Rosen and Barkin's 5-Minute Emergency Medicine Consult (The 5-Minute Consult Series)

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Author: Jeffrey J. Schaider | Stephen R. Hayden | Richard E. Wolfe | Roger M. Barkin | Peter Rosen

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Edito rs

Editors

Jeffrey Schaider MD Associate Professor of Em ergency Medicine Rush Medical College; Chairm an, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Stephen R. Hayden MD Professor of Clinical Medicine, Program Director, Residency Program Departm ent of Em ergency Medicine, University of California San Diego; Editor-in-Chief, Journal of Em ergency Medicine, Medical Center, San Diego, California Richard Wolfe MD Associate Professor Division of Em ergency Medicine, Harvard Medical School; Chief of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Roger M. Barkin MD Professor of Surgery Division of Em ergency Medicine, University of Colorado Health Science Center; Vice President for Pediatric and Newborn Program s and Vice President of Medical Services, Healthone, Denver, Colorado Peter Rosen MD Associate Professor Harvard University; Attending Physician, Beth Israel Deaconess Hospital, Boston, Massachusetts; Attending Physician, St. John's Hospital, Jackson Hole, Wyom ing; Visiting Professor, University of Arizona, Tucson, Arizona

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Secondary Editors Frances R. DeStefano Acquisitions Editor Nicole Demoski Managing Editor David Murphy Project Manager Benjamin Rivera Senior Manufacturing Manager Angela Panetta Marketing Manager Teresa Mallon Design Coordinator TechBooks Production Service Courier Westford Printer

Contributors Barrett Adams M.D. Physician Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona James Adams M.D. Professor and Chair Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Mitchell Adelstein M.D. Assistant Professor Departm ent of Em ergency Medicine, St. Luke's Hospital, New York, New York

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Steven Aks D.O. Associate Professor Departm ent of Em ergency Medicine, Rush University; Director, The Toxikon Consortium , Section of Toxicology, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Amer Aldeen M.D. Attending Physician Departm ent of Em ergency Medicine, Feinburg School of Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Nadeem Al-Duaij M.D. Clinical Fellow Departm ent of Em ergency Medicine, Harvard Medical School, Harvard Affiliated Em ergency Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Paul Allegretti D.O., F.A.C.O.E.P. Associate Professor and Program Director Departm ent of Em ergency Medicine, Midwestern University/Chicago College of Osteopathic, Medicine, Downers Grove, Illinois; Attending Physician, Departm ent of Em ergency Medicine, Provident Hospital of Cook County, Chicago, Illinois Marilyn Althoff M.D. Faculty Departm ent of Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Philip D. Anderson M.D. Assistant Professor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Paul A. Andrulonis M.D. Assistant Medical Director

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Departm ent of Em ergency Medicine, Mem orial Hospital West, Pem broke Pines, Florida Rebecca Apollon M.D. Clinical Associate Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts, Post-Graduate Year 2, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts L. Kristian Arnold M.D. Chief Medical Officer Arlac Health Services, Lexington, Massachusetts Paul Arnold M.D., B.Sc. Clinical Instructor Departm ent of Surgery, University of Toronto; Staff Physician, Departm ent of Em ergency Medicine, University of Health Network, Toronto, Ontario Andrew A. Aronson M.D. Attending Physician Departm ent of Em ergency Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania Veronique Au M.D. Departm ent of Em ergency Medicine, Alta Bates Sum m it Medical Center, Berkeley, California Elisa Aumont M.D. Departm ent of Em ergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi Brandon H. Backlund M.D. Attending Physician Departm ent of Em ergency Medicine, Wahiawa General Hospital, Wahiawa, Hawaii; Attending Physician, Departm ent of Em ergency Medicine, Castle Medical Center, Kailua, Hawaii John Bailitz M.D.

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Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Assistant Program Director, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Amy Baldwin M.D. Physician Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona Adam Z. Barkin M.D. Instructor Departm ent of Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Roger Barkin M.D., M.P.H., F.A.A.P., F.A.C.E.P. Professor of Surgery Division of Em ergency Medicine, University of Colorado Health Science Center; Vice President for Pediatric and Newborn Program s, and Vice President of Medical Services Healthone, Denver, Colorado Suzanne Z. Barkin M.D. Associate Professor of Radiology (Pediatrics) Departm ent of Radiology, Denver Health Medical Center, Denver, Colorado David Barlas M.D. F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Cornell University College of Medicine, New York, New York; Associate Program Director, Departm ent of Em ergency Medicine, New York Hospital Medical Center of Queens, Flushing, New York Eric Barton M.D. Associate Professor of Surgery (EM), Chief Division of Em ergency Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah

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Kathleen Bassett M.D. Assistant Professor of Pediatrics University of Utah School of Medicine, Salt Lake City, Utah Beverly Bauman M.D. F.A.A.P., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Oregon Health and Sciences University, Portland, Oregon Jamil D. Bayram M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical Center, John H. Stroger Hospital of Cook County, Chicago, Illinois B. J. Beck M.S.N., M.D. Clinical Instructor Departm ent of Psychiatry, Harvard Medical School; Clinical Assistant, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts; Staff Psychiatrist, Departm ent of Psychiatry, Anna Jaques Hospital, Newburyport, Massachusetts Kyan J. Berger M.D., F.A.A.E.M. Em ergency Physician Departm ent of Em ergency Medicine, Beverly Hospital and Addison Gilbert Hospital, Beverly, Massachusetts Matthew R. Berkman M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Herbert G. Bivins M.D. Clinical Professor Departm ent of Em ergency Medicine, University of California at Fresno; Program Director, Departm ent of Em ergency Medicine, University Medical Center, Fresno, California Adam Black M.D. Assistant Director

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Departm ent of Em ergency Medicine, St. Elizabeth's Hospital, Chicago, Illinois Paul Blackburn D.O., F.A.C.O.E.P., F.A.C.E.P. Program Director Departm ent of Em ergency Medicine, Maricopa Medical Center, Phoenix, Arizona Keith S. Boniface M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine; Director, Sonography; Assistant Medical Director, Maritim e Medical Access, The George Washington University, Washington, D.C. Michael J. Bono M.D., Ph.D. Professor, Associate Director Departm ent of Em ergency Medicine and Em ergency, Medicine Residency Program , Eastern Virginia Medical School, Norfolk, Virginia Steven H. Bowman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Program Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Jefferson D. Bracey D.O. Clinical Assistant Professor Departm ent of Surgery, University of Nevada School of Medicine, Las Vegas, Nevada; Assistant Medical Director, Departm ent of Em ergency Medicine, St. Rose Dom inican Hospital, Henderson, Nevada Andrea Bracikowski M.D. Associate Professor Departm ents of Em ergency Medicine and Pediatrics, Vanderbilt University Medical Center; Attending Physician, Departm ent of Pediatric Em ergency Medicine, Vanderbilt Children's Hospital, Nashville, Tennessee Kenneth Bramwell M.D.

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Departm ent of Pediatric Em ergency, Medicine, University of Arizona, Tuscon, Arizona Harminder Brar M.D. Resident Physician Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Lorna M. Breen M.D. Assistant in Clinical Medicine Departm ent of Medicine, Colum bia University College of Physicians and, Surgeons; Assistant Attending Physician, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Allison V. Brewer M.D. Senior Resident Departm ent of Em ergency Medicine, Tufts University School of Medicine; Senior Resident, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Judith C. Brillman M.D. Professor of Em ergency Medicine, Assistant Dean Graduate Medical, Education, University of New Mexico, Albuquerque, New Mexico Calvin A. Brown III M.D. Clinical Instructor Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Boston, Massachusetts David F. M. Brown M.D. Assistant Professor Departm ent of Em ergency Medicine, Harvard Medical School; Vice Chairm an, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Lance Brown M.D., M.P.H.

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Associate Professor of Em ergency Medicine and, Pediatrics Departm ent of Em ergency Medicine, Lom a Linda University; Chief, Division of Pediatric Em ergency Medicine, Departm ent of Em ergency Medicine, Lom a Linda University Medical Center and Children's, Hospital, Lom a Linda, California Brian Browne M.D., F.A.C.E.P. Professor Departm ent of Em ergency Medicine and, Medicine; Acting Chairm an, Director, Em ergency Medical Services, University of Maryland Medical Center, Baltim ore, Maryland Sean Bryant M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Attending Physician, Departm ent of Em ergency Medicine, Section of, Medical Toxicology, John H. Stroger Hospital of Cook County, Chicago, Illinois Gary Bubly M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Em ergency Medicine, Brown University School of Medicine; Associate Director, Departm ent of Em ergency Medicine, The Miriam Hospital, Providence, Rhode Island Ann Buchanan M.D. St. David's Hospital, Austin, Texas Robert G. Buckley M.D., M.P.H., F.A.C.E.P Chairm an Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Colleen J. Buono M.D. Em ergency Medical Services Fellow Departm ent of Em ergency Medicine, University of California, San Diego; Clinical Faculty, Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego,

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California Jeffrey A. Bush M.D. Professor of Clinical Medicine Departm ent of Em ergency Medicine, University of California, San Diego; Em ergency Departm ent Medical Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Colleen Campbell M.D. Associate Professor of Em ergency Medicine Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California Michelle Canham M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Taylor Young Cardall M.D. Em ergency Physician Departm ent of Em ergency Medicine, Scottsdale Healthcare, Scottsdale, Arizona Martin J. Carey M.D. Departm ent of Em ergency Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas Keri L. Carstairs M.D. Attending Physician Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Shaun D. Carstairs M.D. Attending Physician Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Ingrid D. Carter D.O.

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Attending Physician Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Wallace Carter M.D. Associate Professor Departm ent of Em ergency Medicine, Weill Medical College of Cornell University; Residency Director, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Austen Chai M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Michael Chamales M.D. Departm ent of Surgery, Texas Tech University Health Sciences Center, Lubbock, Texas Jennifer Chan M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Harvard Affiliated Em ergency Medicine Residency, Boston, Massachusetts Theodore C. Chan M.D. Associate Professor of Medicine Departm ent of Medicine; Medical Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Andrew Chang M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Montefiore Medical Center, Bronx, New York Robert S. Chang M.D. Attending Physician Departm ent of Em ergency Medicine, South Shore Hospital, South Weym outh, Massachusetts

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Anna Cheh M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Hospital, Boston, Massachusetts David Cherkas M.D. Instructor Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine, New York, New York Michele Chetham M.D. Physician Departm ent of Pediatric Medicine, Carepoint, Swedish Medical Center, Denver, Colorado Gordon Chew M.D. Senior Physician Departm ent of Em ergency Medicine, Kaiser Vallejo Medical Center, Vallejo, California Hong K. Choi M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Residency Site Director, Departm ent of Em ergency Medicine, Montefiore Medical Center, Bronx, New York Yi-Mei Chng M.D., M.P.H. Clinical Fellow Departm ent of Em ergency Medicine, Harvard Medical School; Resident, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Teriggi J. Ciccone M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Gregory Ciottone M.D. Director International Section, Departm ent of Em ergency Medicine, Harvard Medical School; Director, Division of Disaster Medicine, Departm ent

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of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Brian Clyne M.D. Assistant Professor Departm ent of Em ergency Medicine, Brown Medical School; Residency Program Director, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Stewart Coffman M.D., F.A.C.E.P. Clinical Assistant Professor Departm ent of Em ergency Medicine, Southwestern University of Texas, Dallas, Texas; Chairm an, Departm ent of Em ergency Medicine, Medical Center of Lewisville, Lewisville, Texas James Colletti M.D. Associate Residency Director Departm ent of Em ergency Medicine, Regions Hospital, St. Paul, Minnesota Christopher B. Colwell M.D., F.A.C.E.P. Associate Professor Departm ent of Surgery, University of Colorado Health Sciences, Center; Associate Director, Departm ent of Em ergency Medicine, Denver Health Medical Center, Denver, Colorado Jim Comes M.D. Associate Professor Departm ent of Em ergency Medicine, University of California-Fresno Medical Education, Program ; Associate Residency Director, Departm ent of Em ergency Medicine, University Medical Center, Fresno, California Matthew D. Cook M.D. Marco Coppola D.O., F.A.C.E.P. Professor Departm ent of Em ergency Medicine, Texas A & M University Health Science System College, of Medicine, College Station, Texas; Medical

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Director, Departm ent of Em ergency Medicine, Las Colinas Medical Center and Questcare Partners, Irving, Texas Kelly Corrigan M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Brian N. Corwell M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Francis L. Counselman M.D. Professor and Chairm an Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Linda C. Cowell M.D. Newton Wellesley Hospital, Norfolk, Massachusetts Richard A. Craven M.D., F.A.C.O.E.M. Associate Professor Departm ent of Fam ily Medicine, Eastern Virginia Medical School, Norfolk, Virginia Kirk Cumpston D.O. Assistant Professor Departm ent of Em ergency Medicine; Assistant Medical Director, Virginia Com m onwealth University, Virginia Poison Center, Richm ond, Virginia Liesl A. Curtis M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Georgetown University Hospital, Washington, D.C. Seric Cusick M.D. Chief Resident Harvard Affiliated Em ergency Medicine; Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Fellow, Division of Em ergency Ultrasound; Clinical

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Instructor, Departm ent of Em ergency Medicine, University of California Irvine Medical Center, Irvine, California Rita Cydulka M.D., M.S. Associate Professor Departm ent of Em ergency Medicine, Case Western Reserve University School of, Medicine; Vice Chair, Departm ent of Em ergency Medicine, MetroHealth Medical Center, Cleveland, Ohio Daniel Davis M.D. Associate Clinical Professor of Medicine Departm ent of Em ergency Medicine; Faculty Physician, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Joanne Davis M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jennifer E. De la Pena M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Peter DeBlieux M.D. Professor of Clinical Medicine Departm ent of Em ergency Medicine, LSUHSC New Orleans; Director of Resident and Faculty Developm ent, Departm ent of Em ergency Medicine, MCLNO Charity Hospital, New Orleans, Louisiana David Della-Giustina M.D., F.A.C.E.P. Departm ent of Military and Em ergency Medicine, Uniform ed Services University of the Health Sciences, Bethesda, Maryland; Chairm an, Departm ent of Em ergency Medicine, Madigan Arm y Medical Center, Tacom a, Washington Paul H. Desan M.D., Ph.D. Assistant Professor Departm ent of Psychiatry, Yale University School of Medicine;

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Director, Psychiatric Consultation Service, Yale New Haven Hospital, New Haven, Connecticutt Paul L. DeSandre D.O. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine, Bronx, New York; Associate Residency Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, New York, New York Diane Devita M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of Washington; Staff Physician, Departm ent of Em ergency Medicine, Madigan Arm y Medical Centerâ€”Fort Lewis, Fort Lewis, Washington Michael K. Doney M.D., M.S., M.P.H. Fellow in International Em ergency Medicine, Adjunct Instructor Departm ent of Em ergency Medicine, The George Washington University, Washington, D.C. Danielle J. Douglas M.D., Ph.D. Associate Professor Departm ent of Surgery, Colum bia University; Chief, Departm ent of Surgery, New York Hospitalâ€”Cornell Medical Center, New York, New York Susan Dufel M.D. Associate Professor Traum atology and Em ergency Medicine, University of Connecticut, Farm ington, Connecticut; Residency Director, Hartford Hospital, Hartford, Connecticut Jonathan A. Edlow M.D. Associate Professor Departm ent of Medicine, Harvard Medical School; Vice Chairm an, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts

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Arunachalam Einstein M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Norbert Elsner M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Associate Director, Departm ent of Em ergency Medicine, Jacobi Medical Center, Bronx, New York Janet Eng D.O., F.A.C.E.P., F.A.C.O.E.P. Medical Toxicologist, Assistant Program Director Massachusetts State University Em ergency Medicine; Residency, Ingham Regional Medical, Lansing, Michigan Stephen K. Epstein M.D., M.P.P. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Timothy Erickson M.D., F.A.C.E.P., F.A.C.M.T., F.A.A.C.T. Professor Departm ent of Em ergency Medicine, University of Chicago at Illinois, Chicago, Illinois Eva Escatel M.D. Senior Resident Em ergency Medicine Residency Program at, MetroHealth Clinic Foundation, Case Western University, Cleveland, Ohio Barnet Eskin M.D., Ph.D. Clinical Assistant Professor Departm ent of Surgery, UMDNJ-New Jersey Medical School, Newark, New Jersey; Attending Em ergency Physician, Departm ent of Em ergency Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Brian Euerle M.D.

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Assistant Professor Division of Em ergency Medicine, University of Maryland School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland James Feldman M.D. Associate Professor of Em ergency Medicine Departm ent of Em ergency Medicine, Boston University School of Medicine; Research Director, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Robert Feldman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Donna Felsenstein M.D. Assistant Professor of Medicine Harvard Medical School, Physician, Departm ent of Medicine/Division of Infectious Disease, Massachusetts General Hospital, Boston, Massachusetts Ian Glen Ferguson D.O. Attending Physician/Clinical Faculty Departm ent of Surgery/Division of Em ergency Medicine, Stanford University Medical Center, Palo Alto, California; Attending Physician/Clinical Faculty, Departm ent of Em ergency Medicine, Santa Clara Valley Medical Center, San Jose, California Maggie Ferng M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois David Feldman M.D. Departm ent of Em ergency Medicine, Boston, Massachusetts James Feldman M.D., F.A.C.E.P. Departm ent of Em ergency Medicine, Boston Medical Center, Boston

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University School of Medicine, Boston, Massachusetts Michelle A. Finkel M.D. Attending Physician Departm ent of Em ergency Medicine, Little Com pany of Mary Hospital, Torrance, California Daniel Firestone M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Christopher Fischer M.D. Chief Resident Beth Israel Deaconess Medical Center, Harvard Affiliated Em ergency Medicine; Residency, Boston, Massachusetts Jonathan Fisher M.D., M.P.H. Instructor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Steven F. Fisher M.D. Physician Departm ent of Em ergency Medicine, Abington Mem orial Hospital, Abington, Pennsylvania Megan Fix M.D. Chief Resident Harvard Affiliated Em ergency Medicine; Residency, Massachusetts General Hospital, Brigham and Wom en's Hospital, Boston, Massachusetts Kelly Anne Foley M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Jessica Freedman M.D.

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Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine, New York, New York Franklin D. Friedman M.D., M.S. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Director, Em ergency Clinical Operations, Departm ent of Em ergency Medicine, Tuftsâ€”New England Medical Center, Boston, Massachusetts Steven Furer M.S., F.A.C.E.P. Attending Physician Departm ent of Em ergency Medicine, The Medical Center of Aurora South, Aurora, Colorado Mary Anne Fuchs M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Ara Gabrielian M.D. Delaram Ghadishah M.D. Assistant Professor Departm ent of Em ergency Medicine, University of California Irvine, Irvine, California Adit A. Ginde M.D. Resident Physician Departm ent of Em ergency Medicine, Harvard Medical School; Resident Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Bret Ginther M.D. Assistant Medical Director Departm ent of Em ergency Medicine, Inland Valley Medical Center, Wildom ar, California Daren Girard M.D. Associate Director Departm ent of Em ergency Medicine, Landm ark Medical Center,

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Woonsocket, Rhode Island Robyn Heister Girard M.D. Kaiser Perm anente South, San Francisco, California Eric Glasser M.D. Clinical Instructor Departm ent of Em ergency Medicine, Georgetown University Hospital, Washington, D.C. Judd L. Glasser M.D. Clinical Instructor Departm ent of Em ergency Medicine, University of California, San Diego; Attending Staff, Director of Pre-Hospital Care, Departm ent of Em ergency Medicine, Tri-City Medical Center, Oceanside, California Laura B. Glicksman M.S., D.M.D. Orthodontist, (Private Practice) Laura B. Glicksm an, M.S., D.M.D., P.C., Needham , Massachusetts Donald C. Goff M.D. Harvard Medical School, Psychotic, Disorders Program , Massachusetts General Hospital, Boston, Massachusetts Jessica R. Goldstein M.D. Senior Instructor Departm ent of Em ergency Medicine, MetroHealth Hospital, Cleveland, Ohio Dolores Gonthier M.D. Consultant MD2 Healthcare Consulting, Inc., Wexford, Pennsylvania J. Scott Goudie M.D. Chief Resident Harvard Affiliated Em ergency Medicine Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Matthew N. Graber M.D., Ph.D. Assistant Professor

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Departm ent of Em ergency Medicine and Departm ent, of Biochem istry, Em ory University School of Medicine, Atlanta, Georgia Charles S. Graffeo M.D. Clinical Professor of Em ergency Medicine, Assistant Program Director Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Ruth Granlund M.D. Physician Departm ent of Em ergency Medicine, Feather River Hospital, Paradise, California Henry J. Grazioso M.D., F.A.A.E.M. Clinical Assistant Professor Departm ent of Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts; Attending Physician, Department of Em ergency Services, Brockton Hospital, Brockton, Massachusetts Ian Greenwald M.D. Assistant Professor Departm ent of Em ergency Medicine, Em ory University, Atlanta, Georgia Shamai A. Grossman M.D., M.S. Assistant Professor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Ian R. Grover M.D. Assistant Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Kama Guluma M.D. Assistant Clinical Professor Departm ent of Em ergency Medicine/Medicine, University of California San Diego, San Diego, California

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Atul Gupta D.O., F.A.A.E.M. Departm ent of Em ergency Medicine, Long Beach Mem orial Medical Center, Miller Children's Hospital, Long Beach, California David A. Guss M.D. Professor Departm ent of Em ergency Medicine, University of California, San Diego; Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Robert S. Hamilton M.D., F.A.A.E.M. Volunteer Clinical Faculty University of California, Davis; Medical Director, Em ergency Services, Merry Medical Center, Redding, Redding, California David Harter M.D. Assistant Residency Director Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Stephen R. Hayden M.D. Professor of Clinical Medicine, Program Director Departm ent of Em ergency Medicine Residency, University of California, San Diego; Editor-in-Chief, Journal of Em ergency Medicine, San Diego, California Robin R. Hemphill M.D., M.P.H. Associate Professor Departm ent of Em ergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Sean O. Henderson M.D. Associate Professor Departm ent of Em ergency Medicine, Keck School of Medicine, University of Southern, California; Vice Chair, Departm ent of Em ergency Medicine, Lactuse Medical Center, Los Angeles, California Gregory W. Hendey M.D., F.A.C.E.P. Associate Professor of Clinical Medicine

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Departm ent of Medicine, University of California, San Francisco, San Francisco, California; Research Director, Departm ent of Em ergency Medicine, University of California, San Francisco, Fresno University Medical Center, Fresno, California David B. Herzog M.D. Professor of Psychiatry (Pediatrics) Departm ent of Psychiatry, Harvard Medical School; Director, Eating Disorders Unit; Child Psychiatry, Services at Massachusetts General Hospital, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Ra'ed A. Hijazi M.D., M.H.A., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, King Saud University of Health Sciences; Deputy Chairm an, Em ergency Departm ent; Division Head, Traum a and Critical Care Director, of Disaster Medicine; Medical Director, Em ergency Medical Services, King Abdulaziz Medical City, National Guard, Riyadh, Saudi Arabia Scot Hill M.D. Assistant Professor Departm ent of Em ergency Medicine, The Mount Sinai School of Medicine; Associate Director, Departm ent of Em ergency Medicine, The Mount Sinai Medical Center, New York, New York Doodnauth Hiraman M.D. Assistant Professor of Medicine Weill Medical College of Cornell University, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Forrest Holden M.D. Em ergency Residency Program Maricopa Medical Center, Phoenix, Arizona Patrick Cline Holland M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Medicine, University of Washington, Medical

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Student/Intern Coordinator, Madigan Arm y Medical Center, Tacom a, Washington Danielle A. Hoover D.O., M.S. Resident Physician Departm ent of Em ergency Medicine, Case Western Reserve University; Resident Physician, Departm ent of Em ergency Medicine, MetroHealth Medical Center/Cleveland Clinic, Foundation/CWRU, Cleveland, Ohio Jeffrey Horton M.D. Physician Departm ent of Em ergency Medicine, Mem orial Hospital, Martinsville, Virginia Mark A. Hostetler M.D., M.P.H Chief Em ergency Medicine, Departm ent of Pediatrics, The University of Chicago School of Medicine; Medical Director, Departm ent of Pediatric Em ergency, The University of Chicago, Com er Children's Hospital, Chicago, Illinois Renee Hsia M.D., M.Sc. Resident Departm ent of Surgery, Division of Em ergency, Medicine, Stanford/Kaiser Em ergency Medicine Residency, Stanford, California Carl K. Hsu M.D. Weill Medical College of Cornell University, New York, New York, Departm ent of Em ergency Medicine, The Brooklyn Hospital Center, Brooklyn, New York J. C. Huffman M.D. Psychiatric Consultation Service, Departm ent of Psychiatry, Massachusetts General Hospital, McLean Hospital and Harvard Medical School, Boston, Massachusetts Timothy Hurtado D.O. Departm ent of Em ergency Medicine, Madiganâ€”University of

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Washington, Tacom a, Washington Anwer Hussain D.O., F.A.A.E.M., F.A.C.O.E.P. Clinical Instructor Departm ent of Em ergency Medicine, Midwestern University, Downers Grove, Illinois; Attending Physician, Departm ent of Em ergency Medicine, Provident Hospital of Cook County, Chicago, Illinois Alec Tuan Huynh M.D. Resident PGY-4 Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California Anthony Huynh M.D. Em ergency Physician Departm ent of Em ergency Medicine, San Clem ente Regional Medical Center, San Clem ente, California James Hwang M.D. Em ergency Ultrasound Fellow Section of Em ergency Medicine/Departm ent of Surgery, Yale University School of Medicine, New Haven, Connecticut Wender Hwang M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jason Imperato M.D., Ph.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School, Boston, Massachusetts; Staff Physician, Departm ent of Em ergency Medicine, Mount Auburn Hospital, Cam bridge, Massachusetts Paul Ishimine M.D. Hagop Isnar M.D. Associate Director Departm ent of Em ergency Medicine, Auburn Mem orial Hospital, Auburn, New York Kenneth Jackimczyk M.D.

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Attending Physician Departm ent of Em ergency Medicine, Maricopa Medical Center, Phoenix, Arizona Safia C. Jackson B.S. Research Assistant Departm ent of Psychiatry, Massachesetts General Hospital, Boston, Massachusetts Irving Jacoby M.D., F.A.C.E.P., F.A.C.P. Professor of Medicine Departm ent of Medicine, University of California, San Diego School of Medicine, La Jolla, California; Attending Physician, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Liudvikas Jagminas M.D., F.A.C.E.P. Assistant Physician Departm ent of Em ergency Medicine, Brown Medical School, Providence, Rhode Island; Physician in Chief, Departm ent of Em ergency Medicine, Mem orial Hospital of Rhode Island, Pawtucket, Rhode Island Thea James M.D. Departm ent of Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts Gregory D. Jay M.D., Ph.D. Associate Professor of Medicine and Em ergency, Medicine, Associate Professor of Engineering Departm ent of Em ergency Medicine, Brown Medical School; Research Director, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island David Jerrard M.D. Associate Professor Departm ent of Em ergency Medicine, University of Maryland, Baltim ore, Maryland

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Albert Jin M.D. Staff Physician Departm ent of Em ergency Medicine, Irvine Regional Hospital and Medical Center, Irvine, California Gary Johnson M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, SUNY Upstate Medical University, Syracuse, New York Jennifer S. Johnson M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Beth Anne Joseph M.D. Assistant Professor University of Connecticut School of Medicine, Departm ent of Em ergency Medicine and Traum atology, Manchester Mem orial Hospital, Manchester, Connecticut Madeline M. Joseph M.D. Associate Professor Departm ent of Em ergency Medicine, University of Florida Health Science Center, Jacksonville; Chief, Departm ent of Pediatric Em ergency Medicine, Shands Hospital, Jacksonville, Florida Pascal Juang M.D. Em ergency Care Unit, Hoag Hospital, Newport Beach, California Joseph H. Kahn M.D., F.A.C.E.P. Associate Clinical Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Director, Medical Student Education, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Christopher S. Kang M.D. Madigan Arm y Medical Center, Tacom a, Washington Tarina Lee Kang M.D.

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Harvard Affiliated Em ergency Medicine Residency, Senior Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts A. Antoine Kazzi M.D., F.A.A.E.M. Chief of Service Em ergency Medicine; Medical Director, The Em ergency Unit, The Am erican University of Beirut, Beirut, Lebanon Ziad N. Kazzi M.D., F.A.A.E.M. Assistant Professor Departm ent of Em ergency Medicine, University of Alabam a, Birm ingham , Birm ingham , Alabam a Samuel Keim M.D. Residency Director Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona Sean P. Kelly M.D. Instructor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Medical Student Clerkship Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Mamata Kene M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego; Resident Physician, Departm ent of Em ergency Medicine, University of California San Diego Medical Center, San Diego, California Elicia Sinor Kennedy M.D., F.A.C.E.P Assistant Professor Clinical Faculty Departm ent of Em ergency Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas Kevin Kern D.O. Attending Physician

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Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois James P. Killeen M.D. Assistant Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego; Clinical Faculty, Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego, California Grace Kim M.D. Assistant Professor Departm ent of Em ergency Medicine, Lom a Linda University; Attending Physician, Departm ent of Em ergency Medicine, Division of Pediatric Em ergency Medicine, Lom a Linda University, Lom a Linda, California Tamaki Kimbro M.D. Departm ent of Em ergency Medicine, Mendocino Coast District Hospital, Fort Bragg, California Jeffrey King M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Em ergency Medicine, Wayne State University; Interim Chief, Departm ent of Em ergency Medicine, Harper University Hospital, Detroit, Michigan Matthew Kippenhan M.D. Clinical Instructor Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine; Staff Physician, Department of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Barry J. Knapp II M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia School of Medicine, Norfolk, Virginia

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Leo Kobayashi M.S Assistant Professor Departm ent of Em ergency Medicine, Brown Medical School; Attending Physician, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Paul Kolecki M.D., F.A.C.E.P. Assistant Professor; Director of Undergraduate Em ergency Medicine Departm ent of Em ergency Medicine, Thom as Jefferson University, Jefferson Medical College, Philadelphia, Pennsylvania Jennifer L. Kolodchak M.D. Clinical Instructor Departm ent of Em ergency Medicine, Rush University Medical School; Attending Physician, Departm ent of Em ergency Medicine, Rush University Medical Center, Chicago, Illinois Amy V. Kontrick M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine, Chicago, Illinois Richard S. Krause M.D. Residency Program Director Departm ent of Em ergency Medicine, University of Buffalo School of Medicine and, Biom edical Sciences, Buffalo, New York Joel Kravitz M.D., F.A.C.E.P., F.R.C.P.S.C. Assistant Professor Departm ent of Em ergency Medicine, Thom as Jefferson University; Assistant Residency Director, Departm ent of Em ergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Lara Kulchycki M.D. Attending Physician Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Alan M. Kumar M.D., F.A.C.E.P.

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Clinical Instructor Departm ent of Medicine, University of Chicago; Attending Physician, Departm ent of Em ergency Medicine, Lutheran General Hospital, Park Ridge, Illinois Dick Kuo M.D. Assistant Professor Departm ent of Surgery, Division of Em ergency, Medicine, University of Maryland School of Medicine; Medical Director, Departm ent of Adult Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland Gregory W. Lampe M.D. Em ergency Physician Departm ent of Em ergency Medicine, Mission Hospital Regional Medical Center, Mission Viejo, California Owen Lander M.D. Assistant Professor Departm ent of Em ergency Medicine, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia Mark Langdorf M.D., M.H.P.E. Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Emi Latham M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Minh V. Le M.D. Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego, California James M. Leaming M.D. Assistant Professor Departm ent of Em ergency Medicine, Tufts School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tuftsâ€”New England Medical Center, Boston, Massachusetts

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Jason M. Lebwohl M.D. Conrow Regional Medical Center, Conrow, Texas JiWon E. Lee M.D. Resident Physician Departm ent of Em ergency Medicine, Rush Medical College; Resident Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Moses S. Lee M.D., F.A.C.E.P., F.A.A.E.M. Assistant Clinical Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Tomas C. Lee Em ergency Physician, Active Staff Physician Departm ent of Em ergency Medicine, Sierra Nevada Mem orial Hospital, Sierra, Nevada Eric Legome M.D. Assistant Professor Departm ent of Em ergency Medicine, New York University School of Medicine, Bellevue Hospital Center; Director/Bellevue Em ergency Medicine Residency, Departm ent of Em ergency Medicine, New York University Hospital/Bellevue Hospital Center, New York, New York Steven Lelyveld M.D., F.A.A.P., F.A.C.E.P. Associate Professor Departm ents of Pediatrics and Medicine, University of Chicago Pritzker School of Medicine; Attending Physician, Departm ents of Pediatric Em ergency Medicine, and Medicine, University of Chicago Corner Children's Hospital, Chicago, Illinois Amy LePage M.D. Chief Resident Departm ent of Em ergency Medicine, Mayo Clinic, Rochester, Minnesota

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Roneet Lev M.D., F.A.C.E.P. Voluntary Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego; Director of Operations, Departm ent of Em ergency Medicine, Scripps Mercy Hospital, San Diego, California Hope W. Levin M.D. Child and Adolescent Psychiatry Fellow Departm ent of Psychiatry, Harvard Medical School; Child and Adolescent Psychiatry Fellow, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts David Levine M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Medical Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Saul Levine M.D. Assistant Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Trevor Lewis M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Director, Observation Em ergency Medicine, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Lazaro Lezcano M.D., F.A.A.P Clinical Assistant Professor of Pediatrics Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Director of Neonatology, Departm ent of Pediatrics/Division of Neonatology, St. Barnabas Hospital, Bronx, New York Richard Lichenstein M.D. Associate Professor

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Departm ent of Pediatrics, University of Maryland School of Medicine; Director, Pediatric Em ergency Medicine, Departm ent of Pediatrics, University of Maryland Hospital for Children, Baltim ore, Maryland Jason Liebzeit M.D. Chief Resident Departm ent of Em ergency Medicine, Northwestern University, McGaw Medical, Center, Chicago, Illinois Alexander T. Limkakeng Jr. M.D. Assistant Professor Departm ent of Em ergency Medicine, Thom as Jefferson University, Jefferson, Medical College; Attending Physician, Department of Em ergency Medicine, Thom as Jefferson University Hospital, Philadelphia, Pennsylvania David A. Listman M.D. Departm ent of Pediatric Em ergency, Medicine, St. Barnabas Hospital, Bronx, New York Shan Liu M.D., M.P.H. Instructor Departm ent of Surgery, Harvard Medical School; Faculty, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Angela Loh M.D. Assistant Chief Departm ent of Em ergency Medicine, Kaiser Perm anente San Jose, San Jose, California Frank LoVecchio M.D. Banner Health, Phoenix, Arizona Lisa Lowe M.D., M.P.H. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Jenny Lu M.D., M.S.

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Resident Physician Departm ent of Em ergency Medicine, University of Illinois at Chicago; Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Boris Lubavin M.D. Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Jon Ludwig M.D. Pacific Em ergency Providers Scripps Mercy Hospital Em ergency, Departm ent, San Diego, California Binh T. Ly M.D. Associate Clinical Professor of Medicine Departm ent of Surgery, University of California, San Diego; Director, Medical Toxicology Fellowship; Associate Director, Em ergency Medicine; Residency, Division of Medical Toxicology, San Diego, California Elizabeth L. Lynch M.D. Assistant Professor Departm ent of Em ergency Medicine, Lom a Linda University Medical Center; Assistant Medical Director, Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Gene Ma M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Medicine, University of California, San Diego, San Diego, California; Quality Assurance Chairm an, Departm ent of Em ergency Medicine, Tri-City Medical Center, Oceanside, California John MacKay Jr. M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas Tech University; Attending Physician, Departm ent of Em ergency Medicine, Thom ason Hospital, El

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Paso, Texas Laura Macnow M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Timothy J. Mader M.D. Associate Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Director of Em ergency, Medicine, Departm ent of Em ergency Medicine, Research, Baystate Medical Center, Springfield, Massachusetts John Mahoney M.D. Associate Professor Departm ent of Em ergency Medicine, University of Pittsburgh School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, UPMC Presbyterian, Pittsburgh, Pennsylvania Mamta Malik M.D. Departm ent of Em ergency Medicine, Rush Medical Center, Chicago, Illinois Gerald Maloney Jr. D.O. Clinical Instructor Departm ent of Em ergency Medicine, Rush Medical College, Medical Toxicology Fellow, Toxikon Consortium , Chicago, Illinois Mark Mandell M.D. Chairm an Departm ent of Em ergency Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Alex Manini M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Julie Marmon M.D.

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Jeffrey Manko M.D. Departm ent of Em ergency Medicine, New York University/Bellevue Medical Center, New York, New York Robert Marsan Jr. M.D., B.S. University of Pennsylvania, Philadelphia, Pennsylvania Kevin J.L. Martens M.D. Resident Physician Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jon D. Mason M.D. Associate Professor Departm ents of Em ergency Medicine and Pediatrics, Eastern Virginia Medical School; Attending Physician, Departm ent of Em ergency Medicine, Sentara Norfolk General Hospital, Norfolk, Virginia Laura Matzkin M.D. Senior Resident Tufts University School of Medicine, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Madeline Matar Joseph M.D. Associate Professor, Director, Pediatric Em ergency Medicine Fellowship Program , Chief Division of Pediatric Em ergency Medicine, University of Florida College of Medicine, Jacksonville, Florida Amal Mattu M.D. Associate Professor and Program Director Departm ent of Em ergency Medicine, University of Maryland School of Medicine, Baltim ore, Maryland Suzan Mazor M.D. Assistant Professor Departm ents of Em ergency Medicine and Pediatrics, Children's Hospital and Regional Medical Center, Sand Point Way, Nebraska Christopher M. McCarthy II M.D.

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Resident Departm ent of Em ergency Medicine, Harvard University, Beth Israel Deaconess Medical Center, Boston, Massachusetts Robert F. McCormack M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Daniel C. McGillicuddy M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Murray J. McLachlan M.D. Michelle S. McMahon-Downer M.D. Instructor in Pediatrics Division of Pediatric Em ergency Medicine, Departm ent of Pediatrics, Boston University School of Medicine; Attending Physician, Pediatric Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Anthony J. Medak M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Howard K. Mell M.D., M.P.H. Resident Departm ent of Em ergency Medicine, Mayo School of Graduate, Medical Education; Resident Physician, Departm ent of Em ergency Medicine, Saint Mary's Hospital/Mayo Clinic, Rochester, Minnesota Moss Mendelson M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School; Chief, Departm ent of Em ergency Medicine, Sentara Hospitals, Norfolk, Norfolk, Virginia

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Fernando G. Mendoza M.D. Instructor in Pediatrics Division of Pediatric Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts Nathan Mick M. D. Medical Director Departm ent of Pediatric Em ergency Medicine, Maine Medical Center, Portland, Maine Scott A. Miller M.D. Clinical Instructor Departm ent of Em ergency Medicine, Rush University Medical Center, Chicago, Illinois Shayle Miller Ph.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Voluntary Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Trevor J. Mills M.D. Program Director Louisiana State University Em ergency Medicine; Residency, Associate Clinical Professor, Louisiana State University Health Science Center, New Orleans, Louisiana Leslie Milne M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Sports Medicine Departm ent, Children's Hospital, Boston, Massachusetts Andrew Milstein M.D., M.S., F.A.C.E.P. Clinical Assistant Professor Departm ent of Surgery, Division of, Em ergency Medicine, University of Maryland, Baltim ore, Maryland; Attending Physician, Departm ent of Em ergency Medicine, Baltim ore Washington Medical Center, Glen Burnie, Maryland

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Elizabeth L. Mitchell M.D. Assistant Professor Departm ent of Em ergency Medicine, Boston University, Boston, Massachusetts Christy Rosa Mohler M.D., F.A.C.E.P., F.A.A.E.M. Em ergency Physician Departm ent of Em ergency Medicine, Scripps Mercy Hospital Chula Vista, Chula Vista, California Robert C. Montana M.D. Providence Everett Medical Center, Everett, Washington Maria Moreira M.D. Associate Program Director The Denver Health Medical Center Residency in, Em ergency Medicine; Clinical Instructor, Departm ent of Surgery, Division of Em ergency Medicine, The University of Colorado Health Sciences Center, Denver, Colorado John W. Morehouse M.D. Jordan Moskoff M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical College; Assistant Director, Adult Em ergency Services, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Matthew B. Mostofi D.O. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts Linda Mueller M.D. Departm ent of Em ergency Medicine, Munster Com m unity Hospital, Munster, Indiana David W. Munter M.D., M.B.A.

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Assistant Clinical Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School; Director and Chair, Departm ent of Em ergency Medicine, DePaul Medical Center, Norfolk, Virginia Michael S. Murphy M.D. Medical Director for Pre-Hospital Care Departm ent of Em ergency Medicine, South Shore Hospital, South Weym outh, Massachusetts Scott B. Murray M.D. Clinical Fellow in Medicine Departm ent of Medicine, Harvard Medical School; Chief Resident, Harvard Affiliated Em ergency Medicine, Beth Israel Deaconess Medical Residency Center, Boston, Massachusetts Veronique Murray M.D. Mark B. Mycyk M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University; Attending Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Eric S. Nadel M.D. Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Boston, Massachusetts Kathleen Nasci M.D. Medical Director Departm ent of Em ergency Medicine, Pennsylvania Hospital, Philadelphia, Pennsylvania Isam Nasr M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Larry A. Nathanson M.D.

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Instructor of Medicine Departm ent of Medicine, Harvard Medical School; Director of Em ergency Medicine Inform atics, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Sean-Xavier Neath M.D., Ph.D. Assistant Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California James Nelson M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Edward Newton M.D. Professor Departm ent of Em ergency Medicine, Keck School of Medicine, University of Southern, California; Chairm an, Departm ent of Em ergency Medicine, Los Angeles California and University of Southern, California Medical Center, Los Angeles, California Ann P. Nguyen M.D. Assistant Professor Departm ent of Em ergency Medicine, New York University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Bellevue Hospital Center and, New York Medical Center, New York, New York Michael W. Nielson M.D. Sean Patrick Nordt M.D. University of California, San Diego, San Diego, California Yasuharu Okuda M.D. Assistant Professor Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine; Associate Residency Director, Departm ent of Em ergency Medicine,

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The Mt. Sinai Hospital, New York, New York Jonathan S. Olshaker M.D. Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Chief, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Jennifer Oman M.D. Associate Clinical Professor of, Em ergency Medicine Departm ent of Em ergency Medicine, University of California Irvine School of, Medicine, Orange, California David Palafox M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas Tech University Health Science Center; Faculty, Departm ent of Em ergency Medicine, Urgent Care Center, Thom ason General Hospital, El Paso, Texas Peter Pang M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University Feinberg, School of Medicine; Staff Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Jennifer M. Park M.D. Instructor of Psychiatry Harvard University; Director, Acute Psychiatry Service, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Lawrence T. Park M.D. Instructor Departm ent of Psychiatry, Harvard Medical School; Director, Inpatient Psychiatry, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Peter J. Park M.D. Attending Physician

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Departm ent of Em ergency Medicine, Naval Medical Center San Diego, San Diego, California Robert A. Partridge M.D., M.P.H., D.T.M., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Brown Medical School; Attending Physician, Departm ent of Em ergency Medicine/Sam uels 2, Rhode Island Hospital, Providence, Rhode Island Raj J. Patel M.D. Assistant Professor Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California; Staff Physician, Departm ent of Em ergency Medicine, Palom ar Medical Center, Escondido, California Rahul Patwari M.D. Attending Physician Departm ent of Em ergency Medicine, Rush University Hospital, Chicago, Illinois Timothy Pavek M.D. St. Vincent Hospital Medical Center, Green Bay, Wisconsin David A. Peak M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Staff Physcian, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts John Pease M.D. Staff Physician Departm ent of Em ergency Medicine, Tripler Arm y Medical Center, Honolulu, Hawaii Bradley F. Peckler M.D. Associate Professor Internal Medicine, Division of Em ergency Medicine, University of South Florida; Attending Physician, Departm ent of Em ergency Medicine, Tam pa General Hospital, Tam pa, Florida

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David A. Perlstein M.D. Clinical Instructor Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Associate Medical Director, Director of Am bulatory Pediatrics, Departm ent of Pediatrics, St. Barnabas Hospital, Bronx, New York Aaron Pessl M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Kelly Pettit M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Benjamin Z. Philips M.D. Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Charles V. Pollack Jr. M.A., M.D., F.A.C.E.P. Professor Departm ent of Em ergency Medicine, University of Pennsylvania School of Medicine; Chairm an, Departm ent of Em ergency Medicine, Pennsylvania Hospital, Philadelphia, Pennsylvania Janet M. Poponick M.D. Assistant Professor Departm ent of Em ergency Medicine, Cast Western Reserve University, MetroHealth Medical Center, Cleveland, Ohio William Porcaro M.D. EMS/Disaster Medicine Fellow Departm ent of Em ergency Medicine, University of Massachusetts Medical School; Attending Physician, Departm ent of Em ergency Medicine, University of Massachesetts Mem orial Healthcare, Worcester, Massachusetts

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Jason J. Prystowsky M.D., M.P.H. Clinical Instructor Departm ent of Em ergency Medicine, Em ory University, Atlanta, Georgia Michelle E. Pyka M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Vittorio Raho M.D. Resident Departm ent of Em ergency Medicine, Harvard Medical School; Resident, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Niels Rathlev M.D. Associate Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Vice Chair, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Wende R. Reenstra M.D., Ph.D. Instructor Departm ent of Medicine, Harvard Medical School; Director Basic Science Research, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Kristine Reid M.D. Departm ent of Em ergency Medicine, York Hospital, York, Maine Ian Reilly M.D. Em ergency Physician Departm ent of Em ergency Medicine, Sharp Mem orial Hospital, San Diego, San Diego, California James W. Rhee M.D. Clinical Instructor Departm ent of Em ergency Medicine, University of Illinois at Chicago, Toxicology Fellow, Toxikon Consortium , Chicago, Illinois

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Christopher Richards M.D. Associate Professor Departm ent of Em ergency Medicine, Oregon Health and Science University, Portland, Oregon Kathy Richardson M.D. Residency Coordinator Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Mark Richmond M.D. Assistant Medical Director Departm ent of Em ergency Medicine, Santa Barbara Cottage Hospital, Santa Barbara, California Steven Riley M.D. Assistant Professor Departm ents of Em ergency Medicine and, Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee Jaime B. Rivas M.D. Physician Departm ent of Em ergency Medicine, Palom ar and Pom erado Hospitals, Escondido, California Matthew Robinson M.D. Clinical Instructor Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Colleen N. Roche M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine, The George Washington University, Washington, D.C. Jedd E. Roe M.D., M.B.A. M.S.F. Residency Director, Associate Professor Departm ent of Em ergency Medicine, University of Alabam a at Birm ingham , Birm ingham , Alabam a

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Joshua Roffman M.D. Carlo L. Rosen M.D. Assistant Professor Departm ent of Medicine, Harvard Medical School; Program Director, Harvard Affiliated Em ergency Medicine Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Peter Rosen M.D. Associate Professor, Attending Physician Beth Israel Deaconess Hospital, Boston, Massachusetts; Attending Physician, St. John's Hospital, Jackson Hole, Wyom ing, Visiting Professor, University of Arizona, Tucson, Arizona Lawrence S. Rosenthal M.D., Ph.D. Associate Professor Departm ent of Cardiology; Director, Section Cardiac Pacing and Electrophysiology, University of Massachusetts Mem orial Medical Center, Worchester, Massachusetts Christopher Ross M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Assistant Program Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Todd C. Rothenhaus M.D. Departm ent of Em ergency Medicine, Boston University Medical Center, Boston, Massachusetts David H. Rubin M.D. Professor of Clinical Pediatrics Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Chairm an and Program Director, Departm ent of Pediatrics, St. Barnabas Hospital, Bronx, New York Scott Rudkin M.D., M.B.A., R.D.M.S. Assistant Clinical Professor

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Departm ent of Em ergency Medicine, University of California, Irvine; Vice Chief of Em ergency Medicine, Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Nate Rudman M.D. Em ergency Physician Departm ent of Em ergency Medicine, Cape Cod Hospital, Hyannis, Massachusetts Gary S. Sachs M.D. Associate Professor of Psychiatry Departm ent of Psychiatry, Massachusetts General Hospital; Director of Bipolar Clinic and, Research Program , Harvard Medical School, Boston, Massachusetts Mark Sagarin M.D. Mt. Auburn Hospital, Cam bridge, Massachusetts Erich Salvacion M.D. Hospitalist, Departm ent of Internal Medicine, Kaiser Perm anente, Bellflower, California Leon D. Sanchez M.D., M.P.H. Clinical Instructor Departm ent of Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Arthur Sanders M.D., M.H.A. Professor Departm ent of Em ergency Medicine, University of Arizona College of Medicine; Attending Physician, Departm ent of Em ergency Medicine, University Medical Center, Tucson, Arizona Kathy Sanders M.D. Assistant Professor Departm ent of Psychiatry, Harvard Medical School; Training Director, Departm ent of Psychiatry, Massachusetts General Hospital, Boston,

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Massachusetts Marcelo Sandoval M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine, Bronx, New York; Chair, Com m ittee on Em ergency/Disaster, Managem ent, Beth Israel Medical Center, New York, New York John Santamaria M.D., F.A.A.P., F.A.C.E.P. Affialiate Professor Departm ent of Medicine, USF School of Medicine, Tam pa, Florida Sally Santen M.D. Assistant Professor Departm ent of Em ergency Medicine, Vanderbilt School of Medicine, Nashville, Tennessee Elaine Sapiro M.D., M.P.H. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Daniel L. Savitt M.D. Associate Professor Departm ents of Em ergency Medicine and Internal, Medicine, Brown University; Director, Departm ent of Em ergency Medicine, The Miriam Hospital, Providence, Rhode Island Assaad J. Sayah M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Chairm an, Departm ent of Em ergency Medicine, Caritas Good Sam aritan Medical Center, Boston, Massachusetts Shari Schabowski M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior

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Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Jeffrey Schaider M.D. Associate Professor of Em ergency Medicine Rush Medical College; Chairm an, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Michael Schmidt M.D. Assistant Professor Departm ent of Em ergency Medicine, Feinburg School of Medicine; Assistant Professor, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Jeffrey I. Schneider M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine, Boston University School of Medicine; Attending Physician, Boston Medical Center, Boston, Massachusetts Hugh Schuckman M.D. Clinical Professor Departm ent of Em ergency Medicine, North East Ohio Universities, College of Medicine, Rootstown, Ohio; Attending Physician, Sum m a Health System s, Akron, Ohio Suzanne Schuh M.D., F.R.C.P.(C), F.A.A.P., A.B.P.E.M. Professor of Paediatrics University of Toronto; Staff Paediatrician and Research Director, Division of Paediatric Em ergency Medicine; Senior Associate Scientist, Research Institute, Hospital for Sick Children, Toronto, Canada Theresa Schwab M.D. Departm ent of Em ergency Medicine, Christ Medical Center, Oak Lawn, Illinois Gary Schwartz M.D. Assistant Professor

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Departm ent of Em ergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee James Scott M.D. Dean School of Medicine and Health Sciences, Deans Office SMHS, George Washington University, Washington, D.C. Michelle Sergel M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical Center; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Nathan Shapiro M.D., M.P.H. Assistant Professor Harvard Medical School, Research Director, Beth Israel Deaconess Medical Center, Boston, Massachusetts Ghazala Q. Sharieff M.D., F.A.C.E.P., F.A.A.E.M., F.A.A.P. Assistant Clinical Professor Children's Hospital and Health Center/University of, California, San Diego, California; Director of Pediatric Em ergency Medicine, Palom ar-Pom erado Hospitals/California Em ergency, Physicians, San Diego, California Philip Shayne M.D. Associate Professor and Residency Director Departm ent of Em ergency Medicine, Em ory School of Medicine, Atlanta, Georgia Lorne Sherman M.D. North Shore University Hospital, Manhasset, New York Scott C. Sherman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Assistant Residency Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois

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Chet Shermer M.D. Clinical Assistant Professor Departm ent of Em ergency Medicine, University of Mississippi Medical Center; Staff Physician, Departm ent of Em ergency Medicine, Mississippi Baptist Medical Center, Jackson, Mississippi Patricia Shipley M.D. Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Lee Shockley M.D. Associate Professor Departm ent of Surgery, Division of Em ergency Medicine, University of Colorado; Medical Director, Departm ent of Em ergency Medicine, The Denver Health Medical Center, Denver, Colorado Robert Sidman M.D. Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Christine Tsien Silvers M.D., Ph.D. Research Associate Children's Hospital Inform atics Program , Children's Hospital, Boston, Massachusetts; Attending Physician, Departm ent of Em ergency Medicine, Caritas Good Sam aritan Medical Center, Brockton, Massachusetts Alison K. Sisitsky M.D. Attending Physician Departm ent of Em ergency Medicine, Newton Wellesley Hospital, Newton, Massachusetts Christian M. Sloane M.D. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego, Medical Center, San Diego, California James Smith M.D. Resident Physician Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency

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Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Rebecca Smith-Coggins M.D. Associate Professor Departm ent of Surgery/Em ergency Medicine, Stanford University, Stanford, California Brian K. Snyder M.D. Associate Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Matthew Solley M.D. Chief Resident Departm ent of Em ergency Medicine, University of California Irvine Medical Center, Orange, California Julia Sone M.D. Physician Departm ent of Surgery, INOVA Fairfax Hospital, Falls Church, Virginia Camie J. Sorensen M.D., M.P.H. Physician Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Matthew T. Spencer M.D. Assistant Professor Departm ent of Em ergency Medicine, University of Rochester School of Medicine and, Dentistry, Rochester, New York Linda L. Spillane M.D. Associate Professor Departm ent of Em ergency Medicine, University of Rochester; Residency Program Director, Departm ent of Em ergency Medicine, Strong Mem orial Hospital, Rochester, New York

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Blake Spirko M.D., F.A.C.E.P., F.A.A.P. Fellowship Director Pediatric Em ergency, Medicine, Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Professor, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Timothy Stallard M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas A & M System Health Sciences Center; Program Director, Em ergency Medicine Residency, Scott and White Mem orial Hospital, Tem ple, Texas Dale W. Steele M.D. Associate Professor Departm ents of Em ergency Medicine and, Pediatrics, Brown Medical School; Attending Physician and Fellowship Director, Departm ent of Pediatric Em ergency Medicine, Hasbro Children's Hospital, Providence, Rhode Island James T. Steen M.D. Senior Resident Departm ent of Em ergency Medicine, University of Iowa, Iowa City, Iowa James M. Stephen M.D. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Directorâ€”Medical Inform atics; Associate Directorâ€”Pediatric Traum a Service, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts T. A. Stern M.D. Psychiatric Consultation Service Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Edward Stettner M.D.

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Assistant Professor Departm ent of Em ergency Medicine, Em ory University; Attending Physician, Departm ent of Em ergency Medicine, Grady Mem orial Hospital, Atlanta, Georgia Helen Straus M.D., M.S. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Stacey A. Suecoff M.D. Assistant Professor Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Director, Departm ent of Pediatric Em ergency Medicine, St. Barnabas Hospital, Bronx, New York John Sullivan M.D. Attending Physician and Core Faculty Departm ent of Em ergency Medicine, Jackson Mem orial Hospital, Miam i, Florida Paul A. Szucs M.D. David Tanen M.D. Director Em ergency Medicine Residency Program , Departm ent of Em ergency Medicine, Naval Medical Center San Diego, San Diego, California Guy Tarleton M.D. Departm ent of Em ergency Medicine, St. Francis Medical Center, Santa Barbara, California Elizabeth Temin M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Adjunct Instructor, Departm ent of Em ergency Medicine, Boston University Medical School; Attending Physician, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts

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Kristine Thompson M.D. Clinical Instructor Departm ent of Em ergency Medicine, Mayo Clinic College of Medicine, Jacksonville, Jacksonville, Florida Trevonne M. Thompson M.D. Medical Toxicology Fellow Toxikon Consortium , John H. Stroger Hospital of Cook County, Division of Occupational Medicine; Clinical Instructor, Departm ent of Em ergency Medicine, University of Illinois at Chicago, Chicago, Illinois Carrie Tibbles M.D. Associate Program Director Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency Medicine Residency; Physician, Beth Israel Deaconess Medical Center, Bostson, Massachusetts Mercedes Torres M.D. Senior Resident Surgery, Departm ent of Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland Susan P. Torrey M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Residency Director, Departm ent of Surgery, Baystate Medical Center, Springfield, Massachusetts Shirin Trachiotis M.D. Departm ent of Em ergency Medicine, Sibley Mem orial Hospital, Washington, D.C. Jason Tracy M.D. Instructor in Medicine Harvard Medical School; Assistant Program Director, Beth Israel Deaconess Medical Center, Boston, Massachusetts

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Clyde Turner M.D. Attending Physician Departm ent of Em ergency Medicine, Darnall Arm y Com m unity Hospital, Fort Hood, Texas Edward Ullman M.D. Attending Physician Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Thomas A. Utecht M.D. Associate Professor of Clinical Medicine University of California, San Francisco; Chief Quality Officer, Com m unity Medical Centers, Fresno, California Sami Uwaydat M.D. Resident Physician Harvey & Bernice Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas Federico E. Vaca M.D., M.P.H. Associate Professor Departm ent of Em ergency Medicine, University of California, Irvine School of, Medicine, Orange, California Tyler F. Vadeboncoeur M.D. Senior Associate Consultant Departm ent of Em ergency Medicine, Mayo Clinic College of Medicine, Em ergency Physician, Departm ent of Em ergency Medicine, St. Luke's Hospital, Jacksonville, Florida Carla Valentine M.D. Attending Physician Departm ent of Em ergency Medicine, Santa Barbara College Hospital, Santa Barbara, California Verena Valley M.D. Departm ent of Em ergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi

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Karen B. Van Hosen M.D. Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California James T. Vandenberg M.D., F.A.A.E.M. Adjunct Clinical Associate Professor Departm ent of Em ergency Medicine, University of Iowa, Iowa City, Iowa; Medical Director, Departm ent of Em ergency Medicine, Great River Medical Center, West Burlington, Iowa P. Yannis Venieris M.D. Gary M. Vilke M.D., F.A.C.E.P., F.A.A.E.M. Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Robert Vissers M.D., F.A.C.E.P. Adjunct Associate Professor Oregon Health & Sciences University; Director, Departm ent of Em ergency Medicine, Legacy Em anuel Hospital, Portland, Oregon David A. Vitberg M.D. Clinical Fellow Critical Care Medicine, Critical Care Medicine Departm ent, National Institutes of Health, Bethesda, Maryland James Walker D.O., M.S. Clinical Professor Departm ent of Surgery, University of Oklahom a HSC; Em ergency Physician, Departm ent of Em ergency Medicine, Oklahom a Heart Hospital, Oklahom a City, Oklahom a Michael Waters M.D. Academ ic Chief Resident Departm ent of Em ergency Medicine, University of California, Irvine School of Medicine, Orange, California Joseph Weber M.D.

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Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Em ergency Medicine Service Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Bruce A. Webster M.D., Ph.D. Chief Departm ent of Em ergency Medicine, Swedish Medical Center, Seattle, Washington Scott G. Weiner M.D., M.P.H. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts Kurt Whitaker M.D. Rebecah M. Wilks M.D. Adjunct Assistant Professor Departm ent of Em ergency Medicine, George Washington University School of Medicine, Washington, D.C. Seth K. Williams M.D. Chief Resident Departm ent of Orthopaedic Surgery, University of California, San Diego, San Diego, California Brandon K. Wills D.O., M.S. Clinical Assistant Professor Departm ent of Em ergency Medicine, University of Washington; Staff Physician, Departm ent of Em ergency Medicine, Madigan Arm y Medical Center, Tacom a, Washington Tracy Wimbush M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Kathleen A. Wittels M.D. Chief Resident

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Harvard Affiliated Em ergency Medicine Residency; Chief Resident, Massachusetts General Hospital, Brigham and Wom en's Hospital, Boston, Massachusetts Peter J. Witucki M.D. Assistant Clincal Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Richard Wolfe M.D. Associate Professor Division of Em ergency Medicine, Harvard Medical School; Chief, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Jeannette M. Wolfe M.D., F.A.C.E.P. Clinical Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Baystate Hospital, Springfield, Massachusetts Jason K. Wong M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Robert Wollard M.D. Adam Wos M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Daniel T. Wu M.D. Assistant Professor Departm ent of Em ergency Medicine, Em ory University School of Medicine, Atlanta, Georgia Christine Yang-Kauh M.D. Clinical Instructor Departm ent of Em ergency Medicine, Weill Medical College of Cornell

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University, New York, New York; Attending Assistant Residency Director, Departm ent of Em ergency Medicine, New York Methodist Hospital, Brooklyn, New York Sandra S. Yoon M.D. Christian Young M.D. Resident Physician Departm ent of Em ergency Medicine, Northwestern University School of Medicine; Resident Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Timothy Young M.D. Richard Zane M.D. Vice Chairm an Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Harvard Affiliated Em ergency Medicine Residency, Boston, Massachusetts Michelle Zell-Kanter Pharm.D., A.B.A.T. TOXIKON Coordinator Section of Clinical Toxicology, Division of Occupational Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Julie Zeller M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Aviva Jacoby Zigman M.D. Physician Departm ent of Em ergency Medicine, Portland Adventist Medical Center, Portland, Oregon Andrew Zigman M.D. Departm ent of Em ergency Medcine, Portland Adventist Medical Center, Portland, Oregon Gary D. Zimmer M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Johns Hopkins University,

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Baltim ore, Maryland; Chairm an, Departm ent of Em ergency Medicine, St. Mary Medical Center, Langhorne, Pennsylvania Karen P. Zimmer M.D. Assistant Professor of Pediatrics Johns Hopkins University, Baltim ore, Maryland David N. Zull M.D., F.A.C.E.P., F.A.C.P. Associate Professor Departm ents of Medicine and Em ergency Medicine, Northwestern University; Co-Director, Em ergency Departm ent, Observation Unit, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Preface

Preface

Rosen and Barkin's 5-Minute Em ergency Medicine Consult uniquely reflects our clinical practices and specialty of em ergency m edicine. It's focus is to provide concise, form atted inform ation that will allow the busy clinician to respond to challenges in a tim ely fashion. The book is m eant to be readily accessible and frequently used in the m idst of the clinical environm ent rather than be read at one's leisure. It is written and edited by practicing clinicians for practicing clinicians. As em ergency physicians, we need references to rem ind us of clinical presentations, differential diagnoses, drugs and dosages and m anagem ent principles that facilitate our clinical judgm ent in synthesizing the vast array of available data. We have attem pted to supplem ent this data bank with a perspective gained through m any years of practice. The book is not m eant to be a diagnostic engine, but rather a place to turn to confirm a diagnosis that is supported by the clinical presentation. Our talented authors discuss each topic as if they were in the m iddle of a busy ED, trying to present a precise and clinically relevant sum m ary to a resident who had queried them on a topic, or with whom they m ight be seeing a patient with a particular problem . We are indebted to them for their com m itm ent to this task. The book is intended to be accurate, pointed, and readily integrated into practice, rather than definitive. This 3rd edition incorporates new inform ation and approaches to m anagem ent, while allowing us to develop new topics that reflect som e of the new challenges we face.

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Rosen and Barkin's 5-Minute Em ergency Medicine Consult will be useful to both novices in em ergency m edicine and experienced clinicians. The inform ation and organization of the book is designed to be optim al in the m iddle of the â€œchaosâ€• that surrounds our clinical settings. The form at and content focuses on the key inform ation that you will need in patient m anagem ent. Clinical acum en, judgm ent, and experience rem ain as the foundation for our clinical practices. It is our hope that this book will serve as a useful and readily used resource and enhance the fulfillm ent of practicing em ergency m edicine. Jeffrey Schaider Stephen R. Hayden Richard Wolfe Roger M. Barkin Peter Rosen

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Ackno w ledgem ents

Acknowledgements

To m y loving wife, Anna, and m y sons Jacob and Isaac, who have always supported and inspired m e. I would like to thank the Cook County Em ergency Medicine Residents and Attendings for their contributions to this textbook and to enhancing m y knowledge and understanding of our unique field. Finally, I want to extend a special thanks to m y friend, Dr. Robert Sim on, who continues to be a role m odel and m entor. J. S. To m y residents, I hope this book helps you where it is needed m ost and gives you the inform ation you need to take better care of your patients. To m y children, Connor, Maia, and Kenny and m y wife Marina thank you for all the love and support and your willingness to allow m e to do the work I love. S. R. H. To the Em ergency Medicine faculty and residents at Beth Israel Deaconess Medical Center R. W. This book is dedicated to the m any talented and devoted clinicians who will hopefully find it useful in their pursuit of excellence in patient care. Your constant focus on your patient's welfare and health is an inspiration to provide tools that facilitate the challenges of working in the em ergency and urgent care setting. Thanks are especially due to the m any authors who help to m ake this book com prehensive, accurate and tim ely. Lippincott's entire editorial team have m ade the process m ove sm oothly through m any steps

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with special thanks to Nicole Dernoski who coordinated the com m unication and com pletion of the m anuscript. R. M. B.

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â†‘ Table of Contents

[+] Abdominal Aortic Aneurysm [+] Abdominal Pain [+] Abdominal Trauma, Blunt [+] Abdominal Trauma, Imaging [+] Abdominal Trauma, Penetrating [+] Abortion, Spontaneous [+] Abruptio Placentae [+] Abscess, Skin/Soft Tissue [+] Abuse, Elder [+] Abuse, Pediatric (Nonaccidental Trauma [NAT]) [+] Acetaminophen Poisoning [+] Acidosis [+] Acromio-Clavicular Joint Injury [+] Acute Coronary Syndrome: Coronary Vasospasm [+] Acute Coronary Syndrome: Drug Induced [+] Acute Coronary Syndrome: Myocardial Infarction [+] Acute Coronary Syndrome: Nonâ€“Q-Wave (Non-ST Elevation) MI

Page 107

[+] Acute Coronary Syndrome: Stable Angina [+] Acute Coronary Syndrome: Unstable Angina [+] Adrenal Insufficiency [+] Airway Management [+] Alcohol Poisoning [+] Alcoholic Ketoacidosis [+] Alkalosis [+] Altered Mental Status [+] Amebiasis [+] Amenorrhea [+] Amphetamine, Poisoning [+] Amputation Traumatic/Replantation [+] Amyotrophic Lateral Sclerosis [+] Anal Fissure [+] Anaphylaxis [+] Anemia [+] Angioedema [+] Ankle Fracture/Dislocation

Page 108

[+] Ankle Sprain [+] Ankylosing Spondylitis [+] Anterior Cruciate Ligament Injury [+] Anticholinergic Poisoning [+] Antidepressant Poisoning [+] Aortic Dissection, Thoracic [+] Aortic Rupture, Traumatic (TAI) [+] Aphthous Ulcers [+] Apnea [+] Appendicitis [+] Arsenic Poisoning [+] Arterial Gas Embolism (AGE) [+] Arterial Occlusion [+] Arthritis, Degenerative [+] Arthritis, Juvenile Idiopathic [+] Arthritis, Monoarticular [+] Arthritis, Rheumatoid [+] Arthritis, Septic

Page 109

[+] Ascites [+] Asthma, Adult [+] Asthma, Pediatric [+] Asystole [+] Ataxia [+] Atrial Fibrillation [+] Atrial Flutter [+] Atrioventricular Blocks [+] Babesiosis [+] Back Pain [+] Bacterial Tracheitis [+] Barbiturates, Poisoning [+] Barotrauma [+] Bartholin Abscess [+] Bell's Palsy [+] Benzodiazepine, Poisoning [+] Beta-Blocker Poisoning [+] Biologic Weapons

Page 110

[+] Bipolar Disorder [+] Bite, Animal [+] Bite, Human [+] Bladder Injury [+] Blow-Out Fracture [+] Boerhaave Syndrome [+] Botulism [+] Bowel Obstruction [+] Bradyarrhythmias [+] Bronchiolitis [+] Bronchitis [+] Bundle Branch Blocks [+] Burns [+] Bursitis [+] Calcium Channel Blocker, Poisoning [+] Candidiasis, Oral [+] Carbamazepine, Poisoning [+] Carbon Monoxide, Poisoning

Page 111

[+] Cardiac Arrest [+] Cardiac Pacemakers [+] Cardiac Testing [+] Cardiac Transplantation Complications [+] Cardiogenic Shock [+] Cardiomyopathy [+] Cardiomyopathy, Hypertrophic [+] Cardiomyopathy, Peripartum [+] Carpal Fractures [+] Carpal Tunnel Syndrome [+] Cauda Equina Syndrome [+] Caustic Ingestion [+] Cavernous Sinus Thrombosis [+] Cellulitis [+] Cerebral Aneurysm [+] Cerebral Vascular Accident [+] Cervical Adenitis [+] Cesarean Section, Emergency

Page 112

[+] Chancroid [+] Chemical Weapons Poisoning [+] Chest Pain [+] Chest Trauma, Blunt [+] Chest Trauma, Penetrating [+] Cholangitis [+] Cholecystitis [+] Cholelithiasis [+] Chronic Obstructive Pulmonary Disease [+] Cirrhosis [+] Clavicle Fracture [+] Cocaine, Poisoning [+] Colon Trauma [+] Coma [+] Compartment Syndrome [+] Congenital Heart Disease, Acyanotic [+] Congenital Heart Disease, Cyanotic [+] Congestive Heart Failure

Page 113

[+] Conjunctivitis [+] Conscious Sedation [+] Constipation [+] Contact Dermatitis [+] Cor Pulmonale [+] Corneal Abrasion [+] Corneal Burn [+] Corneal Foreign Body [+] Cough [+] Croup [+] Cushing Syndrome [+] Cyanide Poisoning [+] Cyanosis [+] Cystic Fibrosis [+] Dacryoadenitis [+] Dacryocystitis [+] Decompression [+] Deep Vein Thrombosis

Page 114

[+] Defibrillators, Implantable [+] Delirium [+] Delivery, Uncomplicated [+] Dementia [+] Dengue Fever [+] Dental Truama [+] Depression [+] Dermatomyositis/Polymyositis [+] Diabetes Insipidus [+] Diabetes Mellitus, Juvenile [+] Diabetic Ketoacidosis [+] Dialysis Complications [+] Diaper Rash [+] Diaphragmatic Trauma [+] Diarrhea, Adult [+] Diarrhea, Pediatric [+] Digoxin, Poisoning [+] Disseminated Intravascular Coagulation

Page 115

[+] Disulfirum Reaction [+] Diverticulitis [+] Diverticulosis [+] Dizziness [+] Domestic Violence [+] Duodenal Trauma [+] Dysfunctional Uterine Bleeding [+] Dysphagia [+] Dyspnea [+] Dystonic Reaction [+] Eating Disorder [+] Ectopic Pregnancy [+] Eczema/Atopic Dermatitis [+] Edema [+] Ehrlichiosis [+] Elbow Injuries [+] Electrical Injury [+] Encephalitis

Page 116

[+] Endocarditis [+] Endometriosis [+] Epididymitis/Orchitis [+] Epidural Abscess [+] Epidural Hematoma [+] Epiglottitis, Adult [+] Epiglottis, Pediatric [+] Epiphyseal Injuries [+] Epistaxis [+] Erysipelas [+] Erythema Infectiosum [+] Erythema Multiforme [+] Erythema Nodosum [+] Esophageal Trauma [+] Ethylene Glycol, Poisoning [+] External Ear Chondritis/Abscess [+] Extremity Trauma, Penetrating [+] Facial Fractures

Page 117

[+] Failure to Thrive [+] Fatigue [+] Feeding Problems, Pediatric [+] Feeding Tube Complications [+] Femur Fracture [+] Fever, Adult [+] Fever, Pediatric [+] Fibrocystic Breast Disease [+] Fibromyalgia [+] Flail Chest [+] Foot Fracture [+] Forearm Fracture, Shaft/Distal [+] Foreign Body, Ear [+] Foreign Body, Esophageal [+] Foreign Body, Nasal [+] Foreign Body, Rectal [+] Fournier Gangrene [+] Fracture, Open

Page 118

[+] Fractures, Pediatric [+] Frostbite [+] Gallstone Ileus [+] Gangrene [+] Gastric Outlet Obstruction [+] Gastritis [+] Gastroenteritis [+] Gastroesophageal Reflux Disease [+] Gastrointestinal Bleeding [+] Î³-GHB, Poisoning [+] Giardia [+] Glaucoma [+] Globe Rupture [+] Glomerulonephritis [+] Gonococcal Disease [+] Gout/Pseudogout [+] Granulocytopenia [+] Guillain-BarrÃ© Syndrome

Page 119

[+] Hallucinogen Poisoning [+] Hand Infection [+] Hazmat [+] Head Trauma, Blunt [+] Head Trauma, Penetrating [+] Headache [+] Headache, Cluster [+] Headache, Migraine [+] Heart Murmur [+] HELLP Syndrome [+] Hematuria/Proteinuria [+] Hemophilia [+] Hemoptysis [+] Hemorrhagic Fevers [+] Hemorrhagic Shock [+] Hemorrhoid [+] Hemothorax [+] Henoch SchÃ¶nlein Purpura

Page 120

[+] Hepatic Encephalopathy [+] Hepatic Injury [+] Hepatitis [+] Hepatorenal Syndrome [+] Hernia [+] Herpes, Genital [+] Herpes Simplex [+] Herpes Zoster [+] Hiccups [+] High Altitude Illness [+] Hip Injury [+] Hirschsprung Disease [+] HIV/AIDS [+] Hordeolum and Chalazion [+] Horner Syndrome [+] Humerus Fracture [+] Hydatidiform Mole [+] Hydrocarbon Poisoning

Page 121

[+] Hydrocele [+] Hydrocephalus [+] Hyperbaric Oxygen Therapy [+] Hypercalcemia [+] Hyperemesis Gravidarum [+] Hyperkalemia [+] Hypernatremia [+] Hyperosmolar Syndrome [+] Hyperparathyroidism [+] Hypertensive Emergencies [+] Hyperthermia [+] Hyperthyroidism [+] Hyperventilation [+] Hyperviscosity Syndrome [+] Hyphema [+] Hypocalcemia [+] HypoGlycemia [+] Hypoglycemic Poisoning

Page 122

[+] Hypokalemia [+] Hyponatremia [+] Hypoparathyroidism [+] Hypothermia [+] Hypothyroidism [+] Idiopathic Thrombocytopenic Purpura [+] Immunizations [+] Immunosuppression [+] Impetigo [+] Inborn Errors of Metabolism [+] Inflammatory Bowel Disease [+] Influenza [+] Intracerebral Hemorrhage [+] Intussusception [+] Iritis [+] Iron Poisoning [+] Irritable Bowel [+] Irritable Infant

Page 123

[+] Irritant Gas Exposure [+] Isoniazid Poisoning [+] Isopropanol Poisoning [+] Jaundice [+] Kaposi Sarcoma [+] Kawasaki Disease [+] Knee Dislocation [+] Labor [+] Labyrinthitis [+] Laceration Management [+] Laryngitis [+] Larynx Fracture [+] Lead Poisoning [+] Legg-CalvÃ©-Perthes Disease [+] Leukemia [+] Lightning Injuries [+] Lithium Poisoning [+] Ludwig's Angina

Page 124

[+] Lunate Dislocation [+] Lyme Disease [+] Lymphadenitis [+] Lymphangitis [+] Lymphogranuloma Venereum [+] Malaria [+] Malgaigne Fracture [+] Mallory-Weiss Syndrome [+] Malrotation [+] Mandibular Fractures [+] Marine Envenomation [+] Mastitis [+] Mastoiditis [+] MDMA Poisoning [+] Measles [+] Meckel Diverticulum [+] Medial Collateral Ligament Strain [+] Medial Meniscus Injury

Page 125

[+] MÃ©niÃ¨re Disease [+] Meningitis [+] Meningococcemia [+] Mercury Poisoning [+] Mesenteric Ischemia [+] Metacarpal Injuries [+] Methanol Poisoning [+] Methemoglobinemia [+] Mitral Valve Prolapse [+] Molluscum Contagiosum [+] Monoamine Oxidase Inhibitor, Poisoning [+] Mononucleosis [+] Multiple Myeloma [+] Multiple Sclerosis [+] Mumps [+] Munchausen's Syndrome [+] Mushroom, Poisoning [+] Myasthenia Gravis

Page 126

[+] Myocardial Contusion [+] Myocarditis [+] Nasal Fractures [+] Near Drowning [+] Neck Injury by Strangulation/Hanging [+] Neck Trauma, Blunt, Anterior [+] Neck Trauma, Penetrating, Anterior [+] Necrotizing Soft Tissue Infections [+] Necrotizing Ulcerative Gingivitis [+] Needle Stick [+] Neonatal Jaundice [+] Neonatal Sepsis [+] Nephritic Syndrome [+] Nephrotic Syndrome [+] Neuroleptic Malignant Syndrome [+] Neuroleptic Poisoning [+] Noncardiogenic Pulmonary Edema [+] Nonsteroidal Anti-inflammatory Poisoning

Page 127

[+] Nursemaid's Elbow [+] Oculomotor Nerve Palsy [+] Opiate Poisoning [+] Opportunistic Infection [+] Optic Artery Occlusion [+] Optic Neuritis [+] Organophosphate Poisoning [+] Osgood-Schlatter Disease [+] Osteogenesis Imperfecta [+] Osteomyelitis [+] Osteoporosis [+] Otitis Externa [+] Otitis Media [+] Otologic Trauma [+] Ovarian Cyst/Torsion [+] Paget's Disease [+] Pancreatic Pseudocyst [+] Pancreatic Trauma

Page 128

[+] Pancreatitis [+] Panic Attack [+] Paraphimosis [+] Parkinson's Disease [+] Paronychia [+] Patellar Injuries [+] Patent Ductus Arteriosus [+] Pediatric Trauma [+] Pediculosis [+] Pelvic Fracture [+] Pelvic Inflammatory Disease [+] Pemphigus [+] Penile Shaft Fracture [+] Peptic Ulcer [+] Perforated Viscous [+] Pericardial Effusion/Tamponade [+] Pericarditis [+] Perilunate Dislocation

Page 129

[+] Periodontal Abscess [+] Periorbital and Orbital Cellulitis [+] Peripheral Neuropathy [+] Peripheral Vascular Disease [+] Perirectal Abscess [+] Peritonsillar Abscess [+] Pertussis [+] Phalangeal Injuries, Foot [+] Phalangeal Injuries, Hand [+] Pharyngitis [+] Phencyclidine, Poisoning [+] Phenytoin, Poisoning [+] Pheochromocytoma [+] Phimosis [+] Pityriasis Rosea [+] Placenta Previa [+] Plant, Poisoning [+] Pleural Effusion

Page 130

[+] Pneumocystis Carinii Pneumonia [+] Pneumomediastinum [+] Pneumonia, Adult [+] Pneumonia, Pediatric [+] Pneumothorax [+] Poisoning [+] Poisoning, Antidotes [+] Poisoning, Gastric Decontamination [+] Poisoning, Toxidromes [+] Polio [+] Polycythemia [+] Postpartum Hemorrhage [+] Postpartum Infection [+] Pre-Eclampsia/Eclampsia [+] Pre-excitation Syndromes [+] Pregnancy, Trauma in [+] Pregnancy, Uncomplicated [+] Priapism

Page 131

[+] Prostatitis [+] Pruritis [+] Pseudotumor Cerebri [+] Psoriasis [+] Psychiatric Commitment [+] Psychosis, Acute [+] Psychosis, Medical vs. Psychiatric [+] Pulmonary Contusion [+] Pulmonary Edema [+] Pulmonary Embolism [+] Purpura [+] Pyelonephritis [+] Pyloric Stenosis [+] QT Syndrome, Prolonged [+] Rabies [+] Radiation Injury [+] Rapid Sequence Intubation [+] Rash

Page 132

[+] Rash, Pediatric [+] Reactive Arthritis [+] Rectal Prolapse [+] Rectal Trauma [+] Red Eye [+] Renal Calculus [+] Renal Failure [+] Renal Injury [+] Reperfusion Therapy, Cardiac [+] Reperfusion Therapy, Cerebral [+] Respiratory Distress [+] Resuscitation, Neonate [+] Resuscitation, Pediatric [+] Retinal Detachment [+] Retropharyngeal Abscess [+] Reye Syndrome [+] Rhabdomyolysis [+] Rheumatic Fever

Page 133

[+] Rib Fracture [+] Ring/Constricting Band Removal [+] Rocky Mountain Spotted Fever [+] Roseola [+] Rubella [+] Sacral Fracture [+] Salicylate Poisoning [+] Sarcoidosis [+] Scabies [+] Scaphoid Fracture [+] Schizophrenia [+] Sciatica/Herniated Disc [+] Seborrheic Dermatitis [+] Seizure, Adult [+] Seizure, Febrile [+] Seizure, Pediatric [+] Sepsis [+] Serum Sickness

Page 134

[+] Sexual Assault [+] Shock [+] Shoulder Dislocation [+] Sick Sinus Syndrome [+] Sickle Cell Disease [+] Sinusitis [+] Skin Cancer [+] Sleep Apnea [+] Slipped Capital Femoral Epiphysis [+] Small-Bowel Injury [+] Smoke Inhalation [+] Snake Envenomation [+] Spider Bite, Black Widow [+] Spider Bite, Brown Recluse [+] Spinal Cord Syndromes [+] Spine Injury: Cervical, Adult [+] Spine Injury: Cervical, Pediatric [+] Spine Injury: Coccyx

Page 135

[+] Spinal Injury: Lumbar [+] Spine Injury: Thoracic [+] Splenic Injury [+] Spondylolysis/Spondylolisthesis [+] Spontaneous Bacterial Peritonitis [+] Sporotrichosis [+] Staphylococcal Scalded Skin Syndrome [+] Sternoclavicular Joint Injury [+] Stevens-johnson Syndrome [+] Sting, Bee [+] Sting, Scorpion [+] Streptococcal Disease [+] Stridor [+] Subarachnoid Hemorrhage [+] Subdural Hematoma [+] Sudden Infant Death Syndrome (SIDS) [+] Suicide, Risk Evaluation [+] Supraventricular Tachycardia

Page 136

[+] Sympathomimetic Poisoning [+] Syncope [+] Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) [+] Synovitis, Toxic [+] Syphilis [+] Systemic Lupus Erythematosus [+] Tachydysrhythmias [+] Temporal Arteritis [+] Temporal Mandibular Joint Injury/Syndrome [+] Tendon Laceration [+] Tendonitis [+] Tenosynovitis [+] Testicular Torsion [+] Tetanus [+] Theophylline Poisoning [+] Thoracic Outlet Syndrome [+] Thrombotic Thrombocytopenic Purpura [+] Thumb Fracture

Page 137

[+] Tibial Plateau Fracture [+] Tibial/Fibular Shaft Fracture [+] Tick Bite [+] Tinea Infections, Cutaneous [+] Toluene Poisoning [+] Toothache [+] Torticollis [+] Toxic Epidermal Necrolysis [+] Toxic Shock Syndrome [+] Toxoplasmosis [+] Transfusion Complications [+] Transient Global Amnesia [+] Transient Ischemic Attack [+] Transplant Rejection [+] Trauma, Multiple [+] Trichomonas [+] Tricyclic Antidepressant, Poisoning [+] Trigeminal Neuralgia

Page 138

[+] Tuberculosis [+] Tularemia [+] Tumor Compression Syndromes [+] Tympanic Membrane Perforation [+] Ultraviolet Keratitis [+] Urethral Trauma [+] Urethritis [+] Urinary Retention [+] Urinary Tract Fistula [+] Urinary Tract Infections, Adult [+] Urinary Tract Infections, Pediatric [+] Urticaria [+] Vaginal Bleeding [+] Vaginal Bleeding in Pregnancy [+] Vaginal Discharge/Vaginitis [+] Valvular Heart Disease [+] Varicella [+] Varices

Page 139

[+] Vasculitis [+] Venous Insufficiency [+] Ventilator Management [+] Ventricular Fibrillation [+] Ventricular Peritoneal Shunts [+] Ventricular Tachycardia [+] Vertebrobasilar Insufficiency [+] Vertigo [+] Violence, Management of [+] Visual Loss [+] Vitreous Hemorrhage [+] Volvulus [+] Vomiting, Adult [+] Vomiting, Pediatric [+] Von Willebrand Disease [+] Warfarin/Coumadin Overdose [+] Warts [+] Weakness

Page 140

[+] West Nile Virus [+] Wheezing [+] Wilmsâ€™ Tumor [+] Withdrawal, Alcohol [+] Withdrawal, Drug [+] Wolff-Parkinson-White Syndrome [+] Wound Ballistics â†‘ Back of Book

[+] Appendix

Page 141

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Ao rtic Aneurysm

Abdominal

Aortic Aneurysm Jason Imperato Carlo L. Rosen

Basics Description 

Focal dilation of the aortic wall with an increase in diam eter by at least 50% (>3 cm )



95% are infrarenal.



Gradual expansion or rupture causes sym ptom s.



Rupture can occur into the intraperitoneal or retroperitoneal spaces.



Intraperitoneal rupture is usually im m ediately fatal.



Average growth rate of 0.2 to 0.5 cm per year



5-year risk of rupture: o

Aneurysm s <4.0 cm : 2%

o

Aneurysm s 4.0â€“5.0 cm : 5%

o

Aneurysm s 5.0â€“6.0 cm : 25%

o

Aneurysm s 6.0â€“7.0 cm : 35%



40â€“50% die before they reach the hospital.



50% of patients who reach the hospital alive survive.



5-year survival after repair is 67%.

Pa ge 1 4 2

Geriatric Considerations 

Risk increases with advanced age.



Present in 4â€“8% of all patients older than 65 years



Peak incidence: o

Men: 5.9% at the age of 80 years

o

Wom en: 4.5% at the age of 90 years

Etiology 



Risk factors: o

Male gender

o

Age >65 years old

o

Fam ily history

o

Cigarette sm oking

o

Atherosclerosis

o

Hypertension

o

Diabetes m ellitus

o

Connective tissue disorders: 

Ehlers-Danlos syndrom e



Marfan syndrom e

Uncom m on causes: o

Blunt abdom inal traum a

o

Infections of the aorta

o

Mycotic aneurysm secondary to endocarditis

Diagnosis Signs and Symptoms 

Unruptured: o

Most often asym ptom atic

o

Abdom inal, back, or flank pain: 

Vague, dull quality

Pa ge 1 4 3





Constant, throbbing, or colicky

o

Abdom inal m ass or fullness

o

Palpable, nontender, pulsatile m ass

o

Intact fem oral pulses

Ruptured: o

o

o

Classic triad: 

Pain



Hypotension



Pulsatile abdom inal m ass



Present in only 30â€“50% of patients

System ic: 

Syncope



Hypotension



Tachycardia



Evidence of system ic em bolization

Abdom en: 

Abdom inal, back, or flank pain



Acute, severe, constant



Radiates to chest, thigh, inguinal area, or scrotum

o



Flank pain radiating to the groin in 10% of cases



Pulsatile, tender abdom inal m ass



Only 75% of aneurysm s >5 cm are palpable



Abdom inal tenderness



Abdom inal bruit



Gastrointestinal (GI) bleeding

Extrem ities: 

Lower-extrem ity pain



Dim inished or asym m etric pulses in the lower extrem ities



Com plications: o

Large em boli: acute painful lower extrem ity

Pa ge 1 4 4

o

Microem boli: cool, painful, cyanotic toes (â€œblue toe syndrom eâ€•)

o

Aneurysm al throm bosis: acutely ischem ic lower extrem ity

o

Aortoenteric fistula: GI bleeding

Essential Workup 



Unstable patients: o

Explorative surgery without further ancillary studies

o

Bedside abdom inal ultrasound

Stable sym ptom atic patients: o

Abdom inal CT

Tests Lab 

CBC



Type and cross-m atch blood



Creatinine



Urinalysis



Coagulation studies

Imaging 

Plain radiographs: o

Abdom inal or lateral lum bar radiographs

o

Only if other tests are unavailable

o

Curvilinear calcification of the aortic wall or a paravertebral soft-tissue m ass indicates abdom inal aortic aneurysm (AAA) in 75% of patients.



o

Cannot identify rupture

o

Negative study does not rule out AAA.

Abdom inal ultrasound: o

Highly sensitive for detecting AAA prior to rupture

o

In em ergent setting, useful to determ ine presence of

Pa ge 1 4 5

AAA only. o

Ultrasound findings consistent with AAA are enlarged aorta greater than 3 cm or focal dilatation of the aorta.

o

Sensitivity has been reported as low as 10% following rupture.

o 

Indicated in the unstable patient

Abdom inal CT scan: o

Contrast is not necessary.

o

Will dem onstrate both aneurysm and site of rupture (intraperitoneal versus retroperitoneal)

o

Allows m ore accurate m easurem ent of aortic diam eter

o 

Indicated in stable patients only

Aortography: o

No use in em ergent evaluation

o

The presence of m ural throm bi can lead to underestim ation of the size of the aorta.

Diagnostic Procedures/Surgery Explorative laparotom y by vascular surgeon P.3

Differential Diagnosis 

Other abdom inal arterial aneurysm s (i.e., iliac or renal)



Renal colic



Biliary colic



Musculoskeletal back pain



Pancreatitis



Cholecystitis



Appendicitis

Pa ge 1 4 6



Bowel obstruction



Perforated viscus



Mesenteric ischem ia



Diverticulitis



GI hem orrhage



Aortic throm boem bolism



Myocardial infarction



Addisonian crisis



Sepsis

Treatment Pre Hospital 

Establish two large-bore IV lines



Rapid transport to the nearest facility with surgical backup



Alert ED staff as soon as possible to prepare the following: o

Operating room

o

Universal donor blood

o

Surgical consultation

Initial Stabilization 

Two large-bore IV lines



Crystalloid infusion



Cardiac m onitor



Early blood transfusion

ED Treatment For patients suspected of sym ptom atic AAA: 

Avoid overaggressive fluid resuscitation; this leads to increased bleeding.



Em ergent surgical consult and operative intervention



Diagnostic tests should not delay definitive treatm ent.

Pa ge 1 4 7

Follow-Up Disposition Admission Criteria All patients with sym ptom atic AAA require em ergent surgical intervention and adm ission.

Discharge Criteria Asym ptom atic patients only

Issues for Referral 

Close vascular surgery follow up m ust be arranged prior to discharge.



Instructions to return im m ediately: o

With any pain in the back, abdom en, flank, or lower extrem ities

o

With dizziness or syncope

References 1. Bessen HA. Abdom inal aortic aneurysm s. In Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO.: Mosby, 2002:1176â€“1186. 2. Ernst CB. Abdom inal aortic aneurysm . N Engl J Med. 1993;328:1167â€“1172. 3. Hallet JW. Managem ent of abdom inal aortic aneurysm s. Mayo Clin Proc. 2000;75:395â€“399. 4. Rogers RL, McCorm ack R. Aortic disasters. Em erg Med Clin N Am . 2004;22:887â€“908. 5. Tayal VS, Graf CD, Gibbs MA. Prospective study of accuracy and outcom e of em ergency ultrasound for abdom inal aortic aneurysm over two years. Acad Em erg Med. 2003;10:867â€“871.

Pa ge 1 4 8

6. Walker JS, Dire DJ. Vascular abdom inal em ergencies. Em erg Med Clin N Am . 1996;14:571â€“591.

Codes ICD9-CM 441.3

ICD10 171.4

Pa ge 1 4 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Pain

Abdominal Pain

Michelle A. Finkel

Basics Description 



Parietal pain: o

Irritating m aterial causing peritoneal inflam m ation

o

Pain transm itted by som atic nerves

o

Exacerbated by changes in tension of the peritoneum

o

Pain characteristics: 

Sharp



Well localized



Abdom inal tenderness



Involuntary guarding



Rebound tenderness



Exacerbated by m ovem ent and coughing

Visceral pain: o

Distention of a viscous or organ capsule or spasm of intestinal m uscularis fibers:

o



Pain is generally poorly localized.



Colicky with intestinal distention



Constant with a distended gallbladder or kidney

Inflam m ation: 

Initially, the pain is poorly localized.

Pa ge 1 5 0



Focal tenderness develops as the inflam m ation extends to the peritoneum or localizers.

o

Ischem ia from vascular disturbances: 

Pain is severe and diffuse with catastrophic vascular em ergencies



Pain is disproportional to the abdom inal exam ination



Referred pain: o

Felt at distant location from diseased organ

o

Due to an overlapping supply by the affected neurosegm ent to the perceived location of pain



Abdom inal wall pain: o

Constant

o

Aching

o

Muscle spasm

o

Involvem ent of other m uscle groups

Etiology 



Peritoneal irritants: o

Gastric juice

o

Fecal m aterial

o

Pus

o

Blood

o

Bile

o

Pancreatic enzym es

Visceral obstruction: o

Sm all intestines

o

Large intestines

o

Gallbladder

o

Ureters and kidneys

o

Visceral ischem ia

o

Intestinal

o

Renal

Pa ge 1 5 1

o 

Splenic

Visceral inflam m ation: o

Appendicitis

o

Inflam m atory bowel disorders

o

Cholecystitis

o

Hepatitis

o

Peptic ulcer disease

o

Pancreatitis

o

Pelvic inflam m atory disease

o

Pyelonephritis



Abdom inal wall pain



Referred pain: o

The possibility of intrathoracic disease m ust be considered in every patient with abdom inal pain.

Diagnosis Signs and Symptoms 

General: o

Anorexia

o

Malaise

o

Tachycardia

o

Hypotension

o

Fever

o

Nausea

o

Vom iting: 

Etiology requiring surgical intervention is less likely when vom iting precedes the onset of pain



Abdom inal: o

Diarrhea

o

Constipation

Pa ge 1 5 2

o

Distended abdom en

o

Abnorm al bowel sounds: 

High-pitched rushes with bowel obstruction



Absence of sound with ileus or peritonitis



Often unreliable

o

Pulsatile abdom inal m ass

o

Rovsing sign: 

Palpation of left lower quadrant causes pain in right lower quadrant (RLQ)

 o

Suggestive of appendicitis

McBurney point tenderness associated with appendicitis: 

Palpation in RLQ two-thirds distance between um bilicus and right anterior superior iliac crest causes pain

o

Murphy sign: 

Pause in inspiration while exam iner is palpating under liver

 o

o

Suggestive of cholecystitis

Psoas sign: 

Pain on extension of the thigh



Suggests inflam m ation around psoas m uscle

Obturator sign 

Pain on rotation of the flexed thigh, especially internal rotation



Inflam m ation around internal obturator m uscle

o

Tender or discolored hernia site

o

Rectal and pelvic exam ination: 

Tenderness with pelvic peritoneal irritation



Cervical m otion tenderness



Adnexal m asses



Rectal m ass or tenderness

Pa ge 1 5 3



Genitourinary: o

Flank pain

o

Dysuria

o

Hem aturia

o

Vaginal bleeding

o

Tender adnexal m ass on pelvis

o

Testicular pain 

May be referred from renal or appendiceal pathology



o

Testicular swelling

o

High-riding testes

o

Transverse lie of testis

Extrem ities: o

Shoulder pain: 

o 

Referred pain from diaphragm atic involvem ent

Pulse deficit or unequal fem oral pulses

Skin: o

Jaundice

o

Herpes zoster

o

Cellulitis

Essential Workup Historical characteristics define the type of pain and suggest underlying causes: 

Nature of onset of pain



Tim e of onset and duration of pain



Location of pain initially and at presentation



Extra-abdom inal radiations



Quality of pain (e.g., sharp, dull, cram py)



Palliative or provocative factors



Relation of associated finding to onset of pain



Changes in bowel habits



History of traum a

Pa ge 1 5 4



Gynecologic history



Visceral obstruction

Tests Lab 

CBC: o

WBC is a poor predictor of surgical disease



Urinalysis



Serum lipase: o

More accurate than a serum am ylase in diagnosing pancreatic disorders



hCG



Serum electrolytes and glucose



Liver function tests



Gonorrhea and chlam ydia cultures should be obtained if a pelvic exam ination is perform ed.

Imaging 

ECG: o

Indicated in patients with epigastric pain with risk factors for coronary artery disease





Kidney, ureter, and bladder (KUB) and upright: o

Indicated prim arily if bowel obstruction is suspected

o

Air-fluid levels and intestinal distention: Bowel obstruction



Ileus



Volvulus



Intussusception

Upright chest radiograph: o





Pneum operitoneum 

Perforated viscus



Extra-abdom inal causes

Ultrasound:

Pa ge 1 5 5

o

Biliary abnorm alities

o

Hydronephrosis

o

Intraperitoneal fluid

o

Aortic aneurysm

o

Pelvic ultrasound

P.5



Abdom inal CT: o

Spiral CT without contrast: 

Determ ines location and size of stone in patients with renal colic

o

CT with IV contrast only: 

o

Vascular rupture suspected in a stable patient

CT with IV and oral contrast: 

Indicated when there is a suspicion of a surgical etiology involving bowel or intraperitoneal hem orrhage

o

CT with rectal contrast only: 





High accuracy reported in detecting appendicitis

IVP: o

Indicated in patients with suspected ureteral calculi

o

More tim e-consum ing than spiral CT

Barium enem a: o

Intussusception

o

Volvulus

Differential Diagnosis 

Parietal pain: o

Abdom inal arterial aneurysm

o

Appendicitis

o

Diverticulitis with perforation or abscess

o

Ruptured ectopic pregnancy

Pa ge 1 5 6



o

Ruptured ovarian cyst

o

Pancreatitis

o

Perforated peptic ulcer

o

Perforated viscus

o

Splenic rupture

Visceral pain: o

Abdom inal epilepsy

o

Abdom inal m igraine

o

Adrenal crisis

o

Early Appendicitis

o

Bowel obstruction

o

Cholecystitis

o

Constipation

o

Depression

o

Diabetic ketoacidosis

o

Diverticulitis

o

Dysm enorrhea

o

Ectopic pregnancy

o

Esophagitis

o

Fecal im paction

o

Fitz-Hughâ€“Curtis syndrom e

o

Gastroenteritis

o

Hepatitis

o

Hirschsprung disease

o

Incarcerated hernia

o

Inflam m atory bowel disease

o

Intussusception

o

Irritable bowel syndrom e

o

Ischem ic bowel

o

Lactose intolerance

o

Lead poisoning

o

Meckel diverticulitis

Pa ge 1 5 7





o

Neoplasm

o

Ovarian torsion

o

Pancreatitis

o

Pelvic inflam m atory disease

o

Peptic ulcer disease

o

Renal/ureteral calculi

o

Sickle cell crisis

o

Splenic infarction

o

Spontaneous abortion

o

Testicular torsion

o

Urinary tract infection

o

Volvulus

Referred pain: o

Myocardial infarction

o

Pneum onia

Abdom inal wall pain: o

Abdom inal wall hem atom a or infection

o

Black widow spider bite

o

Herpes zoster

Pediatric Considerations 



<2 years: o

Hirschsprung disease

o

Incarcerated hernia

o

Intussusception

o

Neoplasm

o

Sickle cell crisis

o

Volvulus

2â€“5 years: o

Appendicitis

o

Incarcerated hernia

o

Meckel diverticulitis

o

Neoplasm

Pa ge 1 5 8

o 

Sickle cell crisis

>5 years: o

Appendicitis

o

Ectopic pregnancy

o

Inflam m atory bowel disease

o

Pelvic inflam m atory disease

Treatment Initial Stabilization 

Em ergent laparotom y: o

Patients who are hem odynam ically unstable with suspected vascular rupture



IV fluids

ED Treatment 

Antiem etics are im portant for com fort.



Narcotics or analgesics should not be withheld.



Antibiotics are needed in potential perforation and in peritonitis.



Surgical consultation based on suspected etiology

Medication (Drugs) 

Am picillin: 0.5â€“2 g IV



Cefotetan 1â€“2 g IV



Cefoxitin: 1â€“2 g IV



Com pazine 5â€“10 m g PO prn nausea



Gentam icin: 1â€“1.7 m g/kg IV



Levofloxacin: 500 m g IV



Metronidazole 15m g/kg IV, loading dose

Pa ge 1 5 9



Ondansetron 4 m g IV prn nausea



Prom ethazine: 12.5â€“25 m g PO/IM/IV

Follow-Up Disposition Admission Criteria 

Surgical intervention



Peritoneal signs



Patient unable to keep down fluids



Lack of pain control



Medical cause necessitating in-house treatm ent (m yocardial infarction, diabetic ketoacidosis)



IV antibiotics needed

Discharge Criteria No surgical or severe m edical etiology found in patient who is able to keep fluid down, has good pain control, and is able to follow detailed discharge instructions.

References 1. Graff LG 4th, Robinson D. Abdom inal pain and em ergency departm ent evaluation. Em erg Med Clin North Am . 2001;19(1):123â€“136. 2. Hendrickson M, Naparst TR. Abdom inal surgical em ergencies in the elderly. Em erg Med Clin North Am . 2003;21(4):937â€“969. 3. Kam in RA, Nowicki TA, Courtney DS, Powers RD. Pearls and pitfalls in the em ergency departm ent evaluation of abdom inal pain. Em erg Med Clin North Am . 2003;21(1):61â€“72 4. Kizer KW, Vassar MJ. Em ergency departm ent diagnosis of abdom inal disorders in the elderly. Am J Em erg Med.

Pa ge 1 6 0

1998;16(4):357â€“362. 5. Mason JD. The evaluation of acute abdom inal pain in children. Em erg Med Clin North Am . 1996;14(3):629â€“643.

Codes ICD9-CM 789.0

ICD10 R10.4

Pa ge 1 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Blunt

Abdominal

Trauma, Blunt Stewart Coffman

Basics Description 

Injury results from a sudden increase of pressure to abdom en.



Solid organ injury usually m anifests as hem orrhage.



Hollow viscous injuries result in bleeding and peritonitis from contam ination with bowel contents.

Etiology 

Sixty percent result from m otor vehicle collisions.



Solid organs are injured m ore frequently than hollow viscous organs.



The spleen is the m ost frequently injured organ (25%), followed by the liver (15%), intestines (15%), retroperitoneal structures (13%), and kidney (12%).



Less frequently injured are the m esentery, pancreas, diaphragm , urinary bladder, urethra, and vascular structures.

Pediatric Considerations

Pa ge 1 6 2



Children tend to tolerate traum a better because of the m ore elastic nature of their tissues.



Owing to the sm aller size of the intrathoracic abdom en, the spleen and liver are m ore exposed to injury because they lie partially outside the bony rib cage.

Diagnosis Signs and Symptoms 

Spectrum from abdom inal pain, signs of peritoneal irritation, to hypovolem ic shock



Nausea or vom iting



Labored respiration from diaphragm irritation or upper abdom inal injury



Left shoulder pain with inspiration (Kehr sign) from diaphragm atic irritation owing to bleeding



Delayed presentation possible with sm all bowel injury

Essential Workup 

Evaluate and stabilize airway, breathing, and circulation (ABCs).



Prim ary objective is to determ ine need for operative intervention.



Exam ine abdom en to detect signs of intra-abdom inal bleeding or peritoneal irritation.



Injury in the retroperitoneal space or intrathoracic abdom en is difficult to assess by palpation.



Rem em ber that the lim its of the abdom en include the diaphragm superiorly (nipples anteriorly, inferior scapular tip posteriorly) and the intragluteal fold inferiorly and encom pass entire circum ference.

Pa ge 1 6 3



Abrasions or ecchym oses m ay be indicators of intra-abdom inal injury: o



Roll the patient to assess the back.

Bowel sounds m ay be absent from peritoneal irritation (late finding).



Foley catheter (if no blood at the m eatus, no perineal hem atom a, and norm al prostate exam ) to obtain urine and record urinary output



Plain film of the pelvis: o

Fracture of the pelvis and gross hem aturia m ay indicate genitourinary injury.

o

Further evaluation of these structures with retrograde urethrogram , cystogram , or intravenous pyelogram



CT m ost useful in assessing need for operative intervention and for evaluating the retroperitoneal space and solid organs: o

Patient m ust be stable enough to m ake trip to scanner.

o 

Also useful for suspected renal injury

FAST (focused abdom inal sonography for traum a) to detect intraperitoneal fluid o

Ultrasonography is rapid, requires no contrast agents, and is noninvasive.

o 

Operator dependent

Diagnostic peritoneal lavage (useful for revealing injuries in the intrathoracic abdom en, pelvic abdom en, and true abdom en) prim arily indicated for unstable patients: o

Positive with gross blood, RBC count of >100,000/m m 3 , WBC count of 500/m m 3 , or presence of bile, feces, or food particles

Tests

Pa ge 1 6 4

Lab 

Hem oglobin/hem atocrit, which initially m ay be norm al owing to isovolem ic blood loss



Type and cross is essential.



Urinalysis for blood: o

Microscopic hem aturia in the presence of shock is an indication for genitourinary evaluation.



Arterial blood gases: o

Base deficit m ay suggest hypovolem ic shock and help guide the resuscitation.

Imaging See Essential Workup.

Diagnostic Procedures/Surgery See Essential Workup.

Differential Diagnosis Lower thoracic injury m ay cause abdom inal pain.

Treatment Pre Hospital 

Aggressive fluid resuscitation is still considered standard of care.



Norm al vital signs do not preclude significant intra-abdom inal pathology.

Initial Stabilization 

Ensure adequate airway: o

Intubate if needed.

o

O 2 100% by nonrebreather face m ask

Pa ge 1 6 5



Two large-bore intravenous lines with crystalloid infusion



Begin infusion of packed RBCs if no response to 2 L of crystalloid.



If patient is in profound shock, consider transfusion of O-negative or type-specific blood.

P.7

ED Treatment 

Continue stabilization begun in field.



Nasogastric tube to evacuate stom ach, decrease distention, and decrease risk of aspiration: o

May relieve respiratory distress if caused by a herniated stom ach through the diaphragm

Medication (Drugs) 

Tetanus toxoid booster: 0.5 m L IM for patients with open wounds



Tetanus im m une globulin: 250 units IM for patients who have not had com plete series



Intravenous antibiotics: broad-spectrum aerobic with anaerobic coverage such as a second-generation cephalosporin

Pediatric Considerations 

Crystalloid infusion is 20 m L/kg if patient in shock.



Packed RBC dose is 1 m L/kg.

Follow-Up

Pa ge 1 6 6

Disposition Admission Criteria 

Postoperative cases



Equivocal findings on diagnostic peritoneal lavage, FAST exam , or CT



Many blunt abdom inal traum a patient benefit from adm ission, m onitoring, and serial abdom inal exam inations.

Discharge Criteria No patient in whom you suspect intra-abdom inal injury should be discharged hom e without an appropriate period of observation despite negative exam ination or im aging studies.

References 1. Am oroso TA. Evaluation of the patient with blunt abdom inal traum a: an evidence based approach. Em erg Med Clin North Am . 1999;17:63â€“75. 2. Brasel KJ, et al. Incidence and significance of free fluid on abdom inal CT in blunt traum a. J Traum a. 1995;44(5):889â€“892. 3. Davis JJ, Cohn I Jr, Nance FC. Diagnosis and m anagem ent of blunt abdom inal traum a. Ann Surg. 1976;183:672â€“678. 4. Holm es JF, et al. Perform ance of helical CT without oral contrast for the detection of gastrointestinal injuries. Ann Em erg Med. 2004;43(1):120â€“128. 5. McGahan JP, Wang L, Richards JR. Focused abdom inal ultrasound for traum a. Radiographics. 2001;21:91â€“99. 6. Stengel D, Bauwens K, Sehouli J, et al. System atic review and m eta-analysis of em ergency ultrasonography for blunt abdom inal traum a. Br J Surg. 2001;88:901â€“912.

Codes

Pa ge 1 6 7

ICD9-CM 868.00

ICD10 S39.9

Pa ge 1 6 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Im aging

Abdominal

Trauma, Imaging Christopher Richards

Basics Description This is a diagnostic procedure; basis for its use will vary with results of exam ination.

Diagnosis Signs and Symptoms 

Abdom inal traum a m ay present in an unstable patient with m ultiple associated injuries or as an isolated injury in a stable patient with no physical findings.



Assessm ent of the abdom en focuses on the need for early surgical m anagem ent; the diagnosis of specific organ injuries should be handled later.

History 

History should include m echanism of injury, restraint use and type, airbag or helm et use, prehospital vital signs, initial m ental status and change in m ental status, and any

Pa ge 1 6 9

prehospital treatm ents perform ed and their effect on patient status. 

AMPLE history (allergies, especially to radiographic contrast agents, m edications, past m edical history, last m eal, events leading up to the injury)

Physical Exam 

Com prehensive physical exam should include com plete bodily exposure and perineal and digital rectal exam s.



Abdom inal stab wounds should be locally explored after local anesthesia; penetration of the abdom inal wall fascia requires further evaluation.



Caution should be taken because the physical exam is accurate in determ ining serious abdom inal injury in only 45â€“50% of cases.

Essential Workup 

See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating)

Tests General approach to im aging in blunt abdom inal traum a: 

The ideal abdom inal im aging study is rapid, inexpensive, sensitive for operative injury; identifies m any nonoperative injuries requiring close observation and follow-up; requires m inim al training to perform and interpret; and does not exist yet.



Ultrasound has becom e the initial screening test of choice for hem odynam ically stable patients; it has replaced diagnostic peritoneal lavage in m any clinical settings.



CT scan is the definitive test for m ost patients, especially children, but requires intravenous contrast m aterial: o

Unstable patients should not be transported for a CT scan.

Pa ge 1 7 0



Most patients require serial physical exam inations and a period of observation even after negative im aging studies.

Imaging Ultrasound 



Advantages: o

Rapid

o

Noninvasive

o

Can be perform ed at patient's bedside

o

Does not require contrast agents or ionizing radiation

Disadvantages: o

Operator dependent

o

Does not reliably identify specific organ injury

o

Not sensitive enough to exclude all injuries. Serial exam ination and observation are required if ultrasound is the sole im aging study.

o

Is not well suited for penetrating injuries; m ay m iss significant bowel injuries not accom panied by hem operitoneum

o 

Indications: o



Does not evaluate spinal or retroperitoneal injuries

Blunt traum a in either stable or unstable patients

Contraindications: o

Absolute: 

Pre-existing indication for exploratory laparotom y

o



Relative: 

Obesity



Subcutaneous em physem a

Positive test: o

Dem onstration of free fluid or obvious solid organ injury (approxim ately 250 m L free fluid required in

Pa ge 1 7 1

adults) 

Adequate exam includes visualization of Morrison pouch, pericardium , both paracolic gutters, and the pelvic rectouterine pouch (pouch of Douglas), and exam of the liver and spleen for parenchym al injuries.



Considerations: o

Positive test result should be followed by CT in a stable patient or by laparotom y in an unstable patient.

o

Institutional factors determ ine which clinical departm ent perform s the study.

CT scan: 

Advantages: o

Sensitivity of 85â€“98%

o

Provides specific organ injury inform ation

o

Allows for sim ultaneous reform atting and reconstruction of spinal structures

o

Fosters nonoperative approach to solid organ injuries

o

Diagnoses retroperitoneal and bony injuries m issed by other m odalities.



Disadvantages: o

Requires intravenous contrast (acute contrast reactions and renal failure)

o

Isolated diaphragm atic, pancreatic, bowel injuries m ay be m issed, especially if perform ed im m ediately after injury.



Indications: o



Hem odynam ically stable patients

Contraindications: o

Absolute: 

Pre-existing indication for exploratory laparotom y

Pa ge 1 7 2

o



Hem odynam ic instability



Previous contrast reaction

Relative: 



Multiple allergies

Considerations: o

Modality of choice in children

o

Many m ultiple-injury patients require CT im aging of the head, spine, chest, or pelvis; m odern equipm ent provides for rapid scanning of m ultiple anatom ic regions in one session.

o

Monitoring m ust be continued in the CT suite; patients should be accom panied by appropriate m edical personnel.

o

Water m ay be substituted for oral contrast, but optim al detection of intestinal injury requires oral contrast and a 2- to 4-hour delay for intestinal opacification.

Diagnostic Procedures/Surgery 

Gunshot wounds to the abdom en require evaluation by a surgeon and will require laparotom y: o

Selective laparotom y is an option for experienced centers.



Diagnostic peritoneal lavage: o

o

Advantages: 

Rapid



Relatively sim ple to perform



97.8% accurate in diagnosing injury

Disadvantages: 

Invasive



Does not identify specific organ injury



1â€“2% com plication rate



May m iss retroperitoneal injuries and

Pa ge 1 7 3

intraperitoneal bladder rupture o

Indications: 

Hem odynam ically unstable patients



Patients requiring em ergent surgery for other conditions (e.g., craniotom y for epidural hem atom a)



Stab wounds that penetrate the abdom inal fascia

o

Contraindications: 

Absolute: pre-existing indication for exploratory laparotom y



Relative: previous abdom inal surgery, severe abdom inal distention, pregnancy, pediatric patients

o

Nasogastric tube and Foley catheter placem ent m andatory before beginning procedure P.9

o

Positive test: 

Aspiration of >10 m L of blood, bile, bowel contents, or urine



Diagnostic peritoneal lavage fluid in the urine or chest tube

o



Blunt traum a with >100,000 erythrocytes/m m 3



Penetrating traum a >1,000 erythrocytes/m m 3

Considerations: 

Favored in stab wound patients when local wound exploration is confirm atory



Favored in unstable blunt traum a patients because it m ay be perform ed sim ultaneously with other em ergency-basis surgical

Pa ge 1 7 4

interventions (e.g., craniotom y for epidural hem atom a) 

Must always be accom panied by serial abdom inal exam s after procedure



In the presence of pelvic fractures, use supraum bilical location.



In pregnancy, consider supraum bilical or open technique.



False-positive results m ay be obtained if perform ed >8 hours after injury.

Differential Diagnosis See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).

Treatment Pre Hospital All patients with a significant m echanism of injury or suspicion of m ajor traum a should be triaged to a facility equipped to m anage such injury.

Pediatric Considerations 

Pediatric patients should be triaged to a pediatric traum a center or to an adult traum a center equipped to m anage children.



CT scan should be considered the diagnostic test of choice in children as a greater percentage of injuries in children will be m anaged nonoperatively.



Diagnostic peritoneal lavage (DPL) is relatively contraindicated.

Initial Stabilization

Pa ge 1 7 5



In unstable patients, m anagem ent of the airway, breathing, and circulation; treatm ent of hypovolem ic shock; and control of m ajor hem orrhage m ust take precedence.



See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).

ED Treatment See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).

Follow-Up Disposition Admission Criteria See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).

Discharge Criteria See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).

References 1. Am oroso TA. Evaluation of the patient with blunt abdom inal traum a: an evidence based approach. Em erg Med Clin North Am . 1999;17:63â€“75. 2. Chiquito PE. Blunt abdom inal injuries. Diagnostic peritoneal lavage, ultrasonography and com puted tom ography scanning. Injury. 1996;27:117â€“124. 3. Pryor JP, Reilly PM, Dabrowski GP, et al. Nonoperative m anagem ent of abdom inal gunshot wounds. Ann Em erg Med. 2004;43(3):344â€“353. 4. Rose JS. Ultrasound in abdom inal traum a. Em erg Med Clin North Am . 2004;22(3):581â€“599. 5. Stengel D, Bauwens K, Sehouli J, et al. Em ergency

Pa ge 1 7 6

ultrasound-based algorithm s for diagnosing blunt abdom inal traum a. Cochrane Database Syst Rev. 2005;18(2):cd004446.

Miscellaneous SEE ALSO: Abdom inal Traum a, Blunt; Abdom inal Traum a, Penetrating

Codes N/A

Pa ge 1 7 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Penetrating

Abdominal

Trauma, Penetrating Stewart Coffman

Basics Description 

Solid organ injury usually results in hem orrhage.



Hollow viscus injury can lead to spillage of bowel contents and peritonitis.



Associated conditions: o

Injury to both thoracic and abdom inal structures occurs in 25% of cases.

Etiology 

Eighty percent of gunshot wounds and 20â€“30% of stab wounds result in significant intra-abdom inal injury. Com m only injured structures include: o

Liver (37%)

o

Sm all bowel (26%)

o

Stom ach (19%)

o

Colon (17%)

o

Major vessel (13%)

o

Retroperitoneum (10%)

o

Mesentery/om entum (10%)

Pa ge 1 7 8

o

Other: 

Spleen (7%)



Diaphragm (5%)



Kidney (5%)



Pancreas (4%)



Duodenum (2%)



Biliary (1%)

Diagnosis Signs and Symptoms 

Penetrating wound from knife, gun, or other foreign object



Spectrum of presentation ranging from localized pain to peritoneal signs: o

High-velocity projectile can cause extensive direct tissue dam age.

o

Secondary m issiles and tem porary cavitation of effected structures

o

Exit wound m ay be larger than entrance wound, but sm all entrance and exit wounds can conceal m assive internal dam age.



Rem em ber the borders of the abdom en: superior from the nipples (anteriorly) or inferior tip of scapula (posteriorly) to inferior gluteal folds.

Essential Workup 

Diagnosis of intra-abdom inal injury from gunshot wounds to the abdom en are m ade by celiotom y in the operating room .



Locally explore stab wounds to abdom en: o

If the wound penetrates anterior fascial layer, the

Pa ge 1 7 9

patient should undergo diagnostic peritoneal lavage or bedside ultrasound. 

Diagnostic laparoscopy is useful in diagnosing diaphragm atic injury and spleen and liver lacerations: o



May help avoid unnecessary surgery.

CT is useful in the evaluation of patients with a suspected retroperitoneal injury: o

Not reliable for detection of hollow viscus or diaphragm atic injuries.



If 10,000 RBC/m m 3 or m ore are found in the diagnostic peritoneal lavage fluid, the patient should undergo laparotom y.



If <10,000 RBC/m m 3 are present, the patient should be observed for 8â€“24 hours for the developm ent of peritoneal signs.

Tests Lab 

Hem oglobin or hem atocrit: o

Repeated m easurem ents to assess for ongoing hem orrhage



Urinalysis for blood to assess for possible genitourinary tract dam age



Arterial blood gases: o

Base deficit m ay be helpful in assessing hypovolem ia and guide volum e resuscitation.



Type and cross-m atch for all patients with significant intra-abdom inal injuries.

Imaging 

Plain film s: o

Obtain after placem ent of m arkers for localization of foreign bodies, m issiles, associated fractures, and

Pa ge 1 8 0

free air. 

Intravenous pyelogram : o



For possible renal injury

Bedside abdom inal ultrasound (FAST: focused abdom inal sonography for traum a): o



May reveal intraperitoneal blood or fluid

CT with IV contrast in experienced facilities and with stable patients: o

For possible retroperitoneal and solid organ injuries

Differential Diagnosis 

In cases of upper abdom inal wounds, consider the possibility of intrathoracic injury.



In cases of wounds to the lower thoracic area, consider the possibility of intra-abdom inal injury.

Treatment Pre Hospital 

Controversies: o

Military antishock trousers (MAST) should not be used.

o

Current standard of care for treatm ent of hypovolem ic shock is volum e resuscitation with crystalloid solutions.



Caution: o

Apply sterile dressings to open wounds and eviscerated bowel.

o

Secure im paled foreign objects in place; do not rem ove them .

Initial Stabilization

Pa ge 1 8 1



Two large-bore intravenous lines with crystalloid infusion



If no response to 2 L of crystalloid, infuse two to four units packed red blood cells: o

May use O-negative blood initially if patient unstable

o

Type-specific and cross-m atched blood when it becom es available



One hundred percent oxygen by nonrebreather face m ask

Pediatric Considerations 

Children in hypovolem ic shock should receive 20-m L/kg boluses of crystalloid.



Children in severe hypovolem ic shock should receive 1 m L/kg of packed red blood cells.



Age younger than 8 years is a relative contraindication for diagnostic peritoneal lavage.

P.11

ED Treatment 

Nasogastric tube placem ent: o

Will decrease aspiration risk

o

Place nasogastric tube before perform ing diagnostic peritoneal lavage to decom press stom ach and reduce risk of iatrogenic injury.

o

May relieve respiratory distress in cases of diaphragm atic injury with herniated abdom inal contents in the thorax





Foley catheter placem ent: o

Insert after ruling out urethral injuries

o

Facilitates rapid assessm ent of genitourinary injury

o

Assists in m onitoring of urinary output

Tetanus toxoid if appropriate; tetanus im m une globulin if

Pa ge 1 8 2

prim ary tetanus series not adm inistered

Medication (Drugs) 

Tetanus toxoid: 0.5 m L intram uscularly



Tetanus im m unoglobulin: 250 units intram uscularly for patients who have not had a com plete series



Intravenous antibiotics: broad-spectrum aerobic with anaerobic coverage such as second generation cephalosporin

Follow-Up Disposition Admission Criteria 

Patients requiring abdom inal surgery



Observe the following patients for at least 8 hours: o

Patients with negative findings on diagnostic peritoneal lavage, CT, or ultrasound. During hospitalization, the following are necessary: 

Frequent abdom inal exam ination



Repeated hem atocrit levels at regular intervals

Discharge Criteria Patients with stab wounds without fascial penetration m ay be discharged after observation in the em ergency departm ent.

References 1. Feliciano DV, Rozycki GS. The m anagem ent of penetrating abdom inal traum a. Adv Surg. 1995;28:1â€“39. 2. Ferrada R, Birolini D. New concepts in the m anagem ent of patients

Pa ge 1 8 3

with penetrating abdom inal wounds. Surg Clin North Am . 1999;79:1331â€“1356. 3. Kirkpatrick AW, et al. The hand-held ultrasound exam ination for penetrating abdom inal traum a. Am J Surg. 2004;187:660â€“665. 4. Leppaniem i A, Haapiainen R. Diagnostic laparoscopy in abdom inal stab wounds: a prospective, random ized study. J Traum a. 2003;55:636â€“645. 5. Thal ER. Evaluation of peritoneal lavage and local exploration in lower chest and abdom inal stab wounds. J Traum a. 1979;17:642. 6. Thom pson JS, Moore EE, Van Duzer-Moore S, et al. The evolution of abdom inal stab wound m anagem ent. J Traum a. 1980;20:478. 7. Velm ahos GC, et al. Selective nonoperative m anagem ent in 1,856 patients with abdom inal gunshot wounds: should routine laparotom y still be the standard of care? Ann Surg. 2001;234:395â€“402.

Codes ICD9-CM 868.00

ICD10 S31.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abo rtio n, Spo ntaneo us

Abortion,

Spontaneous Aviva Jacoby Zigman

Basics Description 

Spontaneous term ination of a <20-week intrauterine pregnancy



Vaginal bleeding in the first trim ester seen in 20â€“25% of pregnant patients: o

50% of these wom en will eventually m iscarry.

Definitions 

Threatened abortion: vaginal bleeding, cervical os is closed, viable intrauterine pregnancy confirm ed



Inevitable abortion: vaginal bleeding, cervical os is open



Incom plete abortion: vaginal bleeding, cervical os is open with partial passage of products of conception (POC) and som e retained POC



Com plete abortion: vaginal bleeding, cervical os closed, com plete passage of POC



Anem bryonic gestation (m issed abortion): nonviable intrauterine pregnancy, os closed, with or without vaginal bleeding

Pa ge 1 8 5

Etiology 

Risk factors include increased age of both the m other and father, increased parity.



Most early m iscarriages are from abnorm alities of the fetus.

Diagnosis Signs and Symptoms 

Lower abdom inal pain, cram ping



Vaginal bleeding with or without passage of clots or products of conception



Dizziness or syncope



Known positive pregnancy test or sexually active with a period of am enorrhea

History 

Last m enstrual period (LMP)



Duration and am ount of bleeding (quantify by num ber of pads used, com pare with norm al m enstrual period for patient)



Passage of clots



Presence of abdom inal pain, fevers, dizziness, or light-headedness

Physical Exam 

Determ ine hem odynam ic status of patient: o

Pregnant patients in late first trim ester have an increased blood volum e.

o

Can lose substantial am ount of blood before having abnorm al vital signs



Pelvic exam :

Pa ge 1 8 6

o

Determ ine whether the internal cervical os is opened or closed

o

Am ount of bleeding

o

Presence of POC

o

Presence of adnexal tenderness or peritoneal irritation can be consistent with an ectopic pregnancy.



Bim anual exam to determ ine the size of the uterus: o

Size of an orange: 6â€“8 weeks

o

Fundus at the sym physis pubis: 12 weeks

o

Fundus at the um bilicus: 16â€“20 weeks

o

Confirm pregnancy with urine or serum testing.

o

Rapid hem oglobin determ ination: type and Rh

Essential Workup 

Pregnancy test as below



Im aging as below

Tests Lab 

Confirm pregnancy with a urine or serum test: o

Urine pregnancy test: m ost are positive at Î²-hCG levels of 50 m IU/m L approxim ately 1 week gestational age and rem ain positive 2â€“3 weeks after induced or spontaneous abortions.



CBC, type and Rh



Type and cross-m atch for wom an with low Hct or signs of active blood loss



Quantitative Î²-hCG if indicated (see below)



Any POC passed should be sent to pathology for confirm ation.

Imaging

Pa ge 1 8 7







Vaginal ultrasound (TVS): o

Gestational sac seen at 5 weeks

o

Cardiac activity seen at 6.5 weeks

Abdom inal ultrasound (TAS): o

Gestational sac at 6 weeks

o

Cardiac activity seen at 8 weeks

Discrim inatory zone: level of Î²-hCG where a norm al IUP should be detected: o

1500â€“2000 for TVS

o

6500 for TAS

Differential Diagnosis 



Positive pregnancy test with vaginal bleeding: o

Cervicitis

o

Ectopic pregnancy

o

Traum a

o

Septic abortions

o

Molar pregnancy

Second- and third-trim ester vaginal bleeding: o

Placenta previa

o

Placental abruption

Treatment Pre Hospital Cautions: 

Patients with SAB/vaginal bleeding can have severe hem orrhage and present in shock, especially at >12 weeks.



Blood pressure drops during the second trim ester of pregnancy with an average of 110/70.

Pa ge 1 8 8



IV fluids, oxygen, and cardiac m onitor

Initial Stabilization 



Stable patients: o

IV

o

Pelvic exam

Unstable patients: o

Oxygen, IV fluids via two large-bore IVs, cardiac m onitor

o

Transfuse PRBC if patient does not stabilize after 2â€“3 L of crystalloid.

o

Gynecologic consultation im m ediately

o

Oxytocin or m ethylergonovine m ay be necessary to control hem orrhage.

o

These patients are at high risk for having ruptured ectopic pregnancies and m ay need em ergent operative intervention.

P.13

ED Treatment 

Threatened abortion: o

Pelvic rest, close follow-up with obstetrics

o

Patients <6.5 weeks pregnant with no docum ented cardiac activity by vaginal ultrasound need to be followed with serial Î²-hCG to assess the viability of the fetus and to rule out ectopic pregnancy.



Inevitable and incom plete abortions: o

Dilation and curettage or evacuation, rem oval of POC at the cervical os to help decrease bleeding and cram ping

o

The confirm ation of POC by pathology rules out

Pa ge 1 8 9

ectopic pregnancy. 

Com plete abortion: o

May treat with m ethylergonovine or oxytocin if bleeding is heavy

o

If quantitative Î²-hCG is <1,000 and the ultrasound is negative, m ay follow-up with obstetrics for serial Î² -hCG to confirm the levels are decreasing



Missed abortion: o

These patients are at risk for dissem inated intravascular coagulation (DIC), especially if fetus is retained >4â€“6 weeks.

o

Obtain CBC, PT/PTT, fibrin-split products (FSP), and fibrinogen levels.

o

These patients m ay be followed closely as outpatients if stable with an early, confirm ed IUP and no evidence of DIC.

o

Patients m ay choose to have a dilation and curettage at a later date or m iscarry at hom e with no intervention; this decision should be done with consultation of ob-gyn.

Medication (Drugs) 

Oxytocin: 20 IU in 1,000 m L of NS at a rate of 20 m IU/m in titrated to decrease bleeding; m ay repeat for a m ax. dose of 40 m IU/m in



Methylergonovine: 0.2 m g IM/PO q.i.d. PRN bleeding



RHO im m une globulin in Rh-negative wom en: o

50 Âµg for wom en with threatened or com plete abortion at <12 weeks

o

300 Âµg for wom en with threatened or com plete abortion at â‰¥12 weeks

Pa ge 1 9 0



Patients need RhoGAM adm inistration within 72 hours to prevent future isoim m unization.

Follow-Up Disposition Admission Criteria 

Suspected unstable ectopic pregnancy (see Ectopic Pregnancy)



Hem odynam ically unstable patients with hypovolem ia or anem ia



DIC



Septic abortions



Suspected gestational trophoblastic disease

Discharge Criteria 

Dilation and curettages can be done in the ED for incom plete and inevitable abortions, and patients m ay be discharged hom e if stable after 2 to 3 hours.



Som e early inevitable m iscarriages can be discharged to com plete their m iscarriages at hom e without a D&C. Discharge with pain m edications and OB/Gyn close FU



Patients with threatened abortions should be told to avoid strenuous activity.



Pelvic rest, i.e., â€œnothing in the vaginaâ€• during active bleeding; m ay increase risk of infection



Patients should be instructed to return to the ED for any increase in bleeding, dizziness, or tem perature >100.4Â°F.



Patients and their partners should be told that early m iscarriages are com m on and that they are not anyone's fault.

Pa ge 1 9 1

References 1. Houry D, Abbott J. Problem s in early pregnancy. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:2413â€“2433. 2. Kuhn G. Em ergencies during pregnancy. In: Tintinalli JE, ed. Em ergency Medicine: a Com prehensive Study Guide. 5th ed. New York: McGraw-Hill; 2000:694â€“702. 3. Turner LM. Vaginal bleeding during pregnancy. Em erg Med Clin North Am . 1994;12:45.

Codes ICD9-CM 634.90

ICD10 003

Pa ge 1 9 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abruptio Placentae

Abruptio

Placentae Rebecah M. Wilks

Basics Description 

Rupture of vessels in the decidua basalis leading to prem ature separation of the norm ally im planted placenta occurring after 20 weeks gestation but prior to delivery of the infant



Incidence/prevalence: o

Approxim ately 1% of all pregnancies

o

30% of bleeding episodes in the second half of pregnancy

o

15% of all fetal deaths

o

6% of all m aternal m orality. Risk of recurrence 10â€“20%



Risk factors: o

Maternal hypertension (>140/90)

o

Traum a

o

Increased parity

o

Previous abruption

o

Tobacco use

Pa ge 1 9 3

o

Cocaine abuse

o

Preterm prem ature rupture of m em branes, especially if associated with intrauterine infection or oligohydram nios

o

Polyhydram nios with rapid decom pression on m em brane rupture

o

Precipitous first twin delivery endangers second twin.

o

Fibroids or other uterine or placental abnorm alities

Genetics Inherited throm bophilias also increase the risk of abruption (factor V Leiden, prothrom bin G20210A gene m utations, protein C or S deficiency, antithrom bin deficiency, and others).

Etiology 

Separation of the placenta from the uterine wall



Dissection of blood into the decidua basalis or m echanical shearing between the placenta and uterus: o

Clot form ation, bleeding, developm ent of dissem inated intravascular coagulation (DIC), and m aternal-fetal com prom ise



Prim ary cause unknown



Spontaneous dissection of blood into the decidua basalis



Blunt abdom inal traum a



Drugs, especially sym pathom im etics

Diagnosis Signs and Symptoms 

Typically in second half of pregnancy



Vaginal bleeding (>80%, usually painful)



Abdom inal pain (>50%)

Pa ge 1 9 4



Uterine cram ps, tenderness, frequent contractions, or tetany



Back pain



Nausea, vom iting

History 

History of recent traum a should be elicited



Recent drug use, particularly cocaine or other sym pathom im etics

Physical Exam 

Signs of hypotensive shock m ay be present.



Uterine tenderness



Nontender uterus m ay occur with com plete abruption



Petechiae, bleeding, and other signs of DIC or coagulopathy



Decreased fetal heart tones and m ovem ent

Pediatric Considerations 

Sterile vaginal exam ination m ust be perform ed with great caution to avoid tissue injury, especially if placenta previa suspected: o

Assess for presence of am niotic fluid (Nitrazine paper turns blue, or ferning of fluid on glass slide)

o

Evaluate for vaginal or cervical lacerations.

o

Bleeding m ay be concealed in 20â€“25%.

Essential Workup 

Blood type, Rh, and cross-m atch



Rapid hem oglobin determ ination



Determ ine fetal heart tones by Doppler.



Fetal m onitoring is sensitive for detecting early fetal distress.



Uterine tocographic m onitoring m ay dem onstrate frequent

Pa ge 1 9 5

contractions and possible tetany.

Tests Lab 

Blood type and Rh



CBC, platelets



PT/PTT (anticipate consum ptive coagulopathy)



Fibrinogen levels (norm ally 450 in latter half of pregnancy)



Fibrinogen <200 m g/dL and platelets <100,000/ÂµL highly suggestive of abruption



Fibrin-split products



Kleihauer-Betke

Imaging 

Ultrasound dem onstrates evidence of abruption in only 50% of cases.



False-negative com m on with posterior abruptions (concealed hem orrhage)



MRI m ost sensitive in detecting sm all or posterior abruption

P.15

Differential Diagnosis 

Placenta previa (typically associated with less pain)



Vasa previa



Bleeding during labor



Vaginal or cervical lacerations



Uterine rupture



Preterm labor



Ovarian torsion



Pyelonephritis

Pa ge 1 9 6



Cholelithiasis/cholecystitis



Pre-eclam psia com plications



Other blunt intra-abdom inal injuries

Treatment Pre Hospital 

Patients with abruption m ay be in shock and need full resuscitative m easures.



Hypotension frequently occurs late in the course of hypovolem ic shock in pregnancy.



In advanced pregnancy, transport in the left lateral recum bent position.

Initial Stabilization 

Airway, breathing, circulation (ABCs), oxygen



Cardiac m onitor



Placem ent of large-bore IVs



IV crystalloid resuscitation

ED Treatment 

Maternal cardiac and tocographic m onitoring



Continuous fetal m onitoring



Transfuse PRBCs, fresh frozen plasm a (FFP), platelets as indicated.



Im m ediate ob-gyn consultation



Tocolysis is generally contraindicated, particularly in severe abruption with coagulopathy or fetal com prom ise.



If abruption is suspected in the setting of traum a, m aternal stabilization is of prim ary im portance: o

All indicated radiographs should be perform ed as needed.

Pa ge 1 9 7

Medication (Drugs) RhoGAM in Rh-negative wom en: 

50 Âµg IM in wom en at <12 weeks gestation



300 Âµg IM in wom en at â‰¥12 weeks gestation

Follow-Up Disposition Admission Criteria 

Patients with abruptio placenta m ust be adm itted for m aternal and fetal m onitoring.



Adm it to ICU setting if DIC, am niotic fluid em bolism , or significant hem orrhage occurs.



Victim s of m ultiple traum a with abruption should be adm itted and m anaged in accordance with traum a protocols.



Transportation to higher traum a or obstetric level of care is appropriate if the patient is stable for transfer.

Discharge Criteria 

Patients with no evidence of abruption or other significant injury m ay be discharged after 4â€“6 hours of norm al m aternal and fetal m onitoring.



Discharge instructions include pelvic rest, no intercourse, no heavy lifting, no prolonged standing.

References 1. Baron F, Hill WC. Placenta previa, placenta abruptio. Clin Obstet Gynecol. 1998;41(3):527â€“532.

Pa ge 1 9 8

2. Gabbe SG, Niebyl JR, Sim pson JL, eds. Obstetrics: Norm al and Problem Pregnancies. 4th ed. New York: Churchill Livingstone; 2002. 3. Gillen-Goldstein J, Lockwood J. Abruptio placentae. UpToDate. Dec 2004;13:1. 4. Marx J, ed. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO: Mosby; 2002.

Codes ICD9-CM 641.20

ICD10 045.9

Pa ge 1 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abscess, Skin/So ft Tissue

Abscess,

Skin/Soft Tissue Nate Rudman

Basics Description 

A localized collection of pus surrounded and walled off by inflam ed tissue



The collection m ay be classified as bacterial or sterile: o

Bacterial: m ost abscesses are bacterial with the m icrobiology reflective of the m icroflora of the involved body part.

o

Sterile: m ore associated with intravenous drug abuse and injection of chem ical irritants

Pathophysiology Microbiology is related to abscess type: 

Dog/cat bites: o

Pasteurella species/anaerobes

o

Usually polym icrobial

o

Capnocytophaga canim orsus: 

Gram -negative rod associated with severe sepsis from dog bites



Im m unocom prom ised patients

Pa ge 2 0 0

 

25% m ortality

Orbital: o

Associated with paranasal sinusitis, hem atogenous spread, or local skin traum a

o

Organism s include staphylococci, streptococci, Haem ophilus influenza, Escherichia coli.

o 

May be polym icrobial

Breast: dependent on type of abscess: o

o

Puerperal: 

Classically occurs during lactation



Located in peripheral wedge



Caused by staphylococci

Duct ectasia: 

Caused by ectatic ducts



Periareolar location



Caused by several organism s (polym icrobial), with a m ix of staphylococci, anaerobic streptococci, bacteroids, and enterococci



Hidradenitis suppurativa: o

Chronic abscesses of apocrine sweat glands: 

o

Groin and axilla

Staphylococcus aureus and Staphylococcus viridans com m on pathogens

o

E. coli and Proteus species m ay be present in chronic disease.



Pilonidal abscess: o

Caused by epithelial disruption of gluteal fold over coccyx



o

Staphylococcal species m ost com m on

o

May be polym icrobial with bacteroides and E. coli

Bartholin abscess: o

Obstruction of Bartholin duct

Pa ge 2 0 1

o

Mixed vaginal flora

o

May include Neisseria gonorrhoeae, Chlam ydia trachom atis, and E. coli



Perirectal: o

Originates in anal crypts and extends through ischiorectal space

o

Inflam m atory bowel disease and diabetes are m ajor predisposing factors.

o

Bacteroides fragilis and E. coli m ost com m on pathogens

o 

Requires treatm ent in operating room

Muscle (pyom yositis): o

Typically occurs in tropics

o

Increasingly com m on in patients with hum an im m unodeficiency virus or diabetes

o 

S. aureus m ost com m on

Intravenous drug abuse: o

Most com m on pathogens staphylococcal species, Streptococcus m illeri, and anaerobes





o

Methicillin-resistant S. aureus (MRSA) com m on

o

Isolates often oral origin

o

May be sterile

Furuncle: o

Arises from infected hair follicle

o

Most com m on on back, axilla, and lower extrem ities

o

Staphylococcal species m ost com m on

o

Com m unity-acquired MRSA increasingly com m on

Carbuncle: o

Larger and m ore extensive than furuncle

o

Often m ultiple in honeycom b pattern on back of neck

o

More com m on in diabetics

o

Usually caused by staphylococci

Pa ge 2 0 2

o 



Com m unity-acquired MRSA increasingly com m on

Paronychia: o

Infection surrounding the nail fold

o

Usually caused by S. aureus

Felon: o

Closed-space abscess in distal pulp of finger

o

Usually caused by S. aureus

Etiology Conditions associated with soft-tissue abscess form ation include the following: 

Soft-tissue traum a



Mam m alian bites



Bacterem ia with hem atogenous seeding



Obstruction of norm al drainage (i.e., sweat glands)



Tissue ischem ia



Intravenous drug use



Endocarditis



Lactation disease



Crohn disease

Diagnosis Signs and Symptoms 

Local: o

Erythem a, tenderness, pain, heat, swelling, fluctuance



System ic: o

Ranges from absent to fever, rigors, hypotension, and altered m entation



Regional lym phadenopathy and lym phangitis m ay occur.

Pa ge 2 0 3



May be associated with surrounding cellulitis

Essential Workup 

History and physical exam ination: o

Identify subcutaneous air and involvem ent of deeper structures.



Gram stain unnecessary for sim ple abscesses in healthy patients



Wound cultures: o

Not indicated in sim ple abscesses unless MRSA is a consideration

o

May help differentiate aerobic from anaerobic infections

o

May be useful in confirm ing com m unity-acquired MRSA in patients with recurrent abscesses

o

May guide specific therapy in a com prom ised host, abscesses of the central face or hand, and treatm ent failures

Tests Lab 

Glucose determ ination is a useful screening test for diabetics.



CK if m yositis suspected



Blood cultures indicated if endocarditis is suspected or patient is system ically ill

Imaging 

Plain film s m ay reveal gas in tissue planes.



Ultrasound, CT, or MRI helpful when diagnosis is in question

Differential Diagnosis 

Cellulitis

Pa ge 2 0 4



Aneurysm (especially with intravenous drug abusers)



Cysts



Hem atom a

P.17

Treatment Pre Hospital Caution: septic patients m ay require rapid transport with intravenous access and volum e resuscitation.

Pediatric Considerations Incision and drainage are painful procedures that often require procedural sedation and analgesia.

Initial Stabilization Septic patient: 

Im m ediate intravenous access



Oxygen



Crystalloid volum e resuscitation



Central venous pressure m onitoring



Mixed venous sam pling



Blood cultures



Early antibiotic therapy

ED Treatment 

Incision and drainage are the m ainstays of treatm ent.



Antibiotics are indicated for the following conditions: o

Sepsis

o

System ic illness

Pa ge 2 0 5

o

Endocarditis

o

Facial abscesses drained into the cavernous sinus

o

Concurrent cellulitis (see Medication)

o

Mam m alian bites

o

Im m unocom prom ised hosts

Medication (Drugs) 

Augm entin (particularly m am m alian bites): 250â€“500 m g PO q8h (pediatric dose: 40â€“80 m g/kg per day divided into three doses)



Cephalexin: 250â€“500 m g PO q8h or 500 m g PO q12h (pediatric dose: 25â€“50 m g/kg per day PO in four doses)



Clindam ycin (MRSA): 150â€“450 m g PO q6h (pediatric dose: 10â€“20 m g/kg per day PO or IV in threeâ€“four divided doses)



Dicloxacillin: 250â€“500 m g PO q6h (pediatric dose: 50â€“100 m g/kg per day in four divided doses)



Erythrom ycin: 500 m gâ€“1 g PO or IV q6h (pediatric dose: 40 m g/kg per day PO divided q6h)



Gentam icin: 5 m g/kg per day IV q24h (pediatric dose: 7.5 m g/kg per day IV divided q8h)



Levaquin: 500 m g IV q24h (contraindicated in children)



Rifam pin (MRSA): 300 m g PO q.i.d. (pediatric dose 10 m g/kg up to 300 m g)



Septra DS (MRSA): one tab PO b.i.d. (pediatric 5 m L susp/10 kg up to 20 m L per dose)



Unasyn: 1.5â€“3.0 g IV q6h (pediatric dose: <40 kg, 300 m g/kg per day divided q6h; â‰¥40 kg, adult dose)



Vancom ycin: 1 g IV q12h (pediatric dose: 40 m g/kg per day IV divided q6h)

Pa ge 2 0 6

Surgery Perirectal abscess requires treatm ent in the operating room .

Follow-Up Disposition In accordance with abscess type and severity of infection

Admission Criteria 

Sepsis



Endocarditis



System ic illness



Perirectal involvem ent



Any abscess requiring incision and dÃ©bridem ent in the operating room

Discharge Criteria Most patients with uncom plicated abscesses can be treated with incision and drainage and close follow-up.

References 1. Benson EA. Managem ent of breast abscesses. World J Surg. 1989;13:753â€“756. 2. Buescher ES. Com m unity-acquired m ethicillin-resistant Staphylococcus aureus in pediatrics. Curr Opin Pediatr. 2005;17(1):67â€“70. 3. Canales FL, Newm eyer WL, Kilgore ES. The treatm ent of felons and paronychias. Hand Clin. 1989;5:515â€“522. 4. Chiedozi LC. Pyom yositis: review of 205 cases in 112 patients. Am J Surg. 1979;137:255â€“259. 5. Loyer EM, DuBrow RA, David CL, et al. Im aging of superficial soft-tissue infections: sonographic findings in cases of cellulitis and

Pa ge 2 0 7

abscess. AJR. 1995;166:149â€“152. 6. Sum m anen PH, Talan DA, Strong C, et al. Bacteriology of skin and soft-tissue infections in intravenous drug users and individuals with no history of intravenous drug use. Clin Infect Dis. 1995;20(Suppl 2):S279â€“282. 7. Talan DA, Citron DM, Abraham ian FM, et al. Bacteriologic analysis of infected dog and cat bites. N Engl J Med. 1999;340:85â€“92.

Codes ICD9-CM 682.9

ICD10 L02.9

Pa ge 2 0 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abuse, Elder

Abuse, Elder

Helen Straus

Basics Description Elder abuse m ay include the following: 





Em otional abuse: o

Insults

o

Hum iliation

o

Threats to institutionalize or abandon

Physical and/or sexual abuse: o

Hitting

o

Slapping

o

Pushing

o

Burning

o

Inappropriate restraining

o

Forced sexual activity

Material exploitation: o

Stealing or coercion involving patient m onies or property



Neglect: o

Behaviors by a patient or caregiver that com prom ise the patient's health or safety

o

Failure to provide adequate food, shelter, hygiene,

Pa ge 2 0 9

and/or m edical attention

Epidemiology Incidence In the United States, one m illion known cases annually (estim ated 5 m illion cases): 

2% reported by physicians

Etiology 

Caregiver stress, dependency, or psychopathology



Victim dependency or dim inishm ent of ability to perform activities of daily living

Diagnosis Essential Workup 

Obtain history without fam ily m em bers/caregivers present: o

Abused elders m ay fear institutionalization if they report caregivers

o

Many m ay feel em barrassm ent and responsibility for abuse

o

Frequently will not volunteer inform ation

o

Ask patient specifically about abuse or neglect (in private)

o

Patient's m edical condition m ay influence quality of history obtained



Obtain history from caregivers/other relatives/friends/neighbors



Docum ent a clear and detailed description of findings including the following: o

Statem ents of the patient as they pertain to the

Pa ge 2 1 0

abuse o

o

Psychosocial history: 

Fam ily and other social relationships



Caregiver burdens/coping m echanism s



Drug/ethanol (EtOH) use



Prior adult protective services reports

Skin and other physical findings: 



Photographic docum entation

Safety assessm ent

Signs and Symptoms Variable, possibly inconsistent, history or physical findings

History 

Not willing or able to obtain adequate food/clothing/shelter



Not providing for personal hygiene/safety



Delay in obtaining m edical care/previously untreated m edical condition



Vague (or im plausible/inappropriate) explanations



Disparities between histories given by patient and caregiver



Caregiver who insists on giving the patient's history



Medication difficulties:





o

Incorrect doses

o

Lost m edications

o

Unfilled prescriptions

Altered interpersonal interactions: o

Withdrawn

o

Indifferent

o

Dem oralized

o

Fearful

o

Substance abuse

Caregiver with:

Pa ge 2 1 1

o

Financial dependence on patient

o

Substance abuse or psychiatric or violence history

o

Controlling behavior (m ay refuse to leave elder alone with physician) or poor knowledge

o

Significant life stressors

o

Relationship issues

o

Financial difficulties

o

Legal problem s

Physical Exam 

Inconsistent findings: o

Patterns or variable-age bruises, burns, lacerations/abrasions

o

Unusual sites of bruising (inner arm , torso, buttocks, scalp)

o 



Poor hygiene (inadequate care of skin, nails, teeth)

Unexplained injuries: o

Bruised or bleeding genital or rectal area

o

Wrist or ankle lesions suggestive of restraint use

Findings perhaps consistent with neglect or delay in seeking/obtaining m edical attention: o

Dehydration

o

Weight loss

o

Decubitus ulcer

o

Malnutrition

Tests Perform any exam ination and laboratory or radiographic studies as indicated by the patient's condition.

Differential Diagnosis Patient m ay present with any chief com plaint: 

Potential differential diagnosis is nonspecific



Abuse best identified by asking patient directly in a setting

Pa ge 2 1 2

apart from caregivers/fam ily and correlating with risk factors and provider findings 

Differentiate findings consistent with other disease causes from abuse/neglect: o

Dehydration

o

Ill-fitting dentures

o

Burns

o

Ecchym oses

o

Insom nia

o

Medication noncom pliance

o

Dem entia

o

Depression

Treatment Pre Hospital Observe details of the patient's environm ent that m ay not be im m ediately available to the hospital care team , including the following: 

Interpersonal interactions at the scene: o

Em barrassm ent

o

Sham e

o

Fear of reprisal, abandonm ent, and/or institutionalization



Conditions in the physical environm ent to determ ine potential danger areas

P.19

Initial Stabilization

Pa ge 2 1 3



ABCs (airway, breathing, circulation)



Treat life-threatening m edical/traum atic conditions as appropriate.

ED Treatment 

May require separation of the patient and the caregiver or fam ily m em ber





Social work referral: o

Safety planning

o

Respite planning for caregiver

o

Adult protective services referral

Com petent elder patients are free to accept or decline treatm ent or disposition despite risks they m ay incur.



General m easures appropriate to the m edical/traum atic conditions identified, including: o

Fluids

o

Medications

o

Surgery

o

Diet

o

Activity

o

Nursing care

o

Physical therapy

Follow-Up Disposition Disposition determ ined by m edical condition and hom e environm ent

Admission Criteria 

Medical condition requiring adm ission



Abuse or neglect renders hom e conditions unsafe.

Pa ge 2 1 4

Discharge Criteria 

Medical condition(s) addressed



Safe environm ent available



Abuse or neglect successfully countered by social services and/or law enforcem ent

Issues for Referral 

Many states have m andatory reporting requirem ents: o

Com ply with area legal requirem ents.



EtOH/drug treatm ent as appropriate



Notify adult protective services.

References 1. Clarke ME, Pierson W. Managem ent of elder abuse in the em ergency departm ent. Em erg Med Clin North Am . 1999;17:631â€“644. 2. Kruger RM, Moon CH. Can you spot the signs of elder m istreatm ent? Postgrad Med. 1999;106:169â€“183. 3. Lachs MS, Pillem er K. Elder abuse. Lancet. 2004;364:1263â€“1272. 4. Levine JM. Elder neglect and abuseâ€”a prim er for prim ary care physicians. Geriatrics. 2003;58(10):37â€“40, 42â€“44. 5. Marshall CE, Benton D, Brazier JM. Elder abuse: using clinical tools to identify clues of m istreatm ent. Geriatrics. 2000;55:42â€“53.

Codes ICD9-CM V61.3

ICD10 T74.1

Pa ge 2 1 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abuse, Pediatric (No naccidental Traum a [NAT])

Abuse, Pediatric (Nonaccidental Trauma [NAT]) Suzanne Z. Barkin

Basics Description 

Child abuse effects up to 14 m illion or 2â€“3% of U.S. children each year.



1,200â€“1,400 children die of m altreatm ent each year in the United States, 80% <5 years and 40% <1 year.



Mandated reporters of suspected abuse or neglect include all health care workers



Risk factors: o

Child: usually <4 years, often handicapped, retarded, or special needs (â€œvulnerable childâ€•), prem ature birth, m ultiple birth

o

Abusive parent: low self-esteem , abused as child, violent tem per, m ental illness history, rigid and unrealistic expectations of child, young m aternal age

o

Fam ily: m onetary problem s, isolated and m obile, m arital instability

o

Poor parentâ€“child relationship, unwanted

Pa ge 2 1 6

pregnancy o

Abuse crosses all religious and socioeconom ic groups

Diagnosis Signs and Symptoms History 

History and m echanism inconsistent with the injury or illness:



o

Unexplained death, apnea, injury

o

Unexplained ingestion or toxin exposure

o

Recurrent injury

Parent/caregiver reluctant to give inform ation or denies knowledge of how injury occurred: o

Discrepancy am ong different caregivers



Developm entally, child unable to experience m echanism



Inappropriate response to injury or illness; delay in seeking care



MÃ¼nchhausen by proxy: o

Recurrent illness without m edical explanation

o

Unexplained m etabolic disorder suspicious for poisoning



Failure to thrive: o

Inadequate caloric intake secondary to poor m aternal bonding/neglect

o

Review of past ED encounters and contact with the patient's prim ary care physician m ay be helpful.

Physical Exam 

Cutaneous bruising/contusions: o

Regular pattern, straight line of dem arcation, regular

Pa ge 2 1 7

angles, slap m arks from fingers, dunking burns (stocking or glove burns or doughnut shaped on buttock), bites, strap, buckle o

Location: buttocks, hips, face (not forehead), arm s, back, thighs, genitalia, pinna

o

Aging: 

Often different ages



Yellow bruises are older than 18 hours



Red, blue and purple, or black color m ay occur from 1 hour after injury to resolution.



Red m ay be present irrespective of age



Bruises of identical age and cause on the sam e person m ay appear to be different.



Skeletal traum a: o

Usually m ultiple, unexplained, various stages of healing

o

Metaphyseal or corner (classic m etaphyseal lesions) fractures (pathognom onic)

o

Skull fractures that cross suture lines

o

Posterior rib fractures (rib fractures alm ost never occur in infants from CPR)

o

Spiral fractures of long bones

o

Subperiosteal new bone form ation

o

Uncom m on fractures (vertebrae, sternum , scapula, spinous process) without significant m echanism



Central nervous system : o

Altered m ental status, seizure

o

Head traum a is leading cause of death in child abuse.

o

Skull fracture; m ust consider child abuse in children <1 year

o

Subdural hem atom a, subarachnoid hem orrhage

o

Shaken baby syndrom e with shearing and rotational

Pa ge 2 1 8

injury 

Ocular findings: o

Retinal hem orrhage or detachm ent

o

Hyphem a

o

Corneal abrasion/conjunctival hem orrhage



Oral traum a



Abdom inal injuries:



o

Lacerated liver, spleen, kidney, pancreas

o

Intram ural hem atom a (duodenal m ost com m on)

o

Retroperitoneal hem atom a

Anogenital/sexual abuse: o

Credible history

o

Contusion, erythem a, open wounds, scarring, foreign m aterial (hair, debris, sem en)

o

Presence of sexually transm itted disease (STD) or pregnancy in child <12 years



Death: o

Unexplained death

Essential Workup 

Form al oral and written report to appropriate child welfare agency



Fam ily and environm ental evaluation, usually in cooperation with responsible child welfare agency



Diagram or photograph of bruises is helpful.

Alert When suspected, health professionals have a legal obligation to report their suspicion to the appropriate authorities.

Tests Lab 

Bleeding screen if there is a history of recurrent bruising

Pa ge 2 1 9

or bruising is the prom inent m anifestation; m ay usually be done electively: CBC, platelets, PT/PTT, bleeding tim e 

If significant blunt traum a, CBC, liver function test (LFT), am ylase, urinalysis



Toxicology, chem istry, and m etabolic screens in children with altered m ental status



Consider other differential considerations.

Imaging 

Global assessm ent: o

Indicated for children <2 years to exclude unsuspected injuries

o

In children 2â€“5 years, in selected cases where physical abuse is strongly suspected

o

In older children, radiographs of individual sites of injury suspected on clinical grounds

o

o

Radiographic skeletal survey: 

Anteroposterior (AP) and lateral skull



Lateral cervical spine



AP and lateral thoracic and lum bar spine



AP and obliques of chest



AP pelvis



AP hum erus, forearm , and hands (bilateral)



AP fem ur, tibia, and feet (bilateral)

If fracture identified, get at least two views, 90 degrees to original view.

o

May need coned-down view of joints for visualization of classic m etaphyseal lesions

o

Skeletal scintigraphy provides adjunctive screening if suspicion exists beyond skeletal survey.



Visceral im aging: o

Suspected thoracoabdom inal injury 

Abdom inal CT scan with IV and oral contrast

Pa ge 2 2 0



Barium upper gastrointestinal (GI) study for gastric and intestinal hem atom a



Neuroim aging: o

Nonenhanced head CT with brain, subdural and bone windowing

o

MRI

o

Adjunctive in evaluation of acute, subacute, and chronic intracranial injury; useful for shear injuries, evolving hem orrhage, contusion, secondary hypoxic/ischem ic injury

P.21

Differential Diagnosis 

General: o



Traum aâ€”accidental or birth/obstetrical

Cutaneous: o

Burnâ€”accidental

o

Infection

o

Im petigo/cellulitis

o

Staphylococcal scalded skin syndrom e

o

Henoch-SchÃ¶nlein purpura

o

Purpura fulm inans/m eningococcem ia

o

Sepsis

o

Derm atitis: contact or photo

o

Hem atologic/oncologic disorder (idiopathic throm bocytopenic purpura [ITP], leukem ia)



o

Bleeding diathesis (hem ophilia, von Willebrand)

o

Nutritional deficiency: scurvy

o

Cultural healing practices (coining, cupping)

Skeletal: o

Osteogenesis im perfecta

Pa ge 2 2 1



o

Nutritional (rickets, copper deficiency, scurvy)

o

Menkes syndrom e

o

Peripheral sensory im pairm ent (indifference to pain)

Ocular: o



Conjunctivitis

Abdom en and genitourinary (GU) tract: o

GI disease (obstruction, peritonitis, inflam m atory bowel disease)

o 

CNS: o





GU tract infection/anom aly

Intoxication, ingestion (CO, lead, m ercury)

Infection: o

Metabolic: hypoglycem ia

o

Epilepsy

Death: o

Sudden infant death syndrom e (SIDS), apparent life-threatening event (ALTE)

Treatment Pre Hospital 

Diagnosis relies on physical evidence in child and inconsistency with the history and m echanism .



Exam ination of the scene m ay be useful: o

Evaluate validity of m echanism s.

o

General appearance of hom e

o

Consistency of history by m ultiple caregivers

o

Evaluation of parentâ€“child interaction

Initial Stabilization As indicated by specific injury

Pa ge 2 2 2

ED Treatment 

Medical and traum a m anagem ent as required



Mandatory reporting to local child welfare agency of any suspected child abuse to determ ine appropriate social disposition: o

This does not im ply 100% certainty. Expedited fam ily, environm ental, and social evaluation



Com m unication with fam ily about report and prim ary concern is child's welfare. o



Security m ay be required to protect child and staff.

Siblings and other household children m ust be exam ined in appropriate tim e fram e.

Follow-Up Disposition Admission Criteria 

Observation and intervention for traum atic injury



Concerns about disposition or lack of availability of child welfare receiving site, if required



Goal m ust always be to ensure safety of child and siblings.

Discharge Criteria 

Adequate ED evaluation and m edical follow-up



Safe setting for child m ust determ ine disposition.



Child (and siblings) m ay require placem ent in foster care.

References 1. Am erican Academ y of Pediatrics, section of radiology. Diagnostic im aging of child abuse. Pediatrics. 2000;105:1345. 2. Duhaim e AC, Christian CW, Rorke LB, et al. Nonaccidental head

Pa ge 2 2 3

injury in infants: the â€œshaken baby syndrom eâ€•. New Eng J Med. 1998;338:1822. 3. Gayle MO, Kissoon N, Hered RW, et al. Retinal hem orrhage in the young child: a review of etiology, predisposed conditions and clinical im plications. J Em erg Med. 1995;13:233. 4. Kleinm an PK, ed. Diagnostic Im aging of Child Abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 5. Schreier HA, Libow JA. Munchausen by proxy syndrom e: a m odern pediatric challenge. J Pediatr. 1994;125:S110â€“115. 6. Schwartz AJ, Ricci LR. How accurately can bruises be aged in abused children? Literature review and synthesis. Pediatrics. 1996;97:254. 7. Steward GM, Rosenberg NM. Conditions m istaken for child abuse. Parts 1 and 2. Pediatr Em erg Med. 1996;12:116.

Miscellaneous SEE ALSO: Traum a, Multiple

Codes ICD9-CM 995.9

ICD10 T74.8

Pa ge 2 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acetam ino phen Po iso ning

Acetaminophen

Poisoning Mark B. Mycyk

Basics Description 

Acetam inophen (APAP) is available alone, in com bination with oral narcotics, and in >100 cold rem edies: o

It is one of the m ost com m on drugs im plicated in intentional and unintentional poisonings.



N-acetyl-p-benzoquinoneim ine (NAPQI) produced when APAP m etabolized by cytochrom e P-450: o

NAPQI norm ally detoxified by glutathione

o

In overdose, glutathione is quickly depleted and NAPQI causes hepatic dam age.

o

N-acetylcysteine (NAC) replenishes the liver's glutathione stores.



Increased risk of toxicity: o

Increased activity of cytochrom e P-450 system (phenobarbital, rifam pin)

o

Patients with poor nutrition have decreased glutathione stores.

Pharmacokinetics

Pa ge 2 2 5



APAP half-life: o

2.5â€“4 hours in a nonoverdose setting

o

>4 hours in overdose



Toxic dose >150 m g/kg acutely



Probable toxic level is 140 Âµg/m L at 4 hours postingestion (see Fig. 1 nom ogram for acute intoxication).



Therapeutic plasm a concentration is 5â€“20 Âµg/m L.

Diagnosis Signs and Symptoms Acute Overdose 



Phase 1: 0.5â€“24 hours postingestion: o

Nausea, vom iting, m alaise

o

Occurs with large overdoses

o

May not be present with sm aller toxic doses

Phase 2: 24â€“72 hours postingestion: o

Decreased GI sym ptom s

o

Hepatic dam age is occurring.

o

Right upper quadrant pain and tenderness

o

Elevation of liver enzym es, PT/INR, bilirubin

o

Oliguria

o

Prolonged (>4 hours) acetam inophen (APAP) half-life im plies hepatic toxicity.



Phase 3: 72â€“96 hours postingestion: o

Critical tim e period in the prognosis

o

Peak liver function abnorm alities

o

Hepatic encephalopathy develops.

o

If the PT/INR continues to rise and/or renal

Pa ge 2 2 6

insufficiency develops beyond the third day postingestion, there is high likelihood that the patient will require hepatic transplantation. 

Phase 4: 96 hours to 10 days postingestion: o

Resolution of hepatic injury or progression to com plete hepatic failure

Fig. 1. Rum ack-Matthew nom ogram . (Adapted from Rum ack BH, Matthew H. Acetam inophen poisoning and toxicity. Pediatrics. 1975;55:871â€“876.

Pa ge 2 2 7

)

Essential Workup 

Ingestion history of all APAP-containing products



Tim e of ingestion



APAP level: o

Obtain 4-hour postingestion level or im m ediately on presentation if >4 hours postingestion.

o

Use Rum ack-Matthew nom ogram as therapeutic guide for single acute overdose.

o

Obtain level, but do not use nom ogram for therapeutic guidance in chronic ingestions or very late ingestions (>24 hours)



Call poison center ([800] 222-1222) or toxicologist.

Tests Lab 

APAP level



Electrolytes, BUN, creatinine, glucose



Liver enzym es: o

Elevated AST is the first abnorm ality detected.

o

AST/ALT levels m ay rise >10,000 in stage III of toxicity.

o

Bilirubin



PT/INR



Pregnancy test

Differential Diagnosis 

Suspect APAP as coingestant with other drugs in overdose.



Causes of acute onset hepatotoxicity: o

Infectious hepatitis

o

Reye syndrom e

o

Am anita sp. m ushroom s toxicity

Pa ge 2 2 8

o

Herbal and dietary supplem ents

o

Other drug ingestions

P.23

Treatment Pre Hospital 

Transport all pill bottles/pills involved in overdose for identification in ED.



Over-the-counter cold rem edies often contain acetam inophen.

Initial Stabilization Airway, breathing, circulation (ABCs): 

Adm inister supplem ental oxygen.



Adm inister naloxone, thiam ine, D50 (or Accu-Chek) for altered m ental status.

ED Treatment 



Supportive care: o

IV fluids

o

Antiem etics

Gastric decontam ination: o

Adm inister a single dose of activated charcoal if recent ingestion.

NAC Administration 

Adm inister if toxic level detected as defined by Rum ack-Matthew nom ogram .



NAC virtually 100% hepatoprotective if initiated within 8

Pa ge 2 2 9

hours of an acute overdose 

NAC available in oral form or IV form



<8 hours postingestion: o

Check APAP level.

o

Initiate NAC if APAP level will not be available within 8 hours of ingestion and toxic ingestion suspected.

o 



Discontinue NAC if APAP level nontoxic.

â‰¥8 hours postingestion: o

Initiate NAC im m ediately if suspected toxic ingestion.

o

Check APAP level.

o

Discontinue NAC if APAP level is nontoxic.

>24 hours postingestion or chronic repeated APAP ingestion o

Initiate NAC if: 

Ingestion >150 m g/kg APAP



Sym ptom atic



Abnorm al hepatic screening panel



Discontinue NAC if APAP falls to nondetectable level and no AST elevation occurs by 36 hours postingestion.



Call poison center ([800] 222â€“1222) or toxicologist for help.

Pregnancy Considerations 

No teratogenicity with NAC



NAC m ay be effective in protecting fetal liver: o

Fetal liver m etabolizes APAP to toxic NAPQI after 14 weeks of gestation.

Alert A shortened oral NAC protocol m ay be considered with poison center or toxicology consultation.

NAC Preparations

Pa ge 2 3 0



Oral NAC: o

Poor taste and odor: 

Dilute to 5% with fruit juice or soft drink to increase palatability.

o

Use antiem etics (m etoclopram ide or ondansetron) liberally to facilitate PO adm inistration.

o

If the patient vom its NAC within 1 hour of adm inistration, repeat the dose.

o

Adm inister NAC as a drip through nasogastric (NG) tube if vom iting continues.

o 

Given q4h

IV NAC (two options): o

Acetadote infusion given per m anufacturer's instructions

o

Oral NAC given by IV route if: 

Oral form not tolerated because of vom iting



Acetadote not available



Contact local poison center or toxicologist for help.

Medication (Drugs) 

Activated charcoal: 1â€“2 g/kg PO



Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2â€“4 m L/kg) IV



Metoclopram ide: Start with 10 m g (peds: 1 m g/kg) IV (1 m g/kg m ax.)



N-acetylcysteine (NAC): 140 m g/kg PO loading (adult and pediatric) followed by 70 m g/kg q4h for 17 additional doses



Acetadote: 21-hour IV infusion (see package insert for dosing)

Pa ge 2 3 1



Naloxone (Narcan): 0.4â€“2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Ondansetron: >80 kg, 12 m g; 45â€“80 kg, 8 m g (peds 0.15 m g/kg) IV



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Hepatotoxic level of APAP requiring full course of NAC therapy (see Treatm ent)



Nontoxic suicide attem pt requiring psychiatric treatm ent

Discharge Criteria Asym ptom atic patients with nontoxic ingestions not requiring full course of NAC therapy

Issues for Referral 

Evidence of significant hepatotoxicity at tim e of ED arrival warrants early evaluation by hepatology and/or transplant service.



Consider substance abuse referral for patients with oral narcotic abuse.



Patients with unintentional (accidental) poisoning require poison prevention counseling.



Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.

References 1. Anker AL. Acetam inophen. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders;

Pa ge 2 3 2

2001:265â€“274. 2. Buckley NA, Whyte IM, O'Connell DL, et al. Oral or intravenous N -acetylcysteine: which is the treatm ent of choice for acetam inophen (paracetam ol) poisoning? J Toxicol Clin Toxicol. 1999;37(6):759â€“767. 3. Dargan PI, Jones AL. Acetam inophen poisoning: an update for the intensivist. Crit Care. 2002;6(2):108â€“110. 4. Jones AL. Mechanism of action and value of N-acetylcysteine in the treatm ent of early and late acetam inophen poisoning: a critical review. J Toxicol Clin Toxicol. 1998;36:277â€“285. 5. Rum ack BH. Acetam inophen m isconceptions. Hepatology. 2004;40(1):10â€“15. 6. Sm ilkstein MJ, Knapp GL, Kulig KW, et al. Efficacy of oral n -acetylcysteine in treatm ent of acetam inophen overdose. Analysis of the national m ulticenter study. N Engl J Med. 1988;319:1557â€“1562. 7. Yip L, Dart RC, Hurlbut KM. Intravenous adm inistration of oral N -acetylcysteine. Crit Care Med. 1998;26:40â€“42.

Codes ICD9-CM 965.4

Pa ge 2 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acido sis

Acidosis

Matthew Robinson

Basics Description Respiratory Acidosis 

Reduced pH owing to alveolar hypoventilation with elevated PaCO 2



Defined as PaCO 2 >45 m m Hg or higher than expected for calculated respiratory com pensation for m etabolic acidosis



Divided into three broad categories: o

Prim ary failure in central nervous system drive to ventilate:

o



Sleep apnea



Anesthesia



Sedative overdose

Prim ary failure in transport of CO 2 from alveolar space:

o



Chronic obstructive pulm onary disease



Myasthenic crisis



Severe hypokalem ia



Guillain-BarrÃ© syndrom e

Prim ary failure in transport of CO 2 from tissue to alveoli:

Pa ge 2 3 4



Severe heart failure

Metabolic Acidosis 

Process that reduces serum pH by decreasing plasm a bicarbonate levels





Prim arily caused by: o

Gain of a strong acid through ingestion or m etabolism

o

Loss of bicarbonate from the body

Metabolic acidosis is clinically evaluated by dividing into two m ain groups: o

Elevated anion gap m etabolic acidosis: 

Bicarbonate reduced through buffering of added strong acid



Anion gap is increased owing to retention of the unm easured anion from the titrated strong acid.

o

Norm al anion gap m etabolic acidosis owing to: 

Kidneys fail to reabsorb or regenerate bicarbonate.



Losses of bicarbonate from gastrointestinal tract (diarrhea)



Ingestion or infusion of substances that release hydrochloric acid

o

No anion gap is observed owing to the absence of any unm easured anion of a titrated acid and secondary chloride retention with HCO 3 - loss.

Etiology Anion Gap Acidosis To rem em ber possible causes, use m nem onic A CAT MUD PILES: 

Alcohol ketoacidosis



Carbon m onoxide or cyanide



Aspirin



Toluene

Pa ge 2 3 5



Methanol



Urem ia



Diabetic ketoacidosis



Paraldehyde



Iron/isoniazid



Lactic acidosis



Ethylene glycol



Starvation

Increased Osmolar Gap To rem em ber possible causes, use m nem onic ME DIE: 

Methanol



Ethylene glycol



Diuretics (m annitol; no acidosis)



Isopropyl alcohol (no acidosis)



Ethanol

Non-Anion Gap Metabolic Acidosis 

Gastrointestinal losses of bicarbonate: o

Diarrhea

o

Villous adenom a

o

Rem oval of sm all bowel, pancreatic or biliary secretions



o

Tube drainage

o

Sm all bowel/pancreatic fistula

Anion exchange resins (i.e., cholestyram ine): o

Ingestion of calcium chloride or m agnesium chloride



Renal loss of bicarbonate



Renal tubular acidosis: o

Type I (distal): hypokalem ic hyperchlorem ic m etabolic acidosis: 

Decreased ability to secrete hydrogen



Serum HCO 3 <15 m Eq/L when untreated

Pa ge 2 3 6

o



Potassium low



Renal stones com m on

Type II (proxim al): hypokalem ic hyperchlorem ic m etabolic acidosis: 

Decreased proxim al reabsorption of HCO 3 - .



Acidosis lim ited by reabsorptive capacity of proxim al tubule for HCO 3 -

o



Serum HCO 3 typically 14â€“18 m Eq/L



Low/norm al potassium .

Type IV (hypoaldosteronism ): hyperkalem ic hyperchlorem ic acidosis: 

Aldosterone deficiency or resistance causing decreased H + secretion



Serum bicarb >15 m Eq/L



Norm al/elevated potassium



Carbonic anhydrase inhibitors



Tubulointerstitial renal disease



Hypoaldosteronism



Addition of hydrochloric acid such as: o

Am m onium chloride

o

Arginine hydrogen chloride

o

Lysine hydrogen chloride

Diagnosis Signs and Symptoms 

Nonspecific findings



Vital signs: o

Tachypnea or Kussm aul respirations with m etabolic acidosis

o

Hypoventilation with respiratory acidosis

Pa ge 2 3 7

o

Tachycardia



Som nolence



Confusion



CO 2 narcosis



Myocardial conduction and contraction disturbances

Essential Workup 

Electrolytes, BUN, creatinine, glucose: o

Decreased bicarbonate with m etabolic acidosis

o

Hyperkalem ia and hypercalcem ia with severe m etabolic acidosis





Arterial blood gases: o

pH

o

CO 2 retention in respiratory acidosis

o

CO level

Calculate anion gap: Na + - (HCO 3 - + Cl - ): o

Correct anion gap for hypoalbum inem ia: 

For every 1 g/dL decrease in album in (from 4.0 g/dL), add 2.5 points to calculated anion gap.



o

Norm al range = 5â€“12 Â± 3 m Eq/L

o

Anion gap >25 m Eq/L is seen only with: 

Lactic acidosis



Ketoacidosis



Toxin-associated acidoses

Calculate the degree of com pensation: o

Expected PaCO 2 = 1.5[HCO 3 - ] + 8

o

If PaCO 2 inappropriately high, patient has a concom itant respiratory acidosis and inadequate com pensation



Respiratory acidosis: o

Acute: expected HCO 3 - increased by 1 m Eq/L for every 10 m m Hg increase in PaCO 2

o

Chronic: expected HCO 3 - increased by 4 m Eq/L for

Pa ge 2 3 8

every 10 m m Hg increase in PaCO 2 

Evaluate the delta gap: o

For every one-point increase in anion gap, HCO 3 should decrease by 1 m Eq/L in sim ple acid/base disorder.



Evaluate by com paring the change in the anion gap (Î”AG) with the change in the HCO 3 - (Î”HCO 3 - ) from norm al: o

If Î”AG > Î”HCO 3 - , then patient has a concom itant m etabolic alkalosis.

o

If Î”HCO 3 - > Î”AG, then patient has concom itant non-anion gap acidosis.

P.25

Tests Lab 

Urinalysis for glucose and ketones



Measure serum osm olality: o

Calculated serum osm olality = 2 Na + glucose/18 + blood urea nitrogen/2.8



Osm olal gap = difference between calculated and m easured osm olality: o



Norm al = <10

Toxicology screen: o

Methanol, ethylene glycol, ethanol, and isopropyl alcohol if increased osm olality gap

o

Aspirin or iron levels for suspected ingestion



Co-oxim etry for CO exposure



Serum ketones or Î²-hydroxybutyrate level



Serum lactate

Alert

Pa ge 2 3 9



Failure to appreciate acidosis in m ixed acid/base disorders



Failure to appreciate inadequate respiratory com pensation for m etabolic acidosis and need for ventilatory support

Differential Diagnosis 

Anion gap acidosis: o

To rem em ber possible causes, use m nem onic A CAT MUD PILES:





Alcohol ketoacidosis



Carbon m onoxide or cyanide



Aspirin



Toluene



Methanol



Urem ia



Diabetic ketoacidosis



Paraldehyde



Iron/isoniazid



Lactic acidosis



Ethylene glycol



Starvation

Increased osm olar gap: o

To rem em ber possible causes, use m nem onic ME DIE : 

Methanol



Ethylene glycol



Diuretics (m annitol)



Isopropyl alcohol



Ethanol

Treatment

Pa ge 2 4 0

Initial Stabilization Airway, breathing, circulation (ABCs): 

Early intubation for severe m etabolic acidosis with progressive/potential weakening of respiratory com pensation



Naloxone, D 5 0 W (or Accu-Chek) and thiam ine if m ental status altered

ED Treatment 

Respiratory acidosis: o

Treat underlying disorder.

o

Provide ventilatory support for worsening hypercapnia.

o

Identify and correct aggravating factors (pneum onia) in chronic hypercapnia.



Metabolic acidosis: o

Identify if concurrent osm olal gap.

o

Treat underlying disorder:

o



Diabetic ketoacidosis



Lactic acidosis



Alcohol ketoacidosis



Ingestion

Correct electrolyte abnorm alities.

IV Fluids Rehydrate with 0.9% norm al saline if patient hypovolem ic.

Medication (Drugs) 

Dextrose: D 5 0 W 1 am p (50 m L or 25 g); (peds: D 2 5 W 4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM

Pa ge 2 4 1

initial dose 

Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Worsening m etabolic acidosis



ICU adm ission if pH <7.1 or if m ental status altered or deteriorated



Respiratory acidosis

Discharge Criteria Resolving or resolved anion gap m etabolic acidosis

References 1. Adrogue HJ, Madias NE. Managem ent of life-threatening acid-base disorders. New Engl J Med. 1998;338:26. 2. Swenson ER. Metabolic acidosis. Respir Care. 2001;46:342. 3. Whittier WL, Rutecki GW. Prim er on clinical acid-base problem solving. Dis Mon. 2004;50:122.

Codes ICD9-CM 276.2 Acidosis

ICD10 E87.2

Pa ge 2 4 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acro m io -C lavicular Jo int Injury

Acromio-Clavicular Joint Injury Lorna M. Breen Wallace A. Carter

Basics Description 

The acrom ioclavicular (AC) joint is located between the lateral end of the clavicle and the m edial end of the acrom ion.



Stabilized by acrom ioclavicular ligam ent, coracoclavicular ligam ent, and attachm ents from deltoid and trapezius m uscles

Etiology 

Injury m ost com m only seen in young, active m ales



Injury often occurs in contact sports.



Most com m on m echanism is a fall or direct blow to shoulder with the arm adducted.



Also fall on an outstretched hand with transm ission of force to the AC joint

Diagnosis

Pa ge 2 4 3

Signs and Symptoms 

Diagnosis of AC joint injury is m ade clinically.



Pain to anterior or superior aspect of the shoulder



Pain exacerbated by m oving arm across the chest, behind the back, or overhead



Classification: o

o

Type 1: 

Sprained AC ligam ent but no ligam ental rupture



Mild tenderness and swelling over AC joint



No radiologic abnorm alities

Type 2: 

AC ligam ent is ruptured and coracoclavicular ligam ents are sprained.



Joint tenderness and slight step-off of AC joint



Radiographs show slight widening of AC joint (norm al distance is 1â€“3 m m ) with the clavicle displaced slightly upward or posteriorly.

 o

AC joint space >6 m m is considered pathologic.

Type 3: 

Acrom ioclavicular and coracoclavicular ligam ents both ruptured



Deltoid and trapezius m uscles are detached.



Distal end of clavicle elevated and shoulder dropped



Radiographs show AC joint widening and increase of the coracoclavicular interspace (>5 m m greater than uninjured side).



Elevation of distal clavicle on radiograph above the acrom ion

o

Types 4, 5, and 6: 

Cause m ore significant pain then types 1, 2, and 3

Pa ge 2 4 4

o



All require operative treatm ent.



Have a greater risk for prolonged disability

Type 4: 

Rupture of acrom ioclavicular ligam ent, coracoclavicular ligam ent, and m uscle attachm ents sim ilar to type 3



Clavicle displaced posteriorly into trapezius m uscle



Posteriorly displaced clavicle m ay be palpable on exam .

o



May cause tenting of skin posteriorly



Best visualized on lateral radiograph

Type 5: 

Rare



Rupture of acrom ioclavicular ligam ent, coracoclavicular ligam ent, and m uscle attachm ents sim ilar to type 3



Clavicle is displaced superiorly (100â€“300% increase in coracoclavicular space).

o



Shoulder droops severely.



Clavicle m ay be palpated subcutaneously.

Type 6: 

Usually associated with severe traum a



Rupture of acrom ioclavicular ligam ent, coracoclavicular ligam ent, and m uscle attachm ents sim ilar to type 3



Clavicle is displaced inferiorly into subacrom ial or subcoracoid location.



On exam , shoulder appears flattened.

Pediatric Considerations 

AC joint injury rarely occurs in isolation in the pediatric population.

Pa ge 2 4 5



When injury does occur, usually is type 1, 2, or 3



In children, there is tight approxim ation of the coracoclavicular and acrom ioclavicular ligam ents to the periosteal tube that protects the AC joint from dislocation.



Distal clavicular fractures are m ore com m on than AC joint dislocations in children.

Physical Exam 

Exam ine in standing or sitting position as supine position can m ask joint instability.



Neck and shoulder joint should be exam ined carefully for radiculopathy or referred pain.



The cross-body adduction test: o

Can confirm AC injury by specifically com pressing the joint

o

Pain caused when arm adducted 90 degrees and elbow flexed 90 degrees is brought across the patient's body

Essential Workup 

History to seek m echanism s that com m only cause AC joint injury



Physical exam to exclude other causes of pain



Radiographic evaluation as outlined below

Tests Imaging 

Specific AC joint view: o

Recom m ended if AC injury suspected

o

Routine views will overpenetrate AC joint and m ay obscure subtle injuries.



Diagnostic inform ation gained from stress views does not justify added cost, patient discom fort, and tim e involved.

Pa ge 2 4 6



Ultrasound m ay be used to exclude AC joint inflam m ation.



CT can be useful (especially in traum a cases) to evaluate bony abnorm alities and fractures.



MRI is very effective for evaluating soft tissue injuries. o

Magnetic resonance angiography (MRA) m ay be used to evaluate associated vascular injuries.

Differential Diagnosis 

Shoulder dislocation



Osteoarthritis



Osteom yelitis



Fractures of acrom ion or clavicle



Rotator cuff injury



Tendinitis



Capsulitis



Cervical radiculopathy

P.27

Treatment Pre Hospital 

Ice packs



Sling im m obilization



Cervical spine im m obilization if indicated

Initial Stabilization 

Sling im m obilization



Ice



Analgesia (NSAIDs, other analgesics)

Pa ge 2 4 7

ED Treatment 

Types 1 and 2: o

Rest, ice, analgesics

o

Brief sling im m obilization (typically 3â€“7 days)

o

Range of m otion and strengthening exercises

o

Discontinue sling usage during painless activities and when pain is under control.



Type 3: o

ED m anagem ent consists of sling im m obilization and early (within 72 hours) orthopedic referral

o

Treatm ent plan is controversial; conservative versus surgical approach.

o

Which approach is chosen m ay depend on general health of patient, level of activity, occupation, hand dom inance, and risk for reinjury.



Types 4, 5, and 6: o

Require early surgical treatm ent

Special Circumstance Potential future com plication of AC joint injury is arthritis of the joint: 

Presents as im pingem ent syndrom e, which causes pain at extrem es of abduction

Pediatric Considerations 



Types 1 and 2: o

Conservative m anagem ent (sling, ice, analgesics)

o

Should heal without m ajor sequelae

Type 3: o

Age <15 years, conservative m anagem ent

o

Age â‰¥15 years m ay require m ore aggressive treatm ent.



Types 4, 5, and 6: o

Operative repair

Pa ge 2 4 8

Medication (Drugs) 

Ibuprofen: 600 m g (peds: 4â€“10 m g/kg) PO q.i.d.



Ketorolac: 30 m g (peds: 0.5 m g/kg up to 30 m g if >6 m onths old) IM/IV q6h (15 m g IM/IV q6h if >65 years old or <50 kg)

Follow-Up Disposition Admission Criteria 

Open injury



Types 4, 5, and 6 require adm ission for operative repair.

Discharge Criteria 

Types 1 and 2 can be discharged with orthopedic referral.



Type 3 should have urgent orthopedic referral.

References 1. Bossart PJ, Joyce SM, et al. Lack of efficacy of weighted radiographs in diagnosing acute acrom ioclavicular separation. Ann Em erg Med. 1988;17:4751. 2. Canale ST. Cam pbell's Operative Orthopaedics. Philadelphia: Mosby; 2003:3179â€“3180. 3. Clarke H, McCann P. Acrom ioclavicular joint injuries. Orthop Clin North Am . 2000;31(2):177â€“187. 4. DeLee JC, Drez D. DeLee and Drez's Orthopaedic Sports Medicine Principles and Practice. Philadelphia: WB Saunders; 2003:912â€“932. 5. Ernberg LA, Potter HG. Radiographic evaluation of the acrom ioclavicular and steroclavicular joints. Clin Sports Med.

Pa ge 2 4 9

2003;22:255â€“275. 6. Garretson RB, William s GR. Clinical evaluation of injuries to the acrom ioclavicular and sternoclavicular joints. Clin Sports Med. 2003;22:239â€“254. 7. Kucher MS. Upper extrem ity injury in the pediatric athlete. Sports Med. 2000;30(2):117â€“135.

Codes ICD9-CM 810.03

ICD10 S43.5

Pa ge 2 5 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: C o ro nary Vaso spasm

Acute Coronary Syndrome: Coronary Vasospasm Shamai A. Grossman J. Scott Goudie

Basics Description 

Spontaneous episodes of chest pain due to coronary artery vasospasm in absence of increase in m yocardial oxygen dem and in either norm al or diseased coronary vessels



Also known as Prinzm etal angina or variant angina



Most com m on in younger patients and m en



Occurs in patients without other cardiac risk factors



Risk factors:



o

Sm oking

o

Hyperinsulinem ia

o

Insulin resistance

Associated with m inim al coronary artery disease: o

Usually has norm al coronary angiogram

Etiology 

Abnorm al vasodilator function in coronary arteries



Focal coronary artery vasospasm

Pa ge 2 5 1



Often adjacent to or at the site of fixed stenoses



Unopposed alpha sym pathetic stim ulation



Sym pathetic stim ulation by endogenous horm ones m ay cause vasoconstriction



Hypersensitivity of coronary arteries due to m ediators of vasoconstriction



May or m ay not be associated with a fixed coronary lesion

Diagnosis Signs and Symptoms 

Chest pain: o

Retrosternal

o

Radiates to neck, jaw, left shoulder, or arm

o

Occurs at rest



Palpitations



Presyncope or syncope



Associated with m igraine headaches and Raynaud disease in a m inority of patients



May occur during cold weather or stress



May be prolonged in duration com pared to typical angina



May be elicited by hyperventilation



May be relieved by exercise



Circadian pattern, m ost com m only in early m orning

Tests ECG: 

Transient ST-segm ent elevation is characteristic



May be followed by ST depression or T-wave inversion



May have associated arrhythm ia during coronary spasm



Heart block with right coronary artery spasm

Pa ge 2 5 2



Ventricular tachycardia with LAD spasm

Lab 

CK-MB and troponin I or T



Toxicologic screen: o

Helpful if cocaine is suspected as etiology of chest pain

Imaging 

Chest radiograph: o

May be helpful to rule out other etiologies such as pneum onia, pneum othorax, or aortic dissection



Thallium scintigraphy m ay be useful to localize area of spasm

Diagnostic Procedures/Surgery 

Exercise stress testing: o



Helpful only if there are underlying fixed stenoses

Coronary angiography: o

Mild atherosclerosis is often the norm

o

Provocative test with ergonovine, acetylcholine, or hyperventilation will induce coronary spasm

Differential Diagnosis 

Angina pectoris



Anxiety and panic disorders



Aortic dissection



Esophageal rupture



Esophageal spasm



Esophagitis



Gastroesophageal reflux



Mitral valve prolapse



Musculoskeletal chest pain



Myocardial infarction

Pa ge 2 5 3



Peptic ulcer disease



Pericarditis



Pneum othorax



Pulm onary em bolism

P.29

Treatment Pre Hospital Treat as any other acute coronary syndrom e

Initial Stabilization 

IV access



Oxygen



Cardiac m onitoring



Vital signs and oxygen saturation

ED Treatment 

All patients with chest pain in which cardiac ischem ia is a consideration should receive an aspirin upon arrival to the ED: o

Possibility of actually increasing severity of episodes in Prinzm etal angina due to inhibiting biosynthesis of naturally-occurring coronary vasodilator prostacyclin



Nitroglycerin should then be adm inistered and is appropriate to help relieve both ischem ic and vasospastic chest pain.



A trial of calcium -channel blockers is indicated if clinical history is consistent with coronary vasospasm



Heparin and beta-blockers are not helpful:

Pa ge 2 5 4

o

Beta-blockers m ay actually be detrim ental due to unopposed alpha-m ediated vasoconstriction.

Medication (Drugs) 

Aspirin: 325 m g PO



Diltiazem : 30â€“60 m g PO



Nitroglycerin, either:



o

0.4 m g sublingual

o

10â€“20 m cg/m in IV, titrating to effect

o

1â€“2 inches of nitropaste

Verapam il: 40â€“80 m g PO

Follow-Up Disposition Admission Criteria 

New-onset chest pain



Rest chest pain (by definition m ost patients with coronary vasospasm )



Accelerated chest sym ptom s

Discharge Criteria Stable (chronic chest pain)

References 1. Braunwald E. Unstable angina: an etiologic approach to m anagem ent [editorial]. Circulation. 1998;98:2219â€“2222. 2. Crea F, Kaski JC, Maseri A. Key references on coronary artery spasm . Circulation. 1994;89:2442â€“2446. 3. Gersh BJ, Braunwald E, Bonow RO. Chronic coronary artery

Pa ge 2 5 5

disease. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular disease. 6th ed. Philadelphia: WB Saunders, 2001;1324â€“1328. 4. Mayer S, Hillis LD. Prinzm etal's variant angina. Clin Cardiol. 1998;21:243â€“246. 5. Orford JL. Coronary artery vasospasm . Med J. 2001;2:111. 6. Prinzm etal M, Kennam er R, Merliss R. A variant form of angina pectoris. Am J Med. 1959;27:375â€“388.

Codes ICD9-CM 413.1

Pa ge 2 5 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: Drug Induced

Acute

Coronary Syndrome: Drug Induced Shamai A. Grossman Jennifer De La Pena

Basics Description Im balance in m yocardial blood supply and oxygen requirem ent

Etiology 

Sym pathom im etics are associated with m yocardial oxygen m ism atch due to induced vasoconstriction: o

Cocaine

o

Cocaethylene is a toxic com pound form ed by hepatic transesterification of alcohol and cocaine further exacerbates the sym pathom im etic effects of cocaine.

o

Am phetam ines (crank)

o

Ephedrine (dietary supplem ent), pseudoephedrine (decongestant)

o

Ma huang (herbal diet supplem ent)

o

Dipivefrin (glaucom a eye drop)

o

Phenylpropanolam ine (nasal decongestant)

o

Epinephrine

o

Methylene 3,4 dioxym etham phetam ine (ecstasy)

Pa ge 2 5 7





Cocaine-induced chest pain also caused by: o

Increased m yocardial workload

o

Accelerated atherosclerosis

o

Activation of platelets and prom otion of throm bosis

Antim igraine therapyâ€”sum atriptan, m ethysergide, ergotam ine, and isom etheptene: o

Vasoconstrictors

o

Particularly with cardiac risk factors or known coronary disease



Calcium channel blockersâ€”nifedipine: o



Beta-blockers (m etoprolol and propanolol): o



Reflex tachycardia and vasoconstriction

Î±-adrenergic m ediated coronary vasospasm

Carbon m onoxide found with gas heaters, sm oke inhalation, furniture stripping with m ethylene chloride: o

Decreasing oxygen-carrying capacity

o

Shifting the oxyhem oglobin dissociation curve to the left

o 

Binding to m yoglobin

Brom ocriptine: o

Vasoconstrictor

o

Used for acrom egaly, Parkinson disease, hyperprolactinem ia, am enorrhea/galactorrhea, lactation cessation

o

Risk increased by predisposing conditions: 

Pregnancy-induced hypertension



Other vasospastic conditions (Raynaud disease or m igraine headaches)



Other dopam inergic agents (dopam ine): o



Vasoconstriction and vasospasm

Sildenafil: o

Vasodilatory properties

Pa ge 2 5 8

o

Transient decreases in supine blood pressure

o

Increase the risk of cardiac event during sexual activity



Oral contraceptives: o

Prothrom botic

o

Higher incidence of MI in young wom en with concom itant sm oking

Diagnosis Signs and Symptoms 

Chest pain



Substernal pressure



Heaviness



Squeezing



Burning sensation



Tightness



Sym pathom im etic toxidrom e sym ptom s: o

Agitation

o

Trem ulousness

o

Tachypnea

o

Tachycardia

o

Hypertension

o

Hypertherm ia

o

Moist skin

o

No urine retention

History 

Recent ingestion of m edication/drug that induces coronary vasospasm



Cardiac risk factors or known cardiac disease

Pa ge 2 5 9

Physical Exam 

Physical exam is usually unrevealing



Blood pressure (BP) is usually elevated during sym ptom s

Essential Workup History is critical in diagnosing and differentiating drug-induced and unusual causes of acute coronary syndrom es.

Tests 

ECG: o

Norm al approxim ately 50% of the tim e

o

Com pare to prior tracings

o

New ST segm ent changes or T-wave inversions

o

1-m m depression of the ST segm ent below the baseline



o

80 m sec from the J point

o

Helpful in diagnosing other etiologies

ECG in carbon m onoxide poisoning: o

Prem ature ventricular contractions:

o

Dysrhythm ias

o

Tachycardia

o

Nonspecific ST-T wave abnorm alities

o

Acute MI: ST elevation or depression

Lab 

Serial cardiac enzym es



Troponin m ay be m ore helpful.



Creatine kinase m ay be elevated in cocaine-induced rhabdom yolysis



Carboxyhem oglobin level for suspected carbon m onoxide (CO) toxicity



Serum toxicology screening

Imaging

Pa ge 2 6 0



Chest radiograph: o

Usually norm al

o

May show cardiom egaly

o

Congestive heart failure

o

May identify other etiologies of chest pain such as pneum onia



Exercise stress testing: Identify underlying atherosclerosis.



A technetium Tc-99m perfusion scan: m yocardial dam age/MI



ECG: wall m otion abnorm alities

Diagnostic Procedures/Surgery 

Gold standard: cardiac catheterization



Most patients will have angiographically norm al coronary arteries.

Differential Diagnosis 

Anxiety



Aortic dissection



Biliary colic



Costochondritis



Esophageal reflux



Esophageal spasm



Herpes zoster



Hiatal hernia



Mitral valve prolapse



Myocardial infarction



Panic disorder



Peptic ulcer disease



Pneum onia



Psychogenic



Pulm onary em bolus

Pa ge 2 6 1



Unstable angina

Treatment Pre Hospital 

Rem ove patient from contam inated environm ent if carbon m onoxide toxicity is a consideration.



IV access



Oxygen



Cardiac m onitoring



Sublingual nitroglycerin for sym ptom relief

Alert 

All chest pain should be treated and transported as a possible life-threatening em ergency.



Avoid Î²-adrenergic antagonists in cases of suspected cocaine use.

Initial Stabilization 

Place patient on a m onitor



IV access should be obtained



O 2 : 100% oxygen



Nitrates

P.31

ED Treatment 

Aspirin



Î²-adrenergic blockers should be avoided in patients who are suspected to have used cocaine.



Benzodiazepines: cocaine use

Pa ge 2 6 2



Reduce BP and heart rate.



Decreasing m yocardial oxygen dem and



Heparin or enoxaparin



Throm bolytics: Use with caution in suspected vasospasm induces acute coronary syndrom e



Cardiac catheterization: diagnostic and/or therapeutic



Carbon m onoxide toxicity:



o

100% O 2

o

Hyperbarics if

o

Carboxyhem oglobin level is >25â€“40%.

o

Any period of com a

o

Neurologic deficits

o

Persistent m etabolic acidosis

o

Pregnant and carboxyhem oglobin level is >15%.

o

Cardiac instability

o

Acute MI, unless hem odynam ically unstable

Half-life of carboxyhem oglobin: o

Room air: 300 m inutes

o

100% O 2 : 90 m inutes

o

Hyperbaric cham ber at 3 ATM: 20 m inutes

Medication (Drugs) 

Aspirin: 160â€“325 m g PO



Enoxaparin (Lovenox): 1 m g/kg SC q12h



Heparin: 80 units/kg IV bolus, then 18 units/kg/hr



Labetalol: 20 m g IV or 100 m g PO



Lorazepam : 1â€“2 m g IV



Metoprolol: 5 m g IV q5m inâ€“q15 m in followed by 25â€“50 m g PO starting dose as tolerated (note: beta-blockers contraindicated in cocaine chest pain)



Morphine: 2 m g IV, m ay titrate upward in 2-m g

Pa ge 2 6 3

increm ents for relief of pain assum ing no respiratory deterioration and SBP >90 m m Hg 

Nitroglycerin: 0.4 m g sublingual



Nitroglycerin: IV drip at 5â€“10 Âµg/m in



Nitropaste: 1â€“2 inches transderm al



Tenecteplase: for 60-kg person, 30 m g; >60â€“69 kg, 35 m g; 70â€“79 kg, 40 m g; 80â€“89 kg, 45 m g, â‰¥90 kg, 50 m g given IV; or Reteplase, 10 units IV over 2 m inutes, repeat in 30 m inutes

Follow-Up Disposition Admission Criteria 

Sim ilar to patients with acute coronary syndrom es of atherosclerotic origin



New-onset chest pain



Rest chest pain



Accelerated chest pain sym ptom s

Discharge Criteria Chronic stable chest pain

References 1. Lai TI, Hwang JJ, Fang CC, Chen WJ. Methylene 3,4 dioxym etham phetam ine-induced acute m yocardial infarction. Ann of Em erg Med. 2003;42(6):759â€“762. 2. Lange RA, Hillis LD. Cardiovascular com plications of cocaine use. N Engl J Med. 2001;345:351â€“358. 3. Manini AF, Kabrhel C, Thom sen. Acute Myocardial Infarction after over-the-counter use of Pseudoephedrine. Ann of Em erg Med.

Pa ge 2 6 4

2005;45(2):213â€“218. 4. Marius-Nunez AL. Myocardial infarction with norm al coronary arteries after acute exposure to carbon m onoxide. Chest. 1990;97:491â€“494. 5. Ottervanger JP, Wilson JH, Stricker BH. Drug-induced chest pain and MI. Reports to a national center and review of the literature. Eur J Clin Pharm acol. 1997;53:105â€“110. 6. Qasim A, Townend J, Davies MK. Esctasy induced m yocardial infarction. Heart. 2001;85(6):E10 7. Tanis BC, van den Bosch MA, Kem m eren JM, et al. Oral contraceptives and the risk of m yocardial infarction. N Engl J Med. 2001;345:1787â€“1793. 8. Wasson S, Jayam VK. Coronary vasospasm and m yocardial infarction induced by oral sum atriptan. Clin Neuropharm ocol. 2004;27(4):198â€“200.

Codes ICD9-CM 411.1

ICD10 I20.9 T88.7

Pa ge 2 6 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: M yo cardial Infarctio n

Acute Coronary Syndrome: Myocardial Infarction Shamai A. Grossman Leon D. Sanchez

Basics Description 

Im balance in m yocardial blood supply and oxygen requirem ent



Acute cardiac ischem ia encom passes a spectrum of disease processes: o

Unstable angina pectoris

o

Acute m yocardial infarction (AMI)

o

ST elevation m yocardial infarction (STEMI)

o

Non-STEMI

Etiology 

Atherosclerotic narrowing of coronary vessels



Vasospasm â€”although this is usually at rest and considered unstable if new onset



Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease



Plaque disruption

Pa ge 2 6 6



Throm bosis



Arteritis: o

Lupus

o

Takayasu disease

o

Kawasaki disease

o

Rheum atoid arthritis



Prolonged hypotension



Anem ia o

Hem oglobin <8 g/dL



Hyperbarism or elevations in carboxyhem oglobin



Coronary artery gas em bolus



Thyroid storm



Structural abnorm alities of coronary arteries: o

Radiation fibrosis

o

Aneurysm s

o

Ectasia



Cocaine- or am phetam ine-induced vasospasm



Cardiac risk factors include: o

Hypercholesterolem ia

o

Diabetes m ellitus

o

Hypertension

o

Sm oking

o

Fam ily history in a first-degree relative less than 55 years old

o

Men, age >55 years

o

Postm enopausal wom en

Diagnosis Signs and Symptoms 

Chest pain:

Pa ge 2 6 7

o

Most com m on presentation of m yocardial infarction (MI)





o

Substernal pressure

o

Heaviness

o

Squeezing

o

Burning sensation

o

Tightness

Anginal equivalents (MI without chest pain): o

Abdom inal pain

o

Syncope

o

Diaphoresis

o

Nausea or vom iting

o

Weakness

May localize or radiate to arm s, shoulders, back, neck, or jaw





Associated sym ptom s: o

Dyspnea

o

Syncope

o

Fatigue

o

Diaphoresis

o

Nausea

o

Vom iting

Sym ptom s are usually reproduced by exertion, eating, exposure to cold, or em otional stress.



Sym ptom s com m only last 30 m inutes or m ore.



Sym ptom s m ay occur with rest or during exertion.



Often preceded by crescendo angina



May be im proved or relieved with rest or nitroglycerin



Sym ptom s generally unchanged with position or inspiration



Positive Levine sign or clenched fist over chest is suggestive of angina.



Blood pressure (BP) is usually elevated during sym ptom s.

Pa ge 2 6 8

Physical Exam 

Physical exam is usually unrevealing.



Occasional physical findings include: o

S3 or S4 due to left ventricular systolic or diastolic sym ptom s

o

Papillary m uscle dysfunction resulting in m itral regurgitation

o

Dim inished peripheral pulses

Essential Workup History is critical in differentiating MI from noncardiac etiologies.

Tests ECG

Lab 

CK-MB and troponin I or T



Hem atocrit



Coagulation profile



Creatinine

Diagnostic Procedures/Surgery See Cardiac Testing

Differential Diagnosis 

Anxiety



Aortic dissection



Biliary colic



Costochondritis



Esophageal reflux



Esophageal spasm



Herpes zoster



Hiatal hernia



Mitral valve prolapse



Myocardial infarction

Pa ge 2 6 9



Panic disorder



Peptic ulcer disease



Pneum onia



Psychogenic



Pulm onary em bolus



Unstable angina

Treatment Pre Hospital 

IV access



Aspirin



Oxygen



Cardiac m onitoring



Sublingual nitroglycerin for sym ptom relief



12-lead ECG, if possible, with transm ission or results relayed to receiving hospital

Alert 

All chest pain should be treated and transported as a possible life-threatening em ergency.



Do not adm inister throm bolytics or heparin if aortic dissection is suspected.

Initial Stabilization 

IV access



Oxygen



Cardiac m onitoring



Oxygen saturation



Continuous BP m onitoring and pulse oxim etry

ED Treatment

Pa ge 2 7 0



STEMI requires reperfusion therapy as soon as possible: o

Throm bolytics should be used if percutaneous coronary intervention is not readily available within a 90-m inute tim e fram e (see Reperfusion Therapy, Cardiac).



Patients with non-STEMI, if started on glycoprotein IIb/IIIa inhibitors and if they subsequently receive a stent, benefit from a PCI within a 48-hour tim e fram e.



Aspirin should be adm inistered first to all patients with suspected MI unless the patient has a known allergy.



If BP is >90â€“100 m m Hg systolic, adm inister sublingual nitroglycerin, nitropaste, or IV nitroglycerin assum ing no ECG criteria of right ventricular infarct: o

Sym ptom s that persist after three sublingual nitroglycerin tablets are strongly suggestive of AMI or noncardiac etiology



Beta-blockers should be adm inistered if no contraindications (e.g., bradyarrhythm ias, heart rate <60, congestive heart failure, hypotension, or obstructive pulm onary disease) are present.



Morphine m ay be given to relieve pain and increase oxygen carrying capacity.



Enoxaparin or heparin is generally appropriate as the next line of therapy.



Angiotensin-converting enzym e inhibitors m ay effect a sm all decrease in m ortality when given acutely.



If non-STEMI is clearly the clinical diagnoses, a glycoprotein IIb/IIIa inhibitor should be started. P.33



Clopidogrel m ay be of benefit acutely when added to

Pa ge 2 7 1

standard therapy by reducing the odds of AMI patients having another occluded artery, or a second heart attack or death by 36% after 1 week of hospitalization. 

Statin therapy reduces clinical events in patients with stable coronary artery disease., this m ay also extend to patients experiencing an acute ischem ic coronary event.



If patient is in cardiogenic shock, patient should be transported to a cardiac catheterization laboratory for angioplasty and intra-aortic balloon pum p as soon as possible (see Congestive Heart Failure).



Ventricular dysrhythm ias: o



See Ventricular Tachycardia

Bradydysrhythm ia associated with hypotension should be treated with atropine or external pacing:



Conduction disturbances: o

First-degree aortic valve (AV) block and Mobitz I (Wenckebach) are often self-lim ited and do not require treatm ent.

o

Mobitz II, com plete heart block, new right bundle branch block (RBBB) in anterior MI, RBBB plus left anterior branch block or left posterior fascicular block, left bundle branch block plus first-degree AV block m ay require a tem porary transvenous pacem aker.

Medication (Drugs) 

Am iodarone: 150 m g IV over 5 m inutes then 0.5 m g/m in



Aspirin: 160â€“325 m g PO



Clopidogrel (Plavix): 300 m g PO load, 75 m g PO per day



Enoxaparin (Lovenox): 1 m g/kg SC q12h



Glycoprotein IIb/IIIa inhibitors:

Pa ge 2 7 2

o

Eptifibatide (Integrilin) 180 Âµg/kg IV over 1â€“2 m inutes, followed by continuous infusion of 2 Âµg/kg/m in up to 72 hours

o

Irofiban (Aggrastat) 0.4 Âµg/kg/m in for 30 m inutes, then 0.1 Âµg/kg/m in for 48â€“108 hours

o

Abcixim ab (ReoPro) for use prior to PCI only: 0.25 m g/kg IV bolus



Heparin 80 units/kg IV bolus, then 18 units/kg/h



Lidocaine: 1.5 m g/kg IV bolus, infusion of 2â€“4 m g/kg/m in



Magnesium : 2 g bolus IV



Metoprolol: 5 m g IV q5m inâ€“q15m in followed by 25â€“50 m g PO starting dose as tolerated (note: beta-blockers contraindicated in cocaine chest pain)



Morphine: 2 m g IV, m ay titrate upward in 2-m g increm ents for relief of pain assum ing no respiratory deterioration and SBP >90 m m Hg



Nitroglycerin: 0.4 m g sublingual



Nitroglycerin: IV drip at 5â€“10 Âµg/m in



Nitropaste: 1â€“2 inches transderm al



Throm bolytics: see Reperfusion Therapy, Cardiac, for dosing

Follow-Up Disposition Admission Criteria 

Patients with an AMI require hospital adm ission.



If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac

Pa ge 2 7 3

enzym es, ECGs, and exercise stress testing and/or cardiac catheterization.

Discharge Criteria No patient with an AMI should be discharged from the ED.

Issues for Referral If PCI is unavailable in the treating institution, and particularly if the patient is in cardiogenic shock, patients should be transported to another hospital if PCI can be underway in less than 90 m inutes.

References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non-ST-segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970â€“1062. 2. Gibson CM. Prim ary angioplasty com pared with throm bolysis: new issues in the era of glycoprotein IIb/IIIa inhibition and intracoronary stenting. Ann Intern Med. 1999;130:841â€“847. 3. Lieu TA, Gurley RJ, Lundstrom RJ, et al. Prim ary angioplasty and throm bolysis for acute m yocardial infarction: an evidence based sum m ary. J Am Coll Cardiol. 1996;27:737â€“750. 4. Ryan TJ, Antm an EM, Brooks NH, et al. ACC/AHA practice guidelines for the m anagem ent of patients with acute m yocardial infarction. J Am Coll Cardiol. 1996;28:1328â€“1428. See also 1999 web update at http://www.acc.org. 5. Schm ig A, Kastrati A, Dirschinger J, et al. Coronary stenting plus platelet glycoprotein IIb/IIIa blockade com pared with tissue plasm inogen activator in acute m yocardial infarction. N Engl J Med. 2000;343:385â€“391. 6. Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for m yocardial infarction with ST-segm ent elevation. N Engl J Med. March 24, 2005;352(12):1179â€“1189. Epub 2005 Mar 9.

Pa ge 2 7 4

Miscellaneous SEE ALSO: Cardiac Testing; Reperfusion Therapy; Unstable Angina

Codes ICD9-CM 410.0

ICD10 I21.9

Pa ge 2 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: No nâ€ “Q-Wave (No n-ST

Acute Coronary Syndrome:

Elevatio n) M I

Nonâ€“Q-Wave (Non-ST Elevation) MI David F. M. Brown Murray J. McLachlan

Basics Description 

Non-ST-elevation m yocardial infarction (NSTEMI) is a part of a clinical syndrom e that includes unstable angina.



Probable cause is the generation of a subtotal coronary occlusion or functional collateral circulation: o



Often indicates an incom plete ischem ic event

Coronary plaque disruption: o

Endothelial disruption exposes subendothelial collagen and other platelet-adhering ligands, von Willebrand factor (vWF), and fibronectin.

o

Release of tissue factors activates factor VII and extrinsic pathway



Throm bus generation: o

Platelet adhesion via glycoprotein (GP) Ia/IIa to collagen; GP Ib to vWF:

Pa ge 2 7 6



Platelet activation: release of ADP, throm boxane A 2 , and serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstriction



Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen m olecules, cross-links platelets form ing local platelet plug

o

Platelet stabilization: throm bin converts fibrinogen to fibrin, provides fibrin m esh, stabilizes platelet aggregate

Etiology 

Coronary throm bosis



Coronary artery spasm , idiopathic or cocaine induced



In situ throm bosis/hypercoagulable states



Em bolic event



Arteritis

Diagnosis Signs and Symptoms History 

Pain: o

Pressure or tightness or heaviness

o

Substernal, epigastric

o

+/- radiation to arm , jaw, back



Nausea, vom iting



Diaphoresis



Cough



Dyspnea



Anxiety

Pa ge 2 7 7



Light-headedness



Syncope

Physical Exam 

Hypertension



Hypotension



Arrhythm ias



S4 heart sound

Essential Workup ECG, cardiac m arkers, chest radiograph

Tests Lab 

Cardiac m arkers: o

Troponins: specific indicators of m yocardial infarction, positive 3â€“6 hours after MI, peaks at 9â€“10 days

o

Creatine kinase (CK): rises following infarction in 4â€“8 hours, peaks at 18â€“24 hours, subsiding at 3â€“4 days; isoenzym e CK-MB m ore specific for cardiac origin

o

Myoglobin: rises within 2â€“6 hours, returns to baseline within 24 hours, highly sensitive but very nonspecific

o

LDH: rises within 24 hours, peaks at 3â€“6 days, baseline at 8â€“12 days



CBC



Serum electrolytes including m agnesium



ESR: nonspecific m arker of inflam m ation, rises within 3 days, elevated for several weeks



PT/PTT/INR for patients on warfarin

Imaging

Pa ge 2 7 8



ECG: o

ST-segm ent depression or transient elevation indicates increased risk

o

T-wave inversion in regional patterns does not increase risk but helps differentiate cardiac pain from non cardiac pain



Chest radiograph: o

To assess heart size, pulm onary edem a/congestion or identify other causes of chest pain



Echocardiography: o

To identify wall m otion abnorm alities and assess left ventricular function



Radionuclide studies: o

Thallium or sestam ibi scanning: identifies viable m yocardium

o

Technetium 99: identifies recently infarcted m yocardium

Differential Diagnosis 

ST-elevation m yocardial infarction



Pulm onary em bolus



Aortic dissection



Acute pericarditis



Pneum othorax



Pancreatitis



Pneum onia



Esophageal spasm /gastroesophageal reflux



Esophageal rupture



Musculoskeletal pain (diagnosis of exclusion)

Treatment

Pa ge 2 7 9

Pre Hospital 

IV access



Oxygen adm inistration



Cardiac m onitoring and treatm ent of arrhythm ias



Aspirin, analgesia, anxiolytics

Initial Stabilization 

Oxygen adm inistration



IV access



Cardiac m onitoring and treatm ent of arrhythm ias

ED Treatment 

Anti-ischem ic therapy to reduce m yocardial dem and and increase m yocardial supply of oxygen: o

Beta-blockers

o

Nitrates

o

Oxygen

o

Morphine sulfate

o

Calcium channel blockers (nondihydropyridinesâ€”e.g., diltiazem , verapam il) m ay be used in patients with ongoing ischem ia and contraindications to beta-blockade.





Antiplatelet therapy to decrease platelet aggregation: o

Aspirin

o

Clopidogrel

o

GP IIb/IIIa inhibitors (eptifibatide, tirofiban): 

When catheterization and PCI is planned



Ongoing ischem ia



Positive initial cardiac m arkers

Antithrom botic therapy to prevent throm bus propagation: o

Low m olecular weight heparin (specifically enoxaparin) preferred over unfractionated heparin



Anxiolytics to suppress sym pathom im etic release

Pa ge 2 8 0

Medication (Drugs) 

Aspirin 162â€“325 m g PO per day



Beta-blockers: o

Atenolol: Start 5 m g IV over 5 m inutes, then 5 m g IV 10 m inutes later, then 50â€“100 m g PO per day (1â€“2 hours after IV doses).

o

Esm olol: 100 m cg/kg/m in IV infusion (titrate by increasing 50 m cg/kg/m in q15m in until effectâ€”to m ax dose 300 m cg/kg/m in)

o

Metoprolol: Start 5 m g IV q5m in Ã— 3, after 15 m inutes begin 25â€“50 m g PO q6h.

o

Propranolol: 0.5â€“1 m g IV then 40â€“80 m g PO q6hâ€“q8h

P.35



Calcium channel blockers o

Diltiazem : start 0.25 m g/kg IV bolus, then 0.35 m g/kg IV after 15 m inutes if needed then 30 m g PO q6h

o

Verapam il: start 5â€“10 m g IV, repeat after 30 m inutes if needed, then 80â€“160 m g PO q8h



Clopidogrel: 300â€“600 m g PO Ã— 1, then 75 m g per day



GP IIb/IIIa inhibitors: o

Abcixim ab: (only just prior to PCI): 0.25 m g/kg IV bolus then 0.125 m cg/kg/m in infusion (m ax 10 m cg/m in) for 12â€“24 hours

o

Eptifibatide: 180 m cg/kg IV bolus then 2 m cg/kg/m in infusion for 72â€“96 hours

o

Tirofiban: 0.4 m cg/kg/m in IV Ã— 30 m in, then 0.1

Pa ge 2 8 1

m cg/kg/m in infusion for 48â€“96 hours 

Heparins: o

Enoxaparin: 1 m g/kg SC q12h, can give 30 m g IV bolus before SC dose (beware of enoxaparin in patients with renal dysfunction) or

o

Unfractionated heparin: 60â€“70 units/kg IV bolus then 12â€“15 units/kg/hr infusion (m ax bolus 5000 units, m ax infusion rate 1000 units/hr (goal is a PTT 50â€“75 seconds)



Lorazepam : 1â€“2 m g IV PRN anxiety



Morphine sulfate 1â€“5 m g IV q5m inâ€“q30m in PRN pain



Nitroglycerin: 0.3â€“0.6 m g SL or 0.4 m g by spray q5m in followed by IV infusion beginning at 10â€“20 m cg/m in if pain persists (m ax. dose 200 m cg/m in)

Follow-Up Disposition Admission Criteria 

All patients with positive cardiac m arkers or significant clinical probability of acute coronary syndrom e



Intensive care unit for m onitoring unstable patients

Discharge Criteria Only those who are ruled out for acute coronary syndrom e/nonâ€“Q-wave infarction can be safely sent hom e.

References 1. Braunwald E, et al. ACC/AHA guideline update for the managem ent of patients with unstable angina and nonâ€”ST-segm ent elevation

Pa ge 2 8 2

m yocardial infarction, 2002, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf. 2. Braunwald E. Application of Current Guidelines to the Management of Unstable Angina and Non-ST-Elevation Myocardial Infarction. Circulation; 108(16 Suppl 1): III28â€“11137, 2003 Oct 21. 3. DeFilippi CR. Evaluating the chest pain patient. Scope of the problem . Cardiol Clin. 1999;17(2):307â€“326. 4. Harrington RA, Becker RC, Ezekowitz M, Meade TW, O'Connor CM, Vorchheim er DA, Guyatt GH. Antithrom botic therapy for coronary artery disease: the Seventh ACCP Conference on Antithrom botic and Throm bolytic Therapy. Chest.126(3 Suppl):513Sâ€“548S, 2004 Sept. 5. Storrow AB. Chest pain centers: diagnosis of acute coronary syndrom es. Ann Em erg Med. 2000;35(5):449â€“461. 6. Tatum JL. Com prehensive strategy for the evaluation and triage of the chest pain patient. Ann Em erg Med. 1997;29(1):116â€“125. 7. Zalenski RJ. National Heart Attack Alert Program position paper: chest pain centers and program s for the evaluation of acute cardiac ischem ia. Ann Em erg Med. 2000;35(5):462â€“471. 8. Zalenski RJ. Evaluation and risk stratification of patients with chest pain in the em ergency departm ent. Predictors of life threatening events. Em erg Med Clin North Am . 1998;16(3):495â€“517, vii.

Codes ICD9-CM 410.9

ICD10 I21.4

Pa ge 2 8 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: Stable Angina

Acute

Coronary Syndrome: Stable Angina Shamai Grossman Tarina Lee Kang

Basics Description 

Chest discom fort that is predictable in nature, occurs with exertion, and im proves with rest



Im balance in m yocardial blood supply and oxygen requirem ents



Canadian Cardiovascular Classificationâ€”class I: ordinary physical activity does not cause sym ptom s.



Canadian Cardiovascular Classificationâ€”class II: sym ptom s that slightly lim it norm al activity such as: o

Walking

o

Clim bing stairs

o

Em otional stress

o

Cold

Etiology 

Cardiac risk factors include: o

Hypercholesterolem ia

o

Diabetes m ellitus

Pa ge 2 8 4

o

Hypertension

o

Sm oking

o

Fam ily history

o

Men: age >35 years

o

Postm enopausal wom en



Atherosclerotic narrowing of coronary vessels



Vasospasm , although this is usually at rest and considered unstable if new onset



Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease



Arteritis: o

Lupus

o

Takayasu disease

o

Kawasaki disease

o

Rheum atoid arthritis



Anem ia: hem oglobin <8 g/dL



Hyperbarism or elevations in carboxyhem oglobin



Structural abnorm alities of coronary arteries:



o

Radiation fibrosis

o

Aneurysm s

o

Ectasia

Cocaine- or am phetam ine-induced vasospasm

Diagnosis Signs and Symptoms 

Chest pain: o

Substernal pressure

o

Heaviness

o

Squeezing

o

Burning sensation

Pa ge 2 8 5

o 

Tightness

May localize or radiate to arm s, shoulders, back, neck, or jaw



May be associated with dyspnea, syncope, fatigue, diaphoresis, nausea, or vom iting



Usually reproduced by exertion, eating, exposure to cold, or em otional stress



Sym ptom s last less than 20 m inutes, but m ore than a few seconds.



Recurrent sym ptom s of 2 m onths duration or m ore



Usually relieved with rest or nitroglycerin



Sym ptom s generally unchanged with position or inspiration



No changes in pattern or frequency of sym ptom s



Occasional anginal equivalents include:



o

Abdom inal pain

o

Syncope

o

Diaphoresis

o

Nausea or vom iting

o

Weakness

Positive Levine sign or clenched fist over chest is suggestive of angina.



Blood pressure is usually elevated during sym ptom s.



Physical exam is usually unrevealing.



Occasional sym ptom s include: o

S3 or S4 due to left ventricular systolic or diastolic sym ptom s

o

Mitral regurgitation or pansystolic m urm ur

o

Dim inished peripheral pulses

Essential Workup 

History is critical in differentiating stable and unstable angina.



ECG:

Pa ge 2 8 6

o

Will be norm al m inim ally 50% of the tim e

o

ST segm ent changes or T-wave inversions m ost often will be unchanged from previous tracings.

o

Must be com pared to prior tracings if available

o

New ST segm ent changes or T-wave inversions are suspicious for unstable angina.

o

Serial ECG tracings that rem ain unchanged m ay assist in differentiating stable from unstable angina.

o

1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, is characteristic of angina



ECG m ay be helpful in diagnosing other causes of chest pain: o

Pericarditis is suggested by diffuse ST elevations followed by T-wave inversions and pulse rate depression.

o

Pulm onary em bolism is suggested by an S1, Q3, T3 pattern; unexplained tachycardia; and signs of right heart strain.

Tests Lab Cardiac enzym es should not be elevated and are not indicated unless the history is suspicious for acute m yocardial infarction (AMI).

Imaging 

Chest radiograph: o

Usually norm al

o

May show cardiom egaly

o

Congestive heart failure is suggestive of unstable angina.

o

May identify other etiologies of chest pain, such as pneum onia

Pa ge 2 8 7



Exercise stress testing m ay help establish the diagnosis of stable angina and provide prognostic inform ation. o

1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischem ia

o

Early positive (within 3 m inutes) stress tests are worrisom e for unstable angina.

o

Six m inutes of exercise utilizing a standard Bruce protocol suggests an excellent prognosis.

o

Exercise stress testing with ECG alone has a sensitivity of 68% and specificity of 77%.

o

Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.

o

Exercise stress testing with thallium -201 or technetium Tc-99m sestam ibi has a sensitivity of 87% and specificity of 64%.

Differential Diagnosis 

Anxiety



Aortic dissection



Biliary colic



Costochondritis



Esophageal reflux



Esophageal spasm



Herpes zoster



Hiatal hernia



Mitral valve prolapse



Myocardial infarction



Panic disorder



Peptic ulcer disease



Pneum onia



Psychogenic

Pa ge 2 8 8



Pulm onary em bolus



Unstable angina

Treatment Pre Hospital 

IV access



Oxygen



Cardiac m onitoring



Sublingual nitroglycerin for sym ptom relief



Aspirin

Initial Stabilization 

IV access



Oxygen



Cardiac m onitoring



Oxygen saturation

ED Treatment 

Aspirin



Sublingual nitroglycerin: o

Sym ptom s that persist after three sublingual nitroglycerins are strongly suggestive of unstable angina, AMI, or noncardiac etiology.



May require adjustm ent of patient's outpatient m edical regim en including adding or changing the dosage of a beta-blocker

P.37

Pa ge 2 8 9

Medication (Drugs) 

Aspirin: 160â€“325 m g



Nitroglycerin: 0.4 m g sublingual



Isosorbide m ononitrate: 20 m g PO b.i.d. or isosorbide dinitrate 5â€“40 m g PO t.i.d. or Nitropatch 1â€“2 inches 10â€“14 hours daily



Metoprolol: 25â€“50 m g PO starting dose: Clopidogrel, in conjunction with standard therapy for ST-segm ent elevation m yocardial infarction, was shown to reduce the odds of AMI patients having another occluded artery or a second heart attack or death by 36% after one week of hospitalization.



Statin therapy reduces clinical events in patients with stable coronary artery disease; this m ay also extend to patients experiencing an acute ischem ic coronary event.

Follow-Up Disposition Admission Criteria 

Patients with stable angina generally do not require hospital adm ission.



If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac enzym es, ECGs, and exercise stress testing.



Patients who require additional adjustm ent of m edication or angioplasty to reduce sym ptom s, and im prove quality of life

Discharge Criteria

Pa ge 2 9 0

By definition, patients who m eet diagnostic criteria of stable angina are safe to discharge.

References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non-ST-segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970â€“1062. 2. Solom on AJ, Gersh BJ. Managem ent of chronic stable angina: m edical therapy, percutaneous translum inal coronary angioplasty, and coronary artery bypass graft surgery. Lessons from the random ized trials. Ann Intern Med. 1998;128:216â€“223. 3. Thadani U. Managem ent of patients with chronic stable angina at low risk for serious cardiac events. Am J Cardiol. 1997;79:2430.

Codes ICD9-CM 413.9

ICD10 I20.9

Pa ge 2 9 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: Unstable Angina

Acute

Coronary Syndrome: Unstable Angina Shamai A. Grossman Leon D. Sanchez

Basics Description 

Im balance in m yocardial blood supply and oxygen requirem ent



Canadian Cardiovascular Classification, Class III: severe lim itations of ordinary physical activity



Class IV: inability to perform any activity without discom fort, sym ptom s m ay be present at rest

Etiology 

Atherosclerotic narrowing of coronary vessels



Vasospasm , although this is usually at rest and considered unstable if new onset



Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease



Plaque disruption



Throm bosis

Pa ge 2 9 2





Arteritis: o

Lupus

o

Takayasu disease

o

Kawasaki disease

o

Rheum atoid arthritis

Anem ia: o

Hem oglobin <8 g/dL



Hyperbarism or elevations in carboxyhem oglobin



Coronary artery gas em bolus



Thyroid storm



Structural abnorm alities of coronary arteries: o

Radiation fibrosis

o

Aneurysm s

o

Ectasia



Cocaine- or am phetam ine-induced vasospasm



Cardiac risk factors include: o

Hypercholesterolem ia

o

Diabetes m ellitus

o

Hypertension

o

Sm oking

o

Fam ily history in a first-degree relative less than age 55

o

Men: age >55 years

o

Postm enopausal wom en

Diagnosis Signs and Symptoms 

Unstable angina is defined by either: o

New-onset sym ptom s

o

Sym ptom s that occur at rest

Pa ge 2 9 3

o 





A change in the patient's usual pattern of angina

Chest pain: o

Most com m on presentation of m yocardial infarction

o

Substernal pressure

o

Heaviness

o

Squeezing

o

Burning sensation

o

Tightness

Occasional anginal equivalents: o

Abdom inal pain

o

Syncope

o

Diaphoresis

o

Nausea or vom iting

o

Weakness

May localize or radiate to arm s, shoulders, back, neck, or jaw



May be associated with dyspnea, syncope, fatigue, diaphoresis, nausea, or vom iting



Sym ptom s are usually reproduced by exertion, eating, exposure to cold, or em otional stress.



Sym ptom s com m only last 15 m inutes or m ore.



Usually im proved or relieved with rest or nitroglycerin



Sym ptom s generally unchanged with position or inspiration



Positive Levine sign or clenched fist over chest is suggestive of angina



Blood pressure (BP) is usually elevated during sym ptom s.

Physical Exam 

Physical exam is usually unrevealing.



Occasional physical findings include: o

S3 or S4 due to left ventricular systolic or diastolic sym ptom s

o

Papillary m uscle dysfunction resulting in m itral

Pa ge 2 9 4

regurgitation o

Dim inished peripheral pulses

Essential Workup History is critical in differentiating m yocardial infarction (MI) from noncardiac etiologies.

Tests 

ECG: o

Will be norm al approxim ately 50% of the tim e

o

ST segm ent changes or T-wave inversions m ost often will be unchanged from previous tracings.

o

Must be com pared to prior tracings if available

o

New ST segm ent changes or T-wave inversions are suspicious for unstable angina.

o

Serial ECG tracings that rem ain unchanged m ay assist in differentiating stable from unstable angina.

o

1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, is characteristic of angina.



ECG m ay be helpful in diagnosing other etiologies of chest pain: o

Pericarditis is suggested by diffuse ST elevations followed by T-wave inversions and PR depression.

o

Pulm onary em bolism is suggested by an S1, Q3, T3 pattern and unexplained tachycardia.

Lab 

CK-MB and troponin I or T



Hem atocrit



Coagulation profile



Creatinine

Imaging

Pa ge 2 9 5



Chest radiograph: o

Usually norm al

o

May show cardiom egaly

o

Congestive heart failure is suggestive of unstable angina.

o

May identify other etiologies of chest pain such as pneum onia



Rest echocardiography m ay establish the diagnosis of acute coronary insufficiency (ACI): o

Has a sensitivity of 70% and specificity of 87% for ACI



Technetium Tc-99 sestam ibi (rest): o

Has a sensitivity of 81% and specificity of 73% for ACI



Exercise stress testing m ay help establish the diagnosis of angina and provide prognostic inform ation when the clinical presentation is equivocal: o

Exercise stress testing with ECG alone has a sensitivity of 68% and specificity of 77%.

o

Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.

o

Exercise stress testing with thallium -201 or technetium Tc-99m sestam ibi has a sensitivity of 87% and specificity of 64%.

o

1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischem ia.

o

Early positive (within 3 m inutes) stress tests are worrisom e for unstable angina.

Diagnostic Procedures/Surgery See Cardiac Testing

Pa ge 2 9 6

Differential Diagnosis 

Acute MI



Anxiety



Aortic dissection



Biliary colic



Costochondritis



Esophageal reflux



Esophageal spasm



Herpes zoster



Hiatal hernia



Mitral valve prolapse



MI



Panic disorder



Peptic ulcer disease



Pneum onia



Psychogenic



Pulm onary em bolus

P.39

Treatment Pre Hospital 

IV access



Aspirin



Oxygen



Cardiac m onitoring



Sublingual nitroglycerin for sym ptom relief

Alert

Pa ge 2 9 7

All chest pain should be treated and transported as a possible life-threatening em ergency.

Initial Stabilization 

IV access



Oxygen



Cardiac m onitoring



Oxygen saturation



Continuous BP m onitoring and pulse oxim etry

ED Treatment 

Aspirin should be adm inistered first to all patients with suspected unstable angina



Sublingual nitroglycerin, nitro paste, or IV nitroglycerin; o

Sym ptom s that persist after three sublingual nitroglycerins are strongly suggestive of unstable angina, acute MI, or noncardiac etiology.



Beta-blockers should be adm inistered if no contraindications (e.g., bradyarrhythm ias or obstructive pulm onary disease) are present.



Morphine m ay be given to relieve pain and increase oxygen-carrying capacity.



Enoxaparin or heparin is generally appropriate as the next line of therapy.



If unstable angina is clearly the clinical diagnoses, a glycoprotein IIb/IIIa inhibitor should be started as well.

Medication (Drugs) 

Aspirin: 160â€“325 m g PO



Enoxaparin (Lovenox): 1 m g/kg SC q12h



Glycoprotein IIb/IIIa inhibitors: o

Eptifibatide (Integrilin): 180 Âµg/kg IV over 1â€“2

Pa ge 2 9 8

m inutes, followed by continuous infusion of 2 Âµg/kg/m in up to 72 hours o

Tirofiban (Aggrastat): 0.4 Âµg/kg/m in for 30 m inutes, then 0.1 Âµg/kg/m in for 48â€“108 hours

o

Abcixim ab (ReoPro): for use prior to percutaneous coronary intervention only, 0.25 m g/kg IV bolus



Heparin: 80 units/kg IV bolus, then 18 units/kg/hr



Metoprolol: 5 m g IV q5m inâ€“q15m in followed by 25â€“50 m g PO starting dose as tolerated (note: beta-blockers contraindicated in cocaine chest pain)



Morphine: 2 m g IV, m ay titrate upward in 2-m g increm ents for relief of pain assum ing no respiratory deterioration and SBP >90 m m Hg



Nitroglycerin: 0.4 m g sublingual



Nitroglycerin: IV drip at 5â€“10 Âµg/m in



Nitropaste: 1â€“2 inches transderm al

Follow-Up Disposition Admission Criteria 

Patients with unstable angina require hospital adm ission.



If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac enzym es, ECGs, and exercise stress testing and/or cardiac catheterization.

Discharge Criteria No patient with unstable angina should be discharged from the ED.

References

Pa ge 2 9 9

1. Boden WE, McKay RG. Optim al treatm ent of acute coronary syndrom es: an evolving strategy. N Engl J Med. 2001;344:1939â€“1942. 2. Braunwald E, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non ST segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970â€“1062. 3. Cannon CP, et al. Com parison of early invasive and conservative strategies in patients with unstable coronary syndrom es treated with the glycoprotein IIb/IIIa inhibitor tirofiban, the TACTICS-throm bolysis in m yocardial infarction 18 investigators. N Engl J Med. 2001;344:1879â€“1887. 4. Lau J, Ioannidis JP, Balk EM, et al. Diagnosing acute cardiac ischem ia in the em ergency departm ent: a system atic review of the accuracy and clinical effect of current technologies. Ann Em erg Med. 2001;37(5):453â€“460. 5. Main C, Palm er S, Griffin S, Jones L, Orton V, Sculpher M, Henderson R, Sudlow C, Hawkins N, Riem sm a R. Clopidogrel used in com bination with aspirin com pared with aspirin alone in the treatm ent of non-ST-segm ent- elevation acute coronary syndrom es: a system atic review and econom ic evaluation. Health Technol Assess. 2004 Oct;8(40):iiiâ€“iv, xvâ€“xvi, 1â€“141.

Miscellaneous SEE ALSO: Cardiac Testing; Myocardial Infarction; Reperfusion Therapy; Stable Angina

Codes ICD9-CM 411.1

ICD10

Pa ge 3 0 0

I20.0

Pa ge 3 0 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Adrenal Insufficiency

Adrenal

Insufficiency Rita Cydulka Eva Escatel

Basics Description 

Inadequate hydrocortisone secretion to m eet body's stress requirem ent



Adrenal deficiency: o

Inadequate cortisol

o

Unresponsive to stim ulation with adrenocorticotropic horm one (ACTH)





Functional hypoadrenalism : o

Inadequate cortisol

o

Partial responsive to stim ulation with ACTH

Addisonian crisis (acute adrenal insufficiency): o

Life-threatening em ergency

o

Precipitated by intensification of: 

Chronic adrenal insufficiency



Acute adrenal hem orrhage



Rapid steroid withdrawal



Treatm ent of hypothyroidism with unrecognized

Pa ge 3 0 2

adrenal disease 

Steroid-dependent patient under stress owing to pregnancy, surgery, traum a, infection, or dehydration

Etiology Primary Adrenal Failure 

Adrenal dysgenesis/im paired steroidogene: o

Congenital hypoplasia

o

Allgrove syndrom e:

o





ACTH resistance



Achalasia



Alacrim a

Glycerol kinase deficiency: 

Psychom otor retardation



Hypogonadism



Muscular dystrophy

o

Congenital hyperplasia

o

Aldosterone synthetase deficiency

o

Mitochondrial disease

Adrenal destruction: o

Autoim m une: 

Autoim m une polyglandular syndrom e types 1 and 2 (alopecia universalis, chronic m ucocutaneous candidiasis, hypoparathyroid, thyroid autoim m unity, diabetes, celiac disease, pernicious anem ia)

 o

Adrenoleukodystrophy

Infectious: 

Granulom atous: tuberculosis



Protozoal and fungal: histoplasm osis, coccidioidom ycosis, candidiasis

Pa ge 3 0 3



Viral: cytom egalovirus, herpes sim plex virus, and HIV

 o

Bacterial

Infiltration: 

Sarcoid



Neoplasm



Hem ochrom atosis



Am yloidosis



Iron depletion



Postadrenalectom y



Hem orrhage: o

Sepsis: particularly m eningococcem ia, Pseudom onas infection



o

Birth traum a/anoxia

o

Pregnancy

o

Seizures

o

Anticoagulants

o

Rhabdom yolysis

Pharm acologic inhibition: o

Etom idate

o

Herbal m edications

o

Ketoconazole

o

Metyrapone

o

Suram in

Secondary Adrenal Failure Pituitary insufficiency: 

Sepsis



Head traum a



Hem orrhage



Infarction (Sheehan syndrom e)



Infiltration: neoplasm , am yloid, sarcoid, hem ochrom atosis



Adrenocorticotropic horm one deficiency

Pa ge 3 0 4



Pharm acologic: glucocorticoid adm inistration, herbal m edications

Tertiary Adrenal Failure 

Hypothalam us insufficiency



Sepsis



Infiltrative: neoplasm , am yloid, sarcoid, hem ochrom atosis



Head traum a

Diagnosis Signs and Symptoms 

Sym ptom s: o

Depression

o

Lethargy

o

Malaise

o

Myalgias

o

Anorexia

o

Abdom inal pain

o

Nausea

o

Vom iting

o

Dehydration (found in prim ary adrenal insufficiency only)

o 

Salt craving

Signs: o

Fever or hypotherm ia

o

Mental status changes

o

Tachycardia

o

Orthostatic blood pressure changes or frank shock

o

Weight loss

o

Goiter

Pa ge 3 0 5

o

Hypogonadism

o

Hyperkalem ia

o

Sodium depletion

o

Eosinophilia

o

Hyperpigm entation (found in prim ary adrenal insufficiency only)

o 

Vitiligo

Addisonian crisis: o

Hypotension and shock

o

Hyponatrem ia

o

Hyperkalem ia

o

Hypoglycem ia

Essential Workup 

Laboratory confirm ation of diagnosis not possible in em ergency departm ent



Adrenal crisis: life-threatening condition: o

High degree of suspicion should prom pt initiation of therapy before definitive diagnosis.



Plasm a cortisol level <20 Âµg/dL accom panied by shock suggests adrenal insufficiency.





Electrolytes: o

Potassium

o

Sodium

BUN, creatinine: o



Elevated owing to dehydration

Serum glucose levels m ay be low.

Tests Lab 

CBC with differential: o

Anem ia

o

Eosinophilia

Pa ge 3 0 6

o 



Lym phocytosis

Arterial blood gases: o

Hypoxem ia

o

Acidosis

Cosyntropin stim ulation test: o

Adrenal deficiency: 

Random serum cortisol <20 Âµg/dL (while stressed)

 o

ACTH stim ulation unresponsive

Functional hypoadrenalism : 

Random serum cortisol = 20 Âµg/dL (while stressed)



Sixty m inutes post ACTH stim ulation <30 Âµg/dL or delta cortisol (60 m inutes - baseline) = 9 Âµg/dL



Search for underlying infection.

Imaging 

ECG



Chest radiograph

Differential Diagnosis 

Sepsis



Shock from any cause



Acute abdom inal em ergency

P.41

Treatment Initial Stabilization

Pa ge 3 0 7



Airway, breathing, and circulation m anagem ent (ABCs)



Cardiac m onitor



Blood pressure support for hypotension: o

Norm al saline (0.9%) IV fluids 500 m Lâ€“1 L (peds: 20 m L/kg) bolus

o

Avoid pressors (if possible): 

May precipitate dysrhythm ias



Supplem ental oxygen to m eet m etabolic needs



Correct hypertherm ia: o

Initiate cooling m easures.

ED Treatment 

Glucocorticoid replacem ent: o

IV hydrocortisone or dexam ethasone

o

Dexam ethasone will not interfere with results of cosyntropin stim ulation tests.



Volum e expansion: o

D 5 W 0.9% norm al saline at rate of 500â€“1,000 m L/h for first 3â€“4 hours

o

Care should be taken to note patient's age, volum e, and cardiac and renal function.



For hypoglycem ia: o



D50W

Treat life-threatening dysrhythm ias secondary to hyperkalem ia with calcium , bicarbonate, and insulin/glucose.



Identification and correction of underlying precipitant

Medication (Drugs) 

Dexam ethasone: 4 m g (peds: 0.15 m g/kg per dose) q12h



Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 1 0 over 1

Pa ge 3 0 8

m inute) IV 

Hydrocortisone: 100 m g (peds: 1â€“2 m g/kg per dose) IV q6h



Insulin (regular): 10 units by IV push



Sodium bicarbonate: 1â€“2 m Eq/kg IV

Follow-Up Disposition Admission Criteria 

All patients with acute adrenal insufficiency



ICU adm ission for patients with unstable or potentially unstable cases

Discharge Criteria Norm al laboratory evaluation with treated adrenal insufficiency

References 1. Chang SS, Liaw SJ, Bullard MJ, et al. Adrenal insufficiency in critically ill em ergency departm ent patients: a Taiwan prelim inary study. Acad Em erg Med. 2001;8:761â€“764. 2. Oelkers W. Adrenal insufficiency. N Engl J Med. 1996;355:1206â€“1212. 3. Rivers E, Blake HC, Dereczyk B, et al. Adrenal dysfunction in hem odynam ically unstable patients in the em ergency departm ent. Acad Em erg Med. 1999;6:626â€“630. 4. Rivers E, Gaspari M, Saad GA, et al. Adrenal insufficiency in high-risk surgical ICU patients. Chest. 2001;119:889â€“896. 5. Ten S, New M, Noel M. Clinical review 130: Addison's disease 2001. J Clin Endocrinol Metab. 2001;86:2909â€“2922.

Codes

Pa ge 3 0 9

ICD9-CM 255.4 Corticoadrenal insufficiency (Addison disease)

ICD10 E27.4

Pa ge 3 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Airw ay M anagem ent

Airway

Management Scott G. Weiner Carlo L. Rosen

Basics Description 

Techniques that ensure adequate oxygenation of a patient



Oral and nasopharyngeal airways:



o

Lift tongue off hypopharynx

o

Facilitate bag-valve-m ask ventilation

o

Insert when gag reflex is absent

Rapid sequence intubation (RSI): o

Preferred m ethod for ED oral intubation (m inim izes aspiration risk)

o

Rapid induction of anesthesia and paralysis

o

Contraindicated in patients who should not be paralyzed

o

A preform ulated backup strategy with alternative airway techniques is recom m ended.



Oral awake intubation: o

Oral intubation with sedation only

o

Ketam ine is the m ost com m on agent used for this

Pa ge 3 1 1

purpose. 

Contraindicated in head injury (m ay elevate intracranial pressure [ICP])





Use with benzodiazepines



Indicated when paralysis is contraindicated

Gum elastic bougie: o

Airway adjunct used when vocal cords are not well visualized

o

Placem ent confirm ed by feeling bougie bum p against tracheal rings

o

Slide endotracheal tube (ET) over bougie, then rem ove bougie.



Laryngeal m ask airway (LMA): o

Used to ventilate until definitive airway is established

o

Inserted blindly into oropharynx and inflated

o

Form s a seal around the glottic structures in the hypopharynx



o

Less protection against aspiration than ET intubation

o

Intubating LMA can be used to place an ET tube.

Fiberoptic intubation: o

ET tube placed over the bronchoscope

o

Nasotracheal or orotracheal approach

o

Indications:

o





Anatom ic lim itations to glottis visualization



Lim ited m obility of m andible or cervical spine



Unstable cervical spine injury

Contraindications: 

Need for im m ediate airway m anagem ent



Significant oropharyngeal blood

Nasotracheal intubation: o

Indications: 

Oral access im paired

Pa ge 3 1 2

o



Unsuccessful oral intubation



Paralysis is contraindicated.



Lim ited cervical m obility

Contraindications: 

Apnea



Anticoagulation



Massive facial, nasal, head traum a



Upper airway abscess



Epiglottitis



Penetrating neck traum a

Cricothyrotom y: o

Incision in cricothyroid m em brane

o

Shiley tracheostom y tube inserted in the airway

o

Indications:

o







Other airway attem pts have failed



Massive facial traum a



Total upper airway obstruction

Contraindications: 

Laryngeal crush injury



Tracheal transection



Expanding zone II or III hem atom a

Percutaneous translaryngeal ventilation (PTV): o

A tem porizing m easure until definitive airway is established

o

Percutaneous placem ent of 12- or 14-gauge catheter through cricothyroid m em brane

o

Interm ittent ventilation via high-pressure oxygen source

o

Indications: 

Failed oral or nasal intubation until cricothyrotom y is com plete

o

Contraindications:

Pa ge 3 1 3

 

Upper airway obstruction preventing expiration

Retrograde tracheal intubation: o

Retrograde advancem ent of guidewire through translaryngeal catheter

o

ET tube advanced over wire once it com es out of the m outh

Diagnosis Signs and Symptoms 

Clinical conditions requiring airway m anagem ent: o

o

o

Failure to m aintain or protect the airway: 

Oropharyngeal swelling



Absent gag reflex



Inability to clear secretions, blood



Stridor

Hypoxia or ventilatory failure: 

Shortness of breath



Altered m ental status



Status epilepticus

Ventilatory control: 

Head injury



Tricyclic overdose

o

Sedation for diagnostic or therapeutic procedures

o

Early m anagem ent if the airway m ight becom e com prom ised

Essential Workup 

Recognition of a difficult airway: o

Anatom ic considerations: 

Short m andible, thick neck, narrow m outh,

Pa ge 3 1 4

large tongue, protruding teeth

o



Congenital syndrom es, acrom egaly



Obesity

Disease states: 

Angioedem a



Rheum atoid arthritis and other arthropathies that decrease cervical spine m obility



Goiter



Laryngeal-tracheal tum ors



History of radiation therapy to the neck



Infections (epiglottitis, supraglottitis, croup, intraoral abscess, retropharyngeal abscess, Ludwig angina)



Profuse upper gastrointestinal hem orrhage



Traum a (facial, neck, cervical spine, laryngeal-tracheal, burns)

o

o



Mallam pati criteria (increasing difficulty): 

Class I: soft palate, uvula, fauces, pillars visible



Class II: soft palate, uvula, fauces visible



Class III: soft palate visible



Class IV: hard palate only

Rule of 3-3-2 (difficult airway if m et): 

Mouth opens <3 fingerbreadths



Horizontal length of m andible <3 fingerbreadths



Thyrom ental distance <2 fingerbreadths

Verification of correct tube placem ent: o

Visualization of tube passing through the vocal cords

o

Auscultate over stom ach, axillae, and anterior lung fields

o

Observe chest wall m ovem ent

o

Condensation in the tube during ventilation

o

End-tidal CO 2 colorim etric device:

Pa ge 3 1 5



Changes color if CO 2 is sensed, indicating tracheal placem ent



Color change m ay not be seen in cardiac arrest

Tests Lab 

Pulse oxim etry should rise after tracheal intubation



Arterial blood gas to m anage ventilator settings after intubation

Imaging Chest radiography: 

To exclude m ainstem bronchus intubation or pneum othorax



Does not rule out esophageal intubation

Differential Diagnosis 

Esophageal intubation



Right or left m ainstem bronchus intubation



Extratracheal placem ent through tear in pyriform sinus or trachea



Pneum othorax

P.43

Treatment Pre Hospital 

Options for patients in respiratory arrest for Advanced life support (ALS) providers: o

Bag-valve m anagem ent (BVM) ventilation followed by

Pa ge 3 1 6

definitive airway m anagem ent in the ED o

Orotracheal intubation

o

Esophageal-tracheal tubes, (e.g., Com bitube): 

A device with two lum ens and two balloons



Ventilates either with tracheal or esophageal intubation



Functions as an ET tube or esophageal obturator depending on placem ent



Contraindicated in children, caustic ingestions, esophageal disease, or in patients with intact gag reflex

o

Laryngeal m ask airway

Initial Stabilization 

Maintain in-line cervical spine im m obilization in traum a



Oxygen, m onitor, IV

ED Treatment 

Rapid sequence intubation



Prepare equipm ent:



o

Suction

o

BVM

o

Various sizes of ET tubes

o

Laryngoscope blades

o

Stylets

o

Medications

Preoxygenation: o



100% FIO 2 for 5 m inutes

Prem edication: o

Prevents physiologic sequelae of intubation

o

Perform ed 2â€“3 m inutes prior to paralytic

o

Defasciculating dose of nondepolarizing agent

o

Fentanyl and lidocaine m ay m inim ize ICP rise and

Pa ge 3 1 7

hem odynam ic response to intubation in head-injured patients. o

Lidocaine decreases airway irritability in reactive airway disease.



Apply cricoid pressure (Sellick m aneuver) to occlude esophagus and prevent aspiration.



Avoid m ask ventilation after preoxygenation to reduce aspiration risk.



Induction/paralysis: o

Adm inistration of induction agent (e.g., etom idate or thiopental)

o

Adm inistration of paralytic agent (e.g., succinylcholine) 

Succinylcholine is relatively contraindicated with anticipated difficult oral intubation, open globe injury, organophosphate poisoning, burns >3 days old, denervation syndrom es, m yopathies, and suspected hyperkalem ia.



Rocuronium can be used in patients with hyperkalem ia.



Intubation: o

After m uscle tone is lost (45â€“60 seconds after succinylcholine)



o

Use a stylet with the ET tube.

o

Place tube through vocal cords.

o

Inflate cuff.

o

Begin ventilation.

o

Confirm correct ET tube placem ent.

Postintubation: o

Benzodiazepines, opiates, or propofol used for continued sedation

o

Vecuronium m ay be used for continued paralysis.

Pa ge 3 1 8

Pediatric Considerations 

Estim ation of ET tube size: 4 + age/4



Uncuffed ET tubes m ay be used in patients <8 years old.



Straight Miller blade is preferred in patients <3 years old



Cricothyrotom y contraindicated in patients <12 years old; PTV is preferred



Use atropine as pretreatm ent to reduce secretions and attenuate vagal effect.



A defasciculating neurom uscular blocking agent is unnecessary for children <5 years old

Medication (Drugs) 

Atracurium : 0.4â€“0.5 m g/kg IV



Atropine: 0.02 m g/kg IV



Diazepam : 2â€“10 m g (peds: 0.2â€“0.3 m g/kg) IV



Etom idate: 0.3 m g/kg IV



Fentanyl: 3 Âµg/kg IV



Ketam ine: 1â€“2 m g/kg IV or 4â€“7 m g/kg IM



Lidocaine: 1.5 m g/kg IV



Midazolam : 1â€“5 m g IV (0.07â€“0.30 m g/kg for induction)



Propofol: 2â€“2.5 m g/kg IV



Pancuronium : 0.01 m g/kg IV (defasciculating dose); 0.1 m g/kg IV (paralyzing dose)



Rocuronium : 1 m g/kg IV



Succinylcholine: 1.5 m g/kg (peds: 2 m g/kg) IV; 2.5 m g/kg IM/SC



Thiopental: 3 m g/kg IV



Vecuronium : 0.01 m g/kg IV (defasciculating dose); 0.1 m g/kg IV (paralyzing dose)

Pa ge 3 1 9

Follow-Up Disposition Admission Criteria All intubated patients should be adm itted to an intensive care unit.

Discharge Criteria Certain ED patients who have been intubated for airway protection or to facilitate diagnostic workup m ay be extubated in the ED after a period of observation and then discharged.

References 1. Blanda M, Gallo UE. Em ergency airway m anagem ent. Em erg Med Clin North Am . 2003 Feb;21(1):1â€“26. 2. Butler KH, Clyne B. Managem ent of the difficult airway: alternative airway techniques and adjuncts. Em erg Med Clin North Am . 2003 May;21(2):259â€“289. 3. Vrocher D, Hopson LR. Basic airway m anagem ent and decision-m aking. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Em ergency Medicine. 4th ed. Philadelphia: WB Saunders, 2003;53â€“67. 4. Walls RM. Airway. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby, 2002: 2â€“21.

Miscellaneous SEE ALSO: Rapid sequence intubation

Codes

Pa ge 3 2 0

ICD9-CM N/A

Pa ge 3 2 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Alco ho l Po iso ning

Alcohol Poisoning

Mark B. Mycyk

Basics Description 

Alcohol is the m ost com m only abused recreational agent am ong em ergency departm ent patients.



Alcohol is com m only associated with ED injury evaluations.

Alcohol Intoxication 

Direct CNS depressant effect



Blood alcohol levels drop by 15â€“40 m g/dL/h depending on individual variables and chronicity of alcohol use.

Alcohol Withdrawal 

Occurs after partial or com plete alcohol abstinence in a chronic alcoholic



CNS excitation



Increased autonom ic catecholam ine release



Decreased inhibitory activity

Diagnosis Signs and Symptoms

Pa ge 3 2 2

Acute Alcohol Intoxication 

Sedation



Relaxation



Euphoria



Mem ory loss



Im paired judgm ent



Ataxia



Slurred speech



Nausea/vom iting



Obtundation/com a

Alcohol Withdrawal Syndrome 

Early or m inor withdrawal: o

<8 hours after last drink (blood alcohol level becom es zero):

o

o

o



Sym ptom s of a hangover



Headache



Nausea/vom iting

12 hours after last drink: 

Mild trem ors/anxiety



Anorexia, nausea, vom iting



Weakness



Myalgias



Vivid dream s/nightm ares

12â€“36 hours after last drink: 

Irritability/agitation



Tachycardia/hypertension



Trem ors in hands and tongue



Alcohol hallucinosis

24â€“48 hours after last drinkâ€”alcohol hallucinosis: 

Visual m ost com m on (bug crawling)



Auditory (buzz, clicks)

Pa ge 3 2 3

 o



Present in m inor and m ajor withdrawal

Alcoholic withdrawal seizures: 

8â€“12 hours after last drink



Brief, spontaneously abating tonic-clonic activity



Precedes delirium trem ens (DTs)

Late alcohol withdrawal or m ajor withdrawal: o

48 hours after last drink

o

DTs: 

Clouded consciousness and delirium (hallm ark)



Confusion/disorientation



Agitation/com bativeness



Tachycardia/hypertension



Hyperpyrexia



Diaphoresis

Essential Workup 

Obtain accurate alcohol drinking and abstinence history.



Investigate for life-threatening causes of seizures: o

Hypoglycem ia

o

Intracranial hem orrhage

o

CNS infection

o

Electrolyte abnorm alities



Evaluate for occult traum a



Monitor all vital signs frequently: o

Elevated tem perature predicts poorer outcom es.

Tests Lab 

Alcohol level if abnorm al m ental status



Urine toxicology screen to exclude coingestants



Electrolytes, BUN, creatinine, and glucose



CBC



Magnesium , calcium , and phosphate

Pa ge 3 2 4



PTT, PT/INR if coagulopathy suspected



Liver function tests if liver disease suspected



Am m onia level if hepatic encephalopathy suspected



Urinalysis for ketones

Imaging 

CT of head if: o

Altered m ental status in greater proportion to intoxication

o

Suspected head traum a

o

Signs of increased intracranial pressure or focal findings on neurologic exam s



o

New-onset seizure

o

Unim proved or deteriorating level of consciousness

EEG differentiates alcohol withdrawal seizures from idiopathic epilepsy.



Chest radiograph if suspected aspiration or pneum onia

Differential Diagnosis Acute Alcohol Intoxication 

Hypoglycem ia



Carbon dioxide narcosis



Mixed-drug overdose



Ethylene glycol, m ethanol, isopropanol poisoning



Hepatic encephalopathy



Psychosis



Severe vertigo



Psychom otor seizure

Alcohol Withdrawal and Seizures 

Sedative-hypnotic withdrawal



Acute intoxication or poisoning: o

Carbon m onoxide

Pa ge 3 2 5



o

Isoniazid

o

Am phetam ine

o

Anticholinergic

o

Cocaine

Idiopathic epilepsy: o

Infection

o

Meningitis

o

Encephalitis

o

Brain abscess



Traum a



Intracranial hem orrhage



CVA



Tum or



Anticonvulsant noncom pliance



Thyroid disorder

Treatment Pre Hospital 

Adm inister benzodiazepines for seizures.



Adm inister com a cocktail for m ental status changes.



C-spine im m obilization if suspected traum a

Initial Stabilization 

Airway, breathing, circulation (ABCs)



Evaluate C-spine if suspected traum a.



IV rehydration with D5 0.5 NS



Adm inister naloxone, thiam ine, and glucose (or Accu-Chek) if altered m ental status.



Benzodiazepines if seizures

P.45

Pa ge 3 2 6

ED Treatment Alcohol Intoxication 

Rehydrate with IV fluids.



Correct electrolyte abnorm alities:





o

Magnesium

o

Potassium

o

Folate

o

Thiam ine

o

Multivitam ins

Alcoholic ketoacidosis: o

Aggressive rehydration with D5 0.5 NS

o

Exclude other causes of acidosis.

Exclude other injuries.

Alcohol Withdrawal Syndrome 

Benzodiazepine is agent of choice (diazepam , lorazepam , chlordiazepoxide): o

Cross-tolerant with alcohol

o

Increases GABA A -m ediated transm ission

o

Anticonvulsant effect

o

Large, frequent doses required with significant withdrawal

o 

May halt progression to DTs

Barbiturates (phenobarbital): o

Cross-tolerant with alcohol

o

Anticonvulsant effect

o

Useful if severe withdrawal or DTs refractory to large doses of benzodiazepines



Beta-blocker (atenolol, labetalol, propranolol): o

Norm alizes vital sign abnorm alities

Pa ge 3 2 7

o

Does not treat CNS com plications of alcohol use or withdrawal



Î±-Agonist (clonidine): o

Centrally acting Î± 2 -adrenergic agonist

o

Norm alizes vital sign abnorm alities

o

Does not treat CNS com plications of alcohol use or withdrawal



Phenytoin: o

Not indicated in alcohol withdrawal seizures

o

Indicated if seizures secondary to idiopathic epilepsy, posttraum atic, or status epilepticus

Medication (Drugs) 

Chlordiazepoxide (Librium ): 25â€“100 m g, PO or IV q6h



Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam : 5â€“10 m g IV q5m inâ€“q10m in until patient calm



Lorazepam : 0.5â€“4 m g IV/IM q5m inâ€“q10m in until patient calm



Naloxone (Narcan): 0.4â€“2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Phenytoin: 15â€“18 m g/kg at 50 m g/m in IV



Propofol: 0.5â€“1.0 m g/kg IV (loading dose), then 5â€“50 Âµg/kg/m in (m aintenance dose)



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up

Pa ge 3 2 8

Disposition Admission Criteria 

Hepatic failure, infection, dehydration, m alnutrition, cardiovascular collapse, cardiac dysrhythm ia, traum a



Hallucinations, abnorm al vital signs, severe trem ors, extrem e agitation



Wernicke encephalopathy



Confusion or delirium

Discharge Criteria 

Clinically sober



Seizure free for 6 hours (with negative workup if first seizure)

Issues for Referral Consider substance abuse referral for patients.

References 1. Chiang C, Wax P. Withdrawal syndrom es. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:582â€“586. 2. D'Onofrio G, Degutis LC. Preventive care in the em ergency departm ent: screening and brief intervention for alcohol problem s in the em ergency departm ent: a system atic review. Acad Em erg Med. 2002;9:627â€“638. 3. D'Onofrio G, Rathlev NK, Ulrich AS, et al. Lorazepam for the prevention of recurrent seizures related to alcohol. N Engl J Med. 1999;340:915â€“919. 4. Kosten TR, O'Connor PG. Managem ent of drug and alcohol withdrawal. N Engl J Med. 2003;348:1786â€“1795. 5. Mayo-Sm ith MF. Pharm acological m anagem ent of alcohol withdrawal. JAMA. 1997;278:144â€“151. 6. McMicken DB, Freedland ES. Alcohol-related seizures. Em erg Med

Pa ge 3 2 9

Clin North Am . 1994;12:1057â€“1079.

Miscellaneous SEE ALSO: Ethylene Glycol, Poisoning; Methanol, Poisoning

Codes ICD9-CM 980.0

Pa ge 3 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Alco ho lic Keto acido sis

Alcoholic

Ketoacidosis Jefferson D. Bracey

Basics Description 

Increased production of ketone bodies due to o

Malnourished and hypovolem ic patient

o

Depleted glycogen stores in the liver

o

Elevated ratio of NADH/NAD due to ethanol m etabolism

o 

Increased free fatty acid production

Elevated NADH/NAD ratio leads to the predom inate production of Î²â€“hydroxybutyrate (BHB) over acetoacetate (AcAc)

Etiology 

Malnourished, chronic alcohol abusers following a recent episode of heavy alcohol consum ption: o

Develop nausea/vom iting/abdom inal pain

o

Leading to the cessation of alcohol ingestion

o

In com bination with decreased caloric intake over the preceding several days



Presentation usually occurs within 12â€“72 hours

Pa ge 3 3 1

Diagnosis Signs and Symptoms 

Dehydration



Fever absent unless there is an underlying infection



Tachycardia due to



o

Dehydration with associated orthostatic changes

o

Concurrent alcohol withdrawal

Tachypnea o

Com m on

o

Deep, rapid, Kussm aul respirations frequently present



Nausea and vom iting



Abdom inal pain o

Usually diffuse with nonspecific tenderness

o

Rebound tenderness, abdom inal distension, hypoactive bowel sounds uncom m on

o

Mandates a search for an alternative, coexistent illness



Decreased urinary output from hypovolem ia



Mental status o

Minim ally altered as a result of hypovolem ia and possibly intoxication

o

Altered m ental status m andates a search for other associated conditions such as 

Head injury, cerebrovascular accident (CVA), intracranial hem orrhage



Hypoglycem ia



Alcohol withdrawal

Pa ge 3 3 2

Essential Workup 

Presence of an increased anion gap m etabolic acidosis secondary to the presence of ketones



Recent history of alcohol consum ption

Tests Lab 

Acid-base disturbance: o

Increased anion gap m etabolic acidosis hallm ark

o

Mixed acid-base disturbance com m on 

Respiratory alkalosis



Metabolic alkalosis secondary to vom iting and dehydration

 o

Hyperchlorem ic acidosis

Mild lactic acidosis com m on 

Due to dehydration and the direct m etabolic effects of ethanol



Profound lactic acidosis should prom pt a search for other disorders such as seizures, hypoxia, and shock

o

Positive urine and serum nitroprusside reaction tests 

May not reflect the severity of the underlying ketoacidosis since BHB predom inates and is not m easured by this test



May becom e m isleadingly m ore positive during treatm ent as m ore AcAc is produced



Electrolytes: o

Decreased serum bicarbonate

o

Hypokalem ia due to vom iting

o

Hypocalcem ia

o

Hypophosphatem ia

o

Glucose

Pa ge 3 3 3

o



Usually m ildly elevated



Hypoglycem ia m ay be present

BUN and creatinine m ildly elevated due to dehydration



CBC: o

Mild leukocytosis

o

Throm bocytopenia and anem ia com m only due to chronic alcoholism



Urinalysis: o



Am ylase/Lipase: o



Elevated with associated pancreatitis

Liver function tests: o



Ketonuria without glucosuria

Mildly elevated LFT

Osm olal gap: o

May be m ildly elevated

o

A level over 20 m osm oL/kg should prom pt evaluation for other ingestions (m ethanol and ethylene glycol)

Imaging 

CXR if suspect associated pneum onia



Abdom inal film s for free air if an acute abdom en is present



CT scan of the head if associated traum a or unexplained altered m ental status

Differential Diagnosis 

Increased anion gap m etabolic acidosis o

Lactic acidosis

o

Carbon m onoxide poisoning

o

Aspirin

o

Methanol

o

Ethylene glycol

o

Paraldehyde

Pa ge 3 3 4

o

Isoniazid

o

Diabetic ketoacidosisâ€”m ore severe hyperglycem ia/diabetic history

o 



Urem ia

Hypovolem ia o

GI bleeding

o

Sepsis

Abdom inal pain o

Pancreatitis

o

GI bleeding

o

Gastritis

o

Hepatitis

o

Perforated ulcer

o

Alcohol withdrawal

Treatment Pre Hospital 

Supportive m easures including IV access with 0.9 NS, oxygen, and cardiac m onitoring



Search for historical clues that m ay suggest other etiologies such as toxic ingestions or diabetic history



Attend to other possible coexistent illnesses such as GI bleeding

Initial Stabilization 

Cardiac m onitor and supplem ent oxygen



Narcan, thiam ine, and dextrose if altered m ental status



Initiate 0.9 NS IV fluids o

500 cc-1 L bolus

o

Prom otes renal excretion of ketone bodies

Pa ge 3 3 5

P.47

ED Treatment 

Antiem etic for vom itingâ€”prom ethazine or prochlorperazine



Benzodiazepines for sym ptom s of alcohol withdrawal



Start dextrose containing solutions (D 5 W 0.9% NS) o

Avoid with significant hyperglycem ia

o

Repletes glycogen stores

o

Decreases production of ketone bodies by stim ulating the production of endogenous insulin

o

More rapid resolution of the m etabolic abnorm alities than saline alone



Thiam ine repletion prior to glucose adm inistration to avoid precipitating Wernicke encephalopathy



Sodium bicarbonate rarely indicated o

Consider in severe acidosis with associated cardiovascular dysfunction or irritability



Electrolyte replacem ent o

Hypokalem ia occurs with treatm ent and should be anticipated



o

Hypophosphatem ia m ay occur with treatm ent

o

Magnesium replacem ent as indicated

Insulin is not indicated and m ay precipitate hypoglycem ia

Medication (Drugs) 

D 5 0 W: one am pule of 50% dextrose (25 g) IVP



Lorazepam (benzodiazepine): 2 m g IV and titrate to effect



Narcan: 2 m g IVP

Pa ge 3 3 6



Prochlorperazine: 5â€“10 m g IVP



Prom ethazine: 12.5â€“25 m g IVP



Thiam ine: 100 m g IVP

Follow-Up Disposition Admission Criteria 

Persistent m etabolic acidosis



Persistent orthostatic hypotension



Persistent nausea and vom iting



Abdom inal pain of uncertain etiology



Com orbid illness requiring adm ission for treatm ent



Monitored bed due to electrolyte abnorm alities requiring continued treatm ent

Discharge Criteria 

Many patients can be m anaged in observation unit over 12 hours



Tolerating oral fluids well



Resolution of m etabolic abnorm alities



No other associated illnesses requiring additional therapy

References 1. Diltoer M, Troubleyn J, Lauwers R, et al. Ketosis and cardiac failure: com m on signs of a single condition. Eur J Em erg Med. 2004;11(3):172â€“175. 2. Hoger J. Severe m etabolic acidosis in the alcoholic: Differential diagnosis and m anagem ent. Hum Exp Toxicol. 1996;15(6):482â€“488. 3. Um pierrez G, DiGirolam o M, Tuvlin J, et al. Differences In

Pa ge 3 3 7

Metabolic and Horm onal Milieu in Diabetic and Alcohol Induced Ketoacidosis. J Crit Care. 2000;15(2):52â€“59. 4. Wrenn KD. Slovis CM, et al. The syndrom e of alcoholic ketoacidosis. Am J Med. 1991;91(2):119â€“128.

Miscellaneous SEE ALSO: Diabetic Ketoacidosis, Acidosis

Codes ICD9-CM 276.2

ICD10 E87.2

Pa ge 3 3 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Alkalo sis

Alkalosis

Matthew Robinson

Basics Description Respiratory Alkalosis 

Elevated serum pH secondary to alveolar hyperventilation and decreased PaCO 2



Hyperventilation occurs through stim ulation of two receptor types: o

Central receptorsâ€”located in the brainstem and respond to decreased CSF pH

o

Chest receptorsâ€”located in aortic arch and respond to hypoxem ia



Increased alveolar ventilation secondary to: o

Disorders causing acidosis

o

Hypoxem ia or

o

Nonphysiologic stim ulation of those receptors by CNS or chest disorders



Rarely life threatening with pH typically <7.50

Metabolic Alkalosis 

Prim ary increase in serum HCO 3 - secondary to loss of H + or gain of HCO 3 -

Pa ge 3 3 9



Pathogenesis requires an initial process that generates a m etabolic alkalosis with a secondary or overlapping process m aintaining the alkalosis.



Generation occurs through one of the following m echanism s: o

Gain of alkali through ingestion or infusion

o

Loss of H + through the GI tract or kidneys

o

Shift of hydrogen ions into the intracellular space

o

Contraction of extracellular fluid (ECF) volum e through loss of HCO 3 - -poor fluids



Renal m aintenance is required to sustain a m etabolic alkalosis secondary to the kidney's enorm ous ability to excrete HCO 3 - . This occurs through the following: o

Decreased glom erular filtration rate (GFR; renal failure, ECF depletion)

o

Elevated tubular resorption of HCO 3 - secondary to hypochlorem ia, hyperaldosteronism , hypokalem ia, ECF depletion



Mortality 45% if pH >7.55 and 80% if pH >7.65

Etiology 

Respiratory alkalosis: o

o

Central nervous system : 

Hyperventilation syndrom e



Pain



Anxiety/psychosis



Fever



Cerebrovascular accident (CVA)



CNS infection (m eningitis, encephalitis)



CNS m ass lesion (tum or, traum a)

Hypoxem ia: 

Altitude



Anem ia

Pa ge 3 4 0

 o

o

o

o



Shunt

Medications/drugs: 

Progesterone



Methylxanthines



Salicylates



Catecholam ines



Nicotine

Endocrine: 

Hyperthyroidism



Pregnancy

Chest stim ulation: 

Pulm onary em bolism



Pneum onia



Pneum othorax

Other: 

Sepsis



Hepatic failure



Heat exhaustion

Metabolic alkalosis: o

Loss of H + : 

Gastrointestinal



Vom iting



Nasogastric suctioning



Bulim ia

o

Antacid therapy

o

Chlorideâ€“losing diarrhea (villous adenom a)

o

Renal loss:

o



Diuretics (loop and thiazide)



Post-chronic hypercapnia



Mineralocorticoid excess



Hyperaldosteronism

Drug/m edication

Pa ge 3 4 1

o

Glucocorticoid excess (Cushing disease)

o

Gitelm an syndrom e

o

Bartter syndrom e

o

H + shift

o

Hypokalem ia

o

Contraction alkalosis: 

Diuretics



Sweat loss in cystic fibrosis

o

HCO 3 - retention

o

NaHCO 3 infusion

o

Milk-alkali syndrom e

o

Blood transfusions

Diagnosis Signs and Symptoms 

Signs and sym ptom s secondary to: o

Arteriolar vasoconstriction

o

Hypocalcem ia secondary to decreased ionized calcium from increased calcium binding to album in

o

Associated hypokalem ia

o

Underlying cause



Weakness



Seizures



Altered m ental status



Tetany



Chvostek Sign



Trousseau Sign



Arrhythm ias



Myalgias



Carpal-pedal spasm

Pa ge 3 4 2



Perioral tingling/num bness



Hypoxem ia



Dehydration

Essential Workup 



Electrolytes: o

Elevated HCO 3 - with m etabolic alkalosis

o

Evaluate for hypokalem ia and hypocalcem ia.

BUN/creatinine: o





Evaluate for renal failure or dehydration.

Arterial blood gases: o

pH

o

PCO 2 decreased in respiratory alkalosis

o

PO 2 for hypoxem ia

Calculate com pensation to identify m ixed acid-base disorders.

Acute Respiratory Alkalosis 

HCO 3 - decreases secondary to intracellular shift and buffering within 10â€“20 m inutes



Expected HCO 3 - decreased by 2 m Eq/dL for each 10 m m Hg decrease in PCO 2

Chronic Respiratory Alkalosis 

HCO 3 - decreased secondary to renal secretion of HCO 3 o



Requires 48â€“72 hours for m axim al com pensation

Expected HCO 3 - decreased by 5 m Eq/dL for each 10 m m HG decrease in PCO 2 o

If HCO 3 - greater than predicted, concom itant m etabolic alkalosis

o

If HCO 3 - less than predicted, concom itant m etabolic acidosis

Metabolic Alkalosis

Pa ge 3 4 3



Expected PCO 2 = 0.9 [HCO 3 - ] + 9: o

If PCO 2 greater than predicted, concom itant respiratory acidosis

o

If PCO 2 less than predicted, concom itant respiratory alkalosis



Urine chloride: o

More accurate m arker than urine Na + for patient's volum e status 

UCl - <20 m Eq/L in volum e depletion



UCl - >40 m Eq/L in euvolem ia or edem atous states

Tests Lab 

Glucose



Ionized calcium



Magnesium level



Urine pregnancy



Additional labs to evaluate underlying cause: o

CBC, blood cultures for sepsis

o

Liver function for hepatic failure

o

Aspirin level

o

Urine toxicology screen

o

Urine diuretics screen (bulim ia)

o

Urine diuretic screen (surreptitious diuretic abuse)

o

Renin level

o

Cortisol level

o

Aldosterone level

o

Thyroid-stim ulating horm one (TSH), T4

o

D-dim er

P.49

Pa ge 3 4 4

Imaging 

Chest radiograph



Head CT



ECG

Differential Diagnosis 

Respiratory alkalosis: o

See etiologies above.

o

It is essential to rule out organic disease prior to diagnosing hyperventilation syndrom e or anxiety states.



Metabolic alkalosis: o

Chloride responsive (urine Cl - <20 m Eq/dL)

o

Loss of gastric secretions

o

Chloride-losing diarrhea

o

Diuretics

o

Post-chronic hypercapnia

o

Cystic fibrosis

o

Chloride resistant

o

Hyperaldosteronism

o

Cushing syndrom e

o

Bartter syndrom e

o

Exogenous m ineralocorticoids or glucocorticoids

o

Gitelm an syndrom e

o

Hypokalem ia

o

Hypom agnesem ia

o

Milk-alkali syndrom e

o

Exogenous alkali infusion/ingestion

o

Blood transfusions

Pa ge 3 4 5

Treatment Initial Stabilization Airway, breathing, circulation (ABCs): 

Early intubation and airway control for obtundation or altered m ental status



IV, oxygen, and cardiac m onitor



Naloxone, D 5 0 W (or Accu-Chek) and thiam ine for altered m ental status

ED Treatment 

Respiratory alkalosis: o

Treat underlying disorder.

o

Rarely life threatening

o

Sedation/anxiolytics for anxiety, psychosis, or drug overdose

o 

Rebreathing into bag for hyperventilation syndrom e

Metabolic alkalosis: o

Treat underlying disorder: 

Antiem etics for vom iting



Proton pum p inhibitors for patients with nasogastric (NG) suction



Rehydrate with 0.9% saline for chloride-responsive alkalosis with signs of volum e depletion.



Potassium chloride for chloride-responsive alkalosis in edem atous states



Follow ventilatory status closely: o

Correct electrolyte abnorm alities.

o

Consider hem odialysis for severe electrolyte abnorm alities.

Pa ge 3 4 6

Medication (Drugs) 

Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: 2% dextrose and water 2â€“4 m L/kg) IV



KCl (K-Dur, Gen-K, Klor-Con): 20â€“120 m Eq PO daily



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 



ICU adm ission if: o

pH >7.55 or altered m ental status

o

Dysrhythm ias

Coexisting m edical illness requiring adm ission

Discharge Criteria Resolving or resolved alkalosis

References 1. Adrogue H. Managem ent of life-threatening acid-base disorders. New Engl J Med. 1998;338:107. 2. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000;11:369. 3. Khanna A. Metabolic alkalosis. Respir Care. 2001;46:354. 4. Whittier W. Prim er on clinical acid-base problem solving. Dis Mon. 2004;50:117.

Codes ICD9-CM 276.23

ICD10

Pa ge 3 4 7

E87.3

Pa ge 3 4 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Altered M ental Status

Altered Mental

Status David F. M. Brown Kathleen A. Wittels

Basics Description 

Dysfunction in either the reticular activating system in the upper brainstem or a large area of one of the cerebral hem ispheres



Definitions: o

Confusion: a behavioral state of reduced m ental clarity, coherence, com prehension, and reasoning

o

Drowsiness: The patient cannot be easily aroused by touch or noise and cannot m aintain alertness for som e tim e.

o

Lethargy: depressed m ental status in which the patient m ay appear wakeful but has depressed awareness of self and environm ent globally; cannot be aroused to full function

o

Stupor: The patient can be awakened only by vigorous stim uli, and an effort to avoid uncom fortable or aggravating stim ulation is

Pa ge 3 4 9

displayed. o

Com a: The patient cannot be aroused by stim ulation and no purposeful attem pt is m ade to avoid painful stim uli.

Etiology 





Hypoxic: o

Severe pulm onary disease

o

Anem ia

o

Shock

o

Intracardiac shunting (especially in pediatrics)

Metabolic: o

Hypoglycem ia

o

Diabetic ketoacidosis

o

Nonketotic hyperosm olar com a

o

Thiam ine deficiency

o

Hyperam m onem ia

o

Urem ia

o

CO 2 narcosis

o

Hyperglycem ia

o

Hyponatrem ia; hypernatrem ia

o

Hypocalcem ia; hypercalcem ia

o

Hypom agnesem ia; hyperm agnesem ia

o

Hypophosphatem ia

o

Acidosis; alkalosis

Toxicologic: o

Ethanol

o

Isopropyl alcohol

o

Methanol

o

Ethylene glycol

o

Salicylates

o

Sedatives and narcotics

o

Anticonvulsants

Pa ge 3 5 0





o

Psychotropics

o

Isoniazid

o

Heavy m etals

o

Carbon m onoxide

o

Cyanide

Endocrine: o

Myxedem a com a

o

Thyrotoxicosis

o

Hypothyroidism

o

Addison disease

o

Cushing disease

o

Pheochrom ocytom a

o

Hyperparathyroidism

Environm ental: o

Hypotherm ia

o

Heat stroke

o

High-altitude cerebral edem a

o

Neuroleptic m alignant syndrom e

o

Malignant hypertherm ia



Intracranial hypertension



Hypertensive encephalopathy



Pseudotum or cerebri



CNS inflam m ation



Meningitis



Encephalitis



Encephalopathy



Cerebral vasculitis



TTP



Subarachnoid hem orrhage



Carcinoid m eningitis



Prim ary neuronal or glial disorders: o

Creutzfeldt-Jakob disease

Pa ge 3 5 1

o

Marchiafava-Bignam i disease

o

Adrenoleukodystrophy

o

Gliom atosis cerebri

o

Progressive m ultifocal leukoencephalopathy



Seizures and postictal state



Supratentorial lesions:



o

Hem orrhage

o

Infarction

o

Tum ors

o

Abscess

Subtentorial lesions: o

Cerebellar hem orrhage

o

Posterior fossa subdural or extradural hem orrhage

o

Cerebellar infarct

o

Cerebellar tum or

o

Cerebellar abscess

o

Basilar aneurysm

o

Pontine hem orrhage

o

Brainstem infarct

o

Basilar m igraine

o

Brainstem dem yelination

Diagnosis Signs and Symptoms Confusion 

Difficulty in m aintaining a coherent stream of thinking and m ental perform ance: o

Rem em ber to consider the level of education and language and possible learning disabilities.

Pa ge 3 5 2



Inattention



Mem ory deficit: o

Inability to recall any of the following: 

The date, inclusive of m onth, day, year, and day of week



The precise place



Item s of universally known inform ation



Why the patient is in the hospital



Address, telephone num ber, or Social Security num ber



Im paired m ental perform ance: o

Difficulty retaining seven digits forward and four backward

o

Difficulty nam ing ordinary objects

o

Serial calculations: 

Holding the result of one calculation in a working m em ory in order to pursue the next step

 

Serial 3-from -30 subtraction test

Disorganized and ram bling language: o

May be m istaken for aphasia

Findings That Suggest an Underlying Cause 

Fever: o

Infectious etiologies, drug toxicities, endocrine disorders, heat stroke



Severe hypertension and decreased heart rate (Cushing reflex): o



Suggestive of an intracranial structural lesion

Hypotension: o

Infectious and toxicologic etiologies, decreased cardiac output



Hypotherm ia:

Pa ge 3 5 3

o

Hypoglycem ia, environm ental factors, Addisonian crisis



Eye resting position: o

Dysconjugate gaze in horizontal plane occurs with drowsiness.

o

Dysconjugate gaze in vertical plane occurs with pontine or cerebellar lesions.

o

Sustained conjugate downward eye deviation occurs with a variety of neurologic disorders.

o

Sustained conjugate upward gaze occurs with hypoxic encephalopathy.

o

Eyes fluttering upwards (Bell phenom enon) occurs with psychogenic com a

o

Ocular bobbing: 

Cyclical brisk conjugate caudal jerks of the globes followed by a slow return to m idposition



Bilateral pontine dam age, m etabolic derangem ent, and brainstem com pression

o

Ocular dipping: 

Slow, cyclical, conjugate, downward m ovem ent of the eyes followed by a rapid return to m idposition

 

Diffuse cortical anoxic dam age

Pupillary exam ination: o

Norm al size, shape, and response to light indicates intact m idbrain function.

o

Nearly all toxic and m etabolic causes of com a leave the pupillary reflexes sluggish but bilaterally intact.



Focal findings: o

Hem iparesis

o

Hem ianopsia

o

Aphasia

Pa ge 3 5 4



o

Myoclonus

o

Convulsions

o

Nuchal rigidity

Asterixis: o

Arrhythm ic flapping trem or (alm ost always bilateral)

o

Caused by m etabolic encephalopathy: 

Hepatic failure or severe renal failure



Anticonvulsant drug ingestion

P.51



Myoclonic jerking and trem or: o

Urem ic encephalopathy: 

Antipsychotic drug ingestion

Tests Lab 

Dextrostix and glucose



CBC



Electrolytes (including calcium )



Blood urea nitrogen, creatinine



Arterial blood gases



Toxicologic screen (including toxic alcohols)



ECG



Urinalysis



Consider LFTs, am m onia, serum osm olarity

Imaging 

Caloric stim ulation of the vestibular apparatus: o

Indicated to assess unresponsive patients

o

Contraindications include tym panic m em brane perforation and cerum en im paction.

o

Irrigate the external auditory canal with 10 cc of

Pa ge 3 5 5

ice-cold water after elevating the head to 30 degrees. o

Bilateral tonic deviation of the eyes toward the stim ulus indicates an intact brainstem .

o

Nystagm uslike quick corrective phases indicates intact cerebral hem ispheres.

o

A norm al response in an unresponsive patient raises the suspicion of psychogenic com a.



CT scan: o

Noncontrast only to rule out hem orrhage and m ass effect



Lum bar puncture (LP): o

Indicated when the etiology rem ains unclear after laboratory and CT scan

o

Em piric antibiotics should be given before LP to avoid any delay in therapy in patients with suspected m eningitis.



MRI (if available): o

Indicated when suspicious of ischem ic stroke within tim e fram e for throm bolysis

Differential Diagnosis 

Locked-in syndrom e: o

Rare disorder caused by dam age to the corticospinal, corticopontine, and corticobulbar tracts resulting in quadriplegia and m utism with preservation of consciousness.

o

Com m unication m ay be established through eye m ovem ents (m aintain vertical eye m ovem ents).





Psychogenic unresponsiveness: o

Conversion reactions

o

Catatonia

Malingering

Pa ge 3 5 6



Akinetic m utism (abulic state)



Dem entia: o

The m ental status waxes and wanes.

o

Attention is preserved in the early stages.

Treatment Pre Hospital 

Airway m anagem ent if loss of airway patency



IV access, supplem ental oxygen, cardiac m onitor



Spine im m obilization if possibility of traum a



Bag-m ask ventilation with cricoid pressure



Endotracheal intubation if no response to com a cocktail



Com a cocktail:



o

Dextrose

o

Naloxone

o

Thiam ine

Look for signs of an underlying cause: o

Medications

o

Medic alert bracelets

o

Docum ent a basic neurologic exam ination

o

GCS

o

Pupils

o

Extrem ity m ovem ents

o

Gross signs of traum a

o

Talk with fam ily/pre-hospital personnel for inform ation

Controversies 

Em pirical dextrose should not be withheld or delayed if Dextrostix is not available

Pa ge 3 5 7

o

Glucose can be safely adm inistered before thiam ine.

o

Glucose does not worsen outcom e in patients with stroke.



Adm inistration of charcoal by pre-hospital personnel

Initial Stabilization 

Intravenous D 5 0



Naloxone



Thiam ine

ED Treatment 

Consider em piric use of antibiotics for altered m ental status of undeterm ined etiology: o

Broad spectrum with good cerebrospinal fluid penetration such as ceftriaxone and vancom ycin



Em piric treatm ent if a toxic ingestion is suspected: o

Activated charcoal

o

Alcohol drip if m ethanol or ethylene glycol is suspected



Correct body tem perature: o

Warm ed hum idified O 2 and IV fluids if hypotherm ic

o

Ice packs and forced air m ovem ent over exposed m oistened skin if severe hypertherm ia



Specific therapy directed at underlying cause

Medication (Drugs) 

Ceftriaxone: 2 g (peds: 50â€“75 m g/kg) IV



Dextrose: 1â€“2 m L/kg of D 5 0 W (peds: 2â€“4 m L/kg D 2 5 W) IV



Diazepam : 0.1â€“0.3 m g/kg slow IV (m ax 10 m g/dose) q10m inâ€“q15m in Ã— three doses



Lorazepam : 0.05â€“0.1 m g/kg IV (m ax 4 m g/dose

Pa ge 3 5 8

q10m inâ€“q15m in) 

Mannitol: 0.5â€“1 g/kg IV



Naloxone: 0.01â€“0.1 m g/kg IV/IM/SC/ET



Thiam ine: 100 m g IM or 100 m g thiam ine in 1,000 m L of IV fluid wide open

Follow-Up Disposition Admission Criteria All patients with acute changes in m ental status require adm ission.

Discharge Criteria 

Treated hypoglycem ia related to insulin therapy with resolved sym ptom s



Chronic altered m ental status (e.g., dem entia) without change from baseline

References 1. Giacino JT, Aschwal S, Childs N, et al. The m inim ally conscious state: definition and diagnostic criteria. Neurology. 2002;58:349â€“353. 2. Kanich W, Brady WJ, Huff JS, Perron AD. Holstege C. Lindbeck G. Carter CT. Altered m ental status: evaluation and etiology in the ED. Am J Em erg Med. 2002;20:613â€“617. 3. Hoffm an RS, Goldfrank LR. The poisoned patient with altered consciousness. Controversies in the use of a â€œcom a cocktail.â€• JAMA. 1995;274:562â€“569. 4. Sam uels MA. The evaluation of com atose patients. Hosp Pract. 1993;28:165â€“182.

Pa ge 3 5 9

Miscellaneous SEE ALSO: Com a

Codes ICD9-CM 293.0 293.81 293.82 294.1 294.8

ICD10 F99

Pa ge 3 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am ebiasis

Amebiasis

Ann P. Nguyen

Basics Description 

Invasive parasitic infection with both intestinal and extraintestinal m anifestations



Endem ic in developing countries



Fifty m illion cases and 40,000â€“100,000 deaths worldwide each year







Fecal-oral transm ission: o

Hum ans are sole reservoir.

o

Up to 90% asym ptom atic carriage

Populations at risk: o

Travelers to and im m igrants from endem ic areas

o

Institutionalized persons

o

Practitioners of anal sexual activity

Risk factors for increased severity of disease and com plications: o

Corticosteroid use

o

Malignancy

o

Malnutrition

o

Pregnancy/postpartum state

o

Extrem es of age

Pa ge 3 6 1

o

HIV disease

Etiology 

Entam oeba histolytica, a nonflagellated protozoa



Biphasic life cycle: o

Ingested as cysts

o

Cysts becom e trophozoites, which cause invasive colitis.

o

Create m ultiple flask-shaped ulcers in the colonic m ucosa and m uscularis

o

Extraintestinal spread is hem atogenous.

Diagnosis Signs and Symptoms Intestinal Disease 

Onset 1 week to 1 m onth postexposure



Acute diarrhea (80% of cases):



o

1â€“4 weeksâ€™ duration

o

Afebrile

o

Occult blood in stool

o

Benign abdom inal exam

Classic dysentery: o

1â€“4 weeksâ€™ duration

o

Bloody m ucoid diarrhea

o

Abdom inal pain

o

Bloating

o

Tenesm us

o

Weight loss

o

Fever (rare)

o

Benign abdom inal exam

Pa ge 3 6 2



Fulm inant colitis: o

Toxic-appearing patient

o

Rigid abdom en (25%)

o

Fever

o

Severe bloody diarrhea

o

Rapid progression to perforated bowel and frank peritonitis

o 

>50% m ortality

Toxic m egacolon: o

Toxic-appearing patient

o

Profuse diarrhea (>10 stools per day)

o

Fever

o

Tachycardia

o

Distended, tym panitic abdom en with signs of peritonitis



o

Associated with corticosteroid use

o

High m ortality

Am ebom a: o

Intralum inal granulated m ass

o

Most com m on in the cecum , ascending colon, and rectosigm oid colon

o 



Tender palpable m ass on exam

Am ebic strictures: o

Owing to chronic inflam m ation and scarring

o

Most com m on in the anus, rectum , or sigm oid colon

o

Cram py abdom inal pain

o

Nausea and vom iting (m ay be feculent)

o

May lead to partial or com plete bowel obstruction

Chronic am ebic colitis: o

Mild recurrent episodes of bloody diarrhea, abdom inal cram ping, tenesm us

o

Weight loss

Pa ge 3 6 3

o

May persist for years

Extraintestinal Disease 

Am ebic liver abscess: o

Most frequent extraintestinal m anifestation (3â€“9% of cases)

o

Single abscess in right lobe (50â€“80%)

o

May develop m onths to years postexposure (m edian of 3 m onths)

o

Fever

o

Cough

o

Right upper quadrant pain

o

Hepatom egaly with point tenderness

o

Rales at right lung base

o

Concurrent diarrhea unusual (20â€“33%)

o

Com plication: rupture into pleural cavity (10â€“20%), peritoneum (2â€“7%) or pericardium (rare)





Extrahepatic am ebic abscess: o

Hem atologic spread

o

Brain

o

Lung

o

Perinephric

o

Splenic

o

Vaginal/cervical/uterine

Cutaneous am ebiasis: o

Perineum and genitalia

o

Well-defined, irregularly shaped friable ulcers

o

Purulent exudate

o

Painful

Pediatric Considerations Children m ore likely than adults to present with fulm inant colitis

Pa ge 3 6 4

Pregnancy Considerations Pregnant patients m ore likely to present with fulm inant colitis

Essential Workup 



History: o

Possible sources of exposure

o

Mem bership in high-risk group

Physical exam : o

Identify evidence of peritonitis, sepsis, or shock.

o

Tender abdom inal m ass m andates workup for liver abscess or am ebom a.

o

Digital rectal exam shows gross or occult blood in >70% of patients.

Tests Lab 

Stool enzym e-linked im m unosorbent assay (ELISA) for E. histolyticaâ€“specific antigen: o

74â€“100% sensitive

o

Stool m icroscopy is insensitive and no longer the test of choice.





Fecal leukocytes and culture: o

Rule out infection owing to enteroinvasive bacteria.

o

Negative in am ebiasis

Serum for anti-E. histolytica antibodies: o

Essential if suspecting liver abscess as these patients rarely shed parasites in their stool



o

90â€“100% sensitive in am ebic liver abscess

o

70â€“90% sensitive in am ebic colitis

CBC: o



Leukocytosis in am ebic liver abscess and peritonitis

Alkaline phosphatase and ALT:

Pa ge 3 6 5

o 

Elevated in am ebic liver abscess

Serum electrolytes, BUN/creatinine if prolonged diarrhea or evidence of dehydration

Imaging 

Abdom inal ultrasound: o

58â€“90% sensitive

o

Evaluate abscess for increased risk of rupture (>5 cm or located in left lobe)



Abdom inal CT or MRI: o

Equivalent to ultrasound for delineating liver abscesses

o

Superior to ultrasound for detecting abscesses in other organs



Head CT or MRI: o

Suspect am ebic brain abscess if patient with known am ebiasis presents with altered m ental status or focal neurologic findings.

o 

Irregular nonenhancing lesions

Chest radiograph: o

Elevated right hem idiaphragm and/or right pleural effusion in liver abscess

Diagnostic Procedures/Surgery 

Colonoscopy with biopsy: o

Provides definitive diagnosis of am ebic dysentery, colitis, am ebom a, and am ebic stricture



Percutaneous fine-needle aspiration of liver abscess: o

Indicated to exclude bacterial abscess if high suspicion for this entity (elderly patient, nondiagnostic serology, failure of antiam ebic therapy)

P.53

Pa ge 3 6 6

Differential Diagnosis 

Intestinal am ebiasis: o

Enteroinvasive bacterial infection (Staphylococcus, E. coli, Shigella, Salm onella, Yersinia, Cam pylobacter)





o

Inflam m atory bowel disease

o

Ischem ic colitis

o

Arteriovenous m alform ation

o

Abdom inal aortic aneurysm

o

Perforated duodenal ulcer

o

Intussusception

o

Diverticulitis

o

Pancreatitis

o

Colorectal carcinom a

Am ebic abscess: o

Bacterial abscess

o

Tuberculous cavity

o

Echinococcal cyst

o

Malignancy

o

Cholecystitis

Cutaneous am ebiasis: o

Carcinom a

o

Sexually transm itted diseases (condylom a acum inata, chancroid, syphilis)

Treatment Initial Stabilization 

Airway, breathing, circulation (ABCs)

Pa ge 3 6 7



IV 0.9 NS if signs of significant dehydration or shock

ED Treatment 

Oral fluids for m ild dehydration



Avoid antidiarrheal agents.



Correct any serum electrolyte im balances.



Stool sam ple for E. histolyticaâ€“specific antigen plus serology for antiâ€“E. histolytica antibodies



If stool or serum is positive for E. histolytica: o

Metronidazole is first-line drug for system ic am ebiasis. 

o

Ninety percent cure rate

Tetracycline for m ild dysentery in m etronidazole-intolerant patients, but will not eradicate hepatic infection

o

Dehydroem etine if m etronidazole fails: 

Must adm it all dehydroem etine patients to a m onitored setting because of the potential for cardiac toxicity and dysrhythm ia

o

Always follow system ic therapy with a lum inal am ebicidal agent to eradicate intestinal colonization (diloxanide furoate, parom om ycin, or iodoquinol).



If stool or serum is negative for E. histolytica: o

Refer to gastroenterologist for colonoscopy with biopsy.

o

Repeat serology in 7 days.

o

Consider em piric course of m etronidazole if high suspicion for am ebiasis and patient is critically ill.



If evidence of peritonitis or sepsis: o

Add IV antibiotic directed against anaerobic and gram -negative bacteria.

o 

Surgery if toxic m egacolon or colonic perforation

If liver abscess is suspected:

Pa ge 3 6 8

o

Ultrasound of hepatobiliary system with concurrent am ebic serology

o

Abdom inal CT scan if ultrasound is equivocal

o

If im aging dem onstrates an abscess but serology is negative, treat with am ebicidals as above and repeat serology in 7 days.

o

Consult surgery for drainage of >5 cm and left lobe abscesses (risk of rupture).

o

If sym ptom s do not im prove after 5 to 7 days of em piric am ebicidal therapy, consider fine-needle aspiration to rule out bacterial liver abscess or hepatom a.

Pregnancy Considerations 

Adm inister m edications with caution in first-trim ester pregnancy, but do not withhold if patient has fulm inant colitis or am ebic abscess.



Erythrom ycin for m ild dysentery in first-trim ester pregnancy

Medication (Drugs) 

Dehydroem etine: 90 m g (peds: 1â€“1.5 m g/kg/24h) IM q24h for 5 days



Diloxanide furoate: 500 m g (peds: 20 m g/kg/24h) PO q8h for 10 days



Erythrom ycin: 500 m g (peds: 30â€“50 m g/kg/24h) PO q6h for 10 days



Iodoquinol: 650 m g (peds: 30â€“40 m g/kg/24h) PO q8h for 20 days



Metronidazole: 750 m g (peds: 30â€“50 m g/kg/24h) PO/IV q8h for 10 days

Pa ge 3 6 9



Parom om ycin: 25â€“30 m g/kg/24h PO q8h for 7â€“10 days



Tetracycline: 250 m g PO q8h for 10 days

Follow-Up Disposition Admission Criteria 

Shock, sepsis or peritonitis



Hypotension or tachycardia unresponsive to IV fluids



Children with >10% dehydration



Severe electrolyte im balance



Patients unable to m aintain adequate oral hydration: o

Extrem es of age, cognitive im pairm ent, significant co-m orbid illness



Fulm inant colitis or toxic m egacolon



Bowel obstruction



Extraintestinal abscesses



Failure of outpatient regim en



Dehydroem etine therapy

Discharge Criteria 

Nontoxic presentation of acute or chronic dysentery



Able to m aintain adequate oral hydration



Dehydration responsive to IV fluids

Issues for Referral Consult surgery if evidence of peritonitis, toxic m egacolon, colonic perforation, or liver abscess >5 cm or located in left liver lobe.

References 1. Blessm an J, Binh HD, Hung DM, et al. Treatm ent of am oebic liver abscess with m etronidazole alone or in com bination with

Pa ge 3 7 0

ultrasound-guided needle aspiration: a com parative, prospective and random ized study. Trop Med Int Health. 2003;8:1030â€“1034. 2. Elzi L, Laifer G, Sendi P, et al. Low sensitivity of ultrasonography for the early diagnosis of am ebic liver abscess. Am J Med. 2004;117:519â€“522. 3. Haque R, Huston CD, Hughes M, et al. Current concepts: am ebiasis. N Engl J Med. 2003;348:1565â€“1573. 4. Hung CC, Deng HY, Hsiao WH, et al. Invasive am ebiasis as an em erging parasitic disease in patients with HIV-1 infection in Taiwan. Arch Int Med. 2005;165:409â€“415. 5. Petri WA. Therapy of intestinal protozoa. Trends Parasitol. 2003;19:523â€“526. 6. Stanley SL. Am oebiasis. Lancet. 2003;361:1025â€“1034. 7. Stauffer W, Ravdin JI. Entam oeba histolytica: an update. Curr Opin Inf Dis. 2003;16:479â€“485. 8. Tanyuksel M, Petri WA. Laboratory diagnosis of am ebiasis. Clin Microbiol Rev. 2003;16:713â€“729.

Miscellaneous SEE ALSO: Diarrhea; Gastroenteritis

Codes ICD9-CM 006.0

ICD10 A06.9

Pa ge 3 7 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am eno rrhea

Amenorrhea

Christy Rosa Mohler

Basics Description Absence of m enstruation

Etiology 



Prim ary: o

Gonadal dysgenesis

o

Chrom osom al abnorm alities

Secondary: o

Pregnancy, breast-feeding, postpartum

o

Asherm an syndrom e (intrauterine adhesions)

o

Dysfunction of the hypothalam ic-pituitary-ovarian axis

o

Endocrinopathies

o

Obesity, starvation, intense exercise

o

Drugs: 

Oral contraceptives, antipsychotics, antidepressants, calcium channel blockers, chem otherapeutic agents, digitalis, m arijuana

o

Autoim m une disorders

o

Ovarian failure

o

Menopause

Pa ge 3 7 2

Diagnosis Signs and Symptoms History 

Prim ary am enorrhea: o

No spontaneous uterine bleeding by age 14 years in the absence of the developm ent of secondary sexual characteristics or by age 16 years with otherwise norm al developm ent



Secondary am enorrhea: o

Absence of m enstrual bleeding for 6 m onths in a wom an with prior regular m enses or for 12 m onths in a wom an with prior oligom enorrhea

Physical Exam 

Low estrogen: atrophic vaginal m ucosa, m ood swings, irritability



High androgen: truncal obesity, hirsutism , acne, m ale-pattern baldness

Essential Workup Pregnancy test

Tests Lab 

If pregnancy test is negative, no further testing is needed em ergently.



May send thyroid-stim ulating horm one (TSH), prolactin, luteinizing horm one (LH), follicle-stim ulating horm one (FSH) for follow-up by gynecology or prim ary care physician

Pa ge 3 7 3

Imaging None needed em ergently

Diagnostic Procedures/Surgery None needed em ergently

Differential Diagnosis Pregnancy P.55

Treatment Pre Hospital If am enorrhea is the result of pregnancy, stabilize patient as appropriate for pregnancy.

ED Treatment Reassurance and referral for follow-up

Medication (Drugs) Defer for gynecology evaluation.

Follow-Up Disposition Admission Criteria No need for adm ission

Pa ge 3 7 4

Discharge Criteria All patients can be discharged with appropriate referral.

Issues for Referral Nonem ergent referral to gynecology

References 1. Prim ary and secondary am enorrhea. In:Stenchever MA, et al., eds. Com prehensive Gynecology. 4th ed. St. Louis, MO: Mosby; 2001:1099â€“1119. 2. Warren MP, Hagey AR. The genetics, diagnosis and treatm ent of am enorrhea. Minerva Ginecol. 2004;56(5):437â€“455.

Codes ICD9-CM N/A

Pa ge 3 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am phetam ine, Po iso ning

Amphetamine,

Poisoning James W. Rhee

Basics Description 

Increased release of norepinephrine, dopam ine, serotonin



Decreased catecholam ine reuptake



Direct effect on Î±- and Î²-adrenergic receptors

Etiology 



Prescription drugs: o

Am phetam ine (Benzedrine)

o

Dextroam phetam ine (Dexedrine)

o

Diethylpropion (Tenuate)

o

Fenfluram ine (Pondim in)

o

Metham phetam ine

o

Methylphenidate (Ritalin)

o

Phenm etrazine (Preludin)

o

Phenterm ine

â€œDesigner drugsâ€•: o

Variants of illegal parent drugs

o

Often synthesized in underground laboratories

o

â€œIceâ€•:

Pa ge 3 7 6



Crystalline m etham phetam ine hydrochloride



Sm oked, insufflated, or injected



Rapid onset; duration several hours

o

â€œCrankâ€•

o

â€œEcstasyâ€• (3,4-m ethylenedioxym etham phetam ine, MDMA, XTC): 

Often used at dances and â€œraveâ€• parties



Dehydration can lead to hypertherm ia, hyponatrem ia, fatality.

o

MDA (3,4-m ethylenedioxyam phetam ine)

o

Methcathinone (â€œcat,â€• â€œJeff,â€• â€œm ulkaâ€•): 

Derivative of cathinone, found in the evergreen tree Catha edulis



Frequently synthesized in hom e laboratories



Does not show up on urine toxicology screens

Diagnosis Signs and Symptoms 

Central nervous system (CNS): o

Agitation

o

Delirium

o

Hyperactivity

o

Trem ors

o

Dizziness

o

Mydriasis

o

Headache

o

Choreoathetoid m ovem ents

o

Hyperreflexia

Pa ge 3 7 7







o

Cerebrovascular accident

o

Seizures and status epilepticus

o

Com a

Psychiatric: o

Euphoria

o

Increased aggressiveness

o

Anxiety

o

Hallucinations (visual, tactile)

o

Com pulsive repetitive actions

Cardiovascular: o

Palpitations

o

Hypertensive crisis

o

Tachycardia or (reflex) bradycardia

o

Dysrhythm ias (usually tachydysrhythm ias)

o

Cardiovascular collapse

Other: o

Rhabdom yolysis

o

Myoglobinuria

o

Acute renal failure

o

Anorexia

o

Diaphoresis

o

Dissem inated intravascular coagulation (DIC)

Essential Workup 

Vital signs: o

o

Tem perature >40Â°C: 

Core tem perature recording essential



Peripheral tem perature m ay be cool.



Indication for urgent cooling



Om inous prognostic sign

Blood pressure: 

Severe hypertension can lead to cardiac and neurologic abnorm alities.

Pa ge 3 7 8

 

Late in course, hypotension m ay supervene.

ECG: o

Signs of cardiac ischem ia

o

Ventricular tachydysrhythm ias

o

Reflex bradycardia

Tests Lab 



Urinalysis: o

Blood

o

Myoglobin

Electrolytes, BUN/creatinine, glucose: o

Hypoglycem ia m ay contribute to altered m ental status.

o

Acidosis m ay accom pany severe toxicity.

o

Rhabdom yolysis m ay cause renal failure.

o

Hyperkalem iaâ€”life-threatening consequence of acute renal failure



Coagulation profile to m onitor for potential DIC: o



Creatine phosphokinase (CPK): o



INR, PT, PTT, platelets

Markedly elevated in rhabdom yolysis

Urine toxicology screen: o

For other toxins with sim ilar effects (e.g., cocaine)

o

Som e am phetam inelike substances (e.g., m ethcathinone) m ay not be detected.



Aspirin and acetam inophen levels if suicide attem pt a possibility



Arterial blood gas (ABG)

Imaging 

Chest radiograph: o

Adult respiratory distress syndrom e

Pa ge 3 7 9

o 

Noncardiogenic pulm onary edem a

Head CT for: o

Significant headache

o

Altered m ental status

o

Focal neurologic signs

o

For subarachnoid hem orrhage, intracerebral bleed

Diagnostic Procedures/Surgery Lum bar puncture for: 

Suspected m eningitis (headache, altered m ental status, hyperpyrexia)



Suspected subarachnoid hem orrhage and CT norm al

Differential Diagnosis 

Sepsis



Thyroid storm



Serotonin syndrom e



Neuroleptic m alignant syndrom e



Pheochrom ocytom a



Subarachnoid hem orrhage



Drugs that cause delirium : o



Anticholinergics: 

Belladonna alkaloids



Antihistam ines

o

Tricyclic antidepressants

o

Cocaine

o

Ethanol withdrawal

o

Sedative/hypnotic withdrawal

o

Hallucinogens

o

Phencyclidine

Drugs that cause hypertension and tachycardia: o

Sym pathom im etics

o

Anticholinergics

Pa ge 3 8 0



o

Ethanol withdrawal

o

Phencyclidine

o

Caffeine

o

Phenylpropanolam ine

o

Ephedrine

o

Monoam ine oxidase inhibitors

o

Theophylline

o

Nicotine

Drugs that cause seizures: o

Carbon m onoxide

o

Carbam azepine

o

Cyanide

o

Cocaine

o

Cholinergics (organophosphate insecticides)

o

Cam phor

o

Chlorinated hydrocarbons

o

Ethanol withdrawal

o

Sedative/hypnotic withdrawal

o

Isoniazid

o

Theophylline

o

Hypoglycem ics

o

Lead

o

Lithium

o

Local anesthetics

o

Anticholinergics

o

Phencyclidine

o

Phenothiazines

o

Phenytoin

o

Propoxyphene

o

Salicylates

o

Strychnine

P.57

Pa ge 3 8 1

Treatment Pre Hospital 

Patient m ay be uncooperative or violent.



Secure IV access.



Protect from self-induced traum a.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Establish IV 0.9% norm al saline (NS) access.



Cardiac m onitor



Naloxone, dextrose (or Accu-Chek), and thiam ine if altered m ental status

ED Treatment 

Decontam ination: o

Gastric lavage: 

Consider if recent (1â€“2 hours) or life-threatening ingestion.



Instill activated charcoal through large-bore orogastric tube both before and after lavage.

o 

Adm inister activated charcoal with sorbitol.

Hypertensive crisis: o

Initially adm inister benzodiazepines if agitated.

o

Alpha-blocker (phentolam ine) as second-line agent

o

Nitroprusside for severe, unresponsive hypertension

o

Avoid beta-blockers, which m ay exacerbate hypertension.



Agitation, acute psychosis:

Pa ge 3 8 2

o 

Adm inister benzodiazepines.

Hypertherm ia: o

Benzodiazepines if agitated

o

Active cooling if tem perature >40Â°C:

o



Tepid water m ist



Evaporate with fan.

Paralysis: 

Indicated if m uscle rigidity and hyperactivity contributing to persistent hypertherm ia





Nondepolarizing agent (e.g., vecuronium )



Avoid succinylcholine.



Intubation; m echanical ventilation

o

Adm inister acetam inophen.

o

Apply cooling blankets.

Rhabdom yolysis: o

Adm inister benzodiazepines.

o

Hydrate with 0.9% NS.

o

Maintain urine output at 1â€“2 m L/m in.

o

Hem odialysis (if acute renal failure and hyperkalem ia occur)



Seizures: o

Maintain airway.

o

Adm inister benzodiazepines.

o

Phenobarbital if unresponsive to benzodiazepines

o

Phenytoin contraindicated

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 100 g PO



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.5

Pa ge 3 8 3

m g/kg) IV 

Lorazepam (benzodiazepine): 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV



Nitroprusside: 1â€“8 Âµg/kg/m in IV (titrated to blood pressure)



Phenobarbital: 15â€“20 m g/kg at 25â€“50 m g/m in until cessation of seizure activity



Phentolam ine: 1â€“5 m g IV over 5 m inutes (titrated to blood pressure)



Sorbitol: 1â€“2 g/kg to a m ax. of 100 g PO m ixed in the activated charcoal slurry (peds: >1 year old: 1â€“1.5 g/kg as a 35% solution to a m ax. of 50 g); avoid repeat doses of sorbitol.



Vecuronium : 0.1 m g/kg IVP

Follow-Up Disposition Admission Criteria 

Hypertherm ia



Persistent altered m ental status



Hypertensive crisis



Seizures



Rhabdom yolysis



Persistent tachycardia

Discharge Criteria 

Asym ptom atic after 6 hours observation



Absence of above adm ission criteria

References

Pa ge 3 8 4

1. Callaway CW, Clark RF. Hypertherm ia in psychostim ulant overdose. Ann Em erg Med. 1994;24:68â€“75. 2. Chan P, Chen JH, Lee MH, et al. Fatal and nonfatal m etham phetam ine intoxication in the intensive care unit. Clin Toxicol . 1994;32:147â€“155. 3. Christophersen AS. Am phetam ine designer drugsâ€”an overview and epidem iology. Toxicol Lett. 2000;112â€“113:127. 4. Doyon S. The m any faces of ecstasy. Curr Opinion Pediatr. 2001;13:170â€“176. 5. Kalant H. The pharm acology and toxicology of â€œecstasyâ€• (MDMA) and related drugs. Can Med Assoc J. 2001;165:917â€“928.

Codes ICD9-CM 969.7

Pa ge 3 8 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am putatio n Traum atic/Replantatio n

Amputation Traumatic/Replantation Matthew Solley Jennifer Oman

Basics Description 

Partial am putations have tissue connecting the distal and proxim al parts and are treated by revascularization.



Com plete am putations have no connecting tissue and m ay be treated by replantation.



Both of the above are treated the sam e from an em ergency standpoint.

Etiology Traum atic am putations result from m achinery, powered hand tools, household appliances, lawnm owers, getting caught between objects, m otor vehicle collisions, crush injuries, blast injuries, gunshot wounds, knives, degloving injuries to digits (ring avulsions), and m am m alian bites.

Diagnosis Signs and Symptoms

Pa ge 3 8 6

History 

Exact tim e of injury critical, as ischem ia tim e predicts success for replantation: o

Warm ischem ia tim e: 

Elapsed tim e since injury without cooling the am putated part



4â€“6 hours for m ajor am putations; 6 to 8 hours for digits

o

Cold ischem ia tim e: 

Elapsed tim e since injury with cooling of am putated part



10â€“12 hours for m ajor am putations; up to 30 hours or longer for digits



Mechanism of injury: o

Clean am putations (with sharp objects) have better prognosis for replantation than crush or avulsion injuries.



Co-m orbid illnesses that hinder successful replantation: o

i.e., diabetes, peripheral vascular disease, rheum atologic disease

Physical Exam 

Assessm ent and docum entation of injured extrem ity is crucial.





Signs of neurologic com prom ise: o

Loss of sensation and two-point discrim ination

o

Loss of active range of m otion

Signs of vascular com prom ise in partial am putations: o

Distal part dusky or cyanotic

o

Delayed capillary refill (>2 seconds)

o

Dim inished or absent pulses (Doppler or palpation)

o

Use Allen test in hand injuries.

Pa ge 3 8 7

o 

Pulse oxim etry m ay be helpful.

Soft tissue: Assess skin, m uscle, tendon, and nail bed integrity.



Identify exposed bone and fractures (gross deform ity, tenderness, crepitus).

Essential Workup Em ergency departm ent workup includes obtaining an accurate history and physical, stabilizing the patient and injured part, and consultation or transfer if replantation is an option.

Tests Lab Preoperative lab studies if needed

Imaging Radiographs of both am putated part and stum p are im portant, but should not delay transport.

Diagnostic Procedures/Surgery Determ ined by surgical consultant for replantation

Differential Diagnosis 

Involves neurologic, vascular, and soft tissue integrity and potential for replantation/revascularization



Do not m iss other m ajor injuries with concurrent traum a.

Treatment Pre Hospital 

Collect all am putated body parts, including pieces of bone, tissue, and skin.



See Initial Stabilization for care of am putated parts during

Pa ge 3 8 8

transport. 

Transport patient and body parts to the nearest m icrovascular replantation center unless other m ajor injuries require transport to the nearest traum a center: o

Air transport from rem ote locations should be considered if ischem ia tim e is of concern.

Initial Stabilization 

Consult surgical specialist as early as possible.



Establish IV access.



Lim it blood loss: o

Elevate injured lim b.

o

Direct pressure using bulky pressure dressing or pressure points if ineffective.

o

Use tourniquet if above m ethods fail to give desired hem ostasis (blood pressure cuff 30 m m Hg greater than systolic blood pressure [SBP]).

o

Partial am putations bleed m ore because of lack of both retraction and spasm of blood vessels.



Avoid further dam age to injured part: o

Avoid vascular clam ps, cautery, vessel ligation, or dÃ©bridem ent.

o

Avoid repeated exam inations of the stum p or am putated part.



Care of am putated part (com plete and partial): o

Rem ove gross contam ination/foreign m aterial.

o

Gently irrigate with saline (avoid antiseptics).

o

Wrap in gauze m oistened with saline.

o

Place in clean, dry plastic bag or specim en cup.

o

Place sealed bag/cup in ice water (half water, half ice) or refrigerate at 4Â°C.

o

Never place directly onto ice or into ice water.

o

Avoid dry ice to prevent freezing.

Pa ge 3 8 9



Care of the stum p: o

Irrigate with saline and cover with saline dam pened gauze

o

Splint if necessary; keep partial am putations as near anatom ic position as possible.



Maintain norm al blood volum e with intravenous fluids or blood products if necessary.

ED Treatment 

Tetanus prophylaxis



Adequate IV analgesia



Patient NPO



Prophylactic antibiotics if devitalized tissue, exposed bone, or contam ination: o



First-generation cephalosporin

All patients are candidates for surgical repair until a specialist deem s otherwise.



Lim it ischem ia tim e of the am putated part (i.e., early transfer if necessary).





Patient considerations in decision to replant: o

Age

o

Occupation/handedness

o

Degree of m otivation

o

General physical condition and underlying diseases

Indications for replantation: o

Thum b, any level (supplies 40% of hand function)

o

Multiple digits

o

Hand am putations through the palm and distal wrist

o

Individual digit distal to flexor digitorum superficialis tendon insertion and proxim al to distal inter-phalangeal joint (DIP)

o

Som e single-digit ring avulsion injuries

o

Arm proxim al to m idforearm (if sharp or m oderately

Pa ge 3 9 0

avulsed) o

Virtually all pediatric am putations (younger patients have lower success rates but better functional outcom es)



Contraindications to replantation: o

Severely crushed or m angled parts

o

Injuries at m ultiple levels

o

Single-digit am putations proxim al to the flexor digitorum superficialis m uscle insertion

o

Am putated parts with tendons avulsed from m usculotendinous junctions

o

Very distal finger am putations (fingertip am putations, see below)

o

Lower extrem ities rarely attem pted and usually in children

o

Unstable patients secondary to other serious injuries or diseases

o

Older patients or those with contraindications to general anesthesia

o 

Inappropriately prolonged ischem ia tim e

Fingertip am putations: m ost com m on type of upper extrem ity am putation: o

Distal to DIP joint

o

Prim ary goals of treatm ent: 

Early functional recovery (coverage of bone, pain free, and sensate tip)



Minim ize pain



Prom ote healing



Cosm esis

P.59

Pa ge 3 9 1

o

Dorsal better prognosis than ventral

o

No exposed phalanx: 

Irrigate with saline, apply petrolatum -soaked gauze and allow to heal by secondary intention (best result in wounds <1 cm 2 ).

o

Sm all am ount of exposed phalanx: 

Shorten bone with rongeur below level of the tissue and close by prim ary intention or allow to heal by secondary intention.



Any bone left exposed requires additional operative procedures and consultation.

o

Considered open fractures if phalanx exposed, thus antibiotics are indicated

o

Preserve nail bed and nail to optim ize function and cosm esis.

o

Treat subungual hem atom as.

o

Splint to prevent traum a to healing fingertip.

o

Consultation required if significant loss of bone or soft tissue for possible graft or flap



Nonlim b am putations (penis, ear, nose): Am putated parts should be cared for sim ilarly as above and em ergently referred to a specialist for replantation: o

Penile am putations: m ost often secondary to self-m utilation and psychiatric illness: 

Successful replantation unlikely beyond 24 hours of cold ischem ia or 6 hours of warm ischem ia

 o

Psychiatric consultation required in all patients

Ear am putations: total or partial am putations relatively uncom m on, with case reports showing som e success

o

Nose am putations: Replantation has been

Pa ge 3 9 2

successfully perform ed with variable results.

Pediatric Considerations 

All pediatric am putations considered for replantation



Fingertip am putations often left to heal by secondary intention: o

Spontaneous regeneration of fingertip occurs in children even with volar fingertip am putations.

o

Pediatric fingertip am putations distal to the lunula of the fingernail can be successfully replanted (unlike adults).

Geriatric Considerations Advanced age not an absolute contraindication to replantation; however, underlying m edical problem s often m ake older patients poor surgical candidates.

Medication (Drugs) Cefazolin: 0.5â€“1.5 g IV or IM q6hâ€“q8h (peds: 25â€“100 m g/kg/d divided q8h, m ax. 6 g/d)

Follow-Up Disposition Admission Criteria Hospitalization is required for all patients undergoing replantation or revascularization.

Discharge Criteria 

Mild fingertip am putations or m ild degloving injuries with adequate repair and stable vasculature

Pa ge 3 9 3



Close surgical or orthopedic follow-up is required.

References 1. Antosia RE, et al. Hand. In: Rosen P, et al. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:525â€“528. 2. Bandi G, et al. Controversies in the m anagem ent of m ale external genitourinary traum a. J Traum a. 2004;56(6):1362â€“1370. 3. Chung KC, et al. Finger replantation in the United States: rates and resource use from the 1996 Healthcare Cost and Utilization Project. J Hand Surg. 2000;25(6):1038â€“1042. 4. Dalsey WC, et al. Managem ent of Am putations. In: Roberts JR, et al. Clinical Procedures in Em ergency Medicine. 4th Edition. Philadelphia, PA: Saunders; 2004:919â€“925. 5. Loder RT. Dem ographics of traum atic am putations in children. Im plications for prevention strategies. J Bone Joint Surg Am . 2004;86-A(5):923â€“928. 6. Martin C, et al. Controversies in the treatm ent of fingertip am putations: conservative versus surgical reconstruction. Clin Orthop Relat Res. 1998;353:63â€“73. 7. Michalko KB, et al. Digital replantation in children. Crit Care Med. 2002;30:S444â€“447. 8. Miller PJ, et al. Replantation of the am putated nose. Arch Otolaryngol Head Neck Surg. 1998;124(8):907â€“910. 9. Soucacos PN. Indications and selection for digital am putation and replantation. J Hand Surg. 2001;26(6):572â€“581.

Codes ICD9-CM 885.0 Traum atic am putation of thum b 886.0 Traum atic am putation of other finger(s) 887.0 Traum atic am putation of arm and hand 895.0 Traum atic am putation of toe(s)

Pa ge 3 9 4

896.0 Traum atic am putation of foot 897.0 Traum atic am putation of leg

Pa ge 3 9 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am yo tro phic Lateral Sclero sis

Amyotrophic

Lateral Sclerosis Richard S. Krause

Basics Description 

Progressive disease of adults m anifested as m uscle weakness, wasting, fasciculations, Babinski sign, and hyperreflexia



Variants with predom inately upper or lower m otor neuron m anifestations also occur.

Etiology 

Etiology of am yotrophic lateral sclerosis (ALS) is unknown.



Pathologically, there is loss of both upper and lower m otor neuron cells



Predilection for the m otor system and sparing of other neurons

Diagnosis Signs and Symptoms 

Most com m only weakness (bilateral) and eventual m uscle

Pa ge 3 9 6

wasting 

Both lower m otor neuron (weakness and wasting with fasciculation) and upper m otor neuron signs (Babinski sign with hyperreflexia)



May begin in either the arm s or the legs: o



Later all lim bs are affected.

Dysphagia or facial dysarthrias (drooling, dysphagia) m ay occur.



Respiratory m uscles and the vocal cords are affected late.



Muscle cram ps and weight loss



Muscle fasciculation is com m on, but m ay not be apparent to the patient.



Extraocular m uscles, sphincters, cognition, and sensation are spared.



Eighty percent of cases begin between ages 40 and 70 years.



Death (usually from respiratory paralysis) occurs within 3â€“5 years of the diagnosis.



Musculoskeletal pain is com m on late in the disease: o

Related to com plications, not prim ary disease

Essential Workup Previously Undiagnosed ALS 

Diagnosis of ALS is clinical and rarely m ade in the ED: o

Recognition of the possibility of this disease is sufficient and m andates referral for workup.



If ALS is suspected, forced vital capacity (FVC) should be perform ed.

Known ALS Patient 

Patients with known disease and progressive sym ptom s: o

Evaluate potentially treatable com plications with lab and im aging studies.

Pa ge 3 9 7



FVC is a sensitive indicator of respiratory m uscle weakness: o

FVC <50% of predicted is considered a sign of advanced disease.

o 

Com pare with the patient's previous baseline.

Chest radiograph m ay reveal aspiration or pneum onia or co-m orbid conditions such as congestive heart failure (CHF)



Pulse oxim etry and blood gas analysis aid in the diagnosis of respiratory failure.



Electrolytes and other blood chem istry tests m ay reveal a treatable cause of increasing weakness.



Cervical spine, other skeletal radiography, or head CT m ay be needed in case of falls (com m on in ALS).

Tests Imaging Electrom yography (EMG) m ay help confirm the diagnosis.

Differential Diagnosis 

Cervical cord com pression: o

Sim ilar sym ptom s but usually acute onset with pain and sensory changes

o 

Spinal MRI or m yelography for diagnosis

Thyrotoxicosis m ay m im ic ALS: o

Usually m arked system ic sym ptom s



Heavy m etal poisoning (lead, m ercury, arsenic)



Syphilis and Lym e disease



Lym phom a m ay have an associated lower m otor neuron syndrom e, which m im ics ALS.

Pa ge 3 9 8

Treatment 

There is no specific therapy for ALS.



Recently, the drug riluzole, a glutam ate release inhibitor, has been shown to extend survival in ALS patients for an average of a few m onths.



Treatm ent issues in the ED revolve around sym ptom atic therapy and identification and treatm ent of com plications.

Pre Hospital Controversies: 

Many patients will have advanced directives: o

Unless im m ediate intervention is essential, intubation should be avoided until directives have been ascertained.

o

Noninvasive m eans of ventilatory support m ay be tried first.

Initial Stabilization 



Respiratory insufficiency or failure: o

Ascertain any advanced directives.

o

Noninvasive ventilatory support

o

Intubation as indicated

Weaning off the ventilator is very difficult: o

Average survival after institution of ventilation is 19 m onths.

ED Treatment 

Sedation and pain control as indicated: o



Joint pain m ay respond to NSAIDs.

Insom nia from pressure pain (owing to im m obility) m ay respond to diphenhydram ine or am itriptyline.



Aspiration or drooling m ay be treated with am itriptyline (dries secretions).

Pa ge 3 9 9



Muscle cram ps m ay respond to baclofen.



Constipation is related to im m obility and diet: o

Treated with laxatives, stool softeners, and dietary changes

P.61

Medication (Drugs) 

Am itriptyline: 25â€“50 m g PO nightly at bedtim e



Baclofen: 10â€“25 m g PO t.i.d.



Diphenhydram ine: 25â€“50 m g PO nightly at bedtim e

Follow-Up Disposition Admission Criteria 

Need for respiratory support



Dehydration, inanition



Unable to be cared for at hom e owing to progression of illness



Com plications (e.g., infection) that require adm ission

Discharge Criteria 

Suspected ALS: Refer for outpatient evaluation if general condition perm its and other serious conditions requiring adm ission are ruled out.



Com plication of known ALS: Discharge if outpatient treatm ent available and stable respiratory status.

Pa ge 4 0 0

References 1. Brooks BR. Natural history of ALS: sym ptom s, strength, pulm onary function, and disability. Neurology. 1996;47(suppl 2):S71â€“S81. 2. Dib M. Am yotrophic lateral sclerosis: progress and prospects for treatm ent. Drugs. 2003;63(3):289â€“310. 3. McGeer E, McGeer P. Pharm acologic approaches to the treatm ent of am yotrophic lateral sclerosis. Biodrugs. 2005;19(1):31â€“37. 4. Rowland LP. Natural history and clinical features of am yotrophic lateral sclerosis and related m otor neuron diseases. In: Calne D, ed. Neurodegenerative Diseases. 1st ed. Philadelphia: WB Saunders; 1994: 507â€“521. 5. Servera E, Sancho J. Appropriate m anagem ent of respiratory problem s is of utm ost im portance in the treatm ent of patients with am yotrophic lateral sclerosis. Chest. 2005;127(6):1879â€“1882.

Codes ICD9-CM 335.20

ICD10 G12.2

Pa ge 4 0 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anal F issure

Anal Fissure

Julia Sone

Basics Description 

Hard stool passes and â€œcutsâ€• anoderm



Linear tear extends from dentate line to anoderm : o

Posterior m idline 95%

o

Anterior m idline 5%

o

Externally: form s skin tag or sentinel pile

o

Internally: form s hypertrophied anal papilla

o

Chronic fissure m ay reveal fibers of internal sphincter with sentinel pile

Etiology 

Stress or an overly tight anal sphincter leads to ischem ia of posterior anoderm .



Diarrhea or hard bowel m ovem ent tears anoderm .



Anal intercourse or sexual abuse m ay be cause.



Lateral fissures indicate underlying causative system ic disease: o

Crohn disease

o

Anal cancer

o

Leukem ia

o

Syphilis

Pa ge 4 0 2

o

Previous anal surgery

Diagnosis Signs and Symptoms 

Bright red blood per rectum usually on toilet paper



Sharp, cutting, or burning pain with bowel m ovem ent: o



May last for hours

Constipation; unable to pass stool owing to pain

History 

Passage of hard stool



Episode(s) of diarrhea

Physical Exam Anal exam : 

Gently retract buttocks and have patient bear down to visualize the fissure.



Severe pain usually prevents a m anual or digital exam : o

Use lidocaine jelly or ELA-Max5, a topical lidocaine ointm ent, before attem pting digital rectal exam .

Pediatric Considerations A clear test tube m ay be used as an anoscope to visualize the anal canal/fissure.

Tests Lab Hem atocrit if severe bleeding by history

Differential Diagnosis 

Crohn disease



Chronic ulcerative colitis

Pa ge 4 0 3



Anorectal carcinom a



Perirectal abscess



Throm bosed hem orrhoid



Sexual abuse



Tuberculosis



Syphilis



Lym phom a



Leukem ia



Previous anal surgery

Treatment ED Treatment 



Oral pain m edication: o

Nonsteroidal anti-inflam m atory drugs

o

Acetam inophen

Topical anesthetics: o

ELA-Max5

o

Lidocaine jelly



Sitz baths (with warm water) to relieve sphincter spasm



Oral m uscle relaxants or diazepam to relieve sphincter spasm

Diet 

High-fiber diet instruction: o

Fiber/bran: 20 g/d

o

Psyllium seeds: 1â€“2 tsp (peds: 0.25â€“1 tsp/d) PO q24h



Encourage consum ption of 10â€“12 8-oz glasses of water per day.

Pa ge 4 0 4

Medication (Drugs) 

Cyclobenzaprine (Flexeril): 10 m g (peds: not indicated) PO t.i.d.



Diazepam (Valium ): 5 m g (peds: 0.12â€“0.8 m g/kg/d) PO t.i.d. PRN for spasm



Diltiazem 2% ointm ent: Apply to fissure b.i.d.



Docusate sodium (Colace): 50â€“200 m g (peds: younger than 3 years, 10â€“40 m g/d; 3â€“6 years, 20â€“60 m g/d; 6â€“12 years, 40â€“150 m g/d) PO q12h



ELA-Max5 (5% lidocaine anorectal cream ): Apply to perianal area q4h PRN pain (pediatric dose: not for those younger than 12 years)



Ibuprofen: 400â€“600 m g (peds: 40 m g/kg/d) PO q6h



Nitroglycerin ointm ent 0.2%: Apply to fissure b.i.d. (peds: not indicated)

P.63

Follow-Up Disposition Admission Criteria None

Discharge Criteria 

Initial treatm ent is conservative therapy for acute anal fissures as an outpatient.



Operative referral for chronic fissures

Pa ge 4 0 5

References 1. Hananel N, Gordon PH. Re-exam ination of clinical m anifestations and response to therapy of fissure-in-ano. Dis Colon Rectum . 1997;40:229â€“233. 2. Mazier WP. Hem orrhoids, fissures and pruritus. Ann Surg Clin North Am . 1994;74:1277â€“1291. 3. Orsay C, Rakinic J. Practice param eters for the m anagem ent of anal fissures (revised). Dis Colon Rectum . 2004;47:2003â€“2007.

Miscellaneous SEE ALSO: Hem orrhoid

Codes ICD9-CM 565.0 Anal fissure

ICD10 K60-2

Pa ge 4 0 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anaphylaxis

Anaphylaxis

Sean-Xavier Neath

Basics Description 

An acute, widely distributed form of shock that occurs within m inutes of exposure to antigen in a sensitized individual



There are approxim ately 400â€“800 deaths annually in the United States attributed to anaphylaxis.



Involves release of bioactive m olecules such as histam ine, leukotrienes, and prostaglandins from inflam m atory cells: o

Mediator release results in increased vascular perm eability, vasodilation, sm ooth-m uscle contractions, and increased epithelial secretion

o

Physiologically, this is m anifested in a decrease in total peripheral resistance, venous return, and cardiac output, as well as intravascular volum e depletion.

Etiology 

IgE-m ediated: o

Antibiotics, particularly penicillin fam ily

o

Venom s, especially bee and wasp

o

Latex

Pa ge 4 0 7

o

Vaccines

o

Foodstuffs (shellfish, soybeans, peanuts, tree nuts, wheat, m ilk, eggs, nitrates/nitrites)



Non-IgE m ediated: o

Iodine contrast m edia

o

Opiates

o

Vancom ycin

o

Quaternary am m onium m uscle relaxants

Pediatric Considerations In children, foods are an im portant trigger for IgE-m ediated anaphylaxis. Milk, egg, wheat, and soy (MEWS) are the m ost com m on food allergens. Peanut allergies are less com m on but can be m ore potent; children can develop anaphylaxis from residual peanut in a candy bar.

Diagnosis Signs and Symptoms 

Sym ptom s begin within seconds to m inutes after contact with an offending antigen.



Anaphylactic reactions alm ost always involve the skin or m ucous m em branes. More than 90% of patients have som e com bination of urticaria, erythem a, pruritus, or angioedem a.



Som e patients m ay have an initial sensation of im pending doom followed by m ore clearly definable sym ptom atology. o

Respiratory: from sneezing and nasal congestion to frank bronchospasm and laryngeal edem a

o

Cardiovascular: hypotension, dysrhythm ias, m yocardial ischem ia

Pa ge 4 0 8

o

Gastrointestinal: nausea, vom iting, diarrhea

o

Ocular: eye itching and tearing, conjunctival injection

o

Hem atologic: activation of intrinsic coagulation pathway som etim es leading to dissem inated intravascular coagulation, throm bocytopenia

o

Neurologic: seizures

Essential Workup 

Diagnosis is m ade based on clinical sym ptom s.



It is im portant not to underestim ate the potential severity of an allergic reaction in its early stages.



ECG should be done in patients with previous cardiac history or ischem ic sym ptom s; consider routinely in the elderly.

Tests Lab The diagnosis of anaphylaxis is m ade on clinical grounds; laboratory tests are usually not useful in aiding diagnosis in the acute setting.

Imaging Hyperinflation can be seen on chest radiograph.

Differential Diagnosis 

Pulm onary em bolism



Acute m yocardial infarction



Airway obstruction



Asthm a



Tension pneum othorax



NSAID reaction



Vasovagal collapse



Hereditary angioedem a



Serum sickness



System ic m astocytosis

Pa ge 4 0 9



Pheochrom ocytom a



Carcinoid syndrom e

Treatment Pre Hospital 

IV access, O2, cardiac and pulse oxim etry m onitoring



Early intubation is param ount as laryngeal edem a and spasm can progress rapidly.



Laryngeal edem a can be m anaged with racem ic epinephrine prior to intubation.



Subcutaneous epinephrine can be adm inistered en route even prior to establishm ent of an IV.

Initial Stabilization 

ABCs



Assure adequate ventilation



Orotracheal intubation is the technique of choice.



Difficult because of laryngeal edem a, spasm , or soft tissue swelling; use advanced airway adjuncts if necessary



Consider blind nasotracheal intubation if soft tissue swelling prohibits an oral approach and there is absence of stridor.



Transtracheal jet insufflation or cricothyrotom y m ay be necessary to control the airway.



Epinephrine IV/SC or endotracheal adm inistration



Direct injection into the venous plexus at the base of the tongue is an option.



Volum e resuscitation with crystalloids or colloids

ED Treatment 

Continuous cardiac and vital sign m onitoring until stable

Pa ge 4 1 0



Persistent bronchospasm can be treated with Î² 2 -agonist bronchodilators.



Hypotension should be treated with volum e repletion.



Vasopressors, MAST garm ents, and Trendelenburg positioning are useful adjuncts.



Antihistam ines (both H 1 and H 2 blockers) have been shown to be helpful in preventing histam ine interactions with target tissues.



Corticosteroids help prevent the progression or recurrence of anaphylaxis.



Glucagon is particularly useful in epinephrine-resistant anaphylaxis from Î²-adrenergic blocking agents.

P.65

Medication (Drugs) Alert 

A patient's concom itant use of a beta-blocker m ay antagonize the effects of epinephrine. For these patients consider glucagon as it increases intracellular cyclic adenosine m onophosphate levels by a m echanism that does not depend upon beta-receptors.



Diphenhydram ine: adultsâ€”50 m g IV; (peds: 1â€“2 m g/kg) slow IVP



Epinephrine: 0.3â€“0.5 m g; use 1:1,000 dilution for SC route and 1:10,000 for IV route (peds: epinephrine 0.01 m g/kg SC/IV)



Racem ic epinephrine: 2.25% solution (0.5 m L placed in a nebulizer in 2.5 m L of norm al saline)

Pa ge 4 1 1



Glucagon: adultsâ€”1â€“2 m g IV/IM/SQ



Hydrocortisone: adults: 500 m g IV (peds: 4â€“8 m g/kg/dose IV)



Methylprednisolone: adultâ€”125 m g IV (peds: 1â€“2 m g/kg IV)



Prednisone: adultâ€”60 m g PO (peds: 1 m g/kg PO)



Ranitidine: adultâ€”50 m g IV or cim etidine 300 m g IV

Follow-Up Disposition Admission Criteria 

Intubated patients or patients in respiratory distress should be adm itted to an intensive care unit setting.



A m onitored bed m ay be necessary for the patient who has not had substantial response to initial therapy.



Patients with significant generalized reactions and persistent sym ptom s should be adm itted for observation for 24 hours.

Discharge Criteria 

Patients with com plete resolution of sym ptom s m ay be discharged after several hours of ED observation.



Patients with allergic reactions should have a follow-up within 48 hours of discharge to evaluate effectiveness of outpatient therapy.



A follow-up visit with an allergist is also recom m ended.



Patients should be advised to carry som e type of treatm ent that can be self-adm inistered in the event of future reactions such as the prefilled syringe EpiPen.



Patients with a known trigger should be counseled on strict

Pa ge 4 1 2

avoidance of that trigger.

Issues for Referral 

Consultation with an allergist/im m unologist is appropriate when desensitization to an antibiotic is being considered for the treatm ent of an infectious process.



When a patient at high risk for contrast reaction needs a contrast study, consultation with the radiologist regarding pretreatm ent and choice of contrast agent is appropriate.



Refer patients who are treated and released from the ED after an episode of anaphylaxis, angioedem a, or urticaria to an allergist for follow-up skin testing and consideration for desensitization.

References 1. Barach EM, et al. Epinephrine for the treatm ent of anaphylactic shock. JAMA. 1984;251:2118. 2. Muellem an RL, Tran TP. Allergy, hypersensitivity and anaphylaxis. In: Marx J, et al. eds. Rosen's Em ergency Medicine. St. Louis, MO: Mosby, 2002;1619â€“1635. 3. Neugut AI, Ghatak AT, Miller RL. Anaphylaxis in the United States: an investigation into its epidem iology. Arch Intern Med. 2001;161:1521. 4. Thom as M, Crawford I. Glucagon infusion in refractory anaphylactic shock in patients on beta-blockers. Em erg Med J. 2005;22:272â€“273.

Miscellaneous SEE ALSO: Angioedem a; Urticaria

Codes ICD9-CM

Pa ge 4 1 3

995.0

ICD10 T78.2

Pa ge 4 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anem ia

Anemia

Paul Allegretti

Basics Description 

Reduction below norm al in the m ass of RBCs: o

Measured by one or m ore of the m ajor RBC com ponents

o

Hgb (hem oglobin): concentration of the m ajor oxygen-carrying com ponent in whole blood

o

Hct (hem atocrit): percent volum e of whole blood occupied by intact RBCs

o

RBC count: RBCs contained in a volum e of whole blood





o

Adult fem ale: Hgb <12 g/dL or Hct <37%

o

Adult m ale: Hgb <14 g/dL or Hct <42%

Norm al blood count values depend on age: o

Birth: Hgb 16.5, Hct 51

o

1 year: Hgb 12, Hct 36

o

6 years: Hgb 12.5, Hct 37

o

Adult m ale: Hgb 14, Hct 42

o

Adult fem ale: Hgb 12, Hct 37

Hgb/Hct depends on oxygen pressure: o

Increased in neonates and people living above 4,000

Pa ge 4 1 5

ft 

Hgb, Hct, and RBC count are concentrations: o

Dependent on RBC m ass and plasm a volum e

o

Values decrease if RBC m ass decreases or plasm a volum e increases.

Etiology 





Never a norm al variant: o

May be the first m anifestation of a system ic disorder

o

Always seek a cause.

Excessive blood loss (m ost com m on cause): o

Traum a

o

GI bleed

o

Menstruation

Hem olysis (increased RBC destruction, RBC lifespan <100 days): o

Hypersplenism

o

Autoim m une hem olytic anem ia

o

Mechanical traum a (prosthetic heart valves, vasculitis, throm botic throm bocytopenic purpura [TTP], hem olytic urem ic syndrom e [HUS], dissem inated intravascular coagulation [DIC])

o

Toxins

o

Infections (m alaria, babesiosis)

o

Mem brane abnorm alities

o

Intracellular RBC abnorm alities (G6PD, sickle cell anem ia, thalassem ia)



Decreased RBC synthesis classified by m easurem ent of RBC size: o

Hypochrom ic/m icrocytic: 

Iron deficiency



Thalassem ia



Sideroblastic

Pa ge 4 1 6

 o

o

Chronic disease

Norm ochrom ic/m acrocytic: 

Hypothyroidism



Folate deficiency



Vitam in B 1 2 deficiency



Liver disease



Myelodysplasia



Certain leukem ias

Norm ochrom ic/norm ocytic: 

Aplastic anem ia



Chronic renal failure



Malignancy



Adrenal insufficiency



Hyperparathyroidism



Alcohol abuse



Acute blood loss

Diagnosis Signs and Symptoms History/Physical General 

Depends on: o



Rapidity of onset: 

Hypovolem ia if acute



Asym ptom atic if m ild and chronic

o

Underlying disease

o

Severity and type of anem ia

Decreased oxygen delivery to tissues: o

Fatigue

Pa ge 4 1 7



o

Decreased exercise intolerance

o

Tachypnea

Hem e-positive stool

Cardiovascular 

Dyspnea on exertion



Chest pain/angina



Syncope



Tachycardia, cardiom egaly, m urm urs



Postural hypotension

Dermatologic 



Skin: o

Cool

o

Pallor

o

Jaundice

o

Purpura

o

Telangiectasia

Spoon-shaped nails (koilonychia)

CNS 

Neuropathy



Altered m ental status

Miscellaneous 

Bone (especially sternal) or joint pain (sickle cell disease)



Hepatom egaly, splenom egaly



Lym phadenopathy



Findings reflect underlying disease



Petechiae



Ecchym osis

Essential Workup 

Hgb/Hct



Vital signs/orthostatics

Pa ge 4 1 8





Determ ine if: o

Bleeding

o

Increased RBC destruction

o

Bone m arrow suppression

o

Iron deficient

Rule out GI m alignancy.

Tests Lab 

CBC



RBC indices: o

Mean corpuscular volum e (MCV; norm al: 80â€“100 Âµm 3 )

o

Mean corpuscular hem oglobin (MCH; norm al: 27â€“34 pg/cell)

o

Mean corpuscular hem oglobin concentration (MCHC; norm al: 33â€“36%)



Platelet count



Throm bocytosis suggests:





o

Iron deficiency

o

Myeloproliferative disorders

o

Inflam m ation

o

Infection

o

Neoplasm

Throm bocytopenia suggests: o

Bone m arrow m alignancy

o

Hypersplenism

o

Sepsis

o

Vitam in B 1 2 or folate deficiency

o

Autoim m une disorders

Reticulocyte count: o

Norm al 0.5â€“1.5% (reticulocytes/1,000 RBCs)

Pa ge 4 1 9

o

Increased retic count: increased erythropoietic response to continued blood loss or hem olysis

o

Stable anem ia with low retic count: im paired RBC production

o

Active hem olysis or blood loss with low retic count: concurrent disorder

o

Low retic count with pancytopenia: aplastic anem ia

o

Low retic count with norm al WBC and platelets: pure RBC aplasia



Reticulocyte index (RI): reticulocyte count (%) Ã— (patient Hct/norm al Hct): o

RI <2% im plies inadequate RBC production.

o

RI >2% im plies increased RBC production with excessive RBC destruction or loss.



WBC: o

Leukopenia with anem ia suggests bone m arrow suppression, hypersplenism , or deficient vitam in B 1 2 /folate



Stool for occult blood



Electrolytes, BUN, creatinine, glucose: o



Chronic renal failure

Urinalysis: o

Hem aturia

o

Hem oglobinuria in hem olytic anem ia

P.67

Workup Strategy 

Hypochrom ic/m icrocytic anem ias: o

Iron

o

Total iron-binding capacity

o

Transferrin saturation

Pa ge 4 2 0

o 



Ferritin

Macrocytic anem ias: o

Folate

o

Vitam in B 1 2

o

Liver function tests

o

Thyroid function tests

Hem olytic anem ia: o

Rapid fall in Hgb

o

Reticulocytosis

o

Fragm ented RBCs

o

Increased LDH

o

Increased indirect bilirubin

o

Decreased serum haptoglobin

o

Coom bs positive

Special Tests 

Peripheral sm ear: o

Helm et cells/schistocytesâ€”m icroangiopathic hem olysis

o

Teardrop cellsâ€”m yelofibrosis

o

Spherocytesâ€”autoim m une hem olysis

o

Leukoerythroblastic patternâ€”bone m arrow replacem ent

o

Bite cellsâ€”oxidative hem olysis

o

RBC parasitesâ€”m alaria or babesiosis

o

Target cellsâ€”liver disease

o

Burr cellsâ€”urem ia

o

Sideroblastsâ€”alcoholism or m yelodysplasia

o

Howell Jolly bodiesâ€”asplenia



Hgb electrophoresis for sickle cell/thalassem ia



Iron, iron-binding capacity, transferrin saturation, ferritin: o

Iron deficiency: 

Ironâ€”decreased

Pa ge 4 2 1

o

o

o



Iron-binding capacityâ€”increased



Transferrin saturationâ€”decreased



Ferritinâ€”decreased

Chronic disease: 

Ironâ€”decreased



Iron-binding capacityâ€”decreased



Transferrin saturationâ€”decreased/norm al



Ferritinâ€”norm al/increased

Thalassem ia: 

Ironâ€”norm al



Iron-binding capacityâ€”norm al



Ferritinâ€”norm al

Sideroblastic anem ia: 

Ironâ€”increased



Iron-binding capacityâ€”norm al



Ferritinâ€”increased

Diagnostic Procedures/Surgery Bone m arrow biopsy evaluates: 

Aplastic anem ia



Myelodysplasia



Bone m arrow m alignancy



Myeloproliferative disorders

Differential Diagnosis 

Dilutional anem ia



Congestive heart failure



Acquired versus inherited anem ia



Blood loss



Nutritional deficiency/m alabsorption



Hem olysis



Toxic bone m arrow suppression



Malignancy

Pa ge 4 2 2



Chronic disease

Pediatric Considerations 

Hem olytic anem ia of the newborn: o

Rh antibody crosses placenta when Rh-negative m other has Rh-positive child.

Pregnancy Considerations 

Physiologic or dilutional anem ia in third trim ester pregnancy: o

25% increase of RBC m ass and 50% increase in plasm a volum e

Geriatric Considerations 

Values for Hgb/Hct in healthy elderly are generally lower than in younger adults.



This lower â€œnorm alâ€• m ust be a diagnosis of exclusion.

Treatment Pre Hospital 

Ongoing blood loss requires close assessm ent and rapid transport.



Multiple large-bore IVs

Initial Stabilization 

Airway, breathing, circulation (ABCs)



Oxygen



IV fluid resuscitation with 0.9% norm al saline (NS) if ongoing loss/hypotension

ED Treatment

Pa ge 4 2 3



Depends on severity of anem ia and acuteness of onset



Transfusion for hem orrhage with unstable vital signs



Most anem ias seen in ED are chronic and do not require im m ediate intervention.

Therapy for Specific Anemia 





Iron deficiency: o

FeSO 4 : 300 m g PO t.i.d.

o

Investigate underlying cause.

o

Increased Hgb expected in 2â€“3 weeks

Renal failure: o

Endogenous erythropoietin is dim inished.

o

Replace with recom binant erythropoietin.

Autoim m une hem olytic anem ia: o

Corticosteroids (prednisone 60 m g/d until response)

o

Im m unosuppressive agents

o

Plasm apheresis

o

Splenectom y if splenic sequestration



Drug-induced hem olytic anem ia: stop offending agent.



Anem ia of chronic disease: treat underlying disease.



Vitam in B 1 2 deficiency: o

Vitam in B 1 2 : 1,000 Âµg IM daily for 1 week, then weekly for 1 m onth, then m onthly

o

Hem atologic param eters norm alize within 2 m onths.

o

Neurologic sym ptom s present >6 m onths m ay be perm anent.



Folate deficiency: o





Folic acid: 1 m g PO daily

Aplastic anem ia: o

Antithym ocyte globulin

o

Bone m arrow transplantation

Sickle cell anem ia: o

Supportive care with oxygen, rehydration, analgesia

Pa ge 4 2 4

o 

Treat precipitating cause.

Leukem ia: o

Bone m arrow replacem ent

Follow-Up Disposition Admission Criteria 

Unstable vital signs



Ongoing blood loss



Sym ptom atic anem iaâ€”angina/dyspnea/syncope



Pancytopenia



Need for transfusion



Need for aggressive evaluation

Discharge Criteria Discharge vast m ajority of stable patients for outpatient workup.

References 1. Braunwald E, et al. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw-Hill; 2001. 2. Hoffm an R, Benz E, Shattil S, et al. Hem atology: Basic Principles and Practice. 3rd ed. New York: Churchill-Livingstone; 2000. 3. McCullough J. Blood and Bone Marrow Pathology. St. Louis, MO: Churchill; 2003. 4. Schrier S. Approach to the Patient with Anem ia. Wellesley, MA: UpToDate; 2004. 5. Scott R. Com m on blood disorders: a prim ary care approach. Geriatrics. 1993;48:72â€“80.

Pa ge 4 2 5

Miscellaneous SEE ALSO: Gastrointestinal Bleeding; Renal Failure; Sickle Cell Disease

Codes ICD9-CM 285.9

ICD10 D64

Pa ge 4 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Angio edem a

Angioedema

Sean-Xavier Neath

Basics Description 

Nonpruritic, well-dem arcated, nonpitting edem a of the derm is



Prim arily involves the periorbital and perioral regions



Sim ilar in pathologic basis to urticaria except that affected tissue lies deeper: o

Urticaria affects superficial tissue and causes irritation to m ast cells and nerves in the epiderm is leading to intense itching.

o

Angioedem a occurs in deeper layers, which have fewer m ast cells and nerves, therefore causing less itching.



There are two types of angioedem a: the classic hereditary form and the acquired form s: o

Hereditary angioedem a (HAE) is an autosom al dom inant disorder caused by a deficiency of C1 esterase inhibtor (C1-INH), which leads to the form ation of bradykinin resulting in angioedem a.

o

The acquired form s dem onstrate norm al quantities and function of C1-INH, but it becom es bound to

Pa ge 4 2 7

circulating antibodies that inactivate it. o

Absolute or functional deficiency of C1-INH from either type results in unopposed activity of the first com ponent of the com plem ent cascade, resulting in higher levels of bradykinin, which incites the form ation of angioedem a.

Genetics 

The prevalence of hereditary angioedem a is estim ated to range from 1:10,000â€“1:150,000.



More than 100 m utations of the C1-INH gene have been reported.

Etiology Typical trigger include: 

Food additives



Food allergies



Drug allergies



Insect stings



Exposure to heat or cold



Exercise



Traum a



Thyroid disease



Diabetes



Lupus



Infections



Contact allergies



ACE inhibitors



NSAIDs, aspirin

Diagnosis

Pa ge 4 2 8

Signs and Symptoms History 

A fam ily history or history of recurrent episodes with the use of particular agents can be useful in the diagnosis.



Abdom inal pain associated with nausea, vom iting, and diarrhea



Attacks of hereditary angioedem a are not associated with hives.



Em otional stress or physical traum a can trigger attacks.

Physical Exam 

The lesions of angioedem a are large, swollen and nonpitting wheals.



The eyelids and lips are frequently involved.



Involvem ent of the pharynx and larynx m ay cause airway obstruction.

Essential Workup 

The diagnosis is m ade of clinical grounds based on the presentation of large nonpitting, nonpruritic wheals.



A fam ily history need not be present to diagnose the disease.

Tests Lab 

CBC with differential, ESR, ANA, rheum atoid factor



Skin biopsy if an urticarial lesion is accessible

Diagnostic Procedures/Surgery Measurem ent of C1-INH levels (not routinely available in EDs): 

Patients affected with hereditary angioedem a have very low levels; carriers will have half-norm al levels.



C4 and C2 levels are low during attacks in both hereditary

Pa ge 4 2 9

and acquired form s

Differential Diagnosis 



Prim ary angioedem a: o

IgE-m ediated allergic reactions

o

Drug reactions

o

Food allergies

o

Inhalation, ingestion, or contact with allergens

o

Panic attacks, globus hystericus

Secondary angioedem a: o

Physical urticaria such as cold, pressure, solar

o

System ic m astocytosis

o

Fam ilial cold urticaria

o

C3b inactivator deficiency

o

Am yloidosis

o

Exercise-induced anaphylaxis

o

Transfusion reaction

o

Collagen vascular disease

o

ACE-inhibitor reaction

Pediatric Considerations Recurrent angioedem a presenting around puberty should raise suspicion of hereditary angioedem a.

Treatment Pre Hospital 

Establish IV access



Early intubation m ay be necessary due to the rapid progression of laryngeal swelling.

Initial Stabilization

Pa ge 4 3 0



Active airway m anagem ent and supportive m easures are the prim ary goals of em ergency treatm ent.



Intubation m ay be necessary in severe cases: o

Orotracheal intubation is the technique of choice but m ay be difficult because of laryngeal edem a, spasm , or soft-tissue swelling.

o

Consider advanced airway adjuncts such as the gum elastic bougie to assist in securing endotracheal tube placem ent;

o

Blind nasotracheal intubation if soft tissue swelling prohibits an oral approach

o

Transtracheal jet insufflation or cricothyrotom y m ay be necessary to control the airway.



Epinephrine, antihistam ines, and steroids in obstructive airway swelling, although patient response can be variable.

ED Treatment 

Airway m anagem ent as above



Acute angioedem a with features of a type I hypersensitivity reaction m ay be treated sim ilarly to an allergic reaction with H1 and H2 blocker along with corticosteroids.



Subcutaneous epinephrine should be used in refractory cases where the benefits outweigh the risks.



For abdom inal attacks consider the addition of parenteral pain relief, antiem etics and IV fluid replacem ent.



Tranexam ic acid (Cyklokapron), an antifibrinolytic agent, is useful in both acute and prophylactic treatm ent.



Epsilon am inocaproic acid (Am icar) another antifibrinolytic agent is considered to be of questionable efficacy.



A C1-INH concentrate is useful during acute attacks.

Pa ge 4 3 1

Alert P.69



While C1-INH is standard therapy in Europe, the U.S. FDA has not approved its use in the United States. Som e patients with HAE in the United States m ay carry vials of the m edication obtained abroad.



Therapy with fresh frozen plasm a (FFP) (as a source of nonpurifiied C1-HN) is advised with caution as it m ay paradoxically worsen som e attacks due to its high concentration of com plem ent com ponents.



Attenuated androgens, such as the anabolic steroids and gonadotropin inhibitor danazol, are used in the long-term prophylactic treatm ent. They m ay not have any effect for 24â€“48 hours in the acute setting.



Angioedem a associated with ACE inhibitors occurs in 0.1â€“0.2% of cases and requires im m ediate withdrawal of the ACE inhibitor and replacem ent with another antihypertensive m edication. ACE inhibitor-related angioedem a usually occurs within a week after starting ACE inhibitor therapy, but m ay occur at any tim e during the use of the m edication.

Medication (Drugs) 

C1-INH: concentrate given in 5% dextrose IV over 10â€“45 m inutes dose: <10 years old 500 U, >10 years old 1000 units; additional infusion and reassessm ent if sym ptom s persist for >2h. This m edication is not currently available in the United States.

Pa ge 4 3 2



Cim etidine: 300 m g IV



Danazol 400â€“600 m g orally up to 1 gm per day Contraindicated in children and pregnancy.



Diphenhydram ine: adult: 50 m g IV.; peds: 1â€“2 m g/kg slow IVP



Epinephrine: 0.3â€“0.5 m g (use 1:1,000 dilution for subcutaneous route, and 1:10,000 for IV route); peds: epinephrine 0.01 m g/kg subcutaneous/IV



Racem ic epinephrine: 2.25% solution (0.5 m L placed in a nebulizer in 2.5 m L of norm al saline)



FFP (if C1-INH is unavailable): adult dosage 2 units



Hydrocortisone: adult: 500 m g IV; peds: hydrocortisone 4â€“8 m g/kg/dose IV.



Methylprednisolone: adult: 125 m g IV.; peds: 1â€“2 m g/kg IV



Prednisone: adult: 60 m g PO; peds: 1 m g/kg PO



Ranitidine: adult: 50 m g IV



Stanozolol: 2 m g orally up to 16 m g per day



o

Discontinued in the United States

o

Contraindicated in children and in pregnancy

Tranexam ic acid: (Cyklokapron) 1 gm orally every 3â€“4 hours for up to 48 hours if necessary

Follow-Up Disposition Admission Criteria 

Patients with system ic sym ptom s that do not resolve com pletely will need to be hospitalized for observation.



A m onitored bed is recom m ended for those with airway

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involvem ent.

Discharge Criteria Patients without system ic sym ptom s who are stable for discharge should been seen in outpatient followup in a few days.

Issues for Referral Patients should be evaluated by an allergist/im m unologist after the initial presentation, especially if there is a fam ily history of angioedem a, or if the angioedem a is accom panied by abdom inal pain, or triggered by traum a.

References 1. Gom pels M, Lock R, Abinun M, et al. C1 inhibitor deficiency: consensus docum ent. Clin Exp Im m . 2005;139:379â€“408. 2. Grattan C, Powell S, Hum phreys F. Managem ent and diagnostic guidelines for urticaria and angio-oedem a. Br J Derm atol. 2001;144:708â€“714. 3. Nadel ES, Brown DF. Angioedem a. J Em erg Med. 1988;16(3):477â€“479. 4. Nzeako UC, Frigas E, Trem aine WJ. Hereditary angioedem a. Arch Intern Med. 2001;161:2417â€“2429. 5. Zuraw B. Current and future therapy for hereditary angioedem a. Clin Im m . 2005;114:10â€“16.

Miscellaneous SEE ALSO: Anaphylaxis; Urticaria

Codes ICD9-CM Angioneurotic edem a/Urticaria 995.1 Hereditary angioedem a 277.6

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ICD10 Angioedem a T78.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankle F racture/Dislo catio n

Ankle

Fracture/Dislocation Binh T. Ly

Basics Description Com m on m echanism s and injury patterns of the ankle

Mechanism of Injury 





Inversion injury: o

Avulsion fracture of the lateral m alleolus

o

Oblique fracture of the m edial m alleolus

Eversion injury: o

Avulsion fracture of the m edial m alleolus

o

Oblique fracture of the fibula

External rotation injury: o

Disruption of the tibiofibular syndesm osis, or a fibular fracture above the plafond

o

Anterior or posterior tibial fracture with separation of the distal tibia and fibula (unstable fracture)



Inversion and external rotation (Maisonneuve fracture): o

Medial m alleolus avulsion fracture or deltoid ligam ent tear

o

Disruption of the tibiofibular syndesm osis

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o

Oblique fracture of the proxim al fibula

Pediatric Considerations 

Ankle fractures in children often involve the physis (growth plate): o

May cause chronic deform ity from growth plate injury

o

In children <10 years of age, growth plate is weaker than epiphysis.



Tillaux fracture: Salter-Harris type III injury of the lateral tibial epiphysis caused by eversion and lateral rotation



Triplane fracture: unusual fracture of distal tibia with fracture lines in three distinct planes (coronal, transverse, sagittal)

Ottawa Ankle Rules. (Adapted from Bachm ann LM. Br Med J. 2003;326:417. ) Available at http://www.bm j.bm jjournals.com /content/vol326/issue7386/im ages/l arge/bacl4176.f2.jpeg.

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Diagnosis Signs and Symptoms 

History of traum a



Local ankle pain, swelling, deform ity



Inability to bear weight



Soft tissue injury, swelling, ecchym osis, skin tenting, skin blanching



Neurovascular com prom ise: o

Dim inished capillary refill

o

Dim inished posterior tibialis (PT) or dorsalis pedis (DP) pulses



Lim ited range of m otion

Essential Workup Physical Exam 

Ottawa ankle rules (Figure): decision rules for ordering radiographs in patients with suspected injury to the ankle and m idfoot. o

Malleolar zone (if either finding is present, then ankle radiographs are indicated): 

Bony tenderness at the posterior edge or distal 6 cm of either m alleoli (points A and B)



Inability to bear weight for four consecutive steps both im m ediately after the injury and in ED

o

Midfoot zone (if either finding is present, then foot radiographs are indicated): 

Bony tenderness at the base of the fifth m etatarsal (point C)



Bony tenderness of the navicular m edially (point

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D) 

Inability to bear weight for four consecutive steps both im m ediately after the injury and in ED



Assess the skin for disruption or ischem ia.



Careful evaluation of distal neurovascular status: o

Capillary refill

o

Palpation or Doppler of dorsalis pedis and posterior tibialis pulses



Palpate proxim al fibula for tenderness, especially when m edial m alleolus or deltoid ligam ent tenderness is present: o

Peroneal nerve is at risk for injury with a Maisonneuve fracture: 

Wraps around the fibular head



Test anterior tibialis and extensor hallucis longus.



Assess sensation in first webspace.

Radiography 

Anteroposterior (AP), lateral, and m ortise (leg internally rotated 20 degrees) views of the ankle if tenderness is elucidated in the m alleolar zone



Evaluate the m ortis view for widening of the m edial clear space >4 m m and tibiofibular clear space >6 m m .



Consider radiographs for the following special circum stances: o

Altered sensorium or dim inished distal lim b sensation

o

Multiple painful and distracting injuries

o

Injuries that occurred 10 days prior to evaluation

Tests Imaging

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

Unstable ankle fractures or dislocations require postreduction radiographs in all three planes after splinting.



AP and lateral radiographs of the tibia and fibula are indicated if a Maisonneuve fracture is suspected clinically.



Stress-testing the ligam ents in a painful ankle is unnecessary in the ED if the patient will be re-exam ined in 3â€“7 days.



Stress radiographs of the ankle are usually unnecessary acutely.



CT scan or MRI: o

Assess the degree of injury to the tibial plafond.

o

Intra-articular pathology

o

Ligam entous injuries

o

Pediatric epiphyseal injuries

P.71

Differential Diagnosis 

Ankle sprain



Achilles tendon injury



Os trigonum fracture



Fifth m etatarsal fracture (Jones fracture)



Peroneal tendon dislocation or injury



Talar fractures



Talar-dom e fracture



Subtalar dislocations



Calcaneal fractures



Foot fractures



Ankle diastasis



Rattlesnake envenom ation

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Pediatric Considerations 

Injury to the growth plates m ay not be apparent on plain radiographs.



Consider im m obilization, nonâ€“weight-bearing status, and orthopedic referral if clinical suspicion warrants, even in the setting of negative radiographs.



CT scan or MRI m ay be warranted to delineate the extent of the injury.



Inform parents of the possibility of growth abnorm alities in patients with injury to the physis.

Treatment Pre Hospital 

Im m obilize with soft splint to reduce pain, bleeding, and further injury.



Cautions: o

Traction devices are usually unnecessary: 

o

Contraindicated with open injuries

Protruding bone should not be reduced; the wound should be covered with a clean dressing.

Initial Stabilization 

Avoid weight bearing



Ice



Com pression



Elevation

ED Treatment Ankle Fracture 

All ankle fractures or dislocations require orthopedic

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consultation or referral. 



Open ankle fractures: o

Rem ove contam inants.

o

Apply m oist sterile dressing.

o

Assess tetanus im m unity.

o

Antibiotics

o

Em ergent orthopedic consultation

Closed ankle fractures: o

Closed reduction, if necessary

o

Im m obilize with a posterior splint.

o

Posterior splint im m obilizes the foot at a 90Â° angle with the application of bulky dressings and covered by volar (posterior) and coaptation (U-shaped stirrup) splinting m aterial.



Stable injury (injury to only one side of the ankle): o

Isolated injury to the lateral m alleolus without m edial involvem ent is virtually always stable.

o 

Apply posterior splint.

Unstable injury (both sides of the ankle are injured): o

Urgent orthopedic consultation

o

Posterior splint as in stable injuries

o

May require open reduction and internal fixation (ORIF) em ergently before significant swelling develops



Neurovascular injury requires em ergent orthopedic consultation.

Ankle Dislocations 

Closed reduction should be perform ed as rapidly as possible to m inim ize ischem ia to the skin and reduce the risk of avascular necrosis of the talus.



Skin tenting and evidence of neurovascular com prom ise are indications for im m ediate reduction, even prior to

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radiographs. 

Most ankle dislocations require ORIF.



After reduction, place a posterior splint.

Medication (Drugs) 

Closed fractures: o



Prim arily analgesics (opioids)

Dislocations or displaced fractures requiring closed reduction: o

Short-acting benzodiazepine (m idazolam 0.05â€“0.1 m g/kg IV) or barbiturate (m ethohexital 1â€“1.5 m g/kg IV) with opioid analgesic



Open fractures: o

Cefazolin: 2 g loading dose (peds: 50 m g/kg) IV

o

Gentam icin: 5â€“7 m g/kg (peds: 2.5 m g/kg) IV

o

Vancom ycin: 1 g loading dose (10 m g/kg in children) if penicillin allergic IV

o

Tetanus toxoid if indicated

Follow-Up Disposition Admission Criteria 

Unstable ankle fractures require urgent orthopedic consultation and m ay require adm ission.



Open ankle fractures and dislocations should be adm itted for dÃ©bridem ent, irrigation, and IV antibiotics.



Ankle dislocations that are treated with either open or closed reduction

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

Concern for com partm ent syndrom e or neurovascular injury

Discharge Criteria Sim ple nondisplaced stable ankle fractures without neurovascular com prom ise m ay be discharged following splinting.

References 1. Bachm ann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to exclude fractures of the ankle and m id-foot: system atic review. Br Med J. 2003;326:417. 2. Duchesneau S, Fallat LM. The Maisonneuve fracture. J Foot Ankle Surg. 1995;34(5):422â€“428. 3. Marsh JL, Saltzm an CL. Ankle fractures. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's Fractures in Adults. 5th ed. Philadelphia: Lippincott William s & Wilkins; 2001: 201â€“283. 4. Moehring HD, Tan RT, Marder RA, et al. Ankle dislocation. J Orthop Traum a. 1994;8:167â€“172. 5. Plint AC, Bulloch B, Osm ond MH, et al. Validation of the Ottawa Ankle Rules in children with ankle injuries. Acad Em erg Med. 1999;6:1005â€“1009.

Codes ICD9-CM 824.8 837.0

ICD10 S82.8 S92.1 S93.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankle Sprain

Ankle Sprain

Taylor Young Cardall

Basics Description 

Injuries to ligam entous supports of the ankle



Ankle joint is a hinge joint com posed of the tibia, fibula, and talus.



Injuries m ay range from stretching with m icroscopic dam age (grade I) to partial disruption (grade II) to com plete disruption (grade III)

Etiology 

Forced inversion or eversion of the ankle



Forceful collisions



85â€“90% of ankle sprains involve lateral ligam ents: o

Anterior talofibular (ATFL)

o

Posterior talofibular (PTFL)

o

Calcaneofibular (CFL)

o

Usually the result of an inversion injury

o

The ATFL is the m ost com m only injured.

o

If the ankle is injured in a neutral position, the CFL is often injured.

o 

The PTFL is rarely injured alone.

Injury to the deltoid ligam ent (connecting the m edial

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m alleolus to the talus and navicular bones) is usually the result of an eversion injury: o

Often associated with avulsion at the m edial m alleolus or talar insertion

o

Rarely found as an isolated injury

o

Suspect associated lateral m alleolus fracture or fracture of the proxim al fibula (Maisonneuve fracture).



Syndesm osis sprains (injury to the tibiofibular ligam ents or the interosseous ligam ent of the leg): o

Occur m ost com m only in collision sports

o

Syndesm osis injuries (â€œhigh ankle sprainsâ€•) have a higher m orbidity and potential for long-term com plications.

Pediatric Considerations 

Children younger than age 10 years with traum atic ankle pain and no radiologic evidence of fracture m ost likely have a Salter-Harris I fracture.



The ligam ents are actually stronger than the open epiphysis.

Diagnosis Signs and Symptoms History 

History m ay predict the type of injury found and should include: o

Tim e of injury

o

Mechanism

o

The presence of a â€œpopâ€• or â€œcrack.â€•

Pa ge 4 4 6

o

History of previous traum a

o

Relevant m edical conditions (e.g., bone or joint disease)

o

Treatm ents attem pted prior to arrival

o

Ability to bear weight subsequent to the injury at scene and ED

Physical Exam 

Aim ed at detecting joint instability and any associated injuries: o

Note the presence or absence of bony tenderness at posterior edge of m edial and lateral m alleoli as well as at the base of the fifth m etatarsal.



Docum ent neurovascular status distal to the injury.



Assess range of m otion and com pare it with the uninjured side.



Stress testing in the ED is often lim ited by pain and m ay im pair detection of ligam ent injury.



The squeeze test helps identify syndesm osis injuries: o

Squeeze tibia and fibula together at the m idcalf; pain felt in the ankle indicates a positive test.

Essential Workup 

The Ottawa Ankle Rules, a selective strategy for obtaining ankle radiographs in adults, suggest that foot or ankle radiographs are unnecessary except when any of the following are present: o

Bony tenderness at the posterior edge of the distal 6 cm or tip of either m alleolus

o

Bony tenderness along the base of the fifth m etatarsal or navicular bone

o

Inability to take four unassisted steps both im m ediately after the injury and in the ED

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

The rules have been prospectively validated by the original authors as well as independently by groups in the United States, the United Kingdom , France, and other countries.

Tests Imaging 

Ankle injuries should be radiographed if there is concern for fracture.



Stress radiographs are rarely useful in the ED and should not be routinely ordered unless requested by a consultant.

Differential Diagnosis 

Ankle fracture (lateral, m edial, or posterior m alleolus) or dislocation



Achilles tendon injury



Maisonneuve fracture



Os trigonum fracture



Fifth m etatarsal fracture (Jones fracture)



Transchondral talar dom e fracture



Peroneal tendon dislocation or injury

P.73

Treatment Pre Hospital Im m obilize ankle as necessary.

Initial Stabilization 

Prevent further injury; avoid weight bearing if painful.

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

RICE (rest, ice, com pression, elevation)

ED Treatment 

The goal of treatm ent is reduction of pain and return to norm al activity without long-term pain or joint laxity.



Existing evidence supports early m obilization and functional treatm ent: o

Unstable ankles (i.e., grade III) or those with severe pain m ay benefit from brief im m obilization followed by early return to functional treatm ent.



Grade I or II sprains can be treated with functional support (elastic bandage, air splint, gel splint, etc.): o

Evidence suggests air or gel splints m ay be superior to elastic bandage dressings.



Grade III sprains can be treated by im m obilization (sugar tong with posterior splint or bulky Jones dressing) and early orthopedic consultation or referral.



Crutches m ay be needed initially for com fort, but encourage weight bearing as tolerated for grades I and II.



Once acute pain and swelling have resolved, strengthening exercises and proprioceptive training (e.g., balance board, sm all circle walking) im prove ankle strength and function and prevent reinjury.



Full sports activities m ay be resum ed only when running and turning are pain free.



Ankle taping, air splints, or gel splints reduce the risk of recurrent injury in high-risk sports such as basketball, volleyball, soccer, and running.

Medication (Drugs) 

Nonsteroidal anti-inflam m atory drugs (NSAIDs) are useful

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in treating acute pain: o 

Ibuprofen: 800 m g (peds: 5â€“10 m g/kg) PO t.i.d.

Narcotic analgesics m ay be required for severe pain.

Follow-Up Disposition Admission Criteria An isolated ankle sprain should not require adm ission.

Discharge Criteria 

Grades I and II sprains should be instructed to follow up with the prim ary care physician in 1â€“2 weeks.



Grade III sprains and syndesm osis injuries should be referred to an orthopedic surgeon or sports m edicine specialist within 7â€“10 days.

Issues for Referral Patient copies of any radiographs obtained m ay facilitate early follow-up.

References 1. Ho K, Abu-Laban RB. Ankle and foot. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:706â€“735. 2. Renstrom PA, Konradsen L. Ankle ligam ent injuries. Br J Sports Med. 1997;31:11â€“20. 3. Stiell IG, McKnight RD, Greenberg GH, et al. Decision rules for use of radiography in acute ankle injuries: refinem ent and prospective validation. JAMA. 1993;269:1127â€“1132. 4. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am .

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2001;18:85â€“113.

Codes ICD9-CM 845.00

ICD10 S93.4

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankylo sing Spo ndylitis

Ankylosing

Spondylitis Paul L. DeSandre

Basics Description 

Inflam m atory disorder, prim arily spinal, with sym m etric sacroiliitis in 100%



Onset 15â€“40 years of age in 90%



Male to fem ale ratio is 3:1.



Inflam m ation at the bony insertions of ligam ents or tendons (entheses)



May have system ic inflam m atory m anifestations such as uveitis



Spondylitis of ankylosing spondylitis (AS) begins at the insertions of the outer fibers of the annulus fibrosus (enthesitis) of the vertebrae: o

Ossification (syndesm ophyte form ation) m ay lead to com plete fusion, ankylosis, of the vertebrae.

o

Extensive spinal involvem ent causes the radiographic appearance of the so-called bam boo spine.

Alert The fused spine is dangerously brittle: significantly increases the

Pa ge 4 5 2

risks for fracture and paralysis.

Genetics HLA-B27 antigen in 90â€“95% of AS patients

Etiology Cytokine inflam m atory process triggered by traum a, infection, or neuroendocrine-im m une abnorm alities in patients genetically predisposed

Diagnosis Signs and Symptoms 

Spinal: Low back pain with sacroiliitis is the m ost com m on presentation:



o

Paralysis from m inor spinal traum a or m anipulation

o

Cauda equina syndrom e

Ocular: Acute anterior uveitis is the m ost com m on extraspinal m anifestation and m ay precede onset of arthritis.



Enthesitis (inflam m ation at tendon or ligam ent insertion): Achilles tendonitis or plantar fasciitis is com m on.



Pulm onary: restrictive lung disease owing to progressive reduction in chest expansion and upper lobe fibrosis



Joints: asym m etric arthritis of large joints of lower extrem ities occasionally



Genitourinary (GU): prostatitis occasionally



Cardiac: aortic valve regurgitation and cardiac conduction defects occasionally

History 

Low back pain, radiating into gluteal areas bilaterally from sacroiliac region, and progressing to involve entire spinal

Pa ge 4 5 3

region; exacerbated by rest and im proved with m ild activity or stooping forward 

Prior history of enthesitis, uveitis, restrictive pulm onary disease, arthritis to lower extrem ity large joints, prostatitis, or aortic valve disease

Physical Exam 

Flattening of the norm al lum bar lordosis



Exaggeration of thoracic kyphosis



Lim itation of spinal flexion



Reduction in chest expansion



Possible aortic valve regurgitation m urm ur

Pediatric Considerations 

Juvenile ankylosing spondylitis (JAS) m ay m im ic a septic process with fever and system ic signs.



Onset of JAS is late childhood or adolescence (usually before age 16 years); prim arily boys.



JAS m ay initially present as aortic regurgitation with fulm inant aortitis and m ay have an association with Takayasu arteritis.



JAS has a m uch greater predilection for extraspinal joints and entheses of the lower extrem ities; exam ine for: o

Asym m etrical arthritis of the joints of the lower extrem ities, especially hip

o

Enthesitis of the Achilles tendon attachm ent at the heel, the plantar fascia attachm ents to the sole of the foot, the patellar ligam ent attachm ent to the tibial tuberosity, and the quadriceps tendon attachm ents to the patella

Essential Workup 

Exclude fracture or nerve injury in any new spinal pain of a patient suspected of AS.

Pa ge 4 5 4



Exclude sepsis or septic joint.



Evaluate for sacroiliitis with pelvic rock test (com pression) or Patrick test (sacroiliac distraction).

Tests Lab 

CBC m ay show m ild leukocytosis with slight to m oderate anem ia and throm bocytosis.



BUN, creatinine, and electrolytes m ay be useful to assess renal involvem ent.



Erythrocyte sedim entation rate (ESR) or C-reactive protein (CRP) m ay be elevated, but are of lim ited use in the ED.

Imaging 

Pelvic radiograph: should be done in any adult patient suspected of undiagnosed ankylosing spondylitis: o

Sacroiliitis is essential to the diagnosis of AS; this is seen initially as subchondral bony erosions on the iliac side of the sacroiliac (SI) joint, which later m anifest as bony proliferation and sclerosis.



Lum bar, thoracic, and cervical spine radiographs to exclude fracture for com plaint of new pain to these areas with or without traum a



CT should be perform ed to further evaluate possible fractures on plain radiographs.



MRI should be perform ed em ergently on any patient with neurologic deficit.



Chest radiograph m ay show patchy inflam m atory infiltrates.

Differential Diagnosis 

Mechanical low back pain is generally im proved with rest

Pa ge 4 5 5

and exacerbated by exercise without signs of system ic inflam m atory process. 

Infectious low back pain is m ore constant, unrem itting, and associated with fever.



Neoplastic low back pain is m ore typical in patients older than age 40 years and m ore constant and unrem itting: o



Night pain is a characteristic sym ptom .

Septic arthritis should be excluded by arthrocentesis if clinically suspected in single joint involvem ent.



Psoriatic arthritis usually presents in a patient with known psoriasis and has m uch greater predilection for the hands and feet.



Reiter disease: the classic triad of arthritis, urethritis, and conjunctivitis: sym ptom onset about 1 m onth after an episode of urethritis or enteritis



Arthritis associated with inflam m atory bowel disease occurs in patients with Crohn disease or ulcerative colitis: o

Prim arily involves knee, elbow, ankle, or wrist, and usually exacerbated by flares of the bowel disease

P.75

Treatment Pre Hospital Alert 

Increased risk of traum atic spinal injury from even m inor injuries



Spinal im m obilization efforts m ust avoid worsening spinal

Pa ge 4 5 6

injury. 

Intubation difficulty (spinal deform ity)



Ventilation difficulty (chest wall restriction)

Initial Stabilization 

Traum a: airway, breathing, circulation (ABCs) while m aintaining im m obilization (including in-line spinal stabilization if intubation required)



Acute traum atic paralysis: m ethylprednisolone IV and im m ediate neurosurgical evaluation

ED Treatment 

Control pain and inflam m ation with nonsteroidal anti-inflam m atory drugs (NSAIDs); steroids or opioids m ay be useful in severe refractory cases.



Exclude infection by clinical presentation, laboratory analysis, and possibly arthrocentesis.



Exclude spinal fracture (use CT for equivocal findings on plain radiographs).

Medication (Drugs) 

Nonselective NSAIDs: o

Ibuprofen: 35 m g/kg/d divided q.i.d., m ax. 50 m g/kg/d (adult: 300â€“800 m g PO t.i.d. or q.i.d.)

o

Indom ethacin: 1â€“2 m g/kg/d divided b.i.d. or q.i.d., m ax. 4 m g/kg/d (adult: 25 m g PO b.i.d. or t.i.d.)

o

Naproxen: 10 m g/kg/d divided b.i.d., m ax. 1,000 m g/d (adult: 250â€“500 m g PO b.i.d)

o

Note: if NSAIDS are poorly tolerated, ineffective, or contraindicated, consider opioid analgesics, m uscle relaxants, or low-dose steroids.

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Alert 

Steroids: o

Methylprednisolone: high-dose protocol for acute paralysis: 30 m g/kg bolus, then 5.4 m g/kg/h for 24 hours total

Follow-Up Disposition Admission Criteria 

Acute neurologic im pairm ent



Pain is intractable.



Sepsis or septic joint cannot be excluded.

Discharge Criteria 

No serious injuries or neurologic deficit



Pain controlled

Issues for Referral 

Additional m edical therapy m ay be useful for chronic treatm ent.



Resting splints for inflam ed joints



Orthoses for enthesitis (such as heel cushion inserts to rest Achilles tendon attachm ent)

References 1. Bracken MB, Shepard MJ, Collins WF, et al. A random ized, controlled trial of m ethylprednisolone or naloxone in the treatm ent of acute spinal-cord injury: result of the second National Acute Spinal Cord Injury Study. New Engl J Med. 1990;322:1405â€“1411. 2. Dougados M, Behier JM, Jolchine I, et al. Efficacy of celecoxib, a cyclooxygenase 2-specific inibitor, in the treatm ent of ankyolsing

Pa ge 4 5 8

spondylitis: a six-week controlled study with com parison against placebo and against a conventional nonsteroidal anti-inflam m atory drug. Arthritis Rheum . 2001;44(1):180â€“185. 3. Dougados M, Dijkm ans B, Khan M, et al. Conventional treatm ents for ankylosing spondylitis. Ann Rheum atol Dis. 2002;61(suppl 3):iii40â€“50. 4. Fleischm ann R, Iqbal I, Slobodin G. Meloxicam . Expert Opin Pharm acother. 2002;3(10):1501â€“1512. 5. Karasick D, Schweitzer ME, Abidi NA, et al. Fractures of the vertebrae with spinal cord injuries in patients with ankylosing spondylitis: im aging findings. AJR Am J Roentgenol. 1995;165:1205â€“1208. 6. Nakstad PH, Server A, Josefsen R. Traum atic cervical injuries in ankylosing spondylitis. Acta Radiol. 2004;45(2):222â€“226. 7. Papadopoulos MC, Chakraborty A, Waldron G. Exacerbating cervical spine injury by applying a hard collar. Br Med J. 1999;319:171â€“172. 8. Pepm ueller PH, Moore TL. Juvenile spondyloarthropathies. Curr Opin Rheum atol. 2000;12(4):269â€“273. 9. Seiper J, Braum J, Rudwaleit M, et al. Ankylosing spondylitis: an overview. Ann Rheum atol Dis. 2002;61(suppl 3):iii8â€“18.

Codes ICD9-CM 720.0

ICD10 M45

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anterio r C ruciate Ligam ent Injury

Anterior

Cruciate Ligament Injury Moss Mendelson

Basics Description 

The anterior cruciate ligam ent (ACL) inserts anterolaterally to the anterior tibial spine and to the posterior aspect of the lateral fem oral condyle: o

Portions are under tension (i.e., at risk) in both flexion and extension.



The ACL prevents excessive anterior m ovem ent, excessive internal rotation of the tibia on the fem ur, or hyperextension of the knee.



Mechanism of injury is often deceleration with flexion and rotation: o

Hyperextension can also occur.

Etiology 

The ACL is the m ost com m only injured ligam ent of the knee: o

Most injuries to the ACL are sports related, especially skiing and football.

o

Noncontact injury is com m on: plant-and-pivot or

Pa ge 4 6 0

stop-and-jum p m echanism . o

Fem ale athletes are m ore susceptible to ACL injury.

Pediatric Considerations 

The ACL is the m ost frequently injured knee ligam ent in children.



Tears of the ACL in children often occur at the insertion site of the ligam ent.

Diagnosis Signs and Symptoms History 

Feeling knee â€œgive way.â€•



Hearing a pop, or feeling a tearing sensation at time of injury



Pain m ost com m on com plaint with ACL rupture



Partial injury m ay not be particularly painful owing to paucity of pain fibers in ACL itself.



Most patients report im m ediate knee dysfunction: o

Som e m ay am bulate despite com plete ACL rupture because of stability from supporting structures.

Physical Exam 

Im m ediate effusion (hem arthrosis within 2â€“3 hours) usually indicates a significant intra-articular injury.



About 70% of acute knee hem arthroses are caused by ACL injury.



Lack of hem arthrosis does not rule out ACL injury: o

Capsular disruption m ay allow extravasation of intra-articular blood.



â€œLockingâ€• m ay occur because of interposition of torn

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cruciate, or associated torn m enisci, or loose body: o

Pseudolocking m ay be present from pain, effusion, or spasm .



Stress testingâ€“always com pare the injured to the uninjured side: o

Asym m etry is m ore reliable than absolute degree of laxity.

o

Lachm an test is m ost reliable: 

Knee flexed 20 degrees, patient supine with thigh supported; tibia is brought forward on the fem ur, one hand holding proxim al tibia, the other stabilizing the fem ur just above the patella.



Pain with no m otion is probable grade 1 injury.



Pain with m otion indicates partial tear or disruption.

 o

Firm end point of m otion suggests partial tear.

Pivot shift test: m ore specific for ACL injury but unreliable without anesthesia; use cautiously in acutely injured knee: 

Patient supine, knee in full extension



Internal rotation of tibia via a hand on foot is applied sim ultaneously with valgus stress from the other hand.



With knee flexion to 20â€“30Â°, the exam iner notices a jerk at the anterolateral corner of the proxim al tibia.

o

Anterior drawer sign: not as sensitive or specific as Lachm an test: 

Knee flexed 90Â°, patient supine, hip flexed 45Â°, foot neutral and stabilized



Anterior m otion is positive.

Pa ge 4 6 2

Pediatric Considerations 

Children and adolescents show m ore laxity on exam than adults.



Ottawa knee rules do not apply to children.

Essential Workup 

Neurovascular evaluation



Exclusion of fractures/dislocations



Valgus/varus stress at 20Â° flexion



Extensor m echanism function



Lachm an test (as described above) is m ost im portant and sensitive test for ACL injury.



Look for signs of associated ligam ent or m eniscus injury: o

Present in about half of patients with ACL injury

Tests Lab 

If cause of knee effusion is uncertain, synovial aspirate can be sent for cell count, Gram stain, and culture and crystals: o



Fat globules in aspirate suggest fracture.

Arthrocentesis usually not indicated except to relieve sym ptom s from tense effusion

Imaging 

Plain film s have low rate of positive findings: Clinical decision rules lim it num ber of negative plain film s obtained.



Ottawa knee rules (apply to adults): plain film s required for patients with any of five findings: o

Age 55 or older

o

Isolated tenderness of patella

o

Tenderness at head of fibula

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o

Inability to flex 90Â°

o

Inability to bear weight both im m ediately and in ED (four steps)



Lateral capsular sign is lateral tibial plateau avulsion fracture, just below joint line: o

Diagnostic for ACL rupture, but present in <10% of ACL injuries



MRI is replacing arthroscopy for definitive im ages of cruciate ligam ents, but is rarely indicated em ergently.

Differential Diagnosis 

Meniscal injury (present in up to 50% of ACL injuries)



Collateral ligam ent injury



Tibial plateau injury

P.77

Treatment Initial Stabilization 

Docum ent neurovascular function.



Im m obilize knee, ice, elevate.

ED Treatment 

Injury is graded by severity: o

Grade 3 is com plete disruption of ligam ent.

o

Grade 2 represents severe stretching with partial tear of ligam ent.

o

Grade 1 is m icroscopic ligam entous dam age with no clinical instability.



General care:

Pa ge 4 6 4

o

First-degree injury m ay be treated with com pressive wrap and weight-bearing as tolerated.

o

More severe grades: Treat with im m obilization and non-weight-bearing with crutches.

o

Ice for first 48 hours, elevation

o

Analgesic

o

Aspiration of a tense hem arthrosis m ay relieve pain.

Pediatric Considerations 

Conservative treatm ent in children is generally associated with poor outcom e.



Controversy exists as to best surgical approach in children.

Medication (Drugs) 

Nonsteroidal anti-inflam m atory drugs (NSAIDs) or narcotic pain m edications are m ainstay.



Motrin: 400â€“600 m g (peds: 5â€“10 m g/kg) PO q.i.d.

Follow-Up Disposition Admission Criteria 

Isolated ACL injury rarely requires em ergent hospitalization.



For suspected com plete ruptures, definitive therapy is often surgical, and orthopedic consultation is appropriate.

Discharge Criteria Most patients can be m anaged as outpatients with appropriate

Pa ge 4 6 5

referral.

Issues for Referral 

Re-exam ination is recom m ended at 48 hours if ED exam is inconclusive or if history suggests m ore significant injury than initial exam dem onstrates (i.e., severe sym ptom s, hearing pop).



Orthopedic referral within 1â€“2 weeks is necessary if significant ligam entous injury is present.



Surgical repair m ay be considered for patients wishing to return to high-level sports or activities.



Controversy and practice variation rem ain prevalent am ong orthopedists caring for ACL-injured patients.

References 1. Beasley LS, Chudik SC. Anterior cruciate ligam ent injury in children: update of current treatm ent options. Curr Opinion Pediatr. 2003;15:45â€“52. 2. Gersoff WK, Clancy WG Jr. Diagnosis of acute and chronic anterior cruciate ligam ent tears. Clin Sports Med. 1988;7(4):727. 3. Harm on K, Ireland M. Gender differences in noncontact anterior cruciate ligam ent injuries. Clin Sports Med. 2000;19(2):287â€“302. 4. Solom on DH, Sim el DL, et al. Does this patient have a torn m eniscus or ligam ent of the knee? Value of the physical exam ination. JAMA. 2001;286:1610. 5. Stiell IG, Greenberg GH, et al. Prospective validation of a decision rule for the use of radiography in acute knee injuries. JAMA. 1996;275:611. 6. Swenson TM, Ham er CD. Knee ligam ent and m eniscal injuries. Orthop Clin North Am . 1995;26:529. 7. Zarins B, Adam s M. Knee injuries in sports. N Engl J Med. 1988;318:950.

Codes

Pa ge 4 6 6

ICD9-CM 959.7

ICD10 S83.5

Pa ge 4 6 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anticho linergic Po iso ning

Anticholinergic

Poisoning Mark B. Mycyk

Basics Description 

Central and peripheral cholinergic blockade



Depending on the drug involved, antagonism occurs at m uscarinic (m ost com m on), nicotinic, or both receptors.



Onset of activity: 15â€“30 m inutes after ingestion



Duration of effect: 2â€“24 hours

Etiology 



Many drugs contain anticholinergic properties: o

Mild at therapeutic doses

o

Life threatening in overdose

Anticholinergic substances: o

Antihistam ines

o

Belladonna alkaloids, synthetic congeners

o

Antiparkinsonian drugs

o

Cyclic antidepressants

o

Antipsychotics (neuroleptics)

o

Mydriatics

o

Skeletal m uscle relaxants (orphenadrine,

Pa ge 4 6 8

cyclobenzaprine) o

Antispasm odics

o

Mushroom sâ€“Am anita m uscaria, A. pantherina

o

Plantsâ€“deadly nightshade, m andrake, henbane

o

Jim son weedâ€“sm oked or ingested

Diagnosis Signs and Symptoms Physical Exam 

Classic toxidrom e: o

â€œMad as a hatterâ€•â€“altered m ental status

o

â€œHot as a hareâ€•â€“hypertherm ia

o

â€œRed as a beetâ€•â€“flushed skin

o

â€œDry as a boneâ€•â€“dry skin and m ucous m em branes

o

â€œBlind as a batâ€•â€“blurred vision secondary to m ydriasis









General: o

Hypertherm ia

o

Altered m ental status

Ocular: o

Unreactive m ydriasis

o

Inability to accom m odate

Cardiovascular: o

Sinus tachycardia

o

Dysrhythm ias (rare except in m assive ingestions)

o

Hypotension/hypertension

o

Cardiogenic pulm onary edem a

Pulm onary:

Pa ge 4 6 9





o

Tachypnea

o

Respiratory failure

GI: o

Decreased/absent bowel sounds

o

Dysphagia

o

Decreased GI m otility

o

Decreased salivation

Genitourinary (GU): o





Urinary retention

Integum ent: o

Decreased sweating

o

Flushed skin

o

Dry skin and m ucous m em branes

CNS: o

Altered m ental status

o

Auditory or visual hallucinations

o

Com a

o

Seizures

Essential Workup Diagnosis based on clinical presentation and an accurate history

Tests Lab 

Urine toxicologic screen to exclude other ingestions



Electrolytes, BUN, creatinine, glucose



CBC



Creatine phosphokinase (CPK) if suspected rhabdom yolysis



Urinalysis



Acetam inophen level: o

Detects occult ingestion (e.g., Tylenol PM)

Imaging

Pa ge 4 7 0

ECG: 

Sinus tachycardia m ost com m on



QRS prolongation



AV blockade



Bundle branch block pattern



Dysrhythm ias

Differential Diagnosis 

Sym pathom im etic intoxication



Withdrawal syndrom e



Acute psychiatric disorders



Sepsis



Thyroid disorder

Treatment Pre Hospital Transport all pills/pill bottles involved in overdose for identification in ED

Initial Stabilization 



Airway, breathing, circulation (ABCs): o

Airway control essential

o

Adm inister supplem ental oxygen.

o

IV access

o

Cardiac m onitor and pulse oxim etry

Naloxone, thiam ine, D 5 0 (or Accu-Chek) if altered m ental status

ED Treatment 

Supportive care: o

IV rehydration with 0.9% norm al saline (NS)

Pa ge 4 7 1

o

Standard aggressive cooling m easures for hypertherm ia

o

Use benzodiazepines for treatm ent of agitation: 

Avoid phenothiazines owing to anticholinergic effects.

o

Treat seizures with benzodiazepines and barbiturates.

o

Dysrhythm ias: 

Use standard antidysrhythm ics.



Avoid class Ia antidysrhythm ic owing to the quinidinelike effect of m any anticholinergic drugs.



Sodium bicarbonate m ay reverse the quinidinelike effects.



Decontam ination: o

Adm inister activated charcoal.

o

Ocular lavage for eyedrop exposure.

o

Jim son weed considerations: 

Gastric decontam ination recom m ended up to 12â€“24 hours after the ingestion of seeds from slowed GI m otility



Consider polyethylene glycol electrolyte solution (GoLYTELY) for seed ingestions if no evidence of obstruction.



Physostigm ine (Antilirium ): o

Reversible acetylcholinesterase inhibitor that crosses the blood-brain barrier

o

Reverses both central and peripheral anticholinergic effects

o

Indicated in the presence of peripheral anticholinergic signs and the following: 

Seizures unresponsive to conventional therapy



Uncontrollable agitation

Pa ge 4 7 2

o

Use with caution owing to risk of dysrhythm ias (especially asystole), seizures, and cholinergic crises:

o



Place on cardiac m onitor.



Observe for cholinergic sym ptom s.

Contraindications: 

Cyclic antidepressant overdose (potentiates toxicity)



Cardiovascular disease



Asthm a/bronchospasm



Intestinal obstruction



Heart block



Peripheral vascular disease



Bladder obstruction

P.79

Medication (Drugs) 

Activated charcoal: 1 m g/kg PO



Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 2 5 over 1 m inute) IV; repeat if necessary



Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV every 10â€“15 m inutes



Dopam ine: 2â€“20 Âµg/kg/m in with titration to effect



Lorazepam : 2â€“4 m g (peds: 0.03â€“0.05 m g/kg) IV every 10â€“15 m inutes



Physostigm ine: 0.5â€“2.0 m g (peds: 0.02 m g/kg) IV over 5 m inutes; repeat if necessary in 30â€“60 m inutes



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Polyethylene glycol electrolyte solution (Colyte, GoLYTELY): 2 L/h (peds: 25â€“40 m L/kg/h) PO or per

Pa ge 4 7 3

nasogastric tube (NGT) until rectal effluent clear 

Propofol: 0.5â€“1.0 m g/kg IV (loading dose), then 5â€“50 Âµg/kg/m in (m aintenance dose)



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

ICU adm ission for m oderate to severe anticholinergic sym ptom s (agitation control, tem perature control, and observation for seizures or dysrhythm ias)



Any patient receiving physostigm ine

Discharge Criteria Mild and im proving sym ptom s of anticholinergic toxicity after 6â€“8 hours of ED observation

Issues for Referral 

Consider substance abuse referral for patients with recreational anticholinergic abuse.



Patients with unintentional (accidental) poisoning require poison prevention counseling.



Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.

References 1. Burns MJ, Linden CH, Graudins A, et al. A com parison of physostigm ine and benzodiazepines for the treatm ent of anticholinergic poisoning. Ann Em erg Med. 2000;35:374â€“381. 2. Ceha LJ, Presperin C, Young E, et al. Anticholinergic toxicity from nightshade berry poisoning responsive to physostigm ine. J Em erg

Pa ge 4 7 4

Med. 1997;15:65â€“69. 3. Delaney KA. Anticholinergics and antihistam ines (H1 antagonists). In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:472â€“477. 4. Hidalgo HA, Mowers RM. Anticholinergic drug abuse. Ann Pharm acother. 1990;24:40. 5. Patel RJ, Saylor T, William s SR, et al. Prevalence of autonom ic signs and sym ptom s in antim uscarinic drug poisonings. J Em erg Med. 2004;26(1):89â€“94. 6. Reilly KM, Chan L, Mehta NJ, et al. System ic toxicity from ocular hom atropine. Acad Em erg Med. 1996;3:868â€“871.

Codes ICD9-CM 971.1

Pa ge 4 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Antidepressant Po iso ning

Antidepressant

Poisoning Gerald Maloney Jr.

Basics Description 

Newer antidepressants, including the atypical antidepressants and selective serotonin reuptake inhibitors (SSRIs), and atypical antipsychotics



Most widely prescribed m edications in the United States



Tricyclic antidepressants (TCAs) covered in separate chapter

Etiology Mechanism 

Selective serotonin reuptake inhibitors: o

Inhibit the reuptake of serotonin at the 5HT1A receptor

o

Older agents include fluoxetine (Prozac).

o

Newer agents include citalopram (Celexa) and escitalopram (Lexapro).



Atypical antidepressants: o

Activity on m ultiple receptor sites, including

Pa ge 4 7 6

serotonin dopam ine and norepinephrine reuptake 

Atypical antipsychotics: o

Multiple receptor sites involved; serotonin, norepinephrine, anticholinergic and antihistam inic effects

o 

Multiple drugâ€“drug interactions

Cardiotoxicity in these agents is owing to sodium and potassium channel blockade, sim ilar to TCAs but less frequent.

Diagnosis Signs and Symptoms SSRIs 



Traditional SSRIs (fluoxetine, paroxetine): o

Seizures

o

Serotonin syndrom e

o

Rarely, QTc prolongation

o

Sedation

Citalopram : o

Seizures

o

Sedation

o

QTc prolongation

o

Active m etabolite is cardiotoxic: 

Exhibits delayed cardiotoxicity (up to 12 hours postingestion)



Escitalopram : o

QTc and QRS prolongation

o

Sedation

Atypical Antidepressants

Pa ge 4 7 7









Venlafaxine: o

Seizures

o

QTc prolongation

Bupropion: o

Sedation

o

Seizures

o

QRS/QTc prolongation

Trazodone: o

Sedation

o

QTc prolongation

o

Hypotension

o

Priapism

Mirtazapine: o

Sedation

o

QTc prolongation

o

Agranulocytosis (usually with chronic dosing)

Atypical Antipsychotics 

All have activity at dopam ine receptors.



Fewer extrapyram idal sym ptom s (EPS) and tardive dyskinesias





Clozapine: o

Sedation

o

Agranulocytosis (in up to 1% taking chronically)

o

Anticholinergic toxidrom e

Olanzapine: o

Fluctuating level of consciousness (LOC) with m iosis

o

Pancreatitis

o

Diabetic ketoacidosis (DKA)

o

Only atypical clearly associated with neurologic m alignant syndrom e (NMS)



Quetiapine: o

QTc prolongation

Pa ge 4 7 8

o 





Sedation up to com a

Risperidone: o

Sedation

o

QTc prolongation (rare)

o

Mild anticholinergic toxidrom e

Ziprasidone: o

Sedation

o

QRS/QTc prolongation

Aripiprazole: o

Lim ited data; m ay see sedation

Essential Workup 

Determ ine agents ingested, dose, and tim e of ingestion: o



Investigate for coingested drugs.

Rapid bedside glucose (Accu-Chek) if altered m ental status

Tests Lab 

Specific drug levels rarely available and usually do not guide clinical m anagem ent



ECG: o



For evaluation of QTc and QRS width

Urine pregnancy: o

In fem ales of childbearing age



Electrolytes, BUN, creatinine, glucose



Serum osm olality: o

Cannot rely on serum osm olality to rule out ingestion of other agents such as toxic alcohols



Routine toxicology screening: o

Rarely alters clinical m anagem ent



Salicylate and acetam inophen levels



Serum EtOH: o

To exclude ethanol intoxication as a cause of altered

Pa ge 4 7 9

m ental status o 

Required if osm oles are m easured

Arterial/venous blood gases (ABG/VBG) o

Check pH.

Imaging 

CT of brain for altered m entation



Chest radiograph

Differential Diagnosis 

Tricyclic antidepressant overdose



Ethanol overdose



Isoniazid overdose



Hypoglycem ia



Hypoxem ia



Hyponatrem ia



Hypocalcem ia



Withdrawal syndrom es



Serotonin syndrom e



Head traum a



Opioid intoxication



Sedative-hypnotic intoxication



DKA

P.81

Treatment Pre Hospital 

In cases of suspected overdose, bring all m edication bottles to hospital with patient.

Pa ge 4 8 0



Airway, breathing, and circulation m anagem ent (ABCs)



O.9% norm al saline (NS) IV fluids for blood pressure stabilization



Benzodiazepines for seizures



In cases of wide-com plex tachycardia, adm inister sodium bicarbonate IV fluid bolus to standard advanced cardiac life support (ACLS) m easures.

Initial Stabilization 

ABCs: o

Adm inister oxygen.

o

Place on cardiac m onitor and m easure pulse oxim etry.

o

Establish IV access with 0.9% norm al saline.

o

Intubation as dictated for airway protection or respiratory status



Rapid bedside glucose determ ination



Naloxone, thiam ine, and D 5 0 W as indicated for altered m ental status: o

Flum azenil is not recom m ended for m ixed-overdose patients, patients with underlying seizure disorder, or patients chronically on benzodiazepines.

ED Treatment 

Patient decontam ination: o

Do not attem pt decontam ination in a patient who does not have a stable airway.

o

Intubation solely for decontam ination purposes, however, is not generally indicated.

o

Activated charcoal in a dose of 50â€“75 g PO or via nasogastric tube (NGT) if the patient is intubated m ay be beneficial in early presenting overdoses.

o

Gastric lavage is not generally indicated for patients

Pa ge 4 8 1

with an isolated overdose of the agents listed in this chapter. 

For QRS widening, adm inister sodium bicarbonate IV bolus.



Treat hypotension unresponsive to IV fluids with norepinephrine rather than dopam ine owing to alpha-1 receptor antagonism .





Treat seizures with: o

Initial therapy: benzodiazepines

o

For refractory seizures: phenobarbital and pyridoxine

Treat sym ptom s of serotonin syndrom e (fever, AMS, tachycardia, rigidity, hyperreflexia) with benzodiazepines, cooling, cyproheptadine.

Medication (Drugs) 

Activated charcoal: 50â€“75 g PO initial dose



D 5 0 W: 25 g (peds: 0.5 g/kg D 5 0 W if <50 kg; 0.5 g/kg D 2 5 W if >50 kg) IV for hypoglycem ia



Diazepam : 5â€“10 m g IV bolus (peds: 0.1 m g/kg IV bolus or 0.5 m g/kg rectal)



Lorazepam : 2â€“4 m g (peds: 0.1 m g/kg) IV bolus



Naloxone: 0.4â€“2 m g (peds: 0.1 m g/kg) initial bolus; m ay repeat up to a total of 10 m g



Norepinephrine: 0.5â€“2 Âµg/kg IV infusion



Phenobarbital: 15â€“20 m g/kg IV m ax. dose is 2 gm ; caution: see respiratory depression with IV loading doses



Pyridoxine: 5 g (peds: 50â€“100 m g) initial IV bolus unless known am ount of isoniazid is given, in which case pyridoxine is gram :gram of INH



Sodium bicarbonate: 1 m Eq/kg IV bolus (adult 8.4%; peds: <50 kg, 4.2%)

Pa ge 4 8 2



Thiam ine: 100 m g (peds: 1 m g/kg) IV or IM

Follow-Up Disposition Admission Criteria 

Com a



Altered m entation



Hem odynam ic com prom ise



ECG changes



Suicidal patients should be on a one:one observation

Discharge Criteria 

Asym ptom atic patients >12 hours postingestion m ay be m edically cleared for psychiatric adm ission



Discharge only asym ptom atic patients >12 hours postingestion who are not suicidal.

References 1. Balit CR, Isbister GK, Hackett LP, et al. Quetiapine poisoning: a case series. Ann Em erg Med. 2003;42(6):751â€“758. 2. Cuenca PJ, Holt KR, Hoefle JD. Seizure secondary to citalopram overdose. J Em erg Med. 2004;26(2):177â€“181. 3. Dart RC, et al. Medical Toxicology. 3rd ed. 2003. 4. Isbister GK, Bowe SJ, Dawson A, et al. Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose. J Toxicol Clin Toxicol. 2004;42(3):277â€“285. 5. Sarko J. Antidepressants, old and new. A review of their adverse effects and toxicity in overdose. Em erg Med Clin North Am . 2000;18(4):637â€“654. Review.

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Miscellaneous SEE ALSO: Tricyclic Antidepressant Poisoning

Codes ICD9-CM 969.3 Poisoning by other antipsychotics, neuroleptics, and m ajor tranquilizers

Pa ge 4 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ao rtic Dissectio n, Tho racic

Aortic

Dissection, Thoracic Jeffrey I. Schneider Jonathan S. Olshaker

Basics Description 

Aortic dissection begins when a jet of blood induces an intim al tear.



Blood then dissects through the m edia under aortic systolic pressure.



It is thought that hypertension is a m ajor factor in the dissection process.



Dissections can start proxim ally at the root and dissect distally to involve any or all branches of the aorta, such as the carotid and subclavian arteries.



The dissection process can also proceed proxim ally to involve the aortic root, the coronary ostia, and the pericardium .



Dissection that progresses proxim ally m ay lead to occlusion of the coronary ostia, aortic valve incom petence, or cardiac tam ponade.



Classification related to portion of aorta involved:

Pa ge 4 8 5

o

o

Stanford classification: 

Type A: ascending aorta



Type B: distal to ascending aorta

DeBakey classification: 

DeBakey I: intim al tear in aortic arch or root



DeBakey II: ascending aorta



DeBakey III: distal to takeoff of left subclavian artery

Etiology 

Any process that affects the m echanical properties of the aortic wall can lead to dissection: o

Hypertension

o

Congenital heart disease (bicuspid aortic valve, coarctation)

o

Aortic wall connective tissue abnorm alities (cystic m edial necrosis)

o

Connective tissue disease (Marfan disease, Ehlers-Danlos syndrom e)

o

Pregnancy

o

Infectious/inflam m atory conditions of the aorta (lupus, syphilis, endocarditis, giant cell arteritis)

o

Tobacco use

Diagnosis Signs and Symptoms History 

Chest pain: o

May be absent in as m any as 15% of patients

o

Substernal if type A dissection

Pa ge 4 8 6



o

Intrascapular is descending thoracic dissection

o

Lum bar if abdom inal aorta involved

o

Starts abruptly

o

Usually described as sharp

o

Most severe at onset

Back pain: o

Com m only interscapular or lum bar



Com bination of chest, back, and abdom inal pain



Neurologic com plaints: o

Visual changes

o

Stroke sym ptom s



Nausea, vom iting



Peak age for occurrence: o

Proxim al dissection: 50â€“55 years

o

Distal dissection: 60â€“70 years

Pregnancy Considerations 

Risk of dissection increases in presence of pregnancy: o

In wom an less than 40 years of age, 50% of dissections occur during pregnancy.

Physical Exam 

Hypertension: o



35â€“40% m ay be norm otensive

Pulse deficits: o

Discrepancies in blood pressure (BP) between lim bs

o

Usually in upper extrem ities



Neurologic/spinal cord deficits



Murm ur of aortic regurgitation: o

Occurs in up to 31% of patients

o

Musical, vibrating quality with variable intensity

Essential Workup ECG:

Pa ge 4 8 7



Useful in ruling in or out ST-elevation m yocardial infarction or ischem ia



Dissection m ay involve coronary ostia and cause m yocardial infarction.



Inferior m yocardial infarction (right coronary artery lesion) is m ore com m on than left coronary artery territory.



Useful for evaluating the presence of left ventricular hypertrophy



A norm al ECG in the presence of severe, acute-onset chest/back pain should heighten one's suspicion of an aortic dissection.

Tests Lab 

Leukocytosis



Hem aturia



Elevated blood urea nitrogen and creatinine



Elevated am ylase secondary to bowel ischem ia



Elevated cardiac enzym es due to m yocardial ischem ia

Imaging 

Chest radiograph: o

Useful in excluding other etiologies such as pneum othorax and pneum onia

o

In dissection, there m ay be a widened m ediastinum or abnorm al aortic contour.

o

An enlarged heart secondary to pericardial fluid (blood) m ay be present.

o

May be com pletely norm al in as m any as 12%â€“18% of cases



Echocardiogram â€”transthoracic or transesophageal: o

Transthoracic:

Pa ge 4 8 8



Not very helpful in the diagnosis of aortic dissection



May be used to evaluate for com plications of a known dissection, such as tam ponade, valvular incom petence, or m yocardial infarction (from ostial occlusion)

P.83

o

Transesophageal: 

May be perform ed in the ED



Patients m ay require intubation.



Provides inform ation regarding extent of dissection and com plications



CT: o

Very useful in defining extent of dissection

o

May also be used in diagnosing clinical entities such as pulm onary em bolism

o

Has a high sensitivity for the diagnosis of aortic dissection and is the diagnostic m odality of choice in m any centers



MRI: o

Highly sensitive and specific

o

Requires patient transport out of ED for extended period of tim e

o

Lack of im m ediate availability m ay be a problem

o

Study of choice in those with renal insufficiency or dye allergy



Aortography: o

High sensitivity and specificity

o

Useful for preoperative planning

o

Difficult to obtain in m any centers

Pa ge 4 8 9



Cardiac catheterization: o

Due of overlap of sym ptom atology with cardiac ischem ia, som e patients m ay have diagnosis m ade by cardiac catheterization when an intim al flap is visualized.

Differential Diagnosis 

Myocardial infarction/ischem ia



Unstable angina



Pneum othorax



Esophageal rupture



Pulm onary em bolism



Pericarditis



Pneum onia



Musculoskeletal pain

Treatment Pre Hospital 

Monitor



IV access

Initial Stabilization 

Two large-bore IV lines



Continuous cardiac m onitoring



Pulse oxim etry



Oxygen



Type and cross

ED Treatment 

BP reduction to reduce shearing forces on aortic wall and slow down the dissection process

Pa ge 4 9 0



Medications: IV beta-blockade and nitroprusside o

Medications are used to control hypertension and cardiac contractility and decrease shearing forces.

o

Esm olol (IV) or labetalol (IV): 

Contraindications: bradycardia, chronic obstructive pulm onary disease, hypotension

o

Nitroprusside (com m only used in conjunction with IV beta-blocker)

o

Caution when using the above together: To prevent an initial increase in shear forces, beta-blocker therapy should be started prior to the addition of nitroprusside therapy



Em ergent surgery: o

Treatm ent of choice for type A dissection

o

Treatm ent for type B dissections in those who have failed m edical therapy



Medical m anagem ent: o

Treatm ent of choice for stable type B dissections

Alert Sym ptom s of aortic dissection m ay be sim ilar to those of cardiac ischem ia/infarction and pulm onary em bolus. Treatm ent with throm bolytics and anticoagulants m ay be harm ful and potentially fatal if aortic dissection is present.

Medication (Drugs) 

Esm olol: 500 Âµg/kg bolus IV, then 25â€“50 m g/kg/m in drip



Labetalol: 10â€“20 Âµg IV every 10â€“15 m inutes, then 2â€“4 m g/h drip



Nitroprusside: 0.5 Âµk/kg/m in IV and titrate upwards to

Pa ge 4 9 1

desired effect

Follow-Up Disposition Admission Criteria 

All patients with aortic dissection should be adm itted to the intensive care unit.



Em ergency cardiothoracic surgery consultation should be obtained, especially in cases of type A dissection.

References 1. Erbel R, et al. Diagnosis and m anagem ent of aortic dissection. Eur Heart J. 2001;22(18):1642â€“1681. 2. Hagan PG, et al. The international registry of acute aortic dissection: New insights into an old disease. JAMA. 2000;283(7):897â€“903. 3. Khan IA, Nair CK. Clinical, diagnostic, and m anagem ent perspectives of aortic dissection. Chest. 2002;122(1):311â€“328. 4. Moore AG, et al. Choice of com puted tom ography, transesophageal echocardiography, m agnetic resonance im aging, and aortography in acute aortic dissection: International registry of acute aortic dissection. Am J Cardiol. 2002;89:1235â€“1238. 5. Rogers RL, McCorm ack R. Aortic disasters. Em erg Med Clin N Am . 2004;(22):887â€“908.

Codes ICD9-CM 441.00

ICD10

Pa ge 4 9 2

171.0

Pa ge 4 9 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ao rtic Rupture, Traum atic (TAI)

Aortic

Rupture, Traumatic (TAI) Kevin J. L. Martens Elizabeth L. Lynch

Basics Description 

Most patients with significant traum a to the aorta die im m ediately.



Patients surviving to the ED usually have a contained rupture (pseudoaneurysm ).



Several theories exist: o

Shear forces arise from unequal rates of deceleration of the relatively fixed descending aorta and the m ore m obile arch.

o

â€œBendingâ€• stress is created by lateral im pact.

o

Twisting of the arch occurs, forcing it superiorly and thus causing it to stretch.

o

Osseous pinch (bony com pression of the thoracic cage) tears m ajor vessels.

o

Water-ham m er pulse wave causes sudden increase in intralum inal pressure.



Most com m on location for rupture (56â€“95%) is the

Pa ge 4 9 4

isthm us at the ligam entum arteriosum . 

Brachiocephalic vessels m ay also be injured.



Innom inate artery is the m ost com m only injured branch of the aorta.



Most tears are transverse, not longitudinal.



Tears m ay be partially or com pletely circum ferential.

Alert 

Rare in patients younger than 15 years; m ay be protected by a m ore com pliant chest wall

Etiology 

Most com m only results from m otor vehicle collisions



Other m echanism s: auto versus pedestrian, airplane crashes, falls from heights >10 ft, crush and blast injuries, direct blow to chest



Cause of death in up to 20% of lethal m otor vehicle collisions



Approxim ately 85% of patients with traum atic aortic rupture (TAI) die before reaching the hospital



Of patients with TAI who survive the initial event, 71â€“84% survive with prom pt diagnosis and treatm ent, 49% die within 24 hours, and 90% die at 4 m onths without treatm ent.



Drivers are 50% m ore likely to sustain TAI than passengers.



Ejection from vehicle doubles the risk.

Diagnosis Signs and Symptoms 

Substernal chest pain

Pa ge 4 9 5



Anterior chest wall contusion



Midscapular pain



Shortness of breath, dyspnea, dysphagia, stridor, hoarseness (owing to expanding hem atom a)



Harsh precordial or m idscapular systolic m urm ur



Acute coarctation syndrom e:



o

Hypertension of upper extrem ity

o

Increased pulse am plitude of upper extrem ities

o

Decreased pulse am plitude in lower extrem ities

o

Cyanosis of lower extrem ities

Paraplegia, anuria, or ischem ic extrem ity pain caused by im paired spinal blood supply



Swelling of neck (extravasation of blood)



Back pain with signs of an acute abdom en

Essential Workup Plain chest radiograph is the prim ary screening tool; high sensitivity and >90% negative predictive value, but low specificity

Tests Lab 

Com plete blood count



Electrolytes



Prothrom bin tim e/partial throm boplastin tim e



Type and cross-m atch (6â€“8 units PRBC)

Imaging 

Plain chest radiograph: o

Findings consistent with m ediastinal hem orrhage, hem atom a, or associated injuries: 

Widened m ediastinum (>8 cm anteroposterior supine at level of aortic arch, >6 cm posteroanterior upright, or >0.25

Pa ge 4 9 6

m ediastinum -width to chest-width ratio) 

Obliteration of aortic knob



Obscured descending aorta



Opacification of aortopulm onary window



Left apical capping



Deviation of trachea to right



Depression of left m ainstem bronchus



Displacem ent of nasogastric tube to right



Widened paraspinal stripe without spinal fracture



Left hem othorax, pleural effusion, pneum om ediastinum

o

Fracture of sternum or first or second ribs

o

Norm al m ediastinum in up to 12%

o

In pediatric patients: The m ost com m on findings are a left apical cap, pulm onary contusion, aortic obscuration, and m ediastinal widening.



Aortography: still considered diagnostic standard: o

Shows location and extent of injury

o

Also diagnoses nonaortic great vessel injuries

o

Can produce false-negative result with throm bosis of a false lum en



Conventional CT: o

May be considered in hem odynam ically stable patients with low suspicion, but whose chest film findings suggest dam age

o 

Angiography indicated with m ediastinal hem atom a

Helical CT-angiography: o

Preferred initial study in stable patients

o

High negative predictive value, but m ay have false-positives

o

Artifact and slice thickness m ay cause a sm all tear to

Pa ge 4 9 7

be m issed. o

Aortography often needed to confirm findings or for equivocal studies



Transesophageal echocardiography: o

Can be done rapidly in the em ergency departm ent

o

Shows isthm us well

o

May not visualize distal ascending aorta or arch well

o

Patients with cervical fractures, m axillofacial, or esophageal injuries are not candidates.

o

Can detect other cardiac injuries (cardiac contusion, pericardial effusion, etc.)



MRI: o

High accuracy, but m any lim itations

o

Lim ited availability, lengthy study tim e

o

Difficulty m onitoring patients

o

Traum a patients often have support devices that cannot enter the m agnetic field.

o

Not widely used in the diagnosis of traum atic aortic injury



Note: Patients at high risk for traum atic aortic injury by clinical suspicion should undergo aortography even if results of other studies are negative.

Pediatric Considerations Presence of large thym us m ay m ake diagnosis of widened m ediastinum difficult.

Differential Diagnosis 

Mediastinal hem atom a owing to other causes



Mediastinal lym phadenopathy



Redundant aorta resulting from hypertension



Ductus diverticulum (norm al variantâ€”bulge at isthm us)

P.85

Pa ge 4 9 8

Treatment Pre Hospital 

Im portant inform ation needs to be gathered from the accident scene:



o

Rate of speed

o

Direction of im pact

o

Dam age to steering wheel

o

Ejection from vehicle

o

Use of safety restraints

o

Driver or passenger affected

Im m ediate transport of any patient with suspected TAI to a level 1 traum a center

Initial Stabilization 

Follow traum a care protocols.



Avoid m aneuvers that m ay result in Valsalvalike response (gagging, straining).

ED Treatment 

Im m ediate consultation with traum a and chest surgeons is m andatory.



Medical therapy of hypertensive patient should be initiated to lower risk of rupture of pseudoaneurysm : o

Negative inotropes (beta-blockers, such as esm olol or labetalol) to target heart rate 60 Â±5 beats per m inute (bpm ); systolic blood pressure, 100â€“120 m m Hg; m ean arterial blood pressure of 70â€“80 m m Hg

Pa ge 4 9 9

o

In patients in whom beta-blockade is contraindicated (sinus bradycardia, second- or third-degree atrioventricular block, congestive heart failure, bronchospasm ), calcium channel blockers m ay be used.

o

Add vasodilators (nitroprusside sodium ) as needed after negative inotropes.

o

For significant hypotension, rapid volum e expansion, including blood, should be given.

o

For refractory hypotension requiring vasopressors, norepinephrine, or phenylephrine are preferred, with dopam ine used to im prove renal perfusion



Central venous catheter



Arterial pressure-m onitoring catheter



Acute coarctation syndrom e is a relative contraindication to antihypertensive therapy.



Peritoneal injuries take precedence.



Concom itant workup of other injuries



TEE m ay be perform ed in OR while correcting abdom inal injuries.

Medication (Drugs) 

Diltiazem : 20 m g (0.25 m g/kg) IV over 2 m inutes; second bolus 25 m g (0.35 m g/kg) in 15 m inutes if needed; infusion 5â€“15 m g/h



Esm olol: 500â€“1,000 Âµg/kg (peds: 100â€“500 Âµg/kg over 1 m inute) IV load; infusion 50â€“150 (peds: 25â€“100 Âµg/kg/m in; repeat load, increase drip 50) (peds: 25 Âµg/kg/m in every 5 m inutes; m ax. 300) (peds: 200 Âµg/kg/m in)



Labetalol: 20 m g IV over 2 m inutes, followed by additional

Pa ge 5 0 0

doses of 40â€“80 m g (peds: 0.2â€“10 m g/kg per dose, m ax. 20 m g per dose) IV every 10â€“15 m inutes, to 300 m g total; start infusion at 2 m g/m in and titrate up to 10 m g/m in (peds: infusion 0.4â€“1 m g/kg/h, m ax. 3 m g/kg/h) 

Nitroprusside: start at 0.3 Âµg/kg/m in; m ax. 10 Âµg/kg/m in



Norepinephrine: 8â€“12 Âµg/m in intravenously (peds: start 0.05â€“0.1 Âµg/kg/m in, m ax. 2 Âµg/kg/m in)



Phenylephrine: 50-Âµg (peds: 5â€“20-Âµg/kg per dose) boluses tension every 10â€“15 m inutes as needed; infusion 100â€“180 Âµg/m in IV (peds: 0.1â€“0.5 Âµg/kg/m in)

Follow-Up Disposition Admission Criteria All patients with aortic injuries m ust be adm itted to the ICU if not taken directly to the OR.

References 1. Britt LD, Weireter LJ, Cole FJ. Newer diagnostic m odalities for vascular injuries: the way we were, the way we are. Surg Clin North Am . 2001;81:1263â€“1279. 2. Feliciano DV. Traum a to the aorta and m ajor vessels. Chest Surg Clin North Am . 1997;7:305â€“323. 3. Gavant ML. Helical CT grading of traum atic aortic injuries. Im pact on clinical guidelines for m edical and surgical m anagem ent. Radiol Clin North Am . 1999;37:553â€“574. 4. Greenberg MD, Rosen CL. Evaluation of the patient with blunt chest traum a: an evidence based approach. Em erg Med Clin North

Pa ge 5 0 1

Am . 1999;17:41â€“62. 5. Lowe LH, Bulas DI, Eichelberger MD, et al. Traum atic aortic injury in children: radiologic evaluation. AJR Am J Roentgenol. 1998;170:39â€“42. 6. O'Connor CE. Diagnosing traum atic rupture of the thoracic aorta in the em ergency departm ent. Em erg Med J. 2004;21:414â€“419. 7. PrÃªtre R, Chilcott M. Blunt traum a to the heart and great vessels. New Engl J Med. 1997;336:626â€“632.

Codes ICD9-CM 901.0 Injury to thoracic aorta 902.0 Injury to abdom inal aorta

ICD10 S25.0 S35.0

Pa ge 5 0 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Aphtho us Ulcers

Aphthous Ulcers

Matthew R. Berkman

Basics Description Ovoid or round ulcerations on the m ucous m em branes of the m outh or genitals

Etiology 

Single etiology: unknown



Etiology likely m ultifactorial with som e correlation with: o

Im m unologic dysfunction; activation of cell-m ediated im m unes system



o

Infection

o

Food hypersensitivities

o

Vitam in deficiency

o

Pregnancy

o

Menstruation

o

Psychologic and genetic factors

Risk factors: traum a, stress, vitam in deficiency, im m unodeficiency



Epidem iology: usually occurs in children and young adults (10â€“30 years old), about 20% of general population

Pa ge 5 0 3

Diagnosis Signs and Symptoms 

Minor aphthous ulcers: o

70â€“90% of all aphthae

o

Sm aller than 10 m m in diam eter; up to five appear at a tim e

o

Painful, shallow ulcers

o

Necrotic centers

o

Raised m argins and erythem atous halos

o

Gray-white pseudom em brane

o

Found on nonkeratinized m ucosa of anterior oral cavity

o

Labial m ucosa, m axillary and m andibular sulci, nonattached gingiva



o

Floor of m outh

o

Ventral surface of tongue

o

Last for 10â€“14 days; do not scar

o

Fever rarely associated

Major aphthous ulcers or Sutton disease: o

10â€“15% of all aphthae

o

Sim ilar in appearance and pain to m inor

o

Larger than 10 m m in diam eter; 1â€“10 ulcers at a tim e

o

Deeper than m inor form

o

Involve all areas of oropharynx including pharynx, soft palate, tonsillar fauces



o

Last for weeks to m onths, heal with scarring

o

Often underlying disease

o

Fever is rarely associated

Herpetiform aphthous ulcers:

Pa ge 5 0 4

o

7â€“10% of all aphthae

o

Multiple sm all clusters

o

Between 1 and 3 m m in diam eter, 10â€“100 at any tim e, m ay coalesce into plaques

o

Herpetiform in nature, but herpes sim plex virus cannot be cultured from lesions.

o

Last for 7â€“30 days; scarring could occur.

Tests History 

Prodrom e of burning or pricking sensation of oral m ucosa 1â€“2 days prior to appearance of ulcers



Inquire about fam ily history of system ic lupus erythem atosus (SLE), inflam m atory bowl disease (IBD), BehÃ§et disease.



Inquire about patient m edical history of SLE, HIV, BID, IBD, BehÃ§et disease or CA

Physical Exam 

See Signs and Sym ptom s



Look for signs of dehydration: o



Vital signs should be within norm al lim its.

Evaluate for signs of secondary infection.

Essential Workup 

Diagnosis is m ade by history and clinical presentation.



Rule out oral m anifestation of system ic disease.



Focus on sym ptom s of eye, m outh, genitalia, skin, gastrointestinal (GI) tract, allergy and diet history.

Tests Lab 

Needed only when other etiologies causing ulcers are suspected

Pa ge 5 0 5



Com plete blood chem istry series



Rapid plasm a reagin test



Fluorescent treponem al antibody-absorption test



Antinuclear antibody test



Tzanck stain: o



Biopsy: o



Inclusion giant cells (herpes virus)

Multinucleated giant cells (Cytom egalovirus)

Fungal cultures: o

Cryptosporidium

Differential Diagnosis 





Traum a: o

Biting

o

Dentures

Drug exposure: o

NSAIDs

o

Nicorandil

Infection: o

o

Herpesvirus: 

Vesicular lesions



Ulcers on attached m ucosa

Cytom egalovirus: 

o

Varicellovirus: 

o

o

Characteristic skin lesions

Coxsackievirus: 

Ulcers preceded by vesicles



Hand, foot, buttock lesions

Syphilis: 

o

Im m unocom prom ised patient

Other skin or genital lesions

Erythem a m ultiform e: 

Lip crusting

Pa ge 5 0 6



Lesions on attached and unattached m ucosa skin lesions

o

Cryptosporidium infection, m ucorm ycosis, histoplasm osis

o 

Necrotizing gingivitis

Underlying disease: o

o

o

o

o

BehÃ§et syndrom e: 

Genital ulceration



Uveitis



Retinitis

Reiter syndrom e: 

Uveitis



Urethritis



HLA-B27-associated arthritis

Sweet syndrom e: 

Fever



Erythem atous skin plaques/nodules



In conjunction with m alignancy

IBD: 

Bloody or m ucous diarrhea



GI ulcerations

Lupus erythem atosus: 

o

Malar rash

Bullous pem phigoid/pem phigoid vulgaris: 

Vesiculobullous lesions on attached and unattached m ucosa

 o

Cyclic neutropenia: 

o

Diffuse skin involvem ent

Periodic fever

Squam ous cell carcinom a: 

Chronicity



Head/neck adenopathy

Pa ge 5 0 7



Im m unocom prom ised patient: o

HIV

o

Agranulocytosis

P.87

Treatment ED Treatment General Measures Sym ptom atic pain relief with analgesics; can use the following for initial pain relief: 

Viscous lidocaine 2%: Applyâ€“ulcer as needed q.i.d.



Sucralfate: 10 m L, swish and swallow or swish and spit q.i.d.



Magnesium hydroxide/diphenhydram ine hydrochloride: 5 m g/5 m L in 1/1 m ix swish and swallow q.i.d.



Dyclonine HCL: 1% solution, 5 m L rinse q.i.d.



5-am inosalicylic acid 5% cream : three tim es a day for 2 weeks



Topical over-the-counter preparations (Orabase, Anbesol)

Medication (Drugs) 

Analgesia: o

5-am inosalicylic acid 5% cream : three tim es a day for 2 weeks

o

Dyclonine HCL 1% solution: 5 m L rinse q.i.d.

o

Magnesium hydroxide/diphenhydram ine

Pa ge 5 0 8

hydrochloride: 5 m g/5 m L in 1/1 m ix swish and swallow q.i.d. o

Sucralfate: 10 m L, swish and swallow or swish and spit q.i.d.

o 

Viscous lidocaine 2%: Apply to ulcer as needed q.i.d.

Prom ote ulcer healing/prevent recurrence (first-line agents): o

Am lexanox 5% paste: 0.5 cm applied to ulcer q.i.d. after m eals

o

Clobetasol 0.05%: 0.5 cm applied to ulcer per day two tim es a day

o

Fluocinonide 0.05% gel: 0.5 cm applied to ulcer up to five tim es a day

o

Triam cinolone 0.1% in Orabase: Apply to ulcer two to four tim es a day until healed.



Second-line agents: o

Prednisone tablets: 40 m g PO per day Ã— 7 days

o

Thalidom ide: 200 m g PO per day Ã— 4 weeks

Follow-Up Disposition Admission Criteria 

Unable to eat or drink after appropriate analgesia



Abnorm al vital signs or evidence of dehydration

Discharge Criteria 

Tolerating fluids



Adequate analgesia



Norm al vital signs

Issues for Referral

Pa ge 5 0 9

Follow up with prim ary care physician if lesions have not resolved within 2 weeks.

References 1. McBride DR. Managem ent of aphthous ulcers. Am Fam Physician. 2000;62:149â€“154. 2. Porter S, Scully C: Aphthous ulcers (recurrent). Clin Evid. 2004;12:360â€“361. 3. Scully C, Gorsky M, Lozada-Nur F. The diagnosis and m anagem ent of recurrent aphthous stom atitis-a consensus approach. Journal of Am erican Dental Association. 2003;134:200â€“207. 4. Shashy RG, Ridley MB. Aphthous ulcers: a difficult clinical entity. Am J Otolaryngol. 2000;21:389â€“393. 5. Ship JA, Chavez EM, Doerr PA, et al. Recurrent aphthous stom atitis. Quintessence Int. 2000;31:95â€“112. 6. Sook BW, Sonis ST. Recurrent aphthous ulcers: a review of diagnosis and treatm ent. J Am Dent Assoc. 1996;127:1202â€“1213.

Codes ICD9-CM 528.2

Pa ge 5 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Apnea

Apnea

James M. Stephen MD

Basics Description 

Cessation of all respiration



Central apnea: o

Disruption in the generation of propagation of respiratory signals in the brainstem and descending neurom uscular pathways



Obstructive apnea: o

Occluding airway m ass

o

Functional obstruction from airway collapse due to positive pressure inspiration.



The apneic patient m ust be aggressively treated or death is im m inent in 4â€“6 m inutes



Apparent life-threatening event (ALTE): o

Episode that is of concern to the caregiver and is associated with a com bination of apnea, color change, change in tone, choking, or gagging

Etiology Adults 

Drug overdose

Pa ge 5 1 1



Severe hypoglycem ia



Cardiac arrest



Airway obstruction



Head or brainstem injury



Pulm onary failure



Near drowning



Sleep apnea

Pediatric 

Central apnea: o

Prem aturity

o

Head traum a

o

Congenital central hypoventilation syndrom e (Ondine curse)



Obstructive apnea: o

Pierre Robin syndrom e

o

Adenotonsillar hypertrophy

o

Foreign body aspiration

o

Laryngom alacia

o

Intralum inal cysts

o

Vocal cord paralysis, central com pression of the abductor vocal cord nerves from hydrocephalus or Chiari type II



o

Bronchiolitis

o

Pneum onia

o

Bronchospasm /Asthm a

o

Seizures

o

Traum a

o

Sepsis/Meningitis

Neonatal: o

Those above plus

o

Apnea of prem aturity

o

Apnea of infancy

Pa ge 5 1 2

o

Suffocation

o

Metabolic abnorm alities

o

Cardiac dysrhythm ias

Diagnosis Alert If the patient is apneic, treatm ent m ust com m ence at once.

Signs and Symptoms Apnea m ay be current, past, or im pending.

History 

Past episodes



Com orbidity



Medications (diabetes)

Pediatric Considerations 

Must assum e ALTE



Was child awake during the event?



Did the child turn red or blue?



Did he or she have seizure activity?



Did the child require stim ulation and/or rescue breaths to recover?



Were there antecedent sym ptom s such as fever or upper respiratory infection?



Any past history of ALTEs in this patient or siblings?

Physical Exam 

Establish unresponsiveness.



Check/Clear out upper airway.



Rem ove or suction any obstruction.



Ensure proper head positioning.

Pa ge 5 1 3



Brief physical assessm entâ€”look for CNS deficits, toxidrom es, traum a, lung disease, fever



Assess im pending apnea.



Fast or slow respirations



Increased work of breathing



Use of accessory m uscles



Abnorm al vital signs



Decreasing O 2 sat

P.89

Essential Workup 

Vital signs with tem perature,



Exam of airway, lung, and heart



Pulse oxim etry



A brief m ental status exam ination

Tests Lab 

Dextrostix



CBC



Electrolytes (including calcium )



Blood urea nitrogen, creatinine



Arterial blood gases



Toxicologic screen (including toxic alcohols)



ECG



Urinalysis



Consider liver function tests, am m onia, serum osm olarity

Pediatric Considerations 

Consider occult sepsis in the neonate.



Consider occult traum a.

Pa ge 5 1 4

Imaging 

Chest radiograph



Upper airway radiographs



Head CT

Diagnostic Procedures/Surgery Endotracheal Intubation

Differential Diagnosis 

Breath-holding spells (voluntary apnea): o

Occur from the first to fourth year of life



Ongoing apnea



Interm ittent apnea



Adult sleep apnea



Periodic breathing m ay be seen in neonates: o

Pauses last <10 seconds,

o

Are not accom panied by change of color or tone

o

Not pathologic

Treatment Pre Hospital 

High-flow oxygen if breathing resum es



Check/Clear out upper airway.



Bag-m ask ventilation with cricoid pressure



Endotracheal intubation if no response to com a cocktail



IV access, supplem ental oxygen, cardiac m onitor



Com a cocktail: o

Dextrose

o

Naloxone

o

Thiam ine

Pa ge 5 1 5



Look for signs of an underlying cause: o

Medications

o

Medic alert bracelets

o

Docum ent a basic neurologic exam ination

o

GCS

o

Pupils

o

Extrem ity m ovem ents

o

Gross signs of traum a

o

Talk with fam ily/prehospital personnel for inform ation

Initial Stabilization 

Establish unresponsiveness



Check/Clear out upper airway.



Rem ove or suction any obstruction.



Ensure proper head positioning



Com a cocktail o

IV D 5 0

o

Naloxone

o

Thiam ine

ED Treatment 

If currently apneic, ventilate with the bag-valve m ask device and high flow oxygen.



Endotracheal intubation is required if apnea persists despite com a cocktail.

Pediatric Considerations IV antibiotics if breathing resum es in infants

Medication (Drugs) 

Ceftriaxone: 2 g (peds: 50â€“75 m g/kg) IV

Pa ge 5 1 6



Dextrose: 1â€“2 m L/kg of D 5 0 W (peds: 2â€“4 m L/kg D 2 5 W) IV



Naloxone: 0.01â€“0.1 m g/kg IV/IM/SC/ET



Thiam ine: 100 m g IM or 100 m g thiam ine in 1,000 m L of IV fluid wide open



Rom azicon: 0.1â€“0.2 m g IV or IM (0.01 m g/kg) titrate to effect. Caution: m ay precipitate seizures.

Follow-Up All patients that were or are apneic m ust be adm itted.

Disposition Patients were or m ay becom e apneic m ust be adm itted to an intensive care unit setting.

Pediatric Considerations All ALTEs m ust be adm itted to a m onitored setting.

References 1. Brooks JG. Apparent life-threatening events. Pediatr Rev. 1996;17:257â€“259. 2. Davies F, Gupta R. Apparent life threatening events in infants presenting to an em ergency departm ent. Em erg Med J. 2002;19:11â€“15. 3. Tintinalli et al, eds. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York, NY: McGraw Hill; 2004: Chapters 12 Basic CPR in Adults, and 14 Pediatric CPR. 4. APLS: The Pediatric Em ergency Medicine Resource. 4th ed. Boston, MA: Jones & Bartlett; 2004.

Codes ICD9-CM

Pa ge 5 1 7

798.4 799.1 518.81 518.82

Pa ge 5 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Appendicitis

Appendicitis

Jennifer Kolodchak

Basics Description 

Acute obstruction of appendiceal lum en results in distension followed by organ ischem ia, bacterial overgrowth, and eventual perforation of the viscus.



Pain m igration: o

Perium bilical pain: Appendiceal distension stim ulates stretch receptors, which relay pain via visceral afferent pain fibers to tenth thoracic ganglion.

o

Localization of pain: As inflam m ation extends to surrounding tissues, pain occurs owing to stim ulation of parietal nerve fibers and localizes to position of appendix.

Pediatric Considerations 

Twenty-eight percent to 57% m isdiagnosis in patients <12 years (nearly 100% in patients <2 years)



Seventy percent to 94% perforation rate in young children (<2 years)

Geriatric Considerations 

Three tim es m ore likely to have perforation owing to

Pa ge 5 1 9

anatom ic changes 

Diagnosis often delayed owing to atypical presentations

Etiology 

Lum inal obstruction of appendix (usually by fecalith)



Appendiceal lum en becom es distended, inhibiting lym phatic and venous drainage.



Bacterial invasion of wall, with edem a and blockage of arterial blood flow



Perforation and spillage of contents into peritoneal cavity, causing peritonitis (usually 24â€“36 hours from onset)



May wall off and form abscess

Diagnosis Signs and Symptoms History 

Abdom inal pain: prim ary sym ptom : o

Norm al location: 

Right lower quadrant (RLQ) pain



Thirty-five percent of patients have appendix located within 5 cm of â€œnorm alâ€• location.

o

o

Retrocecal appendix (28â€“68%): 

Back pain



Flank pain



Testicular pain

Pelvic appendix (27â€“53%): 

o

Long appendix (<0.2%): 



Suprapubic pain

Inflam ed tip m ay cause pain in RUQ or LLQ.

Anorexia

Pa ge 5 2 0



Vom iting



Change in bowel habits: diarrhea (33%), constipation (9â€“33%)



Classic presentation (<75% adults): o

Initially perium bilical pain

o

Followed by anorexia (first sym ptom in 95%) and nausea



o

Localizes to RLQ (1â€“12 hours after onset)

o

Finally, vom iting with fever

Patient position: o

Supine or decubitus with legs (particularly the right) drawn up

o 

Prefer not to m ove

Shuffling gaitâ€”known as â€œappy walkâ€•

Pediatric Considerations 

Presentations often nonspecific and difficult to localize (<50% have classic presentation)



Anorexia, vom iting, and diarrhea m ore com m on (half-eaten m eal hours before com plaints of pain m ay m ore accurately indicate duration of sym ptom s)



Observe child before exam ination for subtle indicators of local inflam m ation: o

Lim ping gait

o

Hesitation to m ove or clim b

o

Flexed right hip

Physical Exam 

Vital signs: o

Often norm al

o

Fever: norm al to m ild elevation (<1Â°F) initially, increases with perforation



Abdom inal exam :

Pa ge 5 2 1

o

Tenderness at McBurney point (one third of distance from right anterior iliac spine to um bilicus)

o

Guarding: 

Voluntary guarding early owing to m uscular resistance to palpation



Involuntary guarding (rigidity) later as inflam m ation progresses and perforation occurs

o

Rebound: 

Pain with any rapid m ovem ent of peritoneum (e.g., bum ping stretcher)



Best assessed by gentle percussion (particularly in children)

o

Specific signs (less useful in pediatrics): 

Rovsing sign: pain in right lower quadrant when palpating left lower quadrant



Psoas sign: increased pain on extension of right hip with patient lying on her or his left side, owing to inflam ed appendix touching iliopsoas m uscle



Obturator sign: pain with passive internal rotation and flexion of right hip



Rectal exam : o



Lim ited value: m ay localize tenderness/m ass

Pelvic exam : o

Im portant to differentiate gynecologic disease

o

Vaginal discharge and/or adnexal tenderness or m ass suggests gynecologic disease.

o

Cervical m otion tenderness when present suggests pelvic inflam m atory disease (PID), but can be seen in up to 25% of wom en with appendicitis.

Pregnancy Considerations 

Enlarging uterus displaces appendix upward and laterally.

Pa ge 5 2 2



Hyperem esis gravidarum and other nonsurgical causes of vom iting should not cause abdom inal tenderness.

Geriatric Considerations Typical signs of peritonitis m ay be absent in elderly.

Essential Workup 

Suggestive history and physical exam sufficient to establish preoperative diagnosis and warrant surgical consultation



Tests listed below m ay be used to assist in diagnosis.



In atypical cases, repeat serial exam s in conjunction with som e of tests listed below have been shown to be effective, with decreased rates of negative appendectom ies and no increase in rates of perforation.

Tests Lab 





CBC: o

WBC >10,000, with left shift (80â€“90%)

o

Norm al WBC does not exclude diagnosis.

C-reactive protein: o

Overall sensitivity 62%, specificity 66%

o

May not be elevated early

o

Increased sensitivity with serial m easurem ents

Urinalysis: o

Generally norm al

o

Mild pyuria, bacteriuria, or hem aturia (20â€“40%)

o

Pyuria present if inflam ed appendix lies near ureter or bladder



Pregnancy test for fem ales of childbearing age

Imaging 

Unnecessary when diagnosis is clear

Pa ge 5 2 3



Most helpful in fem ale patients of childbearing age where diagnosis is often unclear



Abdom inal radiographsâ€”not recom m ended P.91



Ultrasound: sensitivity 75â€“90%; specificity 85â€“95%: o

Noncom pressible appendix 7 m m anteroposterior (AP) diam eter

o

Presence of appendicolith

o

Interruption of continuity of echogenic subm ucosa

o

Periappendiceal fluid/m ass

o

Lim ited by obesity, bowel gas, retrocecal appendix, and operator

o 

Negative study of lim ited use

CT: sensitivity 87â€“100%; specificity 89â€“98%: o

Highest yield using oral and rectal contrast with focused appendiceal technique (5-m m cuts from 3 cm above cecum extending distally 12â€“15 cm )

o

Fat streaking (100%)

o

Appendix 6 m m in diam eter (93%)

o

Focal cecal apical thickening (69%)

o

Defines appendiceal m asses (phlegm on versus abscess)

o

Best study for finding alternative diagnoses

Diagnostic Procedures/Surgery Laparoscopy: 

Diagnostic and therapeutic use



Gross pathology m ay be absent with positive m icroscopic findings.

Differential Diagnosis

Pa ge 5 2 4



Gastroenteritis



Meckel diverticulum



Crohn disease



Diverticulitis



Urinary tract infection



Pelvic inflam m atory disease



Ovarian cyst/torsion



Tubo-ovarian abscess



Renal stone



Testicular torsion



Sickle cell disease (especially in black children)



Mesenteric adenitis



Henoch-SchÃ¶nlein purpura



Diabetic ketoacidosis



Cholecystitis

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Fluid resuscitation with LR or 0.9% norm al saline (NS)

ED Treatment 

Im m ediate surgical consult for convincing history and physical exam : o

Laparoscopic versus open techniques perform ed

o

Negative appendectom y rate of 10% in m ales and 20% in fem ales

o

Percutaneous drainage, IV antibiotics, and possible interval appendectom y in appendiceal abscesses



Preoperative antibiotics (cefoxitin or am picillin/sulbactam )

Pa ge 5 2 5



NPO



Order CT if palpable m ass is present in RLQ to define phlegm on versus abscess.



If diagnosis is uncertain, send serial labs, observe, and repeat exam s (6â€“10% negative appendectom y rate with observation protocols).



Analgesics: o

Adm inistration of analgesics, including narcotics, does not adversely affect abdom inal exam or m ask pathology.

Medication (Drugs) 

Am picillin/sulbactam (Unasyn): 3 g (peds: 100â€“200 m g am picillin/kg/24 h) IV q6h



Cefoxitin (Mefoxin): 2 g (peds: 80â€“100 m g/kg/24 h) IV q6h



Ertapenem (Invanz): 1 g IM/IV per day



Morphine sulfate: 3â€“5 m g (peds: 0.1â€“0.2 m g/kg per dose q2hâ€“q4h) IV, every 15 m inutes titrated to effect



Piperacillin/tazobactam (Zosyn): 3.375 g (peds: 150â€“300 m g/kg/d if <6 m onths; 240â€“400 m g/kg/d if >6 m onths) IV q6h

Follow-Up Disposition Admission Criteria 

Surgical intervention of acute appendicitis



Observation or further diagnostic workup if diagnosis is

Pa ge 5 2 6

uncertain

Discharge Criteria Patients with abdom inal pain thought not to be appendicitis m ay be discharged if they m eet the following criteria: 

Resolved or resolving sym ptom s



Minim al or no abdom inal tenderness



No laboratory/radiologic abnorm alities



Able to tolerate PO intake



Adequate social support and able to return if sym ptom s worsen

References 1. Birnbaum BA, Wilson SR. Appendicitis at the m illennium . Radiology . 2000;215(2):337â€“348. 2. Graffeo CS, Counselm an FL. Appendicitis. Em erg Med Clin North Am . 1996;14:653â€“671. 3. Hendrickson M, Naparst TR. Abdom inal surgical em ergencies in the elderly. Em erg Med Clin N Am . 2003;21:937â€“969. 4. Jones PF. Suspected acute appendicitis: trends in m anagem ent over 30 years. Br J Surg. 2001;88:1570â€“1577. 5. Rothrock SG, Pagane J. Acute appendicitis in children: em ergency departm ent diagnosis and m anagem ent. Ann Em erg Med. 2000;36:39â€“51.

Codes ICD9-CM 540.9 540.0 540.1

ICD10 K37

Pa ge 5 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arsenic Po iso ning

Arsenic Poisoning

Gerald Maloney

Basics Description 

Acute toxicity: o

May be intentional ingestion, m alicious poisoning, or m edication error



Chronic toxicity: o

May be owing to occupational exposures, contam ination of drinking water or food, or use of folk rem edies containing arsenic



Prim arily owing to ingestion



May also be inhalational toxicity from arsine gas

Etiology 

Most arsenic poisonings seen in the ED setting are a result of intentional ingestion or m alicious poisoning.



Sodium arsenate, found in ant killer, m ost com m on acute exposure in United States



Overall, contam inated food/water supplies m ost com m on cause worldwide



Arsenic trioxide has been recently approved as chem otherapy for acute m yelogenous leukem ia (AML).



Melarsoprol used as antitrypanosom al agent in developing

Pa ge 5 2 8

countries 

Found in pesticides, certain folk rem edies (herbal balls), preservatives in wood



Also m ay be released as arsine gas from com bustion of zinc- and arsenic-containing com pounds

Mechanism 

Arsenic exists in several form s: gas (arsine, or Lewisite), organic, elem ental, and inorganic



Inorganic form s m ost frequently encountered toxic exposure



Inorganic in trivalent (arsenite) or pentavalent (arsenate) form s: o

Most pentavalent arsenic converted to trivalent arsenic in body, which is m ore toxic



Trivalent arsenic binds sulfhydryl groups and interferes in hem oglobin production.



Pentavalent arsenic uncouples oxidative phosphorylation.



Both function as cellular poisons.

Diagnosis Signs and Symptoms 



Cardiovascular: o

Prolonged QTc interval

o

Hypotension

o

Dysrhythm ias, prim arily ventricular

o

Nonspecific ST segm ent changes

o

Noncardiogenic pulm onary edem a

Central nervous system : o

Altered m ental status/encephalopathy

Pa ge 5 2 9

o



Peripheral neuropathy: 

Acuteâ€”sensory neuropathy



Subacuteâ€”sensorim otor neuropathy



Peripheral dysesthesias:

o

Muscle weakness up to paralysis

o

Headache

o

Seizures

Gastrointestinal: o

Nausea, vom iting: 

Protracted and m ay be refractory to antiem etics at usual doses



Can have hem orrhagic gastroenteritis; corrosive to GI tract



Rice water diarrhea has been described

o

Abdom inal pain

o

Garlic odor to breath, vom it, stools

o

Causes acute hepatitis; chronically, can cause portal hypertension



Miscellaneous: o

Derm atitis (toxic erythroderm a/hyperpigm ented lesions)

o

Mee lines (white bands across the nails owing to growth arrest caused by arsenic)

o

Hem olytic anem ia (m ore pronounced with arsine gas exposure)

o

Leukopenia (after several days)

o

Increased risk of carcinom a (liver/basal cell/squam ous cell of skin/bronchogenic)

o

Acute rhabdom yolysis

o

Hypothyroidism (antagonizes thyroid horm one)

o

Patchy alopecia

Essential Workup

Pa ge 5 3 0



Spot urine arsenic level



CBC

Tests Lab 

Spot urine arsenic level >1,000 Âµg/L m ay confirm diagnostic suspicion: o



Peaks 10â€“50 hours postingestion

Definitive test is 24-hour urine collection with speciation into organic and inorganic types of arsenic.



Blood levels not routinely helpful owing to short half-life in serum (approxim ately 2 hours)



CBC to check for: o

Anem ia

o

Leukopenia

o

Basophilic stippling



Electrolytes, BUN/creatinine and glucose



Urinalysis to look for evidence of hem olysis/rhabdom yolysis



Liver function tests



Total creatine phosphokinase (CPK) for rhabdom yolysis



Hair and nail arsenic levels: o

Difficult to interpret and not helpful acutely

o

May help determ ine chronicity of exposure in select populations

Imaging 

Plain abdom inal radiographs to look for radio-opaque foreign body



Cranial CT/other studies as indicated by patient's condition

Differential Diagnosis 

Other heavy m etal intoxications

Pa ge 5 3 1



Cyclic antidepressants



Encephalopathy/Korsakoff syndrom e



Hyperem esis gravidarum



Shock



Guillain-BarrÃ© syndrom e



Addison disease



Cholera



Other neuropathies

P.93

Treatment Pre Hospital Alert 

If possible to do so safely, bring containers in suspected overdose/poisoning.



Decontam inate skin.



Support airway/breathing/circulation.



Cardiac m onitoring.

Initial Stabilization 



Airway, breathing, circulation (ABCs): o

Cardiac m onitor

o

Isotonic crystalloids as needed for hypotension

o

Vasopressors if refractory hypotension is present

Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status



Cardiovascular: o

Avoid type 1A antidysrhythm ics:

Pa ge 5 3 2

 o

Exacerbate QTc prolongation

Continuous m onitoring as QTc prolongation is com m on



Neurologic: o

Treat seizures with benzodiazepines.

o

Assist ventilation as needed for respiratory insufficiency owing to neurom uscular weakness.



Renal: o

Urinary alkalinization for rhabdom yolysis

o

Hem odialysis for renal failure

ED Treatment 

Decontam ination: o

If the patient presents within the first hour of ingestion, m ay try orogastric lavage/aspiration

o

Activated charcoal: 75 g

o

If opacities seen on upright abdom inal film , institute whole bowel irrigation at 1â€“2 L/h of polyethylene glycol until abdom inal film s are clear.

o

If derm al exposure, decontam inate skin as first step in m anagem ent.



Ensure that no one else is contam inated and environm ent is evaluated.



Evaluate need for chelation therapy; based on levels, acuity of exposure, sym ptom s:



o

Consultation with a m edical toxicologist advised

o

Agents: 

Dim ercaprol (British Anti-Lewisite)



DMSA (succim er)

Elim ination: o

Hem odialysis not routinely effective 

Consider for patient with renal failure



Must continue chelation through hem odialysis

Pa ge 5 3 3

(HD)

Medication (Drugs) 

Dim ercaprol (British Anti-Lewisite): 3 m g/kg IM q4h for 24 hours, then q6h for the next 24 hours, then q12h until able to tolerate PO: o



Caution: cannot use if patient has peanut allergy

DMSA (succim er): 10 m g/kg PO q8h for 5 days, then q12h for 14 days



Sodium bicarbonate: 1 m Eq/kg IV bolus, followed by infusion of 150 m Eq in 1 L of D 5 W at 150 m L/h: o

Used to treat rhabdom yolysis



Thiam ine: 100 m g IM or IV (peds: 1 m g/kg)



Naloxone: 0.4â€“2.0 m g (peds: 0.1 m g/kg) IV, m ay repeat up to 10 m g for suspected opioid intoxication



Dextrose 50%: 25 g (50 m L) (peds: 0.5 g/kg D 2 5 W) IV for hypoglycem ia

Follow-Up Disposition Admission Criteria Sym ptom atic arsenic exposures should be adm itted to an intensive care setting.

Discharge Criteria 

Asym ptom atic patients with a spot urinary arsenic level <50 Âµg/L m ay be discharged.



Suspected chronic exposures who do not require adm ission should be referred for outpatient evaluation and 24-hour

Pa ge 5 3 4

urine collection. 

Ensure that hom e environm ent is safe for patient prior to discharge.

References 1. Ford M. Arsenic. In: Goldfrank's Toxicologic Em ergencies. 7th ed. McGraw-Hill, New York; 2002. 2. Graem e KA, Pollack CV. Heavy m etal toxicity. Part I: arsenic and m ercury. J Em erg Med. 1998;16(1):45â€“56. 3. Tchounwou PB, Patlolla AK, Centeno JA. Carcinogenic and system ic health effects associated with arsenic exposure: a critical review. Toxicol Pathol. 2003;31(6):575â€“588.

Codes ICD9-CM E950.8 980.8 985.1

Pa ge 5 3 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arterial G as Em bo lism (AG E)

Arterial Gas

Embolism (AGE) Peter J. Park

Basics Description 

Results when air bubbles enter the pulm onary venous return from ruptured alveolae: o

Then propagate through the system ic vasculature

o

Clinical m anifestations dependent on location of air bubbles in system ic vasculature system



Also known as dysbaric air em bolism or cerebral air em bolism

Mechanism 

Overpressurization of lung tissue causing pleural tear with air entering the vascular circulation: o

Air bubbles tend to rise and enter the cerebral vessels where they occlude vascular flow.

o

Boyle's law: At a constant tem perature, pressure (P) is inversely related to volum e (V): 

o

PV = K (constant) or P 1 V 1 = P 2 V 2

As pressure increases/decreases, volum e decreases/increases.

Pa ge 5 3 6

o

Trapped air (in lungs with closed glottis) expands on diver ascent.

Etiology 

Pulm onary atrioventricular (AV) shunts, or as paradoxical em bolism via a patent foram en ovale (up to 30% of the adult population)



Breath-holding during ascent: o

Sym ptom s attributable to a shower of bubbles and m ultiple blood vessel involvem ent



Iatrogenically during placem ent of central venous pressure (CVP) lines, cardiothoracic surgery, or hem odialysis



Penetrating injuries to heart with em ergent repair of cardiac wound

Diagnosis Signs and Symptoms 

Cerebral: o

Dive-related stroke

o

Second leading cause of dive-related death (after drowning)

o

o

Two m ain presentations: 

Apnea and full cardiopulm onary arrest



Any com bination of neurologic deficits

Presentation depends on arterial distribution of gas em bolism 

Change in level of consciousness (40%)



Sensory loss (20%)



Motor deficit (20%)



Paraplegia (10%)

Pa ge 5 3 7

o

o



Seizure (4%)



Visual changes



Aphasia



Paresthesias

Rapid onset: 

8.6% during ascent



83.6% <5 m inutes after surfacing



7.8% between 5 and 10 m inutes after surfacing

Spontaneous im provem ent m inutes after initial deficits m ay occur: 

High incidence of relapse



Im provem ent m ay be transiently related to postural changes that affect distribution of bubbles flowing to brain





Pulm onary: o

Shortness of breath

o

Bloody, frothy sputum

o

Subcutaneous air

Cardiac: o

Myocardial infarction owing to air in coronary vessels

o

Reduced cardiac output owing to air trapped in ventricle

o 

Ham m an sign: crepitus on auscultation of heart

Renal: o

Renal infarction owing to air em bolism

Essential Workup 

Clinical diagnosis: Recognize risk factors and various clinical presentations.





Inquire as to unusual circum stances during ascent: o

Breath-holding

o

Panic/out-of-air situation

Thorough neurologic exam m ust carefully docum ent the

Pa ge 5 3 8

extent of the deficits to the m otor, sensory, cerebellar, and cranial nerves.

Tests Lab 

Serum creatinine kinase activity: o

Marker of the severity of cerebral AGE



CBC



Electrolytes, BUN, creatinine, glucose



Arterial blood gas (ABG) when respiratory sym ptom s are present

Imaging Chest radiograph: 

For evidence of pneum othorax or m ediastinal em physem a (both rare)

Special Studies 

ECG



Echocardiogram : o



Looking for evidence of patent foram en ovale

CT head: o

For altered m ental status

o

Do not delay recom pression for CT when AGE alm ost certain clinically.

Differential Diagnosis 

Cerebrovascular accident (CVA) from causes unrelated to gas em bolism



Neurologic deficits owing to decom pression sickness

P.95

Pa ge 5 3 9

Treatment Pre Hospital 

Cautions: o

Patients who experience sudden neurologic recovery can relapse quickly as bubble positions change.

o

Recognize AGE as potential diagnosis 

Altered m ental status within 10 m inutes of surfacing from com pressed air dive



Sudden neurologic decom pensation following placem ent of central line



Controversies: o

Trendelenburg positioning patients with suspected arterial gas em bolism (AGE) is not effective. 

Hypothesized that elevation of legs could cause air bubbles to m igrate away from cerebral circulation and that increased hydrostatic pressure in brain will shrink bubbles



Trendelenburg positioning m ay in fact increase injury by increasing intracerebral pressure.

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

One hundred percent oxygen by tight-fitting m ask



Intubation for ventilation/protection of airway required



IV access with volum e augm entation

ED Treatment 

Hyperbaric oxygen recom pression therapy (see Hyperbaric Oxygen Therapy) o

For all AGE

o

Arrange transportation to nearest hyperbaric facility.

Pa ge 5 4 0

o

Aircraft capable of cabin pressurization below 1,000 feet barom etric pressure best suited for transfers

o

Prophylactic chest tube for sim ple pneum othorax to prevent conversion to tension pneum othorax during recom pression

o

Fill endotracheal and Foley catheter balloons with water or saline to avoid shrinkage/dam age during recom pression.



Divers Alert Network (DAN): o

Based at Duke University Medical Center

o

Provides 24-hour em ergency hotline for m edical consultation on treatm ent of dive-related injuries and for referrals to hyperbaric cham bers (telephone: [919] 684-8111)

Follow-Up Disposition Admission Criteria Adm it all following initial hyperbaric therapy for observation and re-exam ination.

Discharge Criteria No AGE patients should be discharged from the em ergency departm ent.

References 1. Beckm an TJ. A review of decom pression sickness and arterial gas em bolism . Arch Fam Med. 1997;6(5):491â€“494. 2. Jerrard DA. Diving m edicine. Em erg Med Clin North Am . 1992;10(2):329â€“338.

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3. Kizer KW. Diving m edicine and arterial gas em bolism . In: Auerbach PA, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001. 4. Moon RE, Gorm an DF. Treatm ent of decom pression disorders. In: The Physiology and Medicine of Diving. 5th ed. Philadelphia: WB Saunders; 2003. 5. Sm ith RM, Neum an TS. Elevation of serum creatine kinase in divers with arterial gas em bolism . N Engl J Med. 1994;330:19â€“24. 6. van Hulst RA. Effects of hyperbaric treatm ent in cerebral air em bolism on intracranial pressure, brain oxygenation, and brain glucose m etabolism in the pig. Crit Care Med. 2005;33:841â€“846.

Miscellaneous SEE ALSO: Barotraum a; Decom pression Sickness; Hyperbaric Oxygen Therapy

Codes ICD9-CM 958.0 Em bolism , air (any site):

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arterial Occlusio n

Arterial Occlusion

James M. Leaming

Basics Etiology 

Throm botic: o



Low flow and hypercoagulable states

Em bolic: o

Atrial fibrillation

o

Myocardial infarction

o

Valvular disease

o

Endocarditis

o

Proxim al arterial aneurysm :

o

Atherosclerotic plaques

Diagnosis Alert Elevation, cool com press or ice, or warm com press to the affected extrem ity is contraindicated.

Signs and Symptoms 

The 6 Ps:

Pa ge 5 4 3



o

Pain

o

Pallor

o

Paresthesias

o

Paralysis

o

Pulseless

o

Poikilotherm ia

Chronic: o

Claudication

o

Decreased pulses after physical activity

o

Hairless atrophic skin

o

Poorly healing wounds or ulcers

o

Ankle-brachial index m easurem ent: 

Use a Doppler probe.



Inflate a blood pressure cuff on the arm until radial pulse is no longer heard.



Release valve and note pressure at which the radial pulse returns.



Repeat procedure with the cuff around the calf and note return of the pulse in the dorsalis pedis and posterior tibial arteries.



The ratio of the ankle pressure to radial pressure is the ankle-brachial index: (ABI)



Norm al: 1 or greater



Typical claudication risk: 0.5â€“0.8:



Rest pain/im pending tissue injury: <0.3

Physical Exam Peripheral ischem ic syndrom es m ay result in changes in acid-base status (acidem ia) and electrolyte derangem ent (hyperkalem ia), which are acutely exacerbated on reperfusion.

Essential Workup Acute arterial occlusion is a clinical diagnosis.

Pa ge 5 4 4

Tests Lab 

Electrolytes/Anion gap



Blood urea nitrogen



Creatinine



Com plete blood chem istry



Creatine phosphokinase



Specim en for type and screen

Imaging 

Electrocardiography



Duplex ultrasound



Angiography



Plain film s are of little use in the setting of peripheral vascular disease (PVD).



MRI m ay be of som e clinical benefit due to its high visual detail and can replace traditional arteriography.

Differential Diagnosis 

Lum bar Spine Disorders



Back Pain, Mechanical



Decreased Cardiac Output Owing to Advanced Atherosclerotic Disease



Frostbite



Peripheral Neuropathy



Aneurysm , Abdom inal



Ankle Injury, Soft Tissue



Deep Venous Throm bosis



Septic Throm bophlebitis



Superficial Throm bophlebitis



Traum a, Peripheral Vascular Injuries

P.97

Pa ge 5 4 5

Treatment Pre Hospital Recognition of a potentially lim b-threatening em ergency

ED Treatment 

Prom pt consultation with vascular surgeon



Intra-arterial throm bolytic agents (urokinase plus abcixim ab)



Aspirin



Heparin

Medication (Drugs) 

Aspirin: 325 m g PO; four chewable baby aspirin



Heparin: Weight-based protocol anticoagulation with typical 80 IU/kg loading bolus; 18 IU/kg per hour IV

Follow-Up Disposition Admission Criteria All patients with critical arterial occlusion (ABI < 0.5) should be adm itted after an em ergency consultation with a vascular surgeon.

Discharge Criteria 

Patients with chronic occlusive disease, resolved pain, and

Pa ge 5 4 6

stable ABI m easurem ents 

No other acute m edical issues (e.g., new atrial fibrillation)



Vascular surgical follow-up can be ensured.



Patients should be instructed to return for any recurrent or progressive sym ptom s.

Issues for Referral 

PVD patents in which illness is not so severe or acute as to require inpatient treatm ent m ay be discharged with appropriate follow-up with a vascular surgeon.



Potential effects of various activities and m edications on the course of their illness should be discussed.



Education on sm oking cessation, tem perature extrem es, and vasoconstricting m edications should be considered

References 1. Aufderheide TP: Peripheral arteriovascular disease. In: Em ergency Medicine: Concepts and Clinical Practice. 1998:1826â€“1844. 2. Bassiouny HS. Noninvasive evaluation of the lower extrem ity arterial tree and graft surveillance. Surg Clin North Am . 1995;75:593â€“606. 3. Cooke JP, Ma AO. Medical therapy of peripheral artery occlusive disease. Surg Clin North Am . 1995;75:569â€“579. 4. Feldm an AJ: Acute extrem ity ischem ia and throm bophlebitis. In: Em ergency Medicine: A Com prehensive Study Guide. 4th Howell JM: Acquired diseases of the arteries and veins. In: Em ergency Medicine. 1998:203â€“206. 5. Jackson MR. Antithrom botic therapy in peripheral arterial occlusive disease. Chest. 2001;119:(Suppl 1)283Sâ€“299S. 6. Morgan R, Belli AM. Percutaneous throm bectom y: A review. Eur Radiol. 2002;12:205â€“217. 7. Sem ashko DC. Vascular em ergencies. Mt Sinai J Med. 1997 Sepâ€“Oct;64(4-5):316â€“322.

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8. Working Party on Throm bolysis in the Managem ent of Lim b Ischem ia. Throm bolysis in the m anagem ent of lim b ischem ia. J Intern Med. 1996;240:343â€“355.

Codes ICD9-CM N/A

ICD10 I74.9

Pa ge 5 4 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, Degenerative

Arthritis,

Degenerative Michael K. Doney

Basics Description 

Most com m on progressive joint disease



Found alm ost exclusively in the elderly

Etiology Mechanism 

Repetitive stress to synovial joints associated with age



May be seen in younger patients secondary to joint traum a



Destruction of articular cartilage: o

Reactive changes in joint m argin bone and subchondral sclerosis



Risk factors include age, obesity, traum a, genetics, sex, and environm ent.

Diagnosis Signs and Symptoms

Pa ge 5 4 9



Chronic progressive joint pain: o



Worse with weight bearing, im proved with rest

Asym m etric joint involvem ent: o

Involves hands, knees, hips, spine, and m etatarsophalangeal joints



Morning joint stiffness usually <30 m inutes



Joint deform ity late in presentation with lim ited range of m otion



Heberden nodes at the distal interphalangeal joints



Bouchard nodes at the proxim al interphalangeal joints



Absence of system ic sym ptom s

Essential Workup 

Thorough joint exam ination with assessm ent of range of m otion and functional ability



Radiographic exam ination indicated in setting of traum a to exclude fracture



Synovial fluid analysis in the setting of effusion and warm th/erythem a: o

Differentiate osteoarthritis from gout or septic joint

Tests Lab Synovial fluid exam ination m ay reveal elevated cell count but <1,000 cells/m m 3

Imaging Radiographs: 

Joint space narrowing



Osteophyte form ation



Marginal bone erosion



Subchondral sclerosis

P.99

Pa ge 5 5 0

Differential Diagnosis 

Gout/crystal-induced arthritis



Septic arthritis



Rheum atoid arthritis

Treatment Pre Hospital Im m obilization of affected joint m ay be indicated until fracture is excluded.

ED Treatment 

Pain m anagem ent



Avoidance of unnecessary joint im m obilization

Medication (Drugs) 

Ibuprofen: 400â€“600 m g PO q6h



Acetam inophen: 650 m g PO q6h



Enteric-coated aspirin: 325â€“650 m g PO q6h



Hydrocodone (rarely) 5â€“10 m g PO q6h

Follow-Up Disposition Admission Criteria Rarely indicated in the absence of fracture

Pa ge 5 5 1

Discharge Criteria 

Am bulatory and capable of activities of daily living



Provide instructions for gentle stretching and joint range of m otion exercises.

References 1. Cream er P, Hochberg MC. Osteoarthritis. Lancet. 1997;350:503â€“508. 2. Dearborn JT, Jergesen HE. The evaluation of and initial m anagem ent of arthritis. Prim Care. 1996;23:215. 3. Hochberg MC. Osteoarthritis: clinical features and treatm ent. In: Klippel JH, ed. Prim er on the Rheum atic Diseases. 11th ed. Atlanta: Arthritis Foundation; 1997. 4. Neam e R, Doherty M. Osteoarthritis update. Clin Med. 2005;5(3):207â€“210.

Codes ICD9-CM 715.90

ICD10 M19.9

Pa ge 5 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, Juvenile Idio pathic

Arthritis,

Juvenile Idiopathic Jeannette Wolfe

Basics Description 

Previously called JRA



Affects 60,000â€“250,000 children prevalence about 1 in 1000 girls > than boys for m ost form s, whites > than other races



Persistent unexplained arthritis not caused by traum a or infection that lasts >6 weeks in children younger than 16 years



New nom enclature by International League of Associations for Rheum atology divides juvenile idiopathic arthritis (JIA) into seven subgroups: system ic onset, polyarticular RF + , polyarticular RF - , pauciarticular, psoriatic, enthesitis, other.



Each subtype represents a different disease with different prognosis. Subtypes are based on num ber, type, and sym m etry of joints involved; presence of system ic sym ptom s; skin involvem ent; fam ily history; and lab values

Pa ge 5 5 3



Even with new nom enclature, about 20% of children rem ain unclassified or are classified in m ultiple categories.

Etiology Unknown, but som e subtypes appear to have strong genetic com ponent

Diagnosis Signs and Symptoms Systemic Onset 

10% of cases, girls = boys



Diurnal high fever (>39Â°C) of at least 2 weeks duration, child looks ill during tem perature spike



Accom panied by at least one of the following: o

Rash: m acular papular salm on colored on trunk and axilla, fades with tem perature resolution

o

Lym phadenopathy or hepatosplenom egaly

o

Arthiritis: polyarthralgia, m ay show up weeks to m onths after onset of fever and rash

Pauciarticular 

50% of cases, girls > boys, peak incidence 2â€“3 years old



Child looks healthy, usually insidious onset, joint not particularly painful



Up to four joints involved at 6 m onths: o

Involves larger joints, but hip rarely affected

o

Joints swollen, m ildly tender, with decreased range of m otion (ROM), possibly leg length discrepancy



Uveitis in about 20%, otherwise no system ic involvem ent



Subset term ed extended pauciarticular progresses to greater joint involvem ent after 6 m onths and is associated

Pa ge 5 5 4

with worse prognosis

Polyarticular 

40% of cases, girls > boys, peaks at 2â€“5 and 10â€“14 years



More than 4 joints involved at 6 m onths: o

Arthritis often sym m etrical, sm all or large jointsâ€”com m only knees, wrists, and ankles

o

Decreased ROM of cervical and lum bar spine and tem porom andibular joint (TMJ)



System ic involvem ent rare except for fatigue and anem ia



Older girls with RF + often go on to develop typical adult rheum atoid arthritis (RA) and are placed in separate subtype.

Psoriatic 

Psoriatic rash in patient or first-degree relative



Arthritis; asym m etric large joints of lower extrem ities and back



Dactylitis



Nail pitting

Enthesitis Related (Entheses means pain at the insertion of a muscle or tendon) 

Arthritis; asym m etric large joints of lower extrem ities



Boys > girls, age usually older than 6 years



Sacroiliac (SI) joint pain



Lim ited flexion of lum bar spine



Uveitis



Often FH

Otherwise Unclassified Arthritis not fitting into distinct category

Alert

Pa ge 5 5 5



Child with severe pain and red-hot joint probably does not have new-onset JIA.



Rapid onset of polyarticular joint involvem ent is atypical for JIA, and infectious or reactive cause of arthritis should be ruled out.



Beware of occult infection in patients on JIA m edications other than NSAIDs.

History 

Findings based on specific subtype



New-onset system ic subtype m ost likely to use ED because patients appear acutely ill whereas other subtypes have m ore insidious onset

Essential Workup 

Rule out septic joint and m alignant bone tum or.



Rule out other identifiable causes of joint inflam m ation.



Rule out com plications from long-term drug therapy.

Tests Lab 

CBC, erythrocyte sedim entation rate (ESR); if ill appearance, add blood cultures



Other labs if suspicious of specific subtype: rheum atoid factor (RF), antinuclear antibodies (ANA), HLA-B27, liver function tests (LFTs) o

System icâ€”ESR often elevated, leukocytosis, throm bocytosis, anem ia, m inor AST/ALT elevations, positive RF or ANA rarely seen, increased risk of dissem inated intravascular coagulation (DIC)

o

Pauciarticularâ€”com m on to have positive ANA in young girls; other labs usually norm al; if anem ic or elevated ESR, are probably m isclassified or

Pa ge 5 5 6

pauciarticular extended subtype o

Polyarticularâ€”m ay be anem ic, if positive RF m ore likely to go on to adult RA, ESR m ay be elevated

o

Enthesitisâ€”m ore likely positive HLA; presence of positive RF or positive ANA specifically excludes enthesitis subtype

o

Psoriatic arthritisâ€”presence of positive RF specifically excludes: 

Unfortunately, RF and ESR m ay also be elevated in acute infection unrelated to JIA and RF results m ay be related to assay type

o

Arthrocentesis if concern for septic arthritis: 

5,000â€“8,000 WBC/m m 3 with negative Gram stain and culture typical for JIA

Alert Consider additional labs focused on specific drug therapy toxicity.

Imaging 

Joint radiograph: o

Early presentation: soft tissue swelling, joint effusion

o

Late presentation: osteoporosis, joint destruction, early growth plate closure



Ultrasound: o

Evaluate for sm all effusion, especially if tap considered

Differential Diagnosis 

Traum a



Infection: o

Septic arthritis, viral infection (especially Parvovirus), Lym e disease, rheum atic fever, tuberculosis, subacute endocarditis, m alaria, neisserial infection

Pa ge 5 5 7



Other rheum atic/connective tissue diseases: o

System ic lupus erythem atosus, polyarteritis nodosa, Henoch-SchÃ¶nlein purpura, sarcoid



Neoplasm : o

Be suspicious of neoplasm in severely uncom fortable child with m idshaft bone pain.



Hem atologic disease: o



Sickle cell disease, hem ophilia

Drug reactions

P.101

Treatment Initial Stabilization Toxic-appearing children: IV access, O 2

ED Treatment 

Tailor treatm ent to individual patient's subtype in coordination with rheum atologist.



Nonsteroidal anti-inflam m atory drugs (NSAIDs): o

Used alone in m ild JIA subtype or with other m edications

o

Naproxen com m only first line; responsiveness differs within NSAID subtypes

o

Side effect (SE): gastritis, hepatitis, renal, headache, derm atitis



Disease m odifying anti-rheum atic drug therapy (DMARDs): o

Live vaccines contraindicated in children receiving DMARDs

Pa ge 5 5 8

o

Includes corticosteroids, m ethotrexate, sulfasalozine, and etanercept



Corticosteroids: o

Use judiciously because of long-term com plications, but high-dose pulse therapy m ay be needed in acute attack.

o

SE: gastritis, adrenal suppression, osteopenia, Cushing syndrom e, infection

o

Intra-articular steroids, often provide long-term (6â€“18 m onths) relief for isolated joint pain



Methotrexate: o

Com m only used DMARD, SC route often m ore efficacious than oral



o

Supplem ent with folic acid.

o

SE: liver toxicity, teratogenic

Sulfasalazine: o

Often used in patients with spondyloarthropathy; contraindicated in system ic subtype

o

SE: GI, derm atitis, erythem a m ulitform a, Stevens-Johnson syndrom e, agranulocytosis, hypogam m aglobulinem ia



Etanercept: o

Binds tissue necrosis factor-Î±; has been used successfully for several subtypes of JIA

o 

SE: increased risk of infectious com plications

Other therapies less com m only used: o

Gold, hydroxychloroquine, cyclosporine (used for DIC in system ic subtype), and inflixim ab, adalim um ab, thalidom ide



Antibiotics indicated only if joint is infected

Pa ge 5 5 9

Medication (Drugs) 

Etanercept: 0.4 m g/kg SC twice a week, or 0.8 m g/kg SC once a week



Ibuprofen: 30â€“45 m g/kg divided t.i.d. to q.i.d.



Methotrexate: 5â€“15 m g/m 2 PO/SC or IM once a week



Methylprednisolone: 30 m g/kg daily IV up to 1 g for 1â€“5 days for high-dose pulse steroids



Naproxen: 10â€“20 m g/kg divided b.i.d.



Prednisone: 0.5â€“2 m g/kg PO



Steroid injection: o

Triam cinolone hexacetonide: 1 m g/kg for large joints (m ax. 60 m g), 0.5 m g/kg for sm aller joints, and 1â€“2 m g for hand and foot joints



Sulfasalazine: 30â€“50 m g/kg/d divided b.i.d. to q.i.d.

Follow-Up Disposition Admission Criteria Unclear diagnosis in ill-appearing child or if concern of secondary joint infection

Discharge Criteria 

No evidence of septic joint, system ic infection, or organ failure from drug therapy



Patient appears com fortable.



Appropriate follow-up has been arranged.

Issues for Referral 

Children need long-term follow-up with rheum atologist.



Children with JIA, especially those with a positive ANA or

Pa ge 5 6 0

spine involvem ent, should have frequent eye exam s to rule out uveitis.

References 1. DeWitt E, Sherry D, Cron R. Pediatric rheum atology for the adult rheum atologist. I: therapy and dosing for pediatric rheum atic disorders. J Clin Rheum atol. 2005;11(1):21â€“33. 2. Falcini F, Cim az R. Juvenile rheum atoid arthritis (pediatric and heritable disorders). Curr Opin Rheum atol. 2000;12(5):415â€“419. 3. Groh B. Current concepts in pediatric rheum atology. Curr Opin Orthop. 2003;14(6):385â€“391. 4. Lehm an T. Pauciarticular onset juvenile rheum atic arthritis. UpToDate. 2005; version 13.1. updated Dec 2004 Available at: http://www.uptodate.com . (Last accessed April 2006) 5. Lehm an T. Polyarticular onset juvenile rheum atic arthritis. UpToDate. 2005; version 13.1. updated Dec 2004 Available at: http://www.uptodate.com . (Last accessed April 2006) 6. Petty RE, Southwood TR, Manners P, et al. International League of Associations for Rheum atology classification of juvenile Idiopathic arthritis: second revision, Edm onton, 2001. J Rheum . 2004;31(2):390â€“392.

Codes ICD9-CM 716.90 714.30 719.40

Pa ge 5 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, M o no articular

Arthritis,

Monoarticular Paul Blackburn

Basics Description 

Localized to one joint



Presence of one etiology does not exclude another



Infectious (septic) arthritis o

Hem atogenous spread

o

Contiguous extension (cellulitis, osteom yelitis)

o

Direct inoculation (puncture wound, joint surgery)

o

Predisposing factors: 

Im m unosuppression



IV drug use



Chronic illness



Local pathology (inflam m atory arthritis, traum a, prosthetic joint)



Crystalline: crystal deposition in, around joint o

Gout: uric acid crystals secondary to overproduction, underexcretion

o

Alcoholism , loop diuretics, renal failure, m ales 40â€“50 years old, wom en over 60 years old

Pa ge 5 6 2

o

Pseudogout: calcium pyrophosphate dihydrate (CPPD) crystals 

Most com m on m onoarthritis in elderly; peak incidence fem ales 60â€“70 years old



Increased incidence in elderly, traum a, surgery, hyperparathyroidism , hem ochrom atosis, hypothyroidism patients



Noninflam m atory: o

Osteoarthritis (nonspecific destructive process, cartilage or bone): 

Loss of articular cartilage with reactive changes at joint m argins

o

Greater incidence elderly m en than wom en until 60 years old, then ratio reverses

o

Morbidly obese

o

Congenital hip dysplasia: hip pain in young

o

Traum a: fracture, Charcot joint

Etiology 

Infectious, bacterial: o

Knowledge of local m icrobiology

o

Neisseria gonorrhea

o

Staphylococcus aureus: traum a, IV drug use

o

Salm onella: sickle cell disease

o

Gram -negative organism s, anaerobes: im m unocom prom ised





Infectious, spirochetal: o

Tuberculosis

o

Lym e disease

Infectious, viral: o



More com m only polyarticular

Infectious, fungal: o

More com m only chronic

Pa ge 5 6 3

o 





Im m unosuppressed?

Crystalline: o

Gout (urate)

o

Pseudogout (CPPD)

Inflam m atory: o

Diligent search for underlying conditions

o

Inflam m atory bowel disease

o

Rheum atoid arthritis

o

Psoriatic

o

Reiter syndrom e (seronegative spondylarthropathy)

Noninflam m atory: o

Osteoarthritis: structural disease

o

Traum a: fracture, internal derangem ent, neuropathic arthropathy

o

Tum or: chronic effusion

Pediatric Considerations 



Infectious (rare): hip = knee: o

Escherichia coli: infants

o

Hem ophilus influenzae: 6â€“24 m onths

Noninflam m atory: o

Congenital hip dysplasia

o

Legg-Calve-Perthes:

o



Spontaneous osteonecrosis fem oral head



Age 4â€“9 years



Bilateral 10% cases

Slipped capital fem oral epiphysis in overweight adolescents

Diagnosis

Pa ge 5 6 4

Signs and Symptoms 



Sym ptom s located to one joint: o

Pain

o

Swelling

o

Warm th

o

Erythem a

o

Decreased range of m otion

o

Hyperacute presentation m ost typical

Infectious (septic) arthritis: o

Fever, chills, system ically ill

o

Large joints affected m ore often

o

Adults: knee > hip = shoulder > ankle > wrist

o

Gonorrhea: abdom inal pain, genital discharge

o

Lym e disease: 

Knees or shoulders m ost com m on



Nonspecific constitutional sym ptom s



Centrally clearing expanding skin eruption (erythem a chronicum m igrans)



Crystalline: o

Recurrent, self-lim ited inflam m atory attacks, often of sam e joint

o

Tissue extension appears identical to cellulitis, septic arthritis

o

Gout: First m etatarsophalangeal joint foot (â€œpodagraâ€•) > ankle > tarsal joints > knee

o

Pseudogout: Knee > wrist > ankle = elbow.

o

Tophi: crystalline granulom as overlying affected joints



Inflam m atory: o

Inflam m atory bowel disease: abdom inal pain, bloody diarrhea with m ucous, weight loss

o

Reiter syndrom e: conjunctivitis, urethritis, balanitis

Pa ge 5 6 5

o

Psoriatic arthritis: characteristic skin plaques, â€œsausage digitsâ€•

o 

Chronic: infections (tuberculosis, fungi), tum ors

Noninflam m atory: o

Osteoarthritis: 

Morning stiffness



Following activity (gelling)



Pain relieved by rest:

o

Congenital hip dysplasia: hip pain in young

o

Neuropathic: Charcot joint; swelling, effusion, little pain

o

Traum a: pain, swelling

Essential Workup 

Com plete history; any joint disorder is capable of presenting as m onoarthritis: o

Traum a

o

Surgery

o

STD exposure

o

IV drug abuse

o

Intra-articular injections

o

Im m unosuppression



Meticulous physical exam ination



Establish truly m onoarticular (vs m igratory); exacerbation vs superim posed process



Onset rapidity: o

Seconds to m inutes: traum a, internal derangem ent

o

Hours to 2 days: inflam m atory; bacterial infection, crystalline



Adjunctive diagnostic tests are supportive only

Tests Lab

Pa ge 5 6 6

Arthrocentesis with joint fluid analysis: 

The definitive procedure



Culture is definitive study of the fluid



WBC count with differential varies greatly, nonspecifically; interpret cautiously



Crystal analysis, Gram stain, glucose, viscosity P.103



Serology never confirm s a diagnosis: o

WBC with differential

o

Blood cultures; panculture if suspected gonorrhea, sepsis

o

Acute phase reactant (ESR, CRP)

o

Uric acid can be norm al under all conditions; not helpful

o 

Consider glucose, chem istries, rheum atologic studies

Microscopy with light helpful with gout; polarized light preferred

Imaging 

Plain film s of assistance in selected cases only: o

Infectious: soft tissue swelling, osteoporosis, erosion, joint m argin destruction

o

Crystalline: asym m etric bone erosions, reactive bone form ation, soft-tissue calcification

o

Bone and cartilage disorders: asym m etric joint narrowing, osteophytes, subchondral cysts, loose bodies, fracture



MRI detects bone necrosis or involvem ent o



Study of choice for occult fractures

Nuclear m edicine sensitive tool for deep joints difficult to exam ine, fibrocartilaginous joints, spine

Pa ge 5 6 7



Ultrasound: presence of joint fluid, tissue perfusion, periarticular structures, aspiration guidance



Synovium , bone biopsy: o

Chronic, unexplained, m onoarticular arthritis

o

Gonococcal, m ycobacterial disease is suspected and no fluid available

Differential Diagnosis See Etiology

Treatment Pre Hospital 

Physical im m obilization of the joint, m edication for pain control



Position of com fort



IV placem ent

Initial Stabilization 

None unless underlying illness or traum a m andates



Pain control

ED Treatment 

Septic arthritis: o

Em piric, aggressive IV bactericidal antibiotics for anticipated organism m ay prevent joint destruction

o

Antibiotic selection directed by history and physical 

Adults: ceftriaxone, vancom ycin to cover for staph, strep, and gonococcal arthritis



Treatm ent: 2 weeks IV followed by 2â€“6 weeks of oral antibiotics



Shorter course acceptable only in gonococcal

Pa ge 5 6 8

arthritis o

Knowledge of local m icrobiologic organism s is essential for effective em piric antibiosis

o

o

Methicillin resistance: 

Gonorrhea



IV drug use



Prosthetic joints



Neonates, children less than 2 years

Surgery: open versus closed drainage, frequency of evaluation, treatm ent duration



Crystalline: o

NSAIDs (indom ethacin)

o

Colchicine secondary choice to NSAIDs; do not use IV

o

Prednisone when NSAIDs, colchicine contraindicated

o

Adrenocorticotropic horm one (ACTH) for resistant cases, contraindications to NSAIDS

o

Allopurinol decreases uric acid production; avoid in acute therapy

o 

Probenecid long-term ; uricosuric

Osteoarthritis: o

NSAIDs, analgesics

o

Physical support, rehabilitation

Medication (Drugs) 

ACTH: 40â€“80 IU IM then 40 IU IM q6hâ€“q12h until im provem ent



Allopurinol: 200â€“600 m g q.d.



Ceftriaxone: 1 g IV q.d.



Colchicine: 1 tp 2 m g IV in 20 cc NS over 10 m in; 0.5 m g PO q1h until asym ptom atic, nausea diarrhea develop, or 10 doses

Pa ge 5 6 9



Indom ethacin: 75â€“200 m g per day, divided dosages



Prednisone: 20â€“40 m g PO per day Ã— 3â€“4 days



Probenecid: 250 m g b.i.d. starting; m axim um



Vancom ycin: 1 g IV q12h



Antibiotics and dosage dependent on patient, infectious etiology, severity, duration

Follow-Up Disposition Admission Criteria 





All septic arthritis: o

General m edical/surgical bed

o

Intensive care unit if generalized sepsis

Crystalline: o

Intractable pain

o

Intractable nausea, vom iting, diarrhea

o

Septic joint superim posed on other arthritides

Any joint requiring surgical intervention

Discharge Criteria 

Crystalline tolerating oral NSAIDs



Inflam m atory unless adm ission required by overall disease m anifestations



Osteoarthritis



Medication com pliance



Tim ely follow-up arranged

References 1. Baillieres Best Pract Res Clin Rheum atol. 1999;13:37â€“58. 2. Ho G, Jr. Bacterial arthritis. Curr Opin Rheum atol.

Pa ge 5 7 0

2001;13:310â€“314. 3. Li SF, Henderson J, Dickm an E, Darzynskiewicz R. Laboratory tests in adults with m onoarticular arthritis: can they rule out a septic joint? Acad Em erg Med. 2004;11(3):276â€“280. 4. Mohana-Borges AV. Chung CB. Resnick D. Monoarticular arthritis. Radiologic Clinics of North Am erica. 2004;42(1):135â€“149. 5. Sande MA, Gilbert DN, Moellering RC, Eliopoulos GM, eds. The Sanford Guide To Antim icrobial Therapy. 35th Edition. Hyde Park, VT: Antim icrobial Therapy, Inc. 2005. 6. Siva C, Velazquez C, Mody A, Brasington R. Diagnosing acute m onoarthritis in adults: a practical approach for the fam ily physician. Am Fam Physician. 2003;68(1):83â€“90.

Codes ICD9-CM 716.6

Pa ge 5 7 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, Rheum ato id

Arthritis,

Rheumatoid Hagop Isnar

Basics Description 

Chronic system ic inflam m atory disorder that attacks the joints: o

Nonsuppurative, proliferative synovitis

o

Destruction of the articular cartilage

o

Ankylosis of the joint



Involvem ent of knee is com m on.



Baker cysts m ay be seen in chronic disease.



Involvem ent of spine is lim ited to cervical region: o

May cause atlantoaxial subluxation

o

Rarely results in cord com pression

Pediatric Considerations Juvenile rheum atoid arthritis (JRA) is a distinct entity (see Arthritis, Juvenile Idiopathic).

Genetics 

Genetic predisposition related to HLA-DR4



Fem ale-to-m ale ratio is 3:1.



Typical age of onset is between 30 and 50.

Pa ge 5 7 2

Etiology 

Etiology is unknown.



Possible triggers include infection and autoim m une response.



Prevalence is about 1% of both United States and world population.

Diagnosis Signs and Symptoms 

Malaise, fatigue



Generalized m usculoskeletal pain



After weeks to m onths, patients develop swollen, warm , painful joints.



Often worse in m orning



Joint involvem ent usually sym m etric and polyarticular



Starting in sm all joints of hands and feet: o



Later wrists, elbow, and knees

Distal interphalangeal (DIP) joints of hand generally not involved: o

Presence of swelling in these joints should suggest another type of arthritis.



Synovitis is typically gradual.



Classic joint findings in long-standing disease: o

Metacarpophalangeal (MCP) swelling with ulnar deviation

o 

Swan neck and boutonniere deform ities

Extra-articular com plications: o

Subcutaneous nodules

o

Vasculitis

Pa ge 5 7 3



o

Pericarditis or m yocarditis

o

Pulm onary fibrosis

o

Pneum onitis

o

SjÃ¶gren syndrom e

o

Mononeuritis m ultiplex

Evidence of m ild pericarditis on echocardiogram is found in up to one third of patients.



Patients usually present to ED owing to exacerbations of the disease or com plication in other organ system s: o

Airway obstruction from cricoarytenoid arthritis or laryngeal nodules

o

Heart block, constrictive pericarditis, pericardial effusion with possible tam ponade or m yocarditis

o

Pulm onary fibrosis, pleuritis, intrapulm onary nodules, or pneum onitis

o 

Hepatitis

Neurologic findings m ay result from cervical spine subluxation or ocular m anifestations such as scleritis and episcleritis.





Com plications of chronic steroid use: o

Infections

o

Steroid-induced osteopenia and fractures

Patients m ay present with side effects related to chronic salicylate or nonsteroidal antiinflam m atory drug (NSAID) use such as GI bleeding.



Drugs such as m ethotrexate, gold, or d-penicillam ine also have toxic side effects, m ost com m only gastrointestinal.

Essential Workup 

Prim ary diagnosis of rheum atoid arthritis (RA) is rarely m ade in the ED.



Synovitis should be present for at least 6 weeks; a m inim um of four of the following seven criteria as

Pa ge 5 7 4

established by the Am erican Rheum atism Association m ust be m et to m ake the diagnosis: o

Stiffness of the involved joints in the m orning for at least 1 hour

o

Arthritis in three or m ore joints with effusion or soft tissue swelling

o

Arthritis of joint in hand (wrist, MCP, or proxim al interphalangeal [PIP] joint)

o

Sym m etric arthritis

o

Rheum atoid nodules on extensor surfaces or juxta-articular surfaces

o

Significantly elevated rheum atoid factor

o

Characteristic radiographic changes include erosions and decalcification (not attributable to osteoarthritis).



Other pertinent history: m alaise, weakness, weight loss, m yalgias, bursitis, tendonitis, fever of unknown cause



Initial workup should focus on dem onstrating that other causes of arthritis are not present, especially septic arthritis, reactive arthritis, or gout.



Arthrocentesis of a joint effusion m ay be required.

Tests ECG, chest radiograph, C-spine or extrem ity radiograph, and hem oglobin testing are helpful if patient presents with com plications of RA.

Lab 

CBC: m ild anem ia with leukocytosis and throm bocytosis



Erythrocyte sedim entation rate (ESR): often >30



C-reactive protein



Antinuclear antibodies (ANA) 30â€“40% positive screening tool

Pa ge 5 7 5



Rheum atoid factor: elevated in about 70% of cases



Joint fluid analysis: o

Typically between 4,000 and 50,000 white cells

o

Neutrophil predom inance

o

Microscopic Gram stain of fluid should show no organism s and no crystals.



ECG: conduction defects are rare, but heart block m ay be seen.

Imaging 



Joint radiograph: o

Joint effusion

o

Juxta-articular erosions and decalcification

o

Narrowing of joint space

o

Loss of cartilage

Magnetic Resonance Im aging (MRI) of joints can detect early inflam m ation before plain radiograph



Chest radiographm ay reveal pulm onary fibrosis, pleural changes, nodular lung disease, or pneum onitis: o

Cardiac silhouette m ay show changes related to m yocarditis.



Cervical spine radiograph: o

Atlantoaxial joint subluxation m ay occur.

Differential Diagnosis 

Osteoarthritis



Septic arthritis



Reactive arthritis



Gonococcal arthritis



Lym e disease



Gout



Connective tissue disorders



system ic lupus erythem atosus (SLE), derm atom yositis,

Pa ge 5 7 6

polym yositis, vasculitis, Reiter syndrom e, and sarcoid 

Rheum atic fever



Malignancy

P.105

Treatment Pre Hospital Cervical spine im m obilization and airway support as indicated

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Manage airway with attention to C-spine im m obilization during intubation.



Treat com plications of RA as appropriate.

ED Treatment 

Salicylates or NSAIDs are first-line treatm ent for RA: o

If one NSAID fails, another NSAID from a different chem ical class m ay work better.



Early treatm ent of RA is im portant as joint changes m ay be m ost progressive during the first 18 m onths.

Medication (Drugs) 

Glucocorticoids, m ethotrexate, and other second-line therapies should be initiated by a rheum atologist.



Aspirin (ECASA): adult: 900 m g PO q.i.d. (2.6â€“5.4 g/d); peds: 60â€“90 m g/kg/d q.i.d. up to 3.6 g

Pa ge 5 7 7



Auranofin: 3â€“9 m g/d (peds: 0.15 m g/kg/d up to 9 m g) divided b.i.d.



Celecoxib (Celebrex): 100â€“200 m g PO b.i.d.; peds: N/A



Hydroxychloroquine: adult: 200â€“600 m g/d divided b.i.d.; peds: 6 m g/kg/d up to 600 m g/d



Ibuprofen (Ibuprin, Advil, Motrin): 200â€“800 m g (peds: 10 m g/kg) PO q6h



Leflunom ide (Arava): 100 m g PO daily for 3 days, then m aintenance dose of 10â€“20 m g PO daily; peds: N/A



Methotrexate (Rheum atrex): 0.2â€“0.4 m g/kg PO per week single dose



Prednisone: m aintenance: 5â€“10 m g PO daily; acute exacerbations: 20â€“50 m g PO daily; peds: m aintenance: 0.1 m g/kg/d PO, acute exacerbations: 2â€“5 m g/kg/d PO



Rofecoxib (Vioxx; voluntary m anufacturer withdraw: 25 m g PO daily; peds: N/A



Sulfasalazine: adult: 500â€“1,000 m g PO b.i.d.; peds: 30â€“60 m g/kg/d q.i.d. up to 2 g



Valdecoxib (Bextra): 10 m g PO daily; peds: N/A

Alert Note: Recent studies have shown possibly increased risk of cardiovascular event with NSAID m edications, particularly with COX-2 inhibitors.

Follow-Up Disposition Admission Criteria 

Patients with severe or life-threatening presentations of RA and its com plications should be adm itted to hospital.

Pa ge 5 7 8



Adm ission is warranted when diagnosis is unclear and serious illnesses such as septic joint or system ic vasculitis m ay be present or cannot be ruled out.



Adm ission m ay be required for pain control.



Adm ission m ay be required if patient has inadequate social supports and is unable to m aintain activities of daily living.



Pediatric patients with fever and arthritis should be strongly considered for adm ission.

Discharge Criteria Patients without serious com plications m ay be m anaged as outpatients with appropriate m edications and follow-up.

Issues for Referral All patients should have prim ary physician for further therapy and care as well as appropriate specialty care referral such as rheum atologists, cardiologists, and orthopedics.

References 1. Anaya J, Diethelm L, Ortiz L, et al. Pulm onary involvem ent in rheum atoid arthritis. Sem in Arthritis Rheum . 1995;24(4):242â€“254. 2. Bingham CO. Developm ent and clinical application of COX-2 selective inhibitors for the treatm ent of osteoarthritis and rheum atoid arthritis. Cleve Clin J Med. 2002;69(suppl 1): SI5â€“12. 3. Ilowite NT. Current treatm ent of juvenile rheum atoid arthritis. Pediatrics. 2002;109(1):109â€“115. 4. Jain R, Lipsky P. Treatm ent of rheum atoid arthritis. Adv Rheum . 1997;81(1):57â€“84. 5. King R. Arthritis, rheum atoid. Available at http://www.em edicine.com 6. Leicht M, Harrington T, Davis D. Cricoarytenoid arthritis: a cause of laryngeal obstruction. Ann Em erg Med. 1987;16(8):885â€“888. 7. Sanders S, Harisdangkul V. Leflunom ide for the treatm ent of rheum atoid arthritis and autoim m unity. Am J Med Sci.

Pa ge 5 7 9

2002;323(4):190â€“193. 8. Sm ith JB, Haynes MK. Rheum atoid arthritis: a m olecular understanding. Ann Intern Med. 2002;136(12):908â€“922.

Codes ICD9-CM 714.0

ICD10 M06.9

Pa ge 5 8 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, Septic

Arthritis, Septic

Ziad N. Kazzi A. Antoine Kazzi

Basics Description 



Bacteria can be introduced into a joint by: o

Hem atogenous spread (m ost com m on)

o

Invasive procedures

o

Contiguous infection (e.g., osteom yelitis, cellulitis)

o

Direct inoculation such as plant thorns or nails

Acute inflam m atory process results in WBC m igration into joint.



Synovial hyperplasia, cartilage dam age, and form ation of a purulent effusion



Irreversible loss of function in up to 50%

Pediatric Considerations 

Hip infections are m ost com m on: o

Com m only in patients with otitis m edia or upper respiratory tract infections

o

Com plications of septic arthritis (SA) of hip in children: avascular necrosis, epiphyseal separation, pathologic dislocation, and arthritis



Fifty percent occur in children younger than 3 years old.

Pa ge 5 8 1



Infants present with irritability, fever, and loss of appetite.



Older children present with a lim p or refusal to bear weight or use joint.

Etiology 

Risk factors: o

Old age, infancy

o

Rheum atoid arthritis and degenerative joint disease

o

Intravenous drug user (IVDU), endocarditis

o

Fem ales (gonococcal [GC])

o

Im m unosuppression (AIDS, diabetes, chem otherapy, steroid therapy)

o

Repeated joint injections, pre-existing joint diseases, traum a, or prosthesis



No bacterial pathogen is identified in 10â€“20%.



Most com m on organism s: o

Staphylococcus aureus in adults, hip infections (80%), and patients with rheum atoid arthritis or diabetes

o

Neisseria gonorrhea (GC) m ost com m on in young, healthy, and sexually active patients (m ost com m on source in the U.S.) 

Other pathogens: group A Î²-hem olytic and group B, C, and G streptococci

o

Gram -negative rods (e.g., P. aeruginosa, E. coli) in 10% of cases: 

Com m on in old age, infancy, im m unosuppression, and IVDU (Pseudom onas)



Anaerobes: diabetes, prosthetic joints



Mycobacterial and fungal causes: atypical (e.g., in HIV); m ore indolent course

Pa ge 5 8 2

Diagnosis Signs and Symptoms 

Presents abruptly as a single painful, swollen, warm , and tender joint



Com m on findings include: o

Fever

o

A separate source of infection (e.g., skin)

o

Extrem ely painful joint m otion in all planes

o

A joint effusion (less evident in sacroiliac, hip, and shoulder)





Any joint can be involved: o

Typically a single joint is involved.

o

Most com m only knee, then hip, shoulder, and ankle

Com m only seen in IVDU: sacroiliac costochondral and sternoclavicular joints: o



Vertebral involvem ent such as lum bar facets possible

Hum an and anim al bites, local steroid therapy, and traum a m ay lead to infection in atypical locations.



Polyarticular involvem ent in 10â€“20%: o

Mostly with rheum atoid arthritis; delay in diagnosis from low suspicion and m ore subtle presentations (fever in only 50%)

o 

Patients with sepsis

Gonococcal (GC) SA features: o

Develops in 1â€“3% of untreated gonorrhea and in 42â€“85% of dissem inated GC infection: 

Typically m onoarticular but com m only polyarticular



Migratory polyarthralgia, tenosynovitis (present in 20% of patients with arthritis), and

Pa ge 5 8 3

derm atitis o

Involves sm all joints (e.g., fingers, wrist, elbow, ankle): 

Signs of urethral or vaginal GC infection m ay be present.



Painless m aculopapular lesions on trunk, arm s, legs, and around affected joint

Essential Workup Arthrocentesis 

Perform joint aspiration in any suspected case.



Send fluid for protein and glucose, cell count, Gram stain, and culture.



Typical SA findings: o

A turbid, purulent, or serosanguinous fluid

o

A leukocytosis (50,000â€“150,000/m m 3 ) with a polym orphonuclear predom inance (>75%)

o

Often a decreased glucose and elevated protein level



The appearance of crystals does not rule out SA.



Use special stain or culture m edia when indicated (e.g., GC, anaerobes, fungus, m ycobacterium )



Intra-articular lidocaine reduces the sensitivity of subsequent cultures; im m ediate em ptying of aspirated sam ple into a blood culture flask increases the yield.



In non-GC SA, Gram stain and culture are positive in 50% and 90% of cases, respectively: o



Drops to nearly 10% and 50% in GC SA, respectively

Fluoroscopic, sonographic, or CT guidance can be used in technically difficult aspirations.



CT scan and MRI m ay aid in the diagnosis for joints such as the sacroiliac joint.



Arthrocentesis is contraindicated whenever there is an

Pa ge 5 8 4

underlying joint prosthesis or an overlying skin infection: o

If cellulitis present, use an alternate approach through norm al skin.

Tests Lab 

Nonspecific serum leukocytosis (m ore com m on in children), left shift, and C-reactive protein (CRP) and erythrocyte sedim entation rate (ESR) elevation are usually present.



Urinalysis and culture can reveal a urologic source for the pathogen.



Blood cultures m ay be useful: positive in 50â€“70% of non-GC SA



Culture any potential focus of infection (pharynx, urine, cervix, or anus), particularly when suspecting GC.

Imaging 



Plain radiographs to identify: o

Effusion

o

Baseline status of the joint

o

Contiguous osteom yelitis

o

Concurrent rheum atologic diseases

o

Fractures or foreign body

o

Joint loosening (a late and nonspecific sign)

Ultrasound, CT, and MRI are m ore sensitive: o

Ultrasound m ay be used to guide aspiration of som e joints (e.g., hip) and to detect joint effusions



Scintigraphic techniques are sensitive and specific in diagnosis of SA: o



Often not available through ED

Other tests: o

Bacterial DNA am plification techniques in early

Pa ge 5 8 5

detection of organism s P.107

Differential Diagnosis 

Viral arthritis



Rheum atoid arthritis



Gout or pseudogout



HIV-associated arthritis



Reactive arthritis



Lym e disease



Osteom yelitis



Endocarditis



Traum a



In children: o

Juvenile rheum atoid arthritis

o

Slipped capital fem oral epiphysis

o

Legg-CalvÃ©-Perthes

o

Metaphyseal osteom yelitis

o

Transient synovitis

Pediatric Considerations 

Because of vaccine, H. influenzae is no longer m ost com m on.



S. aureus is m ost com m on.



Group B streptococcus, enterobacteria, and gram -negative rods in the newborn

Treatment Pre Hospital

Pa ge 5 8 6

No specific considerations

Initial Stabilization 

Patient m ay be septic and require resuscitation.



If patient is toxic, do not delay antibiotics for aspiration results.

ED Treatment 

Prom ptly aspirate joint fluid.



Obtain cultures.



Start em piric antibiotics: staphylococcal, streptococcal, and gram -negative coverage; duration of treatm ent recom m ended is 2â€“4 weeks: o

Com bine Î²-lactam aseâ€“resistant penicillin (e.g., nafcillin) with an am inoglycoside (e.g., gentam icin) or a third-generation cephalosporin (e.g., ceftriaxone).

o

Use Vancom ycin instead of penicillin when m ethicillin-resistant S. aureus or penicillin resistant pneum ococci are suspected.

o

Initial guidance by Gram stain, patient's age, risk factors, and com orbid illness is appropriate.

o

When suspecting GC, use a third-generation cephalosporin or a quinolone (e.g., ceftriaxone, ciprofloxacin).

o

Treat patients with sickle cell disease using third-generation cephalosporin (ceftriaxone) and an antistaphylococcal drug (nafcillin, cloxacillin, clindam ycin).

o 

Intra-articular antibiotics are contraindicated.

Early orthopedic consultation to evaluate eligibility for surgical drainage



Pain-control: narcotics and m oderately flexed splinting

Pa ge 5 8 7



Im m unologic therapies are experim ental.



Prosthesis: som e m ay try to preserve it unless it is loose on plain film s.



Patients should be at rest with joint m aintained in optim al position to prevent dam age.

Medication (Drugs) 

Cefotaxim e: 1 g IV q8h; peds: 50 m g/kg q12h



Ceftriaxone: 1 g IV daily; peds: 50 m g/kg



Ciprofloxacin: 400 m g IV q12h



Gentam icin: 2â€“5 m g/kg IV load



Nafcillin: 2 g IV q4h; peds: 25 m g/kg q6h



Piperacillin: 4 g IV q6h



Tobram ycin: 1 m g/kg IV q8h; peds: 2.5 m g/kg q8h



Vancom ycin: 1 g IV q12h; peds: 10 m g/kg q6h

Pediatric Considerations 

Open surgical drainage is the m ethod of choice in pediatric hip SA.



Cover H. influenzae type B if prior im m unization cannot be established.

Follow-Up Disposition Admission Criteria 

All patients with suspected SA should be adm itted until SA is ruled out.



May undergo drainage of their joint as indicated, by serial

Pa ge 5 8 8

aspirations, arthroscopy, or arthrotom y

Discharge Criteria Cases where suspected SA has been adequately ruled out.

References 1. Baker D, Schum acher HR. Acute m onoarthritis. N Engl J Med. 1993;329:1013â€“1019. 2. Deng GM, Tarkowski A. The role of bacterial DNA in septic arthritis. Int J Mol Med. 2000;6:29â€“33. 3. Donatto KC. Orthopedic m anagem ent of septic arthritis. Rheum Dis Clin North Am . 1998;24(2):275â€“286. 4. Goldenberg D. Septic arthritis. Lancet. 1998;35:197â€“202. 5. Greenspan A, Tehranzadeh J. Im aging of infectious arthritis. Radiol Clin North Am . 2001;39(2):267â€“276. 6. Malleson P. Managem ent of childhood arthritis. Part 1: acute arthritis. Arch Dis Child. 1997;76:460â€“462. 7. Shetty AK, Gedalia A. Managem ent of septic arthritis. Indian J Pediatr. 2004;71:819â€“824. 8. Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev. 2002;15(4):527â€“544.

Codes ICD9-CM 711.00

Core Content Code 10.2.1.1

ICD10 M00.9

Pa ge 5 8 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ascites

Ascites

Paul Allegretti

Basics Description 

Pathologic accum ulation of serous fluid in the peritoneal cavity



Portal hypertension (>12 m m Hg) starts fluid retention.



Avid sodium retention state.



Retained sodium and water increases plasm a volum e.



Water excretion becom es im paired.



Increased release of antidiuretic horm one (ADH)



Urinary sodium retention, increased total body sodium , and dilutional hyponatrem ia



Degree of hyponatrem ia correlates with disease severity; prognostic factor.



Decreased plasm a oncotic pressure from hypoalbum inem ia



Peritoneal irritation owing to infection, inflam m ation, or m alignancy

Etiology 

Parenchym al liver disease: o

Cirrhosis and alcoholic hepatitis: 

o

Eighty percent of adult patients

Fulm inant hepatic failure

Pa ge 5 9 0







Hepatic congestion: o

Congestive heart failure

o

Constrictive pericarditis

o

Veno-occlusive disease and Budd-Chiari syndrom e

Malignancies: o

Peritoneal carcinom atosis

o

Hepatocellular carcinom a or m etastatic disease

Infections: o





Tuberculous, fungal, or bacterial peritonitis

Hypoalbum inem ic states: o

Nephrotic syndrom e

o

Malnutrition; album in <2.0 g/dL

Other conditions: o

Pancreatic ascites

o

Biliary ascites

o

Nephrogenous ascites

o

Ovarian tum ors

o

Chylous ascites from lym phatic leak

o

Connective tissue disease

o

Myxedem a

o

Granulom atous peritonitis

Pediatric Considerations 

Most pediatric cases owing to: o

Malignancy (Burkitt lym phom a, rhabdom yosarcom a)

o

Nephrotic syndrom e

o

Malnutrition

Diagnosis Signs and Symptoms

Pa ge 5 9 1



Abdom inal distention, discom fort



Weight gain; som etim es weight loss



Dyspnea



Orthopnea



Edem a



Abdom inal hernias



Muscle wasting



Shifting dullness, flank fullness, fluid wave, puddle sign



Signs and sym ptom s of underlying disease



Stigm ata of chronic liver disease

History 

Risk factors for liver disease



Description of onset of sym ptom s: o

Distinguishes ascites from obesity

o

Patients less tolerant of rapid accum ulation of ascitic fluid



New-onset ascites in known cirrhotic signifies one of the following: o

Progressive liver disease

o

Superim posed acute liver injury (alcohol, viral hepatitis)

o

Hepatocelluar carcinom a

Physical Exam 

Detection difficult in obese patients



Flank dullness is a prom inent physical finding: o

1,500 m L for flank dullness

Essential Workup 

Search for liver disease, congestive heart failure, tuberculosis, m alignancy, other system ic disorders.



Abdom inal paracentesis: o

Mandatory in:

Pa ge 5 9 2





New ascites



Worsening encephalopathy



Fever



Abdom inal pain/tenderness

Determ ine if fluid infected or presence of portal hypertension



Test ascitic fluid for: o

Cell count and differential: 

Most helpful to determ ine infection quickly



Order on every specim en.

o

Album in

o

Protein

o

Gram stain

o

Culture twice in blood culture bottles with 10 m L of fluid



o

Lactate dehydrogenase (LDH)

o

Glucose

o

TB culture

o

Am ylase

o

Triglyceride

o

Cytology

o

Bilirubin

o

Carcinoem bryonic antigen

Spontaneous bacterial peritonitis (SBP): o

Ascitic fluid infection without an intra-abdom inal surgically treatable source

o

Fever, abdom inal pain/tenderness, altered m entation

o

Polym orphonuclear neutrophils (PMNs) >250 cells/m m 3



o

Ascitic fluid protein <1 g/dL

o

Low concentration of opsonins

Secondary bacterial peritonitis:

Pa ge 5 9 3

o

Bacterial peritonitis from a surgically treatable intra-abdom inal source

o

Gut perforation or intra-abdom inal abscess; i.e., perinephric abscess

o

PMNs >250 cells/m m 3 with m ultiple m icro-organism s on Gram stain plus two of the following found with secondary bacterial peritonitis: 

Total protein >1 g/dL



Glucose <50 m g/dL



LDH greater than the upper lim it of norm al for serum

Tests Lab 

CBC



Basic chem istry



Liver function tests



PT, PTT, INR



Arterial blood gas (ABG) or pulse oxim eter



Urinalysis



Urine sodium



Hepatitis panel



Am ylase/lipase



Alpha fetoprotein



Thyroid-stim ulating horm one (TSH)

Imaging 

Ultrasound: o

Confirm ascites, especially if <2 L

o

Evaluate liver, pancreas, spleen, ovaries

o

Guides paracentesis



Doppler study: Evaluate hepatic blood flow



CT scan

Pa ge 5 9 4



Chest radiograph: congestive heart failure (CHF), effusions, cavitary or m ass lesion



Echocardiogram

Diagnostic Procedures/Surgery 

Peritoneoscopy: ascites of unknown cause; especially TB



Paracentesis: o

Clinical diagnosis of SBP without paracentesis is inadequate.

o

Safety of paracentesis: 

Seventy percent of ascitic patients have coagulopathy.



Benefits of a diagnostic paracentesis outweigh the risks.



Paracentesis is still indicated unless dissem inated intravascular coagulation (DIC) is present.



Transfusion of plasm a or platelets prior to paracentesis is not supported.

P.109

Differential Diagnosis 



One of five â€œFâ€• causes of abdom inal swelling: o

Fluid (including cysts)

o

Fat

o

Flatus

o

Fetus

o

Feces

o

Other: organom egaly

Serum -ascites album in gradient (SAAG) = serum album in ascitic album in:

Pa ge 5 9 5

o

Replaced ascitic fluid total protein in the differential diagnosis of ascites

o

SAAG â‰¥1.1 g/dL: 

Ninety-seven percent accurate in predicting portal hypertension

o



Cirrhosis



Alcoholic hepatitis



Cardiac



Liver m etastases



Fulm inant hepatic failure



Portal vein throm bosis



Veno-occlusive disease



Myxedem a



Budd-Chiari



Fatty liver of pregnancy



Spontaneous bacterial peritonitis

SAAG <1.1 g/dL: 

Peritoneal carcinom atosis



Tuberculosis



Pancreatic ascites



Nephrotic syndrom e



Bowel obstruction or infarction



Vasculitis



Postoperative lym phatic leak

Treatment Pre Hospital Sym ptom atic hypotension: airway, breathing, circulation (ABCs), IV 0.9 norm al saline (NS)

Pa ge 5 9 6

Initial Stabilization Sudden increase in abdom inal girth, pain, or fever requires urgent evaluation for possible com plicating factor such as: 

Infection



Hepatom a



Obstruction of hepatic outflow



Decom pensated liver function

ED Treatment 

Successful treatm ent depends on accurate diagnosis of underlying cause.



Treat underlying cause.



Minim ize ascitic fluid and peripheral edem a without causing intravascular volum e depletion.



Early detection of com plications is necessary: o

o

Spontaneous bacterial peritonitis: 

High degree of suspicion



Low threshold for paracentesis



Prom pt therapy

Tense ascites and hydrothorax: 

Supplem ental oxygen



Therapeutic paracentesis or thoracentesis for respiratory distress

o

o

o

Abdom inal hernias: 

Watch for incarceration, ulceration, or rupture.



Therapeutic paracentesis



Surgical consultation

Persistent leak at paracentesis site: 

Rem ove m ore fluid.



Stom al barrier device

Meralgia paresthetica: 

Owing to pressure on the lateral fem oral

Pa ge 5 9 7

cutaneous nerve 

Relieve the pressure by paracentesis or diuresis.



Large-volum e paracentesis: o

5â€“10 L (100 m L/kg)

o

Perform ed safely in the ED with stable hem odynam ics

o

Replace with IV album in (5â€“10 g/L fluid rem oved) if >5 L rem oved.

o 

Monitor the patient for 8 hours prior to discharge.

Nonparacentesis reduction of ascites: o

o

o

Strict sodium restriction: 

<1 g/d



Restrict water if serum sodium <125 m Eq/L

Spironolactone: 

Works best for cirrhotic ascites



Alternatives: am iloride or triam terene

Furosem ide: 

Works best for other causes of ascites



Add to spironolactone in cirrhotics at spironolactone/furosem ide ratio of 100 m g/40 m g.

 o

Add m etolazone for less responsive cases.

Diuretic principles: 

Adm inister diuretics as single m orning dose.



Obtain spot-urine sodium to evaluate response.



Patients with urinary Na >10 m Eq/L are m ore responsive to diuretics.



Diuretic-induced weight loss should not exceed 2 lb/d in patients without edem a and 5 lb/d in patients with edem a.



Monitor electrolytes and renal function.



Avoid hypokalem ia.

Pa ge 5 9 8



Hypokalem ia enhances renal am m onia production, precipitating hepatic encephalopathy.

o

o

Refractory ascites: 

Accounts for 10% of patients



Ensure com pliance with diet and m edications.



Im plem ent peritoneovenous shunt.



Transjugular intrahepatic portosystem ic shunt



Liver transplantation

Avoid nonsteroidal anti-inflam m atory drugs (NSAIDs). 

Dim inish response to diuretics



Decrease renal plasm a flow and glom erular filtration rate (GFR).



Cause sodium retention/reduces urinary Na excretion

o

Treat underlying cause of ascites owing to conditions other than cirrhosis: 

Tuberculosis, CHF

Medication (Drugs) 

Album in: 5â€“10 g/L of fluid rem oved if >5 L rem oved



Am iloride: 10â€“40 m g/d PO



Cefotaxim e: 2 g IV q8h



Furosem ide: 40â€“160 m g/d (peds: 1â€“3 m g/kg) PO



Metolazone: 5 m g/d



Spironolactone: 100â€“400 m g/d (peds: 1â€“6 m g/kg) PO



Triam terene: 100â€“300 m g/d PO

Pa ge 5 9 9

Follow-Up Disposition Admission Criteria 

Fulm inant liver failure



Hepatic encephalopathy



Spontaneous bacterial peritonitis



Hepatorenal syndrom e



GI bleeding



Tense ascites not responding to ED treatm ent

Discharge Criteria 

Patients responding to ED m anagem ent

References 1. Braunwald E, et al. Harrison's Principles of Internal Medicine. 15th Ed. New York: McGraw-Hill; 2001. 2. Feldm an M. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002. 3. Runyon BA. Managem ent of adult patients with ascites caused by cirrhosis. Hepatology. 2004;39:841. 4. Such J. Initial Therapy of Ascites in Patients with Cirrhosis. Wellesley, MA: UpToDate; 2004.

Miscellaneous SEE ALSO: Cirrhosis

Codes ICD9-CM 789.5

ICD10

Pa ge 6 0 0

R18

Pa ge 6 0 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Asthm a, Adult

Asthma, Adult

Eric S. Nadel

Basics Description 





Increased expiratory resistance: o

Bronchospasm

o

Airway inflam m ation

o

Mucosal edem a

o

Mucous plugging

Consequences: o

Air trapping

o

Increased dead space

o

Hyperinflation

Risk factors for life-threatening disease: o

Prior intubations

o

Intensive care unit adm issions

o

Chronic steroid use

o

Hospital adm ission for asthm a during the past year

o

Inadequate m edical m anagem ent

o

Increasing age

o

Ethnicity (African Am ericans)

o

Lack of access to m edical care

Etiology

Pa ge 6 0 2

Mechanism 

Pollen



Dust m ites



Molds



Anim al dander



Other environm ental allergens



Viral upper respiratory infections



Occupational chem icals



Tobacco sm oke



Environm ental change



Cold air



Exercise



Em otional factors



Drugs: o

Aspirin

o

NSAIDs

o

Beta-blockers

Diagnosis Signs and Symptoms 

Wheezing



Dyspnea



Chest tightness



Cough



Tachypnea



Tachycardia



Respiratory distress: o

Posture sitting upright or leaning forward

o

Use of accessory m uscles

Pa ge 6 0 3



o

Inability to speak in full sentences

o

Diaphoresis

o

Poor air m ovem ent

Altered m ental status

Essential Workup 

Prim arily a clinical diagnosis



Measure and follow severity with peak expiratory flow rate (PEFR)



Assess for underlying disease



Pneum onia: o

Pneum othorax

Tests Lab 

Arterial blood gas: o

Not helpful during the initial evaluation

o

The decision to intubate should be based on clinical criteria.

o

Mild-m oderate asthm a: respiratory alkalosis

o

Severe airflow obstruction and fatigue: respiratory acidosis



Pulse oxim etry: o

Less than 90% is indicative of severe respiratory distress

o

Patients with im pending respiratory com prom ise m ay still m aintain saturation above 90% until sudden collapse.



WBC: o

Leukocytosis is nonspecific

o

Pneum onia

o

Chronic steroid use

o

Stress of an asthm a exacerbation

Pa ge 6 0 4

o

Dem argination occurs after adm inistration of epinephrine and steroids.

Imaging 

Peak expiratory flow rate: o

Estim ates the degree of airflow obstruction: 

Norm al peak flow in an adult is 400â€“600



Between 100 and 300 indicates m oderate airway obstruction.



<100 is indicative of severe airway obstruction.



Use serially as an objective m easure of the response to therapy





Forced expiratory volum e (FEV): o

More reliable m easure of lung function than PEFR

o

More operator dependent

o

Difficult to use as a screening tool

o

Often unavailable in the ED

o

Severe airway obstruction: FEV 1 less than 30â€“50%

Chest radiograph: o

Indications: 

Fever



Suspicion of pneum onia



Suspicion of pneum othorax or pneum om ediastinum

o



Foreign body aspiration



First episode of asthm a



Com orbid illness



Diabetes



Renal failure



AIDS



Cancer

Findings: 

Hyperinflation

Pa ge 6 0 5

 

Scattered atelectasis

ECG: o

o

Indicated in patients at risk for cardiac disease: 

Dysrhythm ias



Myocardial ischem ia

Transient changes in severe asthm a: 

Right axis deviation



Right bundle branch block



Abnorm al P waves



Nonspecific ST-T wave changes

Differential Diagnosis 

Congestive heart failure



Myocardial ischem ia



Pulm onary em bolus



Pneum onia



Bronchitis



Bronchiolitis



Croup



Foreign body aspiration



Upper airway obstruction



Angioedem a



Allergic reaction



Chronic obstructive pulm onary disease



Chronic cor pulm onale



Chem ical pneum onitis



Carcinoid tum ors



Sm oke inhalation



Im m ersion injury



Venous air em bolus

Pa ge 6 0 6

Treatment Pre Hospital 

Recognize the â€œquiet chestâ€• as respiratory distress.



Supplem ental oxygen



Continuous nebulized Î²-agonist



Adm inistration of subcutaneous epinephrine



Severe disease with decreased breath sounds

Initial Stabilization 

Im m ediate initiation of inhaled Î²-agonist treatm ent



Intubate for fatigue and respiratory distress.



Steroids

ED Treatment Î²-Adrenergic Agonist 

Mild-m oderate asthm atic: o



Adm inister every 20 m inutes

Severe asthm atic: o

Continuous nebulized treatm ent



Selective Î² 2 -agonists (albuterol)



Subcutaneous Î²-agonist: o

Severe exacerbations

o

Lim ited inhalation of aerosolized m edicine

o

More side effects because of system ic absorption:

o



Tachycardia



Trem ors

Relative contraindications: age >40 years and coronary disease

P.111



Corticosteroids:

Pa ge 6 0 7

o

Reduce airway wall inflam m ation

o

Adm inistered early

o

Onset of action m ay take 4â€“6 hours

o

Adm inister intravenously or orally

o

IV Solu-Medrol in the treatm ent of severe asthm a exacerbation

o

Mild-m oderate exacerbations m ay be treated with oral prednisone.

o

Inhaled corticosteroids are currently not recom m ended as initial therapy.



Oxygen: o





Maintain an oxygen saturation above 90%

Am inophylline: o

Rare utility in acute m anagem ent

o

Toxicity: 

Nausea



Trem or



Anxiety



Palpitations



Tachycardia

Anticholinergic agents: o

If m inim al response to initial Î²-agonist treatm ent

o

Severe airflow obstruction

o

Inhaled anticholinergic agents should be used in conjunction with Î²-agonists.



Magnesium sulfate: o

No benefit in m ild-m oderate asthm a

o

Benefit of m agnesium rem ains unclear in severe asthm a



Heliox: o

Mixture of helium and oxygen (80:20, 70:30, 60:40)

o

Less dense than air

Pa ge 6 0 8

o

Decrease airway resistance.

o

Decrease in respiratory exhaustion

o

Not currently recom m ended for routine use: 







Consider in severe asthm a

Ketam ine: o

Bronchodilator and an anesthetic agent

o

Useful as an induction agent during intubation

o

Contraindications: 

Hypertension



Coronary disease



Pre-eclam psia



Increased intracranial pressure

Halothane: o

Inhalation anesthetics are potent bronchodilators.

o

Refractory asthm a in intubated patients

Intubation of the asthm atic patient: o

Rapid sequence intubation: 

Lidocaine to attenuate airway reflexes



Etom idate or ketam ine as an induction agent



Succinylcholine should be adm inistered to achieve paralysis.



A large endotracheal tube >7 m m should be used to facilitate ventilation.



May need to m echanically exhale for the patient



Perm issive hypercapnia

Medication (Drugs) 

Î²-agonists o

Albuterol: 2.5 m g in 2.5 m L norm al saline q20m in inhaled (peds: 0.1â€“0.15 m g/kg/dose q20m in [m inim um dose 1.25 m g])

Pa ge 6 0 9

o

Epinephrine: adult: 0.3 m g (1:1,000) SC q0.5hâ€“q4.0h Ã— three doses (peds: 0.01 m g/kg up to 0.3 m g SC)

o

Terbutaline: 0.25 m g SC q0.5h Ã— two doses (peds: 0.01 m g/kg up to 0.3 m g SC)



Corticosteroids: o

Methylprednisolone: 60â€“125 m g IV (peds: 1â€“2 m g/kg/dose IV or PO q6h Ã— 24 hours)

o

Prednisone: 40â€“60 m g PO (peds: 1â€“2 m g/kg/day in single or divided doses)



Anticholinergics o

Ipratropium brom ide: 0.5 m g in 3 m L NS q1h Ã— three doses



Magnesium : 2 g IV over 20 m inutes



Am inophylline: 0.6 m g/kg/h IV infusion



Rapid sequence intubation: o

Etom idate: 0.3 m g/kg, or ketam ine: 1â€“1.5 m g/kg

o

Lidocaine: 1â€“1.5 m g/kg

o

Succinylcholine: 1.5 m g/kg

Follow-Up Disposition Admission Criteria 

Persistent respiratory distress



PEFR <100 and m inim al air m ovem ent



Intubated patients

Medical Wards or Observation Unit 

PEFR <40% of predicted



Patients without subjective im provem ent

Pa ge 6 1 0



Patients with continued wheeze and dim inished air m ovem ent



Patients with m oderate response to therapy and no respiratory distress:



o

Factors that should favor adm ission

o

Prior intubation

o

Recent ED visit

o

Multiple ED visits or hospitalizations

o

Sym ptom s for m ore than 1 week

o

Failure of outpatient therapy

o

Use of steroids

o

Inadequate follow-up m echanism s

o

Psychiatric illness

Com plications: o

Pneum othorax

o

Pneum om ediastinum

o

Pneum onia

o

Fatigue

Discharge Criteria 

Patient reports subjective im provem ent



Clear lungs with good air m ovem ent



PEFR or FEV 1 greater than 70% of predicted



Peak flow should be greater than 300.



Adequate follow-up within 48â€“72 hours

References 1. Corbridge TC, Hall JB. The assessm ent and m anagem ent of adults with status asthm aticus. Am J Respir Crit Care Med. 1995;151:1296â€“1316. 2. Guidelines for the diagnosis and m anagem ent of asthm a: National Asthm a Education Program Expert Panel Report. Bethesda, MD: Departm ent of Health and Hum an Services; 1991. NIH 91â€“3042.

Pa ge 6 1 1

3. Jagoda A, Shepherd SM, Spevitz A, et al. Refractory asthm a, part 1: epidem iology, pathophysiology, pharm acologic interventions. Ann Em erg Med. 1997;29:262â€“274. 4. Jagoda A, Shepherd SM, Spevitz A, et al. Refractory asthm a, part 2. Airway interventions and m anagem ent. Ann Em erg Med. 1997;29:275â€“281. 5. Manthous CA. Managem ent of severe exacerbations of asthm a. Am J Med. 1995;99:298â€“308.

Codes ICD9-CM 493

ICD10 J45.9

Pa ge 6 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Asthm a, Pediatric

Asthma, Pediatric

Nathan Shapiro Tarina Lee Kang

Basics Description 

2.7 m illion children (<18 years) affected in the United States



850,000 ED visits per year in the United States



Inflam m atory events, usually viral, lead to bronchoconstriction:



o

Com pounded by hyperreactivity of airways

o

Mediators of the inflam m atory cascade

Airway obstruction produces increased airway resistance and gas trapping:





o

Mucosal edem a

o

Bronchospasm

o

Mucous plugging

Infants m ore vulnerable to respiratory failure: o

Increased peripheral resistance

o

Decreased elastic recoil with early airway closure

o

Unstable rib cage

o

Mechanically disadvantaged diaphragm

Fam ily history of allergy

Pa ge 6 1 3



Medical history of early injury to airway (bronchopulm onary dysplasia, pneum onia, intubation, croup, reflux, passive exposure to sm oking), reactions to foods and drugs, other allergic m anifestations



Environm ental exposures such as pets, sm oke, carpets, dust

Etiology Precipitating/Aggravating Factors 



Infection: o

Viral

o

Bacterial

Allergic/irritant: o

Environm ent: pollens, grasses, m old, house dust m ites, anim al dander

o

Occupational chem icals: chlorine, am m oniaâ€”food and additives

o

Irritants: sm oke, pollutants, gases, aerosols: 

Exercise



Cold weather



Em otional: stress, phobia



Intoxication: beta-blockers, aspirin, nonsteroidal anti-inflam m atory drugs (NSAIDs)

Diagnosis Signs and Symptoms General 

Fatigue, som nolence



Diaphoresis, agitation



Hypoxia, cyanosis

Pa ge 6 1 4



Tachycardia



Dehydration



Pulsus paradoxus

Respiratory 

Wheezing, rales, rhonchi



Cough, acute or chronic



Tachypnea



â€œTight chestâ€•



Dyspnea, shortness of breath with prolonged expiratory phase



Retractions, accessory m uscle use, nasal flaring



Hyperinflation



Often a history of recurrent episodes and chronic restrictions



Com plications: o

Recurrent pneum onia, bronchitis

o

Atelectasis

o

Pneum othorax, pneum om ediastinum

o

Respiratory distress/failure/death

Essential Workup 

Clinical diagnosis based prim arily on physical exam and history; assess ventilation by auscultating air exchange



Follow response to bronchodilator therapy with present illness and past episodes.



Exclude other differential considerations.



Pulse oxim etry: o

Initial SaO 2 <91% (sea level) associated with significant illness: adm ission, relapse, prolonged course

o

Peak flow m eters in cooperative patients (usually >5 years old)

Pa ge 6 1 5

o

<50â€“70% predicts m oderate to severe obstruction.

o

>70â€“90% associated with m ild to m oderate obstruction

o

>90% considered norm al

Tests Lab 

Arterial blood gas (ABG) m ay be an adjunct to pulse oxim etry to m easure oxygenation and clinical exam to assess ventilation; not m andatory or routinely done



CBC as a nonspecific m arker of infection



Theophylline level: only for patients on theophylline (not recom m ended)

Imaging Chest radiograph in the following patients: 

Younger than 1 year of age to exclude foreign body or atelectasis



First episode of wheezing (suggested)



Increasing respiratory distress or m inim al response to therapy



Respiratory distress/failure



Shortness of breath in the absence of wheezing

Differential Diagnosis 

Infection/inflam m ation: o

Bronchiolitis: clinically difficult to differentiate except by age and clinical history

o

Pneum onia: viral, bacterial, chem ical, hypersensitivity

o

Aspiration

o

Lym phadenopathy

o

Anaphylactic reaction

Pa ge 6 1 6







Anatom ic: o

Pneum othorax

o

Foreign body

Vascular disorder: o

Com pression of trachea by vascular anom aly

o

Pulm onary em bolism

o

Congestive heart failure

Congenital disease: o

Cystic fibrosis

o

Tracheoesophageal fistula

o

Bronchogenic cyst



Intoxication: m etabolic acidosis



Neoplasm



Vocal chord dysfunction



Pulm onary edem a

P.113

Treatment Pre Hospital 

Oxygen and oxygen saturation m onitoring



Nebulized Î²-adrenergic agonist: albuterol



Intubate for respiratory failure or severe fatigue.



Rapid transport and good com m unication with ED

Initial Stabilization 

Maintain SaO 2 >90â€“95%.



Î²-adrenergic nebulizer(s): albuterol



Intubate for respiratory failure.

Pa ge 6 1 7

ED Treatment 



Assess patient for signs of potential respiratory failure: o

Cyanosis

o

Severe anxiety or irritability

o

Lethargy, som nolence, fatigue

o

Persistent tachypnea

o

Poor air entry, ventilation

o

Severe retractions

Monitor oxygenation; titrate oxygen saturation to SaO 2 >95% (sea level).





Î²-adrenergic nebulizer: albuterol: o

Frequent or continuous for severe asthm a

o

Levalbuterol m ay require less frequent dosing.

Ipratropium brom ide m ay be added as adjunct to Î²-adrenergic agonists.



Steroid therapy: o

Oral for m oderate exacerbations in those able to take oral m eds

o

Intravenous for severe exacerbations or in those unable to take oral m eds



Subcutaneous epinephrine or terbutaline for severe or refractory asthm a (rarely used)



Magnesium sulfate m ay be useful in severe disease following standard therapy.



Intubate for respiratory failure: o

Ketam ine is a useful induction agent.

Medication (Drugs) 

Albuterol (0.5% solution or 5 m g/m L): o

Nebulizer: 0.015 m g (0.03 m L)/kg per dose, up to 5

Pa ge 6 1 8

m g per dose, q15m inâ€“q30m in as needed o

Metered-dose inhaler (with spacer) (90 Âµg/puff): two puffs q5m inâ€“q10m in, m ax. 10 puffs



Epinephrine (1:1,000) (1 m g/m L): 0.01 m g/kg SC, up to 0.35 m L per dose, q20m in for two doses



Ipratropium brom ide: nebulizer (0.02% inhaled sol 500 Âµg/2.5 m L), 250â€“500 Âµg per dose q6h



Ketam ine (for intubation): 1â€“2 m g/kg IV as induction agent



Levalbuterol (0.63 and 1.25 m g vials): q6hâ€“q8h by nebulizer



Magnesium sulfate: 25 m g/kg per dose IV over 20 m in; m ax. 1.2â€“2 g per dose



Methylprednisolone: 1â€“2 m g/kg per dose IV q6h; m ax. 125 m g per dose



Prednisolone: 1â€“2 m g/kg per dose PO q12h



Prednisone: 1â€“2 m g/kg per dose PO q6hâ€“q12h; m ax. 80 m g per dose



Terbutaline (0.01%): 0.01 m L/kg SC q15m inâ€“q20m in up to 0.25 m L per dose, q20m in for two doses



(available as 15 m g/5 m L)

Follow-Up Disposition Admission Criteria 

Persistent respiratory difficulty: o

Persistent wheezing

o

Increased respiratory rate/tachypnea

o

Retraction and use of accessory m uscles

Pa ge 6 1 9



SaO 2 <93% (sea level) on room air



Peak expiratory flow rate (PEFR) <50â€“70% predicted levels



Inability to tolerate oral m edicines or liquids



Prior ED visit in last 24 hours



Com orbidity:



o

Congenital heart disease

o

Bronchopulm onary dysplasia

o

Cystic fibrosis

o

Neurom uscular disease

Concom itant illness: o

Pneum onia

o

Severe viral infection

Intensive Care Unit Criteria 

Severe respiratory distress



SaO 2 <90% or PaO 2 <60 m m Hg on 40% oxygen



PaCO 2 >40 m m Hg



Significant com plications: o

Pneum othorax

o

Dysrhythm ia

Discharge Criteria 

Good response to therapyâ€”observe in ED 60 m inutes after last treatm ent before discharging: o

PEFR >70% predicted

o

SaO 2 >93% on room air (sea level)

o

Respiratory rate norm al

o

No retractions

o

Clear or m inim al wheezing

o

No or m inim al dyspnea



Good follow-up and com pliance



Discharge treatm ent:

Pa ge 6 2 0

o

Intensive Î²-adrenergic regim en for 3â€“5 days

o

Short course (3â€“5 days) of steroids (2 m g/kg/d) for those presenting with m oderate sym ptom s

o

Follow-up appointm ent 24â€“72 hours

o

Instructions to return for shortness of breath refractory to hom e regim en

o

Long-term therapy should be considered for children with recurrent episodes, persistent sym ptom s, or activity lim itations.

References 1. Baren JM, Zorc JJ. Contem porary approach to the em ergency departm ent m anagem ent of pediatric asthm a. Em erg Med Clin North Am . 2002;20(1):115â€“138. 2. Markoff BA, MacMillan JF Jr, Kum ra V. Discharge of the asthm atic patient. Clin Rev Allergy Im m unol. 2001;20(3):341â€“355. 3. Rowe BH, Brerzlaff JA, Bourdon C, et al. Intravenous m agnesium sulfate treatm ent for acute asthm a in the em ergency departm ent: a review of the literature. Ann Em erg Med. 2000;36:181â€“190. 4. Scarfone RJ, Loiselle JM, Joffe MD, et al. A random ized trial of m agnesium in the em ergency departm ent treatm ent of children with asthm a. Ann Em erg Med. 2000;36:572â€“578. 5. Sm ith SR, Strunk RC. Acute asthm a in the pediatric em ergency departm ent. Pediatr Clin North Am . 1999;46(6):1145â€“1165. 6. Szefler SJ. Asthm a: the new advances. Adv Pediatr. 2000;47:273â€“308.

Miscellaneous SEE ALSO: Bronchiolitis; Pneum onia; Pediatric

Codes

Pa ge 6 2 1

ICD9-CM 493.9

ICD10 J45.0

Pa ge 6 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Asysto le

Asystole

David F. M. Brown

Basics Description 

Absence of cardiac electrical activity



End-stage cardiac rhythm

Etiology 



May occur after progressive dysrhythm ia: o

Bradycardia

o

Prolonged ventricular fibrillation

o

Prolonged pulseless electrical activity

Patient is extrem ely unlikely to survive when asystole occurs outside the hospital: o

Approxim ately 40% will have return of spontaneous circulation and survive to hospital adm ission, but less than 15% survive to hospital discharge.



Prognosis is sim ilarly poor for those patients who develop asystole after countershock for ventricular tachycardia/ventricular fibrillation (VF); <10% survive to hospital discharge.



Potentially reversible causes include: o

Hypoxia

o

Acidosis

Pa ge 6 2 3

o

Hyperkalem ia

o

Hypokalem ia

o

Drug overdose

o

Hypotherm ia

Diagnosis Signs and Symptoms 

Unresponsive patient



Pulseless



No spontaneous respirations

Essential Workup 

Confirm asystole in two lim b leads to exclude ventricular fibrillation.



Confirm lead and cable connections.



Confirm m onitor power is on.



Confirm m onitor gain is up.



Identify reversible causes.

Differential Diagnosis VF

Treatment Pre Hospital 

No intervention should be m ade for patient with valid Do Not Resuscitate docum ent.



No intervention if patient can be verified as dead: o

Rigor m ortis

Pa ge 6 2 4

o

Dependent livedo

o

Injury incom patible with life (decapitation)

Initial Stabilization 

Initiate basic CPR.



Confirm asystole with defibrillator.



Place airway device and confirm placem ent.



Establish IV access.



Confirm asystole in two lim b leads with m onitor.



Consider early transcutaneous pacing (within 3â€“5 m inutes of onset of asystole). P.115



Epinephrine and atropine every 3â€“5 m inutes.



Treat potentially reversible causes.



Sodium bicarbonate if hyperkalem ia or drug overdose suspected



No proven benefit to an em piric single countershock.

ED Treatment Consider stopping resuscitation efforts if the following conditions are m et: 

Adequate CPR



Tracheal intubation



Effective ventilation



IV access



VF excluded



Epinephrine and atropine given: o

Discuss indications of vasopressin versus epinephrine



Reversible causes corrected



Docum ented asystole despite 10 m inutes of above interventions

Pa ge 6 2 5

Medication (Drugs) 

Atropine 1 m g IV every 3â€“5 m inutes



Vasopressin 40 U IV (single dose)



Epinephrine 1 m g IV every 3â€“5 m inutes



Sodium bicarbonate 1 m Eq/kg IV: o

Adm inister only if prim ary acidosis is suspected.

Follow-Up Disposition Admission Criteria All patients with return of spontaneous circulation

Patient Monitoring Intensive care unit for cardiac and blood pressure m onitoring

References 1. Cum m ins RO, Graves JR, Larsen MP, et al. Out-of-hospital transcutaneous pacing by em ergency m edical technicians in patients with asystolic cardiac arrest. N Engl J Med. 1993;328:1377â€“1382. 2. Guidelines 2000 for Cardiopulm onary Resuscitation and Em ergency Cardiovascular Care. Part 6: Advanced cardiovascular life support: 7C: A guide to the International ACLS algorithm s. The Am erican Heart Association in collaboration with the International Liaison Com m ittee on Resuscitation. Circulation. 2000;102:(Suppl. 8) I142â€“157. 3. Niem ann JT, Stratton SJ, Cruz B, Lewis RJ. Outcom e of out-of-hospital postcountershock asystole and pulseless electrical activity versus prim ary asystole and pulseless electrical activity. [see

Pa ge 6 2 6

com m ent].Crit Care Med. 2001;29:2366â€“2370. 4. Wenzel V, Krism er AC, Arntz HR, et al. A com parison of vasopressin and epinephrine for out-of-hospital cardiopulm onary resuscitation. N Engl J Med. 2004;350(2):105â€“113.

Codes ICD9-CM 427.5

ICD10 I46.9

Pa ge 6 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ataxia

Ataxia

Sean P. Kelly

Basics Description 

Ataxia is the inability to perform coordinated m ovem ents.



It is a disorder of coordination and rhythm .



May result from dysfunction at several levels of the cerebellar circuit, including sensory or m otor pathways



Sensory ataxia: o

Proprioceptive sensory pathways to the cerebellum are faulty.





Dorsal root ganglia cells



Posterior colum ns of the spinal cord



Lem niscal system in the brainstem



Thalam us



Parietal cortex

Motor ataxia: o

Sensory pathways are intact, but the integration of proprioceptive data is faulty. 

Cerebellum



Contralateral frontal lobe



Internal capsule



Motor output to the spinal neurons

Pa ge 6 2 8



Different types of ataxia should be distinguished: o

Vertiginous ataxia due to dizziness

o

Cerebellar ataxia due to im balance

o

Spinal cord and m uscular ataxia due to weakness

Etiology 

Acute sym m etric: o





Toxicologic: 

Alcohol



Lithium



Diphenylhydantoin



Barbiturates

o

Acute viral cerebritis

o

Meningitis

o

Hydrocephalus

o

Postinfection syndrom e

o

Hyponatrem ia

o

Hypothyroidism

Acute focal: o

Anterior cerebral artery syndrom e

o

Cerebellar infarction

o

Cerebellar hem orrhage

o

Subdural hem atom a of the posterior fossa

o

Cerebellar abscess

Subacute sym m etric: o

Mercury

o

Hydrocarbons

o

Toluene

o

Vitam in B 1 or B 1 2 deficiency

o

Lym e disease

o

AIDS

o

Toxoplasm osis

o

Mycoplasm a

Pa ge 6 2 9







o

Legionella

o

Bacterial abscesses

o

Creutzfeldt-Jakob disease

Subacute focal: o

Cerebellar gliom a

o

Metastatic tum ors

o

Paraneoplastic syndrom es: 

Breast cancer



Hodgkin disease



Children with neuroblastom as

o

Multiple sclerosis

o

AIDS-related m ultifocal leukoencephalopathy

o

Lym phom a

o

Cervical spondylosis

o

Syringom yelia

o

Guillain-BarrÃ© syndrom e

Chronic: o

Cerebellar degeneration

o

Stable gliosis

o

Inherited and developm ental ataxias: 

Friedreich ataxia and other recessive ataxias



Ataxia-telangiectasia



Autosom al-dom inant cerebellar ataxia

Cerebellar hypoplasia: o

Hartnup disease

o

Niem ann-Pick disease

o

Pyruvate decarboxylase deficiency

o

Dandy-Walker and Arnold-Chiari m alform ation

o

Joubert and Gillespie syndrom es

Signs and Symptoms 

A careful history and physical are essential to classify the ataxia and determ ine the etiology:

Pa ge 6 3 0

o





Onset: 

Hours to daysâ€”acute



Weeks to m onthsâ€”subacute



Yearsâ€”chronic

o

Bilateral, sym m etrical, or focal involvem ent

o

Truncal or lim b ataxia

o

Motor or sensory ataxia (see below)

Perform neurological exam ination: o

Mental status

o

Motor sensory

o

Finger-to-nose

o

Heel-to-shin

o

Rom berg

o

Gait (if possible)

o

Speech

o

Cranial nerves

o

Babinski

Assess for associated signs or sym ptom s of acute, life-threatening disorders such as hem orrhage or stroke:





o

Altered m ental status

o

Headache

o

Focal weakness, num bness, tingling

o

Nausea/vom iting

o

Slurred speech

o

Incontinence

Assess for altered hand coordination (bilaterally): o

Finger-to-nose test

o

Rapid alternating hand m ovem ents

Assess for altered coordination in lower extrem ities (bilaterally): o



Abnorm al heel-to-shin coordination

Assess balance:

Pa ge 6 3 1

o

Ataxia usually results from dysfunction of two out of three of vision, vestibular sense, or proprioception.

o

Evaluated by Rom berg test

o

Positive Rom berg test: unsteady with eyes open, worse with eyes closedâ€”sensory ataxia

o

Negative Rom berg test: unsteady with eyes open, no change with eyes closedâ€”m otor ataxia (cause m ay be in cerebellum )

o

Norm al Rom berg test: no ataxia



Assess gait



Assess for intentional trem or

Specific Syndromes 







Frontal lobe lesions: o

Wide based gait

o

Tendency to fall backward

o

Motor perseveration

o

Grasp and suck reflexes

o

Urinary incontinence

o

Slowness in thinking

o

Headache

o

Altered m ental status

Subcortical lesions: o

Em otional lability

o

Brisk reflexes

o

Dysarthria

o

Dem entia

Brainstem lesions: o

Crossed m otor or sensory findings

o

Internuclear ophthalm oplegia

o

Nystagm us

o

Dysarthria

Cerebellar lesions:

Pa ge 6 3 2





o

Truncal and gait ataxia if m idline lesions

o

Ipsilateral lim b ataxia if hem ispheric lesions

o

Nystagm us

o

Hypotonia

o

Occipital headache

o

Occipital gaze palsy

Posterior colum n dysfunction: o

Positive Rom berg sign

o

Neck and arm pain

o

Positive Babinski sign

o

Loss of vibration and position sense

Peripheral neuropathy: o

Loss of deep tendon reflexes

o

Decreased strength and sensation peripherally

o

Wernicke encephalopathy

o

Encephalopathy

o

Oculom otor dysfunction

o

Gait ataxia

P.117

Essential Workup 

Thorough history and physical exam ination



Tests as described below

Tests Lab 

Blood glucose level



Electrolytes



Toxicology screen



Anticonvulsant drug screen



CBC; consider lum bar puncture if infection, abscess

Pa ge 6 3 3

suspected 

TSH, free T 4 if hypothyroidism suspected

Imaging 

Head CT scan: o

Identifies supratentorial m asses, hem orrhage, or evidence of hydrocephalus

o

If MRI is unavailable, obtain both contrast and noncontrast studies.

o

CT angiogram of the neck can be used to evaluate the neck vessels if MRI/m agnetic-resonance angiography not available



Head MRI: o

Diagnostic study of choice to assess the posterior fossa

o

Excellent study to evaluate for ischem ia, hem orrhage, tum or, edem a or other lesions

o

MR angiogram of the head and neck m ay be indicated if a vertebral basilar artery insufficiency or other vascular abnorm ality is suspected.



Electrom yography: o

Not indicated as part of the em ergency workup

o

Assesses for denervation of peripheral nerves

Diagnostic Procedures/Surgery Lum bar puncture: 

Rarely indicated unless fever or m ental status changes suggest an infectious etiology



Indicated in the evaluation for possible Lym e disease although m ay be done in this setting as an outpatient

Differential Diagnosis 

Stroke



Hem orrhage

Pa ge 6 3 4



Intoxication



Toxicologic



Infection



Electrolyte abnorm alities



Endocrine abnorm alities



Vertebrobasilar Insufficiency



Congenital ataxias



Benign paroxysm al positional vertigo



Acute labyrinthitis



MÃ©niÃ¨re disease



Hydrocephalus



Vitam in deficiency



Neoplasm



Paraneoplastic syndrom e: o

Multiple sclerosis

o

Guillain-BarrÃ© syndrom e



Syringom yelia



Atypical seizure



Com plicated m igraine

Treatment Pre Hospital Alert 

Acute onset of ataxia m ay be due to stroke or hem orrhage: o

Supplem ental oxygen

o

Monitor

o

IV access

o

Observe m ental status carefully; deterioration m ay

Pa ge 6 3 5

warrant field endotracheal intubation

Initial Stabilization 

ABCs



IV access, cardiac m onitor if altered m ental status or cerebellar hem orrhage suspected



Naloxone, dextrose (or rapid fingerstick glucose) if altered m ental status



Em piric thiam ine in chronic alcoholics and poorly nourished patients

ED Treatment Treatm ent should be determ ined by the underlying cause.

Medication (Drugs) 

Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg up to 2 m g) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g IM or 100 m g thiam ine in 1,000 m L of IV fluid wide open

Follow-Up Disposition Admission Criteria 

Acute and subacute ataxia, especially if an underlying etiology cannot be established



Patients who cannot am bulate safely without hom e support



Patients with cerebellar hem orrhage should be adm itted to

Pa ge 6 3 6

the intensive care unit

Discharge Criteria Reversible acute and subacute causes or chronic causes if patient's m ental status is okay and can am bulate without risk of injury: 

Most often due to alcohol, m edications, or cerebellar atrophy

References 1. Baloh RW. Approach to the dizzy patient. In: Baloh RW, ed. Neurotology. Baillieres Clin Neurol. 1994;3:453. 2. Huff JS. Ataxia and Gait Disturbances. In: Tintinalli JE, et al., eds. Em ergency m edicine: a com prehensive study guide. 5th ed. New York: McGraw-Hill, 2000:1449â€“1452. 3. Rosenberg RN. Ataxic disorders. In: Fauci AS, et al., eds. Harrison's principles of internal m edicine. Philadelphia: McGraw-Hill, 1998:2363â€“2368.

Codes ICD9-CM 334.0 334.2 334.3 334.8

ICD10 R27.0

Pa ge 6 3 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Atrial F ibrillatio n

Atrial Fibrillation

Jason K. Wong

Basics Description 

Dysrhythm ia characterized by seem ingly disorganized atrial depolarizations without effective atrial contraction



Caused by m ultiple re-entrant waveform s within the atria



Atrial rate ranges from 350â€“600 beats/m in.



Ventricular rate usually ranges from 160â€“200 beats/m in secondary to blocking by atrioventricular (AV) node: o

Faster rate suggests bypass tract

o

Slower rate suggests abnorm al AV node or presence of AV nodal blocking m edication



Results in loss of organized atrial contractions and rapid ventricular rate:



o

Decrease in cardiac output

o

Em bolus form ation

Affects 2.2 m illion Am ericans: o

Prevalence increasing with age

Etiology 

System ic disease: o

Hypertension

o

Hyperthyroidism

Pa ge 6 3 8



o

Chronic pulm onary disease

o

Pulm onary em bolus

o

Hypoxia

o

Drugs: 

Cocaine



Am phetam ines

o

Acute alcohol ingestion (holiday heart syndrom e)

o

Obesity

Underlying cardiac disease: o

Cardiom yopathy

o

Coronary artery disease

o

Valvular disease: 



Especially m itral

o

Pericarditis

o

Sick sinus syndrom e

o

Myocardial contusion

o

Congestive heart failure (CHF)

o

Congenital heart disease

Idiopathic: o

Absence of any known etiologic factor

o

No clinical or echocardiographic evidence of heart disease

Diagnosis Signs and Symptoms 

Palpitations



Irregularly irregular pulse



Slight variation in intensity of the first heart sound



Absence of a waves in the jugular venous pulse



Pulse deficit with m ore rapid ventricular rates

Pa ge 6 3 9

o

The auscultated or palpated apical rate is faster than the rate palpated at the wrist.

o

Helps differentiate atrial fibrillation (AF) from other supraventricular tachycardias





Decreased cardiac output: o

Weakness

o

Light-headedness

o

Syncope

o

Hypotension

o

Angina

o

Pulm onary edem a

o

Altered m ental status

o

Lower-extrem ity edem a

o

Hepatojugular reflex

Em bolus form ation: o

Acute neurologic injury

o

Mesenteric ischem ia

o

Digit ischem ia

Essential Workup 

History and physical exam : o

Assess for instability and need for im m ediate cardioversion

o

Duration of sym ptom s

o

Evidence of system ic disease or underlying cardiac disease



ECG o

Irregularly irregular R-R intervals

o

No identifiable P waves

o

If rate >200 associated with wide-irregular QRS, consider bypass tract.

Tests

Pa ge 6 4 0

Lab 

CBC



Electrolytes



Cardiac enzym es



Thyroid function



Digoxin level



Ethanol level



Urine drug screen

Imaging 

Chest radiograph



Echocardiogram (ECG)

Differential Diagnosis 

Atrial flutter with variable AV block



Multifocal atrial tachycardia



Sinus rhythm with frequent prem ature atrial contractions



Atrial tachycardia with variable AV block

Treatment Pre Hospital 

IV access



Monitor



Oxygen



Cardioversion: o

In rare settings where patient is unstable

Initial Stabilization 

IV



Oxygen



Monitor

Pa ge 6 4 1



Im m ediate synchronized electrical cardioversion starting at 200 J if the patient is unstable

ED Treatment 

Control rate: o

Not necessary if rate <100 beats/m in or if rhythm spontaneously converts to sinus

o

AV nodal blockers (calcium -channel blockers, beta-blockers, and digoxin) contraindicated if bypass tract suspected 

Younger patients



Wide com plex irregular tachycardia



Adm inistration m ay induce ventricular fibrillation



Use procainam ide to treat stable patients with a bypass tract.



Use electrical cardioversion for unstable patients.

o

Calcium -channel blockers: 

Consider in patient with pulm onary disease



Use cautiously in patient with uncom pensated CHF and second- or third-degree heart block

o



Diltiazem



Verapam il

Beta-blockers: 

Consider in patient with coronary artery disease (CAD)



Use cautiously in patient with uncom pensated CHF, second or third degree heart block, and pulm onary disease



Metoprolol



Propranolol



Esm olol

Pa ge 6 4 2

o

Digoxin: 

Consider in patient with pre-existing CHF



Slow rate of onset

P.119



Treat underlying cause if one is identified



Consider cardioversion in consultation with prim ary care physician or cardiologist: o

Treat all precipitating or reversible causes of AF before antiarrhythm ic treatm ent.

o

Rhythm control does not offer m ortality benefit over rate control: 

However, m ay consider rhythm control for patients with sym ptom atic AF or those with their first episode



Synchronized electrical cardioversion: o

Protocol depends on duration of atrial fibrillation.

o

>48 hours, delayed cardioversion: anticoagulation (INR 2â€“3) for at least 3 weeks, then cardioversion with 200â€“300 J, then anticoagulation for 4 m ore weeks

o

>48 hours, im m ediate cardioversion: IV heparin im m ediately then transesophageal echocardiography to exclude atrial clot then cardioversion then anticoagulation for four m ore weeks; if atrial clot noted on echo, will have to defer to delayed cardioversion protocol

o

<48 hours: IV heparin then cardioversion then anticoagulation for 4 weeks

o

Consider pretreatm ent with anti-arrhythm ic drugs to increase likelihood of success of electrical

Pa ge 6 4 3

cardioversion. 

Chem ical cardioversion: o

Choice of drug depends on history of CHF, high blood pressure, left ventricular hypertrophy, and CAD.

o

Medications m ay be proarrhythm ic and should be used with caution.

o

As with electrical cardioversion, appropriate anticoagulation will be necessary depending on the duration and presence/absence of clot.

o

Ibutilide: 

Requires a norm al QTc, no history of torsades, and correction of hypokalem ia



Posttreatm ent m onitoring for at least 4 hours for possible Torsades de Pointes



o

Quinidine gluconate

o

Procainam ide

o

Flecanide

o

Propafenone

o

Sotalol

Anticoagulation: o

In consultation with prim ary care physician or cardiologist

o

Patients with atrial fibrillation have a five tim es increased risk of stroke without anticoagulation

o

Warfarin: 

Indicated if risk factors for stroke (prior stroke or transient ischem ic attack, significant valvular heart disease, hypertension, diabetes, age older than 65 years, left atrial enlargem ent, CAD, or CHF)

o

Aspirin: 

Patients with contraindications to

Pa ge 6 4 4

anticoagulation and unreliable individuals 

Patients with low stroke risk

Medication (Drugs) 

Digoxin: 0.5 m g IV initially, then 0.25 m g IV q4h until desired effect



Diltiazem : 0.25 m g/kg IV over 2 m inutes; if unsuccessful, repeat in 15 m inutes as 0.35 m g/kg IV over 2 m inutes; an infusion of 5 m g/h is usually started after the initial dose to m aintain rate control



Esm olol: 0.5 m g/kg over 1 m inute; m aintenance infusion at 0.05 m g/kg/m in over 4 m inutes, then 0.1â€“0.2 m g/kg/m in continuously



Heparin: load 80 IU/kg IV; infusion at 18 IU/kg/h



Metoprolol: 5â€“10 m g slow IV push at 5-m inute intervals to total of 15 m g



Propranolol: 0.1 m g/kg IV divided into equal doses at 2- to 3-m inute intervals



Verapam il: 2.5â€“5 m g IV bolus over 2 m inutes; m ay repeat with 5â€“10 m g every 15â€“30 m in to m ax of 20 mg



Procainam ide: 15â€“18 loading dose adm inistered as a slow infusion over 30 m inutes. Maxim um load: 1.5 g. Then 2â€“6 m g/m in infusion.



Quinidine gluconate: 324â€“648 m g PO q8hâ€“q12h hrs



Ibutilide: 1 m g IV for patients >60 kg; 0.01 m g/kg IV for patients <60 kg infused over 10 m inutes; dose can be repeated once if sinus rhythm not restored within 10 m inutes after infusion; patients m ust be m onitored for 4 hrs afterward for QT prolongation, Torsades de Pointes, and ventricular tachycardia

Pa ge 6 4 5



Flecainide: 2 m g/kg IV at 10 m g/m in



Propafenone: 1â€“2 m g/kg IV at 10 m g/m in



Sotalol: 1â€“1.5 m g/kg IV then infused at 10 m g/m in



Warfarin sodium : 2.5â€“5 m g PO per day, dosage adjustm ents based on INR



Aspirin: 50â€“325 m g per day

Alert IV form for flecainide, propafenone, and sotalol not approved for use in United States; m ust be infused slowly.

Follow-Up Disposition Admission Criteria 





Unstable AF: o

Unable to control rate or hem odynam ic stability

o

Cardioversion required in the ED

High risk for stroke: o

Prior cardiovascular accident

o

CHF

o

Rheum atic heart disease

Associated m edical problem s contributing to the AF that require inpatient m anagem ent

Discharge Criteria 

Anticoagulated with HR <120



AF <48 hours and HR<120



AF at low risk for stroke with successful rate control

References 1. Falk RH. Atrial fibrillation. N Engl J Med.

Pa ge 6 4 6

2001;344(14):1067â€“1078. 2. Fuster V, Ryden LE, Asinger RW, et al: ACC/AHA/ESC Guidelines for the Managem ent of Patients with Atrial Fibrillation: Executive Sum m ary a Report of the Am erican College of Cardiology/Am erican Heart Association Task Force on Practice Guidelines and the European Society of Cardiology. Circulation. 2001;104(17):2118â€“2150 3. Saxonhouse SJ, Curtis AB. Risk and benefits of rate control versus m aintenance of sinus rhythm . Am J Cardiol. 2003;91(6A):27Dâ€“32D. 4. Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 5th ed. Philadelphia: WB Saunders. 1997:640â€“704.

Codes ICD9-CM 427.3

ICD10 I48

Pa ge 6 4 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Atrial F lutter

Atrial Flutter

Liesl A. Curtis

Basics Description 

Atrial dysrhythm ia



200,000 new cases each year



Male to fem ale ratio 2:1



A re-entrant circuit in the right atrium is thought to be the underlying m echanism .



Most sensitive rhythm to cardioversion



Seldom occurs in absence of organic heart disease



Less com m on than supraventricular tachycardia (SVT) or atrial fibrillation



Typically paroxysm al, lasting seconds to hours



Often reverts to sinus rhythm or atrial fibrillation



Untreated, m ay prom ote cardiom yopathy

Etiology 

Ischem ic heart disease



Valvular heart diseases



Congestive heart failure



Myocarditis



Cardiom yopathies



Pulm onary em bolus

Pa ge 6 4 8



Other pulm onary disease



Electrolyte abnorm alities



Postoperative following cardiac surgery (often in first postoperative week)



Thyrotoxicosis

Diagnosis Signs and Symptoms 

Palpitations



Syncope/presyncope



Fatigue



Dyspnea



Poor exercise capacity



Tachycardiaâ€”heart rate >150 bpm : o

Most often with a regular pulse



Hypotension



Chest pain



Heart failure

Pediatric Considerations 

Infants do not tolerate atrial flutter well: o

The aortic valve (AV) node is capable of very rapid conduction.

o

Extrem ely rapid ventricular rates can lead to shock or congestive heart failure (CHF).



Atrial flutter can occur in the fetus and young infants without associated cardiac defects: o



Often does not recur beyond neonatal period

Most older children have an underlying cardiac abnorm ality:

Pa ge 6 4 9

o

More likely to recur, m ore difficult to control

Tests Lab 

ECG o

Regular atrial rate between 250 and 350

o

Beat-to-beat uniform ity of cycle length, polarity, and am plitude

o

Sawtooth flutter waves directed superiorly and m ost visible in leads II, III, aVF

o

AV block usually 2:1, but occasionally greater or irregular

o

If rhythm is equivocal, slow the rate to show the presence of flutter waves: 

Vagal m aneuvers



Adenosine



CBC



Electrolytes



Cardiac enzym es



Thyroid function



Ancillary studies are based on the clinical exam ination to determ ine underlying causes.

Imaging 



Chest radiograph: o

Left atrial enlargem ent

o

Cardiom egaly

o

Heart failure

Transesophageal echocardiogram : o

Consider before cardioversion

Differential Diagnosis 

SVT

Pa ge 6 5 0



Sinus tachycardia



Atrial fibrillation



Multifocal atrial tachycardia



Ventricular tachycardia

Treatment Pre Hospital 

IV access



Supplem ental oxygen



Cardiac m onitoring



Unstable patients should be cardioverted in the field:



o

Im m ediate synchronized cardioversion

o

Start with 50 J, then 100 J, 200 J, 300 J, and 360 J

Use of adenosine is controversial: o

Used in som e system s in the field for SVT

o

Unlikely to break atrial flutter

o

May aid in the diagnosis of atrial flutter by unm asking the flutter waves

Initial Stabilization 

Oxygen



Monitor



IV access



Im m ediate synchronized cardioversion starting at 50 J-m in if the patient is unstable

ED Treatment 

Rate control o

Rate control should be instituted prior to giving an antidysrhythm ic to avoid risk of a 1:1 AV conduction ratio and hem odynam ic collapse

Pa ge 6 5 1

o 

May be difficult to achieve

Anticoagulation: o

Sam e guidelines as for atrial fibrillation

o

INR 2â€“3 prior to cardioversion if >48 hours or unknown duration



o

Recom m ended even if negative transesophageal ECG

o

Risk of throm boem bolism ranges from 1.7â€“7%

Patients at higher risk for throm boem bolism include: o

Valvular heart disease

o

Patients who alternate between atrial fibrillation and flutter



o

Left ventricular (LV) dysfunction

o

Prior stroke or throm boem bolism

o

Longer sym ptom duration (>48 hours)

Advanced cardiac life support (ACLS) recom m endations for rate control: o

Cardiac function preserved: 

Calcium channel blocker



Verapam il has higher incidence of sym ptom atic hypotension than diltiazem

o



Beta-blockers



Digoxin

Cardiac function im paired (Ejection fraction (EF) <40% or CHF):

o



Digoxin



Diltiazem



Am iodarone

Preexcited (Wolff-Parkinson-White [WPW] syndrom e) and norm al LV function: 

Am iodarone



Flecainide



Procainam ide

Pa ge 6 5 2

o

o



Propafenone



Sotalol

Preexcited (WPW) and LV dysfunction (CHF): 

Am iodarone



ACLS recom m endations for rhythm conversion:

Cardiac function preserved (use only one): 

Am iodarone



Ibutilide



Efficacy rate of 38â€“76%



Mean tim e to conversion is 30 m inutes



Incidence of sustained polym orphic ventricular tachycardia (VT) 1.2â€“1.7%



Not used in patients with severe structural heart disease, prolonged QT interval or underlying sinus node disease



Observe for 4â€“6 hours after adm inistration for QT prolongation or VT



Flecainide P.121

o

o



Propafenone



Procainam ide

Cardiac function im paired (EF <40% or CHF): 

Consider cardioversion



Am iodarone

Pre-excited (WPW) and norm al LV function: 

Am iodarone



Flecainide



Procainam ide



Propafenone



Sotalol

Pa ge 6 5 3

o



Preexcited (WPW) and LV dysfunction (CHF): 

Am iodarone



Consider cardioversion

Note: In WPW adenosine, beta-blockers, calcium -channel blockers, and digoxin are Class III (can be harm ful): o

Can cause increased ventricular response, which can deteriorate to ventricular fibrillation



Cardioversion: o

50â€“360 J (25 Jâ€“100 J for m ost patients)

o

Sedation when possible

o

Safest and m ost effective m eans of restoring sinus rhythm



Maintenance of sinus rhythm after cardioversion: o

High recurrence rate; up to 70% within first year

o

Am iodarone m ost effective

o

Dofetilide: 

Newer pure class III antiarrhythm ic drug



Recent FDA approval for conversion and m aintenance of sinus rhythm

 o

QT prolongation can occur in 2â€“4% of patients

Percutaneous catheter ablation: 

Acute and long-term success rates exceed 90%



Perm anent cure



Low com plication rate

Pediatric Considerations 

Verapam il is not recom m ended in infants and young children as it is associated with a low cardiac output and serious cardiovascular com prom ise



Digoxin is the first-line drug therapy for pediatric atrial flutter: o

Consider cardioversion as first-line therapy in neonates

Pa ge 6 5 4



Beta-blockers, class IA antiarrhythm ics (procainam ide, quinidine) or am iodarone are alternatives

Medication (Drugs) 

Am iodarone: 150 m g IV over 10 m in, then continuous infusion at 1 m g/m in for 6 hours, then 0.5 m g/m in; supplem ental 150-m g infusions can be dosed PRN to a m axim um daily dose of 2 g (peds: 5 m g/kg IV loading dose over 20â€“60 m in, m ay repeat to m ax of 15m g/kg/day IV)



Atenolol: 5 m g IV over 5 m inutes, m ay repeat in 10 m in if tolerated, then 50 m g PO q12h



Digoxin: Loading dose 10â€“15 ug/kg lean body weight (peds: 8â€“12 Âµg/kg)



Diltiazem : 0.25 m g/kg IV over 2 m inutes followed in 15 m inutes by 0.35 m g/kg IV over 2 m in, m aintenance infusion of 10â€“15 m g/hr titrated to heart rate



Dofetilide: 8 ug/kg IV over 30 m inutes



Esm olol: 0.5 m g/kg over 1 m in; m aintenance infusion at 0.05 m g/kg/m in; can repeat loading dose and increase in increm ents of 0.05 m g/kg/m in q4m in up to 0.3 m g/kg/m in



*,**Flecainide: 2 m g/kg IV at 10 m g/m in



Ibutilide (Corvert): 1 m g IV over 10 m inutes for patients >60 kg; 0.01 m g/kg IV for patients <60 kg infused over 10 m in; dose can be repeated once if norm al sinus rhythm not restored within 10 m inutes after infusion



Metoprolol: 5 m g IV push over 5 m inutes at 5-m inute intervals to total of 15 m g, then 50 m g PO b.i.d.



Procainam ide: 20 m g/m in until arrhythm ia suppressed, hypotension, QRS prolongation of 50%, or total of 17 m g/kg; m ay be given at rate up to 50 m g/m in (peds:

Pa ge 6 5 5

10â€“15 m g/kg IV over 15 m inutes, then 20â€“80 Âµg/kg/m in cont. infusion) 

*,**Propafenone: 1â€“2 m g/kg IV at 10 m g/m in



Propranolol: 0.1 m g/kg in three equal doses by slow IV push at 2- to 3-m inute intervals; not faster than 1 m g/m in (peds: 0.01â€“0.15 m g/kg/dose slow IV push over 5 m inutes, MAX 1 m g/dose)



Quinidine gluconate: 324â€“648 m g PO q8hâ€“q12h



*Sotalol: 1â€“1.5 m g/kg then infused at 10 m g/m in



Verapam il: 2.5â€“5.0 m g IV bolus over 2 m inutes; m ay repeat with 5â€“10 m g every 15â€“30 m inutes to m ax of 20 m g

Alert 

*IV form not approved for use in United States; m ust be infused slowly



**Flecainide and propafenone should not be used in post-MI patients (increased m ortality)

Follow-Up Disposition Admission Criteria 

New-onset atrial flutter requiring antidysrhythm ics



Sym ptom atic (i.e., chest pain that warrants a rule out or cardioversion)



CHF

Discharge Criteria Chronic atrial flutter with good rate control and appropriate anticoagulation

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References 1. Blom strom -Lundqvist C, Scheinm an MM, et al. ACC/AHA/ESC Guidelines for the Managem ent of Patients with Supraventricular Arrhythm iasâ€“Executive Sum m ary. J Am Coll Cardiol. 2003 Oct 15;42(8):1493â€“1531. 2. Ghali WA, Wasil BI, et al. Atrial flutter and the risk of throm boem bolism : A system atic review and m eta-analysis. Am J Med . 2005;118:101â€“107. 3. Khan MH. Oral class III antiarrhythm ics: what is new? Curr Opin Cardiol. 2004;Jan;19(1):47â€“51. 4. International Guidelines 2000 for Cardiopulm onary Resuscitation and Em ergency Cardiovascular Care. Part 6: Advanced cardiovascular life support. Section 5: Pharm acology I: Agents for arrhythm ias. Circulation. 2000;102[suppl I]:I112â€“I128. 5. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharm acologic m anagem ent of supraventricular tachycardias in children. Part 2: atrial flutter, atrial fibrillation, and junctional and atrial ectopic tachycardia. Ann Pharm acother. 1997;31:1347â€“1359. 6. McKee MR. Am iodarone-an â€œoldâ€• drug with new recom m endations. Curr Opin Pediatr. 2003;15(2):193â€“199. 7. Niebauer MJ, Chung MK. Managem ent of atrial flutter. Cardiol Rev. 2001;9(5):253â€“258. 8. Purerfellner H. Recent developm ents in cardiovascular drug therapy: Treatm ent of atrial arrhythm ias with new class III drugs and beyond. Curr Med Chem Cardiovasc Hem atol Agents. 2004; Jan;2(1):79â€“91. 9. http://www.UpToDate.com : Am iodarone: Drug Inform ation. http://www.utdol.com /application/ltopic/print.asp?file=drug_a_k/139 85&drug=true. Accessed 6/13/05. 10. Waldo AL. Treatm ent of atrial flutter. Heart 2000;84(2):227â€“232.

Pa ge 6 5 7

Codes ICD9-CM 427.32

ICD10 I48

Pa ge 6 5 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Atrio ventricular Blo cks

Atrioventricular

Blocks Colleen N. Roche James Scott

Basics Description 

Im paired conduction through the aortic valve (AV) node or His-Purkinje system



First-degree AV block: o

Prolonged conduction through the AV node >0.20 seconds

o 

Ventricular im pulses are not lost.

Second-degree AV block: o

Marked by a failure of som e atrial im pulses to reach ventricles

o

Type I (Wenckebach): 

Usually secondary to conduction deficit in AV node



Generally benign



Progressive prolongation of the pulse-rate (PR) interval until there is a nonconducted P wave and a dropped QRScom plex

Pa ge 6 5 9



May be a com plication of an inferior wall m yocardial infarction (MI)

o

Type II: 

Conduction deficit is usually below the level of the AV node.



PR intervals are constant until a single or m ultiple beats are abruptly dropped.



High likelihood of progression to com plete heart block



Worse prognosis if associated with an acute m yocardial infarction

 

Less com m on than type I

Third-degree AV block: o

Also known as com plete heart block

o

All atrial im pulses are unable to reach the ventricular conducting system ; a ventricular escape pacem aker then takes over, resulting in AV dissociation.

o

Constant PP and RR intervals with variable PR intervals because PP and RR intervals are independent of each other.

o

More severe sym ptom s occur when the block is lower in the conducting system .

o

If secondary to toxicologic agents, often resolves upon om ission of offending toxin

o

Never a benign condition

Etiology 



Essentially due to: o

A structural lesion

o

Increase in inherent refractory period

o

Marked shortening of the supraventricular cycle

MI: o

First-degree block and type I second-degree AV block

Pa ge 6 6 0

m ay be associated with an inferior wall MI: 

10â€“15% of all inferior wall MIs are com plicated by AV blocks.



AV conduction usually returns to norm al with no increased m orbidity or m ortality.

o

Type II second-degree AV block m ay be associated with an anterior wall MI: 

5% anterior wall MIs are associated with AV blocks.



Increased m ortality secondary to ventricular arrhythm ias and left heart failure



Coronary artery disease: o

Chronic ischem ic injury can lead to fibrosis around the AV node



Toxicologic: o

Digoxin

o

Beta-blockers

o

Calcium -channel blockers

o

Am iodarone

o

Procainam ide

o

Class 1C agents: propafenone, encainide, flecainide

o

Clonidine



Congenital



Valvular heart disease



Surgical traum a: o

S/P coronary artery bypass graft or valvular replacem ent



Increased vagal tone



Infectious: o

Syphilis

o

Diphtheria

o

Chagas disease

Pa ge 6 6 1

o

Tuberculosis

o

Toxoplasm osis

o

Lym e disease

o

Myocarditis

o

Endocarditis

o

Rheum atic fever

o

Abscess form ation in interventricular septum



Collagen vascular diseases



Infiltrative diseases: o

Sarcoidosis

o

Am yloidosis

o

Hem ochrom atosis



Cardiom yopathy



Electrolyte disturbances: o

Hyperkalem ia



Myxedem a



Hypotherm ia

Pediatric Considerations 

Occurs in children, but is often asym ptom atic



Associated m ortality is highest in the neonatal period.



Associated with: o

Congenitally acquired m aternal antibodies

o

Congenital heart disease

o

Infectious etiologies, such as rheum atic fever or m yocarditis



Be sure to consider potential toxic ingestions in pediatric patients with new AV block

Diagnosis

Pa ge 6 6 2

Signs and Symptoms History 

First-degree AV block: o



Type I second-degree AV block: o



Asym ptom atic

Pulse irregularities

Type II second-degree AV block and third-degree block: o

Exercise intolerance

o

Palpitations

o

Chest pain

o

Presyncope/syncope

o

Altered m ental status

o

Dyspnea, orthopnea

Physical Exam 

First-degree AV block: o



Type I second-degree AV block: o



No discrete physical exam findings

Regularly irregular pulse

Type II second-degree AV block and third-degree block: o

Irregular pulse

o

Hypotension

o

Confusion

o

Signs of heart failure: 

Rales



Cyanosis



Jugular venous distention

Essential Workup A 12-lead ECG to determ ine the type of block and identify evidence of infarction or drug toxicity: 

First-degree AV block:

Pa ge 6 6 3

o 

PR interval >0.20 seconds

Second-degree AV block: o

Type I: progressive prolongation of PR interval until there is a nonconducted P wave and a dropped QRS; occurs in repeated cycles; QRS is usually narrow P.123

o

Type II: PR interval rem ains constant; atrial im pulses are not conducted interm ittently, giving the appearance of an occasionally dropped ventricular beat; QRS m ay be prolonged depending on the level of the lesion



Third-degree AV block: o

Com plete electrical dissociation: atria and ventricles beat at separate, unrelated rates; constant PP and RR intervals with variable PR intervals

o

QRS duration depends on the level of the pacem aker: pacem akers above the level of the His-Purkinje system result in narrow QRS com plexes, pacem akers below this level produce wide QRS com plexes

Tests Lab 

Electrolytes



Calcium , m agnesium



Cardiac enzym es: o

Especially for type II second-degree and third-degree blocks



Digoxin level

Imaging 

Chest radiograph:

Pa ge 6 6 4

o

May identify cardiom yopathy or congestive heart failure



ECG: o

May identify regional wall m otion abnorm alities or valvular dysfunction

Differential Diagnosis 

Accelerated junctional rhythm



Idioventricular rhythm



Sinus bradycardia

Treatment Pre Hospital 

Transcutaneous pacing for unstable type II second- or third-degree block



Atropine: o

Avoid with type II second-degree block because it m ay precipitate com plete heart block

o

Contraindicated in third-degree heart block with a widened QRS com plex



Attem pts should be m ade at preventing increases in vagal tone.

Initial Stabilization 

Transcutaneous pacem aker: o

o 

Necessary for the unstable patient: 

Profound bradycardia and chest pain



Shortness of breath



Hypotension

Mild sedation is recom m ended beforehand

Atropine:

Pa ge 6 6 5

o

Can be adm inistered in: 

Com plete heart block with a narrow QRS



Sym ptom atic bradycardia

ED Treatment 

First-degree AV block: o

No treatm ent required

o

Close m onitoring to ensure that it does not progress to higher level AV block

o

Evaluate for associated MI, electrolyte abnorm alities, m edication excess.





Type I second-degree AV block: o

Usually no treatm ent needed

o

If sym ptom atic, atropine will enhance AV conduction

Type II second-degree AV block: o

Tem porary transcutaneous or transvenous pacem aker

o 

Atropine and isoproterenol are not effective

Third-degree AV block: o

May transiently respond to atropine

o

Em ergent pacem aker

o

Digoxin-specific antibodies

o

Digoxin overdose with a com plete heart block

o

Glucagon and calcium : 

If beta-blocker or calcium -channel overdose

Medication (Drugs) 

Atropine: 0.5â€“1.0 m g (peds: 0.01â€“0.03 m g/kg) IV every 5 m inutes as necessary



Calcium chloride: 250â€“500 m g (peds: 20 m g/kg) IV



Digoxin-specific antibodies:

Pa ge 6 6 6

o

Serum level Ã— weight (kg) = num ber of vials to be adm inistered



Glucagon: 5â€“10 m g (peds: 50 Âµg/kg IV over 5 m inutes



Isoproterenol: Begin infusion at 2 Âµg/m in and titrate to a m ax 10 Âµg/m in IV (peds: infusion at 0.1 Âµg/kg/m in and titrate to a m ax of 1.5 Âµg/kg/m in).

Follow-Up Disposition Admission Criteria Monitored bed: 

Type II second-degree block



Third-degree block

Discharge Criteria Asym ptom atic first-degree and type I second-degree blocks: 

Ensure follow-up for further outpatient workup.

References 1. Barold SS, Serge S, Hayes DL. Second-degree atrioventricular block: a reappraisal. Mayo Clin Proc. 2001;76(1):4457. 2. Bourke JP. Atrioventricular block and problem s with atrioventricular conduction. Clin Geriatric Med. 2002;18(2). 3. Brady WJ, Harrigan RA. Diagnosis and m anagem ent of bradycardia and atrioventricular block associated with acute coronary ischem ia. Em erg Med Clin North Am . 2001;19:371â€“384. 4. Haushik V, Leon A, Forrester JS, et al. Bradyarrhythm ias, tem porary and perm anent pacing. Crit Care Med 2001;28(10):N121â€“N128. 5. Kaltm an J. Evaluation of the Child with an arrhythm ia. Pediatr Clin

Pa ge 6 6 7

North Am . 2004;54(6). 6. Olgin JE, Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Brunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders, 2001:872â€“876.

Codes ICD9-CM 426.0 426.1

Pa ge 6 6 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Babesio sis

Babesiosis

Philip D. Anderson

Basics Description 

Tick-borne, m alarialike disease caused by an intracellular parasite that invades the red blood cells.



Protozoa pass from tick salivary glands to m am m alian bloodstream .



Erythrocytes are penetrated and infected by parasites that m ature and divide.



RBC m em brane dam age and lysis leads to hem olytic anem ia and hem oglobinuria.



Dam aged RBCs becom e less deform able, enhancing rem oval by spleen.



Asplenic patients are less able to clear infected RBCs, leading to m ore severe disease.



Dam aged RBCs m ay result in m icrovascular stasis with secondary ischem ic organ injury.



Subsequent com plications can include renal failure secondary to acute tubular necrosis, shock, cardiac failure, hypotension, acute respiratory distress syndrom e (ARDS), and dissem inated intravascular coagulation (DIC)



Babesiosis in Europe:

Pa ge 6 6 9

o

Often a fulm inate disease in im m unocom prom ised patients



o

40% m ortality in asplenic patients

o

Bovine strain (Babesia divergens)

North Am erica: o

Usually presents as m ild or subclinical disease in im m unocom petent patients (5% m ortality)

o

Rodent strain (Babesia m icroti) in the Northeastern United States

o

Canine strain (Babesia gibsoni) in the Northwestern United States





Incubation period: o

1â€“4 weeks after tick bite

o

6â€“9 weeks after transfusion

Geographic distribution in the United States: o

Coastal areas of Northeastern United States

o

Em erging clusters: 

Midwest (Minnesota, Wisconsin, Missouri)



West coast (California, Washington)



Seasonal distribution: 80% of hum an cases occur between May and August when tick nym ph populations and hum an outdoor activity are highest.



Risk factors for severe disease: o

Age >40 years

o

Splenectom y

o

Depressed cellular im m unity (HIV, corticosteroid use, other im m unosuppressive drugs)

o

Co-infection with Lym e disease

o

In im m unosuppressed patients, up to 85% of RBCs m ay be infected.

Etiology

Pa ge 6 7 0



Intraerythrocytic protozoa of the genus Babesia



Transm itted to hum ans by the Ixodes tick:



o

Ixodes ricinus in Europe

o

Ixodes scapularis in the United States

o

Anim al reservoirs: 

Cattle in Europe



White-footed m ouse in the United States

I. scapularis: o

Requires a blood m eal to develop through each of it's three developm ental stages.

o

Larvae: 

o

o

Nym phs: 

Feed on hum ans



Nym ph form is 1â€“2 m m in length



Tan color



Patients m ay not recall being bitten

Adult ticks: 

o 

Feed on white-footed m ice

Generally feed on white-tailed deer

Also the vector for Lym e disease and ehrlichiosis

Transfusion-associated infections are possible: o

Parasitem ia not always visible on donor blood sm ear.

o

Risk of transm ission in endem ic areas reported to be 0.17%.

Pregnancy Considerations Transm ission can occur in utero and during delivery; youngest reported case was a 4-week old infant.

Diagnosis

Pa ge 6 7 1

Signs and Symptoms Clinical spectrum ranges from m ild to fulm inate with sym ptom s lasting from weeks to m onths.

History 

Mild flulike illness



Fatigue



Anorexia



Myalgias



Arthralgias



Cough



Nausea



Vom iting



Headache



Em otional lability

Physical Exam 

Conjunctival injection



High-spiking fevers



Shaking chills



Drenching sweats



Rash: o

Uncom m on

o

Petechial or purpuric rash caused by associated throm bocytopenia

o

Erythem a m igrans if concurrent Lym e disease



Respiratory distress



Dark urine



Jaundice



Hepatosplenom egaly



Meningism us



Altered sensorium



Hypotension

Pa ge 6 7 2



ARDS



DIC

Essential Workup 

History of nonspecific febrile illness in any patient with recent outdoor activities or transfusion in an endem ic area during warm weather should prom pt consideration of diagnostic workup for babesiosis, especially if associated with hem aturia, jaundice, anem ia, splenom egaly, and lym phocytosis.



Septic presentation in patients with above history and risk factors (asplenia, im m unocom prom ised, age >40 years) should prom pt consideration of diagnostic workup and em piric treatm ent for babesiosis

Tests Lab 

Nonspecific studies: o

CBC (anem ia, throm bocytopenia, m ild leukopenia, atypical lym phocytosis)

o

Liver function studies (elevated alkaline phosphatase, transam inases, lactate dehydrogenase, bilirubin)

o

Urinalysis (hem oglobinuria, proteinuria)

o

Hem olysis profile (elevated reticulocyte count, decreased serum haptoglobin, hyperbilirubinem ia, elevated lactate dehydrogenase, hem oglobinuria)

o

Elevated blood urea nitrogen, creatinine suggests renal insufficiency

o

Elevated serum potassium m ay result from m assive hem olysis



Specific diagnostic studies: o

Peripheral blood sm ear: 

Microscopy of Giem sa- or Wright-stained thin

Pa ge 6 7 3

sm ears 

Parasites within RBCs can be round, oval, or pear shaped



Most com m on appearance is round (ring form s) to oval (pyriform ) rings with pale blue cytoplasm and red-staining nucleus; extracellular parasites m ay also be seen



Parasites in budding tetrad form ation (Maltese cross) are a rare, but highly suggestive finding of babesiosis.



Level of parasitem ia can range from <1â€“>85%; higher levels m ore com m on in splenectom ized patients

o

Polym erase chain reaction: 

Available for both Babesia m icroti and B. divergens



Higher sensitivity, equal specificity to blood sm ear



Useful in cases with very low levels of parasitem ia

P.125

o

Serology: 

Indirect im m unofluorescent antibody assay



Serum antibody titer usually rises within a few weeks of infection; falls off slowly over m onths



Titers of 1:64 or higher considered positive (acute or prior infection); serology m ay rem ain positive for years



Titers of 1:256 or m ore are indicative of acute infections

Pa ge 6 7 4



Blood and urine cultures if presentation consistent with sepsis



Cerebrospinal fluid analysis if presentation suggestive of CNS infection

Imaging 

Chest radiograph indicated for respiratory com plaints or evidence of hypoxia



Head CT m ay be indicated in setting of altered m ental status.



Abdom inal CT m ay be indicated in setting of splenom egaly and hypotension.



ECG indicated for ischem ic sym ptom s

Differential Diagnosis 

Malaria



Other tickborne diseases:



o

Lym e disease

o

Ehrlichiosis

o

Rocky Mountain spotted fever

o

Colorado tick fever

o

Q fever

o

Tularem ia

o

Relapsing fever

Typhoid fever

Treatment Alert Acute respiratory failure, shock, and m yocardial infarction have been reported as com plications of babesiosis.

Pa ge 6 7 5

Pre Hospital 

Ensure a patent airway



Provide supplem ental oxygen and ventilatory assistance as needed



If patient appears to be in shock, establish IV access and adm inister a fluid bolus of 0.9% norm al saline 500 m L (peds: 20 m L/kg) IV

Initial Stabilization 

Airway m anagem ent, ventilatory support for patients with acute respiratory failure



Pulse oxim etry: hypoxia m ay be present in patients with severe disease.



IV access should be established in patients with evidence or risk factors for severe disease.



IV fluids



Pressor support for patients in shock

ED Treatment 

Start em piric antibiotic therapy with two drug regim en in patients at risk with significant sym ptom s and/or shock



Clindam ycin plus quinine: o

Adverse effects (tinnitus, abdom inal com plaints) or treatm ent failure m ay lim it use.



Atovaquone plus o

Com parable efficacy to clindam ycin-quinine (65% versus 73%) with fewer adverse effects (12% versus 67%) and m ay be used as an alternative



Exchange transfusion as adjunctive therapy in patients with severe sym ptom s or risk factors for severe disease: o

Im m unodeficiency

o

splenia

o

Severe hem olysis

Pa ge 6 7 6



o

B. divergens infection

o

High-level parasitem ia (>10%)

Antibiotic therapy in known m ild or asym ptom atic cases due to risk of transm ission via blood transfusion or recrudescence, especially if risk factors for severe disease are present



Hem odialysis m ay be indicated for patients with acute renal failure



Treat fever with antipyretics

Medication (Drugs) 

Acetam inophen: 325â€“1,000 m g (peds: 40â€“60 m g/kg/24h) PO/PR q4hâ€“q6h PRN



Atovaquone: 750 m g (peds: 40 m g/kg/24h) PO b.i.d. Ã— 7 days



Azithrom ycin: 500 m g (peds: 10 m g/kg up to m ax. 500 m g) PO on day 1, followed by 250 m g (peds: 5 m g/kg up to m ax. 250 m g) PO per day: 6 days



Clindam ycin: 300â€“600 m g (peds: 20 m g/kg/24h in 3 div. doses) PO q8h 7â€“10 days



Ibuprofen: 200â€“400 m g (peds: 20â€“40 m g/kg/24h) PO q6hâ€“q8h PRN



Quinine: 650 m g (peds: 25 m g/kg/24h) PO q8h Ã— 7â€“10 days o

Quinine is contraindicated in pregnancy

Follow-Up Disposition

Pa ge 6 7 7

Admission Criteria 





Patients with severe disease: o

Severe, sym ptom atic anem ia

o

Jaundice

o

Renal insufficiency

o

Respiratory distress

o

DIC

o

Shock

Patients at risk of developing severe disease: o

Im m unodeficiency, asplenia

o

Severe hem olysis

o

B. divergens infection

o

High-level parasitem ia (>10%)

Patients requiring exchange transfusion

Discharge Criteria 

Patients with asym ptom atic or m ild disease



Intact spleen



Able to tolerate oral m edications

Issues for Referral HIV patients m ore likely to relapse following initial treatm ent; should be referred for infectious disease follow up

References 1. Boustani MR, Gelfand JA. Babesiosis. Clin Infect Dis. 1996;22:611â€“615. 2. Boustani MR, Lepore TJ, Gelfand JA, et al. Acute respiratory failure in patients treated for babesiosis. Am J Respir Crit Care Med. 1994;149:1689â€“1691. 3. Dacey MJ, Martinez H, Raim ondo T, et al. Septic shock due to babesiosis. Clin Infect Dis. 2001;33:E37â€“E38. 4. Dorm an SE, Cannon ME, Telford SR III, et al. Fulm inant babesiosis

Pa ge 6 7 8

treated with clindam ycin, quinine, and whole-blood exchange transfusion. Transfusion. 2000;40:375â€“380. 5. Gerber MA, Shapiro ED, Krause PJ, et al. The risk of acquiring Lym e disease or babesiosis from a blood transfusion. J Infect Dis. July 1994;170(1):231â€“234. 6. Hom er MJ, Aguilar-Delfin I, Telford SR III, et al. Babesiosis. Clin Microbiol Rev. 2000;13:451â€“469. 7. Krause PJ, Telford SR III, Spielm an A, et al. Concurrent Lym e disease and babesiosis. Evidence for increased severity and duration of illness. JAMA. 1996;275(Jun 5)(21):1657â€“1660. 8. Krause PJ, Telford SR III, Pollack RJ, et al. Babesiosis: an underdiagnosed disease of children. Pediatrics. June 1992;89(6) Pt 1: 1045â€“1048. 9. Krause PJ, Lepore T, Sikand VK, et al. Atovaquone and azithrom ycin for the treatm ent of babesiosis. N Engl J Med. 2000;343:1454â€“1458. 10. New DL, Quinn JB, Qureshi MZ, Sigler SJ. Vertically transm itted babesiosis. J Pediatr. 1997;131:163. 11. Meldrum SC, Birkhead GS, White DJ, et al. Hum an babesiosis in New York State: an epidem iological description of 136 cases. Clin Infect Dis. Decem ber 1992;15(6):1019â€“1023.

Codes ICD9-CM 08882

ICD10 B60.0

Pa ge 6 7 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Back Pain

Back Pain

Eric Legome

Basics Description 

Low back pain (LBP): o

Refers to pain in the area between the lower rib cage and the gluteal folds, often with radiation into the thighs



Sciatica: o

Pain in the distribution of the lower lum bar spinal roots

o

Often accom panied by neurosensory and m otor deficits



Pain classification: o

Acute if zero to 6 weeks

o

Subacute if 6â€“12 weeks

o

Chronic if >12 weeks

Etiology 

Nonspecific m usculoligam entous source including m uscle, ligam ent, fascia (great m ajority)



Herniation of the nucleus pulposus



Degenerative joints or discs



Spinal stenosis

Pa ge 6 8 0



Anatom ic abnorm alitiesâ€”especially spondylolisthesis



Fractures from traum a and osteoporosis



Underlying system ic diseases (m inority): o

Neoplasm

o

Infections

o

Vascular (dissection, aneurysm and thom bosis)

o

Renal

o

Gastrointestinal

o

Pelvic organ pathology

Diagnosis Signs and Symptoms 

Musculoligam entous: o

Poorly localized and dull back/gluteal pain without radiation past the knee

o

Usually there are no objective neurologic signs.

o

Back spasm is a variable and poorly reproducible finding.



Sciatica: o

Sharp, shooting, well-localized pain

o

Leg com plaints often greater than back

o

May present with: 

Asym m etric deep tendon reflexes



Decreased sensation in a derm atom al distribution

 

Objective weakness

Massive central disc herniation (cauda equina syndrom e): o

Decreased perineal sensation

o

Urinary retention with overflow incontinence

o

Fecal incontinence

Pa ge 6 8 1



Infectious processes: o

Fever

o

Localized percussion tenderness of the vertebral bodies





Bony lesion: o

Continuous pain that does not change with rest

o

Constitutional sym ptom s

Vascular etiology: o

Severe, often â€œripping or tearingâ€• pain

o

May be associated with cold or insensate extrem ities

History 

Can assist with focusing and narrowing differential diagnosis. Helps rule out concerning pathology for pain:



o

Intensity

o

Quality

o

Location and radiation

o

Onset

o

Exacerbating or rem itting factors

o

Social or psychological factors

o

Response to previous therapy

Risk factors for serious disease: o

Fever

o

Constitutional sym ptom s

o

Traum a

o

Age >60 years

o

History of cancer: 

Especially those that m etastasize to bone

o

Chronic steroid use

o

IV drug use

o

Recent instrum entation or bacterem ia

o

Night pain

Pa ge 6 8 2

Physical Exam 

Fever-suggests infectious etiology



Spasm or soft tissue tenderness is a poorly reproducible finding: o

Vertebral tenderness sensitive but nonspecific for infection



Straight leg raiseâ€”elevating the leg while supine reproduces sciatic sym ptom s:



o

Ipsilateral raise highly sensitive but not specific

o

Crossed leg raise highly specific but insensitive

Ankle and great toe dorsiflexion and ankle plantar flexion (L5, S1 nerve roots)



Ankle deep tendon reflexes (S1)



Derm atom al sensory exam ination

Essential Workup 

Thorough history and physical, including detailed neurologic and vascular exam ination



No specific tests are needed for uncom plicated m usculoligam entous or sciatic pain without com plicating factors



Rapid diagnostic testing and vascular consultation for pain concerning aortic etiology

Tests Lab 



Urinalysis for suspected: o

Urinary tract infection (UTI)

o

Pyelonephritis

o

Prostatitis

ESR o

Very sensitive, though nonspecific for infectious or

Pa ge 6 8 3

inflam m atory etiologies o

Used for screening if suspicion exists

Imaging 

Lum bosacral radiograph: o

Significant traum a

o

Age >50 years (som e guidelines recom m end >60)

o

History or signs/sym ptom s of cancer

o

Fever

o

IV drug user

o

Pain at rest

o

Suspicion of ankylosing spondylitis or inflam m atory etiology

o 

Pain that does not im prove after 4 weeks

MRI: o

Suspicion of abscess

o

Rapidly progressing neurologic sym ptom s

o

Urinary retention or fecal incontinence associated with back pain



Abdom inal CT or bedside ultrasound o

Suspicion of abdom inal aortic aneurysm (AAA)

o

CT secondary m odality for diagnosis of abscess, cancer or m assive disc when MRI unavailable.

o 

Test of choice of im aging potential unstable fractures.

Chest CT or transesophageal TEE: o

Suspicion of aortic dissection or aneurysm

Differential Diagnosis 

Spinal originsâ€”in the m ajority of patients no precise anatom ic site is discovered: o

Musculoligam entous (m ajority)

o

Discogenic

o

Fracture

Pa ge 6 8 4



o

Spondylolisthesis

o

Ankylosing spondylitis

o

Osteom yelitis

o

Epidural abscess/hem atom a

o

Neoplasm

Nonspinal causes: o

AAA

o

Prostatitis

o

Upper UTI

o

Abdom inal neoplasm

o

Renal colic

o

Aortic dissection

P.127

Treatment Pre Hospital 

Traum a patients with acute back pain should be im m obilized on a backboard until an unstable fracture can be ruled out.



Rapid transport with IV access for any patient with concerns of vascular etiology

ED Treatment 

NSAIDs for m usculoligam entous pain, renal colic: o

Initial treatm ent of choice, although acetam inophen m ay be preferred due to its preferable side-effect profile.

o

No agent has definitive benefits over others

Pa ge 6 8 5

o 

Recom m end using cost and dosing schedules as guide

Muscle relaxants: o

Possible benefits m ust be balanced by side effects, m ostly sedation and dry m outh



o

Cyclobenzaprine

o

Methocarbam ol

o

Carisoprodol

Efficacy of benzodiazepines for back pain is rarely studied: o



No clear evidence of utility.

Lim ited course of narcotic analgesics for severe pain not relieved by anti-inflam m atory agents or renal colic



Spinal m anipulation: o

A short course (<2 weeks) m ay be helpful in acute LBP without sciatica



Physical therapy/exercise: o

No clear consensus for indications

o

May be helpful in sym ptom atic relief, preventing further episodes and teaching patients



Acupuncture: o

Controversial, probable benefit for chronic m usculoskeletal pain

o 

No clear benefit over other m odalities

Bed rest: o

Unhelpful to speed recovery and m ay im pede im provem ent. If patient requires bed rest acutely or is sym ptom atically im proved, one or two days m ay be recom m ended.



Back exercises: o

Unlikely to be useful in acute phase; m ay assist with prevention of future episodes



Expected recovery to pain-free state: o

Approxim ately 33% within 1 week

Pa ge 6 8 6

o

Approxim ately 90% within 6â€“8 weeks



Recurrence is com m onâ€”about 40%.



ED m anagem ent of aortic dissection geared toward preventing progression of the dissection: o

Reducing the pressure gradient or the force of contraction (dP/dt) by controlling the heart rate and m ean arterial blood pressure

o

Initial control of heart rate with Î²-blockade followed by control of m ean arterial pressure with sodium nitroprusside or com bination therapy with labetalol

Medication (Drugs) 

Acetam inophen: 650â€“1,000 m g PO q4hâ€“q6h



Cyclobenzaprine: 5â€“10 m g PO t.i.d.



Hydrocodone/acetam inophen: 5/500 m g PO q4hâ€“q6h



Ibuprofen: 600â€“800 m g PO q6hâ€“q8h



Naproxen: 250â€“500 m g PO q12h



Oxycodone/acetam inophen: 5/500 m g PO q4hâ€“q6h

Blood Pressure/Heart Rate Control (if concerned for Vascular Etiology) 

Esm olol: 500 Âµg/kg followed by an infusion of 50â€“200 Âµg/kg/m in



Labetalol: has both Î±-blocking and Î²-blocking activity and can be used as m onotherapy; 20 m g IV bolus every 5â€“10 m inutes, increm entally increased to 80 m g until heart rate of 60â€“80 beats/m in has been reached or a total of 300 m g is given



Sodium nitroprusside: 0.3â€“10 Âµg/kg/m in titrate to BP of 100â€“120 systolic

Pa ge 6 8 7

Follow-Up Disposition Admission Criteria 

Severe pain with inability to am bulate



Progressive neurologic deficits



Signs of cauda equina syndrom e



Evidence of infectious, vascular, or neoplastic etiologies

Discharge Criteria Uncom plicated presentation with ability to control pain and am bulate

Pediatric Considerations Back pain is unusual in the pediatric patient; a high suspicion for an infectious etiology m ust be m aintained.

Issues for Referral Urgent neurosurgical or orthopaedic consultation for definite diagnosis or high suspicion for abscess or lesion (disc, neoplasm or other) with rapidly progressive objective neurologic findings

References 1. Brody M. Low back pain. Ann Em erg Med. 1996;27(4):454â€“456. 2. Deyo RA, Rainville J, Kent DL. What can the history and physical tell us about low back pain? JAMA. 1992;268:760â€“765. 3. Deyo RA, Weinstein JN. Low Back Pain. N Engl J Med. 2001;344(5):363â€“370. 4. Sm eal WL, Tyburski M, Alleva J. Discogenic/Radicular Pain. Dis Mon. Decem ber 2004;50:635â€“639. 5. Frym oyer JW. Back pain and sciatica. N Engl J Med. 1988;318:291â€“299. 6. Hagan PG, Nienaber MB, Christoph A, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old

Pa ge 6 8 8

disease. JAMA. 2000;283(7):897â€“903. 7. System ic Review within the Fram ework of the Cochrane Collaboration. Spine. 2003;28(17):1978â€“1992. 8. Van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM. Cochrane Back Review Group. Muscle Relaxants for Non-Specific Low Back Pain: A. 9. van Tulder MW, Scholten RJPM, Koes BW, Deyo RA. Non-steroidal anti-inflam m atory drugs for low-back pain. The Cochrane Database of System atic Reviews 2000.

Codes ICD9-CM 724.2

ICD10 M59.9

Pa ge 6 8 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bacterial Tracheitis

Bacterial

Tracheitis Roger Barkin Gary Bubly

Basics Description 

Usually secondary bacterial infection of dam aged trachea from an antecedent viral infection or instrum entation



Potentially fatal (0â€“20% m ortality rate)



Tracheal m em brane form ation, purulent discharge, subglottic edem a, erosions, with norm al epiglottis



Classically acute in onset, m ay be gradual with prodrom e sim ilar to croup prior to rapid deterioration of airway patency



Slight m ale predom inance



Mean age 5 years; rarely occurs in adults



More com m on in children than epiglottitis owing to success of Haem ophilus influenzae im m unization



More frequent during August through Decem ber

Alert Patients m ay present an insidious course consistent with croup. Rapid deterioration m ay ensue, associated with acute airway obstruction.

Pa ge 6 9 0

Etiology 

Staphylococcus aureus



Moraxella catarrhalis



Streptococcus pneum oniae



Group A streptococcal species



Haem ophilus influenzae type B



Anaerobes



Klebsiella pneum oniae



Pseudom onas aeruginosa



Nocardia



Associated with influenza A and parainfluenza viral infections



Aspergillus, HSV in im m unocom prom ised hosts (HIV)

Diagnosis Signs and Symptoms History Usually preceding viral infection with acute change in course of illness

Physical Exam 

General: o

Toxic appearance

o

Fever

o

Upper airway

o

Hoarseness

o

Sore throat/neck pain

o

Dysphonia: 



Drooling uncom m on

Respiratory: o

Respiratory distress

Pa ge 6 9 1



o

Cyanosis

o

Dyspnea

o

Inspiratory/expiratory stridor

o

Retractions

o

Nasal flaring

o

Barking/brassy cough

o

Wheezing/rhonchi

Com plications: o

o

o

Respiratory: 

Airway obstruction



Subglottic stenosis



Pulm onary edem a



Pneum othorax



ARDS



Endotracheal tube (ETT) plugging

Infection: 

Septic shock



Toxic shock syndrom e



Pneum onia



Retropharyngeal cellulitis

Cardiopulm onary arrest

Essential Workup 

Clinical assessm ent and m anagem ent of airway takes priority over diagnostic workup; secure airway, optim ally in OR under controlled conditions.



Ensure adequate oxygenation before proceeding: o

Pulse oxim etry

Tests Lab 

WBC variably elevated



Blood cultures usually negative

Pa ge 6 9 2



Request tracheal cultures from endoscopist/surgeon.

Imaging Radiographs of neck soft tissue: 

If done, perform in ED; accom pany at all tim es.



Intratracheal m em branes



Tracheal m argin irregularities



Subglottic narrowing



Clouding of tracheal air colum n



Irregular intratracheal densities



Norm al epiglottis

Diagnostic Procedures/Surgery 



Flexible fiberoptic laryngoscopy: o

Perm its direct visualization of epiglottis

o

Mucosal edem a

o

Subglottic edem a, secretions, m em brane

Bronchoscopy: o

Direct visualization of trachea

o

Laryngotracheal inflam m ation and erosions

o

Mucopurulent secretions

o

Mem branes

o

Therapeutic stripping of m em branes

o

Enables direct culture of m aterial

Differential Diagnosis 



Infection: o

Epiglottitis

o

Croup

o

Peritonsillar abscess

o

Retropharyngeal abscess

o

Uvulitis

o

Laryngeal diphtheria

Angioedem a

Pa ge 6 9 3



Intralum inal obstruction: o

Foreign body aspiration



Caustic ingestion



Traum a

P.129

Treatment Pre Hospital 

Assess airway/breathing: o

Supplem ental oxygen

o

Racem ic epinephrine aerosol if easily tolerated

o

Reassurance; avoid agitating child



Bag-valve-m ask (BVM) ventilation if in respiratory failure



Intubate if unable to m aintain airway with BVM and other m easures.



Im m ediate transport



Notify receiving ED of airway status.

Initial Stabilization 

Airway m anagem ent: o

Anticipate difficult airway.

o

Intubation required in 57â€“83%. Active airway m anagem ent ensures stable airway and facilitates suctioning.

o

Intubation should ideally be perform ed in the OR with surgical airway backup.

o

Select an ETT one to two sizes sm aller than usual for age/size.

Pa ge 6 9 4

o

Meticulous ETT care and suctioning.

o

If BVM ventilation needed, use appropriately sized m ask with two-hand seal.

o

Supplem ental hum idified oxygen

ED Treatment 

Continue m onitoring of ventilation and oxygenation.



IV fluids as necessary



Bronchoscopy if not rapidly deteriorating:



o

Assess need for intubation

o

Therapeutic stripping of m em branes

IV antibiotics to cover typical pathogens: o

Cefuroxim e; and nafcillin or vancom ycin

o

Clindam ycin and chloram phenicol for penicillin-allergic patients

Medication (Drugs) 

Cefuroxim e: 50 m g/kg IV; m ax. 3 g



Chloram phenicol: 20 m g/kg IV loading dose



Clindam ycin: 10 m g/kg IV; m ax. 1 g



Nafcillin: 50 m g/kg IV; m ax. 2 g



Racem ic epinephrine: 2.25% solution diluted 1:8 with water in doses of 2â€“4 m L via aerosol



Vancom ycin: 15 m g/kg IV; m ax. 1 g

Follow-Up Disposition Admission Criteria

Pa ge 6 9 5

All patients with suspected or docum ented bacterial tracheitis: 

Adm it to ICU.



Mean ICU length of stay is 2.8 days.

Discharge Criteria None

Issues for Referral Critical care, otolaryngologist, or pulm onologist should be consulted.

References 1. Bernstein T, Brilli R, Jacobs B. Is bacterial tracheitis changing? A 14-m onth experience in a pediatric intensive care unit. Clin Infect Dis . 1998;27:458â€“462. 2. Britto J, Habibi P, Walters S, et al. System ic com plications associated with bacterial tracheitis. Arch Dis Child. 1996;74:249â€“250. 3. Brook I. Aerobic and anaerobic m icrobiology of bacterial tracheitis in children. Pediatr Em erg Care. 1997;13(1):16â€“18. 4. Donnelly BW, McMillan JA, Weiner LB. Bacterial tracheitis: report of eight new cases and review. Rev Infect Dis. 1990;12:729â€“735. 5. Gallagher PG, Myer CM III. An approach to the diagnosis and treatm ent of m em branous laryngotracheobronchitis in infants and children. Pediatr Em erg Care. 1991;7(6):337â€“342.

Miscellaneous See Also: Croup; Epiglottitis, Pediatric

Codes ICD9-CM 464.11 464.10

Pa ge 6 9 6

ICD10 J04.1

Pa ge 6 9 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Barbiturates, Po iso ning

Barbiturates,

Poisoning Sean Patrick Nordt Shaun D. Carstairs David A. Tanen

Basics Description 

Class of sedative-hypnotic agents



Derivatives of barbituric acid



Mechanism : o

Enhances activity of Î³-am inobutyric acid (gam m a-am inobutyric acid [GABA])

o

At high levels, can directly open GABA-A associated calcium channels

o

May inhibit presynaptic release of excitatory neurotransm itters

o

Direct m yocardial depression

o

Inhibition of vascular sm ooth m uscle tone

Diagnosis

Pa ge 6 9 8

Signs and Symptoms 







CNS: o

Lethargy

o

Slurred speech

o

Incoordination

o

Ataxia

o

Com a (can m im ic brain death)

o

Loss of reflexes

Cardiovascular: o

Hypotension

o

Bradycardia

Ophthalm ologic: o

Miosis (generally associated with deep com a)

o

Nystagm us

o

Dysconjugate gaze

Other: o

Respiratory depression

o

Hypotherm ia

o

Bullae or â€œbarb blistersâ€•

Essential Workup 

Check vital signs and gag reflex



Finger stick glucose



Oxygen saturation m onitor/ABG



ECG and continuous cardiac m onitoring



Barbiturate poisoning can m im ic brain death: o

Cannot pronounce patient until barbiturate poisoning has been ruled out in patients in whom it is suspected

Tests Lab 

Electrolytes, blood urea nitrogen/creatinine, glucose:

Pa ge 6 9 9

o 

Calculate anion gap

Urinalysis: o

For m yoglobin

o

For crystalluria (Prim idone)



Creatine phosphokinase for evidence of rhabdom yolysis



Urine toxicology screen



Obtain serum phenobarbital level (if suspected)



Acetam inophen and salicylate levels if suspected suicide attem pt



CBC for other etiologies of altered m ental status



Thyroid function tests

Imaging 

CT scan of head for altered m ental status



Chest radiograph for evidence of aspiration

Diagnostic Procedures/Surgery Lum bar puncture for altered m ental status

Differential Diagnosis 

Sedative-hypnotic poisoning



Carbon m onoxide poisoning



CNS infections



Space-occupying lesions of the head



Hypoglycem ia



Urem ia



Electrolyte im balance (i.e., hyperm agnesem ia)



Postictal state following seizure



Hypothyroidism



Liver failure



Psychiatric illness

Pa ge 7 0 0

Treatment Pre Hospital 

Moderate to severe poisonings require param edic transport.



Intubation often necessary because of respiratory depression or loss of gag reflex



IV access and supplem ental oxygen



Hypotension often requires IV fluids

Initial Stabilization 

ABCs: o

Adm inister supplem ental oxygen

o

Severe poisonings usually require endotracheal intubation



0.9% NS: o

Hypotensive patients require 1â€“2 L IV fluid resuscitation

o

Pressor support m ay be necessary for refractory hypotension



Activated charcoal effectively binds barbiturates and m ay decrease system ic absorption

P.131

ED Treatment 

Adm inister one dose of activated charcoal: o

Consider â€œgut dialysisâ€• with repeated dose activated charcoal (without sorbitol) given q2hâ€“q4h (as long as bowel sounds are present).



Rewarm patient if hypotherm ic (see hypotherm ia chapter).



Treat hypotension resistant to IV fluid bolus with

Pa ge 7 0 1

vasopressors. 

Alkalinize the urine for phenobarbital intoxication to increase excretion (not effective for shorter-acting barbiturates).



Treat hyperkalem ia (from m uscle breakdown) with calcium , sodium bicarbonate, insulin and glucose, and/or potassium -binding agents.





Consider hem odialysis if patient has: o

Decreased or no renal function

o

Prolonged com a

o

Serum phenobarbital level >100 m g/dL

o

Refractory hypotension

Repeat phenobarbital level in 2â€“4 hours to determ ine whether level is increasing.

Medication (Drugs) 

Activated charcoal: 1 g/kg PO



Dopam ine: 5â€“10 m cg/kg/m in titrating to desired effect (to m ax. of 20 m cg/kg/m in)



Sodium bicarbonate: o

Bolus: 1â€“3 am pules (44 m Eq/am pule) IV over 20â€“30 m inutes (peds: 1â€“2 m Eq/kg/dose)

o

Maintenance: 2â€“3 am pules (100â€“150 m Eq) in 1 L D 5 W at 150â€“200 m L/h (peds: 2x m aintenance fluid requirem ents) to achieve a blood pH of 7.45â€“7.50 and m aintain urine output of 2 m L/kg/h (m onitor serum potassium closely)

Follow-Up

Pa ge 7 0 2

Disposition Admission Criteria Intensive care unit adm ission for: 

Com a



Respiratory depression



Hypotension



Hypotherm ia



Rhabdom yolysis

Discharge Criteria Asym ptom atic after m inim um of 6 hours of observation with two consecutive subtoxic phenobarbital levels before discharge

References 1. Frenia ML, Schauben JL, Wears RL, et al. Multiple-dose activated charcoal com pared to urinary alkalinization for the enhancem ent of Phenobarbital elim ination. J Toxicol Clin Toxicol. 1996;34:169â€“175. 2. Lee DC. Sedative-hypnotic agents. In: Goldfrank LR, et al., eds. Goldfrank's Toxicologic Em ergencies., 7th ed. New York: McGraw-Hill, 2002;929â€“945. 3. Pond SM, Olson KR, Osterloh J, et al. Random ized study of the treatm ent of phenobarbital overdose with repeated doses of activated charcoal. JAMA. 1984;251:3104â€“3108.

Miscellaneous See Also: Benzodiazepine, Poisoning; Hypotherm ia

Codes ICD9-CM 967.0

ICD10

Pa ge 7 0 3

T42.3

Pa ge 7 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Baro traum a

Barotrauma

Peter J. Park

Basics Description Injury resulting from the expansion or contraction of gases in an enclosed space

Etiology Mechanism 

Tissue dam age results when a gas-filled space does not equalize its pressure with external pressure.



Boyle's law: At a constant tem perature, pressure (P) is inversely related to volum e (V): o

PV = K (constant) or P 1 V 1 = P 2 V 2

o

As pressure increases/decreases, volum e decreases/increases.



Solid and liquid-filled spaces distribute pressure equally.



Volum e changes experienced during diver ascent are greatest in the few feet nearest the surface.



Gas-filled cavities in the body are subject to expansion/contraction: o

Middle ear: 

Barotraum a of descent

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

Most com m on type of barotraum as



Seen in 30% of inexperienced divers and 10% of experienced divers



Inadequate equalization of pressure between m iddle ear and external ear canal



Eustachian tube provides sole route of pressure equalization for m iddle ear.



Inadequate clearance via eustachian tube leads to increasingly negative pressure gradient across tym panic m em brane (TM)

o

External ear: 

Barotraum a of descent



Pressure cannot equalize throughout canal because of blockage, and relative intracanal vacuum is created as pressure differential across obstruction increases.

o

Inner ear: 

Barotraum a of descent



Results from forceful attem pts at equalizing m iddle ear pressure (Valsalva, Frenzel m aneuvers)



Increased m iddle ear pressure can raise intracranial pressure and cause rupture of round or labyrinth windows, allowing perilym ph to enter m iddle ear.

o

Paranasal sinus: 

Barotraum a of descent



Nasal ostia act as valves to regulate sinus pressure.



If ostia fail to allow pressure equalization, congestion, edem a, and hem orrhage can occur.

o

External objects:

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

Air pockets in dive suit/m ask expand and contract.

o

Teeth; 

o

Air trapped inside a filling

GI: 

Barotraum a of ascent



Swallowed air in GI tract expands as external pressure decreases.

o

Pulm onary: 

Barotraum a of ascent



Lungs expand against closed glottis (breath-holding).



Can lead to pulm onary rupture



Potential arterial gas em bolism (see Arterial Gas Em bolism )



Divers with decreased lung com pliance/increased lung volum es at increased risk (chronic obstructive pulm onary disease [COPD], asthm a)

Diagnosis Signs and Symptoms 

Middle ear (barotitis m edia): o

Begins as clogged sensation

o

Increasingly painful as pressure differential increases across TM

o

Progresses to rupture of TM

o

TM appearance: 

Progresses from TM congestion to edem a to hem orrhage to TM rupture

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

External ear: o

May result from tight-fitting hood, earplug or earwax occluding canal

o

Auditory canal m ucosa becom es edem atous, then hem orrhagic, and ultim ately tears







Inner ear: o

Sudden, severe vertigo

o

Tinnitus

o

Sensineural hearing loss in affected ear

Paranasal sinuses (barosinusitis): o

Sinus congestion

o

Pain

o

Epistaxis

Facial: o

Occlusive dive m ask: conjunctival hem orrhage, facial edem a, and swelling



Extrem ities: o

Tight-fitting dive suit: edem a and erythem a of the skin at locations of air pockets



Teeth (barodontalgia): o





Severe tooth pain: possible air trapped in fillings

GI (aerogastralgia): o

Excessive belching

o

Flatulence

o

Abdom inal distention

Pulm onary (pulm onary barotraum a [PBT], or pulm onary overpressurization syndrom e): o

Dyspnea: â€œthe chokesâ€•

o

Cough productive with frothy red sputum

o

Subcutaneous em physem a

o

Delayed sym ptom s include bull neck appearance, dysphagia, changes in voice character

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Essential Workup 

Head, ears, eyes, nose and throat (HEENT) exam with particular attention paid to TM and auditory canal to determ ine if rupture has occurred



Pulm onary exam looking for signs of subcutaneous em physem a and pneum othorax



Neurologic exam looking for signs of inner ear pathology

Tests Lab Arterial blood gas (ABG) for pulm onary sym ptom s

Imaging 

Sinus im aging: o

CT

o

Plain film s



Chest radiograph for pneum othorax



Abdom inal series (upright, decubitus) for free air from a ruptured viscus

Differential Diagnosis 

Decom pression sickness



Otitis m edia



Otitis externa



Sinusitis

P.133

Treatment

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Pre Hospital 

Cautions: o

For barotraum a of descent, unless air-filled cavity has ruptured, no progression of disease on return to norm al atm ospheric pressure is to be expected.

o

If patient requires air evacuation, m aintain air cabin pressure at 1 atm or fly below 1,000 feet to avoid aggravating barotraum as.

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

One hundred percent oxygen for ill-appearing patients



Intubation for patients with subcutaneous em physem a of neck



Im m ediate needle thoracostom y for evidence of tension pneum othorax

ED Treatment 

Establish IV access for unstable patients.



Control bleeding from ear or nose.



Decongestants for m iddle ear or sinus congestion



Antibiotics with TM or sinus rupture



Analgesics

Medication (Drugs) 

Am oxicillin: 250â€“500 m g (peds: 40 m g/kg/24 h) PO t.i.d.



Oxym etazoline 0.05% (Afrin): 2 or 3 drops/sprays per nostril b.i.d. for 3 days



Pseudoephedrine (Sudafed): 60 m g (peds: 6â€“12 years old, 30 m g; 2â€“5 years old, 15 m g per dose) PO q4hâ€“q6h

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

Trim ethoprim -sulfam ethoxazole (Bactrim DS): 1 tablet double strength (160 m g/800 m g) (peds: 40 m g/200 m g per 5 m L, 5 m L/10 kg per dose) PO b.i.d.

Follow-Up Disposition Admission Criteria 

Pulm onary barotraum as (PBTs)



Inner ear barotraum a with round window rupture or severe vertigo

Discharge Criteria 

Most non-PBT



Ear, nose, and throat (ENT) follow-up for severe TM or sinus pathology

References 1. Becker GD, Parell GJ. Barotraum a of the ears and sinuses after scuba diving. Eur Arch Otorhino. 2001;258(4):159â€“163. 2. Kizer KW. Diving m edicine and barotraum a. In: Auerbach PA, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001. 3. Moon RE, Gorm an DF. Treatm ent of decom pression disorders. In: The Physiology and Medicine of Diving. 5th ed. Philadelphia: WB Saunders; 2003. 4. Raym ond LW. Pulm onary barotraum a and related events in divers. Chest. 1995;107:1648â€“1652. 5. Tetzlaff K, et al. Risk factors for pulm onary barotraum a in divers. Chest. 1997;112(3): 654â€“659.

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Miscellaneous SEE ALSO: Arterial Gas Em bolus; Decom pression Sickness; Hyperbaric Oxygen Therapy

Codes ICD9-CM 993.2 Barotraum a 993.2 Odontalgia 993.0 Otitic 993.1 Sinus

Pa ge 7 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bartho lin Abscess

Bartholin Abscess

Marilyn Althoff Mark Mandell

Basics Description 

The Bartholin glands are located inferiorly on either side of vaginal opening: o



Ducts open on sides of labial vestibule.

Obstruction of duct produces a usually painless cyst: o

Infection of cyst results in abscess form ation.

Epidemiology Prevalence Most com m on in wom en aged 20â€“40 years

Etiology 

Anaerobic and aerobic m icroflora norm ally found in vagina:



o

Bacteroides species

o

Peptostreptococcus species

o

Escherichia coli

o

Other Gram -negative organism s

Occasionally Neisseria gonorrhoeae and Chlam ydia trachom atis

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Diagnosis Signs and Symptoms 

Swollen, painful labia



Tender, fluctuant m ass on posterolateral m argin of vestibule of vagina



Warm th, erythem a

Essential Workup Diagnosis based on findings of tender, localized, fluctuant m ass in region of Bartholin gland

Tests Lab 

Culture m aterial from abscess for gonorrhea and chlam ydia.



Culture cervix for gonorrhea and chlam ydia.

Differential Diagnosis 

Bartholin cyst



Carcinom a of Bartholin gland (rare)



Perineal hernia

Treatment ED Treatment 

Prom pt incision and drainage using local anesthesia with patient in lithotom y position



Narcotic analgesia for patient com fort



Alternative approaches include:

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

o

Sim ple incision and drainage

o

Word catheter m ethod

o

Marsupialization

Antibiotics not necessary after incision and drainage: o

If m ild cellulitis present or patient im m unocom prom ised, broad-spectrum coverage m ay be started.

o

If sexually transm itted disease suspected, treat with antibiotics.



Sim ple incision and drainage: o

After local anesthesia, palpate abscess between thum b and index fingers.

o

Spread vulva apart and m ake stab incision on m ucosal surface of abscess, parallel to hym enal ring.

o

When incising abscess, two tissue layers m ust be penetrated: 

First the labial m ucosa



Then abscess wall



Free flow of pus indicates penetration of abscess wall.

o

Pack wound with gauze.

o

Follow up in 24â€“48 hours for rem oval of packing.

o

Start sitz baths after 24 hours.

o

Consider referral for m arsupialization to avoid recurrence.



Word catheter m ethod: o

Use sm all, inflatable, bulb-tipped Word catheter to treat abscess.

o

May avoid recurrence and m ake m arsupialization unnecessary

o

Stab wound is m ade as with sim ple incision and drainage:

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

It should be just large enough to easily adm it catheter so that balloon does not fall out after inflation.

P.135

o

After inserting bulb tip of catheter, inflate balloon by injecting 2â€“4 m L water using 25-gauge needle (to m inim ize size of puncture): 

Overinflation m ay cause patient discom fort,



Rem edied by withdrawing som e water from balloon

o

Sitz baths m ay be started after 24 hours.

o

Follow-up in 2â€“4 days.

o

Leave catheter in place for 6â€“8 weeks until epithelialization is com plete; after device is rem oved, gland resum es norm al function.

o

Com m on for catheter to fall out prem aturely: 

If this occurs, catheter m ay be reinserted or abscess can heal as with sim ple incision and drainage.



Marsupialization: o

Procedure allows for a perm anent fistula by suturing wound edges of abscess cavity to edges of labial m ucosa: 

Technically m ore challenging in ED and better reserved for specialist.

o

Excise an ellipse of labial m ucosa that overlays cyst cavity.

o

Incision and drainage of abscess

o

Evert edges of abscess and suture them to labial epithelium using absorbable suture:

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

Opening will shrink but rem ain patent.



Packing is not needed.

o

Start sitz baths in 24â€“48 hours.

o

Follow-up within 1 week.

Medication (Drugs) Broad-spectrum coverage: 

Am oxicillin/clavulanic acid: 875 m g PO b.i.d. for 5 days with m etronidazole 500 m g PO b.i.d. for 5 days



Ciprofloxacin: 500 m g PO b.i.d. for 5 days with m etronidazole 500 m g PO b.i.d. for 5 days

Follow-Up Disposition Admission Criteria 

Sepsis



Significant cellulitis



Evidence of necrotizing infection

Discharge Criteria Well-appearing patients m ay be discharged with designated follow-up plan.

References 1. Aghajanian A. Bartholin's duct abscess and cyst: a case control study. South Med J. 1994;87:26â€“29. 2. Brook I. Aerobic and anaerobic m icrobiology of Bartholin's abscess. Surg Gynecol Obstet. 1989;169:32â€“34. 3. Van Bogaert LJ. Managem ent of Bartholin's abscess. World Health

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Forum . 1997;18:(2)200â€“201. 4. Word B. Office treatm ent of cyst and abscess of Bartholin's gland duct. South Med J. 1968;61:514â€“518. 5. Zeger W, Holt K. Gynecologic infections. Em erg Med Clin North Am . 2003;21(3):631â€“648.

Codes ICD9-CM 616.3 Abscess of Bartholin gland

ICD10 N75.1 Abscess of Bartholin gland

Pa ge 7 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bell's Palsy

Bell's Palsy

Robert F. McCormack Richard S. Krause

Basics Description 

Acute, idiopathic peripheral palsy of CN VII (facial nerve)



Com plete recovery in 85% of cases without treatm ent



Degree of deficit correlates with prognosis:



o

Com plete lesions have poorest prognosis.

o

Partial lesions often have excellent results.

Recovery usually begins within 2 weeks (often taste returns first) and is com plete by 2â€“3 m onths: o

Advanced age and slow recovery are poor prognosticators.



Affects m en and wom en equally



Age predom inance between the third and fifth decade (m ay occur at any age)



Incidence 15â€“40 per 100,000 per year

Etiology 

Innervation to each side of forehead is from both m otor cortices: o

Unilateral cortical processes do not com pletely disrupt m otor activity of forehead.

Pa ge 7 1 9

o

Only peripheral or brainstem lesion can interrupt m otor function of just one side of forehead.



Idiopathic by definition, but viral cause (particularly herpes sim plex) suspected



Lym e disease, infectious m ononucleosis (Epstein-Barr virus [EBV] infection), varicella-zoster infections, and others m ay cause peripheral seventh nerve palsy.



Mechanism : edem a and nerve degeneration within stylom astoid foram en

Diagnosis Signs and Symptoms 

Sudden onset of unilateral facial droop, incom plete eyelid closure, and loss of forehead m uscle tone: o

Maxim al deficit by 5 days in alm ost all cases (2 days in 50%)



If forehead m uscle tone is not lost, a central lesion is strongly im plied (i.e., this is not Bell's palsy)



Tearing (68%) or dryness of eye (16%) and less frequent blinking on affected side



The Bell phenom enon (upward rolling of the eye on attem pted lid closure) m ay be seen.



Subjective â€œnum bnessâ€• of the affected side



Abnorm al taste, drooling



Hyperacusis (sensitivity to loud sounds)



Fullness or pain behind m astoid



Viral prodrom e frequently reported

Essential Workup 

Diagnosis is clinical and based on history and physical

Pa ge 7 2 0

exam . 

Motor weakness isolated to seventh nerve distribution: o



Involves both upper and lower face

An otherwise norm al neurologic exam including all cranial nerves and extrem ity m otor function

Tests Lab 

Not helpful in diagnosis of Bell's palsy



Lym e titers are useful when Lym e disease is suspected or in endem ic area



Tests for m ononucleosis (CBC, Monospot) if EBV infection suspected

Imaging 

Not helpful in diagnosis of Bell's palsy



CNS im aging (CT, MRI) useful if CNS pathology is suspected

Differential Diagnosis 

Brainstem events (m ass, bleed, infarct) affecting CN VII alm ost always involve CN VI (abnorm al EOM) and m ay affect long m otor tracts: o

There have been (rare) case reports of isolated CN VII palsy from brainstem disease.



Lym e disease: history of tick bite, erythem a m igrans rash, or endem ic area



Zoster (Ram say-Hunt syndrom e): Look for herpetic vesicles, inquire about tinnitus or vertigo.



Infectious m ononucleosis: look for pharyngitis, posterior cervical adenopathy



Tum ors: parotid, bone, or m etastatic m asses, acoustic neurom a (deafness)

Pa ge 7 2 1



Traum a: Skull fracture or penetrating facial injury m ay dam age CN VII.



Middle ear or m astoid surgery or infection, cholesteatom a



Meningeal infection



Guillain-BarrÃ© syndrom e: other neurologic deficits (e.g., ascending m otor weakness or dim inished deep tendon reflexes [DTRs] present)



Basilar artery aneurysm ; other CN deficits should be present.



Bilateral peripheral CN VII palsy: Consider m ultiple sclerosis, sarcoid, leukem ia, and Guillain-BarrÃ© idiopathic (Bell's) palsy m ay be bilateral in rare cases.



Bell's palsy m ay reoccur; treatm ent is unchanged.

P.137

Treatment Initial Stabilization Patients with an isolated peripheral CN VII palsy are stable.

ED Treatment 

Oral steroids m ay hasten recovery if started within 1 week of onset: o

Com plications of therapy are rare and treatm ent is recom m ended by m any authors.

o 

Som e m eta-analyses question efficacy.

Corneal dam age m ay result from incom plete eyelid closure: o

Lubricating and hydrating ophthalm ic preparations is

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essential/ o 

Eyelid taping at night

Acyclovir with steroids m ay be effective in im proving functional nerve recovery: o



Initiate within 72 hours of sym ptom onset.

Suspected Lym e disease should be treated with doxycycline or am oxicillin.



Surgical decom pression m ay be indicated for com plete lesions that do not im prove; this is controversial.

Medication (Drugs) 

Acyclovir: 400 m g five tim es per day PO for 7 days (peds: no data to support its use) or valacyclovir 1 g PO for 7 days



Lacri-Lube: at bedtim e and PRN; dryness/irritation in affected eye (or equivalent)



Prednisone: 30â€“40 m g PO b.i.d. (or 60 m g PO daily) for 5 days, then taper over 5 days; total 10 days of therapy (peds: 2 m g/kg/d PO [m ax. 60 m g])

Follow-Up Disposition Admission Criteria Isolated peripheral CN VII palsy does not require adm ission.

Discharge Criteria 

Isolated peripheral CN VII palsy m ay be treated on outpatient basis.



Follow-up should be within 1 week.

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References 1. Adour K, et al. Bell's palsy treatm ent with acyclovir and prednisone com pared with prednisone alone. Ann Otol Rhinol Laryngol. 1996;105:371â€“378. 2. Austin JR, et al. Idiopathic facial nerve paralysis: a random ized double blind controlled study of placebo versus prednisone. Laryngoscope. 1993;103:1326â€“1333. 3. Gilden D. Bell's palsy. N Engl J Med. 2004; 351:1323â€“1231. 4. Grogan PM, et al. Practice param eter: steroids, acyclovir, and surgery for Bell's palsy (an evidence-based review). Neurology. 2001; 56(7):830â€“836. 5. Ram sey JR, et al. Corticosteroid treatm ent for idiopathic facial nerve paralysis: a m eta-analysis. Laryngoscope. 2000;110:335â€“341. 6. Salinas R, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2004;4:CD001942.

Codes ICD9-CM 351.0

ICD10 G51.0

Pa ge 7 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Benz o diaz epine, Po iso ning

Benzodiazepine, Poisoning Sean Bryant

Basics Description 

Acts to potentiate activity of Î³-am inobutyric acid (GABA; m ajor inhibitory neurotransm itter) by binding to its own specific site



Facilitates GABA binding to its site



Results in chloride influx, m em brane hyperpolarization, and inhibition of cellular excitation: o

Highly protein bound

o

Large V d

o

Hepatic m etabolism

o

Duration of action is inversely proportional to lipophilicity.

o

Duration of lorazepam > diazepam > m idazolam .

Diagnosis Signs and Symptoms 

CNS:

Pa ge 7 2 5









o

Sedation/drowsiness

o

Slurred speech

o

Com a

o

Delirium

o

Midposition to sm all pupils

Neurom uscular: o

Incoordination

o

Slowed voluntary m ovem ents

o

Ataxia

o

Hypotension

o

Hyporeflexia/areflexia

Cardiovascular: o

Mild depression

o

Rare fatality

Respiratory: o

Mild depression

o

Less depression versus barbiturates

o

Short acting and IV m ay produce depression.

GI: o



Nausea, vom iting, diarrhea

Other: o

Hypotherm ia

o

Com plications m ay include cerebral hypoxia, rhabdom yolysis, pressure-induced neuropathies.

o

No long-term organ toxicity

Essential Workup Diagnosis based on: 

History of ingestion or recent injection



Clinical findings associated with CNS depression



No response to naloxone

Tests

Pa ge 7 2 6

Lab 

Pulse oxim etry



Electrolytes, BUN, creatinine, serum glucose



Urinalysis (UA) for m yoglobin when com a present



Core body tem perature



Arterial blood gas (ABG)



Qualitative urine screen: o

Confirm s exposure m any tim es, but does not indicate or m easure intoxication

o

False-negative test results reported

o

Qualitative im m unoassays detect only benzodiazepines (BZs) that are m etabolized to oxazepam .

o

Those that do not produce this m etabolite (clonazepam , lorazepam , m idazolam , alprazolam ) are not detected on qualitative screen.

o

Do not correlate with clinical state

o

Serum levels not acutely practical

o

Clinical signs and sym ptom s m ore im portant than theoretic LD 5 0 or serum levels



Alcohol(s) level



Barbiturate level



Acetam inophen and salicylate levels



Pregnancy test

Imaging 

ECG



Chest radiograph for aspiration pneum onia

Differential Diagnosis 

Drugs and toxins causing decreased level of consciousness: o

Hypoglycem ics

o

Other sedative-hypnotics (barbiturates)

Pa ge 7 2 7



o

Antidepressant-antipsychotic

o

Narcotics

o

Anticonvulsants

o

Carbon m onoxide/cyanide

o

Alcohols

Nontoxic m edical condition: o

Hypoxem ia

o

Hypotherm ia

o

Head traum a (intracranial bleeding)

o

Infection (m eningitis or encephalitis)

o

Electrolyte and m etabolic disturbances

Treatment Pre Hospital 

Attention to airway and breathing



Cardiac m onitor



IV access



Rapid glucose determ ination



Bring in pill bottles/pills in suspected overdose.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Secure airway and assist ventilation with supplem ental oxygen to prevent hypoxem ia and shock.



o

IV access with 0.9% norm al saline (NS)

o

Cardiac m onitor

Adm inister naloxone, thiam ine, and dextrose if altered m ental status.

P.139

Pa ge 7 2 8

ED Treatment 

Gastric lavage considered only when presents within 1 hour of life-threatening ingestion with protected airway



Activated charcoal (AC) PO or via nasogastric tube (NGT)



No role for diuresis, dialysis, or charcoal hem operfusion



Flum azenil (FZ): o

Com petitive BZ-receptor inhibitor: rapidly reverses BZ-induced com a and respiratory depression

o

Onset within 1â€“2 m inutes; peak at 6â€“10 m inutes; duration 1â€“2 hours (repeated dosing m ay be indicated)

o

Efficacy dependent on dose of BZ being antagonized and dose of FZ used

o

Do not adm inister em pirically as part of any standard protocol therapy or in unknown poisoned patient.

o

Might help avert need of airway intubation

o

May be beneficial in shortening hospital stay or as diagnostic m aneuver

o

Indications include isolated BZ overdose in nonhabituated user.

o

Useful to reverse iatrogenic poisoning (conscious sedation)

o

Contraindications include: 

Coingestions that m ight lower seizure threshold (tricyclic antidepressants [TCAs])



Seizure activity



Allergy



Neurom uscular blockade



Do not use if hypotension, hypoxia, dysrhythm ias, or increased intracranial pressure

Pa ge 7 2 9



May precipitate withdrawal state

Medication (Drugs) 

AC: 1â€“2 g/kg PO/NG (ideal 10:1 ratio)



Dextrose: D 5 0 W one am pule: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



FZ (Rom azicon): o

Initial: 0.2 m g IV over 30 seconds (adult)

o

If no response: 0.3 m g IV after 30 seconds

o

If still no response: 0.5 m g IV and repeat every 1 m inute if needed, to m ax. dose of 3 m g

o

Continuous infusion at 0.2â€“1.0 m g/h if m ultiple repeated doses required to m aintain response

o

Pediatric dosing not established; recom m ended starting dose is 0.01 m g/kg IV, titrate to m ax. dose of 1 m g, continuous infusion at 0.005â€“0.01 m g/kg/h



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IV initial dose



Thiam ine (vitam in B 1 ): 100 m g IV/IM

Follow-Up Disposition Admission Criteria 

Persistent or profound CNS depression



Cardiovascular or respiratory com prom ise



Coingestants with potential delayed toxicity

Discharge Criteria

Pa ge 7 3 0



Discharge after 4- to 6-hour observation period if no signs or sym ptom s of BZ poisoning develop.



If FZ used, observe for additional 2â€“4 hours for recurrent sedation.

Issues for Referral Intentional overdose: 

Psychiatry consultation

References 1. Farrell SE. Benzodiazepines. In: Ford MD, Delaney KA, Ling LJ, et al, eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 2. Lee DC. Sedative-hypnotic agents. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. New York: McGraw-Hill; 2002. 3. Leikin J, Paloucek F. Benzodiazepines, qualitative, urine. In: Poisoning and Toxicology Handbook. Hudson, OH: Lexi-Com p; 2002. 4. Rasanen I, Ojanpera I, Vuori E. Quantitative screening for benzodiazepines in blood by dual-colum n gas chrom atography and com parison of the results with urine im m unoassay. J Anal Toxicol. 2000;24:46â€“53. 5. Spivey WH. Flum azenil and seizures: analysis of 43 cases. Clin Ther. 1992;14:292. 6. Spivey WH, Roberts JR, Derlet RW. A clinical trial of escalating doses of flum azenil for reversal of suspected benzodiazepine overdose in the em ergency departm ent. Ann Em erg Med. 1993; 22:1813â€“1821. 7. Weinbroum A, et al. The use of flum azenil in the m anagem ent of acute drug poisoning: a review. Intensive Care Med. 1991;17:32â€“38.

Codes ICD9-CM 969.4

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ICD10 T42.4

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Beta-Blo cker Po iso ning

Beta-Blocker

Poisoning Janet Eng

Basics Description Normal Physiology Cardiovascular: Î² 1 -receptors: 

ATP converted to cAMP by adenyl cyclase with stim ulation of Î²-receptors



cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasm ic reticulum .



Sarcoplasm ic reticulum releases calcium .



Excitation-contraction coupling occurs.

Effects of Î²-Blockers 

Cardiovascular: o

Decreased excitation/contraction

o

Mem brane stabilizing activity

o

Sodium channel blockade causes a prolongation of the QRS com plex (with som e agents).

o

Prolongation of QTc interval leading to ventricular dysrhythm ias (with som e agents)

o

Intrinsic sym pathom im etic activity

Pa ge 7 3 3

o 

Partial agonist properties (with som e agents)

Neurologic: o

CNS effects with the lipophilic agents (propranolol, m etoprolol, labetalol)

Diagnosis Signs and Symptoms 







Cardiovascular: o

Hypotension

o

Bradycardia

o

Cardiac conduction delays

o

Heart block

o

Heart failure

o

Electrical m echanical dissociation

o

Loss of Î²-selectivity in overdose settings

Neurologic: o

Com a

o

Seizures

Pulm onary: o

Bronchospasm

o

Pulm onary edem a

Metabolic: o

Hypoglycem ia

Essential Workup 

With unknown ingestion: suspect Î²-blocker poisoning with bradycardia/hypotension



ECG: o

Conduction delays

o

First-, second-, or third-degree heart block

Pa ge 7 3 4

o

Bradycardia

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose

Differential Diagnosis 

Calcium channel blocker toxicity



Clonidine toxicity



Digoxin toxicity



Acute m yocardial infarction with heart block

Treatment Pre Hospital CAUTIONS: 

Transport pills and pill bottles when overdose suspected.

Initial Stabilization 

Airway, breathing, circulation (ABCs): o

Airway protection as indicated by m ental status

o

Supplem ental oxygen as needed

o

0.9% norm al saline (NS) IV access

o

Close hem odynam ic m onitoring



Naloxone and thiam ine if altered m ental status



Accu-Chek and treat hypoglycem ia with D 5 0 W.



Treat prolonged seizures with benzodiazepines.

ED Treatment Goals 

Heart rate >60 beats per m inute

Pa ge 7 3 5



Systolic BP >90 m m Hg



Adequate urine output



Im proving level of consciousness

GI Decontamination 

Syrup of ipecac is contraindicated in the em ergency departm ent.



Consider lavage with Ewald tube if ingestion within 1 hour: o

Propranolol m ay cause esophageal spasm producing difficulty with passage and rem oval of gastric lavage tube



Activated charcoal helpful especially in the presence of coingestants

Bradycardia/Hypotension 



Atropine: o

Initial agent

o

Low success rate

Glucagon: o

Adm inister if atropine does not increase heart rate.

o

Prom otes cAMP production through a receptor site other than the Î²-receptor



o

May cause nausea and vom iting

o

Mix with NS or D 5 W

IV fluids: o

Adm inister cautiously in the hypotensive patient

o

Swan-Ganz catheter or central venous pressure (CVP) m onitoring to help follow volum e status



Am rinone: o

Use in conjunction with glucagon to treat sym ptom atic sustained bradycardia.

P.141

Pa ge 7 3 6



Pressor agents: o

Initiate when sym ptom atic hypotension/bradycardia persists after atropine/glucagon.

o

Use invasive m onitoring to help guide therapy.

o

Utility m ay be lim ited owing to Î²-blockade: 

o

Isoproterenol (nonselective Î²-agonist): 

o

Higher doses m ay be required.

Titrate for blood pressure (BP) and heart rate

Epinephrine (potent Î±- and Î²-receptor agonist): 

BP increases as a result of direct m yocardial stim ulation, increase in heart rate, and vasoconstriction

 o 

Use if no BP response with isoproterenol

High-dose dopam ine

Sodium bicarbonate: o

In theory, this is used if there is evidence of prolongation of QRS >100 m s owing to som e of the Î²-blockers also causing sodium channel blockade leading to a prolonged QRS.

o 

Not routinely adm inistered for all Î²-blocker toxicities

Electrical pacing: when other treatm ent options have failed



Insulin: o

Prom otes m ore efficient m yocardial m etabolism

o

May be considered as a treatm ent option

Enhanced Elimination Hem odialysis helpful with water-soluble Î²-blocking agents: 

Nadolol



Atenolol



Sotalol

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Medication (Drugs) 

Activated charcoal: 1 g/kg PO



Am rinone: loading dose 0.75 m g/kg; m aintenance drip 2â€“20 Âµg/kg/m in; titrate for effect



Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5â€“1.0 m g IV (peds: 0.04 m g/kg)



Dopam ine: 2â€“20 Âµg/kg/m in IV



Dextrose: D 5 0 W 1 am pule (50 m L or 25 g; peds: D 2 5 W 2â€“4 m L/kg) IV



Epinephrine: 2 Âµg/m in (peds: 0.1 Âµg/kg/m in); titrate to effect



Glucagon: 3.5â€“5 m g IV (peds: 0.03â€“0.1 m g/kg) bolus followed by 70-Âµg/kg/h infusion



Isoproterenol: 5 Âµg/m in IV and titrate for heart rate effect



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sodium bicarbonate: 1 m Eq/kg IVP



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

ICU adm ission for decreased level of consciousness or hem odynam ic instability (bradycardia, conduction delays, hypotension)



Observation and m onitoring for 24 hours for long-acting or sustained-release preparations owing to the potential

Pa ge 7 3 8

delay in sym ptom s

Discharge Criteria Asym ptom atic 8â€“10 hours after ingestion of short- or im m ediate-release preparation

References 1. DeWitt CR, Waksm an JC. Pharm acology, pathophysiology and m anagem ent of calcium channel blocker and Î²-blocker toxicity. Toxicol Rev. 2004;23:223â€“238. 2. Kerns W, Schroeder D, William s C, et al. Insulin im proves survival in a canine m odel of acute beta-blocker toxicity. Ann Em erg Med. 1997;29:748â€“757. 3. Love J. Acebutolol overdose resulting in fatalities. J Em erg Med. 2000;18:341â€“344. 4. Love J, Howell J. Glucagon therapy in the treatm ent of sym ptom atic bradycardia. Ann Em erg Med. 1997;29:181â€“183.

Miscellaneous SEE ALSO: Calcium Channel Blocker, Poisoning

Codes ICD9-CM 977.9

ICD10 T44.7

Pa ge 7 3 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bio lo gic Weapo ns

Biologic Weapons

Ian Greenwald

Basics Description 

Defined as naturally occurring organism s or toxins that are purified and prepared for m ass dissem ination with intent of causing m ass m orbidity, m ortality, and social disruption



Over 400 potential or actualized etiologic agents capable of being used as biological weapon: o

Characterized by their relatively low cost com pared with other weapons of m ass destruction (WMD), high potency, and their ability to be delivered in stealth m anner

o

Stealth quality of biologic weapons com es from organism 's natural incubation period.



Easy to conceal and difficult to detect: o

Agents often invisible to naked eye, odorless, and tasteless



Patients typically present to various health care facilities with host of com m on com plaints, adding to delay in recognition of covert release of biologic weapon.



Victim s of biologic warfare agents are exposed either via direct cutaneous contact with agent, respiratory inhalation

Pa ge 7 4 0

of aerosolized agent, or via GI tract after poisoning of food or water source.

Etiology 

Bacteria: o

Anthraxâ€”Bacillus anthracis

o

Plagueâ€”Yersinia pestis

o

Choleraâ€”infection from Vibrio cholerae: Presents with severe gastrointestinal sym ptom s and rapidly leads to profound dehydration



o

Tularem iaâ€”Francisella tularensis

o

Brucellosisâ€”organism in the Brucella genus

o

Q feverâ€”Coxiella burnetii

Viruses: o

Sm allpoxâ€”variola virus

o

Viral encephalitidesâ€”m em bers of Alphavirus genus (Venezuelan equine encephalitis, Eastern equine encephalitis, and Western equine encephalitis)

o

Viral hem orrhagic feversâ€”from four fam ilies of viruses, includes illnesses such as Ebola, Marburg, Lassa and dengue fever

Diagnosis Signs and Symptoms 

Health care providers need to be alert to detect illness patterns and diagnostic clues that indicate biologic weapon release.



Indications of intentional release of agent include: o

Geographic clustering of illnesses with individuals who live, work, or attended event in close proxim ity

Pa ge 7 4 1

(if m ultiple people who work in sam e office develop pneum onia, it could potentially represent respiratory pathogen release) o

Unusual age distribution for com m on illness (chickenpoxlike illness am ong adult patients could represent sm allpox release)

o

Two or m ore patients presenting with sim ilar unexplained illnesses (two patients presenting with flaccid paralysis could represent botulinum toxin release)

o

Single case of illness caused by uncom m on agent (sm allpox, inhalational anthrax)

o

High volum e of patients with sim ilar presentation of sym ptom s associated with escalating m orbidity and m ortality

Anthrax 



Inhalational anthrax: o

Fever

o

Chills

o

Fatigue, m alaise, lethargy

o

Cough, usually dry or m inim ally productive

o

Nausea or vom iting

o

Dyspnea

o

Diaphoresis

o

Chest pain

o

Myalgias

o

Tachycardia

o

Fever

o

Meningeal signs

Cutaneous anthrax: o

Skin lesion: 

Painless pruritic papule

Pa ge 7 4 2



Turning into vesicle that ruptures form ing necrotic ulcer

o

Black eschar

o

Surrounding gelatinous nonpitting edem a

Plague 

Abrupt onset



Fever, chills



Cough, hem optysis, dyspnea



Headache



Vom iting



Swollen tender lym ph nodes (buboes)



Skin lesions at site of inoculation (i.e., flea bite)



Confusion



Abdom inal pain



Oliguria



Obtundation



Extensive ecchym osis



Acral gangrene (digits, nose, penis)

Tularemia 

See Tularem ia chapter.



Typhoidal: o

Most likely form of disease when weaponized and delivered by aerosol

o

Fever, headache, m alaise

o

Nonproductive cough

o

Thirty-five percent m ortality if untreated

Q fever 

Incubation period 10â€“40 days



Flulike sym ptom s and pleuritic chest pain for 2â€“10 days



Chest radiograph shows patchy infiltrates.



Definitively diagnosed serologically

Pa ge 7 4 3



Mortality: o

Less than 1% even if untreated

Smallpox 

Incubation period 7â€“17 days (average is 12 days)



Flulike sym ptom s (fever, fatigue, m yalgias, headache) for about 2â€“3 days followed by characteristic rash o

Progresses from m acules to papules to pustular lesions and crusted lesions

o

Starts on face and extrem ities (including palm s/soles) and spreads to trunk in 1 week

o 

Scabs over in 1â€“2 weeks

Mortality: o

30% if untreated

Hemorrhagic Fevers 

See Hem orrhagic Fever chapter.



Incubation period 1â€“3 weeks



Starts as flulike syndrom e with fever, m alaise, m yalgias, headache, and sore throat



Afterward, infectious gastroenteritis syndrom e, rash, and renal/hepatic dysfunction



Finally, hem orrhagic sym ptom s develop around the fifth day followed by shock and death: o

Mortality in 50â€“90% for Ebola if untreated

Essential Workup Suspect bioterrorism if: 

Multiple cases of relatively young, healthy patients who present with flulike syndrom e and within days deteriorate rapidly



Typical cutaneous lesions appear.

Tests

Pa ge 7 4 4

Lab 

CBC



Electrolytes, BUN, creatinine



Arterial blood gas (ABG)



Cerebrospinal fluid (CSF): o

Anthraxâ€”50% with inhalation anthrax develop hem orrhagic m eningitis.



Coagulation studies: o

Plagueâ€”dissem inated intravascular coagulation (DIC)



Blood cultures



Wound cultures



Alert laboratory personnel to potential concerns of clinicians.

P.143

Imaging Chest radiograph: 

Anthraxâ€”m ediastinal widening, pulm onary infiltrate/consolidation, pleural effusion



Plagueâ€”bronchopneum onia

Differential Diagnosis 



Anthrax: o

Influenza

o

Bacterial pneum onia

o

Bacterial m eningitis

o

Brown recluse spider bite

o

Tularem ia

o

Streptococcal/staphylococcal skin infection

Plague:

Pa ge 7 4 5





o

Tularem ia

o

Catscratch disease

o

Lym phogranulom a venereum

o

Chancroid

o

Tuberculosis

o

Streptococcal adenitis

o

Meningitis

o

Encephalitis

o

Sepsis

Sm allpox: o

Varicella

o

Rash starts centrally on trunk and spreads outward: 

Lesions in different stages of developm ent



Rarely involves palm s or soles



Dissem inated m olluscum contagiosum

o

Monkeypox

o

Drug eruptions

Toxins: o

Staphylococcal enterotoxin B: 

Most com m on cause of food poisoning



Can be aerosolized in addition to being placed in food or water reservoir



When inhaled, produces febrile type of illness that can progress to septic shock picture

o

Ricin: 

Plant protein derived from castor beans



Causes rapid progression from upper respiratory congestion to cardiopulm onary collapse



Ingestion is less toxic because GI tract does not absorb it well, but it can lead to local cytotoxic death, shock, and death.

Pa ge 7 4 6

o

Botulinum toxin: 

Initially sym ptom s include cranial nerve dysfunction with descending paralysis that leads to respiratory failure.

o

Mycotoxins: 

Highly toxic com pounds produced by certain species of fungus



Derm al, respiratory, or GI contact can rapidly, lead to m ultiorgan system failure and death.

Treatment Pre Hospital Universal precautions with N-95 m ask

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) fluid bolus for hypotension



Supplem ental oxygen for hypoxem ia



Vasopressors for persistent hypotension.



Respiratory and contact isolation for suspected cases

ED Treatment 

Control fever with acetam inophen.



Initiate therapy for specific disease.

Anthrax 



Initiate antibiotics: o

IV for inhalational or severe cutaneous

o

Antibiotic choice depends on susceptibility.

Antibiotic options: o

Ciprofloxacin

Pa ge 7 4 7

o

Doxycycline

o

Rifam pin

o

Clindam ycin

o

Vancom ycin

Plague 

Antibiotics initiated within 24 hours m inim izes m ortality.



First-line agents: streptom ycin or gentam icin



Add chloram phenicol if signs of m eningitis or unstable patient



Prophylaxis: doxycycline or ciprofloxacin

Q fever 

Recovery occurs within 2 weeks without treatm ent.



Doxycycline shortens duration of illness.

Smallpox 

Supportive therapy



Vaccine given within 4 days of initial exposure decreases chances of contracting sm allpox or developing severe sym ptom s.



Vaccinate m edical staff caring for patient.



Treat secondary bacterial infection.

Tularemia See Tularem ia

Hemorrhagic Fevers See Hem orrhagic Fever

Medication (Drugs) 

Chloram phenicol: 25 m g/kg IV q6h



Ciprofloxacin: 400 m g IV q12h or 500 m g PO b.i.d. (peds: 15 m g/kg b.i.d.)

Pa ge 7 4 8



Clindam ycin: 900 m g IV q12h



Doxycycline: 100 m g (peds: â‰¥45 kg, 100 m g; if weight â‰¤45 kg, 2.2 m g/kg IV) PO/IV q12h



Gentam icin: 5 m g/kg IM or IV q24h (peds: 2.5 m g/kg IV/IM q8h)



Rifam pin: 10 m g/kg IV not to exceed 600 m g/d



Streptom ycin: 1 g (peds: 15 m g/kg) IM q12h



Vancom ycin: 1 gm IV q12h

Follow-Up Disposition Admission Criteria 

Decision to treat patient as inpatient versus outpatient will have to be m ade in context of overall disaster.



Toxic or hypoxic patients require adm ission.



Respiratory isolation

Discharge Criteria Mild, noncontagious illness

References 1. Dennis DT, Inglesby TV, et al. Tularem ia as a biological weapon. JAMA. 2001;285:2763â€“2773. 2. Khan AS, Morse S, Lillibridge S. Public-health preparedness for biological terrorism in the USA. Lancet. 2000;356:1179â€“1182. 3. O'toole T. Em erging illness and bioterrorism : im plications for public health. J Urban Health. 2001;78(2):396â€“402. 4. Centers for Disease Control and Prevention. Recognition of illness associated with the intentional release of a biologic agent. MMWR Morb Mortal Wkly Rep. 2001;50(41):893â€“897.

Pa ge 7 4 9

5. Richards CF, Burstein JL, Waeckerle JF, et al. Em ergency physicians and biological terrorism . Ann Em erg Med. 1999;34(2):183â€“190.

Useful Web Sites http://www.bt.cdc.gov http://www.hopkins-biodefense.org/index.htm l

Miscellaneous SEE ALSO: Botulism ; Hem orrhagic Fever; Tularem ia

Pa ge 7 5 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bipo lar Diso rder

Bipolar Disorder

Paul H. Desan Gary S. Sachs

Basics Description 

Mania: o

Presentation is diverse, from sim ple irritability or cheerfulness to psychosis, delirium , or agitation, which m ay be difficult to recognize as m ania.

o

Full extent of pathology often revealed only by outside inform ants

o

Onset gradual or acute, duration several weeks or m onths; rarely m ay be chronic



Hypom ania: o





Milder sym ptom s without m arked im pairm ent

Mixed m ood: o

Sim ultaneous sym ptom s of m ania and depression

o

Treat in ED as for m ania

Bipolar (form erly m anic depressive) disorder: o

Defined as one or m ore episodes of hypom anic, m anic, or m ixed m ood

o

Possibly with episodes of depressed m ood

o

Bipolar II is used to denote cases where hypom ania

Pa ge 7 5 1

has occurred in the course of the disorder but never m ania. o

Typically begins in the teens or 20s

o

Episodes of abnorm al m ood m ay be m ild or severe, brief or prolonged, infrequent or chronic, chiefly elevated or chiefly depressed in character.

o

Bipolar disorder m ay be readily responsive to treatm ent or nearly intractable.



Schizoaffective disorder also characterized by episodes of altered m ood, but psychotic features present even when m ood is norm al

Etiology Bipolar disorder is typically a prim ary psychiatric disorder with an etiology related to both genetic and environm ental factors; it m ay also present as a secondary disorder, for exam ple, originating after stroke, head traum a, or other neurological process.

Diagnosis Signs and Symptoms History 

Psychiatric history: o

Recent sym ptom s of m ania (often collateral sources critical): elevated, expansive, or irritable m ood; increased energy and activity; decreased need for sleep; irresponsibility, disregard for negative consequences of actions; talkativeness; distractibility; fast thoughts; grandiosity, overconfidence

o

Past m ania or depression

Pa ge 7 5 2

o

Noncom pliance with m ood stabilizer

o

Recent initiation or discontinuation of antidepressant m ay trigger elevated m ood



o

Recent substance abuse

o

Bipolar fam ily history

Medical history: o

Especially endocrine, m etabolic, or neurologic disorders

o

Particularly likely to be secondary to m edical condition if it is the first episode, patient is older than 40 years, there is atypical or m ixed presentation, or abnorm al sensorium

o

Current or recent m edications

Physical Exam 

Appearance: o

Hyperactive, if not agitated

o

Talkative, often with loud, rapid or, â€œpressuredâ€ • speech



Affect: o

Irritable, argum entative, often m ultiple recent argum ents or fights

o

Less com m only euphoric or expansive

o

Often labile with depressed or tearful intervals (m ay confound diagnosis)

o

Patient likely to describe m ood as tense, irritable, or depressed rather than euphoric



Neurovegetative: o

Increased energy, engaged in m ultiple goal-directed activities m any hours per day



o

Racing thoughts

o

Decreased sleep

Thought process:

Pa ge 7 5 3

o 

Rapid, distractible, m ay be incoherent, delirious

Thought content: o

Psychosis possible, either m ood congruent (e.g., such as delusions of grandeur or power) or m ood incongruent (m ay be indistinguishable from other psychotic disorders)



Judgm ent: o

Inflated self-esteem , perhaps to grandiose or psychotic extent

o

Uncharacteristic, irresponsible behavior, such as financial or sexual indiscretions, with inability to recognize negative consequences of actions

o 

Substance abuse is frequent during m ania.

Sensorium : o

Typically norm al

o

Confusion or delirium possible

Essential Workup 

Physical and neurologic exam ; vital signs



Mania m ay present as delirium and need workup of full differential diagnosis of delirium .

Tests Lab 

Toxicologic screen (urine or serum )



Electrolytes



Blood glucose



CBC



TSH



Lithium , carbam azepine, valproate serum levels, if relevant



Other tests as suggested by history or exam

Pa ge 7 5 4

Imaging Head im aging only with suspicion of neurologic etiology

Differential Diagnosis 

Prim ary m ania of bipolar or schizoaffective disorder



Psychosis



Agitated depression



Personality disorders (borderline, narcissistic, antisocial)



Attention deficit disorder



Conduct or interm ittent explosive disorders



Organic brain syndrom e



Intoxication or withdrawal from alcohol or sedative hypnotics



Intoxication with cocaine, am phetam ines, or phencyclidine



Accidental or deliberate toxic overdose



Treatm ent with antidepressants or electroshock therapy in susceptible individuals



Corticosteroid or thyroid horm ones



Anticholinergics



Sym pathom im etics



Treatm ents of parkinsonism



Cyclobenzaprine (Flexeril)



Recent discontinuation of antidepressant m edication



Endocrine or m etabolic disorders (particularly thyroid disease)



Encephalitis



Meningitis



Postictal states



Multiple sclerosis



Post-cerebrovascular accident



CNS tum ors



CNS vasculitis

Pa ge 7 5 5



General paresis

P.145

Treatment Initial Stabilization 



High violence potential: o

Quiet environm ent

o

Prom pt evaluation

o

Nonconfrontational m anner

o

Adequate security backup

o

Physical restraint and sedation as needed

For cooperative agitated patient: o

PO neuroleptics (e.g., haloperidol, consider olanzapine or chlorprom azine as alternate) or PO benzodiazepines (e.g., lorazepam )



For severe or uncooperative agitated patient: o

Synergistic com bination of IM, IV, or PO haloperidol and lorazepam

o

Benztropine for prevention of acute dystonic reaction to haloperidol is not usually required when concurrent benzodiazepine is given.

o

Consider olanzapine, ziprasidone, chlorprom azine, or lorazepam IM as alternative

ED Treatment Outpatient Management 

Neuroleptics for sym ptom atic treatm ent, on tem porary or continuing basis

Pa ge 7 5 6



Agents for sleep



Discontinuation of antidepressant if related to present hypom ania or m ania



Initiation or restart of m ood-stabilizer therapy: o

Action of m ood-stabilizing agents requires days or weeks, even after full serum level attained

Inpatient Management Sedation or initiation of m ood stabilizer in consultation with adm itting psychiatrist

Medication (Drugs) Acute Agitation 

Lorazepam : 2 m g PO/IM (lower dose in m ild agitation or in frail or elderly); m ay repeat every 30 m inutes, generally not to exceed 12 m g/24 hours



Haloperidol: 5 m g PO (lower dose in m ild agitation or in frail or elderly); m ay repeat every 30 m inutes, generally not to exceed 20 m g/24 hours (consider benztropine 1â€“2 m g PO q12hr prophylaxis of dystonic reaction, particularly in continued neuroleptic treatm ent without benzodiazepine or in patients with history of dystonia); consider olanzapine 5â€“10 m g PO or chlorprom azine 50â€“100 m g PO as alternative to haloperidol



Synergistic com bination of haloperidol, 5â€“10 m g IM/IV/PO plus lorazepam 1â€“2 m g IM/IV/PO, repeat every 30 m inutes as required (doses m ay be sm aller in elderly or frail patients)



Olanzapine 10 m g IM, ziprasidone 10 m g IM, or chlorprom azine 50 m g IM m ay be useful parenteral alternatives, perhaps at a lower dose in frail or elderly

Pa ge 7 5 7

(avoid chlorprom azine in hypotension; ziprasidone m ay have m ore QT elongating effect than other neuroleptics but the clinical relevance of such effect at this dose is unclear).

Typical Outpatient Medications 

Benztropine: 1 m g PO b.i.d.



Carbam azepine: 400â€“2,000 m g/d (often in div. doses or in sustained release dose form s)



Clonazepam : 0.5â€“2 m g PO q.h.s. or 0.5â€“2 m g PO b.i.d.



Haloperidol: 0.5â€“5 m g PO b.i.d.



Lam otrigine: 25â€“200 m g/d in 1 or 2 div. doses (typically up to 100 m g/d in patients taking valproate, up to 500 m g/d in patients taking carbam azepine or certain other cytochrom e inducers, but not valproate)

Alert 

Lam otrigine m ust be started by a gradual dose escalation schedule specified by m anufacturer to avoid increased risk of severe derm atological reactions; if resum ed after discontinuation for m ore than five half-lives, the gradual dose escalation schedule m ust be used again.



Lithium : 600â€“3,000 m g/d (often in div. doses or in sustained release dose form s; in acute m ania, initiate at 300 m g PO t.i.d.)



Olanzapine: 1.25â€“30 m g/d, q.h.s. or in div. doses



Perphenazine: 4â€“16 m g PO b.i.d.



Risperidone: 0.5â€“3 m g PO b.i.d.



Valproate (e.g., Depakote): 750â€“3,000 m g/d (often in div. doses; in acute m ania, initiate at 250 m g PO t.i.d.)

Pregnancy Considerations The safety of psychotropic m edications in pregnancy is a com plex

Pa ge 7 5 8

issue, but valproate and carbam azepine m ay pose particular risks in the first trim ester.

Follow-Up Disposition Admission Criteria 

Involuntary hospitalization is required by danger to self: o

Suicidal risk, especially if m ixed or labile m ood or psychotic



o

Unsafe behaviors due to im paired judgm ent

o

Medically unstable

o

Hospitalization diagnostically required

Involuntary hospitalization also required by: o

Risk of behaviors dangerous to others

o

Inability to care for self (unable to obtain basic needs, such as food, clothing, or shelter)

Discharge Criteria 

Patients with m ild sym ptom s m ay be discharged on m edications noted above if: o

Necessary supports to ensure safety are in place

o

Patient is com pliant with treatm ent plan

o

Consultation with outpatient psychiatrist is available within 1â€“3 days



Som e patients who are not legally com m ittable m ay refuse treatm ent; explain availability of future treatm ent to patient and any involved friends or fam ily.

References 1. Allen MH, Currier GW, Hughes DH, et al. The Expert Consensus

Pa ge 7 5 9

Guideline Series: treatm ent of behavioral em ergencies. Postgrad Med . 2001;Spec No: 188. 2. Muller-Oerlinghausen B, Berghofer A, Bauer M. Bipolar disorder. Lancet. 2002;359(9302): 241â€“247. 3. Sachs GS, Printz DJ, Kahn DA, et al. The Expert Consensus Guideline Series: m edication treatm ent of bipolar disorder 2000. Postgrad Med. 2000; Spec No: 1104.

Codes ICD9-CM 296.4 Mania 296.5 Bipolar depression 296.6 Bipolar m ixed state 296.7 Bipolar unspecified 296.89 Bipolar II 295.7 Schizoaffective disorder

ICD10 F31 Bipolar disorder

Pa ge 7 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bite, Anim al

Bite, Animal

Daniel T. Wu

Basics Description 

Most bites are from provoked anim als



Dog bite wounds: o

Large dogs inflict the m ost serious wounds (pit bulls cause the m ost hum an fatalities).

o

Most fatalities in children (70%) due to bites to face/neck

o 

Dogs of fam ily or friends account for m ost bites.

Cat bite wounds: o

Majority from pets known to victim

o

50% infection rate in those seeking care

o

Puncture wounds m ost frequent due to sharp thin teeth causing deep inoculation of bacteria



Cat-scratch disease: o

Three of the following four criteria: 

Cat contact, with presence of scratch or inoculation lesion of the skin, eye, or m ucous m em brane



Positive CSD skin test result



Characteristic lym ph node histopathology

Pa ge 7 6 1



Negative results of laboratory studies for other causes of lym phadenopathy



Rat bite wounds: o

Occur in laboratory personnel or children of low socioeconom ic class

o

Infection rate

o

Rat bites rarely transm it rabies, and prophylaxis not routine

Etiology 

Dog and cat bites: o

Pasteurella m ultocida is the m ajor organism in both 

Twice as likely to be found in cat bites than dog bites



Gram -negative aerobe found in up to 80% of cat infections

 o

Staphylococcus or Streptococcus 

o

Infection appears in <24 hours

Infection appears in >24 hours

Other organism s include anaerobes and Capnocytophaga canim orsus (dogs)



Cat-scratch disease: o



Caused by Bartonella henselae

Rat bites: o

Caused by Spirillum m inus and Streptobacillus m oniliform is

Diagnosis Signs and Symptoms 

Distribution of m am m alian bites:

Pa ge 7 6 2

o

Dog bites represent 80â€“90% of all bites.

o

Cat bites represent 5â€“15% of all bites.

o

Hum an bites represent 2â€“5% of all bites (see Hum an Bite chapter).

o 

Rat bites represent 2â€“3% of all bites.

Dog bites: o

Appearance 

Crush injuries (m ost com m on), tears, avulsions, punctures, and scratches

o

Low rates of infection com pared with cat and hum an bites

o



Infections usually present with: 

Cellulitis



Malodorous gray discharge



Fever



Lym phadenopathy

Cat bites: o

o

Appearance 

Puncture wounds (m ost com m on)



Abrasions



Lacerations

High infection rates (30â€“50%) due to deeper puncture wounds



Cat-scratch disease: o

From the bite/scratch of a cat, dog, or m onkey

o

Sm all m acule or vesicle that progresses to a papule 

Begins several days (3â€“10) after inoculation



Resolves within several days or weeks



Regional lym phadenopathy occurs 3 weeks postinoculation



Tender



Nonsuppurative

Pa ge 7 6 3

 o

Resolves after 2â€“4 m onths

Low-grade fever, m alaise, headache

History 

Anim al's behavior, provocation, location, ownership



Tim e since attack



Past m edical history: conditions com prom ising im m une function, allergies, and tetanus status

Physical Exam 

Record the location and extent of all injuries.



Docum ent any swelling, crush injuries, or devitalized tissue.



Note the range of m otion of affected areas.



Note the status of tendon and nerve function.



Docum ent any signs of infection, including regional adenopathy.



Docum ent any joint or bone involvem ent.

Tests Lab 

Aerobic and anaerobic cultures from any infected bite wound



Cultures not routinely indicated if wounds not clinically infected



Cat-scratch disease o

Presence of elevated titers of Bartonella (Rochalim aea) henselae, or

o

Positive reaction to cat-scratch antigen (CSA) 

Inject 0.1 m L CSA intraderm ally



Induration at the site 48â€“72 hours later equal to or exceeding 5 m m is positive

Imaging

Pa ge 7 6 4

Plain radiograph indications: 

Fracture



Suspect foreign body, e.g., tooth



Baseline film if a bone or joint space has been violated in evaluating for osteom yelitis



For infection in proxim ity to a bone or joint space

Differential Diagnosis 

Hum an bite injuries: hum an teeth cause crush injuries and anim al teeth cause m ore punctures and lacerations.



Bite injuries from other anim als



CSD-caused lym phadenopathy: o

Reactive hyperplasia (leading cause of lym phadenopathy in children younger than 16 years)

o

Infection, chronic lym phadenitis, drug reaction, m alignancy, and congenital conditions

P.147

Treatment Initial Stabilization 

Achieve hem ostasis on any bleeding wound.



Airway stabilization if bite located on face or neck

ED Treatment 

Wound irrigation: o

Copious volum es of norm al saline irrigation with an 18-gauge plastic catheter tip aim ed in the direction of the puncture

o

Avoid injection of saline through tissue planes due to

Pa ge 7 6 5

force of irrigation 

DÃ©bridem ent: o

Rem ove foreign m aterial, necrotic skin tags, or devitalized tissues

o

Do not dÃ©bride puncture wounds

o

Rem ove any eschar present so underlying pus m ay be expressed and irrigated



Wound closure: o

Closing wounds increases risk of infection and m ust be balanced with scar form ation and effect of leaving wound open to heal secondarily.

o

Do not suture infected wounds or wounds >24 hours after injury.

o

Repair of wounds >8 hours: controversial

o

Close facial wounds (warn patient of high risk of infection).

o

Infected wounds, those presenting >24 hours after the event, and deep hand wounds should be left open

o

May approxim ate the wound edges with Steri-Strips and perform a delayed prim ary closure



Antibiotic indications: o

Infected wounds

o

Cat bites

o

Hand injuries

o

Severe wounds with crush injury

o

Puncture wounds

o

Full-thickness puncture of hand, face, or lower extrem ity

o

Wounds requiring surgical dÃ©bridem ent

o

Wounds involving joints, tendons, ligam ents, or fractures

o

Im m unocom prom ised patients

Pa ge 7 6 6

o

Wounds presenting >8 hours after the event



Elevate injured extrem ity.



Tetanus prophylaxis

Rabies Immunoprophylaxis 

Not required if rabies not known or suspected



Rodents (squirrels, ham sters, rats, m ice) and rabbits rarely transm it the disease.



Skunks, raccoons, bats, and foxes represent the m ajor reservoir for rabies.



Recom m ended in following situations: o

Dog or cat in rabies-known area unable to be quarantined for 10 days

o

Previously healthy dog or cat becom es ill while being quarantined (and awaiting results of rabies fluorescent antibody test)

o

An ill dog or cat while awaiting rabies test results (to be continued or halted based on results of rabies test)



Active im m unization: o

Hum an diploid cell vaccine (HDCV): 1 m L IM on days 1, 3, 7, 14, and 28 after exposure



Passive im m unization: o

Hum an rabies im m une globulin (HRIG): 20 IU/kg

o

Up to one half in area around wound with the rest IM

Cat-Scratch Disease 

Analgesics



Apply local heat to affected nodes.



Avoid lym ph node traum a.



Disease usually self-lim iting



Antibiotics controversial, consider if severe disease is present or im m unocom prom ised victim

Pa ge 7 6 7

Medication (Drugs) 

Am oxicillin/clavulanic acid (Augm entin): 500â€“875 m g (peds: 40 m g/kg/24 hr) PO b.i.d. (first line for all three anim als)



Am picillin/sulbactam (Unasyn): 1.5â€“3.0 g IV q6h



Cefoxitin (Mefoxin): 2.0 g IV q8h



Cefuroxim e axetil (Ceftin): 500 m g PO b.i.d.



Clindam ycin (Cleocin): 300 m g PO q6h; 900 m g IV q8h



Ciprofloxacin (Cipro): 500 m g PO b.i.d.; 400 m g IV q12h



Doxycycline (Vibram ycin): 100 m g PO b.i.d.



Im ipenem /cilastatin (Prim axin): 0.5â€“1.0 g (peds: 50 m g/kg/24h) IV q6h



Piperacillin/tazobactam (Zosyn): 3.375 g IV q6h



Ticarcillin/clavulanic acid (Tim entin): 3.1 g IV q6h



Trim ethoprim -sulfam ethoxazole (Bactrim ): 1 tablet (peds: 6â€“12 m g TMP, 30â€“60 m g SMX/kg/24h) PO b.i.d.

Follow-Up Disposition Admission Criteria 

All bites: o

Infected wounds at presentation

o

Severe/advancing cellulitis/lym phangitis

o

Signs of system ic infection

o

Infected wounds that have failed to respond to outpatient (PO) antibiotics



Cat-scratch disease:

Pa ge 7 6 8

o

Prolonged fever, system ic sym ptom s, and/or m arked lym phadenopathy

Discharge Criteria 

Healthy patient with localized wound infection: discharge on antibiotics with 24-hour follow-up.



48-hour follow-up for noninfected wounds

References 1. Brook I. Microbiology and m anagem ent of hum an and anim al bite wound infections. Prim Care. 2003;30(1):25â€“39, v. 2. Galloway RE. Mam m alian bites. J Em erg Med. 1998;6:325â€“331. 3. Griego RD, et al. Dog, cat, and hum an bites: a review. J Am Acad Derm atol. 1995;33: 1019â€“1029. 4. Klein JD. Cat scratch disease. Pediatr Rev 1994; 15(9):348â€“353. 5. Pickering L, Red Book: 2003 Report of the Com m ittee on Infectious Diseases. Am er Academ y of Pediatrics 2003. 26th edition. 6. Sm ith PF, et al. Treating m am m alian bite wounds. J Clin Pharm Ther. 2000;25:85â€“99.

Miscellaneous See also: Rabies

Codes ICD9-CM 879.8

ICD10 T14.1

Pa ge 7 6 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bite, Hum an

Bite, Human

Daniel T. Wu

Basics Description 

Third m ost com m on bite (after dogs and cats)



Most bites (up to 75%) occur during aggressive acts



15â€“20% are related to sexual activity (love nips)



Two types of bites: o

Occlusional bites: laceration or crush injury to affected body part:

o



Occurs when hum an teeth bite into the skin



Sam e risk of infection as other wounds

Clenched-fist injuries: (CFIs; m ost serious type): present as sm all wounds over m etacarpophalangeal joints in dom inant hand (fight bites) 

Sustained from a clenched fist striking the m outh and teeth of another person



With joint relaxation from the clenched position: o

Puncture site sealed

o

Oral bacteria inoculated in the anaerobic setting within the joint

o

Bacterial inoculation carried by the tendons deeper into the potential spaces of the hand

Pa ge 7 7 0

o

Increases chances for a m ore extensive infection

Etiology 

Aerobic and anaerobic organism s: o

o

Most com m on 

Streptococcus



Staphylococcus

Anaerobes (about 50%): 

Eikenella corrodens



Haem ophilus influenzae



Neisseria species



Corynebacterium



E. corrodens exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides, and gram -negative organism s

Diagnosis Signs and Symptoms 



Location: o

Upper extrem ities (60â€“75%)

o

Head and neck (15â€“20%)

o

Trunk (10â€“20%)

o

Lower extrem ities (about 5%)

Frequent com plications: o

Cellulitis

o

Serious deep-space infections (septic arthritis and osteom yelitis)

o

Fractures and tendon injuries

o

Hand bites have highest rates of infection.

History

Pa ge 7 7 1



Tim e of injury



Patient allergies



Relevant m edical history (im m une status)



Last tetanus shot



HIV, Hepatitis B status of person inflicting bite

Physical Exam 

Record the location and extent of all injuries.



Docum ent any swelling, crush injuries, or devitalized tissue.



Note the range of m otion of affected areas.



Note the status of tendon and nerve function.



Docum ent any signs of infection, including regional adenopathy.



Docum ent any joint or bone involvem ent.

Tests Lab 

Aerobic and anaerobic cultures from any infected bite wound



Cultures not indicated if wounds not clinically infected

Imaging Plain radiograph indications: 

Fracture



Suspect foreign body, e.g., tooth



Baseline film if a bone or joint space has been violated in evaluating for osteom yelitis



For infection in proxim ity to a bone or joint space

Differential Diagnosis Bite injuries from anim als: 

Sharper teeth cause m ore punctures and lacerations than hum an teeth, which usually cause m ore crush-type injuries

Pa ge 7 7 2

Pediatric Considerations 

In suspected sexual abuse: o

Check for a central area of bruising or â€œhickeyâ€• from suction



Linear abrasions or bruises on both the dorsal and palm ar/plantar surfaces of the hand or foot: o

Highly suggestive of bite m arks

o

Lesions on one extrem ity should prom pt a search for lesions on the other extrem ities.



An intercanine distance of >3 cm indicates perm anent dentition (present only if the attacker is older than 8 years)



If abuse suspected: o

Rub a saline-m oistened swab in the wound to collect any saliva and then place in a paper envelope for analysis

o

Obtain photographs.

Treatment Initial Stabilization ABCs: ensure patent airway and adequate peripheral tissue perfusion

ED Treatment 

Wound irrigation: o

Copious volum es of norm al saline irrigation with an 18-gauge needle or plastic catheter tip aim ed in the direction of the puncture

o

Care should be taken not to inject fluid into the tissues



DÃ©bridem ent:

Pa ge 7 7 3

o

Rem ove any foreign m aterial, necrotic skin tags, or devitalized tissues.

o

Do not dÃ©bride puncture wounds.

o

Rem ove any eschar present so that underlying pus m ay be expressed and irrigated.



Closed-fist injuries: o

Im m obilize

o

Splint in a position of function that m aintains the m axim al length of ligam ents and intrinsic m uscles.

o

Use a bulky hand dressing.

o

Consultation with hand surgeon regarding operative irrigation/exploration of wound

o

Elevation for several days until any edem a resolved

o

Sling for outpatients

o

Place the hand in a tubular stockinette attached to an IV pole for inpatients.

o

Adm inister antibiotics



Do not perform prim ary repair of avulsion wounds.



Wound closure: o

Closing wounds increases risk of infection and m ust be balanced with scar form ation and effect of leaving wound open to heal secondarily.

o

Do not suture infected wounds or wounds >24 hours after injury.

o

Repair of wounds >8 hours after bite: controversial

o

Close facial wounds up to 24 hours after bite (warn patient of high risk of infection).

o

Infected wounds and those presenting >24 hours should be left open.

o

May approxim ate the wound edges with Steri-Strips and perform a delayed prim ary closure

o

Do not suture closed-first injuries.

Pa ge 7 7 4



Prophylactic antibiotics controversial for low-risk bites P.149



Antibiotics for outpatients with: o

Moderate to severe injuries with crush injury or edem a

o

Involvem ent of the bone or a joint

o

Hand bites

o

Wounds near a prosthetic joint

o

Underlying disease (diabetes, prior splenectom y, or im m unosuppression) that increases the risk of developing a m ore serious infection



Tetanus prophylaxis



Refer for possible testing/surveillance for HIV infection.

Medication (Drugs) 

Am oxicillin/clavulanic acid (Augm entin): 500/125 m g (peds: 40 m g/kg/24h) q8h PO



Cefoxitin (Mefoxin): 1â€“2 g (peds: 80â€“160 m g/kg/24h) q6h IV



Ciprofloxacin (Cipro): 500â€“750 m g q12h PO or 400 m g q12h IV o



Poor anaerobic coverage

Clindam ycin (Cleocin): 150â€“450 m g (peds: 8â€“20 m g/kg/24h) PO q6h or 600â€“900 m g (peds: 20â€“40 m g/kg/24h) IV q8h o



No coverage against E. corrodens

Dicloxacillin (Pathocil): 500 m g (peds: 50 m g/kg/24h) PO q6h



Penicillin (Penicillin VK): 500 m g (peds: 50 m g/kg/24h) PO

Pa ge 7 7 5

q6h 

Ticarcillin/clavulanic acid (Tim entin): 3.1 g q4hâ€“q6h



Trim ethoprim -sulfam ethoxazole (Septra DS): 1 tablet q12h (peds: 8 m g/kg trim ethoprim and 40 m g/kg sulfam ethoxazole per day divided into two daily doses) PO o

Poor anaerobic coverage

Follow-Up Disposition Admission Criteria 

Infected wounds at presentation



Severe/advancing cellulitis/lym phangitis



Signs of system ic infection



Infected wounds that have failed to respond to outpatient (oral) antibiotics

Discharge Criteria 

Healthy patient with localized wound infection: discharge on antibiotics with 24-hour follow-up



48-hour follow-up for noninfected wounds

Geriatric Considerations 

Hum an bite m arks rarely occur accidentally; good indicators of inflicted injury.



Consider elder abuse

Pediatric Considerations 

Hum an bite m arks rarely occur accidentally; good indicators of inflicted injury



Consider child abuse.

References

Pa ge 7 7 6

1. Brook I. Microbiology and m anagem ent of hum an and anim al bite wound infections. Prim Care 2003;30(1):25â€“39, v. 2. Broder J, et al. Low risk infection in selected hum an bites treated without antibiotics. Am er Jour of Em erg Med 2004;22(1):10â€“13. 3. Pickering L, Red Book: 2003 Report of the Com m ittee on Infectious Diseases. Am er Academ y of Pediatrics 2003. 26th edition. 4. Sm ith PF, et al. Treating m am m alian bite wounds. J Clin Pharm Ther. 2000;25:85â€“99.

Miscellaneous SEE ALSO: Bite, Mam m al

Codes ICD9-CM 879.8

ICD10 T14.1

Pa ge 7 7 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bladder Injury

Bladder Injury

Roneet Lev

Basics Description 

Blunt traum a is the m ost com m on m echanism .



10â€“15% of pelvic fractures have bladder injury.



95% of bladder ruptures have pelvic fracture.



Mortality: 17â€“22% overall; 60% if com bined intraperitoneal/extraperitoneal rupture

Etiology Mechanism 

Traum a, 82%



Blunt traum a: m otor vehicle accident (MVA; 87%), falls (7%), assault (6%)



Penetrating: GSW (85%), stabbings (15%)



Iatrogenic 14%: TURP and urologic procedures, gynecologic procedures, obstetric procedures, abdom inal procedures, hernia repair, intrauterine device (IUD), orthopedic hip procedures, biopsies, indwelling Foley



Intoxication 2.9%



Spontaneous <1%

Classification

Pa ge 7 7 8



Extraperitoneal bladder rupture (62%): o

Associated with pelvic fractures (10â€“15% of pelvic fractures have bladder injury)

o 



Caused by blunt force or fracture fragm ents

Inraperitoneal bladder rupture (25%): o

Direct com pression of distended bladder

o

Caused by rupture of the dom e of the bladder

Com bined extraperitoneal and intraperitoneal rupture (12%): o



Highest m ortality owing to associated injuries

Bladder contusion: o

Dam age to endothelial lining or m uscularis layer with intact bladder wall

o

Gross hem aturia after extrem e physical activity (long distance running)

o

Gross hem aturia with norm al im aging

o

Usually resolves without intervention

Pediatric Considerations 

In children the bladder is an intra-abdom inal organ and descends into the pelvis by age 20 years.



Intraperitoneal rupture is m ore com m on in children than adults because the bladder is an abdom inal organ.



Bladder injury is m ore com m on in children than in adults because the pediatric bony pelvis is less rigid and transm its m ore force to adjacent structures.

Diagnosis Signs and Symptoms Triad:

Pa ge 7 7 9



Gross hem aturia



Suprapubic pain



Difficulty voiding

History Establish potential m echanism .

Physical Exam Evaluate urethral m eatusâ€”if blood is present, do not insert Foley catheter until retrograde urethrogram (RUG) is perform ed.

Essential Workup 

History of traum a or procedures



Evaluate urethral m eatus for blood.



Urinalysis (UA)



Retrograde cystography

Tests Lab 

Urinalysis: o

Gross hem aturia in 95â€“100% of patients with significant bladder or urethral traum a

o 

Microscopic hem aturia in 5%

BUN and creatinine: o

The BUN can be elevated from resorption of urine within the peritoneum .



Electrolytes: o

Hyperkalem ia and hypernatrem ia m ay result from resorption of urine within the peritoneum .

Imaging 

Retrograde cystography is the m ethod of choice to diagnose a ruptured bladder.



If urethral injury is suspected, the cystogram is perform ed after a RUG.

Pa ge 7 8 0



CT scan and IVP are not sensitive enough to evaluate bladder injuries.

Cystography Technique 

Kidneys/ureter/bladder (KUB) scout film



Infuse 100 m L of diluted contrast via Foley into bladder. Contrast m aterial needs to be diluted: 30% or 6:1 saline; otherwise it is too dense.



Plane film is repeated to evaluate early extravasation.



If initial film is norm al, fill rest of bladder with diluted contrast: o

350 m L total for adult

o

3â€“5 m L/kg or 60 m L + (age in years Ã— 30) for children

o 

or until discom fort

It is essential to have a bladder full of contrast for diagnosis; it is not sufficient to place contrast and clam p Foley in antegrade fashion.



Cystogram film s taken in AP, lateral, and oblique views (oblique m ay be difficult in traum a and CT is often used)



Em pty bladder and obtain a postdrainage film .



Postdrainage film is essentialâ€”13% of bladder ruptures are seen on postdrainage film ; a distended bladder m ay hide extravasation.

Cytography Interpretation 

Extraperitoneal rupture: tear drop- or star-shaped form



Intraperitoneal rupture: outlining of bowel or contrast within the paracolic gutters

Differential Diagnosis 

Peritoneal traum a



Urethral traum a



Renal or ureteric traum a

Pa ge 7 8 1

P.151

Treatment Pre Hospital Do not attem pt bladder catheterization in the field.

Initial Stabilization 

Airway, breathing, circulation (ABCs)



Early urologic consultation

ED Treatment 

Urologic consultation is needed when bladder rupture is diagnosed:



Extraperitoneal ruptures m ay be m anaged by catheter drainage o

20 F Foley or larger for 7â€“10 days

o

80% of lacerations will seal in 3 weeks.



Intraperitoneal ruptures require surgical exploration.



Bladder contusions do not need any specific interventions.

Medication (Drugs) Broad-spectrum antibiotics for intraperitoneal rupture

Follow-Up Disposition

Pa ge 7 8 2

Admission Criteria 

Concurrent m ajor traum a requiring adm ission or observation



Surgical intervention required

Discharge Criteria 

Bladder contusion with no rupture or other m ajor traum a requiring adm ission



Most cases of bladder rupture will require adm ission; discharge only after clearance by urology and no other associated injuries.

References 1. Corriere, JN. Traum a to the lower urinary tract. In: Gillenwater, Grayhack, Howards, et al. Adult and Pediatric Urology. 3rd ed. St Louis, MO: Mosby-Year Book; 1991. 2. Gibbs MA, Schnieder R. Genitourinary traum a. In: Ferrera PC, Colucciello SA, Marx JA, et al. Traum a Managem ent an Em ergency Medicine Approach. St. Louis, MO: Mosby; 2001. 3. Harwood-Nuss AL, Sandler CM. Genitourinary traum a. In: Rosen P, Doris PE, Barkin RM, et al, eds. Diagnostic Radiology in Em ergency Medicine. St. Louis, MO: Mosby-Year Book; 1992. 4. McAninch JW, Santucci RA. Genitourinary traum a. In: Walsch PC, Retik, AB, Vaughan ED, et al. Cam bell's Urology. 8th ed. Philadelphia: WB Saunders; 2002. 5. Schneider RE. Genitourinary traum a. In: Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Codes ICD9-CM 867.0

Pa ge 7 8 3

ICD10 S37.2

Pa ge 7 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Blo w -Out F racture

Blow-Out Fracture

Shari Schabowski

Basics Description 

Defined as an orbital floor fracture without orbital rim involvem ent



Caused by blunt traum a to the orbit: o

Typically caused by a projectile less than half the size of the fist



Force transm itted through the orbital structures to the weakest structural point: the orbital floor: o



Results in fracture of the orbital floor

Orbital floor serves as roof to air-filled m axillary and ethm oid sinuses: o

Com m unication between the spaces results in orbital em physem a.



Orbit contains fat, which holds the globe in place: o

Orbital floor fracture m ay result in herniation of the fat on the inferior orbital surface into the m axillary or ethm oid sinuses.

o

Leads to enophthalm os owing to orbital volum e loss

o

Sinus congestion and fluid collection occur secondary to edem a.

Pa ge 7 8 5



Infraorbital nerve runs through the bony canal 3 m m below the orbital floor: o

Injury results in hypoesthesia of the ipsilateral cheek.

o

Distinguished from hypoesthesia owing to swelling by testing for decreased sensation on the ipsilateral gingiva, which is within the infraorbital nerve distribution



Inferior rectus and the inferior oblique m uscle run along the orbital floor: o

Restriction of these extraocular m uscles occurs because of entrapm ent within the fracture, contusion, or cranial nerve dysfunction.

o

Diplopia on upward gaze

o

Inability to elevate the affected eye norm ally on exam



Medial rectus located above the ethm oid sinus: o

Less com m only entrapped

o

Diplopia on ipsilateral lateral gaze

Etiology Most com m only caused by projectiles sm all enough to fit within the bony orbit

Pediatric Considerations 

Orbital floor fractures: extrem ely unlikely before 7 years of age



Lack of pneum atization of the paranasal sinuses; therefore, orbital floor is not as weak a point in the orbit.



Orbital roof fractures with associated CNS injuries m ore com m on

Pa ge 7 8 6

Diagnosis Signs and Symptoms 

Periorbital tenderness, swelling, ecchym osis



Im paired ocular m obility or diplopia: o

Restricted upward gaze owing to inferior rectus entrapm ent

o

Restricted ipsilateral lateral gaze with m edial rectus entrapm ent



Infraorbital hypoesthesia: o

Caused by com pression/contusion of infraorbital nerve

o 

May extend to upper lip

Enophthalm os: o

Globe set back owing to orbital fat displaced through fracture.



Periorbital em physem a: o

From the ethm oid or m axillary sinus



Norm al visual acuity (unless associated ocular injury)



Epistaxis

Associated Injuries 

Ocular injuries: o

o

Ruptured globe: 

Incidence 5â€“10% of blow-out fractures



Ophthalm ologic em ergency

Subconjunctival hem orrhage: 

Com m on

o

Corneal abrasion/laceration

o

Hyphem a

o

Iridodialysis

o

Traum atic iridocyclitis (uveitis)

o

Traum atic m ydriasis

Pa ge 7 8 7





o

Retinal detachm ent

o

Vitreous hem orrhage

o

Com pressive orbital em physem a

o

Retrobulbar hem orrhage

o

Optic nerve injury

Associated facial fractures: o

Nasal bones

o

Zygom atic arch fracture

Cervical spine or intracranial injuries

Late Complications 

Sinusitis



Orbital infection



Perm anent restriction of extraocular m ovem ent



Enophthalm os

Essential Workup Thorough ophthalm ologic exam ination: 

Visual acuity (should not be affected)



Test extraocular m ovem ents for disconjugate gaze or diplopia.



Palpate bony structures for evidence of step off.



Test sensation in inferior orbital nerve distribution.



Exam ine lid and adnexa.



Careful attention not to place pressure on the globe until ruptured globe excluded



Slit-lam p and funduscopic exam ination to identify associated injuries

Tests Lab Preoperative laboratory studies if indicated

Imaging

Pa ge 7 8 8



Plain radiographs: o

Facial film s

o

Orbits

o

Waters view and exaggerated Waters view: 

Classic teardrop sign illustrates herniated m ass of orbital contents in the ipsilateral m axillary sinus.



Opacification of or air fluid level in the ipsilateral m axillary sinus (less specific)



Orbital floor bony fracture



Lucency in orbits consistent with orbital em physem a



o

Diagnostic in up to 97%

o

Ten percent false-positive and false-negative rate

CT orbits: excellent alternative: o

If diagnosis in question and for follow-up

o

Defines involved anatom y

o

Obtain 1.5-m m cuts.

P.153



Forced duction test: o

Distinguishes nerve dysfunction from entrapm ent

o

Topical anesthesia applied to the conjunctiva on the opposite side, and the globe is pulled away from the expected point of entrapm ent; if the globe is not m obile, the test is positive.

Pediatric Considerations 

Im m ature facial skeleton with lack of pneum atization of the paranasal sinuses m akes plain radiographs of lim ited value.



Orbital CT: study of choice

Pa ge 7 8 9

Differential Diagnosis 

Retrobulbar hem orrhage



Periorbital contusion/ecchym osis



Cranial nerve palsy



Ruptured globe



Orbital cellulitis



Periorbital cellulitis

Treatment Pre Hospital 

Metal protective eye shield if possible globe injury



Place in supine position.

Initial Stabilization Initial approach and im m ediate concerns: 

Rule out ruptured globe.



Assess for associated intracranial or cervical spine injuries.



Test visual acuity: o

Decreased visual acuity suggestive of associated ocular injury

ED Treatment 

Apply cool com presses for the first 24â€“48 hours to decrease swelling to m inim ize or reverse herniation and avoid surgical intervention.



Avoid Valsalva m aneuvers and nose blowing to prevent com pressive orbital em physem a.



Prophylactic antibiotics to prevent infection



Nasal decongestants



Analgesics

Pa ge 7 9 0



Tetanus prophylaxis

Medication (Drugs) 

Am oxicillin: 250â€“500 m g PO t.i.d. for 10â€“14 days



Cephalexin: 250â€“500 m g PO q.i.d. for 10â€“14 days



Erythrom ycin: 250â€“500 m g PO q.i.d. for 10â€“14 days



Phenylephrine nasal spray: b.i.d. for 10â€“14 days

Follow-Up Disposition Admission Criteria Rarely indicated except with: 

Severe herniation of orbital contents threatening vision



Cosm etically enophthalm os typically >5 m m



Associated injuries that m andate adm ission

Discharge Criteria 

Consultation with facial traum a service: o

Arrange follow-up evaluation within 1â€“2 weeks of injury and to determ ine need for surgery



Im m ediate ophthalm ology evaluation if patient has evidence of visual loss or within 24 hours for com plete retinal evaluation



Need for surgical intervention: o

Rarely indicated im m ediately

o

Eighty-five percent resolve without surgical intervention.

o

Typically observe for 10â€“14 days until swelling resolves

Pa ge 7 9 1

o

Surgery indications: 

Persistent diplopia



Restricted extraocular m ovem ents



Cosm etically significant enophthalm os

References 1. Burm JS, Chung CH, Oh SJ. Pure orbital blowout fracture: new concepts and im portance of m edial orbital blowout fracture. Plast Reconstr Surg. 1999;103(7):1839â€“1849. 2. Hatton MP, Watkins LM, Rubin PA. Orbital fractures in children. Ophthalm ol Plast Reconstr Surg. 2001;17(3):174â€“179. 3. Koltai PJ, Am jad I, Meyer D. Orbital fractures in children. Arch Otolaryngol Head Neck Surg. 1995;121:1375â€“1379. 4. Linden JA, Renner GS. Traum a to the globe. Em erg Med Clin North Am . 1995;13(3):581â€“605.

Codes ICD9-CM 829.0

ICD10 S02.3

Pa ge 7 9 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bo erhaave Syndro m e

Boerhaave

Syndrome Robert C. Montana

Basics Description 

Spontaneous esophageal rupture: o

o

From sudden com bined increase in both: 

Intra-abdom inal pressure



Negative intrathoracic pressure

Causes com plete, full-thickness (transm ural), longitudinal tear in distal esophagus at left posterolateral aspect



Esophagus has no serosal layer (which norm ally contains collagen and elastic fibers): o

Results in weak structure vulnerable to perforation and m ediastinal contam ination

o

Esophageal wall is further weakened by conditions that dam age m ucosa (esophagitis of various causes)



Significant m orbidity/m ortality (m ost lethal GI tract perforation): o

Owing to explosive nature of tear

o

Owing to alm ost im m ediate contam ination of

Pa ge 7 9 3

m ediastinum with contents of esophagus

Etiology 

Associated with: o

Forceful vom iting and retching

o

Heavy lifting

o

Seizures

o

Childbirth

o

Blunt traum a

o

Induced em esis

o

Laughing



Com m on in m iddle-aged m en



Alcoholism , ingesting large m eals, and peptic ulcer disease



Second m ost com m on cause of esophageal rupture after iatrogenic perforation from instrum entation

Pediatric Considerations Described in fem ale neonates but rarely seen

Diagnosis Signs and Symptoms History 

Often no classic sym ptom s



Most com m on sym ptom s: o





Chest or epigastric pain after vom iting/retching

Mackler triad: o

Vom iting/retching

o

Chest pain

o

Subcutaneous em physem a

Retrosternal chest pain present in m ost patients: o

Often pleuritic

Pa ge 7 9 4

o

Radiates to back or left shoulder

o

Worsens with swallowing



Odynophagia



Swallowing m ay precipitate coughing.

Physical Exam 

Dyspnea



Diaphoresis



Subcutaneous em physem a in neck and chest wall



Mediastinal crackling on auscultation (Ham m an sign)



Pleural effusions



Tachypnea



Fever



Shock, in m ore severe cases



If untreated, m ediastinitis will develop and abscesses will form .



Not usually associated with bleeding

Essential Workup 

Upright chest radiographs (preferably posteroanterior and lateral views if tolerated) evaluating for: o

Pneum om ediastinum

o

Subcutaneous em physem a

o

Pleural effusion (left side)

o

Pneum othorax

o

Widened m ediastinum

o

Hydropneum othorax

o

Em pyem a

o

Free peritoneal air

o

Naclerio â€œVâ€• sign: 

V-shaped radiolucency seen through the heart (air in left lower m ediastinum )



Esophagram identifies leak in esophagus:

Pa ge 7 9 5

o

Initially use water-soluble contrast m aterial

o

If esophagus is intact, use barium contrast for better detail.

o

Aids in decision of which type of surgical approach

o

If negative and high suspicion, repeat with patient in left and right decubitus positions.

Tests Lab 

CBC



PT/PTT



Blood cultures



Pleural effusion:



o

Am ylase content

o

pH (<6)

o

Undigested food particles

ECG

Imaging 

Endoscopy: o

Controversial

o

Can extend perforation and/or introduce air into m ediastinum



CT chest: o

Sensitive for identifying free air, periesophageal fluid, m ediastinal widening, but does not isolate lesion

o

Indicated if esophagram cannot be obtained

o

Evaluates other intrathoracic structures

P.155

Pa ge 7 9 6

Differential Diagnosis 

Myocardial infarction



Pneum othorax



Pericarditis



Pneum onia



Pancreatitis



Ruptured abdom inal viscus



Dissecting aortic aneurysm



Pulm onary throm boem bolism



Mesenteric throm bosis



Cholecystitis



Spontaneous pneum om ediastinum (clinically benign)



Lung abscess

Treatment Pre Hospital 

Airway control m ust be established if patient unresponsive or airway patency in jeopardy.



Establish two large-bore intravenous catheters and treat hypotension with 0.9% norm al saline.



Avoid opiates until patient is in ED to avoid com plication of hypotension.

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

Airway control: 100% oxygen or intubate patient if unresponsive or airway patency is in jeopardy.



Establish intravenous access and treat hypotension: o

Adm inister 1-L (20-m L/kg) bolus with 0.9% norm al saline (or lactated Ringer solution).

Pa ge 7 9 7

o

Initiate dopam ine if blood pressure does not respond to fluids.

o

Central catheter placem ent if condition of patient rem ains unstable for m ore efficient delivery of fluids and m onitoring of central venous pressure

ED Treatment 

NPO



Careful placem ent of a nasogastric tube to decom press the stom ach



Bladder catheter to m onitor urine output



Expedient diagnosis to decrease incidence of m orbidity/m ortality



Prom pt surgical consultation



Definitive treatm ent:



o

Surgical repair of perforation

o

Adequate drainage

Initiate broad-spectrum antibiotics directed against oral m icroflora and gastrointestinal pathogens: o

Am picillin/sulbactam plus gentam icin

o

Im ipenem /Cilastatin

Medication (Drugs) 

Am picillin/sulbactam : 3.0 g IV per bolus q6h



Dopam ine: 2â€“20 Âµg/kg/m in IV per bolus



Gentam icin: 2 m g/kg load, then 1.7 m g/kg IV per bolus q8h or 5.1 m g/kg IV per bolus once daily (assum ing norm al renal function)



Im ipenem /Cilastatin: 250â€“500 IV q6h

Pa ge 7 9 8

Follow-Up Disposition Admission Criteria 

All cases of Boerhaave syndrom e m ust be adm itted to surgical intensive care unit after definitive surgical repair of lesion.



Surgery should be perform ed directly from ED without delay.

Discharge Criteria None

References 1. Jagm inas L, Silverm an RA. Boerhaave syndrom e presenting with abdom inal pain and right hydropneum othorax. Am J Em erg Med. 1996;14:53â€“55. 2. Ma G, Jacoby I. Spontaneous esophageal rupture. J Em erg Med. 2000;18:257â€“258. 3. Troum S, Lane CE, Dalton ML Jr. Surviving Boerhaave's syndrom e without thoracotom y. Chest. 1994;106:297â€“298. 4. Younes Z, Johnson DA. The spectrum of spontaneous and iatrogenic esophageal injury: perforations, Mallory-Weiss tears, and hem atom as. J Clin Gastroenterol. 1999;29:306â€“317.

Codes ICD9-CM 530.4 Perforation of esophagus

ICD10 K22.3 Perforation of esophagus

Pa ge 7 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bo tulism

Botulism

Philip Shayne

Basics Description 

Caused by a polypeptide, heat-labile exotoxin produced by Clostridium botulinum : o



Most potent poison known

Toxin blocks neurom uscular transm ission in cholinergic nerve fibers.



Sym ptom s occur by inhibition of acetylcholine release from presynaptic nerve m em branes: o

Dam age is perm anent.

o

Recovery is by form ation of new synapses through sprouting from the axon.



Onset: 12â€“36 hours after exposure: o

Death can occur in 24 hours.



Slow recovery; sym ptom s often persist for m onths



Mortality:



o

Untreated: 60â€“70%

o

With supportive care: 10â€“15%

Three m ajor types: food-borne botulism , wound botulism , and infantile botulism (see Pediatric Considerations)



Food-borne botulism :

Pa ge 8 0 0

o

Occurs by ingestion of preform ed toxin; im properly canned food facilitates the necessary anaerobic conditions.

o

Conditions required for exposure: 

Food product contam inated with C. botulinum bacilli or spores



Proper conditions for germ ination of spores exist.



Tim e and conditions perm it production of toxin before eating.



Food not heated sufficiently to destroy botulism toxin



Toxin-containing food ingested by susceptible host



Wound botulism : o

Clinical evidence of botulism after traum a with a resultant infected wound and no history suggestive of food-borne illness



o

Botulinum isolated in about 50%

o

Wounds usually contam inated with soil

o

Seen rarely in chronic drug abusers

Other types: o

Hidden botulism is an adult variant of infantile botulism seen in com prom ised hosts (rare).

o

Inadvertent botulism seen rarely from reactions to botulism toxin used therapeutically: 

Sym ptom s sim ilar to those of classic botulism

Pediatric Considerations 

Infantile botulism occurs from the ingestion of C. botulinum spores, which germ inate in the gut and produce the toxin.



Ninety percent occur in children younger than 6 m onths.

Pa ge 8 0 1



Progresses for 1â€“2 weeks, then stabilizes for 2â€“3 weeks before receding: o



Usually subacute presentation with low m ortality

Slower onset is attributed to the toxin being produced locally as opposed to being ingested in one dose



C. botulinum spores found in honey: o

Honey not recom m ended for children younger than 6 m onths

Etiology 

C. botulinum is a large spore-form ing, usually gram -positive, strictly anaerobic bacilli ubiquitous in nature.



Each strain produces antigenically distinct toxins, designated types A through G: o

Types A, B, and E are responsible for m ost hum an cases.

Diagnosis Signs and Symptoms History 

Ingestions



Im m une status (AIDS, cancer, chronic illness)

Physical Exam 

Food-borne botulism (classic botulism ): o

Most com m on: 

Diplopia



Blurred vision



Bulbar weakness: dysphagia, dysarthria, dysphonia

Pa ge 8 0 2

o

Subsequent sym m etric, descending weakness or paralysis of the extrem ities (hallm ark of the disease)

o

No sensory deficit

o

Patient rem ains awake/alert; m entation unaffected.

o

Ventilatory insufficiency from weakness of respiratory m uscles

o

Autonom ic dysfunction (sym pathetic and parasym pathetic):







Dry m outh



Blurred vision



Orthostatic hypotension



Constipation



Urinary retention

o

Nausea and vom iting with food-borne botulism only

o

Afebrile

Wound botulism : o

Finding sim ilar to food-borne botulism

o

May be febrile

Infantile botulism : o

Constipation

o

Weakness

o

Poor suck

o

Lethargy

o

Hypotonia

o

Flaccid facial expression

o

Respiratory difficulty

Essential Workup 

Diagnosis is entirely clinical.



Workup focuses on differentiation from other conditions causing general paralysis.



Notify public health officials of diagnosis.

Pa ge 8 0 3

Tests Lab 

CBC



Electrolytes, BUN/creatinine, glucose: o



Arterial blood gas (ABG): o





Check for hypokalem ia.

For signs of respiratory insufficiency

Toxin detection in: o

Blood

o

Feces

o

Gastric contents

o

Suspected food and containers

Anaerobic blood cultures

Imaging CT/MRI of brain: 

Norm al

Diagnostic Procedures/Surgery 



Cerebrospinal fluid (CSF) testing: o

Norm al

o

Helps differentiate from Guillain-BarrÃ© syndrom e

Electrophysiologic studies: o

Norm al nerve conduction with dim inished evoked m uscle action potential



Edrophonium testing m ay be positive, but not to the degree seen in m yasthenia gravis.

P.157

Differential Diagnosis 

Myasthenia gravis (less acute)

Pa ge 8 0 4



Lam bert-Eaton m yasthenic syndrom e (less acute)



Polio (fever and asym m etric)



Guillain-BarrÃ© (sim ultaneous sensory findings and elevated spinal fluid protein)



Tick paralysis



Magnesium intoxication



Hypokalem ic periodic paralysis



Diphtheritic neuropathy

Pediatric Considerations Often m isdiagnosed as dehydration, sepsis, or Reye syndrom e

Treatment Alert 

Death is invariably from progressive ventilatory failure: o

Intubate as soon as respiratory insufficiency noted.

Initial Stabilization 

Early intubation and ventilatory support is the key to survival.



Respiratory difficulties occur rapidly.

ED Treatment 

Trivalent ABE antitoxin: o

IV adm inistration as soon as the diagnosis is m ade, without waiting for laboratory confirm ation

o

Use should be preceded by testing for hypersensitivity to horse serum



Nasogastric (NG) suctioning if ileus is profound



With wound botulism , perform wound dÃ©bridem ent even if it appears to be healing.

Pa ge 8 0 5



Antibiotics for specific infectious com plications

Medication (Drugs) Trivalent botulism antitoxin: two vials (approxim ately 10,000 IU each of types A, B, and E) IV

Pediatric Considerations 

Antitoxin is rarely indicated for infantile botulism .



Antibiotics: o

Ineffective in eradicating organism from the intestine

o

Release of toxin in the gut through bacterial cell lysis m ay worsen neurologic sym ptom s.

Follow-Up Disposition Admission Criteria Adm it patients with suspected botulism poisoning to m onitored bed: 

ICU adm ission for any respiratory deficiency

Discharge Criteria Clinical course of botulism poisoning is unpredictable; it can becom e rapidly progressive and fatal: 

Discharge only patients with a prolonged period of progressive recovery from sym ptom s

References 1. Bleck TP. Clostridium botulinum . In: Mandell GI, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 4th ed. New York: Churchill-Livingstone; 1995. 2. Cherington M. Clinical spectrum of botulism . Muscle Nerve.

Pa ge 8 0 6

1998;21:701â€“710. 3. Darling RG, Catlett CL, Huebner, et al. Threats in bioterrorism I: CDC category A agents. Em erg Med Clin N Am . 2002;20:273â€“309. 4. Hatheway CL. Botulism : the present status of the disease. Curr Top Microbiol Im m unol. 1995;195: 55â€“75. 5. Mechem CC, Walter FG. Wound botulism . Vet Hum Toxicol. 1994;36(3):233â€“237. 6. Midura TF. Update: infant botulism . Clin Microbiol Rev. 1996;9(2):119â€“125. 7. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidem iologic review. Ann Intern Med. 1998;129(3):221â€“228. 8. Wigginton JM, Thill P. Infant botulism : a review of the literature. Clin Pediatr. 1993;32(11):669â€“674.

Codes ICD9-CM 005.1

Pa ge 8 0 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bo w el Obstructio n

Bowel Obstruction

Jenny Lu

Basics Description 

Obstruction of norm al flow of intestinal contents owing to m echanical or nonm echanical causes



Obstruction leads to rapid increase in both anaerobic and aerobic bacteria, with resultant increase in m ethane and hydrogen production.



Distended bowel becom es progressively edem atous, and increased intestinal secretions cause further distention.



Retrograde peristalsis causes vom iting.

Etiology 



Sm all bowel: o

Adhesions: m ost com m on

o

Hernias

o

Neoplasm s

o

Strictures: inflam m atory bowel

o

Traum a: bowel wall hem atom a

o

Miscellaneous: (e.g., ascaris infection)

Large bowel: o

Carcinom a

o

Volvulus

Pa ge 8 0 8

o

Diverticular disease

o

Inflam m atory bowel disease

o

Ischem ic colitis

Diagnosis Signs and Symptoms History 

Previous surgery, m alignancy, constipation, cathartic use



Abdom inal pain:



o

Interm ittent when early

o

Constant with strangulated obstruction

Vom iting: o

Bile-stained em esis with proxim al obstruction

o

Feculent em esis with distal obstruction



Obstipation



Stool caliber changes

Physical Exam 

Vital signs: o

Tachycardia, hypotension with significant volum e depletion



o

Fever with strangulation or perforation

o

Hypotherm ia with sepsis

Abdom inal exam ination: o

Distention

o

Variable tenderness, often diffuse

o

Hyperactive and high-pitched bowel sounds when early; hyperactive when late

o

Ischem ic or gangrenous bowel if pain out of proportion to findings

Pa ge 8 0 9

o

Peritoneal signs indicate strangulation or perforation.



Hernia (ventral, inguinal, fem oral)



Rectal exam : o

Rectal m ass

o

Blood in stool, gross or occult

Geriatric Considerations 

Abdom inal pain variable in elderly



Nausea/vom iting and abdom inal pain are com m on sym ptom s in elderly patients with acute m yocardial infarctions: o

Abdom inal distention, obstipation, and colicky pain suggests GI cause.

Pediatric Considerations 

Intussusception: o

Leading cause of intestinal obstruction in infants

o

Most com m on between 3 and 12 m onths of age



Incarcerated inguinal/um bilical hernia



Malrotation with volvulus: o

Can occur as early as 3â€“7 days of age

o

Double bubble sign seen on plain radiograph owing to partial obstruction of duodenum , resulting in air in stom ach and in first part of duodenum



Pyloric stenosis: o

Progressive, projectile, nonbilious, postprandial vom iting



o

Male/fem ale ratio: 5:1 incidence

o

Onset usually 2â€“5 weeks of age

Other causes include duodenal atresia, Hirschsprung, im perforate anus.

Essential Workup Careful history and physical exam

Pa ge 8 1 0

Tests Lab 

CBC: o



Leukocytosis com m on

Electrolytes, BUN/creatinine, glucose: o

Hypokalem ia

o

Hypochlorem ic m etabolic alkalosis

o

Prerenal azotem ia



Urinalysis



Am ylase/lipase



Stool hem e test



Type and cross-m atch



PT/PTT



ECG in patients at risk of coronary artery disease



Liver panels to exclude hepatic/biliary pathology

Imaging 



Upright chest radiograph: o

Evaluate for lung pathology.

o

Check for free air beneath diaphragm .

Plain abdom inal radiographs, flat and upright (75% sensitivity) o

Distended loops of bowel (norm al sm all bowel <3 cm in diam eter)

o

Distended cecum >13 cm indicates potential rupture.

o

Air fluid levels

o

â€œString of pearlsâ€• sign if sm all bowel loops nearly com pletely fluid filled

P.159



Abdom inal CT for detecting neoplastic causes of

Pa ge 8 1 1

obstruction (90% sensitivity for SBO):



o

Identify early strangulation

o

Delineate other causes of pain

Ultrasound (US): o

More sensitive and specific than plain film s for sm all bowel obstruction but not as accurate as CT

Diagnostic Procedures/Surgery Upper GI/barium enem a: 

If carcinom a or m ass lesion suspected as cause

Differential Diagnosis 

Paralytic ileus



Pseudo-obstruction (Ogilvie)



Perforated ulcer



Pancreatitis



Cholecystitis



Colitis



Mesenteric ischem ia



Urem ia

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) or lactated ringers (LR) IV fluid resuscitation for significant volum e depletion and strangulated or perforated bowel:



o

Adults: 1 L bolus

o

Peds: 20 m L/kg bolus

Correct electrolyte abnorm alities, especially hypokalem ia.

Pa ge 8 1 2

ED Treatment 

Intravenous fluids (IVFs)



Nasogastric tube (NGT)



Foley catheter to m onitor urine output



Surgical consultation



Antibiotics for suspected strangulated/perforated bowel: o

Antibiotic choices to cover gram -negative aerobic and anaerobic organism s:

o

o

Single agent: 

Piperacillin/tazobactam



Am picillin/sulbactam



Meropenem or im ipenem

Com bination regim en: 



Analgesics o



Metronidazole PLUS ciprofloxacin or ceftriaxone

Morphine sulfate

Antiem etics: o

Odansetron

o

Prom ethazine

Medication (Drugs) Antibiotics: 

Piperacillin-tazobactam (Zosyn): 3.375 g (peds: 150â€“400 m g/kg/24h IV div. q6hâ€“q8h) IV q4hâ€“q6h



Am picillin-sulbactam (Unasyn): 1.5â€“3 g (peds: 100â€“400 m g/kg/24h IV div. q6h) IV q6h



Meropenem (Merrem ): Adult: 1 g (peds: 60â€“120 m g/kg/24h IV q8h) IV q8h



Im ipenem -cilastatin (Prim axin): 250â€“1000 m g (peds: 50â€“100 m g/kg/24h IV q6hâ€“q12h) IV q6hâ€“q8h

Pa ge 8 1 3



Metronidazole (Flagyl): 1 g IV, then 500 m g IV q6h (peds: 7.5â€“30 m g/kg/24h IV div. q6hâ€“q8h)



Ciprofloxacin (Cipro): 400 m g IV q12h



Ceftriaxone (Rocephin): 1â€“2 g (peds: 25â€“75 m g/kg/d IV up to 2 g div. q12hâ€“q24h) IV q24h

Analgesics: 

Morphine sulphate: 2â€“10 m g/dose (peds: 0.1â€“0.2 m g/kg IV/IM/SC q2hâ€“q4h) IV/IM/SC q2hâ€“q6h PRN

Anti-em etics: 

Odansetron (Zofran): 4 m g (peds: 0.1 m g/kg IV div. q8h) IV q4hâ€“q8h PRN OR



Prom ethezine (Phenergan) 12.5â€“25 m g (peds: >2 yrs: 0.25â€“1 m g/kg/d IV/IM/PR div. q4hâ€“q6h PRN) IV/IM/SC q4h

Follow-Up Disposition Admission Criteria All patients with suspected/confirm ed intestinal obstruction should be adm itted with early surgical consultation.

References 1. Adam so W. Bowel Obstruction in the Newborn. Em edicine [on-line reference]. Available at http://www.em edicine.com /ped/topic2857.htm . Last updated June 15, 2004. 2. Elsakr R. Antim icrobial treatm ent of intra-abdom inal infections. Dig Dis 1998;16: 47â€“60. (DOI: 10.1159/000016848) 3. Kim ura K, Loening-Baucke V. Bilious vom iting in the newborn: rapid diagnosis of intestinal obstruction. Am Fam Physician. 2000;61:

Pa ge 8 1 4

2791â€“2798. 4. McCabe C. Obstruction, Large Bowel. Em edicine [on-line reference]. Available at http://www.em edicine.com /EMERG/topic65.htm . Last updated April 2005. 5. Nobie B. Obstruction, sm all bowel. Em edicine [on-line reference]. Available at http://www.em edicine.com /em erg/topic66.htm . Last accessed Novem ber 2005. Last updated Septem ber 2005. 6. Quickel R, Hodin RA. Clinical Manifestations and Diagnosis of Sm all Bowel Obstruction. UpToDate [on-line reference]. Available at http://www.uptodate.com . Last updated Februray 2005. 7. Quickel R, Hodin RA. Treatm ent of Sm all Bowel Obstruction. UpToDate [on-line reference]. Available at http://www.uptodate.com . Last updated January 2006. 8. Sanson TG, O'Keefe KP. Evaluation of abdom inal pain in the elderly. Em erg Med Clin North Am . 1996;14:615â€“627. 9. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865.

Codes ICD9-CM 560.9

ICD10 K57.6

Pa ge 8 1 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bradyarrhythm ias

Bradyarrhythmias

Adam Z. Barkin

Basics Description 

Defined as heart rate less than 60



Can be norm al variant



May present without sym ptom s

Etiology 

Sinus node dysfunction: o

Sick sinus syndrom e: 



Intrinsic disease: o



May alternate with tachycardia

Fibrous tissue replaces pacem aker cell

Extrinsic causes: o

Î²-blockers

o

Calcium channel blockers

o

Digoxin

o

Anti-arrhythm ics

o

Hypoxia

o

Hypotherm ia

o

Increased intracranial pressure

o

Increased vagal tone

o

Hypothyroid

Pa ge 8 1 6



o

Hyperkalem ia

o

Hypokalem ia

o

Hypoglycem ia

Atrioventricular node dysfunction: o

First degree aortic valve block: 

Pulse rate prolongation greater than 0.2 seconds

o



Every P wave conducts a QRS com plex.



May not be bradycardic

Second degree AV block, type Iâ€”Mobitz I (Wenckebach):

o

o





Progressive prolongation of PR segm ent



P wave eventually fails to conduct



Often grouped beating



Î²-blocker or calcium channel blocker toxicity



Digitalis



Inferior wall ischem ia



Increased vagal tone



Myocarditis

Second degree AV block, type IIâ€”Mobitz II: 

PR segm ents are constant



Interm ittent failure to conduct a QRS com plex



Anteroseptal ischem ia



Sclerodegenerative disease



Risk of third-degree heart block

Third-degree AV blockâ€”com plete heart block: 

Dissociation of atrial and ventricular activity



Cardiac ischem ia



Î²-blocker or calcium channel blocker toxicity



Digitalis toxicity



Hyperkalem ia

Junctional bradycardia:

Pa ge 8 1 7

o

Loss of atrial rhythm , atrioventricular pacem aker takes over at 45â€“60 im pulses per m inute



o

Î²-blocker or calcium channel blocker toxicity

o

Digitalis toxicity

o

Cardiac ischem ia

Idioventricular bradycardia: o

Loss of both sinoatrial and atrioventricular nodal activity; bundle branch or Purkinje network takes over at 30â€“40 im pulses per m inute

o

Myocardial infarction

o

Cardiac tam ponade

o

Severe acidem ia

o

Preterm inal rhythm

Pediatric Considerations Hypoxia is the m ost com m on cause.

Pregnancy Considerations Can see bradycardia in setting of ectopic pregnancy

Diagnosis Signs and Symptoms 

Asym ptom atic



Weakness



Syncope



Lightheaded/dizzy



Falls



Hypotension



Palpitations

History 

Medication changes

Pa ge 8 1 8



Urine output



Traum a related to falls

Physical Exam 

Mental status



Perfusion state

Essential Workup 

Twelve-lead electrocardiogram and continuous cardiac m onitoring



Pulse oxim etry



Blood pressure m onitoring

Tests Lab 

Serum glucose



Serum potassium



Serum electrolytes



Blood urea nitrogen



Creatinine



Cardiac enzym es



Digoxin level, if relevant



Thyroid function tests

Imaging Chest radiograph

Diagnostic Procedures/Surgery 

Transcutaneous pacing



Transvenous pacing

Differential Diagnosis 

Norm al variant



Î²-blocker toxicity



Calcium channel blocker toxicity

Pa ge 8 1 9



Digoxin toxicity



Hypoxia



Hypotherm ia



Hyperkalem ia



Hypokalem ia



Hypoglycem ia



Renal failure



Cardiac ischem ia



Increased intracranial pressure



Hypothyroidism

Treatment Pre Hospital 

Treat the patient, not the heart rate.



Epinephrine/atropine: o

May increase the rate but lead to increased ischem ia

o

Should be used only in patients with evidence of hypoperfusion

o

Atropine usually does not affect heart rate in third-degree heart block.



Transcutaneous pacing: o

Initiated for poor perfusion that cannot be corrected by other m eans

o

Must obtain ventricular capture, dem onstrated by a palpable pulse



Hypotherm ia: Avoid m edication or pacing.



Pediatrics: Correct hypoxem ia before attem pting to increase the heart rate.

P.161

Pa ge 8 2 0

Initial Stabilization 

ABC's



Apply pacing pads



Oxygen therapy



IV access

ED Treatment 

Atropine and/or epinephrine for sym ptom atic or unstable bradycardia



Isoproterenol for hem odynam ically unstable bradycardia



D 5 0 for hypoglycem ia



Î²-blocker or calcium channel blocker overdose o



Calcium gluconate and glucagon

Calcium , D 5 0 , insulin and sodium bicarbonate for hyperkalem ia



Digoxin antibodies for digoxin toxicity



Initiate treatm ent of ischem ia associated with the bradyarrhythm ia.



Correct acid-base disturbances



Tem porary transvenous pacing wire if other therapy is not successful

Medication (Drugs) 

Atropine: 0.5â€“1 m g (peds: 0.02 m g/kg; m in. dose of 0.1 m g) IV q3â€“5m in; m ax. dose of 0.04 m g/kg



Calcium gluconate: 1,000 m g (40â€“60 m g/kg) IV



D 5 0 : 25 g (peds: 1 cc/kg) IV



Epinephrine: 0.5â€“1 m g (peds: 0.01â€“0.03 m g/kg) IV q3â€“5m in; 1â€“4 m cg/m in (peds: 0.1â€“1 m cg/kg/m in) IV infusion

Pa ge 8 2 1



Glucagon: 0.05â€“0.15 m g/kg IV; 2â€“5 m g/h IV infusion



Isoproterenol infusion: 1â€“4 m cg/m in IV

Follow-Up Disposition Admission Criteria 



Intensive care unit: o

Hem odynam ically unstable bradycardia

o

Transvenous pacer

o

Pressor therapy

o

Acute m yocardial infarction or ischem ia

o

After/ongoing em ergent antidote treatm ent

Telem etry: o

Hem odynam ically stable bradycardia

Discharge Criteria Asym ptom atic sinus bradycardia

References 1. Birkhahn RH, Gaeta TJ, Tloczkowski J, et al. Em ergency m edicine-trained physicians are proficient in the insertion of transvenous pacem akers. Ann Em erg Med. 2004;43:469â€“474. 2. Brady WJ, Harrigan RA. Diagnosis and m anagem ent of bradycardia and atrioventricular block associated with acute coronary ischem ia. Em erg Med Clin North Am . 2001;19:371â€“384. 3. Kaushik V, Leon AR, Forrester JS, et al. Bradyarrhythm ias, tem porary and perm anent pacing. Crit Care Med. 2000: 28:N121â€“128. 4. Mangrum JM, DiMarco JP. The evaluation and m anagem ent of bradycardia. NEJM. 2000;342: 703â€“709.

Pa ge 8 2 2

Miscellaneous SEE ALSO: Acute Coronary Syndrom e; Î²-Blocker Overdose; Calcium Channel Blocker Overdose; Digoxin Overdose; Hyperkalem ia

Codes ICD9-CM 427.8

ICD10 I49.8

Pa ge 8 2 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bro nchio litis

Bronchiolitis

Suzanne Schuh

Basics Description Lower respiratory tract infection by airway inflam m ation and bronchoconstriction with wheezes/tachypnea and respiratory distress and upper respiratory prodrom e

Etiology 

Respiratory syncytial virus (RSV) in 85â€“90% of cases



Influenza



Parainfluenza



Adenovirus

Diagnosis Signs and Symptoms 

Age younger than 2 years



Nasal congestion



Cough



Wheezing



Crackles

Pa ge 8 2 4



Respiratory distress m anifested by nasal flaring, retractions, grunting



Fever usually <39.5Â°C



Cyanosis (rare)

Essential Workup 

Clinical diagnosis



Defining viral cause m ay be useful for cohorting in hospital if adm itted.



Assess ventilation clinically.



Pulse oxim etry: o

Confirm s proper oxygenation on continuing basis

o

Follows trends over the course of illness

Tests Lab 

Most patients need no specific tests beyond oxim etry.



Nasopharyngeal aspirate/wash: o

Viral cultures

o

Fluorescent antibodies

o

Com m ercial kits are available.

o

Consider when: 

Clinical sym ptom s suggestive of other causey (pertussis, chlam ydia)



Critically ill child



Coexisting signs suggesting bacterial sepsis (but positive aspirate does not rule out coexisting sepsis)



Bronchopulm onary dysplasia or chronic lung disease



Coexistent cardiac disease



Prem aturity



Other conditions warranting antiviral therapy

Pa ge 8 2 5

(rare)

Imaging Chest radiographs: 

Usually hyperinflation, airway disease, atelectasis, variable infiltrate



Minority have airway plus airspace disease; pneum onia usually viral



Rarely changes m anagem ent acutely



Consider when: o

Need to exclude other diagnoses such as congestive heart failure (CHF), aspiration, congenital airway anom aly (rare)

o

Chronic course with lack of resolution over 2â€“3 weeks

o

Critically ill infants with im pending respiratory failure

o

Atypical presentation in toxic or deteriorating child

o

Not indicated in typical clinical presentation

Differential Diagnosis 

Asthm a/recurrent virus-induced wheezing: severe bronchiolitis requiring hospitalization, and fam ily history of atopy are risk factors for future asthm a.



Pertussis: no respiratory distress between coughing spasm s, no wheezing



Bacterial pneum onia: often toxic appearance, no wheezing, isolated airspace disease (consolidation) with no airway abnorm ality on chest radiograph



Foreign body: sudden onset of sym ptom s, usually afebrile



CHF: pre-existing clinical red flags (failure to thrive [FTT], feeding problem s)

Pa ge 8 2 6

Treatment Pre Hospital Alert 

Young infants have lim ited respiratory reserve and decom pensate rapidly with little warning.



Monitor cardiorespiratory status and oxygenation.



Supplem ental oxygen if saturation 92% and/or severe distress



Watch for apneic pauses: o

Greatest risk in children younger than 3 m onths, prem ature



Bag-m ask ventilation if recurrent apneas

Initial Stabilization 

Pediatric advanced life support



Em ergent intubation if recurrent apneas, im pending respiratory failure

ED Treatment 

Supplem ental oxygen if oxygen saturation 92% (sea level)



Parenteral hydration if dehydration (rare) or severe respiratory distress P.163



Bronchodilators (albuterol, racem ic epinephrine, L-epinephrine, levalbuterol): o

Trial of bronchodilators warranted in all but m ildest cases

o

Evidence for variable and m odest clinical response but no evidence of im pact on hospitalization/econom ics

Pa ge 8 2 7

o

Trial of two to three consecutive treatm ents

o

Continue only if clear response with decrease in respiratory distress.

o

Racem ic epinephrine or L-epinephrine m ay be useful in m oderate to severe distress if poor response to albuterol or levalbuterol; cannot be used after discharge.



Steroids: o

Controversial

o

Dexam ethasone

o

Recent ED study suggests superior clinical efficacy and 50% lower hospitalization rate 4 hours after treatm ent in children with m oderate or severe disease; optim al duration of therapy is unknown.



Antibiotics: o

Alm ost never indicated since viral cause

o

Consider if associated signs of focal bacterial disease (otitis), radiographic evidence of isolated lobar consolidation without airway disease (usually bacterial pneum onia rather than bronchiolitis), significant toxicity, sepsis



Ribavirin: o

May rarely be indicated in the early course of hospitalization in children with severe underlying chronic disease

o

No role in ED m anagem ent

Medication (Drugs) 

Albuterol: 0.5 m L (2.5 m g) per dose via nebulizer with 3 m L norm al saline (NS) q20â€“30m in, or 400â€“500 Âµg per dose via m etered-dose inhaler (MDI)/spacer

Pa ge 8 2 8

q20â€“30m in 

Dexam ethasone: 0.6 m g/kg per dose PO; m ay be given parenterally if not tolerated orally



L-Epinephrine: 2.5 m L (1:1,000 solution) via nebulizer in 2 m L NS



Levalbuterol: 0.31â€“1.25 m g (unit dose vial) via nebulizer



Racem ic epinephrine: 0.25â€“0.75 m L via nebulizer in 3 m L NS



Ribavirin (Virazole): continuous inhalation 12â€“20/24h for 3â€“5 days

Follow-Up Disposition Admission Criteria 

Need for supplem ental oxygen



Inability to self-hydrate



Apnea



Severe underlying chronic lung disease or cardiac disease



Persistent severe respiratory distress after several doses of Î² 2 -agonists therapy or 4 hours after corticosteroids



Significant com orbidity/suspicion of alternative diagnosis/underlying system ic disease/im m unodeficiency or im m unosuppressive therapy



Strongly consider in infants younger than 8 weeks

Discharge Criteria 

Feeding well



Acceptable room air saturation



Absence of significant respiratory distress

Pa ge 8 2 9



Follow-up available within 24 hours

References 1. Dawson KP, Long A, Kennedy J, et al. The chest radiograph in acute bronchiolitis. J Paediatr Child Health. 1990;26:290â€“311. 2. Gadom ski AM, Lichensttein R, Horton L, et al. Efficacy of albuterol in the m anagem ent of bronchiolitis. Pediatrics. 1994;93:907â€“912. 3. Kellner JD, Ohlsson A, Gadom ski AM, et al. Efficacy of bronchodilator therapy in bronchiolitis. A m eta-analysis. Arch Pediatr Adolesc Med. 1996;150(11):1166â€“1167. 4. Menon K, Sutcliffe T, Klassen TP. A random ized trial com paring the efficacy of epinephrine with salbutam ol in the treatm ent of acute bronchiolitis. J Pediatr. 1995;126:1004â€“1007. 5. Reionen T, Korppi M, Pitkakangas S, et al. The clinical efficacy of nebulized racem ic epinephrine and albuterol in acute bronchitis. Arch Pediatr Adolesc Med. 1995;149:686â€“692. 6. Roosevelt G, Sheehan K, Grupp-Phelan J, et al. Dexam ethasone in bronchiolitis: a random ized controlled trial. Lancet. 1996;348:292â€“295. 7. Schuh S, Coates AL, Binnie R, et al. Efficacy of oral dexam ethasone in outpatients with acute bronchiolitis. J Pediatr. 2002;140:27â€“32.

Miscellaneous SEE ALSO: Asthm a, Pediatric

Codes ICD9-CM 466.1.9

ICD10 J21.9

Pa ge 8 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bro nchitis

Bronchitis

Robin R. Hemphill

Basics Description 

Hyperem ia and edem a of the m ucous m em branes



Production of m ucopurulent exudates



Im pairm ent of the productive function of the cilia, lym phatics, and phagocytes



Airway obstruction from : o

Edem a

o

Secretions

o

Bronchial m uscle spasm

Etiology 

Viral infections are the prim ary cause of bronchitis: o

Parainfluenza

o

Influenza A and B

o

Respiratory syncytial virus

o

Hum an m eta pneum ovirus

o

Echovirus

o

Coronavirus

o

Adenovirus

o

Coxsackievirus

o

Rhinovirus

Pa ge 8 3 1

o

Measles and herpes viruses (can cause severe viral bronchitis)



Particularly severe or long-lasting bronchitis: o

Mycoplasm a pneum oniae

o

Chlam ydia pneum oniae

o

Bordetella pertussis: 

Rates of pertussis are increasing, even in the fully im m unized population (little protection rem ains after 10 years).



Other bacteria have not been conclusively proven to cause bronchitis except in those with chronic lung disease.

Diagnosis Signs and Symptoms History 

Com plaints that m ay precede upper respiratory tract infection (URTI) sym ptom s:



o

Malaise

o

Chills

o

Myalgias

o

Coryza

o

Sore throat

Onset of URTI sym ptom s: o

Mile dyspnea

o

Cough, initially dry and nonproductive

o

Cough, later becom es m ucoid or m ucopurulent

o

Chest pain or burning related to cough

o

Initial sym ptom s im prove after 3â€“5 days, with 1â€“3 weeks of residual cough and m alaise

Pa ge 8 3 2

Physical Exam 

Fever, not usually above 102Â°F (38.5Â°C)



Tachypnea



Mild hem optysis



Wheezing



Rales



Scattered rhonchi



Pulm onary function tests are frequently abnorm al

Essential Workup 

The diagnosis is clinical



Pulse oxim etry



Influenza A and B testing if identification of these organism s is required for treatm ent or reporting



Evaluate for pertussis: o

Acute cough illness lasting 14 days or m ore in a person with paroxysm al cough, posttussive vom iting, or inspiratory whoop

o

14 days or m ore of cough within an outbreak setting

Tests Lab 

Influenza A and B testing m ay help im m ediately confirm clinical suspicion.



In m ost cases, no specific test will help m ake the diagnosis im m ediately.



Viral or bacterial cultures are rarely helpful.



CBC m ay show leukocytosis, but this is a nonspecific finding.



Pertussis m ay be confirm ed using polym erase chain reaction (PCR) testing, but diagnosis will be delayed.

Imaging

Pa ge 8 3 3

Chest radiograph: 

No evidence of consolidation



Indications: o

Shortness of breath

o

Hypoxia

o

Chest pain

o

Heart rate >100 beats/m inute

o

Respiratory rate â‰¥ 24 breaths/m inute

o

Tem perature â‰¥ 38Â°C

o

Focal findings on chest exam ination

o

Elderly patient with m ultiple com orbid conditions

o

Hypoxia

o

14 days or m ore of cough

Diagnostic Procedures/Surgery None specific

Differential Diagnosis 



Acute and subacute <8 weeks: o

Pneum onia

o

Reactive airway disease

o

Aspiration

o

Acute sinusitis

o

Bacterial tracheitis

o

Occupational exposure

Chronic >8 weeks: o

Asthm a

o

Gastroesophageal reflux disease

o

Chronic bronchitis

o

Bronchiectasis

o

ACE inhibitor use

o

Bronchogenic carcinom a

o

Carcinom atosis

Pa ge 8 3 4

o

Sarcoidosis

o

Left ventricular failure

o

Aspiration syndrom e

o

Psychogenic/habit

Pediatric Considerations 

Aggressive initial m anagem ent of these patients is seldom required.



Adm inister oxygen if the patient is hypoxic.



Fluids m ay be adm inistered if the patient is dehydrated.

P.165

Treatment Pre Hospital 

Maintain adequate oxygenation



Bronchodilators if wheezing is present

Initial Stabilization 

Aggressive initial m anagem ent of these patients is seldom required.



Adm inister oxygen if the patient is hypoxic.



Fluids m ay be adm inistered if the patient is dehydrated.

ED Treatment 

Bronchitis is usually a viral process; treatm ent is sym ptom atic.



Cough suppressants m ay be considered.



Î²-adrenergic inhaler for patients with severe cough or wheezing

Pa ge 8 3 5



Am antadine m ay be used in known outbreaks of influenza A.



Oseltam ivir (Tam iflu) and zanam ivir (Relenza) m ay be considered in patients with recent onset of influenza.



Antibiotics: o

Generally, antibiotics are not indicated (even when secretions are purulent).

o

Antibiotics do not im prove overall illness duration, activity lim itation, or work loss in healthy patients with no underlying lung disease.

o

Consider use in those patients who have recurrence of fever after initial im provem ent.



Sym ptom atic control with antipyretics and analgesics



Although patients should be encouraged to stop sm oking, the use of tobacco is not an indication for antibiotics unless the patient has a known history of em physem a.

Medication (Drugs) 

Albuterol: 0.5 m L in a 0.5% solution nebulized q6h



Am antadine: 100 m g PO per day, m ust be given within 48 hours of sym ptom onset



Oseltam ivir (Tam iflu) and zanam ivir (Relenza) within 48 hours of sym ptom onset for influenza-related bronchitis: o

Zanam ivir: 10 m g inhalation q12h Ã— 5 days (no pediatric dosing)

o

Oseltam ivir: 75 m g PO b.i.d. (peds: 2 m g/kg) Ã— 5 days



Erythrom ycin should be given to proven cases of pertussis and to household contacts of those with proven pertussis.



Yearly influenza vaccinations should be encouraged in health care providers and in the high-risk population

Pa ge 8 3 6

(elderly, im m unocom prom ised, chronic lung disease).

Pediatric Considerations 

Use of acetam inophen rather than aspirin for analgesia.



Repeated bouts in children should lead to referral for com plete evaluation of the respiratory tract.

Follow-Up Disposition Admission Criteria 

Underlying significant cardiopulm onary com prom ise



Significant hypoxia



Ill patient with unclear diagnosis

Discharge Criteria 

No pulm onary com prom ise should be present.



Instruct patients, particularly high-risk patients, to return if no im provem ent or worsening of sym ptom s occurs.



Bed rest



Fluids



Aspirin or acetam inophen

References 1. Aagaard E, Gonzales R. Managem ent of acute bronchitis. Infect Dis Clinic N Am . 2004; 18:919â€“937. 2. Gonzoles R, Sande MA: Uncom plicated acte bronchitis. Ann Intern Med. 2000;133:981â€“991. 3. Hirschm ann JV: Antibiotics for com m on respiratory tract infections in adults. Arch Intern Med. 2002; 162:256â€“264. 4. Linder JA, Sim s I: Antibiotic treatm ent of acute bronchitis in sm okers. A system ic review. J Gen Inern Med. 2002;17:230â€“234.

Pa ge 8 3 7

5. Stephens MM, Nashelsky J: Do inhaled beta-agonists control cough in URIs or acute bronchitis? J Fam Prac. 2004;53:662â€“663. 6. Ward MA: Em ergency departm ent m anagem ent of acute respiratory tract infections in adults. Sem Resp Infec. 2002:17:65â€“71.

Miscellaneous SEE ALSO: Cough; Shortness of Breath

Codes ICD9-CM 466 490

ICD10 J40

Pa ge 8 3 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bundle Branch Blo cks

Bundle Branch

Blocks Keith S. Boniface James Scott

Basics Description 

Blockage of intraventricular electrical im pulses through the right and left bundles



Com plete bundle branch block: o

Absence or delay of conduction down one bundle, with norm al conduction down the other bundle

o

Affected ventricle depolarizes from m uscle to m uscle in a slower and m ore disorganized fashion.

o

Quasi-random signal (QRS) com plex at 120 m sec or longer



Incom plete bundle branch block: o

Delayed depolarization, but less than com plete bundle branch block

o

QRS com plex less than 120 m sec and 100 m sec or longer



Right bundle branch block: o

Delayed depolarization of the right ventricle

Pa ge 8 3 9



Left bundle branch block: o

Delayed depolarization of the left ventricle

o

Left bundle branch block can be caused by delay of conduction in m ain left bundle or delay in both fascicles of the left bundle.

o

Causes early activation of the right side of the septum and the right ventricular m yocardium (so explaining loss of â€œseptal Qâ€• on ECG)

o

Left bundle branches into two fascicles: 

Left anterior fascicle: Initial septal activation proceeds inferiorly, anteriorly, and to the right.



Left posterior fascicle: rare; activation begins in the m idseptum and finishes in inferior and posterior walls.



Bifascicular block: o

Right bundle branch block with concom itant block of the left anterior or left posterior fascicle

Etiology 

Myocardial infarction



Cardiom yopathy



Hypertension



Age-related fibrosis of Purkinje fibers



Valvular disease



Exercise induced



Congenital/atrial septal defect



Brugada syndrom e (right bundle branch block): cause of sudden cardiac death in otherwise healthy patients



Chagas disease (especially Central/South Am erica)



Postoperative, following cardiac surgery



Drugs: o

Beta-blockers

o

Calcium blockers

Pa ge 8 4 0

o

Tricyclic antidepressants

o

Type Ia and Ic antiarrhythm ics

o

Digitalis

Diagnosis Signs and Symptoms 

Asym ptom atic



Right bundle branch block: split S 2 that persists with expiration



Left bundle branch block: reversed/paradoxic split S 2



Syncope



Chest pain

Essential Workup Electrocardiography: 

Right bundle branch block: o

Com plete: QRS com plex â‰¥ 0.12 seconds; incom plete: â‰¤ 0.10 seconds QRS com plex â‰¤ 0.12 seconds

o

rsrâ€², rsRâ€², rSRâ€² in V 1 or V 2 (M shape)

o

Wide and deep S wave in V 5 through V 6

o

Brugada syndrom e: RBBB and ST-segm ent elevation in V 1 through V 3



Left bundle branch block: o

Broad slurred R waves in leads V 5 through V 6 , aVL, and I

o

Sm all/absent R wave in V 1 through V 2 and deep S waves

o

Absence of norm al q waves in leads V5 through V6 and I

Pa ge 8 4 1



Left anterior fascicular block: o

QRS com plex <120 m sec, axis -45Â° to -90Â°

o

Deep S wave in leads II, III, aVF, qR in leads aVL and I



Left posterior fascicular block: o

QRS <120 m s, axis â‰¥120

o

RS waves in leads I and aVL, qR in leads II, III, and aVF

o

Exclusion of other things causing right axis deviation (right ventricle overload, right ventricular hypertrophy, lateral infarction)

Tests Lab 

Potassium if hyperkalem ia is suspected



Cardiac enzym es if ischem ia is suspected

Imaging 

Chest radiograph study: o

May reveal cardiac enlargem ent or congestive heart failure



Electrophysiologic testing: o

Especially for unexplained syncope in patient with structural heart disease, as part of inpatient workup

P.167

Differential Diagnosis 

Ventricular tachycardia



Myocardial infarction: o

Criteria for diagnosing m yocardial infarction with left bundle branch block: ST-segm ent elevation â‰¥1

Pa ge 8 4 2

m m concordant with QRS: 

ST-segm ent elevation â‰¥5 m m discordant with QRS



ST-segm ent depression â‰¥1 m m in leads V 1 through V 3



Hyperkalem ia



Ventricular hypertrophy



Drug effects (see Etiology section)

Treatment Pre Hospital Cautions: 

Monitor: difficult to diagnose from single lead



Avoid confusing with ventricular tachycardia or ischem ia.



Treat patient; bundle branch block requires no specific therapy.

Initial Stabilization 

Standard treatm ent for sym ptom s of ischem ia, shortness of breath, and syncope



Bifascicular block and sym ptom atic high-degree atrioventricular block: o

Apply transcutaneous pacing pads to back and chest.

o

IV sedation and analgesia

o

Gradually increase current until capture is achieved.

ED Treatment 

Asym ptom atic: none



Throm bolysis for sym ptom s suggestive of m yocardial infarction and new bundle branch block



Transvenous pacem aker indications:

Pa ge 8 4 3

o

Bifascicular block and type II second- or third-degree atrioventricular block

o

Alternating left and right bundle branch block

Follow-Up Disposition Admission Criteria 

Concern about m yocardial ischem ia



Syncope



Bundle branch block with advanced atrioventricular block or com plete heart block

Discharge Criteria Asym ptom atic or incidental finding of bundle branch block

Issues for Referral At discharge, patient should be referred to cardiologist for underlying disease.

References 1. Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045â€“2050. 2. Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segm ent elevation in leads V1 through V3: a m arker for sudden death in patients without dem onstrable structural heart disease. Circulation. 1998;97:457â€“460. 3. Gregoratos G, Abram s J, Epstein AE, Freedm an RA, Hayes DL, Hlatky MA, Kerber RE, Naccarelli GV, Schoenfeld MH, Silka MJ, Winters SL. ACC/AHA/NASPE 2002 guideline update for im plantation of cardiac pacem akers and antiarrhythm ia devices: a report of the

Pa ge 8 4 4

Am erican College of Cardiology/Am erican Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Com m ittee on Pacem aker Im plantation). 2002. Available at: http://www.acc.org/clinical/guidelines/pacem aker/pacem aker.pdf 4. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of acute m yocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasm inogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med. 1996;334:481â€“487. Erratum in: N Eng J Med. 1996; 334:931.

Codes ICD9-CM 426.2 to 426.5

ICD10 I45.4

Pa ge 8 4 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Burns

Burns

Michael Waters Scott Rudkin

Basics Description Burn injuries represent an acute disruption of the skin.

Etiology Burns can be classified into six categories: 

Scaldâ€”hot liquids, grease, or steam



Contactâ€”hot or cold surfaces



Therm alâ€”fire or flam es



Radiation burns



Chem ical burns



Electrical burns

Diagnosis Signs and Symptoms 

Most burns will have external signs of integum entary dam age.



Inhalation injury:

Pa ge 8 4 6



o

Facial burns

o

Carbonaceous sputum

o

Pharyngeal injection

o

Wheezing

o

Hoarseness

o

Singed nasal hair

Electrical burns m ay have m inim al external findings.

History 

Inform ation from em ergency m edical services (EMS), fam ily, friends, or witnesses m ay be required.



Medical history, surgical history, m edications, allergies, social history, tetanus im m unization status



Carbon m onoxide poisoning with exposure to com bustion



Cyanide poisoning from burning wool, silk, nylon, and polyurethane found in furniture and paper

Physical Exam 

Focus on airway, breathing first, then head-to-toe secondary survey for concurrent injuries.



Evaluate face and oropharynx for signs of inhalation injury.



Assess need for im m obilization of cervical spine.



Eye exam ination for corneal burns



Determ ine severity of partial- and full-thickness burns by assessing size and depth of burn: o

Estim ate surface area involved.

Pediatric Considerations Specific patterns of injury m ay indicate nonaccidental injury (stockinglike or glovelike appearance of wounds, cigarette burns, etc.)

Essential Workup

Pa ge 8 4 7

The severity of the burn should be assessed by determ ining the size and depth.

Size 

Reported as percent involvem ent of total body surface area (TBSA) in one of three ways:



1â€”Rule of nines: o

TBSA of body parts is estim ated by m ultiples of 9%; applies to adults only.

o

o

Adult estim ates of percentage of TBSA: 

Head and neck: 9



Arm s: right, 9; left, 9



Legs: right, 18; left, 18



Trunk: front, 18; back, 18



Perineum , palm s: 1

In infants and children, the head contributes m ore to the percentage of TBSA and legs contribute less.

o



Infants/children: 

Head and neck: 18



Arm s: right, 9; left, 9



Legs: right, 14; left, 14



Trunk: front, 18; back, 18

2â€”Lund and Browder chartâ€”divides body into areas and assigns percentage of BSA based on age



3â€”Palm surface areaâ€”patient's palm is approxim ately 1% of TBSA: o

Estim ate size in term s of num ber of patient's palm s that cover burn.

o

Helpful in assessing sm aller, scattered burns

Depth 

Superficial or first-degree burns (epiderm is only): local erythem a and pain only, no blisters; healing occurs in

Pa ge 8 4 8

several days 

Partial-thickness or second-degree burns (epiderm is and derm is): divided into superficial partial-thickness and deep partial-thickness burns: o

Superficial partial-thickness: epiderm is and superficial derm is: 

Skin is red, m oist, painful, good capillary refill, develop blisters

 o

Heals in 14â€“21 days

Deep partial-thickness: epiderm is and deep derm is: 

Skin m ay be blistered, with derm is white to yellow; absent capillary refill, and pain sensation

 

Heals via epithelialization within 3â€“12 weeks

Full-thickness or third-degree burns (epiderm is and derm is, extends into subcutaneous tissue): o

Skin is charred, leathery and pale, no blisters.

o

Sensation absent

o

Lesions will not heal spontaneously; needs surgical repair and skin grafting.

o

Full-thickness burns with dam age to underlying m uscle or fourth-degree burns:

o

Full-thickness plus involvem ent of underlying fascia, m uscle, bone, and other tissues

o

Requires extensive dÃ©bridem ent

o

Resultant disability

Tests Lab 

For severe burns, obtain CBC, serum electrolytes, glucose, BUN, creatinine, and PT/PTT, type and cross-m atch, pregnancy test (fem ale)

Pa ge 8 4 9



Blood gas with carbon m onoxide level for closed space or inhalation exposures



Cyanide level if suspected

Imaging 

Chest radiograph



Fiber optic bronchoscopy to assess inhalation injury

Differential Diagnosis 

Electrical injury



Chem ical injury



Associated traum a or intoxication

Treatment Pre Hospital 

Stop the burning process, rem ove sm oldering clothes/jewelry.



Establish patent airway; frequent reassessm ent: o

Intubate early for signs of respiratory distress.



Initiate early IV fluid therapy.



Relieve pain.



Protect the wound with clean sheets.



Transport to burn center (for m ajor burns) if transport tim e shorter than 30 m inutes.



Im m obilize spine if decreased sensorium or traum a.

Initial Stabilization 

Airway control param ount: o

Early intubation for patients with signs of upper airway injury, significant nasolabial burns, or circum ferential neck burns

Pa ge 8 5 0



IV access, supplem ental 100% oxygen, m onitor, pulse oxim etry



Evaluation for concurrent injuries



Provide adequate analgesia.

ED Treatment Fluid Resuscitation: Partial and Full-thickness Burns (>20% TBSA) 

Parkland form ula: 4 m L of lactated Ringer solution or norm al saline (NS) per kilogram per percentage of BSA burned IV; one half of this total is given in the first 8 hours and the rem aining half over the next 16 hours: o

Exam ple: 70-kg patient with a 40% TBSA burn requires 4 m L Ã— 70 kg Ã— 40% = 11,200 m L over 24 hours, with 5,600 m L over first 8 hours or 700 m L/h.



For large burns, >20% TBSA, IV fluid therapy should be guided by invasive hem odynam ic m onitoring or urine output; m aintain urine output of 0.5 to 1.0 m L/kg/h for adults and 1.0â€“1.5 m L/kg/h for children.

P.169

Escharotomy 

Circum ferential burn eschar m ay lead to neurovascular com prom ise: o

Monitor pulses; m ay need Doppler flow probe.

o

Elevate burned extrem ity.

o

If circulation is com prom ised, escharotom y incisions on extrem ities should be m ade m edially and laterally along the long axis of the lim b just to the

Pa ge 8 5 1

subcutaneous layer through the entire length of the burn eschar. 

A circum ferential burn of the chest wall m ay prevent adequate ventilation unless escharotom y is perform ed: o

Make longitudinal incisions at anterior axillary line from the second rib to the level of the twelfth rib; connect with two transverse incisions across the chest.

Wound Care 

Cover the wounds with sterile m oist saline dressings.



If disposition is delayed, cleanse with sterile saline or poloxam er 188 product (e.g., Shur-Clens), dÃ©bride blisters except those on palm s or soles, and apply topical antibacterial agent (e.g., silver sulfadiazine, bacitracin, or m afenide acetate).



Do not delay transfer to burn unit for wound care.



Prophylactic antibiotics not indicated

Outpatient Management of Minor Burns 

Sterile technique for cleansing and dÃ©bridem ent



Rem ove loose, necrotic skin; dÃ©bride broken, tense, or infected blisters.



Topical antibacterial agents: (e.g., silver sulfadiazine, bacitracin, m afenide acetate) recom m ended in deep partial-thickness or full-thickness burns only



Three-layer burn dressings should keep the wound m oist and absorb exudate: o

Inner layer should be nonadherent porous m esh gauze saturated with a non-petroleum -based lubricant, or use a m ild ointm ent (e.g., bacitracin or Polysporin) under a nonadherent porous gauze.

o

The next layer should be fluffed coarse-m esh gauze.

Pa ge 8 5 2

o

The outer wrap should keep the dressing in place without constricting.

o 

Dressings should be changed at least daily.

Silver wound dressings (Silverlon and Acticoat): o

Thin coating of m etallic silver applied to knitted fabric backing

o

Requires dressing to rem ain m oist

o

May leave on for up to 3 days

Pediatric Considerations 

Parkland form ula underestim ates fluid requirem ents in children; the Galveston form ula m ay be used instead: 5,000 m L/m 2 BSA burned plus 2,000 m L/m 2 .



TBSA of 5% dextrose in lactated Ringer solution IV over the first 24 hours, half in the first 8 hours and the other half over the next 16 hours



Consider nonaccidental traum a, particularly with burns on the back of hands or feet, buttocks, the perineum , and the legs.



Avoid hypotherm ia: o

Children have greater BSA/m ass ratio and lose heat m ore rapidly.



Avoid hypoglycem ia: o

Children are m ore prone to hypoglycem ia owing to lim ited glycogen stores.

Pregnancy Considerations 

Significant m orbidity to m other and child



Fluid requirem ents m ay exceed estim ations.



Fetal m onitoring and early obstetric consultation recom m ended

Pa ge 8 5 3

Medication (Drugs) 

Bacitracin ointm ent: Apply to wound oneâ€“four tim es per day.



Mafenide (Sulfam ylon) acetate cream : Apply to wound one or two tim es per day.



Morphine: 0.1â€“0.2 m g/kg titrated to effect for pain control after shock



Silverlon and Acticoat: Cut sheet to size of burn; m oisten with sterile water.



Silver sulfadiazine cream : Apply to wound one or two tim es per day.



Tetanus toxoid or im m unoglobulin: 0.5 m L IM; 250 U IM once along with toxoid

Follow-Up Disposition Admission Criteria N/A

Injuries Requiring Admission 

Partial-thickness burns of noncritical areas (not the eyes, ears, face, hands, feet, or perineum ) involving 10â€“20% of BSA in adults (older than 10 years and younger than 50 years)



Partial-thickness burns of noncritical areas involving 5â€“10% of BSA in children younger than 10 years



Suspicion of nonaccidental traum a



Patients unable to care for wounds in outpatient setting (e.g., hom eless patients)

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Injuries Requiring Transfer and Admission to a Burn Center 

Partial-thickness and full-thickness burns involving â‰¥10% of BSA in patients younger than 10 years or older than 50 years



Partial-thickness and full-thickness burns over >20% of BSA in any patient



Full-thickness burns involving >5% of BSA



Partial-thickness and full-thickness of face, hands, feet, genitalia, perineum , or m ajor joints



Electrical burns, including lightning injury



Significant chem ical injury



Inhalation injury



Burn injury in patients with pre-existing illness that could com plicate m anagem ent



Burn injury in patients with a concom itant traum a or social barrier

Discharge Criteria Partial-thickness burns of <15% of BSA in adults (<10% in children) involving noncritical areas only and in patients able to m anage wounds as outpatients and follow up reliably

References 1. Com m ittee on Traum a, Am erican College of Surgeons. Guidelines for the operation of burn units. Resources for Optim al Care of the Injured Patient 1999.1998:55. 2. Holm C, et al. A clinical random ized study on the effects of invasive m onitoring on burn resuscitation. Burns. 2004;30(8):798â€“807. 3. Kavanagh S, et al. Care of burn patients in the hospital. Burns. 2004;30(8):A2â€“6.

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4. Schwartz LR. Therm al burns. In: Tintinalli JE, Kelen GD, Stapczynski JS. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill, 2004:1220â€“1226. 5. Tom pkins D, et al. Care of out patient burns. Burns. 2004;30(8):A7â€“9.

Codes ICD9-CM 940.0â€“949.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bursitis

Bursitis

Kelly Pettit

Basics Description 

Bursae are synovial fluid-filled sacs: o

Approxim ately 150 located between bones, ligam ents, tendons, m uscles, and skin

o

Provide lubrication to reduce friction during m ovem ent



Bursitis is inflam m ation of a bursae caused by traum a (acute or chronic), repetitive use, prolonged pressure, infection, crystal deposition, or system ic disease.



Affected joints: o

Potentially any bursa m ay be affected.

o

Com m only affected joints: 

Shoulder



Elbow: usually secondary to traum a



Wrist and hand



Hip: m ore com m on in elderly



Knee: secondary to traum a or arthritis



Foot: calcaneal bursitis is alm ost always secondary to im properly fitting shoes/heels.

Etiology

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

Traum a (m ost com m on cause): o

Specific traum atic event or repetitive use of associated joints



Infection: m ay be obvious or m icroscopic: o

Higher risk with diabetes, chronic alcohol abuse, urem ia, gout, im m unosuppression

o

90% caused by staphylococci



Crystal deposition: calcium phosphate, urate



System ic disease: rheum atoid arthritis, gout, ankylosing spondylitis, psoriatic arthritis, lupus, rheum atic fever

Diagnosis Signs and Symptoms History 

Acute onset, but m ay be chronic (especially in hip)



Elicit history of traum a, overuse, or prolonged pressure.



Screen for system ic disease.

Physical Exam 

Localized pain that worsens with m ovem ent of structures adjacent to affected bursae



Often reduced active range of m otion (ROM) with preserved passive ROM



Localized swelling m ay be present with superficial bursal involvem ent.



Overlying erythem a, warm th, or skin traum a m ay be present with infectious bursitis.



May have low-grade tem perature

Essential Workup 

Full assessm ent of adjacent m usculoskeletal structures

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

Any suspicion of infection warrants aspiration of bursae (especially olecranon and prepatellar bursae).



Aspiration of hip and other deep bursae m ay be guided in ED by ultrasound or deferred to interventional radiology, orthopedics, or rheum atology.

Tests Lab 

Serum labs: o

Suspected infection: CBC with differential

o

Evaluation of related system ic disease (e.g., uric acid level for gout)

o 

Send serum glucose if bursal fluid aspiration is done.

Bursal fluid analysis: o

Send fluid for cell count with differential, glucose, total protein, crystal determ ination, Gram stain, and culture.

o

Because infection and inflam m ation m ay be difficult to differentiate, cultures m ust always be sent.

o

Norm al fluid: Fluid is clear yellow with 0â€“200 WBCs, 0 RBCs, low protein, and glucose is sam e as serum .

o

Traum atic bursitis: Fluid is bloody/xanthochrom ic with <1,200 WBCs, m any RBCs, low protein, and norm al glucose.

o

Infective bursitis: Fluid is cloudy yellow with >50,000 WBCs, few RBCs, slightly increased protein, and decreased glucose; bacteria on Gram stain.

o

Rheum atoid and m icrocrystalline inflam m ation: fluid is yellow, can be cloudy, and has 1,000â€“40,000 WBCs, few RBCs, slightly increased protein, and variable glucose; use polarizing m icroscope to

Pa ge 8 5 9

identify crystals.

Imaging 

Radiographs m ay dem onstrate chronic arthritic changes or calcium deposits: o

Recom m ended when traum a is involved to rule out fracture or foreign body



MRI and ultrasound m ay aid in diagnosis of deep bursitis and in defining the extent of infectious bursitis.

Differential Diagnosis 

Arthritis, gout



Tendonitis, fasciitis, epicondylitis



Fracture, tendon/ligam ent tear, contusion, sprain



Osteom yelitis



Also in hips: neuritis, lum bar spine disease, sacroiliitis

Treatment Pre Hospital May be difficult to distinguish from fractures; suspicious joints should be im m obilized, particularly in the setting of traum a.

Initial Stabilization Im m obilize joint if pain severe: 

Shoulders should not be im m obilized for >2â€“3 days because of the risk of adhesive capsulitis.

P.171

ED Treatment 

Noninfectious bursitis:

Pa ge 8 6 0

o

Rest and rem oval of aggravating factors (e.g., avoid direct pressure and repetitive use)

o

Ice affected areas for 10 m inutes, four tim es a day until im proved; m ay alternate with heat.

o

Nonsteroidal anti-inflam m atory drugs (NSAIDs) for at least 7 days; best if continued for 5 days after im provem ent to help prevent recurrence

o

If no im provem ent within 5â€“7 days and infection has been ruled out (by culture), injection of lidocaine and steroids m ay be considered: 

Mix 2 m L of 2% lidocaine with 20â€“40 m g of depoglucocorticoid and inject 1â€“3 m L of this m ixture into the bursae using sterile technique.



Steroid injections should not be repeated until at least 4 weeks have passed, and no m ore than two injections into one joint should be perform ed without rheum atologic or orthopedic consultation.



Septic bursitis: o

Olecranon: Aspiration and antibiotics m ay be sufficient with close follow-up.

o

Other m ajor bursae: antibiotics and drainage of bursae (leaving in perforated drainage catheter can reduce period of treatm ent and avoid eventual bursectom y)

o

Base antibiotic choice on the Gram stain: 

Penicillinase-resistant antistaphylococcal drug m ay be used if Gram stain result is negative or shows gram -positive cocci.



If gram -negative organism s are found, blood cultures should be done and another prim ary source for the infection should be sought.

Pa ge 8 6 1

o

Antibiotics should be continued for 5â€“7 days beyond the sterilization of bursal fluid.



Treat associated diseases as needed (e.g., gout).

Medication (Drugs) 

NSAIDs (m any choices; a few are listed here): o

Diclofenac: 50 m g PO b.i.d./t.i.d.

o

Ibuprofen: 600 m g PO q6h (peds: 5â€“10 m g/kg PO q6h)



o

Ketorolac: 30 m g IV/IM q6h or 10 m g PO q4hâ€“q6h

o

Piroxicam : 20 m g PO daily

Corticosteroids: o

Methylprednisolone acetate: 20â€“40 m g single intrabursal injection

o

Triam cinolone acetonide: 20â€“40 m g single intrabursal injection

Follow-Up Disposition 

Most patients m ay be treated as outpatients.



Most patients respond to therapy in 3â€“4 days and m ay follow up within a week.



Septic bursitis requires repeated bursal aspiration every 3â€“5 days until sterile.

Admission Criteria 

Patients with high fevers, chills/rigors, large surrounding cellulitis, unable to take oral antibiotics, failed outpatient therapy, or im m unosuppressed

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

Unusual organism s, extrabursal prim ary site, or deep bursal involvem ent

Issues for Referral Rheum atology or orthopedic referral is recom m ended for patients who do not respond to intrabursal steroids or recurrent bursitis.

References 1. Butcher JD, et al. Lower extrem ity bursitis. Am Fam Physician. 1996;53(7):2317â€“2324. 2. Chau CL, Griffith JF. Musculoskeletal infections: ultrasound appearances. Clin Radiol. 2005;60(2):149â€“159. 3. Greene WB, ed. Essentials of Musculoskeletal Care. 2nd ed. Rosem ont, IL: Am erican Academ y of Orthopedic Surgeons; 2001: 20â€“23, 335â€“337, 368â€“370, 402â€“403. 4. Gutierrez G, Burroughs M, Poddar S. Clinical inquiries. Does injection of steroids and lidocaine in the shoulder relieve bursitis? J Fam Pract. 2004;53(6):488â€“492. 5. Larsson L, Baum J. The syndrom es of bursitis. Bull Rheum Dis. 1986;36(1):1â€“8.

Codes ICD9-CM 727.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C alcium C hannel Blo cker, Po iso ning

Calcium

Channel Blocker, Poisoning Janet Eng

Basics Description Three Classes of Calcium Channel Blockers 

Phenylalkylam ines (verapam il): o

Vasodilation resulting in a decrease in blood pressure (BP)

o

Negative chronotropic and inotropic effects: reflex tachycardia not seen with a drop in BP.



Dihydropyridine (nifedipine): o

Decreased vascular resistance resulting in a drop in BP

o

Little negative inotropic effect: reflex tachycardia occurs.



Benzodiazepine (diltiazem ): o

Decreased peripheral vascular resistance leading to a decrease in BP

o

Heart rate (HR) and cardiac output initially increased

o

Direct negative chronotropic effect, which leads to a fall in HR

Pa ge 8 6 4

Effects of Calcium Channel Blockade 

Calcium plays key role in cardiac and sm ooth m uscle contractility.



Calcium channel blockers (CCBs) prevent: o

The entry of calcium , resulting in a lack of m uscle contraction

o

The norm al release of insulin from pancreatic islet cells, resulting in hyperglycem ia

Diagnosis Signs and Symptoms 





Cardiovascular: o

Hypotension

o

Bradycardia

o

Reflex tachycardia (dihydropyridine)

o

Conduction abnorm alities/heart blocks

Neurologic: o

CNS depression

o

Com a

o

Seizures

Metabolic: o

Hyperglycem ia

Essential Workup ECG: 

Bradycardia (tachycardia with nifedipine)



Conduction delays: QRS-com plex prolongation



Heart blocks

Tests

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Lab 

Ionized calcium level when adm inistering calcium



Digoxin level if patient taking digoxin (dictate safety of calcium adm inistration)



CBC



Electrolytes, BUN, creatinine, glucose: o



Hyperglycem ia/m etabolic acidosis m ay occur.

Toxicology screen if coingestants suspected

Differential Diagnosis 

Î²-Blocker toxicity



Clonidine toxicity



Digitalis toxicity



Acute m yocardial infarction with heart block

Treatment Pre Hospital Cautions: 

Transport pill/pill bottles to ED.



Calcium for bradycardic/unstable patient with confirm ed CCB overdose

Initial Stabilization Airway, breathing, circulation (ABCs): 

Airway protection as indicated



Supplem ental oxygen as needed



0.9% norm al saline (NS) IV access



Hem odynam ic m onitoring

ED Treatment

Pa ge 8 6 6

Goals 

Heart rate >60 beats/m inute



Systolic BP >90 m m Hg



Adequate urine output



Im proving level of consciousness

GI Decontamination 

Syrup of ipecac: contraindicated in the ED



Activated charcoal: o

May be helpful, especially in the presence of coingestants



Whole bowel irrigation: o

Beneficial with ingestion of sustained-release preparations

o

Contraindicated in hem odynam ically unstable patients

P.173

Calcium 

First-line agent for CCB toxicity



Calcium chloride (10%): o

Contains 1.36 m Eq Ca 2 + /m L (three tim es m ore calcium than calcium gluconate)

o

Can cause tissue necrosis and sloughing with extravasation

o 

Very irritating to veins

Calcium gluconate (10%): o

Contains 0.45 m Eq Ca 2 + /m L

o

Does not cause tissue necrosis as calcium chloride does

o

Calcium gluconate: preferred agent in an acidem ic

Pa ge 8 6 7

patient 

Follow serum calcium levels if repeated doses of calcium adm inistered.



Contraindicated in digoxin toxicity because calcium can produce serious adverse effects in digoxin toxicity

Bradycardia/Hypotension 

IV fluids: o

Adm inister cautiously in the hypotensive patient.

o

Swan-Ganz catheter or central venous pressure (CVP) m onitoring to help follow volum e status



Atropine usually ineffective



Pressor agents: o

No clear evidence that one agent is m ore effective than another

o

Institute invasive m onitoring to help guide treatm ent.

o

Dopam ine: 

Î² 1 -Receptor agonist at low doses, which causes a positive inotropic effect on the m yocardium



Î±-Receptor agonist at higher doses, which leads to vasoconstriction

o

Epinephrine: 



Potent Î±- and Î²-receptor agonist

Glucagon: o

Prom otes cAMP production through a receptor site other than the Î²-receptor





o

May cause nausea and vom iting

o

Mix with NS or 5% dextrose in water.

Am rinone: o

Selective phosphodiesterase III inhibitor

o

Indirectly increases cAMP

Electrical pacing: when other treatm ent options have

Pa ge 8 6 8

failed 

Insulin: o



Prom otes m ore efficient m yocardial m etabolism

Hypertonic sodium bicarbonate: o

Potential treatm ent in the future

Medication (Drugs) 

Am rinone: loading dose 0.75 m g/kg; m aintenance drip 2â€“20 Âµg/kg/m in; titrate for effect



Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5â€“1.0 m g IV (peds: 0.04 m g/kg)



Calcium chloride: 10 m L of 10% solution slow IVP (peds: 0.2â€“0.25 m L/kg; repeat in 10 m inutes if necessary) followed by infusion 20â€“50 m g/kg/h



Calcium gluconate: 10 m L of 10% solution slow IVP (peds: 1 m L/kg; m ay repeat in 10 m inutes if necessary)



Dopam ine: 2â€“20 Âµg/kg/m in; titrate to effect



Epinephrine: 2 Âµg/m in (peds: 0.1 Âµg/kg/m in); titrate to effect



Glucagon: 3.5â€“5 m g (peds: 0.03â€“0.1 m g/kg) IV bolus followed by 70 Âµg/kg/h infusion



GoLYTELY WBI: 2 L/h PO or by nasogastric tube (NGT) for 4â€“6 hours or until rectal effluent is clear (peds: 40 m L/kg/h)



Insulin: 1 IU/kg bolus IV followed by 0.5â€“1.0 IU/kg/h titrated to clinical response

Follow-Up

Pa ge 8 6 9

Disposition Admission Criteria 

Adm it sym ptom atic patients to a m onitored bed for hem odynam ic m onitoring.



Adm it all patients who ingested sustained-release CCBs for 24 hours of observation and m onitoring owing to the potential delay in sym ptom s.

Discharge Criteria Discharge asym ptom atic patients 8 hours after ingestion of im m ediate-release preparation.

References 1. Boyer EW, Shannon MW. Treatm ent of calcium channel blocker intoxication with insulin infusion. New Engl J Med. 2001;344:1721â€“1722. 2. Kalm an S, Berg S, Lisander B. Com bined overdose with verapam il and atenolol: treatm ent with high doses of adrenergic agonists. Acta Anaesthesiol Scand. 1998;45:379â€“382. 3. Salhanick SD, Shannon MW. Managem ent of calcium channel antagonist overdose. Drug Safety. 2003;26:65â€“79. 4. Tanen DA, Ruha AM, Curry SC, et al. Hypertonic sodium bicarbonate is effective in the acute m anagem ent of verapam il toxicity in swine m odel. Ann Em erg Med. 2000;36:547â€“553.

Miscellaneous SEE ALSO: Î²-Blocker, Poisoning

Codes ICD9-CM 977.9

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ICD10 T46.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C andidiasis, Oral

Candidiasis, Oral

Howard K. Mell Kristine M. Thompson

Basics Description 

Infection of oral m ucosa with any species of Candida, m ost com m only Candida albicans



Candida norm ally present as oral flora in 20â€“60% of the healthy population.



Several variations exist, ranging in severity from superficial and localized to severe system ic disease with 50% m ortality.



In im m unocom petent individuals, a benign course is the norm .



Often recurrent in im m unocom prom ised patients



May represent an early m anifestation of AIDS in HIV-infected patients

Etiology 

Usually overgrowth of Candida albicans from alterations in intraoral environm ent



Antim icrobial treatm ent



Changes in salivary flow (anticholinergic m edications, steroid inhalers, psychotropics, and others)

Pa ge 8 7 2



Presence of dentures or other orthodontic appliances



Interruption of epithelial barrier (cheek biting)



Endocrinopathies (diabetes, hypothyroidism )



Im m unosuppression (iatrogenic, congenital, or acquired)

Acute Pseudomembranous Candidiasis (Thrush) 

Com m only occurs with other serious underlying conditions (diabetes, leukem ia, AIDS)



Frequently m edication induced in the im m unocom petent

Acute and Chronic Atrophic Candidiasis Occurs in up to 60% of denture wearers

Angular Cheilosis 

Often seen with intraoral candidal infection



Loss of skin barrier from repetitive irritation



Often superinfected with Staphylococcus epiderm idis

Hyperplastic Candidiasis 

Im m unosuppressed individuals



High incidence of m alignant degeneration in tobacco users

Geriatric Considerations 

Candida organism s are norm ally present as oral flora in up to 80% of elderly or those in long-term care facilities.



The presence of dentures or other orthodontic appliances can lead to the overgrowth of candida.



Angular cheilosis is m ore com m on in the elderly secondary to facial wrinkling.

Pediatric Considerations 

Acute pseudom em branous candidiasis (thrush) is com m on in infancy likely because of im m aturity of their im m une system and lack of m ature oral flora.

Pa ge 8 7 3



The source of infection is believed to be m aternal birth canal.

Diagnosis Signs and Symptoms Pseudomembranous Candidiasis (Thrush) 

Painless white m ucosal plaques



Adherent but rem ovable



Erythem atous base



May becom e confluent and curdlike



Anorexia

Atrophic Candidiasis (Denture Stomatitis) 

Burning sensation in m outh or on tongue



Erythem atous with few, if any, white patches



Usually lim ited to the denture-bearing m ucosa

Angular Cheilosis 

Cracking and erythem a at the corners of the m outh



Lesion can be asym ptom atic, pruritic, or painful.

Hyperplastic Candidiasis 

Chronic, invasive ulcers



Typically on lateral borders of tongue or buccal m ucosa

Essential Workup 

Determ ine whether there is a cause for a breakdown of host factors.



If no reason is found, evaluate for possible HIV infection or diabetes.



Exclude a system ic infection.

Pa ge 8 7 4

Tests Lab 

CBC if suspect severe infection



Glucose testing



Potassium hydroxide (KOH)/fungal culture

P.175

Differential Diagnosis 

Hairy leukoplakia



Hyperkeratosis



Lichen planus



Squam ous cell carcinom a



Adherent food/m ilk

Treatment ED Treatment 



Topical antifungal m edications: o

Clotrim azole

o

Itraconazole

o

Nystatin

o

Com bine with topical steroid for angular cheilosis.

System ic agents (should be reserved for those with disease resistant to topical therapy):



o

Fluconazole

o

Itraconazole

o

Ketoconazole

Analgesia:

Pa ge 8 7 5

o

â€œMagic m outhwashâ€•: 

Form ulas vary by institution; one com m only used is equal parts viscous lidocaine, diphenhydram ine elixir, and m agnesium alum inum hydroxide.

Medication (Drugs) Pediatric Considerations 

Dissolve troche in nipple of bottle.



Mix suspensions with fruit juice and freeze into popsicle.



Apply suspensions to affected areas with cotton-tipped swab.

Topical 

Clotrim azole: 10-m g troche five tim es daily (children >3 years)



Itraconazole: 10 m L solution (peds: 5 m g/kg/d, m ax. 600 m g/d) swish and swallow daily



Nystatin oral suspension: 6 m L (peds: infants 2 m : PO; children 4â€“6 m L PO) swish and swallow four tim es daily



Nystatin/triam cinolone ointm ent: Apply twice daily.



Nystatin troche: 1 or 2 troches (peds: infants one-half troche, children 1 troche) 4â€“5 tim es daily

Systemic 

Fluconazole: 200 m g day 1, then 100 m g (peds: <14 days old 6 m g/kg, then 3 m g/kg; >14 days old 12 m g/kg, then 6 m g/kg, m ax. 400 m g daily) PO daily



Itraconazole solution: 200 m g (peds: 5 m g/kg/d) PO twice daily



Ketoconazole: 200 m g (peds: 5â€“10 m g/kg) PO daily

Pa ge 8 7 6



Nystatin: one or two tabs (peds: use oral suspension as above) PO three tim es daily

Follow-Up Disposition Admission Criteria 

Inability to tolerate oral intake owing to discom fort



Newly diagnosed im m unocom prom ised state



System ic infection

Discharge Criteria Patients with candidiasis that does not threaten the patient's hydration status m ay be discharged with close follow-up.

References 1. Fotos PG, Lilly JP. Clinical m anagem ent of oral and perioral candidosis. Derm atol Clin. 1996;14:273â€“280. 2. Glick M. Viral and fungal infections of the oral cavity in im m unocom petent patients. Infect Dis Clin North Am . 1999;13(4):817â€“831. 3. McGee D. Topical and local anesthesia. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Em ergency Medicine. 4th ed. St. Louis, MO: WB Saunders; 2004. 4. Messadi DV, Waibel JS, Mirowski GW. White lesions of the oral cavity. Derm atol Clin. 2003;21(1):63â€“78. 5. Patel NJ, Sciubba J. Oral lesions in young children. Pediatr Clin North Am . 2003;50(2):469â€“486. 6. Shay K, Truhlar MR, Renner RP. Oropharyngeal candidosis in the older patient. J Am Geriatr Soc. 1997;45(7):863â€“870.

Codes

Pa ge 8 7 7

ICD9-CM 112.0

ICD10 B37.0

Pa ge 8 7 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arbam az epine, Po iso ning

Carbamazepine, Poisoning James W. Rhee

Basics Description 



Therapeutic uses of carbam azepine: o

Anticonvulsant

o

Treatm ent of chronic pain

o

Migraine prophylaxis

o

Mood stabilizer

Mechanism : o

Anticholinergic

o

Sim ilarities to phenytoin and tricyclic antidepressants (TCAs)

o

Sodium channel blocker

o

Decreases synaptic transm ission

Etiology Toxicity m ay occur from : 

Suicide attem pt



Accidental ingestion



Supratherapeutic dosing



Drugâ€“drug interaction

Pa ge 8 7 9

Diagnosis Signs and Symptoms 

Neurologic m anifestations com m on



Cardiotoxicity rare, except in m assive overdose



CNS:







o

Ataxia

o

Dizziness

o

Drowsiness

o

Nystagm us

o

Hallucinations

o

Com bativeness

o

Com a

o

Seizures

Respiratory system : o

Respiratory depression

o

Aspiration pneum onia

Cardiovascular system : o

Hypotension

o

Conduction disturbances (m ostly in elderly)

o

Supraventricular tachycardia

o

Sinus tachycardia or bradycardia

o

ECG changes: 

Prolongation of PR, QRS, and QTc intervals



T-wave changes

Miscellaneous: o

Anticholinergic m anifestations: 

Decreased bowel sounds



Mydriasis



Flushing



Urinary retention

Pa ge 8 8 0

o

Neurom uscular changes: 

Trem or



Slurred speech



Myoclonus



Choreiform and choreoathetoid m ovem ents

Pediatric Considerations Higher incidence of neurologic m anifestations

Essential Workup 

Continuous cardiac m onitor



Serum carbam azepine level: o

Therapeutic, 6â€“12 Âµg/L

o

Levels >25â€“40 Âµg/m L associated with serious toxicity:

o



Com a



Seizures



Respiratory failure



Conduction defects

Serum levels do not clearly predict clinical toxicity: 

Active m etabolite carbam azepine epoxide not m easured



Neurologic m anifestations depend on CNS (not serum ) level.

o

Serial levels m ay be needed owing to erratic absorption of carbam azepine.



ECG: o

Conduction delays: 

Increased QRS interval



Increased PR interval

o

Dysrhythm ias

o

Sinus tachycardia (m assive carbam azepine overdose)

o

Bradydysrhythm ia (often seen in elderly with m ild

Pa ge 8 8 1

increase in carbam azepine level) 

Serum acetam inophen level (to evaluate for coingestion in a suicide attem pt)

Tests Lab 

CBC: o



Leukopenia or leukocytosis

Electrolytes, BUN/creatinine, glucose: o

Hyperglycem ia

o

Hypokalem ia

o

Hyponatrem ia



Arterial blood gases (ABGs)



Urinalysis: o

Glucosuria

o

Ketonuria



Pregnancy test



ALT, AST, bilirubin, alkaline phosphatase: o

May be m ildly elevated

o

Usually not clinically significant

Imaging Chest radiograph: 

Aspiration pneum onia



Pulm onary edem a

Differential Diagnosis 

Drugs that cause decreased m ental status: o

Alcohol

o

Anticholinergics

o

Barbiturates

o

Benzodiazepines

o

Lithium

Pa ge 8 8 2



o

Opiates

o

Phenothiazines

Drugs that cause seizures: o

Alcohol withdrawal

o

Anticholinergics

o

Cam phor

o

Isoniazid

o

Lithium

o

Phenothiazines

o

Sym pathom im etics

o 



Am phetam ine



Cocaine

TCAs

Drugs that cause abnorm al m ovem ent: o

Antihistam ines

o

Butyrophenones

o

Caffeine

o

Cocaine

o

Levodopa

o

Meperidine

o

Phencyclidine

o

Phenothiazines

o

Phenytoin

o

TCAs

Treatment Pre Hospital 

Do not adm inister ipecac.



Intubate if significant respiratory depression or airway com prom ise.

Pa ge 8 8 3



Secure IV access.



Get com plete inform ation about all products potentially ingested.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Intravenous access and fluid resuscitation if hypotensive



Oxygen



Cardiac m onitor



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status

P.177

ED Treatment 

General m anagem ent: o

Gastric lavage: 

Consider if recent ingestion (<1â€“2 hours) and significantly decreased m ental status.



Few patients will need gastric lavage.



Instill activated charcoal through orogastric tube before and after lavage.

o

Activated charcoal: 

Adm inister sorbitol with first dose (only) of activated charcoal.



Adm inister with caution if GI activity is decreased.

 o

Contraindicated if bowel sounds are absent

Multidose activated charcoal: 

Decreases m ean half-life of carbam azepine



Binds unabsorbed drug in GI tract



Interrupts enterohepatic circulation

Pa ge 8 8 4

 o

Do not give additional sorbitol.

Charcoal hem operfusion: 

Rem oves only sm all am ount of ingested dose



Patients usually do well with supportive care without hem operfusion.



Indicated in cases of clinical deterioration or lack of im provem ent with good supportive care









Respiratory depression: o

Intubation

o

Ventilatory support

Hypotension: o

Bolus with intravenous isotonic crystalloid solution

o

Norepinephrine if unresponsive to IV fluids

Seizures: o

Diazepam (drug of choice)

o

Phenobarbital (if diazepam ineffective)

o

Phenytoin not effective in m ost toxic seizures

Cardiac conduction delay: o

QRS widening (>100 m sec): 

Sodium bicarbonate (to overcom e sodium channel blockade)



Psychiatric consultation if suicide attem pt

Medication (Drugs) 

Activated charcoal (initial bolus): slurry 1â€“2 g/kg up to 100 g PO m ixed with sorbitol (below)



Dextrose: D 5 0 W 1 am pule: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Multidose activated charcoal: 25 g (peds: 0.25 g/kg) q2h PO after bolus dose (above)

Pa ge 8 8 5



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV/IM initial dose



Norepinephrine: 4â€“12 Âµg/m in (peds: 0.05â€“0.1 Âµg/kg/m in) IV titrated to effect



Sodium bicarbonate 1 or 2 am ps IV push (peds: 1â€“2 m Eq/kg)



Sorbitol: 1â€“2 g/kg to m ax. 100 g (peds: older than 1 year old, 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed with activated charcoal slurry (first dose only)

Follow-Up Disposition Admission Criteria 

Decreased m ental status at any tim e, even if resolving: o

Observe at least 24 hours for late relapse.



Seizures



Cardiac dysrhythm ias



Lack of psychiatric clearance after suicidal ingestion

Discharge Criteria 

Asym ptom atic after 6 hours of observation



Norm al m ental status



Norm al or baseline ECG



GI m otility present



Psychiatric clearance (after suicidal ingestion)

Issues for Referral 

Suicidal patients need psychiatric evaluation referral.



Supratherapeutic dosing will need ongoing m onitoring by physician treating underlying disorder.

Pa ge 8 8 6

References 1. Bridge TA, Norton RL, Robertson WO. Pediatric carbam azepine overdoses. Pediatr Em erg Care. 1994;10:260â€“263. 2. Deshpande G, Meert KL, Valentini RP. Repeat charcoal hem operfusion treatm ents in life threatening carbam azepine overdose. Pediatr Nephrol. 1999;13:775â€“777. 3. Hojer J, Malm lund H, Berg A. Clinical features in 28 consecutive cases of laboratory confirm ed m assive poisoning with carbam azepine alone. J Toxicol Clin Toxicol. 1993;31:449â€“458. 4. Schm idt S, Schm itz-Buhl M. Signs and sym ptom s of carbam azepine overdose. J Neurol. 1995;242: 169â€“173. 5. Seym our JF. Carbam azepine overdose: features of 33 cases. Drug Safety. 1993;8:81â€“88. 6. Wason S, Baker RC, Carolan P, et al. Carbam azepine overdose: the effects of m ultiple dose activated charcoal. J Toxicol Clin Toxicol. 1992;30:39â€“48.

Codes ICD9-CM 966.3

Pa ge 8 8 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arbo n M o no xide, Po iso ning

Carbon

Monoxide, Poisoning Trevonne M. Thompson

Basics Description 

Carbon m onoxide (CO) is a colorless, odorless, nonirritating gas.



Binds to hem oglobin to form carboxyhem oglobin: o

Decreases oxygen-carrying capacity

o

Decreases oxygen release to tissue owing to shift of oxyhem oglobin dissociation curve to the left



Direct cellular toxin



Binds to other hem e-containing proteins: o

Cytochrom es: 

o

Im pairs cellular oxygen utilization

Myoglobin: 

Im pairs cardiac and skeletal m uscle function

Etiology 

Endogenous: o



Result of norm al m etabolism

Incom plete com bustion of carbonaceous fossil fuel: o

Internal com bustion engines

Pa ge 8 8 8



o

Natural gas

o

Heaters

o

Indoor grills

o

Fireplaces

o

Furnaces

o

Accidental fires

o

Tobacco sm oke

Methylene chloride: o

Found in som e solvents for paint rem oval and furniture stripping

o

Endogenously converted to carbon m onoxide after exposure

o

Peak carboxyhem oglobin levels delayed after exposure

o

Half-life is approxim ately two tim es that of inhaled carbon m onoxide.

Diagnosis Signs and Symptoms History 



CNS: o

Headache

o

Dizziness

o

Ataxia

o

Confusion

o

Syncope

o

Seizures

GI: o

Nausea

Pa ge 8 8 9

o 



Cardiovascular: o

Chest pain

o

Palpitations

Respiratory: o



Vom iting

Dyspnea

Ophthalm ologic: o

Decreased visual acuity

Physical Exam 







CNS: o

Acute encephalopathy

o

Seizures

o

Com a

Cardiovascular: o

Tachycardia

o

Prem ature ventricular contractions

o

Dysrhythm ias

o

Myocardial ischem ia/infarction

Respiratory: o

Tachypnea

o

Noncardiogenic pulm onary edem a

Ophthalm ologic: o



Retinal hem orrhage

Other: o

Respiratory alkalosis

o

Rhabdom yolysis

o

Lactic acidosis

Essential Workup 

History: o

Maintain a high index of suspicion.

o

Sym ptom s m ay be m ild, nonspecific.

Pa ge 8 9 0

o

Inquire about the following: 

Sim ilar sym ptom s in other household m em bers



Malfunctioning furnaces



Use of space heaters, open ovens for supplem ental heat

 



Ill pets

Arterial blood gas: o

Norm al PaO 2

o

Norm al calculated oxygen saturation

o

Low m easured oxygen saturation

o

Metabolic acidosis in severe cases

Carboxyhem oglobin level: o

Measure as soon as possible.

o

Level m ay not reflect clinical severity: 

Patient m ay be critically ill despite unim pressive carboxyhem oglobin level.



May be m isleadingly low if significant tim e has passed since exposure



Norm al range is 0â€“3% (up to 10% in sm okers).

Tests Lab 

Pulse oxim etry: o

Falsely elevated reading

o

Device cannot distinguish oxyhem oglobin from carboxyhem oglobin.



Electrolytes: o

Metabolic acidosis and elevated anion gap associated with increased clinical severity



Urinalysis: o

Myoglobinuria m ay indicate rhabdom yolysis.

Pa ge 8 9 1



Cardiac enzym es: o

When m yocardial ischem ia/infarction suspected



Pregnancy test



ECG: o

Carbon m onoxide m ay precipitate m yocardial ischem ia/infarction.

o

Dysrhythm ias

o

Nonspecific ST-segm ent and T-wave abnorm alities

P.179

Imaging 

Chest radiography: o



Pulm onary edem a

CT scan of the head: o

To evaluate for intracranial causes of altered m ental status when indicated

o

Bilateral globus pallidus low-density lesions m ay be clue to CO poisoning in unclear cases.

Differential Diagnosis 

Viral illness/viral syndrom e



Meningitis/encephalitis



Intracranial hem orrhage



Gastroenteritis



Migraine headache



Tension headache



Ethanol intoxication



Sedative-hypnotic overdose



Cyanide poisoning



Salicylate overdose



Toxic alcohol exposure

Pa ge 8 9 2

Treatment Initial Stabilization 

Evaluate and m anage airway, breathing, circulation (ABCs).



Establish IV access.



100% oxygen



Cardiac m onitor



Dextrose, naloxone, thiam ine when indicated for altered m ental status

ED Treatment 

Oxygen: o

Adm inister 100% norm obaric oxygen: 

o

Via face m ask or endotracheal tube

Continue oxygen therapy until carboxyhem oglobin level <5â€“10%

o

Half-life of carboxyhem oglobin: 

Approxim ately 300 m inutes in am bient air



Approxim ately 90 m inutes in 100% norm obaric oxygen



Approxim ately 20 m inutes at 3 atm (hyperbaric oxygen)



Hyperbaric oxygen: o

o

Dose: 

100% oxygen at 3 atm for 45 m inutes



May be repeated

Benefits: 

Decreases half-life of carboxyhem oglobin



Increases dissolved oxygen

Pa ge 8 9 3



May decrease m ortality and long-term neurologic sequelae

o

o

Potential adverse effects: 

Tym panic m em brane rupture



Pneum othorax



Seizure



Decom pression sickness



Pulm onary edem a

Indications for use: 

Altered m ental status/com a



Focal neurologic deficits



Seizures



Cardiovascular com prom ise (infarction, persistent dysrhythm ia)



Persistent m etabolic acidosis



Carboxyhem oglobin level >40%



Carboxyhem oglobin level 20â€“70 consult a hyperbaricist



Pregnancy with carboxyhem oglobin level >10%

Pregnancy Considerations 

Fetal hem oglobin has higher affinity for CO than adult hem oglobin.



Fetal carboxyhem oglobin levels 10â€“15% higher than m aternal levels



Delayed clearance of fetal carboxyhem oglobin com pared to m aternal



Treat pregnant patients with 100% norm obaric oxygen for five tim es as long as it takes to reduce m aternal levels below 10%.



Treat with hyperbaric oxygen if level >15%.

Pa ge 8 9 4

Medication (Drugs) 

Dextrose: D 5 0 W one am pule (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m g/kg) IV



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Persistent sym ptom s after 4 hours of treatm ent with 100% oxygen



Evidence of m yocardial ischem ia or cardiac instability



Seizures



Persistent m etabolic acidosis



Syncope



Rhabdom yolysis

Discharge Criteria 

Asym ptom atic after 4 hours of observation



Absence of aforem entioned adm ission criteria



Psychiatric clearance if suicidal exposure

Issues for Referral Need for hyperbaric oxygen

References 1. Gorm an D, Drewry A, et al. The clinical toxicology of carbon m onoxide. Toxicology. 2003;187:25â€“38. 2. Kao LW, Nanagas KA. Carbon m onoxide poisoning. Em erg Med Clin North Am . 2004;22(4): 985â€“1018. 3. Weaver LK, Hopkins RO, et al. Hyperbaric oxygen for acute carbon

Pa ge 8 9 5

m onoxide poisoning. N Engl J Med. 2002;347:1057â€“1067.

Miscellaneous SEE ALSO: Hyperbaric Oxygen

Codes ICD9-CM 986

Pa ge 8 9 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Arrest

Cardiac Arrest

Todd C. Rothenhaus

Basics Description 

Sudden death: o

Death within 24 hours of sym ptom onset

o

Initial presentation in 50% of patients with cardiovascular disease



Return of spontaneous circulation (ROSC) achieved in 9â€“65%



1â€“20% of patients survive to discharge



Factors affecting survival:



o

Initial rhythm

o

Tim e to successful defibrillation

Incidence of re-arrest in neurologically intact survivors: o

30% at 1 year and 60% at 5 years

Etiology 



Acute coronary ischem ia: o

Underlying etiology in 50% of arrests

o

Myocardial irritability leads to ventricular fibrillation

Prim ary dysrhythm ia: o

Congenital and acquired electrical abnorm alities

o

Hypertrophic/dilated cardiom yopathy

Pa ge 8 9 7

o

Myocarditis



Cardiac rupture



Pericardial tam ponade



Metabolic abnorm alities



Noncardiac etiologies: o

Consider especially in cases of pulseless electrical activity



o

Tension pneum othorax

o

Hem orrhage

o

Massive pulm onary em bolus

o

Sepsis

o

Severe acidosis

Drugs or toxins: o

Antidysrhythm ics

o

Digoxin

o

Beta-blockers

o

Calcium channel blockers

o

Tricyclic antidepressants

o

Cocaine

o

Heroin

Diagnosis Signs and Symptoms 

Unresponsiveness



Pulselessness



Shallow, gasping respirations m ay persist for a few m inutes



Occasionally preceded by: o

Chest pain

o

Dyspnea

Pa ge 8 9 8



o

Palpitations

o

Seizure activity

Im m ediately prior to arrest: o

Shock or hypotension

o

Im paired m entation

Essential Workup 

â€œQuick lookâ€• using paddles of a cardiac defibrillator



Determ ine rhythm

Tests Lab Indicated only when successful ROSC is achieved: 

Electrolytes



Blood urea nitrogen/creatinine



Creatinine kinase with isoenzym es, cardiac troponin



Arterial blood gas (avoid arterial puncture in throm bolysis candidates).



CBC



Therapeutic drug levels



Toxicological testing

Imaging 

ECG: o





Establish or rule out acute coronary syndrom e

Chest radiograph: o

Endotracheal tube position

o

Cardiac silhouette

o

Pneum othorax

ECG: o

Pericardial effusion

o

Wall m otion abnorm ality

o

Valvular dysfunction

Pa ge 8 9 9

Differential Diagnosis Sudden loss of consciousness with a palpable pulse: 

Syncope



Seizure



Acute stroke



Hypoglycem ia



Acute airway obstruction



Head traum a



Toxins

Treatment Pre Hospital 

Prom pt initiation of standard CPR or active com pression-decom pression CPR (ACD-CPR)



Confirm underlying rhythm



Early defibrillation of ventricular tachycardia (VT) or ventricular fibrillation (VF):



o

Autom ated external defibrillator

o

EMT-D or layperson

Consider CPR before defibrillation in cases of if arrest >5 m inutes.







Secure airway and provide adequate respirations: o

Endotracheal intubation

o

Laryngeal m ask airway

Post-resuscitation care: o

Identify cause of arrest

o

12-lead ECG

o

Monitor vital signs

Transport to the closest facility:

Pa ge 9 0 0

o

If return of spontaneous circulation, consider transport to center equipped for interventional cardiac care.

o 

Pediatric critical care center for children

Term ination of resuscitative efforts: o

Persistent, confirm ed asystole

o

Prolonged arrest

Initial Stabilization 

Initiate advanced cardiac life support (ACLS).



Perform standard CPR as long as no pulse is palpable.



Consider ACD-CPR: o

Stop CPR only briefly to check cardiac rhythm or intubate.



Secure the airway



Obtain IV access



Cardiac m onitor



Therapy based on the underlying rhythm according to ACLS protocols

P.181

ED Treatment Pulseless VT or VF 





Im m ediate defibrillation with up to three countershocks: o

200 J

o

200â€“300 J

o

360 J

If defibrillation is unsuccessful: o

Epinephrine

o

Vasopressin

If refractory to defibrillation and epinephrine:

Pa ge 9 0 1

o

Am iodarone

o

Lidocaine

o

Procainam ide

o

Magnesium for Torsades de Pointes

Asystole 

Dism al prognosis if this is the presenting rhythm



Confirm in two or m ore leads



Epinephrine



Atropine



Consider transcutaneous pacing for severe brady-asystolic rhythm .

Pulseless Electrical Activity 

Epinephrine



Atropine



Treat for reversible cause of pulseless electrical activity o

Pneum othorax

o

Cardiac tam ponade

o

Hypoxia

o

Pulm onary em bolus

o

Hypovolem ia (hem orrhage)

Post-Resuscitation 

Treat the underlying cause of the arrest.



ECG to establish presence of acute coronary syndrom e: o

Im m ediate catheterization or throm bolysis for ACS



Ventilatory support



Continue antidysrhythm ic therapy.



Correct electrolyte abnorm alities.



Initiate volum e resuscitation and provide inotropic support as needed.

Pa ge 9 0 2

Medication (Drugs) 

Am iodarone: 300 m g (peds: 5 m g/kg) IVP



Atropine: 1 m g (peds: 0.02 m g/kg) IV q3â€“5m in up to 0.04 m g/kg



Epinephrine: 1 m g (peds: 0.01 m g/kg) IVP q3â€“5m in



Lidocaine: 100 m g (peds 1 m g/kg) IVP, then 2â€“4 m g/m in (peds: 20â€“50 Âµg/m in) IV continuous infusion



Magnesium : 1â€“2 g (peds: 25â€“50 m g/kg) slow IV



Procainam ide: 20 m g/m in slow IV to a total of 1 g or until arrhythm ia is suppressed; m aintenance infusion 1â€“4 m g/m in (peds: 15 m g/kg over 30 m in, then 20â€“80 Âµg/kg/m in IV)



Sodium bicarbonate: 1 m Eq/kg slow IV



Vasopressin: 40 U IVP (adults with VT/VF only)

Follow-Up Disposition Admission Criteria Return of spontaneous circulation: 

Coronary care unit or intensive care unit



Postresuscitation care

References 1. Am erican Heart Association. Guidelines 2000 for cardiopulm onary resuscitation and em ergency cardiovascular care. Circulation. 2000;102(Suppl): I-1â€“I-384. 2. Dorian P, Cass D, Schwartz B, et al. Am iodarone as com pared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884â€“890.

Pa ge 9 0 3

3. Hallstrom AP, Ornato JP, Weisfeldt M, et al. Public-access defibrillation and survival after out-of-hospital cardiac arrest. N Engl J Med. 2004;351:637â€“646. 4. Nolan JP, Morley PT, Vanden Hoek TL, et al. Therapeutic hypotherm ia after cardiac arrest: an advisory statem ent by the advanced life support task force of the International Liaison Com m ittee on Resuscitation. Circulation. 2003;108:118â€“121. 5. Stiel IG, Hebert PC, Wells GA, et al. Vasopressin versus epinephrine for inhospital cardiac arrest: a random ised controlled trial. Lancet. 2001;358:105â€“109. 6. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulm onary resuscitation to patients with out-of-hospital ventricular fibrillation: a random ized trial. JAMA. 2003;289:1389â€“1395. 7. Zoll PM, Linenthal AJ, Gibson W, et al. Term ination of ventricular fibrillation in m an by externally applied electric countershock. N Engl J Med. 1956;254:727â€“732.

Codes ICD9-CM 798 427.5

Pa ge 9 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Pacem akers

Cardiac

Pacemakers Susan P. Torrey

Basics Description Equipment 

Perm anent, im planted pacem aker has three com ponents o

A battery-powered energy source: 

o

Lithium batteries last 7â€“10 years

Generator: 

A sophisticated com puter with m any program m able param eters

o

Leads connected to the right ventricle and/or right atrium : 

These typically sense electrical activity and pace the m yocardium .



Pacem aker m agnet: o

Placed over pulse generator

o

Converts pacer to asynchronous m ode

o

Useful if no pacer spikes on presenting rhythm

o

A depleted battery will result in decrease in m agnet rate by 10%.

Pa ge 9 0 5

Pacemaker Terminology 

Fixed m ode: o

The pacem aker is set to fire at a set rate regardless of patient's underlying rhythm .

o 

Occasionally seen in old pacers

Dem and m ode: o

The pacem aker fires only when necessary.

o

It senses the underlying rhythm .

o

It will only pace the atria or ventricle if the intrinsic rhythm is absent.



Sensing: o

Refers to the pacem aker's ability to determ ine whether the heart is being intrinsically paced



All pacem akers have a five-letter code to describe their function.



For ED purposes, only the first three letters of the code are necessary: o

First letter in code indicates cham ber being sensed by pacem aker:

o



A: atria



V: ventricle



D: dual (both cham bers)

Second letter in code indicates cham ber that can be paced:

o



A: atria



V: ventricle



D = dual (both cham bers)

Third letter in code describes pacem aker's response to sensed intrinsic com plex: 

T: trigger (a sensed beat results in a pacing response as when a sensed atrial beat provokes a subsequent ventricular beat)

Pa ge 9 0 6



I: inhibit (a sensed beat precludes pacem aker function)



D: dual (a pacem aker is capable of both functions)

 o

O: no response

The m ost com m on pacem akers are VVI (single lead) and DDD (two leads).

Pacemaker-Associated Complications 

Pacem aker-associated infection: o

Infection of pacem aker com ponents often associated with endocarditis

o

Staphylococcus epiderm idis and Staphylococcus aureus account for >90% of infections

o

Transesophageal echo is the preferred diagnostic m ethod.





Venous throm bosis: o

Very com m on (overall incidence 30â€“50%)

o

Sym ptom atic, acute obstruction is rare (<3%)

o

Pulm onary em bolism is rare

Pacem aker failure to pace or discharge im pulse: o

Com ponent failure is rare.

o

Battery depletion is rare with routine checks; it is not abrupt.

o

Lead fracture or disconnection

o

Oversensing of m uscular activity or external electrical interference



Pacem aker failure to capture m yocardium : o

Lead dislodgm ent is com m on cause: 

Change in cardiac or quasi-random signal (QRS) m orphology

o

Twiddler syndrom e: 

Unintentional m anipulation of pacem aker

Pa ge 9 0 7

generator, causing lead to dislodge from m yocardium o

o 

Elevated m yocardial threshold: 

Hyperkalem ia



Ischem ia

Failure to sense intrinsic depolarization

Pacem aker-m ediated tachycardia: o

Occurs with dual-cham ber pacem akers

o

A re-entry rhythm using generator and intrinsic conduction system

o

Maxim um rate typically 140 beats/m in due to built-in safeguards



Runaway pacem aker: o

Rare; triggered by battery depletion or com ponent failure

o

Often rapid rates (>200 beats/m in) with hem odynam ic com prom ise

Diagnosis Signs and Symptoms 

Pacem aker failure: o

Bradycardia

o

Syncope

o

Hypotension, progressive to shock and hem odynam ic collapse

o

Fatigue and weakness

o

Dyspnea on exertion or shortness of breath secondary to congestive heart failure

o

Ischem ic chest pain

o

Altered level of consciousness

Pa ge 9 0 8





Pacem aker-induced tachycardia: o

Dyspnea

o

Ischem ic chest pain

o

Lightheadedness

o

Syncope

Pacem aker syndrom e: o

Sym ptom s related to asynchronous aortic valve contractions

o

Lightheadedness

o

Dyspnea

o

Palpitation

o

Syncope

Physical Exam 

General cardiac exam ination



Heart exam for m urm urs



Lung exam for congestive heart failure



Chest wall exam at generator site

Tests Lab 

Serum potassium



Arterial blood gas



Serum levels of antidysrhythm ic drugs

Imaging Chest radiograph: 

Evaluate problem with pacer lead(s) and position.



Fractured lead



Lead dislodgm ent



Perforation

P.183

Pa ge 9 0 9

Essential Workup 

12-lead ECG to assess whether there is any obvious evidence of pacem aker failure



Metabolic workup to determ ine whether an acquired m edical condition led to an elevated m yocardial threshold



ECG with pacer m agnet: o

Assess m agnet rate

o

Particularly useful when the baseline ECG does not reveal pacer spikes

o

The m agnet activates asynchronous pacing m ode.

o

Produces pacer spikes at a preprogram m ed rateâ€”regardless of the intrinsic rhythm : 

If the m agnet rate equals the preprogram m ed rate set at im plantation, the pacer is okay.



If the m agnet rate is >10% slower than at im plantation, the battery is depleted.



If there are no pacer spikes, there is significant pacem aker m alfunction.

Treatment Initial Stabilization 

Oxygen adm inistered via 100% nonrebreather



Intubation as needed



Intravenous access



Advanced cardiac life support drugs as per usual protocol



Defibrillation: Avoid placing paddles over generator.



Transcutaneous pacem aker in hem odynam ically unstable patients with pacem aker failure

Pa ge 9 1 0

ED Treatment 

Pacem aker failure: o

Transcutaneous pacem aker

o

Tem porary transvenous pacem aker 

Obtain central IV access with a Cortis introducer.



Perform the procedure under fluoroscopy if possible.



Set the pulse generator to asynchronous m ode.



Turn the output dial all the way up.



Advance the catheter through the central venous access Cortis until you see a QRS com plex on the m onitor.



Check the fem oral pulse.



If you have a pulse and see a QRS com plex, the pacer is â€œcapturing.â€•



Slowly turn the output dial down until you lose the QRS com plex (capture threshold).



Turn the output dial up to 2 or 3 tim es the capture threshold.



Continuous ECG m onitoring facilitates correct placem ent.



Treat hyperkalem ia (see Hyperkalem ia)



Runaway pacem aker: o

AV node blocking or reprogram m ing

o

In extrem e situation, m ay need to disconnect lead from generator surgically

Medication (Drugs) Adenosine: 6 m g IV bolus

Pa ge 9 1 1

Follow-Up Disposition Admission Criteria 

Perm anent pacem aker failure



Suspicion of infection involving pacem aker com ponents

Discharge Criteria 

Asym ptom atic pacem aker m alfunction



A cardiologist has interrogated the pacem aker

References 1. Cardall TY, Brady WJ, Chan TC, et al. Perm anent cardiac pacem akers: Issues relevant to the em ergency physician, parts I and II. J Em erg Med. 1999;17:479â€“489, 697â€“709. 2. Griffin J, Sm ithline H, Cook J. Runaway pacem aker: A case report and review. J Em erg Med. 2000;19:177â€“181. 3. Kusum oto FM, Goldschlager N. Cardiac pacing. N Engl J Med. 1996;334:89â€“98. 4. Stone KR, McPherson CA. Assessm ent and m anagem ent of patients with pacem akers and im plantable defibrillators. Crit Care Med. 2004;32:155â€“165.

Codes ICD9-CM 429.4

Pa ge 9 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Testing

Cardiac Testing

Shamai A. Grossman Jonathan Fisher

Basics Description 

Testing is indicated for em ergency patients at risk for acute cardiac ischem ia (ACI) and heart failure (HF): o

Spectrum of disease processes, including acute m yocardial infraction (AMI) and unstable angina pectoris

o

About 10% of ED visits are cardiac related, m ost with chest pain.

o

10% of ED m alpractice claim s are due to m issed diagnosis of AMI.

o

2â€“8% of patients presenting to the ED with chest pain are sent hom e with AMI.

o

History, physical exam , and ECG m iss 1â€“4% of all AMIs.



Various approaches to differentiation of chest pain m ay be em ployed: o

History is the critical com ponent.

o

All m odalities beyond history and ECG are adjuncts to diagnosing the etiology of chest pain.

Pa ge 9 1 3

Etiology 

Cardiac risk factors include: o

Hypercholesterolem ia

o

Diabetes m ellitus

o

Hypertension

o

Sm oking

o

Fam ily history

o

Men >35 years old

o

Postm enopausal wom en



Atherosclerotic narrowing of coronary vessels



Vasospasm , although this is usually at rest and considered unstable if new onset



Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease



Anem ia: hem oglobin <8 g/dL



Hyperbarism or elevations in carboxyhem oglobin



Medication-induced vasospasm or cocaine- and stim ulant-induced vasospasm

Diagnosis Signs and Symptoms 

Chest pain: o

Substernal pressure

o

Heaviness

o

Squeezing

o

Burning sensation

o

Tightness

o

May localize or radiate to arm s, shoulders, back, neck, or jaw

Pa ge 9 1 4





Associated findings: o

Dyspnea

o

Syncope

o

Fatigue

o

Diaphoresis

o

Nausea or vom iting

Usually reproduced by exertion, eating, exposure to cold, or em otional stress



Anginal sym ptom s last fewer than 20 m inutes but m ore than a few seconds.



Myocardial infarction should be considered if sym ptom s last longer than 20 m inutes.



Usually relieved with rest or nitroglycerin



Sym ptom s generally unchanged with position or inspiration.





Occasional anginal equivalents include: o

Abdom inal pain

o

Dyspnea

o

Syncope

o

Diaphoresis

o

Nausea or vom iting

o

Weakness

Positive Levine sign or clenched fist over chest is suggestive of angina.



Blood pressure is usually elevated during sym ptom s.



Physical exam is usually unrevealing.



Occasional physical findings include: o

S3 or S4 due to LV systolic or diastolic sym ptom s

o

Mitral regurgitation or pansystolic m urm ur

o

Dim inished peripheral pulses

Essential Workup 

History is critical in differentiating stable and unstable

Pa ge 9 1 5

angina. 

Single ECG: o

Norm al in m ost cases of ACI

o

ST-segm ent changes or T-wave inversions m ost often are unchanged from previous tracings.

o

Must be com pared with prior tracings if available

o

New ST-segm ent changes or T-wave inversions are suspicious for unstable angina.

o

1-m m depression of the ST segm ent below the baseline, 80 m illiseconds from the J point, is characteristic of angina.

o

New bundle branch block (right or left) is suggestive of AMI



Continuous or serial ECG: o

Alone has a sensitivity of 21â€“25% and specificity of 92â€“99% for ACI

o

Alone has a sensitivity of 39% and specificity of 88% for AMI



ECG m ay be helpful in diagnosing other etiologies of chest pain: o

Pericarditis is suggested by diffuse ST-segm ent elevations followed by T-wave inversions and PR depression.

o

Pulm onary em bolism is suggested by an S1, Q3, T3 pattern and unexplained tachycardia.

Tests Lab 

Cardiac enzym es: o

Indicated if the history is suspicious for AMI

o

Should not be abnorm al in unstable angina

o

Should not be elevated and are not indicated in

Pa ge 9 1 6

stable angina o

Creatine kinase: 

Single value on presentation has sensitivity of 37% and specificity of 87% for AMI



Serial values have sensitivity of 66â€“99% and specificity of 68â€“84% for AMI

o

Creatine kinase-Mb 

Single value on presentation has sensitivity of 42% and specificity of 97% for AMI.



Serial values have sensitivity of 79% and specificity of 96% for AMI.

o

Myoglobin: 

Single value on presentation has sensitivity of 49% and specificity of 91% for AMI.



Serial values have sensitivity of 89% and specificity of 87% for AMI.

o

Troponin I: 

Single value on presentation has sensitivity of 39% and specificity of 93% for AMI.



Serial values have sensitivity of 90â€“100% and specificity of 83â€“96% for AMI.

o

Troponin T: 

Single value on presentation has sensitivity of 39% and specificity of 93% for AMI



Serial values have sensitivity of 93% and specificity of 85% for AMI.

o

Brain natriuretic peptide (BNP): 

Useful for predicting heart failure



A cut off of >100 pg/m L diagnosed HF with a sensitivity of 90% and specificity of 76%



Unclear significance of elevated BNP in setting of ACI

Pa ge 9 1 7

Imaging 

Chest radiograph: o

Usually norm al

o

May show cardiom egaly

o

Congestive heart failure is suggestive of unstable angina.

o

May identify other etiologies of chest pain such as pneum onia

P.185



Echocardiography m ay establish the diagnosis of ACI: o

Rest echocardiography has a sensitivity of 70% and specificity of 87% for ACI.

o

Rest echocardiography has a sensitivity of 93% and specificity of 66% for AMI.



Technetium -99m sestam ibi (rest): o

Has a sensitivity of 81% and specificity of 73% for ACI

o

Has a sensitivity of 92% and specificity of 67% for AMI



Exercise stress testing m ay help establish the diagnosis of angina and provide prognostic inform ation. o

1-m m depression of the ST segm ent below the baseline, 80 m illiseconds from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischem ia.

o

Early positive (within 3 m inutes) stress tests are worrisom e for unstable angina.

o

Six m inutes of exercise using a standard Bruce protocol suggests an excellent prognosis

o

Exercise stress testing with ECG alone has a

Pa ge 9 1 8

sensitivity of 68% and specificity of 77%. o

Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.

o

Exercise stress testing with thallium -201 or technetium -99m sestam ibi has a sensitivity of 87% and specificity of 64%.



Cardiac catheterization is considered the gold standard: o

A history of a negative catheterization does not exclude AMI.

Differential Diagnosis 

Aortic dissection



Anxiety



Biliary colic



Costochondritis



Esophageal spasm



Esophageal reflux



Herpes zoster



Hiatal hernia



Mitral valve prolapse



Myocardial infarction



Peptic ulcer disease



Psychogenic



Panic disorder



Unstable angina



Pneum onia



Pulm onary em bolus

Treatment Pre Hospital

Pa ge 9 1 9



IV access



Oxygen



Cardiac m onitoring



Out-of-hospital ECG: o

Alone has a sensitivity of 76% and specificity of 88% for ACI

o

Alone has a sensitivity of 68% and specificity of 97% for AMI



Sublingual nitroglycerin for sym ptom relief

Caution All chest pain should be treated and transported as a possible life-threatening em ergency.

Initial Stabilization 

IV access



Oxygen



Cardiac m onitoring



Oxygen saturation

ED Treatment See Acute Coronary Syndrom e: Stable Angina; Acute Coronary Syndrom e: Unstable Angina; and Acute Coronary Syndrom e: Myocardial Infarction for m ore detail

Guidelines for Cardiac Testing 

History suggestive of acute cardiac syndrom e: o



ECG or first set of cardiac enzym es abnorm al: o



Adm it patient; consider cardiology consult,

Ongoing chest pain or pressure: o



Obtain ECG and first set of cardiac enzym es.

Obtain pain sestam ibi or echocardiogram

Pain sestam ibi or echocardiogram abnorm al: o

Adm it patient; consider cardiology consult.

Pa ge 9 2 0



Second set of cardiac enzym es abnorm al: o

Adm it patient; consider cardiology consult.

o

History suggestive of acute cardiac syndrom e, ECG nondiagnostic, enzym es norm al.

o

Ancillary testing

o

Standard exercise testing (ETT)

o

Stress echocardiogram or sestam ibi (abnorm al or uninterpretable ECG) 

Pharm acologic ETT (i.e., dobutam ine echocardiogram or dipyridam ole [Persantine] sestam ibi [patient unable to exert])

o

Ancillary testing abnorm al: 

Adm it patient or cardiology consult.

Medication (Drugs) Patient should not be started on new antianginal m edication before stress testing in the ED.

Follow-Up Disposition Admission Criteria 

History suggestive of cardiac etiology for chest pain



Abnorm al or changed ECG



Positive cardiac enzym es



Positive rest im aging



If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac enzym es, ECGs, and exercise stress testing.

Pa ge 9 2 1



Early positive stress test



If the patient has an otherwise positive stress test, the decision for adm ission should be m ade in consultation with the prim ary care physician or cardiologist.

Discharge Criteria Patients who m eet the following criteria are safe to discharge: 

History not suggestive of cardiac etiology for chest pain



Norm al ECG



Norm al cardiac testing

References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the m anagem ent of patients with unstable angina and non-ST-segm ent elevation m yocardial infarction: A report of the Am erican College of Cardiology/Am erican Heart Association Task Force on Practice Guidelines. Circulation. 2002;106(14):1893â€“1900. 2. Ioannidis JPA, Salem D, Chew PW, et al. Accuracy and clinical effect of out-of-hospital electrocardiography in the diagnosis of acute cardiac ischem ia: a m eta-analysis. Ann Em erg Med. 2001;37:461â€“470. 3. Ioannidis JPA, Salem D, Chew PW, et al. Accuracy of im aging technologies in the diagnosis of acute cardiac ischem ia in the em ergency departm ent: a m eta-analysis. Ann Em erg Med. 2001;37:471â€“477. 4. Lau J, Ioannidis JPA, Balk EM, et al. Diagnosing acute cardiac ischem ia in the em ergency departm ent: a system atic review of the accuracy and clinical effect of current technologies. Ann Em erg Med. 2001;37:453â€“460.

Pa ge 9 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Transplantatio n C o m plicatio ns

Cardiac

Transplantation Complications Barrett Adams Samuel Keim

Basics Description 

Cardiac transplant recipients are a unique population with increased risk for cardiac ischem ia, heart failure, as well as general risks as an im m unocom prom ised host.



2,200 cardiac transplants per year in the United States



1-year survival 85â€“90%; 5-year survival approxim ately 75%



Typical im m unosuppresive therapy to control rejection is a â€œtriple drugâ€• regim e often including steroids.



Frequent biopsies are used initially to evaluate rejection; echocardiography often used in children.



Com plications occur m ost com m only in the first 6 weeks after cardiac transplantation

Etiology 

Rejection: o

Hyperacute rejection: 

Occurs within m inutes of transplantation

Pa ge 9 2 3



Rare, due to ABO or other graft/host m ajor incom patibility

 o

o



Aggressive and im m ediately fatal to graft

Acute rejection: 

Lym phocyte infiltration and m yocyte destruction



Most com m on in first 6 weeks



May occur at any tim e



75% prevalence

Chronic rejection: 

Fibrosis and graft vascular disease



Long-term com plication



Incom pletely understood etiology



No effective therapy

Cardiac allograft vasculopathy: o

Analogous to accelerated coronary artery disease in native hearts

o

Lim its long-term survival, leading cause of m ortality after 1 year

o

Im m une-m ediated atherosclerosis, form of chronic rejection



Infections: o

First m onth: 

Bacterial infections are m ost com m on cause of m ortality during this high-risk tim e period:



Pneum onia (Pseudom onas, Legionella, other gram -negative organism s)

o



Mediastinitis



Wound infection



Urinary tract infection

First year: 

Opportunistic and conventional infections



Cytom egalovirus (CMV)

Pa ge 9 2 4





Herpes sim plex virus (HSV)



Legionella



Fungal infections



Pneum ocystis carinii

Medication toxicity: o

Cyclosporine, Neoral (2nd generation cyclosporine), Tacrolim us:

o

o

o





Nephrotoxicity (30% incidence)



Hepatotoxicity



Neurotoxicity



Hyperlipidem ia, diabetogenic

Azathioprine, Mycophenolate Mofetil: 

Bone m arrow suppression



Leukopenia

Sirolim us: 

Hyperlipidem ia



Wound healing

Steroids: 

Osteoporosis



Cushing's disease

Neoplasm s: o

Secondary to im m unosuppression

o

10â€“100 tim es m ore com m on versus general population

o

Skin and lip cancer

o

Lym phom as

o

Kaposi sarcom as

o

Solid organ neoplasm s

Pediatric Considerations 

If the patient is not on steroids, bacterem ia risk is sim ilar to that in the general population.



High incidence of pneum onia

Pa ge 9 2 5



Patients on steroids m ay not show m eningeal signs.

Diagnosis Signs and Symptoms Acute Rejection 

Nonspecific sym ptom s predom inate because the heart is usually denervated: o

Fatigue

o

Dyspnea

o

Low-grade fever

o

Nausea

o

Vom iting



May be difficult to differentiate between infection



Signs of heart failure: o

Tachypnea

o

Rales

o

Hypoxia

o

S3

o

Murm ur

o

Edem a

Allograft Vasculopathy 

As early as 3 m onths after transplantation (20â€“50% incidence by 5 years)





Insidious onset: o

Fatigue

o

Cough

o

Dyspnea

Acute onset: o

Heart failure

Pa ge 9 2 6



o

Sudden death

o

Infarction

Denervated hearts do not present with typical angina.

Infection (Opportunistic and Conventional) 

Fever



Skin lesions (zoster)



CMV: o

o

Mild (flu-like illness) 

Fever



Nausea



Malaise

Severe: 

Pneum onitis (13â€“50% m ortality)



Hepatitis



Gastroenteritis



Profound leukopenia

Pediatric Considerations 

Higher risk for post-transplant lym phoproliferative disease with Epstein-Barr virus seroconversion



Like adults, at risk for allograft vasculopathy and its associated cardiac ischem ia

Essential Workup 

Assess for signs of rejection, cardiac dysfunction, and infarction:



o

ECG

o

Cardiac enzym es

o

Chest radiograph

o

Echocardiography

Possible rejection requires biopsy-consult transplant team .

Pediatric Considerations

Pa ge 9 2 7

Norm al fever workup plus chest radiograph and ECG; if on steroids, perform LP

Tests Lab 

Electrolytes: o



Cyclosporine effects: 

Increased blood urea nitrogen, creatinine



Hyperkalem ia



Metabolic acidosis



Hyponatrem ia

CBC: o

Relative eosinophilia m ay indicate rejection over infection



Blood and urine culture if febrile



Lum bar puncture if seizures, altered m ental status, or severe headache



Consider: o

BNP (expect baseline elevation)

o

CMV titers

o

Urine antigen test

o

Cyclosporine trough level

P.187

Imaging 

ECG o

Tachycardia

o

20% decrease in total voltage (nonsensitive)

o

Note that norm al rhythm for denervated heart is sinus 90â€“110 beats/m in

o

Depending on transplant surgical technique, m ay see

Pa ge 9 2 8

two P waves (native and donor heart): 

Native P waves do not correspond to quasi-random signal



Chest radiograph: o

Cardiom egaly

o

Pulm onary edem a

o

Pleural effusions

o

Com pare with previous (healthy donor heart m ay appear large in sm all recipient)



Echocardiography: o

Decreased m itral deceleration tim e

o

Initial diastolic dysfunction

o

Biventricular enlargem ent

o

Mitral/tricuspid regurgitation

Differential Diagnosis 

Rejection



Infection



Ischem ia



CMV



Viral illness



Malignancy



Cyclosporine toxicity

Treatment Initial Stabilization ABCs: 

IV access



Oxygen



Monitor

Pa ge 9 2 9



Intubation



Defibrillation/pacing



Vasopressors as required



Arrhythm ias: o

Advanced cardiac life support

o

Bradycardia does not respond to atropine; use isoproterenol

ED Treatment 

Hem odynam ically significant rejection: o

Methylprednisolone

o

May also require OKT3 or other antiâ€“T-cell antibody therapy





Infarct/vasculopathy: o

Aspirin

o

Heparin

o

Possible angioplasty

o

Likely need retransplantation

CMV: o



HSV: o



Search for CMV infection with culture, serology

Fever without a source: o



Oral or IV acyclovir

Gastroenteritis: o



Em piric IV ganciclovir

Consult infectious disease or transplantation team

Headache: o

Threshold for CT scan and lum bar puncture should be low (m eningitis, abscess)



Serious illness/traum a/operation: o



Steroid burst

Lim it NSAID use because risk for renal insufficiency from cyclosporine and tacrolim us.

Pa ge 9 3 0

Medication (Drugs) 

Acyclovir: 5â€“10 m g/kg IV q6h; genital herpes: 400 m g PO t.i.d. Ã— 7â€“10 days; varicella: 20 m g/kg up to 800 m g PO q.i.d. for 5 days



Ceftriaxone: 50 m g/kg IV



Cyclosporine, Cellcept, Tacrolim us, Sirolim us, Neoral, Azathioprine, Mycophenolate Mofetil: per transplantation team



Ganciclovir: 5 m g/kg b.i.d. for 2â€“3 weeks (adjust for renal function)



Isoproterenol: 1â€“4 m cg/m in, titrate to effect; m ax. 10 m cg/m in



Methylprednisolone: 1 g IV; peds: 10â€“20 m g/kg IV



OKT3, Daclizum ab or other antibody therapy: per transplant team

Follow-Up Disposition Admission Criteria 

Hem odynam ically significant rejection



Vasculopathy/ischem ia



New dysrhythm ia



Poorly controlled hypertension



Congestive heart failure



Dyspnea



Hypoxia



Tem perature >38Â°C in adult or child on steroids

Pa ge 9 3 1



Suspected CMV (unexplained fever, gastroenteritis, or interstitial pneum onitis)



Not tolerating oral m edicines



Syncope

Discharge Criteria 

Mild rejection



Only in consultation with transplantation team



Fever in nontoxic child: o

Do not give children stress dose steroids

References 1. Chinnock R, Sherwin T, Robie S, et al. Em ergency departm ent presentation and m anagem ent of pediatric heart transplant recipients. Pediatr Em erg Care. 1995;11(5):355â€“360. 2. Deng MC. Cardiac transplantation. Heart. 2002;87:177â€“184. 3. Johnson MR. Clinical follow-up of the heart transplant recipient. Curr Opin Cardiol. 1995;10:180â€“192. 4. Massad MG. Current trends in heart transplantation. Cardiology. 2004;101:79â€“92. 5. Mill MR, Grady MS. Cardiac transplantation. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency m edicine: a com prehensive study guide. 6th ed. San Francisco: McGraw-Hill; 2000:422â€“428. 6. Miniati DN, Robbins RC, Reitz BA. In:Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine, 6th ed. Philadelphia: WB Saunders; 2001:615â€“631. 7. Mueller XM. Drug im m unosuppression therapy for adult heart transplantation. Ann Thorac Surg. 2004;77:363â€“371. 8. Poston RS, Griffith BP. Heart transplantation. J Intensive Care Med . 2004;19:3â€“12. 9. Vulsteke A, Wallwork J. The heart-transplanted patient in the intensive care unit: last news before the m illennium . Cur Opinion in Crit Care. 1999;5(5):422â€“426.

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Codes ICD9-CM 996.83 Com plications of transplanted Heart. Transplant failure or rejectionâ€”Use additional code to identify nature of com plication, such as: 078.5 Cytom egalovirus [CMV] infection

Pa ge 9 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardio genic Sho ck

Cardiogenic Shock

Nadeem Al-Duaij

Basics Description 

Inadequate tissue perfusion due to cardiac dysfunction



Underlying m echanism s in acute m yocardial infarction (AMI): o

o

o

Pum p failure: 

â‰¥40% left ventricle (LV) infarct



Infarct in pre-existing LV dysfunction



Reinfarction

Mechanical com plications: 

Acute m itral regurgitation



Ventricular septal defect



LV rupture



Pericardial tam ponade

Right ventricular (RV) infarction



6â€“7% of patients with AMI develop cardiogenic shock



Cutting-edge: o

Role of a system ic inflam m atory response in the pathophysiology of cardiogenic shock

o

Recent evidence suggests that nitric oxide synthase inhibition m ay reduce m ortality.

Pa ge 9 3 4

Etiology 

AMI



Sepsis



Myocarditis



Myocardial contusion



Valvular disease



Cardiom yopathy



Left atrial m yxom a



Drug toxicity: o

Beta-blocker

o

Calcium channel blocker

o

Adriam ycin

Diagnosis Signs and Symptoms 

ABCs and vital signs: o

Patent airway (early)

o

Labored breathing and tachypnea (early); respiratory failure (late)

o

Diffuse crackles or wheezing

o

Hypoxia

o

Hypotension: 

Systolic blood pressure <90 m m Hg



Decline by at least 30 m m Hg below baseline level



o

Tachycardia

o

Weak pulses

General: o

Cyanosis

Pa ge 9 3 5



o

Pallor

o

Diaphoresis

o

Dulled sensorium

o

Decrease in body tem perature

o

Urine flow of less than 20 m L/h

Neck: o



Jugular venous distention

Cardiac: o

Ischem ic chest pain

o

Systolic apical blowing m urm ur

o

Gallop rhythm : 

S3 reflects severe m yocardial dysfunction



S4 is present in 80% patients in sinus rhythm with AMI

o

Systolic click: 





Suggests rupture of the chordae tendinae

Abdom inal: o

Epigastric pain

o

Nausea and vom iting

Neurologic: o

Obtundation

Essential Workup 

Obtain history from patient, fam ily, or EMS for clues to possible etiology.



Perform rapid survey and stabilize ABCs.



Ancillary studies further define the type and degree of cardiac injury and determ ine the indications for em ergent catheterization or surgical intervention.

Tests Electrocardiogram 

Norm al ECG does not rule out AMI.

Pa ge 9 3 6



Findings of AMI (ST-elevations in two or m ore contiguous leads)



May occur in non-ST-elevation acute coronary syndrom e



Dysrhythm ias



LV hypertrophy

Chest Radiography 

Pulm onary congestion



Pleural effusion



Cardiom egaly



Pneum onia



Pneum othorax



Pericardial effusion

Emergent Echocardiography 

Transthoracic echocardiography (TTE) with color Doppler



LV contractility looking for hypokinesis, akinesis or dyskinesis



Acute m itral regurgitation or septal defects



RV dilatation, tricuspid insufficiency, high pulm onary artery and RV pressures suggest pulm onary em bolism



RV hypokinesis or akinesis, RV dilatation, norm al pulm onary pressures suggest RV infarction



Pericardial effusion, right atrium or RV diastolic collapse suggest cardiac tam ponade

P.189

Lab 

B-type natriuretic peptide (BNP): o

Diagnostic and prognostic value



Creatine kinase (CK), CK-Mb, troponin



Electrolytes and renal function

Pa ge 9 3 7

o 

CBC: o



Acute renal failure is a strong predictor of m ortality

Identify anem ia or elevated WBC

Drug levels (e.g., digoxin)

Differential Diagnosis 





Obstructive shock: o

Tension pneum othorax

o

Cardiac tam ponade

o

Pulm onary em bolism

o

Spontaneous esophageal rupture

o

Air em bolus

Distributive shock: o

Sepsis

o

Anaphylaxis

o

Addisonian crisis

o

Neurogenic shock

Hypovolem ic shock: o

Hem orrhage

o

Gastrointestinal losses

o

Dehydration

o

Burns

Treatment Pre Hospital 

ABCs, IV access, O 2 , m onitor



Consider fluid bolus if no crackles.



Aspirin



Nitroglycerin or m orphine sulfate for chest pain in absence of hypotension

Pa ge 9 3 8



Transport AMI patients to facility with 24-hour cardiac revascularization capability.

Initial Stabilization 

ABCs



Two large bore peripheral IV lines



Cardiac m onitor



Endotracheal intubation for airway com prom ise: o

Consider etom idate for induction (m inim al effect on blood pressure)



Fluid challenge (100â€“250 m L norm al saline) in absence of pulm onary congestion



Foley catheter to m onitor urine output

ED Treatment 

AMI: o

Aspirin

o

Heparin

o

Throm bolysis if percutaneous coronary intervention or bypass surgery not available

o

GP IIb/IIIa inhibitors prior to percutaneous coronary intervention



Hypotension: o

Dopam ine, firstline vasopressor

o

Norepinephrine m ay be used for hypotension unresponsive to dopam ine or intra-aortic balloon pum p (IABP), or for tachycardia.



Nonhypotensive patient: o

Dobutam ine m ay be used. It has additive effect when used with dopam ine; com bine with nitroprusside in acute m itral regurgitation

o

Milrinone m ay be considered in conjunction with dobutam ine or dopam ine.

Pa ge 9 3 9



Pulm onary edem a: o

Nitroglycerin drip or furosem ide in the nonhypotensive patient



Prom pt cardiology consultation is crucial for the initiation of the following therapies: o

IABP im proves survival when com bined with revascularization.

o

Early revascularization is the single m ost im portant life-saving m easure.

Medication (Drugs) 

Dobutam ine: 3â€“5 Âµg/kg/m in, titrate to 20â€“50 Âµg/kg/m in as needed IV



Dopam ine: 3â€“5 Âµg/kg/m in, titrate to 20â€“50 Âµg/kg/m in as needed IV



Furosem ide: 40â€“80 m g/d (peds: 1 m g/kg IV or IM, not to exceed 6 m g/kg) IV or IM



Milrinone: 50 Âµg/kg loading dose, 0.375â€“0.75 Âµg/kg/m in continuous infusion IV



Nitroglycerin: 10â€“20 Âµg/m in (pedis: 0.1â€“1 Âµg/kg/m in) IV



Nitroprusside: 0.3 Âµg/kg/m in, titrate to a m ax. of 10 Âµg/kg/m in IV



Norepinephrine: 2 Âµg/m in, titrate up as needed IV

Follow-Up Disposition Admission Criteria

Pa ge 9 4 0

All patients in cardiogenic shock require adm ission to a critical care unit.

References 1. Hochm an JS. Cardiogenic shock com plicating acute m yocardial infarction: expanding the paradigm . Circulation. 2003;107:2998â€“3002. 2. Menon V, Hochm an JS. Treatm ent of cardiogenic shock com plicating acute m yocardial infarction. UpToDate v13.1. Accessed April 14, 2005. 3. Peacock WF, Weber JE. Cardiogenic shock, in Tinitinalli JE, Kelen GD, Stapczynski JS (eds): Em ergency Medicine: A Com prehensive Study Guide. McGraw-Hill Com panies, Inc.; 2004:242.

Miscellaneous SEE ALSO: Shock; Myocardial Infarction

Codes ICD9-CM 785.51

Pa ge 9 4 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardio m yo pathy, Hypertro phic

Cardiomyopathy, Hypertrophic L. Kristian Arnold

Basics Description 

Hypertrophic cardiom yopathy (HCM): o

Hypertrophied (regionally or globally), nondilated left ventricle (LV) in the absence of another cause of LV hypertrophy such as hypertension or aortic stenosis

o

Originally described in 1950s as subaortic outflow track obstruction known as idiopathic hypertrophic subaortic stenosis 

Current understanding: 75% of HCM patients have no significant resting outflow tract gradient.

o

Now defined as prim arily genetic disorder of the sarcom ere

o

Predom inant abnorm ality identified (one third of cases) in young (<35 years old) athletes suffering sudden atraum atic death

o

Manifests in all ages, from neonate to elderly: 

Average age of diagnosis is 30â€“40 years old.



Usually m ore severe with younger age at

Pa ge 9 4 2

diagnosis  

Adolescence m ost com m on onset of hypertrophy

Structural abnorm ality: o

Irregular, m arked ventricular wall thickening with disarray of m yofibrils in the thickened regions and fibrin deposition 

Som e evidence of progressive wall thinning with age associated with decreased death from arrhythm ia

 o

Som e phenotypes with later age onset

Thickening usually asym m etric involving the septum to a greater extent than the free ventricular wall

o

Atrial dilation secondary to diastolic filling stiffness

Genetics 

First cardiac disorder for which genetic basis identified



Autosom al dom inantly inherited disorder: o

More than 10 associated genes found: 

Most encode proteins for sarcom ere



More than 200 distinct m utations recognized

o

Variable penetrance

o

Variable phenotypic expression

o

Som e genotypes significantly m ore lethal: 



Routine screening im practical at present

Prevalence about 1 in 500 general population: o

Based on echocardiographic diagnosis

Etiology N/A (see Genetics)

Diagnosis

Pa ge 9 4 3

Signs and Symptoms History 

Sym ptom s correlate with exertion, Valsalva m aneuver, or suddenly assum ing upright positionâ€”all activities that decrease venous return or ventricular filling.



Severity depends on the location and degree of ventricular wall thickening.



Shortness of breath



Dyspnea on exertion



Exertional or postprandial angina



Presyncope



Syncope



Congestive heart failure (CHF)



Cardiovascular collapse



Dysrhythm ias: o

Paroxysm al atrial fibrillation: 

Often leads to significant, rapid clinical deterioration when present with CHF

o

Supraventricular tachycardia

o

Nonsustained ventricular tachycardia (VT) occurs in young adults.

o

Bradydysrhythm ia less com m on

o

VT or ventricular fibrillation m ay lead to sudden death.



Prior therapy for known HCM m ight include surgery or alcohol injection to reduce septal bulk:



o

Potential for conduction blocks

o

Potential septal rupture

Known cases with higher risk of arrhythm ia m ay have im planted defibrillators.

Pediatric Considerations

Pa ge 9 4 4

Due to potential increasing severity in adolescence, any young child with syncope without clear cause should have m ore extensive, focused history for fam ilial sudden death and possible referral for evaluation.

Physical Exam 

No or subtle physical findings



Most findings in patients with outflow tract obstruction: o

Loud, left-sided S4

o

Double apical cardiac im pulse at the m id to upper sternum

o

Murm ur: 

Crescendo-decrescendo m idsystolic m urm ur at the left sternal edge



Radiation to aortic and m itral areas, not to neck or axilla



Increasing in intensity with Valsalva m aneuver or standing up



Quieter with recum bency, swatting, or handgrips

 o

Frequent associated m itral regurgitation

With m ore severe obstruction, a m ore apparent m urm ur with radiation to the left sternal border

o

Radiation to the axilla if there is associated m itral insufficiency

Tests ECG findings: 

Norm al in 15% of patients



ST segm ent and T wave abnorm alities



LV hypertrophy with strain, with quasi-random signal (QRS) com plexes that are tallest in the m idprecordial leads

Pa ge 9 4 5



Large Q waves, particularly in infero-lateral leads



Left atrial enlargem ent



Short pulse rate with slurred upstroke of QRS

Lab Clinical laboratory testing is of no assistance.

Imaging 

Chest radiograph: o

Norm al

o

Bulge along left heart border representing hypertrophy of free wall of LV



o

Right or left atrial enlargem ent

o

Pulm onary vascular redistribution

Transthoracic cardiac echo/Doppler: o

Establishes the diagnosis of HCM (standard >15 m m wall thickness in adults)

o

Dem onstrates systolic outflow obstructions and diastolic filling abnorm alities



Nuclear MRI supplem ents indeterm inate echocardiography and is a better definition of patchy hypertrophy.



Stress thallium and PET evaluate ischem ia.

Diagnostic Procedures/Surgery No ED-based procedures are of diagnostic utility

Differential Diagnosis 

Vagal and other causes of syncope and presyncope (if HCM is considered, it m ust be ruled out because it is m uch m ore likely to be fatal with repeat episodes)



Aortic stenosis



Pulm onic stenosis



Ventricular septal defect



Mitral regurgitation

Pa ge 9 4 6



Mitral valve prolapse



Arteriosclerotic coronary vascular disease



Differentiate in patients presenting with CHF or angina: o

More om inous in the setting of HCM

P.193

Treatment Pre Hospital Alert Consider HCM in patients who decom pensate during standard treatm ents for CHF, ischem ia, or supraventricular tachycardia, and in young athletes who collapse during or just after exertion.

Initial Stabilization 

ABCs



IV catheterization



Supplem ental oxygen



Cardiac m onitor



Pulse oxim etry

ED Treatment 

Depends on type of presentation: dysrhythm ia, cardiac failure or ischem ia



Underlying principle to understand sensitivity to any situation that m ay im pair cardiac filling: o

Do not place in seated or Fowler position: 



Patient m ay need to rem ain supine.

Standard CHF or anginal vasodilator therapy m ay lead to

Pa ge 9 4 7

cardiovascular collapse; if this occurs, treat with fluid bolus. 

Attention to any hypovolem ia as sm all degree m ay significantly im pair cardiac output.



Control heart rate and im prove diastolic filling (underlying principle in treating HCM-associated CHF and angina): o

Beta-blockers: 

Mainstay of therapy



Decrease dysrhythm ias and lower elevation of pressure gradient across the LV outflow tract

o

Calcium -channel blockers: 

Verapam il reduces obstruction by decreasing contractility and im proving diastolic relaxation and filling.



Nifedipine relatively contraindicated due to vasodilatation



Dysrhythm ia m anagem ent: o

Beta-blockers and calcium -channel blockers first line for supraventricular dysrhythm ias

o

Am iodarone: 

Drug of choice for ventricular dysrhythm ias



Used when beta-blockers and calcium -channel blockers fail

o

Disopyram ide: 

Effective for supraventricular and ventricular dysrhythm ias

o

Electrical cardioversion: 

Use early in HCM with new atrial fibrillation and CHF

Medication (Drugs)

Pa ge 9 4 8



Most em ergency presentations associated with this disorder that require any ED treatm ent other than frank resuscitation are likely to either be tachydysrhythm ia that will require or warrant electrical therapy or CHF.



Am iodarone: 150 m g over 10 m inutes, then 360 m g over 6 hours, then 540 m g over next 18 hours (peds: 5 m g/kg IV over 1 hour in 1m g/kg bolus aliquots, off-label use per m anufacturer, but class IIb for VT with a pulse and class indeterm inate for VF and pulseless VT, per Am erican Heart Association. Do not use in infants.)



Diltiazem : 0.25 m g/kg (peds: contraindicated <12 years old) IV over 2 m inutes; m ay repeat in 15 m inutes at 0.35 m g/kg



Propranolol: 1â€“3 m g (peds: 0.01â€“0.1 m g/kg slow IV push over 10 m inutes; not to exceed dose 1 m g/dose) slow IV bolus



Verapam il: 2.5 m g (peds: >1 year: 0.1â€“0.2 m g/kg/dose over 2 m inutes; repeat q10m inâ€“q30m in as needed; not to exceed 5 m g/dose [first dose] or 10 m g/dose [second dose]) IV bolus over 1â€“2 m inutes, m ay repeat as 5.0 m g in 15â€“30 m inutes

Follow-Up Disposition Admission Criteria 

Consider for unexplained syncope, especially in younger adults.



Telem etry adm ission for dysrhythm ia



Intensive care unit adm ission:

Pa ge 9 4 9

o

Syncopal episodes

o

CHF

o

Angina

o

Hem odynam ically significant tachydysrhythm ia

Discharge Criteria When increased m yocardial wall thickness is an incidental finding during the ED evaluation for another presentation: 

No history of fam ilial sudden death or personal history of syncope



Need urgent follow-up with a cardiologist



Counsel against any activities that m ay decrease diastolic filling pending follow-up.

References 1. Charron P, Dubourg O, Desnos M, et al. Diagnostic Value of Electrocardiography and Echocardiography for Fam ilial Hypertrophic Cardiom yopathy in a Genotyped Adult Population. Circulation. 1997;96(1):214â€“219. 2. Doolan A, Langlois N, Sem sarian C. Causes of sudden cardiac death in young Australians. Med J Australia. 2004;180(3):110â€“112. 3. Elliott P, McKenna WJ. Hypertrophic cardiom yopathy. Lancet. 2004;363(9424):1881â€“1891. 4. Maron BJ, McKenna WJ, Danielson GK, et al. Am erican College of Cardiology/European Society of Cardiology Clinical Expert Consensus Docum ent on Hypertrophic Cardiom yopathy: a report of the Am erican College of Cardiology Foundation Task Force on Clinical Expert Consensus Docum ents and the European Society of Cardiology Com m ittee for Practice Guidelines. J Am Coll of Cardiol. 2003;42(9):1687â€“1713. 5. Maron BJ, Pelliccia A, Spirito P. Cardiac disease in young trained athletes. Insights into m ethods for distinguishing athlete's heart from structural heart disease, with particular em phasis on hypertrophic

Pa ge 9 5 0

cardiom yopathy. Circulation. 1995;91(5):1596â€“1601. 6. Maron BJ, Seidm an JG, Seidm an CE. Proposal for contem porary screening strategies in fam ilies with hypertrophic cardiom yopathy. J Am Coll Cardiol. 2004;44(11):2125â€“2132. 7. McKenna WJ, Sadoul N, Slade AK, et al. The prognostic significance of nonsustained ventricular tachycardia in hypertrophic cardiom yopathy. Circulation. 1994;90(6):3115â€“3117. 8. Spirito P, Rapezzi C, Autore C, et al. Prognosis of asym ptom atic patients with hypertrophic cardiom yopathy and nonsustained ventricular tachycardia. Circulation. 1994;90:2743â€“2747. 9. Spirito P, Seidm an CE, McKenna WJ, et al. The m anagem ent of hypertrophic cardiom yopathy. N Engl J Med. 1997;336(11):775â€“785. 10. Tham an R, Gim eno JR, Reith S, et al. Progressive left ventricular rem odeling in patients with hypertrophic cardiom yopathy and severe left ventricular hypertrophy. J Am Coll Cardiol. 2004;44(2):398â€“405. 11. Wigle ED, Rakowski H, Kim ball BP, et al. Hypertrophic cardiom yopathy. Clinical spectrum and treatm ent. Circulation. 1995;92(7):1680â€“1692. 12. Wyeth-Ayerst. Letter to health care professionals. 21 March, 2001. Available at http://www.fda.gov/m edwatch/SAFETY/2001/cordarone_deardoc.pdf. Accessed: June 15, 2005.

Codes ICD9-CM 425.4 Other prim ary cardiom yopathies. 425.1 Hypertrophic obstructive cardiom yopathy (Hypertrophic Sub-aortic Stenosis)

Pa ge 9 5 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardio m yo pathy, Peripartum

Cardiomyopathy, Peripartum Richard Wolfe

Basics Description 

Onset of m yocardial failure during last m onth of pregnancy or first 5 m onths after delivery: o

Absence of a specific cause

o

Absence of a history of cardiac disease



Occurs in 1 of every 3,000â€“15,000 pregnancies



Classified as a form of dilated cardiom yopathy



About 50% of cases resolve spontaneously.



Mortality rates are 18â€“56%.



Risk factors:



o

Older wom en

o

Multiparous wom en

o

Twin births

o

Prolonged tocolytic therapy

o

Obesity

o

Pre-eclam psia

o

African or Haitian origin

System ic and pulm onary em bolism m ore frequent than with other form s of cardiom yopathy

Pa ge 9 5 2



Factors indicating a poor prognosis: o

Lower left ejection fraction at 6 m onths postpartum

o

Onset >2 weeks postpartum

o

Age >30 years

o

African Am erican descent

o

Multiparity

Etiology Various causes are suggested but rem ain unproved: 

Viral infection leading to m yocarditis, in presence of im m unosuppression during pregnancy



Im m unologic response to an unknown m aternal or fetal antigen



Maladaptive response to the hem odynam ic stresses of pregnancy



Stress-activated cytokines



Prolonged tocolysis



Selenium deficiency

Diagnosis Pre Hospital Differentiate pulm onary edem a from acute reactive airway disease.

Signs and Symptoms 

Dyspnea



Chest pain



Orthopnea



Cough



Paroxysm al nocturnal dyspnea



Anorexia



Fatigue

Pa ge 9 5 3



Jugular venous distention



Gallop rhythm



Mitral regurgitation m urm ur



Loud P2



Pulm onary rales



Peripheral edem a



Ascites



Hepatom egaly



Hepatojugular reflux

Essential Workup 



Chest radiograph views: o

Pulm onary venous congestion

o

Cardiom egaly

ECG: o

Nonspecific

o

Left ventricular hypertrophy

o

Left atrial enlargem ent

o

T-wave flattening or inversion

o

Arrhythm ias

o

Ventricular ectopy (40%)

o

Atrial fibrillation (20%)

Tests Lab 

Electrolytes: o

Generally norm al



Blood urea nitrogen, creatinine



CBC: o

Mild postpartum anem ia m ay contribute to fatigue and dyspnea.



Creatine kinase with m uscle and brain fraction



Beta natriuretic peptide (BNP):

Pa ge 9 5 4

o

Useful for distinguishing between heart failure due to diastolic and/or systolic dysfunction and a pulm onary cause of dyspnea

o

BNP >100 pg/m L diagnosed heart failure with a sensitivity of 90%, a specificity of 76%, and a predictive accuracy of 83%. BNP of â‰¤50 pg/m L has a high negative predictive value.

Imaging 

ECG: o

Dem onstrates cham ber enlargem ent and decreased ejection fraction



Chest radiograph film : o

Cardiom egaly

o

Effusions (usually right sided)

o

Three phases of pulm onary findings: 

Stage I: pulm onary redistribution to upper lung fields (cephalization)



Stage II: interstitial edem a with Kerley B lines



Stage III: alveolar edem a



Bilateral confluent perihilar infiltrates leading to classic butterfly pattern



May be asym m etric and m istaken for pneum onia



Echocardiography: o

Criteria for the diagnosis were established by Hibbard et al. 

Ejection fraction less than 45% or M-m ode fractional shortening of less than 30%



End-diastolic dim ension that is greater than 2.72 cm /m 2

o 

Exclude valvular pathology and cardiac tam ponade

Endom yocardial biopsy:

Pa ge 9 5 5

o

Indicated to assess for m yocarditis and steroid therapy

Differential Diagnosis 

Other causes of dilated cardiom yopathy: o

Ischem ia

o

Infarction

o

Valvular rupture or disease

o

Chronic hypertension

o

Fam ilial

o

Toxins: 

o

o

Ethanol, anthracyclines, cocaine, drug allergy

Metabolic: 

Thiam ine



Selenium



Hypothyroidism



Thyrotoxicosis



Hypophosphatem ia

Infectious: 

Viral



Parasitic



Rickettsial



Bacterial



Fungal

P.195

o

System ic disorders: 

Sarcoidosis



Scleroderm a



System ic lupus erythem atosus

o

Eosinophilic Myocarditis

o

Neurom uscular dystrophies

Pa ge 9 5 6

o

Mitochondrial cardiom yopathies



Pulm onary em bolism



Pneum onia



Asthm a



Cardiac ischem ia



Anem ia



Hyperthyroidism



Constrictive pericarditis



Pericardial tam ponade



Nephrotic syndrom e



Cirrhosis

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent: 

Prom pt evaluation of respiratory and hem odynam ic status



Control airway as needed.



Supplem ental oxygen



Continuous positive airway pressure, as needed

ED Treatment Prepartum therapy: 

Am lodipine: o

A dihydropyridine calcium -channel blocker that has been shown to im prove survival in nonischem ic cardiom yopathy patients



Nitrates



IV furosem ide



Digoxin to control rate due to atrial fibrillation



Postpartum therapy:

Pa ge 9 5 7



Add angiotensin-converting enzym e inhibitors (enalapril) or angiotensin II receptor blockers.



Anticoagulation therapy often recom m ended: o

30% of cases com plicated by system ic or pulm onary em bolism

o

During pregnancy, use subcutaneous heparin rather than warfarin, which causes birth defects.



For severe sym ptom s or lack of response to standard therapy:



o

Dobutam ine

o

Dopam ine

o

Nitroprusside

Im m unosuppressive therapy: o

Advocated for patients who fail to im prove within 2 weeks of standard m edical therapy

o

Prednisone with cyclosporine or azathioprine

o

Im m unoglobulin therapy

o

Rem ains controversial

Medication (Drugs) 

Am lodipine: 2.5â€“10 m g PO daily



Am rinone: 0.75 m g/kg IV load; 5â€“10 Âµg/kg per m inute IV



Bum etanide: 0.5â€“2.0 m g IV



Digoxin: 1 m g IV load over 1 day; 0.125â€“0.375 m g per day PO



Dobutam ine: 2â€“10 Âµg/kg per m inute IV



Dopam ine: 2â€“20 Âµg/kg per m inute IV



Enalapril: 0.625â€“1.25 m g intravenously; 2.5â€“20 m g per day PO



Furosem ide: 20â€“100 m g IV

Pa ge 9 5 8



Metoprolol: 12.5 m g b.i.d. PO



Morphine sulfate: 2â€“4 m g IV q5m in



Nitroglycerin: 0.4 m g sublingual; 1â€“2 in. of nitroglycerine paste; 5â€“20 Âµg per m inute IV, m axim um of 100â€“200 Âµg per m inute IV



Nitroprusside: 0.5â€“10 Âµg/kg per m inute IV

Follow-Up Disposition Admission Criteria 

Patients with pulm onary edem a, cardiogenic shock, or evidence of ischem ia should be adm itted to intensive care unit.



All sym ptom atic patients with new onset of peripartum cardiom yopathy should be adm itted.

Discharge Criteria 

Mild left ventricular dysfunction



Established history of peripartum cardiom yopathy: o

Mild fluid overload attributable to excessive salt intake

o

Com plete resolution of sym ptom s following ED treatm ent

o

No evidence of cardiac ischem ia

References 1. Brown CS. Peripartum cardiom yopathy: A com prehensive review. Am J Obstet Gynecol. 1998;178:409â€“414. 2. Hibbard JU, Lindheim er M, Lang RM. A m odified definition for peripartum cardiom yopathy and prognosis based on

Pa ge 9 5 9

echocardiography. Obstet Gynecol. 1999;94(2):311â€“316. 3. Murali S, Baldisseri MR. Peripartum cardiom yopathy. Crit Care Med. 2005;33:S340â€“S346. 4. Pearson GD, Veille JC, Rahim toola S, et al. Peripartum cardiom yopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recom m endations and review. JAMA. 2000;283:1183â€“1188.

Codes ICD9-CM 674.8

ICD10 090.3

Pa ge 9 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardio m yo pathy

Cardiomyopathy

Elizabeth Temin James Feldman

Basics Description 

Diseases of the m yocardium associated with cardiac dysfunction.



Dilated cardiom yopathy: o

Dilated and im paired contraction of the left or both ventricles

o

Idiopathic dilated cardiom yopathy accounts for 25% of all cases of heart failure.





Hypertrophic cardiom yopathy: o

Left or right asym m etric ventricular hypertrophy

o

Usually involves the interventricular septum

Restrictive cardiom yopathy: o

Restrictive filling and reduced volum e of either or both ventricles

o 

Norm al or near-norm al systolic function

Arrhythm ogenic right ventricular cardiom yopathy: o

Progressive fibrofatty replacem ent of the right ventricular m yocardium

o

Relative sparing of the septum

Pa ge 9 6 1



Unclassified cardiom yopathy: o

Disorders such as fibroelastosis that do not fit into a dom inant pattern



Specific cardiom yopathy: o

Heart m uscle disease associated with a system ic disease or condition

Pediatric Considerations 

Genetic: 20â€“30%



Acquired



Idiopathic

Pregnancy Considerations 

Onset during last m onth of pregnancy to 5 m onths postpartum



No identifiable cause



Depressed systolic function

Etiology 



Dilated: o

Idiopathic

o

Viral

o

Genetic/Toxic

o

Im m une

Hypertrophic: o





Fam ilial disease with autosom al dom inance

Restrictive: o

Idiopathic

o

Am yloid

Arrhythm ogenic right ventricular: o

Fam ilial disease with dom inant and recessive patterns



Specific: o

Infectious

Pa ge 9 6 2



o

Lym e disease

o

Viral

o

Chagas disease

o

HIV

Toxic agents: o

Alcohol

o

Chem otherapeutic agents



Peripartum period



Metabolic



o

Hyperthyroidism

o

Pheochrom ocytom a

o

Am yloid

General system s diseases: o

Lupus

o

Scleroderm a

o

Neurom uscular diseases

Pediatric Considerations 

Idiopathic



Genetic:



o

Inborn errors of m etabolism

o

Malform ation syndrom es

o

Neurom uscular disease

o

Fam ilial isolated cardiom yopathy disorders

Acquired: o

Vitam in and/or trace m ineral deficiencies

o

Electrolyte disturbances

o

Endocrine disorders

o

Toxins

o

Collagen vascular disease

o

Im m unologic disease

o

Malignancy

o

Morbid obesity

Pa ge 9 6 3

o

Myocarditis

o

Pulm onary disease

o

Kawasaki disease

o

Infection

o

Radiation

o

Congenital heart disease

o

Asphyxia

Diagnosis Signs and Symptoms History 





Antecedent illness or exposure: o

Chem otherapy

o

HIV

o

Lym e disease

o

Viral

Underlying system ic condition: o

Hem ochrom atosis

o

Sarcoidosis

o

Pregnancy

Fam ily history: o

Fam ilial sudden death

o

Exertional com plaints (syncope, dyspnea)

Dilated Cardiomyopathy 



General: o

Fatigue

o

Weakness

Respiratory: o

Dyspnea on exertion

Pa ge 9 6 4

o 



Cardiac: o

Chest pain

o

S4 gallop is alm ost always present.

o

S3 gallop only after cardiac decom pensation occurs

o

Jugular venous distention (JVD)

o

Dysrhythm ias

o

Mitral or tricuspid regurgitation

Abdom en: o



Enlarged, pulsatile liver

Extrem ities: o



Orthopnea

Peripheral edem a

System ic em boli

Hypertrophic Cardiomyopathy â€”See Cardiom yopathy, Hypertrophic

Restrictive Cardiomyopathy 







General: o

Exercise intolerance

o

Weakness

Respiratory: o

Dyspnea

o

Pulm onary congestion

Cardiac: o

Exertional chest pain is usually absent

o

JVD with Kussm aul sign (rise with inspiration)

o

Apex is usually easily palpated

o

Mitral regurgitation

Abdom inal: o

Increased abdom inal girth

o

Right upper-quadrant pain

o

Ascites

Pa ge 9 6 5

o 

Hepatom egaly

Extrem ities: o

Edem a

o

Peripheral edem a

Arrhythmogenic Right Ventricular Cardiomyopathy 

Dizziness



Near syncope and syncope



Palpitations



Sudden death



Ventricular arrhythm ias



Congestive heart failure (CHF)

Pediatric Considerations 

Irritability



Hepatom egaly



Generalized m uscle weakness



Acute biochem ical crisis



Hypoglycem ia



Metabolic acidosis



Hyperam m onem ia



Cyanosis



Encephalopathy



Dysm orphic features

Pregnancy Considerations See Cardiom yopathy, Peripartum

Tests Lab 

CBC



Electrolytes, blood urea nitrogen, creatinine, liver function tests

Pa ge 9 6 6



Cardiac enzym es



Brain (B-type) natriuretic peptide: level >100 pg/m L



Serologies



Not useful in the ED

P.191

Imaging 

Chest radiograph: o

o

Dilated cardiom yopathy: 

Cardiom egaly



Pulm onary congestion



Pleural effusions

Hypertrophic cardiom yopathy: 

o



See Cardiom yopathy, Hypertrophic

Restrictive cardiom yopathy: 

Norm al cardiac silhouette



Pulm onary congestion

ECG: o

o

Hypertrophic cardiom yopathy: 

Left ventricle (LV) hypertrophy



Abnorm al septal Q waves

Dilated, Lym e, Chagas, and toxic cardiom yopathies: 

Atrial fibrillation



Heart block



Conduction abnorm alities



Pseudoinfarct pattern with pathologic Q waves can be seen in anterior and inferior leads without coronary artery disease.



Em ergency transthoracic 2D echocardiogram ; o

Depressed LV ejection fraction

o

Excludes pericardial tam ponade

Pa ge 9 6 7





Form al transthoracic Doppler echocardiography: o

Study of choice in patients with cardiom yopathy

o

Identification of underlying disease

Nuclear scintigraphy: o

Indicated when ECG is indeterm inate

o

Direct determ ination of the thickness of the septum and free wall

o 

Alternative assessm ent to echo

CT and MRI distinguish between constrictive pericarditis and restrictive cardiom yopathy.

Diagnostic Procedures/Surgery Cardiac catheterization: 



Dilated cardiom yopathy: o

Suspicion of ischem ia

o

Treatable system ic disease

Hypertrophic cardiom yopathy: o

Assessm ent of hem odynam ic abnorm alities

o

Endom yocardial biopsy

o

Evaluation for m yocarditis or define etiology

Pediatric Considerations 

Electrolytes



pH



Glucose



Am m onia level



Cardiac output



Dysm orphic evaluation



ECG



Echocardiogram : o

Genetic workup; see individual causes

Differential Diagnosis 

Other causes of dyspnea:

Pa ge 9 6 8

o

Chronic obstructive pulm onary disease

o

Anem ia

o

Asthm a

o

Interstitial lung disease

o

Pulm onary em bolism

o

Pericardial tam ponade: 

Valvular heart disease

o

Ischem ic heart disease

o

Hypothyroidism

o

Constrictive pericarditis, com m only confused with restrictive cardiom yopathy



Other causes of syncope: o

Hypovolem ia

o

Heat disorder

o

Hypoglycem ia

Treatment Pre Hospital 

Monitor



Oxygen



Hypertrophic cardiom yopathy, known or suspicion:



o

Avoid or use a lower dose of nitroglycerine.

o

Cardioversion if deterioration due to atrial fibrillation

LV heart failure: o

Oxygen

o

Nitroglycerine spray

o

Furosem ide

o

Morphine

Initial Stabilization

Pa ge 9 6 9

Airway, breathing, and circulation: 

Control airway as needed.



Supplem ental oxygen



Continuous positive airway pressure

ED Treatment 



Anticoagulation: o

Dilated cardiom yopathy

o

Standard treatm ent of atrial fibrillation

o

System ic em bolization

Lim ited ED experience with agents effective in hypertrophic cardiom yopathy: o

Disopyram ide to reduce obstruction

o

Am iodarone to convert and m aintain sinus rhythm



Standard treatm ent of CHF



Standard treatm ent of dysrhythm ias

Pediatric Considerations 

Keep NPO until inborn errors of m etabolism ruled out.



IV fluids: o

D10 should be given until defects in the protein or fatty acid m etabolism pathways can be ruled out.

o

IV fluids need to be given slowly to avoid rapid fluid shifts to the extravascular space.



Do not give any products with lactate to avoid worsening any m etabolic acidosis or lactic academ ia.



Antioxidants and vitam in cofactors



L-Carnitine to increase m itochondrial energy m etabolism



Standard treatm ent of CHF



Dichloroacetate acutely lowers acetic acid levels in patients with m itochondrial disorders.

Pa ge 9 7 0

Medication (Drugs) 

Am iodarone: 5 m g/kg over 10 m inutes



Carnitine: (peds: 50â€“300 m g/kg/d PO or IV)



Digoxin: start 0.125 m g



Disopyram ide: 100â€“200 m g PO q6h.



Furosem ide: 20â€“40 m g IV to a m ax. of 200 m g on subsequent doses (peds: 1 m g/kg IV q12hâ€“q24h)



Heparin: load 80 IU/kg IV.; then 18 IU/kg/h



Milrinone: bolus 50 Âµg/kg IV over 10 m inutes, then 0.375â€“0.75 Âµg/kg/m in IV



Morphine: 2â€“5 m g IV



Nesiritide: bolus 2 Âµg/kg IV, then 0.01 Âµg/kg/m in IV with a m axim um of 0.03 Âµg/kg/m in



Nitroglycerine: 5 Âµg/m in IV titrate to SBP



Verapam il: 2.5â€“10 m g IV over 2 m inutes; m ax. 20 m g (peds: <1 yr, 0.1â€“0.2 m g/kg IV over 2 m inutes; m ay repeat one tim e in 30 m inutes.

Admission Criteria 

New or suspected cardiom yopathy



Syncope where dysrhythm ias or HCM are possible etiologies.



Fam ilial history of prem ature sudden death



Cardiogenic shock: o

Consider transfer to a cardiac center capable of m echanical support and cardiac transplantation.

Discharge Criteria 

Diagnosed cardiom yopathy with m ild CHF that im proves with ED therapy



Restrictive or hypertrophic cardiom yopathy



Cardiology consultation for discharge planning

Pa ge 9 7 1

Issues for Referral Patients with ejection fraction (EF) <35% m ay require referral for single cham ber im plantable cardioverter defibrillator and resynchronization therapy with atrial-synchronized biventricular pacing.

References 1. Nishim ura RA, Holm es DR Jr. Hypertrophic obstructive cardiom yopathy. N Engl J Med. 2004;350:1320â€“1327. 2. Pearson GD, Veille JC, Rahim toola S, et al. Peripartum cardiom yopathy: National Heart, Lung and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recom m endations and review. JAMA. 2000;283:1183â€“1188. 3. Pisani B, Taylor DT, Mason JW. Inflam m atory m yocardial diseases and cardiom yopathies. Am J Med. 1997;102:459â€“469. 4. Schwartz ML, Cox GF, Lin AE, et al. Clinical approach to genetic cardiom yopathy in children. Circulation. 1996;94:2021â€“2038. 5. Wynne J, Braunwald E. The cardiom yopathies and m yocarditises. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 7th ed. Philadelphia, PA: WB Saunders, 2006.

Codes ICD9-CM 425.4 425.5 425.7 428

ICD10 I42 I43

Pa ge 9 7 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arpal F ractures

Carpal Fractures

Colleen Campbell

Basics Description 

Scaphoid (carpal navicular) is the m ost com m only fractured carpal: o



Followed by capitate and lunate fractures

Fractures of the carpal bones com m only occur with dislocations at the wrist or CMC joint: o

Capitate fractures occur as part of the scaphocapitate syndrom e

o



Scaphoid waist fracture



Proxim al capitate +/- distal radius fx

Ham ate fractures: 

May occur with associated rupture of flexor tendons of ring and sm all fingers

Etiology 

Crush injury or direct blow



Fall on an outstretched hand (FOOSH)



Lunate fractures m ay occur as a result of repetitive traum a: o

Wrist held in hyperextension

Pa ge 9 7 3

Pediatric Considerations 

Injuries are rare in children.



Bones are incom pletely calcified in children: o

Fractures m ay be m ore difficult to detect.

Diagnosis Signs and Symptoms History 

Usually FOOSH



Direct traum a to the hand or wrist



Repetitive m otion injury

Physical Exam 

Pain in wrist or dorsum of hand



Ham ate fractures m ay cause pain in ulnar palm region.



Swelling



Decreased range of m otion of the wrist

Essential Workup 

A com plete physical exam ination of the entire upper extrem ity and shoulder girdle: o



Evaluate for associated injuries.

Neurovascular exam is essential.

Tests Imaging 

Anterior-posterior, lateral, oblique views of the hand and wrist



Special views (e.g., scaphoid views) m ay be obtained for m ost of the carpals if physical exam ination is suspicious.

Pa ge 9 7 4



CT scan m ay be necessary to diagnose fractures of the scaphoid, trapezium , and trapezoid, as radiographs are often nondiagnostic.



One area in which com parison with a good radiographic atlas m ay be very helpful

Differential Diagnosis 

Metacarpal base fracture



Distal radius or ulna fracture



Lunate or perilunate dislocation

Pediatric Considerations 

Be wary of epiphyseal injuries of the distal radius: o

Children rarely get sim ple sprains or fractures of the wrist.

Treatment Initial Stabilization 

Any patient with a wrist or hand injury should be referred to a physician or ED: o



Fractures m ay be easily m issed.

Patients with swelling or significant pain at the wrist or hand: o

Should be splinted to the elbow

o

Extrem ity elevated

o

Ice applied



Assess for other, m ore serious injuries.



Prevent contam ination of any lacerations overlying the area.

P.197

Pa ge 9 7 5

ED Treatment 

Isolated fractures of the carpals (except the scaphoid) are very rare: o

Manage with sugar-tong splinting from the forearm to the distal hand.



Suspected scaphoid fractures: o

Snuffbox tenderness but negative initial radiograph

o

Require im m obilization by splint of the forearm , wrist, thum b, and hand (thum b spica splint).



o

Im m obilize for 10â€“14 days.

o

Then repeat radiograph.

Chip fractures off the dorsal triquetrum : o



Treated with sim ple im m obilization splinting

Associated injuries such as lunate or perilunate dislocation should be sought.





Ham ate fractures: o

Rare but m ay be associated with ulnar artery injury

o

Allen test of hand circulation im portant

Open carpal fracture: o

Requires high pressure irrigation as soon as possible

o

Parenteral antibiotics as well as im m ediate orthopedic consultation

Medication (Drugs) 

Mild oral analgesics, oral narcotics, NSAIDs for patient com fort



Proper splinting will relieve m ost of the pain for these injuries.

Pa ge 9 7 6

Follow-Up Disposition Admission Criteria 

Open fractures are adm itted for early operative irrigation and dÃ©bridem ent.



Patients with injuries requiring surgical m anagem ent (open reduction) frequently are adm itted for early intervention.



Most displaced or intra-articular fractures require percutaneous or open reduction and internal fixation.

Discharge Criteria 

Closed, nondisplaced carpal fractures treated with adequate splinting of entire forearm m ay be discharged to have orthopedic follow-up in several days.



Nondisplaced fractures require 6â€“8 weeks in a short arm cast for healing.

References 1. Geissler WB. Carpal Fractures in Athletes. Clin Sports Med. 2001;Jan20(1):167â€“168. 2. Goddard N. Carpal Fractures in Children. Clin Orthop Relat Res. 2005;Mar(432):73â€“76. 3. Tan V, Benedjiklian PK, Weiland AJ. Closed Reduction of Hand Fractures. J Orthop Traum a. 2005;Sep19(8):518â€“523. 4. Yaghoubian R, Goebel F, Musgrave DS, Sotereanos DG. Diagnosis and m anagem ent of Acute Fracture Dislocation of the Carpus. Ortho Clin Nam . 2001;Apr3(2):295â€“305.

Codes ICD9-CM 814.00

Pa ge 9 7 7

814.01

ICD10 NEC S62.1

Pa ge 9 7 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arpal Tunnel Syndro m e

Carpal Tunnel

Syndrome Matthew T. Spencer Linda L. Spillane

Basics Description 

The m edian nerve, flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus are located in the carpal tunnel.



Area bound by the carpal bones and the transverse carpal ligam ent



Com pression of the m edian nerve causes sym ptom s.

Etiology 

Occupational/overuse syndrom esâ€”high im pact, repetitive m otion



Traum a



Pregnancy, birth control pills



Granulom atous disease: tuberculosis, sarcoidosis



Mass lesions with m edian nerve com pression



Osteophytes



Am yloid



Multiple m yelom a

Pa ge 9 7 9



Rheum atoid arthritis



Endocrine disorders: hypothyroidism , diabetes m ellitus, acrom egaly



Chronic hem odialysis



Idiopathic

Pediatric Considerations 

Idiopathic cause rare in children; m ost cases have correctable cause including: o

Traum a

o

Mucolipidosis

o

Ham artom a of the m edian nerve

o

Anom alous flexor digitorum superficialis (FDS)

o

Hem ophilia with hem atom a

Diagnosis Signs and Symptoms History 

Num bness/paresthesias in m edian nerve distribution: o

Thum b, index, m iddle, and radial aspect of ring finger



Pain: o

Location: wrist or hand, som etim es radiating to elbow, forearm , or shoulder

o

Often worse at nightâ€”relieved by â€œshaking outâ€ • the hand

o

Exacerbated by repetitive wrist m ovem ent and by activities in which the wrist is flexed (e.g., driving)

Physical Exam 

Weakness of the abductor pollicis brevis and opponens

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m uscles: o

Innervated by the recurrent branch of the m edian nerve

o

Patient m ay com plain of dropping things or having decreased fine m otor control.

o 



Sensitivity of 29%; specificity of 80%, on average

Loss of two-point discrim ination: o

Late finding, highly specific

o

Sensitivity of 24%; specificity of 94%

Atrophy of thenar m uscles: o

Late finding, highly specific

o

Sensitivity of 18%; specificity of 94%

Essential Workup 

History of characteristic nocturnal pain and paresthesias in the m edian nerve distribution.



Muscle weakness and thenar wasting are later findings.



Provocative testing: o

Phalen test: 

Wrist flexion for 60 seconds produces num bness or tingling in the m edian nerve distribution.

 o

Sensitivity of 68%; specificity of 73%

Tinel sign: 

Gentle tapping over the m edian nerve at wrist produces tingling in the fingers in the m edian nerve distribution.

 o

Sensitivity of 50%; specificity of 77%

Carpal com pression test: 

Thum b pressure applied over the proxim al carpal ligam ent produces tingling in the fingers in the m edian nerve distribution.

 o

Sensitivity of 64%; specificity of 83%

Tourniquet test:

Pa ge 9 8 1



Blood pressure (BP) cuff inflated to just above the patient's systolic blood pressure for 2 m inutes produces paresthesias in the m edian nerve distribution.



Sensitivity of 59%; specificity of 61%

Tests Lab 

Not indicated in m ost cases



Thyroid function studies; rheum atoid factor and im m une panel if indicated by history and physical exam

P.199

Imaging 

Wrist radiograph if traum a or degenerative arthritis suspected



CT in select cases: o



May show encroachm ent of carpal tunnel

MRIâ€”displays the soft tissues well but m ay not be justified in ED owing to tim e and cost: o

Findings: palm ar bowing of transcarpal ligam ent, flattened m edian nerve, m edian nerve or synovial swelling, fluid in carpal tunnel, signal abnorm ality of m edian nerve



Ultrasound can be diagnostic: o

Findings: m edian nerve swelling at proxim al canal, m edian nerve flattening at distal canal, bowing of transcarpal ligam ent

Diagnostic Procedures/Surgery Nerve conduction studies and electrom yography are criterion

Pa ge 9 8 2

standard tests.

Differential Diagnosis 

Cervical nerve root com pression: o

Origin of m edian nerve is at the sixth and seventh cervical roots.

o

Sym ptom s are aggravated by erect posture and neck m ovem ent.



Hand-arm vibration syndrom e: o

Characterized by Raynaud, num bness and tingling in ulnar and m edian nerve distributions when exposed to cold or vibration, weakened grip, and upper extrem ity m yalgias

o

Associated with prolonged exposure to vibration



Thoracic outlet obstruction



Osteoarthritis of the first carpom etacarpal joint



Brachial plexitis



Generalized neuropathy



Syringom yelia

Treatment Initial Stabilization None necessary

ED Treatment 

Splint wrist in neutral position (0 degrees).



Aspirin or nonsteroidal anti-inflam m atory drugs (NSAIDs)



Avoidance of repetitive wrist m ovem ent



Wrist splint to be worn at night until follow-up



Apply heat to involved wristsâ€”heating pad, hot water bottle, low-level heat wraps

Pa ge 9 8 3



Referral to occupational m edicine for ergom etric testing if caused by repetitive m otion, and tendon gliding or nerve gliding exercises



May need referral to a hand surgeon for consideration of surgical release of transverse carpal ligam ent using either open or endoscopic technique

Medication (Drugs) 

NSAIDs (there are m any choices; a few are listed below): o

Ibuprofen: 600 m g (peds: 5â€“10 m g/kg) PO q6h

o

Ketorolac: 30 m g IV or IM q6h or 10 m g PO q4hâ€“q6h



o

Diclofenac: 50 m g PO b.i.d. or t.i.d.

o

Piroxicam : 20 m g PO daily

Local corticosteroid injection provides transient relief in two thirds of patients (m any different regim ens): o

Hydrocortisone: 25â€“100 m g

o

Methylprednisolone: 40 m g

o

Prednisolone suspension: 20â€“40 m g

o

Triam cinolone: 20 m g

Follow-Up Disposition Discharge Criteria Discharge to hom e with appropriate referral to either patient's prim ary care physician or directly to a specialist in occupational m edicine or hand surgery.

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References 1. Al-Qattan MM, Thom pson HG, Clarke HM. Carpal tunnel syndrom e in children and adolescents with no history of traum a. J Hand Surg. 1996;21B(1):108â€“111. 2. Kanaan N, Sawaya RA. Carpal tunnel syndrom e: m odern diagnostic and m anagem ent techniques. Br J Gen Pract. 2001;51:311â€“314. 3. MacDerm id JC, Wessel J. Clinical diagnosis of carpal tunnel syndrom e: a system atic review. J Hand Ther. 2004;17(2):309â€“319. 4. Michlovitz SL. Conservative interventions for carpal tunnel syndrom e. J Orthop Sports Phys Ther. 2004;34(10):589â€“600. 5. O'Gradaigh D, Merry P. Corticosteroid injection for the treatm ent of carpal tunnel syndrom e. Ann Rheum Dis. 2000;59:918â€“919. 6. Sternbach G. The carpal tunnel syndrom e. J Em erg Med. 1999;17:519â€“523. 7. Whitley JM, McDonnell DE. Carpal tunnel syndrom e. A guide to prom pt intervention. Postgrad Med. 1995;97(1):89â€“96.

Codes ICD9-CM 354.0 G56.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C auda Equina Syndro m e

Cauda Equina

Syndrome Kyan J. Berger

Basics Description Com pression of lum bar and sacral nerve fibers in cauda equina region: 

Nerve fibers below conus m edullaris



Fibers end at L1-2 interspace.

Risk Factors 

Neoplasm



IV drug use

Etiology 



Herniated disc m ost com m on: o

L4â€“L5 discs > L5â€“S1 > L3â€“L4

o

Most com m on in fourth and fifth decades of life

Mass effect from : o

Myelom a, lym phom a, sarcom a, m eningiom a, neurofibrom a, hem atom a

o

Spine m etastases (breast, lung, prostate, thyroid, renal)

Pa ge 9 8 6

o

Epidural abscess (especially in IV drug users)



Blunt traum a



Penetrating traum a



Spinal anesthesia

Diagnosis Signs and Symptoms History 

Low back pain



Sciatica/radicular pain (unilateral or bilateral)



Lower extrem ity num bness or weakness



Difficulty am bulating owing to weakness or pain



Bladder or rectal dysfunction: o

Retention or incontinence

Physical Exam 

Lum brosacral tenderness



Lower extrem ity sensory or m otor deficits: o

May be asym m etric

o

Decreased foot dorsiflexion strength

o

Decreased quadriceps strength



Decreased deep tendon reflexes



Saddle hypalgesia or anesthesia



Decreased anal sphincter tone

Essential Workup 

Neurologic exam m ost essential: o

Straight-leg raise

o

LasÃ¨gue sign: 

With patient supine, flex hip and dorsiflex foot.



Pain or spasm in posterior thigh indicates nerve

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irritation. o

Perineal sensation

o

Rectal tone

o

Anal wink: reflex contraction of external anal sphincter with gentle stroking of skin lateral to anus



Postvoid residual volum e: o

Estim ate by bladder catheterization or using ultrasound.

o

Greater than 50â€“100 m L is considered abnorm al.

o

Residual increases with age.

o

Diagnosis unlikely if norm al

Tests Lab 

Based on differential diagnoses



CBC, urinalysis, erythrocyte sedim entation rate (ESR)

Imaging 

Radiographs of lum bosacral (LS) spine



MRI of spine is definitive study.



CT m yelogram if MRI unavailable

Differential Diagnosis 

Osteoarthritis, LS strain, sciatica



Vertebral fracture (pathologic and nonpathologic)



Osteom yelitis



Spinal epidural abscess



Conus m edullaris or higher cord com pression



Ankylosing spondylitis, spinal stenosis



Abdom inal aortic aneurysm dissection



Vascular claudication



Hip pathology



Acute transverse m yelitis

Pa ge 9 8 8

P.201

Treatment Pre Hospital 

Manage airway and traum atic injuries as indicated.



If evidence of traum a, patient should be transported with full spine im m obilization.

Alert Even in nontraum a patient, consider spinal im m obilization given possibility of unstable lesion.

Initial Stabilization 

Spine im m obilization if traum a or unstable spine lesion suspected



Analgesia



NPO until evaluated by neurosurgery

ED Treatment 

Repeat neurologic exam inations to detect progression.



For acute spinal cord traum a (<8 hours), begin high-dose m ethylprednisolone protocol.



Im m ediate neurosurgical consultation in all cases



Controversy exists regarding urgency of decom pression: o

Recom m endations range from within 6 hours of onset to within 24 hours.

Medication (Drugs)

Pa ge 9 8 9



Methylprednisolone (high-dose steroid protocol): 30 m g/kg IV bolus, then 5.4 m g/kg/h infusion over next 23 hours



Morphine sulfate: 2â€“4 m g (peds: 0.1 m g/kg per dose q5m in PRN; m ax. 15 m g) IV/SC q5m in PRN



Ondansetron: 4â€“8 m g (peds: 0.15 m g/kg [up to 4 m g] IV q8h PRN nausea)



Prom ethazine HCl: adult: 25â€“50 m g IV q4h

Follow-Up Disposition Admission Criteria 

All patients with acute cauda equina syndrom e m ust be adm itted to neurosurgical service.



Patients have good prognosis with rapid surgical decom pression.



Treatm ent should not be delayed.



Patients presenting late (>48 hours) also benefit from surgical decom pression.

Discharge Criteria Patients with established cauda equina syndrom e with prior com plete evaluation and no new neurologic deficits m ay be discharged with close follow-up with their neurosurgeon.

References 1. Della-Giustina DA. Em ergency departm ent evaluation and treatm ent of back pain. Em erg Med Clin North Am . 1999;27:877â€“893. 2. Green BA, et al. Spinal cord injury in adults. In: Youm ans JR, et al., eds. Neurological Surgery. 4th ed. Philadelphia: WB Saunders;

Pa ge 9 9 0

1996:1969â€“1940. 3. Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrom e: outcom e and im plications for m anagem ent. Br J Neurosurg. 2003;17(2):164â€“167. 4. Miller DW, et al. General m ethods of clinical exam ination. In: Youm ans JR, et al., eds. Neurological Surgery. 4th ed. Philadelphia: WB Saunders; 1996:40. 5. Shapiro S. Medical realities of cauda equina syndrom e secondary to lum bar disc herniation. Spine. 2000;25(3):348â€“352.

Codes ICD9-CM 344.60

ICD10 G83.4

Pa ge 9 9 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C austic Ingestio n

Caustic Ingestion

Paul Kolecki

Basics Description Alkalis 

Dissociate in the presence of H 2 O to produce hydroxy (OH ) ions, which leads to liquefaction necrosis



Post-ingestionâ€”m ainly dam ages the esophagus: o



Gastric dam age can occur (see acids).

Esophageal dam age (in the order of increasing dam age) consists of:



o

Superficial hyperem ia

o

Mucosal edem a

o

Superficial blisters

o

Exudative ulcerations

o

Full-thickness necrosis

o

Perforation

o

Fibrosis with resulting esophageal strictures

Do not directly produce system ic com plications

Acids 

Dissociate in the presence of H 2 O to produce hydrogen (H + ) ions, which leads to a coagulation necrosis with eschar

Pa ge 9 9 2

form ation 

Post-ingestionâ€”dam ages the stom ach because of rapid transit tim e through esophagus: o



Esophageal dam age can occur (see alkalis).

Gastric dam age (in the order of increasing dam age) consists of:



o

Edem a

o

Inflam m ation

o

Im m ediate or delayed hem orrhage

o

Full-thickness necrosis

o

Perforation

o

Fibrosis with resulting gastric outlet obstruction

Well-absorbed and can cause hem olysis of RBCs and a system ic m etabolic acidosis

Etiology 

Direct chem ical injuries



Injuries occur secondary to acid and alkali exposures.



Many caustic agents (acids and alkalis) are found in com m on household and industrial products.



Caustic substances: o

Am m onia hydroxide: 

o

Form aldehyde: 

o

o

Em balm ing agent

Hydrochloric acid: 

o

Glass cleaners

Toilet bowel cleaners

Hydrofluoric acid: 

Glass etching industry



Microchip industry



Rust rem overs

Iodine: 

Antiseptics

Pa ge 9 9 3

o

Phenol: 

o

o

Antiseptics

Sodium hydroxide: 

Drain cleaners



Drain openers



Oven cleaners

Sodium borates, carbonates, phosphates, and silicates:

o



Detergents



Dishwasher preparations



Sodium hypochlorite



Bleaches

Sulfuric acid: 

Car batteries

Diagnosis Signs and Symptoms 

Oropharyngeal: o

Pain

o

Erythem a

o

Burns

o

Erosions

o

Ulcers

o

Drooling

o

Hoarseness

o

Stridor

o

Aphonia

o

Absence of visible lesions in the oropharynx does not exclude visceral injuries.



Pulm onary:

Pa ge 9 9 4







o

Tachypnea

o

Cough

o

Pneum onitis if aspirated

Gastrointestinal: o

Pain

o

Em esis or hem atem esis

o

Melena, dysphagia

o

Odynophagia

o

Esophageal or gastric perforation

o

Peritonitis owing to perforation

Cardiovascular: o

Tachycardia

o

Hypotension

o

Orthostatic changes

Hem atologic: o







Acid ingestion can cause RBC hem olysis.

Derm atologic: o

Pain

o

Erythem a

o

First, second, or third-degree burns

Ocular: o

Pain

o

Erythem a

o

Injection

o

Corneal burns

o

Full-thickness corneal dam age

Metabolic: o

Metabolic acidosis

Essential Workup 

History of or signs and sym ptom s of an exposure



Absence of oropharyngeal lesions does not exclude visceral injury.

Pa ge 9 9 5

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose



Arterial blood gas



Blood cultures: o



If m ediastinitis or peritonitis suspected

Type and cross-m atch.

Imaging Chest and abdom inal radiographs for: 

Esophageal or gastric perforation

Diagnostic Procedures/Surgery 

Esophageal and gastric endoscopy: o

For sym ptom atic patients to determ ine the extent of injury

o

Perform within the first 12â€“24 hours after ingestion.

o

Not recom m ended in the presence of respiratory distress without proper airway m anagem ent

o

Not recom m ended in the presence of severe pharyngeal dam age



Radiographic oral contrast im aging not recom m ended acutely: o

May be used in follow-up for assessm ent for strictures

Differential Diagnosis 

Chem ical injuries from corrosives, acids, alkalis, desiccants, vesicants, and oxidizing and reducing agents



Foreign body ingestion



Upper airway infection or angioedem a

Pa ge 9 9 6

P.203

Treatment Pre Hospital 

For oral burns or sym ptom s: Rinse m outh liberally with water or m ilk.





Water or m ilk can be given to following patients: o

Able to drink

o

Not com plaining of significant abdom inal pain

o

Do not have airway com prom ise or vom iting

Copious irrigation for ocular or derm al exposure

Initial Stabilization 

Airway, breathing, circulation (ABCs): o

Prophylactic intubation if there is any evidence of respiratory com prom ise

o 

Blind nasotracheal intubation contraindicated

Treat hypotension with 0.9% norm al saline (NS) IV fluid resuscitation.

ED Treatment 

Decontam ination: o

Derm al or ocular exposure: 

Im m ediate and thorough irrigation with water or 0.9% NS until physiologic pH attained



Alkalis typically require m ore irrigation than acids.

o

Ipecac, activated charcoal, gastroesophageal lavage, and a neutralizing acid or base are all contraindicated

Pa ge 9 9 7

with caustic ingestions. 

Dilution: o

Water or m ilk in the first 30 m inutes of ingestion: 

Especially useful for solid caustic alkali ingestions



Excessive intake m ay induce vom iting and worsen esophageal dam age.

o

If respiratory distress, intubate before dilution.

o

Contraindicated if esophageal or gastric perforation suspected



Keep patient NPO (nothing by m outh) if oral exposure.



Broad-spectrum antibiotics if m ediastinitis or peritonitis suspected



Antiem etics for nausea and vom iting



Treat derm al exposures according to standard burn recom m endations.



Detailed exam ination for ocular exposures



Intravenous H 2 blockers for sym ptom atic relief



Gastroenterology and surgical consultation



Benefit of corticosteroids following esophageal dam age is controversial: o

May prevent the form ation of esophageal stricture

o

May prom ote bacterial invasion, im m une suppression, and tissue softening

o

The decision to initiate corticosteroids requires input from entire team caring for patient.

o

Initiate broad-spectrum antibiotics if corticosteroids are given.



Laparoscopy or laparotom y for perforation and full-thickness necrosis



Topical hydrofluoric acid exposure (options depend on severity and location):

Pa ge 9 9 8

o

Intraderm al injection of 5% calcium gluconate (0.5 m L/cm 2 of skin with 30-gauge needle)

o

Intra-arterial infusion of 10 m L of 10% calcium gluconate in 40 m L D 5 W over 4 hours

Medication (Drugs) 

Methylprednisolone: 40 m g q8h IV (peds: 2 m g/kg/d IV); the course of therapy is 14â€“21 days followed by a corticosteroid taper



Prochlorperazine (Com pazine): 5â€“10 m g IV (peds: 0.13 m g/kg per dose IM)



Ranitidine (Zantac): 50 m g IV q6hâ€“q8h

Follow-Up Disposition Admission Criteria 

All sym ptom atic patients



Nonaccidental ingestion

Discharge Criteria 

Asym ptom atic patients who accidentally ingested and are able to swallow without difficulty



Minim al oropharyngeal pain with a corresponding visible lesion; no drooling; no respiratory com prom ise; no deep throat, chest, or abdom inal pain; and able to swallow without difficulty

References 1. Anderson KD, Rouse TM, Randolph JG. A controlled trial of

Pa ge 9 9 9

corticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323:10:637â€“640. 2. Nagi B, Kochar R, Thapa BR, et al. Radiological spectrum of late sequelae of corrosive injury to upper gastrointestinal tract. A pictorial review. ACTA Radiologica. 2004;1:712. 3. Rao RB, Hoffm an RS. Caustics and batteries. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:1323â€“1340.

Codes ICD9-CM 983.2 983.1

ICD10 T54.9

Pa ge 1 0 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C averno us Sinus Thro m bo sis

Cavernous

Sinus Thrombosis Edward Stettner

Basics Description 

Throm bosis of a branch of the m ajor intracerebral venous drainage system



Most com m only infectious



Spreads from odontogenic or sinus infectious source.



Less frequently occurs with hypercoagulable states

Anatomy 

Three prim ary sites of throm bosis: o

Cavernous sinus: m ost com m on: 

Drainage from superficial venous system



Superolateral to the sphenoid sinus and surrounds the sella



Cranial nerves (CN) III, IV, V1, and V2 traverse the lateral wall of the sinus.



CN VI and the internal carotid artery occupy the m edial portion of the sinus.

o

Can also involve transverse sinus and superficial sagital sinus

Pa ge 1 0 0

Pathophysiology 

Hem atogenous spread of facial, otic, or neck infection into venous drainage system



Bacterial overgrowth leads to inflam m ation and coagulation, resulting in throm bosis.



Venous engorgem ent of cavernous sinus can effect adjacent structures: o

Ophthalm oplegia from inflam m ation of CN III, IV, or VI

o

Pupillary fixation from CN III

o

Sensory deficits or parasthesias of forehead or cheek from CN V1 and V2

Etiology Septic 

Cavernous sinus: o

Thirty percent m ortality

o

Midface infection spreads into cavernous sinus

o

Maxillary dental infection and sphenoid sinusitis are m ost com m on.





Lateral: o

Twenty-five percent m ortality

o

Prim arily disease of young children

o

Spread from otogenic source

o

Otitis m edia or m astoiditis

Superior sagital: o

Extrem ely rare, with 80% m ortality

Aseptic 

Less com m on



Granulom atous conditions (tuberculosis [TB])



Inflam m atory disorders

Pa ge 1 0 0



From m ass effect (tum ors at base of skull, aneurysm s)



Hypercoagulable states (postoperation, m alignancy, nephritic syndrom e, pregnancy, oral contraceptives)

Complications 

Blindness can result from : o

Central retinal artery occlusion

o

Central retinal vein occlusion

o

Septic em boli

o

Arteritis

o

Ischem ic optic neuritis

o

Glaucom atous optic atrophy

o

Corneal ulceration from loss of corneal reflex



Hearing loss from otic invasion



Local spread can cause m eningitis or intracranial abscess



Pituitary necrosis and insufficiency from local invasion



Sepsis can develop from system ic hem atogenous seeding: o

Septic em boli

o

Adult respiratory distress syndrom e (ARDS)

Pediatric Considerations 

Children m ay present with nonspecific sym ptom s such as decreased energy, vom iting, fever.



Have high level of suspicion for any child with recent otitis or pharyngitis with worsening sym ptom s, declining m ental status, or signs of increased intracranial pressure: o

Hypertension, bradycardia, lethargy, vom iting, gait instability



More com m on in the neonatal period where diagnosis can be extrem ely difficult to m ake

Pa ge 1 0 0

Diagnosis Signs and Symptoms Signs 

Headache



Fever if infectious cause



Ocular or retrobulbar pain



Facial swelling



Visual disturbance



Facial dysesthesias



Lethergy and alteration in consciousness

Symptoms 

Ptosis



Chem osis with retinal vein engorgem ent



Facial or periorbital edem a



Ophthalm oplegia



Retinal hem orrhage or papilledem a



Altered level of consciousness or com a



Seizures



Sepsis with cardiovascular instability or collapse

Essential Workup Clinical diagnosis based on: 

Sym ptom s of venous obstruction



Ophthalm oplegia



Sepsis or m eningitis



Sym ptom s that becom e unilateral and spread to becom e bilateral are diagnostic.

Tests Lab 

Neither sensitive nor specific

Pa ge 1 0 0



CBC: o

Leukocytosis



PT/PTT/INR



Erythrocyte sedim entation rate (ESR) elevated in 50â€“60%



Lum bar puncture/cerebrospinal fluid (CSF): o

To evaluate fever and altered m ental status

o

CSF with elevated protein and WBC

Imaging 

CT scan: o

Can be norm al early in disease course

o

Findings include: 

Nonspecific abnorm alities



May identify original source of infection (e.g., sinusitis)



Delayed filling of involved sinus



Filling defect of sinus owing to throm bosis



Dilated superior ophthalm ic vein



Associated intracranial hem orrhage



Signs of increased intracranial pressure (ICP): sm all ventricles, loss of sulci



MRI with m agnetic resonance angiography (MRA)/m agnetic resonance venography (MRV): o

Diagnostic m odality of choice

o

Direct visualization of intracranial vessels and sinuses

o

Capable of visualizing throm bus as any stage

P.205

Differential Diagnosis 

Meningitis

Pa ge 1 0 0



Encephalitis



Intracranial abscess



Periorbital and orbital cellulitis



Bacterem ia



Migraine



Pseudotum or cerebri



Intracranial hem orrhage



Tolosa-Hunt syndrom e: o

Rare granulom atous inflam m ation of cavernous sinus

Alert 

This can be an extrem ely difficult diagnosis to m ake.



Maintain a high level of suspicion in toxic-appearing patients with recent ear/nose/throat (ENT) infections, or in patients with refractory headache and risk factors for hypercoagulability or intracranial infection.

Treatment Pre Hospital Alert 

Patients can be altered and unstable.



May require rapid assessm ent and stabilization of airway, breathing, and circulation (ABCs)

Initial Stabilization 

Careful assessm ent of m ental status with intubation for airway protection as needed



Aggressive fluid resuscitation for cardiovascular instability

ED Treatment 

High level of suspicionâ€”difficult diagnosis to m ake

Pa ge 1 0 0



Broad-spectrum antibiotics with m ultiple drug regim ens: o

Cover for gram -positives, gram -negatives, as well as anaerobes.

o

Nafcillin or vancom ycin (for m ethicillin resistant staphlococcal aureus [MRSA]) plus ceftriaxone: 

Add m etronidazole or clindam ycin in significant infections.



Surgical consultation for drainage of prim ary site of infection (e.g., dental abscess or sinusitis)



Heparin: o

May im prove m orbidity and m ortality in cavernous throm bosis

o

Controversial in transverse and sagital throm bosis owing to higher risk of subsequent hem orrhage

o 

Adm inister only after ruling out bleed on CT scan.

System ic steroids: o

Believed to be of benefit with concom itant pituitary insufficiency



Appropriate m anagem ent of increased ICP as needed

Medication (Drugs) 

Ceftriaxone: 2 g (peds: 80â€“100 m g/kg daily to b.i.d.) IV daily



Clindam ycin: 300â€“900 m g (neonates: 10â€“20 m g/kg/24h IV div. q6hâ€“q12h; peds: 25â€“40 m g/kg/24h div. q6hâ€“q8h) IV q6hâ€“q12h



Metronidazole: 500 m g (neonates: 7.5â€“30 m g/kg/24h IV div. q12hâ€“q24h; peds: 30 m g/kg/24h IV div. q6h) IV q6h



Nafcillin: 1â€“2 g (peds: 50â€“75 m g/kg/24h IV div. b.i.d.â€“t.i.d. depending on age) IV q4h



Vancom ycin: 1 g (peds: 10â€“20 m g/kg IV b.i.d.â€“t.i.d.

Pa ge 1 0 0

depending on age) IV q12h

Follow-Up Disposition Admission Criteria 

All patients with sinus throm bosis need adm ission to a m onitored setting.



Consider ICU adm ission.



Neurologic and neurosurgical consultation.

Discharge Criteria None

References 1. Cannon ML, Antonio BL, McCloskey JJ, et al. Cavernous sinus throm bosis com plicating sinusitis. PediatrCcrit Care Med. 2004;5(1):86â€“88. 2. Carvalho KS, Garg BP. Cerebral venous throm bosis and venous m alform ations in children. Neurol Clin North Am . 2002;20:1061â€“1077. 3. Eustis HS, Mahm ood FM, Wato C, et al. Im aging in ophthalm ology. I: MR im aging and CT of orbital infections and com plications in acute rhinitis. Radiol Clin North Am . 1998;36(6):1165â€“1183. 4. Heilpern KL, Lorber B. Infectious disease em ergencies: focal intracranial infections. Infect Dis Clin North Am . 1996;10(4):879â€“898. 5. Sztajunkrycer M, Jauch EC. The difficult diagnosis: unusual headaches. Em erg Med Clin North Am . 1998;16(4):741â€“760.

Codes ICD9-CM

Pa ge 1 0 0

325 Phlebitis and throm bophlebitis of intracranial venous sinuses 671.5 Other phlebitis and throm bosis 437.6 Nonpyogenic throm bosis of intracranial venous sinus

ICD10 S36.4

Pa ge 1 0 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ellulitis

Cellulitis

John Mahoney Dolores Gonthier

Basics Description 

Acute, spreading erythem atous superficial infection of skin and subcutaneous tissues: o

Variety of pathogens

o

Extension into deeper tissues can result in necrotizing soft tissue infection.



Progressive spread of erythem a, warm th, pain, and tenderness



Predisposing factors: o

Lym phedem a

o

Tinea pedis

o

Open wounds

o

Pre-existing skin lesion (furuncle)

o

Prior traum a or surgery

o

Retained foreign body

o

Vascular or im m une com prom ise

o

Injection drug use

Etiology 

Sim ple cellulitis:

Pa ge 1 0 1

o

Group A streptococci

o

Staphylococcus aureusâ€”including resistant strains; see below



Extrem ity cellulitis after lym phatic disruption o

Non-group A Î²-hem olytic streptococci (groups C, B, G)



Cellulitis in diabetics: o

Can be polym icrobial with S. aureus, streptococci, gram -negative bacteria, and anaerobes, especially when associated with skin ulcers





Periorbital cellulitis: o

S. aureus

o

Streptococcal species

Buccal cellulitis: o

Haem ophilus influenzae type B

o

Anaerobic oral flora, associated with intraoral laceration or dental abscess



Nosocom ial m ethicillin-resistant S. aureus: o

Risk factors: recent hospital or long-term care adm ission, surgery, injection drug use, vascular catheter, dialysis, recent antibiotic use, unresponsive infection

o 

Resistant to m ost antibiotics (see Treatm ent)

Com m unity-acquired m ethicillin-resistant S. aureus (CA-MRSA): o

No identified risk factor

o

Different antibiotic susceptibility than nosocom ial MRSA: 

Trim ethoprim -sulfam ethoxazole (TMP/SMX) and clindam ycin m ay be effective.

o

Variable, rising local prevalence should be considered when starting em piric antibiotic therapy.

Pa ge 1 0 1

o 

Suspect in unresponsive infections

Less com m on causes: o

Clostridia

o

Anthrax

o

Pasteurella m ultocidaâ€”com m on after cat and dog bites

o

Eikenella corrodensâ€”hum an bites

o

Pseudom onas aeruginosa:

o



Hot-tub folliculitisâ€”self-lim ited



Foot puncture wound



Ecthym a gangrenosum in neutropenic patients

Erysipelothrix speciesâ€”raw fish, poultry, m eat or hide handlers

o

Aerom onas hydrophilaâ€”freshwater swim m ing

o

Vibrio speciesâ€“seawater or raw seafood

Pediatric Considerations 

Facial cellulitis in children: o

Streptococcus pneum oniae

o

H. influenzae type B, although incidence declining since introduction of HIB vaccine





Perianal cellulitis: o

Group A streptococci

o

Associated or antecedent pharyngitis or im petigo

Neonates: o

Group B streptococci

Diagnosis Signs and Symptoms 

Com m on to all syndrom es:

Pa ge 1 0 1



o

Pain, tenderness, warm th

o

Erythem a

o

Edem a or induration

o

Fever/chills

o

Tender regional lym phadenopathy

o

Lym phangitis

o

Accom panying subcutaneous abscess possible

o

Superficial vesicles

Buccal cellulitis: o

Odontogenic cases m ore serious: 

Toothache, sore throat, or facial swelling



Progressive extension into soft tissues of neck with fever, erythem a, neck swelling, and dysphagia

Pediatric Considerations 

Facial cellulitis in children: o

Erythem a and swelling of the cheek and eyelid

o

Rapidly progressive

o

Usually unilateral

o

Upper respiratory tract sym ptom s

o

Risk for cavernous sinus throm bosis and perm anent optic nerve injury



Perianal cellulitis: o

Erythem a and pruritus extending from the anus several centim eters onto adjacent skin

o

Pain on defecation

o

Blood-streaked stools

Essential Workup 

Cellulitis is a clinical diagnosis.



Physical exam ination to reveal infection source.

Tests

Pa ge 1 0 1

Lab 

White blood count unnecessary



Gram stain and culture to focus antim icrobial selection and reveal resistant pathogens (MRSA): o

Aspirate point of m axim al inflam m ation or punch biopsy.

o 

Consider in treatm ent failures.

Blood culture: o

Usually negative in uncom plicated cellulitis

o

May identify organism in patients with: 

Lym phedem a



Buccal or periorbital cellulitis



Salt water or freshwater source



Fever or chills

Imaging 

Plain radiographs m ay reveal abscess form ation, subcutaneous gas, or foreign bodies: o

Extension to bone (osteom yelitis) not visualized early on plain radiographs



Extrem ity vascular im aging (Doppler ultrasound) can help rule out deep venous throm bosis.



CT or MRI can help rule out necrotizing fasciitis.

Differential Diagnosis 

Necrotizing fasciitis



Lym phangitis or lym phadenitis



Throm bophlebitis or deep venous throm bosis (DVT): o



Differentiation from cellulitis: 

Absence of initial traum atic or infectious focus



No regional lym phadenopathy



Presence of risk factors for DVT

Insect bite

Pa ge 1 0 1



Allergic reaction



Acute gout or pseudogout



Ruptured Baker cyst



Herpetic whitlow



Neoplasm



Phytophotoderm atitis



Prom inent response to sm allpox vaccination



Erythem a chronicum m igrans lesion of Lym e disease



Sm allpox vaccination, norm al variant of usual reaction to vaccination



Differential diagnosis of facial cellulitis: o

Allergic angioedem a

o

Conjunctivitis

o

Contusion

Pediatric Considerations 

Differential diagnosis of perianal cellulitis: o

Candida intertrigo

o

Psoriasis

o

Pinworm infection

o

Child abuse

o

Behavioral problem

o

Inflam m atory bowel disease

P.207

Treatment Initial Stabilization Airway com prom ise possible with deep extension of facial or neck

Pa ge 1 0 1

cellulitis

ED Treatment 

General principles: o

Consider local prevalence of MRSA and other resistant pathogens in addition to usual causes.

o

Usual outpatient treatm ent: 7â€“10 days

o

Cool com presses for com fort

o

Analgesics

o

Extrem ity elevation

o

Treat predisposing tinea pedis with topical antifungal such as clotrim azole.



Sim ple cellulitis: o

Outpatient: oral dicloxacillin; alternatives: oral m acrolide, cephalexin, or levofloxacin

o 

Extrem ity cellulitis after lym phatic disruption: o



Inpatient: IV nafcillin or equivalent

Sam e as sim ple cellulitis

Cellulitis in diabetics: o

Outpatient: am oxicillin/clavulanate or clindam ycin

o

Inpatient: IV am picillin/sulbactam or im ipenem cilastatin or equivalent







Periorbital cellulitis in adults: o

Outpatient: oral dicloxacillin or azithrom ycin

o

Inpatient: IV vancom ycin

Buccal cellulitis in adults: o

Outpatient: oral am oxicillin/clavulanate

o

Inpatient: IV ceftriaxone

o

Odontogenic source: 

Drainage essential



Coverage for anaerobes: clindam ycin

Facial cellulitis in children: o

IV ceftriaxone

Pa ge 1 0 1





Perianal cellulitis: o

Outpatient: oral penicillin VK

o

Inpatient: IV penicillin G (aqueous)

Anim al or hum an bite: o



Foot puncture wound: o



Oral am oxicillin/clavulanate

Oral or IV ciprofloxacin or IV ceftazidim e

Methicillin-resistant Staphylococcus aureus: o

Nosocom ial MRSA: IV vancom ycin or oral or IV linezolid

o

Com m unity-acquired MRSA: 

Add oral TMP/SMX to em piric treatm ent or use oral clindam ycin alone.



More severe: IV clindam ycin or IV vancom ycin

Medication (Drugs) 

Am oxicillin/clavulanate: 500â€“875 m g (peds: 45 m g/kg/24h) PO b.i.d. or 250â€“500 m g (peds: 40 m g/kg/24h) PO t.i.d.



Am picillin/sulbactam : 1.5â€“3 g (peds: 100â€“300 m g/kg/24h up to 40 kg; over 40 kg give adult dose) IV q6h



Azithrom ycin: (adults and peds) 10 m g/kg up to 500 m g PO on day 1, followed by 5 m g/kg up to 250 m g PO daily on days 2â€“5



Ceftazidim e: 500â€“1,000 m g (peds: 150 m g/kg/24h; m ax., 6 g/24h; use sodium form ulation in peds) IV q8h



Ceftriaxone: 1â€“2 g (peds: 50â€“75 m g/kg/24h) IV daily



Cephalexin: 500 m g (peds: 50â€“100 m g/kg/24h) PO q.i.d.



Ciprofloxacin: (adult only) 500â€“750 m g PO b.i.d. or 400 m g IV q8hâ€“q12h



Clindam ycin: 450â€“900 m g (peds: 20â€“40 m g/kg/24h)

Pa ge 1 0 1

PO or IV q8h 

Dicloxacillin: 125â€“500 m g (peds: 12.5â€“25 m g/kg/24h) PO q6h



Erythrom ycin base: (adult) 250â€“500 m g PO q.i.d.



Im ipenem cilastatin: 500â€“1,000 m g (peds: 15â€“25 m g/kg) IV q6h; m ax. 4 g/24h or 50 m g/kg/24h, whichever is less



Levofloxacin: (adult only) 500â€“750 m g PO or IV daily



Linezolid: 600 m g PO or IV q12h (peds: 30 m g/kg/24h div. q8h)



Nafcillin: 1â€“2 g IV q4h (peds: 50â€“100 m g/kg/24h divided q6h); m ax. 12 g/24h



Penicillin VK: 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q6h



Penicillin G (aqueous): 4 m U (peds: 100,000â€“400,000 U/kg/24h) IV q4h



Trim ethoprim /sulfam ethoxazole (TMP/SMX): 1 DS tab PO q12h (peds: 6â€“10 m g/kg/24h TMP div. q12h)



Vancom ycin: 1 g IV q12h (peds: 10 m g/kg IV q6h; dosing adjustm ents required younger than age 5 years); check serum levels

Follow-Up Disposition Admission Criteria 

Toxic appearing



Tissue necrosis



History of im m une suppression



Concurrent chronic m edical illnesses

Pa ge 1 0 1



Unable to take oral m edications



Unreliable patients

Discharge Criteria 

Mild infection in a non-toxic-appearing patient



Able to take oral antibiotics



No history of im m une suppression or concurrent m edical problem s



No hand or face involvem ent



Has adequate follow-up within 24 to 48 hours

References 1. Givner LB, Mason EO, Barson WJ, et al. Pneum ococcal facial cellulites in children. Pediatrics. 2000;106(5):e61. 2. Moran GJ, Talan DA. Com m unity-acquired m ethicillin-resistant Staphylococcus aureus: is it in your com m unity and should it change practice? Ann Em erg Med. 2005;45:321â€“322. 3. Padm anabhan R, Fraser T. The em ergence of m ethicillin-resistant Staphylococcus aureus in the com m unity. Cleve Clin J Med. 2005;72(3):235â€“241. 4. Swartz MN. Cellulitis. New Engl J Med. 2004;350:904â€“912. 5. Swartz MN, Pasternack, MS. Cellulitis and subcutaneous tissue infections. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:1172â€“1194.

Miscellaneous SEE ALSO: Abscess, Skin/Soft Tissue; Lym phadenitis; Lym phangitis; Necrotizing Fasciitis

Codes ICD9-CM

Pa ge 1 0 1

682.9

ICD10 L03.9

Pa ge 1 0 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C erebral Aneurysm

Cerebral

Aneurysm Veronique Au Rebecca Smith-Coggins

Basics Description 

Abnorm al, localized dilation or outpouching of cerebral artery wall: o



Occurs in 5â€“10% of population

Rupture of saccular aneurysm s account for 5â€“15% of strokes.



Of those that rupture: o

Forty percent occur at anterior com m unicating artery (ACA)

o

30% at internal carotid (IC)

o

20% in m iddle cerebral artery (MCA)

o

5â€“10% in vertebrobasilar artery (VBA) system

Etiology 

â€œCongenital,â€• saccular, or berry aneurysm s m ost com m on (90%): o

Develop at weak points in arterial wall and bifurcations of m ajor cerebral arteries

Pa ge 1 0 2



o

Incidence increases with age.

o

Multiple in 20â€“30%

o

Increased incidence: Polycystic kidney disease



Cerebral arteriovenous m alform ation



Type III collagen deficiency



Fibrom uscular dysplasia



Ehlers-Danlos syndrom e



Marfan syndrom e



Pseudoxanthom a elasticum



Neurofibrom atosis



Moyam oya disease



Coarctation of the aorta



Tuberous sclerosis



Sickle cell disease



Osler-Weber-Rendu syndrom e



Î±1-Antitrypsin deficiency



System ic lupus erythem atosus

Arteriosclerotic, fusiform or dolichoectatic (7%): o





More com m on in peripheral arteries

Inflam m atory (m ycotic): o

Ten percent of patients with bacterial endocarditis



Traum atic, associated with severe closed head injury



Neoplastic, em bolized tum or fragm ents

Pediatric Considerations 

Although rare in children, m ore likely to be giant (>25 mm)



Occur in the posterior circulation

Diagnosis

Pa ge 1 0 2

Signs and Symptoms 

Com m only asym ptom atic before rupture



Sentinel headaches occur in 30â€“60% of patients before rupture: o

Can be unilateral



Seizures, syncope, or altered level of consciousness



Com pression of adjacent structures m ay cause neurologic sym ptom s: o

Anterior com m unicating artery aneurysm s: 

Optic tract: altitudinal field cut or hom onym ous hem ianopsia

o



Optic chiasm : bitem poral hem ianopsia



Optic nerve: unilateral am blyopia

Aneurysm s at internal carotidâ€“posterior com m unicating artery junction: 

Oculom otor nerve: fixed and dilated pupil, ptosis, diplopia, and tem poral deviation of eye with inability to turn eye upward, inward, or downward

o

Aneurysm s in cerebral cortex m ay produce focal deficits, including hem iparesis, hem isensory loss, visual disturbances, aphasia, and seizures.



Rupture results in subarachnoid hem orrhage: o

Headache: severe (â€œworst headache everâ€•) with sudden onset (â€œthunderclapâ€•)

o



Different from prior headaches



Classically without focal deficits

Nuchal rigidity (m ost com m on sign) secondary to blood in cerebrospinal fluid (CSF)

Essential Workup 

Com plete neurologic exam ination

Pa ge 1 0 2



Em ergent noncontrast head CT scan will diagnose 90â€“95% of subarachnoid hem orrhages.



Lum bar puncture with CSF analysis if CT scan is negative

Tests Lab 

Coagulation studies



Baseline com plete blood chem istry with platelets and differential



Electrolytes



Renal and liver function tests



Arterial blood gases

Imaging 

Chest radiographs for pulm onary edem a



Four-vessel cerebral angiography rem ains gold standard.



Magnetic resonance angiography



Helical CT scanning m ay be useful in detecting aneurysm s >3 m m .



Transcranial Doppler ultrasound m ay be useful in detecting vasospasm .

Differential Diagnosis 

Neoplasm



Arteriovenous m alform ation



Optic neuritis



Migraine



Meningitis



Encephalitis



Hypertensive encephalopathy



Hyperglycem ia or hypoglycem ia



Tem poral arteritis



Acute glaucom a

Pa ge 1 0 2



Subdural hem atom a



Epidural hem atom a



Intracerebral hem orrhage



Throm boem bolic stroke



Air em bolism



Sinusitis

Treatment Pre Hospital Cautions: 

Neurologic exam ination in the field can be extrem ely helpful.





Assess: o

Level of consciousness

o

Glasgow com a scale score

o

Gross m otor deficits

o

Speech abnorm alities

o

Gait disturbance

o

Facial asym m etry

o

Other focal deficits

Patients with subarachnoid hem orrhage m ay need em ergent intubation for rapidly deteriorating level of consciousness.



Patients m ust be transported to a hospital with em ergent CT scanning and intensive care unitâ€“level treatm ent.

P.209

Initial Stabilization

Pa ge 1 0 2



Managem ent of airway, breathing, and circulation: o

Supplem ental oxygen

o

Rapid-sequence intubation m ay be required for airway protection or for controlled ventilation.

o 

Continuous cardiac m onitoring and pulse oxim etry

For altered m ental status, check blood glucose im m ediately, give D 5 0 (if glucose is low), naloxone, and thiam ine.



Managem ent of acute hypertension is essential; this m ay be accom plished with labetalol, nicardipine, nitroprusside, or hydralazine.



Prevention of acute increases in intracranial pressure from vom iting should be accom plished with antiem etics.



Seizures should be m anaged acutely with intravenous benzodiazepines and phenytoin.

ED Treatment Following initial stabilization, the m ajor goals of early treatm ent of ruptured or leaking aneurysm s are to prevent rerupture, cerebral vasospasm , and hydrocephalus (see: Subarachnoid Hem orrhage).

Pediatric Considerations Aneurysm s in children have a high rate of hem orrhage and should be repaired early.

Medication (Drugs) 

Diazepam : 5â€“10 m g IV q10â€“15m in m ax., 30 m g (peds: 0.2â€“0.3 m g/kg q5â€“10m in m ax. 10 m g)



Docusate sodium : 100 m g PO b.i.d.



Hydralazine: 10â€“20 m g IV q30m in



Labetalol: 20â€“30 m g/m in IV bolus, then 40â€“80 m g q10m in m ax. 300 m g; follow with continuous infusion

Pa ge 1 0 2

0.5â€“2 m g/m in 

Lorazepam : 2â€“4 m g IV q15m in PRN (peds: 0.03â€“0.05 m g/kg per dose; m ax. 4 m g per dose)



Nicardipine 5 m g/h IV infusion, increase by 2.5 m g/h q5â€“15m in m ax. 15 m g/h (peds: dosing unavailable)



Nim odipine: 60 m g PO/nasogastric q4h



Nitroprusside: 0.25â€“10 Âµg/kg per m inute (adult and peds)



Phenytoin: 15â€“20 m g/kg IV load at m ax. 50 m g/m in; m ax. 1.5 g (adult and peds); m aintenance 4â€“6 m g/kg/d IV/IM



Prochlorperazine: 5â€“10 g IV/IM q6hâ€“q8h (peds: 0.2 m g/kg/d IM in 3 or 4 div. doses); m ax. 40 m g/d

Surgery Optim al tim ing for angiography and surgery rem ain controversial, but trend is toward early surgery to decrease incidence of rebleeding and cerebral vasospasm .

Follow-Up Disposition Admission Criteria 

Any patient with acute aneurysm al subarachnoid hem orrhage should be adm itted, preferably to intensive care unit.



Any patient with sym ptom atic unruptured aneurysm should receive adm ission and urgent neurosurgical consultation, given high rate of rupture.

Discharge Criteria

Pa ge 1 0 2



Patients with incidentally discovered asym ptom atic intracranial aneurysm s m ay be discharged with close neurosurgical follow-up.



Note that overall risk of rupture is 1â€“2% per year and that critical size at which risk for rupture outweighs risk for surgery is controversial (classically 10 m m , but probably in the 4- to 8-m m range).

References 1. Barrow DL, Reisner A. Natural history of intracranial aneurysm s and vascular m alform ations. Clin Neurosurg. 1993;40:3â€“39. 2. Barsan WG, Kothari R. Stroke. In: Rosen P, et al. eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1997:2184â€“2197. 3. Becker KJ. Epidem iology and clinical presentation of aneurysm al subarachnoid hem orrhage. Neurosurg Clin N Am . 1998;9:435â€“444. 4. Bederson JB, Awad IA, Wiebers DO, et al. Recom m endations for the m anagem ent of patients with unruptured intracranial aneurysm s: a statem ent for healthcare professionals from the Stroke Council of the Am erican Heart Association. Stroke. 2000;31:2742â€“2750. 5. Edlow JA, Caplan LR. Avoiding the pitfalls in the diagnosis of subarachnoid hem orrhage. New Engl J Med. 2000;1:29â€“36. 6. Mitchell P, Gholkar A, Vindlacheruvu RR, et al. Unruptured intracranial aneurysm s: benign curiosity or ticking bom b? Lancet Neurol. 2004;3:85â€“92. 7. Victor M, Ropper AH. Cerebrovascular diseases. In: Adam s RD, Victor M, eds. Principles of Neurology. 5th ed. New York: McGraw-Hill; 1993. 8. Wijdicks EF, Kallm es DF, Manno EM, et al. Subarachnoid hem orrhage: neurointensive care and aneurysm repair. Mayo Clinic Proc. 2005;80:550â€“559. 9. White PM, Wardlaw JM, Easton V. Can noninvasive im aging accurately depict intracranial aneurysm s? A system atic review.

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Radiology. 2000;217:361â€“370.

Miscellaneous SEE ALSO: Subarachnoid Hem orrhage

Codes ICD9-CM 437.3 Cerebral Aneurysm , Nonruptured

ICD10 I67.1 Subarachnoid Haem orrhage from Middle Cerebral Artery

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C erebral Vascular Accident

Cerebral

Vascular Accident Veronique Au Rebecca Smith-Coggins

Basics Description Interruption of blood flow to a specific brain region: 

Neurologic findings determ ined by specific area affected



Onset m ay be sudden and com plete, or stuttering and interm ittent

Risk Factors 

Diabetes



Sm oking



Hypertension



Coronary artery disease



Peripheral vascular disease



Oral contraceptive use



Polycythem ia vera



Sickle cell anem ia



Deficiencies of antithrom bin III, protein C, or protein S

Etiology

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

May be ischem ic (throm botic or em bolic) or hem orrhagic (intracranial or subarachnoid hem orrhage)



Throm botic stroke is caused by occlusion of blood vessels: o

Clot form ation at an ulcerated atherosclerotic plaque is m ost com m on.

o

Sludging (sickle cell anem ia, polycythem ia vera, protein C deficiency)

o

Arterial dissection, arteritis (giant cell, Takayasu), or fibrom uscular dysplasia



Em bolic stroke is caused by acute blockage of a cerebral artery by a piece of foreign m aterial from outside the brain, including: o

Cardiac m ural throm bi associated with m itral stenosis, atrial fibrillation, cardiom yopathy, congestive heart failure, or m yocardial infarction

o

Prosthetic heart valves or abnorm al native valves

o

Atherosclerotic plaques in the aortic arch or carotid arteries



o

Atrial m yxom a

o

Ventricular aneurysm s with ventricular throm bi

Global ischem ic or hypotensive stroke is caused by an overall decrease in system ic blood pressure: o

Sepsis

o

Hem orrhage

o

Shock

Pediatric Considerations Usually attributable to underlying disease process such as sickle cell anem ia, leukem ia, or a blood dyscrasia

Diagnosis

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Signs and Symptoms 

Aphasia



Hem iparesis, hem iplegia



Hem isensory loss



Dysarthria, dysphagia



Facial droop



Ataxia, clum siness



Visual loss, photophobia, diplopia



Headache



Nausea, vom iting



Vertigo, dizziness



Altered level of consciousness, confusion, agitation



Cardiac dysrhythm ias, m urm urs



Cheyne-Stokes breathing, apnea



Hypertension



Transient ischem ic attacks: o

Focal neurologic deficits that com pletely resolve in <24 hours

o 



Precede m ost throm botic cerebral vascular accidents

Anterior cerebral artery: o

Contralateral hem iplegia (lower â†’ upper)

o

Hem isensory loss

o

Apraxia

o

Confusion

o

Im paired judgm ent

Middle cerebral artery: o

Contralateral hem iplegia (upper â†’ lower)

o

Hem isensory deficits

o

Hom onym ous hem ianopsia

o

Dysphasia

o

Dysarthria

o

Agnosia

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



Posterior cerebral artery: o

Cortical blindness in half the visual field

o

Visual agnosia

o

Altered m ental status

o

Im paired m em ory

o

Third nerve palsy

o

Hem iballism us

Vertebrobasilar system : o

Im paired vision, visual field defects, nystagm us, diplopia

o

Vertigo, dizziness

o

Crossed deficits: ipsilateral cranial nerve deficits with contralateral m otor and sensory deficits





Basilar system : o

Quadriplegia

o

Locked-in syndrom e

o

Com a

Watershed area (boundary zone between anterior, m iddle, and posterior circulation): o

Contralateral hem iplegia (upper extrem ity)

o

Contralateral hem isensory loss (upper extrem ity)

o

Face and speech spared

Essential Workup 

Detailed neurologic exam inationâ€”consider calculating National Institutes of Health stroke scale (NIHSS).



Em ergent noncontrast head CT scan to distinguish ischem ic from hem orrhagic events: o

May be norm al in first 24â€“48 hours of ischem ic stroke



If CT is norm al and subarachnoid hem orrhage is suspected, em ergent lum bar puncture is indicated.



Electrocardiogram to evaluate for dysrhythm ias and

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presence of m yocardial infarction 

Rapid glucose determ ination

Tests Lab 

Baseline com plete blood count, electrolytes, renal function tests, liver function test, prothrom bin tim e, partial throm boplastin tim e



Urinalysis: o

Hem aturia is seen in subacute bacterial endocarditis with em bolic stroke.



Sedim entation rate: o

Elevated in subacute bacterial endocarditis, vasculitis, hyperviscosity syndrom es



Cardiac enzym es

Imaging 

Noncontrast head CT



Chest radiography



Echocardiography



Carotid ultrasonography



MRI can detect ischem ia <2 hours after onset.

Differential Diagnosis 

Intracranial bleeding



Hypoglycem ia



Seizure disorderâ€”Todd paralysis



Myocardial infarction or congestive heart failure



Panic attacks, depression



Head traum a P.211

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

Encephalitis



Meningoencephalitis



Peripheral neuropathy



Intracranial abscess



Migraine



Air em bolism



Transient ischem ic attack



Hypertensive encephalopathy



Neoplasm



Subdural hem atom a



Giant cell arteritis



Takayasu arteritis

Treatment Pre Hospital Alert 

Patients m ay have difficulty m oving or com m unicating after cerebral vascular accident.



Neurologic exam ination in field is helpful: o

Should include assessm ent of consciousness level, Glasgow com a scale score, gross m otor deficits, speech abnorm alities, gait disturbance, facial asym m etry, and other focal deficits



Hyperglycem ia m ay exacerbate an ischem ic insult: o

Perform rapid blood glucose testing before adm inistration of glucose-containing fluids.

Initial Stabilization 

Manage airway, achieve vascular access: o

Supplem ental oxygen 2â€“4 L via nasal cannula

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o

Rapid-sequence intubation m ay be required for airway protection or controlled ventilation to decrease intracranial pressure.



o

Intravenous access

o

Cardiac m onitoring and pulse oxim etry

For altered m ental status, give naloxone and thiam ine and check blood glucose.

ED Treatment 

Treat elevated blood pressure (BP) with labetalol, nicardipine, nitroprusside, or hydralazine: o

Systolic BP >220â€“240 m m Hg or diastolic BP >130â€“150 m m Hg on repeated m easurem ents

o

If indicated for other concurrent problem s (m yocardial infarction, aortic dissection, congestive heart failure, hypertensive encephalopathy)

o

Initial goal is systolic BP <180 m m Hg, diastolic <110 m m Hg.



Control seizures with benzodiazepines, then phenytoin.



Maintain euvolem ia and norm otherm ia.



Throm bolytics: o

Ischem ic stroke only; adm inister within 3 hours of sym ptom onset (see Reperfusion Therapy, Cerebral)

o

Contraindications: 

Hem orrhage on CT



Recent stroke



Surgery or traum a <14 days ago



Systolic BP >185 m m Hg; diastolic BP >110 m m Hg



Bleeding diathesis



Anticoagulation/throm bocytopenia



Intracranial neoplasm



Seizure at stroke onset

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o



Rapidly im proving sym ptom s



Pregnancy



Internal bleed <3 weeks ago

Avoid anticoagulants and antiplatelet drugs for 24 hours.



Treat increased intracranial pressure and cerebral edem a: o

Elevate head of bed 30Â°

o

Controlled ventilation to keep partial pressure of carbon dioxide 35â€“40 m m Hg

o 

Mannitol

Urgent neurosurgic decom pression m ay be required with brainstem com pression in cases of vertebrobasilar stroke or hem orrhage.



In patients with com pleted or m inor strokes, aspirin m ay prevent recurrence.

Medication (Drugs) 

Aspirin: 81 m gâ€“325 m g PO daily



Clopidogrel: 75 m g PO daily



Diazepam : 5 m g IV q5â€“10m in m ax. 20 m g



Enalapril: 0.675â€“1.25 m g IV



Hydralazine: 10â€“20 m g IV q30m in



Labetalol: 15â€“20 m g per m inute IV bolus, then 40â€“80 m g q10m in m ax. 300 m g; follow with continuous infusion 0.5â€“2 m g per m inute



Mannitol (15â€“25% solution): 0.5â€“2 g/kg IV over 5â€“10 m inutes, then 0.5â€“1 g/kg q4hâ€“q6h (adult and peds)



Nicardipine: 5 m g/h IV infusion, increase by 2.5 m g/h q5â€“15m in m ax. 15 m g/h (peds: dosing unavailable)



Nitroprusside: 0.25â€“10 Âµg/kg per m inute (adult and

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peds) 

Trim etaphan: 1â€“4 m g per m inute



Tissue plasm inogen activator: 0.9 m g/kg IV; m ax. 90 m g, with 10% of dose given as bolus and rem ainder infused over 60 m inutes

Follow-Up Disposition Admission Criteria 

Patients with acute cerebral vascular accident should be adm itted to hospital.



Indications for intensive care unit: o

Severely decreased level of consciousness

o

Hem odynam ic instability

o

Life-threatening cardiac dysrhythm ias

o

Significantly increased intracranial pressure

Discharge Criteria 

Patients who present with com pleted strokes that are days to weeks old m ay be discharged if they are able to function independently or have adequate social support.



Patients with m ultiple prior strokes who experience relatively m inor new episodes m ay also be treated on outpatient basis if sim ilar criteria are m et and stroke is com pleted.

References 1. Adam s HP, Brott TG, Furlan AJ, et al. Guidelines for throm bolytic therapy for acute stroke: a supplem ent to the guidelines for the m anagem ent of patients with acute ischem ic stroke. A statem ent for

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healthcare professionals from a Special Writing Group of the Stroke Council. Am erican Heart Association. Circulation. 1996;94:1167â€“1174. 2. Barsan WG, Kothari R. Stroke. In: Rosen P, Barkin R, eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1997: 2184â€“2197. 3. Brott TG, Clark WM, Fagan SC, et al. Stroke: The First Hours. Guidelines for Acute Treatm ent. Englewood, CO: National Stroke Association; 2000. 4. Fulgham JR, Ingall TJ, Stead LG, et al. Managem ent of acute ischem ic stroke. Mayo Clin Proc. 2004;11:1459â€“1469. 5. Hacke W, Donnan G, Fieschi C, et al. Association of outcome with early stroke treatm ent: pooled analysis of ATLANTIS, ECASS, and NINDS rt-PA stroke trials. Lancet. 2004;363:768â€“774. 6. Hacke W, Kaste M, Fieschi C, et al. Random ised double-blind placebo-controlled trial of throm bolytic therapy with intravenous alteplase in acute ischaem ic stroke (ECASS II). Lancet. 1998;352:1245â€“1251. 7. Naradzay JFX, Gaasch WR. Acute stroke. Em erg Med Clin North Am . 1995;14:197â€“216. 8. NINDS rt-PA Stroke Study Group. Tissue plasm inogen activator for acute ischem ic stroke. N Engl J Med. 1995;333:1581â€“1587. 9. http://www.ninds.nih.gov/doctors

Codes ICD9-CM 436 Acute but ill-defined cerebrovascular disease

ICD10 I64 Stroke, not specified as hem orrhage or infarction

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ervical Adenitis

Cervical Adenitis

Kristine Reid Julie Zeller

Basics Description 

Cervical adenitis is an acute bacterial infection of a cervical lym ph node, often arising after a prior bacterial infection of the head or neck area.



Prim arily a pediatric disease with 70â€“80% of patients falling in the 1- to 4-year-old age group: o

It is becom ing m ore com m on in adults owing to im m unocom prom ised disease states (HIV, cancer, transplant patients).



Any cervical node can becom e infected: o

Cervical nodes act as the final com m on pathway for lym phatic drainage of all areas of the head and neck.

o

Initial lym phadenopathy results after bacterial invasion of regional areas of the head and neck and causes local lym ph nodes to swell secondary to hyperplasia of sinusoidal cells and infiltration of lym phocytes.

o

If the infection is not contained, the bacteria enter the lym ph system and proliferate (lym phadenitis).

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o

Pus form s when neutrophils are incited, and an abscess develops when host defenses are unable to clear infection.

Etiology 

About 50â€“80% of cases are a result of group A Î²-hem olytic Streptococcus and Staphylococcus aureus.



Mycobacteria tuberculosis (TB): o

Scrofula or tuberculous lym phadenitis

o

Rarely seen

o

Usually a chronic lym phadenitis in the posterior cervical nodes

o

Purified protein derivative (PPD) is usually strongly reactive.

o 

Treatm ent m edical

Atypical m ycobacteria (nontuberculous): o

More com m only seen

o

Usually a chronic lym phadenitis in the subm andibular or anterior cervical nodes



o

PPD test results are unreliable.

o

Treatm ent is prim arily surgical.

Bartonella henselae (catscratch disease): o

Subacute lym phadenitis

o

Has indolent course but usually spontaneously resolves



Anaerobes: o

Consider in lym ph nodes draining infections of the teeth or gingiva



Rarer organism s: o

Haem ophilus influenzae

o

Yersinia pestis

o

Nocardia species

o

Francisella tularensis

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o

Brucella m elitensis

o

Mycoplasm a pneum oniae

o

Treponem a pallidum

o

Actinom yces israelii

Pediatric Considerations 

One of the m ost com m on causes of a neck m ass in a child



Overall, group A Î²-Streptococcus and Staphylococcus aureus m ost com m on causes



In neonates, group B Streptococcus and Staphylococcus aureus m ost com m on



Group B streptococcal cellulitis-adenitis syndrom e: o

Neonates with fever, subm andibular or facial cellulitis, and an ipsilateral otitis

o 

94% incidence of concurrent bacterem ia

Staphylococcus aureus associated with m ore indolent course and higher frequency of suppuration

Geriatric Considerations 

Consider m alignancy over infection in this population, especially in the absence of fever, leucocytosis, etc.



Fixed, nontender, hard node m ost likely not cervical adenitis

Diagnosis Signs and Symptoms 

Enlarged, tender cervical lym ph node



Usually unilateral and solitary



Warm th and erythem a of overlying skin



Early in course firm but later possibly fluctuant node



With or without fever

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

Malaise



Irritability in infants and children



Usually a concurrent head and neck infection: o

Pharyngitis, tonsillitis, peritonsillar abscess

o

Otitis m edia, otitis externa

o

Dental infection

o

Im petigo, scalp infection

Essential Workup 

Cervical adenitis is a clinical diagnosis.



Identify prim ary source of infection in head and neck area (e.g., otitis, tonsillitis).



If no prim ary inflam m atory source of infection in head and neck: o

Address possible TB exposure with PPD.

o

Look for signs of system ic disease and viral illness.

Tests Lab 

Unnecessary if a treatable prim ary source of infection confirm ed



Blood cultures for toxic-appearing patients



Sepsis workup in neonates



If cause unclear, the following lab tests m ay help to discern a nonbacterial cause (see Differential Diagnosis): o

Leukocyte count with differential

o

Monospot

o

Throat cultures

o

Antibody titers (Epstein-Barr virus, cytom egalovirus, toxoplasm osis)

Diagnostic Procedures/Surgery 

Needle aspiration:

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o

All fluctuant nodes should be aspirated.

o

Send for gram and acid-fast stains, aerobic and anaerobic cultures, m ycobacteria, and fungi.

o

If any suspicion of tuberculous lym phadenitis, the node should not be aspirated owing to risk for sinus developm ent and chronic drainage.



Intraderm al skin testing: o

Mycobacteria, catscratch disease

Imaging 

Chest radiograph study, lateral neck, or Panorex: o

Helpful if source of infection unclear or to rule out a deep space infection

o 

Chest radiograph study to screen for TB

CT or MRI of neck: o

Helpful in delineating em bryonic developm ental m asses or ruling out deep space infections



Ultrasound: o

Can differentiate cystic from solid structures, but other findings nonspecific

o

Can identify deep cavity abscess if not palpable on exam



Excisional biopsy

P.213

Differential Diagnosis 

Lym phadenopathy (inflam m ation of node but no bacterial infection) can be a sign of m any system ic diseases; usually these nodes are m ultiple and bilateral.



Viral infections are a com m on cause: o

Respiratory viruses (adenoviruses, rhinoviruses,

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enteroviruses) o

Epstein-Barr virus, herpes sim plex virus, varicella-zoster virus, cytom egalovirus

o 

Mum ps, rubella, rubeola

Specific pediatric diseases with cervical adenitis in their diagnostic criteria: o

Kawasaki disease

o

Kikuchi disease

o

Periodic fever, aphthous stom atitis, pharyngitis, and cervical adenitis known by m nem onic PFAPA



Toxoplasm osis



Congenital cysts: o

Brachial cleft cysts, thyroglossal duct cysts, cystic hygrom as



Malignancies: o

Leukem ia, lym phom a, rhabdom yosarcom a, thyroid carcinom a

o

Rare cause of a nonspecific lum p in children (<2% overall)



Other system ic diseases: o

Lupus, sarcoidosis

Treatment Initial Stabilization Airway m anagem ent: 

Rare cases of airway com prom ise

ED Treatment 

Treatm ent directed toward the prim ary source of infection in the head and neck:

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o

If unsure of cause, treat for group A Streptococcus and Staphylococcus aureus.



Aspirate all fluctuant nodes.



Many oral antibiotics are effective: o

Cephalexin

o

Dicloxacillin

o

Am oxicillin/Clavulanic acid

o

Erythrom ycin (not as effective against Staphylococcus aureus)



Affected patients with suspected dental, periodontal, or anaerobic causes of illness:



o

Clindam ycin

o

Penicillin V

o

Am oxicillin/Clavulanic acid

Treatm ent should be for at least 10 days, even if sym ptom s resolve sooner



Warm , m oist com presses



Analgesics as needed

Medication (Drugs) 

Am oxicillin/clavulanic acid: 250â€“500 m g (peds: 20â€“40 m g/kg/24h) PO q8h



Cefazolin: 1â€“2 g (peds: 25â€“50 m g/kg/24h) IV q8h



Cephalexin: 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q6h



Clindam ycin: 300 m g (peds: 8â€“25 m g/kg/24h) PO q6h



Clindam ycin: 600â€“900 m g (peds: 20â€“40 m g/kg/24h) IV q8h



Dicloxacillin: 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q6h



Erythrom ycin: 250â€“500 m g (peds: 40 m g/kg/24h) PO

Pa ge 1 0 4

q6h 

Nafcillin: 1â€“2 g (peds: 50â€“200 m g/kg/24h) IV q4hâ€“q6h



Penicillin VK: 250â€“500 m g (peds: 25â€“50 m g/kg/24) PO q6h

Follow-Up Disposition Admission Criteria 

Neonates



Patient appears ill.



Im m unocom prom ised



Inability to take PO



Not im proving on oral antibiotics

Discharge Criteria 

Most patients can be discharged on oral antibiotics.



Close follow-up with a recheck in 2â€“3 days



Ability to take PO antibiotics and fluids



Return to the ED if: o

Sym ptom s worsen

o

Abscess develops

o

Voice changes

o

Dyspnea develops

o

System ic sym ptom s develop

References 1. Chesney P. Cervical adenopathy. Pediatr Rev. 1994;15:276â€“284. 2. Maraqa NF, Rathore MH. Lym phadenitis. In: Harwood-Nuss A. The Clinical Practice of Em ergency Medicine. 3rd ed. Philadelphia:

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Lippincott William s & Wilkins; 2001:1284â€“1286. 3. Santam aria JP, Abrunzo TJ. Ear, nose and throat disorders. In: Pediatric Em ergency Medicine. 2nd ed. St. Louis, MO: Mosby; 1997:732â€“735. 4. Shaikh, U. Lym phadenitis. Em edicine. http://www.em edicine.com /ped/topic32.htm .

Codes ICD9-CM 289.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C esarean Sectio n, Em ergency

Cesarean

Section, Emergency James Walker Michael Chamales

Basics Alert 

The sole indication for ED physician to perform em ergency perim ortem cesarean section is gravid fem ale (>24 weeksâ€™ gestation) in cardiopulm onary arrest who has not responded to initial resuscitative m easures, regardless of cause.



The m ost im portant predictor of fetal survival is length of tim e between m aternal cardiac arrest and cesarean delivery: o

Cesarean section should begin within 4 m inutes of m aternal arrest.

o 

Goal is delivering fetus within 1 m inute.

Obtain im m ediate consultations from obstetrics, pediatrics (and surgery, if traum a related): o

Do not defer or delay perform ing procedure until arrival of consultants.



Do not perform em ergent cesarean section if patient is

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<24 weeksâ€™ gestation.

Etiology 

Traum a (penetrating or blunt): o



Major cause of m aternal m ortality

Pulm onary em bolus: o

Throm boem bolism is num ber one cause of nontraum atic m aternal m ortality.



Cerebral vascular accident



Am niotic fluid em bolism



Dissem inated intravascular coagulation



Placenta previa



Eclam psia



Miscellaneous m edical disorders: o

Asthm a

o

Congestive heart failure

o

Myocardial Infarction

o

Drug overdose

Diagnosis Signs and Symptoms Gravid fem ale (>24 weeksâ€™ gestation determ ined by uterine fundal height) who is in cardiopulm onary arrest

Essential Workup 

Physical exam ination for apnea and pulselessness in obviously gravid fem ale



Quickly evaluate for reversible causes of cardiopulm onary arrest: o

Tension pneum othorax

o

Pericardial tam ponade

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o

Supine hypotension syndrom e (com pression of inferior vena cava by enlarged uterus)



Assess gestational age by uterine fundal height.



Distance from pubis to fundus in centim eters is roughly equivalent to gestational age in weeks.



Ultrasonography is beneficial if im m ediately available to assess fetus.

Tests Imaging 

None necessary to establish cardiopulm onary arrest



Do not waste tim e by attem pting to find fetal heart tone.

Differential Diagnosis Cardiopulm onary arrest is final com m on pathway: 

Evaluate for underlying cause.

Treatment Pre Hospital Cautions: 

Minim al scene tim e, â€œscoop and runâ€•



Place the patient in the left lateral decubitus position to avoid com pression of inferior vena cava (supine hypotension syndrom e)



Traum a patient requiring spinal im m obilization o

Uterus can be m anually displaced to left.

o

Backboard can be wedged to keep right hip elevated 45 degrees.

Initial Stabilization 

Standard resuscitation m easures:

Pa ge 1 0 5



o

Em ergency intubation

o

High-flow oxygen

o

Cardiac and blood pressure m onitoring

o

Two large-bore peripheral intravenous lines 

Fluid resuscitation



O-negative blood if indicated

Fetal survival correlates with m aternal survival and adequacy of initial m aternal resuscitation.



If patient is at <24 weeksâ€™ gestation, use advanced cardiac life support and advanced traum a life support protocols directed at m aternal resuscitation; do not perform em ergent cesarean section.



If patient is >24 weeksâ€™ gestation, use 4-m inute rule: o

Perform advanced cardiac life support or advanced traum a life support for 4 m inutes.

o

If no response, proceed to im m ediate em ergency cesarean section.

o

Goal is to deliver fetus within 1 m inute.

o

If it is obvious there is no chance for m aternal survival, begin perim ortem cesarean section im m ediately.

P.215

ED Treatment 

Call for im m ediate obstetric, surgical, and pediatric consultations: o

Do not delay perform ing procedure while waiting for consultants.



Ensure a Foley catheter has been inserted to decom press bladder.



Perform cesarean section:

Pa ge 1 0 5

o

Use linea nigra as landm ark for vertical m idline incision.

o

Incise abdom inal wall from pubic hairline to 5 cm above um bilicus.

o

This incision should pass through fascial and peritoneal layers.

o

Retract urinary bladder inferiorly against pubic sym physis.

o

Make sm all vertical incision in lower uterine segm ent, just cephalad to urinary bladder.

o

Extend incision cephalad with scissors. 

Insert your free hand into uterus.



Lift uterine wall away from fetus to avoid fetal injury.

o

Deliver fetus.

o

Clam p um bilical cord in two places and cut between the two clam ps.

o

Manually deliver placenta.

o

Perform neonatal resuscitation as indicated.

o

Im m ediately reassess m aternal vital signs because occasionally spontaneous circulation m ay return.

o

Continue m aternal resuscitation as appropriate.

o

Suture uterus with running lock stitch using no. 0 polyglactin suture.

o

Suture fascia and peritoneum with running stitch using no. 0 polyglactin suture.

o

Close the skin with staples or suture

o

Adm inister broad-spectrum antibiotics.

Follow-Up

Pa ge 1 0 5

Disposition Admission Criteria 

The infant should be adm itted to neonatal ICU.



If m aternal resuscitation is successful, patient should be adm itted to appropriate ICU.

Discharge Criteria Neither infant nor m other should be discharged from ED.

References 1. Boyd R, Teece S. Towards evidence based em ergency m edicine: best BETs from the Manchester Royal Infirm ary. Perim ortem caesarean section. Em erg Med J. 2002;19:324â€“325. 2. Dildy GA, Clark SL. Cardiac arrest during pregnancy. Obstet Gynecol Clin North Am . 1995;22:303â€“314. 3. Gianopoulos JG. Em ergency com plications of labor and delivery. Em erg Med Clin North Am . 1994;12:201â€“217. 4. Katz VL, Dotters DJ, Droegenueller W. Perim ortem caesarean delivery. Obstet Gynecol. 1986;68: 571â€“576. 5. Lanoix R, Akkapeddi V, Goldfeder B. Perim ortem caesarean section: case reports and recom m endations. Acad Em erg Med. 1995;2: 1063â€“1067. 6. Stallord TC, Burns B. Em ergency delivery and perim ortem C-section. Em erg Med Clin North Am . 2003;21:679â€“693.

Codes ICD9-CM 669.7 Cesarean delivery, without m ention of indication

ICD10 O82.1 Delivery by em ergency cesarean section

Pa ge 1 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hancro id

Chancroid

Norbert Elsner

Basics Description 

Sexually transm itted genital ulcerative disease: o



Increased risk for HIV infection

A com m on cause of genital ulceration in Africa, southeast Asia, and Latin Am erica: o

Uncom m on in United States where HSV > syphilis >> chancroid, but likely underreported

Etiology Causative agent: Haem ophilus ducreyi: 

Highly infectious bacterium

Diagnosis Signs and Symptoms 



Begins as single erythem atous papule or pustule: o

Quickly erodes into painful chancres (1â€“20 m m )

o

Soft and friable with ragged, irregular borders

Prim ary ulcer usually excavated

Pa ge 1 0 5



Moist, granulation tissue at base



Purulent or hem orrhagic exudate



Location: o

Male: 

Penile shaft, glans, internal surface of foreskin, anus

o

Fem ale: 

Cervix, vagina, vulva, perineum , anus



Occurs 4â€“7 days (m edian) after exposure



Incubation period 3â€“10 days (range 1â€“35 days)



Inguinal adenopathy: o

In approxim ately 50% of m en; less com m on in wom en

o

Appears 3â€“14 days after initial ulcer

o

Unilateral (usually)

o

Painful

o

Suppurative large nodes (buboes)

o

May rupture and form chronic draining sinuses



Dysuria, dyspareunia secondary to contact with lesions



Variants: o

Phagedenic: 

Secondary superinfection (especially fusospirochetal) and rapid extensive tissue destruction

o

Giant chancroid: 

o

Very large single ulcer

Serpiginous ulcer: 

Rapidly spreading, indolent, shallow ulcers in groin or thigh

o

Follicular: 

Multiple sm all ulcers with perifollicular distribution

Pa ge 1 0 5

Essential Workup 

Clinical diagnosis based on appearance is often inaccurate, and lab tests difficult or unavailable, so consider:



CDC case definitions: o

Definite: positive culture of H ducreyi

o

Probable: typical signs, sym ptom s of chancroid PLUS negative darkfield exam for T. pallidum PLUS negative syphilis serology PLUS negative culture for HSV (or clinical exam atypical for herpes).

Tests Lab 

Gram stain unreliable (positive in 50â€“80%) o

Gram -negative coccobacilli: linear or â€œschool-of-fishâ€• pattern



Culture extrem ely difficult (positive in 0â€“80%); requires com plex m edia o

Obtain specim en from 

Base of ulcer



Needle aspiration of inguinal node by placing needle through norm al skin (to avoid form ation of fistula)



Polym erase chain reaction (PCR) assay: sensitive and specific, but not widely available



RPR o

Coinfection with syphilis is com m on

o

Part of CDC guidelines for probable clinical diagnosis of chancroid



Herpes sim plex virus (HSV) culture o

Part of CDC guidelines for probable clinical diagnosis of chancroid



HIV testing

Pa ge 1 0 5

Differential Diagnosis Infectious: 

Syphilis (T. pallidum ) o



Herpes genitalis (H. sim plex) o



Vesicular, m ultiple, recurrent

Granulom a inguinale or Donovanosis (C. granulom atis) o



chancre usually painless, indurated, clean

Ulcer m argins elevated; + induration

Lym phogranulom a venereum (C. trachom atis) o

Often single lesion; tender, fluctuant, unilateral lym phadenopathy

Non-Infectious: 

Drug eruption



Less com m on: o

Pyoderm a gangrenosum ; BehÃ§et's disease

Treatment Initial Stabilization Usual precautions for patient exam and handling of specim ens

ED Treatment Antibiotics: 

Ceftriaxone: single IM dose



Azithrom ycin: single PO dose



Ciprofloxacin: PO Ã— 3 days P.217

Pa ge 1 0 5





Erythrom ycin: PO Ã— 7 days o

Recom m ended for HIV positive or pregnant patients

o

Requires m ultiple doses

o

GI side effects

Needle aspiration of suppurative nodes (>5 cm diam eter): o

To prevent chronic sinus drainage from spontaneous rupture



o

Use 18-gauge needle through lateral intact skin.

o

May require repetition

Recom m end concurrent HIV, syphilis, HSV testing and follow-up testing in 3 m onths if initially negative.

Medication (Drugs) 

Azithrom ycin: 1 g PO Ã— 1



Ceftriaxone: 250 m g IM Ã— 1



Ciprofloxacin: 500 m g PO b.i.d. for 3 days



Erythrom ycin: 500 m g PO q.i.d. for 7 days

Follow-Up Disposition Discharge Criteria 

Sexual abstinence or condom use until lesions healed



Clinical course: o

Sym ptom s im prove within 2 days of treatm ent.

o

Ulcers im prove within 3â€“7 days.

o

Possible delayed resolution in those HIV-positive or uncircum cised

Issues for Referral

Pa ge 1 0 5

Exam ine and treat sexual partners if contact within 10 days of sym ptom onset

References 1. Centers for Disease Control and Prevention. Sexually Transm itted Diseases Treatm ent Guidelines 2002. Available at http://www.cdc.gov/std/treatm ent. 2. Lewis DA. Chancroid: clinical m anifestations, diagnosis and m anagem ent. Sex Transm Inf. 2003;79:68â€“71. 3. Schlossberg D. Current Therapy of Infectious Disease. Philadelphia: WB Saunders; 2002. 4. Chancroid. UpToDate Online. 2005;v13.1. Available at http://www.utdol.com .

Codes ICD9-CM 099.0

Pa ge 1 0 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hem ical Weapo ns Po iso ning

Chemical

Weapons Poisoning Kirk Cumpston

Basics Description Chem ical agents that affect CNS, pulm onary, cardiovascular, derm al, ocular, or GI system s when exposed to victim s

Etiology 

Blood agents: cyanide: o

Inhibition of cellular respiration by binding to ferric ion in cytochrom e oxidase a-a3 and uncoupling oxidative phosphorylization



Blister agents: sulfur m ustard, nitrogen m ustard, lewisite, phosgene oxim e: o

Alkylation and cross-linking of purine bases of DNA and am ino acids resulting in change in structure of nucleic acid, proteins, and cellular m em branes



Lacrim ators and riot control agents: 1-chloroacetophenone (CN; Mace), o-chlorobenzilidine m alononitrile (CS), oleoresin capsicin-pepper spray (OC), chloropicrin, adam site (DM) o

Mucous m em brane irritators

Pa ge 1 0 6



Pulm onary irritants (choking agents): o

High water solubility: am m onia: 

Mucous m em brane irritation of eyes and upper airway

o

Interm ediate water solubility: chlorine: 

Form s hydrochloric acid, hydrochlorous acids, which form free radicals causing upper airway and pulm onary irritation

o

Low water solubility: phosgene: 

Mild irritant effects initially, then delayed pulm onary edem a as late as 24 hours



Direct pulm onary dam age after hydrolysis in lungs to hydrochloric acid



Nerve agents o

Anticholinesterase inhibitorsâ€”causes cholinergic overstim ulation at m uscarinic, nicotinic, and central nervous system sites

o

Incapacitating agents: 3-quinuclidinyl benzilate (BZ): 

Anticholinergic (antim uscarinic)

Diagnosis Signs and Symptoms 

Blood agents (cyanide and cyanogens): o

Vital signs: 

Tachypnea and hyperpnea (early); respiratory depression (late)



Hypertension and tachycardia (early); hypotension and bradycardia (late)

 o

Death within seconds to m inutes

Central nervous system :

Pa ge 1 0 6

o

o





Headache



Mental status changes



Seizures

Pulm onary: 

Dyspnea



Noncardiogenic pulm onary edem a



Cyanosis uncom m on

Gastrointestinal: 

Odor of bitter alm onds (som etim es)



Burning in m outh and throat



Nausea, vom iting

Blister agents (m ustards, lewisite): o

General: 

o

Mortality, 2â€“4%

Derm atologic: 

Skin erythem a, edem a, pruritus can appear 2â€“24 hours after exposure.



Necrosis and vesiculation appear 2â€“18 hours after exposure.

o

Head, eyes, ears, nose, and throat (HEENT): 

Airway occlusion from sloughing of debris



Laryngospasm , sore throat, sinusitis



Eye pain, photophobia, lacrim ation, blurred vision, blepharospasm , periorbital edem a, conjunctival edem a, corneal ulceration

o

o

Pulm onary: 

Bronchospasm , tracheobronchitis



Respiratory failure



Hacking cough

Gastrointestinal: 

o

Nausea, vom iting

Hem atologic:

Pa ge 1 0 6

 

Leukopenia

Lacrim ators and riot control agents (tear gases): o

o

o

HEENT: 

Eye pain



Lacrim ation



Blepharospasm



Tem porary blindness

Derm atologic: 

Skin irritation



Papulovesicular derm atitis (tear gas)



Superficial burns

Pulm onary: 

Cough



Chest tightness



Dry throat



Sensation of suffocation



Pulm onary edem a when exposed to high concentrations without ventilation



Pulm onary irritants (choking agents): o

o

HEENT: 

Eye pain, lacrim ation, blepharospasm



Tem porary blindness

Derm atologic: 

o

Skin irritation, dry throat, nasal irritation

Pulm onary: 

Shortness of breath, cough, bronchospasm



Chest pain



Pulm onary edem a as late as 24 hours from exposure (phosgene)



Nerve agents (sarin, tabun, som an, VX): o

SLUDGEBAM syndrom e 

Salivation

Pa ge 1 0 6



Lacrim ation



Urination



Defecation



Gastrointestinal cram ps



Em esis



Bronchorrhea, bronchoconstriction, bradycardia (m ost life threatening)

o



Abdom inal upset



Miosis

HEENT: 

Miosis



Hypersecretion by salivary, sweat, lacrim al, and bronchial glands

o

o

o

o



Central nervous system : 

Irritability, nervousness



Giddiness



Fatigue, lethargy, depression



Ataxia, convulsions, com a

Pulm onary: 

Bronchoconstriction



Bronchorrhea

Gastrointestinal: 

Nausea, vom iting, diarrhea



Cram py abdom inal pains



Urinary and fecal incontinence

Musculoskeletal: 

Fasciculations, skeletal m uscle twitching



Weakness



Flaccid paralysis

Incapacitating agents (BZ): o

Anticholinergic (antim uscarinic) toxidrom e: 

Hot as a hare

Pa ge 1 0 6



Dry as a bone



Red as a beet



Blind as a bat



Mad as a hatter



Hypertension



Tachycardia



Hyperpyrexia



Urinary retention



Decreased bowel sounds

Essential Workup 

History and sym ptom s key to type of agent exposure



Physical exam ination: o

Cyanide (bitter alm onds, com atose, hypotensive, m etabolic acidosis)

o

Mustard (faint, sweet odor of m ustard or garlic, blisters, sloughing of skin, dyspnea)

o

Check for SLUDGEBAM syndrom e.

o

Lacrim ators (eye irritation, lacrim ation, blepharospasm )

o

Choking agents (dyspnea, bronchospasm )

Tests Lab 

Arterial blood gases: o

Cyanide: 

Decreased atrioventricular (AV) oxygen saturation gap



Lactic acidem ia with high anion gap m etabolic acidosis



Arterialization of venous blood



Cyanide levels cannot be perform ed in clinically relevant tim e fram e.

Pa ge 1 0 6

P.219



CBC: o

Leukopenia, throm bocytopenia, anem ia with significant m ustard exposure



Electrolytes, BUN, creatinine, glucose



Urinalysis



Creatine phosphokinase (CPK)



Lactate for cyanide



Erythrocyte cholinesterase activity for nerve agents

Imaging Chest radiograph for pulm onary edem a

Differential Diagnosis 

Asthm a



Chronic obstructive pulm onary disease



Stevens-Johnson syndrom e



Toxic epiderm al necrolysis



Pem phigus vulgaris



Scalded skin syndrom e



Organophosphate or carbam ate pesticide poisoning



Botulism



Radiation poisoning



Reactive airway disease



Congestive heart failure



Anaphylactoid reaction



Other anticholinergic agent

Treatment

Pa ge 1 0 6

Pre Hospital 

Avoid contam ination of environm ent and clinicians: o

Use level A or level B personal protective equipm ent.

o

Decontam ination: 

Derm al wet decontam ination prim arily for nerve and blistering agents



Dry decontam ination (rem oval of clothing and jewelry) for other agents



Adm inister atropine even if patient is tachycardic because condition m ay result from hypoxia.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Patient decontam ination: o

Brush off powder from chem ical.

o

Irrigate skin and eyes with copious am ounts of water or saline.

o 

Rem ove and dispose of clothing in double bags.

Protection for health care workers: o

Level A or B personal protective suit

o

Chem ical-resistant suit

o

Heavy rubber gloves and boots, neoprene gloves



Adm inister oxygen.



Place on cardiac m onitor and m easure pulse oxim etry.



Establish IV access with 0.9% norm al saline.

ED Treatment 

Blood agents: o

One hundred percent oxygen

o

Benzodiazepines for seizures

o

Cyanide antidote kit, m ay be repeated

o

Hydroxocobalam in available in Europe as cyanide antidote

Pa ge 1 0 6



Blister agents: o

Supportive care

o

Standard burn m anagem ent

o

Atropine to relieve eye pain

o

Monitor fluids, electrolytes, com plete blood chem istry.

o

Monitor com plete blood count for nadir.

o

Supportive care for sepsis, anem ia, hem orrhage

o

Granulocyte colony-stim ulating factor (G-CSF) for neutropenia



Choking agents, lacrim ators, riot control agents: o

Supportive care, bronchodilators

o

Eye irrigation

o

Chest radiograph and careful m onitoring for respiratory com plications

o

Phosgenes require m onitoring for delayed pulm onary edem a for 24 hours



Nerve agents: o

o

Supportive care: 

One hundred percent oxygen



Frequent airway suctioning

Atropine 2 m g IV every 5 m inutes until reversal of bronchorrhea, bronchoconstriction, and hypoxem ia: 

Antagonizes m uscarinic effects and som e central nervous system but no effect on skeletal m uscle weakness or respiratory failure



Pupillary response and heart rate are not useful m easures of adequate atropinization.



Stop atropine after patient regains consciousness and spontaneous ventilation (m ay need for periodic relapses); give as m uch as it takes to reverse respiratory com prom ise.

Pa ge 1 0 6

o

Pralidoxim e chloride (2-PAM or Protopam ): 

Regenerates cholinesterase by reversing phosphorylation (unless aging has occurred)



Reduces abnorm al skeletal m uscle m ovem ents, im proves skeletal m uscle weakness, and reverses flaccid paralysis



May repeat first dose or start on continuous infusion



If im provem ent from first dose, repeat 60â€“90 m inutes later.

o 

Diazepam : Give for seizures

Incapacitating agents (BZ): o

Supportive care

o

Aggressive IV fluid hydration

o

Benzodiazepines for agitation and increased m uscular activity

o

Consider physostigm ine in consultation with a poison center.

Medication (Drugs) 

Albuterol using nebulizer: 2.5 m g in 2.5 m L norm al saline (peds: 0.1â€“0.15 m g/kg per dose)



Atropine: 2 m g IM or IV (6 m g in severely intoxicated patients; peds: 0.02â€“0.08 m g/kg), then q5â€“10m in titrate to clinical effect



Diazepam : 5â€“10 m g IV over 3â€“5 m inutes (peds: 0.2â€“0.4 m g/kg up to 10 m g over 2â€“3 m inutes)



Hydroxocobalam in: 5 g IV (available in France)



Cyanide antidote kit: o

Inhale am yl nitrite am pule for 30 seconds every m inute until sodium nitrite given.

Pa ge 1 0 7

o

Sodium nitrite: 10 m L of 3% solution or 300 m g IV over 3â€“5 m inutes (peds: 0.15â€“0.33 m L/kg)

o

Monitor m ethem oglobin levels to keep <30%.

o

Sodium thiosulfate: 50 m L IV of 25% solution or 12.5 g (peds: 1.65 m L/kg)



Pralidoxim e chloride (2-PAM, Protopam ): 1â€“2 g IV over 20â€“30 m inutes or 600 m g IM (diluted with water or saline to concentration of 300 m g/m L) given with first three atropine doses (peds: 25â€“50 m g/kg per dose IV), repeat in 2 hours if m uscle weakness has not been relieved, and in 4- to 6-hour intervals if necessary. Continuous infusion of 500 m g/h has been used for organophosphate poisoning.

Follow-Up Disposition Admission Criteria 



Intensive care unit adm ission for: o

Blood agents

o

Nerve agents

o

Blister agents

o

Severe choking or lacrim ating agents

Adm it to hospital to watch for developing com plications: o

Blister, choking, lacrim ating agents, incapacitating agents

Discharge Criteria Riot control exposures: 

Observe in ED for 6 hours and discharge if sym ptom s resolve.

Pa ge 1 0 7



High/interm ediate water solubility gas exposures can be discharged in 6 hours if asym ptom atic.

References 1. Davis K, Aspera G. Exposure to liquid sulfur m ustard. Ann Em erg Med. 2001;37:653â€“656. 2. Ford M, Delaney K, Ling L, et al. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 3. Keyes DC. Chem ical warfare agents. In: Dart RC, et al., eds. Medical Toxicology. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 2004:1777â€“1794. 4. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002. 5. Suchard JR. Chem ical and biological weapons. In: Goldfrank LR, et al., eds. Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:1527â€“1551.

Pa ge 1 0 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hest Pain

Chest Pain

Kelly Corrigan

Basics Description 

One of the m ost frequent chief com plaints in the ED



There is a wide differential diagnosis of life-threatening etiologies as well as benign conditions often with m inim al physical findings.



Chest wall pain: o

Inflam m ation of skin and subcutaneous structures of the chest wall

o



Pain is reproduced by: 

Palpation



Horizontal flexion of the arm s



Extension of the neck



Vertical pressure on the head

Pleuritic pain: o

Inflam m ation or traum a to the ribs, cartilage, m uscles, nerves, pleural or pericardial surface

o

Pain increased by breathing, laughing, coughing, sneezing

o

Tenderness to palpation m ay be present

o

Diaphragm atic pleurisy:

Pa ge 1 0 7



Sharp shooting pains in the epigastrium , lower restrosternal area, or shoulder intensified by thoracic m ovem ent



Deep visceral pain: o

Upper thoracic visceral pain: 

Pain caused by visceral structures served by sensory fibers originating from T1â€“T4



May involve the m yocardium , pericardium , the ascending aorta, pulm onary artery, m ediastinum , and esophagus



Pain is generally precordial.



Pain is deep, visceral, and poorly localized.



Characteristics vary from severe and crushing to m ild, burning, or indigestion

o

Lower thoracic visceral pain: 

Pain caused by visceral structures served by sensory fibers originating from T5â€“T6



May involve the descending aorta, diaphragm atic m uscles, the gallbladder, the pancreas, the duodenum , and the stom ach



Pain is generally located to the xiphoid region and in the back.

Etiology Chest Wall Pain 

Chest wall hem atom a



Chest wall laceration



Throm bophlebitis of the thoracoepigastric vein



Xiphisternal arthritis



Adiposis Dolorosa



Breast abscess, fibroadenosis, carcinom a

Pleuritic pain:

Pa ge 1 0 7



Chest-wall twinge syndrom e: o

Brief episodes of sharp anterior chest pain lasting 30 seconds to three m inutes, aggravated by deep breathing and relieved by shallow respirations

o

Cause unknown



Costochondritis



Epidem ic pleurodynia: o

Sudden severe pains with shifting of loci associated with fever and headache

o 

Caused by a viral infection

Diaphragm atic pleurisy: o

Splenic rupture

o

Subdiaphragm atic abscess



Esophageal rupture



Herpes zoster



Intercostal m yositis



Intercostal neuralgia



Pectoralis m inor strain



Pericarditis



Pleuritis



Pulm onary em bolism



Pneum othorax



Pneum onia



Pneum onitis



Rib fractures



Rib periostitis



Slipping cartilage

Upper Thoracic Visceral Pain 

Coronary artery disease



Pericarditis



Myocarditis



Stress-induced cardiom yopathy

Pa ge 1 0 7



Cardiac syndrom e X: o

Anginalike chest pain, often with signs of cardiac ischem ia in the absence of coronary artery disease.



Thoracic aortic dissection



Esophagitis



Esophageal spasm



Gastroesophageal reflux disease



Esophageal hyperalgesia



Abnorm al m otility patterns and achalasia



Esophageal rupture and m ediastinitis

Lower Thoracic Visceral Pain: 

Dissection of the descending aorta



Peptic ulcer disease



Pancreatitis



Cholecystitis



Splenic rupture



Subdiaphragm atic abscess

Diagnosis Signs and Symptoms Coronary Artery Disease 

Shortness of breath



Pressure



Squeezing pain



Radiation to arm , jaw



Tachycardia or bradycardia



Diaphoresis



Nausea



Vom iting

Pa ge 1 0 7



Signs of congestive heart failure (CHF)



Anxiety

Aortic Dissection 

Sudden onset of pain with m axim al intensity early



Tearing pain



Radiation to back and/or flank



Hypertension



Differential pulses



Associated neurological changes (i.e., visual changes)

Pulmonary Embolism 

Pleuritic pain



Shortness of breath



Anxiety



Diaphoresis



Tachypnea



Tachycardia



Low-grade fever



Localized rales



Wheezing

Acute Pericarditis 

Substernal pain



Varies with respiration



Increased with recum bency



Relieved by leaning forward



Anxiety



Anorexia



Fever



Pericardial friction rub

History 

The history is the m ost im portant tool to distinguish

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between the various etiologies. 

Have the patient define the key features: o

Duration

o

Location: 

Retrosternal



Subxiphoid



Diffuse

P.221

o

o

o

Frequency: 

Constant



Interm ittent



Sudden versus delayed onset

Precipitating factors: 

Exertion



Stress



Food



Respiration



Movem ent

Tim ing: 

Context of onset of pain (i.e., at rest, exertional)

 o

o

Duration of pain

Quality: 

Burning



Squeezing



Dull



Sharp



Tearing



Heavy

Associated sym ptom s:

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

Shortness of breath



Diaphoresis



Nausea



Vom iting



Jaw pain



Back pain



Radiation



Palpitations



Change to focal or generalized weakness



Fatigue

Tests Lab 

Creatine kinase, with m uscle and brain subunits (CK-MB) and troponin T or I: o

They have a high positive predictive value.

o

If negative initially, they cannot be used to rule out m yocardial infarction (MI).

o

Serial troponin studies rule out MI and significantly decrease the probability of significant ischem ia.



D-Dim er: o

Sensitive but poor specificity for physical exam ination

o

Increased sensitivity with enzym e-linked im m unosorbent assay m ethods

o 

Indicated for low risk patient

Serum lipase: o

If an atypical presentation of pancreatitis is suspected

Imaging 

Ultrasound: o

Test of choice for pericardial and valvular disease

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o

May be helpful in acute ischem ic coronary artery disease by showing wall m otion abnorm alities if there is no prior infarction

o

Transesophageal echocardiography can be used in diagnosis of aortic dissection, especially in unstable patients and those unable to tolerate contrast.

o

Right ventricular dilation and hypokinesia m ay suggest pulm onary em bolus.



Stress echocardiogram : o

Chest pain centers

o

Stable patients in whom MI has been ruled out with serial enzym es and ECGs over 6â€“12 hours



Helical CT scan: o

Sensitive for aortic dissection

o

Useful in stable patient

o

Som e centers are using in diagnosis of pulm onary em bolus and in stable cardiac effusion



Ventilation/Perfusion scan: o

Useful in pulm onary em bolus

o

Must have norm al chest radiograph

o

Can rule in or out based on high probability or norm al scan in the patient with high or low pretest probability, respectively

o 

Angiography: o



Otherwise, further testing based on clinical suspicion

Useful in dissection, especially in stable patients

MRI: o

Mostly used to follow stable dissections or aneurysm s over tim e

ECG 

Inexpensive and available



Obtain and interpret within 10 m inutes of arrival

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

See specific etiologies

Chest radiograph 

Pneum othorax



Pneum onia



A com plication of ischem ic heart disease such as CHF



Aortic dissection: o

Widened m ediastinum seen in about 55â€“62% of patients

o

A pleural effusion is found in about 20% of patients.

o

Apical capping

o

Aortic knob obliteration

o

A norm al chest radiograph is found in 12â€“15% of patients.



Acute pericarditis: o

Usually norm al unless m assive effusion enlarges cardiac silhouette



Esophageal rupture: o

Usually will show m ediastinal air

o

May have left pleural effusion

Differential Diagnosis See Etiology

Treatment Pre Hospital 

IV access



Cardiac m onitoring



Oxygen



Baby aspirin



Pain control:

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

o

Nitrates

o

Morphine

All chest pain should be treated and transported as a possible life-threatening em ergency.

Initial Stabilization 

ABCs



IV



Oxygen



Cardiac m onitoring

ED Treatment 

IV, oxygen, and m onitoring



Treatm ent varies based on suspected etiologies:

Medication (Drugs) 

Alum inum and m agnesium hydroxide: 15 to 30 m L PO q2hâ€“q4h



Aspirin: 160â€“325 m g PO



Cim etidine: 300 m g IV or PO q6h



Donnatal: 5â€“10 m L PO q6h



Esm olol: 50 Âµg/kg bolus, then 50â€“200 Âµg/m in drip



Labetalol: 20 m g IV every 10 m inutes up to 300 m g



Metoprolol: 5 m g IV every two hours up to 15 m g



Morphine sulfate: 2â€“4 m g every five m inutes



Nitroglycerin: 0.4 m g sublingual, or 1â€“2 inches of nitro paste, or drip at 5â€“10 Âµg/m in and titrate to effect



Nitroprusside: 0.3â€“10 Âµg/kg/m in drip



Propranolol: 1â€“2 m g IV every 2 m inutes

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Follow-Up Disposition Admission Criteria Dependent on the risk for life-threatening cardiopulm onary etiologies

Discharge Criteria Very low risk for untoward event if discharge is planned

References 1. ACC/AHA Guidelines for the Managem ent of Patients with unstable Angina and Non-ST-Segm ent Elevation MI: Executive Sum m ary and Recom m endations. Circulation. 2000;102:1193. 2. Davis K, Aspera G. Exposure to liquid sulfur m ustard. Ann Em erg Med. 2001;37:653â€“656. 3. Thoracic: Respiratory, Cardiovascular, and Lym phatic Sym ptom s. In: LeBlond RF, DeGowin RL, Brown DD, et al, eds. DeGowin's Diagnostic Exam ination McGraw-Hill Professional. 8th ed. (March 26, 2004). 4. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002. Clinical Toxicology. Philadelphia: WB Saunders; 2001.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hest Traum a, Blunt

Chest Trauma,

Blunt Lisa G. Lowe

Basics Description 

Significant source of m orbidity and m ortality in the United States



Approxim ately 12 thoracic traum a victim s per m illion population per day



Approxim ately 33% of these injuries require hospital adm ission.



Directly responsible for 20â€“25% of all deaths attributed to traum a



Contributing cause of death in 25% of patients who die from other traum atic injuries

Etiology 

Com m on m echanism s of injury include: o

Motor vehicle collisions (70â€“80%)

o

Motorcycle collisions

o

Pedestrians struck by a m otor vehicle

o

Falls from great heights

o

Assaults

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o 

Blast injuries

Injuries can result from direct blunt force to the chest or from forces related to rapid deceleration.

Diagnosis Signs and Symptoms 

Obvious contusion, wound, or other defect of the chest wall: o

Paradoxical chest wall m ovem ent suggests flail chest segm ent.



Usually occurs in com bination with other injuries



Hypotension



Som e patients with severe intrathoracic injuries, such as traum atic aortic disruption, m ay have no visible external signs of traum a.

History 

Tim e of injury



Mechanism of injury



Estim ates of m otor vehicle accident (MVA) velocity and deceleration



Loss of consciousness



Chest pain



Pain with deep inspiration or cough



Dyspnea

Physical Exam 

Unilaterally absent breath sounds



Crepitus or subcutaneous air in the chest wall



Decreased or absent breath sounds



Tenderness to palpation on the chest wall

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

Jugular venous distention



Hyperresonance to percussion on involved side

Essential Workup 

Check airway, breathing, and circulation (ABCs) to determ ine the patient's stability.





Focused exam ination of the chest: o

Respiratory effort and rate

o

Chest wall excursion

o

Crepitus

o

Subcutaneous air

o

Breath sounds and heart sounds

o

Presence of jugular venous distention

Obtain a supine chest radiograph im m ediately: o

Avoid an upright chest radiograph because of the potential for other injuries (especially spinal injuries).



Electrocardiogram and m onitor to detect m yocardial ischem ia or dysrhythm ias

Tests Lab 

Baseline hem oglobin



Pulse oxim etry



Arterial blood gas



Serum lactate



Type and cross-m atch



Coagulation profile



Cardiac enzym es if concerned for cardiac contusion



Periodic chem istry panel for patients receiving significant fluid resuscitation

Imaging

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

Chest radiograph is the initial radiologic study of choice: o

If chest radiograph reveals widened m ediastinum and patient hem odynam ically stable, repeat film in upright position.



Chest CT is m ore specific for pneum othoraces and pulm onary contusions/occult injuries.



Chest CT with contrast, or aortic angiogram , is useful in identifying aortic and large vessel injuries.



Esophagram m ay be useful for possible esophageal injury (e.g., pneum om ediastinum )



Electrocardiogram if sternal tenderness is present or abnorm alities on cardiac m onitor

Diagnostic Procedures/Surgery 

If patient's condition is unstable, em ergency thoracotom y m ay be necessary to repair a traum atic aortic disruption.



If there are signs of tam ponade and patient is stable, perform an echocardiogram on an urgent basis.



If there are signs of pericardial tam ponade and patient is unstable, em ergent pericardiocentesis m ay be necessary, followed by im m ediate transport to the OR for a pericardial window.



Bronchoscopy for possible upper airway injuries (e.g., large persistent air leak after chest tube)



Bedside ultrasound is up to 90% sensitive for identifying pericardial injuries or hem othoraces.

Pregnancy Considerations 

In pregnant patients, rem em ber to use the least am ount of radiation available and to shield the uterus during im aging when possible.



See Pregnancy, Traum a in, for details.

Differential Diagnosis

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

Sim ple pneum othorax



Tension pneum othorax



Open pneum othorax



Hem othorax



Rib fractures



Flail chest



Pulm onary contusion



Myocardial contusion



Myocardial rupture



Pericardial tam ponade



Traum atic aortic disruption



Esophageal injury



Large vascular injury (subclavian, pulm onary artery)



Tracheobronchial injury



Diaphragm atic injury

Pediatric Considerations Rib cage is highly elastic in children and can withstand significant forces without overt signs of external traum a, but such patients m ay have m ajor internal injuries.

Treatment Pre Hospital 

All patients with any signs of life in the field should be transported to a traum a center.



Full spinal precautions



Needle decom pression for tension pneum othorax: o

Unilaterally absent breath sounds

o

Hypotension

o

Jugular venous distention

Pa ge 1 0 8

o 

Hyperresonance to percussion

If large open pneum othorax exists, tape occlusive dressing on three sides; a totally occlusive dressing m ay produce a tension pneum othorax



Do not delay transport to hospital for intravenous access: o

IV access can be established en route.

Initial Stabilization 

ABCs m anagem ent; intubate patient early if signs of respiratory insufficiency, shock, or altered m ental status exist.



Resuscitation attem pts should be initiated only in patients who arrive in the ED with vital signs.



Any patient who presents in blunt traum atic arrest is not likely to survive a thoracotom y in the ED, and is therefore not indicated in this group. P.223



If the patient's condition is unstable and clinically shows signs of a tension pneum othorax, perform needle thoracostom y and place a chest tube im m ediately after: o

Do not wait to obtain a chest radiograph.

o

Place chest tube on the affected side or bilaterally if injury site is unclear.



Oxygen by nonrebreather face m ask for stable patients



Obtain vascular access, preferably two large intravenous lines (>18 gauge).



Maintain spinal im m obilization.

ED Treatment 

Tube thoracostom y if pneum othorax or hem othorax is identified:

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o

36-French chest tube in an adult

o

In children use the largest tube that the intercostal space will accom m odate.



Provide resuscitation with isotonic fluids and blood products as necessary: o

Aggressive fluid resuscitation m ay be harm ful if severe pulm onary contusions exist.



Workup for associated intra-abdom inal injuries (e.g., with diagnostic peritoneal lavage, abdom inal ultrasound, abdom inal CT scan): o

Patients with chest traum a frequently have concom itant intra-abdom inal injuries.

Medication (Drugs) 

Tetanus booster if indicated



Methylprednisolone (for signs of spinal cord injury): 30 m g/kg intravenously over 1 hour, followed by a continuous drip of 5.4 m g/kg/h for next 23 hours



Judicious doses of short-acting analgesics (fentanyl 1â€“2 Âµg/kg IV, m orphine 0.1 m g/kg IV) as needed for pain control

Follow-Up Disposition Admission Criteria 

Patients with conduction blocks, frequent ectopy, or ischem ic changes visible on ECG should be adm itted to a m onitored setting for possible m yocardial contusion.

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

Hem odynam ically unstable patients should go to the operating room on an em ergency basis for thoracotom y or laparotom y.



More than 1,000â€“1,500 m L of blood drawn out of the chest tube on initial insertion indicates need for thoracotom y.



More than 200 m L of blood per hour from chest tube for several hours suggests the need for operative intervention.



Patients with significant rib fractures should be adm itted for pain control: o



Epidural catheter

Patients who lose vital signs in the ED should undergo rapid open thoracotom y.

Discharge Criteria Patients with clinically insignificant chest wall contusions and an initial negative upright chest radiograph m ay be observed for 6 hours in the ED and have a repeat radiograph; if the repeat radiograph reveals no pneum othorax, hem othorax, or pulm onary contusion and the patient is able to breathe deeply and to cough, he or she m ay be discharged.

Issues for Referral 

Notify traum a surgeon prom ptly about patients with significant injuries requiring surgical intervention or adm ission.



The following are indications for em ergent surgical referral: o

Traum atic thoracotom y with loss of chest wall integrity

o

Blunt diaphragm atic injuries

o

Massive air leak following chest tube insertion

Pa ge 1 0 9

o

Massive hem othorax or continued high rate of blood loss via the chest tube (i.e., 1,500 m L on insertion of tube or continued loss of 200â€“300 m L/h

o

Radiographically or endoscopically confirm ed tracheal, m ajor bronchial, or esophageal injury

o

Gastrointestinal tract contents recovered on chest tube placem ent

o

Cardiac tam ponade

o

Radiographic confirm ation of a great vessel injury

o

Em bolism or m issile into pulm onary artery or heart

References 1. Adam s JE 3rd, Davila-Rom an VG, Bessey PQ, et al. Im proved detection of cardiac contusion with cardiac troponin I. Am Heart J. 1996;131(2):308â€“12. 2. Fabian TC, Davis KA, Gavant ML, et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227(5):666â€“676; discussion 676â€“677. 3. Feliciano DV. The diagnostic and therapeutic approach to chest traum a. Sem in Thorac Cardiovasc Surg. 1992;4:156â€“162. 4. Karm y-Jones R, Jurkovich GJ. Blunt chest traum a. Curr Probl Surg. 2004;41(3):211â€“380. 5. Mansour KA. Traum a of the diaphragm . Chest Surg Clin North Am . 1997;7(2):373â€“383. 6. Sartorelli KH, Vane DW. The diagnosis and m anagem ent of children with blunt injury of the chest. Sem in Pediatr Surg. 2004;13(2):98â€“105. 7. Sim on BJ, Leslie C. Factors predicting early in-hospital death in blunt thoracic aortic injury. J Traum a. 2001;51(5):906â€“910; discussion 911.

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Miscellaneous SEE ALSO: Chest Traum a, Penetrating; Flail Chest; Pregnancy, Traum a in; Traum a, Multiple

Codes ICD9-CM 862.8 Multiple and unspecified intrathoracic organs, without m ention of open wound into cavity

ICD10 S29.9 Unspecified injury of thorax

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hest Traum a, Penetrating

Chest Trauma,

Penetrating Mamata Kene

Basics Etiology 

Gunshot wounds or stab wounds m ost com m on



Im palem ent on a sharp object from a fall can occur.

Diagnosis Signs and Symptoms 

Object im paled in the chest wall



Obvious wound in the chest wall with or without bleeding



Chest pain



Dyspnea



Respiratory distress



Altered m ental status from hypoxem ia



Absent or altered breath sounds on one or both sides



Hypotension



Jugular venous distention

Essential Workup

Pa ge 1 0 9



Perform routine assessm ent of airway, breathing, and circulation.





Rapid exam ination: o

Respiratory effort and rate

o

Chest excursion

o

Crepitus

o

Subcutaneous air

o

Breath sounds and heart sounds

Upright chest radiograph is preferred for identifying a pneum othorax: o

Supine chest radiograph should be taken first if spinal precautions m ust be m aintained.



Baseline hem oglobin



Pulse oxim etry



Arterial blood gas



Serum lactate



Type and screen

Tests Lab 

Perform echocardiogram if signs of tam ponade present or if wound is close to the heart.



ECG

Imaging 

With gunshot wounds, other areas (abdom en, pelvis) should be im aged: o

total num ber of wounds and bullets m ust be the sam e.



Arteriogram of aortic arch, carotid arteries, or subclavian artery if great vessel injury is suspected



Esophageal Gastrografin swallow or endoscopy to identify esophageal perforation

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

Bronchoscopy to identify tracheobronchial injuries

Differential Diagnosis 

Sim ple pneum othorax



Tension pneum othorax



Open pneum othorax



Hem othorax



Rib fractures



Flail chest



Pulm onary contusion



Myocardial contusion



Myocardial rupture



Pericardial tam ponade



Traum atic aortic disruption



Esophageal injury



Large vessel injury



Tracheobronchial injury



Diaphragm atic injury



Intra-abdom inal injury



Spinal cord injury

Treatment Pre Hospital 

Cautions: o

All patients with signs of life in the field according to reports from EMS personnel should be transported to a traum a center.

o

Full spinal im m obilization if spinal injury suspected

o

Never rem ove objects im paled in the chest because exsanguination m ay follow.

Pa ge 1 0 9

o

Needle decom pression m ay be necessary if tension pneum othorax suspected: 

Unilaterally absent breath sounds, hypotension, jugular venous distention

o

If large open pneum othorax exists, occlusive dressing taped on three sides: 

A totally occlusive dressing m ay produce a tension pneum othorax.



Controversies: o

Do not delay transport to hospital to obtain intravenous access: 

Intravenous access m ay be established en route.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent: o

Intubate for signs of serious chest injury, obvious respiratory distress, or hypotension.



Oxygen by nonrebreather face m ask for patients in stable condition



Obtain vascular access, two peripheral large-bore intravenous lines (>18 gauge), and fluid resuscitation as needed: o

Two-liter isotonic fluid bolus initially

P.225



For tension pneum othorax, perform a needle thoracostom y and place a chest tube im m ediately: o



Do not wait to get a chest radiograph.

For pericardial tam ponade, perform an em ergency pericardiocentesis: o

Followed by rapid transport to the operating room for

Pa ge 1 0 9

a pericardial window 

Maintain spinal im m obilization if indicated.

ED Treatment 

Notify traum a surgeon about patient's arrival.



Tube thoracostom y if a pneum othorax or hem othorax is identified: o

36-gauge chest tube in an adult

o

In children use largest tube intercostal space will accom m odate.



Fluid resuscitation as necessary: o

Contused lung parenchym a will have leaky capillary beds, and aggressive crystalloid resuscitation m ay aggravate pulm onary dysfunction.



Any wound with an entry or exit site below the nipple or the posterior tip of the scapula is concerning for an intra-abdom inal injury: o

Work up with a diagnostic peritoneal lavage (DPL), ultrasound, CT scan, exploratory laparotom y, or laparoscopy.

o 

DPL positive with 5,000 RBC

Describe the nature of wounds accurately: o

Retain any bullet fragm ents, clothes, or tissue rem oved from the wound.



Probing a chest wound is contraindicated because it can create a pneum othorax or worsen hem orrhage.



Im paled objects should be rem oved only in the operating room .



Tetanus booster if indicated

Medication (Drugs)

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

Methylprednisolone (for spinal cord injury): 30 m g/kg IV over 1 hour, followed by a continuous drip of 5.4 m g/kg/h for 23 hours



Sm all doses of short-acting analgesics (fentanyl, 1â€“2 Âµg/kg IV, m orphine 0.1 m g/kg IV) or sedatives (m idazolam , 0.05 m g/kg intravenously) as needed for pain control and sedation



Treat with intravenous antibiotics if wound grossly contam inated (e.g., cephalexin 1 g IV).

Follow-Up Disposition Admission Criteria 

All patients with penetrating chest traum a should be adm itted.



A patient who has signs of life in the field but no blood pressure on arrival in the ED should have an em ergency thoracotom y perform ed by the m ost experienced person present: o

If the source of bleeding is controlled and there are signs of cardiac activity, the patient should go to the operating room for form al operative repair.



Hem odynam ically unstable patients should go im m ediately to the operating room .



Any patient with intrathoracic penetration should have a chest tube placed and should be adm itted to a m onitored setting.



More than 1,000â€“1,500 m L of blood drawn out of the chest tube on initial insertion indicates the need for

Pa ge 1 0 9

thoracotom y. 

More than 200 m L of blood per hour from a chest tube for several hours suggests the need for surgical intervention.



Patients with large, persistent air leaks usually require surgery.



Patients with significant rib fractures should be adm itted and have an epidural catheter placed for pain control and pulm onary toilet.

Discharge Criteria Patients with isolated m inor chest wounds and a norm al chest radiograph can be observed for 6 hours in the ED and have a repeat radiographic study; if no intrathoracic penetration is suspected, the patient can be discharged.

References 1. Baillot R, Dontigny L, Verdant A, et al. Penetrating chest traum a: a 20-year experience. J Traum a. 1987;27:994â€“997. 2. Degiannis E, Bowley DM, Westaby S. Penetrating cardiac injury. Ann R Coll Surg Engl. 2005;87(1):61â€“63. 3. Ivatury RR, Cayten CG. The Textbook of Penetrating Traum a. Baltim ore: William s & Wilkins; 1996. 4. Mandavia DP, Joseph A. Bedside echocardiography in chest traum a. Em erg Med Clin North Am . 2004;22(3):601â€“619. 5. Mansour KA. Traum a of the diaphragm . Chest Surg Clin N Am . 1997;7(2):373â€“383. 6. Millham FH, Grindlinger GA. Survival determ inants in patients undergoing em ergency room thoracotom y for penetrating chest injury. J Traum a. 1993;34:332â€“336.

Codes ICD9-CM 862.9 Multiple and unspecified intrathoracic organs, with open wound

Pa ge 1 1 0

into cavity

ICD10 S21.9 Open wound of thorax, part unspecified

Pa ge 1 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ho langitis

Cholangitis

Robert G. Buckley

Basics Description 

Partial or com plete obstruction of the com m on bile duct owing to gallstones, tum or, cyst, or stricture



Increased intralum inal pressure in biliary tree



Bacterial m ultiplication results in bacterem ia and sepsis.



Purulent infection of biliary tree, which m ay involve the liver and gallbladder



Mirizzi syndrom e is defined as com m on bile duct obstruction owing to extrinsic com pression from gallbladder or cystic duct edem a or stones.

Etiology 



Bacterial sources of infection include: o

Ascending duodenal source

o

Gallbladder infection

o

Portal venous seeding

o

Hem atogenous spread with hepatic secretion

o

Lym phatic spread

Bacterial organism s include: o

Anaerobes (Bacteroides and Clostridium species)

o

Intestinal coliform (Escherichia coli)

Pa ge 1 1 0

o 

Enterococcus

AIDS sclerosing cholangitis characterized by: o

Papillary stenosis

o

Sclerosing cholangitis

o

Extrahepatic biliary obstruction

o

Cytom egalovirus (MV), Cryptosporidium , and m icrosporidia isolated, but causal role not established

Diagnosis Signs and Symptoms History 

Charcot triad: o

Classic presentation of fever and chills; right upper quadrant (RUQ) pain and jaundice found in only 50â€“70%

o

Addition of shock and altered m ental status denotes a m ore advanced form of biliary sepsis known as Reynold pentad



Abdom inal pain present in >70%â€” localizing to RUQ.



AIDS sclerosing cholangitis presents with sim ilar sym ptom s but with m ore chronic indolent course and near-norm al serum bilirubin levels.

Physical Exam 

Fever found in >90%



Peritoneal findings found in 30%



Clinically apparent jaundice m ay be absent in up to 40%.

Essential Workup 

ECG in patients at risk for coronary artery disease

Pa ge 1 1 0



CBC



Liver function test (LFT)



Am ylase, lipase



Urinalysis



Blood cultures



Gallbladder ultrasound or hepatoim inodiacetic acid (HIDA) scan

Tests Lab 

CBC: o

Leukocytosis with left shift unless im m unocom prom ised or severe sepsis



LFTs consistent with cholestasis: o

Elevated direct bilirubin and alkaline phosphatase

o

Minim al elevation of transam inases (<200 IU/m L)

o

Changes m ay lag sym ptom onset by 24â€“48 hours.



Am ylase and lipase norm al or m ildly elevated



Urinalysis positive for bilirubin

Imaging 

Ultrasound detects the level of ductal obstruction and the presence of gallstone etiology.



Radionuclide scanning (HIDA): o

Indicates obstruction when tracer not found in duodenum within 1 hour

o

More sensitive than ultrasound in detecting obstruction in the first 24â€“48 hours before ductal dilation occurs



Abdom inal radiograph and chest radiograph: o

Useful to rule out intestinal obstruction, perforation, or pneum onia

o

20% gallstones radiopaque

Pa ge 1 1 0

Diagnostic Procedures/Surgery Em ergency invasive biliary im aging and drainage (surgical, percutaneous, or endoscopic retrograde cholangiopancreatography [ERCP]) if no response to m edical treatm ent in 12â€“24 hours P.227

Differential Diagnosis 

Acute cholecystitis



Hepatitis or hepatic abscess



Acute pancreatitis



Right pyelonephritis



Right lower lobe pneum onia or pulm onary em bolism



Perforated duodenal ulcer



Appendicitis



Sepsis with nonspecific elevation of LFTs



Fitz-Hugh and Curtis syndrom e

Treatment Pre Hospital Stabilize septic shock.

Initial Stabilization 

Im m ediate IV fluid resuscitation for dehydration, hem odynam ic com prom ise, and sepsis



Vasopressors (dopam ine) for hypotension refractory to volum e replacem ent

ED Treatment 

Broad-spectrum antibiotics for coliform s, anaerobes, and

Pa ge 1 1 0

enterococcus such as: o

Am picillin/sulbactam plus am inoglycoside (e.g., gentam icin)

o

Piperacillin/tazobactam plus am inoglycoside (e.g., gentam icin)

o

Substitute levofloxacin (Levaquin; peds: clindam ycin) and m etronidazole in penicillin allergy.

o

Substitute aztreonam for am inoglycoside in renal insufficiency.



NPO



Nasogastric (NG) suctioning if protracted vom iting or ileus



IV fluid (0.9% norm al saline [NS]) replacem ent and m aintenance



Narcotic analgesia if hem odynam ically stable and diagnosis reasonably established



Im m ediate surgical consultation



Em ergency invasive biliary drainage procedure (surgical, percutaneous, or ERCP) if no response to m edical treatm ent in 12â€“24 hours

Medication (Drugs) 

Am picillin/sulbactam : 3.0 g (peds: 200 m g/kg/24h) intravenous piggyback (IVPB) q6h



Aztreonam : 2 g (peds: 120 m g/kg/24h) IVPB q6h



Clindam ycin: 600â€“900 m g (peds: 25â€“40 m g/kg/24h) IVPB q6hâ€“q8h



Dopam ine: 2â€“20 Âµg/m in IVPB; titrate to m aintain blood pressure (BP)



Gentam icin: 1.5â€“2.0 m g/kg (peds: 6â€“7 m g/kg/24h) IVPB q8h; follow levels



Levaquin: 500 m g IVPB q24h; contraindicated in peds

Pa ge 1 1 0



Meperidine: 0.5 m g/kg intravenous push (IV) titrated up to 2.0 m g/kg for pain relief



Metronidazole: 500 m g (peds: 30 m g/kg/24h) IVPB q6h



Piperacillin/tazobactam : 3.375 m g (peds: 300 m g/kg/24h) IVPB q6h



Prom ethazine: 12.5â€“25 m g (1â€“2 m g/kg/24h) q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

All patients with acute cholangitis should be adm itted with im m ediate surgical and gastroenterologic consultation.



Adm it patients with signs of septic shock to the ICU

Discharge Criteria None

References 1. Hanau LH, Steigbigel NH. Cholangitis: pathogenesis, diagnosis and treatm ent. Curr Clin Top Infect Dis. 1995;311:99â€“105. 2. Lai EC, Mok FP, Tan ES, et al. Endoscopic biliary drainage for severe acute cholangitis. N Engl J Med. 1992;326:1582â€“1586. 3. Mahajani RV, Uzer MF. Cholestasis: cholangiopathy in HIV-infected patients. Clin Liver Dis. 1999;3:669â€“684. 4. Moscati RM. Cholelithiasis, cholecystitis, and pancreatitis. Em erg Med Clin North Am . 1996;14:719â€“737. 5. Westphal JF, Brogard JM. Biliary tract infections: a guide to treatm ent. Drugs. 1999;57:81â€“91.

Pa ge 1 1 0

Miscellaneous SEE ALSO: Cholecystitis; Cholelithiasis

Codes ICD9-CM 576.1

ICD10 K83.0

Pa ge 1 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ho lecystitis

Cholecystitis

Robert G. Buckley

Basics Description Cholecystitis is defined as inflam m ation of the gallbladder.

Etiology 

Acute calculous cholecystitis: o

Owing to bile stasis secondary to prolonged obstruction by a gallstone (see Cholelithiasis) in the gallbladder neck, cystic duct, or com m on bile duct

o

Leads to increased intralum inal pressure and m ucosal dam age

o

Release of inflam m atory m ediators results in distention, edem a, and increased vascularity.

o

Coliform s and anaerobes lead to infectionâ€”prim ary causal role is controversial.



Acalculous cholecystitis: o

Ten percent of cases

o

Underlying critical illness leads to biliary stasis and m ucosal ischem ia.

o

Subsequent m ucosal inflam m ation and infection

Pediatric Considerations

Pa ge 1 1 0



Acute calculous cholecystitis extrem ely rare in childhood (see Cholelithiasis)



Acalculous cholecystitis m ore com m on than calculous form in children: o

Associated with system ic bacterial infections, scarlet fever, Kawasaki disease, and parasitic infections

Diagnosis Signs and Symptoms History N/A

Acute Calculous Cholecystitis 

Dull, aching, epigastric, or right upper quadrant (RUQ) pain: o

Radiation to tip of right scapula, acrom ion, or thoracic spine

o

Duration >6 hours m ore suggestive of cholecystitis than uncom plicated biliary colic



As inflam m ation progresses, parietal peritoneal irritation leads to sharp, localized pain.



Nausea, vom iting, fever, and chills often reported, but absent in m ost cases



Jaundice in 20%



History of prior attacks of biliary colic or known gallstones favors diagnosis.

Acalculous Cholecystitis 

Occurs in critically ill patients (burns, sepsis, traum a, or postoperative)



Localized pain and tenderness frequently absent

Pa ge 1 1 1



Often presents with sym ptom s of generalized sepsis of unknown source

Physical Exam 

Murphy sign: o

Inspiratory arrest with gentle palpation of RUQ owing to increased pain

o 

Found in m ost cases

Localized parietal peritoneal signs: o

Percussion tenderness

o

Rebound

o

Found as the disease progresses

Essential Workup 

ECG in patients at risk for coronary artery disease



CBC



Liver function test (LFT)



Am ylase, lipase



Urinalysis



Hum an chorionic gonadotropin (hCG)



Gallbladder ultrasound or HIDA scan

Tests Lab 

CBC: o

WBC >12,000 cells/m m 3 supports diagnosis, but m ay be norm al in m ore than half of cases



LFTs: o

Transam inases, bilirubin, am ylase, and lipase m ay be m inim ally elevated, but are generally norm al.

o

Disproportionate elevation of direct bilirubin and alkaline phosphatase com pared with transam inases suspicious for com m on duct obstruction or cholangitis

Pa ge 1 1 1

Imaging 

Ultrasound: o

Generally the first-line im aging procedure

o

Positive findings include gallbladder wall thickening (>5 m m ) or pericolic fluidâ€”sensitivity, 90%; specificity, 80%.

o 

Optim al if patient NPO >8 hours

Radionuclide scanning (HIDA) o

Most useful when clinical suspicion rem ains high despite equivocal findings on ultrasound or when acalculous cholecystitis suspected

o

Positive when tracer seen in sm all bowel but inflam ed gallbladder fails to visualize



o

Sensitivity, >95%; specificity, 90%

o

False-positive results increase in nonfasting state.

Abdom inal radiographs: o

Exclude intestinal perforation or obstruction

o

Air in the gallbladder wall consistent with em physem atous cholecystitis

o

Gallstones radiopaque in up to 20%

Differential Diagnosis 

Biliary colic



Hepatitis or hepatic abscess



Cholangitis



AIDS sclerosing cholangitis



Pancreatitis



Duodenal perforation



Peptic ulcer disease



Gastritis



Duodenal perforation



Right lower lobe pneum onia, pleurisy, or pulm onary

Pa ge 1 1 1

infarction 

Myocardial infarction



Abdom inal aortic aneurysm



Appendicitis



Fitz-Hugh and Curtis syndrom e



Pyelonephritis

P.229

Treatment Initial Stabilization 

IV, oxygen, cardiac m onitoring until m yocardial ischem ic cause excluded



Initiate IV fluid therapy for dehydration, hem odynam ic com prom ise, or sepsis.

ED Treatment 

Broad-spectrum antibiotics for coliform s, anaerobes, and enterococcus: o

Am picillin/sulbactam

o

Piperacillin/tazobactam

o

Add am inoglycoside if sepsis or cholangitis suspected (see Cholangitis).



Alternative antibiotics for penicillin allergic: o

Adults: levofloxacin (Levaquin) and m etronidazole

o

Peds: Clindam ycin with am inoglycoside



NPO



IV fluid replacem ent and m aintenance



Antiem etics (prom ethazine) if vom iting

Pa ge 1 1 1



Nasogastric (NG) suctioning if refractory vom iting or ileus



Narcotic analgesics (m eperidine) with antiem etic (prom ethazine): o

Adm inister for refractory pain once diagnosis is reasonably established

o

Morphine sulfate m ay lead to spasm at sphincter of Oddi (clinical significance not well established).



Anticholinergics (glycopyrrolate) com m only used despite lack of clinical trials proving benefit



Surgical consultation

Medication (Drugs) 

Am picillin/sulbactam : 3.0 g (peds: 200 m g/kg/24h) intravenous piggyback (IVPB) q6h



Clindam ycin: 600â€“900 m g (peds: 25â€“40 m g/kg/24h) IVPB q6h to q8h



Gentam icin: 1.5â€“2.0 m g/kg (peds: 6â€“7 m g/kg/24h) IVPB q8h; follow levels



Levaquin: 500 m g IVPB q24h; contraindicated in peds



Meperidine: 0.5 m g/kg intravenous push (IVP) titrated up to 2.0 m g/kg for pain relief



Metronidazole: 500 m g (peds: 30 m g/kg/24h) IVPB q6h



Piperacillin/tazobactam : 3.375 m g (peds: 300 m g/kg/24h) IVPB q6h



Prom ethazine: 12.5â€“25 m g IV (1â€“2 m g/kg/24h) q4hâ€“q6h

Follow-Up

Pa ge 1 1 1

Disposition Admission Criteria 

All cases of cholecystitis should be adm itted for parenteral antibiotics, analgesia, fluid replacem ent, and cholecystectom y in 24â€“72 hours.



Unstable patients (gallbladder perforation or sepsis) require im m ediate surgery.

Discharge Criteria N/A

References 1. Horton JB, Bilhartz LE. Gallstones and its com plications. In: Feldm an, M. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002: 1065â€“1090. 2. Mahajani RV, Uzer MF. Cholestasis: cholangiopathy in HIV-infected patients. Clin Liver Dis. 1999;3:669â€“684. 3. Silen W. Cholecystitis and other causes of acute pain in the right upper quadrant of the abdom en. In: Silen W, ed. Cope's Early Diagnosis of the Acute Abdom en. 20th ed. Oxford, UK: Oxford University Press; 2000:128â€“137. 4. Singer AJ, McCracken G, Henry MC, et al. Correlation am ong clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis. Ann Em erg Med. 1996;28:267â€“272.

Miscellaneous SEE ALSO: Cholangitis; Cholelithiasis

Codes ICD9-CM

Pa ge 1 1 1

575.10

ICD10 K81.9

Pa ge 1 1 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ho lelithiasis

Cholelithiasis

Robert G. Buckley

Basics Description 

Sym ptom s arise when gallstones pass through the cystic or com m on bile ducts leading to im pedance of norm al bile flow and gallbladder spasm .



Biliary dyskinesia produces sym ptom s identical to biliary colic in the absence of stones.

Etiology 



Cholesterol stones: o

Most com m on type of gallstone

o

Form when solubility exceeded

Pigm ent stones: o

20%

o

Com posed of calcium bilirubinate

o

Associated with clinical conditions such as hem olytic anem ias that lead to increased concentration of unconjugated bilirubin



Incidence increases with age and favors fem ales to m ales 2:1.



Gallstones are exceedingly rare in childhood and are m ost com m only associated with sickle cell disease, hereditary

Pa ge 1 1 1

spherocytosis, or other hem olytic anem ias that result in pigm ent stone form ation. 

Biliary sludge: o

Nonstone, crystalline, granular m atrix

o

Associated with rapid weight loss, pregnancy, ceftriaxone or octreotide therapy, and organ transplantation

o

May develop sym ptom s identical to cholelithiasis and its com plications

Diagnosis Signs and Symptoms History 

Dull, aching epigastric or right upper quadrant (RUQ) pain: o

Arising over 2â€“3 m inutes, continuous (rather than colicky), and lasting from 30 m inutes to 6 hours before dissipating

o

May radiate to the tip of right scapula, acrom ion, or thoracic spine

o

Often correlated with ingestion of large, fatty m eal



Anorexia



Nausea and vom iting



Afebrile: o

Fever and chills suggest cholecystitis or cholangitis

Physical Exam 

Tenderness to deep palpation but without rebound



Murphy sign (inspiratory arrest during deep palpation of the RUQ) m ay be present during the episode of colic, but should resolve when sym ptom s pass.

Pa ge 1 1 1

Essential Workup 

Obtain ECG on those whose pain m ay be owing to m yocardial ischem ia.



CBC



Liver function tests (LFTs)



Am ylase, lipase



Urinalysis



Hum an chorionic gonadotropin (hCG)

Tests Lab 

CBC: o

White blood cell count (WBC) usually norm al, but m ay elevate after vom iting

o 

Leukocytosis suggestive of cholecystitis or cholangitis

LFTs: o

Usually norm al

o

Elevation suggests com m on duct obstruction, cholangitis, cholecystitis, or hepatitis.



Am ylase/lipase: o

Norm al or m inim ally elevated with passage of gallstone

o

Elevation in context of severe persistent epigastric pain suggests pancreatitis.



Urinalysis: o

Exclude nephrolithiasis or pyelonephritis.

o

Bilirubinuria suggests com m on duct obstruction or hepatitis.

Imaging 

Ultrasound: o

Detects gallstones with sensitivity and specificity

Pa ge 1 1 1

>90% o

Dilation of com m on bile duct >10 m m indicates obstruction, but m ay be norm al with acute obstruction.

o

Gallbladder wall thickening >5 m m or pericolic fluid 90% sensitive and 80% specific for cholecystitis

o

Accuracy enhanced in fasting patient with noncontracted gallbladder



Radionuclide scanning (HIDA) o

Cannot detect gallstones

o

Passage of tracer into sm all intestine without visualization of gallbladder highly diagnostic of cystic duct obstruction and cholecystitis; sensitivity and specificity roughly 95%

o

Failure of tracer to pass into duodenum suggests com m on bile duct obstruction.



Plain radiographs: o

Not helpful in diagnosing uncom plicated cholelithiasis

o

Exclude intestinal perforation or intestinal obstruction

o

Up to 20% of gallstones radiopaque

o

Reveal rare com plications such as air in gallbladder wall in em physem atous cholecystitis or air-filled gallbladder in biliary-enteric fistula



CT scanning: o

Less sensitive than ultrasound to detect gallstones

o

Most useful to exclude other causes of upper abdom inal pain such as aortic aneurysm , perihepatic abscess, or pancreatic pseudocyst

Differential Diagnosis 

Myocardial infarction



Abdom inal aortic aneurysm



Acute cholecystitis, cholangitis, or choledocholithiasis

Pa ge 1 1 2



Renal colic or pyelonephritis



Duodenal ulcer perforation



Acute pancreatitis



Intestinal obstruction



Peptic ulcer disease, gastritis, or gastroesophageal reflux



Right lower lobe pneum onia, pleurisy, or pulm onary infarction



Hepatitis or hepatic abscess



Fitz-Hugh and Curtis syndrom e

P.231

Treatment Initial Stabilization IV access

ED Treatment 

IV hydration with 0.9% norm al saline (NS) if vom iting



NPO



Parenteral nonsteroidal anti-inflam m atory drugs (NSAIDs; ketorolac) m ay lessen biliary spasm , but m ay exacerbate peptic causes of pain.



Narcotic analgesics (m eperidine) with antiem etic (prom ethazine): o

Adm inister for refractory pain once diagnosis is reasonably established.

o

Morphine sulfate m ay lead to spasm at sphincter of Oddi (clinical significance not well established).



Anticholinergics (glycopyrrolate) com m only used despite

Pa ge 1 1 2

lack of clinical trials proving benefit

Medication (Drugs) 

Glycopyrrolate (anticholinergic): acutely, 0.2 m g intravenous push (IVP) q10m in up to 3 doses until pain relieved, 2 m g PO t.i.d. for recurrent colic



Ketorolac: 60 m g IM or 30 m g (peds: start 0.5 m g/kg for first dose up to 1 m g/kg/24h) IV q6h. In elderly: 30 m g IM or 15 m g IV



Meperidine: 0.5 m g/kg intravenous push (IVP) titrated to pain relief up to 2.0 m g/kg IV



Morphine sulfate: 2â€“5 m g IV titrated to pain relief



Prom ethazine: 12.5â€“25 m g (1â€“2 m g/kg/25h) intravenous push (IVP) q4h to q6h

Follow-Up Disposition Admission Criteria Adm ission and surgical or gastroenterologic consultation for evidence of: 

Acute cholecystitis



Acute cholangitis



Com m on duct obstruction



Gallstone pancreatitis

Discharge Criteria 

Lack of clinical, laboratory, or radiographic evidence of cholecystitis, cholangitis, com m on duct obstruction, or pancreatitis

Pa ge 1 1 2



Resolution of all pain and tenderness



Ability to tolerate oral fluids

Issues for Referral General Surgery referral for all cases of biliary colic with docum ented cholelithiasis

References 1. Ahrendt SA, Pitt HA. Biliary tract: calculous biliary disease. In: Townsend CM Jr, ed. Sabiston Textbook of Surgery. 17th ed. Philadelphia: WB Saunders; 2004:1597â€“1642. 2. Elta GH. Motility and dysm otility of the biliary tract and sphincter of Oddi. In: Feldm an, M. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002: 1043â€“1050. 3. Ko CW, Sekijim a JH, Lee SP. Biliary sludge. Ann Intern Med. 1999;130:301â€“311. 4. Moscati RM. Cholelithiasis, cholecystitis and pancreatitis. Em erg Med Clin North Am . 1996;14:719â€“737. 5. Silen W. The colics. In: Silen W, ed. Cope's Early Diagnosis of the Acute Abdom en. 20th ed. Oxford, UK: Oxford University Press; 2000:142â€“149.

Miscellaneous SEE ALSO: Cholangitis; Cholelithiasis

Codes ICD9-CM 572.4

ICD10 K80.2

Pa ge 1 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hro nic Obstructive Pulm o nary Disease

Chronic

Obstructive Pulmonary Disease Adam Z. Barkin

Basics Description 

A disease characterized by airflow obstruction due to several processes: o

Em physem a: irreversible alveolar destruction with loss of airway elastic recoil

o

Chronic bronchitis: airway inflam m ation without alveolar destruction

o

Reactive airway disease: reversible bronchospasm , m ucous plugging, and m ucosal edem a



Chronic obstructive pulm onary disease (COPD) affects about 15 m illion people in the United States.

Genetics Î± 1 -antitrypsin deficiency

Etiology 

Sm oking is the overwhelm ing cause: o



COPD develops in 15% of sm okers.

Air pollution

Pa ge 1 1 2



Airway hyperresponsiveness



Î± 1 -Antitrypsin deficiency



Acute exacerbations: o

Viral or bacterial infections

o

Pollutants

Diagnosis Signs and Symptoms History 

Dyspnea on exertion



Cough



Sputum production



Fatigue



Wheezing



Orthopnea



Altered m ental status



Carbon dioxide narcosis

Physical Exam 

Wheezing



Retractions



Poor air m ovem ent



Cyanosis



Prolonged expiratory phase



Barrell chest



Lower extrem ity edem a



Jugular venous distension



S3 and S4 gallops

Tests

Pa ge 1 1 2

Lab 

CBC: o

Elevated hem atocrit m ay indicate chronic hypoxem ia.

o

Increased neutrophils and elevated WBC m ay indicate infection.





Arterial blood gas: o

Retaining carbon dioxide

o

Acidosis

o

Oxygenation

Beta natriuretic peptide: o

Differentiate between COPD and congestive heart failure (CHF)



Sputum sam ple



Theophylline level as needed

Imaging 

Chest radiography: o



Pneum othorax, pneum onia, CHF, lobar collapse

Chest CAT scan: o

When needed to evaluate for pulm onary em bolus or further characterize disease

Diagnostic Procedures/Surgery 

Pulse oxim etry



ECG



Pulm onary function tests



Echocardiography: o

To diagnose left or right ventricular failure or strain

Differential Diagnosis 

Pneum othorax



CHF



Pneum onia

Pa ge 1 1 2



Pulm onary em bolus



Upper airway obstruction



Asthm a



Restrictive lung disease



Acute respiratory distress syndrom e



Pleural effusions



Acute coronary syndrom e



Pericardial effusion



Metabolic derangem ent

Treatment Pre Hospital 



Supplem ental oxygenation: o

100% via nonrebreather

o

Do not withhold for fear of CO 2 retention.

Initiate nebulized bronchodilator therapy.

Initial Stabilization 

Oxygen therapy: o

Maintain oxygen saturation >90â€“92%.

o

Patients at risk for CO 2 narcosis are those with slow respiratory rate.

o

Monitor closely for ventilation suppression.

P.233





Noninvasive ventilation: o

May prevent intubation

o

May help resolve hypercarbia

Intubation for airway control:

Pa ge 1 1 2

o

Indicated if clinical tiring, altered m ental status, or the inability to com ply with em ergent therapy

o

Ineffective ventilation

o

CO 2 narcosis

ED Treatment 

Continuous ECG and pulse oxim etry m onitoring



Bronchodilator therapy o

Î²-agonists: 

o

Anticholinergics: 





o

Anti-inflam m atory effects

o

Reduce relapses

o

Methylprednisolone or prednisone

Antibiotics: Fever, increased sputum production and/or dyspnea

Methylxanthines: o



Ipratropium brom ide

Corticosteroids:

o 

Albuterol

Controversial

Ventilator settings: o

Allow sufficient expiratory tim e to m inim ize air trapping and subsequent barotraum a.

o

Perm issive hypercapnia

Medication (Drugs) 

Albuterol: 2.5 m g nebulized q10â€“30m in



Azithrom ycin: 500 m g PO/IV once then 250 m g PO per day for 4 days



Ceftriaxone: 1 g IV q24h



Ipratropium brom ide: 0.5 m g nebulized q6h

Pa ge 1 1 2



Levofloxacin: 500 m g PO/IV q24h



Methylprednisolone: 125 m g IV q6h



Prednisone: 40â€“60 (1â€“2 m g/kg) m g PO per day for 5 days



Terbutaline: 0.25 m g SC q30m in

Follow-Up Disposition Admission Criteria 



Intensive care unit adm ission: o

Intubated patients

o

CO 2 narcosis with oxygen saturation <90%

o

Clinical tiring in the ED

o

Severe acidosis

o

Concom itant cardiac or pulm onary disease

o

Acute coronary syndrom e

o

Arrhythm ia

o

CHF

o

Pulm onary em bolism

Regular hospital bed: o

COPD patients with an additional pulm onary insult: 

Pneum onia



Lobar collapse



Increased work of breathing



Exercise intolerance



Failure to im prove in ED



Failed outpatient treatm ent

Discharge Criteria 

Mild flare

Pa ge 1 1 2



Resolution in ED



Am bulatory oxygen saturation >92%

References 1. Mandavia DP, Dailey RH. Chronic obstructive pulm onary disease. In: Marx J, et al. (eds). Rosen's em ergency m edicine: Concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby; 2002: 956â€“969. 2. McCullough PA, Hollander JE, Nowak RM, et al. Uncovering heart failure in patients with a history of pulm onary disease: Rationale for the early use of B-type natriuretic peptide in the Em ergency Departm ent. Acad Em erg Med. 2003;10:198â€“204. 3. Wouters EFM. Managem ent of severe COPD. Lancet. 2004;364:883â€“895. 4. Sutherland ER, Cherniack RM. Managem ent of chronic obstructive pulm onary disease. New Eng J Med. 2004;350:2689â€“2697.

Miscellaneous SEE ALSO: Asthm a; Congestive Heart Failure; Dyspnea; Pulm onary Em bolism

Codes ICD9-CM 491.2

ICD10 J44.9

Pa ge 1 1 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C irrho sis

Cirrhosis

Paul Allegretti

Basics Description 

Progressive process of inflam m ation, cellular injury and necrosis, diffuse fibrosis, and form ation of regenerative nodules



Loss of lobular and vascular architecture



Irreversible in advanced stages



Intrahepatic portal hypertension owing to increased resistance at the sinusoid, com pression of the central veins, and anastom osis between the arterial and portal system s



Markedly reduced life expectancy



Tenth leading cause of death in the United States

Etiology 

Chronic alcohol abuse (m ost com m on cause in U.S.)



Chronic viral hepatitis, B or C (second m ost com m on cause in U.S.)



Autoim m une hepatitis



Biliary cirrhosis, prim ary (PBC) or secondary (sclerosing cholangitis)



Metabolic:

Pa ge 1 1 3





o

Hereditary hem ochrom atosis

o

Wilson disease

o

Porphyria

Drugs: o

Acetam inophen

o

Methotrexate

o

Am iodarone

o

Methyldopa

Hepatic congestion: o

Right-sided heart failure

o

Pericarditis

o

Budd-Chiari syndrom e (hepatic venous outflow obstruction)



Infiltrative: o

Sarcoidosis

o

Am yloidosis

o

Nonalcoholic steatohepatitis (NASH)



Hepatocellular carcinom a, diffusely infiltrating



Infections: o

Brucellosis

o

Echinococcosis

o

Tertiary syphilis

o

Schistosom iasis

Pediatric Considerations 

Congenital



Arteriohepatic dysplasia, biliary atresia, cystic fibosis, Î± 1 -antitrypsin deficiency



Metabolic



Fructosem ia, tyrosinem ia, galactosem ia, glycogen storage diseases



Infectious



Congenital hepatitis B

Pa ge 1 1 3

Diagnosis Signs and Symptoms 

May be silent



Insidious onset with nonspecific findings: o

Malaise

o

Fatigue

o

Anorexia

o

Nausea and vom iting

o

Weight loss

o

Pruritus

o

Hyperpigm entation



Jaundice



Fetor hepaticus



Asterixis



Hypotension



Cruveilhier-Baum gartnen m urm ur



Renal insufficiency



Spider telangiectasias



Palm ar erythem a



Dupuytren contractures



Parotid and lacrim al gland enlargem ent



Nail changes



Terry nails



Muehrcke lines



Clubbing



Fem inization: o

Testicular atrophy

o

Im potence

o

Loss of libido

Pa ge 1 1 3

o

Gynecom astia



Ascites



Am enorrhea



Abdom inal collateral circulation including caput m edusae



Hepatom egaly



Splenom egaly



Abdom inal discom fort or tenderness



Fever



Com plications



When com plications develop, patient is considered to have decom pensated disease: o

Ascites

o

Spontaneous bacterial peritonitis (SBP)

o

Hepatic encephalopathyâ€”m ay be precipitated by:

o



GI bleed



Infections



Increased dietary protein



Hypokalem ia



Sedatives



Constipation



Azotem ia



Alkalosis

Variceal hem orrhage: 

One third of patients with varicies bleed.



Each bleeding episode carries a 33% m ortality rate.



Hepatic venous pressure gradient >12 m m Hg increases risk of bleed.

o

Portal hypertensive gastropathy or peptic ulcer disease

o

Hepatorenal failure: 

Caused by decreased renal perfusion during

Pa ge 1 1 3

severe decom pensated cirrhosis 

May be iatrogenic: secondary to diuretics, nonsteroidal anti-inflam m atory drugs (NSAIDs), IV contrast, am inoglycosides, large-volum e paracentesis

 o

High m ortality rate

Hepatopulm onary syndrom e: 

Intrapulm onary vascular dilation and hypoxia



Results in increased alveolar-arterial gradient

Essential Workup Detailed historical and physical exam search for clues to liver disease

Tests Lab 



CBC: o

Anem ia

o

Macrocytosis

o

Leukopenia and neutropenia

o

Throm bocytopenia

Im paired liver function: o

High bilirubin

o

Low album in

o

High globulins

o

Prolonged prothrom bin tim e

o

Varying degrees of dissem inated intravascular coagulation (DIC)

o 

Hypoglycem ia

Increased liver enzym es: o

Aspartate alanine am inotransferase (AST, SGOT), alanine am inotransferase (ALT, SGPT)â€” reflect injury

o

Ratio of AST:ALT â‰¥2.0 in alcoholic liver disease

Pa ge 1 1 3

o

Alkaline phosphatase and 5â€²-nucleotidase reflect cholestasis.

o

Gam m a-glutam yltranspeptidase (GGT)

o

May be norm al in inactive cirrhosis



Electrolytes, BUN, and creatinine



Hyponatrem ia: o



Renal dysfunction and hepatorenal syndrom e

Arterial blood gases or pulse oxim eter for: o

Suspected pneum onia

o

Congestive heart failure

o

Hepatopulm onary syndrom e

P.235



Search for cause: o

Hepatitis B surface antigen

o

Hepatitis C antibody

o

Antinuclear antibody (ANA) and anti-sm ooth m uscle antibody (autoim m une hepatitis)

o

Antim itochondrial antibody (prim ary biliary cirrhosis)

o

Serum iron, transferrin saturation, and ferritin (hem ochrom atosis)

o

Ceruloplasm in (Wilson disease)

o

Î± 1 -Antitrypsin deficiency

o

Serum im m une electrophoresis (high im m unoglobulin M [IgM] in PBC)

o

Cholesterol (chronic cholestasis)

o

Alpha fetoprotein (hepatocellular cancer)

Imaging 

Ultrasound for liver architecture, biliary obstruction, ascites, portal vein throm bosis, splenom egaly



CT scan to explore abnorm al finding on ultrasound

Pa ge 1 1 3



MRI role unclear and lim ited



Chest radiograph for pleural effusion, cardiom egaly, and congestive heart failure (CHF)

Diagnostic Procedures/Surgery 

Esophagogastroduodenoscopy (EGD) indicated for upper GI bleeding or variceal surveillance



Variceal ligation or endoscopic sclerotherapy



Cholangiogram for suspected biliary obstruction



Liver biopsy to confirm diagnosis



TIPS (transjugular intrahepatic portal system ic shunt)

Differential Diagnosis 





Ascites: o

Increased right heart pressure

o

Hepatic vein throm bosis

o

Peritoneal m alignancy/infection

o

Pancreatic disease

o

Thyroid disease

o

Lym phatic obstruction

Upper GI bleeding: o

Peptic ulcer disease (PUD)

o

Gastritis

Encephalopathy: o

Metabolic

o

Toxic

o

Intracranial process

Treatment Pre Hospital 

Naloxone, dextrose (or Accu-Chek), and thiam ine for

Pa ge 1 1 3

altered m ental status 

Reverse hypotension with IV fluids to prevent acute ischem ic hepatic injury.

Initial Stabilization Treat com plications such as GI bleeding or hepatic encephalopathy.

ED Treatment 

For suspected variceal bleed: o

IV octreotideâ€”analog of som atostatin (splanchnic vasoconstrictor)

o

IV vasopressin with sim ultaneous nitroglycerin has been used, but has high com plication rate. 

Nitroglycerin decreases vasoconstriction of vasopressin.

o

Reverse coagulopathy: 

Fresh-frozen plasm a 1 IU/h until bleeding is controlled



Desm opressin (DDAVP)â€”im proves bleeding tim e and prolonged partial throm boplastin tim e

o

Balloon tam ponade with Sengstaken-Blakem ore tube or a variant for variceal com pression (rarely used anym ore, prophylactic intubation recom m ended)

o 

Em ergent endoscopic sclerotherapy

Initiate broad-spectrum antibiotics in suspected sepsis or spontaneous bacterial peritonitis (SBP):



o

Cefotaxim e

o

Ticarcillin-clavulanate

o

Piperacillin-tazobactam

o

Am picillin-sulbactam

Treat com plicating conditions such as ascites, hepatic encephalopathy, SBP.



Treat pruritus with:

Pa ge 1 1 3

o

Diphenhydram ine 25â€“50 m g IM/IV q4h

o

Cholestyram ine, ursodeoxycholic acid, or rifam pin

o

Naloxone infusion 0.2 Âµg/kg/m in for tem porary relief for extrem e cases



For prolonged PT, adm inister vitam in K, 10 m g PO daily for 3 days.



Relieve biliary obstruction (e.g., stricture) by endoscopic, radiologic, or surgical m eans.



Provide nutritious diet; high in calories and adequate in protein (1 g/kg), unless there is com plicating hepatic encephalopathy (HE)



Beta-blocker (propranolol) for large esophageal varices: o

Titrated to pulse rate of 60 or 25% reduction of resting pulse



o

With or without isosorbide dinitrate

o

Decreases rebleeeding rate

o

May delay or prevent occurrence of first bleed

Consult transplantation coordinator whenever post-liver transplantation patient presents to the ED with liver dysfunction, suspected sepsis, or possible treatm ent-related com plication.

Specific Therapy 

Hem ochrom atosis: phlebotom y or deferoxam ine (iron-chelating agent)



Autoim m une hepatitis: prednisone with or without azathioprine



Chronic hepatitis B or C: alpha interferon (avoid in decom pensated cirrhosis)



Prim ary biliary cirrhosis: ursodeoxycholic acid



Wilson disease: penicillam ine



The only cure for m ost advanced cirrhosis is liver transplantation.

Pa ge 1 1 3

Medication (Drugs) 

Azathioprine: 1â€“2 m g/kg PO



Cefotaxim e: 1â€“2 g q6hâ€“q8h (peds: 50â€“180 m g/kg/d q6h) IV



Cholestyram ine: 4 g PO one to six tim es per day



Desm opressin (DDAVP): 0.3 Âµg/kg in 50-m L saline infused over 15â€“30 m inutes



Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2â€“4 m L/kg) IV



Naloxone (Narcan): 0.2â€“2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Octreotide: 25â€“50 Âµg IV bolus followed by 50 Âµg/hr IV infusion



Piperacillin-tazobactam : 3.375 g IV q6h (peds: 100â€“400 m g/kg/d divided q6hâ€“q8h; renal dosing required)



Prednisone: 40 m g (peds: 1â€“2 m g/kg) PO daily



Propranolol: 40 (initial) to 240 m g (peds: 1â€“5 m g/kg/d) PO t.i.d.



Rifam pin: 600 m g (peds: 10â€“20 m g/kg) PO daily



Thiam ine: 100 m g (peds: 50 m g) IV or IM



Ursodeoxycholic acid: 8â€“10 m g/kg/d t.i.d.

Follow-Up Disposition Admission Criteria 

Acute decom pensation or com plicating conditions



First presentation with clinically evident cirrhosis, unless

Pa ge 1 1 4

close outpatient workup is possible 

Advanced grades hepatic encephalopathy, sepsis, active GI bleed, and hepatorenal and hepatopulm onary syndrom es require ICU.

Discharge Criteria Most patients with com pensated cirrhosis can be treated as outpatients.

References 1. Braunwald E, et al. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw-Hill; 2001. 2. Feldm an M. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002. 3. Goldberg, E. Diagnostic Approach to the Patient With Cirrhosis. Wellesley, MA: UpToDate; 2004. 4. Goldberg, E. Overview of Com plications, Prognosis, and Managem ent of Cirrhosis. Wellesley, MA: UpToDate; 2004. 5. Runyon BA. Treatm ent of patients with cirrhosis and ascites. Sem in Liver Dis. 1997;17:249. 6. Sanyal A. Prim ary Prophylaxis against Variceal Hem orrhage in Patients with Cirrhosis. Wellesley, MA: UpToDate; 2004.

Miscellaneous SEE ALSO: Ascites, Varices; Hepatic Encephalopathy; Hepatitis; Spontaneous Bacterial Peritonitis

Codes ICD9-CM 571.5

Pa ge 1 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C lavicle F racture

Clavicle Fracture

Sean Patrick Nordt Jeffrey Manko

Basics Description 

Clavicle fractures account for 5% of all fractures in all age groups



80% of clavicle fractures involve the m iddle third



15% occur in the distal third



5% occur in the m edial third

Classification 

Group I: m iddle-third fractures



Group II: distal-third fractures: o

Type I: coracoclavicular ligam ents are intact (nondisplaced).

o

Type II: severing of the coracoclavicular ligam ents (conoid)

o

Type III: articular surface involvem ent of the acrom ioclavicular joint



Group III: m edial (proxim al)-third fractures

Etiology Mechanism

Pa ge 1 1 4



Direct traum a to the clavicle



Fall on the lateral shoulder



Fall on the outstretched hand

Pediatric Considerations 

Most com m on of all pediatric fractures



May occur in newborns secondary to birth traum a

Diagnosis Signs and Symptoms History 

Local pain, tenderness, and swelling over the fracture site



Crepitus is often present owing to the clavicle's subcutaneous position



Arm held in adduction against the chest wall with resistance to m otion



Shoulder displaced anteriorly and inferiorly

Physical Exam 

Palpate the clavicle for tenderness, crepitus, and swelling.



Exam ine the hum erus and shoulder joint for other fractures, dislocations, or subluxations.



Determ ine whether the fracture is open or closed.



Evaluate for associated injuries (often serious and life threatening) that m ust be excluded: o

Skeletal injuries: 

First rib fracture with underlying aortic injury



Sternoclavicular joint separation/fracture-dislocation



Acrom ioclavicular joint separation/fracture-dislocation

Pa ge 1 1 4



Cervical spine injuries

Tests Imaging 

AP radiographs of both clavicles are m andatory and m ust include:



o

Upper third of the hum erus

o

Shoulder girdle (rule out other fractures)

o

Upper lung fields (rule out pneum othorax)

Oblique and apical lordotic views: o

May be helpful, especially for m edial and distal clavicle fractures that are not easily visualized on the AP view



Stress views (weight-bearing) for distal clavicle fractures are no longer routinely recom m ended.



Angiography: o

Should be perform ed if there is any evidence or suspicion of vascular injuries (m ost com m only subclavian vessels)

Differential Diagnosis 

Distal fractures: Consider acrom ioclavicular separation.



Medial fractures: Consider sternoclavicular separation.



Shoulder fracture-dislocation

Treatment Pre Hospital 

Ice packs to affected area



Pain m anagem ent using either narcotics or NSAIDs



Im m obilize affected side in a sling.

Pa ge 1 1 4

Initial Stabilization Airway m anagem ent and resuscitate as indicated

ED Treatment 

Open fracture: uncom m on occurrence, but usually requires open dÃ©bridem ent and internal fixation (obtain im m ediate orthopaedic referral)



Closed fracture: if severely displaced, attem pt closed reduction and im m obilize depending on type of fracture: o

Middle third: 

If nondisplaced, a sling or shoulder im m obilizer is enough to provide support



Controversy exists as to whether closed reduction is necessary because the alignm ent is rarely m aintained regardless of splinting technique.



To perform a closed reduction, 1% lidocaine should be injected into the fracture hem atom a. The shoulders are pulled upward, outward, and backward, and the fracture is then m anipulated into place.



Sedation m ay be given to alleviate pain or anxiety.

o



A figure-of-eight splint is then applied.



Ice should be applied for the first 24 hours.



Analgesia (narcotics or NSAIDs) for pain

Distal third type I: 

Ice for the first 24 hours.



Im m obilization with a sling or shoulder im m obilizer.



Orthopaedic referral



Analgesia (narcotics or NSAIDs) for pain

Pa ge 1 1 4



Early range of m otion

P.237

o

Distal third type II: 

Ice for the first 24 hours.



Im m obilization with a sling or shoulder im m obilizer.



Orthopaedic referral (m ay require operative repair)



Analgesia (narcotics or NSAIDs) for pain

o

Distal third type III: sam e as type II

o

Medial (proxim al) third: 

Ice for the first 24 hours.



Im m obilization in a sling or shoulder im m obilizer for support





Analgesia (narcotics or NSAIDs) for pain



Orthopaedic follow-up

Reassess neurovascular status after all splints are applied.

Pediatric Considerations 

Children who do not cooperate with the figure-of-eight splint should be referred to an orthopaedic surgeon for possible shoulder spica placem ent.



Most children will tolerate a shoulder im m obilizer best.

Medication (Drugs) 

Acetam inophen: 500â€“1,000 m g PO q6h PRN, (peds: 15â€“20 m g/kg PO q6h PRN)



Ibuprofen: 600â€“800 m g PO q6h PRN with m eals, (peds: 5â€“10 m g/kg PO q6h PRN)

Pa ge 1 1 4

Follow-Up Disposition Admission Criteria 

Open fracture



Associated injuries that are potentially life threatening

Discharge Criteria 

Isolated closed clavicle fracture without other injuries



Appropriate support services at hom e (especially for elderly patients)



Orthopaedic follow-up



Adequate pain m anagem ent

Issues for Referral Open fracture, com plex injury, signs of neurovascular injury require im m ediate orthopaedic referral.

References 1. Anderson K. Evaluation and treatm ent of distal clavicle fractures. Clin Sports Med. 2003;22:319â€“326. 2. Eiff MP. Managem ent of clavicle fractures. Am Fam Physician. 1997;55:12â€“128. 3. Heckm an J, Bucholz R. Rockwood and Green's fractures in adults. 5th ed. Philadelphia: Lippincott William s & Wilkins, 2001. 4. Post M. Current concepts in the treatm ent of fractures of the clavicle. Clin Orthop. 1989;245:89â€“101. 5. Sim on RR, Koenignsknecht SJ. Em ergency orthopedics: the extrem ities. 4th ed. McGraw-Hill.

Codes

Pa ge 1 1 4

ICD9-CM 810.00

ICD10 S42.0

Pa ge 1 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o caine, Po iso ning

Cocaine,

Poisoning Steven Aks

Basics Description 

Sym pathom im etic



Inhibits neurotransm itter reuptake at the nerve term inal



Metabolism : o

Hepatic degradation

o

Nonenzym atic hydrolysis

o

Cholinesterase m etabolism

Etiology 

IV, nasal, oral adm inistration of cocaine



Oral ingestion: o

Body stuffers: 

Ingest hastily wrapped packets in attem pt to evade police

o

Body packers: 

Ingest cocaine packets to sm uggle the drug using couriersâ€™ oral, rectal, and vaginal cavities



Cocaine is wrapped carefully in packets

Pa ge 1 1 4

containing large am ounts of drug.

Diagnosis Signs and Symptoms 

Sym pathom im etic toxidrom e



Cardiovascular:



o

Hypertension

o

Tachycardia

o

Chest pain (angina)

Respiratory: o

Tachypnea

o

Pleuritic chest pain:

o 





Pneum om ediastinum



Pneum othorax



Bronchitis



Pulm onary infarction

Cough

Central nervous system (CNS): o

Agitation

o

Trem ulousness

o

Com a

o

Seizures

o

Stroke

Miscellaneous: o

Hypertherm ia (poor prognosis)

o

Lim b ischem ia (inadvertent intra-arterial injection)

o

Corneal ulcerations (heavy crack sm okers): 

Owing to local chem ical and therm al irritation that disrupts corneal epithelium

o

Rhabdom yolysis

Pa ge 1 1 5

Essential Workup 

Recognition of the sym pathom im etic toxidrom e caused by cocaine: o



Distinguish from anticholinergic toxidrom e.

Toxidrom e recognition: o

o

o

Sym pathom im etic: 

Heart rate (tachycardia)



Blood pressure (increased)



Moist skin



Bowel sounds present



Tem perature (increased)



No urinary retention

Anticholinergic: 

Heart rate (tachycardia)



Blood pressure (increased)



Dry skin



Bowel sounds dim inished



Tem perature (increased)



Urinary retention present

History of route of drug ingestion: 

If oral ingestion, inquire how the packets were wrapped to determ ine leakage potential.

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose



Urinalysis dip for m yoglobin



Cardiac enzym es (troponin, creatine phosphokinase) for:



o

Anginal chest pain

o

Abnorm al results on ECG

Creatine phosphokinase (CPK) for evidence of

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m yoglobinuria

Imaging 

ECG: o

For anginal chest pain

o

Consider possibility of m yocardial infarction with cocaine-related chest pain.



Chest radiograph: o

For chest pain or shortness of breath

o

Check for pneum om ediastinum , pneum othorax, aortic rupture.



Abdom inal radiograph: o

For body packers/stuffers

o

Usually produces negative result for stuffers because drug is loosely packed in cellophane

o

Positive for packers because drug is densely packed and usually radiopaque



CT of the abdom en with contrast: o

When unreliable history of body packers/stuffers and negative on abdom inal frontal radiograph



CT brain scan: o

For altered m ental status or severe headache

o

Detects cerebral ischem ia or hem orrhage

Differential Diagnosis 

Other agents with sym pathom im etic effects



Theophylline



Caffeine



Am phetam ines



Albuterol



Tricyclic antidepressants



Antihistam ines



Phencyclidine (PCP)

Pa ge 1 1 5



Thyrotoxicosis



Neuroleptic m alignant syndrom e



Hallucinogens

Treatment Pre Hospital 

Cautions o

Establish IV access

o

Cardiac m onitor 

Chest pain m ay be ischem ic



Benzodiazepine therapy to control agitation



When drug is used as a â€œspeedballâ€• (com bination of heroin and cocaine), adm inister naloxone in increm ents to reverse com a

Initial Stabilization 

Check airway, breathing, and circulation (ABCs).



Establish IV access.



Establish cardiac m onitor.



Provide therapy with naloxone (Narcan), thiam ine, dextrose (or Accu-Check) for altered m ental status.

P.239

ED Treatment 

Supportive care for m ildly sym ptom atic patients



Benzodiazepines:



o

For agitation and trem or

o

Initial agents for hypertension and tachycardia

Cooling m easures for hypertherm ia:

Pa ge 1 1 5

o 



Evaporative-convective m ethod

Treat rhabdom yolysis: o

Hydrate with 0.9% norm al saline (NS)

o

Alkalinization with IV bicarbonate in severe cases

Cardiac chest pain: o

Aspirin

o

Nitrates

o

Oxygen

o

Opiates

o

Avoid Î²-blockers because of unopposed Î±-stim ulation

o

Angiography/angioplasty/throm bolysis for acute m yocardial infarction



Hypertension/tachycardia: o

Benzodiazepine initial agent

o

Use Î±-blocking agent (phentolam ine) as sole agent or com bine with Î²-blocker (propranolol, esm olol) if unresponsive to benzodiazepine. 

Use labetalol cautiously (does not have equal Î±- and Î²-blocking properties).

o

IV nitroglycerin/nitroprusside for severe unresponsive hypertension



Body packer/stuffers: o

Treat asym ptom atic or m inim ally sym ptom atic body packers and body stuffers: 

Oral activated charcoal



Whole-bowel irrigation with polyethylene glycol-electrolyte lavage solution

o

Consult with surgeons about sym ptom atic body packers and stuffers: 

If toxicity is not easily m anaged with previously suggested pharm acologic therapy, rem ove the

Pa ge 1 1 5

drug packets intraoperatively.

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Dextrose: D 5 0 W 1 am pule (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam : 5 m g increm ental doses IV



Esm olol: 50â€“200 Âµg/kg/m in IV infusion titrated to effect



Lorazepam : 2 m g increm ental doses IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg up to 2 m g) IV or IM initial dose



Nitroglycerin: 10â€“100 Âµg/m in IV infusion



Nitroprusside: 0.3 Âµg/kg/m in IV (titrate to effect up to 10 Âµg/kg/m in)



Phentolam ine: 5 m g IV q15â€“24m in (titrate to clinical effect)



Polyethylene glycol (GoLYTELY): 4 L PO over 4 hours until com plete bowel evacuation

Follow-Up Disposition Admission Criteria 

Altered m ental status



Abnorm al vital signs: Heart rate >100 beats per m inute, diastolic blood pressure >120 m m Hg, or hypotension



Hypertherm ia



Cocaine-induced m yocardial ischem ia

Pa ge 1 1 5



Body stuffers and body packers



Intensive care unit adm ission for m oderate to severe toxicity

Discharge Criteria 

Mental status and vital signs norm al after 6 hours of observation



Body packers or stuffers with confirm ed expulsion of packets and no clinical signs of toxicity.

References 1. Hollander JE. The m anagem ent of cocaine-associated m yocardial ischem ia. N Engl J Med. 1995;33:1267. 2. Hollander JE, Hoffm an RS. Cocaine. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. 6th ed. Stam ford, CT: Appleton & Lange; 1998: 1071â€“1089. 3. June R, Aks S, Keys N, et al. Medical outcom e of cocaine bodystuffers. J Em erg Med. 2000;18:221â€“224. 4. Lange RA, Hillis LD. Cardiovascular com plications of cocaine use. N Engl J Med. 2001;345:351â€“358.

Codes ICD9-CM 968.5 Surface (topical) and infiltration anesthetics

ICD10 T40.5 Cocaine

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o lo n Traum a

Colon Trauma

Rebecca Apollon Blake Spirko

Basics Description 

Traum a that perforates the colon inflam es the cavity in which it lies.



Peritoneal inflam m ation from hollow viscus perforation often requires hours to develop.



Mesenteric tears from blunt traum a cause hem orrhage and bowel ischem ia.



Delayed perforation from ischem ic or necrotic bowel m ay occur.



Peritonitis and sepsis m ay develop from the extravasated intralum inal flora.



Ascending and descending colon segm ents are retroperitoneal.



The left colon has a higher bacterial load than the right.



Morbidity and m ortality increase if the diagnosis of colon injury is delayed.

Etiology 

Penetrating abdom inal traum a: o

The colon is the second m ost com m only injured organ

Pa ge 1 1 5

in penetrating traum a.



o

Gunshot wounds have the highest incidence.

o

Transverse colon is m ost com m only injured.

o

Often presents with peritonitis

Blunt abdom inal traum a: o

Colon rarely injured in blunt traum a

o

Burst injury occurs from com pression of a closed loop of bowel.

o

Intestine m ay be squeezed between a blunt object (lap belt) and vertebral colum n or bony pelvis.

o

Sudden deceleration m ay produce bowel-m esenteric disruption and consequent devascularization.

o

With deceleration, the sigm oid and transverse colon are m ost vulnerable.



Transanal injury: o

Iatrogenic endoscopic or barium enem a injury

o

Foreign bodies used during sexual activities m ay reach and injure the colon.

o

Com pressed air under high pressure such as at autom obile repair facilities can perforate the colon even if the com pressor nozzle is not inserted anally.



Swallowed sharp foreign bodies (toothpick) m ay penetrate the colon, particularly the cecum , appendix, and sigm oid: o

Most foreign bodies pass without com plications.

Pediatric Considerations Unlike adults, children have an equal frequency of blunt and penetrating colon injuries.

Diagnosis

Pa ge 1 1 5

Signs and Symptoms 

Colon traum a is generally associated with other intra-abdom inal and extra-abdom inal injuries, com m only to the sm all intestine.



Injuries of significant severity m ay have m inim al early findings.



It is uncom m on to determ ine specific organ injury on physical exam .



Assess on exam ination: o

Abdom en for peritoneal signs

o

Ecchym osis or hem atom a on lower abdom en from lap-belt com pression

o

Ecchym osis on epigastric region from steering-wheel com pression

o

Grey Turner sign (flank hem atom as) resulting from retroperitoneal bleeding.

o

Foreign bodies or blood on digital rectal exam ination (particularly in the presence of pelvic fracture).

o

Note: Abdom inal wall ecchym osis or hem atom a is not always present despite existing injury.

o

Note: Bowel sounds are not helpful.

Essential Workup 

Serial abdom inal exam ination because inflam m ation takes tim e to develop.



Abdom inal CT with contrast is the best diagnostic study in stable patients.



Ultrasound and diagnostic peritoneal lavage (DPL) are helpful in the potentially unstable patient.

Tests 

No individual test or com bination of currently available diagnostic m odalities is adequate to detect blunt colonic

Pa ge 1 1 5

injury. 

Signs of peritoneal irritation owing to intestinal injury typically develop hours after the event.

Imaging 

CT is m ore useful for detecting penetrating versus blunt colon injury.



CT with triple contrast allows intraperitoneal and retroperitoneal visualization.



Oral contrast is not essential in blunt abdom inal traum a CT evaluation.



Although CT m ay m iss colon injuries, abnorm al findings are typical.



CT is only m oderately sensitive at identifying hollow viscus injury.



Hollow viscus injury associated CT findings include extralum inal gas or contrast, m esenteric fat streaking, and free fluid without solid organ injury.



Water-soluble enem a with fluoroscopy is useful if other test results are inconclusive.



Plain abdom inal radiographs can show indirect signs such as intraperitoneal and retroperitoneal free air.



FAST ultrasound exam does not evaluate for enteric injury and retroperitoneal hem orrhage.



See Abdom inal Traum a, Blunt; Abdom inal Traum a, Im aging.

Diagnostic Procedures/Surgery 

DPL or ultrasound in addition to CT will increase sensitivity.



In blunt traum a, DPL will often not detect retroperitoneal injuries and enteric injury as intra-abdom inal bleeding is lim ited.

Pa ge 1 1 6



Fecal or vegetable m aterial on DPL analysis indicates hollow viscus injury.



Lavage white cell response m ay be negative secondary to delayed peritoneal inflam m ation.



In hollow viscus injury, lavage white blood cell count: red blood cell count ratio is higher than that seen with solid-organ injuries.

Differential Diagnosis 

Other intra-abdom inal injuries



A fractured pelvis m ay present sim ilarly to intraperitoneal injuries in children.

P.241

Treatment Pre Hospital 

Cautions: o

Follow standard prehospital guidelines for traum a treatm ent (airway, breathing, andcirculation [ABCs]).

o

Do not rem ove penetrating foreign bodies.

o

Do not attem pt to replace eviscerated bowel; cover with m oist saline dressings.

o

Obtain history regarding m echanism of injury, vehicular dam age, and seat belt use.



Controversies: o

Use of intravenous crystalloid resuscitation is still considered the standard of care.

Initial Stabilization

Pa ge 1 1 6



Refer to topic on Abdom inal Traum a.



ABCs should precede abdom inal evaluation.



Aggressive m anagem ent with intravenous crystalloid resuscitation and blood replacem ent as needed.

ED Treatment 

Early surgical consultation; surgery is definitive treatm ent.



Cover eviscerated bowel in m oist saline gauze, in a nondependent position.



Adm inister broad-spectrum antibiotics to cover gram -negative aerobic and anaerobic bacteria.



The efficacy of m ultiple-agent and single-agent antibiotic regim ens is sim ilar.



Ensure tetanus prophylaxis.

Medication (Drugs) 

Am picillin: 2 g (peds: 50 m g/kg) IV q6h plus gentam icin 2 m g/kg (peds: 2.5 m g/kg) IV q8h plus m etronidazole 500 m g IV q6h (peds: use clindam ycin 25â€“40 m g/kg IV q24h div. q6hâ€“q8h)



Aztreonam : 2 g IV q8h (peds: 90â€“120 m g/kg IV q24h div. q6hâ€“q8h) plus clindam ycin 900 m g IV q8h (peds: use clindam ycin 25â€“40 m g/kg IV q24h div. q6hâ€“q8h)



Cefoxitin: 2 g IV q8h (peds: 40 m g/kg IV q6h)



Piperacillin/tazobactam : 4.5 g (peds: 75 m g/kg) IV q8h

Follow-Up Disposition

Pa ge 1 1 6

Admission Criteria 

Colon injuries require adm ission for surgical repair.



All penetrating foreign bodies m ust be rem oved to prevent sepsis.



Patients with abdom inal ecchym osis require hospital adm ission and observation because of potential for undiagnosed hollow viscus injury.

Discharge Criteria 

Patients in whom serious abdom inal injury is not suspected and with com pletely norm al abdom inal exam ination, norm al hem odynam ic status, and no other injury m ay be considered for discharge with appropriate precautions.



If there is any doubt about the possibility of colon injury, the patient should be adm itted and observed.

References 1. ACEP Clinical Policies Com m ittee and Clinical Policies Subcom m ittee on Acute Blunt Abdom inal Traum a. Clinical policy: critical issues in the evaluation of adult patients presenting to the em ergency departm ent with acute blunt abdom inal traum a. Ann of Em erg Med. 2004;43:278â€“290. 2. Asbun H, Irani H, Roe EJ, et al. Intra-abdom inal seatbelt injury. J Traum a. 1990;30:189â€“193. 3. Carrillo EH, Som berg LB, Ceballos CE, et al. Blunt traum atic injuries to the colon and rectum . J Am Coll Surg. 1996;183:548â€“552. 4. Fealk M, Osipov R, Foster K, et al. The conundrum of traum atic colon injury. Am J Surg. 2004;188(6): 663â€“670. 5. Killeen KL, Shanm uganathanm K, Poletti PA, et al. Helical com puted tom ography of bowel and m esenteric injuries. J Traum a. 2001;51(1):26â€“36. 6. McCabe C, Warren R. Traum a: an annotated bibliography of the

Pa ge 1 1 6

literatureâ€”2001. Am J Em erg Med. 2002;20(4):352â€“366. 7. Stokes M, Jones D. ABC of colorectal diseases: colorectal traum a. Br Med J. 1992;305:303â€“306. 8. William s MD, Watts D, Fakhry S. Colon injury after blunt abdom inal traum a: results of the EAST Multi-Institutional Hollow Viscus Injury Study. J Traum a. 2003;55(5):906â€“912.

Codes ICD9-CM 863.40 Colon, unspecified site

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o m a

Coma

Gregory D. Jay Linda C. Cowell

Basics Description 

Light com a: o



Deep com a: o



Responds to noxious stim uli

Does not respond to pain

Unresponsiveness: o

Loss of either arousability or cognition: 

Loss of arousal



Arousal is prim arily a brain-stem function.



Im pairm ent of the reticular activating system



Loss of cognition



Requires dysfunction of both cerebral hem ispheres

o

o

Stupor: 

Deep sleep, although not unconsciousness



Exhibits little or no spontaneous activity



Awaken with stim uli



Little m otor or verbal activity once aroused

Obtundation:

Pa ge 1 1 6



Mental blunting with m ild or m oderate reduction in alertness

o

o

Delirium : 

Floridly abnorm al m ental status



Irritability



Motor restlessness



Transient hallucinations



Disorientation



Delusions

Clouding of consciousness: 

Disturbance of consciousness



Im paired capacity to:



think clearly



perceive, respond to, and rem em ber current stim uli

Etiology 

Diffuse brain dysfunction (69%): o

o

Lack of nutrients: 

Hypoglycem ia



Hypoxia

Poisoning: 

Ethanol



Isopropyl alcohol



Ethylene glycol



Methanol



Salicylates



Sedative-hypnotics



Narcotics



Anticonvulsants



Isoniazid



Heavy m etals



Opiates

Pa ge 1 1 6

o

o

o

o

o



Anticholinergics



Lithium



Phenylcyclidine



Cyanide



Carbon m onoxide

Infection: 

Bacterial/Tuberculous/Syphilitic m eningitis



Encephalitis



Falciparum m eningitis



Typhoid fever



Rabies

Endocrine disorders: 

Myxedem a com a



Thyrotoxicosis



Addison disease



Cushing disease



Pheochrom ocytom a

Metabolic disorders: 

Hepatic encephalopathy



Urem ia



Porphyria



Wernicke encephalopathy



Am inoacidem ia



Reye syndrom e



Hypercapnia

Electrolyte disorders: 

Hypernatrem ia, hyponatrem ia



Hypercalcem ia, hypocalcem ia



Hyperm agnesem ia, hypom agnesem ia



Hypophosphatem ia



Acidosis, alkalosis

Tem perature regulation:

Pa ge 1 1 6





Hypotherm ia



Heat stroke



Neuroleptic m alignant syndrom e



Malignant hypertherm ia

o

Urem ia

o

Postictal state, status epilepticus

o

Psychiatric

o

Shock

o

Fat em bolism

o

Hypertensive encephalopathy

Supratentorial lesions (19%): o

o

o

Hem orrhage (15%): 

Intraparenchym al hem orrhage



Epidural hem atom a



Subdural hem atom a



Subarachnoid hem orrhage

Infarction (2%): 

Throm botic arterial occlusion



Em bolic arterial occlusion



Venous occlusion

Tum or or abscess (2%): 

Hydrocephalus



Herniation



Hem orrhage from erosion into adjacent blood vessels



Subtentorial lesions (12%): o

Infraction

o

Hem orrhage

o

Tum or

o

Basilar m igraine

o

Brain-stem dem yelination

Pa ge 1 1 6

Diagnosis Signs and Symptoms History Ongoing disturbance of consciousness

Physical Exam 

No spontaneous eye opening



Lack of response to painful stim uli



No m otor activity



Regular cardiorespiratory function



Glasgow Com a Scale (GCS) scoring: o

o

Eye opening (E) 

Spontaneously: 4



To verbal com m and: 3



To pain: 2



No response: 1

Best m otor response (M) to verbal com m and 

o

o

Obeys: 6

Best m otor response to painful stim ulus 

Localizes to pain: 5



Withdraws to pain: 4



Flexionâ€”abnorm al: 3



Extensionâ€”abnorm al: 2



No response: 1

Best verbal response (V): 

Oriented and converses: 5



Disoriented and converses: 4



Verbalizes: 3



Vocalizes: 2



No response: 1

Pa ge 1 1 6

o 

GCS = E + M + V

Hypotherm ia: o

Infection, hypoglycem ia, m yxedem a com a, alcohol and sedative-hypnotic poisoning



Fever: o

Infection, thyrotoxicosis, anticholinergics, sym pathom im etics, neuroleptic m alignant syndrom e, hypothalam ic hem orrhage



Hypertension: o



Structural lesion, hypertensive encephalopathy

Hypotension: o

System ic disease

o

Sepsis should be highly considered

HEENT 

Mydriasis: o





Miosis: o

Narcotics

o

Anticholinergics

o

Pontine lesion

Loss of pupillary reflexes or unequal pupils: o



Organophosphates

Structural lesions

Evidence of head traum a: o

Contusions

o

Hem atom as

o

Lacerations

o

Hem otym panum

P.243



Neck: o

Nuchal rigidity

Pa ge 1 1 7

o

Meningitis

o

Subarachnoid hem orrhage

Neurologic 





Decorticate posturing: o

Flexion of elbows and wrists

o

Adduction and internal rotation of shoulders

o

Supination of the forearm s

o

Suggests severe dam age above the m idbrain

Decerebrate posturing: o

Extension of elbows and wrists

o

Adduction and internal rotation of shoulders

o

Pronation of the forearm s

o

Suggests dam age at the m idbrain or diencephalon

Asym m etric m ovem ents: o



Structural lesions

Persistent twitching of an extrem ity: o

Status epilepticus

Essential Workup 

Detect and treat reversible causes



Im m ediate exclusion of com alike states: o

Noting resistance to passive opening of eyelids, fluttering of eyelids when stroked, abrupt eyelid closure, eye m ovem ents by saccadic jerks (rather than roving), or finding the eyes rolled back

o

Provocation of nystagm us with ice-water caloric testing

o

Before paralyzing a patient for intubation, an attem pt should be m ade to detect a locked-in syndrom e.

o

Dem onstrating that the patient is able to blink on verbal com m and will establish this diagnosis.

o

Intubation is still indicated to prevent aspiration.

Pa ge 1 1 7

Tests Lab 

Dextrostix



CBC



Electrolytes

Imaging Head CT scan: 

Diagnosis of hem orrhage and m idline shift



CT angiography for suspected cerebrovascular accident

Diagnostic Procedures/Surgery 

Lum bar puncture: o

All patients with com a of unknown etiology, particularly if fever is present

o

Antibiotics m ay be adm inistered for as long as 68 hours before lum bar puncture.

o

CT scan should be perform ed before lum bar puncture if there is evidence of increased intracranial pressure, a m ass lesion, pre-existing traum a, or focal findings. 

Risk of tonsillar herniation in patients with a m ass lesion is very sm all.



Electroencephalography: o

Perform ed to rule out suspected seizure activities

o

Little use in the em ergency evaluation

o

Unlike electroencephalogram studies perform ed in a laboratory, lighting will cause artifacts.

Differential Diagnosis 

Locked-in syndrom e



Psychogenic unresponsiveness



Stupor

Pa ge 1 1 7



Catatonia



Akinetic m utism

Treatment Pre Hospital 

Airway m anagem ent if loss of airway patency



Endotracheal intubation if no response to com a cocktail



IV access



Dextrose or Dextrostix



Narcan



Monitor



Look for signs of an underlying cause: o

Medical alert bracelets

o

GCS

o

Pupils

o

Extrem ity m ovem ents

Initial Stabilization 

Airway m anagem ent



Em piric use of naloxone



Em piric dextrose: o

Adm inister if serum glucose cannot be m easured at the bedside

o

Can safely be adm inistered before thiam ine

o

Does not worsen outcom e in patients with stroke

ED Treatment 

Specific therapy directed at underlying cause once identified: o



Adm inister glucose, thiam ine, naloxone, flum azenil

Screen for drug overdose

Pa ge 1 1 7



CT scan



Consider em piric use of antibiotics for com a of undeterm ined etiology: o

Broad-spectrum with good cerebrospinal fluid penetration such as ceftriaxone



Adm inister m annitol if clinical or radiographic evidence of im pending herniation



Stop seizure activity with benzodiazepines, phenytoin, and phenobarbital.



Em piric treatm ent for a toxic ingestion: o

Activated charcoal

o

Fom epizole for suspected m ethanol or ethylene glycol ingestion



Spinal tap



Correct body tem perature: o

Aggressive rewarm ing for patients with core tem perature between 32â€“35Â°C and invasive rewarm ing for <32Â°C

o

Ice packs and forced air m ovem ent over exposed wetted skin if severe hypertherm ia

Medication (Drugs) 

Ceftriaxone: 100 m g/kg IV



Dextrose: 1â€“2 m L/kg of D 5 0 W IV; neonate: 10 m L/kg D 1 0 W IV; peds: 4 m L/kg D 2 5 W IV



Diazepam : 0.1â€“0.3 m g/kg slow IV (m ax: 10 m g/dose) q10â€“15m in Ã— 3 doses



Flum azenil: 0.20 m g IV every m inute Ã— 1â€“5 doses



Fom epizole: 15 m g/kg IV



Lorazepam : 0.05â€“0.1 m g/kg IV (m ax: 4 m g/dose q10â€“15m in)

Pa ge 1 1 7



Mannitol: 0.25â€“1.0 g/kg IV over 20 m inutes



Naloxone: 0.01 m g/kg IV/IM/SC/ET



Narcan: 0.4â€“2.0 m g IV/IM/SQ



Phenobarbital: 10â€“20 m g/kg IV



Phenytoin: 18â€“20 m g/kg IV/IO or fosphenytoin 15â€“20 m g/kg IV/IO



Physostigm ine: 0.06â€“0.08 m g/kg IV



Thiam ine: 100 m g IM or 100 m g thiam ine in 1,000 m L of IV fluid wide open

Follow-Up Disposition Admission Criteria All patients who do not have a readily identifiable and com pletely reversible cause should be adm itted.

Discharge Criteria Com atose patients with correctable hypoglycem ia and opiate toxicity who respond com pletely to aggressive ED treatm ent

References 1. Ellenhorn MJ, ed. Ellenhorn's m edical toxicology: diagnosis and treatm ent of hum an poisoning. Baltim ore, MD: William s & Wilkins, 1997:16â€“19. 2. Ferrera PC, Chan L. Initial m anagem ent of the patient with altered m ental status. Am Fam Physician. 1997;55(5):1773â€“1780. 3. Plum F, Posner J. The diagnosis of stupor and com a. 3rd ed. Philadelphia, PA: FA Davis, 1986. 4. Wolfe R, Brown D. Com a. In: Marx J, ed. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO:

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Mosby, 2002: 137â€“144.

Miscellaneous SEE ALSO: Altered Mental Status

Codes ICD9-CM 780.01

ICD10 R40.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o m partm ent Syndro m e

Compartment

Syndrome Chet Shermer

Basics Description 

Elevated tissue pressure in closed spaces that com prom ises blood flow through capillaries



Norm al tissue pressure is <10 m m Hg.



Capillary blood flow in a com partm ent is com prom ised at pressures >20 m m Hg.



Muscles and nerves can develop ischem ic necrosis at pressures >30 m m Hg.



When distal pulses are dim inished on exam , m uscle necrosis is probably present.



The four com partm ents of the leg are m ost frequently involved, but com partm ent syndrom e can occur in the arm , forearm , hand, foot, shoulder, buttocks, and thigh.

Etiology 

Decreased com partm ent size: circum ferential cast, burn eschar, or m ilitary antishock trousers (MAST)



Increased com partm ent contents: com pression of the com partm ent from edem a or hem atom a caused by direct

Pa ge 1 1 7

traum a, fracture, overexertion of m uscles, postischem ic tim e, or lim b com pression during prolonged recum bency

Diagnosis Alert 

Keep the extrem ity at the level of the heart to prom ote arterial flow but not dim inish venous return.



Do not use ice if com partm ent syndrom e is suspectedâ€”it m ay com prom ise m icrocirculation.

Signs and Symptoms 

Severe, constant pain over the com partm ent that is disproportionate to extent of injury



Pain increases with active contraction and passive stretching.



Muscle weakness



Hypesthesia



Six P's: pain, pressure, paresis, paresthesia, and pulses present

History 

Elicit above sym ptom s.



Six P's

Physical Exam 

Tenderness of m uscle com partm ent



Assess m otor and neurologic function.

Tests Imaging Radiographs should be perform ed if fracture is suspected.

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Diagnostic Procedures/Surgery 

Measurem ent of com partm ent pressures with a system such as the Stryker IC pressure m onitor system (Stryker Surgical, 420 East Alcott Street, Kalam azoo, MI 49001), using an 18-gauge needle or continuous pressure m onitoring with the attachm ent for an indwelling catheter



Technique is as follows: o

Prep overlying skin with antiseptic solution.

o

Local anesthetic can be infiltrated into the subcutaneous tissue only, taking care not to inject intram uscularly.

o

The needle used for pressure m easurem ents is advanced through the skin until a popping sensation is felt when the fascia is pierced.

o

0.2 m L of saline is injected to clear the lum en of the needle, and the intracom partm ental pressure m easurem ent is then read.

o

To ascertain correct placem ent of the needle within the com partm ent, external pressure m ay be applied over the m uscle com partm ent, or the m uscles can be passively stretched to increase the intracom partm ental pressure transiently; once these m aneuvers are discontinued, the pressure should drop to baseline and stabilize.

Differential Diagnosis 

Chronic com partm ent syndrom e



Fascial hernia



Stress fracture



Arterial occlusion



Neuropraxia



Deep vein throm bosis

Pa ge 1 1 7



Cellulitis



Osteom yelitis



Tenosynovitis



Synovitis

P.245

Treatment Initial Stabilization 

Acutely injured extrem ities that are casted should have the cast univalved and spread, and underlying cast padding should be cut.



Keep the extrem ity at the level of the heart.

ED Treatment 

Acute com partm ent syndrom e is a surgical em ergency.



Mainstay of treatm ent is fasciotom y, particularly for com partm ent pressures >30â€“40 m m Hg.

Medication (Drugs) 

Medications are not helpful, including steroids or vasodilators, in the treatm ent of com partm ent syndrom e.



Pain m edication is essential after diagnosis is m ade or consultant evaluation is begun.

Follow-Up

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Disposition Admission Criteria 

Em ergent orthopedic or surgical consultation for com partm ent pressures >30 m m Hg



For com partm ent pressures >20 m m Hg but <30 m m Hg, surgical consultation should be sought and the patient adm itted.



For com partm ent pressures between 15 and 20 m m Hg, serial m easurem ent of pressures should be taken; if the patient cannot be relied on to return for repeat m easurem ents, the patient should be adm itted.

Discharge Criteria Com partm ent pressure <10â€“15 m m Hg: patients should be given sym ptom atic treatm ent and instructed to return for increased pain, swelling, developm ent of paresthesias.

References 1. Mabee JR. Com partm ent syndrom e: a com plication of acute extrem ity traum a. J Em erg Med. 1994;12(5):651â€“656. 2. Mayeda DV. Knee and lower leg. In: Rosen P, ed. Em ergency Medicine: Concepts and Clinical Practice. 3rd ed. St. Louis, MO: Mosby; 1992. 3. Mubarak SJ, Hargens AR: Com partm ent syndrom es and Volkm an's contracture. Philadelphia: WB Saunders; 1981. 4. Reis ND, Better OS. Mechanical m uscle-crush injury and acute m uscle-crush com partm ent syndrom e. J Bone Joint Surg Br. 2005;87(4): 450â€“453.

Codes ICD9-CM 958.8

Pa ge 1 1 8

ICD10 T79.6

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ngenital Heart Disease, Acyano tic

Congenital

Heart Disease, Acyanotic Ara Gabrielian Robert Woolard

Basics Description N/A

Pathophysiology 

Left to right shunt (LRS): o

Anom alous connection between pulm onary and system ic circulation

o

Becom es apparent in first few weeks of life when pulm onary vascular resistance falls

o

Recirculation of oxygenated blood trough the pulm onary vasculature

o

Pulm onary overload that leads to congestive heart failure (CHF)

o

Severity of shunt varies with size of lesion, relative pressure gradients, and age of patient.

o

Results in accelerated renninangiotensin and sym pathetic input

o

Increased m etabolic needs lead to poor growth

Pa ge 1 1 8

despite adequate caloric intake, 

Ductal dependent lesions: o

In fetal circulation, oxygenated pulm onary artery blood enters the system ic circulation.

o

After birth, decreasing pulm onary artery pressure and increasing aortic pressure reverses flow.

o

Increasing P02 through the patent ductus arteriosus (PDA)

o

PDA causes it to close.

o

Closure of the ductus coincides with onset of sym ptom s in ductal dependent lesions.

o

Sym ptom s usually present in the first 2 weeks of life.

o

Consider tolerating m ild hypoxia until prostaglandin is adm inistered for ductal dependent lesions.

Presentation 

CHF: o





Increased preload (LRS, valvulopathy)



Increased afterload (obstructive)



Decreased inotropy (coronary perfusion)



Dysrhythm ia (heart block)

o

Excess pulm onary shunting leads to edem a

o

Lym phatic drainage overwhelm ed

o

Decrease diffusion across alveoli

o

Poor oxygenation and lung com pliance

Shock-producing congenital heart disease (CHD): o



Poor m yocardial perform ance

Often left ventricle obstructive lesion 

May not respond to fluid resuscitation



Often are ductal dependent lesion

o

â€œGray babyâ€•

o

Precipitous deterioration

Syncope and sudden death:

Pa ge 1 1 8

o

Syncope in CHD is a consequence of reduced cerebral oxygenation.

o

Often presents as syncope during exercise

o

Most com m only due to an obstructive lesion or a dysrhythm ia

o

Conduction abnorm alities result in dysrhythm ias and sudden death.



Adult patients: o

Patients with CHD m ay present as older children and adults: 

Mild lesions



Multiple lesions counterbalance each other



Com pensatory m echanism s



May present for the first tim e as adults with patients who have poor access to healthcare

Alert 

Increased m ortality and m echanical ventilation rates in CHD with respiratory syncytial virus infection



Presenting age of CHD can vary significantly, with 60% presenting in the first m onth of life.

Etiology 



LRS: o

Atrial septal defect

o

Ventricular septal defect

o

Endocardial cushion defect

o

PDA

o

Partial anom alous pulm onary venous return

Obstructing lesions causing shock: o

Hypoplastic left heart syndrom e

o

Critical coarctation of the aorta

o

Critical aortic regurgitation or stenosis

Pa ge 1 1 8



Arrhythm ia: o

Hypertrophic obstructive cardiom yopathy

o

Aortic stenosis

o

Anom alous left coronary artery (m ost com m on cause of sudden death)

o

Congenital heart block

o

Right ventricular dysplasia

Diagnosis Signs and Symptoms History 

Asym ptom atic



Lethargy



Poor feeding



Poor growth



Shortness of breath



Chest pain



Unexplained interm ittent irritability



Fam ily history of sudden death before age 50 years (HOC)



Syncope with exercise

Physical Exam 



General: o

Sm all for stated age

o

Tachypnea

o

Tachycardia

o

Hypotension

Skin: o

Diaphoresis

o

Pallor

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

o

Cool m oist extrem ities

o

Scalp edem a

o

Skin m ottling

o

Cool and pale extrem ities

Cardiovascular: o

Left displacem ent of cardiac im pulse

o

Gallop S3/S4

o

JVD

o

Systolic ejection m urm ur along the lower left sternal border





o

Prom inent peripheral pulses

o

Apical diastolic flow rum ble with significant LRS

o

Delayed capillary refill

o

Dim inished or absent fem oral pulses

Respiratory: o

Rales or wheezing

o

Retractions

o

Orthopnea

Abdom en: o

Hepatom egaly

o

Splenom egaly

o

Ascites

Essential Workup 

Cardiology consult with echocardiography in sym ptom atic patient



Consider early involvem ent of CT surgery

Tests Lab 

Arterial blood gas analysis



CBC



Chem istries

Pa ge 1 1 8



Glucose, blood urea nitrogen, Creatinine



Cardiac enzym es



Brain natriuretic peptide

P.247

Imaging Chest radiograph: 

Pulm onary edem a



Cardiom egaly



Left or right ventricular hypertrophy

Diagnostic Procedures/Surgery 



ECG: o

Left or right ventricular hypertrophy

o

Absent left ventricular forces

o

Absent anterior forces

o

Dysrhythm ias

o

ST-T wave changes

Echocardiogram : o

Most definitive diagnostic tool

o

Start with transthoracic echo

o

May require transesophageal echo

o

Left or right ventricular hypertrophy

o

Dilated cardiom yopathy

o

Doppler flow m ay reveal regurgitation or stenosis.

o

Estim ate pressure gradients across valves.

o

Evaluate for wall m otion abnorm ality.

o

Measure heart cham ber size.

Differential Diagnosis 

Hem atologic: o

Thalassem ia

Pa ge 1 1 8

o 





Sickle cell

Infectious: o

Pneum onia/Acute respiratory distress syndrom e

o

HIV cardiom yopathy

Autoim m une: o

Kawasaki m yocarditis

o

Acute rheum atic fever

Metabolic: o

CF

o

Hyponatrem ia (form ula dilution)

o

Hypoglycem ia

o

Addison disease

o

Adrenal insufficiency

Treatment Initial Stabilization 

ABCs



Establish IV/IO access.



Use oxygen with caution (see Description: Ductal Dependent Lesions).



Monitor

ED Treatment 

Treat apnea with m echanical ventilation.



Provide supplem ental oxygen if it does not agitate the patient (consider blow-by).



Treat hypotension with fluids.



Adm inister prostaglandin E 1 (PGE 1 ) to all sym ptom atic newborns: o

Continuous IV infusion

Pa ge 1 1 8

o

Prom otes reopening of the ductus arteriosus

o

Provides tem porary com pensation in m ost patients younger than 2 weeks of age

o

o

Side effects of PGE 1 

Apnea



Hypotension



Fever



Restlessness

The overall benefits to m ost patients presenting in distress far outweigh the potential risks or side effects.







Inotropic support for shock caused by CHD: o

Epinephrine

o

Norepinephrine

o

Dobutam ine

o

Dopam ine

o

Am rinone

CHF: o

Digoxin

o

Diuretics

o

Dobutam ine

o

Sym pathom im etics

o

Nitroglycerin

o

ACE-I

o

Nitroprusside

Sym ptom atic patients with hypertrophic obstructive cardiom yopathy:



o

Give 10â€“20 m L/kg NS IV.

o

Adm inister propranolol IV.

Prohpylactic Abx therapy: o

Dental procedures

o

Skin infections

Pa ge 1 1 9

o

Colonoscopy

o

Genitourinary tract instrum entation

Medication (Drugs) 

Am rinone 0.5â€“2.0 m g/kg, followed by 5â€“10 Âµg/kg/m in IV infusion



Digoxin requires dosing chart: o

Dose varies with age and weight

o

Loading dose (50% of total)

o

Two follow-up doses (25% each of total dose)



Dobutam ine: 5â€“20 m cg/kg/m in IV



Dopam ine: 2â€“20 m cg/kg/m in IV



Enalaprilat: 0.005â€“0.01 m g/kg q8hâ€“q24h IV



Epinephrine: 0.1â€“2 m cg/kg/m in IV



Morphine sulfate: 0.05â€“0.2 m g/kg SQ or IV



Nitroglycerin: 2â€“10 m cg/kg/m in IV



Norepinephrine: 0.1â€“2 m cg/kg/m in IV



Propranolol: 0.1 m g/kg IV



Prostaglandin E 1 : 0.05 Âµg/kg/m in

Follow-Up Disposition 

All sym ptom atic patients with newly diagnosed CHD should be adm itted.



Cardiologic and surgical consultation

Admission Criteria Adm it to pediatric intensive care unit: 

CHD with vital sign abnorm alities

Pa ge 1 1 9



Requiring m echanical ventilation



Requiring continuous infusions



Known CHD with sym ptom atic or suspected respiratory syncytial virus



Patients with worsening CHF

Discharge Criteria Known CHD with absence of vital sign abnorm alities or concerning sym ptom s

Issues for Referral Cardiology referral for syncope: 

Syncope during exercise



Lack of prodrom al sym ptom s prior to syncope



Fam ily history of sudden death



Abnorm al ECG findings

References 1. Braunwald: Heart disease. 6th ed. Philadelphia: WB Saunders; 2001:1505â€“1582. 2. Berm an: Nelson Textbook of Pediatrics. 17th ed. Elsevier, 2004. 3. Fleisher: Textbook of Pediatric Em ergency Medicine. 4th ed. Lipincott William s & Wilkins, 2000. 4. Garson: The Science and Practice of Cardiology. 2nd ed. Baltim ore: William s & Wilkins, 1998. 5. Marx: Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. Mosby, Inc., 2002: 2278â€“2295. 6. Park: Pediatric Cardiology for Practitioners. 4th ed. Mosby, Inc., 2002. 7. Teitel, et al. Changes in the pulm onary circulation during birth-related events. Pediatr Res. 1990;27:372.

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Miscellaneous SEE ALSO: McCollough M. Com m on com plaints in the first 30 days of life. Em erg Med Clin North Am . 2002;20(1):2748.

Codes ICD9-CM 745.1 745.2 745.3 746.2 746.85

ICD10 Q24.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ngenital Heart Disease, C yano tic

Congenital

Heart Disease, Cyanotic David Cherkas Robert Woolard

Basics Description 

Aberrant em bryonic developm ent of the heart or great arteries: o

Fixed right-to-left shunt leads to central cyanosis.

o

Hypoperfusion and vasoconstriction cause peripheral cyanosis.



Certain conditions trigger cyanosis in older children and adults with congenital heart disease (CHD): o

Cardiac shunt obstruction

o

Pulm onary disease

o

Decreased system ic vascular resistance

o

Fever

o

Dehydration

Etiology 

Tetralogy of Fallot: o

Right ventricle (RV) outflow stenosis, RV hypertrophy (RVH), ventricular septal defect (VSD), overriding

Pa ge 1 1 9

aorta o 

Decreased pulm onary blood flow

Transposition of great arteries: o

A parallel circulatory system

o

The aorta arises from the RV.

o

Two thirds have m ixing through a patent ductus arteriosus; one third have m ixing through a ventricular septal defect.



o

Increased pulm onary blood flow

o

Presents from birth to the first week of life

Truncus arteriosus: o

A single great artery leaves the heart to provide system ic, pulm onary, and coronary circulations.



o

Increased pulm onary blood flow

o

Associated with DiGeorge syndrom e

Tricuspid atresia: o

No direct com m unication between the right atrium (RA) and RV

o

Obligatory right-to-left atrial shunt

o

RV developm ent dependant on VSD

o

Decreased pulm onary blood flow

o

Presents in the first to fourth week of life



Pulm onary valve stenosis



Norm al RV with tricuspid regurgitation



Decreased pulm onary blood flow



Right-to-left atrial shunting



Pulm onary atresia:



o

RV hypertrophy and cardiom egaly

o

Right-to-left shunting through a patent foram en ovale

Ebstein anom aly: o

Downward displacem ent of the tricuspid valve into the RV due to an anom alous attachm ent of the

Pa ge 1 1 9

tricuspid leaflets o

Resultant sm all RV

o

Associated with pulm onary stenosis and a patent foram en ovale

o

Decreased pulm onary blood flow

o

Severe form s m ay present early and are associated with poor outcom es.



Totally anom alous pulm onary venous return o

All pulm onary venous flow returns to the RA, either directly or through the system ic venous system .

o

Increased pulm onary blood flow

o

Sym ptom s generally appear within the first year of life.

Diagnosis 



Most com m on initial presentation to ED: o

Congestive heart failure (CHF)

o

Circulatory collapse/cyanosis

Most com m on presentation to ED in patients with diagnosis of congenital heart disease (CHD): o

Respiratory tract infection

o

CHF

Signs and Symptoms 

Central cyanosis: o

Visible in lips, nailbeds, m ucosa, ears, and m alar regions

o



Seen with right-to-left shunt 

Increases with agitation



Associated with warm skin

Minim al change with 100% O 2

Pa ge 1 1 9





Peripheral cyanosis: o

Blue nail beds and lips

o

Pink m ucosa

o

Cool extrem ities

Differential cyanosis: o

Always indicates the presence of CHD

o

Upper body pink, lower body blue

o

Coarctation of the aorta or interruption of aortic arch

o

Right-to-left flow through the ductus arteriosus

o

Upper body blue, lower body pink: 

Transposition of the great arteries and coarctation of the aorta

o

Lethargy



Clubbing



Right-to-left shunting is not associated with a m urm ur: o

Harsh continuous m urm ur of a patent ductus arteriosus at left sternal border



o

Pleural effusion

o

Decreased breath sounds

CHF: o



Rales

Hepatom egaly o

Scalp edem a

o

Ascites

Tetralogy of Fallot 

Hypercyanotic spells or â€œTet spellsâ€•: o

Follows events that decrease the system ic vascular resistance 

Wakening



Feeding



Defecation



Systolic ejection m urm ur inversely proportional

Pa ge 1 1 9

to severity 

Soft, continuous m urm ur usually audible on auscultation of anterior and posterior chest

Pulmonary Valve Stenosis 

Jugular venous Î±-waves



Presystolic hepatic pulsations



Systolic ejection m urm ur proportional to severity

Totally Anomalous Pulmonary Venous Return 

Fixed, widely split second heart sound



Soft, systolic ejection m urm ur along the left sternal border



Mid-diastolic m urm ur along the lower left sternal border

Essential Workup 

Differentiate central, peripheral, and differential cyanosis



Chest radiograph to assess pulm onary blood flow



ECG to assess for ventricular hypertrophy



Exclude noncardiac causes of cyanosis in newborns.



Cardiology consult and echocardiogram

Tests Lab 

Arterial blood gas analysis: o

Helps to distinguish pulm onary disease from cardiac disease in the cyanotic newborn



CBC



Erythrocytosis identifies chronically cyanotic patients.

Imaging 

Chest radiograph: o

With decreased pulm onary flow and RV hypertrophy 

o

Tetralogy of Fallot (boot-shaped heart)

With decreased pulm onary flow and left ventricle (LV) hypertrophy

Pa ge 1 1 9

 o

Severe tricuspid atresia with atrial septal defect

With increased pulm onary flow and RV hypertrophy: 

Hypoplastic left heart syndrom e



Transposition of the great vessels (â€œegg on a stringâ€•)



Total anom alous pulm onary venous return (â€œsnowm an signâ€•)

o

With increased pulm onary flow and biventricular hypertrophy: 

o

Truncus arteriosus

Box- or funnel-shaped heart 

Ebstein anom aly

P.249



Echocardiogram : o

Should be perform ed em ergently in all infants with suspected and undiagnosed CHD

Diagnostic Procedures/Surgery ECG: 



Right axis deviation, RA hypertrophy o

Tetralogy of Fallot

o

Total anom alous pulm onary venous congestion

o

Hypoplastic left heart syndrom e

o

Transposition of the great vessels

o

Pulm onary stenosis

o

Tricuspid and pulm onary atresia

Left ventricular (LV) hypertrophy: o



Severe tricuspid atresia with atrial septal defect

Biventricular hypertrophy: o

Truncus arteriosus

Pa ge 1 1 9

Differential Diagnosis 

Central cyanosis: o



Im proves with oxygen and activity



Pneum onia



Pulm onary edem a



Pneum othorax



Lung agenesis



Bronchopulm onary dysplasia



Chronic obstructive lung disease

o

Hypoventilation

o

CNS depression:

o

o

o



Prim ary lung disease of any kind:



CNS traum a



Drugs



Sepsis, m eningitis

Upper airway obstruction: 

Tracheal rings



Epiglottitis

Hypotonia: 

Spinal cord insults



Neurom uscular disease



Drugs

Abnorm al or excessive hem oglobin: 

Polycythem ia



Methem oglobinem ia



Sulfa-hem oglobinem ia

Peripheral cyanosis: o

Shock

o

Sepsis

o

Hypotherm ia

Pa ge 1 2 0

Treatment Pre Hospital Alert 

Avoid 100% nonrebreather m asks in cyanotic newborns.



High oxygen tensions prom ote ductal closure.

Initial Stabilization 

Cyanosis or hypotension in the neonate: o

Endotracheally intubate all sym ptom atic patients.

o

The FIO 2 delivered should be no higher than 0.40 for patients with possible ductal-dependent CHD.



Place air filters on the IV lines of all patients with CHD.

ED Treatment 

Adm inister prostaglandin E 1 (PGE 1 ) to all sym ptom atic newborns: o

Continuous IV infusion

o

Prom otes reopening of the ductus arteriosus

o

Provides tem porary com pensation in m ost patients less than 2 weeks of age

o

Not effective in m anaging total anom alous pulm onary venous return

o

May exacerbate pulm onary and tricuspid valve regurgitation in patients with Ebstein anom aly

o 

Dose-dependent hypotension

The overall benefit to m ost patients presenting in distress far outweigh the potential risks or side effects.



Cyanosis in the child or adult with known CHD: o

Adm inister 10â€“20 m L/kg NS IV if dehydration seem s likely.

Pa ge 1 2 0

o

Provide supplem ental oxygen if pulm onary disease is suspected.

o

Treat fever with antipyretics.



Adm inister antibiotics if pneum onia is suspected.



Patients with Tet spells: o

Provide a calm ing environm ent.

o

Place patient in the knee-chest position to increase system ic vascular resistance and prom ote left-to-right shunting.

o

Provide supplem ental oxygen if it does not agitate the patient.



Inotropic support for shock caused by CHD: o

Dobutam ine or dopam ine



Adm inister antibiotics if sepsis or pneum onia is suspected.



Am picillin and gentam icin

Medication (Drugs) 

Acetam inophen: 15 m g/kg PO or PR



Am picillin: 50 m g/kg IV



Dobutam ine: 5â€“20 Âµg/kg/m in IV



Dopam ine: 5â€“20 Âµg/kg/m in IV



Gentam icin: 2.5 m g/kg IV



Ibuprofen: 10 m g/kg PO



Morphine sulfate: 0.1â€“0.2 m g/kg SQ or IV



Phenylephrine: 0.5â€“5 Âµg/kg/m in IV



Propranolol: 0.1 m g/kg IV



Prostaglandin E 1 : 0.05â€“0.1 Âµg/kg/m in



Sodium bicarbonate: 1â€“2 m Eq/kg IV

Pa ge 1 2 0

Follow-Up Disposition Admission Criteria 

All newborns with suspected CHD: o

Adm it to pediatric intensive care unit.

o

Surgical consultation for cardiac repair



Children and adults with an acute worsening of cyanosis



Known CHD with sym ptom atic or suspected respiratory syncytial virus



Patients with worsening CHF

Discharge Criteria 

Patients with tetralogy of Fallot who respond to m inim al intervention: o



Calm ing and knee-chest positioning

Close follow-up

References 1. Friedm an WF, Silverm an N. Congenital heart disease in infancy and childhood. In: Braunwald E, ed. Heart disease. 6th ed. Philadelphia, PA: WB Saunders, 2001:1505â€“1582. 2. Grifka R. Cyanotic Congenital Heart Disease with Increased Pulm onary Blood Flow. Ped Clin North Am . 1999;(2):405â€“425. 3. McCollough M. Com m on com plaints in the first 30 days of life. Em erg Med Clin North Am . 2002;20(1):274â€“278. 4. Savitsky E, Alejos J, Votey S. Em ergency Departm ent Presentations of Pediatric Congenital Heart Disease. J Em erg Med. 2003;24(3):239â€“245. 5. Toepper WC. Cardiac disorders. In: Marx J (ed). Rosen's em ergency m edicine: concepts and current practices. 5th ed. St Louis, MO: Mosby, 2002: 2278â€“2295. 6. Waldm an J, Wernly J. Cyanotic Congenital Heart Disease with

Pa ge 1 2 0

Decreased Pulm onary Blood Flow in Children, Ped Clin North Am 1999;(2):385â€“404.

Miscellaneous SEE ALSO: Cyanosis

Codes ICD9-CM 745.1 745.2 745.3 746.2 746.85

Pa ge 1 2 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ngestive Heart F ailure

Congestive

Heart Failure Benjamin Z. Philips Robert A. Partridge

Basics Description 

Inability of the ventricle to fill with (diastolic) or eject (systolic) blood. As a result, the heart fails to maintain adequate circulation to satisfy tissue m etabolism .



Low-output failure: o

Decreased cardiac output secondary to m yocardial m uscle failure



High-output failure: o

Cardiac output is norm al or high.

o

Output is insufficient to fulfill the requirem ent of m etabolizing tissue.

o

Hyperthyroidism

o

Pregnancy

o

Anem ia

o

A-V fistula

o

Berberi

o

Paget disease

Pa ge 1 2 0

o 

Severe anem ia

Acute congestive heart failure (CHF): o

Rapidly progressive failure state (hours to days)

o

Usually caused by a precipitating event

o

The heart does not have the reserve to com pensate for the added burden.



Chronic CHF (weeks): o



Slowly progressive failure state

Left-sided failure: o

Hem odynam ic burden placed on left ventricle

o

Results in back up of pressure and fluid behind the involved cham ber

o 

Pulm onary congestion occurs

Right-sided failure: o

Hem odynam ic burden placed on right ventricle

o

Results in back up of pressure and fluid behind the involved cham ber

o

Hepatic enlargem ent, jugular venous distention (JVD), dependent edem a occurs.



CHF affects about 2% of the United States populationâ€”nearly 4.8 m illion Am ericans.



Nearly 60% of health care expenditures are for hospital care.



Total cost of heart failure care for 2004 was $25.8 billion.



Most com m on inpatient diagnosis over the age of 65, accounting for at least 20% of adm issions in this age group.



The incidence of CHF increases twofold for each decade of life, rising m ore steeply with age in wom en than in m en.



The presence of CHF increases the likelihood of m ortality: o

Eight tim es for m en

o

Five tim es for wom en

Pa ge 1 2 0



Diastolic dysfunction associated with better prognosis versus systolic dysfunction

Etiology 





Decreased m yocardial contractility: o

Ischem ia

o

Infarction

o

Cardiom yopathy

o

Myocarditis

o

Dysrhythm ias

o

Decreased contractile efficiency: Drug related



Metabolic disorder

Pressure overload states: o

Hypertension

o

Valvular abnorm alities

o

Congenital heart disease

Restricted cardiac output: o





Myocardial infiltrative disease

Volum e overload: o

Dietary indiscretion (sodium overload)

o

Drugs leading to sodium retention (glucocorticoids, NSAIDs, nasal decongestants, vasodilators)



Thyrotoxicosis



Pregnancy



Severe anem ia

Diagnosis Signs and Symptoms 

General:

Pa ge 1 2 0



o

Fatigue

o

Weakness

o

Anxiety

o

Shortness of breath

o

Cough

o

Malaise

o

Lightheadedness

Left heart failure: o

Dyspnea

o

Orthopnea

o

Paroxysm al nocturnal dyspnea

o

Decreased exercise tolerance

o

Rales and/or wheezing (â€œcardiac asthm aâ€•)

o

Pleural effusion (usually right sided)

o

Dullness at lung bases

o

S3 gallop (secondary to decreased left ventricle com pliance)



o

S4 m ay be present

o

Laterally displaced apical im pulse

Right heart failure: o

Dyspnea on exertion

o

JVD

o

Hepatic enlargem ent/tenderness (m ay lead to right upper quadrant pain)



o

Nausea

o

A positive abdom ino-jugular reflex

o

Ascites

o

Dependent edem a

Severe im pairm ent: o

Confusion

o

Tachypnea

o

Sinus tachycardia

Pa ge 1 2 0

o

Mild hypotension

o

Palpable dicrotic notch

o

Cool, pale, cyanotic extrem ities (result of decreased perfusion and increased oxygen extraction)

o

Pulsus alternans

o

Frothy sputum

o

Cheyne-Stokes respirations

Essential Workup 

The chest radiograph is essential in confirm ing the diagnosis and assessing severity.



Classic radiologic progression often not found.



Twelve-hour radiographic lag from onset of sym ptom s m ay occur.



Radiographic findings m ay persist for several days despite clinical im provem ent.

Tests 

Arterial blood gas: o

Rarely needed for em ergency m anagem ent when pulse oxim etry is available



Electrolytes: o

Generally norm al before treatm ent

o

Obtained to establish baseline when initiating therapy with diuretics and/or angiotensin-converting enzym e inhibitors

o 

CBC: o



Anem ia can be a cause or exacerbating factor.

Beta natriuretic peptide (BNP) and creatinine: o



Hyperkalem ia with severe low output states

Elevation in severe CHF

Liver function tests: o

May increase suggesting hepatic congestion

Pa ge 1 2 0



Thyroid function tests: o

Specifically in patients >65 years old or patients in atrial fibrillation



Cardiac enzym es: o

May be useful if ischem ia or infarction is presum ed to be the underlying cause



BNP: o

Approved by FDA

o

Useful for distinguishing between heart failure due to diastolic and/or systolic dysfunction and a pulm onary cause of dyspnea

o

Evaluated in the Breathing Not Properly Study of 1,583 patients presenting to an ED or urgent care facility with a com plaint of acute dyspnea 

In the study, a BNP >100 pg/m L diagnosed heart failure with a sensitivity of 90%, a specificity of 76%, and a predictive accuracy of 83%. BNP of â‰¤50 pg/m L has a high negative predictive value.

o

BNP >500 pg/m L m ost consistent with heart failure.

P.251



Plasm a N-pro-BNP: o

Active BNP cleaved from C term inal end of a prohorm one, creating pro-BNP and the N-term inal fragm ent, N-pro-BNP.

o

In norm al subjects, plasm a concentrations of BNP and N-pro-BNP are sim ilar.

Imaging 

Chest radiograph: o

Cardiom egaly

Pa ge 1 2 1

o 

Effusions (usually right sided)

Three phases of pulm onary findings: o

Stage I: pulm onary redistribution to upper lung fields (cephalization)

o

Stage II: interstitial edem a with Kerley B lines

o

Stage III: alveolar edem a

o

Bilateral confluent perihilar infiltrates leading to classic butterfly pattern

o 

May be asym m etric and m istaken for pneum onia

ECG: o

Underlying cardiac ischem ia

o

presence of dysthym ias

o

Left ventricular hypertrophy

o

Heart block

o

Norm al ECG has high negative predictive value for systolic dysfunction.



Echocardiography: o

Acute valvular pathology

o

Pericardial tam ponade

o

Pericardial thickening in constrictive pericarditis

o

Ventricle size

o

Regional wall m otion abnorm alities

o

Cardiac output

Differential Diagnosis 

Left-sided CHF: o

Acute exacerbation of chronic obstructive pulm onary disease

o

Asthm a exacerbation

o

Acute respiratory distress syndrom e

o

Pneum onia

o

Bronchitis

o

Constrictive pericarditis

Pa ge 1 2 1



o

Valvular disease

o

Pericardial tam ponade

o

Coarctation of aorta

Right-sided CHF: o

Nephrotic syndrom e

o

Cirrhosis

o

Left-side heart failure

o

Pulm onary em bolism

Treatment Pre Hospital 

IV access



Supplem ental oxygen: o

100% nonrebreather m ask



Cardiac m onitor



Pulse oxim etry



ECG



Sublingual nitrates for active chest pain without hypotension



Furosem ide



Endotracheal intubation m ay be required in severe cases.

Initial Stabilization 

IV access



Supplem ental oxygen



Elevate head of the bed with the patient's legs dependent to reduce venous return.



Cardiac m onitor



Pulse oxim etry



Control airway as needed:

Pa ge 1 2 1

o

Continuous positive airway pressure/bilevel positive: 

Higher incidence of m yocardial infarction (MI) reported with BiPAP; studies not conclusive

 o

May decrease the need for intubation

Endotracheal intubation for im pending respiratory failure

ED Treatment 

Norm otensive or hypertensive patients: o



Rapid-acting nitrates: 

Sublingual nitroglycerin



Nitro paste



IV nitroglycerin

Failure of sublingual nitroglycerin and nitro paste to provide relief: o

Morphine sulfate

o

IV diuretics: 

o

Furosem ide (Lasix) or bum etanide (Bum ex)

Sodium nitroprusside for afterload reduction m ay be required for severe persistent hypertension.





Hypotensive patients: o

Avoid nitrates, m orphine, and diuretics.

o

Agents that increase m yocardial contractility: 

Dopam ine



Dobutam ine



Norepinephrine



Am rinone



Milrinone

In less severe or chronic cases of low-output CHF: o

Angiotensin-converting enzym e (ACE) inhibitors such as enalapril im prove hem odynam ic and increase exercise capacity.

o

Use in conjunction with other diuretics.

Pa ge 1 2 1



Acutely decom pensated heart failure: o

Nesiritide

o

Recom binant DNA form of hum an BNP

o

Vasodilation of arteries and veins, reducing preload and afterload.

o

Prom otes free water and sodium loss

o

Reduces aldosterone levels and inhibits rennin-angiotensin system

Medication (Drugs) 

Am rinone: 0.75 m g/kg IV load; 5â€“10 m cg/kg/m in IV



Aspirin: 325 m g PO/PR if acute MI is suspected



Bum etanide (Bum ex): 1â€“3 m g IV



Dobutam ine: 2â€“10 m cg/kg/m in IV, m ax. of 40 m cg/kg/m in



Dopam ine: 2â€“20 m cg/kg/m in IV, m ax. of 50 m cg/kg/m in



Enalapril: 0.625â€“1.25 m g IV; 2.5â€“20 m g/d PO



Furosem ide (Lasix): no prior useâ€”40 m g IVP; prior useâ€”double 24-hour dose (80â€“180 m g IV); no effect in 30 m inutesâ€”redouble dose



Morphine sulfate: 2â€“4 m g IV q5m in



Nitroglycerin: 0.4 m g sublingual; 1â€“2 inches of nitro paste; 5â€“20 m cg/m in IV, m ax. of 100â€“200 m cg/m in IV



Nitroprusside: 0.3â€“10 m cg/kg/m in IV (starting dose), m ax. of 10 m cg/kg/m in



Nesiritide: 2 m cg/kg bolus, then infusion of 0.01 m cg/kg per m in

Follow-Up

Pa ge 1 2 1

Disposition Admission Criteria 



Intensive care unit: o

Pulm onary edem a

o

Cardiogenic shock

o

Concom itant MI or ischem ia

Medical wards: o

New-onset CHF

o

Sym ptom s not relieved by aggressive ED therapy

Discharge Criteria 

Mild exacerbation of chronic CHF: o



Responds to treatm ent

Close follow-up should be arranged with continuation of diuretic, vasodilator, or ACE inhibitor therapy

References 1. Am erican Heart Association. Heart Disease and Stroke Statistics 2004 Update. Dallas, TX: Am erican Heart Association; 2003. 2. Felker GM, O'Connor CM. Inotropic therapy for heart failure: an evidence based approach. Am Heart J. 2001;142(3):393â€“401. 3. Maisel AS, et al. Rapid m easurem ent of B-type natriuretic peptide in the em ergency diagnosis of heart failure. N Engl Med. 2002;347:161. 4. Mehta S, Jay GD, Woolard RH. Random ized, prospective trial of bilevel versus continouous positive airway pressure in acute pulm onary edem a. Crit Care Med. 1997;25(4):620â€“628. 5. Sm ith TW, et al. Managem ent of heart failure. In: Braunwald E, ed. Heart disease. 5th ed. Philadelphia, PA: WB Saunders, 1997:492â€“514. 6. Wilson PW, Vasan RS: Epidem iology and causes of heart failure. http://www.uptodate.com 2004.

Pa ge 1 2 1

Codes ICD9-CM 428.0

ICD10 I50.0

Pa ge 1 2 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o njunctivitis

Conjunctivitis

Jessica Freedman

Basics Description Inflam m ation of the conjunctiva arising from a broad group of clinical causes

Etiology Bacterial 

Staphylococcus aureus



Streptococcus pneum oniae



Haem ophilus influenza



Gonococcal: o



Ophthalm ic em ergency

Chlam ydia: o

Transm ission occurs via autoinoculation from genital secretions.

o

Often occurs in newborns

Viral 

Adenovirus m ost com m on: o

Frequently associated with upper respiratory infections or exposure to som eone with a red eye



Herpes sim plex virus:

Pa ge 1 2 1

o

Recurrent ocular infection occurs in 25% patients within 2 years.

o

Use of steroids is contraindicated.

Allergic Frequent history of allergy, atopy, nasal sym ptom s

Contact Related 

Most vision-threatening cause of â€œred eyeâ€•



May be owing to chem ical irritation, hypersensitivity from preservatives, m edications



Pseudom onas com m only im plicated organism : o

May be found in patients using saliva to clean contact lenses

Diagnosis Signs and Symptoms General 

Red eye (conjunctival irritation)



Gritty, foreign body sensation



Discharge



Eyelid sticking (worse on arising)



Conjunctival edem a (chem osis) and eyelid edem a

Bacterialâ€”General Mucopurulent or purulent discharge

Gonococcal 

Hyperacute, copious purulent discharge: o

Discharge starts 12 hours after inoculation.



Severe chem osis



Eyelid swelling:

Pa ge 1 2 1

o 

Tender preauricular lym phadenopathy

Invades intact conjunctiva and cornea within 24 hours and causes ulcerations, scarring, and perforations leading to blindness

Chlamydia 

Lacrim ation



Mucopurulent discharge



With or without photophobia



Concom itant genital infection (>50%)



Transm ission occurs via autoinoculation from genital secretions.

Viralâ€”General 

Watery, m ucous discharge, lacrim ation



Gritty feeling or foreign body sensation in eye



Pinpoint subconjunctival hem orrhages: o

Tarsal conjunctiva m ay have a bum py appearance.

Herpes Simplex Virus (HSV) 

Acute follicular conjunctival reaction



Skin lesions or vesicles along eyelid m argin or periocular skin



Corneal involvem entâ€”dendritic lesion

Herpes Zoster Virus (HZV) 

Associated with pain or paresthesias of the skin



Rash or vesicles involving the distribution of cranial nerve V1



Dendritic characters on cornea



Rarely vesicles or ulcers form on the conjunctiva.

Allergic 

Hallm ark: itching



Red conjunctiva

Pa ge 1 2 1



Watery discharge



Papillary hypertrophy



Frequent history of allergy, atopy, nasal sym ptom s

Contact Related Acute sym ptom s result of corneal ulceration: 

Norm al visual acuity and intraocular pressures

Essential Workup 



History for: o

Onset of inflam m ation

o

Environm ental or work-related exposure

o

Ill contacts

o

Sexual activity, discharge, rash

o

Use of over-the-counter m edicines or cosm etics

o

System ic diseases

Careful physical exam ination including slit-lam p exam ination including fluorescein staining

Tests Lab 

Bacteriologic studies: o

Not indicated in routine cases

o

Indications: 

Ophthalm ia neonatorum (except chem ical)



Suspected gonococcal ophthalm ia



Com prom ised host



Signs and sym ptom s of system ic disease



Refractory to treatm ent within 48â€“72 hours (with good com pliance)



Positive Gram stain for gram -negative intracellular diplococci: o

Sufficient to initiate system ic and topical treatm ent

Pa ge 1 2 2

for gonococcal disease 

Rapid plasm a reagent (RPR): o

For suspected cases of sexually transm itted disease

Differential Diagnosis 

Dry eye



Foreign body



Corneal abrasion



Allergies or hypersensitivity



Nasolacrim al obstruction



Anterior uveitis



Acute angle-closure glaucom a (m ost serious cause)



Scleritis or episcleritis



Subconjunctival hem orrhage

Treatment Initial Stabilization 

Initiate em piric antibiotic therapy with broad-spectrum topical agent.



System ic therapy for gonococcal, chlam ydial, and m eningococcal conjunctivitis, ophthalm ia neonatorum , and all severe infections regardless of cause



Manage herpetic eye infections in consultation with an ophthalm ologist.

ED Treatment 

Rem ove discharge from the eye(s): o

Contact lens wearers should discontinue use and throw away affected contact lenses.

o

Contact lens wearers should discontinue use until: 

Eye is white.

Pa ge 1 2 2





Antibiotic therapy is com pleted.



No discharge for 24 hours

o

Frequent hand washing

o

No sharing of towels, tissues, cosm etics, linens

Bacterial conjunctivitis: o

Antibioticsâ€”topical: 

Can use ointm ent or drops



Continue therapy for 48 hours after clearing of sym ptom s.



Discontinue therapy and obtain cultures if no im provem ent in 48â€“72 hours (with good com pliance).

o

Antibioticsâ€”system ic: 

Parenteral therapy m andatory for gonococcal infection



Chlam ydia requires system ic treatm ent of sexual partners and parents of neonates.

P.253





Viral conjunctivitis: o

No specific antiviral therapy

o

Lim ited use of topical antihistam ine or decongestant

Allergic conjunctivitis (there m ay be a lag tim e of up to 2 weeks for im provem ent with these agents): o

Antihistam ine or decongestant drops (naphazoline [Naphcon-A])

o

Mast cell stabilizer/antihistam ine or nonsteroidal anti-inflam m atory drug (NSAID) ophthalm ic drops as second line



Noninfectious: o

Eye lubricant drops or ointm ent

Pa ge 1 2 2



Em piric treatm ent: o

Topical antibiotic ointm ent or drops

Medication (Drugs) 

General: o

All contact lens wearers require pseudom onal coverage.

o

Bacitracin ophthalm ologic ointm ent (no pseudom onal coverage)

o

Ciprofloxacin: 0.35% 1 drop q1hâ€“q6h (has antipseudom onal properties; m ay be used in children)

o

Erythrom ycin: 0.5% ointm ent

o

Gentam icin: 0.3% ointm ent q3hâ€“q4h or drops q1hâ€“q4h (has antipseudom onal coverage)

o

Sulfacetam ide: 10% 1 drop q1hâ€“q6h (lacks pseudom onal coverage)

o 

Tobram ycin ointm ent

Chlam ydia: o

Doxycycline: 100 m g PO b.i.d. for 3 weeks

o

Erythrom ycin: 500 m g PO q.i.d. for 3 weeks (peds: 50 m g/kg/d PO in four div. doses for 14 days)

o 

Tetracycline: 250â€“500 m g PO q.i.d. for 3 weeks

Gonococcal: o

Adults: 

Ceftriaxone: 1 g IV or IM daily for 3â€“5 days or as needed



Erythrom ycin: 500 m g PO q.i.d. for 2â€“3 weeks or doxycycline 100 m g PO b.i.d. for 2â€“3 weeks



Plus topical antibiotics as above

Pa ge 1 2 2

o

Neonates: 

Penicillin G 100,000 IU/kg/d in 4 div. doses for 7 days or ceftriaxone 25â€“50 m g/kg/d IV for 7 days



Viral o

Artificial tears

o

Naphcon-A or Visine AC 1 or 2 drops q.i.d. PRN for no m ore than 1 week





HSV or HZV: o

Trifluorothym idine: 1% five tim es per day, or

o

Vidarabine: 3% ointm ent five tim es per day

Allergic: o

Naphazoline (Naphcon-A): 1 drop b.i.d.â€“q.i.d. or Visine AC



o

Acular: 1 or 2 drops b.i.d.

o

Crom olyn sodium 4% (Crolom ): 1 drop q.i.d.

Noninfectious and nonallergic: o

Eye lubricant drops or ointm ent: artificial tears or Lacri-Lube



Em piric treatm ent: o

Erythrom ycin ointm ent 0.5% (half inch q.i.d.)

o

Sulfacetam ide 10% ophthalm ic drops (1 or 2 drops q.i.d.) for 5â€“7 days

Pediatric Considerations 

Often a m anifestation of system ic disease in infants



Neonates becom e infected during passage through the birth canal.



Gonococcal, herpetic, chlam ydial organism s m ost com m on



Ophthalm ia neonatorum is conjunctivitis within the first 4 weeks of life.



Chlam ydia trachom atis is not eradicated by silver nitrate.



Som e newborns treated with erythrom ycin still develop

Pa ge 1 2 2

conjunctivitis. 

Ointm ent is preferred over drops because of difficulty with adm inistration of drops.

Follow-Up Disposition Admission Criteria Known or suspected gonococcal infection (any age group)

Discharge Criteria Close follow-up for all cases

References 1. Alteveer JG, McCans KM. The red eye, the swollen eye, and acute vision loss. Em erg Med Pract. 2002;4(6):27. 2. Bertolini J, Pelucio M. The red eye. Em erg Med Clin North Am . 1995; 13(3):561â€“579. 3. Kunim oto D, Kanitkar K, Makar M. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Diseases. 4th ed. Philadelphia: Lippincott William s & Wilkins; 2004. 4. Leibowitz HM. The red eye. New Engl J Med. 2000;343:345.

Codes ICD9-CM 372.30

ICD10 H10.9

Pa ge 1 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o nscio us Sedatio n

Conscious

Sedation Christopher Ross

Treatment Initial Stabilization Preparation 

Perform a com plete history and physical.



Have patient positioned in area with accessibility to appropriately sized resuscitation equipm ent: o

Breathing m asks, Am bu bag with m ask, oropharyngeal and nasal airways, laryngoscopes, endotracheal tubes, and stylets appropriate for size of patient

o

Defibrillator

o

Em ergency cart with all available m edications necessary to resuscitate the patient including flum azenil and naloxone



Apply cardiorespiratory m onitor, pulse oxim eter, and blood pressure m onitor.



Gather m edicines that will be used in procedure, label, and place at bedside.



Assem ble reversal agents if applicable.

Pa ge 1 2 2



Apply appropriate oxygen delivery device (cannula or m ask) and keep oxygen saturation >95%



Assem ble wall suction unit and catheters



Acquire inform ed consent.

Sedation Agents and Techniques 

Can be adm inistered by various m eans (e.g., IV, IM, PO, rectal (PR), sublingual, transm ucosal, and intranasal)



Adm inister m edications and titrate to effect.



Adm inister local or regional anesthesia if applicable.



Perform the procedure.



Closely observe and m onitor patient during entire course of procedure as well as the recovery period afterwards.



Monitor patient until awake, alert, and back to baseline.



Benzodiazepines: o

Provide anxiolysis and am nesia but not analgesia, so that for painful procedures m ust not be the sole agent.

o

Midazolam is a negative inotropic and m ay induce hypotension.

o

Effects m ay be reversed with flum azenil.

o

Midazolam : 

Dosage (IV): 0.05â€“0.15 m g/kg (single m ax. dose, 2 m g) with subsequent increm ental doses at 3-m inute intervals to desired effect or to a total of 0.2 m g/kg



Dosage (IM): 0.05â€“0.2 m g/kg



Dosage (PO): 0.5â€“0.75 m g/kg (m ax. of 15 m g)



Dosage (nasal): 0.2â€“0.5 m g/kg (m ax. of 5 m g)

 o

Duration of action: 30â€“90 m inutes

Diazepam (largely replaced by shorter-acting

Pa ge 1 2 2

m idazolam ):

o





Dosage (IV): 0.1â€“0.2 m g/kg (m ax. 10 m g)



Dosage (PO): 0.2â€“0.3 m g/kg



PR: 0.5 m g/kg



Duration of action: 2â€“6 hours

Cautions for benzodiazepines: 

Respiratory depression



Hypotension



Excessive sedation



Effects augm ented by opioids

Sedative-hypnotics: o

Chloral hydrate: 

Dosage (PO): 20â€“100 m g/kg with usual dose of 50â€“75 m g/kg (m ax. 2 g)



Dosage (PR): Not recom m ended owing to erratic absorption



Duration of action: 2â€“4 hours (effects up to 24 hours)



Tim e of onset: 30â€“45 m inutes

Alert 

Nausea, vom iting, and paradoxic delirium /excitem ent



Not reversible



Serious effects of airway obstruction and death have been reported. o



No analgesia

Pentobarbital: o

Dosage (IV): 2â€“5 m g/kg

o

Dosage (IM): 4 m g/kg

o

Duration of action: 30â€“60 m inutes

o

Onset: IV m ode acts within 30 seconds, and patient is appropriately sedated within 5 m inutes

o

Titrated sm all increm ental dosing:

Pa ge 1 2 2



Central nervous system and respiratory depression

 

No analgesia

Narcotics: o

Can be adm inistered with an anxiolytic for sedation for painful procedures

o

Fentanyl: 

Dosage (IV): 1â€“3 Âµg/kg with onset in 1â€“3 m inutes



Transm ucosal (oral lozenge [Oralet] allows patient to suck on drug, which then can be rem oved by physician or patient when adequate sedation achieved): 10â€“15 Âµg/kg with onset in 15â€“20 m inutes



Duration of action: 30 m inutes



Respiratory depression



Chest wall rigidity



Use less than one-third dose in children younger than 6 m onths.

 

Em esis with transm ucosal preparation

Nitrous oxide: o

Provides analgesia, anxiolysis, and sedation without the need for IV placem ent

o

Adm inistered in a 50% N 2 O/O 2 concentration by inhalation: 

Onset of action: 30â€“60 seconds and peaks at 5 m inutes



Duration of action: 3â€“5 m inutes after ceasing inhalation



Side effects rare



Potent sedation if previous narcotic in past 4 hours

Pa ge 1 2 2



Nausea and vom iting



Pregnancy



Pneum othorax or bowel obstruction

P.255



Ketam ine: o

Produces analgesia, am nesia, and sedation owing to its dissociative effect

o

Spontaneous respirations and airway reflexes m aintained: 

Dosage (IV): 0.5â€“1.0 m g/kg (use m idazolam 0.05 m g/kg and atropine 0.01 m g/kg concurrently) with onset of action 5â€“10 m inutes



Dosage (IM): 2.0â€“4.0 m g/kg (com bine atropine and m idazolam in sam e syringe) with onset of action 15â€“25 m inutes



Dosage (PO): 5â€“10 m g/kg (use m idazolam 0.5 m g/kg and atropine 0.02 m g/kg) with onset of 30â€“45 m inutes



Duration of action: IV (15â€“45 m inutes); IM (30â€“90 m inutes); PO (60â€“120 m inutes)

o

Causes hypertension and tachycardia, so do not use if hypertension or cardiovascular disease

o

Increases intracranial and intraocular pressure, so do not use with head injury or penetrating globe injury

o

Stim ulates salivary and tracheobronchial secretions, so m ust be adm inistered with an anticholinergic such as atropine

o

Em ergence reactions with hallucinations reported, but are less frequent in children younger than 10

Pa ge 1 2 3

years; the incidence can be reduced by prem edicating the patient with m idazolam . o 

Not for use in children younger than 3 m onths old

Propofol: o

Produces am nesia and sedation but not analgesia: 

Onset of action: seconds



Dosage: 0.5â€“1.0 m g/kg bolus (usually given as 20-m g boluses every 10 seconds in adults until desired effect is obtained) followed by infusion of 50â€“75 Âµg/kg/m in; effective total dosages for adults range from 20â€“150 m g





Duration of action: <2 m inutes



Dose-related respiratory depressant



Deep sedation



Hypotension



Transient apnea



Pain at injection site

Reversal agents: o

Naloxone: 

Opioid antagonist



For reversal of respiratory depression, apnea, and severe hypotension



Dosage: 0.1â€“0.2 m g/kg IV/IM in increm ental doses (to total of 2 m g) q1â€“2m in to the desired reversal effect; usual adult dose of 1â€“2 m g effective



Duration of action: 20â€“45 m inutes



Use sm aller doses on patients who are dependent on opioids to prevent withdrawal reactions.



Flum azenil: o

Benzodiazepine antagonist

Pa ge 1 2 3

o

Reverses CNS depression and som e degree of respiratory depression

o

Dosage: 0.01 m g/kg per dose (m ax. initial dose 0.2 m g) repeated at 1-m inute intervals to desired effect or m ax. 0.05 m g/kg or 1.0 m g

o

Duration of action: 20â€“45 m inutes

o

Not to be used in patients with chronic benzodiazepine therapy or tricyclic antidepressant therapy because of seizures

Follow-Up Disposition Admission Criteria 

Postprocedural sedation



Inability to walk



No responsible adult to accom pany patient hom e



Reason for undergoing conscious sedation still present



Postprocedure com plication

Discharge Criteria 

Patient is awake, alert, and at baseline.



Stable hem odynam ically



Am bulatory 30 m inutes before discharge



Able to urinate



Able to retain oral fluids



Pain controlled



Discharged with follow-up instructions both for the necessitating procedure and for conscious sedation



Under observation of a responsible person and have transportation from the hospital

Pa ge 1 2 3

Complications 

Postprocedural sedation



Hem odynam ic instability



Seizures



Respiratory com plications such as aspiration or depression

References 1. Fleisher G, et al. Guidelines For Pediatric Sedation. Dallas, TX: Am erican College of Em ergency Physicians;1998. 2. Marx JA, et al. Rosen's Em ergency Medicine: Clinical Concepts and Practice. 5th ed. St. Louis, MO: Mosby; 2002. 3. Reichm an E, Sim on R. Em ergency Medicine Procedures. McGraw-Hill; 2004. 4. Tintinalli J. Em ergency Medicine: A Com prehensive Study Guide. 5th ed. New York: McGraw-Hill;2000.

Pa ge 1 2 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o nstipatio n

Constipation

Julia Sone

Basics Description Less than two bowel m ovem ents per week

Pediatric Considerations 

Three percent of pediatric outpatient visits are because of defecation disorders.



Children with cerebral palsy often develop functional constipation.



Most com m on cause of fecal retention and soiling in children is functional fecal retention: o

Caused by fears associated with defecation

o

Associated with irritability, abdom inal cram ps, decreased appetite, early satiety

Etiology 

Metabolic and endocrine: o

Diabetes

o

Urem ia

o

Porphyria

o

Hypothyroidism

o

Hypercalcem ia

Pa ge 1 2 3







o

Pheochrom ocytom a

o

Panhypopituitarism

o

Pregnancy

Functional and idiopathic: o

Colonic irritable bowel syndrom e

o

Diverticular disease

o

Colonic inertia

o

Megacolon/m egarectum

o

Pelvic intussusception

o

Nonrelaxing puborectalis

o

Rectocele/sigm oidocele

o

Posthysterectom y syndrom e

o

Descending perineum

Pharm acologic: o

Analgesics

o

Anesthetics

o

Antacids

o

Anticholinergics

o

Anticonvulsants

o

Antidepressants

o

Antihypertensives

o

Calcium channel blockers

o

Diuretics

o

Ferrous com pounds

o

Laxative abuse

o

Monoam ine oxidase inhibitors

o

Opiates

o

Paralytic agents

o

Parasym patholytics

o

Phenothiazines

o

Psychotropics

Neurologic:

Pa ge 1 2 3



o

Central Parkinson disease

o

Multiple sclerosis

o

Cerebrovascular accidents

o

Spinal cord lesions/injury

o

Peripheral Hirschsprung disease

o

Chagas disease

o

Neurofibrom atosis

o

Autonom ic neuropathy

Mechanical obstruction: o

Neoplasm

o

Stricture

o

Hernia

o

Volvulus

Diagnosis Signs and Symptoms 

Constipation is a sym ptom , not a disease.



Passage of hard stool



Straining/difficulty passing stool



Infrequent bowel m ovem ents



Abdom inal distention/bloating



Firm /hard stool on digital rectal exam : o



May have em pty rectal vault

Diarrhea (liquid stool passes around firm feces)

Essential Workup Thorough history and physical exam : 

Medical, surgical, and psychiatric investigation and date of onset



Note abdom inal distention, hernias, tenderness, or m asses

Pa ge 1 2 3



Com plete anorectal exam for anal stenosis, fissure, neoplasm , sphincter tone, perineal descent, tenderness, spasm

Tests Lab 

Only necessary when considering m etabolic/endocrine disorders



CBC if inflam m atory or neoplastic origin



Electrolytes and calcium indicated if at risk of:



o

Hypokalem ia

o

Hypocalcem ia

Thyroid function test if patient appears to be hypothyroid

P.257

Imaging 

Rarely indicated unless an underlying process suspected



Abdom inal radiograph:



o

Large am ount of feces in colon

o

Dilated colon

Barium enem a study: o

Diverticulosis

o

Megarectum

o

Megacolon

o

Hirschsprung disease

o

Stricture

Differential Diagnosis 

See Etiology



Bowel obstruction

Pa ge 1 2 3

Treatment ED Treatment 



Clean out colon: o

Enem as, suppositories

o

Manual disim paction of hard stool

o

Laxatives

Maintain bowel regim en: o

Increase noncaffeinated fluids (8â€“10 cups per day).

o

Increase dietary fiber intake (20 g/d).

o

Stool softeners

o

Exercise

o

Change m edications causing constipation.

Medication (Drugs) 

Enem as: o

Fleet: 120 m L (peds: 60â€“120 m L) per rectum (PR)

o

Mineral oil: 60â€“150 m L (peds: 5â€“11 years old, 30â€“60 m L; older than 12 years, 60â€“150 m L) PR daily

o 

Tap water: 100â€“500 m L PR

Fiber supplem ents: o

Methylcellulose: 1 tbs in cup water PO daily to t.i.d.

o

Psyllium : 1â€“2 tsp in cup of water/juice (peds: younger than 6 years, 1/4â€“1/2 tsp in 2 oz water or juice; 6â€“11 years, 1/2â€“1 tsp in 4 oz water or juice; older than 12 years, 1â€“2 tsp in cup water or juice) PO daily to t.i.d.



Laxatives (osm otic):

Pa ge 1 2 3

o

Lactulose: 15â€“30 m L (peds: 1 m L/kg) PO daily to b.i.d.

o

Polyethylene glycol: 17 g (peds: 0.8 g/kg/d dissolved in 4â€“8 oz of liquid) PO daily dissolved in liquid



Laxatives (stim ulant): o

Bisacodyl: 10â€“15 m g PO daily (peds: younger than 3 years, 5 m g PR daily; 3â€“12 years, 5â€“10 m g PO/PR daily; older than 12 years, 5â€“15 m g PO daily or 10 m g PR daily)

o

Cascara sagrada: 5 m L (peds: infants, 1.25 m L; 2â€“12 years, 2.5 m L; older than 12 years, 5 m L) PO at bedtim e on an em pty stom ach

o

Castor oil: 15â€“60 m L (peds: 2â€“12 years, 5â€“15 m L) PO daily; do not take at bedtim e

o

Senna: 2â€“4 tabs PO daily to t.i.d. (peds: 2â€“6 years, 1/2â€“1 tab PO daily to b.i.d.; 6â€“12 years, 1â€“2 tabs PO daily to b.i.d.; older than 12 years, 2â€“4 tabs PO daily to b.i.d.)



Stool softeners: o

Docusate sodium : 100 m g (peds: 3â€“5 m g/kg/d in divided doses) PO daily to b.i.d.

o 

Mineral oil: 15â€“45 m L (peds: 5â€“15 m L) PO daily

Suppositories: o

Glycerin: 1 adult (peds: infant, 1 infant suppository) PR PRN

Follow-Up Disposition Admission Criteria

Pa ge 1 2 3



Patients with severe abdom inal pain, nausea, and em esis



Neurologically im paired, elderly, m orbidly obese who cannot be cleaned out in the ED or hom e



Bowel obstruction/peritonitis

Discharge Criteria 

No co-m orbid illness requiring adm ission



Pain free



Adequately cleaned out

References 1. Prather C, Ortiz-Cam acho C. Evaluation and treatm ent of constipation and fecal im paction in adults. Mayo Clin Proc. 1998;73(9):881â€“887. 2. Rasquin-Weber A, Hym an PE, Cucchiara S, et al. Childhood functional gastrointestinal disorders. Gut. 1999; 45(suppl II):II60â€“II68. 3. Talley N. Differentiating functional constipation from constipation-predom inant irritable bowel syndrom e: m anagem ent im plications. Rev Gastroenterol Disord. 2005;5(1):1â€“9.

Codes ICD9-CM 564.0

ICD10 K59.0

Pa ge 1 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ntact Derm atitis

Contact

Dermatitis Jeffrey Horton

Basics Description 

Irritant: o

Eczem atous eruption (superficial inflam m atory process prim arily in epiderm is)

o

Direct injury to skin resulting in nonim m unologic inflam m atory reaction with erythem a, dryness, cracking, or fissuring 

May see vesicles



Usually owing to repeated exposure to m ild irritant (e.g., water, soaps, heat, friction)

o



Lesions itch or burn: 

Usually gradual onset with indistinct borders



Most often seen on hands

Allergic: o

Delayed hypersensitivity reaction (requires prior sensitization)

o

Local edem a, vesicles, erythem a, pruritus, or burning:

Pa ge 1 2 4



Usually corresponds to exact distribution of contact (e.g., watchband)

o

Onset usually within 12â€“48 hours with prior sensitization; m ay take 14â€“21 days for prim ary exposure

Pediatric Considerations 

Allergic contact derm atitis is less frequent in children, especially infants, than in adults.



Major sources of pediatric contact allergy: o

Metals, shoes, preservatives or fragrances in cosm etics, topical m edications, and plants



Circum oral derm atitis: seen in infants and sm all children; m ay result from certain foods (irritant or allergic reaction)

Etiology 

Irritant (80% of contact derm atitis), for exam ple: o

Soaps, solvents

o

Chem icals

o

Certain foods

o

Urine, feces

o

Continuous or repeated exposure to m oisture (hand washing)

o 

Course paper, glass, wool fibers

Allergic, for exam ple: o

Plants, poison ivy, oak, sum ac (rhus derm atitis): 

Com m on form of allergic contact derm atitis



Direct: reaction to oleoresin from plant



Indirect: contact with pet or clothes with oleoresin on surface or fur or in sm oke from burning leaves



Lesions m ay appear up to 3 days after exposure with prior sensitization (12â€“21 days after

Pa ge 1 2 4

prim ary exposure) and m ay persist up to 3 weeks. 

Fluid from vesicles is not contagious and does not produce new lesions.

o

Cem ent (prolonged exposure m ay result in severe alkali burn)

o

Metals (especially nickel)

o

Solvents, epoxy

o

Chem icals in rubber (e.g., elastic waistbands) or leather

o

Lotions, cosm etics

o

Topical m edications (e.g., neom ycin, hydrocortisone, benzocaine, paraben)

o 

Som e foods

Shoe derm atitis: o

Com m on; identify by lesions lim ited to distal dorsal surface of foot usually sparing the interdigital spaces



Photoderm atitis: o

Inflam m atory reaction from exposure to irritant (frequently plant sap) and sunlight

Diagnosis Signs and Symptoms History 

Date of onset



Tim e course



Pattern of lesions



Relationship to work



New products (e.g., lotions and cosm etics), m edications,

Pa ge 1 2 4

and jewelry

Physical Exam 

Special attention to character and distribution of rash



Acute lesions: skin erythem a and pruritus: o

May see edem a, papules, vesicles, bullae, serous discharge, or crusting



Subacute: vesiculation less pronounced



Chronic lesions: m ay see scaling, lichenification, pigm entation, or fissuring with little to no vesiculation; m ay have characteristic distribution pattern

Tests Lab No specific tests in ED are helpful.

Imaging No specific tests in ED are helpful.

Diagnostic Procedures/Surgery 

Patch testing: o



Generally not done in ED; refer to subspecialist.

When tinea is suspected, m ay use Wood lam p for fluorescence

Differential Diagnosis 

Atopic derm atitis: associated with fam ily history of atopy



Seborrheic derm atitis: scaly or crusting â€œgreasyâ€• lesions



Num m ular derm atitis: coinlike lesions



Intertrigo: derm atitis in which skin is in apposition



Infectious eczem atous derm atitis: derm atitis with secondary bacterial infection, usually Staphylococcus aureus



Cellulitis: warm , blanching, painful lesion

Pa ge 1 2 4



Im petigo: yellow crusting



Scabies: intensely pruritic, frequently interdigital with tracks



Psoriasis: silvery adherent, scaling, lesions well delineated, affecting extensor surfaces, scalp, and genital region



Herpes sim plex: groups of vesicles, painful, burning



Herpes zoster: painful, follows derm atom al pattern



Bullous pem phigoid: diffuse bullous lesions



Tinea: m axim al involvem ent at m argins, fluoresces under Wood lam p



Pityriasis alba: discrete, asym ptom atic, hypopigm ented lesions



Urticaria: pruritic raised lesions (wheal) frequently with surrounding erythem a (flare)



Acroderm atitis enteropathica: vesiculobullous lesion of hands and feet, associated with failure to thrive, diarrhea, and alopecia



Letterer-Siwe tum or (Langerhans cell histiocytosis): o



Associated with hepatosplenom egaly and adenopathy

Dyshidrotic derm atitis (eczem a)

P.259

Treatment Initial Stabilization Rarely required in absence of concom itant pathology

ED Treatment

Pa ge 1 2 4

General 

Prim arily sym ptom atic



Wash area with m ild soap and water



Rem ove or avoid offending agent (including washing clothes)



Cool, wet com presses; especially effective during acute blistering phase



Antipruritic agents: o

Topical: 

Calam ine lotion, corticosteroids (do not penetrate blisters); avoid benzocaine or hydrocortisone-containing products, which m ay further sensitize skin.

o 

System ic: antihistam ines, corticosteroids

Alum inum acetate (Burrows) solution: weeping surfaces

Irritant Dermatitis 

Rem ove offending agent



Decrease wet/dry cycles (hand washing)



Bland em ollient



Topical steroids for severe cases (ointm ent preferred) m edium to high potency (hands) b.i.d. for several weeks

Allergic Dermatitis 



Topical steroids (ointm ent preferred) b.i.d. 2â€“3 weeks: o

Face: low potency

o

Arm s, legs, trunk: m edium potency

o

Hands and feet: high potency

Oral steroids for severe cases

Rhus Dermatitis 

Follow general m easures plus: o

Aseptic aspiration of bullae m ay relieve discom fort.

Pa ge 1 2 4

o

Severe reaction: system ic corticosteroids for 2â€“3 weeks with gradual taper: 

Prem ature term ination of corticosteroid therapy m ay result in rapid rebound of sym ptom s.

Shoe Dermatitis Follow general m easures plus: 

Wear open-toe, canvas, or vinyl shoes.



Control perspiration: change socks, use absorbent powder.

Medication (Drugs) Systemic 

Antihistam ine (H 1 -receptor antagonist, first and second generation)



Cetirizine (Zyrtec): adult and children older than 6 years, 5â€“10 m g PO daily (peds: age 2â€“6 years, 2.5 m g PO daily to b.i.d.) o

Diphenhydram ine hydrochloride (Benadryl): 25â€“50 m g IV/IM/PO q6h PRN (peds: 5 m g/kg/24h div. q6h PRN)

o

Fexofenadine (Allegra): 60 m g PO b.i.d. or 180 m g PO daily (peds: age 6â€“12, 30 m g PO b.i.d.)

o

Hydroxyzine hydrochloride (Atarax): 25â€“50 m g PO IM up to q.i.d. PRN (peds: 2 m g/kg/24h PO div. q.i.d. or 0.5 m g/kg IM q4hâ€“q6h PRN

o

Loratadine (Claritin): 10 m g PO b.i.d.

o

For refractory pruritus: doxepin: 75 m g daily m ay be effective.



Corticosteroid: o

Prednisone: 40â€“60 m g PO daily (peds: 1â€“2 m g/kg/24h, m ax. 80 m g/24h) div. daily/b.i.d.

Pa ge 1 2 4

Topical 

Alum inum acetate (Burrows) solution: Apply topically for 20 m inutes t.i.d. until skin is dry.



Calam ine lotion: q.i.d. PRN



Topical corticosteroid



Triam cinolone: ointm ent 0.025, 0.1%; cream 0.025, 0.1%; lotion 0.025, 0.1% t.i.d. or q.i.d.

Follow-Up Disposition Admission Criteria Rarely indicated unless severe system ic reaction or significant secondary infection

Discharge Criteria 

Sym ptom atic relief



Adequate follow-up with prim ary care physician (PCP) or derm atologic specialist

References 1. Habif TP. Skin Disease Diagnosis and Treatm ent. 2nd ed. China: Mosby; 2005. 2. Habif TP. Clinical Derm atology. St Louis, MO: Mosby; 1996: 81â€“99. 3. Hurwitz S. Clinical Pediatric Derm atology. Philadelphia: WB Saunders; 1993: 68â€“82. 4. Juckett G. Plant derm atitis. Postgrad Med 1996;100(3):159â€“171. 5. White IR. Occupational derm atitis. Br Med J. 1996;313:487â€“489. 6. Wolf R, Wolf D. Contact derm atitis. Clin Derm atol. 2000;18(6):661â€“666.

Pa ge 1 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o r Pulm o nale

Cor Pulmonale

Jedd E. Roe

Basics Description 

Ventricular failure confined to the right ventricle: o

Right ventricular hypertrophy or dilation is an adaptive response to pulm onary hypertension, which predom inately occurs as a result of alveolar hypoxia.



The pulm onary circulation is a low-resistance, low-pressure system : o

The pulm onary arteries are thin walled and distensible.

o

Mean pulm onary arterial pressure is usually 12â€“15 m m Hg

o

Norm al left-arterial pressure is 6â€“10 m m Hg.

o

The resulting pressure difference driving the pulm onary circulation is only 6â€“9 m m Hg.





Three factors affect pulm onary arterial pressure: o

Cardiac output

o

Pulm onary venous pressure

o

Pulm onary vascular resistance

Pulm onary hypertension can arise through a num ber of m echanism s:

Pa ge 1 2 4

o

A m arked increase in cardiac output

o

Left-to-right shunt secondary to congenital heart disease

o

Hypoxia: 

Most com m only causes pulm onary vascular resistance to increase



The resulting hypercapnia and acidosis induce additional vasoconstriction.



Pulm onary venous pressure increases.



A com pensatory rise is seen in the pulm onary arterial system so flow is m aintained across the pulm onary vascular bed.

o

Pulm onary em bolus causes a sim ilar change by increasing resistance to pulm onary blood flow.

o

Left ventricular failure achieves the sam e result by directly influencing pulm onary venous pressure.

o

Dram atic rises in blood viscosity or intrathoracic pressure im pede blood flow.



Functional classification of pulm onary arterial hypertension based on New York Heart Association criteria: o

Class Iâ€”Pulm onary arterial hypertension without lim itation of physical activity

o

Class IIâ€”Pulm onary arterial hypertension resulting in slight lim itation of physical activity (e.g., ordinary activity causes sym ptom s such as dyspnea on exertion)

o

Class IIIâ€”Pulm onary arterial hypertension resulting in m arked lim itation of physical activity (e.g., less than ordinary activity causes sym ptom s such as dyspnea on exertion)

o

Class IVâ€”Pulm onary arterial hypertension resulting in an inability to carry out any physical activity

Pa ge 1 2 5

without sym ptom s (signs of cor pulm onale are present)

Incidence 

Approxim ately 86,000 patients die from chronic obstructive pulm onary disease (COPD) each year: o

Associated right ventricular failure is a significant factor in m any of these cases.



In patients older than 50 years with COPD, 50% develop pulm onary hypertension and are at risk of developing cor pulm onale.



The course of cor pulm onale is generally related to the progression of the underlying disease process.



Once biventricular failure is noted, life expectancy is usually
Etiology 

Chronic hypoxia: o

COPD

o

Chronic hypoxia at high altitude

o

Sleep apnea: 

Prim ary pulm onary hypertension



Cystic fibrosis



Congenital heart disease: o

Left-to-right shunts



Severe anem ia



Pulm onary em bolism



Collagen vascular diseases



Thoracic deform ities: o

Kyphoscoliosis



Obesity



Mitral stenosis



Pulm onary venoocclusive disease

Pa ge 1 2 5





Increased blood viscosity: o

Polycythem ia vera

o

Leukem ia

Increased intrathoracic pressure: o

COPD

o

Mechanical ventilation with positive end-expiratory pressure

Diagnosis Signs and Symptoms 

Exertional dyspnea



Easy fatigability



Weakness



Syncope



Cough



Hem optysis



Wheezing



Hoarseness



Weight gain



Jugular venous distention: o

Prom inent A and V waves



Hepatom egaly



Ascites



Hepatojugular reflex



Peripheral edem a



Left parasternal heave on cardiac palpation



Pulm onic com ponent of the second heart sound increases in intensity.

Tests

Pa ge 1 2 5

Lab 



Pulse oxim etry or arterial blood gas: o

Resting PO 2 40â€“60 m m Hg

o

Resting PCO 2 often 40â€“70 m m Hg

Hem atocrit: o



Frequently elevated

B-natriuretic peptide: o

May be helpful in distinguishing biventricular failure from respiratory disease



Other laboratory tests are not generally useful.

Imaging 

Chest radiograph: o

Signs of pulm onary hypertension: 

Large pulm onary arteries (>16â€“18 m m )



An enlarged right-ventricular silhouette



Shows abnorm alities in >90% of patients in the detection of cor pulm onale, but does not indicate the severity of disease



Pleural effusions do not occur in the setting of cor pulm onale alone.



ECG o

Right-axis deviation

o

Tall, peaked P waves (P pulm onale)

o

Right-ventricular hypertrophy (specific not sensitive)

o

Transient changes due to hypoxia

o

Right precordial T-wave flattening

o

ST-segm ent depression in segm ents II, III, and arteriovenous fistula



Echocardiographyâ€”the noninvasive diagnostic m ethod of choice: o

Right ventricular dilation or hypertrophy in the

Pa ge 1 2 5

setting of norm al left ventricular dim ensions o

Assessm ent of tricuspid regurgitation

o

Doppler quantization of pulm onary artery pressure, right ventricular ejection fraction



Ventilation/perfusion scans or pulm onary angiography: o



Useful in the setting of acute cor pulm onale

CT or MRI: o

Delineates size and shape of the ventricles and pulm onary arteries

o 

Detection of larger pulm onary em boli

Right heart catheterization: o

The m ost precise estim ate of pulm onary vascular hem odynam ics

o

Gives accurate m easurem ents of pulm onary arterial pressure and pulm onary capillary wedge pressure

Differential Diagnosis 

Prim ary disease of the left side of the heart



Congenital heart disease



Hypothyroidism



Cirrhosis

P.261

Treatment Pre Hospital 

Supportive therapy: o



Supplem ental oxygen

To an endpoint of 90% arterial saturation:

Pa ge 1 2 5



o

IV access

o

Cardiac m onitoring

o

Pulse oxim etry

Treat bronchospasm from associated respiratory disease: o



Î²-agonist nebulizers

Caution: o

Vasodilators and diuretics do not have a role in the field.

o

Severely hypoxic patients m ay require ETT intubation

Initial Stabilization ED therapy is directed at the underlying disease process and reducing pulm onary hypertension.

ED Treatment 

Supplem ental oxygen sufficient to raise arterial saturation to 90%: o

Im proving oxygenation reduces pulm onary arterial vasoconstriction and right ventricular afterload.

o

The im proved cardiac output enhances diuresis of excess body water.

o

Care m ust be taken to m onitor the patient's ventilatory status and PCO 2 , as hypercapnia m ay reduce respiratory drive and cause an acidosis.



Diuretics, such as furosem ide, m ay be added cautiously to reduce pulm onary artery pressure by contributing to the reduction of circulating blood volum e.



Patients should be m aintained on salt and fluid restriction.



There is no role for digoxin in the treatm ent of cor pulm onale.



Bronchodilator therapy is particularly helpful for those patients with COPD: o

Selective Î²-adrenergic agents such as subcutaneous

Pa ge 1 2 5

terbutaline 0.25 m g SC o

Bronchodilator affects and reduces ventricular afterload.

o

Theophylline m ay play a role to im prove diaphragm atic contractility and reduce m uscle fatigue. 

While controversial, anticoagulation in the form of warfarin has been recom m ended to m aintain a target international norm alized ratio between 1.5â€“2.5.



In the future, nitric oxide adm inistration for patients with severe disease m ay becom e an adjunctive therapy initiated in the ED.





Acutely decom pensated COPD patients: o

Early steroid therapy

o

Antibiotic adm inistration

In general, im provem ent in the underlying respiratory disease results in im proved right ventricular function.

Medication (Drugs) 

Furosem ide: 20â€“60 m g IV (peds: 1 m g/kg m ay increase by 1 m g/kg/q2h not to exceed 6 m g/kg)



Terbutaline: 0.25 m g SC

Follow-Up Disposition Admission Criteria 

New-onset hypoxia

Pa ge 1 2 5



Anasarca



Severe respiratory failure



Adm ission criteria for the underlying disease process

Discharge Criteria 

Patients without hypoxia or a stable oxygen requirem ent



Close follow-up as long as the underlying etiology has responded to acute m anagem ent

References 1. Braunwald E. Heart Failure and Cor pulm onale. In: Kasper D, et al, eds. Harrison's textbook of m edicine. 16th ed. New York: McGraw-Hill, 2005: 1355â€“1359. 2. Hum bert M, Sitbon O, Sim onneau G. Treatm ent of Pulm onary Arterial hypertension. N Engl J Med. 2004;351:14:1425â€“1436. 3. Schwam E. B-Type Naturietic Peptide for Diagnosis of Heart failure in Em ergency Departm ent Patients: A Critical Appraisal 4. Weitzenblum E. Chronic Cor Pulm onale. Heart. 2003;89:225â€“230.

Codes ICD9-CM 415.0 415.1 416 416.0 416.1 416.8 416.9

ICD10 I27.9 I26.0

Pa ge 1 2 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o rneal Abrasio n

Corneal Abrasion

Kevin Kern

Basics Description 

Traum atic desquam ation of portions of corneal epithelium



Focal epithelial loss secondary to rem oval of corneal foreign body



Previous corneal transplant, corneal surgery, or radial keratotom y: o

Predisposes patient to m ore severe injury after m inor traum a to eye

Etiology 

Contusive force



Direct contact injury: o

Hum an fingernail

o

Branches

o

Fingers/toes

o

Hairbrushes/com bs

o

Sand/stones

o

Metallic object

o

Snow

o

Pens/pencils

o

Toys

Pa ge 1 2 5



o

Activated charcoal

o

Airbag deploym ent

Mechanical action of eyelid: o

Blinking or rubbing eye with loose foreign body (scratches on windshield)



Projectiles at high speeds (m etal workers): o

Carefully exam ine for globe perforation (Seidel test positive, teardrop pupil)



Poorly fitting contact lens or prolonged contact lens use: o

Extended-wear soft contact lenses increase infection rate 10â€“15% over daily-wear contact lenses.

Pediatric Considerations 







Signs and sym ptom s m ay differ: o

Excessive crying

o

Conjunctival erythem a

o

Tearing

o

Eye rubbing

o

Lid edem a

o

Grunting respiration

Younger than 12 m onths: o

Frequently no history of eye traum a

o

Often no eye signs

Older than 12 m onths: o

More often will have history of m inor eye traum a

o

Positive eye signs

o

No excessive crying

Com pression injuries to cornea associated with birth: o

Localized edem a

o

Corneal clouding

o

Clear within hours

Pa ge 1 2 5

Diagnosis Signs and Symptoms 

Severe ocular pain



Tearing/ocular discharge



Blepharospasm



Foreign body sensation



Photophobia



Conjunctival injection



Blurred vision



Headache

Essential Workup 

History: o

Past ocular traum a

o

Ocular/periocular surgery

o

Pre-existing visual im pairm ent

o

Glasses

o

Contact lens use (extended wear has increased risk of corneal ulcer)

o

Tim e of onset

o

Associated sym ptom s

o

Treatm ent before visit

o

Use of safety glasses (pounding, drilling, grinding m etal)

o 

System ic disease (diabetes, autoim m une disorders)

Com plete eye exam : o

Visual acuity

o

Evert upper lids to check for retained foreign body

o

Bright white light for visual inspection of cornea to rule out infiltrate/edem a/loss of corneal luster

Pa ge 1 2 6

o

Slit-lam p to evaluate anterior segm ent and depth of abrasion

o

Fluorescein to identify area of dam aged corneal epithelium : 

Dam aged area appears bright green using blue Wood lam p.

o

Funduscopic exam ination of retina and m acula

Tests Pediatric Considerations Handheld slit-lam p and Wood lam p: helpful in exam ination of pediatric eye

Differential Diagnosis 

Herpes sim plex virus keratitis



Recurrent corneal erosion syndrom e



Ultraviolet keratitis (snow blindness)



Corneal ulcer



Corneal dystrophy (inherited)



More extensive injury than corneal abrasion: o

Laceration of cornea

o

Perforation of cornea

o

Hyphem a

o

Iris prolapse

o

Lens disruption

Treatment Initial Stabilization 

Instill topical anesthetic (proparacaine/tetracaine).



Consider cycloplegic for intense pain owing to ciliary

Pa ge 1 2 6

spasm (hom atropine 5%).

ED Treatment 

Exam ination



Rem oval of superficial foreign body



Pain control (topical/oral):



o

Diclofenac (topical)

o

Ketorolac (topical)

o

Oral narcotics

o

Cool com presses

Cycloplegic (optional): o

Cyclopentolate (m ydriasis 1â€“2 days)

o

Tropicam ide (m ydriasis 6 hours)

o

Hom atropine 5%

P.263



Antibiotic ointm ent/drop options: o

Ciprofloxacin

o

Erythrom ycin

o

Gentam icin

o

Sulfacetam ide

o

Tobram ycin/TobraDex

o

Contact lens wearers m ust be covered for Pseudom onas: 



Use am inoglycoside or quinolone.

Eye patch: o

Controversial regarding efficacy

o

No patch required for sm all abrasions

o

Never patch contact lens-related injury.

o

Never patch infection-prone injury: 

Fingernail



Vegetable m atter

Pa ge 1 2 6

 o

Rem oval of wood particles

Patch nonâ€“contact lensâ€“related abrasions >10 m m 2 only or recurrent corneal erosions

o

Collagen shields/soft bandage contact lenses (currently under investigation)





Disadvantages of patching: o

Rem oves binocular vision/reduces visual field

o

Uncom fortable

o

Increases corneal tem perature

o

Decreases corneal oxygenation

o

Slows re-epithelialization

o

Decreases tear exchange

o

Prolongs healing

Tetanus prophylaxis: o

When contam inants include dirt, fecal m aterial, or saliva

o

Routine tetanus not necessary

Medication (Drugs) 

Ciprofloxacin: 0.35% 1 drop q.i.d.



Cyclopentolate: 0.5%, 1.0%, or 2.0% drops (m ydriasis 1 or 2 drops t.i.d.)



Diclofenac: 0.1% drops 1 drop q.i.d.



Erythrom ycin: 0.5% ointm ent q.i.d.



Gentam icin: 0.3% ointm ent q.i.d.



Gentam icin: 0.3% 2 drops q6h



Hom atropine: 5% solution 2 drops b.i.d.



Ketorolac: 0.5% drops 1 drop q.i.d.



Proparacaine: 0.5% 1 drop once



Sulfacetam ide: 10% drops 2 drops q.i.d.



Sulfacetam ide: 10% ointm ent q.i.d.

Pa ge 1 2 6



TobraDex: suspension 0.1%/0.3% 2 drops q4hâ€“q6h



Tobram ycin: 0.3% drops 2 drops q6h



Tobram ycin: 0.3% ointm ent q6h



Tropicam ide: 0.5%, 1.0% drops (m ydriasis 6 hours) 1 drop q4h

Follow-Up Disposition Admission Criteria Associated injuries requiring adm ission

Discharge Criteria 

All sim ple corneal abrasions



Follow-up in 24â€“48 hours with ophthalm ologist for re-exam ination and ongoing care



Follow-up with ED when access to specialist is lim ited

Issues for Referral All corneal burns should be referred to ophthalm ologist within 12â€“24 hours.

References 1. Alteveer JG, McCans KM, eds. The red eye, the swollen eye, and acute visual loss. Em erg Med Pract. 2002:4(6). 2. Calder LA, Fergusson D. Topical nonsteroidal anti-inflamm atory drugs for corneal abrasions: Meta-analysis of random ized trials. Acad Em erg Med. 2005;12:467â€“473. 3. Khaw PT, Shah P, Elkington AR. Injury to the eye. Br Med J. 2004;328:36â€“38. Available at http://www.bm j.com . 4. Le Sage N, Verreault R, Rochette LM. Efficacy of eye patching for traum atic corneal abrasions. Ann Em erg Med. 2001;38:129â€“134.

Pa ge 1 2 6

5. Micheal JG, Hug D, Dowd MD. Managem ent of corneal abrasions in children: a random ized clinical trial. Ann Em erg Med. 2002;40:67â€“72. 6. Mukherjee P, Sivakum ar A, Mackway-Jones K. Tetanus prophylaxis in superficial corneal abrasions. Em erg Med J. 2003;20:62â€“64. 7. Upadhyay MP, Karm acharya PC, Koirala S, et al. The Bhaktapur eye study: ocular traum a and antibiotic prophylaxis for the prevention of corneal abrasions in Nepal. Br J Ophthalm ol. 2001;85:388â€“392. 8. Weavers CS, Terrell KM. Evidence based em ergency m edicine. Update: do ophthalm ic nonsteroidal anti-inflam m atory drugs reduce the pain associated with sim ple corneal abrasions without delaying healing? Ann Em erg Med. 2003;41:134â€“140.

Miscellaneous SEE ALSO: Red Eye

Codes ICD9-CM 918.1 Corneal abrasion 370.00 Corneal ulcer, unspecified 930.9 Eye foreign body, external, unspecified

ICD10 S05.0

Pa ge 1 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o rneal Burn

Corneal Burn

Kevin Kern

Basics Description 

Inappropriate exposure of cornea to chem icals, heat, cold, electrical, or radiant energy causing dam age to the cornea and often extending to adjacent structures



Severity of injury related to duration of exposure, type of agent, anion concentration, pH level of solution



Alkalis: o

Cause im m ediate rise in pH level

o

Highly soluble in lipids, so rapidly penetrate the eye, causing severe corneal injury and continue to penetrate over tim e if no intervention undertaken

o

Penetration can occur in <1 m inute.

o

Exception: calcium alkalis penetrate relatively poorly secondary to soap form ation; can cause corneal opacification, so m ay appear worse but actually have better prognosis than other alkali burns.



Acids: o

Im m ediately coagulate proteins of corneal epithelium

o

Cause opacification

o

Coagulation produces barrier to deeper penetration.

Pa ge 1 2 6

o

Exception: Lipophilicity of hydrofluoric acid causes it to act sim ilar to a base with m ore rapid penetration



Therm al burns: o

Cause direct injury to cornea

o

Dam age prim arily depends on duration and intensity of heat.

o

Globe often spared secondary to blinking, Bell phenom enon (eyes roll up and outward), tears, protective bony structure of orbit



Electrical injury: o

Occurs with current flow through head, with input at or near eye

Etiology 

Alkalis: o

Am m onia: 

Fertilizer, refrigerant, household am m onia, cleansing agents

o

Potassium hydroxide: 

o

Magnesium hydroxide: 

o

Sparklers, flares, fireworks

Lye: NaOH: 

o

Caustic potash

Caustic soda, drain cleaners

Lim e: CaOH 2 : 

Fresh lim e, quicklim e, calcium hydrate, slaked lim e, hydrated lim e, plaster, m ortar, cem ent, whitewash

o

Nonspecific alkali: 



Motor vehicle airbag on inflation releases alkali.

Acids: o

Sulfuric acid: H 2 SO 4 : 

Car battery acid

Pa ge 1 2 6

o

o



Sulfurous acid: H 2 SO 3 : 

Preservatives (fruit and vegetable)



Bleach



Refrigerants

Hydrofluoric acid: HF: 

Etching silicon/glass



Cleaning brick



Electropolishing m etals



Control of ferm entation in breweries



Com m ercial/household rust rem oval

Therm al: o

Hot liquids, m olten m etal

o

Flam es

o

Hot sm oke/gases

o

Flash burn

o

Steam

o

Cigarette burns

Pediatric Considerations Consider child abuse or neglect.

Diagnosis Signs and Symptoms 

Severe ocular pain



Photophobia



Lacrim ation



Foreign body sensation



Conjunctival injection



Corneal edem a



Corneal opacification

Pa ge 1 2 6



Im paired visual acuity



Lim bal blanching



Lens opacification



Vesicles clear fluid (hypotherm al injury)



Vesicles hem orrhagic fluid



Necrosis of iris, ciliary body

Essential Workup History 

Type of exposure



Duration of exposure



Tim e of onset



Tim e irrigation initiated



Pre-existing visual im pairm ent



Protective eyewear



Contact lens use



Treatm ent before arrival

Physical Exam Com plete eye exam (after irrigation): 

Visual acuity



Bright white light for visual inspection of cornea/conjunctivae/lim bus



Slit-lam p to evaluate anterior segm ent inflam m ation



Fluorescein to identify dam aged corneal epithelium



Check for lenticular clarity.



Fundus exam



Measure intraocular pressure (especially in delayed presentation).



Lid/eyelash exam



Check pH with acid/alkali burns with litm us paper or pH indicator on urine dipstick

Pa ge 1 2 6

Differential Diagnosis 



Infection: o

Viral keratitis

o

Corneal ulcer

Corneal erosion syndrom e: o

Corneal foreign body

o

Corneal abrasion

o

Hypotherm al injury

Pediatric Considerations Handheld slit-lam p and Wood lam p helpful in exam ination of child's eye

Treatment Pre Hospital 

Irrigate at scene 15â€“30 m inutes unless other coexisting life-threatening conditions require im m ediate transfer.



Continuous irrigation en route to hospital with norm al saline

Initial Stabilization 

Chem ical exposure: o

Irrigate with any available diluting substance but preferably water or norm al saline.



Therm al exposure: o

Cool m oist dressing with overlying ice packs

P.265

ED Treatment

Pa ge 1 2 7



Chem ical exposure: alkalis/acids/m ace: o

Continuous irrigation to achieve pH 7.3â€“7.5 (1â€“2 L via a Morgan lens over 30â€“60 m inutes)

o

pH should be evaluated at 5 and 30 m inutes after irrigation to ensure norm alization of pH.

o

Evaluate fornices in detail and eye in full range of m otion to ensure rem oval of all particulate chem ical substance.

o

Topical anesthetic (proparacaine)

o

Antibiotic prophylaxis for Staphylococcus/Pseudom onas until epithelialization is com plete:

o



Gentam icin ointm ent plus erythrom ycin or



Bacitracin

Cycloplegics to m inim ize posterior synechiae form ation: 

Cyclopentolate 1%



Atropine 1%

o

Oral analgesics

o

If increased intraocular pressure: 

Im m ediate ophthalm ologic consultation



Adm inister acetazolam ide 125 m g PO q.i.d. and tim olol 0.5% drops b.i.d.

o

Topical steroids to control anterior uveitis (consult ophthalm ology)

o

Eye patch (consult ophthalm ology)

o

May require surgical intervention if frank corneal penetration

o

Ophthalm ologic consultation by phone in m ild injuries

o

Im m ediate ophthalm ologic consultation in all m oderate to severe injuries; if unavailable at your hospital, arrange transfer to closest eye center

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o

Hydrofluoric acid: 

Treat as above, plus 1% calcium gluconate eyedrops

 

System ic analgesia for 24 hours

Therm al exposure: o

Frequent m oist dressing changes

o

Antibiotics drops q.i.d.

o

Generous lubricant application

o

Moisture cham ber when extensive injury to eyelid

o

Steroids (consult ophthalm ologist; do not use for >1 week)



Electrical Injury: o

Irrigation

o

Wound care

o

Antibiotic ointm ent

o

Cycloplegic (if anterior uveitis)

o

Analgesia

Pediatric Considerations 

Patching poorly tolerated



May require system ic analgesia for com plete exam ination

Medication (Drugs) 

Artificial tears



Atropine: 0.5%, 1.0%, 2.0% drops (cycloplegia 5â€“10 days, m ydriasis 7â€“14 days) 1 drop t.i.d.



Bacitracin ointm ent: q.i.d.



Ciprofloxacin: 0.35% 1 drop q.i.d.



Cyclopentolate: 0.5%, 1.0%, 2.0% drops (cycloplegia 1â€“2 days, m ydriasis 1â€“2 days) 1 drop t.i.d.



Erythrom ycin: 0.5% ointm ent q.i.d.

Pa ge 1 2 7



Gentam icin: 0.3% ointm ent q.i.d.



Gentam icin: 0.3% drops 1 drop q6h



Proparacaine: 0.5% drops 1 drop



Sulfacetam ide: 10% ointm ent q.i.d.



Sulfacetam ide: 10% drops q.i.d.



Tobram ycin: 0.3% ointm ent q6h



Tobram ycin: 0.3% drops q6h



Tropicam ide: 0.5%, 1.0% drops (cycloplegia none; m ydriasis 6 hours) 1 drop

Follow-Up Disposition Admission Criteria 

Intractable pain



Increased intraocular pressure



Corneal penetration requiring im m ediate surgical intervention



Hydrofluoric acid burn; adm it for 24 hours of system ic analgesia



Suspected child abuse

Discharge Criteria 

All m ild corneal burns



Mandatory follow-up with ophthalm ologist in 12â€“24 hours; arrange before patient discharge

References 1. Bouchard CS, Morno K, Perkins J, et al. Ocular com plications of therm al injury. J Traum a. 2001;50:79â€“82. 2. Hooper M. Prom pt treatm ent for chem ical eye injuries. Nurs Stand

Pa ge 1 2 7

. 1997;11:40â€“43. 3. Keller G, Kuckelkorn R, Redbrake C, et al. Em ergency treatm ent of chem ical and therm al eye burns. Acta Ophthalm ologica Scandinavica. 2002;80:4. 4. Khaw PT, Shah P, Elkington AR. Injury to the eye. Br Med J. 2004;328:36â€“38. Available at http://www.bm j.com . 5. Lipshy KA, Wheeler WE, Denning DE. Ophthalm ic therm al injuries. Am Surg. 1996;62:481â€“483. 6. Markoff DD, Chacko D. Ophthalm ologic em ergencies. In: Em ergency Medicine Reports Textbook of Adult and Pediatric Em ergency Medicine. Atlanta: Am erican Health Consultants; 2000;1011â€“1021. 7. Michel FK, Sulewski ME. Focused assessm ent of the patient with eye traum a: the essentials. Topics Em erg Med. 2000;22:1â€“8. 8. Watts DD, Kokiko J. Air bags and eye injuries: assessm ent and treatm ent. J Em erg Nursing. 1999;25:572â€“574.

Miscellaneous SEE ALSO: Corneal Abrasion; Red Eye

Codes ICD9-CM 940.4 Other burn of cornea and conjunctival sac 940.3 Acid chem ical burn of cornea and conjunctival sac 940.2 Alkaline chem ical burn of cornea and conjunctival sac

ICD10 T26.1 Burn of cornea and conjunctival sac

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o rneal F o reign Bo dy

Corneal Foreign

Body David A. Harter

Basics Description 

Com m on com plaint: Som ething fell, flew, or otherwise landed in m y eye. o

Hot, high-speed projectiles m ay not produce pain initially.



Corneal epithelium disrupted: o

Abrasion if only epithelium disrupted

o

Scar if deeper layers of cornea involved

Etiology 



Poorly tolerated: o

Organic m aterial (plant m aterial, insect parts)

o

Inorganic m aterial that oxidizes (iron, copper)

Well tolerated: o

Inert objects (paint, glass, plastic, fiberglass, nonoxidizing m etals)

Pa ge 1 2 7

Diagnosis Signs and Symptoms 

Foreign body sensation



Eye pain



Conjunctiva and sclera injection



Tearing



Blurred or decreased vision



Photophobia



Visible foreign body or rust ring



Iritis

Essential Workup 

Injury history to determ ine type of foreign body and likelihood of perforation



Com plete eye exam : o

Visual acuity

o

Visual fields

o

Extraocular m ovem ents

o

Lids and lashes

o

Pupils

o

Sclera

o

Conjunctiva

o

Fundi: 

Slit-lam p



Fluorescein exam



Perform Seidel test (visualization of flow of aqueous through corneal perforation during fluorescein slit-lam p exam ination)



Intraocular pressure if no evidence of perforation



Exclude intraocular foreign body: o

Suspect intraocular foreign body with high-speed

Pa ge 1 2 7

m echanism s such as m achine operated or ham m ering m etal on m etal.

Tests Imaging 

Ocular CT or B-m ode ultrasound (US) when suspect intraocular foreign body



Orbital plain radiograph to screen for intraocular m etallic foreign body

Differential Diagnosis 

Conjunctival foreign body



Corneal abrasion



Corneal perforation with or without intraocular foreign body



Corneal ulcer



Keratitis

Treatment Pre Hospital Place a Fox shield and position the patient upright.

Initial Stabilization Apply topical anesthetic to stop eye discom fort and assist in exam ination.

ED Treatment 

Deep foreign bodies: o

Refer those penetrating the Bowm an m em brane (next layer under epithelium ) to an ophthalm ologist, because perm anent scarring m ay occur.

Pa ge 1 2 7



Superficial foreign bodies: o

Irrigation rem oval technique: 

Apply topical anesthetic



Try to wash foreign body off cornea by directing a stream of 0.9% norm al saline (NS) at an oblique angle to cornea.

o

25-gauge needle or foreign-body (FB) spud rem oval technique: 

Using slit-lam p to im m obilize patient's head and allow good visualization.



Hold needle (bevel up) with thum b and forefinger, allowing other fingers to be stabilized on the patient's cheek.



Lift foreign body off cornea, keeping needle parallel to corneal surface.



Rust rings rem oval: o

Within 3 hours, iron-containing foreign bodies oxidize, leaving a rust stain on adjacent epithelial cells.

o

Rem oval recom m ended as rust rings delay healing and act as an irritant focus

o

Rem ove with needle or pothook burr either at sam e tim e as foreign body or delayed 24 hours

P.267



Postrem oval therapy: o

Recheck Seidel test to exclude corneal perforation.

o

Treat resultant corneal abrasion with antibiotic drops.

o

Initiate cycloplegic agent when suspect presence of keratitis.

o

Update tetanus.

Pa ge 1 2 7

o

Initiate analgesia (nonsteroidal anti-inflam m atory drug [NSAID] or acetam inophen with codeine).

Pediatric Considerations May require sedation to facilitate exam and foreign body rem oval

Medication (Drugs) 

Cyclopentolate 1â€“2%: 1 drop t.i.d. (lasts up to 2 days)



Gentam icin ophthalm ic: 2 drops q6h



Hom atropine 2% or 5%: 1 drop daily (lasts up to 3 days)



Sulfacetam ide 10%: 1 drop q6h



Tobram ycin ophthalm ic: 2 drops q6h

Follow-Up Disposition Admission Criteria Globe penetration

Discharge Criteria 

All corneal foreign bodies



Ophthalm ologist follow-up in 24 hours for: o

Rust ring rem oval

o

Vegetative m aterial rem oval owing to risk of ulceration

References 1. Khaw P, Shaw P, Elkington A. ABC of eyes. Injury to the eye. Br Med J. 2004;328:36â€“38. 2. Levine L. Pediatric ocular traum a and shaken infant syndrom e. Pediatr Clin N Am . 2003;50:137â€“148.

Pa ge 1 2 7

3. Rhee D, Pyfer M. The Wills eye m anual: office and em ergency room diagnosis and treatm ent of eye disease. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 1999:24â€“26. 4. Santen S, Scott J. Ophthalm ologic procedures. Em erg Med Clin North Am . 1995;13(3):681â€“694.

Codes ICD9-CM 930

Pa ge 1 2 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ugh

Cough

Alison K. Sisitsky

Basics Description 

A sudden spasm odic contraction of the thoracic cavity resulting in violent release of air from the lungs and usually accom panied by a distinctive sound: o

Deep inspiration

o

Glottis closes

o

Expiratory m uscles contract

o

Intrapulm onary pressures increase

o

Glottis opens

o

Air expiration at high pressure

o

Secretion and foreign m aterial excretion

o

Vocal cord vibration with tracheobronchial walls, lung parenchym a, and secretions



Defense m echanism to clear the airway of foreign m aterial and secretions: o

Voluntary or involuntary

o

Reflex involves respiratory tissue receptor activation of afferent neurons to the central cough center followed by efferent output to the respiratory m uscles.

Pa ge 1 2 8

o

Mechanical receptors in larynx, trachea, and carina sense touch and displacem ent.

o

Chem ical receptors in larynx and bronchi are sensitive to gases and fum es.

o

Activated by irritants, m ucus, edem a, pus, and therm al stim uli.

Etiology 

Acuteâ€”<3 weeks: o

Com m on cold

o

Bacterial sinusitis

o

Allergic rhinitis

o

Environm ental irritant rhinitis

o

Pertussis

o

Exacerbation of chronic obstructive pulm onary disease





o

Pneum onia

o

Left ventricular failure

o

Asthm a

o

Pulm onary em bolism

Subacute: 3â€“8 weeks: o

Postinfectious cough

o

Bacterial sinusitis

o

Asthm a

o

Pulm onary em bolism

Chronicâ€”>8 weeks: o

Postnasal drip

o

Asthm a

o

Gastroesophagal reflux disease (GERD)

o

Chronic bronchitis

o

Bronchiectasis

o

Eosinophilic bronchitis

o

Angeotestin converting enzym e (ACE) inhibitor use

Pa ge 1 2 8

o

Bronchogenic carcinom a

o

Carcinom atosis

o

Sarcoidosis

o

Left ventricular failure

o

Aspiration syndrom e

o

Psychogenic/habit

Diagnosis Signs and Symptoms History 

Sputum production: o

Frothy (pulm onary edem a)

o

Mucopurulent

o

Suggestive of bacterial pneum onia or bronchitis but also seen with viral infections

o

Rust colored (pneum ococcal pneum onia)

o

â€œCurrant jellyâ€• (Klebsiella pneum onia)

o

Hem optysis



Posttussive syncope or em esis (suggests pertussis)



Shortness of breath



Chest pain



Chills/fever



Night sweats



Wheezing



GERD: o

Heartburn

o

Dysphagia

o

Regurgitation

o

Belching

Pa ge 1 2 8

o 

Early satiety

Malignancy: o

Weight loss

o

Poor appetite

o

Fatigue

Physical Exam 

Vital signs



Abnorm al breath sounds: o

Absence or decreased: reduced airflow vs. overinflation

o

Rales (crackles): popping or rattling when air opens closed alveoli 

o

Moist, dry, fine, coarse

Rhonchi: snoringlike sounds when large airways are obstructed

o

Wheezes: high-pitched sounds produced by narrowed airways

o 

Stridor: upper airway obstruction

Evidence of respiratory distress: o

Use of accessory m uscles

o

Abdom inal breathing

Essential Workup 



Com plete m edical history: o

Duration

o

Associated sym ptom s

o

Sm oking exposure

o

ACE inhibitor use

o

HIV/Im m unocom prom ised state

o

Potential exposure to tuberculosis

ECG: o

History of cardiac disease

Pa ge 1 2 8

o

Associated chest pain or abnorm al vital signs

o

Lack of infectious sym ptom s

Tests Lab Order according to presenting signs and sym ptom s: 

WBC count with differential



Sputum gram stain, cultures, and sensitivities



Acid fast bacilli (AFB) culture



CD4 count



Pertussis titers



D-dim er

Imaging 



Chest radiograph: o

For im m unosuppressed patient

o

Abnorm al lung sounds on exam

o

Ill appearing

o

Change in chronic cough

o

Continued cough after discontinuation of ACE inhibitor

CT of chest: o

Abnorm al chest radiograph

o

Assess for pulm onary em bolism

P.269

Diagnostic Procedures/Surgery 

Peak flow



Bronchoscopy: o

For unknown m ass on chest radiograph

o

Hem optysis

o

Suspected cancer

Pa ge 1 2 8

Differential Diagnosis See Etiology

Pediatric Considerations 







Most frequent causes: o

Asthm a

o

Sinusitis

o

GERD

Less com m on causes: o

Tracheobronchom alacia

o

Mediastinal tum or

o

Acyanotic congenital heart disease

o

Ventricular septal defect

o

Patent ductus arteriosus

o

Pulm onary stenosis

o

Tetralogy of Fallot

o

Lodged foreign body

o

Chronic aspiration of m ilk

o

Environm ental exposure

Consider: o

Neonatal history

o

Feeding history

o

Growth and developm ental history

o

Allergies

o

Eczem a

o

Sleep disorders

Indications for chest radiograph: o

Suspicion of foreign body ingestion

o

Suspect aspiration

Pa ge 1 2 8

Treatment Initial Stabilization Assess airway, breathing, and circulation.

ED Treatment Specific treatm ent related to cause: 

Respiratory infection: Consider antibiotics, decongestants, and antitussives.



Asthm a: inhaled Î² 2 -agonist and steroid



GERD: H 2 -blockers, proton pum p inhibitors, and antacids



Malignancy: supportive care

Medication (Drugs) 

Antitussives: o

Benzonatate (Tessalon Perles): 100â€“200 m g PO q6h

o

Codeine: 10â€“20 m g (peds: 1â€“1.5 m g/kg/d) PO q4hâ€“q6h

o

Dextrom ethorphan: 10â€“20 m g (peds: 1 m g/kg/d) PO q6hâ€“q8h

o

Hydrocodone: 5â€“10 m g (peds: 0.6 m g/kg/d q6hâ€“q8h) PO q6hâ€“q8h



Bronchodilators: o

Albuterol: 2.5 m g in 2.5 NS (peds: 0.1â€“0.15 m g/kg/dose q20 m in) q20m in inhaled

o

Ipratropium : 0.5 m g in 3 m L NS (peds: nebulizer 250â€“500 Âµg/dose q6h) q3h



Decongestants: o

Chlorpheniram ine: 4â€“12 m g (peds: 2 m g PO q4â€“6h) PO q4hâ€“q12h

o

Phenylpropanolam ine: 25â€“50 m g (peds:

Pa ge 1 2 8

6.25â€“12.5 m g PO q4h) PO q4hâ€“q8h 

Mucolytics: o

Guaifenesin: 5â€“20 m L (peds: 5â€“10 m L/dose if older than 6 years; 2.5â€“5 m L/dose if younger than 6 years) PO q4h



Steroids: o

Dexam ethasone: 2 sprays/nostril b.i.d.

o

Methylprednisolone: 60â€“125 m g IV (peds: 1â€“2 m g/kg/dose IV/PO q6h)

o

Prednisone: 40â€“60 m g (peds: 1â€“2 m g/kg/d q6hâ€“q12h) PO

Follow-Up Disposition Admission Criteria 

Hypoxem ia or critical illness



Suspected tuberculosis with positive chest radiograph result



Im m unocom prom ised with fever



Risk of bacterem ia or sepsis

Discharge Criteria 

Oxygenation at baseline for patient



Oral m edications



Safe environm ent at hom e

References 1. Barkin R, Rosen P. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby-Year Book Inc., 1998. 2. Irwin RS. Managing cough as a defense m echanism and as a

Pa ge 1 2 8

sym ptom . Chest. 1998;114(2):133Sâ€“181S. 3. Irwin RS. Prim ary care: the diagnosis and treatm ent of cough. N Engl J Med. 2000;343(23):1715â€“1721. 4. http://www.nlm .nih.gov/m edlineplus

Codes ICD9-CM 786.2

ICD10 R05

Pa ge 1 2 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ro up

Croup

Dale W. Steele

Basics Description 

Viral infection of the upper and lower respiratory tract



Most com m only presents in children 6 m onths to 3 years: o

Laryngotracheitis/laryngotracheo-bronchitis

o

Inspiratory stridor owing to extrathoracic airway obstruction

o

Expiratory wheeze suggests lower airway involvem ent.

o

Inflam m atory edem a of subglottic region

o

Narrowest part of pediatric airway



May progress to respiratory failure



Spasm odic croup: o

Sudden onset at night without viral prodrom e

o

Consistent response to m ist or cool night air

o

Often recurrent

o

May represent allergic reaction to viral antigen

Etiology 

Parainfluenza types 1, 2, and 3



Influenza A and B



Adenoviruses

Pa ge 1 2 9



Respiratory syncytial virus



Measles



Mycoplasm a pneum oniae



Herpes sim plex

Diagnosis Signs and Symptoms History 

Nonspecific upper respiratory prodrom e with or without fever



Duration of illness: o

Prior airway m anipulation

o

Possibility of foreign body aspiration



Previous episodes



Im m unization status (Haem ophilus influenzae Type b [HIB]; diphtheria, pertussis, and tetanus [DPT])

Physical Exam 

Toxic appearing?



Preferred position?



Quality of cry/voice?



Drooling/trism us/lim ited neck extension?



Mental status



Stridor at rest, increased work of breathing?



Hydration status:



Westley croup score (m axim um total points: 17) o

Stridor (inspiratory or biphasic) 

0 = None



1 = Audible with stethoscope at rest



2 = Audible without stethoscope at rest

Pa ge 1 2 9

o

o

o

o

Retractions: 

0 = None



1 = Mild



2 = Moderate



3 = Severe

Air entry: 

0 = Norm al



1 = Decreased



2 = Severely decreased

Cyanosis: 

0 = None



4 = With agitation



5 = At rest

Level of consciousness: 

0 = Norm al



5 = Altered

Essential Workup N/A

Tests Lab 

Pulse oxim etry



Other tests are not routinely indicated.

Imaging Anteroposterior (AP) and lateral neck radiographs: 

Steeple sign indicates narrowing of subglottic trachea.



Not routinely indicated, unless atypical presentation or clinical course



Subject to m isinterpretation



Should not delay definitive visualization and intubation in OR in child with concern for epiglottitis or bacterial

Pa ge 1 2 9

tracheitis 

Monitor child during im aging, if done.

Differential Diagnosis 

Infection: o

Bacterial tracheitis

o

Retropharyngeal or parapharyngeal abscess

o

Epiglottitis

o

Peritonsillar abscess

o

Diphtheria



Foreign body (airway or esophageal)



Angioedem a



Vocal cord paralysis



Congenital airway anom aly: o

Laryngom alacia



Acquired subglottic stenosis



Therm al injury to upper airway



Hem angiom a



Laryngeal papillom atosis



Vocal cord dysfunction (adolescents)

P.271

Treatment Pre Hospital 

Allow child to m aintain position of com fort.



Defer interventions that m ay distress child such as: o

IV access

o

IM injections

Pa ge 1 2 9



If severe distress: o

Im m ediate nebulized epinephrine with hum idified oxygen

Initial Stabilization 

Oxygen (via blowby) for suspected or docum ented hypoxia



Mist therapy often used, but of unproven efficacy



Dexam ethasone: o

Indicated in patients with stridor at rest and those receiving epinephrine

o

Effective even in m ild croup (Westley croup score â‰¤2)



Nebulized racem ic epinephrine or L-epinephrine if any distress or stridor at rest: o

L-epinephrine containing only the active isom er; has been shown to be therapeutically equivalent to racem ic epinephrine



If poor response to nebulized racem ic epinephrine or L-epinephrine: o



Consider trial of heliox.

Heliox, when available, has been used to decrease the work of breathing in patients with an incom plete response to epinephrine.



If im pending or existing respiratory failure despite aforem entioned therapy: o

Tracheal intubation by m ost experienced person available

o

Use uncuffed endotracheal tube (ETT) 0.5â€“1.0 m m sm aller than usual size.



If epiglottitis suspected: o

Ideally, to OR for inhalational anesthesia, direct laryngoscopy, and intubation

o

Surgeon standing by for em ergent tracheostom y

Pa ge 1 2 9

ED Treatment See Initial Stabilization

Medication (Drugs) 

Racem ic epinephrine 2.25%: 0.25â€“0.5 m L nebulized in 2.5 m L norm al saline (NS)



L-epinephrine 1:1,000: 5 m L (5 m g) nebulized



Dexam ethasone: single dose of 0.6 m g/kg (m ax. 10 m g) PO (use crushed tablet with flavored syrup). As effective when given PO, IV, or IM



Heliox (70% helium : 30% oxygen m ixture adm inistered via face m ask or tent house)



Antibiotics: not indicated

Follow-Up Disposition Admission Criteria 

Young infants, pre-existing upper airway obstruction



Persistent stridor at rest unresponsive to nebulized epinephrine



Recurrent stridor 3â€“4 hours after initial treatm ent with epinephrine and dexam ethasone. Children should norm ally be observed for a m inim um of 3 hours after adm inistration of epinephrine.



Pediatric intensive care unit (PICU): o

Persistent severe obstruction

o

Need for frequent epinephrine treatm ents and/or

Pa ge 1 2 9

heliox o

Tracheal intubation with assisted ventilation

Discharge Criteria 

Norm al oxygenation in room air



No stridor at rest after brief observation or



No recurrent stridor 3â€“4 hours after nebulized epinephrine



Reliable caretaker, com m unication, transport

Issues for Referral Concern for underlying anatom ic abnorm ality

References 1. Bjornson L, Klassen TP, William son J, et al. A random ized trial of a single dose of oral dexam ethasone for m ild croup. N Engl J Med. 2004;351:1306â€“1313. 2. Ham m er J. Acquired upper airway obstruction. Paediatr Respir Re. 2004;5:25â€“33. 3. Johnson D. Croup. Clin Evid. 2004;12:401â€“426. 4. Ledwith CA, Shea LM, Mauro RD. Safety and efficacy of nebulized racem ic epinephrine in conjunction with oral dexam ethasone and m ist in the outpatient treatm ent of croup. Ann Em erg Med. 1995;25:331â€“337. 5. Neto GM, Kentab O, Klassen TP, et al. A random ized controlled trial of m ist in the acute treatm ent of m oderate croup. Acad Em erg Med. 2002;9:873â€“879. 6. Rittichier KK, Ledwith CA. Outpatient treatm ent of m oderate croup with dexam ethasone: intram uscular versus oral dosing. Pediatrics. 2000;106:1344â€“1348. 7. Waism an Y, Klein BL, Boenning DA, et al. Prospective random ized double-blind study com paring L-epinephrine and racem ic epinephrine aerosols in the treatm ent of laryngotracheitis (croup). Pediatrics. 1992;89:302â€“306.

Pa ge 1 2 9

8. Weber JE, Chudnofsky CR, Younger JG, et al. A random ized com parison of helium -oxygen m ixture (heliox) and racem ic epinephrine for the treatm ent of m oderate to severe croup. Pediatrics. 2001;107:e96.

Codes ICD9-CM 464.4

ICD10 J05.0

Pa ge 1 2 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ushing Syndro m e

Cushing

Syndrome Hugh Schuckman

Basics Description 

Cushing disease: pituitary adenom a producing excess adrenocorticotropic horm one (ACTH)



Cushing syndrom e: excessive glucocorticoid effects

Genetics 

Multiple endocrine neoplasia type I



Carney com plex (pigm ented lentigines, atrial m yxom a, germ -cell tum ors with Cushing disease)

Etiology 

Most com m only exogenous adm inistration of glucocorticoids either therapeutically or surreptitiously



Pituitary adenom a secreting ACTH



Adrenal production of cortisol from adenom a, carcinom a, or m icronodular disease



Tum or-producing ectopic ACTH: o

Sm all cell lung carcinom a: 

Most com m on

Pa ge 1 2 9

o

Uterine cervical carcinom a

o

Islet cell tum or of pancreas: 

Multiple endocrine neoplasia (MEA) I-type syndrom e

o

Medullary thyroid cancer

o

Pheochrom ocytom a

o

Ganglioneurom a

o

Melanom a prostate carcinom a

o

Carcinoid tum or: 

Lung



Pancreas



GI tract



Thym us



Ovary

Diagnosis Signs and Symptoms Alert 

The m ost im portant aspect of Cushing syndrom e in the ED is recognizing the potential for addisonian (adrenal) crisis during periods of stress.



Although nonem ergent, the early recognition of Cushing syndrom e m ay prevent m orbidity and m ortality.

Pediatric Considerations Suspect if increasing in obesity while falling off in height on the growth chart

Pregnancy Considerations Cushing syndrom e rarely com plicates pregnancy, but has been associated with severe pre-eclam psia and HELLP syndrom e (h

Pa ge 1 2 9

em olysis, elevated liver function, and low platelets).

History 

Cushing disease previously diagnosed



Prior use of corticosteroids



Characteristic appearance should lead to questions concerning change in weight, facial appearance, hirsutism , or psychiatric sym ptom s.

Physical Exam 

Diagnosis suggested by: o

Abnorm al fat deposition with m oon facies

o

Buffalo hum p

o

Central obesity with thin extrem ities

o

Supraclavicular fat deposition

o

Above findings raise suspicion in a stressed patient of potentially developing addisonian (adrenal) crisis



Hypokalem ia while not on diuretic therapy



Cardiovascular:



o

Uncontrolled hypertension

o

Myocardial infarction

Neurologic: o

Atherosclerotic or em bolic stroke

o

Pseudotum or cerebri (prim arily with exogenous glucocorticoid adm inistration)

o

Spinal lipom atosis with cord or nerve-root com pression



Gastroenterologic: o

Peptic ulcers

o

GI hem orrhage

o

Pancreatitis (prim arily with exogenous glucocorticoid adm inistration)

o

Fatty liver

Pa ge 1 3 0





Psychiatric: o

Toxic psychosis

o

Mood disorders (40%)

o

Depression

o

Mem ory im pairm ent

o

Euphoria

Musculoskeletal: o

Myopathy (proxim al weakness)

o

Pathologic fractures

o

Osteoporosis

o

Aseptic necrosis hum eral or fem oral heads (prim arily with exogenous glucocorticoid adm inistration)

o 

Delayed bone age

Endocrine: o

Glucose intolerance

o

Hyperlipidem ia

o

Am enorrhea, fem ale with m ale pattern balding, or hirsutism





Hem atologic: o

Increased neutrophils

o

Decreased lym phocytes and eosinophils

o

Opportunistic infections

Ophthalm ologic: o

Cataracts (prim arily with exogenous glucocorticoid adm inistration)

o

Glaucom a (prim arily with exogenous glucocorticoid adm inistration)



Derm atologic: o

Purple striae >1 cm in diam eter

o

Hyperpigm entationâ€”especially of buccal m ucosa (from excess ACTH production)

o

Facial plethora

Pa ge 1 3 0

o

Thin skin

o

Im paired wound healing

o

Ecchym oses

o

Acne

o

Hyperhidrosis

Essential Workup 

Cannot confirm diagnosis in ED



Anticipate im pending addisonian (adrenal) crisis: o

Most frequent and com m on problem with Cushing syndrom e is its recognition in patient with intercurrent illness to prevent acute addisonian crisis.



Search for life-threatening conditions: o

Myocardial infarction

o

Stroke

o

Sepsis

o

Pathologic fracture

o

Uncontrolled DM

o

Psychiatric em ergency necessitating adm ission

P.273

Tests Lab 



Electrolytes, BUN, creatinine, glucose: o

Hypokalem ia

o

10% with m etabolic alkalosis

o

Dim inished glucose tolerance (75%): 

50% have glycosuria.



20% overt diabetes m ellitus (DM)

CBC: o

Increased WBCs

Pa ge 1 3 0

o

Decreased eosinophils

Imaging 

ECG for m yocardial ischem ia



Chest radiograph for tum or-causing ectopic ACTH



Plain film s if suspect possible pathologic fractures

Diagnostic Procedures/Surgery N/A

Nonemergent Testing 

MRI for pituitary tum or



CT for adrenal carcinom a, adenom a, or hyperplasia



Dexam ethasone-suppression test (follow-up study with prim ary physician): o

If suspicion of endogenous Cushing syndrom e exists

o

Low-dose (screening test): 1 m g at 11:00 PM with an 8 AM cortisol level drawn: 

Low specificity



Decrease false-positive results by stopping alcohol, estrogens, spironolactone, phenytoin, and barbiturates.

o

High-dose dexam ethasone-suppression test needed to confirm the diagnosis: 

2 m g q.i.d. of dexam ethasone with cortisol level 6 hours later



Com pare day 2 urine-free cortisol and 17-hydroxyketosteroids with baseline levels.

Differential Diagnosis 

Alcohol-induced pseudoâ€“Cushing syndrom e



Obesity



Psychiatric states: o

Depression

Pa ge 1 3 0



o

Obsessive-com pulsive disorder

o

Panic disorder

Physiologic states: o

Chronic stress

o

Third-trim ester pregnancy

o

Chronic strenuous exercise

Treatment Pre Hospital 

Acute addisonian (adrenal) crisis under stress m ay develop with iatrogenic Cushing syndrom e.



Patients m ay have extrem ely labile behavior with violent behavior.



Cause of death in untreated Cushing syndrom e is: o

Infection

o

Stroke

o

Myocardial infarction

Initial Stabilization 

Anticipate addisonian (adrenal) crisis.



Initiate treatm ent for associated com plications: o

Myocardial infarction

o

Stroke

o

Psychiatric stabilization

ED Treatment 

IV rehydration



Glucose-lowering agents for hyperglycem ia



Appropriate cultures and antibiotics for suspected infection



Antihypertensive agents for uncontrolled blood pressure (BP)

Pa ge 1 3 0



Adm inister steroids (hydrocortisone) with iatrogenic Cushing if patient under stress to prevent addisonian crisis.



Medications to lower cortisol levels (brom ocriptine, ketoconazole, am inoglutam ide, m etapyrone): o

Used rarely with severe sym ptom s in patients awaiting surgery

o

Institute under the direction of an endocrinologist.

Definitive Therapy 

Iatrogenic: o

Taper steroids as rapidly as possible,

o

Calcium , vitam in D, and estrogen supplem entation if possible



Pituitary Cushing: o

Transsphenoidal surgery

o

Radiation for surgical failures and a few select patients



Adrenal adenom a/carcinom a: o

Adrenal resection with m edical therapy for m etastatic lesions not resectable



Ectopic ACTH: o

Tum or resection (if possible) with m edical therapy for m etastatic lesions not resectable

Medication (Drugs) Hydrocortisone: 100 m g (peds: 1â€“2 m g/kg) IV q6h if adrenal crisis

Follow-Up

Pa ge 1 3 0

Disposition Admission Criteria 



Com plications that require adm ission such as: o

Myocardial infarction

o

Stroke

o

Sepsis

o

Pathologic fracture

o

Uncontrolled DM

o

Psychiatric em ergency

Im pending addisonian (adrenal) crisis

Discharge Criteria Well-appearing, stable patient without adm ission criteria

Issues for Referral 

Any patient suspected of Cushing syndrom e for further evaluation.



Conditions secondary to Cushing requiring treatm ent

References 1. Goldm an L, Bennett JC, eds. Cecil's Textbook of Medicine. 22nd ed. Philadelphia: WB Saunders; 2000. 2. Greenspan FS, Gardner DG. Basic and Clinical Endocrinology. 7th ed. Lange Publishers. 2003. 3. Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. Philadelphia: Mosby; 2002. 4. Wallach J, ed. Interpretation of Diagnostic Tests. 7th ed. Boston: Little, Brown and Com pany; 2000.

Codes ICD9-CM 255.0

ICD10

Pa ge 1 3 0

E24.9

Pa ge 1 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C yanide Po iso ning

Cyanide Poisoning

Kirk Cumpston

Basics Description 

Toxicity through inhalation, derm al, or GI tract absorption



Intracellular toxin that inhibits aerobic m etabolism through interruption of oxidative phosphorylation: o



Leads to decreased O 2 utilization and ATP production

Inhibits antioxidant defense enzym es; contributes to oxidative dam age



Stim ulates neurotransm itter release in CNS/peripheral nervous system (PNS)

Cyanide Detoxification Rhodanese: hepatic m itochondrial enzym e responsible for the m etabolism : 

Com bines cyanide (CN) with sulfur (rate-lim iting step) covalently (irreversible) to form less toxic and water-soluble thiocyanate (T-CN)



Form s less toxic reversible cyanhem oglobin when com bined with hem oglobin (Fe 2 + )



Form s nontoxic cyanocobalam in (B 1 2 ) when com bined with hydroxocobalam in (B 1 2 a )



Rate of CN rem oval requires adequate bioavailability of

Pa ge 1 3 0

sulfur com pounds (thiosulfate [TS]).

Etiology 

Fires: o

Com bustion by-product of natural and synthetic products



Vehicle exhaust



Industry:



o

Metal plating, m icrochip m anufacturing

o

Chem ical synthesis

o

Plastic m anufacturing

o

Pesticides

Solvents: o

Artificial nail rem over

o

Metal polishes



By-product of nitroprusside m etabolism (nonenzym atic)



By-product of Pseudom onas aeruginosa and pyocyaneus infections



Am ygdalin (converted by intestinal flora to CN)-containing plants (apricot and peach pits, apple and pear seeds, and cassava)



Jewelry m aking

Diagnosis Signs and Symptoms 

Derm al exposure: standard decontam ination



Oral exposure: can be caustic, 50 m g has caused death.



Inhalational exposure: o

50 parts per m inute causes anxiety, palpitations, dyspnea, headache.

Pa ge 1 3 0

o 

100â€“135 ppm <1 hour is lethal

Heart and brainâ€”m ost sensitive organsâ€”first to show m anifestation of toxicity







CNS: o

Headache

o

Confusion

o

Syncope

o

Seizures

o

Com a

Cardiovascular: o

Dyspnea

o

Chest pain

o

Cardiorespiratory collapse and death

Other: o

Nausea/vom iting

Essential Workup 

History of exposure (not routinely available)



Clinical clues (frequently absent): o

Peculiar odor of bitter alm onds

o

Bright red (arterialization) retinal vessels

o

Abrupt onset and/or deteriorating toxic effects

o

Lactic acidosis

o

High venous O 2 saturation (owing to blocked cellular O 2 consum ption); arterialization of venous blood gases

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose: o



Anion gap acidosis

Liver profile

Pa ge 1 3 1



Creatine phosphokinase (CPK)



Carboxyhem oglobin (CO) level



Methem oglobin (MH) level



CN level: o

Supports clinical diagnosis if perform ed in tim ely fashion

o

Analyze sam ple im m ediately after venipuncture because CN in vitro production and transform ation are both tim e and tem perature dependent:

o

Levels >0.5â€“1 m g/L: toxic

o

Levels 2.5â€“3.0 m g/L: fatal



Thiocyanate level



Blood gas determ inations: o

Increased arterial saturation gap (calculated direct [m easure] O 2 saturation [cooxim eter])

o

Elevated m ixed venous O 2 : MvO 2 (norm al about 35â€“40)

o

Elevated m ixed venous O 2 saturation (cooxim eter): Sm vO 2 (norm al about 75%)

o

Decreased arteriovenous O 2 difference: AVO 2 D (norm al about 3â€“4.8 m L/dL)



Elevated lactate level >8 m m ol/L

Imaging Chest x-ray

Differential Diagnosis 

Carbon m onoxide



Hydrogen sulfide



Methem oglobinem ia (MH)



Sulfhem oglobinem ia



Inert gases â€œasphyxiantsâ€•



Causes of high anion gap m etabolic acidosis

Pa ge 1 3 1

Treatment Pre Hospital 

Rem ove source of CN.



Prevent others from becom ing contam inated.



Rem ove and bag all contam inated clothing and wash affected areas copiously with soap and water. If vapor contam ination, rem oval of clothing m ay be all that is necessary.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o



Adm inister 100% oxygen: 

Even in presence of norm al PaO 2



Acts synergistically with antidotes

Gastric decontam ination for oral ingestions if within 1 hour: o

Perform gastric lavage and adm inister activated charcoal (AC) if ingestion of CN or CN-containing products and no contraindications.

o

Do not induce em esis.

P.275

ED Treatment Cyanide Antidote Kit 

Adm inister if m anifesting significant CN toxicity with persistent high anion gap m etabolic acidosis and narrow arteriovenous O 2 difference, and hypotension.

Pa ge 1 3 1



Adm inistration often instituted em pirically; CN levels not im m ediately available



Contents: am yl nitrite pearls, sodium nitrite, and TS



Nitrite action: o

Induce a CN-scavenging MH by oxidizing hem oglobin (Fe 2 + to Fe 3 + ), which attracts extracellular CN away from the m itochondria-form ing CN-MH, which is less toxic.

o 



Do not adm inister em pirically or prophylactically.

TS action: o

Substrate for the enzym e rhodanase

o

Com bines with CN to form a less toxic T-CN

o

May adm inister em pirically

Use clinical response and not m ethem oglobin levels to guide nitrite adm inistration.



Side effects of nitrites: o

Hypotension (nitrite-induced vasodilation)

o

MH: 

Does not function as O 2 transporter



Im pairs oxygen delivery



Elevated level leads to further tissue hypoxia.

Hydroxocobalamin (B 12a ) 

Alternate safe antidote



Binds to CN: o

Form s nontoxic cyanocobalam in (B 1 2 ); renally excreted





Advantages: o

No m ethem oglobin induction

o

Does not cause hypotension

Lim itations: o

Large am ount needed to successfully treat poisoned patients (50 g B 1 2 a :1 g CN)

Pa ge 1 3 1

o

Use of TS com bined with B 1 2 a m ay reduce am ount of B 1 2 a required.

o

Available only in Europe

Combined TS and B 12a Therapy 



Victim s of sm oke inhalation m ay have com bination of: o

CN toxicity

o

MH

o

CO toxicity

Avoid further reduction in oxygen transport; initially treat with TS and/or B 1 2 a until CO and MH levels are known.

Hyperbaric Oxygen Therapy 

Maxim izes tissue oxygenation despite toxic MH level



Use as adjunct to aforem entioned antidotes in severe cases or when antidotes have failed.

Antidote Alternatives 

Not yet FDA approved



Do not institute em pirically because of toxicity.



Dicobalt edetate: o

Inactivates CN by chelation

o

Associated with hypertension, dysrhythm ias, and m etabolic acidosis



Dim ethylam inophenol: o

Induces a m uch faster scavenging m ethem oglobinem ia

o

Nephrotoxic

Medication (Drugs) 

AC: 1â€“2 g/kg PO



Hydroxocobalam in (B 1 2 a ): o

Dose equivalent to 50 tim es am ount of CN exposure

Pa ge 1 3 1

infused in 30 m inutes o

Em piric single dose, 4â€“5 g (50 m g/kg) IV in D 5 W

o

Prophylactic IV infusion at 25 m g/h in Nipride usage

Cyanide Antidote Kit (Eli Lilly Antidote Kit) 

Am yl nitrite pearls: o

Crush one or two am pules in gauze and hold close to nose, in lip of face m ask, or within Am bu bag

o

Inhale for 30 seconds to 1 m inute until IV access obtained.



Sodium nitrite (NaNO 2 ): 10 m L (300 m g) (peds: 0.15â€“0.33 m L/kg) IV as 3% solution over 5â€“20 m inutes: o

May repeat once at one-half dose within 30â€“60 m inutes



o

Keep MH level <30%.

o

Dilute; infuse slowly if hypotensive.

Sodium thiosulfate: 50 m L: 12.5 g (peds: 0.95â€“1.95 m L/kg) IV over 10â€“15 m inutes of 25% solution: o

Half initial dose m ay be given after 30â€“60 m inutes.

Follow-Up Disposition Admission Criteria ICU adm ission of all sym ptom atic exposures

Discharge Criteria 

Asym ptom atic patients after at least 4 hours of observation



Survival after 4 hours of acute exposure usually associated

Pa ge 1 3 1

with com plete recovery

References 1. Baud F, Borron S, Megarbane B, et al. Lactic acidosis in cyanide poisoning: pathophysiology and clinical considerations. J Toxicol Clin Toxicol. 2001;39:244. 2. Eyer P. Therapeutic im plications of the toxicokinetics and toxicodynam ics in cyanide poisoning. J Toxicol Clin Toxicol. 2000;38(2):212â€“214. 3. Ford M, Delaney K, Ling L, et al. Clinical Toxicology. Philadelphia: WB Saunders; 2001:705â€“711. 4. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Corp; 2002:424â€“426, 665.

Codes ICD9-CM 989.0

ICD10 T65.0

Pa ge 1 3 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C yano sis

Cyanosis

Michael S. Murphy

Basics Description 

Caused by abnorm al elevations of hem oglobin or hem oglobin derivatives:



o

Reduced hem oglobin >5 g/dL

o

Methem oglobin >1.5 g/dL

o

Sulfhem oglobin >0.5 g/dL

The am ount of oxyhem oglobin does not affect the blood's color.



Cyanosis is m ore com m on in patients with polycythem ia.



Cyanosis is less com m on in patients with anem ia.



Methem oglobinem ia cyanosis presents with norm al PO 2 and chocolate-colored blood.

Etiology Central Cyanosis/Decreased Saturation 

Im paired pulm onary function: o

Hypoventilation: 

Pneum onia



Chronic obstructive pulm onary disease



Pulm onary edem a

Pa ge 1 3 1

o

o

Ventilation/perfusion m ism atch: 

Asthm a



Pulm onary em bolus

Diffusion problem s: 



Interstitial lung disease

Anatom ic shunts: o

o

Congenital cardiac causes: 

Transposition



Tetralogy

Pulm onary arteriovenous fistula: 

o

Hereditary hem orrhagic telangiectasia

High-altitude related, with decreased atm ospheric pressure at 16,000 feet



Low-oxygen affinity hem oglobin m utants: o

Hb Kansas

o

Beth Israel

o

St. Mande

Central Cyanosis/Hemoglobin Abnormalities 

Methem oglobinem ia: o

o



Congenital: 

Cytochrom e b5 reductase deficiency



Hem oglobin M disease

Most cases are acquired: 

Aniline dyes



Chloroquine, prim aquine



Dapsone



Local anesthetic agents such as lidocaine



High doses of m ethylene blue



Naphthalene



Nitrites, nitroglycerine



Sulfonam ides

Sulfhem oglobin:

Pa ge 1 3 1

o

Generally benign

o

Irreversible alteration of hem oglobin

o

Caused by m any m edications: 

Dim ethyl sulfoxide



Paint



Phenacetin



Phenazopyridine



Phenylenediam ine



Phenylhydroxylam ine



Sulfanilam ide



Sulfapyridine



Sulfathiazole



Sulfur com pounds

Peripheral Cyanosis 

Vasoconstriction to cold air or water



Arterial obstruction seen in em boli or Raynaud



Venous obstruction throm bophlebitis



Decreased cardiac output com pensatory vasoconstriction

Differential Cyanosis 

Lower extrem ities involved, but upper extrem ities spared



Patent truncus arteriosus or pulm onary hypertension

Pediatric Cyanosis 

Cardiac: o

o

Cyanotic congenital defects: 

Tetralogy of Fallot



Transposition of great vessels



Truncus arteriosus



Pulm onary and tricuspid atresia



Ebstein anom aly

Total anom alous pulm onary venous return: 

Pulm onary stenosis

Pa ge 1 3 1

 

Any right-to-left shunting

Respiratory: o

o

Upper airway disorders 

Croup:



Bacterial tracheitis



Epiglottitis



Retropharyngeal abscess



Foreign body



Traum a

Lower airway disorders: 

Asthm a



Bronchiolitis



Pneum onia



Cystic fibrosis



Pulm onary edem a/congestive heart failure



Pulm onary em bolism



Chest wall injury



Pleural disorders such as pneum othorax or diaphragm atic hernia



Neurologic: o

CNS injury/lesions

o

Infection

o

Seizure

o

Toxins

o

Breath holding

o

Hem oglobinopathy

Diagnosis Signs and Symptoms 

A bluish discoloration of the skin and m ucous m em branes:

Pa ge 1 3 2

o

Chocolate color: 

o

Slate gray color: 

o 



Methem oglobinem ia

Methem oglobinem ia or sulfhem oglobin

Varies based on skin thickness or pigm ent

Central or generalized: o

Visible in lips, nailbeds, ears, or m alar regions

o

Peripheral or local cyanosis:

o

Lim ited to extrem ities

Differential cyanosis: o

Lower extrem ities involved, but upper extrem ities spared

o

Clubbing

o

Dyspnea

o

Fatigue

o

Headache

o

Occupational exposure or use of certain chem icals or drugs



Asym ptom atic: o

Suggests m ethem oglobinem ia

Essential Workup 

Assess airway and ventilation as first priority: o



Stabilize airway and provide adequate ventilation.

Investigate hypoxem ia causes: o

Cardiac and respiratory m ost com m on

o

Consider m ethem oglobinem ia.

Tests Lab 

Pulse oxim etry: o

Does not assess ventilation

o

Results inaccurate with:

Pa ge 1 3 2





Abnorm al hem oglobins



Nail polish



Pigm ented skin



Hypoperfusion



Used of vital dyes

Arterial blood gas: o

Oxygen tension

o

Measured hem oglobin saturation

o

Cyanosis in face of norm al PO 2 , think m ethem oglobinem ia



o

Blood in m ethem oglobinem ia is chocolate color.

o

Methem oglobin level

Com plete blood chem istry: o



Check hem oglobin.

Hyperoxia test for congenital cyanosis of newborn: o

If PO 2 fails to increase to 100 m m Hg after 100% O 2 , suspect congenital heart disease.

P.277

Imaging 

Chest radiograph to investigate respiratory or cardiac pathology:





o

Inspiratory/Expiratory views if foreign body

o

Expiratory view if occult pneum othorax suspected

Radiograph of neck for upper airway disorders: o

Foreign body

o

Steeple sign (croup)

o

Prevertebral swelling (retropharyngeal abscess)

o

Epiglottic swelling

ECG: o

Dysrhythm ia, injury, or ischem ia

Pa ge 1 3 2



Echocardiography: o

Bubble study if septal defect/shunt suspected

o

Wall m otion/valvular abnorm alities

o

Pericardial fluid

Differential Diagnosis 



Hyperpigm entation: o

Drugs or m etals

o

Chronic high-dose chlorprom azine

o

Minocycline

o

Argyria (silver deposits)

o

Tattoos

Polycythem ia

Treatment Pre Hospital 

Assess and establish patent airway.



Correct any airway obstruction.



Recognize an incorrectly placed airway.



One hundred percent O 2 using a nonrebreathing device



Ensure adequate ventilation.



Recognize need to establish definitive airway.



Protect cervical spine if traum a suspected.



IV line, m onitor, pulse oxim etry



Albuterol nebulizer for bronchospasm



Racem ic epinephrine nebulizer for severe croup



Managem ent of pulm onary edem a per protocol

Initial Stabilization 

Oxygen supplied through a 100% nonrebreathing device



Im m ediately assess and address airway issues.

Pa ge 1 3 2

ED Treatment General m easures: 

Recognize and m anage cardiopulm onary disorders.



Methylene blue for m ethem oglobinem ia exceeding 30%: o

Do not use if patient has G6PD deficiency.

Medication (Drugs) 

Albuterol nebulized: 0.03 m L/kg (5 m g/m L)



Dexam ethasone: (for croup) 0.6 m g/kg IV/IM



Furosem ide: 1.0 m g/kg IV q6h



Magnesium : 2.0 g IV over 10 m inutes (40 m g/kg IV over 20 m inutes)



Methylene blue: 1â€“2 m g/kg IV of 1% solution over 5 m inutes



Methylprednisolone: 1â€“2 m g/kg IV q6h



Morphine: 2â€“4 m g IV (0.05â€“0.1 m g/kg IV g2h PRN)



Nitroglycerine: 0.4 m g sublingually or IV (0.5â€“5 Âµg/kg/m in IV)



Prostaglandin E 1 : 0.05â€“0.1 Âµg/kg/m in IV; m axim um 0.4 Âµg/kg/m in



Racem ic epinephrine nebulized: 0.05 m L/kg

Follow-Up Disposition Admission Criteria Most affected patients should be adm itted to hospital: 

Intensive care unit adm ission is required for any instability

Pa ge 1 3 2

or cyanosis.

Discharge Criteria Reversible causes of hypoxia: 

Reactive airway disease responsive to Î²-agonists



Pulm onary edem a in patient with known congestive heart failure but no suspicion of m yocardial injury and diuresis

References 1. Braunwald E. Hypoxia, polycythem ia, and cyanosis. In: Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994:178â€“183. 2. Mansouri A, Lurie A. Concise review: m ethem oglobinem ia. Am J Hem atol. 1993;42:7â€“12. 3. Stack A. Cyanosis. In: Synopsis of Pediatric Em ergency Medicine. 4th ed. Philadelphia, PA: Lippincott William s & Wilkins; 2002:64â€“67. 4. Wright RO, Lewander WJ, Woolf AD. Methem oglobinem ia: etiology, pharm acology, and clinical m anagem ent. Ann Em erg Med. 1999;34:646â€“656.

Codes ICD9-CM 782.5 Cyanosis

Pa ge 1 3 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ystic F ibro sis

Cystic Fibrosis

Roger Barkin

Basics Description 

Defect of the cystic fibrosis transm em brane conductance regulator (CFTR)



CFTR functions as an ATP-regulated chloride channel that regulates the activity of chloride and sodium channels on the cell surface: o

Abnorm al electrolyte transport in exocrine glands and secretory epithelia

o

Decreased exocrine pancreatic function with m alabsorption

o

Thickened m ucus, recurrent pulm onary infections, and progressive obstructive dam age to the lungs



Occurs in 1:3,500 live births



More prevalent in white populations (1/2,500)



Diagnosed in the first decade of life in about 70% of cases



Approxim ately 30,000 children and young adults in United States have CF.



Median life expectancy in the United States is about 30 years.



Approxim ately 40% of CF patients are older than 18 years

Pa ge 1 3 2

of age. 

10 m illion Am ericans are unknown, asym ptom atic carriers of the defective gene.

Alert An acute or chronic respiratory problem in a patient with CF requires pulm onary consultation.

Genetics Recessively inherited genetic disease, involving the CFTR gene on the long arm of chrom osom e 7: 

Different m utations produce variable phenotypes.



Classic disease is hom ozygous for the DF508 m utation.

Etiology Com m on organism s in patients with pneum onia; often m ultiple drug resistance: 

Pseudom onas aeruginosa o

Prevalence increases with age; 70% of adults are chronically infected.



Haem ophilus influenzae



Staphylococcus aureus



Burkholderia cepacia:



Prevalence 5%



Associated with rapid clinical deterioration



Aspergillus

Diagnosis Signs and Symptoms 

General: o

Failure to thrive

o

Recurrent respiratory tract infections

Pa ge 1 3 2





o

Anasarca in infancy

o

Salty taste of skin

Head, ears, eyes, nose and throat (HEENT): o

Nasal polyps

o

Severe headaches owing to sinusitis

Pulm onary: o

Persistent, dry hacking paroxysm al cough

o

Recurrent pneum onitis or bronchiolitis in the first year of life





o

Wheezing

o

Hem optysis

o

Pneum onia

o

Respiratory distress

o

Pneum othorax

o

Most com m on cause of hospitalization

Cardiac: o

Congestive heart failure (CHF)

o

Cor pulm onale

o

Pulm onary hypertension

GI: o

Abdom inal pain

o

Distal ileal obstructive syndrom e or â€œm econium ileus equivalentâ€•



o

Cholelithiasis

o

Pancreatitis

o

Ileocecal intussusception

o

Foul sm elling, fatty stools

o

Jaundice

o

Cirrhosis or cholelithiasis

o

Rectal prolapse

o

Hem atem esis

Extrem ities:

Pa ge 1 3 2



o

Bone pain

o

Edem a

o

Joint effusions

Cardiorespiratory failure is m ost com m on cause of death.

Essential Workup 

Test patients with chronic or unusual respiratory and GI com plaints.



Prior culture results m ay be helpful in patients with known CF.

Tests Lab 

Sweat chloride test: o

Chloride concentration >80 m Eq/L

o

With classic signs and sym ptom s, a positive test result confirm s the diagnosis.







Stool sam ple: o

Trypsin or chym otrypsin absent or dim inished

o

Increased fat in 72-hour fecal fat excretion

Im m unoreactive trypsin (IRT): o

Defines increased risk and/or diagnosis

o

May be falsely positive or negative

Cytogenetic analysis: o

Indicated if sym ptom s are highly suggestive, but sweat test result is negative

o

Positive if two abnorm al genes present

o

Genotyping, however, cannot establish the diagnosis.

o

Detects 70 of 500 CTFR m utations

o

Am eliorating or neutralizing second m utation m ay be present.



CBC: o

Throm bocytopenia

Pa ge 1 3 2



Serum electrolytes: o



Hyponatrem ic, hypochlorem ic alkalosis

Serum glucose: o

Hyperglycem ia and new-onset diabetes occurs prim arily in adolescents and adults; ketoacidosis is rare.



Liver function tests and PT: o

Indicated when CF is com plicated by hem atem esis or signs of liver failure





ABG: o

Hypoxem ia

o

Metabolic alkalosis

Sputum culture: o

Determ ine whether pseudom onal colonization is present.

o

Studies indicated in patients at high risk with a difficult diagnosis



Sem en analysis: o

Azoosperm ia

o

Nasal potential-difference m easurem ents

o

Com plex and tim e-consum ing study

Imaging 

Chest radiograph: o

Hyperaeration

o

Peribronchial thickening

o

Atelectasis

o

Hilar lym phadenopathy

o

Possible pneum othorax

o

Bronchiectasis

o

Blebs

o

Com pare with previous chest radiograph for acute pulm onary deterioration.

Pa ge 1 3 3

P.279



Abdom inal radiographs: o

Indicated if abdom inal pain, vom iting, or abdom inal distention



o

Distal ileal obstruction syndrom e

o

Intussusception

Barium enem a: o



Indicated if suspicion of intussusception

Sinus film s: o

Lim ited use because routine sinus film s are always cloudy

o

CT scan is needed to assess sinuses.

Diagnostic Procedures/Surgery Bronchoalveolar lavage: 

High percentage of neutrophils and absolute neutrophil count



Unnecessary in patients with obvious pulm onary sym ptom s

Differential Diagnosis 





Respiratory: o

Asthm a

o

Recurrent pneum onia

o

Bronchiectasis

o

Pertussis

o

Im m unodeficiency

GI: o

Chronic diarrhea

o

Gastroenteritis

o

Milk allergy

Elevated electrolyte levels in sweat:

Pa ge 1 3 3

o

Fucosidosis

o

Glycogen storage disease type I

o

Mucopolysaccharidosis

o

Hypothyroidism

o

Vasopressin-resistant diabetes insipidus

o

Adrenal insufficiency

o

Fam ilial cholestasis

o

Fam ilial hypoparathyroidism

o

Malnutrition

o

Ectoderm al dysplasia

o

Atopic derm atitis

o

Infusion of prostaglandin E 1

Treatment ED Treatment 

Stabilize airway, breathing, and circulation (ABCs): o

Correct fluid, respiratory, electrolyte, and glucose abnorm alities.





Pneum othorax: o

Observe if <5â€“10%

o

Thoracostom y

Consultation with the prim ary CF physician or pulm onary specialist



Right heart failure: o





Diuretics

Hem optysis: o

Blood products as indicated

o

Ventilatory support

Distal ileal obstructive syndrom e: o

Usually requires surgery

Pa ge 1 3 3

o

Blood products are used for the correction of coagulation abnorm alities, and red cells m ay be required for replacem ent in hem atem esis.

o

Early consultation with an endoscopist to find the cause and help with therapy of hem atem esis is useful.

o

Intussusception can be corrected with barium enem a, but at tim es requires surgery,

o

Manual reduction of rectal prolapse; surgical consult for difficult case or for recurrence



o

Pulm onary toilet/physical therapy

o

Mucous thinning inhaled agents

Antibiotics: o

Based on culture and sensitivity

o

Pneum onia

o

S. aureus:

o



Cephalothin



Nafcillin

H. influenzae: 

o

Ticarcillin and clavulanate

P. aeruginosa: 

Tobram ycin and ticarcillin



Azithrom ycin m ay have adjunctive role.



Inhaled tobram ycin (adults: 300 m g b.i.d.) has been shown to im prove pulm onary function and decrease risk of hospitalization.

o

S. aureus and P. aeruginosa: 

o

P. aeruginosa and Burkholderia cepacia: 

o

Ticarcillin and tobram ycin

Ceftazidim e and ciprofloxacin

B. cepacia: 

Chloram phenicol

Pa ge 1 3 3



Trim ethoprim -sulfam ethoxazole

o

Sinusitis:

o

Antibiotics based on cultures and sensitivities



Future directions



Genetically engineered enzym es to thin m ucous in lungs



Gene therapy

Medication (Drugs) 

Azithrom ycin: 10 m g/kg PO loading; 5 m g/kg PO daily



Ceftazidim e: 50â€“75 m g/kg IV q8h



Cephalothin: 25â€“50 m g/kg IV q6h



Chloram phenicol: 15â€“20 m g/kg IV q6h



Gentam icin: 3 m g/kg IV q8h



Nafcillin: 25â€“50 m g/kg IV q6h



Ticarcillin: 100 m g/kg IV q6h



Trim ethoprim -sulfam ethoxazole: 5â€“25 m g/kg IV q12h



Note: Because m any patients are undernourished, pharm acokinetics of antibiotics (especially am inoglycosides, penicillins, and cephalosporins) m ay be altered, requiring careful m onitoring.

Follow-Up Disposition Admission Criteria 

Pulm onary exacerbation with significant deterioration from baseline, resistant bacteria, failure of outpatient therapy



Hem optysis



Hem atem esis

Pa ge 1 3 3



Intussusception or unexplained abdom inal pain



Hyperglycem ia

Discharge Criteria 

Close follow-up to verify the sensitivities of culture results and change therapy as needed



Avoid hot weather.



Oral salt supplem ents during tim es of profuse sweating



Chloride sweat test of newly diagnosed child with CF

Issues for Referral All patients with cystic fibrosis should be followed by a pediatric pulm onary center to ensure com prehensive m anagem ent. Consultation is appropriate during acute exacerbations.

References 1. Farrell DM, Kosorok MR, Rock MT, et al. Early diagnosis of cystic fibrosis through neonatal screening prevents severe m alnutrition and im proves long term growth. Pediatrics. 2001;107:113. 2. Nishioka GJ, Cook PR. Paranasal sinus disease in patients with cystic fibrosis. Otolaryngol Clin North Am . 1996;29(1):193â€“205. 3. Ram sey BW. Managem ent of pulm onary disease in patients with cystic fibrosis. N Engl J Med. 1996;335(3):179â€“188. 4. Ram sey BW, Pepe MS, Quan TJ. Interm ittent adm inistration of inhaled tobram ycin in patients with cystic fibrosis. N Engl J Med. 1999;340:24â€“30. 5. Stern RC. The diagnosis of cystic fibrosis. N Engl J Med. 1997;336:487â€“490.

Codes ICD9-CM 277.0

ICD10

Pa ge 1 3 3

E84.9

Pa ge 1 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dacryo adenitis

Dacryoadenitis

Shari Schabowski

Basics Description 

Inflam m ation of lacrim al gland



Prim ary infection of lacrim al gland: o

Secondary to contiguous spread from bacterial conjunctivitis or periorbital cellulitis



Uncom m on

Etiology Noninfectious Most diseases causing inflam m ation of lacrim al gland are not infectious: 

Autoim m une diseases



SjÃ¶gren syndrom e



Sarcoidosis



Tum or: o

More than 25% of all lacrim al gland swelling

Infectious 

Infection m ay be prim ary or m ay occur secondary to contiguous spread from bacterial conjunctivitis or periorbital cellulites.

Pa ge 1 3 3



Acute, suppurative: o



Bacteria m ost com m on cause in adults: 

Staphylococcus aureus



Streptococci



Chlam ydia trachom atis



Neisseria gonorrhoeae

Chronic dacryoadenitis: o

Viruses m ost com m on cause in children: 

Mum ps



Measles



Epstein-Barr virus



Cytom egalovirus



Coxsackievirus



Varicella-zoster virus

Diagnosis Signs and Symptoms 

May present as sudden-onset, unilateral eyelid erythem a or indolent swelling (bilateral uncom m on)



Swelling and tenderness greatest in tem poral aspect of upper lid under orbital rim : o

Mass m ay be palpable.

o

May be associated with: 

Extensive cellulitis



Conjunctival discharge



Increase or decrease in tear production



Ipsilateral conjunctival injection and chem osis



Ipsilateral preauricular adenopathy



Norm al visual acuity, slit-lam p, and funduscopic exam s



Chronic form : slowly progressive, painless swelling

Pa ge 1 3 3

without system ic sym ptom s

Pediatric Considerations Slowly enlarging m ass m ay be derm oid.

Essential Workup 

Determ ine likelihood of gonorrhea as cause: o



High-risk system ic illness and visual loss

Com plete eye exam , including visual acuity, slit-lam p, and funduscopic exam s

Tests Lab 

Gram stain and culture of drainage: o



May identify pathogen and guide therapy

CBC

Imaging 

Radiographic studies generally unnecessary



Orbital CT: o

If diagnosis unclear, to rule out orbital cellulitis, tum or, or other cause

Differential Diagnosis 

Autoim m une diseases



Lacrim al gland tum or



Hordeolum



Periorbital (preseptal) cellulitis



Severe blepharitis



Orbital cellulitis



Acute conjunctivitis



Acute dacryocystitis



Insect bite



Traum atic injury

Pa ge 1 3 3

Treatment Initial Stabilization Exclude orbital cellulitis

ED Treatment 

Cool com presses to decrease inflam m ation and pain



Antibiotics: o

o

Oral for m ild infection: 

Cephalexin



Am oxicillin/clavulanate

Intravenous for severe infection: 

Cefazolin



Ticarcillin/clavulanate



Analgesics



Tetanus toxoid if necessary



Incision and drainage rarely necessary except in very severe cases: o

Perform with consultation to facial surgery service or ophthalm ology

P.281

Pediatric Considerations 

Cool com presses



Analgesics



If cause unclear, treat with antibiotics as with adults.

Medication (Drugs)

Pa ge 1 3 4



Am oxicillin/clavulanate (Augm entin): 500 m g (peds: 20â€“40 m g of am oxicillin/kg/24h) PO q8h



Cephalexin: 500 m g (peds: 25â€“100 m g/kg/24h) PO q.i.d.



Cefazolin: 500â€“1,000 m g (peds: 50â€“100 m g/kg/24h) IV q6hâ€“q8h



Ticarcillin/clavulanate: 3.2 g (peds: 200â€“300 m g of ticarcillin/kg/24h) IV q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

Acutely ill, toxic appearance



Im m unocom prom ised

Discharge Criteria Patient appears well and can tolerate oral antibiotics.

References 1. Boruchoff SA, Boruchoff SE. Infections of the lacrim al system . Infect Dis Clin North Am . 1992;6:925â€“932. 2. Brook I, Frazier EH. Aerobic and anaerobic m icrobiology of dacryoadenitis. Am J Ophthalm ol. 1998;125:552â€“554. 3. Kanski JJ. Clinical Ophthalm ology. Oxford, England: Butterworth-Heinem ann; 1994:66â€“69. 4. Rhee DJ, Pyfer MF, Rhee DM. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. Philadelphia: Lippincott William s & Wilkins; 1999. 5. Rubin S, Hallagan L. Lids, lacrim als, and lashes. Em erg Med Clin North Am . 1995;13:631â€“648.

Pa ge 1 3 4

Miscellaneous SEE ALSO: Dacryocystitis

Codes ICD9-CM 375.00 Dacryoadenitis

ICD10 H04.0 Dacryoadenitis

Pa ge 1 3 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dacryo cystitis

Dacryocystitis

Shari Schabowski

Basics Description 

Suppurative infection involving the lacrim al sac which is located below the m edial aspect of the eye and accessed through lacrim al ducts in the inner canthus

Epidemiology 

Occurs m ost com m only in infants and postm enopausal wom en



Congenital nasolacrim al obstruction owing to stenosis occurs in approxim ately 2â€“4% of full-term newborns (presents as acute dacryocystitis).

Etiology 

Under norm al conditions, tears drain via pum ping action at lacrim al duct, m oving tears to lacrim al sac and then to m iddle turbinate and into sinuses.



Sym ptom s begin when duct to lacrim al sac becom es partially or com pletely obstructed: o

Stasis in this conduit results in overgrowth of bacteria and infection.



May also occur secondary to traum a, a dacryolith, after

Pa ge 1 3 4

nasal or sinus surgery, or with chronic inflam m ation 

Infection m ay be recurrent and m ay becom e chronic.



Most com m on bacteria: ocular and sinus flora



Staphylococcus aureus is m ost com m on organism in acquired acute dacryocystitis.

Pediatric Considerations 

Congenital nasolacrim al obstruction owing to stenosis presents as acute dacryocystitis.



Most com m on organism in congenital dacryocystitis: Streptococcus pneum onia

Diagnosis Signs and Symptoms 

Unilateral, red, painful, swollen m ass extending inferiorly and m edially from inner canthus



Epiphora or excessive tearingâ€”hallm ark sym ptom



Discharge from punctum



Cellulitis extending to lower lid in som e cases



Low-grade fever m ay be present, but patient rarely appears toxic.

Essential Workup 

Apply pressure to m ass: Expression of purulent m aterial from punctum confirm s diagnosis.



Com plete eye exam , including visual acuity, slit-lam p, and funduscopic exam s.



Exam ine nasal passages.

Tests Lab

Pa ge 1 3 4

Tests of expressed m aterial (used to help direct specific antibiotic treatm ent) 

Gram stain



Culture and sensitivity



Chocolate agar plating

Imaging CT of orbit/sinus to evaluate deep tissue extension, particularly with recurrent cases

Differential Diagnosis 

Insect bite



Traum atic injury



Acute ethm oid sinusitis



Acute m axillary sinusitis



Periorbital (preseptal) cellulitis



Orbital cellulitis



Acute conjunctivitis



Acute blepharitis

Treatment Initial Stabilization 

Confirm diagnosis by expressing purulent m aterial.



Begin treatm ent to avoid extension of infection to adjacent structures.



Determ ine whether sym ptom s are recurrent.

ED Treatment 

Drainage of infected sac is essential: o

Warm com presses and gentle m assage to relieve obstruction

Pa ge 1 3 4

o

May facilitate outflow from obstructed tract with nasal introduction of vasoconstricting agent





Incision and drainage in severe cases: o

Typically done by ophthalm ology

o

Avoid in ED when possible.

o

May result in fistula form ation

Duct instrum entation to facilitate drainage is not indicated in acute setting (controversial): o

Reserve instrum entation for nonacute setting, if necessary at all.

o

Only 50% of adults show im provem ent after m anipulation.

o

Manipulation while duct is inflam ed m ay cause injury to duct and perm anent obstruction from scarring and stenosis.



Topical ophthalm ic antibiotic drops to prevent secondary conjunctivitis



System ic antibiotics to resolve infection and prevent spread to adjacent structures:



o

Oral for m ild infection

o

Intravenous when febrile or severe infection

Analgesics

P.283

Pediatric Considerations 

Newborns respond well to m assage and topical antibiotics in about 95% of cases.



If no resolution in first year of life, m ay require probing of duct by ophthalm ologist



Children <4 years old who develop dacryocystitis: o

At increased risk for Haem ophilus influenzae infection

Pa ge 1 3 4

if not im m unized o

Haem ophilus influenzae type B carries high risk for bacterem ia, septicem ia, and m eningitis.

o

Treat afebrile, well-appearing children with responsible parent with oral cefaclor or am oxicillin/clavulanate.

o

Adm inister cefuroxim e intravenously in acutely ill patients.

Medication (Drugs) 

Am oxicillin/clavulanate (Augm entin): 500 m g (peds: 20â€“40 m g of am oxicillin/kg/24h) PO q8h



Cefaclor: 500 m g (peds: 20â€“40 m g/kg/24h) PO t.i.d.



Cefazolin: 500â€“1,000 m g (peds: 50â€“100 m g/kg/24h) IV q6hâ€“q8h



Cefuroxim e: 750â€“1,500 (peds: 50â€“100 m g/kg/24h) m g IV q8h



Cephalexin: 500 m g (peds: 25â€“100 m g/kg/24h) PO q.i.d.



Cocaine hydrochloride: 4% topical solution single-dose nasal spray



Erythrom ycin ophthalm ic ointm ent: 2 drops q.i.d. to affected eye



Tetracaine and phenylephrine topical solution single-dose nasal spray



Ticarcillin/clavulanate: 3.2 g (peds: 200â€“300 m g of ticarcillin/kg/24h) IV q4hâ€“q6h



Trim ethoprim -polym yxin ointm ent: 2 drops q.i.d. to affected eye

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Follow-Up Disposition Admission Criteria 

Adults: o

Febrile or toxic appearance

o

Concom itant m edical problem s including diabetes or im m unosuppression

o

Extensive cellulitis

o

Suspicion of adjacent spread with deep tissue involvem ent or m eningitis



Children: o

Acutely ill appearance

o

Concom itant m edical problem s

o

Extensive cellulitis

o

High risk for Haem ophilus influenzae

o

If reliable follow-up within 24 hours cannot be arranged

Discharge Criteria Well-appearing, healthy individual

Complications 

Mucocele



Fistula form ation



Conjunctivitis with or without corneal involvem ent



Facial, periorbital, or orbital cellulitis

References 1. Boruchoff SA, Boruchoff SE. Infections of the lacrim al system . Infect Dis Clin North Am . 1992;6:925â€“932. 2. Kanski JJ. Clinical Ophthalm ology. Oxford, England: Butterworth-Heinem ann; 1994:66â€“69. 3. Lueder GT. Neonatal dacryocystitis associated with nasolacrim al

Pa ge 1 3 4

duct cysts. J Pediatr Ophthalm ol Strabism us. 1995;32:102â€“106. 4. Rhee DJ, Pyfer MF, Rhee DM. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. Philadelphia: Lippincott William s & Wilkins; 1999. 5. Rubin S, Hallagan L. Lids, lacrim als, and lashes. Em erg Med Clin North Am . 1995;13:631â€“648. 6. Thom pson CJ. Review of the diagnosis and m anagem ent of acquired nasolacrim al duct obstruction. Optom etry. 2001;72:103â€“111.

Miscellaneous SEE ALSO: Dacryoadenitis

Codes ICD9-CM 375.30 Dacryocystitis, unspecified

ICD10 H04.3 Acute and unspecified inflam m ation of lacrim al passages

Pa ge 1 3 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Deco m pressio n

Decompression

Peter J. Park

Basics Description 

Multisystem ic disease process resulting from escape of nitrogen bubbles out of solution into body fluids and tissues



Also known as â€œthe bendsâ€• or caisson disease

Etiology Mechanism 

Sequence of events: o

Increases in am bient pressure cause increase in partial pressure of nitrogen inspired (per Henry's law, below).

o

Nitrogen accum ulates in tissues in increasing concentrations the longer am bient pressures rem ain elevated.

o

Decom pression sickness (DCS) results when am bient pressure keeping nitrogen in solution decreases too rapidly (on ascent), preventing gradual rem oval of excess body burden of nitrogen.

o

As the nitrogen rem oval gradient is overwhelm ed,

Pa ge 1 3 5

tissues becom e supersaturated and bubble form ation occurs. 

Henry's law: o

Am ount of gas that will dissolve in a solution is directly proportional to partial pressure of that gas.

o

Increases in partial pressure result in larger am ount of gas dissolved in tissue.

o

Decreases in partial pressure result in gas com ing out of solution.



Dalton's law: o

Total pressure exerted by a m ixture of gases is equal to the sum of the partial pressure of each of the com ponent gases.



Bubble location determ ines clinical effects: o

Blood flow obstruction and tissue ischem ia from intravascular bubbles

o

Tissue distention and com pression from interstitial bubbles

o

Com pression of arterioles, nerves, and lym phatics

o

Endothelial dam age leading to stim ulation of coagulation and clotting cascades

o

Bubbles sensed as foreign by host defenses leading to release of chem otactic and other factors



Risk factors for DCS: o

Greater depth (increased am bient pressures), longer bottom tim e, and quicker rate of ascent

o

Proper use of dive tables and com puters does not elim inate risk for DCS.

o

Increased incidence with age and weight (higher body fat), hypotherm ia, dehydration, exercise, m ultiple dives in a day



Airplane flight following diving can precipitate DCS owing

Pa ge 1 3 5

to lower cabin pressure.

Diagnosis Signs and Symptoms 

Cutaneous: o

Scarlatiniform , erysipeloid, or m ottled rash: 

o

Cutis m arm orata

Peau d'orange appearance owing to lym phatic obstruction



Musculoskeletal: o

Pain: 

â€œThe bendsâ€•



Dull, deep m uscular aching



Often in a joint (elbow and shoulder m ost com m on)



Typically not exacerbated by m ovem ent or reproduced with palpation

o 



No external physical signs of traum a

GI: o

Nausea and vom iting

o

Abdom inal pain

Pulm onary: o

Shortness of breath

o

Chokes triad is thought to be owing to bubbles in pulm onary vascular tree:





Substernal pressure



Cough



Dyspnea

CNS: o

Weakness and fatigue

Pa ge 1 3 5

o

Num bness and paresthesia

o

Agitation

o

Headache

o

Dizziness

o

Vertigo

o

Convulsion

o

Bladder and/or bowel incontinence

o

Lethargy

o

Visual disturbances

o

The staggers: 

Vestibular system and posterior colum n involvem ent

Essential Workup 

Clinical diagnosis: Recognize risk factors and various clinical presentation.



Careful neurologic exam to docum ent possible waning sym ptom s



Trial of pressure: o

Rapid relief of sym ptom s upon recom pression in a hyperbaric cham ber m ay be only way to diagnose DCS conclusively.

Tests Lab 

CBC: o

Increased hem atocrit secondary to hem oconcentration



Electrolytes, BUN, creatinine, glucose



Urinalysis



Arterial blood gas (ABG) and pulse oxim etry: o

Monitor oxygenation.

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Imaging 



Chest radiograph: o

Concom itant pulm onary barotraum a

o

Aspiration pneum onia

Head CT when altered m ental status or neurologic deficit

Differential Diagnosis 

Musculoskeletal injury unrelated to bubble form ation



Inner or m iddle ear barotraum as



Arterial gas em bolism



Cerebrovascular accident (CVA)

P.285

Treatment Pre Hospital 

Cautions: o

Recognize DCS: 

Postdive extrem ity pain often attributed to m uscle strain



Serious neurologic com plaints often m inim ized because diver does not consider DCS

o

Tim e after surfacing to presentation of DCS: 

Fifty percentâ€”sym ptom s within 1 hour



Ninety-five percentâ€”sym ptom s within 12 hours



Sixty percent of neurologic DCS within 10 m inutes



Controversies:

Pa ge 1 3 5

o

In-water recom pression: 

Return injured diver/patient to depth where sym ptom s are am eliorated.

o



Extrem ely difficult



Need large am ount of surface support

Corticosteroids and lidocaine: 

No controlled studies dem onstrating benefit

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Provide norm obaric (100%) oxygen via m ask or endotracheal tube (ETT): o

Increases inert gas (nitrogen) elim ination from tissues, reducing gas bubble size

o 

Increases oxygen delivery to injured tissue

Early recom pression in hyperbaric cham ber

ED Treatment 

IV rehydration with 0.9% norm al saline (NS) to m aintain goal urine output of 1â€“2 m L/kg/h: o

Diver usually dehydrated owing to diuretic effect of pressure, exercise, breathing dry com pressed air

o

Increased fluid assists with gas rem oval and dissolution of nitrogen.



Hyperbaric oxygen recom pression therapy (see Hyperbaric Oxygen Therapy): o

For all DCS except for cutaneous

o

Arrange transportation to nearest hyperbaric facility.

o

Aircraft capable of full pressurization m aintaining barom etric pressure below 1,000 feet best suited for transfers

o

Prophylactic chest tube for sim ple pneum othorax to prevent conversion to tension pneum othorax

Pa ge 1 3 5

o

Fill endotracheal and Foley catheter balloons with water or saline to avoid shrinkage/dam age during recom pression.



Divers Alert Network (DAN): o

Based at Duke University Medical Center

o

Provides 24-hour em ergency hotline for m edical consultation on treatm ent of dive-related injuries and for referrals to hyperbaric cham bers ([919] 684-8111)



Analgesics

Follow-Up Disposition Admission Criteria Refer all patients with suspected or diagnosis DCS for hyperbaric therapy.

Discharge Criteria 

Patients not requiring hyperbaric treatm ent



Stable patients with m ild sym ptom s m ay be discharged postâ€“hyperbaric oxygen treatm ent



Air travel m ay exacerbate sym ptom s as am bient pressure decreases.

References 1. Bakker DJ. Treatm ent of the accidents induced by hyperbaric pressure. In: 7th European Consensus Conference on Hyperbaric Medicine. 2004. 2. Bartlett RB. Diving em ergencies. In: Critical Decisions in Em ergency Medicine. Vol. 10, No. 10, Lesson 20. Dallas, TX:

Pa ge 1 3 5

Am erican College of Em ergency Physicians; 1997. 3. Kizer KW. Diving m edicine and dysbarism . In: Auerbach PA, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001. 4. Moon RE, Gorm an DF. Treatm ent of decom pression disorders. In: The Physiology and Medicine of Diving. 5th ed. Philadelphia: WB Saunders; 2003. 5. Newton HB. Neurologic com plications of scuba diving. Am Fam Physician. 2001;63:2211â€“2218.

Miscellaneous SEE ALSO: Arterial Gas Em bolism ; Barotraum a; Hyperbaric Oxygen Therapy

Codes ICD9-CM 993.3 Decom pression sickness

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Deep Vein Thro m bo sis

Deep Vein

Thrombosis Jonathan A. Edlow

Basics Description 

A constant balance exists between intravascular clot form ation and clot dissolution, clot form ing when the form er overpowers the latter. Clot can be superficial (to the fascia) or deep. The latter is called deep vein throm bosis (DVT). DVT can be upper or lower extrem ity and distal or proxim al (to the popliteal vein).



About 600,000â€“2,000,000 new cases present annually



Prevalence increases with advancing age in the general population.



Diagnosis is m ore accurate using active surveillance rather than clinical suspicion.



Com m on in both m edical and surgical hospitalized patients



Pulm onary em bolism (PE) and DVT are different ends of the clinical spectrum of the sam e disease process.

Pediatric Considerations DVT in children is unusual, but when cases do occur, search for an underlying reason for hypercoagulability. Also, upper-extrem ity DVT

Pa ge 1 3 5

is associated with central IV lines in children.

Etiology 

Three generic factors prom ote clotting



Hypercoagulable states: o

Cancer

o

Nephrotic syndrom e

o

Sepsis

o

Inflam m atory conditions: 

o

Ulcerative colitis

Increased estrogen: 

Pregnancy



Oral contraceptives

o

Antiphospholipid syndrom e

o

Protein S, C, and antithrom bin III deficiencies, Factor V Leiden, prothrom bin gene m utations, others





Stasis: o

Prolonged bed rest

o

Im m obility (such as from a cast)

o

Long plane, car or train ride

o

Neurologic disorders with paralysis

o

Congestive heart failure

o

Obesity

Vascular dam age: o

Traum a

o

Surgery

o

Central lines: 



Especially with upper extrem ity DVT

Multifactorial issues: o

Advancing age: 

Prior DVT or PE

Pregnancy Considerations

Pa ge 1 3 5

Pregnancy is a risk factor for DVT, especially in the third trim ester and the two weeks postpartum .

Geriatric Considerations Age in and of itself is a risk for DVT (and PE). As with m any diseases, the presentation m ay be atypical in the elderly.

Genetics Im portant with respect to som e of the risk factors; ask about fam ily history of clotting.

Diagnosis Signs and Symptoms 

Leg swelling: o

Greater than 1 cm difference is usually significant.



Leg warm th and redness



Leg pain and tenderness



Palpable cord



In superficial throm bophlebitis, a red pipe cleaner-like cord m ay be visible and palpable.



Arm swelling, warm th, or tenderness: o



Upper extrem ity or subclavian vein involved

Phlegm asia cerulea dolens: o

Cold, tender, swollen, and blue leg (secondary arterial insufficiency)



In phlegm asia alba dolens: o

Cold, tender, and white leg (secondary arterial insufficiency)

Essential Workup 

Determ ination of a patient's clinical (pretest) risk is a key step in a workup for DVT.

Pa ge 1 3 6



A careful history and physical exam , interpreted in the context of the risk factor profile, is the m ost im portant driver of subsequent diagnostic evaluation.

Tests Lab 

D-dim er testing: o

D-dim er, a byproduct of endogenous clot form ation, is becom ing increasingly used in evaluation of patients for DVT and PE.

o

Only useful when the result is negative (to exclude DVT). Positive D-dim er does not m ake the diagnosis; it only m andates further testing.

o

Methods of m easuring D-dim er levels: 

Latex agglutination (first generation tests) are not sufficiently sensitive and should not be used.



Microlatex agglutination tests (2nd generation test) show som e prom ise but rem ain insufficiently tested as com pared with other m ethods.



Whole-blood latex agglutination (Sim pliRED) is valuable if negative in low probability patients (using Well criteria).



Enzym e-linked im m unosorbent assay testing gives a quantitative result and has been validated in large clinical studies in ED patients.

Imaging 

Contrast venography: o

Once the im aging test of choice; now rarely perform ed because it is invasive, is expensive, and has com plications.

Pa ge 1 3 6

o

Involves injection of contrast m edium into a leg vein, the inflam m ation from which can cause throm bophlebitis in several percent of patients undergoing the procedure.

o

Reactions to the contrast dye m ay also cause reaction.



Radionuclide venography: o

Radionuclide venous im aging is under investigation.

o

This test is not com m only used in routine clinical practice.



Im pedance plethysm ography: o

Another uncom m only used test, which can m iss sm aller distal clots



Com pression ultrasound: o

Standard first-line diagnostic test

o

It exam ines the veins. Norm al veins com press; those with clots do not.

o

Color Doppler can be useful for identifying the vein but does not add substantially to accuracy.

o

Duplex scanning refers to the com bination of com pression B-m ode ultrasound and color Doppler.

o

Has a sensitivity in the high 90% range

o

Should be repeated (or followed up with contrast venography) in high-risk patients with negative ultrasounds

P.287

Differential Diagnosis 

Superficial throm bophlebitis



Cellulitis



Torn m uscle and/or ligam ents (including plantaris and

Pa ge 1 3 6

gastrocnem ius tears) 

Ruptured Baker cyst



(Bilateral) edem a secondary to heart, liver, or kidney disease



(Unilateral) edem a from abdom inal m ass (gravid uterus or tum or) or lym phedem a



Postphlebitic syndrom e (from prior throm bophlebitis)

Treatment Initial Stabilization In cases of phlegm asia cerulean, or alba dolens: 

IV access



Supplem ental oxygen



Surgical or vascular consultation

ED Treatment 

System ic anticoagulation: o

In patients without contraindications

o

Use either unfractionated heparin or low-m olecular-weight heparin (LMWH)

o

Carefully selected patients can be prim arily treated with LMWH as outpatients.



Warfarin: o

Started shortly after a heparin has been adm inistered

o

Not before heparin because of the theoretic risk for inducing a transient hypercoagulable state

o

Xim elagatran, a direct oral throm bin inhibitor, is effective, but not FDA-approved at the present tim e because of concern about hepatotoxicity.



Vena cava filters:

Pa ge 1 3 6

o

Indications: 

Contraindications to system ic anticoagulation



New throm boem bolic event while on adequate anticoagulation

o

Vena cava filters (or um brellas) can be placed transcutaneously, usually by a vascular surgeon or radiologist.

o

Em piric filter placem ent m ay be useful in certain settings: 

Ongoing risk such as cancer



Risk for a recurrent PE could be fatal because of poor cardiopulm onary reserve or a recent PE.

o

Random ized data suggest that filter placem ent is no m ore effective than anticoagulation.

o

Filters can also be deployed in the superior vena cava in the setting of upper-extrem ity DVT.



Throm bolysis: o

Rarely indicated

o

Roughly a threefold increase in bleeding com plications

o

Catheter-adm inistered lytic therapy is used m ore com m only in upper extrem ity DVT.



Throm bectom y: o

Occasionally recom m ended for patients with extensive disease

o 

Consult a vascular surgeon.

Septic throm bophlebitis: o

Surgical excision of the vein or IV antibiotics

Medication (Drugs) 

Enoxaparin: 1 m g/kg SQ b.i.d. for outpatients (or

Pa ge 1 3 6

inpatients); a dose of 1.5 m g/kg SQ per day is FDA-approved for inpatients. 

Heparin (unfractionated): 80 U/kg bolus followed by an 18 U/kg/h drip, with the activated partial throm boplastin tim e (aPTT) titrated 2â€“2.5 tim es norm al



Tinzaparin: 175 IU/kg SQ per day



Warfarin: 5 m g/d with a prothrom bin tim e being checked on the third day

Follow-Up Alert When the clinical suspicion is high but the ultrasound is negative, rem em ber to advise the patient to follow-up with his or her prim ary care physician, and to have a follow-up ultrasound in 5â€“10 days.

Disposition Admission Criteria 

Patients with DVT unable to receive LMWH as an outpatient



Patients with concom itant PE or other serious diseases



Patients thought to be at especially high bleeding risk



Patients with phlegm asia

Discharge Criteria 

Outpatient treatm ent with a LMWH: o

No serious concom itant disease that requires hospitalization

o

Patient has m eans of com m unication and transportation to return to the hospital if needed.

o

Patient (or fam ily m em ber) is willing and able to

Pa ge 1 3 6

inject the m edication. o

Patient needs hem atocrit, platelet count, and international norm alized ratio (INR) checked in two to three days.

o

aPTT does not need to be checked.

o

Heparin-induced throm bocytopenia is less com m on with the LMWH but still occurs.

o 

INR needs to be checked at about day three.

Patients with superficial or distal throm bophlebitis can be discharged with close follow-up.

Issues for Referral 

Consult vascular surgery if there is any question about arterial insufficiency.



Consider need for inferior vena cava filter in patients who have contraindications to full anticoagulation or form new clots on adequate anticoagulation.

References 1. Brown DFM. Treatm ent options for DVT. Em erg Med Clin North Am . 2001;19:913â€“923. 2. Decoussis MN, et al. A clinical trial of vena cava filters in the prevention of pulm onary em bolism in patients with proxim al deep-vein throm bosis. N Engl J Med. 1998;333:409â€“415. 3. Hirsh J, Hoak J. Managem ent of DVT and PE. Circulation. 1996;93:2212â€“2245. 4. Kelly J, Hunt BJ. Role of D-dim ers in diagnosis of venous throm boem bolism . Lancet. 2002;359(9305):456â€“458. 5. Levine M, et al. A com parison of LMWH adm inistered prim arily at hom e with unfractionated heparin adm inistered in the hospital for proxim al DVT. N Engl J Med. 1996;334:677â€“681. 6. Kyrle PA and Eichinger, S; Deep venous throm bosis. Lancet 2005;365(9465):1163â€“74.

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7. Tracy JA and Edlow, JA; Ultrasound diagnosis of DVT. Em erg Med Clin North Am . 2004;22:775â€“796.

Codes ICD9-CM 451.9

ICD10 I80.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Defibrillato rs, Im plantable

Defibrillators,

Implantable Robert Sidman Lawrence S. Rosenthal

Basics Description 

Therapy related (im plantable cardioverter defibrillator [ICD] fires):



o

Appropriate

o

Inappropriate

Device/site related: o

Wound infection

o

Pocket hem atom a

o

Vascular occlusion

Etiology 

Therapy related: o

Appropriate therapies: 

Ventricular fibrillation (VF): Consider acute coronary syndrom e



Ventricular tachycardia (VT): Consider prior infarct

o

Inappropriate therapies:

Pa ge 1 3 6

o



Atrial fibrillation



Atrial flutter



Other supraventricular tachycardias (SVT)



Lead related

Phantom shocks: 

Patient awakened from sleep by a perceived shock



Device/site related: o

Wound infection: 

Staphylococcus aureus (m ost aggressive and seen early)



Staphylococcus epiderm idis (m ore indolent and later)



Escherichia coli, Pseudom onas species, and Streptococcal species (less com m on)

o

Pocket hem atom as

o

Vascular (venous throm bosis/em bolism secondary to im pedance of venous flow as a result of the ICD lead[s])

Diagnosis 



Therapy related: o

Based on sym ptom s before shock

o

Based on device interrogation

o

12-lead ECG: 

Ongoing ischem ia



Cardiac enzym es

Device/site related: o

Exam ination of surgical wound

o

Exam ination of upper extrem ities

Pa ge 1 3 6

Signs and Symptoms 

Therapy related: o

o



Appropriate ICD therapies: 

Syncope or near syncope



Lightheadedness or dizziness



Shortness of breath



Palpitations (non-SVT)



Chest discom fort or pain



Diaphoresis

Inappropriate therapies: 

Palpitations (SVT)



Lead related fractures, inappropriate sensing

Device/site related: o

o

o

Wound infection: 

Purulent drainage



Warm th



Erythem a



Pain



Fluctuance



Skin erosion



Fever

Hem atom a at the insertion site (pocket hem atom a): 

Pain (m ild)



Swelling

Vascular (throm boem bolic phenom ena): 

Unilateral swelling in upper extrem ity



Superficial varicosities

History 

Therapy related: o



Recent angina, heart failure

Device related:

Pa ge 1 3 7

o

Recent im plant (<14 days)

o

Skin traum a to wound

o

Lead related: 

Repetitive arm m otions



â€œTwiddler's syndrom eâ€• (inadvertent m anipulation of the device)

o

Vascular: 

Recent im plant



Multiple leads

Physical Exam 



Therapy related: o

Vital signs

o

Evidence of heart failure/acute coronary sydrom e: 

Displaced point of m axim al im pulse



Left ventricular heave



Presence of an S3 or S4



Presence of basilar rales



Dullness to percussion



Determ ination of jugular venous pressure



Hepato-jugular reflex



Peripheral edem a

Device/site related: o

o

Exam ination of wound/pocket: 

Dem arcation of pocket (erythem a)



Purulent drainage

Exam ination of affected upper extrem ity

Essential Workup 

Therapy related: o

ICD interrogation will determ ine whether therapy was appropriate and can determ ine lead fracture if present.

Pa ge 1 3 7

o

ECG (transient ST-segm ent changes and elevations of the cardiac enzym es m ay be seen after shock delivery and do not necessarily indicate m yocardial dam age)

o 

Chest radiograph m ay diagnose lead fracture.

Device/site related: o

Signs and sym ptom s of local verses system ic infection

o

Upper extrem ity swelling suggests venous throm bosis.

Tests Lab 



Therapy related: o

12-lead ECG

o

Cardiac enzym es

Device related: o

CBC with differential

o

Blood cultures

o

Do not aspirate pocket

Imaging 

PA and lateral chest radiograph: o

Lead fractures

o

Lead dislodgm ent



Vascular ultrasound of upper extrem ity



MRI absolutely contraindicated: o

Magnetic field m ay dam age ICDs

Diagnostic Procedures/Surgery 

Therapy related: o

Device interrogation by electrophysiologist/cardiologist

Pa ge 1 3 7

o 

Application of m agnet inhibits therapies

Device/Site related (pocket hem atom a/infection): o

Referral to surgeon/electrophysiologist

o

Aspiration of device pocket is not recom m ended.

o

Electrocautery should generally be avoided in patients with ICDs unless device is deactivated with program m ing or with m agnet application.



External defibrillation is safe, but avoid shock directly over ICD (see below).

P.289

Differential Diagnosis 

Therapy related: o

Appropriate therapies: 

o

VT/VF

Inappropriate therapies: 

SVT



Atrial fibrillation/atrial flutter



Lead m igration

o

Phantom shocks

o

Lead dysfunction: im proper sensing due to lead dislodgem ent or lead fracture



Device/site related: o

Pocket infection: 

Local cellulites



Suture abscess

o

System ic infection

o

Pocket hem atom a

Pa ge 1 3 7

Treatment Pre Hospital 

Therapy related: o

IV access

o

Continuous ECG m onitoring

o

Advanced cardiac life support (ACLS) protocols

o

Treatm ent of underlying ischem ia and/or heart failure:





Diuretics



Oxygen



Aspirin



Nitroglycerine

Device related: o

Supportive care

Initial Stabilization 



Therapy related: o

ACLS protocols

o

Magnet application inhibits ICD therapies.

Device related: o

Pain m anagem ent

o

Supportive care: 

Warm packs



Analgesics



Elevation of affected extrem ity

ED Treatment Patients with devices should receive treatm ent according to standard ACLS protocols. Care should be taken not to deliver external shocks directly over the device as it m ay shunt energy away from the heart.

Pa ge 1 3 7

Medication (Drugs) 

Therapy related: o

Appropriate therapies: 

VT/VF storm m ay require IV antiarrhythm ic agents



Am iodarone 150 or 300 m g IVP followed by an infusion 1 m g/kg/hr for six hours, then reduce to 0.5 m g/kg/hr. Can rebolus (150 m g) as often as required



Treat underlying ischem ia and heart failure (beta blockers, aspirin, ACE inhibitors/ACE receptor blockers, diuretics)

o

Inappropriate therapies: 

Treatm ent of SVT to prevent ICD shocks with beta blockers or calcium -channel blockers



Lopressor: 5 m g IV as needed to control heart rate



Diltiazem : 5â€“20 m g IV, then a m aintenance drip to control heart rate



Lead-related problem s m ay require further surgical intervention or device reprogram m ing, m agnet application will inhibit therapies.



Device related: o

o

Antibiotics, obtain blood cultures first: 

Cefazolin: 1 g IV q8h



Vancom ycin: 1 g IV q12h



Cefalexin: 500 m g PO q.i.d.

Warfarin for docum ented venous occlusion, international norm alized ratio two to three for three m onths

Pa ge 1 3 7

Follow-Up 

Therapy related: o



Cardiologist or electrophysiologist

Device related: o

Surgeon or cardiologist/electrophysiologist

Disposition Admission Criteria 

Therapy related: o

Ongoing/suspected cardiac ischem ia or heart failure

o

Multiple ICD shocks and initiation of antiarrhythm ic agents for VF/VT or other SVT

o

Treat underlying process and consult with electrophysiologist whether im m ediate interrogation is warranted.



Device/site related: o

Skin erosion

o

Wound dehiscence

o

System ic infection/endocarditis

o

Need for lead revision

o

Expanding pocket hem atom a

o

Upper extrem ity throm bosis

Discharge Criteria 

Therapy related: o

If patient is hem odynam ically stable without evidence of active ischem ia or heart failure, interrogation usually not required: 

Single shock therapy



Consult with electrophysiologist and arrange appropriate follow up.

Pa ge 1 3 7

o 

Device reprogram m ed to avoid inappropriate therapy

Device/site related: o

Localized infection

o

No signs of skin erosion

o

Pocket not expanding: 

Prophylactic antibiotics are not indicated for pocket hem atom as.

o 

Wound stable

Appropriate follow up

Issues for Referral Most ICD related issues require follow up with an electrophysiologist.

References 1. Dim arco, John P. Im plantable Cardioverter-Defibrillators NEJM 2003;349(19):1836â€“1847. 2. Scher, David L. Troubleshooting pacem akers and im plantable cardioverter-defibrillators. Current Opinion in Cardiology. January 2004;19(1):36â€“46. 3. Munter D. Assessm ent of im planted pacem aker/AICD devices. In: Roberts J, Hedges G, eds. Clinical procedures in em ergency m edicine . 4th ed. Philadelphia, PA: WB Saunders, 2003. 4. Peters R, Gold M. Cardiac arrhythm ias: im plantable cardiac defibrillators. Med Clin North Am . 2001;85(2):343â€“367. 5. Pinski S. Scientific reviews: em ergencies related to im plantable cardioverter-defibrillators. Crit Care Med. 2000;28(10):N174â€“180.

Codes ICD9-CM Therapy related MI410.9 VT 427.1 VF 427.41

Pa ge 1 3 7

Palpitations 785.1 Chest pain 786.5 CHF 428.0 Syncope and collapse 780 Chronic ischem ic heart disease 414.8 Device related Infection due to cardiac device 996.61 with im plant date.

Pa ge 1 3 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Delirium

Delirium

Arthur Sanders

Basics Description 

Syndrom e caused by m ultiple m edical disorders



Delirium is caused by underlying m edical condition.



Pathophysiology unknown: o

Diffuse derangem ents of cerebral acetylcholine

o

CNS dopam ine, Î³-am inobutyric acid, and serotonin m ay be involved.

Etiology 

Life threats: o

Withdrawal from barbiturates

o

Wernicke encephalopathy

o

Hypoxia and hypoperfusion of the brain

o

Hypertensive crisis

o

Hypoglycem ia

o

Hypertherm ia or hypotherm ia

o

Intracranial bleed or m ass

o

Acute coronary syndrom es

o

Meningitis or encephalitis

o

Poisoning or m edications

o

Status epilepticus

Pa ge 1 3 7

o 

Sepsis

General categories of disorders causing delirium : o

Medications

o

Drug abuse

o

Intoxication

o

Withdrawal

o

Metabolic abnorm alities

o

CNS pathology

o

Hypoperfusion from cardiovascular disease

o

Hypoxem ia

o

Vitam in deficiencies

o

Endocrinopathies

o

Infections

o

Toxins

o

Collagen vascular illnesses

Geriatric Considerations 

Com m on presentation in older ED patients



Up to 10% of older ED patients m ay have delirium .



Many patients will present with subtle sym ptom s and vague chief com plaints: o

Fall, dizzy, or not feeling well



Waxing and waning sym ptom s



Cause m ay be life-threatening condition.

Diagnosis Signs and Symptoms 

Disturbed consciousness: o

Hyperalert

o

Lethargic

Pa ge 1 3 8



o

Stupor

o

Com a

Cognitive changes: o

Disorientation

o

Im paired m em ory

o

Disorganized thinking and speech

o

Misperceptions, illusions, delusions, and hallucinations



Tim e course: o

Hours to days

o

Fluctuating course



Reduced awareness of environm ent



Inattention: o

Difficulties in focusing, shifting, and m aintaining attention

o

Restlessness

o

Distractibility

o

Lability

Essential Workup 

Awareness of delirium as syndrom e is key.



Confusion assessm ent m ethod: o

Acute onset or fluctuating course

o

Inattention

o

Disorganized thinking

o

Altered level of consciousness



Vital signs and physical exam ination



Neurologic exam ination with careful attention to changes in m ental status



Ancillary studies to determ ine underlying cause

Tests Lab

Pa ge 1 3 8



Electrolytes, calcium



BUN and creatinine



Glucose



CBC



Toxicology screens



Further studies based on signs and sym ptom s: o

Arterial blood gases

o

Liver function tests

o

Thyroid tests, thyroid-stim ulating horm one m easurem ent

o

Cardiac enzym es

Imaging 

ECG



Head CT scan



Lum bar puncture



Chest radiograph

P.291

Differential Diagnosis 

Cardiovascular diseases producing hypoperfusion



Pulm onary diseases causing hypoxia



Metabolic abnorm alities



Infections



Environm ental illness



Adverse drug event



Drug or alcohol withdrawal



Psychiatric illness



Dem entia



CNS disorders

Pa ge 1 3 8

Treatment Pre Hospital 

Intravenous access: o

Pulse oxim etry to m onitor respiratory status 

Glucose m easurem ent



ECG m onitoring



Naloxone (Narcan) if associated respiratory insufficiency



Monitor patient: o

Advanced life support (ALS) transport with all m edications





Look for signs of an underlying cause: o

Medications

o

Medical alert bracelets

Docum ent basic neurologic exam ination: o

Glasgow com a scale score

o

Pupils

o

Extrem ity m ovem ents

Initial Stabilization 

Most patients with delirium do not need m edications acutely.



Treatm ent is based on cause of delirium .



Chem ical sedation in severely agitated patients: o

Benzodiazepines

o

Neuroleptics

o

If withdrawal is likely, consider lorazepam .

ED Treatment 

Diagnosis and treatm ent of underlying m edical condition



Thiam ine is adm inistered to alcoholic and m alnourished patients.

Pa ge 1 3 8



For patients who are significantly agitated, treatm ent of agitation m ay help facilitate ED workup: o

Benzodiazepines

o

Neuroleptics

Medication (Drugs) 

Alprazolam : 0.25â€“0.5 m g PO



Haloperidol: 5â€“10 m g IV or IM



Lorazepam : 0.5â€“2 m g IV, IM, or PO



Thiam ine: 100 m g IV, IM, or PO

Follow-Up Disposition Admission Criteria 

When cause is unclear, adm it.



If delirium has not resolved, adm it.

Discharge Criteria 

Treatable cause is found and treated.



Mental status clears while in the ED: o

Reliable caregivers and follow-up

References 1. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients presenting with altered m ental status. Ann Em erg Med. 1999;33:251â€“280. 2. Hustey FM, Meldon SW. The prevalence and docum entation of im paired m ental status in elderly em ergency departm ent patients. Ann Em erg Med. 2002;39:248â€“253.

Pa ge 1 3 8

3. Inouye SK, van Dyck CH, Alessi CA, et al. Clarifying confusion: the confusion assessm ent m ethod: a new m ethod for detection of delirium . Ann Intern Med. 1990;113:941â€“948. 4. Kalbfleisch N. Altered m ental status. In: Em ergency Care of the Elder Person. St. Louis, MO: Beverly Cracom Publications, 1996:119â€“142. 5. Murphy BA. Delirium . Em erg Med Clin North Am . 2000;18:243â€“252.

Codes ICD9-CM 780.09

ICD10 F05.9

Pa ge 1 3 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Delivery, Unco m plicated

Delivery,

Uncomplicated James Walker

Basics Etiology 

Delivery in ED is rare: o

Incidence of ED deliveries in United States is not known.

o

Health care system s in which patients have little prenatal care tend to have greater incidence of ED deliveries.



ED deliveries usually occur in one of following three scenarios: o

Multiparous patient with history of prior rapid labor

o

Nulliparous patient who does not recognize sym ptom s of labor

o

Patients with lack of prenatal care, lack of transportation, or prem ature labor

Diagnosis

Pa ge 1 3 8

Signs and Symptoms 

True labor presents as uterine contractions occurring at least every 5 m inutes and lasting 30â€“60 seconds.





Signs and sym ptom s of im pending delivery: o

Ruptured m em branes (am niotic sac)

o

Bloody show (loss of m ucous plug)

o

Urge to push or to have bowel m ovem ent

Signs of im m inent delivery: o

Fully effaced and dilated cervix (about 10 cm in term infant)



o

Palpable fetal parts

o

Bulging of perineum

o

Widening of vulvovaginal area

Significant vaginal bleeding with labor dem ands im m ediate assessm ent for placenta previa or abruption.

Essential Workup 

Bim anual pelvic exam is m ost useful tool to assess presence of labor and possibility of im m inent delivery: o

Assess dilation, station, and effacem ent.

o

Bim anual exam should not be done with vaginal bleeding until ultrasound can rule out placenta previa.



Fetal heart tones (FHTs) should be obtained by Doppler.

Tests Lab 

If patient is in active labor, CBC, blood typing, and Rh screen should be sent: o

Kleihauer-Betke testing should be ordered after delivery if Rh-negative m other gives birth to Rh-positive child.

Pa ge 1 3 8

o

Rh im m unoglobulin can be adm inistered to m other within 72 hours of delivery.



Urinalysis if there is concern about urinary tract infection or pre-eclam psia

Imaging 

Im aging studies are not needed for uncom plicated vaginal deliveries.



Third-trim ester vaginal bleeding should have em ergent ultrasound to evaluate for placental abruption or placenta previa.

Differential Diagnosis 

Braxton Hicks contractions: o

Irregular uterine contractions that do not result in cervical dilation or effacem ent



Muscular low back pain



Round uterine ligam ent pain



Other causes of abdom inal pain, such as torsion of the ovary, appendicitis, nephrolithiasis

Treatment Pre Hospital 

Place patients in left lateral recum bent position.



Em ergency m edical services (EMS) personnel should be adequately trained and have proper equipm ent available for delivery.



EMS transportation of high-risk obstetric patients before delivery: o

Lower neonatal m orbidity and m ortality

o

Faster and less expensive when com pared with

Pa ge 1 3 8

transportation of neonate after delivery 

Use of air transport for obstetric patients has been shown to be safe and effective: o

If altitude during flight can result in hypoxia for fetus, pregnant patients should be placed on supplem ental oxygen.

Initial Stabilization 

Im m ediate pelvic exam ination to assess for cervical dilation, effacem ent, station, or presenting parts



Patients in active labor should be transferred to Labor and Delivery im m ediately unless delivery is im m inent.



If patient is com pletely dilated and fetal parts are on perineal verge, prepare for ED delivery.

ED Treatment 

Obstetrician should be notified that delivery will be occurring in ED.



If patient is high risk or fetus is <36 weeks gestational age, pediatrician or neonatologist and NICU should be notified.



Begin IV saline and supplem ental oxygen, and place patient in lithotom y position.





Assem ble obstetric (OB) pack: o

Bulb syringe

o

Two sterile Kelly clam ps

o

Sterile Mayo scissors

o

Um bilical clam p

Neonatal resuscitative equipm ent should also be available. P.293



If tim e perm its, sterilize vaginal area with povidone-iodine

Pa ge 1 3 8

(Betadine). 

Uncom plicated vaginal delivery should occur as follows: o

As crowning occurs, deliver head in controlled fashion, guiding it through introitus with each contraction.

o

Routine episiotom y is not necessary; however, if perineum is tearing, perform m idline episiotom y by placing two fingers behind perineum and m ake straight incision toward (but not including) rectum with sterile Mayo scissors.

o

After fetal head is delivered, quickly suction nasopharynx, then feel around neck for nuchal cord: 

If present, m anually reduce over head.



If nuchal cord is too tight, double clam p, cut cord, and deliver infant im m ediately.

o

Apply gentle downward pressure on fetal head with uterine contractions: 

Deliver anterior shoulder.



Posterior shoulder and rem ainder of infant will rapidly deliver.

o

After delivery, infant should be held at level of uterus and oropharynx suctioned again.

o

Double clam p cord with sterile Kelly clam ps and cut between them .

o

Infant should be stim ulated, warm ed, and dried: 

If cyanosis is present, infant should be given oxygen and resuscitated.

o

Place um bilical clam p.

o

Placenta will spontaneously deliver in 20â€“30 m inutes: 

Observe m other closely for postpartum hem orrhage.

Pa ge 1 3 9

o

Uterine m assage can aid in separation of placenta from uterus and lim it uterine atony: 

Avoid placing traction on um bilical cord because this can lead to inversion of uterus or rupture cord.

o

If patient has severe bleeding and placenta is not passing spontaneously, patient should be taken im m ediately to operating room .

o

After delivery of placenta, it should be exam ined for any irregular or torn areas suggestive of retained placental products.



In uncom plicated delivery, use of drugs is not necessary: o

Massage of uterus is all that is needed to facilitate cessation of bleeding after placenta has been delivered.



Postpartum uterine bleeding is com m on: o

Uterus, vagina, and perineum should be inspected for laceration.

o

If no laceration is found, assum e uterine atony.

o

If uterus does not contract in response to uterine m assage, adm inister oxytocin IV.

o

Continued m assage of uterus m ay be helpful if bleeding still persists; then give m ethylergonovine m aleate (Methergine) IM.

o

If bleeding is not responding to these m easures, then carboprost trom etham ine (Hem abate) can be adm inistered IM.

Medication (Drugs) 

Carboprost trom etham ine (Hem abate): 0.25 m g IM q15â€“q60m in (up to 2 doses)

Pa ge 1 3 9



Methylergonovine m aleate (Methergine): 0.2 m g IM



Oxytocin: 20â€“20 IU in 1 L of crystalloid infused at 250â€“500 m L/h IV

Follow-Up Disposition Admission Criteria 

All wom en with uncom plicated deliveries and no significant postpartum bleeding should be adm itted to Labor and Delivery or postpartum unit for care and m onitoring.



Obtain pediatric or neonatal consultation and adm it to neonatal intensive care unit:



o

All infants with respiratory distress

o

Gestational age <36 weeks

o

Weight <5 pounds

o

Low Apgar scores

Term infants with none of above com plications m ay be adm itted to the nursery or with m other to com bined m aternal-fetal unit.

Discharge Criteria Adequate recovery from delivery

References 1. Doan-Wiggins L. Em ergency childbirth. In: Roberts J, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 3rd ed. Philadelphia: WB Saunders; 1998:988â€“1015. 2. Druelinger L. Postpartum em ergencies. Em erg Med Clin North Am . 1994;12:219â€“225. 3. Gianooulod JG. Em ergency com plications of labor and delivery.

Pa ge 1 3 9

Em erg Med Clin North Am . 1994;12:201â€“217. 4. Mallon WK, Henderson S. Labor and Delivery. In: Marx JA, et al., eds. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO: Mosby; 2002:2460â€“2484. 5. Zlatnik FJ. Norm al labor and delivery and its conduct. In: Scott J, et al., eds. Danforth's Obstetrics and Gynecology. 7th ed. Philadelphia: WB Saunders; 1998:988â€“1015.

Codes ICD9-CM 650.0

ICD10 O80.9

Pa ge 1 3 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dem entia

Dementia

David A. Guss

Basics Description 

Progressive degenerative process of the CNS



Prevalence 1% at age 60 years to 30â€“50% by age 85 years



Pathophysiology varies, dependent on cause.



Prim ary dem entia:



o

Neurofibrillary tanglesâ€”Alzheim er

o

Gliosisâ€”Pick

Secondary dem entia: o

Ischem icâ€”m ultiinfarct dem entia

o

Subcortical degenerationâ€”Parkinson, Wilson

o

Toxic, m etabolic, nutritional derangem entsâ€”vitam in B1 2

o

Prionsâ€”Creutzfeldt-Jakob

o

Virusâ€”HIV dem entia

o

Bacterialâ€”syphilis

o

Vasculitisâ€”system ic lupus erythem atosus (SLE), throm botic throm bocytopenic purpura (TTP)



Characterized by gradual decline in cognitive functioning: o

Generally evolves over period of years

Pa ge 1 3 9

o

Course is highly variable, m onths to years in duration.





Prim ary dem entia: o

Alzheim er disease

o

Lewy body variant

o

Pick

o

Binswanger

Secondary dem entia o

See Differential Diagnosis

Genetics Increased risk of Alzheim er disease in first-degree relatives of patients with Alzheim er

Etiology 



Prim ary dem entia: o

Alzheim er disease

o

Lewy body variant

o

Pick

o

Binswanger

Secondary dem entiaâ€”see Differential Diagnosis

Diagnosis Signs and Symptoms Acquired loss of cognitive function leading to im pairm ent of daily functioning, m ay be associated with the following: 

Loss of m em oryâ€”short followed by long term



Im pairm ent of abstract thinking



Im paired judgm ent and im pulse control



Agnosiaâ€”inability to recognize objects



Aphasiaâ€”language disorder

Pa ge 1 3 9



Apraxiaâ€”inability to perform m otor functions



Agitation



Apathy



Depression



Inappropriate behavior



Declining personal hygiene and appearance



Urinary or fecal incontinence

History Full and com plete history: 

Must include input from fam ily and friends



Com plete list of m edications



Co-m orbid diseases



Prior history of sim ilar behavior



Onset and progression

Physical Exam Full and com plete physical exam : 

Head-to-toe evaluation, all organ system s



Meticulous neurologic exam ination: o

Mental status evaluation

o

Cranial nerves

o

Reflexes

o

Motor, sensory, cerebellar, gait

Essential Workup 

Must elim inate acute reversible or exacerbating factors



Extent of workup is related to history and course of illness: o

Extensive evaluation for new diagnosis

o

Directed evaluation for sudden change of dem entia

o

Lim ited evaluation for stable disease previously assessed

Pa ge 1 3 9

Tests Lab 

Extent of evaluation dependent on patient condition and suspected cause





New diagnosis or sudden deterioration: o

CBC

o

Erythrocyte sedim entation rate (ESR)

o

C-reactive protein (CRP)

o

Glucose

o

Electrolytes

o

BUN, creatinine

o

Liver enzym es

o

Urinalysis

o

Toxicology screen

o

Thyroid-stim ulating horm one

o

Vitam in B 1 2 level

o

Syphilis serology (RPR)

o

HIV

o

Blood cultures if fever present

o

Antinuclear antibody if SLE suspected

Established diagnosis with stable disease: No tests m ay be required.

Imaging 

New diagnosis or sudden deterioration in established dem entia:



o

Chest radiograph if infection considered

o

Head CT, without and with contrast

o

Electroencephalogram if suspicion of seizure disorder

o

Head MRI in selected cases

Established diagnosis with stable disease: Studies m ay not be required.

Pa ge 1 3 9

Diagnostic Procedures/Surgery Lum bar puncture and cerebrospinal fluid (CSF) analysis, syphilis serology

Differential Diagnosis 



Toxic, m etabolic, nutritional: o

Narcotics, sedatives, hypnotics

o

Alcohol

o

Heavy m etals

o

Dehydration

o

Hypotherm ia, hypertherm ia

o

Hypoglycem ia, hyperglycem ia

o

Hyponatrem ia, hypernatrem ia

o

Hypercalcem ia

o

Thiam ine deficiency

o

Vitam in B 1 2 deficiency

o

Niacin deficiency

Infections: o

Urinary tract infection (UTI)

o

Pneum onia

o

Sepsis

o

Meningitis, encephalitis



Seizuresâ€“frontal lobe status



Head traum a: o

Bilateral chronic subdural hem atom as

o

Pugilistic dem entia



Norm al pressure hydrocephalus



Stroke



Tum or



Vasculitis: o

SLE

o

TTP

Pa ge 1 3 9



Depression

Treatment Pre Hospital 

Obtain history from friends, fam ily.



Provide for patient and staff safety.



Manage agitation.



Attentiveness to co-m orbid conditions



Treat acute toxic and m etabolic disorders: o

Hypoglycem ia

o

Hypotherm ia

o

Hypertherm ia

Initial Stabilization 

Ensure adequate airway.



Adm inister O 2 if hypoxic.



Ensure norm al vital signs.



Establish intravenous access if required.



In agitated patients, provide for patient and staff safety.

P.295

ED Treatment 

Evaluate for reversible causes of altered m ental status.



Consider full differential diagnosisâ€”evaluate and treat appropriately: o

Treat hypoglycem ia with oral or IV dextrose.

o

Treat narcotic overdose or excess with naloxone.

o

Rewarm if hypotherm ic.

o

Antipyretic for hypertherm ia

Pa ge 1 3 9

o

Intravenous fluids for dehydration

o

Correct electrolyte abnorm alities.

o

Adm inister antibiotics for infection: 

UTI and pneum onia m ost com m on occult infections

o



Treat seizures: 

Lorazepam for status epilepticus



Phenytoin for long-term m anagem ent

Sedation for agitation: o

Start with low doses and increase as necessary to achieve clinical result.

o

Neuroleptics; haloperidol, risperidone, ziprasidone

o

Benzodiazepinesâ€”lorazepam , m idazolam



Soft restraints if chem ical sedation ineffective



Attem pt to lim it num ber of m edications: o

Reduced likelihood of toxicity

o

Reduced likelihood of drugâ€“drug interaction

o

If agitation not an issue, elim inate all sedative-hypnotics



Treat depression.

Medication (Drugs) 



Alzheim er agentsâ€”always start at lowest dose: o

Donepezil: 5â€“10 m g PO at bedtim e

o

Rivastigm ine: 1.5â€“6 m g PO b.i.d.

o

Galantam ine: 4â€“12 m g PO b.i.d.

o

Tacrine: 10â€“40 m g PO q.i.d.

o

Mem antine: 5 m g PO q.i.dâ€“10 m g PO b.i.d.

Am itriptyline: 10â€“50 m g PO b.i.d. o

Start with lowest dose

o

Oversedation a problem

Pa ge 1 4 0

o

May worsen dem entia

o

Useful in patients who cannot sleep



Dextrose: 25 g slow IVP



Droperidol: 0.625â€“2.5 m g IVâ€”advantage, rapid onset; disadvantage, risk for QT prolongation, requires prolonged EKG m onitoring



Fluoxetine: 20â€“60 m g PO daily; start with lowest dose



Haloperidol: 0.5â€“2 m g PO b.i.d.; start with lowest dose 0.5â€“2.5 m g IM or IV if rapid onset required



Lorazepam : 0.5â€“1 m g IV, 0.5â€“2 m g PO



Midazolam : 0.5â€“2 m g IV slow push



Naloxone: 0.4â€“2 m g IVP



Risperidone: 0.5â€“2 m g PO b.i.d.; start with lowest dose



Ziprasidone: 20â€“80 m g PO b.i.d., 10â€“20 m g IM q4h; start with lowest dose

Follow-Up Disposition 

Prim ary dem entia is characterized by slow, steady progression: o

Course is generally 5â€“10 years from diagnosis to death.



Can fluctuate as consequence of intervening illness and com orbid conditions



Cholinesterase m edications can im prove functional status in patients with Alzheim er disease.



Careful attention to m edications, secondary illnesses, and prom pt intervention for infections can im prove quality of life and longevity.



Death is generally consequence of infection, cardiovascular

Pa ge 1 4 0

disease, or injury.

Admission Criteria 

Unstable vital signs



Significant com orbid condition requiring parenteral m edications:



o

Pneum onia

o

UTI

o

Fluid and electrolyte disorder

Uncertain diagnosis requiring evaluation and m anagem ent that is not suitable for outpatients



Inadequate hom e support coupled with inability to arrange suitable placem ent from ED

Discharge Criteria 

Stable vital signs



No significant co-m orbid conditions



Secure diagnosis or elim ination of life-threatening organic disease



Adequate hom e support



Reliable access to follow-up care

Issues for Referral Insurance, transportation, assistance

References 1. Conn DK. Cholinesterase inhibitors, com paring the options for m ild to m oderate dem entia. Geriatrics. 2001;56:56â€“57. 2. Geldm acher DA, Whitehouse PJ. Evaluation of dem entia. N Engl J Med. 1996;335:330â€“336. 3. Rossor M. Dem entia. In: Bradley WG, ed. Neurology in Clinical Practice. 3rd ed. Boston: Butterworth-Heinem ann; 2000:1703â€“1743. 4. Silverm an JM, Ciresi G. Variability of fam ilial risk of Alzheim er

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disease across the late life span. Arch Psych. 2005;62:565â€“573 5. Sm ith J, Seirafi J. Organic brain syndrom e. In: Marx JA, ed. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO:Mosby; 2002:1468â€“1485. 6. Tune LE. Risperidone for the treatm ent of behavioral and psychological sym ptom s of dem entia. J Clin Psychiatry. 2001;62(suppl 21):29â€“32.

Codes ICD9-CM 290.0 294.1 331.0

ICD10 F03

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dengue F ever

Dengue Fever

Jessica Freedman

Basics Description 

Dengue fever occurs secondary to dengue viral infection.



Poorly understood im m unopathologic response causes dengue hem orrhagic fever (DHF) and dengue shock syndrom e (DSS).



DHF and DSS usually occur in patients with previous exposure to dengue virus.



Hem orrhagic m anifestations occur after defervescence of fever.



Vascular perm eability increases.



Plasm a extravasates into extravascular space, including pleural and abdom inal cavities.



Bleeding tendency



Shock m ay ensue.



Dissem inated intravascular coagulation (DIC) m ay develop.



Dengue fever, DHF, and DSS are all self-lim ited.

Etiology 

Occurs in tropical regions: Asia, Africa, Central and South Am erica, and the Caribbean

Pa ge 1 4 0



Caused by dengue virus serotypes 1 through 4



Transm itted by m osquitoes: Aedes aegypti and Aedes albopictus



Incubation period of 4â€“7 days

Diagnosis Signs and Symptoms 



Fever: o

Abrupt in onset rising to 39Â°C or higher

o

2â€“7 days duration

o

Biphasic, returning to alm ost norm al after 2â€“7 days

o

Associated with frontal or retro-orbital headache

Rash: o

Generalized m aculopapular rash occurs with onset of fever.

o

After 3â€“4 days, rash becom es diffusely erythem atous.

o

Faded areas appear.

o

Areas of desquam ation m ay appear.

o

After defervescence of fever, scattered petechiae m ay develop over trunk, extensor surfaces of lim bs, and axillae.

o 



Palm s and soles spared

Musculoskeletal: o

Arthralgias and m yalgias after onset of fever.

o

Severe lum bar back pain

GI: o

Anorexia

o

Nausea and vom iting

o

Abdom inal pain (som etim es severe)

Pa ge 1 4 0



o

Altered taste

o

Hepatom egaly/ascites

o

GI bleeding

Miscellaneous: o

Epistaxis

o

Gingival bleeding

o

Hem optysis

o

Hypotension

o

Narrowed pulse pressure (<20 m m Hg)

Essential Workup 

Prim arily a clinical diagnosis



Suspect in endem ic areas.



Suspect in patients with history of travel.

Tests Lab 



CBC: o

Throm bocytopenia

o

Elevated hem atocrit

Electrolytes, BUN, creatinine o



Elevated BUN

Liver function tests: o

Elevated aspartate transam inase (AST; or serum glutam ic-oxaloacetic transam inase [SGOT])



Coagulation profiles: o

Prolonged INR, prothrom bin tim e (PT), and partial throm boplastin tim e (PTT)

o

Low fibrinogen: 



D-Dim er

Virus isolation or detection of dengue virusâ€“specific antibodies (available in only a few laboratories) through hem agglutination inhibition (HI) assay

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Imaging 

Chest radiograph: o



Pleural effusions

Tourniquet test: o

Inflate blood pressure (BP) cuff to m edian BP in patient's extrem ity.

o

Test is positive when three or m ore petechiae appear per square centim eter



World Health Organizationâ€“required criteria for diagnosis of DHF: o

Fever

o

Positive tourniquet test or bleeding phenom enon

o

Hepatom egaly

o

Shock

o

Throm bocytopenia (<100,000/m m 3 )

o

Increased vascular perm eability as evidenced by an elevated hem atocrit (>20%)

Differential Diagnosis 

Viral illness



Influenza



Rubella



Measles



Hepatitis



Appendicitis



Meningitis



Malaria



Rocky Mountain spotted fever



Typhoid

P.297

Pa ge 1 4 0

Treatment Initial Stabilization 

IV access



IV crystalloids for hypotension



O 2 and m onitor for unstable patients

ED Treatment 

Treatm ent is supportive.



Intravenous fluids



Acetam inophen (Tylenol) for fever



Analgesics for pain



Platelet transfusion for severe throm bocytopenia



DIC therapy, if necessary

Pediatric Considerations 

Neonatal dengue can occur by vertical transm ission if m other infected 0â€“8 days before delivery: o

Infants m ay develop DHF or DSS because of passive m aternal im m unity.



DHF and DSS m ost com m on in children 7â€“12 years of age

Follow-Up Disposition Admission Criteria 

ICU adm ission for the following: o

Hypotension

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

o

DIC

o

Throm bocytopenia

o

Hem oconcentration

Regular adm ission for the following: o

15 years of age or younger

o

All patients with previous dengue exposure

o

Any patient where close follow-up is not available

Discharge Criteria 

Close follow-up guaranteed



Tolerating PO



Pain controlled

References 1. Isturiz RE, Gubler DJ, del Castillo JB. Dengue and dengue hem orrhagic fever in Latin Am erica and the Caribbean. Infect Dis Clin North Am . 2000;14(1):121â€“140. 2. Kautner I, Robinson MJ, Kuhnle U. Dengue virus infection: epidem iology, pathogenesis, clinical presentation, diagnosis and prevention. J Pediatr. 1997;131(4):516â€“524. 3. Mandell GL, Bennett JE, Dolin R. eds. Principles and Practice of Infectious Diseases. 6th ed. New York: Churchill Livingstone; 2004.

Codes ICD9-CM 061

ICD10 A90

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dental Truam a

Dental Truama

Brian N. Corwell

Basics Description Permanent Teeth 

Thirty-two total (4 central and 4 lateral incisors, 4 canines, 8 prem olars, 12 m olars)



Num ber from 1â€“32 starting with upper right third m olar (1) to upper left third m olar (16) and lower left third m olar (17) to lower right third m olar (32)



Often easier to describe the involved tooth anatom ically



Tooth fractures (classified according to the depth of penetration using the Ellis classification system ): o

Class I fracture: 

Involves only m inor chipping of the superficial enam el

o



Fracture line has uniform , chalky white surface.



Painless to tem perature, air, percussion

Class II fracture: 

Involves enam el and dentin



Fracture line will have ivory or pale-yellow appearance com pared to whiter enam el.



Sensitive to tem perature, air, percussion

Pa ge 1 4 1

o

Class III fracture (true dental em ergency): 

Involves enam el, dentin, and pulp



Pulp has pinkish, red, fleshy hue within surrounding dentin.



Blush of blood after wiping tooth surface indicates pulp violation.



May be either exquisitely painful or desensitized (if neurovascular supply disrupted)

Concussed Teeth 

Tooth without obvious injury other than sensitivity to percussion



Subluxed teeth



Abnorm al m obility to gentle m anipulation



Alveolar bone fractures



Fractures of tooth-bearing portions of m andible, m axilla



Diagnosed clinically from exposed bone or radiographically with a panorex



Bite m alocclusion, painful bite, tooth m obility en bloc

Etiology 

Age periods of greatest predilection: o

Toddlers (falls and child abuse)

o

School-aged children and preteens (bicycle and playground accidents)

o

Adolescents (athletic events, altercations and m otor vehicle collisions)



Sporting dental injury greatly reduced with m outh guard use



Assault



Laryngoscopy



Dom estic violence



Multiple traum a

Pa ge 1 4 1



Motor vehicle, m otorcycle, bicycle accidents



Certain predisposing anatom ic factors increase risk: o

Anterior overbite >4 m m increases risk for fracture two to three tim es

o

Short upper lip, m outh breathing, incom petent upper lip, physical disabilities

Diagnosis Signs and Symptoms 

History of oral or facial traum a (abrasions, contusions, or lacerations)



Oral or facial pain: o

Tooth pain (m ay indicate pulp exposure or inflam m ation)



Tooth looseness, m obility, or avulsion



Exacerbating factors (m ay indicate pulp exposure or inflam m ation):



o

Difficulty opening and closing jaw

o

Chewing

o

Drinking

o

Extrem es of tem perature

o

Pain on palpation

Bite m alocclusion (suggests displaced teeth or m axillary or m andibular fracture)

Essential Workup 

Mechanism : o

Sufficient m echanism necessitates com plete evaluation for m ultiple traum a and associated local injuries (e.g., jaw fracture)

Pa ge 1 4 1



Exact tim e of injury



Inspect each tooth surface and percuss for m obility, sensitivity or fracture.



Assess for m alocclusion and m idface instability



Account for all m issing teeth, tooth fragm ents, and prostheses (m ay have been swallowed, aspirated, em bedded into adjacent soft tissue or im pacted into alveolus).



Inspect oral cavity carefully: o

Adjacent soft tissue injuries

o

Fractures to alveolar bone, m andible, or m axilla

o

Associated injuries: 

Salivary glands



Ducts



Nerves (test tooth sensitivity by tapping with tongue blade in addition to testing m ental and infraorbital nerve function)



Blood vessels

Tests Imaging 



Plain dental radiograph: o

Ellis class III fractures

o

Assess for associated root or alveolar fracture

Panorex: o

Indicated for suspected associated m andibular fracture:





Foreign bodies



Displacem ent of teeth



Alveolar or jaw fractures

Chest radiograph: o

Indicated for unaccounted teeth or tooth fragm ents

Pa ge 1 4 1



CT: o

Indicated for suspected condyle fractures (m ay be m issed by plain film )

Diagnostic Procedures/Surgery Bronchoscopy: 

Indicated for rem oval in cases of dental aspiration

Differential Diagnosis Rule out other significant concurrent facial or system ic injuries.

Treatment Pre Hospital 

Maintain a patent airway.



Account for all teeth.

Avulsed Teeth 

Im m ediately reim plant tooth if possible: o

Tim e is tooth: Each m inute tooth is out of socket reduces tooth viability by 1%



o

Best chance of success if done in <30 m inutes

o

Poor tooth viability if avulsed m ore than two hours

Alternatively, place tooth in a transport solution (listed from m ost to least desirable, i.e., likelihood of preservation of tooth viability): o

Hanks balanced salt solution (HBSS): 

Balanced pH culture m edia available com m ercially in the Save-a-Tooth kit



Works well even after 30 m inutes avulsion or with dry tooth

o

Cold m ilk

Pa ge 1 4 1

o

Saliva (place tooth in patient or parent's m outh)

o

Saline

o

Never use tap water or dry transport (will cause cell dam age).

Initial Stabilization 

Ensure patent airway.



Control bleeding by having the patient bite on gauze.



Account for all teeth and tooth fragm ents.



Re-im plant avulsed tooth im m ediately.

ED Treatment Tooth Fractures Managem ent determ ined by fracture extent and patient's age.

Ellis Class I 

No em ergency treatm ent indicated.



File/Sm ooth all sharp edges with an em ery board (preventing further injury to soft tissue).



Dental referral for cosm etic repair (nonem ergent)



Tooth can be restored later to norm al appearance (for patient reassurance).

P.299

Ellis Class II 

Treatm ent goal is to prevent bacterial pulp contam ination through exposed dentin (naturally porous): o

Dressing of calcium hydroxide paste (Dycal)

o

Tooth surface should be dried prior to application.

o

Followed by covering with dry foil, a m etal band, or enam el-bonded plastic



Pain control

Pa ge 1 4 1



Dental referral within 24 hours



In children <12 years of age: o

Protective dentin layer is thinner, placing pulp at greater risk of infection.

o

Dress in calcium hydroxide paste and cover in foil

o

Dental referral urgent

Ellis Class III 

Im m ediate dental/oral surgeon referral



Children with prim ary teeth: o



Nerve block, pulpotom y by dentist

Adults and older children: o

Nerve block (for significant pain)

o

Dentist to provide root canal to avoid abscess form ation

o

If dental/oral surgeon is not im m ediately available: 

Place a piece of m oist cotton over the exposed pulp



Cover with dry dental foil or seal with tem porary root canal sealant



Avoid topical anesthetics (m ay lead to sterile abscess).

Subluxed Tooth 

Analgesia and reduce to norm al position



If tooth m inim ally m obile, treat with soft diet.



Markedly m obile teeth require 10â€“14 days of stabilization by dentist or other specialist

Tooth Avulsion 

Treatm ent based on age of patient and am ount of tim e since avulsion



Gently rinse (do not scrub or sterilize) in saline or tap water.



Adm inister local anesthesia.

Pa ge 1 4 1



Gently suction and irrigate socket to rem ove clots.



Re-insert holding the tooth only by the crown using firm but gentle pressure.



If tooth dry for >30 m inutes outside m outh, soak in HBSS for 30 m inutes before reim planting.



Once tooth inserted, have patient bite down onto folded gauze to help m aneuver tooth into proper position.



Stabilize with a splint or periodontal pack such as a Coe-Pak: o

Mix resin and catalyst in even am ounts to a firm consistency.

o

Apply to anterior and posterior surface of the avulsed tooth and adjacent two teeth.



Prophylactic antibiotic coverage for 5â€“7 days



Tetanus im m unization as necessary



Liquid diet for 72 hours, then advance to soft diet



Definitive stabilization by a dentist



Avulsed prim ary teeth are never replaced because of potential for ankylosing facial deform ity and dam age to root bed.



Patients should be referred to pedodontist.

Concussed Teeth Soft diet and follow-up with dentist

Displaced Teeth 

Reposition to norm al anatom ic position by hand with anesthesia and splint



Soft diet, analgesia, no straws, warm saline rinses t.i.d., dental follow-up in <24 hours

Alveolar Bone Fracture 

Pain control



Oral surgery/dental consultation for reduction and fixation

Pa ge 1 4 1

(arch bar) 

Prophylactic antibiotic coverage



Tetanus im m unization as necessary



Liquid diet, advance to soft m echanical, no straws, warm rinses t.i.d.

Medication (Drugs) 

Acetam inophen with codeine (Tylenol No. 3): 2 tablets PO q4hâ€“q6h PRN (peds: codeine: 0.5â€“1.0 m g/kg/dose [m ax. 30â€“60 m g] PO q4hâ€“q6h



Acetam inophen with oxycodone (Percocet): 1â€“2 tablets PO q4hâ€“q6h PRN (peds: oxycodone: 0.1 m g/kg/dose [m ax. 10 m g/dose] PO q4hâ€“q6h



Clindam ycin (use if penicillin allergic): 300 m g PO q6h (peds: 10â€“20 m g/kg/24h PO q6h)



Erythrom ycin: adult: 500 m g PO q6h (peds: 30â€“50 m g/kg/24h [m ax. 2 g] PO q6h)



Penicillin V: 500 m g PO q6h (peds: 25â€“50 m g/kg/24h [m ax. 3 g] PO q6h)



Tetanus prophylaxis for dirty wounds, avulsed/intruded teeth and for deep lacerations

Follow-Up Disposition Admission Criteria 

Adm ission for other associated injuries



Suspected child or elder abuse and no safe available environm ent

Pa ge 1 4 1

Discharge Criteria 

Isolated dental fractures, Ellis class I: o



Avulsions, Ellis class II: o



Follow-up with a dentist (elective)

Dental follow-up within 24 hours

Ellis class III fractures: o

Require im m ediate dental referral secondary to the risk for tooth loss and abscess form ation



Advise all patients that involved teeth m ay die and/or require future root canal therapy.

References 1. Am sterdam JT. Traum atic dental em ergencies. In: Rosen P, et al., eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002:902â€“905. 2. Baum ann BM, Thom as LB. Dental injuries. In: Harwood-Nuss A, et al., eds. The clinical practice of em ergency m edicine. 3rd ed. Philadelphia, PA: Lippincott William s & Wilkins, 2001:475â€“480. 3. Medford HM, Curtis JW. Acute care of severe tooth fractures. Ann Em erg Med. 1983;12:364â€“365. 4. Powers MP. Diagnosis and m anagem ent of dentoalveolar injuries. In: Fonseca RJ, Walker RV, eds. Oral and m axillofacial traum a. Philadelphia, PA: WB Saunders, 1991:323â€“358.

Codes ICD9-CM 525

ICD10 S09.9

Pa ge 1 4 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Depressio n

Depression

Kathy Sanders

Basics Description Major depression: 

Psychiatric illness with depressed m ood and neurovegetative signs and sym ptom s lasting two weeks or m ore



Significant associated m orbidity and m ortality



Clinician should try to recognize this disorder in the m edically ill.

Etiology 

Major depression with suicidal ideations: o

Biological illness associated with derangem ents in several neurotransm itter system s of the brain, including serotonin



Causes of neurobiological derangem ent include: o

Genetic predisposition

o

Medical illness

o

Effects of m edications

o

Chronic unrem itting stressors in a predisposed individual



Wom en are twice as likely to have m ajor depression than

Pa ge 1 4 2

m en: o

Men are m ore likely to com plete suicide successfully

Pediatric Considerations 

Depressed children and adolescents are difficult to diagnose because the criteria are not as easily recognized





Indicators of m ajor depression in children: o

Irritability

o

Changes in school, hom e, and social functioning

o

Social withdrawal

o

Substance abuse

Consultation with a child psychiatrist is crucial in further assessm ent and disposition

Diagnosis Signs and Symptoms 

Wide variety of presentations: o

Dram atically in suicidal crisis

o

Quietly with som atic com plaints, panic attacks, or psychosocial distress



Vague som atic com plaints: o

Weakness, m alaise

o

Weight loss

o

Headache

o

Back pain



Dim inished sense of self-esteem



Loss of interest in or lack of enjoym ent of pleasurable activities



Loss of energy



Poor appetite

Pa ge 1 4 2



Sleep disturbance



Decreased attention span



Irritability

Essential Workup 

Eliciting the signs and sym ptom s of m ajor depression is key to m aking the diagnosis.



DSM-IV diagnostic criteria include: o

The presence of depressed m ood or loss of interest or pleasure for two weeks or longer accom panied by at least five of the following criteria: 

Weight loss or gain



Insom nia or hypersom nia



Psychom otor agitation or retardation



Fatigue or loss of energy



Feelings of excessive guilt or worthlessness



Dim inished thinking or concentration or indecisiveness



Suicidal ideation or preoccupation with death

Tests Lab 

May be needed for m edical screening based on the initial presentation



CBC



Electrolytes, blood urea nitrogen, creatinine, glucose



Liver function tests



Thyroid screen

Differential Diagnosis Depressivelike Psychiatric Illnesses Dysthym ia: 

Adjustm ent reactions

Pa ge 1 4 2



Bereavem ent



Acute reactions to stress

Medical Causes of Depression 









Drug induced: o

Antihypertensives

o

Oral contraceptives

o

Steroids

o

Cim etidine and ranitidine

o

Sedative-hypnotics

o

Cocaine and am phetam ine

o

Beta-blockers

o

Metoclopram ide

Endocrine disorders: o

Thyroid

o

Adrenal

o

Diabetes m ellitus

o

Hyperparathyroid

Tum ors: o

Pancreatic

o

Lung

o

Brain

Neurologic disorders: o

Dem entia (early phase)

o

Epilepsy

o

Huntington's disease

o

Multiple sclerosis

o

Parkinson's disease

o

Stroke

o

Subdural hem atom a

o

Syphilis

Infections: o

Hepatitis

Pa ge 1 4 2



o

Influenza

o

Mononucleosis

Nutritional disorders: o

Folate deficiency

o

Pellagra

o

Vitam in B 1 2 deficiency



Electrolyte disturbances



End-stage renal pulm onary and cardiovascular disease



Chronic pain syndrom es

Treatment Initial Stabilization One-to-one nursing, or restrain any potentially suicidal patient for patient safety

ED Treatment Psychological Management 

Em pathetic listening to understand the stressors involved in the depression helps focus and encourage patients.



Em phasizing that depression is a treatable condition is reassuring as well as helpful in developing a treatm ent alliance.

Initiation of Psychotropic Medications 

Use for diagnosed neurovegetative, m ajor depression



Decision to initiate antidepressant m edication should be for patients with established follow-up and only with enough m edication given until the next appointm ent.



Low-dose benzodiazepines or neuroleptics m ay be used for associated agitation, insom nia, or psychosis.

Pa ge 1 4 2



Usually takes weeks for antidepressant m edications to resolve m ajor depression.



Choice of drug for the initiation of antidepressant therapy depends on:



o

Efficacy

o

Side-effect profile of the agent

o

Potential lethality if used to overdose

o

Com pliance factors

Selective serotonin reuptake inhibitors (citalopram , escitalopram , fluoxetine, sertraline, paroxetine) o

Well tolerated

o

Side effects include 

Mild nausea



Decreased appetite



Agitation



Som nolence



Sexual dysfunction



Minim al overdose potential

o

Starting dose is often final dose

o

Sertraline better tolerated in the m edically ill but m ay be titrated to 150â€“200 m g

P.301



Tricyclic antidepressants (am itriptyline, im ipram ine, nortriptyline): o

Side effects include: 

Anticholinergic effects



Postural hypotension



Sedation



Decreased seizure threshold



Overdoses of as little as 1 g of tricyclic

Pa ge 1 4 2

antidepressant can be fatal o 

Nortriptyline is best tolerated and effective

Monoam ine oxidase inhibitors (phenelzine, tranylcyprom ine): o

Dietary restrictions to avoid hypertensive crisis

o

Best prescribed by psychiatrist

Medication (Drugs) 

Am itriptyline: initial 25â€“50 m g PO per day



Citalopram 20â€“40 m g PO per day



Escitalopram 10 m g PO per day



Fluoxetine: 20 m g PO per day



Im ipram ine: initial 25â€“50 m g PO per day



Nortriptyline: initial 25 m g PO per day



Paroxetine: 20 m g PO per day



Phenelzine: 15 m g PO TID



Sertraline: 50 m g PO per day



Tranylcyprom ine: 10 m g PO t.i.d.

Follow-Up Disposition Admission Criteria 

Patient is suicidal or at high risk for suicide o

See Suicide, Risk Evaluation



Minim al or unreliable social supports



Previous history of suicide or poor treatm ent response



Sym ptom s so severe that continual observation or nursing supportive care is required

Pa ge 1 4 2



Psychotic features



Civil com m itm ent for psychiatric hospitalization is necessary if the patient is refusing treatm ent and is suicidal or otherwise judged to be at-risk to harm self or others.

Discharge Criteria 

Low suicide risk



Adequate social support



Close follow-up available

Issues for Referral 

Insurance carrier determ ines inpatient disposition.



Options for any level of care are specified by the patient's insurance coverage



Outpatient followup appointm ents with m ental health provider are im portant if discharging rather than adm itting. Waiting tim es for appointm ents m ay m ake this difficult



Use of case m anagem ent or social services in ED for disposition issues

References 1. APA practice guidelines for the treatm ent of patients with m ajor depressive disorder, 2nd ed. Washington DC: APPI, 2000. 2. Cassem NH et al. Mood disordered patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. 5th ed. St. Louis, MO: Mosby, 2004. 3. Rosenbaum JF, Arana GW, Hym an SE, Labbate LA, Fava M. Drugs for the Treatm ent of Depression. In: Rosenbaum JF, Arana GW, Hym an SE, Labbate LA, Fava M, eds. Handbook of psychiatric drug therapy. 5th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2005:55â€“120.

Pa ge 1 4 2

4. Stern TA, Herm an JB, Slavin PL, eds. MGH Guide to Prim ary Care Psychiatry, 2nd ed. New York: McGraw-Hill, 2004.

Codes ICD9-CM 311

ICD10 F32.9

Pa ge 1 4 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Derm ato m yo sitis/Po lym yo sitis

Dermatomyositis/Polymyositis Sean-Xavier Neath

Basics 

DM/PM is a system ic inflam m atory m yopathy.



Progression of m uscle weakness over weeks to m onths



Respiratory insufficiency from respiratory m uscle weakness



Aspiration pneum onia owing to a weak cough m echanism , pharyngeal m uscle dysfunction, and esophageal dysm otility



Cardiac m anifestations include m yocarditis and congestive heart failure (CHF).



Arthralgias of the hands, wrists, knees, and shoulders



Ocular m uscles are not involved, and facial m uscle weakness m ay be seen in advanced cases.

Etiology 

The exact cause is unknown, although an autoim m une m echanism is thought to be largely responsible.



Incidence about 1:100,000 with a fem ale preponderance



Association with HLA-B8 and HLA-DR3



There m ay be an association between PM and viral, bacterial, and parasitic infections.

Pa ge 1 4 2



DM/PM occurs with collagen vascular disease about 20% of the tim e.



Deposition of com plem ent is the earliest and m ost specific lesion, followed by inflam m ation, ischem ia, m icroinfarcts, necrosis, and destruction of the m uscle fibers.

Pediatric Considerations 

Although DM is seen in both children and adults, PM is rare in children.



Juvenile form m ay include vasculitis, ectopic calcifications (calcinosis cutis), and lipodystrophy.



The juvenile form m ay be associated with coxsackievirus.

Diagnosis Signs and Symptoms History 

Polym yositis (PM) is distinguished from derm atom yositis (DM) by the absence of rash.



Patients with PM present with m uscle pain and proxim al m uscle weakness.



DM presents with skin rash, m uscle pain, and weakness.



Constitutional sym ptom s include weight loss, fever, anorexia, m orning stiffness, m yalgias, and arthralgias.



Often note fatigue doing custom ary tasks: o

Brushing hair, clim bing stairs, reaching above the head, rising from a chair

o 

May also com plain of dysphagia, dyspnea, and cough

Progressive weakness of the proxim al lim b and girdle m uscles is seen early; distal m uscle weakness can occur late in the disease.

Pa ge 1 4 3

Physical Exam Skin findings of DM: 

Skin rash occurs with or precedes m uscle weakness.



Heliotrope rash (lilac discoloration) on the upper eyelids associated with edem a



Gottron sign: violaceous or erythem atous papules over the extensor surfaces of the joints, particularly knuckles, knees, and elbows



Shawl sign: a V-shaped erythem atous rash occurring on the back and shoulders



Periungual telangiectasias: nail-bed capillary changes that include thickened irregular and distorted cuticles



â€œMachinist handsâ€•: darkened horizontal lines across the lateral and palm ar aspects of the fingers

Tests 

Serum m uscle enzym es: o

Creatine phosphokinase (CPK)

o

Lactate dehydrogenase (LDH), aldolase, aspartate transam inase (AST), and serum glutam ic-oxaloacetic transam inase (SGOT)



ECG and urinalysis



Diagnostic criteria established in 1975 by Bohan and Peter: o

Sym m etric proxim al m uscle weakness with dysphagia and respiratory m uscle weakness

o

Elevation of serum m uscle enzym es

o

Electrom yographic features of m yopathy

o

Muscle biopsy showing features of inflam m atory m yopathy

o

Confidence lim its for diagnosis (typical rash m ust be seen for diagnosis of DM) 

Definite diagnosis: three or four criteria

Pa ge 1 4 3





Probable diagnosis: two criteria



Possible diagnosis: one criterion

Newer diagnostic criteria using the MHC/CD8 com plex m ay prove to be m ore specific for this diagnosis.

Imaging 

Chest radiograph m ay show interstitial lung disease, evidence of aspiration pneum onia, CHF, or cardiom yopathy.



Electrom yogram (EMG) studies show m yopathic potentials that are not specific for DM/PM.



Pulm onary function tests are useful in following the progression of interstitial lung disease.



Renal biopsies of patients m ay show focal proliferative glom erulonephritis.



Muscle biopsy is the definitive test: o

In PM, inflam m atory infiltrates are often endom ysial, although they m ay be perivascular.

o

In DM, inflam m atory infiltrates are m ostly perivascular and include a high percentage of B cells.

P.303

Differential Diagnosis 

Collagen vascular diseases



Muscular dystrophies, spinal m uscular atrophy, m yasthenia gravis, am yotrophic lateral sclerosis, poliom yelitis, Guillain-BarrÃ© syndrom e



Hypothyroidism , hyperthyroidism , Cushing syndrom e



Drug-induced: colchicine, zidovudine (AZT), penicillam ine, ipecac, ethanol, chloroquine, corticosteroids



Toxoplasm osis, trichinosis, coxsackievirus, HIV, influenza,

Pa ge 1 4 3

Epstein-Barr virus 

Hypokalem ia, hypercalcem ia, hypom agnesem ia, vasculitis, paraneoplastic neurom yopathy, hypereosinophilic m yalgia syndrom e

Treatment Initial Stabilization 

Intubation and m echanical ventilation as required



Nasogastric (NG) suction to prevent aspiration



Pneum othorax has been described as a rare occurrence in childhood DM.

ED Treatment 

Elevate head of the bed to prevent aspiration.



Begin high-dose corticosteroids to suppress inflam m ation and im prove m uscle weakness.



Avoid triam cinolone and dexam ethasone because there is an associated m yopathy.



Efficacy of prednisone determ ined by objective increase in m uscle strength



Im m unosuppressive m edications



Azathioprine is lim ited by GI intolerance and bone m arrow suppression.



Cyclosporine has been used but with lim ited success.



Methotrexate



Do not treat CPK level.

Medication (Drugs) 

Azathioprine: 3 m g/kg/d PO for 4â€“6 m onths

Pa ge 1 4 3



Methotrexate: 15â€“25 m g PO per week; (peds: 0.5â€“1 PO m g/kg per weekâ€“not to exceed adult dose)



Prednisone: 60 m g/d PO (peds: 1â€“2 m g/kg/d PO)



Intravenous im m unoglobulin (IVIG), m ycophenolate, cyclosporine, cyclophospham ide are increasingly used by rheum atologists.

Follow-Up Disposition Admission Criteria Respiratory insufficiency, aspiration pneum onia, m uscle weakness, weakened cough m echanism s, and pharyngeal dysfunction, CHF

Discharge Criteria 

Well-appearing patients with no respiratory dysfunction and no risk for aspiration



Patients who can take oral corticosteroids and im m unosuppressive agents as outpatients

Issues for Referral Consultation with a rheum atologist should be m ade when the diagnosis is suspected for assistance with definitive diagnosis and further treatm ent.

References 1. Bohan A, Peter JB. Polym yositis and derm atom yositis. N Engl J Med. 1975;292:344â€“347. 2. Caro I. Derm atom yositis as a system ic disease: collagen vascular diseases. Med Clin North Am . 1989;73(5):1181â€“1191. 3. Dalakas M. Inflam m atory disorders of m uscle: progress in polym yositis, derm atom yositis and inclusion body m yositis. Curr Opin

Pa ge 1 4 3

Neurol. 2004;17:561â€“567. 4. Pachm an L. Juvenile derm atom yositis: im m unogenetics, pathophysiology, and disease expression. Rheum Dis Clin North Am . 2002;28(3):579. 5. Shearer P, Jagoda A. Derm atom yositis. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1525â€“1526.

Miscellaneous SEE ALSO: Hypokalem ia; Hypothyroidism ; Myasthenia Gravis; System ic Lupus Erythem atosus

Codes ICD9-CM 710.4 710.3

Pa ge 1 4 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diabetes Insipidus

Diabetes Insipidus

Rahul Patwari

Basics Description 

Excessive urinary loss of solute-free water (polyuria)



Often characterized by excessive fluid intake (polydipsia)



Two types: o

Central DI (CDI; failure or deficiency of arginine vasopressin [AVP] release): 

Four types: 

No AVP to release (loss or m alfunction of posterior pituitary neurons)



Defective osm oreceptorsâ€”release AVP only in response to severe dehydration

o



Elevated threshold for AVP release



Subnorm al am ount of AVP released

Nephrogenic DI (lack of renal response to AVP): 

Differentiate from prim ary polydipsia.

Genetics 

Central DI: Fam ilial cases have been reported (autosom al dom inant).



Nephrogenic DI: usually X-linked recessive in m ales

Pa ge 1 4 3

Etiology 

Central DI: o

Any condition that disrupts the osm oreceptor-hypothalam us-hypophyseal axis: 

Traum a (skull fractures, hem orrhage)



CNS neoplasm â€”DI can be considered a tum or m arker.



Pituitary adenom as



Craniopharyngiom as



Germ inom as



Pinealom as



Metastatic tum ors



Leukem ia



Histiocytosis X



Sarcoidosis

o

Congenital CNS defects

o

Pituitary or hypothalam ic surgery

o

CNS infections (e.g., m eningitis, encephalitis)

o

Pregnancy (Sheehan syndrom e)

o

Idiopathic (autoantibodies, occult tum or)

o

Wolfram syndrom e (DI, diabetes m ellitus, optic atrophy, deafness)



Nephrogenic DI: o

Congenital renal disorders

o

Obstructive uropathy

o

Renal dysplasia

o

Polycystic kidney disease

o

System ic disease with renal involvem ent

o

Sickle cell disease

o

Sarcoidosis

o

Am yloidosis

o

Drugs:

Pa ge 1 4 3

o



Am photericin



Phenytoin



Lithium (persists past discontinuation of drug)



Am inoglycosides



Methoxyflurane



Dem eclocycline

Electrolyte disorders: 

Hypercalcem ia



Hypokalem ia

Pregnancy Considerations 

Sheehan syndrom e



Release of placental vasopressinase



Desm opressin (dDAVP) resists this vasopressinase.

Diagnosis Signs and Symptoms History 

Polyuria (up to 16â€“24 L/d of urine): o



Polydipsia (often craves cold fluids): o



Note the voiding frequency.

Note the am ount of PO fluid intake per day.

Signs and sym ptom s of hypothalam ic tum ors: o

Headache

o

Visual disturbances

o

Growth disturbances

o

Cachexia

o

Obesity

o

Hyperpyrexia

o

Sleep disturbances

Pa ge 1 4 3



o

Sexual precocity

o

Em otional disturbances

Drug intake

Physical Exam 

Signs of dehydration



Signs of traum a

Pediatric Considerations 

Polyuria and polydipsia m ay not be recognized by caregivers until sym ptom s of dehydration develop.



Neonatal diabetes insipidus: o

Often present at birth

o

If unrecognized, dehydration and hypernatrem ia m ay cause perm anent CNS dam age.





In infants: o

Irritability

o

Poor feeding

o

Growth failure

o

Interm ittent high fever

o

Abnorm al behavior (hyperactivity, restlessness)

In children: o

Enuresis

Essential Workup 





Clinical diagnosis in the ED: o

Elevated serum sodium concentration

o

Copious am ounts of dilute urine

History: o

Am ount of PO fluid intake per day

o

Voiding frequency

o

Medication use history

Physical exam : o

Signs of dehydration

Pa ge 1 4 3

o

Signs of traum a

Tests Lab 





Serum and urine osm olality: o

High serum osm olality

o

Low urine osm olality

Electrolytes, BUN, creatinine, and glucose: o

Hypernatrem ia

o

Hypercalcem ia

o

Hypokalem ia

CBC: o



Anem ia m ay be a sign of a neoplasm .

Serum and urine AVP tests are expensive and unnecessary in the ED.

Imaging 

As needed to evaluate for traum a or search for neoplasm s



Chest radiograph



CT of brain



MRI of pituitary axis

Diagnostic Procedures/Surgery N/A

Dehydration Test 

Unnecessary in the em ergency setting



Can be dangerous in cases of hypotension or sm all children



Perform ed as a confirm atory test for those receiving treatm ent



Method: o

No PO fluids for 3 hours or until urine osm olality stabilizes

o

Determ ine plasm a osm olality.

Pa ge 1 4 4

o

Should be >288 m m ol/kg

o

AVP 5 units (or desm opressin 1 Âµg SC or 10 Âµg intranasally)

o

Check urine osm olality at 0 m inutes, 30 m inutes, and 60 m inutes afterward.



Interpretation: o

In norm al patients: 

Osm olality will not change >9%.



Endogenous AVP will increase osm olality to m axim um .

 o

Exogenous AVP has no effect.

In central DI: 

Osm olality rises >9%.



No or little endogenous AVP



Exogenous AVP has significant concentrating effect.

o

In nephrogenic DI: 

Osm olality does not change.



Renal tubules are insensitive to AVP.

Differential Diagnosis 

Prim ary water deficit: o

Inadequate access to free water

o

Increased insensible water loss (e.g., prem ature infants)

o 

Inadequate breast-feeding

Prim ary sodium excess: o

Excessive sodium bicarbonate during resuscitation

o

Hypernatrem ic enem as

o

Ingestion of seawater

o

Hypertonic saline adm inistration

o

Accidental substitution of salt (sodium chloride [NaCL]) for glucose in infant form ulas

Pa ge 1 4 4



o

Intentional salt poisoning

o

High breast m ilk sodium

Prim ary polydipsia (psychogenic polydipsia): o

Solute-induced polyuria

o

Diuretic use

o

Resolving acute renal failure

o

Uncontrolled diabetes m ellitus

P.305

Treatment Pre Hospital 

Manage airway, breathing, and circulation (ABCs).



IV access and fluids if signs of dehydration exist

Initial Stabilization 

Manage ABCs.



Manage traum atic injuries accordingly.



High index of suspicion for head traum a

ED Treatment 

Correction of hypotension: o

Use of 0.9% NaCl is indicated for shock.

o

Intravascular losses represent only about one twelfth of total water losses.



Correction of initial water deficit: o

Sym ptom atic hypertonicity (seizures, com a): 

P o s m should be corrected aggressively 1 to 2 m Osm /kg/h to about 330 m Osm /kg



To a level of Na = 160 or until asym ptom atic

Pa ge 1 4 4

o

Asym ptom atic hypertonicity with Na <160: 

To prevent cerebral edem a, should be corrected m ore slowly



o

Fluid calculations

o

D 5 W is fluid of choice.

Isotonic and without sodium : o

Rem em ber to check potassium (K) and glucose frequently.

o

Current water deficit = (0.6) (lean body weight [LBW]) (1-140/Na s )

o

Total body water = (0.6) (LBW) - (current water deficit)

o

Fluid rate = (total body water) (correction rate)/(Na s )

o

Correct at a rate of 0.5â€“1 m m ol/L/h

o

Sam ple calculation: 

Na = 160, LBW = 70 kg, patient asym ptom atic



Current water deficit = (0.6) (70 kg) (1 140/160) = 5.25 L



Total body water = (0.6) (70 kg) - 5.25 = 36.75 L



Correct at 0.5 m m ol/L/h



Fluid rate = (0.5) (36.75)/160 = 114 m L/h of D 5 W



Chronic treatm ent: o

Usually initiated by adm itting physician after confirm ation of diagnosis



Central DI (vasopressin deficient): o

Arginine vasopressin (aqueous vasopressin): 

Half-life is too short.



May induce coronary vasospasm



Used only for dehydration test

Pa ge 1 4 4

o

o

Lysine vasopressin (lypressin): 

Can be given intranasally



Frequent instillation needed

Desm opressin: 

Drug of choice to control sym ptom s



Adm inister intranasally b.i.d. in dosage necessary to control polyuria or polydipsia.



Caution in postoperative patients as cerebral edem a m ay develop

o

Chlorpropam ide (Diabinese) 

Enhances effect of vasopressin at renal tubule



May stim ulate AVP release



Useful only in partial CDI



Clofibrate stim ulates the release of endogenous vasopressin.



Nephrogenic DI: o

Thiazide diuretics

o

Induce natriuresis.

o

Dietary sodium restriction

o

Restrict solutes and avoid excessive drinking to prevent water intoxication.

o

Avoid alcohol (especially beer) intake.

o

Check daily weights.

o

Nonsteroidal anti-inflam m atory drugs (NSAIDs; indom ethacin)

Medication (Drugs) 

Aqueous arginine vasopressin: 5â€“10 U SC in the unconscious patient from head traum a or postop



Chlorpropam ide (Diabinese): 200â€“500 m g PO daily



Clofibrate (Atrom id-S): 500 m g PO q6h

Pa ge 1 4 4



Desm opressin: 10â€“20 Âµg intranasally; 2â€“4 Âµg SC or IV; 0.1 m g PO



Hydrochlorothiazide (HCTZ): 50 m g PO daily



Lypressin nasal spray: 1â€“2 nasal spray t.i.d.â€“q.i.d. as needed

Follow-Up Disposition Admission Criteria 

Patients requiring dDAVP testing or a trial of water restriction



Severe dehydration



Electrolyte abnorm alities



Associated traum a

Discharge Criteria 

Known diagnosis of DI



Stable electrolytes



Adequately hydrated

References 1. Behrm an RE, ed. Nelson Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000. 2. Braunwald E, et al. Diabetes insipidus. In: Braunwald E, ed. Harrison's Principles of Internal Medicine. New York: McGraw-Hill; 2002. 3. Goroll AH, ed. Prim ary Care Medicine. 4th ed. Philadelphia: Lippincott William s & Wilkins, 2000. 4. Lee CC. Em ergency departm ent presentation of pituitary apoplexy. Am J Em erg Med. 2000;18(3):328â€“331.

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5. Rose BD. Diabetes Insipidus. Wellesley, MA: 2005. 6. Sainz Bueno, JA, et al. Transient diabetes insipidus during pregnancy: a clinical case and review of the syndrom e. Eur J Obstet Gynecol. 2005;118: 251â€“254. 7. Singer I, et al. The m anagem ent of diabetes insipidus in adults. Arch Int Med. 1997;157: 1293â€“1301. 8. Zink BJ. Traum atic brain injury outcom e: concepts for em ergency care. Ann Em erg Med. 2001;37(3): 318â€“332.

Miscellaneous SEE ALSO: Head Traum a; Hypernatrem ia

Codes ICD9-CM 253.5

ICD10 E23.2

Pa ge 1 4 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diabetes M ellitus, Juvenile

Diabetes

Mellitus, Juvenile Madeline M. Joseph

Basics Description 

Decrease in effective circulating insulin



Increase in counterregulatory horm ones including glucagon, catecholam ines, cortisol, and growth horm one



Hyperglycem ia owing to: o

Decreased peripheral glucose utilization

o

Increased hepatic gluconeogenesis



Hyperosm olality and osm otic diuresis



Ketoacidosis produced by increased lipolysis, with ketone body (Î²-hydroxybutyrate, acetoacetate) production, causes ketonem ia and m etabolic acidosis.



Potassium deficit: o

Intracellular shifts into extracellular space owing to hydrogen ion exchange.

o

Loss from osm otic diuresis

Etiology Mechanism

Pa ge 1 4 4



Im m une-m ediated pancreatic islet Î²-cell destruction



Precipitating events leading to diabetic ketoacidosis (DKA): o

Infection

o

Stress

o

Pregnancy

o

Psychiatric disorders, including eating disorders

o

Medication noncom pliance, inappropriate interruption of insulin pum p therapy, or treatm ent error



Risk factors for cerebral edem a: o

Attenuated rise in m easured serum sodium during DKA therapy (unrelated to the volum e or sodium content of intravenous fluid or rate of change in serum glucose)

o

Bicarbonate treatm ent for acidosis correction

o

Hypocapnia

o

Increased serum urea nitrogen

o

No association with degree of hyperglycem ia

Diagnosis Signs and Symptoms 

Polydipsia



Polyuria



Polyphagia



Weight loss, unexplained



Diabetic ketoacidosis (DKA): o

Initial presentation in 20â€“40% of patients

o

Nausea

o

Vom iting

o

Abdom inal pain, often resolving with reduction in

Pa ge 1 4 4

ketosis



o

Hyperpnea

o

Ketotic breath

o

Dehydration

o

Shock

Cerebral edem a: o

The incidence ranges from 0.87â€“1.1%.

o

Cerebral edem a accounts for 57â€“87% of all DKA deaths.

o

Headache

o

Gradual decrease or deterioration in level of consciousness

o

Inappropriate slowing in pulse rate

o

Increase in blood pressure

Essential Workup 

For DKA: o

Hourly vital signs and neurologic checks

o

Frequent blood chem istries

o

ECG m onitoring (in severe DKA) to assess T waves for evidence of hyperkalem ia/hypokalem ia

o

Accurate fluid input and output. Consider urinary catheterization in patients with im paired level of consciousness.

Tests Lab 

For DKA: o

Glucose, serum , and bedside hyperglycem ia

o

Urinalysis: 

Glycosuria



Ketonuria



Exclude urinary tract infection.

Pa ge 1 4 4

o

Blood chem istries every 2â€“4 hours until acidosis has resolved (m ore frequent as clinically indicated in the m ore severe cases)

o

Electrolytes and venous pH

o

Anion gap m etabolic acidosis: 

Potassium â€”high or norm al (artifactual owing to extracellular shift)



Sodium â€”low or norm al (m ay be artifactual owing to hyperglycem ia)



Bicarbonateâ€”low

o

Serum ketonesâ€”elevated

o

Serum osm olality

o

CBC: 

White blood cell count often elevated owing to stress or infection

o

Calcium

o

Phosphate

o

Cultures as indicated

Differential Diagnosis 

Infection: o

Urinary tract infection

o

Gastroenteritis

o

Appendicitis

o

Sepsis



Ingestion (salicylates, alcohols, glycols)



Diabetes insipidus

P.307

Pa ge 1 4 5

Treatment Pre Hospital For DKA: 

Monitor airway, breathing, and circulation (ABCs).



Airway protection



Establish intravenous access and initiate fluid therapy.

Initial Stabilization For DKA: 

Oxygen



Cardiac m onitor



Intravenous access and volum e resuscitation

ED Treatment For DKA 

Fluid replacem ent: o

Assum e fluid deficit of 10% of body weight

o

Initial volum e expansion with 10â€“20 m L/kg of 0.9% NaCl; m ay repeat to achieve hem odynam ic stability

o

Correct 50% of fluid deficit over first 8 hours, rem ainder over 24â€“48 hours.

o 

Do not give >3 L/m 2 over first 24 hours.

Begin intravenous insulin infusion after ketoacidosis confirm ed: o

Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h

o

Adjust rate to drop serum glucose m axim um of 100 m g/dL/h.

o

Add dextrose to infusion fluid when serum glucose <300 m g/dL.

o

Change to subcutaneous insulin when no longer significantly acidotic and able to eat.

Pa ge 1 4 5



Replace potassium and phosphate losses: o

Verify adequate urine output.

o

Add to fluids as KCl and K 3 PO 4 in equal am ounts.

o

Large doses of K + m ay be necessary; guide therapy by frequent m onitoring of K + .



Monitor serum sodium : o

Risk for cerebral edem a if Na + fails to rise as glucose falls



Bicarbonate therapy: o

Not recom m ended in m ost cases since generally it does not alter outcom e and it increases risk for cerebral edem a with its use

o

Use it with caution in patients with severe acidosis (pH <6.9) in whom peripheral vasodilation and decreased cardiac contractility m ay further im pair tissue perfusion and in potentially life-threatening hyperkalem ia.

o

Treat cerebral edem a as needed: 

Recognize early, if present.



Usually occurs 8â€“12 hours after onset of treatm ent



Mortality rate, 90%



Decrease fluid adm inistration.



Endotracheal intubation and ventilation: Avoid aggressive hyperventilation since it has been associated with poor outcom e in DKA-related cerebral edem a (sim ilar to that found in head traum a).

 o

Mannitol

Hypertonic saline (3%) 5â€“10 m L/kg over 30 m inutes m ay be an alternative to m annitol.

Pa ge 1 4 5

Medication (Drugs) 

Insulin drip: start 0.1 U/kg/h IV.



Mannitol: 0.25â€“1 g/kg IV

Follow-Up Disposition Admission Criteria 

For DKA: o

o

Intensive care unit (ICU): 

Altered m ental status



Shock or cardiac dysrhythm ia



Initial glucose >700 m g/dL



Initial pH <7.0

Inpatient unit: 

Stable new-onset diabetic patients requiring intensive education



Patients with ketoacidosis not m eeting requirem ents for ICU care



Com pliance concerns or other social issues

Discharge Criteria 

Known diabetic patients who respond well to therapy with norm alization of glucose, pH, and ketosis



Tolerating oral fluids



Reliable parents



Reliable follow-up within 24 hours including appropriate education

References

Pa ge 1 4 5

1. Finberg L. Why do patients with diabetic ketoacidosis have cerebral swelling, and why does treatm ent som etim es m ake it worse? Arch Pediatr Adolesc Med. 1996;150:785. 2. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edem a in children with diabetic ketoacidosis. N Engl J Med. 2001;344:264â€“269. 3. Green SM, Rothrock SG, Ho JD, et al. Failure of adjunctive bicarbonate to im prove outcom e in severe pediatric diabetic ketoacidosis. Ann Em erg Med. 1998;31:41â€“48. 4. Hale PM, et al. Factors predicting cerebral edem a in young children with diabetic ketoacidosis and new onset type I diabetes. Acta Paediatr. 1997;86:626â€“631. 5. Harris GD, et al. Minim izing the risk of brain herniation during treatm ent of diabetic ketoacidosis: a retrospective and prospective study. J Pediatr. 1990;117:22â€“31. 6. Kam at P, et al. Use of hypertonic saline for the treatm ent of altered m ental status associated with diabetic ketoacidosis. Pediatr Crit Care Med. 2003;4:239â€“242. 7. Klekam p J, Churchwell KB, Ho JD, et al. Diabetic ketoacidosis in children: initial clinical assessm ent and treatm ent. Pediatr Ann. 1996;25:387â€“393. 8. Marcin JP, et al. Factors associated with adverse outcom es in children with diabetic ketoacidosis-related cerebral edem a. J Pediatr. 2002;141:793â€“797. 9. Rewers A, et al. Predictors of acute com plications in children with type 1 diabetes. JAMA 2002;287:2511â€“2518.

Codes ICD9-CM 250.1

ICD10 E10

Pa ge 1 4 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diabetic Keto acido sis

Diabetic

Ketoacidosis Joseph Weber

Basics Description Insulin deficiency and excess of counterregulatory horm ones (catecholam ines, glucagon, growth horm one, and cortisol) resulting in: 

Dehydration (osm otic, hyperglycem ic, diuresis, and decreased oral intake)



Acidosis (anion gap m etabolic acidosis)



Ketone form ation (unrestrained lipolysis and ketogenesis)



Hyperglycem ia (unrestrained glycogenolysis and gluconeogenesis)



Electrolyte disturbances (hypokalem ia, hypo/hypernatrem ia, hypophosphatem ia)

Etiology 

Medication noncom pliance (>50%)



New-onset diabetes (type I or II)



Underlying m edical illness (increased counterregulatory horm ones and insulin resistance): o

Infectious process

Pa ge 1 4 5



o

Myocardial infarction

o

GI bleed

o

CNS event

Pregnancy (relative insulin deficiency and counterregulatory horm one excess)



Medications (protease inhibitors and atypical antipsychotics: olanzapine, clozapine)



Alcohol abuse

Diagnosis Signs and Symptoms History 

Medication noncom pliance



Polyuria, polydipsia



Weakness



Abdom inal pain, nausea, vom iting



Altered m ental status



Chest pain



Febrile illness

Physical Exam 

Tachycardia



Hypotension (dehydration, sepsis)



Tachypnea (hyperpnea)



Kussm aul respirations



Hypertherm ia/hypotherm ia (coexisting infection)



Dehydration:



o

Poor skin turgor

o

Dry m ucous m em branes

Odor of ketones on breath

Pa ge 1 4 5



Diffuse abdom inal tenderness

Essential Workup 

Diagnostic criteria: o

pH < 7.3, with ketonem ia

o

Bicarbonate <15 m Eq/L

o

Glucose >250 m g/dL



Bedside glucose m easurem ent



Venous blood gas



Urine dip for ketones



Serum electrolytes, glucose, BUN/creatinine



Search for precipitating cause.

Tests Lab 

Serum glucose m easurem ent: o



Confirm bedside test.

Electrolyte m easurem ent: o

Increased anion gap m etabolic acidosis: [Na - (Cl + HCO 3 )] >12

o

Sodium : 

Pseudohyponatrem ia (from hyperglycem ia) correction factorâ€”add 1.6 m Eq/L to the m easured sodium for every 100 m g/dL of blood glucose >100 m g/dL.

o

Potassium : 

Initial serum level m ay be norm al to high owing to extracellular shift as com pensation for acidosis.



Total body deficit usually 3â€“5 m Eq/kg



As acidosis im proves, for every 0.1 increase in the pH, serum potassium decreases 0.5 m Eq/L.



Can drop precipitously with insulin and fluids

Pa ge 1 4 5

o

Bicarbonate: 

Usually <15 m Eq/L



May be higher owing to coexisting volum e contraction alkalosis



BUN/creatinine: o

Usually shows pre-renal azotem ia owing to dehydration



Serum ketones: o

Must be present to m ake diagnosis of DKA. Î²-Hydroxybutyrate is the predom inant ketoacid, but acetoacetate and acetone are also present. Î²-Hydroxybutyrate is not m easured by m ost hospitals serum and urine ketone tests (nitroprusside reaction m easures only acetoacetate and acetone), thus there is a theoretical risk of m issing the presence of ketones using these tests

o

However, urine ketone dip test (UKDT) is 97% sensitive for presence of serum ketones and a negative UKDT has a negative predictive value of 100% in ruling out the presence of DKA.





Urinalysis: o

Ketonuria, glucosuria

o

Pregnancy (UhCG)

Venous blood gas: o

Essential to assess patient's pH

o

pH correlates well with arterial pH.

o

Avoids need for repeated arterial sticks

o

Arterial blood gas (ABG) should be perform ed if oxygenation/ventilation need assessm ent.



Serum osm olarity o

May be m easured in the lab and calculated

o

Calculated: 2(Na) + glucose/18 + BUN/2.8 (norm al

Pa ge 1 4 5

285â€“300 m Osm /L) o 



Significant hyperosm olarity >320

CBC: o

Leukocytosis m ay be present without infection.

o

If left shift in differential, suspect infection.

Other lab tests: o

Am ylaseâ€”elevation is nonspecific in DKA.

o

Lipaseâ€”elevation specific for pancreatitis

o

Calcium , Mg, Phosphate: all usually decreased as is K +

Imaging 

CT headâ€”to rule out other causes of altered m ental status



Chest radiographâ€”if pneum onia suspected as precipitant or hypoxia present



ECGâ€”to rule out ischem ia as a precipitant, and look for signs of hyper/hypo K +

Differential Diagnosis 

Other causes of anion gap acidosis



Use ACAT MUD PILES m nem onic: o

Alcoholic ketoacidosis

o

Carbon m onoxide/cyanide

o

Aspirin

o

Toluene

o

Methanol

o

Urem ia

o

Diabetic ketoacidosis

o

Paraldehyde

o

Iron/isoniazid

o

Lactic acidosis

o

Ethylene glycol

o

Starvation/sepsis

Pa ge 1 4 5



Hyperglycem ic hyperosm olar nonketotic syndrom e

P.309

Treatment Pre Hospital 

Fluid bolus often initiated in field



Quantify am ount given by param edics to guide further ED fluids

Initial Stabilization 

Airway, breathing, and circulation (ABCs) for patients with altered m ental status



Com a cocktail for AMS: naloxone, thiam ine, Accu-Chek



0.9% norm al saline (NS) bolus for hypotension/tachycardia

ED Treatment 

Cardiac m onitor and pulse oxim etry for patients with abnorm al vitals



Fluids: o

Average adult water deficit is 100 m L/kg (5â€“10 L).

o

Initial 1- to 2-L bolus of 0.9% NS to restore intravascular volum e over first hour.

o

If corrected serum sodium is low, continue with 0.9% NS, giving 1â€“2 m ore liters over the next 2â€“4 hours.

o

If corrected serum sodium is norm al or elevated, use 0.45% NS giving 1â€“2 m ore liters over next 2â€“4 hours.

o

Be careful to avoid fluid overload in patients with

Pa ge 1 4 6

cardiac disease. o

Avoid precipitous falls in serum sodium /osm olality as this m ay contribute to cerebral edem a.

o 

Total fluid replacem ent should take 24â€“36 hours.

Insulin: o

Reverses ketogenic state and downregulates counterregulatory horm ones

o

Adm inistered as continuous IV infusion of regular insulin at 0.1 units/kg/h: 

Adjust infusion in response to changes in glucose and anion gap

o

Continue until pH >7.3 and resolution of anion gap.

o

Serum glucose will fall sooner than resolution of acidosis and should be kept >250 m g/dL with glucose-containing fluids such as D 5 , 45% NS.



Potassium : o

Adm inistration is essential.

o

Total body deficit of 3â€“5 m Eq/kg

o

Will drop precipitously with adm inistration of fluid and insulin

o

Adm inister KCl, 10 m Eq/h IV once renal function is established and K + is known to be <5.5 m Eq/L.

o

May need to give up to 20â€“40 m Eq/h IV in cases where initial K + is < 3.5 m Eq/L

o

Som e advocate checking K + before initiating insulin to avoid severe hypokalem ia.

o

Should m easure q1hâ€“q2h during first 4â€“6 hours of therapy



Bicarbonate: o

No studies have shown clinical benefit in DKA, and its routine use is not advocated.

o

Com plications include hypokalem ia, alkalosis,

Pa ge 1 4 6

cerebral acidosis, and edem a. o

Som e advocate its use for pH <7.0 with cardiac instability.







Phosphate: o

Not routinely replaced during initial ED therapy

o

May supplem ent if <1.0 m g/dL

o

Adm inister as potassium phosphate.

Magnesium : o

May supplem ent if <1.2 m g/dL

o

Adm inister 2 g MgSO 4 IV over 1 hour.

Identify and treat precipitating cause.

Pediatric Considerations 

Fluids: o

Average fluid deficit is 100 m L/kg.

o

Initial 10â€“20 m L/kg bolus of 0.9% NS to restore intravascular volum e

o

May repeat once in severely dehydrated children

o

Should not exceed 40â€“50 m L/kg of fluid in first 4 hours of therapy

o

Replace rem ainder of deficit at 1.5â€“2.0 tim es m aintenance over 24â€“36 hours.

o

Overzealous fluid adm inistration thought to contribute to cerebral edem a



Cerebral edem a: o

Occurs in 1â€“2% of children with DKA

o

Causes 31% of deaths associated with DKA

o

Exact causes unclear

o

Suspect with com a, fluctuating m ental status, bradycardia, hypertension, severe headache, decreased urine output. or quickly falling corrected Na + or osm olality to below norm al levels

o

Mannitol 0.25â€“1.0 g/kg IV over 30 m inutes should

Pa ge 1 4 6

be given im m ediately and can be repeated hourly. o

Fluid rate should be decreased and other supportive m easures instituted.

Medication (Drugs) 

D 5 0 : 1 am p (25 g) of 50% dextrose IVP (peds: 2â€“4 m L/kg D 2 5 )



Insulin (100 units regular insulin in 100 m L NS) run at 0.1 U/kg/h



MgSO 4 : 2 g of 20% solution

Follow-Up Disposition Admission Criteria 

ICU adm ission for pH <7.0, altered m ental status, serious co-m orbid illness and extrem es of age (<2 years or >60 years)



Monitored unit for m oderate DKA (pH 7.01â€“7.24) with CHF or cardiac history



General floor (nurses skilled with insulin infusions) for m oderate DKA without com orbidities



Observation unit (<23 hours adm ission) for m ild DKA (pH 7.25â€“7.30) without precipitating illness

Discharge Criteria 

Resolution of anion gap acidosis



Tolerating oral fluids



No evidence of precipitating event



Clear instructions on hom e insulin regim en

Pa ge 1 4 6



Close prim ary care follow-up arranged

References 1. Am erican Diabetes Association: Position statem ent: hyperglycem ic crises in diabetes. Diabetes Care. 2004;27(suppl 1). 2. Kitabchi AE, et al. Managem ent of hyperglycem ic crises in patients with diabetes. Diabetes Care. 2001;24(1):131â€“153. 3. Ma OJ, et al. Arterial blood gas results rarely influence em ergency physician m anagem ent of patients with suspected diabetic ketoacidosis. Acad Em erg Med. 2003;10(8):836â€“841. 4. White, NH. Managem ent of diabetic ketoacidosis. Rev Endocr Metab Disord. 2003;4:343â€“353.

Miscellaneous SEE ALSO: Hyperosm olar Syndrom e

Pa ge 1 4 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dialysis C o m plicatio ns

Dialysis

Complications Christopher B. Colwell

Basics Description Dialysis com plications m ay be: 

Vascular access related (infection, bleeding)



Non-vascular access related (hypotension)



Peritoneal (abdom inal pain)

Etiology Vascular Access Related 

Infections: o

Often caused by Staphylococcus aureus

o

Can present with signs of localized infection or system ic sepsis



Throm bosis or stenosis: o

Often presents with loss of bruit or thrill over access site

o

Needs to be addressed quickly (within 24 hours) to avoid loss of access site



Bleeding:

Pa ge 1 4 6

o

Can be life threatening

Non-Vascular Access Related 

Hypotension: o

Most com m on com plication of hem odialysis

o

After dialysis: often owing to acute decrease in circulating blood volum e

o

During dialysis: hypovolem ia (m ore com m only) or onset of cardiac tam ponade owing to com pensated effusion suddenly becom ing sym ptom atic after correction of volum e overload:

o

Myocardial infarction, sepsis, dysrhythm ias, hypoxia

o

Hem orrhage secondary to anticoagulation, platelet dysfunction of renal failure



Shortness of breath: o

Volum e overload

o

Developm ent of dyspnea during dialysis owing to: tam ponade, pericardial effusion, hem orrhage, anaphylaxis, pulm onary em bolism , air em bolism



Chest pain: o

Ischem ic: 

Dialysis creates acute physiologic stressor with transient hypotension and hypoxem ia and increased m yocardial oxygen dem and.

o

Pleuritic: 



Pericarditis, pulm onary em bolism

Neurologic dysfunction: disequilibrium syndrom e: o

Rapid decrease in serum osm olality during dialysis leaves brain in com paratively hyperosm olal state.

Peritoneal 

Peritonitis: o

Owing to contam ination of peritoneal dialysate or

Pa ge 1 4 6

tubing during exchange o

Staphylococcus aureus or Staphylococcus epiderm is (70%)



Perforated viscus with abdom inal pain that can be severe, fever, brown or fecal m aterial in effluent, or localized tenderness



Fibrinous blockage of catheter resulting from infection or inflam m ation

Diagnosis Signs and Symptoms Vascular Access Related 

Bleeding from puncture sites



Loss of bruit in graft



Local infection, cellulitis, fever



Decreased sensation and strength distal to access

Non-Vascular Access Related 

Hypotension before, during, or after procedure



Palpitations



Syncope



Chest pain:



o

Ischem ic

o

Pleuritic

Hem orrhage: o

Gastrointestinal

o

Pleural

o

Retroperitoneal



Shortness of breath:



Neurologic sym ptom s (disequilibrium syndrom e):

Pa ge 1 4 6

o

Headache

o

Malaise

o

Seizures

o

Com a

Peritoneal 

Abdom inal pain



Cloudy dialysis effluent



Nausea and vom iting



Exudates or inflam m ation at insertion site of Tenckhoff catheter

Essential Workup 

Careful physical exam : o

Com plete set of vital signs including auscultated blood pressure, pulse, respiratory rate, accurate tem perature, and pulse oxim etry

o

Careful physical exam for occult infectious sources (odontogenic, perirectal abscess)

o

Auscultation of lungs for evidence of infection (rhonchi) or volum e overload (rales)

o

Search for other evidence of volum e overload (edem a).

o

Careful cardiac exam including listening for m urm urs or rubs







Infection: o

Blood and wound cultures

o

Cell count, Gram stain, culture of peritoneal fluid

Bleeding: o

CBC to evaluate anem ia and platelet count

o

Coagulation studies

Chest pain or shortness of breath: o

ECG

Pa ge 1 4 6



o

Chest radiograph

o

Arterial blood gas

o

Cardiac enzym es (if appropriate, based on history)

Neurologic dysfunction: o

CT of brain for intracranial hem orrhage

Tests Lab 

Electrolytes, BUN, and creatinine



Glucose



CBC

Imaging 



Echocardiogram for suspected: o

Pericarditis

o

Effusion

o

Tam ponade

Ultrasonography of access for possible clotted graft or fistula



Peritoneal catheterogram for catheter blockages



CT scan for pulm onary em bolism : o

Dialysis patients are at risk for both bleeding and clotting problem s.

o

Problem atic in renal insufficiency owing to contrast dye load: 

Can be done in renal failure, but contrast is then a fluid bolus and m ay need to be dialyzed off



Com m unicate contrast load to renal team as dialysis m ay need to occur for longer-thannorm al duration.

Differential Diagnosis

Pa ge 1 4 6



Hypotension: o

Hypovolem ia

o

Cardiogenic shock, acute m yocardial infarction, tam ponade, prim ary dysrhythm ias

o

Electrolyte abnorm alities leading to dysrhythm ias (hyperkalem ia and hypokalem ia)

o

Em bolism : air or pulm onary

o

Vascular instability: autonom ic neuropathy, drug related, dialysate related





Neurologic com plications: o

Cerebrovascular accident

o

Intracranial bleed

o

Meningitis or abscess

o

Disequilibrium syndrom e

o

Urem ia

o

Hypernatrem ia or hyponatrem ia

o

Hyperglycem ia or hypoglycem ia

o

Hypoxem ia

Peritoneal com plications: o

Peritonitis

o

Hernia incarceration

o

Perforated viscus

o

Acute abdom inal process: appendicitis, cholecystitis

P.311

Treatment Pre Hospital

Pa ge 1 4 7

Alert 

Do not perform intravenous access and blood pressure (BP) m easurem ent in extrem ity with functioning access.



Run intravenous fluids slowly and keep to m inim um , if possible.



Adm inister furosem ide in pulm onary edem a (anuric patients: use high doses â‰¤200 m g).

Initial Stabilization Check airway, breathing, and circulation.

Vascular Access Related Bleeding: 

Firm pressure to site(s): o

Do not totally occlude graft; m ay cause clotting.

o

Will likely need pressure applied for at least 5â€“10 m inutes to stop even m inor bleeding

o 

Docum ent presence of thrill postpressure.

Apply Gelfoam .

Non-Vascular Access Related 



Hypotension: o

Search for underlying cause.

o

Vasopressors, fluids

Shortness of breath: o

Preload and afterload reduction with nitrites and angiotensin-converting enzym e (ACE) inhibitors.



o

Attem pt diuresis if fluid overload is suspected cause.

o

Arrange for dialysis.

Hyperkalem ia: o

Adm inister intravenous calcium , bicarbonate, insulin, and glucose when appropriate (see Hyperkalem ia).

o

Monitor cardiac rhythm .

Pa ge 1 4 7



o

Adm inister ion-exchange resin (Kayexalate).

o

Arrange for dialysis.

Neurologic com plications: o

Adm inister naloxone, thiam ine, dextrose (or Accu-Chek) for altered m ental status.

o

Control seizures with benzodiazepines.

ED Treatment Vascular Access Related 

Infection: o





Initiate antistaphylococcal intravenous antibiotics.

Clotted access: o

Analgesia

o

Warm com presses

o

Vascular surgery consult

Hem orrhage: o

Control bleeding.

o

Correct coagulopathies.

o

Adm inister intravenous fluids and blood products.

Non-Vascular Access Related 

Electrolyte im balances: o

Treat hypercalcem ia or hyperm agnesem ia with saline infusion if tolerated (dilution).

o

Diuresis with furosem ide after preload and afterload reduction (nitroglycerin, enalapril)

o 



Arrange for dialysis.

Volum e overload: o

Attem pt diuresis with nitrites and furosem ide,

o

Arrange for dialysis.

Pericardial effusion or tam ponade: o

Em ergent pericardiocentesis m ay be necessary in unstable patient.

Pa ge 1 4 7

o 

Arrange for dialysis.

Acute m yocardial infarction: o

Throm bolytics or angioplasty if patient is appropriate candidate

o 

Nitrates to decrease m yocardial workload

Disequilibrium syndrom e: o

Rule out other causes of altered m ental status.

o

Generally resolves over tim e

Peritoneal 

Peritonitis: intravenous or intraperitoneal antibiotics



Culture catheter or tunnel infection, visible exudates:



o

Oral antibiotics (antistaphylococcal)

o

If recurrent or tunnel, m ay need to be unroofed

o

Meticulous site care

Perforated viscous: o

Intravenous antibiotics

o

Surgical consultation

Medication (Drugs) 

Calcium gluconate: 1 g slowly IV (cardioprotective in hyperkalem ia with widened QRS com plex))



Cefazolin: 1 g IV or IM followed by 250 m g/2 L bag for 10 days (peritonitis)



Captopril: 25 m g sublingually



Dextrose D 5 0 W: one am p: 50 m L or 25 g (peds: dextrose D 25

W: 2â€“4 m L/kg) IV



Dopam ine: 2â€“20 Âµg/kg/m in IV



Enalapril: 1.25 m g IV



Furosem ide: 20â€“100 m g IV (m ay require doses of â‰¥30 m g to effect diuresis in chronic renal failure)

Pa ge 1 4 7



Insulin: 5â€“10 U regular insulin IV (with D 5 0 for hyperkalem ia)



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg)IV or IM initial dose



Nitroglycerin: 0.4 m g sublingually; 5â€“20 Âµg/m in IV



Sodium bicarbonate: 1 m Eq/kg up to 50â€“100 m Eq IV PRN



Sodium polystyrene sulfonate (Kayexalate): 1 g/kg up to 15â€“60 g PO or 30â€“50 g retention enem a q6h PRN (for hyperkalem ia)



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM



Tobram ycin: 1.7 m g/kg IV or IM followed by 10 m g/2 L bag for 10 days (peritonitis)



Vancom ycin: 1 g IV or IM followed by 50 m g/2 L bag for 10 days (peritonitis)

Follow-Up Disposition Admission Criteria 

ICU adm ission: o

Severe hyperkalem ia

o

Pulm onary edem a

o

Volum e overload

o

Persistent hypotension

o

Uncontrolled seizures

o

Acute m yocardial infarction

o

Cardiovascular accident

o

Pericarditis

o

Sepsis

Pa ge 1 4 7

o 

Peritonitis with toxic or system ic sym ptom s

Regular adm ission: o

Fever

o

Vom iting

o

Peritonitis without toxic or system ic sym ptom s

o

Nonâ€“life-threatening electrolyte disturbances

o

Inability to provide self-care for continuous am bulatory peritoneal dialysis with antibiotics

Discharge Criteria 

Mild infections of access site



Sam e-day surgery for som e throm bectom y procedures



Hem ostasis at puncture sites

References 1. Feldm an HI, Held PJ, Hutchinson JT, et al. Hem odialysis vascular access m orbidity in the United States. Kidney Int. 1993;43(suppl 41): S1091â€“S1096. 2. Kahn IH, Catto GRD. Long-term com plications of dialysis: infection. Kidney Int. 1993;43(suppl 41): S143â€“S148. 3. Wolfson AB, Maenza RL. Renal failure. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1380â€“1390. 4. Sinert R, Spektor M. Renal failure and dialyisis patients. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency Medicine: A Com prehensive Guide. 6th ed. New York: McGraw-Hill; 2004: 599â€“606.

Miscellaneous SEE ALSO: Renal Failure; Hyperkalem ia

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diaper Rash

Diaper Rash

Amy LePage Kristine Thompson

Basics Description 

Also known as diaper derm atitis



Very com m on derm atologic disorder of infancy



Most com m on in first 4 weeks and again at 8â€“12 m onths



Incidence in adults unknown but com m on am ong incontinent patients



Prim ary irritant/contact derm atitis: o

Outer skin layers are broken down, leading to inflam m ation and loss of protective barrier function.

o

Secondary fungal or bacterial infection can cause m ore severe form s of diaper derm atitis.

Etiology 

Irritants: o

Moisture: 

Prolonged overhydration owing to infrequent diaper changes, poorly absorbing diapers, or cloth diapers

o

Friction: 

Diaper rubbing on skin or loose-fitting diaper

Pa ge 1 4 7

o

Chem icals: 

Prolonged exposure to stool enzym es and urine



Scents or m oisturizers in wipes or soap



Diaper m aterial or adhesive used to hold diaper in place



Infection: o

Candida albicans: 

Isolated in up to 80% of infants



Overgrowth com m on after system ic antibiotic use

o

Bacterial

o

Often com plication of other causes of derm atitis: 

Staphylococcus aureus, Streptococcus, Escherichia coli are com m on; Peptostreptococcus and Bacteroides m ay also be encountered.



Seborrheic diaper derm atitis



Atopic diaper derm atitis

Diagnosis Diagnosis often em piric based on appearance of rash

Signs and Symptoms History Child m ay cry with diaper changes or wiping diaper area.

Physical Exam 

Irritant



Beefy-red confluent patches with distinct borders at diaper edges, typically sparing skin folds



Infectious:

Pa ge 1 4 7

o

Candidaâ€”dem arcated erythem atous rash with satellite pustules or papules, typically involves skin folds

o

Bacterialâ€”superficial erosions with yellow crust and occasionally bullae



Seborrheic diaper derm atitis: o

Lesions with erythem atous base and greasy yellow or gray scale

o

Infant will likely have sim ilar lesions on other body surfaces, especially scalp.



Atopic diaper derm atitis: o

Sim ilar appearance to irritant derm atitis, but lesions also on other body surfaces such as the face



Variations include: o

Jacquet form â€”erosive variant usually seen with persistent diarrhea

o

Psoriasiform â€”erythem a, silvery surface scales and spared skin folds; also likely to have sim ilar lesions on other body surfaces

Essential Workup 

Inquire about diaper-changing habits and urinary and fecal habits.



Exam ine other body areas to identify associated rashes.



Consider child abuse or neglect: o

Child's overall hygiene

o

Burns or other traum a

Tests Lab 

Laboratory evaluation usually not necessary for m anagem ent of diaper derm atitis



Bacterial cultures usually not indicated except in

Pa ge 1 4 7

com plicated cases 

Skin surface scrapings with KOH prep and/or culture m ay help distinguish between Candida and atypical seborrheic derm atitis: o

Look for budding yeast and/or pseudohyphae

Differential Diagnosis 

Child abuse or neglect



Infection: o

Im petigo

o

Scabies

o

Herpes sim plex

o

Varicella

o

Congenital syphilis



Psoriasis



Atopic derm atitis



Seborrheic derm atitis



Allergic contact derm atitis



Papular urticaria



Bullous pem phigoid

P.313

Treatment ED Treatment 

Environm ental adjustm ents: o

Education of parents and caregivers is essential.

o

Frequent diaper changes, up to q1h for neonates and q3hâ€“q4h for infants and adults

Pa ge 1 4 7

o

Gentle rinsing of affected area with warm water or saline

o

Avoid harsh soaps or alcohol wipes.

o

Leave area uncovered as m uch as possible; allow tim e to air dry.

o

Highly absorbant diapers have less incidence of diaper rash than cloth diapers.

o

New diapers that are â€œbreathableâ€• or contain top sheet of zinc oxide/petroleum and steryl alcohol lining have been shown to decrease incidence.



Barrier cream s: o

Many preparations available containing zinc oxide, petroleum , lanolin

o

Should be applied after each diaper change and continued after rash resolves to m inim ize recurrence

o

If Candidal infection present, apply over antifungal m edication.



Corticosteroids: o

For m oderate to severe cases not responding to other therapy

o

Should not be stronger than 1% hydrocortisone: anything stronger can cause serious side effects

o 

Discontinue after 3â€“5 days

Antifungals: o

Nystatin cream , powder, or ointm ent: 

Expect im provem ent in 1â€“2 days



Ointm ent best tolerated on m acerated skin

o

Clotrim azole applied topically after diaper change

o

Miconazole applied topically after diaper change

o

Lotion is preferred in intertriginous areas.

o

Cream should be applied sparingly to avoid m aceration effects.

Pa ge 1 4 8

o

Ciclopirox applied topically after diaper change

o

Antifungal agent also found to have som e antibacterial activity and anti-inflam m atory properties

o

Currently indicated for children >10 years, but recent studies dem onstrate safety in infants as well

o

Consider oral agent if concurrent cutaneous or oral candidiasis is present or in recalcitrant case because stool m ay be colonized with C. albicans.



Antibacterials: o

Typically concurrent with other therapies

o

Mupirocin (Bactroban) applied after diaper changes

o

System ic antibiotics rarely needed

Medication (Drugs) 

Ciclopirox 0.77% cream , gel, or suspension: applied topically twice daily after diaper change



Clotrim azole 1% cream : applied topically twice daily after diaper change



Hydrocortisone 0.5â€“1% topical cream : applied three or four tim es daily



Miconazole topical 2% cream : applied twice daily after diaper change



Mupirocin 2% ointm ent or cream (Bactroban): applied topically three to five tim es daily after diaper changes (for infants >3 m onths of age)



Nystatin 100,000 U/g cream , powder, or ointm ent: apply twice daily after diaper change.

Pa ge 1 4 8

Follow-Up Disposition Admission Criteria 

Evidence of child abuse or neglect



Evidence of sepsis

References 1. Gupta AK, Skinner AR. Managem ent of diaper derm atitis. Int Soc Derm . 2004;43:830â€“834. 2. Sires UL, Mallory SB. Diaper derm atitis: how to treat and prevent. Postgrad Med. 1995;98:79â€“84. 3. Ward DB, Fleischer AB Jr, Feldm an SR, et al. Characterization of diaper derm atitis in the United States. Arch Pediatr Adolesc Med. 2000;154(9): 943â€“946. 4. Wolf R, Wolf D, Tuzun B, et al. Diaper derm atitis. Clin Derm atol. 2000;18(6):657â€“660.

Codes ICD9-CM 691.0

ICD10 L22

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diaphragm atic Traum a

Diaphragmatic

Trauma Robert S. Hamilton

Basics Description 

Penetrating injury: o

Violation of the diaphragm by penetrating object (knife and gunshot wounds)

o 

May involve any portion of diaphragm

Blunt injury: o

Increased intra-abdom inal or intrathoracic pressure is transm itted to diaphragm , causing rupture.

o

Injuries are typically in radial orientation: 

Posterolateral area of the left side of the diaphragm



Em bryologic point of weakness



Injuries are frequently between 5 cm and 15 cm in length.



Diaphragm atic defects do not heal spontaneously because of pleuroperitoneal pressure gradient: o

May exceed 100 cm H 2 O during m axim al respiratory effort

Pa ge 1 4 8

o

Prom otes herniation of abdom inal contents through rent in diaphragm and into chest

Epidemiology Incidence Estim ated to be 1â€“6% in all patients sustaining m ultiple-system traum a

Etiology 

Lateral torso im pact is three tim es m ore likely to result in ipsilateral diaphragm atic rupture than frontal im pact.



Suspect diaphragm atic injury: o

Penetrating traum a to thoracoabdom inal area

o

Injuries that cross plane of the diaphragm

Diagnosis Alert 

In acute phase, there m ay be no abdom inal visceral herniation: o

This injury m ay even be m issed on initial laparotom y or laparoscopy.

Signs and Symptoms 

Vary depending on whether phase is acute, latent, or obstructive: o

Acute: 

Tachypnea



Hypotension



Absence of breath sounds



Abdom inal distention



Bowel sounds in chest

Pa ge 1 4 8

o

Latent: 

Abdom inal discom fort from interm ittent herniation of abdom inal contents into thorax

o





Abdom inal pain that is worse postprandially



Exacerbated by lying supine



Pain radiating to left shoulder



Nausea, vom iting, or belching

Obstructive: 

Severe abdom inal pain



Obstipation



Nausea, vom iting



Abdom inal distention

Strangulated abdom inal organs m ay perforate and spill abdom inal contents into chest.



Respiratory com prom ise, sepsis, and death

Essential Workup Chest radiograph m ay reveal herniated loops of bowel or other abdom inal viscera in thorax: 

Pathognom onic finding is presence of nasogastric tube above diaphragm .



Findings are often nonspecific: o

Unilaterally elevated diaphragm

o

Mediastinal shift away from affected side

o

Unilateral pleural thickening

o

Areas of atelectasis or consolidation at bases

o

Sm all hem othorax or pneum othorax



50% of initial chest radiographs m ay be norm al.



Diagnosis m ay be difficult in latent phase because of interm ittent nature of herniation.



Contrast studies of gastrointestinal tract m ay be helpful.

Tests

Pa ge 1 4 8

Lab 

If diagnostic peritoneal lavage (DPL) is perform ed: o

Red blood cell count of 5,000 RBC/m m 3 is considered positive.



No laboratory studies confirm or rule out presence of diaphragm atic injury.

Imaging 

Gastrointestinal contrast studies are the m ost useful in diagnosing chronic herniation of abdom inal contents through diaphragm .



Ultrasound m ay be used, particularly on right side with accom panying hepatic herniation.



Conventional CT is rarely diagnostic and has poor sensitivity.



New m ultidetector CT (MDCT) has had m uch better success at diagnosing subtle diaphragm atic injuries.



MRI m ay be useful.

P.315

Diagnostic Procedures/Surgery 

Diagnostic pneum operitoneography: o

Air is injected through DPL catheter.

o

Pneum othorax on subsequent chest radiograph is diagnostic of diaphragm atic injury.

o

Poorly tolerated by unstable patients and m ay require chest tube placem ent



Thoracoscopy and laparoscopy are potentially valuable tools, both diagnostically and therapeutically.

Differential Diagnosis

Pa ge 1 4 8



Atelectasis



Hem othorax



Pneum othorax



Pulm onary contusion



Gastric dilation, intra-abdom inal fluid



Traum atic pneum atocele



Subdiaphragm atic abscess



Intrathoracic cyst



Em pyem a



Congenital eventration of the diaphragm

Treatment Alert 

Herniation of abdom inal contents into chest wall m ay m im ic hem othorax or tension pneum othorax: o

Bowel sounds in chest m ay help distinguish.

o

Be suspicious of diaphragm atic injury with lateral com pression of chest: 

Be cautious in placem ent of needle or tube thoracostom ies.

o

Fecal thorax has been reported with bowel rupture.

Initial Stabilization 

Follow advanced traum a life support (ATLS) protocols



If respiratory distress is present, im m ediate placem ent of a nasogastric tube m ay decom press herniated abdom inal contents.

ED Treatment 

Palpate within the chest wall com pletely for visceral organs before placing chest tube.

Pa ge 1 4 8



Patients with visceral perforations are septic and need aggressive resuscitation and antibiotic therapy.



Early surgical intervention is param ount.



Thoracoscopy or laparoscopy is useful in selected injuries and patients.



Em piric broad-spectrum antibiotics are indicated in the case of perforated viscera.

Medication (Drugs) 

Gram -negative aerobes: o



Gentam icin: Adults/peds: 2â€“5 m g/kg IV initial dose

Gram -negative anaerobes: o

Clindam ycin: 900 m g (peds: 20â€“40 m g/kg/24h) IV q8h

o

Metronidazole: 1 g (peds: 15 m g/kg) IV load, then 500 m g (peds: 7.5 m g/kg) IV q6h



Both aerobic and anaerobic: o

Am picillin/sulbactam : 1.5â€“3 g (peds: 100â€“400 m g/kg/24h) IV q6h

o

Cefotetan: 2 g (peds: 40â€“80 m g/kg/24h) IV q12h

o

Cefoxitin: 2 g (peds: 80â€“160 m g/kg/24h) IV q12h

o

Ticarcillin/clavulanate: 3.1 g (peds: 50 m g/kg per dose) IV q6h

Follow-Up Disposition Admission Criteria 

Patients with suspicion for diaphragm atic injury m ust be

Pa ge 1 4 8

adm itted to traum a surgeon. 

Patients should be adm itted to m onitored or intensive care unit setting.

Discharge Criteria Patients with diaphragm atic injury or any significant suspicion for it m ust not be discharged from ED.

References 1. Blaivas M, Brannam L, Hawkins M, et al. Bedside em ergency ultrasonographic diagnosis of diaphragm atic rupture in blunt abdom inal traum a. Am J Em erg Med. 2004;22(7):601â€“604. 2. Kanowitz A, Markovchick V. Esophageal and diaphragm atic traum a. In: Rosen's Em ergency Medicine: Concepts and Clinical Practice. 4th Ed. St. Louis, MO: Mosby; 1998:546â€“554. 3. Mansour KA. Traum a to the diaphragm . Chest Surg Clin North Am . 1997;7(2):373â€“383. 4. Mirvis SE. Diagnostic im aging of acute thoracic injury. Sem in Ultrasound CT MR. 2004;25(2): 156â€“179. 5. Rosati C. Acute traum atic injury of the diaphragm . Chest Surg Clin North Am . 1998;8(2):371â€“379. 6. Shah R, Sabanathan S, Mearns AJ, et al. Traum atic rupture of the diaphragm . Ann Thorac Surg. 1995;60(5):1444â€“1449. 7. Sharm a OP, Duffy B. Transdiaphragm atic intercostals hernia: review of the world literature and presentation of a case. J Traum a. 2001;50(6): 1140â€“1143. 8. Vallina VL, Norwood S, McAuley C, et al. Laparoscopic diaphragm rupture repair. Surg Endosc. 2002;16(5):869.

Codes ICD9-CM 862.0 Injury to other and unspecified intrathoracic organs

ICD10

Pa ge 1 4 8

S27.8

Pa ge 1 4 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diarrhea, Adult

Diarrhea, Adult

Isam Nasr Harminder Brar

Basics Description Bowel m ovem ents characterized as frequent (m ore than three per day), loose and watery owing to an infectious or toxin exposure

Etiology N/A

Infectious 

Viruses: o



50â€“70% of all cases

Invasive bacteria: o

Cam pylobacter: 

Contam inated food or water, wilderness water, birds, and anim als

o



Most com m on bacterial diarrhea



Gross or occult blood is found in 60â€“90%.

Salm onella: 

Contam inated water, eggs, poultry, or dairy products



Typhoid fever (Salm onella typhi) characterized

Pa ge 1 4 9

by unrem itting fever, abdom inal pain, rose spots, splenom egaly, and bradycardia o

Shigella: 

o

Vibrio parahaem olyticus: 

o

Fecal or oral route

Raw and undercooked seafood

Yersinia: 

Contam inated food (pork), water, and m ilk



May present as m esenteric adenitis or m im ic appendicitis



Bacterial toxin: o

Escherichia coli: 

Major cause of traveler's diarrhea



Ingestion of food or water contam inated by feces

o

o

o

Staphylococcal aureus: 

Most com m on toxin-related disease



Sym ptom s 1â€“6 hours after ingesting food

Bacillus cereus: 

Classic sourceâ€”fried rice left on steam tables



Sym ptom s within 1â€“36 hours

Clostridium difficile: 

Antibiotic-associated enteritis linked to pseudom em branous colitis



Incubation period within 10 days of exposure or initiation of antibiotics

o

o

Aerom onas hydrophila: 

Aquatic sources prim arily



Affects children younger than 3 years of age



Fecal leukocytes absent

Cholera: 

Caused by enterotoxin produced by Vibrio

Pa ge 1 4 9

cholerae 

Profuse watery stools with m ucus (classic appearance of rice-water stools)



Protozoa: o

Giardia lam blia: 

Most com m on cause of parasite gastroenteritis in North Am erica



High-risk groups: travelers, children in day care centers, institutionalized people, hom osexual m en, and cam pers who drink untreated m ountain water

o

Cryptosporidium parvum : 

o

Com m only carried in patients with AIDS

Entam oeba histolytica (entam ebiasis): 

5â€“10% extraintestinal m anifestations (hepatic am ebic abscess)

Pediatric Considerations 

Most are viral in origin and self-lim ited.



Rotavirus accounts for 50%.



Shigella: infections associated with seizures



Focus evaluation on state of hydration.

Diagnosis Signs and Symptoms History 

Loose, watery bowel m ovem ents



Bloody stools with m ucus



Abdom inal pain and cram ps, tenesm us, flatulence



Fever, headache, m yalgias

Pa ge 1 4 9



Nausea, vom iting



Dehydration, lethargy, and stupor

Physical Exam 

Dry m ucous m em branes



Abdom inal tenderness



Perianal inflam m ation, fissure, fistula

Essential Workup 

Digital rectal exam ination to determ ine presence of gross or occult blood



Fecal leukocyte determ ination: o

Present with invasive bacteria

o

Absent in protozoal infections, viral, toxin-induced food poisoning

Tests Lab 



CBCâ€”indications: o

Significant blood loss

o

System ic toxicity

Electrolytes, glucose, BUN, creatinineâ€”indications: o

Lethargy, significant dehydration, toxicity, or altered m ental status

o

Diuretic use, persistent diarrhea, chronic liver or renal disease



Stool cultureâ€”indications: o

Presence of fecal leukocytes

o

Historical m arkers: im m unocom prom ised, travel, hom osexual

o

Public health: food handler, day care or health care worker, institutionalized



Blood culturesâ€”indications:

Pa ge 1 4 9

o

Suspected bacterem ia or system ic infections

o

Ill patients requiring adm ission

o

Im m unocom prom ised

o

Elderly patients and infants

Imaging Abdom inal radiographs: 

No value unless obstruction or toxic m egacolon suspected

Differential Diagnosis 

Ulcerative colitis



Crohn disease



Mesenteric ischem ia



Diverticulitis, anal fissures, hem orrhoids



Irritable bowel syndrom e



Milk and food allergies



Malrotation with m idgut volvulus



Meckel diverticulum



Intussusception



Appendicitis



Drugs and toxins: o

Mannitol

o

Sorbitol

o

Phenolphthalein

o

Magnesium -containing antacids

o

Quinidine

o

Colchicine

o

Mushroom s

o

Mercury poisoning

P.317

Pa ge 1 4 9

Treatment Pre Hospital 

Difficult IV access with severe dehydration



Avoid exposure to contam inated clothes or body substances.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



IV fluid with 0.9% norm al saline (NS) resuscitation for severely dehydrated

ED Treatment 

Oral fluids for m ild dehydration (Gatorade/Pedialyte)



IV fluids for: o

Hypotension, nausea and vom iting, obtundation, m etabolic acidosis, significant hypernatrem ia or hyponatrem ia

o

0.9% NS bolus: 500 m Lâ€“1 L (peds: 20 m L/kg) for resuscitation, then 0.9% NS or D 5 W 0.45% NS (peds: D 5 W 0.25% NS) to m aintain adequate urine output







Bism uth subsalicylate (Pepto-Bism ol): o

Antisecretory agent

o

Effective clinical relief without adverse effects

Kaolin-pectin (Kaopectate): o

Reduces fluidity of stools

o

Does not influence course of disease

Antim otility drugs: diphenoxylate (Lom otil), loperam ide (Im odium ), paregoric, and codeine o

Appropriate in noninfectious diarrhea

o

Initial use of sparse am ounts to control sym ptom s in infectious diarrhea

Pa ge 1 4 9

o

Avoid prolonged use in infectious diarrheaâ€”m ay increase duration of fever, diarrhea, and bacterem ia and m ay precipitate toxic m egacolon



Antibiotics for Infectious pathogens: o

Cam pylobacter: quinolones or erythrom ycin

o

Salm onella: quinolones or trim ethoprim -sulfam ethoxazole (TMP-SMX)

o

Typhoid fever: ceftriaxone

o

Shigella: quinolone, TMP-SMX, or am picillin

o

Vibrio parahaem olyticus: tetracycline or doxycycline

o

Clostridium difficile: vancom ycin

o

Escherichia coli: quinolones or TMP-SMX

o

Giardia lam blia: m etronidazole or quinacrine

o

Entam oeba histolytica (entam ebiasis): iodoquinol or m etronidazole

Medication (Drugs) 

Am picillin: 500 m g (peds: 20 m g/kg/24 h) PO or IV q6h



Bactrim DS (TMP-SMX): 1 tab (peds: 8â€“10 m g TMP/40â€“50 m g SMX/kg/24h) PO or 4â€“5 m g/kg TMP IV b.i.d.



Ceftriaxone: 1 gram (peds: 50â€“75 m g/kg/12h) IM or IV b.i.d.



Ciprofloxacin (quinolone): 500 m g PO or 400 m g IV b.i.d. (older than 18 years)



Doxycycline: 100 m g PO or 100 m g IV b.i.d.



Erythrom ycin: 500 m g (peds: 40â€“50 m g/kg/24h) PO q.i.d.



Iodoquinol: 650 m g (peds: 30â€“40 m g/kg/24h) PO t.i.d.



Metronidazole: 250 m g (peds: 35 m g/kg/24h) PO t.i.d. (older than 8 years)

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

Quinacrine: 100 m g (peds: 6 m g/kg/24h) PO t.i.d.



Tetracycline: 500 m g PO or IV q6h



Vancom ycin: 500 m g (peds: 10â€“50 m g/kg/24h) IV q.i.d.

Follow-Up Disposition Admission Criteria 

Hypotension, unresponsive to IV fluids



Significant bleeding



Signs of sepsis or toxicity



Intractable vom iting or abdom inal pain



Severe electrolyte im balance or m etabolic acidosis



Altered m ental status



Children with >10â€“15% dehydration

Discharge Criteria 

Mild cases requiring oral hydration



Dehydration responsive to IV fluids

References 1. Dupont HL. What's new in enteric infectious diseases at hom e and abroad. Curr Opinion Infect Dis. 2005;18:407â€“412. 2. Gough JE, Clem ent PA. Diarrhea. In: Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO; 2002:200â€“208. 3. Hogan D. The em ergency departm ent approach to diarrhea. Em erg Med Clin North Am . 1996;14(4): 673â€“694. 4. Reisdorff E, Pflug V. Infectious diarrhea: beyond supportive care. Em erg Med Rep. 1996;17(14): 141â€“150. 5. Surawicz CM. Infectious causes of chronic diarrhea. Gastroenterol

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Clin North Am . 2001; 30(3):679â€“692.

Miscellaneous SEE ALSO: Gastroenteritis

Codes ICD9-CM 787.91

ICD10 A09

Pa ge 1 4 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diarrhea, Pediatric

Diarrhea,

Pediatric Richard Lichenstein

Basics Description 

One of the m ost com m on pediatric com plaints; second only to respiratory infections in overall disease frequency



Leading cause of illness and death in children worldwide



Acute infectious enteritis (AIE): o

Vom iting and diarrhea

o

Children <5 years in the United States typically have two episodes annually.

o

Responsible for about 10% of all pediatric ED visits and hospital adm issions



Acute change in the â€œnorm alâ€• bowel pattern that leads to increased num ber or volum e of stools and lasts <7 days; World Health Organization (WHO) defines case as three or m ore loose or watery stools per day. o

Chronic if the diarrhea persists for >2 weeks

Etiology Acute Enteritis

Pa ge 1 5 0



Infectious: o

Viruses: 70â€“80% of cases: 

Rotavirus and norovirus (Norwalk) viruses in the winter m onths

 o

o 

Enteroviruses in the sum m er and early autum n

Bacteria: 10â€“20% 

Escherichia coli



Cam pylobacter



Salm onella



Shigella



Yersinia enterocolitica



Clostridium difficile

Parasites: 5%

Food poisoning: o

Escherichia coli (EHEC -O157:H7;ETEC)

o

Staphylococcus aureus

o

Cyclospora cayetanensis (raspberries)

o

Cryptosporidiosis (water-borne)

o

Clostridium perfringens

o

Vibrio species (seafood and fish)

P.319



Postinfectious



Milk allergy



Associated with life-threatening infections:



o

Hem olytic urem ic syndrom e (HUS)

o

Toxic m egacolon

Associated with other infections: o

Otitis m edia

o

Urinary tract infection

Chronic Diarrhea

Pa ge 1 5 0



Osm otic: (increased sorbitol or fructose from fruit juices) o



Lactose intolerance

Secretory: o

Increased secretion owing to secretagogues (bacterial toxins, failure reabsorption, horm one-producing tum ors)



Altered m otility: o



Increased gut transit (irritable bowel syndrom e)

Exudative diarrhea: o

Inflam m atory conditions where there is disruption of the m ucosa of the intestines (inflam m atory bowel disease, Henoch-SchÃ¶nlein purpura, bacterial colitis)



Malabsorption (cystic fibrosis)

Diagnosis Signs and Symptoms 

Frequent, loose stools: o

Watery

o

Bloody

o

Mucoid



Signs of dehydration reflect loss of total-body water



Categorization of degree of dehydration: o

o

Mental status: 

Mild (<5%): alert



Moderate (5â€“10%): irritable



Severe (â‰¥15%): lethargic

Mucous m em brane: 

Mild: variably dry



Moderate: dry

Pa ge 1 5 0

 o

o

o

o

o

o

Severe: dry

Skin turgor: 

Mild: norm al



Moderate: variably reduced



Severe: reduced

Anterior fontanel: 

Mild: norm al



Moderate: depressed



Severe: depressed

Blood pressure: 

Mild: norm al



Moderate: variably orthostatic



Severe: orthostatic or decreased

Pulse: 

Mild: norm al



Moderate: tachycardia



Severe: m arkedly tachycardic

Capillary refill: 

Mild: <2 seconds



Moderate: 2â€“3 seconds



Severe: â‰¥4 seconds

Urine output: 

Mild: decreased



Moderate: oliguria



Severe: oliguria/anuria



Fever



Abdom inal pain, distention



Vom iting



Tenesm us



Im paired nutritional status or abnorm al growth param eters

Essential Workup

Pa ge 1 5 0



Gross exam ination of stool



Guaiac and Wright stain for fecal leucocytes: o

Watery diarrhea without blood or m ucus associated with viral enteritis or related to bacterial enterotoxins

o

Diarrhea with blood or m ucus suggests an enteroinvasive inflam m atory or cytotoxin- m ediated process (Salm onella, invasive E. coli).

o

Microscopic exam ination of a Wright-stained sm ear of the m ucoid part of stool revealing >5 fecal leucocytes per high-power field is suggestive of bacterial infection: 

Shigella



Salm onella



Cam pylobacter



Yersinia



Invasive E. coli

Tests Lab 

Serum electrolytes, BUN, creatinine assist in the assessm ent of m oderate to severe dehydration.



Urinalysis assists in the assessm ent of dehydration.



Stool pH <5.5 or positive stool-reducing substances in viral infection



Stool culture: o

Unnecessary in m ost cases unless there is a high likelihood of identifying bacterial pathogens (positive guaiac and/or fecal leucocytes) for which the clinical course and period of contagion m ay be altered by antibiotic therapy



Consider urine culture in febrile children â‰¤12 m onths

Pa ge 1 5 0

Imaging 

Abdom inal ultrasound for intussusception



Air contrast enem a often diagnostic and therapeutic for intussusception



Abdom inal CT for conditions such as appendicitis

Differential Diagnosis 

Infectious: o

o



Bacterial gastroenteritis 

Tem perature >39Â°C



Toxic clinical appearance



Cram py abdom inal pain



Bloody m ucoid stools

Viral gastroenteritis 

Seasonal epidem ics



Guaiac-negative stool

o

Parasitic (Giardia lam blia)

o

Chronic diarrhea

Postinfectious: o

Follows acute or bacterial or viral gastroenteritis; often associated with m alabsorption, especially lactose

o 

C. difficile m ay follow use of antibiotics.

Noninfectious: o

Milk allergy 

Hem e-positive stool



Vom iting

o

Malrotation with m idgut volvulus

o

Inflam m atory bowel disease

o

Intussusception 

â€œCurrant jellyâ€• stool



Abdom inal m ass

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Treatment Initial Stabilization 

For severely dehydrated children in shock or near shock, intravenous or intraosseous access with 20 m L/kg 0.9% norm al saline (NS) and 1 g/kg dextrose if hypoglycem ic



Pulse oxim etry



Endotracheal intubation m ay be required for children in shock.

ED Treatment 

For m ild to m oderate dehydration, correct dehydration using oral rehydration therapy (ORT), 50 m L/kg and 100 m L/kg, respectively, over a 4-hour period: o

Replace ongoing losses with 10 m L/kg of ORT for each stool.



For m oderate to severe dehydration, correct dehydration using parenteral fluids com bining m aintenance and deficit requirem ents.



If diarrhea is not associated with dehydration, use 10 m L/kg of ORT for each stool alone.



Antibiotics only for defined acute enteritis: o

Cam pylobacter jejuni: 

o

Salm onellaâ€”uncom plicated: 

o

Erythrom ycin

No antibiotics

Salm onellaâ€”com plicated (infant <6 m onths old, dissem inated, bacterem ia, im m unocom prom ised host, enteric fever) 

Am picillin or trim ethoprim -sulfam ethoxazole

Pa ge 1 5 0

(TMP-SMX) for 10 days o

Shigella: 

o

Yersinia: 

o

TMP-SMX for 5 days

E. coliâ€”enteroadherent: 

o

None

E. coliâ€”enteroinvasive: 

o

Metronidazole or vancom ycin for 7 days

E. coliâ€”enterotoxigenic, enteropathogenic: 

o

None

C. difficileâ€”severe and or prolonged enteritis: 

o

None or TMP-SMX for 5 days

C. difficileâ€”carrier: 

o

TMP-SMX for 5 days

Neom ycin for 5 days

G. lam blia: 

Furazolidone or m etronidazole for 7 days; nitazoxanide for 3 days



Antidiarrheal agents not recom m ended, although som e prom ising studies suggest that loperam ide m ay be helpful: o

Alter intestinal m otility (loperam ide, opiates, opiate-atropine com binations)

o

Alter secretion (bism uth subsalicylate)

o

Adsorb fluid and toxins (kaolin-pectin, fiber, activated charcoal, attapulgite)

o

Alter intestinal m icroflora (Lactobacillus- containing com pounds, probiotics)

o

Im proves transport of water and electrolytes and replaces zinc lost in m alnourished children (Zinc)

Post-ED Diet 

On rehydration, feed children with diarrhea age-appropriate diets.

Pa ge 1 5 0



Well-tolerated foods: o

Rich in com plex carbohydrates (rice, potatoes, bread)

o

Lean m eats

o

Yogurt

o

Fruits

o

Vegetables

o

Full-strength m ilk and form ula unless there is a strong suspicion of lactose intolerance



Avoid fatty foods and foods high in sim ple sugars.

Medication (Drugs) 

Am picillin: 50â€“200 m g/kg/24h IV/PO q6h



Erythrom ycin: 40 m g/kg/24h PO q6h; 10â€“20 m g/kg/24h IV q6h



Furazolidone: 6 m g/kg/24h PO q6h



Metronidazole: 15 m g/kg/24h PO t.i.d.



Neom ycin: 50â€“100 m g/kg/24h PO q6hâ€“q8h



Nitazoxanide: 100 m g PO b.i.d. (age 1â€“3 years); 200 m g PO b.i.d. for older



TMP-SMX: 8â€“10 m g/kg/24h as TMP PO b.i.d.



Vancom ycin: 40â€“50 m g/kg/24h PO q6h



Loperam ide (not for use in children <6 years old or in those with hem e-positive stools): age 6â€“8 years, 2 m g PO b.i.d.; age 8â€“12 years, 2 m g PO t.i.d.

Follow-Up Disposition

Pa ge 1 5 0

Admission Criteria 

Surgical abdom en



Inability to tolerate oral fluids



Ten percent dehydration or greater



Suspected com plicated Salm onella enteritis



Toxic-appearing child

Discharge Criteria 

Im provem ent in the patient's condition



Caregivers of child can follow through with appropriate ORT and diet.



Caregivers able to report signs and sym ptom s of dehydration

Issues for Referral 

Im m unocom prom ised host



Conditions associated with com plications such as seizures



Hypernatrem ic dehydration

References 1. Bonadio WA. Acute infectious enteritis in children. Em ergency departm ent diagnosis and m anagem ent. Em erg Med Clin North Am . 1995;13:457â€“472. 2. Kaplan MA, Prior MJ, McKonly KI, et al. A m ulticenter random ized controlled trial of a liquid loperam ide product versus placebo in the treatm ent of acute diarrhea in children. Clin Pediatr. 1999;38:579â€“591. 3. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis am ong children: oral rehydration, m aintenance, and nutritional therapy. MMWR Recom m Rep. 2003;52(RR-16):1â€“16. 4. Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Em erg Infect Dis. 199;5:607â€“625. 5. Provisional Com m ittee on Quality Im provem ent, Subcom m ittee on

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Acute Gastroenteritis. Practice param eter: the m anagem ent of acute gastroenteritis in young children. Pediatrics. 1996;97:424â€“436. 6. Ram aswam y K. Infectious diarrhea in children. Gastroenterol Clin North Am . 2001;30:611â€“624. 7. Salazar-Lindo E, Santisteban-Ponce J, Chea-Woo E, et al. Racecadotril in the treatm ent of acute watery diarrhea in children. N Engl J Med. 2000;343: 463â€“467.

Miscellaneous SEE ALSO: Vom iting, Pediatric

Codes ICD9-CM 787.91

Pa ge 1 5 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Digo xin, Po iso ning

Digoxin, Poisoning

Kirk Cumpston

Basics Description Acute Digitalis Effects (Elevated Levels in Children and Intentional Overdose) 

Inhibits sodium -potassium ATPase pum p in cell m em branes



Allows m ore calcium ions to enter cell and cardiac cells to contract m ore strongly



Increases K + extracellularly



Increases vagal tone



Slows atrioventricular (AV) node conduction (vagotonic)



Increases autom aticity and conduction system refractory period



Bradydysrhythm ias

Chronic Digitalis Effects (Therapeutic to Toxic Levels in Elderly Patients) 

Inhibits sodium -potassium ATPase pum p in cell m em branes



Increases intracellular calcium

Pa ge 1 5 1



Increases vagal tone



Increases autom aticity



Usually hypokalem ic secondary to diuretic use



Tachydysrhythm ias

Etiology 

Digoxin/digitoxin pharm aceuticals



Plants and anim als containing cardiac glycosides: o

Foxglove

o

Oleander

o

Lily of the valley

o

Dogbane

o

Red squill

o

Cane toad, Colorado River toad

Diagnosis Signs and Symptoms 

Toxicity onset: 2 hours after PO ingestion and 15 m inutes following IV



Toxicity: o

Occurs with norm al digoxin levels (chronic)

o

May be absent with elevated digoxin levels (acute)

Cardiovascular 

Dysrhythm ias: o

Paroxysm al atrial tachycardia (PAT) with AV block

o

Bidirectional ventricular tachycardia is pathognom onic:

o



Classic dysrhythm ia



Uncom m on

Prem ature ventricular contractions (PVCs) m ost

Pa ge 1 5 1

com m on o

Nonparoxysm al accelerated junctional tachycardia

o

Ventricular tachycardia (VT)

o

Atrial fibrillation

o

Bigem iny

o

Bradycardia

o

Nonparoxysm al atrial tachycardia

o

AV blocks

o

Sinus arrhythm ia

o

Prem ature atrial contraction



Congestive heart failure (CHF) exacerbation



Hypotension



Shock



Cardiovascular collapse



Syncope

CNS 



Mental status changes: o

Agitation

o

Lethargy

o

Psychosis

Visual perception: o

Blurred

o

Scotom a

o

Green to yellow halo

o

Photophobia

o

Hallucinations

o

Color perception changes

GI 

Anorexia



Nausea and vom iting



Diarrhea

Pa ge 1 5 1



Abdom inal pain

General 

Headache



Weakness



Light-headedness

Essential Workup 

ECG: o



For dysrhythm ia

Digoxin level: o

Norm al range: 0.5â€“2.0 ng/m L

o

Distribution after oral intake not com plete until 6 hours; therefore, a 6-hour level is m ost accurate steady state concentration.

o

False elevations possible with spironolactone use, pregnancy, hyperbilirubinem ia, chronic renal failure, liver failure, congestive heart failure

o

May be falsely elevated after digoxin Fab fragm ents given

Tests Lab 

Electrolytes, BUN, creatinine, glucose: o

Hypokalem ia contributes to digitalis toxicity.

o

Hyperkalem ia seen in acute toxicity and correlates with acute digitalis m ortality better than digoxin serum levels.

o

Follow K + serially.



Calcium , m agnesium



Serum digoxin concentration should not be obtained after digoxin-specific antibody Fab fragm ents have been adm inistered because it will be inaccurate.

Pa ge 1 5 1

Differential Diagnosis 

Overdoses: o

Calcium channel blockers

o

Beta-blockers

o

Quinidine, procainam ide

o

Clonidine

o

Organophosphates

o

Antidysrhythm ics

o

Other antihypertensives



Prim ary cardiac dysrhythm ias



Acute gastroenteritis

Treatment Pre Hospital Alert 

If cardioversion is necessary for tachydysrhythm ias, use low levels (50 J): o

May precipitate refractory tachydysrhythm ias

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

IV, oxygen, m onitor: o



IV fluid bolus if hypovolem ic

Adm inister naloxone, thiam ine, dextrose, for altered m ental status.

ED Treatment Cardiac Arrest Resuscitation 

Defibrillate for ventricular fibrillation, pulseless VT.



Standard advanced cardiac life support (ACLS) protocol

Pa ge 1 5 1



Adm inister digoxin-specific antibody Fab fragm ents (Digibind), up to 20 vials IV push (IVP).



MgSO 4 , 2 g IVP



Continue resuscitation for 30 m inutes after digoxin-specific antibody Fab fragm ents.

General Measures 

Gastric lavage if <1 hour after acute ingestion and history of significant ingestion, hem odynam ically stable, and airway stabilization: o

May cause bradycardia, asystole

o

Use caution if bradycardia or AV block present.

o

Consider atropine pretreatm ent.



Avoid ipecac and induction of em esis.



Activated charcoal if acute ingestion



Potassium replacem ent to achieve level >4.0 m Eq/L in chronic overdose: o

Use with caution if bradycardia or AV block.



Replenish m agnesium .



Treat hyperkalem ia with insulin, dextrose, bicarbonate, sodium polystyrene sulfonate: o

Calcium contraindicated

Dysrhythmia Management 

First choice is digoxin-specific antibody Fab fragm ents. If these are not im m ediately available, initiate the following: o

o

o

Lidocaine: 

For ventricular dysrhythm ias without AV block



Not harm ful but not very effective

For bradydysrhythm ias: 

Atropine



Pacing for sym ptom atic bradydysrhythm ia

Beta-blockade (propranolol, esm olol) for

Pa ge 1 5 1

supraventricular tachycardia: 

Avoid with AV block, bradycardia.

P.321



o

MgSO 4 for ventricular dysrhythm ias

o

Quinidine, procainam ide contraindicated

Cardioversion is last resort for severe, life-threatening tachydysrhythm ia: o

Start at low energy 10â€“50 J, then increase to high levels if ineffective.

o 

Safe if digoxin level <2.0 ng/m L

Pacem aker

Digoxin-Specific Antibody Fab Fragments (Digibind, Digi Fab) 

Indications: o

Serum digoxin concentration â‰¥15 ng/m L at any tim e or â‰¥10 ng/m L at steady state (6h)

o

Ingestion of >10 m g in adults or 0.2 m g/kg or 4 m g in children

o

Hyperkalem ia >5.0â€“5.5 m Eq/L

o

Hem odynam ically unstable or life-threatening dysrhythm ias

o

Ventricular tachycardia, ventricular fibrillation

o

Atrial tachycardia

o

Variable AV block

o

Bradycardia with no response to atropine

o

Hypotension



Onset: 20â€“30 m inutes



Digoxin levels m ay increase, decrease, or stay in therapeutic range after therapy owing to Fab digoxin

Pa ge 1 5 1

com plexes. 

Renal clearance of drugâ€“antibody com plexes: o

Too large to be rem oved by dialysis



Second dose if rebound toxicity



Com plications: o

Exacerbation of CHF

o

Hypokalem ia

o

Afibrillation with rapid ventricular response

Medication (Drugs) 

Activated charcoal slurry: o



1 m g/kg if within 1 hour

Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5â€“1.0 m g IV (peds: 0.04 m g/kg)



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Digoxin-specific antibody Fab fragm ents: o

40-m g vial neutralizes 0.6 m g of digoxin.

o

If am ount ingested known: 

Num ber of vials needed equals am ount ingested m g/0.6.

o

If steady serum level known: 

Num ber of vials needed equals serum digoxin level m ultiplied by patient's weight in kg/100.

o



If neither am ount ingested or serum level known: 

Acute toxicity: 10â€“15 vials adults or children



Chronic toxicity: 2â€“3 vials adults

o

Bolus for cardiac arrest

o

Additional doses as needed

Insulin and glucose: 10 U (peds: 0.25 U/kg) regular insulin plus 50 m L 50% (peds: 1 g/kg) dextrose IV

Pa ge 1 5 1



Lidocaine: 1 m g/kg IV, then 0.5 m g/kg q10m in to m ax. 3 m g/kg



Magnesium sulfate: 2 g (peds: 25â€“50 m g/kg per dose) IVPB



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM



Propranolol: 1 m g (peds: 0.01â€“0.1 m g/kg) IV



Sodium polystyrene sulfonate (Kayexalate):



o

Oral: 15 g m ixed with water or 50 m L of sorbitol

o

Rectal enem a: 50 g in 200 m L of sorbitol

o

Peds: 1.0 g/kg PO or per rectum (PR)

Sorbitol: 1â€“2 g/kg to m ax. 100 g (peds: >1 year old: 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO



Thiam ine: 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

ICU: o

Unstable cardiovascular status in acute or chronic toxicity



Telem etry: o

Asym ptom atic or m ildly sym ptom atic dysrhythm ia

o

High risk for developing toxicity

Discharge Criteria 



Acute/chronic ingestion: o

Digoxin level <2.0 ng/m L

o

Asym ptom atic for 6 hours and no ECG abnorm alities

Chronic exposure: o

Digoxin level <2.0 ng/m L and asym ptom atic

Pa ge 1 5 1

o

Asym ptom atic for 6 hours and no ECG abnorm alities

References 1. Bism uth C, Gaultier F, Conso Efthym iou ML. Hyperkalem ia in acute digitalis poisoning: prognostic significance and therapeutic im plications. J Toxicol Clin Toxicol. 1973;6(2): 153â€“162. 2. Ford M, Delaney K, Ling L, et al. Clinical Toxicology. Philadelphia: WB Saunders; 2001:379â€“389. 3. Goldfrank L, Flom enbaum N, Lewin N, et al. Goldfrank's Toxicologic Em ergencies. 6th ed. Stam ford, CT: Appleton & Lange; 1998:791â€“798. 4. Hickey A, Wenger T, Carpenter V, et al. Digoxin im m une Fab therapy in the m anagem ent of digitalis intoxication: safety and efficacy results of an observational surveillance study. J Am Coll Cardiol. 1991;17:590â€“598. 5. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:484â€“488. 6. Mauskopf J. Cost-effectiveness analysis of the use of digoxin im m une Fab (ovine) for treatm ent of digoxin toxicity. Am J Cardiol. 1991;68: 1709â€“1714.

Codes ICD9-CM 972.1

ICD10 T46.0

Pa ge 1 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dissem inated Intravascular C o agulatio n

Disseminated Intravascular Coagulation Steven H. Bowman

Basics Description 

Norm al coagulation: series of local reactions am ong blood vessels, platelets, and clotting factors



Dissem inated intravascular coagulation (DIC) is system ic activation of coagulation and fibrinolysis by som e other prim ary disease process.



Coagulation system activation results in system ic circulation of throm bin and plasm in.



Role of throm bin in DIC: o

Throm bin circulates and converts fibrinogen to fibrin m onom er.

o

Fibrin m onom er polym erizes into fibrin (clot) in the circulation.

o

Clots cause m icrovascular and m acrovascular throm bosis with resultant peripheral ischem ia and end organ dam age.

o

Platelets becom e trapped in clot with resultant

Pa ge 1 5 2

throm bocytopenia. 

Role of plasm in in DIC: o

Plasm in circulates system ically converting fibrinogen into fibrin degradation products (FDPs).

o

FDPs com bine with fibrin m onom ers.

o

FDPâ€“m onom er com plexes interfere with norm al polym erization and im pair hem ostasis.

o 

FDPs also interfere with platelet function.

Acute DICâ€”uncom pensated form : o

Clotting factors used m ore rapidly than body can replace them

o

Hem orrhage predom inant clinical feature, which overshadows ongoing throm bosis



Chronic DICâ€”com pensated form : o

Body able to keep up with pace of clotting factor consum ption

o

Throm bosis predom inant clinical feature

Etiology 

Precipitated by m any disease states



Com plications of pregnancy:



o

Retained fetus

o

Am niotic fluid em bolism

o

Placental abruption

o

Abortion

o

Eclam psia

Sepsis: o

Gram -negative (endotoxin m ediated m eningococcem ia)

o 

Gram -positive (m ucopolysaccharide m ediated)

Traum a: o

Crush injury

o

Severe burns

Pa ge 1 5 2

o 





Severe head injury

Malignancy: o

Metastatic disease

o

Leukem ia

Intravascular hem olysis: o

Transfusion reactions

o

Massive transfusion

Throm bocytopenia: o

Throm botic throm bocytopenic purpura

o

Idiopathic throm bocytopenic purpura

Diagnosis Signs and Symptoms 



Excessive bleeding: o

Petechiae

o

Purpura

o

Hem orrhagic bullae

o

Wound bleeding

o

Epistaxis

o

Hem optysis

o

Gastrointestinal bleeding

Excessive throm bosis: o

Large vessels

o

Microvascular throm bosis and end organ dysfunction

o

Cardiac, pulm onary, renal, hepatic, CNS

o

Throm bophlebitis

o

Pulm onary em bolus

o

Nonbacterial throm botic endocarditis

o

Gangrene

o

Ischem ic infarcts of kidney, liver, CNS, bowel

Pa ge 1 5 2



Acute DIC: o



Hem orrhagic com plications predom inate.

Chronic DICL: o

Throm botic com plications predom inate.

Essential Workup 

Depends on precipitating illness



Diagnosis generally not m ade in ED

Tests Lab 









Platelet count: o

Decreased

o

<100,000/m m 3

o

May be norm al in chronic DIC

Prothrom bin tim e (PT)/partial throm boplastin tim e (PTT): o

Increased

o

May be norm al in chronic DIC

Fibrinogen: o

Decreased

o

Less than 150 m g/dL in 70%

o

May be norm al in chronic DIC

FDPs: o

Increased

o

Greater than 40 Âµg/m L

D-Dim er: o





Increased

CBC/peripheral sm ear: o

Red cell fragm ents

o

Low platelets

o

Peripheral sm ear confirm s disease in chronic DIC

Electrolytes, BUN, creatinine, glucose: o

Elevated BUN, creatinine owing to renal insufficiency

Pa ge 1 5 2



Arterial blood gases (ABGs): o

Oxygen, acid base status

Imaging 

Chest radiograph for suspected pneum onia



Head CT for altered m ental status

Differential Diagnosis 

Inherited coagulation disorders: o





Factor deficiencies

Other acquired coagulation disorders: o

Anticoagulant therapy

o

Drugs

o

Hepatic disease

Platelet dysfunction

P.323

Treatment Initial Stabilization 



Airway m anagem ent and resuscitation m easures: o

Control bleeding

o

Establish IV access

o

Restore and m aintain circulating blood volum e.

Initiate therapy of precipitating disease: o

Antibiotics in sepsis

o

Evacuate uterus of retained dead fetus.

o

Chem otherapy in m alignancy

o

DÃ©bridem ent of devitalized tissue in traum a

Pa ge 1 5 2

ED Treatment Overview 

Therapy of DIC is controversial and should be individualized based on:



o

Age

o

Hem odynam ic status

o

Severity of hem orrhage

o

Severity of throm bosis

Involve adm itting service before initiating specific DIC therapy.



Replace depleted blood com ponents: o

Fresh frozen plasm a (FFP): 

For prolonged PT



Provides clotting factors and volum e replacem ent

 o

Dose: 2 U or 10â€“15 m L/kg

Platelets: 

If platelet count <20,000 or platelet count <50,000 with ongoing bleeding

 o

Dose: 1 U/10 kg body weight

Cryoprecipitate: 

Higher fibrinogen content than whole plasm a



For severe hypofibrinogenem ia (<50 m g/dL) or for active bleeding with fibrinogen <100 g/dL





Dose: 8 U

o

Washed packed cells

o

Album in

o

Nonclotting volum e expanders

Inhibition of intravascular clottingâ€”heparin o

Use is controversial.

o

Consider when throm bosis predom inates.

Pa ge 1 5 2

o

May be effective in m ild to m oderate DIC

o

Efficacy undeterm ined in severe DIC

o

Possible indications: 

Purpura fulm inans (gangrene of digits, extrem ities)



Acute prom yelocytic leukem ia



Dead fetus syndrom eâ€”several weeks after intrauterine fetal death



Throm boem bolic com plications of large vessels



Before surgery with m etastatic carcinom a

Antithrom bin concentrates (controversial): o





Used alone or in com bination with heparin

Inhibition of fibrinolysis: o

Block secondary com pensatory fibrinolysis that accom panies DIC

o

Use com plicated by severe throm bosis

o

Use only when DIC accom panied by prim ary fibrinolysis:

o



Prom yelocytic leukem ia



Giant hem angiom a



Heat stroke



Am niotic fluid em bolism



Metastatic carcinom a of prostate

Initiate in extrem e cases only: 

Profuse bleeding not responding to replacem ent therapy



Excessive fibrinolysis present (rapid whole blood lysis/short euglobulin lysis tim e)



Î·Am inocaproic acid (EACA)

Medication (Drugs)

Pa ge 1 5 2

Heparin: 

Low-dose regim en: 5â€“10 U/kg/h IV for chronic DIC



High-dose regim en: 10,000 U bolus followed by 1,000 U/h; 20,000â€“30,000 U q24h via constant infusion

Follow-Up Disposition Admission Criteria Severe precipitating illness in com bination with DIC requires ICU adm ission.

Discharge Criteria None

References 1. Bick RL. Dissem inated intravascular coagulation: current concepts of etiology, pathophysiology, diagnosis, and treatm ent. Hem atol Oncol Clin North Am . 2003;17(1):149â€“176. 2. Bick RL. Dissem inated intravascular coagulation: objective clinical and laboratory diagnosis, treatm ent and assessm ent of therapeutic response. Sem in Throm b Hem ost. 1996;22(1):69. 3. Gusset A, et al. In: Lee G, et al., eds. Clinical Hem atology. 10th ed. Philadelphia: Lippincott William s & Wilkins; 1999:1733â€“1780. 4. Rodgers GM. Acquired coagulation disorders. In: Lee G, et al., eds. Wintrobe's Clinical Hem atology. 11th ed. Philadelphia: Lippincott William s & Wilkins; 2004:1675â€“1687. 5. Seligsohn U. Dissem inated intravascular coagulation. In: Beutler E, et al., eds. William s Hem atology. 6th ed. New York: McGraw-Hill; 2001;22(1):1677â€“1679.

Codes

Pa ge 1 5 2

ICD9-CM 286.6

ICD10 D65

Pa ge 1 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Disulfirum Reactio n

Disulfirum

Reaction Sean Bryant

Basics Description 

Inhibits various enzym es, and its active m etabolites exert additional effects.



Disulfiram -ethanol reaction: o

Usually occurs 8â€“12 hours after taking the drug; should not be observed >24 hours after dosing

o

Com petitively and irreversibly inactivates aldehyde dehydrogenase

o

Ethanol m etabolism is blocked, resulting in accum ulation of acetaldehyde.

o

Acetaldehyde produces release of histam ine resulting in vasodilation and hypotension.

o

Severe reactions m ay occur in drinkers with ethanol levels of 50â€“100 m g/dL.

o

Severity and duration of reaction is proportional to am ount of ethanol ingested.



Disulfiram blocks dopam ine Î²-hydroxylase and lim its synthesis of norepinephrine from dopam ine:

Pa ge 1 5 3

o

Relative excess of dopam ine m ay contribute to altered behavior.

o

Relative depletion of norepinephrine m ay contribute to hypotension.



Disulfiram m etabolite (carbon disulfide) interacts with pyridoxal 5-phosphate: o

Dim inishes concentration of pyridoxine available for form ation of Î³-am inobutyric acid (GABA) in central nervous system

o

Potentially lowers seizure threshold

o

Carbon disulfide is also cardiotoxic, hepatotoxic, and inhibits cytochrom e P-450 (CYP2E1).



Disulfiram m etabolites m ay chelate im portant m etals (copper, zinc, iron) essential in various enzym e system s.



Disulfiram m etabolites m ay cause peripheral neuropathies that are dose and duration dependent.

Etiology 

Disulfiram is used as deterrent in treatm ent of chronic ethanol abuse.



Many users of the m edication wear m edical alert bracelet.



Other agents producing disulfiram like reactions: o

o

Antibiotics: 

Cephalosporins



Nitrofurantoin



Metronidazole

Oral hypoglycem ics: 

o

o

Sulfonylureas

Industrial agents: 

Carbon disulfide



Hydrogen sulfide

Mushroom s: 

Coprinus atram entarius

Pa ge 1 5 3



Clitocybe clavipes

Diagnosis Signs and Symptoms 



Disulfiram overdose: o

Sym ptom s rare with <3 g ingested

o

10â€“30 g m ay be lethal.

o

Tachycardia, hypotension, tachypnea

o

Abdom inal pain, diarrhea, garlic or rotten-egg breath

o

Agitation, irritability, ataxia

o

Dysarthria, hallucinations

o

Lethargy, com a, seizures, flaccidity

o

Parkinsonlike syndrom e

Disulfiram -ethanol reaction: o

Hypotension, tachycardia, tachypnea

o

Flushing of face, neck, torso

o

Pruritus, diaphoresis, sensation of warm th

o

Nausea, vom iting, abdom inal pain, diarrhea

o

Headache, ataxia, confusion, anxiety, dizziness

o

Dyspnea, pulm onary edem a, chest pain, dysrhythm ias, m yocardial infarction

Essential Workup Suspect disulfiram -ethanol reaction with the following: 

Typical signs and sym ptom s are present.



Treatm ent for chronic ethanol abuse in conjunction with recent ethanol ingestion, or exposure to ethanol-containing foods or m edications

Tests Lab

Pa ge 1 5 3



Ethanol level



Electrolytes, BUN, creatinine, and glucose



Liver function tests if hepatitis is suspected



Creatine phosphokinase (CPK) if considering rhabdom yolysis in light of seizures or agitation



Urinalysis (m yoglobin)

Imaging 

ECG to assess cardiac ischem ia



CT scan or MRI: o

Indicated with altered m ental status/seizure

o

Basal ganglia ischem ia and infarction have been reported.



EEG: o

Diffuse slowing without focal abnorm alities has been seen in cases of acute toxicity with com a.

Differential Diagnosis 

Sepsis



Meningitis, encephalitis



Cardiogenic shock secondary to acute coronary syndrom e



Anaphylactoid/anaphylactic reaction



Gastroenteritis/pancreatitis with dehydration



Ethanol withdrawal

Pediatric Considerations 

Acute poisonings yield m ainly severe CNS toxicity.



Ataxia, weakness, lethargy, seizures



Reye syndrom e-like encephalopathy in severe cases



Adult sym ptom s m ay also be present.

P.325

Pa ge 1 5 3

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Airway protection if necessary

o

Supplem ental oxygen

o

Mechanical ventilation as needed

o

Resuscitation with 0.9% norm al saline intravenously for hypotension



Pressor support with norepinephrine for refractory hypotension

ED Treatment 

Supportive care is key to m anagem ent.



No specific antidote available



GI decontam ination:





o

Activated charcoal in cases of disulfiram overdose

o

Gastric lavage is unnecessary.

Alleviation of flushing: o

Antihistam ines (H 1 and H 2 antagonists)

o

Prostaglandin inhibitors (indom ethacin, ketorolac)

Antiem etics for intractable vom iting (ondansetron, m etoclopram ide)



Seizures: o

Benzodiazepines (diazepam , lorazepam )

o

Pyridoxine (for disulfiram overdose)

o

4-Methylpyrazole: 

Inhibits ethanol m etabolism at alcohol dehydrogenase enzym e



Has no indication for disulfiram â€“ethanol reactions or disulfiram overdose

Pa ge 1 5 3



Hem odialysis: o

Consider after m assive ingestion of disulfiram and ethanol with refractory hypotension.

o

No studies docum enting beneficial effect

Medication (Drugs) 

Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Diphenhydram ine: 25â€“50 m g (peds: 1â€“2 m g/kg) IV



Indom ethacin: 50 m g PO (peds: 0.6 m g/kg PO for age >14 years)



Lorazepam : 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV



Metoclopram ide: 10 m g (peds: 1â€“2 m g/kg) IV



Norepinephrine: 4 m L in 1,000 m L of D 5 W, infused at 0.1â€“0.2 Âµg/kg/m in



Ondansetron: 4 m g (peds: 0.1 m g/kg for >2 years old) IV



Pyridoxine: 1 g (peds: 500 m g) IV, repeat PRN

Follow-Up Disposition Admission Criteria 

ICU adm ission for m echanical ventilation, com a, refractory hypotension requiring pressors, cardiac ischem ia, refractory seizures, and severe agitation



Persistent vom iting, abdom inal pain, or flushing



Elderly patients or those who have pre-existing cardiac disease

Discharge Criteria 

Mild reactions that resolve with supportive care after

Pa ge 1 5 3

observation period of 8â€“12 hours: o

Sym ptom s m ay recur on rechallenge with ethanol up to 7â€“10 days after last dose of disulfiram or agents that cause disulfiram like reactions.

o

Abstain from ethanol use until at least 2 weeks after last dose of such agents.



Appropriate follow-up needed to assess developm ent of hepatic or neurologic sequelae

References 1. Enghusen Poulsen H, Loft S, Anderson JR, et al. Disulfiram therapy adverse drug reactions and interactions. Acta Psychiatr Scand. 1992;86:59â€“66. 2. Kuffner EK. Disulfiram and disulfiram -like reactions. In: Goldfrank LR. Goldfrank's Toxicologic Em ergencies. McGraw-Hill; 2002;971â€“979. 3. Johansson B. A review of the pharm acokinetics and pharm acodynam ics of disulfiram and its m etabolites. Acta Psychiatr Scand. 1992;86:15â€“26. 4. Leikin J, Paloucek F. Disulfiram . In: Poisoning and Toxicology Handbook. Hudson, OH: Lexi-Com p; 2002;502â€“503. 5. Park CW, Rissio S. Disulfiram ethanol induced delirium . Ann Pharm acother. 2001;35:32â€“35. 6. Petersen EN. The pharm acology and toxicology of disulfiram and its m etabolites. Acta Psychiatr Scand. 1992;86:7â€“13. 7. Watson WA. Disulfiram . In: Clinical Toxicology. Philadelphia: WB Saunders; 2001;591â€“594.

Miscellaneous SEE ALSO: Alcohol Poisoning

Pa ge 1 5 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diverticulitis

Diverticulitis

Robert C. Montana

Basics Description Perforation of diverticulum : 

Microscopic or m acroscopic

Etiology 

Fecal m aterial in diverticulum hardens, form ing fecalith.



Fecalith abrades m ucosa or com prom ises blood supply, causing inflam m ation.



Inflam m ation causes m icroperforation of bowel wall: o

Peridiverticulitis: inflam m ation of wall not extending beyond serosa (uncom plicated diverticulitis)

o

Pericolic abscess: serosal perforation, yet inflam m ation rem ains localized (com plicated diverticulitis)

o

Peritonitis: serosal perforation with generalized spread of inflam m ation (com plicated diverticulitis)



Com plications: o

Bowel obstruction

o

Fistulas after recurrent attacks

o

Colovesical fistula (m ost com m on) presents with dysuria, frequency, urgency, pneum aturia, and

Pa ge 1 5 3

fecaluria.

Diagnosis Signs and Symptoms History 

Sym ptom s develop over hours to days



Anorexia



Nausea, vom iting



Low-grade fever



Malaise



Abdom inal pain: o

Persistent

o

Initially vague

o

Becom es localized to left lower abdom en



Abdom inal distention



Diarrhea (colon irritation) or constipation (inflam m atory obstruction)



Flatulence, heartburn



Urinary frequency: o

Owing to contact of inflam ed colon against bladder

Physical Exam 

Tenderness at left lower quadrant with occasional m ass palpated (phlegm on): o

Phlegm onâ€”inflam ed bowel loops or abscess



Bowel sounds norm al, increased, or decreased



Rectal tenderness with hem e-positive stool: o



Massive gross rectal bleeding (rare)

Peritoneal signs if: o

Perforation has occurred

Pa ge 1 5 3



Unrem arkable exam ination if: o

Elderly

o

Im m unocom prom ised

o

Taking corticosteroids

Essential Workup 

CBC: o

Elevated WBC with left shift

o

Iron deficiency anem ia suggests underlying carcinom a cause.



CT of abdom en: o

Preferred diagnostic m odality

o

Better than contrast studies at diagnosing extralum inal processes (e.g., diverticulitis)

o

o

o

Diagnostic criteria include: 

Wall thickening >5 m m



Inflam m ation of pericolic fat



Pericolic abscess

Nondiagnostic criteria include: 

Stricture



Diverticula



Fistula

Ability to diagnose nondiverticular causes of abdom inal pain

o

CT-guided percutaneous needle aspiration of localized abscesses avoids further surgery.

o

Avoid PO/PR (per rectum ) contrast

Tests Lab 

Urinalysis: o

WBC/RBC com m on

o

Colovesical fistula results in WBC, bacteria, or feces.

Pa ge 1 5 3



Blood cultures: o

If hospitalized with peritonitis

Imaging 



Abdom inal (supine and upright) and chest radiographs: o

Perforation indicated by free air

o

Obstruction indicated by airâ€“fluid levels

Endoscopy: o

Not necessary to diagnose acute illness

o

Rigid sigm oidoscopy aids in diagnosing nondiverticular causes of abdom inal pain (spasm , stricture, edem a, pus, or peri diverticular erythem a).



Ultrasonography: o

For diagnosing colonic wall thickening, inflam m ation, m ass, abscess, or fistula



o

Greatly operator dependent

o

Not reliable in presence of intestinal gas

Barium enem a: o

Indicated after resolution of acute illness to rule out fistula or other colonic pathology (e.g., carcinom a)



Avoid endoscopic procedures and contrast studies in acute cases so as not to cause perforation: o

In select cases, water-soluble contrast m ay be safe alternative.

Differential Diagnosis 

Colon carcinom a with perforation



Ischem ic colitis



Bacterial colitis



Appendicitis o

Left-sided pain if peritonitis from ruptured appendix

o

Right-sided diverticular pain with cecal diverticulum (rare) or redundant sigm oid colon

Pa ge 1 5 4



Inflam m atory bowel disease



Irritable bowel syndrom e



Ruptured or torsed ovarian cyst



Pancreatic disease



Pelvic inflam m atory disease



Peptic ulcer disease



Renal colic

Treatment Pre Hospital Avoid opiates in abdom inal pain when underlying cause is unclear.

Initial Stabilization 

Rehydration with 0.9% norm al saline (NS) to replace intravascular volum e depletion



Bowel rest: o

NPO

o

Nasogastric tube (NG) tube if persistent vom iting or bowel obstruction present

ED Treatment 

Uncom plicated diverticulitis: o



Most respond to m edical therapy.

Com plicated diverticulitis: o

Most require percutaneous drainage or surgery.

Analgesia 



Anticholinergics (dicyclom ine): o

Reduces colonic spasm

o

Does not m ask underlying pathology

Opiates for m ore aggressive pain m anagem ent (IV

Pa ge 1 5 4

m orphine or dem erol although m orphine can cause colonic spasm ): o

If hem odynam ically stable

o

When not dependent on repeat abdom inal exam inations for diagnostic or therapeutic decisions

P.327

Antibiotics 

Mild, uncom plicated cases (peridiverticulitis): o

Outpatient oral agents include: 

Ciprofloxacin or Levaquin plus m etronidazole or clindam ycin



Trim ethoprim -sulfam ethoxazole (TMP-SMX) DS plus m etronidazole

 o

Am oxicillin/clavulanate

Duration of therapy is 7â€“10 days or until afebrile for 3â€“5 days.



Moderate uncom plicated and m ild com plicated cases: o

Inpatient parenteral therapy includes: 

Ceftriaxone or other third-generation cephalosporin plus m etronidazole or clindam ycin



Am picillin/sulbactam



Piperacillin/tazobactam



Ticarcillin/clavulanate



Ciprofloxacin or Levaquin plus m etronidazole or clindam ycin

 

Aztreonam

Com plicated cases (with peritonitis from perforation): o

Im ipenem /cilastatin

o

Meropenem

o

Aztreonam plus m etronidazole or clindam ycin

Pa ge 1 5 4

o

Gentam icin plus m etronidazole or clindam ycin plus/m inus am picillin

o

Trovafloxacin (alternative)

Surgery 

Em ergent surgery: o

Indicated for generalized peritonitis from perforation

o

Two-stage procedure with resection of diseased segm ent of colon and proxim al colostom y followed later with reanastom osis



Elective surgery: o

Indicated for: 

Multiple recurrent attacks without generalized peritonitis



Fistula form ation



Intractable pain



Unresolved obstruction



Failure of m edical therapy



Single serious attack in patient younger than 40 years of age (controversial)

o

One-stage procedure following resolution of inflam m ation from m edical therapy



Peridiverticular abscess drainage: o

Indicated if well circum scribed and easily accessible

o

Accom plished by CT- or ultrasound-guided percutaneous needle aspiration

Outpatient Therapy 

Clear liquids with follow-up in 2 or 3 days



When acute condition has resolved: o

High-fiber, low-fat diet to decrease recurrence of attacks

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Medication (Drugs) 

Am oxicillin/clavulanate: 500/125 m g PO t.i.d. or 875/125 m g PO b.i.d.



Am picillin: 2.0 g IV q6h



Am picillin/sulbactam : 3.0 g IV q6h



Cefotetan: 2.0 g IV q12h



Cefoxitin: 2.0 g IV q8h



Ciprofloxacin: 400 m g IV q12h or 500 m g PO b.i.d.



Dicyclom ine: 20 m g PO q.i.d. (up to 40 m g PO q.i.d.) or 20 m g IM q.i.d. (not for IV use)



Gentam icin: m ultiple daily dose (MDD) regim en, 2.0 m g/kg load, then 1.7 m g/kg IV q8h, or once-daily dose (OD) regim en, 5.0â€“7.0 m g/kg IV q24h (assum ing norm al renal function)



Im ipenem /cilastatin: 500 m g IV q6h



Meropenem : 1 g IV q8h



Meperidine: 50â€“100 m g IM q3hâ€“q4h PRN or 25â€“50 m g IV and titrate to clinical response



Metronidazole: 1 g (15 m g/kg) IV load then 500 m g IV q8h or 500 m g PO q8h



Morphine sulfate: 2â€“10 m g/70 kg body weight IV push slowly



Piperacillin/tazobactam : 3.375 g IV q6h or 4.5 g IV q8h



Ticarcillin/clavulanate: 3.1 g IV q6h



Trim ethoprim -sulfam ethoxazole DS: one tablet PO b.i.d.



Trovafloxacin: 300 m g IV for first dose, then 200 m g IV/PO daily

Follow-Up

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Disposition Admission Criteria 

Intractable pain



High fever



Peritonitis



Failure to respond to outpatient m anagem ent



Im m unocom prom ised or steroid-dependent patients



Extrem e of age



Uncertainty of diagnosis

Discharge Criteria Mild cases (low-grade fever, m ild discom fort) of known diverticular disease

References 1. Am brosetti P, et al. Acute left colonic diverticulitis in young patients. J Am Coll Surg. 1994;179:156â€“160. 2. Ferzoco LB, Raptopoulos V, Silen W. Acute diverticulitis. N Engl J Med. 1998;338:1521â€“1526. 3. Freem an SR, McNally PR. Gastrointestinal em ergencies: diverticulitis. Med Clin North Am . 1993;77:1149â€“1165. 4. Gilbert DN, Moellering RC, Sande MA, eds. The Sanford Guide to Antim icrobial Therapy. 32nd ed. Hyde Park, VT: Jeb C. Sanford, Publisher; 2002. 5. Kohler L, et al. Diagnosis and treatm ent of diverticular disease: results of a consensus developm ent conference. The Scientific Com m ittee of the European Association for Endoscopic Surgery. Surg Endosc. 1999;13(4):430â€“436. 6. Vignati PV, et al. Long-term m anagem ent of diverticulitis in young patients. Dis Colon Rectum . 1995;38:627â€“629.

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Miscellaneous SEE ALSO: Diverticulosis

Codes ICD9-CM 562.11

ICD10 K57.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diverticulo sis

Diverticulosis

Robert C. Montana

Basics Description 

Single (diverticulum ) or m ultiple (diverticula) colonic wall outpouchings from colonic m uscle dysfunction



Sequence: o

Insufficient am ounts of dietary fiber cause dim inished stool bulk.

o

Increased colonic contractions to propel stool through colon cause increase in intralum inal pressure.

o

Increased pressure forces m ucosa and subm ucosa to herniate through m uscularis propria at its weakest point of artery (vasa recta) penetration site.

Etiology 

Occurs anywhere in GI tract, although generally a colonic disease:



o

Left sided m ore than right sided

o

Sigm oid colon is m ost com m on site.

Pseudodiverticula: o

Outpouchings of m ucosa and subm ucosa only

o

Most com m on form of colonic diverticula

o

True congential diverticula (uncom m on) contain all

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bowel wall layers. 

Incidence directly related to increase in age



Com m on in Western society, owing to refined diet and low fiber intake



Com plications: o

Massive arterial bleeding usually from right colon: 

Fecalith (dry, hard stool) erodes through arterial branch.

o

Inflam m ation (diverticulitis)

Diagnosis Signs and Symptoms History 

Thorough history and physical exam ination essential to avoid excessive workup







Clinical patterns: o

Asym ptom atic (70â€“85%)

o

Sym ptom atic (painful)

o

Hem orrhagic (5â€“15%)

Chronic or interm ittent left lower quadrant pain: o

Often precipitated by eating

o

Som etim es relived by flatulence or bowel m ovem ent

Painless brisk hem atochezia (m aroon stools or bright red blood)



Constipation (or diarrhea)



Dyspepsia



Diverticulitis and diverticular bleeding are separate entities and rarely coexist.

Physical Exam

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





Abdom inal palpation: o

Tenderness in left lower quadrant

o

Firm sigm oid colon in left lower quadrant

Rectal exam : o

Predom inantly reveals hem e-negative stool

o

Bleeding typically m ild

Fever: absent

Essential Workup Thorough history and physical exam ination essential to avoid excessive workup

Tests Lab 

Asym ptom atic diverticulosis: o



Requires no testing

Uncom plicated painful disease (no peritoneal signs) with known history: o



Requires no workup

Uncom plicated painful disease (no peritoneal signs) without previous history: o

Requires workup to rule out carcinom a (if weight loss, anorexia, hem e-positive stool)



o

CBC for leukocytosis or anem ia

o

Urinalysis to exclude hem aturia or pyuria

Hem orrhagic diverticulosis: o

CBC

o

Electrolytes, BUN, creatinine, glucose, calcium

o

Type and cross for 4 U of packed red blood cells (PRBCs)

o

Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), international norm alized ratio (INR)

o

ECG

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Imaging 

Uncom plicated painful diverticulosisâ€”outpatient options: o

Flexible sigm oidoscopy, then barium enem a: 

Sigm oidoscopy: Rule out carcinom a (before barium studies for optim al visualization).



Barium enem a: Search for classic diverticula and exclude carcinom a or polyps.

o 

Colonoscopy

Hem orrhagic diverticulosis: o

Anoscopy: 

o

If m ild bleeding, to rule out hem orrhoids

Proctosigm oidoscopy: 

If no blood in stool above rectum , assum e rectal bleed.

o

Colonoscopy: 

Bleeding cannot be excessive (difficult to visualize pathology).



Allows for therapeutic intervention



Usually done prior to radionuclide im aging or angiography

o

Radionuclide im aging: 

Safe, no bowel prep needed



Poor localization of bleeding site



Ideal for detecting interm ittent bleeding, owing to long half-life of radioisotope (24â€“36 hours)

o

Angiography: 

No bowel prep needed



Localizes site of bleeding (m ore exact after radionuclide scanning)

 o

Allows for therapeutic intervention

Barium enem a: 

Rarely indicated

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

Identifies diverticula but not bleeding (can hinder visualization of other im aging techniques)

P.329

Differential Diagnosis 

Painful diverticulosis: o

Irritable bowel syndrom e (alm ost identical clinical presentation)



o

Diverticulitis

o

Colon carcinom a

o

Crohn disease

o

Urologic (renal colic)

o

Gynecologic (ruptured or torsed ovarian cyst)

Hem orrhagic diverticulosis: o

Hem orrhoids

o

Anal fissure

o

Proctitis

o

Colitis

o

Carcinom a

o

Polyps

o

Ischem ic enteritis

o

Angiodysplasia

o

Am yloidosis

o

Vascular-enteric fistula

o

Upper GI source

Treatment

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Pre Hospital 

Avoid opiates in abdom inal pain when underlying cause is uncertain.



Establish two large-bore intravenous lines with 0.9% norm al saline (NS) if significant rectal bleeding/hem odynam ic instability.



For hypotension: o

1â€“2 L (20 m L/kg) bolus 0.9% NS intravenously

o

Trendelenburg position

Initial Stabilization Hem orrhagic diverticulosis (m assive): 

Airway control (100% oxygen or intubate if unresponsive)



Intravenous access with at least one large-bore catheter or two if unstable



0.9% NS bolus 1â€“2 L (20 m L/kg) for hypotension



Central catheter placem ent if unstable following initial fluid resuscitation for m ore efficient delivery of fluids and m onitoring of central venous pressure



Nasogastric tube to rule out upper GI bleed



Bladder catheter to m onitor urine output



Transfuse O-negative red blood cells im m ediately if im pending arrest.



Consult surgeon (m ost diverticular bleeding stops spontaneously).

ED Treatment 

Uncom plicated sym ptom atic diverticulosis: o

High-fiber diet and/or hydrophilic bulk laxative (e.g., psyllium )

o

Warm com presses to abdom en

o

Reassurance

o

Avoid cathartic laxatives.

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o

No evidence to support use of antispasm odic (dicyclom ine)



Hem orrhagic diverticulosis (m assive): o

Initial stabilization (see above)

o

Monitor fluid status (input/output).

o

Prepare for radionuclide scan followed by angiography if necessary.

o

Surgical intervention for segm ental colectom y if bleeding on radionuclide scan

o

Consider selective angiography with injection of vasopressin to control bleeding.

o

Em bolization not recom m ended for colonic hem orrhage

Medication (Drugs) Dicyclom ine: 20 m g PO/IM q.i.d. (not for IV use)

Follow-Up Disposition Admission Criteria 

ICU if unstable with m assive hem orrhagic diverticulosis



Mild or interm ittent hem orrhagic diverticulosis that is otherwise stable, to determ ine site of bleeding and to evaluate need for definitive treatm ent

Discharge Criteria 

Uncom plicated, sym ptom atic diverticulosis



Stable with trace hem e-positive stool, negative gastric aspirate, no anem ia, and no other com plaints

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References 1. Bono MJ. Gastrointestinal em ergencies. Part I: lower gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):547â€“556. 2. Kim YI, Marcon NEl. Injection therapy for colonic diverticular bleeding. A case study. J Clin Gastroenterol. 1993;17(1):46â€“48. 3. Kohler L, Sauerland S, Neugebauer E. Diagnosis and treatm ent of diverticular disease: results of a consensus developm ent conference. The Scientific Com m ittee of the European Association for Endoscopic Surgery. Surg Endosc. 1999;13(4):430â€“436. 4. McGuire HH. Bleeding colonic diverticula: a reappraisal of natural history and m anagem ent. Ann Surg. 1994;220(5):653â€“656.

Miscellaneous SEE ALSO: Diverticulitis; Gastrointestinal Bleeding

Codes ICD9-CM 562.10 Diverticulosis of colon

ICD10 K57.9 Diverticular disease of intestine, part unspecified, without perforation or abscess

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diz z iness

Dizziness

Mitchell Adelstein Jonathan Edlow

Basics Description 

Nonspecific feeling that m ay define a whirling sensation, a tendency to fall, feeling faint, weakness, or feeling confused



May be caused by a num ber of problem s: o

o

o

Vertigo: 

Vestibular dysfunction



Cerebellar disease

Disequilibrium : 

Suggests a structural CNS disorder



Multiple sensory deficits

Near syncope/syncope: 

Cardiovascular insufficiency



Faintness that is postural or paroxysm al suggests a cardiovascular disorder

o

Weakness

o

Psychiatric illness: 

Constant, ill-defined dizziness unrelated to posture suggests a psychogenic etiology

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Etiology Vertigo 



Peripheral (85%): o

Benign paroxysm al positional (m ost com m on)

o

Acute labyrinthitis

o

MÃ©niÃ¨re disease

o

Vestibule neuritis

o

Acoustic neurom a

o

Ototoxic drugs: 

Am inoglycosides



Antim alarials



Erythrom ycin



Furosem ide

o

Otitis m edia and serous otitis with effusion

o

Foreign body in ear canal

Central (15%): o

Cerebellar hem orrhage

o

Vertebral basilar artery insufficiency

o

Cerebellar traum a

o

Cerebellopontine angle tum or

o

Tem poral lobe epilepsy

o

Vertebral basilar m igraines

o

Multiple sclerosis

o

Subclavian steal syndrom e

o

Drugs suppressing the reticular activating system : 

Sedative hypnotics



Anticonvulsants

Disequilibrium 

Multiple sensory defects



Frontal lobe disorder: o

Tum ors:

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







Meningiom a



Gliom a



Metastatic tum or

o

Anterior cerebral artery syndrom e

o

Hydrocephalus

Subcortical disorders: o

Multiple strokes

o

Ataxic hem iparesis

Brainstem disorders: o

Stroke

o

Multiple sclerosis

Cerebellar disorders: o

Cerebellar hem orrhage, infarct, tum or

o

Spinocerebellar degeneration

o

Alcoholism

o

Acute cerebellitis

Cardiac and Vascular Insufficiency 

Hypovolem ia



Orthostatic hypotension



Anem ia



Myocardial ischem ia



Structural cardiac or valvular disease



Cardiac dysrhythm ias: o

Preexcitation

o

Prolonged QT syndrom e

o

Hypokalem ia

o

Supraventricular tachycardia

o

Ventricular dysrhythm ia



Pulm onary em bolism :



Subarachnoid hem orrhage



Hypoglycem ia



Hypoxia

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

Hypercarbia



Hyperventilation syndrom e



Vasovagal episode

Other 

Psychogenic: o

Anxiety

o

Hyperventilation syndrom e

o

Depression



Chronic fatigue syndrom e



Fam ilial periodic paralysis



Hypothyroidism

P.331

Diagnosis Signs and Symptoms 



Dizziness is used to describe a wide range of sym ptom s: o

Abnorm al sensation of m otion

o

Feeling faint or fainting

o

Lightheadedness

o

Unsteadiness

Classify dizziness into one of four categories by asking the patient to explain the sensation without using the word dizzy: o

Vertigo: 

Abnorm al sensation of m ovem ent and position in space



Nystagm us

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Alert 

Vertical nystagm us is abnorm al and should elicit concern for a central etiology:



o

Nausea

o

Vom iting

o

Diaphoresis

Disequilibrium : o

Disorder of coordination and rhythm

o

Loss of equilibrium

o

May include sensory deficits such as peripheral neuropathy





Near syncope/syncope: o

Diaphoresis

o

Palpitations

o

Pallor during the episode

Other: o

Depression

o

Fatigue

o

Weakness

o

Hyperventilation

Essential Workup Must be tailored to each individual patient's signs and sym ptom s

Tests Lab 

Hem atocrit, if suspected anem ia/blood loss



Glucose in setting of DM



Electrolytes in setting of volum e depletion



Toxicologic screen, if suspected exposure/ingestion

Imaging 

CT scan if central vertigo or ataxia is present

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

Magnetic-resonance angiogram if vertebral basilar insufficiency is suspected

Diagnostic Procedures/Surgery ECG to detect cardiac causes of near syncope and weakness

Differential Diagnosis See Etiology

Treatment Initial Stabilization 

Supplem ental oxygen



Stabilization should be determ ined by m ore specific classification of dizziness based on the history, physical exam ination, and ancillary studies.

ED Treatment Treatm ent should be determ ined by the underlying cause.

Medication (Drugs) 

Diazepam : 2.5â€“5 m g IV. q8h or 2â€“10 m g PO q8h



Diphenhydram ine: 25â€“50 m g IV, IM, or PO q6h



Meclizine: 25 m g PO q6h PRN



Prom ethazine: 12.5 m g IV q6h or 25â€“50 m g PO, IM, or PR q6h

Follow-Up Disposition

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Admission Criteria Adm ission or discharge of patients with dizziness should be based on the underlying etiology or associated sym ptom s.

Issues for Referral Referral for com pletion of workup as an outpatient to a prim ary-care physician or a neurologist

References 1. Baloh RW. Approach to the dizzy patient. In: Baloh RW, ed. Neurotology. Baillieres Clin Neurol. 1994;3:453. 2. Brown JJ. A system atic approach to the dizzy patient. Neurol Clin. 1990;8:209â€“224. 3. Herr RD, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Em erg Med. 1989;18:664. 4. Olshaker S. Vertigo. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St Louis: Mosby; 2002:123â€“131. 5. Pigott DC, Rosco CJ. The dizzy patient: an evidence-based diagnosis and treatm ent strategy. Em erg Med Pract. 2001;3(3):120. 6. Walker JS, Barnes SB. Dizziness. Em erg Med Clin North Am . 1998;16(4):845â€“875.

Miscellaneous SEE ALSO: Vertigo

Codes ICD9-CM 386 780.2

ICD10

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R42

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Do m estic Vio lence

Domestic Violence

Jim Comes

Basics Description 

Intim ate partner violence and abuse is the infliction or the threat of physical harm against an intim ate partner.



Occurs in dating, m arried, cohabiting, or separated relationships



Intim ate partner violence and abuse is a pattern of assaultive and coercive behaviors that include physical, sexual, and psychologic attacks against the victim .



The perpetrator uses these tactics to attain com pliance from and to control the victim .



Tactics used by perpetrators to gain power and control over their partners include: o

Pushing

o

Shoving

o

Slapping

o

Punching

o

Kicking

o

Choking

o

Holding

o

Tying down

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

Verbal abuse: o

Threatening harm (including toward children or pets), intim idation, or destruction of property

o

Isolating the victim physically or socially

o

Degrading or hum iliating behavior

o

Attem pting to force or forcing the victim to perform sexual acts against his or her will or without protection against pregnancy

o

Causing physical harm during sex or assaulting genitalia

Etiology 

Most victim s are wom en, and m ost perpetrators are m en.



Partners in sam e-sex relationships and m en m ay also be victim s.



Most rapes and assaults of wom en are by known assailants.

Diagnosis 

Diagnosis and recognition in the ED, clinic, or office rem ains difficult and problem atic.

Signs and Symptoms 



Traum atic injuries: o

Sm all subset of presenting com plaints

o

Fractures

o

Contusions

o

Lacerations

o

Penetrating and blunt traum a to body

Psychiatric: o

Chronic pain syndrom es

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o

Physical sym ptom s related to stress

o

Anhedonia

o

Insom nia

o

Anorexia

o

Som atic com plaints

o

Anxiety

o

Depression and suicidal ideation

Alert 

Clinical clues: o

History not com patible with exam

o

Repeat visits for the sam e chief com plaint

o

Delay in seeking care

o

Any injury during pregnancy

o

Interaction between wom an and partner that suggests interpersonal problem s

o

Evidence of traum a not attributable to a m otor vehicle accident

o

Multiple sym ptom s without obvious physical findings

History 

Short screening questions of all fem ale patients m ay be an effective m eans of identifying victim s of dom estic violence.



Screening should be direct, nonjudgm ental, supportive, and private.

Differential Diagnosis 

Partner violence m ay be the acute precipitant of the patient's reason for presenting to the ED, or it m ay be part of the patient's past or present social history.



There is no traum atic or nontraum atic presentation that is pathognom onic for intim ate partner violence.

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Treatment Initial Stabilization 

Provide tim ely and appropriate m edical attention.



Maintain advocacy by expressing m essages of support and validating victim 's dilem m a.

P.333

ED Treatment 

Docum ent in the chart the victim 's allegations in his or her own words.



Diagram or photograph injuries (after consent) and incorporate them into the clinical record.



Address the patient's safety in returning to the sam e hom e environm ent: o

Im portant determ inants in predicting future danger include violence that is increasing in frequency and severity, threats of hom icide or suicide by the partner, or the availability of a lethal weapon.



With the aid of social services or dom estic violence advocates, review the patient's options:



o

Outpatient victim services

o

Em ergency shelter inform ation

o

Hotlines

o

Restraining order inform ation

o

Legal services

Mandatory reporting requirem ents vary am ong states: o

Som e states require the health-care practitioner to m ake a verbal and written report if he or she

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suspects wound or physical injury results from assaultive and abusive conduct. o

Determ ine how local authorities respond to reports of intim ate partner violence and abuse from health-care practitioners.

o

Recognize that m andatory reporting requirem ents m ay place the victim in m ore danger and create ethical dilem m as for the physician when the victim does not want the case reported to police or social service agencies.

Medication (Drugs) 

Acetam inophen: 650â€“975 m g PO



Meperidine: 1.0â€“1.8 m g/kg/dose IV or IM



Morphine sulfate: 0.1 m g/kg/dose IV or IM

Follow-Up Disposition Admission Criteria 

A victim whose life is in im m inent danger and who cannot be safely discharged (to his or her hom e, fam ily, friends, or shelter) m ay need to be adm itted to the hospital (under an assum ed nam e).



Use appropriate adm ission guidelines depending on degree of traum a sustained.

Discharge Criteria A victim whose safety is ensured and whose injuries can be m anaged as an outpatient m ay be discharged.

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References 1. Abbott J. Injuries and illnesses of dom estic violence. Ann Em erg Med. 1997;29:781â€“785. 2. Hayden SR, Barton ED, Hayden M. Dom estic violence in the em ergency departm ent: how do wom en prefer to disclose and discuss the issues? J Em erg Med. 1997;15:1â€“5. 3. Hym an A, Schillinger D, Lo B. Laws m andating reporting of dom estic violence: do they prom ote well-being? JAMA. 1995;273:1781â€“1787. 4. Salber PR, Taliaferro E.Intim ate partner violence and abuse. In: Rosen's Em ergency Medicine Concepts and Clinical Practice 5th ed. St. Louis, MO.: Mosby; 2002:863â€“875. 5. Salber PR, Taliaferro E. The Physician's Guide to Dom estic Violence. Volcano, Calif.: Volcano Press; 1995.

Codes ICD9-CM V15.49 Other V15.41 History of Physical Abuse

ICD10 R45.6 Physical Violence

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Duo denal Traum a

Duodenal Trauma

Hagop Isnar

Basics Description 

Characteristics of duodenum : o

12 inches long

o

C shaped

o

Divided into four sections: 

o

Last three sections intraperitoneal

Lies m ostly over first three lum bar vertebrae



Second section is m ost com m only injured.



Types of injury:



o

Duodenal wall hem atom a

o

Wall perforation

o

Hem orrhage

Incidence of duodenal injury is about 5% of all intra-abdom inal injuries.





Penetrating traum a accounts for 85% of duodenal injuries: o

Mortality ranges from 13â€“28%.

o

Associated with exsanguination

Blunt duodenal injuries have higher m ortality: o

If injury is diagnosed in <24 hours, m ortality rate is about 11%.

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o

If >24 hours has passed, m ortality rate approaches 40%.

o

Late m ortality usually from sepsis

Pediatric Considerations 

Most duodenal injuries are secondary to recreational injuries (e.g., bicycle handlebar injuries).



Intram ural duodenal hem atom as m ay occur in nonaccidental traum a: o

If suspected, then prom pt referral to appropriate child protective agencies is required along with m edical treatm ent.



In children, hem atom a is m ost com m only seen in first portion of duodenum .

Diagnosis Signs and Symptoms 

Com plaints m ay be m inim al with vague abdom inal, flank, and back pain.



High gastrointestinal obstruction m ay be seen with duodenal hem atom as.

History Penetrating or blunt abdom inal traum a

Physical Exam Elicit tenderness or ecchym osis of upper abdom en or penetrating wounds to right upper quadrant or lower chest.

Tests Lab 

Laboratory tests are of little value.

Pa ge 1 5 7



Fifty percent of patients with duodenal injuries have elevated serum am ylase.

Imaging 

Upright chest and abdom inal radiographs m ay show: o

Intraperitoneal air

o

Retroperitoneal air

o

Air in biliary tree

o

Scoliosis to right

o

Loss of psoas shadow

o

Air around right kidney

o

Injecting air into nasogastric tube m ay dem onstrate retroperitoneal air m ore clearly.

o

Intram ural hem atom as without leakage m ay have coiled spring appearance.



CT with contrast: o

Perhaps best diagnostic test that shows sm all am ounts of retroperitoneal gas and extravasated contrast m aterial

o

Sausage-shaped m ass in duodenal wall strongly suggests hem atom a.

Diagnostic Procedures/Surgery Diagnostic peritoneal lavage (DPL): 

Often positive for blood, bile, or bowel content



Negative lavage does not exclude injury.

Differential Diagnosis 

Injury to hollow organs (stom ach, sm all and large intestines)



Liver and biliary tree injuries



Vascular injuries (aortic and m esenteric arteries as well as venous injuries)



Postoperative com plications from prior duodenal surgery

Pa ge 1 5 7

or injury repair such as infection and suture line dehiscence

Treatment Pre Hospital 

Follow traum a protocols.



Im portant to have prehospital personnel provide clear description of m echanism of injury and to transport to appropriate facility

Initial Stabilization 

Airway m anagem ent, resuscitation as needed



Aggressive fluid therapy with warm ed norm al saline or lactated Ringer solution if patient hypotensive



Central line m ay be needed for unstable patients.



Nasogastric decom pression



Early traum a surgical consultation

ED Treatment 

Tetanus and antibiotic prophylaxis for penetrating wounds



Definitive treatm ent involves laparotom y with exploration of duodenum for injuries.



Broad-spectrum antibiotics to prevent sepsis in patients with perforation

P.335

Medication (Drugs)

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

Cefoxitin: 2 g (peds: 40 m g/kg) IV plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or



Cefotetan: 2 g (peds: 20 m g/kg) IV plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or



Clindam ycin: 600 m g IV (peds: 20â€“40 m g/kg/d IV in 3â€“4 div. doses) plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or



Ceftriaxone: 1â€“2 g IV (peds: 50â€“75 m g/kg/d in 2 div. doses, not to exceed 2 g) plus m etronidazole: 15 m g/kg IV

Follow-Up Disposition Admission Criteria 

All patients with duodenal injuries need adm ission to traum a surgical service.



Minor duodenal hem atom as that do not require im m ediate surgery m ay require nasogastric decom pression for obstruction (up to 7 days) and observation for possible expansion or rupture of the hem atom a.

Discharge Criteria No patient with identified traum atic duodenal injury should be discharged from the Em ergency Departm ent without Traum a Surgical consultation.

References 1. Carrillo EH, Richardson JD, Miller FB, et al. Evolution in the m anagem ent of duodenal injuries. J Traum a. 1996;40:1037â€“1046. 2. Cogbill TH, Moore EE, et al. Conservative m anagem ent of duodenal traum a: a m ulticenter perspective. J Traum a.

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1990;30:1469â€“1475. 3. Degiannis E, Boffard K. Duodenal injuries. Br J Surg. 2000;87:1473â€“1479. 4. Ivatury RR, Nassoura ZE, Sim on RJ, et al. Com plex duodenal injuries. Surg Clin North Am . 1996;76:797â€“812. 5. Tyburski JG, Dente CJ, Wilson RF, et al. Infectious com plications following duodenal and/or pancreatic traum a. Am Surg. 2001;67:227â€“230.

Codes ICD9-CM 863.21 Duodenum

ICD10 S36.4

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysfunctio nal Uterine Bleeding

Dysfunctional Uterine Bleeding Christy Rosa Mohler

Basics Description Excessive (>80 m L) or prolonged vaginal bleeding without dem onstrable organic cause

Etiology 

Unopposed estrogen stim ulation of proliferative endom etrium



Anovulatory (m ost com m on): o

Alteration of neuroendocrinologic function

o

Obesity

o

Very low calorie diets, rapid weight change, intense exercise

o

Psychologic stress

o

Most com m on in postm enarchal, prem enopausal wom en



Ovulatory

Pediatric Considerations Anovulatory bleeding com m on in adolescence owing to im m aturity of the hypothalam ic-pituitary-ovarian axis

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Diagnosis Signs and Symptoms History 

Vaginal bleeding that is significantly changed from a patient's norm al pattern



Abnorm al uterine bleeding in the absence of system ic or structural disease: o

Includes bleeding between norm al m enstrual cycles, change in norm al pattern of m enstrual cycle, increased or decreased am ount of m enstrual bleeding

Physical Exam 

Mild to m oderate bleeding on pelvic exam



Pallor, tachycardia, hypotension, orthostasis in severe cases

Alert It is rare for wom en to be hem odynam ically unstable sim ply from dysfunctional uterine bleeding; if such instability is present, concern is for ectopic pregnancy or other cause for hem orrhage.

Essential Workup Pregnancy test

Tests Lab 

CBC, prothrom bin tim e (PT), partial throm boplastin tim e (PTT), bleeding tim e



May send iron studies, thyroid-stim ulating horm one (TSH), luteinizing horm one (LH), follicle-stim ulating horm one

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(FSH), prolactin level, cervical cultures for routine follow-up by prim ary m edical doctor (PMD)/gynecology

Imaging Pelvic ultrasound m ay show uterine, tubal, or ovarian abnorm ality; m ay be needed to rule out differential diagnoses.

Diagnostic Procedures/Surgery 

Dilation and curettage (D & C) m ay be required for heavy bleeding unresponsive to other interventions.



Refer for endom etrial biopsy if older than 35 years of age

Differential Diagnosis 

Pregnancy com plications: o

Threatened, incom plete, or spontaneous abortion; ectopic or m olar pregnancy



Infectious: o

Vaginitis, cervicitis, pelvic inflam m atory disease (PID)



Coagulopathies: o

Von Willebrand disease, idiopathic throm bocytopenic purpura, platelet defects, thalassem ia



Medications: o

Warfarin, aspirin, oral contraceptives, tricyclic antidepressants, m ajor tranquilizers



System ic illness: o

Adrenal, hepatic, renal or thyroid dysfunction, diabetes m ellitus, other endocrinopathies



Anatom ic lesions: o

Fibroids, endom etriosis, polyps, endom etrial hyperplasia, neoplasm



Intrauterine devices



Traum a

P.337

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Treatment Pre Hospital IV crystalloid boluses as needed for hypotension, tachycardia secondary to heavy bleeding

Initial Stabilization Airway, breathing, and circulation (ABCs): 

Packed RBCs for significant bleeding unresponsive to crystalloids

ED Treatment 

Observation usually adequate if bleeding m ild



IV crystalloid, packed red blood cells for continued bleeding or hem odynam ic instability



Gynecology consultation if bleeding is severe and unresponsive to crystalloids, m edications o

D & C m ay be necessary for hem odynam ic instability.

o

Hysteroscopy or hysterectom y for continued heavy bleeding unresponsive to other m easures

Medication (Drugs) 

Conjugated estrogen (Prem arin) for heavy bleeding, hem odynam ic instability: o

2.5 m g PO q.i.d.

o

25 m g IV, repeat in 3 hours if needed: 

Intravenous dosing has not been shown to be

Pa ge 1 5 7

superior to oral route. o

Medroxyprogesterone acetate (Provera) 10 m g PO per day is added when bleeding subsides.



Oral contraceptive pills o

Ethinyl estradiol 35 Âµg and norethindrone 1 m g PO q.i.d. for 1 week



Medications m ay be deferred in m ild cases with referral to gynecology.

Follow-Up Disposition Admission Criteria 

Significant blood loss



Continued bleeding



Unresponsive hem odynam ic instability for D & C or operative treatm ent

Discharge Criteria Most patients can be discharged with gynecology referral once bleeding is controlled and patient is hem odynam ically stable.

References 1. Abnorm al uterine bleeding. In: Stenchever MA, et al., eds. Com prehensive Gynecology. 4th ed. St. Louis, MO: Mosby; 2001:1079â€“1098. 2. Albers JR, Hull SK, Wesley RM. Abnorm al uterine bleeding. Am Fam Phys. 2004;69(8):1915â€“1927. 3. Bradford JC, Kyriakedes CG. Vaginal bleeding. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosbyâ€“Year Book; 2002:226â€“233.

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4. Morrison LJ, Spence JM. Obstetrics and gynecology: vaginal bleeding and pelvic pain in the non pregnant patient. In: Tintinalli JE, ed. Em ergency Medicine: a Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004: 647â€“653.

Codes ICD9-CM 626.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysphagia

Dysphagia

Timothy J. Mader Allison V. Brewer

Basics Description Dysphagia: 

Difficulty swallowing



Im paired passage of solids or liquids from the oral cavity to the stom ach

Etiology 



Mechanism : o

Can be neurom uscular or m echanical

o

Frequency and severity increase with advancing age

Classification: o

Oropharyngeal (transfer) dysphagia: 

Difficulty transferring from the oropharynx to the proxim al esophagus (difficulty initiating a swallow)



Easier to swallow solids versus liquids



Im m ediate, within seconds of swallowing



Sensation of the bolus not passing below the cervical esophagus



Nasal or oral regurgitation

Pa ge 1 5 8



Coughing or choking (indicating aspiration)



Gurgling noise after swallowing (suggests Zenker diverticulum )



Vocal quality changes



Usually a neurom uscular disorder resulting in bulbar m uscle weakness or im paired coordination

o

Esophageal (transport) dysphagia: 

Failure of norm al transit through the esophagus



Retrosternal sticking sensation 10â€“15 seconds after swallowing



Nocturnal regurgitation



Drooling or regurgitation of undigested food and liquid (characteristic of esophageal obstruction)



Usually obstructive but consider m otility disorders

o

Functional dysphagia: 

Diagnosis of exclusion



Full workup without evidence of m echanical or neurom uscular pathology

 



Sym ptom s >12 weeks

Odynophagia: o

Pain with swallowing

o

Separate, but often related, entity

Pain pattern: o

Voluntary striated m uscle in the upper one-third transitions to involuntary nonstriated m uscle in the lower two-thirds

o

Som atic nerve fibers in the upper esophagusâ€”excellent pain localization

o

Afferents, from the vagus nerve along with the cervical and thoracic sym pathetic ganglia, innervate

Pa ge 1 5 8

the lower esophagusâ€”poor pain localization o

Visceral pain from the lower esophagus m ay be difficult to distinguish from that of acute coronary syndrom e.

Pediatric Considerations 

Pediatric dysphagia: o

Wide range of feeding and swallowing difficulties

o

Multifactorial pathophysiology:

o 



Neurom uscular developm ent



Anatom ical changes from infancy to childhood

Esophageal disorders m ost com m on etiology

Classification: o

Oral phase: 

Im paired ingestion/m astication and transfer to posterior pharynx

o

Pharyngeal phase: 

Im paired swallow m echanism and transport of m aterial through pharynx with appropriate airway closure (requires intact sensory and m otor m echanism s to prevent aspiration)

o

Esophageal phase: 

Im paired transport of m aterial from esophagus to stom ach

Diagnosis Signs and Symptoms History Three im portant questions: 

What causes sym ptom s?

Pa ge 1 5 8

o

Solids and liquids suggests a neurom uscular disorder.

o

Solids only or progression from solids to liquids suggests a m echanical abnorm ality.



Are sym ptom s interm ittent or progressive? o

Interm ittent sym ptom s suggest rings or webs.

o

Progressive sym ptom s suggest peptic or m alignant strictures.

o 

Motility disorders can be interm ittent or progressive.

Are there concom itant sym ptom s? o

Odynophagia or chest pains

o

Chronic cough or nocturnal wheezing

o

Nasopharyngeal regurgitation

o

Weight loss

o

Chronic heartburn

o

Hem atem esis

Physical Exam 

Often unrem arkable



Oropharyngeal inspection



Pulm onary and cardiac auscultation



Neurologic exam with em phasis on cranial nerves

Tests ECG 

Consider cardiac etiology for chest discom fort



Heart and esophagus share a com m on neural pathway.

Lab No specific studies are indicated.

Imaging 

Chest radiograph: o

Food dilating the esophagus

o

Aspiration pneum onitis

Pa ge 1 5 8

o

Extrinsic com pressing m ass



Soft tissue lateral neck radiograph



Cineradiography barium swallow (liquid or bread soaked):



o

Defines esophageal anatom y

o

Assesses function

o

Do not perform if endoscopy anticipated

CT of the head: o

Indicated for new-onset neurom uscular dysphagia

Diagnostic Procedures/Surgery 

Endoscopy: o

Indicated to relieve obstruction and inspect the esophageal anatom y



Esophageal m anom etry



Fiberoptic endoscopic evaluation of swallowing



Electrom yography

P.339

Differential Diagnosis 

Oropharyngeal: o

o

o

Infectious: 

Derm atom yositis



Infectious pharyngitis



Lym e disease



Botulism

Mechanical: 

Malignancy



Pharyngeal pouch



Congenital

Medications: 

Anticholinergics

Pa ge 1 5 8

o

o 



Metoclopram ide



Am inoglycosides



Am iodarone



Phenothiazines



Procainam ide



Penicillam ine



HMG-CoA reductase inhibitors



Potassium



Ferrous sulfate



Aspirin and NSAIDs

Neurom uscular: 

Cerebrovascular accident



Multiple sclerosis



Am yotrophic lateral sclerosis



Parkinson disease



Huntington chorea



Myasthenia gravis



Cranial nerve palsy



Cricopharyngeal spasm

Psychological/Behavioral

Esophageal: o

o

Mechanical: 

Foreign body



Peptic esophageal stricture



Neoplasm



Schatzki ring



Esophageal webs



Diverticula



Radiation injury

Motor: 

Scleroderm a



Achalasia

Pa ge 1 5 8

o

o



Diffuse esophageal spasm



Nutcracker esophagus



Nonspecific m otor disorders

Inflam m atory: 

Eosinophilic esophagitis



Pill esophagitis

Extrinsic: 

Cardiovascular abnorm alities (vascular rings, thoracic aneurysm , left atrial enlargem ent, aberrant subclavian artery)



Mediastinal m ass



Cervical osteophytes

Treatment Pre Hospital 

Vigilant airway attention



Position of com fort with suction available

Initial Stabilization 

Vigilant airway attention



Position of com fort with suction available



NPO



0.9% NS 500 m L (peds: 20 m L/kg) IV fluid bolus for significant dehydration

ED Treatment 

Nitroglycerin for esophageal spasm



Glucagon for im pacted foreign body



Treat com plications: o

Airway obstruction

o

Aspiration, pneum onia, lung abscess

Pa ge 1 5 8

o 

Dehydration, m alnutrition

Dietary m odifications: o

Thickened liquids for neurom uscular disorder

o

Thin liquids for m echanical disorders

Medication (Drugs) 

Glucagon: 1 m g IV followed by second dose of 1 m g after 5 m inutes if there is no im provem ent in sym ptom s



Nitroglycerin: 0.4 m g SL q5m in repeated up to 3 tim es

Follow-Up Disposition Admission Criteria 

Esophageal obstruction



Com prom ised fluid or nutrition status



Inability to protect airway



Sym ptom s cannot be distinguished from cardiac ischem ia.

Discharge Criteria 

Well-hydrated patient



Urgent neurology, otolaryngology, or gastroenterology referral arranged for further evaluation and treatm ent

References 1. Baker BM. Sym ptom s, diagnosis, and m anagem ent of dysphagia. J Ky m ed Assoc. 1998;96(9):362â€“367. 2. Cefalu CA. Diagnosing and treating dysphagia. Provider. 1999;25(11):7172â€“7475. 3. Miller CK, Willging JP. Advances in the evaluation and

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m anagem ent of pediatric dysphagia. Cur Op in Otolaryn and Head and Neck Surg. 2003;11(6):442â€“446. 4. Owen W. Dysphagia (Clinical review: ABC of the upper gastrointestinal tract). Brit Med J. 2001;323(7317):850â€“853. 5. Rothstein RD. A system atic approach to the patient with dysphagia. Hosp Pract. 1997;32(3):169â€“175. 6. Swann LA, Munter DW. Esophageal em ergencies. Em erg Med Clin North Am . 1996;14(3):557â€“570.

Codes ICD9-CM 787.2

ICD10 R13

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dyspnea

Dyspnea

Elizabeth L. Mitchell

Basics Description 

Dyspnea com es from the Greek word for â€œhard breathing.â€•



Often described as â€œshortness of breathâ€•



Usually an unconscious activity, dyspnea is the subjective sensation of breathing, from m ild discom fort to feelings of suffocation.

Etiology 

Dyspnea usually reflects an im pairm ent in ventilation, perfusion, m etabolic function, or CNS drive.



Mechanism s that control breathing: o

Control centers: 

Brainstem and cerebral cortex affect both autom atic and voluntary control of breathing.

o

Chem o, stretch, and irritant sensors: 

CO 2 receptors located centrally and PO 2 receptors located peripherally



Mechanoreceptors lie in respiratory m uscles and respond to stretch.



Intrapulm onary m echanoreceptors respond to

Pa ge 1 5 9

chem ical irritation, engorgem ent, and stretch. o

Effectors of respiratory center output are in the respiratory m uscles and respond to central stim ulation to m ove air in and out of the thoracic cavity.

o

Motor-sensory control of the diaphragm and m uscles of respiration are controlled by C-3â€“C-8 nerves and T-1â€“T-12 nerves



Derangem ents of any of these neurosensory pathways produces dyspnea: o

Many etiologies for the sensation of dyspnea are due to the com plex nature of m echanism s that control breathing.

Diagnosis Signs and Symptoms 

Difficult, labored, or uncom fortable breathing



Upper airway:





o

Stridor

o

Upper-airway obstruction

Pulm onary: o

Tachypnea

o

Accessory m uscle use

o

Wheezing

o

Rales

o

Asym m etric breath sounds

o

Poor air m ovem ent

Cardiovascular: o

S3 gallop

o

Murm ur

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o 

CNS: o



Jugular venous distention

Altered levels of consciousness

General o

Diaphoretic/cool versus hot/dry skin

o

Pallor

o

Upright patient position

o

Clubbing

o

Cyanosis

o

Edem a

o

Ketotic breath odor

Essential Workup 

Pulse oxim etry: o

May be falsely elevated due to increased ventilation or carbon m onoxide



Chest radiograph: o

For diagnosis of pulm onary conditions

o

Assess heart size and evidence of congestive heart failure (CHF)



Arterial blood gas: o

Oxygenation

o

Calculate arterial-alveolar gradient:

o



A-a (at sea level) = 150 - (PO 2 - PCO 2 )/0.8



Norm al = 5â€“20

Assess degree of acidosis.

Tests Lab 

CBC: o

Evaluation of anem ia

o

Neutrophil count helpful in evaluation of infectious processes

Pa ge 1 5 9



Electrolyte, blood urea nitrogen, creatinine, glucose: o

Consider when specific m etabolic derangem ents are suspected

o

B-natriuretic peptide May be elevated in CHF



Toxicology screen



Methem oglobin/Carboxyhem oglobin level



Thyroid function tests



D-dim er (ELISA): o

Useful for excluding pulm onary em bolus if norm al

Imaging 

ECG for suspected m yocardial ischem ia, CHF



Ventilation-perfusion scan or CT pulm onary angiogram for suspected pulm onary em bolism



Soft-tissue neck radiograph or fiberoptic visualization for suspected upper airway obstruction



Echocardiography for suspected pericardial effusion/tam ponade



Peak expiratory flow/spirom etry to assess for reactive-airway disease



Tensilon test for suspected m yasthenia gravis

P.341

Differential Diagnosis 



Upper airway: o

Epiglottitis

o

Laryngeal obstruction

o

Tracheitis or tracheobronchitis

o

Angioedem a

Pulm onary: o

Airway m ass

Pa ge 1 5 9

o

Asthm a

o

Bronchitis

o

Chest wall traum a

o

CHF

o

Drug-induced conditions (e.g., crack lung, aspirin overdose)







o

Effusion

o

Em physem a

o

Metastatic disease

o

Pneum onia

o

Pneum othorax

o

Pulm onary em bolism

o

Pulm onary hypertension

o

Restrictive lung disease

Cardiovascular: o

Arrhythm ia

o

Coronary artery disease

o

Intracardiac shunt

o

Left ventricular failure

o

Myxom a

o

Pericardial disease

o

Valvular disease

Neurom uscular: o

CNS disorders

o

Myopathy and neuropathy

o

Phrenic nerve and diaphragm atic disorders

o

Spinal cord disorders

o

System ic neurom uscular disorders

Other: o

Acidosis

o

Altitude

o

Anaphylaxis

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o

Anem ia

o

Thyroid disorders

o

Psychogenic

o

Sepsis

Pediatric Considerations 

Unique conditions in differential diagnosis for age <2 years: o

Croup

o

Congenital anom alies of the airway

o

Congenital heart disease

o

Foreign-body aspiration

o

Nasopharyngeal obstruction

o

Shock

Treatment Pre Hospital 

Place all patients on supplem ental oxygen, pulse oxim etry, and cardiac m onitor.



Initiate therapy for suspected cause of dyspnea when indicated:



o

Asthm a

o

Chronic obstructive pulm onary disease

o

CHF

Intubate patients in the face of im pending respiratory failure

Initial Stabilization 

ABCs



Im m ediate intubation for im pending respiratory distress

Pa ge 1 5 9

ED Treatment 

ABCs



Im m ediate intubation for im pending respiratory distress

Follow-Up Disposition Admission Criteria 

Assisted ventilation



Hypoxia



A-a gradient >40



Medical condition requiring hospital therapy

Discharge Criteria 

Adequate oxygenation



Stable m edical illness that can be m anaged as outpatient

References 1. De Peuter S, Van Diest I, Lem aigre V, et al. Dyspnea: the role of psychological processes. Clin Psychol Rev. 2004;Sep24(5):557â€“581. 2. Manning HL, Mahler DA. Pathophysiology of dyspnea. Monaldi Arch Chest Dis. 2001;Aug56(4):325â€“30. 3. Michelson E, Hollrah S. Evaluation of the patient with shortness of breath: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):221â€“237. 4. Schwartzstein RM, Manning HL. Pathophysiology of dyspnea. N Engl J Med. 1995;12(3):1547â€“1552. 5. Tobin MJ. Dyspnea: pathophysiologic basis, clinical presentation, and m anagem ent. Arch Intern Med. 1990;8:1604â€“1612. 6. Weism an IM, Zeballos RJ. Clinical evaluation of unexplained dyspnea. Cardiologia. 1996;41(7):621â€“634.

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Miscellaneous SEE ALSO: Respiratory Distress

Codes ICD9-CM 786.09

ICD10 R06.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysto nic Reactio n

Dystonic Reaction

Kenneth Jackimczyk

Basics Description 

Norm al pattern of CNS neurotransm ission m aintained by balance between dopam inergic and cholinergic receptors: o

Certain drugs disrupt this balance, leading to involuntary m uscle spasm s.



Although the spasm s are uncom fortable and frightening, they are not life threatening.

Etiology 

Usually occur after patient has taken antipsychotic, antiem etic, or antidepressant drug



Incidence of dystonic reactions in patients taking neuroleptics is 2â€“25%, depending on the agent.



Neuroleptic agents: o

Phenothiazine (Thorazine, Mellaril, Prolixin, Com pazine, Stelazine, Phenergan)



o

Thioxanthenes (Navane)

o

Butyrophenones (Haldol, Droperidol)

o

Indole (Moban)

o

Dibenzoxipine (Loxitane)

Antiem etic agents:

Pa ge 1 5 9



o

Metoclopram ide (Reglan)

o

Trim ethobenzam ide (Tigan)

Other agents: o

Cyclic antidepressants

o

Antihistam ines

o

Doxepin

o

Cim etidine

o

Prozac

o

Cocaine

o

Ketam ine

o

Chloroquine

o

Lithium

o

Phencyclidine

Pediatric Considerations Children are particularly vulnerable to dystonic reactions when dehydrated or febrile.

Diagnosis Signs and Symptoms General 

Usually occurs within hours of ingestion: o

Alm ost always within first week after exposure to offending drug



Age: o

Twice as com m on in m ales

o

Uncom m on in older patients

o

Children are m ore susceptible.



Difficulty with vocalization



Com pletely alert and able to answer questions

Pa ge 1 5 9



Involuntary m uscle spasm s usually involving the face, neck, and trunk (see Physical Exam )

History Ingestion of antipsychotic, antiem etic, or other drug within week of sym ptom onset

Physical Exam 

Characteristic m otor spasm s occur.



Oculogyric crisis: o

Involves eye and periorbital m uscles

o

Starts as blepharospasm

o

Evolves into painful upward or lateral deviation of eyes



Buccolingual crisis: o

Involves facial m uscles and tongue

o

Bizarre grim acing

o

Trism us

o

Tongue protrusion

o

Dysphagia

o

Dysarthria

o

Rarely causes spasm of pharynx and larynx that can be severe enough to cause stridor



Torticollic crisis: o



Tortipelvic crisis: o



Twisting of neck

Abdom inal wall m uscle spasm

Opisthotonos: o

Involves m uscles of trunk and back

o

Twisting and arching of spine

Essential Workup 

Clinical diagnosis is based on characteristic signs and sym ptom s with history of possible drug exposure.

Pa ge 1 6 0



Diagnosis is confirm ed by response to treatm ent.

Differential Diagnosis 





Tardive dyskinesia: o

Com plication of chronic antipsychotic therapy

o

Usually choreiform m ovem ents

Akathisia: o

Involuntary m otor restlessness

o

May appear agitated

Seizure: o

History of prior seizures

o

Not responsive to verbal stim uli

o

Tonic-clonic-type m otor m ovem ents rather than spasm



Hysteria or pseudoseizure: o

History of precipitating em otional event

o

Tonic-clonic m otor activity rather than sustained spasm



Tetanus



Strychnine poisoning



Chronic dystonias: o

Cerebral palsy, fam ilial choreas

o

Usually history of dystonia is associated with chronic neurologic process.



Scorpion envenom ation: o

Oculogyric crisis and opisthotonos are com m on m anifestations of scorpion envenom ation.

o 

Patient lacks history of drug exposure.

Meningitis and encephalitis m ay present with atypical seizures that m im ic dystonic reaction.

P.343

Pa ge 1 6 0

Treatment Pre Hospital 

Rarely life threatening



Direct attention toward spasm of larynx and tongue to be sure dystonic reaction is not causing respiratory com prom ise



Ask fam ily and friends about ingestions of antipsychotic m edications, antiem etics, and recreational drugs.



Transport pill bottles.

Initial Stabilization Stabilize airway to prevent spasm of larynx or tongue from causing respiratory com prom ise.

ED Treatment 

Adm inister diphenhydram ine (Benadryl) or benztropine m esylate (Cogentin): o

Rapid resolution of m uscular spasm by restoring cholinergic-dopam inergic balance in CNS

o

IV adm inistration is preferred route of treatm ent.

o

Onset of relief in 2â€“5 m inutes

o

Com plete resolution of sym ptom s in 15 m inutes

o

IM adm inistration is alternate route of treatm ent.

o

Begins to work in 15â€“30 m inutes

o

Continue oral adm inistration for 3 days to prevent redevelopm ent of sym ptom s.



Diazepam (Valium ): o

Adm inister in cases of dystonia unresponsive to adequate doses of anticholinergic m edications.

o

Failure to respond to standard treatm ent should lead

Pa ge 1 6 0

physician to consider other diagnoses.

Medication (Drugs) 

Benztropine m esylate (Cogentin): 1â€“2 m g either IV (over 2 m inutes) or IM followed by 1â€“2 m g PO b.i.d. for 3 days: o

Not to be used in children <3 years old

o

For children >3 years old: 0.02 m g/kg IV (over 2 m inutes) or IM followed by 0.02 m g/kg PO b.i.d. for 3 days



Diphenhydram ine (Benadryl): 1â€“2 m g/kg up to 100 m g either IV (over 2 m inutes) or IM followed by 25â€“50 m g (peds: 1â€“2 m g/kg) PO q6hâ€“q8h for 3 days, or



Diazepam : 5â€“10 m g IV followed by 5 m g PO q4hâ€“q6h as necessary for 3 days

Follow-Up Disposition Admission Criteria None

Discharge Criteria 

Discharge after resolution of sym ptom s.



Patient should not drive or perform tasks that require full alertness while taking sedating m edications.

References 1. Diederich NJ, Goetz CG. Drug-induced m ovem ent disorders. Neurol Clin. 1998;16:125â€“139.

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2. Gallagher EJ. Neurologic principles. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. New York: McGraw-Hill, 2002:282â€“301. 3. Manognerra AS. Dystonic reactions. In: Harwood-Nuss A, ed. The Clinical Practice of Em ergency Medicine. Philadelphia: Lippincott William s & Wilkins; 2005:1622â€“1624. 4. Van Harten PN, Hoek HW, Kahn RS. Acute dystonia induced by drug treatm ent. Br Med J. 1999;319:623â€“626.

Codes ICD10 G24.0

Pa ge 1 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Eating Diso rder

Eating Disorder

David B. Herzog Hope W. Levin Safia C. Jackson

Basics Description Anorexia Nervosa (AN) 

Refusal to m aintain body weight at or above a m inim ally norm al weight for age and height



Failure to m ake expected weight gain during a period of growth



Intense fear of gaining weight or becom ing fat, even though underweight



Disturbance in the way body weight or shape is experienced



Undue influence of body weight and shape on self-evaluation



Denial of seriousness of low body weight



In postm enarchal fem ales, am enorrhea for three consecutive cycles

Bulimia Nervosa (BN) 

Recurrent episodes of binge eating characterized by:

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o

Eating a larger than usual am ount of food in a discrete period of tim e

o

A sense of loss of control over eating during the episode



Recurrent inappropriate com pensatory behaviors used to prevent weight gain: o

Self-induced vom iting

o

Misuse of laxatives

o

Diuretics

o

Enem as or other m edications

o

Fasting

o

Excessive exercise

Binge Eating Disorder (BED) 

Recurrent episodes of binge eating characterized by: o

Eating a larger than usual am ount of food in a discrete period of tim e

o

A sense of loss of control over eating during the episode



Binge-eating episodes associated with three or m ore of the following: o

Eating m uch m ore rapidly than norm al

o

Eating until feeling uncom fortably full

o

Eating large am ounts of food when not feeling physically hungry

o

Eating alone because of being em barrassed by how m uch one is eating

o

Feeling disgusted with oneself, depressed, or very guilty after overeating

o 

Marked distress regarding binge eating

Prevalence: o

AN: 0.5% of the United States fem ale population

o

BN: 2% of the United States fem ale population

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o

BED: 2% of the United States fem ale population

Etiology 

Eating disorders result from a com bination of genetic, neurochem ical, developm ental, psychological, and sociocultural factors.



Typical age of onset for AN is bim odal at 13â€“14 years and 17â€“18 years.



AN com m only onsets in a teenager whose initial dieting behavior escalates into an obsessive preoccupation with weight and thinness.



BN and BED com m only onset in late adolescence or early adulthood.



BN com m only onsets in an individual who: o

Has attem pted m any diets and failed

o

May have learned purging behaviors from a friend or fam ily m em ber



BED is associated with a history of obesity, weight cycling, and dieting.

Diagnosis Signs and Symptoms 

Endocrine/m etabolic com plications: o

Electrolyte im balances

o

Hypotherm ia

o

Am enorrhea

o

Sleep disturbance

o

Growth retardation

o

Osteoporosis

o

Nutritionally based osteoporosis

Pa ge 1 6 0











Cardiovascular problem s: o

Arrhythm ias

o

Bradycardia

o

Hypotension

o

QTC prolongation

o

Ipecac cardiom yopathy

Renal com plications: o

Hypokalem ia

o

Edem a

Hem atologic com plications: o

Anem ia

o

Leukopenia

o

Throm bocytopenia

Gastrointestinal com plications: o

Decreased m otility

o

Intestinal dilatation

Neurological com plications: o

Potentially irreversible structural brain changes

Physical Exam 

Weight, body m ass index [weight in kg/(height in m eters) 2 ]



Vital signs



Dry skin



Lanugo: o

A soft, downy body hair that develops on the chest and arm s



Breast atrophy



Parotid swelling, subm andibular swelling



Hypercarotenem ia



Abnorm al dentition



Abrasions of dorsum of hand

Pa ge 1 6 0

Essential Workup 

Clinical diagnosis



Medical evaluation



Physical exam ination



Nutritional assessm ent



Psychiatric interview:



o

Concurrent psychiatric illness

o

Suicide risk assessm ent

o

Explore psychosocial context

Fam ily evaluation when patient lives with her or his fam ily

Tests Lab 

Com plete blood count



Electrolytes, blood urea nitrogen, creatinine, glucose



Liver function tests



Calcium , m agnesium , phosphorus



Am ylase



Consider checking thyroid-stim ulating horm one



ECG



Consider cardiac ECHO if substantial weight loss

Differential Diagnosis 

Mood disorders



Obsessive-com pulsive disorder



Borderline personality disorder



Medical conditions o

Crohn disease

o

Diabetes m ellitus

o

Thyroid disease

o

Cancer

Pa ge 1 6 0

Treatment Initial Stabilization 

ABCs



IV 0.9% NS 1 L bolus (peds: 20 m L/kg) for severe dehydration



Accu-Chek, correct hypoglycem ia with dextrose



Correct hypokalem ia



Warm ing blankets for severe hypotherm ia

ED Treatment Labs, physical exam ination, psychiatry consultation (including assessm ent of suicide risk), and m edical stabilization P.345

Medication (Drugs) 

Escitalopram (Lexapro): 10â€“20 m g q.i.d. daily for BN



Fluoxetine (Prozac): 20â€“60 m g every AM for treatm ent of BN and relapse prevention in AN



Olanzapine (Zyprexa): 2.5â€“10 m g q.i.d. daily for AN



Sertraline (Zoloft): 50â€“200 m g q.i.d daily for BN

Follow-Up Disposition Admission Criteria

Pa ge 1 6 1





Medical risk: o

Extrem ely low weight

o

Rapid weight loss

o

Serum electrolyte im balance

o

Cardiac disturbance

o

Marked orthostatic hypotension

o

Bradycardia <40

o

Tachycardia >110

o

Hypotherm ia <97Â°

Psychiatric risk: o

Severe depression

o

Suicidality

o

Severe denial

o

Severe im pairm ent in functioning

o

Toxic fam ily environm ent

o

Psychosis

o

Refractory sym ptom s

Discharge Criteria 

Medically and psychologically safe enough to be m anaged on an outpatient basis



Referral to outpatient treatm ent providers is crucial.



Outpatient treatm ent requires a m ultim odal, m ultidisciplinary team approach com posed of a: o

Psychiatrist and/or psychologist

o

Nutritionist, preferably one who specializes in eating disorders



o

Pediatrician or internist

o

Fam ily therapist

o

Group therapist

Outpatient treatm ent: o

Establish m odest goals and clear param eters, including expected weight gain for anorexic patients

Pa ge 1 6 1



Psychotherapy: o

Cognitive behavioral therapy and interpersonal psychotherapy are the m ost effective form s of psychotherapy for BN.

o

Cognitive behavioral therapy, fam ily therapy, and psychodynam ic therapies are all useful for AN.

o

Fam ily therapy is the preferred therapy for teenagers with AN.



Pharm acotherapy: o

Only indicated within the context of psychotherapy, especially with com orbid psychopathology

o

Antidepressant m edications are shown to significantly reduce binging and purging behaviors.

o

Selective serotonin reuptake inhibitors (fluoxetine is the best studied and has a Food and Drug Adm inistration indication)

o

No accepted pharm acologic treatm ent of AN

o

Case studies suggest that second-generation antipsychotics m ay be helpful.

o

There is no clear evidence for specific treatm ent of osteoporosis in AN apart from nutritional calcium supplem entation.



Prognosis: o

AN and BN

o

20% chronic course

o

30% im prove

o

50% recover

o

Mortality rate 5.6% per decade for AN

References 1. Anonym ous. Practice guideline for the treatm ent of patients with eating disorders (revision). Am erican Psychiatric Association. Practice guideline for eating disorders. Am J Psychiatry. 2000;157:139.

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2. Becker AE, Grinspoon SK, Klibanski A, et al. Eating disorders. N Engl J Med. 1999;340:1092â€“1098. 3. Herzog DB, Beresin EV, Charat VE. Anorexia nervosa. In: Weiner JM, ed. Textbook of child and adolescent psychiatry, 3rd ed. Washington, DC: Am erican Psychiatric Publishing, 2004. 4. Kreipe RE, Birndorf SA. Eating disorders in adolescents and young adults. Psychiatr Clin North Am . 2000;84:1027â€“1049. 5. Mehler PS. Clinical practice: Bulim ia nervosa. N Engl J Med. 2003;28:349:875â€“881. 6. Miller KK, Grinspoon SK, Ciam pa J, Hier J, Herzog DB, Klibanski A. Medical findings in outpatients with anorexia nervosa. Arch Intern Med. 2005;165:561â€“566. 7. Misra M, Aggarwal A, Miller KK, Alm azan C, Worley M, Soyka LA, Herzog DB, Klibanski A. Effects of anorexia nervosa on clinical, hem atologic, biochem ical, and bone density param eters in com m unity-dwelling adolescent girls. Pediatrics. 2004;114:1574â€“1583. 8. Yager J, Devlin MJ, Halm i KA, Herzog DB, Mitchell JE, Powers PS, Zerbe KJ. Guideline watch: Practice guideline for the treatm ent of patients with eating disorders, 3rd edition. Arlington, VA: Am erican Psychiatric Association. Available online at http://www.psych.org/psych_pract/treatg/pg/EatingDisorders3e_PG_ 04-28.06.pdf.

Codes ICD9-CM 307.50

ICD10 F50

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ecto pic Pregnancy

Ectopic Pregnancy

Aviva Jacoby Zigman

Basics Description 

Im plantation of fertilized ovum outside of uterus: o





Most com m only fallopian tube

Abdom inal and peritoneal im plantations: o

Associated with higher m orbidity

o

Difficulty in diagnosis

o

Tendency to bleed

Incidence is 16.8 cases per 1,000 pregnancies.

Etiology Risk factors include: 

Wom an >35 years old



African Am erican



Previous fallopian tube dam age from infections, such as pelvic inflam m atory disease (PID)



Previous tubal surgery, i.e., tubal ligation



History of previous ectopic pregnancy



History of intrauterine device (IUD) use



Diethylstilbestrol (DES) exposure



In vitro fertilizations



43% of wom en with ectopic pregnancies have no risk

Pa ge 1 6 1

factors.

Diagnosis Signs and Symptoms 

Classic triad of am enorrhea, vaginal bleeding, and abdom inal pain are present in only 15% of wom en with ectopic pregnancies: o

Am enorrhea (75â€“95%)

o

Abdom inal pain (80â€“100%): 

Frequently unilateral

o

Abnorm al vaginal bleeding (50â€“80%)

o

Sym ptom s of pregnancy (10â€“25%)

o

Orthostatic hypotension, dizziness, and syncope (5â€“35%)

o

Abdom inal tenderness (55â€“95%)

o

Adnexal tenderness (75â€“90%)

o

Adnexal m ass (35â€“50%)

o

Cervical m otion tenderness (43%)

Physical Exam 

Evaluate for signs of peritoneal irritation.



Pelvic exam : o

Note uterine size.

o

Adnexal size

o

Adnexal tenderness

o

Presence of tissue in vaginal vault

o

Cervical OS open or closed

Essential Workup Pregnancy testing: 

Wom en of potential childbearing age with vaginal bleeding

Pa ge 1 6 1

or abdom inal pain m ust have urine or serum pregnancy test. 

Do not forget to include patients with history of recent elective or spontaneous abortion, tubal ligations, or IUD use.

Vital Signs Unstable 

Type and cross-m atch, hem atocrit (Hct)



Bedside ultrasound (US), if im m ediately available, sim ultaneous with resuscitation



Consult gynecology and prepare for im m ediate surgical intervention.

Vital Signs Stable 

Rapid hem oglobin determ ination



Type and Rh



Ultrasonography

Tests Lab 

Urine pregnancy tests can detect Î²-hum an chorionic gonadotropin (Î²-hCG) levels of 25â€“50 m IU/L: o

Î²-hCG levels of 25 m IU/L can be detected with serum tests.

o

For pregnant patients with no dem onstrable intrauterine pregnancy (IUP)



Quantitative serum Î²-hCG; for diagnosis and follow-up: o

Doubles every 2 days in norm al early pregnancy (early pregnancy <10,000 Î²-hCG m IU/L, 8 days to 7 weeks)

Ultrasound in Conjunction with Quantitative Î²-hCG 

Patients with Î²-hCG levels >6,500 m IU/L and no

Pa ge 1 6 1

intrauterine gestational sac seen on ultrasound have 100% chance of having ectopic pregnancy. 

Patients with Î²-hCG levels >6,500 m IU/L with intrauterine gestational sacs present have 94% chance of having norm al pregnancy.



Patients with Î²-hCG <2,000 m IU/L are too early to have gestational sac seen by abdom inal ultrasound and thus cannot be ruled out for ectopic pregnancy.



Patients with Î²-hCG >2,000 and <6,500 m IU/L should have IUP visualized on transvaginal US; suspect ectopic pregnancy if IUP is absent.

Imaging Ultrasonographic evidence of IUP m akes ectopic pregnancy very unlikely: 

Positive IUP is indicated by double-ringed gestational sac, yolk sac, or fetal pole, and heartbeat seen in uterus.



Transvaginal ultrasound; gestational sac at 5 weeks, cardiac activity at 6.5 weeks



Transabdom inal ultrasound; gestational sac at 6 weeks, cardiac activity at 8 weeks



Com plex adnexal m ass and fluid in cul-de-sac seen in 22% of ectopics and has 94% positive predictive value when present.



Positive pregnancy test with no confirm ed IUP and fluid in pelvis; high risk for bleeding ectopic pregnancy

Differential Diagnosis 



Positive pregnancy test with vaginal bleeding: o

Spontaneous abortion

o

Cervicitis

o

Traum a

Positive pregnancy test with no evidence of IUP:

Pa ge 1 6 1



o

Com pleted spontaneous abortion

o

Early threatened abortion

Positive pregnancy test with evidence of IUP, abdom inal pain, or adnexal tenderness: o

Septic abortion

o

Threatened abortion

o

Corpus luteal cyst

o

Ovarian torsion

o

Urinary tract infection (UTI)

o

Nephrolithiasis

o

Gastroenteritis

o

Appendicitis

Treatment Pre Hospital Cautions: 

Fem ale patients of childbearing age presenting in shock m ay have unrecognized ruptured ectopic pregnancy.

Initial Stabilization 

Vital signs unstable: o

Airway m anagem ent, resuscitate as needed

o

Fluid therapy with two large-bore IVs, oxygen, and m onitor

o

Type specific, or O-negative blood if hypotensive after initial fluid bolus

o

Consult gynecology and transport to OR im m ediately for surgery.

P.347

Pa ge 1 6 1



Vital signs stable: o

Evidence of ectopic pregnancy on ultrasound: 

Obstetric-gynecologic evaluation for surgery versus outpatient m ethotrexate treatm ent

o

For patients in whom future fertility is desired, m ethotrexate is the best option; otherwise surgery is the definitive treatm ent. 

Methotrexate: initiated only in conjunction with obstetric consultant and close followup



Reliable patients with unruptured ectopic pregnancies <4.0 cm



Î²-HCG levels <6,000â€“15,000



Contraindications are renal, hepatic, or pulm onary dysfunction; active peptic ulcer disease; blood dyscrasias; and Hct <30.



Most com m on dosing, single dose (50 m g/m 2 ); serial Î²-hCG on days 2, 4, and 7. If <15% decline in Î²-hCG between days 4 and 7, second dose is given.



Most com m on side effects are worsening abdom inal pain, nausea, vom iting, and diarrhea.



Worsening abdom inal pain usually occurs 3â€“7 days after m ethotrexate initiation. These are usually tubal m iscarriages; however, follow-up ultrasounds are essential to rule out ectopic rupture.

 o

Most com m on com plication, tubal rupture in 4%

No evidence of ectopic pregnancy (early IUP or early ectopic): 

Desired pregnancy: Î²-hCG levels in norm al

Pa ge 1 6 1

early IUP should double every 2 days; stable, reliable patients m ay be followed for serial Î²-hCG tests in conjunction with obstetrician-gynecologist. 

Undesired pregnancy: dilation and curettage (D&C) to evacuate uterus and confirm presence of products of conception

Medication (Drugs) RhoGAM in Rh-negative wom en: 50 Âµg IM in wom en â‰¤12 weeks pregnant; 300 Âµg IM in wom en >12 weeks pregnant

Follow-Up Disposition Admission Criteria 

Any patient with confirm ed ectopic pregnancy who is hem odynam ically unstable



Unreliable patients with increased risk factors, no available ultrasound, Î²-hCG >6,500 with no evidence of IUP should be adm itted for observation and serial Î²-hCG tests.

Discharge Criteria Decision for outpatient m anagem ent should be m ade in conjunction with obstetrician-gynecologist: 

Hem odynam ically stable and reliable patients with workup that cannot rule out ectopic pregnancy: o

Strict follow-up for serial Î²-hCG tests every 2 days

o

Patients should be recorded in logbook with phone

Pa ge 1 6 2

num bers to ensure follow-up. 

Ectopic precautions: Patients should return to em ergency room im m ediately for: o

Increasing abdom inal pain

o

Vaginal bleeding

o

Syncope or dizziness

o

Patients should not be left alone until diagnosis of ectopic pregnancy can be safely ruled out.

o

Fam ily and friends should also be instructed on warning signs and sym ptom s of ruptured/bleeding ectopic pregnancies.

References 1. Am erican College of Obstetricians and Gynecologists. Practice Bulletin No. 3: Medical Managem ent of Tubal Pregnancy. Author; 1998. 2. Hockberger RS. Ectopic pregnancy. Em erg Med Clin North Am . 1987;5:481. 3. Houry D, Abbott JT. Acute com plications in pregnancy. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 4. Kaplan BC, et al. Ectopic pregnancy: prospective study with im proved diagnostic accuracy. Ann Em erg Med. 1996;28:10. 5. Krause RS, David MJ. Ectopic pregnancy. In: Tintinalli et al. Em ergency Medicine a Com prehensive Study Guide. 5th ed. McGraw-Hill, 2000. 6. Lipscom b GH, Stovall TG, Ling FW. Nonsurgical treatm ent of ectopic pregnancy. N Engl J Med. 2000;343(18):1325â€“1329. 7. Stovall TG, Ling FW. Single dose m ethotrexate: an expanded clinical trial. Obstet Gynecol. 1993;168:1759â€“1765.

Codes ICD9-CM

Pa ge 1 6 2

633.9

ICD10 O00.9

Pa ge 1 6 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ecz em a/Ato pic Derm atitis

Eczema/Atopic

Dermatitis Jon Ludwig James Nelson

Basics Description 

Chronic disease with acute flares



Superinfection with bacteria (especially Staphylococcus aureus) com m on



Altered cell-m ediated im m unity predisposes to infection with herpes sim plex virus (eczem a herpeticum ), m olluscum contagiosum , com m on warts, and fungi.

Genetics Fam ily history of atopy (asthm a, allergic rhinitis) 30â€“70% of the tim e: 

If both parents are atopic, the incidence of atopic derm atitis (AD) in their child is 79%.

Etiology Allergic etiology; preferential T helper 2 (TH2)â€“m ediated production of IL-4, which increases IgE and circulating eosinophils

Pa ge 1 6 2

Diagnosis Signs and Symptoms History 

Itching



Distribution varies with age: o

Infancy: tends to be m ore widespread with facial and scalp involvem ent; from 8â€“12 m onths, extensor surface involvem ent

o

Childhood: wrists, ankles, antecubital and popliteal fossae

o

Adolescents/adults: flexor areas, hands, feet, face, and neck

Physical Exam 

Chronic disease: hyperpigm entation, hypopigm entation, lichenification, and scaling



Acute flares: o

Mild/m oderate: erythem atous, scaly patches with crusting and excoriation

o 

Severe: diffuse, exfoliative erythroderm a

Other exam findings com m only associated with AD include: o

Dennie-Morgan folds (infraorbital grooves)

o

Pityriasis alba (dry, white patches to the face and upper body)

o

Hyperlinear palm s

o

Follicular accentuation

o

Keratosis pilaris (flesh-colored, keratotic papules on upper arm s, thighs, buttocks)

o

Derm atographism

Pediatric Considerations

Pa ge 1 6 2



Occurs in 10â€“15% of children <5 years of age



Onset <6 m onths of age in 48â€“75% of patients

Tests Lab 

Serum IgE levels and eosinophils are often elevated.



CBC with differential and blood cultures if febrile or toxic appearing

Diagnostic Procedures/Surgery Generally reserved for settings outside of the ED: 

Patch testing can help distinguish AD from contact derm atitis.



Radioallergosorbent test (RAST) can som etim es help identify allergic triggers.



Skin biopsy m ay help rule out other disorders.

Differential Diagnosis 

Seborrheic derm atitis



Allergic contact derm atitis



Irritant derm atitis



Psoriasis



Scabies



Wiskott-Aldrich syndrom e



Hyperim m unoglobulin E syndrom e

Treatment Initial Stabilization Treat septic shock if present

ED Treatment

Pa ge 1 6 2



Treatm ent is twofold: chronic m aintenance and control of acute flares.



Chronic m aintenance: o

Avoid excessive bathing.

o

Use of tepid water and m ild soaps

o

Frequent use of em ollients (Eucerin cream , Aquaphor ointm ent)

o

Avoidance of irritants: tobacco sm oke, wool or other harsh fabrics, feather/down bed products, stuffed anim als, dust m ites, and pets

o

Avoidance of allergic precipitants: m ilk, egg, peanut, soy, wheat, fish

o

Probiotics (Lactobacillus rham nosus) reduced sym ptom s in children by 56%.

o 

Reduction of perspiration

Control of acute flares: o

Em ollients

o

Mild disease/face: hydrocortisone 2.5% ointm ent (low potency)

o

Moderate disease: triam cinolone 0.1% ointm ent (m oderate potency)

o

Severe disease: fluocinonide 0.05% ointm ent (high potency)

o

System ic corticosteroids are rarely used owing to the chronicity of AD and the high likelihood of relapse on discontinuation.

o

Topical im m unom odulator m edications: topical pim ecrolim us and tacrolim us



Antihistam ines: diphenhydram ine, hydroxyzine, Zyrtec, Claritin, or Allegra to help reduce itching



Bacterial superinfection: cephalexin, cefazolin

P.349

Pa ge 1 6 2

Medication (Drugs) 

Aquaphor ointm ent: apply to affected areas b.i.d.



Cefazolin: 1 g (peds: >1 m onth 50â€“100 m g/kg/24h; <1 m onth, see PDR) IV q8h



Cephalexin: 500 m g (peds: 25â€“100 m g/kg/24h) PO q6h



Cetirizine: 5â€“10 m g (peds: 2.5â€“5 m g) PO daily



Diphenhydram ine: 25â€“50 m g (peds: 5 m g/kg/24h) PO or IV q6h



Eucerin cream : apply to affected areas b.i.d.



Fexofenadine: 60 m g (peds: >12 years) PO daily to b.i.d.



Fluocinonide 0.05% ointm ent: apply to affected areas of body b.i.d. (high potency)



Hydrocortisone 2.5% ointm ent: apply to affected areas of body/face b.i.d. (low potency)



Hydroxyzine: 25â€“100 m g (peds: 2 m g/kg/24h) PO q4hâ€“q6h



Loratadine: 10 m g (peds: <30 kg: 5 m g) PO daily



Pim ecrolim us 1% cream : Apply to affected areas b.i.d. (peds: >2 years of age).



Tacrolim us ointm ent: 0.1%: (peds: >2 years of age: 0.03%) apply to affected areas b.i.d.



Triam cinolone 0.1% ointm ent: apply to affected areas of body b.i.d. (m id potency).

Follow-Up

Pa ge 1 6 2

Disposition Follow-up with prim ary physician or derm atology referral for problem atic cases

Admission Criteria Severe secondary infection

Discharge Criteria Nearly all patients m ay be discharged with appropriate follow-up instructions.

References 1. Boguniewicz M, Eichenfield LF, Hultsch T. Current m anagem ent of atopic derm atitis and interruption of the atopic m arch. J Allergy Clin Im m unol. 2003;112(6 suppl):S140â€“150. 2. Hanifin J, Ling M, Langley R, et al. Tacrolim us ointm ent for the treatm ent of atopic derm atitis in adult patients Part I: efficacy. J Am Acad Derm atol. 2001;44(1 suppl):S28â€“38. 3. Leung DY, Bieber T. Atopic derm atitis. Lancet. 2003;361:151â€“60. 4. Odom RB, Jam es WD, Berger TG, eds. Andrewsâ€™ Diseases of the Skin. 9th ed. Philadelphia: WB Saunders; 2001 (8th ed. 2000:69â€“95). 5. Paller A, McCalister R, Doyle J, et al. Atopic derm atitis in pediatric patients: perceptions of physicians and parents. Paper presented at: Annual Meeting of the Am erican Academ y of Derm atology; March 2000; San Francisco, CA. 6. Sieberry G, Iannone R, eds. The Harriet-Lane handbook. 15th ed. St. Louis, MO: Mosby; 2001 (14th ed. 2000:908â€“909).

Codes ICD9-CM 619.8

Pa ge 1 6 2

ICD10 L30.9 L20.9

Pa ge 1 6 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Edem a

Edema

Laura Macnow

Basics Description 

Clinically apparent accum ulation of extravascular fluid due to a derangem ent in the balance of oncotic and hydrostatic forces: o

Increase in venous hydrostatic pressure: 

System ically, as with congestive heart failure



Locally, as with deep vein throm bosis

o

Increase in lym phatic hydrostatic pressure

o

Decrease in oncotic pressure:

o



System ically from hypoalbum inem ia



Locally from increased capillary perm eability

Increased venous hydrostatic pressure or decreased oncotic pressure results in pitting edem a

o

Protein-rich extravasated fluid results in nonpitting edem a





Lym phedem a



Increased capillary perm eability

In certain disorders, there is no clear relation to Starling forces: o

Myxedem a

Pa ge 1 6 3

o

Idiopathic (cyclic) edem a 

Worsened with heat



More com m on in wom en



Not necessarily related to m enses

Etiology Generalized 

Right heart failure



Constrictive pericarditis



Acute glom erulonephritis



Renal failure



Salt retention: o

Steroids/estrogens/progestins

o

NSAIDs

o

Antihypertensives (especially vasodilators)

o

Lithium

o

Cyclosporine

o

Insulin

o

Acute withdrawal of diuretics



Idiopathic (cyclic) edem a



Cirrhosis



Nephrotic syndrom e



Protein-losing enteropathy



Starvation



Pregnancy

Localized 

Throm bophlebitis



Chronic lym phangitis



Cellulitis



Baker cyst



Vasculitis



Angioedem a:

Pa ge 1 6 3

o

Allergic

o

Acquired



Hypothyroidism (m yxedem a)



Mechanical traum a



Therm al injuries



Radiation injuries



Chem ical burns



Hem iplegia



Com pressive or invasive tum or



Postsurgical resection of lym phatics



Postirradiation



Filariasis

Diagnosis Signs and Symptoms 

Weight gain of several kilogram s



Discom fort in the affected areas



Swelling



Tenderness



Pitting edem a: o

Increased venous hydrostatic pressure or decreased oncotic pressure



Nonpitting edem a: o

Protein-rich extravasated fluid

Generalized Edema (Anasarca) 

Edem a is m ost prom inent in dependent areas: o

Feet

o

Sacrum

o

Bilateral lower extrem ities

Pa ge 1 6 3

o 





Face/periorbital (especially in the m orning)

Cardiac: o

Dyspnea

o

Orthopnea

o

Paroxysm al nocturnal dyspnea

o

Increased jugular venous pressure

o

Rales

o

S3 gallop

Renal: o

Anorexia

o

Puffy eyelids

o

Frothy urine

o

Oliguria

o

Dark urine

o

Hem aturia

o

Hypertension

Hepatic: o

Jaundice

o

Spider angiom as

o

Palm ar erythem a

o

Gynecom astia

o

Testicular atrophy

Localized 

Ascites



Hydrothorax



History of traum a: o



Mechanical, therm al, radiation

Infectious/Inflam m atory: o

Chills

o

Fever

o

Erythem a

o

Increased warm th

Pa ge 1 6 3







Allergic: o

Pruritus

o

Hives

o

Involvem ent of the lips and the oral m ucosa

Myxedem a: o

Pretibial nonpitting edem a

o

Dry waxy swelling of skin and subcutaneous tissues

o

Periorbital m ost com m on (puffy eyes)

o

Nondependent areas

o

Fatigue

o

Cold intolerance

o

Weight gain

o

Constipation

o

Slowed deep-tendon reflex relaxation

Idiopathic: o

Diurnal weight gain/loss

Pregnancy Considerations 

Com m on secondary to horm onally m ediated fluid retention



When involving hands and face, m ay be early sign of pre-eclam psia





Dependent edem a: o

Usually in late pregnancy

o

From im pedance of venous return

Diuretics contraindicated

Essential Workup Diagnostic studies should be directed by the underlying etiology suggested by the history and physical exam ination. P.351

Tests

Pa ge 1 6 3

Lab 





Renal etiology suspected: o

Electrolytes

o

Blood urea nitrogen and creatinine

o

Urinalysis

o

Urine electrolytes and protein

Hepatic etiology suspected: o

Serum album in

o

Liver function tests

o

Prothrom bin tim e and partial throm boplastin tim e

Myxedem a suspected: o

Thyroid function tests

Imaging 



Cardiac etiology suspected: o

ECG

o

Chest radiograph

o

Echocardiography

Localized edem a to an extrem ity: o

Ultrasound (duplex scanning) or contrast venography

Differential Diagnosis 

Cellulitis



Contact derm atitis



Diffuse subcutaneous infiltrative process



Lym phedem a



Obesity

Treatment Initial Stabilization

Pa ge 1 6 3

See ED Treatm ent.

ED Treatment 

Treatm ent should be directed toward the underlying cause.



Diuretics are indicated in cases of generalized edem a but are not required em ergently.

Medication (Drugs) 

Am iloride: 5â€“20 m g PO q.i.d.



Captopril: 12.5â€“100 m g PO t.i.d. (m ax. 450 m g/d)



Furosem ide: 20â€“80 m g IV/PO q.i.d. (m ax. 600 m g/d)



Hydrochlorothiazide: 25â€“200 m g PO q.i.d.



Spironolactone: 25â€“200 m g PO q.i.d.

Follow-Up Disposition Admission Criteria 

Base the decision to adm it the patient on the underlying etiology.



Inability to am bulate without adequate hom e support



Hypoxia

Discharge Criteria 

Patient should be advised to decrease salt intake.



Elastic support stockings

References 1. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387â€“395. 2. Braunwald E. Edem a. In: Braunwald E., et al., eds. Harrison's principles of internal m edicine. 16th ed. New York: McGraw-Hill,

Pa ge 1 6 3

2005. 3. Chertow GM: Approach to the patient with edem a. In: Braunwald E, Goldm an L, eds. Prim ary Cardiology. 2nd ed. Philadelphia: Saunders, 2003. 4. Kay A, Davis DL. Idiopathic edem a. Am J Kidney Dis. 1999;34:405â€“423.

Codes ICD9-CM 782.3

ICD10 R60.9

Pa ge 1 6 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ehrlichio sis

Ehrlichiosis

Jonathan A. Edlow

Basics Description 

Relatively recently described tick-borne hum an infection that presents as a nonspecific febrile illness



Several form s of ehrlichiosis, but two predom inate in North Am erica.: o

Hum an m onocytic ehrlichiosis (HME), first described in 1987

o

Hum an granulocytic ehrlichiosis (HGE), first described in 1994

o

Both are tick-borne, but have different vectors and geographical ranges. Other species have been reported, but presently, HME and HGE are the im portant ehrlichial hum an pathogens.



HME: o

Vector tick: Am blyom m a am ericanum (Lone Star tick)

o

Geographical range: central, southern, and m id-Atlantic states with range expanding to parts of New England



HGE:

Pa ge 1 6 3

o

Vector tick: Ixodes scapularis (deer tick)

o

Geographical range: east coast, m id-central states, and Pacific Northwest (sam e area as Lym e disease)

Etiology Two distinct species of obligate intracellular organism s: 

The taxonom y of these pathogens has changed in recent years as m ore DNA and ribosom al RNA data becom e available.



HME is caused by the organism Ehrlichia chaffeensis.



HGE is caused by Anaplasm a phagocytophila (a new nam e as of 2002).

Diagnosis 

Signs and sym ptom s of HME and HGE are sim ilar.



Since both of these are new diseases: o

Many patients who are infected undergo asym ptom atic seroconversion.

o

The spectrum reported m ay overrepresent the m ore severely affected patients.



With any tick-borne infection, patients can be coinfected by m ore than one pathogen from the sam e tick bite: o

May have com plicated presentation of two different diseases

Signs and Symptoms History 

The season and other epidem iologic context are im portant in diagnosing tick-borne diseases: o

Most com m only present from April through October

o

Variability is likely owing to changes in weather

Pa ge 1 6 3

patterns from year to year and from region to region. 

Sym ptom onset between 1 and 2 weeks (m edian 9â€“10 days) following the tick bite: o

Bite of the larger Lone Star tick is m ore likely to be recalled by the patient than that of the sm aller deer tick.







Abrupt onset of: o

Fever

o

Chills

o

Headache

o

Myalgias

o

Malaise

Rash: o

HME (35â€“40% of cases)

o

HGE (approxim ately 5% of cases)

o

Often delayed

Sym ptom s m ay relate to com plications of ehrlichiosis such as: o

Adult respiratory distress syndrom e

o

Renal failure

o

Hypotension and shock

o

Rhabdom yolysis

o

GI disturbances

o

CNS or peripheral nervous system (PNS) involvem ent

Physical Exam 

Fever



Rash: o

May be m acular, m aculopapular, or petechial

o

May be absent during first week of illness



Lym phadenopathy



Hepatosplenom egaly

Pa ge 1 6 4





Neurologic findings: o

Abnorm al m ental status

o

Meningism us

o

Nystagm us

Pulm onary findings (rales, rhonchi) depending on pulm onary com plications.

Alert 

Ehrlichiosis is a potentially fatal tick-borne illness that is usually diagnosed clinically.



Consider diagnosis in all patients with nonspecific febrile illnesses, especially during the warm m onths of the year, and definitely if there is a history of tick bite.

Tests Lab 



CBC: o

Leukopenia

o

Throm bocytopenia

o

Anem ia

Hepatic transam inases: o



Often elevated 2â€“6 norm al

Indirect im m unofluorescence antibody test: o

Usual test available

o

Threshold for a positive test is usually m ade by the individual lab testing the serum .



Wright stain of peripheral blood: o

Morula m ay be seen: 

Sm all intracytoplasm ic ehrlichial DNA inclusion bodies



Diagnostic



Sensitivity of seeing m orulae depends on who is looking, for how long, and the im m unologic

Pa ge 1 6 4

com petence of the patient. 

Found m ore com m only in HGE (approxim ately 50%) than in HME (approxim ately 10â€“15%).



Culture and polym erase chain reaction test (PCR): o



Not routinely available

Antibody titer tests: o

Not available in real tim e

Imaging 

Head CT for encephalopathy



Chest radiograph for fever/dyspnea

Differential Diagnosis 



Most tick-borne illnesses: o

Rocky Mountain spotted fever

o

Lym e disease

o

Babesiosis

Many viral and bacterial infections, and num erous other infectious diseases, especially early in their course, can initially present with an undifferentiated febrile illness sim ilar to ehrlichiosis.



Mononucleosis



Throm botic throm bocytopenia purpura



Hem atologic m alignancy



Cholangitis



Pneum onia

P.353

Treatment

Pa ge 1 6 4

Initial Stabilization Airway, breathing, and circulation (ABCs)

ED Treatment 

Initiate antibiotics: o

Doxycycline: 

Drug of choice



Children who are severely affected should also receive doxycycline.

o

Rifam pin for: 

Pregnant patients



Allergy to doxycycline



Mildly affected children younger than 9 years of age



Patients who are pregnant, allergic to doxycycline, or who are m ildly affected can be given rifam pin for 7â€“10 days.



Initiate therapy for other tick-borne diseases that m ay have been cotransm itted

Medication (Drugs) Doxycycline: 

Adults: 100 m g IV/PO q12h



Children: (severely affected) 3 m g/kg q12h if less than 45 kg; older children can be dosed as adults.

Pediatric Considerations Despite the fact that doxycycline is generally contraindicated in patients younger than 9 years old, it is the drug of choice in young children who are severely affected by ehrlichiosis. In less affected children, rifam pin has been used successfully.

Pa ge 1 6 4

Pregnancy Considerations Rifam pin can be used to treat pregnant wom en with ehrlichiosis.

Follow-Up Disposition Admission Criteria 

Significant com orbidities/severely affected



Cannot take PO antibiotics



Im m unosuppressed

Discharge Criteria Healthy appearing

References 1. Edlow JA. Bull's Eye: Unraveling the Medical Mystery of Lym e Disease. New Haven, CT: Yale University Press; 2004. 2. Olano JP, Walker DH. Hum an ehrlichioses. Med Clin North Am . 2002;86:375â€“392. 3. Ram sey AH, Belongia EA, Gale CM, et al. Outcom es of treated HGE cases. Em erg Infect Dis. 2002;8(4):398â€“401. 4. Stone JH, Kerry D, Aram G, et al. Hum an m onocytic ehrlichiosis. JAMA. 2004;292:2263â€“2270.

Miscellaneous SEE ALSO: Lym e Disease; Rocky Mountain Spotted Fever; Tick-Borne Diseases

Pa ge 1 6 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Elbo w Injuries

Elbow Injuries

Christian M. Sloane

Basics Description Bony Injuries 

Supracondylar fracture: o

Most com m on in children

o

Peak ages 5â€“10 years, rarely occurs after age 15 years

o

Extension type (98%): FOOSH (fall on out stretched h and) with fully extended or hyperextended arm : 

Type 1: m inim al or no displacem ent



Type 2: slightly displaced fracture; posterior cortex intact



Type 3: totally displaced fracture; posterior cortex broken

o

Flexion type: blow directly to flexed elbow: 

Type 1: m inim al or no displacem ent



Type 2: slightly displaced fracture; anterior cortex intact



Type 3: totally displaced fracture; anterior cortex broken



Radial head fracture:

Pa ge 1 6 4

o

Usually indirect m echanism , i.e., FOOSH

o

Radial head driven into capitellum

Soft Tissue Injuries 



Elbow dislocation: o

Second only to shoulder as m ost dislocated joint

o

Most are posterior.

Medial/lateral epicondylitis: o

Overuse injuries usually related to rotary m otion at elbow

o

Involving attachm ent points of hand and wrist flexor/extensor groups to elbow

o

Plum bers, carpenters, tennis players, golfers

o

Pain m ade worse by resisted contraction of particular m uscle groups

Pediatric Considerations 

Subluxed radial head (nursem aid's elbow): o

Twenty percent of all upper extrem ity injuries in children

o

Peak age 1â€“4 years; occurs m ore frequently in fem ales than m ales

o

Sudden longitudinal pull on forearm with forearm pronated

Etiology 

Mechanism aids in determ ining expected injury.



Traum a predom inates.



Most elbow injuries caused by indirect traum a transm itted through bones of forearm (FOOSH)



Direct blows account for very few fractures or dislocations.

Pa ge 1 6 4

Diagnosis Signs and Symptoms How patient carries arm m ay give clues to diagnosis.

Bony Injuries Supracondylar fracture: 

Flexion type: o

Patient supports injured forearm with other arm and elbow in 90Â° flexion.

o 

Loss of olecranon prom inence

Extension type: o

Patient holds arm at side in S-type configuration.

Soft Tissue Injuries 



Elbow dislocations: o

Posterior: abnorm al prom inence of olecranon

o

Anterior: loss of olecranon prom inence

Radial head subluxation: o

Elbow slightly flexed and forearm pronated, resists m oving arm at elbow



Medial/lateral epicondylitis: o

Gradual onset of dull ache over inner/outer aspect of elbow referred to forearm

o

Pain increases with grasping and twisting m otions.

Essential Workup 

Radiographs



Assess wrist and shoulder for associated injury.



Evaluate neurovascular status of lim b.



Assess skin integrity.



Exam ine for com partm ent syndrom e, which is m ore com m on in supracondylar fractures.

Pa ge 1 6 4

Alert 

Injuries to ipsilateral upper lim b, particularly fractures to m idshaft hum erus and distal forearm , are com m on.



Evaluate for associated neurovascular injuries (up to 20%).

Tests Lab None specific for elbow injuries

Imaging 

Not usually necessary if overuse injury suspected



Routine anteroposterior (AP) and lateral; add oblique for assessm ent of subtle injuries to radial head/distal hum erus.



Fat pad sign: o

Seen with intra-articular injuries

o

Norm ally, anterior fat pad is narrow radiolucent strip anterior to hum erus.

o

Posterior fat pad is norm ally not visible.

o

Anterior fat pad sign indicates joint effusion/injury when raised and becom es m ore perpendicular to anterior hum eral cortex (sail sign).

o

Posterior fat pad sign indicates effusion/injury: 

In adults, posterior fat pad sign im plies radial head fracture.



In children, it im plies supracondylar fracture.

Pediatric Considerations 

Fractures in children often occur through unossified cartilage, m aking radiographic interpretation confusing.



A line drawn down anterior surface of hum erus should always bisect the capitellum in lateral view.

Pa ge 1 6 4



If any bony relationships appear questionable on radiographs, obtain com parison view of uninvolved elbow.



Suspect nonaccidental traum a if history does not fit injury.



Ossification centers: first appears: o

Capitellum : 3â€“6 m onths

o

Radial head: 3â€“5 years

o

Medial epicondyle: 5â€“7 years

o

Trochlea: 9â€“10 years

o

Olecranon: 9â€“10 years

o

Lateral epicondyle: 9â€“13 years

Differential Diagnosis 

Sprain/strain



Effusion



Contusion



Bursitis



Arthritis

P.355

Treatment Pre Hospital Appropriate splinting

Initial Stabilization Im m obilization to prevent further injury before taking radiographs is essential.

ED Treatment 

Orthopedic consultation is recom m ended for all but

Pa ge 1 6 4

nondisplaced, stable fractures that can generally be splinted with 24- to 48-hour orthopedic follow-up. 

Fractures generally requiring orthopedic consultation: o

Transcondylar, intercondylar, condylar, epicondylar fractures

o

Fractures involving articular surfaces such as capitellum or trochlea



Supracondylar fractures: o

Type 1 can be handled by ED physician with 24- to 48-hour orthopedic follow-up.

o

Elbow m ay be flexed and splinted with posterior splint.

o

Types 2 and 3 require im m ediate orthopedic consult.

o

Reduce these in ED when fracture is associated with vascular com prom ise.



Anterior dislocation: o

Reduce im m ediately if vascular structures com prom ised.

o 

Then flex to 90Â° and place posterior splint.

Posterior dislocation: o

Reduce im m ediately if vascular structures com prom ised.

o 

Then flex to 90Â° and place posterior splint.

Radial head fracture: o

Minim ally displaced fractures m ay be aspirated to rem ove hem arthrosis; instill bupivacaine (Marcaine) and im m obilize.

o 

Other types should have orthopedic consult.

Radial head subluxation: o

In one continuous m otion, supinate and flex elbow while placing slight pressure on radial head.

o

Often will feel click with reduction

Pa ge 1 6 5

o

If exam suggests fracture but radiograph is negative, splint and have patient follow up in 24â€“48 hours for re-evaluation.



Medial/lateral epicondylitis: o

Severe cases can be splinted.

o

Rest, heat, anti-inflam m atory agents

Alert 

Neurovascular injuries to num erous structures that pass about the elbow, including anterior interosseus nerve, ulnar and radial nerve, brachial artery



Volkm ann ischem ic contracture is com partm ent syndrom e of forearm .

Medication (Drugs) 

Conscious sedation is often required to achieve reductions; see Conscious Sedation.



Ibuprofen: 600â€“800 m g (peds: 5â€“10 m g/kg) PO t.i.d.



Naprosyn: 250â€“500 m g (peds: 10â€“20 m g/kg) PO b.i.d.



Tylenol with codeine no. 3: 1 or 2 tabs (peds: 0.5â€“1 m g/kg codeine) PO q4hâ€“q6h



Morphine sulfate: 0.1 m g/kg IV q2hâ€“q6h

Follow-Up Disposition Admission Criteria 

Vascular injuries, open fractures



Fractures requiring operative reduction or internal fixation

Pa ge 1 6 5



Adm it all patients with extensive swelling or ecchym osis for overnight observation and elevation to decrease risk for com partm ent syndrom e.

Discharge Criteria 

Stable fractures or reduced dislocations with none of above features



Splint and arrange orthopedic follow-up in 24â€“48 hours.



Uncom plicated soft tissue injuries

References 1. Anderson BC. Office Orthopedics for Prim ary Care: Diagnosis and Treatm ent. 2nd ed, Philadelphia: WB Saunders; 1999. 2. McCarty LP, Ring D, Jupiter JB. Managem ent of distal hum erus fractures. Am J Orthop. 2005;34(9):430â€“438. 3. Minkowitz B, et al. Supracondylar hum erus fractures: current trends and controversies. Orthop Clin North Am . 1994;25:4. 4. Nicholson DA, et al. ABC of em ergency radiology: the elbow. Br Med J. 1993;307:23. 5. Sim on R, Koenigsknecht S. Em ergency Orthopedics: The Extrem ities. 4th ed. East Norwalk, CT: Appleton & Lange; 1996.

Codes ICD9-CM 959.3

ICD10 S59.9

Pa ge 1 6 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Electrical Injury

Electrical Injury

Scot Hill

Basics Description 

Ohm 's law: Voltage (V) = current (I) Ã— resistance (R): o

Am perage (electron flow or current) is proportional to voltage (potential difference) and inversely proportional to resistance.





Levels of electrical exposure in voltage: o

Telephone lines: 65 V

o

Household circuits: 110 V

o

Electrical range or dryer: 220 V

o

Household power lines: 220 V

o

Subway third rail: 600 V

o

Residential trunk line: 7,620 V

Alternating current (AC): o

Has periodic reversal of electron flow (60 Hz in U.S.)

o

Found in residential power supply

o

Can produce tetanic m uscle contraction, prolonging contact

o

More likely to result in ventricular fibrillation at household current level



Direct current (DC):

Pa ge 1 6 5

o

Continuous electron flow in one direction

o

Defibrillators and pacem akers, industrial sources

o

Single forceful contraction, tends to throw patient from source

o 

More likely to result in asystole

Factors that increase severity of injury: o

High voltage (>600 V considered high voltage)

o

Higher current (am perage)

o

Lower resistance (wet skin 10 tim es less resistant than dry skin) allows m ore penetration.

o

Higher resistance m ay m ean m ore conversion of electricity to heat, m ore necrosis.

o

Longer tim e of contact with source (AC >DC)

o

Current pathway through susceptible vital organs (brain, spinal cord, heart)



Trim odal distribution of electrical injuries: o

Toddlers (household outlets and cords)

o

Teenagers (risk-taking behavior)

o

Adults (work-related injuries)

Etiology 

Types of electrical injury: o

o

Prim ary electrical phenom ena: 

Cardiac arrhythm ias



Muscle contractions and tetany

Tissue destruction: 

Electrotherm al burn m ay cause skin or deep tissue coagulation necrosis.



Burns from noncontact arcing



Burns from burning cloths or equipm ent



Minor visible injuries m ay be m isleading for extensive deep tissue injury.

o

Secondary injury from traum a:

Pa ge 1 6 5





Supraphysiologic m uscle contraction



Fall or being thrown

Tissue resistance: o

Blood and nerves least resistant

o

Fat and bone m ost resistant

o

Skin interm ediate resistance: 

o

Wet skin 10 tim es less resistant

More resistance m eans less flow, m ore conversion to heat.

Diagnosis Signs and Symptoms 



Sym ptom s and effects of electricity: o

0.2â€“2 m A AC: tingling sensation

o

1â€“4 m A AC: pain

o

6â€“22 m A AC: unable to let go/local tetany

o

30â€“50 m A AC: diaphragm /intercostal tetany

o

100 m A AC: ventricular fibrillation

o

1,000 m A AC: ventricular standstill

Severity ranges from m inor cutaneous burns to crush-type traum a involving deep tissues: o



Minor skin burns m ay m ask m ajor deep injury.

Cardiac: o

Cardiac standstill/asystole is leading cause of death from DC and high-voltage AC.

o

o

Ventricular fibrillation: 

Most com m on lethal dysrhythm ia



Induced by AC at household current 60 Hz

Other dysrhythm ias: sinus tachycardia, atrial fibrillation, and prem ature ventricular contractions

Pa ge 1 6 5

 o

Usually resolve spontaneously

Myocardial dam age occurs rarely: 

Generally epicardial, not transm ural



Dam age does not follow distribution of coronary arteries.

 

ECG will not show standard injury patterns.

Respiratory com prom ise m ay occur from : o

Brain injury causing respiratory center inhibition

o

Tetanic contraction of chest wall/diaphragm m uscles

o

Prolonged paralysis of respiratory m uscles

o

Postcardiac arrest respiratory arrest

o

Traum atic lung injury

o

Lung tissue itself appears resistant to electrical injury, probably owing to air content



Neurologic: o

o



Acute: 

Respiratory arrest



Am nesia



Altered m ental status, seizures, com a



Localized paresis up to/including quadriplegia

Delayed: 

Ascending paralysis



Transverse m yelitis



Am yotrophic lateral sclerosis



Reflex sym pathetic dystrophy

Vascular: o

Throm bosis in slow-m oving venous system owing to coagulation

o

Intim al injury in fast-m oving arterial system m ay lead to acute or delayed arterial m alfunction.

o 

Com partm ent syndrom es secondary to edem a

Renal failure secondary to m yoglobinuria

Pa ge 1 6 5



Orthopedic injuries result from : o

Supraphysiologic m uscle contraction from electrostim ulation





o

Secondary injury from traum a

o

Classically described injuries: 

Vertebral colum n fracture



Posterior shoulder dislocation



Fem oral neck fracture

Ophthalm ologic: o

Corneal burns

o

Intraocular hem orrhage

o

Uveitis

o

Retinal injuries

o

Delayed effects: 

Optic nerve atrophy



Cataracts (onset 4â€“6 m onths postinjury)

Derm atologic: o

Burns from current, arcing, or clothes burning

o

Contact/ground woundsâ€”hands, feet, and head m ost com m on sites

o

Kissing burns from current exit and re-entry on flexor surfaces

P.357

Pediatric Considerations 

Oral com m issure burn: o

Results from child biting electrical cord

o

Associated with bleeding from labial artery 3â€“5 days after injury

o

May heal with significant contractures

Pa ge 1 6 5

Pregnancy Considerations 

Fetus m uch less resistant to electrical shock than m other: o

All pregnant patients m ust undergo period of fetal m onitoring.

Essential Workup 

ECG



Urinalysis for m yoglobin



Cardiac m onitor: o

Prolonged m onitoring is probably not necessary in asym ptom atic patients with norm al ECG, no dysrhythm ias, and exposure to <240 V.

Tests Lab 

For m ost exposures to household current, no testing is indicated.



Urinalysis for m yoglobinuria



Creatinine kinase, electrolytes, blood urea nitrogen, creatinine:



o

Positive urine m yoglobin

o

High-voltage exposures

o

Provides baseline renal function

o

Hyperkalem ia owing to cell traum a.

o

Metabolic acidosis with significant injury

Cardiac m arkers in: o

Abnorm al ECG or dysrhythm ia

o

High-voltage exposures

Imaging Dictated by clinical need

Differential Diagnosis 

Therm al burns from electrical arcing flash injuries versus

Pa ge 1 6 5

deep electrotherm al injury 

Instability owing to traum atic injuries versus electrical burns

Treatment Pre Hospital 

Assum e traum atic injury in unstable or unconscious patient: o



Spinal precautions for transport

Standard basic life support/advanced cardiac life support care



Early cardiopulm onary resuscitation (CPR) in post-electric shock arrest m ay allow tim e for heart to restart.

Alert Care m ust be exercised at scene to ensure that rescuers do not contact live electrical sources.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Local wound care for therm al burns



Im m obilize/reduce fractures and dislocations.

ED Treatment 

Intravenous fluid resuscitation: o

Larger fluid volum es m ay be required owing to extensive third spacing in injured m uscle.

o

Rapid adm inistration to reach urine output of 1 m L/kg/h

o

Titrate to urine output and central venous pressure m easurem ent.

Pa ge 1 6 5

o 

Foley catheter

Prevent renal failure from m yoglobinuria: o

Maintain good urine output.

o

Intravenous bicarbonate increases solubility of m yoglobin in urine.

o

Furosem ide/m annitol

o

Monitor renal function.



Tetanus prophylaxis



Pain control as required

Medication (Drugs) 

Bicarbonate: one am pule IV, then two am pules added to 1 L of D 5 W to m aintain urine pH >7.45



Furosem ide: 0.5 m g/kg IV



Mannitol: 25 g (peds: 0.25â€“0.5 m g/kg) IV bolus, then 12.5 m g/kg/h IV titrated to urine flow >1 m L/kg/h

Follow-Up Disposition Admission Criteria 

Docum ented loss of consciousness



Dysrhythm ias, abnorm al ECG, or evidence of m yocardial dam age



Suspicion of deep tissue dam age



Myoglobinuria or acidosis



Burn criteria for adm ission



Traum atic injuries requiring adm ission

Discharge Criteria

Pa ge 1 6 6



Minor, low-voltage injury (<240 V) with no associated injuries and norm al ECG



Stable in ED after period of observation

Issues for Referral 

Burn wound care



Ophthalm ology

References 1. Bailey B, Gaudreault P, Thivierge R, et al. Cardiac m onitoring of children with household electrical injuries. Ann Em erg Med. 1995;25:612â€“617. 2. Fish R. Electrical injuries. Part III: cardiac m onitoring indications, the pregnant patient, and lightning. J Em erg Med. 2000;18:181â€“187. 3. Price TG, Cooper M. Electrical and lightning injuries. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:2011â€“2016. 4. Rai J, Jeschke M, Barrow R, et al. Electrical injuries: a 30-year review. J Traum a. 1999;46:933â€“936. 5. Subin J, Venkata B. Electrical and lightning injuries. Crit Care Clin. 1999;15:319â€“331.

Miscellaneous SEE ALSO: Burns; Lightening Injury; Rhabdom yolysis

Codes ICD9-CM 994.8 Electrocution and nonfatal effects of electric current E925 Electric current accident

Pa ge 1 6 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Encephalitis

Encephalitis

Arunchalam Einstein

Basics Description 

Acute infectious inflam m ation of the brain



20,000 cases in United States annually



Mortality 10%



Inflam m atory reaction occurs within brain parenchym a with destruction of neurons, parenchym al edem a, and petechial hem orrhages.



Route of CNS infection usually hem atogenous; search for another site



Neural m igration occurs with rabies, herpes sim plex virus (HSV), and varicella-zoster encephalitis.

Etiology 

Viral is m ost com m on.



50% of cases have no identifiable cause.

Specific Viruses 

HSV: o

10â€“20% of all encephalitides

o

Prim ary or reactivation

o

Early treatm ent im proves prognosis.

Pa ge 1 6 6



Arbovirus: o

10â€“15% of all encephalitides

o

Zoonotic transm ission (m osquitoes, ticks) in warm m onths

o

o

Eastern equine causes fulm inant encephalitis: 

Tropism for the hippocam pus



Abrupt onset of headache, fever, vom iting

Western equine occurs m ostly in the western two thirds of the United States: 

Often preceded by nonspecific upper respiratory/GI tract sym ptom s

o

Japaneseâ€”m ost prevalent arboviral encephalitis worldwide: 

Indolent course of fever, headache, m yalgias, and fatigue followed by confusion, delirium , m asklike facies, and parkinsonism s, seizures, brainstem dysfunction, com a, and death



Flavivirus: o

West Nile virusâ€”increased incidence in North Am erica: 

Found in m osquitoes and birds



Febrile illness, often with rash



Headache



Lym phadenopathy



Polyarthropathy



Increased m orbidity/m ortality in elderly patients



Enteroviral: o

Occurs m ainly in children <10 years old

o

Relatively benign course with little or no long-term sequelae



Measles encephalitis:

Pa ge 1 6 6

o

Occurs several days to 2â€“3 weeks after prim ary infection and rash, or after years of latent infection

o

Abrupt onset and rapid progression to com a

o

Seizures com m on (50â€“60%)

o

Postim m unization incidence of 1 per 1 m illion vaccinated



HIV encephalitis: o

Lower CD4 counts predispose to encephalitis.

o

Typical features include m otor spasticity and dem entia.

o

Involvem ent of white m atter with extensive neural degeneration



Rhabdovirus: rabies

Nonviral 

Mycoplasm a pneum oniae



Toxoplasm a gondii



Rickettsia rickettsii



Mycobacterium tuberculosis



Borrelia burgdorferi



Coccidioides im m itis



Leptospirosis

Immunocompromised/HIV Patients 

Histoplasm a



Cryptococcus neoform ans



Varicella-zoster



Listeria m onocytogenes



Cytom egalovirus



Toxoplasm a gondii



Hum an herpesvirus type 6 (HHV-6)

Pa ge 1 6 6

Diagnosis Signs and Symptoms 

Often begins with a preceding flulike illness over a few days: o

Mild headache, fever, sore throat, reduced appetite, m yalgias



Altered level of consciousness, drowsiness, com a



Im paired cognitive ability and personality change, hallucinations, psychosis



Restlessness, agitation, irritability, delirium



Rash: o

Lym e disease

o

Rocky Mountain spotted fever

o

Varicella

o

Herpes sim plex virus (HSV)



Seizures



Fever, headache, vom iting, possible m eningism us



Focal neurologic deficits, trem or, ataxia, cranial nerve palsies (m ore com m on than m eningitis)



Papilledem a on funduscopy



Clinical picture varies from m ild headache and m ild cognitive/em otional lability to severe agitation, seizures, com a, perm anent neurologic sequelae, and death.



Clinical course of sym ptom s m ay be slow m oving or rapidly progressive.

Essential Workup Lum bar punctureâ€”cerebrospinal fluid (CSF) analysis for: 

Cell count/chem istry: o

Elevated WBC, predom inantly lym phocytes

o

Elevated protein

o

Glucose (norm al in viral disease)

Pa ge 1 6 6

o

Gram stain with or without India ink for suspected/confirm ed HIV



Viral and bacterial cultures (fungi if indicated by history)



Antigen assays for o

HSV

o

Cryptococcus

o

Toxoplasm osis

o

Other viral antigen and antibody assays if available (enterovirus, adenovirus, cytom egalovirus, m um ps, and varicella-zoster)

P.359

Tests Lab 

CBC o

WBC usually elevated; however, a norm al WBC does not rule out infection



Electrolytes, glucose, BUN, creatinine



Bacterial and viral blood cultures



Liver function tests, am m onia level if hepatic failure suspected



Carboxyhem oglobin level if CO poisoning suspected



Toxicology screen if ingestion suspected in differential



Polym erase chain reaction (PCR) o

Confirm viral nucleic acids in CSF

o

HSV, varicella, enteroviruses, others

Imaging 

CT scan: o

To rule out traum a, hem orrhagic conditions, and m ass lesions

Pa ge 1 6 6

o

Cerebral edem a m ay be the only finding consistent with encephalitis.

o

HSV m ay show parenchym al hem orrhagic areas of the frontal and tem poral lobes, along with edem a.



MRI: o

Hypodense tem poral lobes in HSV

Differential Diagnosis 

Meningitis



Brain abscess



Sepsis



Stroke (hem orrhagic or ischem ic)



Head injury



Subarachnoid hem orrhage



Encephalopathy (hepatic, urem ic)



Metabolic: o

Electrolyte abnorm alities (Na 2 + , K + , Cl - , Ca 2 + , Mg 2 + , phosphate)

o

Hypoglycem ia

o

Hyperglycem ic nonketotic com a



Neoplastic



Drugs/toxins



Carbon m onoxide (CO) inhalation

Treatment Initial Stabilization 

Airway, breathing, and circulation (ABCs): o

Intubate patients who are obtunded/com atose/absent gag reflex.



Naloxone, thiam ine, glucose (or Accu-Chek) for altered

Pa ge 1 6 6

m ental status 

For signs of raised intracranial pressure on funduscopy or CT:



o

Hyperventilate to PCO 2 of 25â€“30 m m Hg

o

Adm inister m annitol.

o

Neurosurgical consult for suspected hydrocephalus

Run IV saline at KVO or half-m aintenance to avoid cerebral edem a.

ED Treatment 

Seizure control: o

Abort with diazepam .

o

Initiate antiseizure m edication (dilantin or phenobarbital) if m ore than one seizure has occurred.



No specific treatm ent for m ost viral encephalitides: o



Steroid use controversial

Treat HSV encephalitis with acyclovir IV: o

Initiate if considered likely based on clinical grounds, CT, and CSF findings



Initiate ganciclovir for suspected im m unocom prom ised related infections (cytom egalovirus [CMV], HHV-6)



Adm inister antibiotic to cover for m eningitis if diagnosis uncertain, especially when rash present (e.g., m eningococcem ia, rickettsia)

Medication (Drugs) 

Acyclovir: 5â€“10 m g/kg IV q8h, m ax. 15 m g/kg/d (peds: 30 m g/kg/24h IV q8h)



Diazepam : 5 m g IV (peds: 0.1â€“0.2 m g/kg IV or per rectum [PR]) per dose



Dilantin: loading dose 15 m g/kg IV to a m ax. 1 g

Pa ge 1 6 6



Ganciclovir: 5 m g/kg IV q12h



Mannitol: 0.5â€“1 g/kg of a 20% solution to run IV over 20â€“30 m inutes



Phenobarbital: load 15â€“20 m g/kg to 300â€“800 m g IV at 25â€“50 m g/m in

Follow-Up Disposition Admission Criteria All patients

References 1. Kim berlin DW, Whitley RJ. Viral encephalitis. Pediatr Rev. 1999;20:192â€“198. 2. Mandell GL, ed. Principles and Practice of Infectious Disease. 5th ed. New York: Churchill Livingstone; 2000. 3. Morgenstern LB, ed. Encephalitis. In: Neurologic Clinics. Vol. 17, No. 4. Philadelphia: WB Saunders; 1999. 4. Rakel RE, ed. Conn's Current Therapy 2002. 5th ed. Philadelphia: WB Saunders; 2002. 5. Solom on T. Flavivirus encephalitis. New Engl J Med. 2004;351:370â€“378.

Miscellaneous SEE ALSO: Meningitis

Codes ICD9-CM

Pa ge 1 6 6

323.9

ICD10 G04.9

Pa ge 1 6 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Endo carditis

Endocarditis

Michael S. Murphy

Basics Description 

A m icrobial infection of the endothelial surface of the heart



Characterized by the vegetation (a throm bus with superim posed m icroorganism s)



Older population



Frequently affects m en



Fewer patients at present dem onstrate the classic signs once noted by Osler



Risk factors: o

Poor dental hygiene

o

IV drug abuse (IVDA): 

Greater risk than rheum atic heart disease or prosthetic valves

o



Predilection for right-sided heart valves



Risk factor for recurrent endocarditis

Structural heart disease serves as com m on vegetative site due to altered intracardiac flow:

o



Mitral valve prolapse



Aortic valve dysfunction

Congenital heart disorders in the pediatric

Pa ge 1 6 7

populations: 

Tetralogy of Fallot



Aortic stenosis



Patent ductus arteriosus



Ventricular septal defects



Aortic coarctation

o

Prosthetic valves

o

Indwelling catheters

o

Any m echanical devices m ay serve as a portal of entry or attachm ent for m icroorganism s.

Etiology 



Major categories: o

Bacterial endocarditis

o

Prosthetic valve endocarditis

o

Nonbacterial throm botic endocarditis: 

Malignancy



Urem ia



Burns



System ic lupus erythem atosus

Com m on organism s: o

Streptococcus viridans 

Found in oropharynx, com m on agent in native valve endocarditis

o

Streptococcus bovis: 

Com m on association with colonic polyps or gastrointestinal m alignancy

o

Streptococcus pneum oniae: 

Causes rapid valvular destruction, abscess, and congestive heart failure (CHF)



Risk factor: alcoholism

o

Staphylococcus epiderm idis

o

Staphylococcus aureus

Pa ge 1 6 7



Seen in all populations, especially IVDA and toxic illness

 o

Som etim es m etastatic

Enterococci: 

Seen in young wom en and old m en following instrum entation or infection

o

Candida and Aspergillus 

Found in IVDA, prosthetic valves, or im m unocom prom ised patients

o

HACEK (Haem ophilus species)

o

Culture-negative endocarditis (Q fever, psittacosis, Bartonella, brucellosis)

Diagnosis Signs and Symptoms General 

Fever: o

Most com m on sym ptom

o

Often absent in certain settings: 

Elderly



CHF



Severe debility



Chronic renal failure



Flulike illness



Chills



Sweats



Rigors



Malaise

Head, Eyes, Ears, Nose, and Throat

Pa ge 1 6 7

Retinal hem orrhages or Roth spots

Respiratory 

Dyspnea



Cough

Cardiac A new or changing m urm ur in 80â€“85% of patients

Abdominal 

Abdom inal or back pain



Splenom egaly (15â€“50%)

Extremities 

Myalgias



Arthralgias



Digital clubbing

Neurologic Septic em bolization (stroke or m ycotic aneurysm )

Skin Cutaneous vasculitic lesions: 

Mucosal and conjunctival petechiae



Splinter hem orrhages



Osler nodes: o



Erythem atous, painful tender nodules

Janeway lesions: o

Erythem atous or hem orrhagic, m acular or nodular lesions, a few m illim eters in diam eter on the hands and feet

Essential Workup 

Identify risk factors for endocarditis in patients with fever of unknown etiology.



Blood cultures

Pa ge 1 6 7



Echocardiography is needed to confirm the diagnosis.

Tests Lab 



CBC: o

Anem ia (som etim es hem olytic)

o

Leukocytosis (with granulocytosis and bandem ia)

Blood cultures: o

Multiple sets (three sets over a tim e period) should be obtained before antibiotic adm inistration.



Elevated sedim entation rate and C-reactive protein (lacks specificity)



Urinalysis: o

Microscopic hem aturia

Imaging 

Chest radiography: o

CHF

o

Septic pulm onic em boli, which m ay be seen in right-sided endocarditis



ECG: o



Arrhythm ia, new heart block

Echocardiography: o

Acute valvular pathology

o

Abscess

o

Vegetations

o

Transesophageal echocardiography provides greater sensitivity.

Differential Diagnosis 

Rheum atic fever



Atrial m yxom a



Acute pericarditis

Pa ge 1 6 7



Myocardial infarction



Aortic dissection with regurgitant valve



Throm botic throm bocytopenic purpura



System ic lupus erythem atosus



Occult neoplasm with m etastasis



Septicem ia

P.361

Treatment Initial Stabilization 

Monitor for signs of heart failure



Operative repair if:



o

Severe valvular dysfunction causing failure

o

Unstable prosthesis

o

Perivalvular extension with intracardiac abscess

o

Antim icrobial therapy failure

o

Large or fungal vegetations

Antibiotic therapy: o

IV, bactericidal, and em piric, pending culture results

o

Native valve or congenital abnorm ality:

o



Penicillin G + nafcillin + gentam icin



Vancom ycin + gentam icin

Prosthetic valve or history of IVDA: 

Vancom ycin + gentam icin + rifam pin



Nafcillin + gentam icin + rifam pin (if m ethicillin-resistant S. aureus [MRSA] is not suspected)



If MRSA vancom ycin failure/intolerant consider

Pa ge 1 6 7

daptom ycin or quinupristin-dalfopristin 

Vancom ycin-resistant enterococcus faecium consider quinupristin-dalfopristin

o

Fungal: 

o

Am photericin B

HACEK: 

Ceftriaxone

Medication (Drugs) 

Am photericin B: o

Test dose 0.1 m g/kg up to 1 m g slow IV.

o

Wait 2â€“4 hours.

o

If tolerated, begin 0.25 m g/kg IV and advance to 0.6 m g/kg IV q.i.d.



Ceftriaxone: 2 g IV q.i.d.



Daptom ycin 4 m g/kg IV q.i.d.



Gentam icin: 1 m g/kg IV q8h



Nafcillin: 2 g IV q4h



Penicillin G: 20 m illion IU IV q.i.d.



Quinupristin-dalfopristin: 7.5 m g/kg IV q12h



Rifam pin: 600 m g PO q.i.d.



Vancom ycin: 15 m g/kg IV q12h

Follow-Up Disposition Admission Criteria 

Patients with risk factors who exhibit pathologic criteria or clinical findings

Pa ge 1 6 7



All IV drug users with fever



Adm it patients with cardiovascular instability to an intensive care unit/m onitored setting.

Discharge Criteria None

Expected Course Most patients will defervesce within 1 week.

Complications 

Cardiac: CHF, valve abscess, pericarditis, fistula



Neurologic: em bolic stroke, abscess, hem orrhage



Em bolization: CNS, pulm onary, ischem ic extrem ities



Mycotic aneurysm s: cerebral or system ic



Renal: infarction, nephritis, abscess



Metastatic abscess: kidney, spleen, tissue

References 1. Berbari E, Cockerill F, et al. Infective endocarditis due to unusual or fastidious m icroorganism s. Mayo Clin Proc. 1997;72:532â€“542. 2. Hogevik H, Alestig K. Fungal endocarditis: a report on seven cases and a brief review. Infection. 1996;24(1):17â€“21. 3. Karchm er A, Alestig K. Infective endocarditis. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 5th ed. Philadelphia: WB Saunders, 1996;1997:1077â€“1104. 4. Mylonakis E, Calderwood S. Infective endocarditis in adults. N Engl J Med. 2001;345(18):1318â€“1330. 5. Salm an L, Prince A, et al. Pediatric infective endocarditis in the m odern era. J Pediatr. 1993;122:847â€“853.

Codes ICD9-CM 421

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ICD10 I38

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Endo m etrio sis

Endometriosis

Christy Rosa Mohler

Basics Description Ectopic endom etrial tissue with cyclic horm onal responsiveness

Etiology 

Theories include retrograde m enstruation, im m unologic factors, and m etaplastic transform ation.



Invades tissues, spreads locally and hem atogenously

Pediatric Considerations Not seen before m enarche

Genetics Fam ilial disposition suggested by clinical, population, and twin studies

Diagnosis Signs and Symptoms History 

Pelvic or back pain, usually cyclic



Dysm enorrhea m ay be severe.

Pa ge 1 6 8



Dyspareunia



Infertility

Physical Exam 

Pelvic exam nonspecific: o

Rarely im m obile tender uterus or nodular m asses are present.



Abdom inal exam typically benign unless ruptured endom etriom a produces peritoneal signs



Endom etriosis has been found in the lungs, brain, and m any nonperitoneal sites; signs and sym ptom s can vary greatly depending on location of lesions.

Essential Workup 

Pregnancy test



Rule out other, life-threatening diagnoses, as directed by history and physical exam .

Tests Lab Pregnancy test

Imaging Pelvic ultrasound, CT, and MRI m ay show ovarian endom etriom as, but rarely reveal im plants.

Diagnostic Procedures/Surgery Laparoscopy usually required for definitive diagnosis

Differential Diagnosis 

Appendicitis



Ectopic pregnancy



Ovarian cysts



Ovarian torsion



Pelvic inflam m atory disease/tubo-ovarian abscess

Pa ge 1 6 8



Menstrual cram ps/m ittelschm erz



Inflam m atory bowel disease



Irritable bowel disease



Sm all bowel obstruction



Diverticulosis



Gastroenteritis

P.363

Treatment Initial Stabilization 

Manage hypotension initially with isotonic IV fluid.



For severe bleeding not responsive to IV fluid, m ay need transfusion of packed red blood cells (PRBC)

ED Treatment 

Analgesia



Gynecology consultation for large or ruptured endom etriom as



Oral contraceptives, gonadotropin-releasing horm one agonists (e.g., leuprolide [Lupron]), or other horm onal treatm ent m ay be started in consultation with the prim ary care physician or gynecologist.

Medication (Drugs) 

Acetam inophen: 650 m g to 1 g PO



Ibuprofen: 400â€“800 m g PO



Ketorolac: 30 m g IM/IV

Pa ge 1 6 8



Morphine: 4â€“8 m g IM/IV or equivalent analgesic

Follow-Up Disposition Admission Criteria 

Intractable pain



Unclear diagnosis to follow serial exam s or for further workup and treatm ent



Ruptured endom etriom a with peritoneal signs

Discharge Criteria Most patients with a clear exacerbation of endom etriosis can be discharged with gynecology referral once pain is controlled.

References 1. Dart R. Acute pelvic pain. In: Marx JA, et al, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosbyâ€“Year Book; 2002:219â€“226. 2. Giudice LC, Kao LC. Endom etriosis. Lancet. 2004;364:1789â€“1799. 3. Morrison LJ, Spence JM. Gynecology and obstetrics: abdom inal and pelvic pain in the non pregnant patient. In: Tintinalli JE, ed. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:655â€“657.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epididym itis/Orchitis

Epididymitis/Orchitis Matthew D. Cook

Basics Description Epididymitis 

Definition: inflam m ation or infection of the epididym is



Rare in prepubertal boys



Pathogenesis: o

o

Initial stages: 

Cellular inflam m ation begins in vas deferens



Descends to lower pole of epididym is

Acute phase: 

Epididym is is swollen and indurated in upper and lower poles.

 o

Sperm atic cord thickened

Testis m ay becom e edem atous owing to passive congestion or inflam m ation.

o

Resolution: 

May be com plete without sequelae



Peritubular fibrosis m ay develop, occluding ductules



Com plications:

Pa ge 1 6 8

o

Two thirds of m en have atrophy due to partial vascular throm bosis of testicular artery.

o

Abscess and infarction rare (5%)

o

Incidence of infertility with unilateral epididym itis unknown: 

50% with bilateral epididym itis

Orchitis 

Definition: inflam m ation or infection of the testicle: o

Usually from direct extension of the sam e process within the epididym is

o

Isolated testicular infection is rare: 

Can result from hem atogenous spread of bacteria or following m um ps infection



Categories: o

Pyogenic bacterial orchitis secondary to bacterial involvem ent of epididym is

o

Viral orchitis: 

Most com m only due to m um ps



Rare in prepubertal boys; occurs in 20â€“30% of postpubertal boys with m um ps.



Occurs 4â€“6 days after parotitis but can occur without parotitis.



Unilateral in 70% of patients



Usually resolution in 6â€“10 days



30â€“50% of testes involved have residual atrophy; rarely affects fertility.

o

Granulom atous orchitis: 

Syphilis



Mycobacterium and fungal diseases



Usually occurs in im m unocom prom ised host

Etiology

Pa ge 1 6 8

Epididymitis 

Children: o

Coliform or pseudom onal urinary tract infections

o

Sexually transm itted diseases rare in prepubertal m ales

o

Associated with predisposing abnorm alities of lower urinary tract



Young m en, age <35 years: o

Usually sexually transm itted

o

Chlam ydia trachom atis (28â€“88%) with severe inflam m ation with m inim al destruction

o

Neisseria gonorrhoeae (3â€“28%)

o

Coliform bacteria (7â€“24%): 

Highly destructive with tendency for abscess



Coliform bacteria m ore com m on in insertive partners in anal intercourse

o

Ureaplasm a urealyticum (sole organism in only 6% of cases)



Older m en, age >35 years: o

Com m only associated with underlying urologic pathology (benign prostatic hypertrophy, prostate cancer, strictures)

o

May have acute or chronic bacterial prostatitis

o

Coliform bacteria m ore com m on (23â€“67%), especially after instrum entation



o

Chlam ydia trachom atis (8â€“80%)

o

Klebsiella and Pseudom onas species

o

Neisseria gonorrhoeae (15%)

o

Gram -positive cocci

Drug related: o

Am iodarone-induced epididym itis: 

Usually with am iodarone levels higher than

Pa ge 1 6 8

therapeutic levels 

Granulom atous: o

Syphilis or m ycobacterial and fungal causes: 

May be presenting feature of Mycobacterium tuberculosis in high prevalence regions

 

Urine cultures often negative for M. tuberculosis

Vasculitis: o

Polyarteritis nodosa

o

BehÃ§et disease

o

Henoch-SchÃ¶nlein purpura

Orchitis 



Pyogenic bacterial orchitis: o

Escherichia coli

o

Klebsiella pneum oniae

o

Pseudom onas aeruginosa

o

Staphylococci

o

Streptococci

Viral orchitis: o

Mum ps: 

20% m ay develop epididym oorchitis



Rarely associated with live-attenuated m um ps vaccine

o 

Coxsackie A and lym phocytic choriom eningitis virus

Granulom atous orchitis: syphilis and m ycobacterial and fungal diseases



Fungal orchitis: o

Blastom ycosis in endem ic regions

o

Invasive candidal infections in im m unosuppressed hosts



Posttraum atic orchitis: inflam m ation

Pa ge 1 6 8

Diagnosis Signs and Symptoms History 

Gradual onset of m ild to m oderate testicular or scrotal pain, usually unilateral



Progressive scrotal swelling



Dysuria (30%):



o

Recent urinary tract infection

o

History of abnorm al bladder function

Urethral discharge: o

Of patients with gonococcal epididym itis, 21â€“30% did not com plain of urethral discharge

o

No dem onstrable urethral discharge in 50%



Fever (14â€“28%)



Recent urethral instrum entation or catheterization

Physical Exam 

Tenderness in groin, lower abdom en, or scrotum



Scrotal skin com m only erythem atous and warm (60%)



Early: o



May feel swollen, indurated epididym is

Later: o

May not be able to distinguish epididym is from testis



Sperm atic cord m ay be edem atous.



Intact crem asteric reflex and Prehn sign: o

Pain relief with testicular elevation

o

Com m only observed but not specific



Coexistent prostatitis is rare (8%)



Pyogenic bacterial orchitis: o

Patients usually are acutely ill.

Pa ge 1 6 8

o

Fever

o

Intense discom fort

o

Swelling of testicle

o

Often reactive hydrocele

Essential Workup 

Must differentiate from testicular torsion



Early consultation with urologist if strong suspicion of testicular torsion

Tests Lab 

CBC: o



Often leukocytosis in range of 10,000â€“30,000/m m 3

Urinalysis and culture: o

15â€“50% of patients with epididym oorchitis have pyuria

o

24% of patients have positive urine bacterial cultures

o

Urine chlam ydial enzym e im m unoassay low sensitivity (50â€“70%)



Urethral swab (50â€“73% have dem onstrable urethritis despite m inority of sym ptom s): o

Gram stain and culture

o

Chlam ydia testing

o

Avoid bladder em ptying within two hours of tests (lowers sensitivity)

o 

Especially for postpubertal and sexually active

Blood culture if system ically ill

P.365

Imaging

Pa ge 1 6 8



Ultrasonography: color Doppler im aging: o

82â€“100% sensitivity, 100% specificity in detecting testicular torsion or decreased blood flow

o

o

Epididym oorchitis: 

Hyperem ia



Increased vascularity and blood flow

Advantages: 

Can evaluate for epididym itis or other causes of scrotal pain

 o



70% sensitivity, 88% specificity for epididym itis

Disadvantages: 

Highly exam iner dependent



Difficult in infants or children

Testicular scintigraphy: o

Radionuclide study to assess perfusion

o

90â€“100% sensitivity, 89â€“97% specificity in detecting testicular torsion

o

Inflam m atory processes have increased flow and uptake

o

o

False-positive scans: 

Large fluid collections in scrotum



Abscess



Hydrocele, hem atocele



Bowel herniation

False-negative scans: 

Early torsion



Spontaneous detorsion



Sm all children or infants

Diagnostic Procedures/Surgery Surgical indications: 

Scrotal abscess



If another scrotal problem , such as torsion, cannot be

Pa ge 1 6 9

excluded 

Suspected or proved ischem ia caused by severe epididym itis



Patient with solitary testicle



Scrotal fixation: indicates severe inflam m ation and potential suppuration

Differential Diagnosis 

Testicular torsion



Testicular tum or



Torsion of testicular appendages



Traum a to scrotum



Acute hernia



Acute hydrocele

Treatment Pre Hospital 

IV access



IV fluids, especially if system ically ill

Initial Stabilization 

IV access



IV fluids, especially if system ically ill

ED Treatment 

Antibiotics: o

Cover for chlam ydial and gonococcal etiologies if adult or presum ed sexually transm itted

o

Cover for coliform etiology: 

Child, or adult >35 years of age



Insertive partner in anal intercourse

Pa ge 1 6 9



Presum ed nonsexually transm itted

o

Adjust according to culture and sensitivity

o

Treat sexual partners



Bed rest and scrotal support



Ice packs



Analgesics and ant inflam m atories

Medication (Drugs) Age <35 Years or Sexually Active Postpubertal Males 

Prim ary: ceftriaxone 250 m g IM for one day, plus doxycycline 100 m g PO b.i.d. for 10 days



Alternative: ofloxacin 300 m g PO b.i.d. for 10 days

Age >35 Years or Insertive Partners in Anal Intercourse 

Prim ary: ciprofloxacin 500 m g PO b.i.d. or 400 m g IV b.i.d. (or ofloxacin 300 m g PO b.i.d. or levofloxacin 750 m g PO/IV per day) for 10â€“14 days



Alternative: am picillin/sulbactam 3 g IV q6h or cefotaxim e 2 g IV q8h or ceftriaxone 2 g IV per day

Children 

Azithrom ycin: 10 m g/kg PO day 1, 5 m g/kg PO per day 2 through 10 or TMP-SMX 4 m g/kg TMP and 20 m g/kg SMX b.i.d. for 10â€“14 days



Avoid quinolones and tetracyclines in children.

Follow-Up

Pa ge 1 6 9

Disposition Admission Criteria 

Surgical indications present



Older age group if it is the only way to ensure appropriate workup: o

Many will have underlying urologic pathology.



System ically ill, fever, nausea, vom iting



Scrotal abscess



Intractable pain

Discharge Criteria 

Fails to m eet adm ission criteria



Patient with good follow-up



Able to take oral antibiotics

Issues for Referral Urologic consultation and follow-up: 



Children need workup for urologic abnorm alities: o

Voiding cystourethrography

o

Renal ultrasound

If bacteriuria present, exam ination of lower tract with cystoscopy after treatm ent com pleted

References 1. Herberner TE. Ultrasound in the assessm ent of the acute scrotum . J Clin Ultrasound. 1996;24:405â€“421. 2. Kass EJ, Lundak B. The acute scrotum . Pediatr Clin North Am . 1997;44:1251â€“1266. 3. Luzzi GA, O'Brien TS. Acute epididym itis. Br J Urol Int. 2001;87:747â€“755. 4. Marcozzi D, Suner S. The nontraum atic acute scrotum . Em erg Med Clin North Am . 2001;19:547â€“568.

Codes

Pa ge 1 6 9

ICD9-CM 604.90

ICD10 N45.9

Pa ge 1 6 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epidural Abscess

Epidural Abscess

Richard S. Krause

Basics Description 

Pyogenic infection of epidural space



Most com m on in thoracic spine, followed by lum bar and cervical areas

Etiology 

Focus of infection is present followed by either hem atogenous spread (approxim ately 50%) or direct extension.



Most com m on source is skin infection: o



Staphylococcus aureus accounts for >50% of cases: o



Any pyogenic infection m ay be source.

Streptococcus is second m ost com m on.

Haem ophilus influenzae, gram -negative bacilli, m ycobacteria, anaerobic and m ixed infections also occur.



May occur after lum bar puncture (usually follows m ultiple attem pts)

Pediatric Considerations 

Children present sim ilar to adults with back pain, fever, and neurologic signs as well as nonspecific system ic

Pa ge 1 6 9

sym ptom s. 

Infants m ay exhibit only fever, irritability, and associated m eningitis.



Sphincter disturbance is frequently seen.



Most cases are secondary to hem atogenous spread.



Location and bacteriology sim ilar to adults

Diagnosis Fever and severe back pain represent â€œred flagâ€• for potentially serious condition: 

If pain is radicular or there is neurologic disturbance, likelihood of epidural abscess is increased.

Signs and Symptoms 



Classic presentation: o

Severe, progressive back pain (often radicular)

o

Fever

o

Neurologic deficit: 

Weakness or paralysis



Sensory level



Sphincter disturbance

May present with signs and sym ptom s of sepsis without prom inent back pain



Occurs at all ages including infants: o



Peak is at ages 60â€“70 years

Most patients have predisposing condition: o

IV drug abuse

o

Diabetes

o

Malignancy

o

Chronic steroids

o

Chronic alcoholism

Pa ge 1 6 9

o 

Instrum entation or spinal surgery

May occur in absence of identifiable predisposing factors

Essential Workup 

History should include predisposing conditions when this diagnosis is suspected.



Physical exam for source of infection, localized spinal tenderness, and neurologic findings:



o

Especially decreased sphincter tone

o

Saddle anesthesia

o

Lower extrem ity weakness

Voided urine followed by postvoid catheterization: o

Younger adults should have <50 m L postvoid residual urine.

o

Older adults m ay norm ally have higher residuals up to 100 m L.



Erythrocyte sedim entation rate (ESR) as below



MRI with and without gadolinium contrast is the diagnostic test of choice: o

When not available, obtain CT m yelogram or CT with IV contrast (least sensitive).

o

Suspected epidural abscess is true neurosurgical em ergency and requires em ergent im aging.

Tests Lab 

ESR is alm ost always elevated (approxim ately 100%), but is nonspecific: o

Norm al ESR m akes diagnosis m uch less likely.



C-reactive protein nearly always elevated.



Blood cultures are often positive (approxim ately 60%).



Leukocytosis with left shift is com m on (approxim ately 70%).

Pa ge 1 6 9



Cerebrospinal fluid (CSF) is often abnorm al, but is nondiagnostic; routine lum bar puncture should be avoided when epidural abscess is suspected (m ay cause m eningitis).

Imaging 

MRI is at least 90% sensitive: o



Shows high-intensity lesion on T2 im aging

Myelography and CT m yelography are also sensitive, but risk dissem ination.



Plain film s are usually abnorm al but nonspecific: o

May dem onstrate occult traum atic injury

Differential Diagnosis 

Diagnosis is difficult owing to rarity of condition and nonspecific sym ptom s: o

Multiple physician encounters com m only precede diagnosis.

o

Most com m on initial diagnosis is benign m usculoskeletal pathology



Early presentation: m uscular or ligam entous pain, degenerative arthritis, com pression fracture, discogenic pain





Back pain with fever, system ic signs and sym ptom s: o

Vertebral osteom yelitis

o

Spinal tum or

o

Meningitis

o

Spinal subdural abscess

o

Discitis

o

Pyelonephritis

Back pain with neurologic signs and sym ptom s: o

Cord com pression

o

Cord ischem ia

Pa ge 1 6 9

o

Disc herniation

Pediatric Considerations Fever and back pain should be urgently investigated with MRI when epidural abscess is suspected. P.367

Treatment Pre Hospital Spinal im m obilization if traum a suspected or neurologic deficits present

Initial Stabilization 

Broad-spectrum parenteral antibiotics early for signs of sepsis: o

Must include coverage for S. aureus, streptococci, and gram -negative rods



Ceftriaxone and clindam ycin are appropriate initial coverage.

ED Treatment 

Urgent im aging essential when diagnosis is considered



Delay in definitive treatm ent is associated with poor outcom e.



If unable to localize lesion on physical exam , consider im aging entire spine.



Urgent neurosurgical consultation or transfer for definitive therapy (surgical decom pression) after diagnosis and antibiotic prescription:

Pa ge 1 6 9

o

Som e cases have been treated nonsurgically (prolonged antibiotics).

Medication (Drugs) 

Ceftriaxone: 1â€“2 g IV q12h



Clindam ycin: 600â€“900 m g IV q8h

Follow-Up Disposition Admission Criteria 

Suspected epidural abscess should be adm itted; MRI is needed em ergently; transfer patient if necessary.



Patients with spinal epidural abscess require adm ission to facility with neurosurgical capability.

Discharge Criteria Patients with epidural abscess should not be discharged.

References 1. Davis DP, Wold RM, Patel RJ. The clinical presentation and im pact of diagnostic delays on em ergency departm ent patients with spinal epidural abscess. J Em erg Med. 2004;26(3):285â€“291. 2. Huang RC, Durbhakula MM. Spinal epidural abscess. Contem p Spine Surg. 2005;6(5):31â€“36. 3. Lyu R, et al. Spinal epidural abscess successfully treated with percutaneous, com puted tom ography-guided, needle aspiration and parenteral antibiotic therapy: case report and review of the literature. Neurosurgery. 2002;51(2):509â€“512. 4. Martin MJ, Yuan HA. Neurosurgical care of spinal epidural,

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subdural, and intram edullary abscesses and arachnoiditis. Orthop Clin North Am . 1996;27(1):125â€“136. 5. Rubin G, et al. Spinal epidural abscess in the pediatric age group: case report and review of the literature. Pediatr Infect Dis J. 1993;12:1007â€“1011. 6. Siddiq F, et al. Medical vs surgical m anagem ent of spinal epidural abscess. Arch Int Med. 2004;164:2409â€“2412. 7. Soehle M, Wallenfang T. Spinal epidural abscesses: clinical m anifestations, prognostic factors, and outcom es. Neurosurgery. 2002;51(1):79â€“87.

Codes ICD9-CM 324.9

ICD10 G06.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epidural Hem ato m a

Epidural

Hematoma Colleen Campbell

Basics Description 

Direct skull traum a



Inward bending of calvarium causes bleeding when dura separates from skull: o

Middle m eningeal artery is involved in bleed >50% of tim e.



o

Meningeal vein is involved in one third.

o

Diploic venous sinus bleed is seen in <10%.

Skull fracture is associated in 75% of cases, less com m only in children.



Greater than 50% have epidural hem atom a (EDH) as isolated head injury: o

Most com m only associated with subdural hem atom a (SDH) and cerebral contusion



Classic CT finding is lenticular, unilateral convexity, usually in tem poral region



It usually does not cross suture lines, but m ay cross m idline.

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Etiology 

Accounts for 1.5% of traum atic brain injury (TBI)



Male/fem ale incidence is 3:1.



Peak incidence is second to third decade of life.



Motor vehicle accidents (MVAs), assault, and falls are m ost com m on causes: o

Of all blunt m echanism s, assault has highest association with intracranial injury requiring neurosurgical intervention.



Uncom m on in very young (younger than 5 years) or elderly patients



Mortality is 12% and is related to preoperative condition.

Pediatric Considerations 

Head injury is the m ost com m on cause of death and acquired disability in childhood.



Falls, pedestrian-struck bicycle accidents are m ost com m on causes:



o

Most severe head injuries in children are from MVA.

o

Always consider possibility of nonaccidental traum a.

Less than 50% have altered level of consciousness (LOC): o

If EDH in differential diagnosis (DD), CT should be obtained



Bleeding is m ore likely to be venous.



Good outcom e in 95% of children younger than 5 years

Diagnosis Signs and Symptoms History 

Altered or deteriorating LOC

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

LOC: 85% will have at som e point in course o



Only 11â€“30% will have a lucid interval.

Nausea and vom iting: 40%

Pediatric Considerations 

Many tim es the only clinical sign is drop in hem atocrit (Hct) of 40% in infants.



Bulging fontanel with vom iting, seizures, or lethargy also suggest EDH in infants.



Less than 50% of children have LOC at tim e of injury.



Posterior fossa lesions are seen m ore com m only in children.

Physical Exam 

Pupillary dilation: 20â€“40%: o



Usually on sam e side as lesion (90%)

Hem iparesis m ore than one third: o

Usually on opposite side from lesion (80%)

Essential Workup Head im aging as below

Tests Lab 

Arterial blood gas (ABG), CBC, chem istry, PT/PTT



Blood ETOH and drug screen as appropriate

Imaging 

Noncontrast CT of head: o

Adm ission perfusion CT m ay help predict prognosis.

o

Lenticular, biconvex hem atom a with sm ooth borders m ay be seen.

o 

Most com m only seen in tem poral parietal region

Plain film s m ay show skull fractures: o

CT with bone windows is m ore often used.

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

Spine series



Further workup of traum a as indicated

Pediatric Considerations Ultrasound (US) m ay be used for diagnosis in infants with open fontanels.

Differential Diagnosis 

History of recent head traum a lends itself to the diagnosis: o



Traum a m ay be m inor in infants and toddlers.

Consider other diagnosis: o

SDH

o

Cerebral concussion/contusion

o

Intracerebral bleed

o

Diffuse axonal injury

o

Subdural hygrom a

o

Shaken baby syndrom e

o

Toxic, m etabolic, or infectious causes

Treatment Pre Hospital 

Head-injured patients have im proved outcom e when triaged to regional traum a centers.



Spinal im m obilization is essential.



Ensure adequate oxygenation throughout transport: o

Intubation and airway protection m ay be necessary.

Initial Stabilization 

Prevent hypoxia and hypotension: o

Rapid-sequence intubation for signs of deterioration or increased intracranial pressure (ICP)

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o

Controlled ventilation to PCO 2 of 35â€“40 m m Hg

o

Avoid hyperventilation unless signs of brain herniation are present.

o

Avoid induction agents, which m ay increase ICP (e.g., ketam ine).



Elevate head of bed 15â€“20% after adequate fluid resuscitation.



Perform rapid neurologic assessm ent: o

o 

Glasgow com a scale (GCS) score: 

14â€“15; m inor head injury



9â€“13; m oderate head injury



Less than 8; severe

Reflexes; pupils, corneal, gag, brain stem reflexes

Secondary survey will reveal coexisting injury in >50%.

ED Treatment 

Early surgical intervention (<4 hours) in com atose patients with EDH im proves m eaningful survival: o

Burr hole is placed at fracture site or side with ipsilateral pupillary dilation.

o

Rapid craniectom y is occasionally perform ed if bleeding is not controlled at site of burr hole.

P.369



Nonsurgical intervention in asym ptom atic patients is associated with high rate of deterioration; >30% require surgical intervention.



Maintain euvolem ia with isotonic fluids: o

Arterial line placem ent for close m onitoring of MAP, PO 2 , PCO 2

o 

Foley catheter to m onitor input/output (I/O) status

Control ICP:

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o

Prevent pain, posturing, and increased respiratory effort: 

Sedation with benzodiazepines



Neurom uscular blockade with vecuronium or pancuronium in intubated patients



Etom idate is good induction agent.



Barbiturate com a should be initiated for refractory increased ICP in neurosurgical ICU.

o

Mannitol m ay be used once euvolem ic: 

Shown to increase MAP less than coronary perfusion pressure (CPP) and cerebral blood flow (CBF), as well as decrease ICP



Keep osm olality between 295 and 310.



Use furosem ide (Lasix) as adjunct only if no risk of hypovolem ia.

o

Treat hypertension: 



Labetalol or hydralazine

Treat hyperglycem ia if present: o

Associated with increased lactic acidosis and m ortality in patients with TBI



Treat and prevent seizures: o





Diazepam and dilantin

Not considered helpful: o

Steroids

o

Antibiotic prophylaxis

o

Hyperventilation in absence of herniation

o

Fluid restriction

o

Calcium channel blockers

Factors associated with poor outcom e: o

Age greater than 40 years

o

Increased adm ission base deficit

o

Large hem atom a with rapid expansion

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o

Increased m idline shift

o

Lower adm ission GCS or unconsciousness at presentation

o

Postoperative ICP >3

o

Prolonged anisocoria

o

Associated brain injuries or concom itant traum a injuries

Pediatric Considerations 

Hem odynam ically significant blood loss can result from scalp lacerations and subgaleal hem atom as: o

Direct pressure and control of bleeding is indicated.

Medication (Drugs) 

Diazepam : 5â€“10 m g (peds: 0.1â€“0.2 m g/kg) IV



Dilantin: adult/peds: load 18 m g/kg at 25â€“50 m g/m in



Etom idate: 3 m g/kg IV



Furosem ide (Lasix): adults/peds: 0.5 m g/kg IV



Hydralazine: 10/m g/h IV (peds: safety not established)



Labetalol: 15â€“30 m g/h IV (peds: safety not established)



Lidocaine: as preinduction agent, 1.5 m g/kg IV



Mannitol: adults/peds: 0.25â€“1 g/kg IV q4h



Pentobarbital: 1â€“5 m g IV q6h



Thiopental: as induction agent, 20 m g/kg IV



Versed: 2â€“4 m g/h IV PRN (peds: 0.15 m g/kg IV)

Pediatric Considerations Hypertonic saline has been shown to be beneficial in som e pediatric studies (1.7â€“3%).

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Follow-Up Disposition Admission Criteria All patients with CT abnorm ality or altered LOC should be adm itted to ICU setting with frequent neurologic assessm ent: 

Patients should have repeated CT exam ination in 12â€“24 hours or if clinical deterioration occurs.



Patients at increased risk of deterioration include those with rapid bleeds, associated skull fracture, or lower GCS or neurologic deficits.

Discharge Criteria Adm ission is necessary for all patients with EDH.

References 1. Dias MS. Traum atic brain and spinal cord injury. Pediat Clin North Am . 2004;51(2):272â€“303. 2. Marik PE. Managem ent of head traum a. Chest. 2002;122(2):699â€“711. 3. Ono JI, et al. Outcom e prediction in severe head injury: analyses of clinical prognostic factors. J Clin Neurosci. 2001;8(2):120â€“123. 4. Stieg PE, Kase CS. Neurologic em ergencies: intracranial hem orrhage: diagnosis and em ergency m anagem ent. Neurol Clin. 1998;16(2):373â€“390. 5. Vincent JL, Berre J. Prim er on m edical m anagem ent of severe brain injury. Crit Care Med. 2005;33(6):1392â€“1399. 6. Zink BJ. Traum atic brain injury outcom e: concepts for em ergency care. Ann Em erg Med. 2001;37(3):318â€“332.

Codes ICD9-CM 852.40

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ICD10 S06.4

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epiglo ttis, Pediatric

Epiglottis,

Pediatric Beverly Bauman

Basics Description 

Inflam m ation of the epiglottis and surrounding supraglottic region, which is potentially life threatening owing to airway obstruction



Children are at greater risk of upper airway obstruction owing to: o

Decreased cross-sectional area of the upper airway (resistance is proportional to the inverse of the radius to the fourth power)

o

Loose attachm ent of m ucosal surface and increased vascularity of m ucosa allows for edem a

o 

Dynam ic collapse of the airway

A precipitous decline in the incidence of childhood epiglottitis since the introduction of the Haem ophilus influenzae vaccination, although vaccine failure m ay result in rare cases am ong children who have been im m unized



In the post-Hib vaccine era, the m ean age for this disease has increased, and it is now m ore com m only seen in

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adolescents and adults than in toddlers or young school-aged children. 

May occur throughout the year

Alert All patients with suspected epiglottis require intensive m onitoring and intervention. Rapid progression of airway obstruction m ay occur.

Etiology 

Infection: o

H. influenzae type B

o

S. pneum oniae

o

Group A Î²-hem olytic Streptococcus

o

Staphylococcus aureus

o

Viruses

o

Less com m on infections include Klebsiella, Pseudom onas, Candida



Caustic



Therm al



Traum atic



Posttransplant lym phoproliferative disorder

Diagnosis Signs and Symptoms History 

Usually fulm inant presentation without prodrom al illness



General: o

Irritability, throat pain, fever, noisy breathing

o

Progressive toxicity and respiratory distress

Physical Exam

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





General: o

Toxic appearing

o

High fever is typical.

Throat: o

Drooling

o

Dysphagia

o

Muffled â€œhot potatoâ€• voice

Respiratory: o

Rapidly progressive respiratory distress (dyspnea in only one third of adults)

o

Children usually prefer to sit upright, leaning forward with open m outh (â€œtripod sniffing positionâ€•) to m axim ize air entry.

o

Subtle stridor that m ay progress to severe stridor (stridor in only 10% of adults)



Com plications: o

Airway obstruction is the m ost severe com plication.

o

Epiglottic abscess

o

Associated pneum onia and atelectasis

Essential Workup 

Epiglottitis is a clinical diagnosis.



Indirect laryngoscopy or any attem pts to directly visualize the epiglottis are not indicated in children with suspected epiglottis unless perform ed in a controlled environm ent (In adolescents or adults, use of fiberoptic nasopharyngoscope m ay be indicated for patients without im pending airway obstruction).



If infection is suspected, obtain cultures of the epiglottis during laryngoscopy after airway is secure.

Tests Lab

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

Avoid laboratory tests until airway is controlled.



Throat cultures after control of airway



Blood cultures after airway is secure: o

Often positive if H. influenzae is the pathogen

Imaging Radiographs of the soft tissue lateral neck: 

Usually not necessary to m ake the diagnosis



Create additional risk by delaying stabilization of the airway, prom oting airway obstruction by agitating the patient, and often rem oving the child from the ED to an uncontrolled environm ent



Variable findings: o

Norm al

o

Swelling of the epiglottis (â€œthum bprint signâ€•) and often supraglottic region

o

Ballooned hypopharynx

o

Obliteration of vallecula

o

EW/C3W (epiglottic width to third cervical vertebral body width) ratio of >0.5

Diagnostic Procedures/Surgery Laryngoscopy: 

In a controlled environm ent whenever possible



Cultures of the epiglottis during laryngoscopy after the airway is secured m ay help identify pathogens and direct treatm ent.



Epiglottis will appear swollen, inflam ed, reddened.

Differential Diagnosis 

Other infectious processes: o

Bacterial tracheitis

o

Mononucleosis

o

Diphtheria

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o

Pertussis

o

Croup or laryngotracheobronchitis (prim arily in younger children, but there is a significant overlap in the ages of presentation)

o

Ludwig angina

o

Peritonsillar infection

o

Retropharyngeal abscess



Anaphylactic reaction with angioedem a



Foreign body in upper airway



Laryngeal traum a



Laryngospasm



Inhalation or aspiration of toxins (e.g., hydrocarbons)



Airway burns (have been related to crack cocaine)



Hyperventilation



CNS disorders

Treatment Pre Hospital Degree and m ode of intervention m ust reflect degree of obstruction, tim e and m eans of transport, capability of care providers, etc. Consult and notify receiving hospital.

Initial Stabilization Airway m anagem ent if patient is in extrem is: 

Bag-valve-m ask ventilation with 100% O 2 with cricoid pressure often provides adequate ventilation and tim e to prepare for intubation and m ove to a controlled setting such as the OR.



Oral intubation: o

Use an endotracheal tube (ETT) size that is one or

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two sizes sm aller than indicated by age or length. o

Direct com pression of the anterior neck in the glottic region m ay help visualize air bubbles at the opening of the swollen glottis.



If oral intubation fails: o

Em ergent cricothyrotom y or needle cricothyrotom y if age older than 10â€“12 years

o

Needle cricothyrotom y if age younger than 10â€“12 years

P.373

ED Treatment 

One hundred percent O 2 as tolerated by patient



Allow child to rem ain in position of com fort and do not force child to lie down, which m ay worsen airway obstruction.



Although not proven, racem ic epinephrine or L-epinephrine by nebulizer m ay tem porize sym ptom s while plans for a definitive airway are rapidly arranged. It m ust be done with caution to avoid agitating the child.



Avoid procedures that agitate the child such as IV access and blood draws.



Em piric invasive airway m anagem ent m ay be indicated: o

Patients with rapidly progressive respiratory difficulty, tachypnea, worsening throat pain, tachycardia, or hypoxem ia

o

Patients at high risk of acute obstruction (e.g., children with im m unodeficiency disorders)



Intubate in OR or controlled environm ent by m ost skilled person.



Use inhalational anesthesia before intubation.

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

Have appropriate various diam eters of endotracheal tubes available to accom m odate the inflam ed supraglottic region.



Surgical backup is required in case intubation is not possible; then em ergency tracheotom y or cricothyrotom y can be perform ed.



Equipm ent for intubation and for a surgical airway or needle cricothyrotom y m ust be available at the bedside.



Adm inister IV antibiotics: Second- or third-generation cephalosporins are active against Î²-lactam aseâ€“producing H. influenzae.



Steroids are controversial but frequently adm inistered, particularly in patients with chem ical or therm al epiglottitis.

Medication (Drugs) 

Am picillin/Sulbactam : 100â€“200 m g/kg/24h q6h IV



Am picillin: 100â€“200 m g/kg/24h q6h IM/IV; given with chloram phenicol



Cefotaxim e: 150 m g/kg/24h q8h IV



Ceftriaxone: 100 m g/kg/24h q12h IV



Chloram phenicol: 75â€“100 m g/kg/24h q6h IV



Decadron: 0.6 m g/kg/d (m ax. 10 m g) IV



Epinephrine, racem ic: 0.05 m L/kg (m ax. 0.5 m L) q30m in in 2.5 m L norm al saline (NS) via nebulizer



L-Epinephrine, 1:1,000: 0.5 m L/kg (m ax. 5 m L) q30m in via nebulizer



Rifam pin for contact prophylaxis: 20 m g/kg (m ax. 600 m g) daily for 4 days

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Follow-Up Disposition Admission Criteria Patients with suspected or proven epiglottitis should be adm itted to ICU after stabilization of airway and adm inistration of antibiotics and fluids.

Discharge Criteria 

Rifam pin prophylaxis m ay be indicated for close contacts of H. influenzae epiglottitis. If the household has children younger than 12 m onths of age or children who are unim m unized, incom pletely im m unized, or im m unosuppressed, prophylaxis is indicated for nonpregnant household contacts. Child care center contacts should receive prophylaxis when two or m ore cases of Hib invasive disease have occurred within 60 days.



All cases of invasive H. influenzae disease should be reported to the local or state public health departm ent.

Issues for Referral Critical care or pulm onary consult on all patients

References 1. Am erican Academ y of Pediatrics. Haem ophilus influenzae infections. In: Pickering LK, ed. Red Book: 2003 Report of the Com m ittee on Infectious Diseases. 26th ed. Elk Grove Village, IL: Am erican Academ y of Pediatrics; 2003:293â€“301. 2. Dam m M, Eckel HE, Jungehulsing M, et al. Managem ent of acute inflam m atory childhood stridor. Otolaryngol Head Neck Surg. 1999;121(5):633â€“638.

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3. Frantz T, Ragson B, Quesenberry C. Acute epiglottitis in adults: analysis of 129 cases. JAMA. 1994;272:1358â€“1360. 4. Rothrock S, et al. Radiologic diagnosis of epiglottitis: objective criteria for all ages. Ann Em erg Med. 1990;19:978â€“982. 5. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Hem ophilus influenzae type B era: changing trends. Laryngoscope. 2004;114:557â€“560. 6. Stroud RH, Friedm an NR. An update on inflam m atory disorders of the pediatric airway: epiglottitis, croup and tracheitis. Am J Otolaryngol. 2001;22(4):268â€“275.

Miscellaneous SEE ALSO: Bacterial Tracheitis; Epiglottis, Adult

Codes ICD9-CM 464.3 464.30 464.31

ICD10 J05.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epiglo ttitis, Adult

Epiglottitis, Adult

Jonathan Fisher Owen Landers

Basics Description Rapidly progressive inflam m ation of the epiglottis and surrounding tissues leading to airway com prom ise

Alert Patients with respiratory distress are at high risk for com plete airway obstruction. Surgical airway m anagem ent m ay be required.

Mechanism 

Inflam m ation of supraglottic structures: o

Epiglottis: 

Involvem ent of this is of prim ary airway concern.



May be prim ary or secondary from adjacent structures



o

Vallecula

o

Arytenoids

Uncom m on: o

Incidence is rising in adults, while decreasing in children.

Pa ge 1 7 2

o

Unclear whether this is true incidence versus im proved diagnosis



Im m une com prom ised patients m ay be particularly fulm inant, with m inim ally associated sym ptom s and unusual pathogens, such as candida.



Com plications: o

Total airway obstruction

o

Retropharyngeal abscess

o

Acute respiratory distress syndrom e

o

Pneum onia

o

Em pyem a

Etiology 

Infectious causes: o

Haem ophilus influenzae B, also type A and nontypable strains





o

Haem ophilus parainfluenzae

o

Streptococcus pneum oniae

o

Staphylococcus aureus

o

Group A strep

o

Herpes sim plex

o

Neisseria m eningitis

o

Cytom egalovirus

o

Num erous other uncom m on agents

Physical agents: o

Chem ical burns

o

Therm al burns

o

Toxic or illicit drug inhalation

Traum a, instrum entation

Diagnosis

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Signs and Symptoms 

General: o

Fever

o

Upper respiratory tract infection sym ptom s 



Prodrom e absent in significant num ber of cases

o

Toxic appearance

o

Drooling

Head, eyes, ears, nose, throat: o

Dysphagia

o

Muffled voice

o

Voice change: 

â€œHot potatoâ€• voice



Hoarseness

o

Foreign body sensation in throat

o

Associated tonsillar, peritonsillar, uvula findings

o

â€œCherry redâ€• epiglottis is classic, m ay be pale and edem atous in up to 50 percent.



o

Hyoid/thyroid cartilage tender to gentle palpation

o

Lym phadenopathy

Respiratory: o

Respiratory com prom ise

o

Subjective sense of obstructed airway

o

Stridor

o

Sudden loss of airway

o

May be m ore indolent in adults than pediatrics; rapid progression to total airway occlusion still seen in adults

Essential Workup 

If significant respiratory distress: o

Avoid invasive diagnostic procedures

o

Manage em pirically with antibiotics and control of

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airway 

Portable lateral soft-tissue x-ray

Pediatric Considerations 

Children with a high suspicion of epiglottitis are at risk of com plete airway obstruction and should be quickly transferred to a setting where the airway can be definitively m anaged in a surgical setting.



Staff capable of m anaging the airway should accom pany the child until the airway has been secured.



IV insertion, adm inistration of antibiotics, and obtaining blood work should follow airway m anagem ent.



A needle cricothyrotom y m ay be required in extrem e situations in young children.

Tests Lab 

CBC with differential



Blood cultures



Cultures of pharynx: o

Only if no signs of respiratory distress

Imaging 

Portable lateral soft-tissue x-ray: o

Epiglottic â€œthum bâ€• sign: 

o

Thickening of the epiglottis

â€œValleculaâ€• sign: 

The vallecula is norm ally well delineated, deep, and roughly parallel to the pharyngotracheal air colum n.



Absence of a deep and well-defined vallecula, approaching the level of the hyoid bone

o

Swelling of the arytenoids and aryepiglottic folds

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o

Prevertebral soft-tissue swelling

o

Significant false-negative with im aging

o

If suspected with negative film results, rule out with indirect visualization



CT: o

Indicated when a laryngoscopic evaluation cannot be perform ed or if coexistent soft-tissue com plications are suspected

Diagnostic Procedures/Surgery 

Avoid prior to airway m anagem ent if any signs of respiratory distress are present, including stridor



Nasopharyngoscopy (m ini-fiberoptic scope)



Indirect laryngoscopy

Differential Diagnosis 

Croup



Airway foreign body



Anaphylaxis



Paradoxic vocal cord dysfunction



Angioedem a



Laryngitis



Pharyngitis



Oropharyngeal abscess (peritonsillar or retropharyngeal)



Bacterial tracheitis



Congenital anom aly

P.371

Treatment

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Pre Hospital 

Transport patients in position of com fort



Supplem ental oxygen as tolerated; avoid increasing anxiety



Intubation indicated only if patient is in severe respiratory distress: o

Likely difficult airway and significant chance of exacerbating com prom ise with laryngoscopy attem pts



Inhaled agents, racem ic epinephrine, and Î²-agonists have no dem onstrated value.

Initial Stabilization 

ABCs



Be prepared with all equipm ent on hand for definitive airway m anagem ent, including a surgical airway, from presentation until diagnosis is ruled out or transport to intensive care setting.



Exam ination of the airway can trigger airway obstruction.



Orotracheal intubation in patients with signs of obstruction or significant respiratory distress: o

Respiratory distress/airway failure m ay develop precipitously.

o

Consider ear-nose-throat/surgical consult if patient's condition perm its for possible difficult/surgical airway.



Needle jet insufflation m ay be a life-saving tem porizing m easure if a surgical airway is not im m ediately attainable with failed intubation.

ED Treatment 

Hum idified oxygen support



IV access, hydration as indicated

Pa ge 1 7 2



Begin antibiotic coverage em pirically: o

o

o

First line: 

Cefotaxim e



Ceftriaxone

Second line: 

Am picillin/sulbactam



Trim ethoprim -sulfam ethoxazole

Consider adding increased coverage against Staph Aureus:





Nafcillin



Vancom ycin

Corticosteroids controversial

Medication (Drugs) 

Am picillin/sulbactam : 3 g IV initially, then 200â€“300 m g/kg/d in 4 div. doses



Cefotaxim e: 1â€“2 g IV initially, then 180 m g/kg/d in 4 div. doses



Ceftriaxone: 1â€“2 g IV initially, then 100 m g/kg/d in 2 doses



Trim ethoprim -sulfam ethoxazole: 320 m g IV initially, then 4â€“5 m g/kg IV q12h



Nafcillin: 150â€“200 m g/kg IV per day in 4 div. doses



Vancom ycin: 40â€“60 m g/kg IV per day in 3 div. doses if concern for MRSA



Rifam pin prophylaxis: o

Adults: 600 m g PO per day for 4 days

o

>1 m onth of age: 20 m g/kg PO per day for 4 days

o

<1 m onth of age: 10 m g/kg PO per day for 4 days

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Follow-Up Disposition Admission Criteria Any patient with a suspected or confirm ed diagnosis of epiglottitis should be adm itted to an intensive care unit setting for IV antibiotics and airway m anagem ent.

Discharge Criteria 

Patients should not be discharged unless the diagnosis has been ruled out by visualization of the supraglottic structures by a physician fam iliar with physical appearance of the disease.



Close contacts should receive prophylactic treatm ent with rifam pin.

References 1. Carey MJ. Epiglottitis in adults. Am J Em erg Med. 1996;14:421â€“424. 2. Ducic Y, Herbert PC, MacLachlan L, et al. Description and evaluation of the vallecula sign: a new radiologic sign in the diagnosis of adult epiglottitis. Ann Em erg Med. 1997;30:16. 3. Melio FR. Upper respiratory tract infections. In: Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice, 5th ed. Philadelphia: Mosby, 2001. 4. Woods, CR. Epiglottitis. In: Rose, BD, ed. UpToDate, Wellesley, MA: 2005.

Codes ICD9-CM 464.3 464.30

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464.31

ICD10 J05.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epiphyseal Injuries

Epiphyseal

Injuries Steven F. Fisher Daniel L. Savitt

Basics Description 

Occur m ost frequently in distal radius, phalanges, and distal tibia



More com m on than sprains in children: o

Physis relatively weak com pared with ligam ents or m etaphyseal bone

o 

Ligam ents often insert into epiphyses.

Com m on m echanism s: o

Shearing

o

Tension

o

Com pression



Most com m on during peak growth



More com m on in m ales



Salter-Harris classification: o

Type I: 

Fracture line confined to physis



Epiphyseal separation from m etaphysis

Pa ge 1 7 2

 o

No growth disturbance

Type II: 

Fracture propagates along physis, and fragm ent from m etaphysis accom panies displaced epiphysis.

o



Periosteum torn opposite m etaphyseal fragm ent



Most com m on epiphyseal fracture



No growth disturbance

Type III: 

Fracture through a portion of physis extending through epiphysis and articular surface



Phalanges and distal tibia m ost com m only affected



Requires anatom ic alignm ent owing to displacem ent of both physis and articular surface



Growth disturbance m ay occur despite anatom ic reduction.

o

Type IV: 

Fracture originates at articular surface.



Extends through physis and into m etaphysis



Distal hum erus and distal tibia m ost com m only affected



Anatom ic reduction essential and frequently requires surgical intervention

 o

Growth arrest is com m on.

Type V: 

Results from crush injuries to physis



No im m ediately visible radiographic alteration



Often found in retrospect with prem ature physeal closure



Usually involves knee or ankle

Pa ge 1 7 3

 o

Growth arrest is com m on.

Type VI (not described in original Salter-Harris classification): 

Involves periosteum surrounding physis



Reactive form ation of bone external to growth plate causing tethering of epiphysis to m etaphysis and restricting further expansion at physis



May result from ligam entous avulsion or therm al injuries

o

Type VII (not described in original Salter-Harris classification): involves epiphysis only

Etiology Traum atic injury, often without specific history in young children

Diagnosis Signs and Symptoms 

Pain and localized, often pinpoint, tenderness



Lim ited m obility of affected joint



Swelling



Ecchym osis



Bony deform ities

Complications Long-term com plications: 

Overreduction



Bone growth disturbances



Reduced joint m obility

Essential Workup 

Assess pulses and capillary filling distal to injury.

Pa ge 1 7 3



Evaluate distal m otor and sensory function.



Verify integrity of skin overlying injury.



Address and m anage coexisting injuries.

Tests Imaging 

Plain radiography of injured extrem ity: o

Type I fractures: 

May appreciate a slightly separated physis or an associated joint effusion; usually unrem arkable radiograph



Consider com parison views of contralateral joint to detect sm all defects.



Callus m ay be present on subsequent follow-up film s.

o

Types II through IV: film s diagnostic of fracture

o

Types V and VI: 

Initial film often norm al



Subsequent radiographs m ay reveal prem ature bone arrest.





Radionuclide bone scan: o

Rarely necessary

o

Fractures m ust be â‰¥24â€“48 hours old.

o

Valuable adjunct if child abuse is suspected.

CT scan: helpful in assessing integrity of articular surfaces in type III and IV fractures



MRI: o

If diagnosis rem ains equivocal and identification of a specific fracture would alter m anagem ent

o

Allows for early detection of growth arrest

Differential Diagnosis 

Strain

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

Sprain



Contusion

P.375

Treatment Pre Hospital 

Im m obilize lim b in position found.



Apply ice or cold packs to injury.



Assess injured extrem ity for neurologic and vascular function.



Consider concom itant injuries.

Initial Stabilization 

Control hem orrhage.



Apply sterile dressings to open wounds.



Analgesia

ED Treatment 

Reduction/alignm ent required: o

Displacem ent to achieve anatom ic alignm ent

o

Vascular or neurologic com prom ise distal to injury requires intervention.



Im m obilization: o

Splint m ust im m obilize joints proxim al and distal to injury in anatom ic alignm ent.

o 

Elevate injured lim b.

Open fractures: o

Intravenous antibiotics for Staphylococcus aureus, group A streptococcus, and potentially anaerobes

Pa ge 1 7 3

after culture



o

Copious irrigation with saline

o

Sterile dressing

o

Orthopedic consultation

Consultation: o

Types III and higher

Medication (Drugs) 

Cefazolin: 25â€“50 m g/kg/d IV/IM q6hâ€“q8h



Clindam ycin: 20â€“40 m g/kg/d IV q6hâ€“q8h



Fentanyl: 2â€“3 Âµg/kg IV; transm ucosal lollipops 5â€“15 Âµg/kg, m ax. 400 m g, contraindicated if <10 kg



Morphine: 0.1 m g/kg IV/IM

Follow-Up Disposition Admission Criteria 

Open fractures



Open surgical reduction required



Type III and IV fractures

Discharge Criteria 

Type I, II, V, VI, and VII epiphyseal injuries



Splint for com fort



Analgesics



Ice packs



Elevation of affected lim b



Follow-up film m ay be useful.



Patient teaching:

Pa ge 1 7 3



Casts



Splints



Fractures

Patient Monitoring Orthopedic follow-up within 1 week, often with follow-up film

References 1. England SP, Sundberg S. Managem ent of com m on pediatric fractures. Pediatr Clin North Am . 1996;43:991â€“1012. 2. Morrissy RT, Weinstein SL. Lovell and Winter's Pediatric Orthopaedics. 5th ed. Philadelphia: Lippincott William s & Wilkins; 2001. 3. Perron AD, Miller MD, Brady WJ. Orthopedic pitfalls in the ED: pediatric growth plate injuries. Am J Em erg Med. 2002;20:50â€“54. 4. Rogers LF, Poznanski AK. Im aging of epiphyseal injuries. Radiology. 1994;91:297â€“308. 5. Salter R, Harris W. Injuries involving the epiphyseal plate. J Bone Joint Surg. 1963;45A:587.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epistaxis

Epistaxis

Christopher M. McCarthy II

Basics Description 

Anterior epistaxis (90% of cases): o

Source: Kiesselbach plexus of anterior inferior nasal septum

o 

Generally unilateral

Posterior epistaxis (10% of cases): o

Source: posterolateral branch of sphenopalatine artery

Etiology 

Local factors: o

Traum a (including postoperative, facial traum a from MVC)

o

Nose picking (especially com m on in children)

o

Dry nasal m ucosa (low hum idity)

o

Environm ental irritants (am m onia, gasoline, sulfuric acid, glutaraldehyde)

o

Inflam m ation and local hyperem ia from allergic or infectious rhinitis

o

Neoplasia (e.g., papillom a and polyp)

o

Nasal foreign body

Pa ge 1 7 3



System ic factors: o

Atherosclerosis of nasal vasculature

o

Barotraum a

o

Hypertension (data supporting association is controversial)

o

Coagulopathy (fam ilial): hem ophilia A or B, von Willebrand disease

o

Coagulopathy (acquired): throm bocytopenia, liver disease, renal failure/urem ia

o

Drug induced (salicylates, NSAIDs, heparin, coum adin)

o

Diabetes m ellitus

o

Alcoholism

o

Hereditary hem orrhagic telangiectasia (Osler-Weber-Rendu disease)

Diagnosis Signs and Symptoms History 

Intensity and am ount of bleeding from nare(s)



Com plaints of vom iting or coughing blood



Recurrence of epistaxis



Known tum ors or coagulopathy



Presence of system ic disease exacerbated by blood loss (coronary artery disease, chronic obstructive pulm onary disease)

Physical Exam 

Anesthetize nasopharynx prior to exam with cotton swab soaked in anesthetic and vasoactive agent (lidocaine,

Pa ge 1 7 3

cocaine, oxym etolazine, etc.â€”see below). 

Attem pt to identify bleeding source with nasal speculum (i.e., Kiesselbach plexus versus posterior source).



Blood in m outh or oropharynx



Tachycardia



Hypotension



Airway com prom ise

Essential Workup 

Assess stability: airway com prom ise, hypovolem ia.



Determ ine source (anterior versus posterior).



Consider underlying coagulopathy.

Tests Lab Consider for severe bleeding or suspected coagulopathy: 

Type and cross-m atch, hem atocrit, PT, PTT, blood urea nitrogen

Imaging Direct visualization of nasal m ucosa with nasal speculum : 

Pretreat with topical vasoconstricting agent and anesthetic



Ensure adequate lighting (i.e., headlam p) and suction

Differential Diagnosis 

Hem atem esis



Hem optysis

Pediatric Considerations 

Posterior epistaxis is rare in children; consider further workup for bleeding diatheses.



Consider nasal foreign bodies or neoplasm such as juvenile angiofibrom a or papillom a.

Pa ge 1 7 3

Treatment Pre Hospital 

Stable patients: Patient should bend forward at the waist, pinch nares closed, and spit out blood rather than swallow it.



Unstable patients: o

Intubation, if airway is com prom ised

o

IV access

o

Crystalloid resuscitation, if signs of hypovolem ia

Initial Stabilization 

Secure the airway in patients who are unconscious, have m ajor facial traum a, or are otherwise at risk of obstruction or aspiration.



Treat hypotension with crystalloids and blood products, if necessary, and ensure adequate IV access.

ED Treatment 

Universal precautions against blood/fluid contam ination



Anterior source: o

Instruct patient to bend forward at waist, pinch nares closed for 15 m inutes, and spit out blood rather than swallow it.

o

If bleeding persists, use bayonet forceps to place cotton pledgets soaked in vasoconstricting and anesthetic agents (see list below) into affected nares.

o

Visualize source of bleeding and cauterize lim ited area with silver nitrate or trichloroacetic acid.

o

Consider Gelfoam or Surgicel packing over cauterized site.

o

Consider anterior packing with Vaseline ribbon gauze

Pa ge 1 7 3

coated with Bacitracin if cautery is unsuccessful, ensuring that both ends protrude from nares and that the strip is rem oved by 48 hours. o

Merocel synthetic sponge tam pon is an alternative to ribbon gauze packing.

o

After anterior packing, persistent new bleeding m ay be a sign of inadequate packing or posterior source.

o

All patients with nasal packing in place should be prescribed an anti-Staphylococcal antibiotic (am oxicillin-clavulanate, cephalexin, trim ethoprim -sulfam ethoxazole) for the duration that the packing rem ains in place for prevention of both acute sinusitis and toxic shock syndrom e.

P.377



Posterior source: o

Posterior packing with balloon device such as Nasostat, Epistat; these are not left in for m ore than 3 days, with antibiotic prophylaxis for anterior packing

o

If com m ercial packs are unavailable, a Foley catheter m ay be directed into posterior nasopharynx until the tip visible in m outh. The balloon is then inflated and the catheter retracted until the balloon is lodged in the posterior nasopharynx. The catheter is then held in place by um bilical clam p.



Com plications of posterior packing: o

Pressure necrosis of posterior oropharynx (do not overfill balloon)

o

Nasal traum a

o

Vagal response

Pa ge 1 7 4

o

Aspiration

o

Infection

o

Hypoxia

o

Endoscopic cautery by otolaryngology is also useful and m ay obviate need for adm ission.

Medication (Drugs) 

Vasoactive solutions: o

4% cocaine

o

1:1 m ixture of 2% tetracaine and epinephrine (1:1,000)

o

1:1 m ixture of oxym etazoline 0.05% (Afrin) and lidocaine solution 4%

o

Phenylephrine (Neo-Synephrine)



Am oxicillin-clavulanate potassium : 250 m g PO q8h



Cephalexin: 250 m g PO q6h



Clindam ycin: 150 m g PO q6h



Trim ethoprim -sulfam ethoxazole: 160/800 m g PO q12h

Follow-Up Disposition Admission Criteria 

Severe blood loss requiring transfusion



Severe coagulopathy that places the patient at risk of further blood loss



Posterior nasal packing: otolaryngology consult and adm ission for supplem ental oxygen, sedation, and observation; possible further surgical intervention (e.g.,

Pa ge 1 7 4

arterial ligation or em bolization) 

Patients with packing who cannot be relied upon to follow up in a tim ely m anner

Discharge Criteria 



Stable patients: o

Use Afrin nasal spray for 2 days

o

Lubricate nares with an antibiotic ointm ent

o

Hum idify air

o

Avoid nose picking

Return to ED for bleeding not controlled by pressure, fever, difficulty breathing, or vom iting.

Issues for Referral Refer all patients with packing to a specialist within 48 hours.

References 1. Evans JA, Rothenhaus TC. Epistaxis. In: Wolfson AB et al, eds. Harwood-Nussâ€™ Clinical Practice of Em ergency Medicine. 4th ed. Philedelphia: Lippincott William s & Wilkins, 2005:185â€“190. 2. Frazee TA, Hauser MS. Nonsurgical m anagem ent of epistaxis. J Oral Maxillofac Surg. 2000;58:419â€“424. 3. Kucik C, Klenny T. Managem ent of Epistaxis. Am erican Fam ily Physician. 2005;71:305â€“377. 4. Middleton P. Episaxis. Em ergeny Medicine Australasia. 2004;16:428â€“440. 5. Pfaff JA, Moore GP. Otolaryngology. In: Marx J, Hockberger R, Walls R, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis: Mosby, 2002:933â€“935. 6. Tan LS, Calhoun KH. Epistaxis. Med Clin North Am . 1999;83:43â€“56.

Codes ICD9-CM

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784.7

ICD10 R04.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erysipelas

Erysipelas

Irving Jacoby

Basics Description Superficial cellulitis of the skin with prom inent lym phatic involvem ent

Pediatric Considerations 

Hem ophilus influenza Type b causes facial cellulitis in children that m ay appear sim ilar to erysipelas: o

Should be considered in unim m unized children

o

Many will be bacterem ic and require adm ission.

o

Cefuroxim e or other appropriate Hem ophilus influenza coverage is im portant.

o

Hem ophilus influenza is m uch less com m on with the vaccine.



Group B streptococci can cause erysipelas in the newborn.



Can develop from infection of um bilical stum p

Etiology 

Group A Î²-hem olytic streptococcus is the causative organism (uncom m only, group C or G streptococci).



Portals of entry are com m only skin ulcers, local traum a or abrasions, psoriatic or eczem atous lesions, or fungal infections.

Pa ge 1 7 4

Diagnosis Signs and Symptoms 

Most com m on sites of involvem ent are the face (5â€“20% of cases), lower legs (70â€“80% of cases), and ears.



Skin has an intense fiery red color, earning the nam e â€œSaint Anthony's fire.â€•



Predilection for infants, children, and the elderly



System ic sym ptom s m ay include m alaise, fever, chills, nausea, and vom iting.



Traum atic portal of entry on skin is not always apparent.



Rarely there m ay be an associated periorbital cellulitis or cavernous sinus involvem ent.

History 

Facial erysipelas m ay follow an upper respiratory tract infection.



Predilection for areas of lym phatic obstruction



Thirty percent recurrence rate within 3 years, owing to lym phatic obstruction caused by an episode of erysipelas

Physical Exam 

The involved skin is an edem atous, indurated (peau d'orange), painful, well-circum scribed plaque with sharp, clearly dem arcated edge.



Classical butterfly rash on cheeks and across nose when affecting face



Vesicles and bullae m ay be present in m ore serious infections.

Essential Workup 

The diagnosis is clinical based on the characteristic skin

Pa ge 1 7 4

findings and the clinical setting. 

Needle-aspirate wound cultures are seldom positive and not indicated.



Positive blood cultures in 3â€“5%; leukocytosis is com m on; when com plicating infected ulcers, cultures are positive in 30%.

Tests Lab 

Swabs of the skin are not indicated for culture, as they will show only skin organism s.



CBC, differential blood cultures should be perform ed in diabetics and other high-risk populations. o

Check glucose in diabetics as infection m ay disrupt control.

Differential Diagnosis 

Allergic inflam m ation



Cellulitis



Contact derm atitis



Fam ilial Mediterranean fever



Herpes zoster, second division of fifth central nerve



Im petigo



Viral exanthem



Diffuse inflam m atory carcinom a of the breast

P.379

Treatment

Pa ge 1 7 4

Pre Hospital Wearing gloves, followed by hand washing when m anaging patients, to decrease risk of transm ission of streptococcal carriage

Initial Stabilization Patients m ay be toxic and in need of intravenous fluid resuscitation or pressure support.

ED Treatment Appropriate antibiotic therapy, treatm ent should be for 10 days: 

Patients with extensive involvem ent should be adm itted for parenteral antibiotic treatm ent.



When parenteral antibiotics used, can switch to oral m edication when patient is stable and showing signs of response



Mild cases: patients can be discharged on oral therapy if nontoxic appearing, good com pliance, and close follow-up can be ensured.



Penicillin is the drug of choice when clearly the sym ptom s are consistent with erysipelas.



If there is difficulty in distinguishing from cellulitis, staphylococcal coverage should be added. o

Use penicillinase-resistant penicillin or first-generation cephalosporin

o

If in com m unity with high incidence of m ethicillin-resistant S. aureus (MRSA), use vancom ycin or other anti-MRSA coverage.

Medication (Drugs) 

Cefuroxim e: peds: 50â€“100 m g/kg/d PO div. q8h



Cephalexin: adult: 500 m g PO q6h (peds: 40 m g/kg/d PO

Pa ge 1 7 4

div. q8h) 

Dicloxacillin: adult: 500 m g PO q6h (peds: 30â€“50 m g/kg/d PO div. q6h)



Erythrom ycin ethylsuccinate: adult: 250â€“500 m g PO q6h (peds: 40 m g/kg/d PO in div. doses q6h)



Penicillin G: adult: 2 m illion U q4h IV (peds: 25,000 U/kg IV q6h)



Penicillin G, procaine: 600,000 U q12h IM



Penicillin V: adult: 500 m g PO q6h (peds: 25â€“50 m g/kg/d div. q6hâ€“q8h)

Follow-Up Disposition Admission Criteria 

Patients with extensive involvem ent, fever, toxic appearance, or those who live alone will require adm ission for IV antibiotics.



Children m ore often require adm ission. Blood cultures, intravenous antibiotics, including coverage for H. influenza , should be initiated for patients who have not been im m unized.

Discharge Criteria 

Minim al facial involvem ent



Nontoxic appearing



Not im m unosuppressed



Able to tolerate and com ply with oral therapy



Adequate follow-up

References

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1. Bisno Al, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. 1996;334:240â€“244. 2. Kahn RM, Goldstein EJ. Com m on bacterial skin infections. Postgrad Med. 1993;93(6):175â€“182. 3. Morris A. Cellulitis and erysipelas. Clin Evid. 2004 Dec;(12):2271â€“2277.

Codes ICD9-CM 035

Core Content Code 3.2.1.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a Infectio sum

Erythema

Infectiosum Kathlene Bassett Alec Tuan Huynh

Basics Description 

Characteristic viral exanthem also known as fifth disease: o

Based on historical order of com m on exanthem s described

o

Measles (first disease), scarlet fever (second), rubella (third), Duke disease (fourth), roseola (sixth)



School-aged children age 3â€“12 years typically infected

Etiology 

Caused by hum an parvovirus B19



Incubation period typically 4â€“14 days



Seasonal predilection for late winter and spring



Spreads via respiratory transm ission



Sixty percent of adults have serologic evidence of prior infection.

Pa ge 1 7 5

Diagnosis Signs and Symptoms History 

Mild constitutional sym ptom s (fever, headache)



Contagious only until appearance of facial rash



Rash begins within 1 week.

Physical Exam 

Three stages: o

o

o

Stage 1: 

Malar blush (â€œslapped cheekâ€•) in 75%



Warm , erythem atous, and nontender



Asym ptom atic



Contagious

Stage 2: 

Nonspecific m aculopapular eruption



1â€“4 days after facial rash



More prom inent on extrem ities than trunk



Usually spares palm s and soles



May be pruritic

Stage 3: 

Fading rash on sixth day



Usually with central clearing leaving characteristic lacy reticulated pattern



Can last up to several weeks



Rash m ay recur secondary to cutaneous vasodilation, especially during periods of stress, exercise, sun exposure, and bathing.



Com m on com plications: o

Arthritis or hypersensitivity derm atitis in adults

o

Transient aplastic crisis in patients with hem olytic

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anem ias (classically sickle cell disease): 

Fever, pallor, lethargy, hepatosplenom egaly, heart failure

Pregnancy Considerations 

Nonim m une hydrops fetalis in pregnancy: o

About 60% pregnant wom en are susceptible to infection.

o

30% risk of transplacental infection when infected

Essential Workup Clinical diagnosis based on characteristic signs and sym ptom s

Tests Lab 

Usually no workup necessary



CBC if concern for aplastic crisis



IgM antibody assay rarely available, but confirm s acute infection

Differential Diagnosis 

Scarlet fever



Rubella



Roseola



Infectious m ononucleosis



Echovirus



Coxsackie virus



Drug eruptions

P.381

Pa ge 1 7 5

Treatment Initial Stabilization Airway, breathing, and circulation (ABCs) for septic or ill-appearing infant

ED Treatment 

No specific antiviral treatm ent or vaccine is available.



Sym ptom atic treatm ent with fluids and acetam inophen



Hospitalization and respiratory isolation for aplastic crisis

Follow-Up Disposition Admission Criteria 

Aplastic crisis



Hydrops fetalis



Toxic appearance



Severe arthritis

Discharge Criteria 

Nearly all patients



Patients are no longer contagious following facial rash and m ay return to school or day care.

References 1. Adam s DM, Ware RE. Parvovirus B19: how m uch should you worry? Contem p Pediatr. 1996;13(4): 85â€“96. 2. Anderson MJ, Higgins PG, Davis LR, et al. Experim ental parvoviral infection in hum ans. Infect Dis. 1985;152:257â€“265. 3. Hurwitz S. Clinical Pediatric Derm atology. 2nd ed. Philadelphia: WB Saunders; 1993.

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4. Ussery X, Dem m ler G. Hum an parvovirus B19. Sem in Pediatr Infect Dis. 1996;7(2):89â€“96. 5. Young NS, Brown KE. Parvovirus B19. New Engl J Med. 2004;350:586â€“597.

Codes ICD9-CM 057.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a M ultifo rm e

Erythema

Multiforme Gregory W. Hendey Thomas A. Utecht

Basics Description 

A rash caused by a hypersensitivity reaction: o

May occur in response to various m edications, infections, or other illness



Divided into m ajor and m inor types: o

Erythem a m ultiform e m ajor: separate disease pattern that includes m ore severe disorders (see Toxic Epiderm al Necrolysis and Stevens-Johnson syndrom e)

o

Erythem a m ultiform e m inor is characterized by a benign, self-lim ited rash, generally not associated with acute, serious illness; sim ply referred to as erythem a m ultiform e



Most often affects children and young adults (>50% younger than 20 years)



Males are affected m ore often than fem ales.

Etiology

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

Hypersensitivity reaction, probably transient autoim m une defect



Herpes sim plex virus is the m ost com m on precipitant (>70%).



Other causes include idiopathic, m edications (antibiotics: penicillin, sulfur-based, phenytoin, and others), m alignancy, and Mycoplasm a infections.

Diagnosis Signs and Symptoms History 

Prodrom e: infrequent system ic sym ptom s (m ild fever/m alaise), antecedent (within 3 weeks) herpes sim plex virus (HSV) in m ost cases



Usually not associated with severe system ic illness

Physical Exam Characteristic rash: 

Lesions: sym m etric dull red m acules and papules, evolving into round, well-dem arcated target lesions with central clearing



Multiform e refers to the evolution of the rash through various stages at different tim es.



Distribution: extrem ities, dorsal hands and feet, extensor surfaces, especially elbows and knees. It is one of the few rashes that involve palm s and soles.



Spread: from extrem ities toward trunk



Mucosal involvem ent: often involves m ild blistering or erosions on the lips or m outh



Duration: usually 1â€“4 weeks, but m ay becom e chronic or

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recurrent

Essential Workup Com plete history and physical exam , with special attention to the skin, genitourinary system , recent infectious sym ptom s, and recent m edications

Tests Lab No specific laboratory tests needed

Imaging No specific im aging is helpful.

Diagnostic Procedures/Surgery 

Skin biopsy reveals m ononuclear cell infiltrate around upper derm al blood vessels, without leukocytoclastic vasculitis and necrosis of epiderm al keratinocytes.



Biopsy is not necessary in m ost cases.

Differential Diagnosis 

System ic lupus erythem atosus



Fixed drug eruption



Pityriasis rosea



Secondary syphilis



Erythem a m igrans



Urticaria

P.383

Treatment

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Pre Hospital Not contagious and does not require isolation or postexposure prophylaxis for exposed personnel

Initial Stabilization Generally benign and self-lim ited, requiring no initial stabilization

ED Treatment 

Attem pt to identify, treat, or rem ove underlying cause or precipitant.



Sym ptom atic: cool com presses, antipruritics

Medication (Drugs) 

Antipruritic agents: o

Cetirizine (Zyrtec): 10 m g PO daily (peds: 2.5â€“5 m g)

o

Diphenhydram ine: 25â€“50 m g (peds: 5 m g/kg/24h) PO q6hâ€“q8h

o

Hydroxyzine: 25 m g PO q6h to q8h (peds: 2 m g/kg/24h)



Antiviral therapy: o

If HSV infection is present, see Herpes for specific treatm ent options.

Follow-Up Disposition Admission Criteria Adm ission is not needed unless required for another concurrent disorder.

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Discharge Criteria Erythem a m ultiform e is a benign disorder that does not require adm ission.

References 1. Assier H, Bastuji-Garin S, Revuz J, et al. Erythem a m ultiform e with m ucous m em brane involvem ent and Stevens-Johnson syndrom e are clinically different disorders with distinct causes. Arch Derm atol. 1995;131:539â€“543. 2. Foster J. Erythem a m ultiform e. Available at http://www.em edicine.com , updated January 5, 2005. 3. Kerob D, Assier-Bonnet H. Recurrent erythem a m ultiform e unresponsive to acyclovir prophylaxis and responsive to valacyclovir continuous therapy. Arch Derm atol. 1998;134:877â€“878. 4. Leaute-Labreze C, Lam ireau T, Chawki D, et al. Diagnosis, classification, and m anagem ent of erythem a m ultiform e and Stevens-Johnson syndrom e. Arch Dis Child. 2000;83:347â€“352. 5. Weston WL. What is erythem a m ultiform e? Pediatr Ann. 1996;25(2):106â€“109.

Miscellaneous SEE ALSO: Stevens-Johnson Syndrom e; Toxic Epiderm al Necrolysis

Codes ICD9-CM 695.1

ICD10 L51.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a No do sum

Erythema

Nodosum Herbert G. Bivins Theresa Schwab

Basics Description 

Characterized by m ultiple sym m etric, nonulcerative tender nodules on the extensor surface of the lower extrem ities typically in young adults



Peak incidence in third decade, m ore com m on in wom en (4:1)



Nodules are round with poorly dem arcated edges and vary in size from 1â€“10 cm .



Skin lesions are initially red, becom e progressively ecchym otic appearing as they resolve over 3â€“6 weeks.



Lesions are caused by inflam m ation of the septa between SC fat nodules (septal panniculitis).



Spontaneous regression of lesions within 3â€“6 weeks



Major disease variants include: o

Erythem a nodosum m igrans (usually m ild unilateral disease with little or no system ic sym ptom s)

o

Chronic erythem a nodosum (lesions spread via

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extension, and associated system ic sym ptom s tend to be m ilder)

Etiology 

Im m une-m ediated response; 30â€“50% of the tim e etiology is idiopathic.



Often a m arker for underlying disease; specific etiologies include: o

Drug reactions (oral contraceptives, sulfonam ides, penicillins)

o

Infections including streptococcal, m ycobacterium tuberculosis (TB), atypical m ycobacteria, and coccidioidom ycosis, hepatitis, syphilis, chlam ydia, Rickettsia, Salm onella, Cam pylobacter, Yersinia, parasites, and leprosy

o

System ic diseases such as sarcoidosis, inflam m atory bowel disease, BehÃ§et, and connective tissue disorders

o

Malignancies such as lym phom a and leukem ia

o

Catscratch disease

o

HIV infection

o

Rarely can be caused by vaccines for hepatitis and TB (BCG)



Typically erythem a nodosum begins 2â€“3 weeks after the onset of pharyngitis in children.

Diagnosis Signs and Symptoms 

Tender erythem atous nodules sym m etrically distributed on extensor surface of lower legs

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

Lesions occasionally occur on fingers, hands, arm s, calves, and thighs.



In bedridden patients, dependent areas m ay be involved.



Fever, m alaise, leukocytosis, arthralgias, arthritis, and unilateral or bilateral hilar adenopathy with any form of the disease

Essential Workup Careful history and physical exam directed at detecting precipitating cause

Tests Lab CBC, erythrocyte sedim entation rate (ESR), appropriate chem istry tests; TB and coccidioidom ycosis skin tests m ay be useful initial screening tests for lym phom a, leukem ia, TB, and cocci.

Imaging 

Chest radiograph can serve as initial screen for sarcoidosis.



Definitive diagnosis m ade by deep elliptical biopsy and histopathologic evaluation (punch biopsy m ay be inadequate)

Differential Diagnosis 

Erythem a nodosum m igrans and chronic erythem a nodosum



Any type of panniculitis can resem ble erythem a nodosum .



Differences can be determ ined histopathologically.



Other disorders include periarteritis nodosum , m igratory throm bophlebitis, superficial varicose throm bophlebitis, scleroderm a, system ic lupus erythem atosus, Î± 1 -antitrypsin deficiency, BehÃ§et syndrom e, lipodystrophies, leukem ic infiltration of fat, and

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panniculitis associated with steroid use, cold, and infection.

Treatment Pediatric Considerations 

Rare in children, streptococcal pharyngitis is the m ost likely etiology.



Catscratch disease should be considered.

Initial Stabilization Airway, breathing, and circulation (ABCs); IV, oxygen, m onitoring as appropriate

ED Treatment 

Treatm ent should be directed at underlying disease.



Supportive therapies including analgesics



Treatm ent of the underlying pathology and disappearance of the lesions within 1â€“2 m onths



Specific therapies such as potassium iodide and system ic corticosteroids are used only when the underlying process is known.



System ic corticosteroids are contraindicated in presence of certain underlying infections such as TB or coccidioidom ycosis, which m ay dissem inate with their use.

P.385

Medication (Drugs)

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

Aspirin: 650 m g PO q4hâ€“q6h PRN (peds: contraindicated)



Ibuprofen: 300â€“800 m g PO q8h (peds: 5â€“10 m g/kg PO q6h)



Indom ethacin: 25â€“50 m g PO q8h



Potassium iodide/SSKI (used for resistant disease; contraindicated in hyperthyroidism ): 900 m g PO daily for 3â€“4 weeks



System ic corticosteroids (prednisone): 40 m g PO dailyâ€”duration determ ined by prim ary physician

Follow-Up Disposition Admission Criteria Dictated by the severity of sym ptom s and the etiologic agent

Discharge Criteria 

Nontoxic patients, able to take oral fluids without difficulty



Scheduled follow-up should be arranged.

References 1. Barbier SC, Faucher R. Erythem a nodosum and adenopathy in a 15-year-old boy: uncom m on signs of cat scratch disease. Arch Pediatr . 2005;12(3):295â€“297. 2. Gonzalez-Gay MA. Erythem a nodosum : a clinical approach. Clin Exp Rheum atol. 2001;19:365â€“368. 3. Myerson MS. Erythem a nodosum leprosum . Int J Derm atol. 1996;35(6):389â€“392. 4. Psychos DN, Voulgari PV. Erythem a nodosum : the underlying conditions. Clin Rheum atol. 2000;19:212â€“216.

Codes

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ICD9-CM 695.2

ICD10 L52

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Eso phageal Traum a

Esophageal

Trauma Susan Dufel

Basics Description 

Adult esophagus is approxim ately 25â€“30 cm in length.



It begins at hypopharynx posterior to larynx at level of cricoid cartilage.



On either side of this slit are piriform recesses: o



May be site for foreign body to lodge

Sites of esophageal narrowing: o

Cricopharyngeal m uscle (upper esophageal sphincter)

o

Crossover of left m ain stem bronchus and aortic arch

o

Gastroesophageal junction (lower esophageal sphincter)

o 

Areas of disease (cancer, webs, or Schatzki ring)

Upper third of esophagus is striated m uscle: o

Initiates swallowing



Middle portion is m ixture of striated and sm ooth.



Distal portion is sm ooth m uscle.



It is fixed structure, but can becom e displaced by other organs:

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o

Goiter

o

Enlarged atria

o

Mediastinal m asses

Etiology Mechanism 

External forces or agents (30%): o

Penetrating:leading to tears:stab wounds, m issile wounds

o

Perforation: 

Foreign bodies via direct penetration



Pressure necrosis



Chem ical necrosis



Instrum entation

o

Blunt: m otor vehicle accident

o

Caustic ingestions/burns: 

Acid pH <2, alkali pH >12 accidental or intentional



Alkali: liquefaction necrosis causing burns, airway edem a or com prom ise, perforation, chronic stricture, and cancer



Acid: coagulation necrosis, therm al injury, and dehydration causing perforation, ulceration, and infection, m ore likely to perforate than alkali

o

Swallowed foreign bodies: coins, bones, buttons, m arbles, pins, button batteries

o

Food bolus im paction: 

Most com m on type is m eat



In adults, often associated with prisoners, psychiatric patients, intoxicated patients, or edentulous patients



Iatrogenic (55%):

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o

Perforation secondary to instrum entation, endoscopy m ost com m on cause

o

Nasotracheal intubation/nasogastric tube m ost com m on cause in em ergency departm ent



Increased gastric pressure (15%): o

Large pressure differences between thorax and intra-abdom inal cavity 

o

May lead to lacerations or perforation

Mallory-Weiss syndrom e 

Longitudinal tears in distal esophageal m ucosa with bleeding

o

Boerhaave syndrom e: 

Spontaneous esophageal rupture



Full thickness rupture of distal esophagus



Classically after alcohol or large m eals and vom iting

Pediatric Considerations 

Accounts for 75â€“80% of swallowed foreign bodies: o



Typically in infants ages 18â€“48 m onths

Entrapm ent usually at upper esophageal sphincter

Diagnosis Signs and Symptoms 

General: o

Dysphagia: difficulty swallowing

o

Odynophagia: pain with swallowing

o

Chest pain: angina like, often pleuritic, severe, and unrelenting

o

Hoarseness

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o 







Dyspnea

Tears or perforations: o

Bleeding

o

Hem atem esis

Ingestions/foreign bodies: o

Drooling or excessive salivation

o

Choking, gagging, vom iting, stridor, or wheezing

o

Inability of food or liquid to pass

Caustic ingestions: o

Oral pain

o

Abdom inal pain

o

Vom iting

o

Drooling

Esophagus injury scale: o

I: contusion/hem atom a; partial thickness

o

II: laceration â‰¤50% circum ference

o

III: laceration >50% circum ference

o

IV: segm ental loss or devascularization <2 cm

o

V: segm ental loss or devascularization >2 cm

History 

History of ingestions (type, tim e, am ount)



History of protracted vom iting



History of inability to swallow after eating, foreign body sensation in throat



History of penetrating traum a

Physical Exam 

Tears or perforations: o

Subcutaneous air at base of neck

o

Ham m an crunch: 

Systolic crunching sound secondary to air in m ediastinum

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

o

Shock

o

Septicem ia

o

Peritonitis

Penetrating traum a: o

Associated neck, chest, or abdom inal injury with traum a:





Most com m only trachea



Associated with penetrating/blunt traum a

Caustic ingestions: o

Airway edem a leading to stridor

o

Oral burns

Essential Workup High level of suspicion and early diagnosis are key: 

Mortality <5% for perforation if repaired within 24 hours; 75% if delayed



Early endoscopy for caustic ingestions



Chest radiograph

Tests Lab 

CBC in cases of gastrointestinal bleeding



Type and cross for any extensive bleeding or if patient is OR candidate



Coagulation studies



Electrolytes for protracted vom iting or prolonged foreign body retention



Arterial blood gas (ABG) for acid ingestions

Imaging 

Chest radiograph for foreign body or perforation: o

Pneum om ediastinum

o

Widened m ediastinum

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

o

Pneum othorax

o

Pleural effusion

Lateral cervical spine film s for foreign body or perforation: o

Retropharyngeal air or fluid

o

Cervical em physem a



Fiberoptic nasopharyngoscopy for foreign body rem oval:



Esophagram for foreign bodies or suspected perforation: o

Ten percent to 25% false-negative rate

o

Current recom m endations for water-soluble contrast first if perforation likely

o

Barium m ay lim it visibility for later endoscopy: 

o

o

More irritating if extravasates into m ediastinum

Water-soluble contrast provides better visibility: 

Less reaction if extravasates into m ediastinum



May cause chem ical pneum onitis if aspirated

Nonionic contrast m ay be safest, but is m ore expensive.



Endoscopy for suspected perforation, caustic ingestions, and esophageal foreign body rem oval

P.387

Differential Diagnosis 





Pulm onary: o

Tracheal injury

o

Pneum othorax

Cardiovascular: o

Myocardial infarction

o

Aortic dissection

o

Spontaneous pneum om ediastinum

Other esophageal em ergencies: o

Peptic stricture

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o

Esophageal neoplasm

o

Schatzki ring

o

Diverticula

o

Achalasia

o

Diffuse esophageal spasm

o

Nutcracker esophagus

o

Gastroesophageal reflux

o

Esophagitis

Treatment Pre Hospital Alert 

Chest pain should be presum ed cardiac until proven otherwise



Airway protection, frequent suctioning



Intravenous crystalloid if patient is hypotensive, vom iting, or if hem atem esis is present



Avoid neutralizing agents in caustic ingestions as that m ay worsen injury



Avoid copious am ounts of oral fluids in caustic ingestions to prevent em esis.

Initial Stabilization 

Manage airway and resuscitate as needed



Intravenous access, m onitoring



Early intubation for penetrating neck and chest wounds



Frequent suctioning of copious secretions



Fluid replacem ent

ED Treatment

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General Measures 

Foreign bodies/food im paction: o

Eighty percent pass, 20% need endoscopy, <1% need surgery

o

Glucagon m ay be tried: 1 m g IV and repeated in 20 m inutes

o

Nitroglycerin or nifedipine m ay be tried.

o

Carbonated beverages in com bination with glucagons m ay be helpful

o

Valium m ay be of benefit for foreign bodies in the upper (striated m uscle) esophagus

o

Gastrointestinal consultation and endoscopic extraction if not relieved



Caustic ingestions: o

Em esis/lavage contraindicated

o

Im m ediate decontam ination with m ilk

o

Avoid neutralizing agents as they m ay cause exotherm ic reaction

o

Gastrointestinal consultation for early endoscopy to provide prognostic inform ation



Tears/perforations: o

Partial-thickness tears usually heal spontaneously.

o

Gastrointestinal consultation m ay be needed for diagnosis (endoscopy).

o

Perforation requires surgical consultation for thoracotom y and prim ary repair

o

Broad-spectrum parenteral antibiotics for perforation

Pediatric Considerations 

Certain swallowed foreign bodies require gastrointestinal consultation and endoscopic rem oval: o

Sharp objects: fish bones, straight pins, razor blades,

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pencil o 

Caustic objects: button batteries

Other objects m ay pass on their own if below the lower esophageal sphincter and require follow-up only: o

Coins, buttons, m arbles

o

Open safety pins m ay pass spontaneously if blunt end forward 

Consult pediatric gastrointestinal specialist

Medication (Drugs) 

Foreign bodies/food im pactions: o

Glucagon: 1â€“2 m g (peds: 0.02â€“0.03 m g/kg) IV; m ay repeat once in 20 m inutes



o

Nitroglycerin: 0.4 m g sublingually

o

Valium : 5â€“10 m g (peds: 1â€“2 m g) IV

Ingestions: o



Antibiotics if perforated

Perforation: o

Cefoxitin: 1â€“2 g (peds: 100â€“160 m g/kg/24h) IV q6hâ€“q8h

o

Gentam icin: 1.0â€“1.7 m g/kg (peds: 1.5â€“2.5 m g/kg/24h) IV q8h

Follow-Up Disposition Admission Criteria 

Caustic ingestion



Sharp foreign bodies

Pa ge 1 7 7



Airway com prom ise



Penetrating neck or chest traum a



Evidence of sepsis, m ediastinitis, or esophageal perforation



Significant bleeding



Inability to tolerate oral fluids

Discharge Criteria 

Self-lim ited bleeding from partial-thickness tear



Foreign body or food im paction that has passed lower esophageal sphincter

References 1. Poley JW, Steyerberg EW, et al. Ingestion of acid and alkaline agents:outcom e and prognostic value of early upper endoscopy. Gastrointest Endosc. 2004;60(3):372â€“377. 2. Richardson JD, Miller FB, Carrillo EH, et al. Com plex thoracic injuries. Surg Clin North Am . 1996;76:725â€“748. 3. Shanm uganathan K. Im aging diagnosis of nonaortic thoracic injury. Radiol Clin North Am . 1999;37:533â€“551. 4. Stack L, Munter D. Foreign bodies in the gastrointestinal tract. Em erg Med Clin North Am . 1996;14:557â€“570. 5. Swann L, Munter D. Esophageal em ergencies. Em erg Med Clin North Am . 1996;14:557â€“570.

Miscellaneous SEE ALSO: Boerhaave Syndrom e; Foreign Body, Esophageal; Mallory-Weiss Syndrom e; Neck Traum a, Anterior Blunt and Penetrating

Codes ICD9-CM

Pa ge 1 7 7

862.22 862.32 Esophagus

ICD10 S27.8 S19.8 S11.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ethylene G lyco l, Po iso ning

Ethylene

Glycol, Poisoning Kirk Cumpston

Basics Description 

Peak levels in 1â€“4 hours



Half-life, 2.5â€“4.5 hours



Less than 20% excreted unm etabolized by kidneys



Three stages (m ay overlap): o

First stage: 1â€“12 hours after ingestion: 

Central nervous system depression



Gastrointestinal sym ptom s



Worsening acidosis



Com a



Convulsions



Cerebral edem a



Tetany and m yoclonus secondary to hypocalcem ia

o

o

Second stage: 12â€“36 hours after ingestion: 

Cardiopulm onary sym ptom s



When m ost deaths occur

Third stage: 36â€“72 hours after ingestion:

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

Oliguria



Flank pain



Acute renal failure



Bone m arrow suppression and pancytopenia

Pathophysiology Metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase ultim ately to oxalic acid: 

Results in aldehyde and acid m etabolites



Directly toxic to central nervous system , heart, lungs, and kidneys

Etiology 



Ethylene glycol-containing products: o

Antifreeze

o

Solvents

Minim um reported lethal dose is 30 m L of 100% ethylene glycol.

Diagnosis Signs and Symptoms 



Cardiovascular: o

Tachycardia/bradycardia/other dysrhythm ias

o

Hypertension/hypotension

Central nervous system : o

Inebriation/irritability

o

Ataxia

o

Obtundation

o

Com a

o

Cerebral edem a

o

Convulsions

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





o

Peripheral nervous system

o

Cranial nerve abnorm alities

Gastrointestinal: o

Nausea/vom iting

o

Abdom inal pain

Pulm onary: o

Hyperventilation/tachypnea/Kussm aul respiration

o

Pulm onary edem a

Renal: o

Acute renal failure

o

Costal-vertebral angle tenderness

o

Crystalluria

Essential Workup 

History of all substances ingested



Drawn sim ultaneously: o

Arterial blood gas

o

Serum ethylene glycol, m ethanol, isopropyl alcohol, and ethanol levels

o

Electrolytes, BUN/creatinine, glucose

o

Measured serum osm olality (by freezing point depression)

o

Serum calcium , phosphorus, m agnesium

Tests Lab 



Determ ine the anion gap: o

Anion gap = (Na + ) - (Cl - + HCO 3 - )

o

Norm al anion gap is 8â€“12.

Determ ine osm ol gap: o

Osm ol gap = m easured osm olality - calculated osm olarity

o

Increased osm ol gap: >10

Pa ge 1 7 7

o

Calculated osm olarity = 2(Na + ) + glucose/18 + blood urea nitrogen/2.8 + ethanol (in m g/dL)/4.6

o

Calculated to screen for ethylene glycol ingestion because toxic alcohol levels are not com m only available in tim ely m anner from m ost clinical laboratories

o

Most useful early in course of ethylene glycol poisoning or with concurrent ethanol ingestion

o

With concurrent ethanol ingestion, osm ol gap tends to be larger and acidosis tends to be less severe because relatively less ethylene glycol has been converted to acid-producing m etabolites.

o

Norm al osm ol gap does not rule out ethylene glycol ingestion.

o

Late presentation after ethylene glycol ingestion m ay m anifest itself with only an elevated anion gap without a significant osm ol gap.



Ethylene glycol, m ethanol, isopropyl alcohol levels



Ethanol level: o

Measured to determ ine am ount of ethanol bolus necessary to attain therapeutic level, and to determ ine coingestants



Urinalysis: o

Envelope-shaped oxalate crystals: insensitive but specific finding. Absence of urine calcium oxalate crystals does not rule out ethylene glycol exposure.

o

Ketones m ay be owing to isopropyl alcohol ingestion, starvation, or diabetic ketoacidosis.

Diagnostic Procedures/Surgery Wood lam p inspection of urine or gastric contents: 

Detects presence of fluorescein, a com m on antifreeze additive

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

Insensitive and not specific m arker of antifreeze ingestion: o

Absence of urinary fluorescence does not rule out ethylene glycol exposure.

Differential Diagnosis 

Increased osm ol gap: o

Methanol

o

Ethanol

o

Diuretics (m annitol, glycerin, propylene glycol, sorbitol)



o

Isopropyl alcohol

o

Ethylene glycol

o

Acetone, am m onia

o

Propylene glycol

Elevated anion gap m etabolic acidosis: A CAT MUDPILES o

Alcoholic ketoacidosis

o

Cyanide, CO, H 2 S, others

o

Acetam inophen-associated fulm inant hepatic failure

o

Toluene

o

Methanol, m etform in

o

Urem ia

o

Diabetic ketoacidosis

o

Paraldehyde, phenform in

o

Iron, INH

o

Lactic acidosis from other causes

o

Ethylene glycol

o

Salicylates

P.389

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Treatment Pre Hospital Bring containers of all possible ingestants.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Supplem ental oxygen, cardiac m onitor, secured intravenous line with 0.9% norm al saline



D 5 0 W (or Accu-Chek), naloxone, and thiam ine for altered m ental status

ED Treatment Prevent Further Ethylene Glycol Absorption 

Gastric lavage with nasogastric tube: o

If <1 hour since ingestion, if patient is in com a, or if history of large ingestion



Ipecac contraindicated



Initial dose of activated charcoal for potential coingestants, but unlikely to help if only ethylene glycol: o

Activated charcoal adsorbs ethylene glycol poorly.

Prevent Ethylene Glycol Conversion to Toxic Metabolites 

4-Methylpyrazole (4-MP, Antizol): o

Initiate before ethylene glycol level returns, if accidental ingestion greater than a sip or intentional ingestion or altered m ental status associated with unexplained osm ol gap or elevated anion gap acidosis.

o

Com petitive inhibitor of alcohol dehydrogenase

o

Disadvantage over ethanol: 

More expensive

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o

Advantages over ethanol: 

Easy dosing



No need for continuous infusion



No inebriation/central nervous system depression



No hypoglycem ia, hyponatrem ia, or hyperosm olality



Not necessary to check ethanol levels



Reduction in degree of nursing care and m onitoring



Ethanol therapy: o

Initiate before ethylene glycol level returns, if potentially toxic ingestion is suspected.

o

Ethanol: greater affinity than ethylene glycol for alcohol dehydrogenase

o

Slows conversion to toxic m etabolites

o

Indications: 

History of accidental ethylene glycol ingestion of greater than a sip or intentional ethylene glycol ingestion



Altered m ental status associated with unexplained osm ol gap or elevated anion gap m etabolic acidosis

o

Goal: serum ethanol level of 100â€“150 m g/dL

o

Continue ethanol therapy until ethylene glycol level is zero.

Enhance Elimination 

Hem odialysis: o

Decreases elim ination half-life of ethylene glycol and rem oves toxic m etabolites

o

Indications: 

Severe acidosis or osm ol gap

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

No ethylene glycol levels with m etabolic acidosis, and clinical suspicion of significant ingestion

o



Persistent electrolyte or fluid disturbance



Renal insufficiency



Pulm onary edem a



Cerebral edem a



Serum ethylene glycol level >25â€“50 m g/dL

Continue hem odialysis until ethylene glycol level approaches zero.



Adm inister thiam ine, pyridoxine, and m agnesium : o

Thiam ine, pyridoxine, and m agnesium are cofactors in m etabolism of ethylene glycol that m ay prom ote conversion to nontoxic m etabolites.

o

No hum an data supporting this theory

Correct Secondary Disorders 

Ensure adequate urine output via intravenous fluids.



Sodium bicarbonate therapy for acidem ia with pH <7.1



Monitor/replace calcium : o

Deposition of calcium into tissues can result in hypocalcem ia.

Medication (Drugs) 

Activated charcoal: 1 g/kg PO



Dextrose: D 5 0 W one am pul: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Ethanol: o

Oral: 50% ethanol solution (100-proof liquor) via nasogastric tube 

Loading dose: 1.5 m L/kg

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

Maintenance dose: 0.2â€“0.4 m L/kg/h



Maintenance dose during hem odialysis: 0.4â€“0.7 m L/kg/h

o

Intravenous: 10% ethanol in D 5 W: 

Loading dose: 7.5 m L/kg over 30â€“60 m inutes



Maintenance infusion: 1â€“2 m L/kg/h



Maintenance infusion during hem odialysis: 2â€“3.5 m L/kg/h



4-Methylpyrazole: o

Loading dose: 15 m g/kg slow infusion over 30 m inutes

o

Maintenance dose: 10 m g/kg q12h for 4 doses, then 15 m g/kg q12h until ethylene glycol levels are reduced to <20 m g/dL

o

Dosing related to hem odialysis: 

Do not adm inister dose at beginning of dialysis if last dose was <6 hours previously.



Adm inister next dose if last dose was >6 hours previously.



Dose q4h during dialysis.



If tim e between last dose and end of dialysis was <1 hour from last dose, do not adm inister new dose.



If tim e between last dose and end of dialysis was 1â€“3 hours from last dose, adm inister one half of next scheduled dose.



If tim e between last dose and end of dialysis was >3 hours from last dose, adm inister next scheduled dose.



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Pyridoxine: 100 m g/d for 2 days



Sodium bicarbonate: 1â€“2 m Eq/kg in D 5 W IV

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

Thiam ine: 100 m g (peds: 50 m g) IV or IM per day for 2 days

Pediatric Considerations 

Measure fingerstick glucose hourly to m onitor for ethanol-induced hypoglycem ia.



Monitor serum chem istry for hyponatrem ia if patient is on ethanol drip.

Follow-Up Disposition Admission Criteria 

All patients with significant ethylene glycol ingestion, even if initially asym ptom atic



ICU adm ission for seriously ill patients



Transfer to another facility if hem odialysis or 4-Methylpyrazole is indicated but not readily available.

Discharge Criteria Asym ptom atic patient with isolated ethylene glycol ingestion, if serum ethylene glycol level is undetectable and no m etabolic acidosis

References 1. Barceloux D, Krenzelok E, Olson K, et al. Am erican Academ y of Clinical Toxicology Practice Guidelines on the Treatm ent of Ethylene Glycol Poisoning. Ad Hoc Com m ittee. J Toxicol Clin Toxicol. 1999;37:537â€“560. 2. Brent J, McMartin K, Phillips S, et al. Fom epizole for the treatm ent of ethylene glycol poisoning. N Engl J Med. 1999;340:832â€“838. 3. Ford M, McMartin K. Ethylene glycol and m ethanol. In: Clinical Toxicology. Philadelphia: WB Saunders; 2001:757â€“767.

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4. Leikin J, Paloucek F. Alcohol. In: Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:201â€“202. 5. Leikin J, Paloucek F. Ethylene glycol. In: Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:556â€“557. 6. Leikin J, Paloucek F. Fom epizole. In: Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:599â€“600.

Codes ICD9-CM 982.8 Other non-petroleum -based solvents

ICD10 T52.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > External Ear C ho ndritis/Abscess

External Ear

Chondritis/Abscess Assaad J. Sayah

Basics Description Inflam m ation and infection of the pinna

Etiology Mechanism 



Cartilage of the external ear is easily dam aged due to: o

Lack of overlying subcutaneous tissue

o

Relative avascularity

o

Exposed position

Chondritis: o

Most com m only a secondary com plication of otic traum a and burns

o

Onset is often insidious and m ay be delayed until apparent healing has occurred.



Disfiguration of the pinna occurs without proper treatm ent: o

Ranges from being a shriveled, cauliflowerlike ear to com plete loss of the external ear and possible

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stenosis of the auditory m eatus.

Causes 



Com m on causes of chondritis include: o

Chem ical or therm al burns

o

Frostbite

o

Hem atom a form ation

o

Mastoid surgery

o

Hum an bites

o

Deep abrasions

o

External otitis

o

High piercing of the ear lobe

Bacteria involved: o

Pseudom onas aeruginosa

o

Staphylococcus

o

Proteus

Diagnosis Signs and Symptoms 

Initially a dull pain that increases in severity



Pinna: o

Painful

o

Exquisite tenderness

o

Erythem atous

o

Warm th

o

Loss of contours caused by edem a often with sparing of the lobule.



Increase of the auriculocephalic angle



Fluctuant areas develop with eventual breakdown and suppuration.

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

Entire ear involvem ent if untreated: o

Disfigurem ent can occur.



Fever



Chills

Essential Workup Clinical diagnosis: 

Typical physical findings in com bination with aforem entioned causes

Tests Lab Only if system ic signs of infection: 

CBC



Blood cultures

Treatment ED Treatment General Postinjury Preventive Measures 

Prevention of chondritis is of the utm ost im portance: o

Difficult m anagem ent and disfiguring potential



Avoid pressure to the injured ear



Minim ize active dÃ©bridem ent of eschars and crusts



Gentle washing twice daily with antibacterial soap and water followed by com plete drying and application of topical antibiotics



Keep hair away from the ear



Oral antibiotics for m inor cases of early ear-lobe inflam m ation



Parenteral antibiotics and early surgical drainage for

Pa ge 1 7 9

patients with chondritis

Medication (Drugs) 

Cephalexin: 500 m g (peds: 50 m g/kg/d) PO q.i.d.



Ciprofloxacin: 500 m g PO b.i.d. (adult)



Dicloxacillin: 500 m g (peds: 25 m g/kg/d) PO q.i.d.



IV antibiotics for severe infection



Apply topical antibiotics when there's a break in skin barrier.

P.391

Follow-Up Disposition Admission Criteria 

Edem a, erythem a, and significant ear tenderness



Toxic patient with fever and chills



Im m unocom prom ised patient

Discharge Criteria Stable patient without system ic signs with close ear-nose-throat (ENT) follow-up

ENT Consult 

For chondritis, abscess, and necrosis of the involved cartilage



Early surgical drainage for chondritis



Aggressive early m anagem ent m ay prevent gross ear

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deform ity.

References 1. Bentrem DJ, Bill TJ, Him el HN, et al. Chondritis of the ear: a late sequela of deep partial thickness burns of the face. J Em erg Med. 1996;14:469â€“471. 2. More DR, Seidel JS, Bryan PA. Ear-piercing techniques as a cause of auricular chondritis. Pediatr Em erg Care. 1999;15(3):189â€“192. 3. Staley R, Fitzgibbon JJ, Anderson C. Auricular infections caused by high ear piercing in adolescents. Pediatrics. 1997;99:610â€“611.

Codes ICD9-CM 733.99

ICD10 H60.0 M94.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Extrem ity Traum a, Penetrating

Extremity

Trauma, Penetrating Gary M. Vilke

Basics Description Penetrating injury to extrem ity

Diagnosis Signs and Symptoms 

Entry and exit wound (if present), lacerations



High-m uzzle-velocity gunshot wounds: o

Produce shockwave that results in significant tissue injury

o

Often exit wound dem onstrates m ore tissue dam age than entrance wound.



Vascular injury: o

Arterial injury: 

Decreased or absent distal pulse



Distal ischem ic changes



Expanding hem atom a

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 o

Bruit or thrill over injury

Presence of distal pulse does not exclude proxim al vascular injury.





Neurologic injury: o

Paresthesias

o

Decreased or absent m otor function

o

Dim inished sensation distal to injury

Musculoskeletal injury: o

Visible deform ity

o

Ligam entous laxity in joints adjacent to injury suggests tendon injury

o

Effusion in adjacent joint indicates fracture or ligam entous injury.



Com partm ent syndrom e: o

Suggested by severe and constant pain over involved com partm ent

o

Pain on active and passive extension or flexion of distal extrem ity

o

Weakness, pain on palpation of com partm ent

o

Hypesthesia of nerves in com partm ent

o

Pulselessness and pallor are late findings.

History 

Mechanism of injury: o

Stab or puncture

o

Gunshot

o

Laceration

o

Bite

o

High-pressure injection injury



Age of wound



Circum stances of wounding: o

Assault

o

Self-inflicted wound

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o 

Dom estic violence

Co-m orbid conditions: o

Im m unosuppression or diabetes

o

Valvular heart disease

o

Asplenia

o

Peripheral vascular disease

Physical Exam 

Note location, length, depth, and shape of prim ary wound and exit wound, if present.



Vascular injury: o

Com pare distal pulses by palpation and with Doppler study.

o

Assess capillary refill: 

o

Abnorm al if >2 seconds

Ankle-brachial index (ABI): 

Take blood pressure (BP) in calf and arm (involved extrem ity).



Systolic pressure difference of >10 m m Hg suggests vascular injury.

o

Expanding hem atom a, bruit, or thrill over injury also indicates vascular injury.



Neurologic injury: o



Assess distal m otor function and sensory function: 

Two-point discrim ination



Light touch



Proprioception

Musculoskeletal injury: o

Note associated crush, tendon, or ligam entous injury and bony deform ity.



o

Exam ine adjacent joints for range of m otion.

o

Assess for com partm ent syndrom e.

Explore wound for foreign body

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Tests Lab 

Culture of acute wounds is not indicated.



Wounds with signs of infection m ay be cultured to guide antibiotic choice.

Imaging 

Radiograph to evaluate for radiopaque foreign body or underlying fracture: o



Minim um anteroposterior (AP) and lateral views

Radiolucent foreign bodies m ay be located by fluoroscopy, ultrasound (US), or CT.



Arteriogram is indicated when vascular injury is suspected and im m ediate vascular surgery is not required.

Treatment Pre Hospital Cautions: 

Control hem orrhage with direct pressure over site.



Elevate extrem ity.



Evaluate neurovascular status.



Leave im paled objects in place and stabilize in current position.



Pain control

Initial Stabilization 

Manage airway and resuscitate as indicated.



Expose wound com pletely and rem ove constricting clothing or jewelry.



Control hem orrhage with direct pressure.

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

Blind clam ping within wound and prolonged tourniquet use are not recom m ended.

P.393

ED Treatment 

Pain control



Com plete neurologic assessm ent before local anesthesia



Prolonged soaking of wounds, particularly with cytotoxic agents, is not recom m ended.



Rem ove any visible debris and dÃ©bride devitalized tissue.



Most im portant is copious high-pressure irrigation with saline.



Tetanus prophylaxis



Stab wounds and gunshot wounds should receive single dose of cefazolin in ED.



Im m obilize extrem ity if there is suspicion of significant vascular injury, tendon injury, fracture, or joint violation.



Loss of pulse or distal ischem ia requires em ergent surgery: o



Do not delay surgical m anagem ent for arteriogram .

Lacerations m ay be closed if they have been adequately cleaned, have m inim al tissue loss, and are seen within 6â€“8 hours of injury: o

Delayed prim ary closure is alternative for older or contam inated wounds.



Puncture or gunshot wounds should not be closed prim arily.

Special Considerations 

Plantar puncture wounds:

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o

Exam ine wound carefully under bright light.

o

Rem ove any foreign m aterial.

o

Clean wound carefully: 

Coring wound is controversial and should be reserved for rem oval of devitalized tissue or im bedded debris.

o

Probing or high-pressure irrigation of puncture wound will only force particulate m atter further into wound.

o

Prophylactic antibiotics are not recom m ended (unless patient is diabetic or im m unocom prom ised).

o

Close follow-up is necessary to assess for infection from unseen foreign body: 

If not treated with aggressive dÃ©bridem ent, can lead to osteom yelitis



High-pressure injuries of hand: o

Orthopedic evaluation in ED is essential because wounds that appear trivial on surface m ay have product track up tendon sheaths into m ore proxim al aspects of hand.

o

Som e paints and other products are radiopaque, and plain radiographs m ay dem onstrate extent of spread.



Soft tissue foreign bodies (FB): o

Sm all inert FB in wound, including bullets, not easily retrievable and not in close proxim ity to joint, tendon, vessel, or nerve can be left in place with close follow-up.

o

FB in hands and feet should be referred to specialist as they often m igrate and becom e or rem ain sym ptom atic.

o

Organic m aterials (thorns, wood, spines, clothing) should be rem oved as are very reactive.

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Medication (Drugs) 

Tetanus prophylaxis: TD 0.5 m L IM



Wounds >12 hours old, especially of hands and lower extrem ities, crush wounds with devitalized tissue, contam inated wounds: o

Cefazolin: 1 g IV/IM (peds: 20â€“40 m g/kg IV/IM single dose in ED)

o

Cephalexin: 500 m g PO (peds: 25â€“50 m g/kg/d) q.i.d. for 7 days or 

Am oxicillin/clavulanate: 875/125 m g PO (peds: 25 m g/kg/d) b.i.d. for 7 days

o

Erythrom ycin: 333 m g PO t.i.d. (peds: 40 m g/kg/d q6h for 7 days)



Contam inated wounds in patients with pre-existing valvular heart disease: o

Cefazolin: 1 g IV/IM, then cephalexin, 500 m g PO q.i.d. for 7 days

o

If penicillin allergic:

o

EES: 800 m g PO, then 400 m g PO q6h for 7 days or 

Clindam ycin: 300 m g PO q6h for 7 days

Follow-Up Disposition Admission Criteria 

Em ergent surgical consultation and adm ission are required for any penetrating wounds with potential for vascular com prom ise, associated com partm ent syndrom e, and joint penetration.

Pa ge 1 7 9



High-m uzzle-velocity penetrating gunshot wounds



Diabetic or im m unocom prom ised patients with contam inated wounds

Discharge Criteria Penetrating extrem ity injuries not requiring surgical intervention m ay be discharged after appropriate wound care with instructions to elevate extrem ity, keep wound clean, and to return for recheck in 24â€“48 hours or for any signs of infection.

References 1. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients presenting with penetrating extrem ity traum a. Ann Em erg Med, 1999;33:612â€“636. 2. Haverstock BD, Grossm an JP. Puncture wounds of the foot. Evaluation and treatm ent. Clin Podiatr Med Surg. 1999;16(4):583â€“596. 3. Modrall JG, Weaver FA, Yellin AE. Diagnosis and m anagem ent of penetrating vascular traum a and the injured extrem ity. Em erg Med Clin North Am . 1998;16:129â€“144. 4. Newton E. Peripheral vascular injuries. In: Marx JA, et al, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 456â€“467. 5. Schnall SB, Mirzayan R. High pressure injuries to the hand. Hand Clin. 1999;15(2):245â€“248.

Codes ICD9-CM 959.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F acial F ractures

Facial Fractures

David W. Munter

Basics Description 

Typically blunt traum a from m otor vehicle accidents, direct blows, or falls



Consider physical assault and dom estic violence, especially in wom en and children



Open fractures com m on



Many facial fractures are com plex and are not easily classified

Etiology 

Le Fort fractures involve the m axilla and are classified as: o

Le Fort I: transverse fracture of m axilla below nose but above teeth through lateral wall of m axillary sinus to lateral pterygoid plate

o

Le Fort II: pyram idal fracture from nasal and ethm oid bones through zygom aticom axillary suture and m axilla, often involving m axillary sinuses and infraorbital rim s

o

Le Fort III: craniofacial disjunction with elongated, flattened face owing to fractures through frontozygom atic suture, orbit, base of nose, and

Pa ge 1 8 0

ethm oid bone o

Le Fort IV: includes frontal bone in addition to Le Fort III

o

A patient m ay have different level Le Fort fractures on each side of the face.



Zygom atic arch fractures often occur in two or three places and can involve the orbit and m axilla (tripod fracture).



Inner plate frontal sinus fractures are associated with cerebrospinal fluid (CSF) leaks and ocular injuries.



Orbital fractures m ost com m only involve the orbital floor (blow-out fracture), and are com m only associated with ocular injuries.

Pediatric Considerations 

Maxillofacial fractures rarely seen in children younger than 6 years; suspect nonaccidental traum a.



Falls and m otor vehicle accidents account for m ost cases.



High incidence of associated head injury

Diagnosis Signs and Symptoms 

Most posttraum atic deform ities of the face represent underlying fractures.



Pain, swelling, ecchym osis, and deform ity



CSF rhinorrhea, facial hem orrhage, epistaxis, raccoon eyes



Facial anesthesia with nerve entrapm ent or injury



Associated injuries; tooth, m andible, eye, tear duct, skull, and neck

Pa ge 1 8 0



Bluish fluid-filled sac overlying nasal septum is a septal hem atom a and is critical to detect.

Physical Exam 

Im m ediately assess airway.



Most im portant: o

Palpate entire face for tenderness, step-offs, depressions, and crepitus.

o

Check for m andibular injuries or m alocclusion.

o

Nasal speculum exam for septal hem atom a or CSF leak

o

Assess for areas of facial anesthesia.

o

Careful eye exam including funduscopic exam ; obtain a visual acuity; assess for telecanthus (intercanthal width >30 to 35 m m ), upward dysconjugate gaze (indicative of ocular m uscle entrapm ent in an orbital floor blow-out fracture)



Le Fort fractures are assessed by placing thum b and index finger of one hand on the bridge of the nose and pulling upper teeth with other hand: o

Le Fort I: m ovem ent of hard palate and m axillary dentition only (your hand on the nose will not feel m ovem ent)

o

Le Fort II: m ovem ent of hard palate, m axillary dentition, and nose (your hand on the nose will feel m ovem ent)

o

Le Fort III: m ovem ent of entire m idface

Pediatric Considerations Sedation with diazepam or m idazolam m ay be needed to perform an adequate exam .

Tests

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Imaging 

Com puted tom ography (CT) scanning is the im aging m odality of choice for com plex facial injuries.



Obtain radiographs of any area of tenderness, crepitus, depression, or deform ity, with the exception of isolated nasal injuries.



A Waters view is a good screening exam ; Caldwell and lateral facial film s are less helpful: o

May show fractures, asym m etry, or blood in the sinuses, or the classic teardrop opacity in the m axillary sinus representing an orbital floor blow-out fracture



Jug-handle views (subm ental vertex) m ay be needed to view zygom atic arch fractures.

Differential Diagnosis 

Nasal fracture



Zygom a fractures (arch or tripod fracture)



Le Fort fracture



Skull fractures including frontal sinus fractures and cribriform plate fractures



Nasofrontoethm oid com plex fractures



Mandibular fractures



Associated injuries to teeth, neck, brain



Contusions or lacerations without underlying fractures

Treatment Pre Hospital Alert

Pa ge 1 8 0



Airway control takes precedence: o

Attem pt chin lift, jaw thrust, and suctioning first.

o

Underlying injuries m ay m ake these attem pts as well as use of bag/valve/m ask (BVM) device unsuccessful.

o

Severe facial fractures m ay preclude oral intubation.

o

Nasotracheal intubation contraindicated in m assive facial or nasal traum a

o

Cricothyroidotom y perform ed if intubation using rapid-sequence induction (RSI) cannot be perform ed.



If associated injuries are present, protect cervical spine.

P.395

Initial Stabilization 

Aggressively m anage airway: RSI is initial airway m anagem ent of choice in facial injuries; use etom idate or m idazolam and vecuronium , rocuronium , or succinylcholine for rapid-sequence induction.



Surgical airway (cricothyroidotom y or needle cricothyroidotom y) m ay be required if RSI is unsuccessful.



Nasotracheal intubation is contraindicated in m ost facial fractures.



Protect cervical spine until clinically or radiographically cleared.



Once airway is secure, other m ajor injuries take precedence over facial injuries.



Bleeding m ay be difficult to control and m ay require posterior packing if direct pressure does not work.

ED Treatment 

Consult ear, nose, throat specialist; plastic surgery; or oral surgery for com plex fractures, including all Le Fort

Pa ge 1 8 0

fractures and frontal sinus fractures involving the posterior table. 

Antibiotics (cefazolin or clindam ycin in penicillin-allergic patients) for open fractures and CSF leak



Tetanus prophylaxis



Parenteral pain m edication (m orphine or fentanyl)



A septal hem atom a m ust be drained in the ED: o

Anesthetize, aspirate with an 18- to 20-gauge needle, and pack both nares with Vaseline gauze.

o

Discharge on am oxicillin or erythrom ycin with recheck in 24 hours by ear, nose, and throat specialist.



Nondisplaced zygom atic fractures can be discharged with analgesics (acetam inophen or ibuprofen); refer displaced zygom a and tripod fractures that are otherwise stable for outpatient reduction in 2â€“3 days after swelling is reduced.



Overlying lacerations with sim ple fractures can be sutured in the em ergency departm ent; if patient is discharged, treat with am oxicillin or erythrom ycin.

Pediatric Considerations 

Surgical cricothyroidotom y should not be perform ed in children younger than 8 years: o

Needle cricothyroidotom y with jet ventilation m ay be perform ed.



Children are at high risk of associated injuries.



Repair of facial fractures should not be delayed m ore than 3â€“4 days (rapid healing of facial fractures and the risk of m alunion and cosm etic deform ity).

Pa ge 1 8 0

Medication (Drugs) 

Acetam inophen: 650 m g (peds: 10â€“15 m g/kg) PO q4h



Am oxicillin: 250 m g (peds: 40â€“80 m g/kg/24h) PO q8h



Cefazolin: 1 g (peds: 50â€“100 m g/kg/24h) IV or IM



Clindam ycin: 600â€“900 m g (peds: 25â€“40 m g/kg/24h) PO q8h



Diazepam : 5â€“10 m g (peds: 0.1â€“0.2 m g/kg) IV



Erythrom ycin: 500 m g (peds: 30â€“50 m g/kg/24h) PO q.i.d.



Etom idate: 0.2â€“0.3 m g/kg (peds: 0.2â€“0.3 m g/kg) IV



Fentanyl: 2â€“10 Âµg/kg (peds: 2â€“3 Âµg/kg) IV



Ibuprofen: 600â€“800 m g (peds: 20â€“40 m g/kg/24h) PO t.i.d.â€“q.i.d.



Ketam ine: 1â€“2 m g/kg (peds: 1â€“2 m g/kg) IV



Midazolam : 2â€“5 m g (peds: safety not established, but 0.02â€“0.05 m g/kg per dose has been used) IV



Morphine sulfate: 0.1â€“0.2 m g/kg (peds: 0.1â€“0.2 m g/kg) IV q1hâ€“q4h titrated



Rocuronium : 0.6â€“1.2 m g/kg (peds: 0.6 m g/kg) IV



Succinylcholine: 1â€“1.5 m g/kg (peds: 1â€“2 m g/kg) IV



Vecuronium : 0.1â€“0.3 m g/kg (peds: 0.1â€“0.3 m g/kg) IV

Follow-Up Disposition Admission Criteria 

Significant associated traum a



Airway com prom ise



Le Fort II and III fractures



CSF leak

Pa ge 1 8 0



Posterior table frontal sinus fractures



Most open fractures, excluding sim ple nasal fractures with lacerations

Discharge Criteria 

No evidence of significant head, neck, or other injuries



Closed fractures of the zygom a or anterior table of the frontal sinus with appropriate follow-up in 24â€“36 hours



Septal hem atom as that have been drained in the em ergency departm ent require follow-up in 24 hours.



Refer displaced zygom a and tripod fractures that are otherwise stable for outpatient reduction in 2â€“3 days after swelling is reduced.

References 1. Chang EL, Bernardino CR. Update on orbital traum a. Curr Opinion Ophthalm ol. 2004;15(5):411â€“415. 2. Druelinger L, Guenther M, Marchand EG. Radiographic evaluation of the facial com plex. Em erg Med Clin North Am . 2000;18:393â€“410. 3. Ellis E, Scott K. Assessm ent of patients with facial fractures. Em erg Med Clin North Am . 2000;18:411â€“447. 4. Ferreira P, Marques M, Pinho C, et al. Midfacial fractures in children and adolescents: a review of 492 cases. Br J Oral Maxillofac Surg. 2004;42(6):501â€“505. 5. Iiada S, Koso M, Sugivia T, et al. Retrospective analysis of 1502 patients with facial fractures. Int J Oral Maxillofac Surg. 2001;30:286â€“290. 6. Ng M, Saadat D, Sinha UK. Managing the em ergency airway in LeFort fractures. J Craniom axillofac Traum a. 1998;4(4):38â€“43. 7. Sun JK, LeMay DR. Im aging of facial traum a. Neuroim aging Clin N Am . 2002;12(2):295â€“309.

Codes

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ICD9-CM 801.1 Closed with cerebral laceration and contusion 802.4 Malar and m axillary bones, closed

ICD10 S02.9

Pa ge 1 8 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ailure to Thrive

Failure to Thrive

David A. Listman

Basics Description 

Not a single disease, but a description of a group of sym ptom s



Inadequate physical growth: o

Usually diagnosed earlier than age 2 years

o

Broadly divided into: 

Organic (underlying m edical condition)



Nonorganic (no underlying m edical condition)

o

Found in all socioeconom ic groups

o

Poverty increases risk of failure to thrive (FTT).

o

May result in long-term growth, behavioral, and developm ental difficulties

Genetics Many genetic syndrom es can contribute

Etiology Many diseases with unique causes resulting in one or m ore of: 

Inadequate caloric intake



Inadequate caloric absorption



Excessive caloric expenditure

Pa ge 1 8 1

Diagnosis Signs and Symptoms 

Failure to achieve or m aintain a growth rate appropriate for age



Weight less than two standard deviations below norm al for age (corrected for prem aturity)



Weight that crosses downward through two m ajor percentiles (m ajor percentiles are 5th, 10th, 25th, 50th, 75th, and 90th percentiles) on standard growth chart (see References below) o

Weight loss initially followed by im paired growth in length/height and finally head circum ference



Can m anifest as: o

Reduced m uscle m ass

o

Loss of subcutaneous fat

o

Alopecia

o

Derm atitis

o

Chronic disease

o

Marasm us

o

Kwashiorkor

History 

Detailed feeding history: o

o

Breast-feeding: 

Prior breast-feeding experience



Frequency of feedings



Length of feedings



Fam ily support for breast-feeding

Form ula:

Pa ge 1 8 1



Type of form ula (m ilk, soy, elem ental, prem ie follow-up)



How form ula is prepared (ready to feed, powder, liquid concentrate)











Frequency of feedings



Volum e per feeding

o

Solid foods

o

Vom iting associated with feeds

o

Urine and stool output

Gestational history: o

Maternal m edical com plications

o

Drug or alcohol use

Birth history: o

Com plications

o

Birth weight

Developm ental history: o

Achievem ent of appropriate m ilestones

o

Child's perceived tem peram ent

Psychosocial history: o

Fam ily com position

o

Fam ily/social support

o

Stresses

o

Maternal depression

o

Abuse or neglect

Physical Exam 

Weight, length/height, head circum ference: o

Plotted on appropriate growth chart: 



Include as m any prior growth points as possible.

Dysm orphic features: o

Cardiac disorders

o

Pulm onary disorders

o

Gastrointestinal disorders

Pa ge 1 8 1



Skin exam to include signs of child abuse

Essential Workup 

Detailed history and physical exam



Growth param eters plotted on appropriate growth charts



Observation of fam ilyâ€“child interaction



Direct observation of feeding



CBC, electrolytes, urinalysis, lead level

Tests Lab 

CBC



Infections:



o

Anem ia

o

Leukem ia/m alignancy

o

Lead level

o

Lead poisoning

Chem istry panel (electrolytes, BUN, creatinine, glucose, liver function, protein, album in, calcium , phosphate, m agnesium ):





o

Hydration and acidosis

o

Metabolic disorders

o

Diabetes m ellitus

o

Renal disease

o

Blood gas analysis

o

Renal tubular acidosis

o

Inborn errors of m etabolism

Urinalysis with culture: o

Renal disease

o

Infection

HIV

Imaging

Pa ge 1 8 1

Chest radiograph: 

Tuberculosis



Pneum onia



Cardiom egaly

Diagnostic Procedures/Surgery 

pH probe: o



Sweat chloride test: o



Gastroesophageal reflux

Cystic fibrosis

Tuberculin skin testing

P.397

Differential Diagnosis Organic Causes 



GI: o

Malabsorption syndrom es

o

Celiac disease

o

Cystic fibrosis

o

Food allergy

o

Inflam m atory bowel disease

o

Hepatobiliary disease

o

Hepatitis

o

Cirrhosis

o

Biliary Atresia

o

Obstructive disease

o

Pyloric stenosis,

o

Malrotation

o

Hirschsprung disease

o

Gastroesophageal reflux

Cardiac

Pa ge 1 8 1











o

Congenital heart disease

o

Cyanotic

o

Congestive

o

Acquired heart disease

Pulm onary o

Bronchopulm onary dysplasia

o

Obstructive sleep apnea

o

Chronic lung disease

o

Cystic fibrosis

Hem atologic/oncologic: o

Iron deficiency anem ia

o

Thalassem ia

o

Lead poisoning

o

Leukem ia

Renal: o

Chronic renal insufficiency

o

Renal tubular acidosis

o

Recurrent urinary tract infections (UTIs)

Neurologic/CNS o

Hydrocephalus

o

Hypertonia/hypotonia

o

Generalized weakness (i.e., spinal m uscular atrophy)

Im m unologic o





AIDS

Endocrine: o

Diabetes m ellitus

o

Thyroid/parathyroid disease

o

Adrenal disease

o

Growth horm one deficiency

o

Hypopituitarism

o

Hypophosphatem ic rickets

Infectious:

Pa ge 1 8 1





o

Tuberculosis

o

Parasite

Genetic/congenital o

Fetal alcohol syndrom e

o

Sm ith-Lem li Opitz syndrom e

o

Cleft lip/palate

o

Inborn errors of m etabolism

Toxic

Nonorganic Causes Parentâ€“child dysfunction: 

Motherâ€“infant bonding problem s



Maternal m ental illness/substance abuse



Inexperienced m other



Breast-feeding difficulties



Im proper form ula preparation



Chaotic fam ily environm ent



Child abuse or neglect



MÃ¼nchhausen syndrom e by proxy

Treatment Initial Stabilization 

Check for hypoglycem ia



Fluid resuscitation when dehydrated



Supportive/nonjudgm ental environm ent

ED Treatment 

Recognize/identify child with FTT.



Rule out organic abnorm alities: o



Organic causes m ay have specific treatm ents.

Social services consult

Pa ge 1 8 1



Breast-feeding consult: o

Advise on appropriate feeding.

Medication (Drugs) Dependent on underlying cause

Follow-Up Disposition Admission Criteria 

Organic cause requiring m edical adm ission



Nonorganic causes to observe caregiverâ€“child interaction



Nonorganic causes to observe weight while m onitoring oral intake



Child abuse/neglect



Severe dehydration, m alnutrition, or electrolyte im balance

Discharge Criteria 

Case appropriately m anaged by prim ary care physician



Follow-up is ensured.

Issues for Referral Subspecialty referral depending on cause

References 1. Bithoney WG, Dubowitz H, Egan H. Failure to thrive/growth deficiency. Pediatr Rev. 1992;13:453â€“460. 2. Gahagan S, Holm es R. A stepwise approach to evaluation of undernutrition and failure to thrive. Pediatr Clin North Am . 1998;45(1):169â€“187. 3. Shah MD. Failure to thrive in children. J Clin Gastroenterol.

Pa ge 1 8 1

2002;35(5):371â€“374.

Miscellaneous SEE ALSO: Centers for Disease Control and Prevention, National Center for Health Statistics: Growth charts. Available at http://www.cdc.gov/growthcharts. Accessed April 23, 2005.

Codes ICD9-CM 783.41

Pa ge 1 8 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F atigue

Fatigue

Matthew Mostofi

Basics Description 

A subjective state of overwhelm ing, sustained exhaustion and decreased capacity for physical and m ental work, which is not relieved by rest



Fatigue occurs with or without objective findings on physical exam .



Fatigue is a com m on com plaint in people with and without system ic disease, which m akes this com plaint a challenge to practicing physicians.

Etiology 

The specific m echanism s of fatigue are unknown.



Hem atological:





o

Anem ia

o

Leukem ia

Endocrine: o

Thyroid disorders

o

Adrenal insufficiency

o

Diabetes

o

Pregnancy

Malignancy:

Pa ge 1 8 1

o 



Paraneoplastic syndrom es

Psychiatric: o

Chronic pain

o

Em otional distress

o

Depression

o

Eating disorders

o

Chem ical dependency

o

Withdrawal syndrom es

Sleep disorders: o

Insom nia

o

Sleep apnea



Cardiac and pulm onary disorders



Infections acute and chronic



Rheum atic and autoim m une disorders



Nutritional deficiencies including electrolyte abnorm alities



Physical inactivity and deconditioning



Medications



Chronic fatigue syndrom e: o

Sym ptom com plex which is defined by the Centers for Disease Control and Prevention

o

Severe fatigue lasting greater than 6 m onths

o

No definable organic disease

o

Presence of associated physical sym ptom s: 

Headache,



Arthralgias



Sleep disturbances



Lym phadenopathy



Exercise intolerance



Myalgias

Pa ge 1 8 2

Diagnosis Signs and Symptoms 

Fatigue is a subjective com plaint of exhaustion or tired sensation that interferes with norm al activities of life, and sym ptom s do not resolve with sleep.



There are no specific signs of fatigue, but frequently physical signs m ay hint at the underlying cause of com plaint.

History 

Onset, pattern, duration of fatigue



Associated sym ptom s: fever, night sweats, weakness, dyspnea, weight loss/gain, sleep patterns



Past m edical and surgical history



Psychiatric history: em otional and m ental stressors, depression



Social history: alcohol, drug use, m ajor life events



Medications



Full review of system s

Essential Workup 

Because fatigue is a subjective com plaint, the essential workup is directed at identification of an underlying cause.



Vital signs review, including pulse oxim etry

Tests Lab 

Lab evaluation should be directed by findings of history and physical exam .



CBC: o



Screen for anem ia or leukem ia

Serum glucose:

Pa ge 1 8 2

o

Both hyperglycem ia and hypoglycem ia can present with fatigue.



Pregnancy test



Electrolytes with blood urea nitrogen/creatininer



Thyroid-stim ulating horm one: o



Screen for hypothyroidism

Urine drug screen

Imaging Im aging/special test: special tests are reserved for evaluation of abnorm al physical exam findings or history suggesting further evaluation.

Differential Diagnosis 



Infection: o

Bacterem ia

o

Urosepsis

o

Pneum onia

o

Viral syndrom es

o

Abscess

o

Epstein-Barr virus, Monospot

o

Cytom egalovirus

o

HIV

o

Hum an herpes virus-6

Im m unologic/connective tissue: o

Rheum atologic (rheum atoid arthritis, system ic lupus erythem atosus, juvenile rheum atoid arthritis)



o

Osteoarthritis

o

Fibrom yalgia

o

Myasthenia gravis

o

Lam bert-Eaton syndrom e

Neoplastic: o

Solid or hem atologic cancers

Pa ge 1 8 2











Metabolic: o

Electrolyte abnorm alities

o

Mitochondrial diseases

o

Brom ism

Hem atologic: o

Anem ia

o

Hypovolem ia

o

Hem oglobinopathy

Endocrine: o

Hyperthyroid or hypothyroid

o

Adrenal insufficiency

o

Diabetes

o

Hypoglycem ia

Neurologic: o

Multiple sclerosis

o

Cerebrovascular accident

o

Am yotrophic lateral sclerosis

Cardiovascular: o

Myocardial infarction

o

Cardiom yopathy

o

Congestive heart failure

P.399





Pulm onary: o

Pneum onia

o

Chronic obstructive pulm onary disease

o

Asthm a

o

Sleep apnea

Gastrointestinal: o

Reflux

o

Peptic ulcer disease

Pa ge 1 8 2

o

Liver disease



Autonom ic dysfunction



Lifestyle:





o

Excessive or insufficient exercise

o

Obesity

Psychiatric: o

Major depression

o

Anxiety

o

Grief

o

Stress

Medication related: o

Drug interactions

o

Com m only caused by blood pressure, cardiovascular, psychiatric, and narcotic m edications



Dehydration

Treatment Initial Stabilization 

ABCs



Adm inister supplem ental oxygen for hypoxia



IV fluid bolus for signs of dehydration

ED Treatment 

Treatm ent should be directed to correction of the underlying cause of fatigue: o

Identify and treat any infectious process.

o

Correct m etabolic and hem atologic disturbances.

o

Diagnose progressive neurologic disease and acute psychiatric crisis.

o

Initiate workup for endocrine and neoplastic disease.

Pa ge 1 8 2

o 

Stop any offending m edications or toxins.

Most cases will not have identifiable cause, so reassurance and close follow up is required.



Recom m end appropriate diet, exercise regim en, and consistent sleep cycles.

Follow-Up Disposition Admission Criteria 

Underlying disease requiring IV m edication or m onitoring



Failure to thrive as outpatient



Unable to provide for self

Discharge Criteria 

Able to care for self



Serious disturbances have been excluded.



Adequate follow-up is arranged.

References 1. Buchwald D, Wener MH, Pearlm an T, et al. Markers of inflam m ation and im m une activation in chronic fatigue and chronic fatigue syndrom e. J Rheum atol. 1997;24(2):372â€“376. 2. Dickinson CJ. Chronic fatigue syndrom e etiological aspects. Eur J Clin Invest. 1997;27(4):257â€“267. 3. Fukuda K. The chronic fatigue syndrom e: a com prehensive approach to its definition and study. International Chronic Fatigue Syndrom e Study Group. Ann Intern Med. 1994;121(12):953â€“959. 4. Maul AC. Chronic fatigue syndrom e. Im m unol Invest. 1997;26(1â€“2):269â€“273. 5. Morrison RE, Keating HJ. Fatigue in prim ary care. Obstet Gynecol

Pa ge 1 8 2

Clin. 2001;28(2). 6. Manzullo EF, Escalante CP. Research into Fatigue. Hem /Onc Clinics of North Am . 2002;16(3).

Codes ICD9-CM 780.7

ICD10 R53

Pa ge 1 8 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F eeding Pro blem s, Pediatric

Feeding

Problems, Pediatric Niels Rathlev Fernando G. Mendoza

Basics Description 

Feeding requires coordinated series of actions involving several com ponents: o

Getting food into oral cavity: appetite, food-seeking behavior, ingestion

o

Swallowing food: oral and pharyngeal phases

o

Ingestion and absorption: esophageal swallowing, gastrointestinal phase



Infant requires m inim um of 100â€“120 calories/kg/d; form ula and hum an breast m ilk provide 20 calories/oz.



Minor feeding difficulties reported in 25â€“50% of norm al children

Etiology 

Behavioral issues: o

Poor environm ental stim ulation

o

Dysfunctional feederâ€“child interaction

o

Selective food refusal

Pa ge 1 8 2





o

Rum ination

o

Phobias

o

Conditioned em otional reactions

o

Depression

o

Poverty (inadequate food available)

Conditioned dysphagia: o

Gastroesophageal reflux

o

Aspiration

o

Fatigue (heart or lung disease)

Structural abnorm alities of the oropharynx, larynx, and trachea: o

Retrognathic jaw

o

Cleft lip/palate

o

Choanal atresia

o

Posterior tongue placem ent

o

Macroglossia

o

Ankyloglossia

o

Pierre Robin sequence

o

Esophageal strictures or stenosis

o

Tonsillar hypertrophy

o

Retropharyngeal m ass or abscess

o

Laryngeal cleft

o

Laryngom alacia

o

Tracheotom y

o

Laryngeal cyst

o

Subglottic stenosis

o

Tracheom alacia

o

Tracheoesophageal cleft

o

Tracheoesophageal com pression from vascular ring/sling

o

Tracheoesophageal fistula

o

Esophageal stricture, web, or ring

Pa ge 1 8 2







o

Esophageal m ass or tum or

o

Foreign body

o

Vascular ring

Neurologic conditions: o

Cerebral palsy

o

Muscular dystrophies

o

Myasthenia gravis

o

Cranial nerve dysfunction

o

Arnold-Chiari m alform ation

o

Mental retardation/developm ental disabilities

o

Brainstem injury

o

Pervasive developm ental disorder

o

Infant botulism

o

Brainstem gliom a

o

Polym yositis/derm atom yositis

Cardiorespiratory problem s: o

Congestive heart failure

o

Cyanotic heart disease

Metabolic dysfunction: o

Hereditary fructose intolerance

o

Organic acidem ias

o

Urea cycle disorders

o

Dum ping syndrom e

Diagnosis Signs and Symptoms 

Sym ptom s: o

Food refusal

o

Failure to thrive

o

Oral aversion

Pa ge 1 8 2



o

Recurrent pneum onia

o

Chronic lung disease

o

Recurrent em esis

Signs: o

Vital signs variable

o

Hydration variable

o

Growth (especially weight) velocity slow; im paired nutritional status

o

Cough, tachypnea, color change

o

Oropharyngeal inflam m ation, infection, or anatom ic abnorm ality

o

Chest: evidence of aspiration

o

Neurologic status: abnorm al m uscle tone, reflexes, m ental status

History 

Define nature of problem s: o

Frequency, duration, and quantity of feeding

o

Onset, duration, and severity

o

Findings during feeding: cough, dyspnea, color change, vom iting, spitting



Variability in feeding patterns is typical; parental im pression of norm al feeding for their infant is best guide: o

Full-term healthy infant usually has 2â€“3 oz of form ula every 2â€“3 hours.

o

Breast-fed baby eats 10â€“20 m inutes on each breast every 2â€“3 hours.

o

One-m onth-old norm ally eats 4 oz every 4 hours.



Poor weight gain



Irritability

Physical Exam 

Observation of feeding: neurom uscular tone, posture,

Pa ge 1 8 3

position; patient m otivation; oral structure and function; efficiency of oral intake 

Ability to handle oral secretions



Pace of feeding



Tongue and jaw m ovem ents



Num ber of swallows to clear a bolus



Noisy airway sounds after swallowing



Gagging, coughing, or em esis during feeding

Essential Workup 

Medical and dietary history



Observation: o

Caretaker feeding child

o

Parentâ€“child interactions

Tests Lab 

Initial assessm ent if child failing to thrive or dehydrated: o

CBC, urinalysis, electrolytes, BUN, glucose

o

Consider erythrocyte sedim entation rate (ESR) and thyroid functions.



Oxim etry if suspected cardiopulm onary concerns



Chest radiograph if suspect aspiration or respiratory cause



Cultures of blood, urine, and CSF if concern of infection



Urine for organic acids if concern for m etabolic disorders

P.401

Imaging 

Chest x-ray film if suspected cardiopulm onary concerns



Fluoroscopy, contrast radiographs, endoscopy, and ultrasonography m ay be needed on an individual basis to

Pa ge 1 8 3

define nature of swallowing, reflux, and associated conditions. 

Direct visualization with nasopharyngeal scope or GI endoscopy



MRI if concerns for brainstem , skull base, or spinal problem s

Diagnostic Procedures/Surgery May need a m ultidisciplinary swallow study involving speech pathologist, pediatrician, and potentially an otolaryngologist

Differential Diagnosis 

Fam ily dysfunction, stress leading to potential neglect



Difficulty getting food into oral cavity: o

Depression or other behavioral issues

o

Deprivation

o

Infection of oropharynx (e.g., herpes or aphthous ulcers)

o

CNS or endocrine disease: 

Thyroid dysfunction



Adrenal dysfunction

o

Sensory deficit

o

Neurom uscular disease

o

Continued dysphagia and fatigue because of overwhelm ing infection (sepsis, m eningitis, urinary tract infection)

o

Anem ia

o

Cardiopulm onary disease: 

Congestive heart failure (CHF)



Congenital heart disease



Bronchopulm onary dysplasia



Bronchiolitis



Pneum onia

Pa ge 1 8 3



Difficulty swallowing: o

Anatom ic abnorm alities of oropharynx or esophagus: congenital or acquired

o

Cardiopulm onary disease

o

Neurom uscular disorder

o

Disorder of esophagus: 

Peristaltic abnorm ality



Mucosal inflam m ation



Esophagitis



Reflux

Treatment Pre Hospital Assess vital signs and hydration; resuscitate as necessary.

Initial Stabilization Resuscitation as required

ED Treatment Observe feeding session with prim ary caretaker. Note: 

Gagging



Coughing



Em esis



Noisy airway sounds



Ability to handle secretions

General Measures 

Speech pathologist m ay be helpful.



Behavioral therapy m ay be needed.

Pa ge 1 8 3

Follow-Up Disposition Admission Criteria 

Suspected system ic infection



Moderate to severe dehydration



Significant failure to thrive, particularly in infants <3 m onths



Decom pensated cardiopulm onary disease



Severe esophagitis or reflux



Sym ptom atic anem ia or endocrine dysfunction



Negligent caretaker

Discharge Criteria 

Dem onstrated ability to tolerate oral feedings



Weight gain if failure to thrive



Reliable caretaker and follow-up



Com plications: o

Poor nutrition m ay lead to im paired brain developm ent, im m unocom prom ise, and other long-term adverse outcom es.

Issues for Referral If significant feeding disorder, m ay need consultation with otolaryngologist and speech pathologist

References 1. Burklow KA, Phelps AN, Schultz JR, et al. Classifying com plex pediatric feeding disorders. J Pediatr Gastroenterol Nutr. 1998;27:143â€“147. 2. Rudolph CD, Link DT. Feeding disorders in children. Pediatr Clin North Am . 2002;49(1):97â€“112. 3. Rudolph CD. Feeding disorders in infants and children. J Pediatr. 1994;125:S116â€“S124.

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Codes ICD9-CM 783.3 Feeding difficulties and m ism anagem ent

ICD10 R63.3, P92.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F eeding Tube C o m plicatio ns

Feeding Tube

Complications Jennifer Kolodchak

Basics Description 

Extubation: o

Accidental or intentional

o

More com m on with nasoenteric tubes com pared with percutaneous endoscopic gastrostom y tubes, gastrostom y tubes (G tubes), or jejunostom y tubes (J tubes)



Occlusion: o

Owing to sm all diam eter: 

Most com m on with nasoenteric tubes



Polyurethane tubes and solution with high pH level less likely to occlude

o

Owing to pill fragm ents (especially if enteric coated or sustained release)

o

Physical incom patibilities between form ula and m edications: 

o

Adherence of form ula residue to inner wall

Essential to rule out m alposition, fracture, and

Pa ge 1 8 3

dislodgm ent 

Peristom al wound infections: o

o

Risk factors: 

Malnutrition



Poor wound healing



Stom al leak



Local irritation



Poor wound care



Im m unosuppression



Diabetes m ellitus



Obesity

Excessive traction on tube: 

Leads to delayed m aturation of gastrocutaneous tract



Stom a leak: o

Problem atic with distal obstruction (m echanical or dysm otility); m ore com m on with high gastric residual



Aspiration pneum onia: o

At risk: 

Im paired cough/gag reflex



Delayed gastric em ptying owing to ileus



Obstruction



Gastroparesis (in diabetes m ellitus or head traum a)



Gastroesophageal reflux (frequent with large nasoenteric tube)



Diarrhea: o

o

Medication induced: 

Antibiotics



Sorbitol or m agnesium -containing m edications

Overgrowth of Clostridium difficile, other bacteria, or Candida

Pa ge 1 8 3

o 

Form ula-related/high-osm olar feeds

Form ula intolerance: o

Residual of 150â€“200 m L suggests gastrointestinal m otility dysfunction: 

Delivery is too rapid.

o

High osm olarity

o

Lactose or fat intolerance

o

Low serum album in

Diagnosis Signs and Symptoms 

Extubation: o



Occlusion: o



Tube rem oved from source

Unable to pass liquid through tube

Tube m igration: o

Distal displacem ent of percutaneous endoscopic gastrostom y tube

o

Obstruction at or distal to pylorus

o

Dum ping syndrom e

o

Ischem ia

o

Intussusception

o

Evidence of distal prolapse on external tube (if m arked)





Peristom al wound infections: o

Cellulitis

o

Necrotizing fasciitis

o

Abscess form ation

Stom a leak: o

Leakage of feedings/gastrointestinal tract contents

Pa ge 1 8 3

around stom a o 







Aspiration pneum onia: o

Cough

o

Dyspnea

o

Hypoxia

o

Food coloring in pulm onary secretions

o

Fever

Misplacem ent of nasoenteric tube in pulm onary tree: o

Pneum othorax

o

Hydrothorax

o

Pleural effusion

o

Bronchopleural fistula

Diarrhea: o

Frequent loose stools

o

Dehydration

Esophageal bezoars: o



Usually m ild and short lived

Form ula and sucralfate

Intolerance to enteral nutrition: o

High residuals

o

Associated with increased risk of aspiration

Essential Workup Careful exam ination of feeding tube site and position of feeding tube within wound

Tests Lab 

Peristom al wound infections: o



CBC for significant infections

Aspiration pneum onia: o

Arterial blood gas or pulse oxim eter

o

CBC

Pa ge 1 8 3



o

Electrolytes, BUN/creatinine, glucose

o

Urine analysis

o

Blood and sputum culture

Diarrhea: o

Stool for white blood cells/culture/C. difficile toxin

Imaging Chest radiographs: 

For nasoenteric tube position



Aspiration pneum onia



Tube m igration: endoscopy or upper gastrointestinal Gastrografin study to confirm m igration of tube into gastrointestinal tract

Treatment Pre Hospital Alert If extubation of tube has occurred, transport tube with patient to facilitate easier replacem ent.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Intravenous fluid resuscitation for dehydration/sepsis

ED Treatment Extubation 



Nasoenteric tube: o

Replaced in em ergency departm ent

o

Confirm position by radiograph before use.

Percutaneous endoscopic gastrostom y (PEG) tube and gastrojejunal (G-J) tube:

Pa ge 1 8 4

o

Takes up to 6 weeks for gastrocutaneous tract/fistula to m ature

o

Im proper or aggressive attem pt at tube replacem ent could lead to disruption of gastrocutaneous tract and subsequent peritonitis.

o

PEG tube in place >1 week before extubation: 

Replace in em ergency departm ent (m ay use a Foley catheter).



Confirm by Gastrografin study if doubt about placem ent.



Secure catheter to abdom inal wall to prevent distal m igration.

o

PEG tube in place <1 week before extubation: 

Fistula m ay not close prom ptly.



Do not replace in em ergency departm ent.



Watch for signs of peritonitis owing to intraperitoneal leak of gastric contents.



May need hospital adm ission and endoscopic tube replacem ent

o

Surgical gastrostom y (G tube) or jejunostom y (J tube): 

Managem ent sim ilar to that for PEG tube except fistula m ay take up to 3 weeks to heal properly



Early dislodgm ent within first 3 days requires em ergency surgical consult and antibiotic coverage for peritonitis.



May need endoscopic replacem ent if <3 weeks old

P.403

Occlusion

Pa ge 1 8 4



Attem pt gentle irrigation with norm al saline, water, or carbonated soda.



If irrigation fails, replace tube.



Do not use m eat tenderizer or pancreatic enzym es.

Tube Migration 



If retraction of tube is possible and well tolerated: o

Secure tube externally.

o

Discharge hom e after brief trial of tube feeding.

If feeding is not tolerated, or if there are signs of persistent obstruction or peritonitis: o

Adm it with consult to appropriate service (surgical/gastrointestinal).



If external tube is cut (accidental or intentional): o

Inner bum per usually passes through gastrointestinal tract.

o

Cases of obstruction, subsequent perforation, and peritonitis have been reported, especially in children.

Peristomal Wound Infections 

Local wound care with hydrogen peroxide



Antibiotics: o

First-generation cephalosporin (cefazolin or cephalexin)

o

Am picillin/sulbactam

o

Am oxicillin/clavulanic acid



Outpatient m anagem ent for m ilder cases



More severe cases require surgical consult for possible drainage/dÃ©bridem ent and inpatient care.



Prophylactic use of antibiotic (cefazolin) before tube placem ent decreases wound infection.

Stoma Leak 

Change from interm ittent to continuous delivery.

Pa ge 1 8 4



Decrease rate of infusion.



Adm inister prokinetic agents (e.g., m etoclopram ide, cisapride, or erythrom ycin).



Local care: o

Keep site clean and dry.

o

Use sucralfate powder or stom a adhesive powder.

Aspiration Pneumonia 

Stop enteral feeding.



Adm inister oxygen and broad-spectrum antibiotics.



Endotracheal intubation with m echanical ventilation for respiratory failure and airway protection when indicated



Prevent by: o

Elevation of head of bed

o

Monitoring gastric residual

o

Use of continuous infusion at graduated rate

o

Use of prokinetic agent

Diarrhea 

Manage cause.



Correct fluid and electrolyte im balance.



Try isotonic, hypotonic, or fat- or lactose-free form ulas.



High-fiber form ula if aforem entioned m easures fail



Antim otility agents: o

Loperam ide

o

Kaopectate

o

Cholestyram ine

Formula Intolerance Prokinetic agents prom ote gastric em ptying.

Medication (Drugs) 

Am oxicillin/clavulanic acid (Augm entin): 500â€“875 m g

Pa ge 1 8 4

(peds: 25â€“45 m g/kg/24h q12h) PO b.i.d. 

Am picillin/sulbactam : 1.5â€“3 g (peds: 100â€“200 m g/kg/24h) IV q6h



Cefazolin (Ancef, Kefzol): 500 m gâ€“1 g (peds: 25â€“100 m g/kg/24h) IV q6h



Cephalexin (Keflex): 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q.i.d.



Cholestyram ine: 2â€“4 g (peds: >6 years 80 m g/kg t.i.d.) PO b.i.d.â€“q.i.d.



Kaopectate: 30 m L (peds: 3â€“6 years old, 7.5 m L;6â€“12 years old, 15 m L) PO after each loose bowel m ovem ent up to 7 tim es per day



Loperam ide (Im odium ): 4 m g initially, then 2 m g (peds: 1 m g t.i.d. if 13â€“20 kg; 2 m g b.i.d. if 20â€“30 kg; 2 m g t.i.d. if >30 kg) PO up to 16 m g/d



Metoclopram ide: 5â€“10 m g (peds: 0.1â€“0.2 m g/kg to m ax. 0.8 m g/kg/d) PO/IV/IM q.i.d. (30 m inutes before feeds and every night)

Follow-Up Disposition Admission Criteria 

Percutaneous endoscopic gastrostom y tube extubation within 1 week of placem ent



Surgical gastrostom y (G tube) or jejunostom y (J tube) extubation within 3 days of placem ent



Significant peristom al wound infection with fever/leukocytosis



Aspiration pneum onia

Pa ge 1 8 4



Diarrhea associated with dehydration



Peritonitis

Discharge Criteria Successful replacem ent of extubated feeding tube

References 1. Flem ing CR. Enteral nutrition. Gastrointest Dis Today. 1996;5:1â€“9. 2. Kirby DF, Delegg MH, Flem ing CR. Am erican Gastroenterological Association technical review on tube feeding for enteral nutrition. Gastroenterology. 1995;108:1282â€“1301. 3. MacLaren R. Intolerance to intragastric enteral nutrition in critically ill patients: com plications and m anagem ent. Pharm acotherapy. 2000;20:1486â€“1498. 4. McClave SA, Chang WK. Com plications of enteral access. Gastroentestinal Endosc. 2003;58:739â€“751. 5. Rassias AF, Ball PA, Corwin HL. A prospective study of tracheopulm onary com plications associated with the placem ent of narrow-bore enteral feeding tubes. Crit Care. 1998;2:25â€“28. 6. Sam uels LE. Nasoenteric teeding tubes. In: Roberts JR, Hedges JR, eds, Clinical Procedures in Em ergency Medicine. 4th ed. Philadelphia: WB Saunders; 2004. 7. Schapira GD, Edm undowicz SA. Com plications of percutaneous endoscopic gastrostom y. Gastrointest Endosc Clin North Am . 1996;6:409â€“422.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F em ur F racture

Femur Fracture

Colleen J. Buono

Basics Description Fractures classified according to: 







Location: o

Proxim al third (subtrochanteric region)

o

Middle third

o

Distal third (distal m etaphyseal-diaphyseal junction)

Geom etry: o

Spiral

o

Transverse

o

Oblique

o

Segm ental

Extent of soft tissue injury: o

Open

o

Closed

Degree of com m inution: Winquist and Hansen classification: o

Grade I: fracture with sm all fragm ent <25% width of fem oral shaft; stable lengthwise and rotationally

o

Grade II: fracture with 25â€“50% width of fem oral shaft; stable lengthwise; m ay or m ay not have

Pa ge 1 8 4

rotational stability o

Grade III: fracture with >50% width of fem oral shaft; unstable lengthwise and rotationally

o

Grade IV: circum ferential loss of cortex; unstable lengthwise and rotationally

Etiology 

Usually requires m ajor, high-energy traum a



Patients are m ostly young adults with high-energy injuries (m otor vehicle accidents [MVAs], gunshot wounds [GSWs], falls): o

Spiral fractures with falls from height



Consider pathologic fracture if m inor m echanism



Can occasionally be due to stress fracture from repetitive activity



Com plications include com partm ent syndrom e, fat em bolism , adult respiratory distress syndrom e (ARDS), hem orrhage

Pediatric Considerations 

Seventy percent of fem oral fractures in children <3 years old are the result of nonaccidental traum a (NAT).



Spiral fractures of the fem ur strongly suggest NAT.

Diagnosis Signs and Symptoms History 

Thigh pain, deform ity, swelling, shortening



Patient unable to m ove hip or knee



Com m only presents as m ultitraum a: o

Chest, abdom inal, pelvic, hip, knee injury, including

Pa ge 1 8 4

dislocation

Physical Exam 

Rarely open fracture unless injury is due to penetrating traum a



Patient m ay be hypotensive due to hem orrhage into the thigh.



Patient m ay have im paired circulation in the foot due to vascular com prom ise, com partm ent syndrom e.

Essential Workup 

Radiographs (see below)



Assess distal pulses, palpate com partm ents, evaluate sensation and m otor function.



If pulses are not equal or palpable, bedside Doppler or angiography m ay be necessary.



Search for associated injuries with m ultisystem traum a.



In suspected NAT, obtain skeletal survey or bone scan.

Tests Lab CBC, type and cross-m atch

Imaging 

AP pelvis, true lateral of the hip, AP and lateral views of the fem ur, com plete knee series



Baseline chest radiograph, other film s as indicated by traum a protocols

Differential Diagnosis 

Hip fracture or dislocation



Knee fracture or dislocation



Thigh contusion or hem atom a

Pa ge 1 8 4

Treatment Pre Hospital 

Im m obilization of the extrem ity and application of a traction splint can be im portant for tam ponade of further blood loss into the thigh: o

Backboard im m obilization, rigid splinting, support of extrem ity for position of com fort





Contraindications to traction: o

Fractures close to the knee

o

Fracture or dislocation of the ipsilateral hip

o

Fractures of the pelvis

o

Fractures of the lower leg

Do not attem pt to reduce open fractures in the field; cover open wounds with sterile dressings.



Monitor closely for developm ent of hem orrhagic shock as thigh can contain four to six units of blood.

Initial Stabilization 

Airway, chest, abdom inal injuries take precedence.



Monitor blood pressure continuously for signs of hem orrhagic shock.

ED Treatment 

Maintain lower extrem ity stability.



Rem ove splint and clothing.



Pain control: o

Isolated fem ur injuries: parenteral analgesia

o

Multitraum a or pediatric patients: fem oral nerve block



Orthopedic consultation necessary for all fem ur fractures: o

Em ergent if neurovascular com prom ise

Pa ge 1 8 4

o

Open fractures m ust go directly to the OR for irrigation and dÃ©bridem ent.



Antibiotics: o

Fractures requiring surgery: cefazolin

o

If open fracture with laceration, extensive soft tissue dam age, contam ination: add gentam icin/tobram ycin, tetanus.

o

If highly contam inated wound: add penicillin G to cover clostridial species.



Fem ur fractures with dim inished or absent distal pulses, an expanding hem atom a, or a palpable pulsatile m ass require im m ediate angiography or fem oral artery exploration.



Skeletal traction should be applied if the patient will not go to the OR im m ediately.

P.405

Medication (Drugs) Antibiotics 

Cefazolin: 1 g IM/IV q6hâ€“q8h (peds: 25â€“50 m g/kg IM/IV div. q6hâ€“q8h m ax. 1 g)



Gentam icin/tobram ycin: 3â€“5 m g/kg/day IV/IM div. 18h (peds: 2â€“2.5 m g/kg q8h)



Penicillin G: 2 m illion IU IV q4h (peds: 100,000â€“400,000 IU/kg/d IV div. q4hâ€“q6h to m ax. 24 m illion IU in 24 h)

Moderate Sedation 

Etom idate: 0.1â€“0.3 m g/kg IV once (not recom m ended for younger than 12 years of age)



Fentanyl: 50â€“100 m cg IV over 1â€“2 m inutes once

Pa ge 1 8 5

(peds: >6 m onths 1â€“2 m cg/kg IV once) 

Ketam ine: not recom m ended in adults due to em ergence reaction (peds: 1.0â€“2 m g/kg IV, 4 m g/kg IM once)



Methohexital: 1â€“1.5 m g/kg IV once (peds: not recom m ended) Midazolam : 0.07 m g/kg IM or 1 m g slowly q2â€“3m in up to 5 m g m ax. (peds: 0.25â€“1.0 m g/kg PO once to a m ax.) of 20 m g PO; 6 m o to 5 yr: 0.05â€“0.1 m g/kg IV titrate to m ax. of 0.6 m g/kg 6â€“12 yr: 0.025â€“0.05 m g/kg IV titrate to m ax. of 0.4 m g/kg



Propofol: 40 m g IV q10sec until induction; 5â€“60 m cg/kg/m in IV continuous infusion

Pain Control 

Hydrom orphone: 0.5â€“2.0 m g IM/SC/slow IV q4hâ€“q6h PRN; titrate for pain control (peds: 0.015 m g/kg per dose IV q4hâ€“q6h PRN)



Morphine: 2â€“10 m g IV q4h; titrate for pain control (peds: 0.1 m g/kg IV q4h; titrate for pain control to m ax. 15 m g/dose)

Pediatric Considerations 

Assess m arkers for nonaccidental traum a: o

Delay in presentation

o

History of m echanism inconsistent with the injury

o

Isolated traum a to the thigh, associated burns, bruises, or linear abrasions



Assess for dislocation of the fem oral capital epiphysis.



Depending on the age of the patient and the fracture type, pediatric fem oral fractures m ay not require operative treatm ent.

Pa ge 1 8 5

Follow-Up Disposition Admission Criteria 

All fem ur fractures m ust be adm itted except as noted below in Discharge Criteria.



Any suspicion of nonaccidental traum a in children

Discharge Criteria In certain rare circum stances of pathologic fracture or fem ur fractures in patients who are not am bulatory and would not undergo operative fixation, discharge can be considered in consultation with orthopedics if adequate pain control can be achieved and proper follow-up ensured.

References 1. Abarbanell N. Prehospital m idthigh traum a and traction splint use: recom m endations for treatm ent protocols. Am J Em erg Med. 2001;19:137â€“140. 2. Brien W, et al. Managem ent of gunshot wounds to the fem ur. Orthop Clin North Am . 1995;26(1):133â€“138. 3. Buckley S. Current trends in the treatm ent of fem oral shaft fractures in children and adolescents. Clin Orthop. 1997;338:60â€“73. 4. The Harriet Lane Handbook. Fifteenth Edition. 2000, Mosby, Inc. Saint Louis, Mo. 5. Rockwood C, et al. Fractures of the fem oral shaft. In: Rockwood and Green's Fractures in Adults and Children. Philadelphia: Lippincottâ€“Raven Publishers; 1991: Chapter 19. 6. Rudm an N, McIlm ail D. Em ergency departm ent evaluation and treatm ent of hip and thigh injuries. Em erg Med Clin North Am . 2000;18:29â€“66.

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7. Tarascon Pocket Pharm acopoeia 2006 Edition. Tarascon Publishing, Lom poc, CA. 8. Ward K, Yealy D. System ic analgesia and sedation in m anaging orthopedic em ergencies. Em erg Med Clin North Am . 2000;18:141â€“166.

Miscellaneous SEE ALSO: Hip Injury

Codes ICD9-CM 821.00

Core Content Code 18.4.13.1.7

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ever, Adult

Fever, Adult

Henry J. Grazioso

Basics Description 

Fever represents an elevation in the body's set therm oregulatory point.



Core tem perature is regulated by the anterior hypothalam us at 37Â°C Â± 2Â°C.



Fever is caused by increased prostaglandin E 2 (PGE 2 ) synthesis in the hypothalam us.



Autonom ic discharge from hypothalam us raises core tem perature through shivering and derm al vasoconstriction.



Norm al circadian variation in core tem perature occurs with nadir in early m orning and peak in late afternoon.



Both exogenous and endogenous factors can raise the body's set therm oregulatory point: o

Endogenous factors include IL-1 and IL-6, tum or necrosis factor, and IFN-Î³

o

Exogenous factors include endotoxin (lipopolysaccharide) and other toxins and m etabolites produced by infectious organism s.

Etiology

Pa ge 1 8 5



Any infectious process m ay present with fever: o

Cardiac (endocarditis, pericarditis)

o

Respiratory (pneum onia, upper respiratory tract infection, sinusitis)

o

Genitourinary (urinary tract infection, pyelonephritis, prostatitis)

o

Gastrointestinal (infectious diarrhea, gastroenteritis, hepatitis, pancreatitis, appendicitis)

o

CNS (m eningitis, encephalitis)

o

Skin and connective tissue (cellulitis, abscess, osteom yelitis)

o

Gynecologic (pelvic inflam m atory disease)

o

System ic (Epstein-Barr virus, cytom egalovirus, HIV, sepsis, insect vector-borne disease, biological weapons)

o 

Iatrogenic (indwelling catheters, prostheses)

Drugs: Nearly all drugs m ay cause fever: o

Antiarrhythm ics (procainam ide, quinidine)

o

Antibiotics (penicillins, sulfonam ides, erythrom ycin, isoniazid, nitrofurantoin)

o

Anticonvulsants (barbiturates, carbam azepine, phenytoin)

o

Antidepressants (TCAs, m onoam ine oxidase inhibitors)

o

Antihistam ines (H 1 and H 2 antagonists)

o

Antihypertensives (nifedipine, hydralazine, m ethyldopa, captopril, hydrochlorothiazide)



o

Drugs of abuse (cocaine, am phetam ines)

o

NSAIDs

o

Others (allopurinol, heparin, m eperidine)

System ic inflam m atory: o

Collagen vascular diseases

Pa ge 1 8 5





o

Rheum atic fever

o

Rheum atoid arthritis

o

System ic lupus erythem atosus

o

Vasculitis

o

Polym yalgia rheum atica

o

Tem poral arteritis

o

Granulom atous diseases

o

Sarcoidosis

o

Inflam m atory bowel disease

o

Sickle cell disease

o

Hem olytic anem ia

Neoplastic disease: o

Lym phom as and leukem ias

o

Hepatom a

o

Metastatic carcinom as

o

Atrial m yxom as

Endocrine: o

Hyperthyroidism or thyrotoxicosis

o

Pheochrom ocytom a



Pulm onary em bolus



Fam ilial Mediterranean fever



CNS lesions



Fever of unknown origin: o

Defined as fever >38.3Â°C for at least 3 weeks as an outpatient and 3 days of inpatient evaluation or three outpatient visits without determ ining etiology

o

A diagnosis of exclusion is rarely m ade in the ED.

Diagnosis Signs and Symptoms

Pa ge 1 8 5

History 

Chills, shivering, and rigors: o

Mechanism s to raise body core tem perature



Fatigue



Malaise



Myalgias



Night sweats: o

Suggestive of lym phom a, solid tum or, chronic inflam m atory disease, or tuberculosis (TB)



Anorexia



Specific fever patterns: o

Relapsing fevers: febrile episode with alternating afebrile intervals

o

Seen in m alaria, Borrelia infections, rat-bite fever, and lym phom a (Pel Ebstein fevers)

o

Rem ittent fever: tem perature falls daily but does not return to norm al

o

Seen in TB and viral diseases

o

Interm ittent fevers: exaggerated circadian rhythm

o

Seen in system ic infections, m alignancy, and drug fever

o

Reversal of norm al circadian patterns

o

Som etim es seen in typhoid fever and dissem inated TB

Physical Exam 

Elevated core tem perature: o

Tem perature >38Â°C (100.4Â°F) rectally or 37.5Â°C (99.5Â°F) orally

o

Lower thresholds in patients older than 65 years, as the febrile response is not as strong



Diaphoresis:

Pa ge 1 8 5

o

Absence of diaphoresis with severe hypertherm ia suggests anticholinergic poisoning or heat stroke.



Muscle rigidity: o

Found in patients with neuroleptic m alignant syndrom e or serotonin syndrom e



Changes in heart rate: o

Tachycardia is com m only seen.

o

Tem perature pulse dissociation (relative bradycardia) is seen in typhoid, brucellosis, psittacosis, leptospirosis, Legionnaire disease, Lym e disease, and factitious fevers.



Changes in m ental status: o

Can range from irritability to frank delirium and obtundation



Rash: o

Type of lesions and distribution can offer im portant clues to diagnosis.

o

Petechial rashes concerning for m eningococcem ia and Rocky Mountain spotted fever



Signs of hyperthyroidism : o

Goiter

o

Exophthalm os

Essential Workup 

Core tem perature is m ost acutely m easured rectally.



Careful history and physical exam (PE) necessary to determ ine need for further diagnostic testing: o

History should elicit any sick contacts, previous infections, recent travel, m edications, anim al exposure, and im m unization status.

Tests Lab

Pa ge 1 8 5



CBC: o

Com m only perform ed, but rarely helpful in m anagem ent of fever in the ED

o

Im portant in determ ining neutropenia in patients with risk factors

o

Differential WBC count is unreliable but m ay give clues to certain etiologies.

o

Neutrophilia and bandem ia suggestive of bacterial infection

o

Lym phocytosis suggestive of typhoid, TB, brucellosis, and viral disease

o

Atypical lym phocytosis seen in m ononucleosis, cytom egalovirus, HIV, rubella, varicella, m easles, and viral hepatitis

o

Monocytosis suggestive of TB, brucellosis, viral illness, and lym phom a

o

Platelet count <150,000 m ay be predictor of sepsis.

P.407



Erythrocyte sedim entation rate is generally not useful in ED diagnosis of fever: o

Very high values suggestive of endocarditis, tem poral arteritis, TB, and polym yalgia rheum atica



C-reactive protein is nonspecific and m inim ally useful in ED workup.



Urinalysis and urine culture: o



Helpful if fever etiology is uncertain after PE

Blood cultures: o

Obtain for patients with signs of sepsis or altered m ental status and ill-appearing patients

o

Ideally should be attained before antim icrobial

Pa ge 1 8 5

therapy, but antibiotics should be started im m ediately in unstable patients or patients with altered m ental status

Imaging 

Chest radiograph: o

In patients with PE finding of cardiopulm onary disease and patients with unclear fever source



CT scanning, MRI, or m ay be indicated based on history, physical, and lab findings.

Diagnostic Procedures/Surgery 

Lum bar puncture for patients with headache, m eningeal signs, or change in m ental status



Surgical intervention as indicated by prior workup

Differential Diagnosis 

Failure of therm oregulatory system s: o

Core tem peratures >41Â°C m ore com m on in these states



o

Neuroleptic m alignant syndrom e

o

Malignant hypertherm ia

o

Serotonin syndrom e

o

Heat stroke

Factitious fever

Treatment Pre Hospital 

No specific field interventions required



Monitoring and IV access should be obtained in the field for unstable patients or patients with altered m ental status.

Pa ge 1 8 6

Initial Stabilization 

Im m ediate treatm ent rarely required



Airway control, breathing and circulatory support for unstable patients



Initiate broad-spectrum antibiotic treatm ent im m ediately for im m unocom prom ised patients and patients with unstable vital signs or profound m ental status changes.

ED Treatment 

Antipyretics: o

Acetam inophen, NSAIDs, or salicylates: 

Inhibit the cyclooxygenase enzym e, thereby blocking synthesis of prostaglandins.

o

Most febrile patients do not require antipyretic m edication other than for com fort.

o

Selected patients require m ore aggressive antipyretic interventions:





Pregnant wom en



Patients with history of seizure disorders



Patients with significant cardiac disease



Hem odynam ically unstable patients



Patients with altered m ental status

Glucocorticoids: o

Inhibit phospholipase A 2 blocking prostaglandin synthesis.

o

Indicated only in chronic inflam m atory conditions; contraindicated in infectious etiologies



Em piric antibiotics for unstable or im m unocom prom ised patients



External cooling m echanism rarely indicated

Pa ge 1 8 6

Medication (Drugs) 



Antipyretics: o

Acetam inophen (B): 650 to 1,000 m g PO/PR q4â€“6h

o

Aspirin (D): 650 m g PO q4h

o

Ibuprofen (B): 800 m g PO q6h

Em piric antibiotics (dosage, interval assum e norm al renal function): o

Unstable, nonneutropenic patients with unidentified source of fever: 

Gentam icin (D) or tobram ycin (D): 2 m g/kg IV load then 1.7 m g/kg q8h plus piperacillin/tazobactam (B) 3.375 g IV q4h or ticarcillin/clavulanate (B) 3.1 g IV q4h



Im ipenem /cilastatin (C): 500 to 1,000 m g IV q8h

 o

Meropenem (B): 1 g IV q8h

If asplenic: 

Consider Cefotaxim e (B) 2 g IV q8h or Ceftriaxone (B) 2 g IV q12h

o

If neutropenic and low risk (24/7 access to hospital; no focal findings, structural lung disease, fungal infection, or dehydration; hem odynam ically stable; 16
Ciprofloxacin(C): 750 m g PO b.i.d. plus am oxicillin/clavulanate (B) 875 m g PO b.i.d.

o

If neutropenic and high risk: 

Cefepim e(B): 2 g IV q8h



Ceftazidim e(B): 2 g IV q8h



May treat as above for nonneutropenic patients

Pregnancy Considerations Pregnancy safety categories are shown in parentheses.

Pa ge 1 8 6

Follow-Up Disposition Admission Criteria 

Patients with unstable vital signs require intensive care unit adm ission.



Certain high-risk groups generally require adm ission for fever: o

High risk neutropenic patients or patients with known m alignancy



o

Im m unosuppressed or im m unocom prom ised patients

o

Asplenic patients

o

IV drug abusers (high risk of endocarditis)

Lower thresholds for adm ission in patients older than 60 years and diabetics

Discharge Criteria Im m unocom petent patients with stable vital signs and an identified source of fever with appropriate outpatient treatm ent and follow-up m ay be safely discharged.

References 1. Gelfand JA, Dinarello CA. Fever and hypertherm ia. In: Fauci AS, Braunwald E, Isselbacher KJ, et al. eds. Harrison's principles of internal m edicine. 14th ed. New York: McGraw-Hill, 1998:84â€“90. 2. Gilbert DN, et al. eds. The Sanford guide to antim icrobial therapy. 34th ed. Hyde Park, VT: Antim icrobial Therapy, Inc., 2004. 3. Kam al A, Kauffm an CA. Fever of unknown origin. Postgrad Med. 2003;114(3):69â€“75. 4. Knockaert DC, Vanderschueren S, Blockm ans D. Fever of unknown

Pa ge 1 8 6

origin in adults: 40 years on. J Intern Med. 2003;253:263â€“275. 5. Mackowiak PA. Concepts of fever. Arch Intern Med. 1998;158:1870â€“1881. 6. McKinnon HD Jr, Howard T. Evaluating the febrile patient with a rash. Am Fam Phys. 2000;62(4):804â€“815. 7. Mendelson M. Fever in the im m unocom prom ised host. Em erg Med Clin North Am . 1998;16(4):761â€“778. 8. Plaisance KI, Mackowiak PA. Antipyretic therapy. Arch Intern Med. 2000;160:449â€“456. 9. Roth AR, Basello GM. Approach to the adult patient with fever of unknown origin. Am Fam Phys. 2003;68(11):2223â€“2228.

Codes ICD9-CM 780.6

ICD10 R50.9

Pa ge 1 8 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ever, Pediatric

Fever, Pediatric

Nathan Mick David Peak

Basics Description 

Fever is defined as a tem perature of 38Â°C (100.4Â°F) rectally: o

Oral and tym panic tem peratures are generally 0.6â€“1.0Â°C lower.



Tym panic tem peratures are not accurate in children younger than 6 m onths.



Axillary tem peratures are generally unreliable.



After 3 m onths of age, significant fever is defined as a tem perature of 39Â°C.



Children who are afebrile but have a reliable history of docum ented fever should be considered to be febrile to the degree reported.

Etiology 

Bacterem ia (Haem ophilus influenzae type B and Streptococcus pneum oniae vaccines have decreased incidence of invasive Haem ophilus and pneum ococcal disease), viral exanthem (varicella, roseola, rubella), coxsackievirus (hand-foot-m outh disease), abscess.

Pa ge 1 8 6



CNS: m eningitis, encephalitis



Head, eyes, ears, neck and throat (HEENT): otitis m edia, facial cellulitis, orbital/periorbital cellulitis, pharyngitis (group A Î²-hem olytic streptococcus, herpangina, adenovirus pharyngoconjunctival fever), viral gingivostom atitis (herpes and coxsackievirus), cervical adenitis, sinusitis, m astoiditis, conjunctivitis, peritonsillar/retropharyngeal abscess



Respiratory: croup (param yxovirus), epiglottitis, bronchiolitis (respiratory syncytial virus [RSV]), pneum onia, em pyem a



Cardiovascular: purulent pericarditis, endocarditis, m yocarditis



Genitourinary (GU): cystitis, pyelonephritis



GI: bacterial diarrhea, intussusception, appendicitis, hepatitis



Extrem ity: osteom yelitis, septic arthritis, cellulitis



Miscellaneous: Kawasaki disease, vaccine (DPT) reaction, heat exhaustion/stroke, factitious, fam ilial dysautonom ia, thyrotoxicosis, collagen vascular disease, vasculitis, rheum atic fever, m alignancy, drug induced, overbundling (recheck 15 m inutes after unbundling)

Diagnosis Signs and Symptoms 

Clinical appearance m ust be evaluated.



Toxicity associated with lethargy, poor perfusion, hypoventilation/hyperventilation, weak cry, decreased PO intake; purpuric or petechial rash



Altered m ental status:

Pa ge 1 8 6

o

Lethargy presenting with decreased level of consciousness

o

Irritability

o

Im paired interaction with environm ent, parents, physician, toys



Physical exam (PE) to search for underlying condition



Febrile seizures



Tem peratures >42Â°C often have a noninfectious cause.



Serious infection m ay occur in the absence of fever.



Antipyretics m ay change findings without im pacting underlying disease.



Approxim ately 20% of children will have fever without source after history and PE.

Essential Workup 

Oxygen saturation as m andatory 5th vital sign



Resuscitate as appropriate.



Determ ine duration of illness, degree and level of fever, use of antipyretics, past m edical history, drug allergies, vaccination status, recent m edications/antibiotics, birth history if younger than 6 m onths of age, exposures, feeding, activity, urine/bowel habits, travel history, and relevant review of system s.



Search for underlying condition.



Initiate antipyretic therapy.

Tests Lab 

CBC with differential



Urinalysis and culture in all m ale infants younger than 6 m onths, uncircum cised infants younger than 12 m onths, and fem ales younger than 2 years



Blood culture:

Pa ge 1 8 6

o

The developm ent of autom ated blood culture system s has led to m ore rapid detection of bacterial pathogens.



Cerebrospinal fluid (CSF) for cell counts/culture for children toxic or 0â€“28 days of age; consider for nonâ€“toxic-appearing children 28â€“90 days of age as well as older in whom m eningitis m ust be excluded.



Stool for WBCs and culture when diarrhea present

Imaging 

Chest radiograph to exclude pneum onia if patient tachypneic or hypoxic



Lum bar puncture as indicated



Other studies as indicated to evaluate for underlying infection

Differential Diagnosis See Etiology

Treatment Pre Hospital 

Resuscitate as appropriate.



Begin cooling with antipyretics or tepid towels.

Initial Stabilization 

Treat any life-threatening conditions.



Antipyretic therapy



Evaporative cooling techniques such as sponge bath have m inim al role.

P.409

Pa ge 1 8 6

ED Treatment 

Focal infections require evaluation and treatm ent.



Toxic children require prom pt septic workup and appropriate antibiotics.



All potential life-threatening conditions m ust be excluded before treating a m inor acute illness, which is m ore com m on.



Infants 0â€“28 days old need a full septic workup: CBC, urinalysis (UA), cultures (blood, urine, CSF), lum bar puncture, chest radiograph:



o

Antibiotics: cefotaxim e and am picillin

o

Adm it

Nontoxic infants 28â€“90 days old need workup, selective antibiotic use (ceftriaxone), and re-evaluation within 24 hours of adm ission: o

H. influenzae type B and S. pneum oniae incidence has declined significantly with widespread vaccination.

o

It is currently reasonable to perform blood culture and urine culture with selective lum bar puncture, coupled with ceftriaxone IM in low-risk patients (see definition under Disposition) if re-evaluation in 24 hours is ensured.

o

Lum bar puncture is optional in this setting, but should be done if em piric antibiotics (ceftriaxone) are given to ensure that subsequent re-evaluation is not com prom ised.

o

Presence of respiratory syncytial virus in this age group decreases the risk of bacterem ia and m eningitis, but the rate of urinary tract infections is still appreciable.

Pa ge 1 8 6



Children 3 m onths to 3 years of age are evaluated selectively; antibiotic use is individualized for specific identifiable infections and pending appropriate cultures: o

Nontoxic children with tem peratures >39Â°C and no identifiable infection receive urinalysis/culture as indicated, chest radiograph as indicated, CBC/blood culture, and selective em piric antibiotics.

o

Children with WBC >15,000/m m 3 and no identifiable infection m ay benefit from em piric antibiotics pending culture results, especially if not vaccinated with H. influenzae type B and pneum ococcal vaccines.



Im m unocom prom ised children need aggressive evaluation, as do children with fever and petechiae/purpura.

Medication (Drugs) 

Acetam inophen: 15 m g/kg per dose PO/PR (per rectum ) q6h



Am oxicillin: 50 m g/kg/d PO t.i.d.



Am picillin: 150 m g/kg/d IV q4hâ€“q6h



Cefotaxim e: 100 m g/kg/d IV q6hâ€“q8h



Ceftriaxone: 50â€“100 m g/kg/d IV/IM q12h



Ibuprofen: 10 m g/kg per dose PO q6h



Penicillin V: 25â€“50 m g/kg/d PO b.i.d.â€“q.i.d.

Follow-Up Disposition Admission Criteria 

All toxic patients

Pa ge 1 8 7



Infants 0â€“28 days of age with tem perature >38Â°C



Nontoxic infants 28â€“90 days of age with tem perature >38Â°C who do not m eet low-risk criteria (see definition under Discharge Criteria)



Poor com pliance or follow-up

Discharge Criteria 

Infants 28â€“90 days of age m eeting low-risk criteria: o

No prior hospitalizations, chronic illness, antibiotic therapy, prem aturity

o

Reliable, m ature parents with hom e phone, available transport, therm om eter, and living in relative proxim ity to ED

o

No evidence of focal infection (except otitis m edia); non-toxic appearing; norm al activity, perfusion, and hydration with age-appropriate vital signs

o

Norm al WBC (5â€“15,000/m m 3 ), urine (negative Gram stain of unspun urine or leukocyte esterase or <5 WBC/high power field (HPF)), stool (<5 WBC/HPF) if perform ed, and CSF (<8 WBC/m m 3 and negative Gram stain) if perform ed



Infants 3â€“36 m onths of age who are nontoxic and previously healthy with good follow-up:



o

Antipyretics

o

Consider ceftriaxone and close follow-up.

Follow-up by phone in 12â€“24 hours and re-evaluate in 24â€“48 hours with parental instructions to return if concerns develop or patient worsens.

References 1. Abram son JS, Baker CJ, Fisher MC. Am erican Academ y of Pediatrics. Com m ittee on Infectious Diseases. Technical report: prevention of pneum ococcal infections, including the use of

Pa ge 1 8 7

pneum ococcal conjugate and polysaccharide vaccines and antibiotic prophylaxis. Pediatrics. 2000;106:367â€“376. 2. Baraff LJ. Managem ent of fever without source in infants and children. Ann Em erg Med. 2000;36:602â€“614. 3. Bulloch B, Craig WR, Klassen TP. The use of antibiotics to prevent serious sequelae in children at risk for occult bacterem ia: a m eta-analysis. Acad Em erg Med. 1997;4:679â€“683. 4. Lee GM, Harper MB. Risk of bacterem ia for febrile young children in the post-Haem ophilus influenzae type b era. Arch Pediatr Adolesc Med. 1998;152:624â€“628. 5. Levine DA, Platt SL, Dayan PS, et al. Risk of serious bacterial infection in young febrile infants with respiratory syncytial virus infections. Pediatrics. 2004;113:1728â€“1734. 6. Mandl KD, Stack AM, Fleisher GR. Incidence of bacterem ia in infants and children with fever and petechiae. J Pediatr. 1997;131:398â€“404.

Codes ICD9-CM 780.6

ICD10 P81.9

Pa ge 1 8 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ibro cystic Breast Disease

Fibrocystic

Breast Disease Michael W. Nielsen

Basics Description 



Fibrocystic change occurs in the breast in conjunction with: o

Pain

o

Nipple discharge

o

Nodularity sufficient to cause suspicion of cancer

Term fibrocystic breast disease should be considered synonym ous with fibrocystic change (FCC).



FCC: o

Increased num ber of cysts or fibrous tissue in a norm al breast

o

Most com m on of all benign breast conditions

o

FCC occurs in approxim ately 60% of wom en

o

Palpable thickening or lum piness in the breast

o

Often associated with pain and tenderness

o

Sym ptom s are m ore prom inent during the prem enstrual phase and tend to im prove with the onset of m enses.

o

Often becom es progressively worse until m enopause

Pa ge 1 8 7

o

Breast pain is m ost likely caused by rapid expansion of a sim ple cyst.

o

Breast pain alone is a rare sym ptom of cancer: 

o

Accounts for only 0.2â€“2% of cases

There are three indistinct clinical stages of FCC, with significant overlap: 

The three stages are term ed m azoplasia, adenosis, andcystic.



Each stage has predom inant histological findings.

o

Synonym (s): Adenosis; Benign breast disease; Cystic m astitis; Fibrocystic disease; Mam m ary dysplasia

Etiology 

Enhanced or exaggerated reaction by breast tissue to cyclic levels of ovarian horm ones: o

FCC m ay be caused by im balance of the ratio of estrogen to progesterone.

o

FCC m ay occur secondary to increased daily prolactin production.



Most com m on in wom en between 30 and 50 years old: o

May be carried into m enopausal age with horm one replacem ent therapy



Decreased incidence in wom en taking birth control pills



Risk factors are controversial and m ay include: o

Fam ily history

o

Diet, including high fat intake

o

Methylxanthine-containing substances: 

Coffee, tea, cola, and chocolate

Diagnosis

Pa ge 1 8 7

Signs and Symptoms History 

Breast pain (m astodynia) and tenderness: o

Persistent or interm ittent

o

Especially occurs during prem enstrual phase of norm al m enstrual cycle



o

Pain is usually bilateral.

o

Pain m ay radiate to shoulders and upper arm s.

Lum piness, nodularity: o



May be localized or generalized

Increased engorgem ent and breast density: o

Breasts described as being dull and heavy.

o

Fluctuations in the size of the cystic areas



Occasional spontaneous nipple discharge



Nipple sensation changes, itching



Fam ily history of cysts is com m on

Physical Exam 

Palpate the four breast quadrants while patient is sitting and lying down.



Identify discrete, m obile breast m asses, rounded with sm ooth borders.



Exam ine for regional nodes.



FCCs feel doughy with vague nodularity.



Usually m ore m arked in the upper outer quadrants



Sm all groups of cysts often described as palpating a â€œplate full of peasâ€•



Larger cysts have consistency of a balloon filled with water.

Essential Workup 

Clinical exam ination:

Pa ge 1 8 7

o

Ideally seven to nine days after first day of m enses, when breasts are least congested



Ultrasonography: o

Can differentiate cystic from solid breast m asses

o

Useful in m asses that appear on m am m ography

o

Benign cystic m asses typically have uniform outer m argin without asym m etry or irregular thickness of the cyst wall.

o

There are no echoes centrally, and posterior wall enhancem ent is noted.

o

Can assist in aspiration of deep cysts and nonpalpable cysts

o

Can be used to conservatively follow cyst size

Tests Lab 

Prolactin, thyroid-stim ulating horm one (if galactorrhea present)



Cyst aspiration cytology or biopsy of m ass

Imaging Mam m ography: 

Mam m ographic findings of benign processes of the breast can appear as m alignant



Mam m ogram s can be difficult to interpret in wom en less than 35 years: o



Due to breast tissue density

To avoid artifacts, should be perform ed either before aspiration or 7â€“10 days after

P.411

Pa ge 1 8 7

Diagnostic Procedures/Surgery 

Fine needle aspiration: o

Should com pletely evacuate cyst

o

Can be done for sym ptom atic or large m asses

o

Allows differentiation between cystic and solid m asses

o 

Cells sent for cytology can diagnose cancer

Excisional biopsy: o

Indicated for solid lum ps that are not proven benign

Differential Diagnosis 





Benign breast m asses: o

Solitary papillom as

o

Sim ple fibroadenom as

o

Duct ectasia

o

Breast abscess

o

Mastitis

Malignant breast m asses: o

Ductal hyperplasia without atypia

o

Sclerosing adenosis

o

Diffuse papillom atosis

o

Com plex fibroadenom as

o

Atypical hyperplasia

Chest wall pain: o

Costochondritis

o

Anxiety

o

Referred pain of cardiac or gastrointestinal origin

Treatment ED Treatment

Pa ge 1 8 7



Conservative therapy: o

Support bra: 

Reduces tension on supporting ligam ents of breast

 o

May reduce inflam m atory response and edem a

Mild diuretic for two to three days before onset of m enses

o 

NSAIDs

Dietary changes; controversial: o

Restricting dietary fat (to 25% of total calories) and elim inating caffeine



o

Increasing vitam in E and vitam in B 6

o

Herbal preparations such as prim rose oil

Horm onal therapy: o

Should be prescribed by prim ary care physician to enable follow-up during course of treatm ent

o

Oral contraceptives can decrease the sym ptom s of FCC, particularly after one year.

o

Danazol: 

Synthetic androgen



Greater anabolic than androgenic activity



Only FDA-approved drug for treatm ent of m astalgia

o

Brom ocriptine (inhibits prolactin productions) or tam oxifen (a partial estrogen antagonist) used if patient unresponsive to danazol



Surgical intervention: o

If a nodule in a breast rem ains, excision is recom m ended regardless of m am m ographic or ultrasound findings

o

If a large cyst recurs after aspiration on two occasions, it should be excised and studied

Pa ge 1 8 7

histologically. o

Refer to general surgeon.

Medication (Drugs) 

Danazol: 100â€“400 m g/d b.i.d. for 6 m onths



Brom ocriptine: 2.5â€“5 m g/d b.i.d.



Tam oxifen: 10â€“20 m g/d per day.



Oral contraceptives

Follow-Up Disposition Discharge Criteria 

Patients m ay be discharged if the diagnosis is fibrocystic changes.



Encourage patient to keep a breast pain record chart to determ ine whether pain is cyclic.



It is im portant for patient satisfaction, as well as patient health and disease prevention, to ensure follow-up for all patients with breast m asses.



Encourage regular breast self-exam ination, annual physical exam s, and annual m am m ogram s, if appropriate.

Issues for Referral 

Referral to a general surgeon should be provided to diagnostically elim inate possibility of cancer.



Lum ps that persist throughout m enses and are not cyclical should be further investigated with im aging and a fine needle biopsy.

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References 1. Fine RE, Staren ED. Updates in breast ultrasound. Surg Clin N Am . 2004;84:1001â€“1034. 2. London SJ, Connolly JL, Schnitt SJ, Colditz GA. A prospective study of the developm ent of benign breast disease and the risk of breast cancer. JAMA. 1992;267:941. 3. Marchant DJ. Benign breast disease. Obstet Gynecol Clin North Am . 2002;29:1. 4. Rastelli A. Breast pain, fibrocystic changes, and breast cysts. Probl Gen Surg. 2003;20(4):17â€“26. 5. Zera RT, et al. Atypical hyperplasia, proliferative fibrocystic change, and exogenous horm one use. Surgery. 2001;130(4):732.

Codes ICD9-CM 610.1

ICD10 N60.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ibro m yalgia

Fibromyalgia

Jennifer S. Johnson

Basics Description 

Nonarticular, noninflam m atory form of m uscular rheum atism :



o

Widespread pain

o

Tender points (not trigger points)

o

Fatigue

o

Sleep disturbance

o

Lim ited physical findings

Not diagnosis of exclusion, m ay occur with other rheum atic diseases



Painful sym ptom s believed to be m uscular in origin



Abnorm alities identified as possible m echanism : o

Decreased ATP/phosphocreatine level

o

Prolonged m uscle ischem ia/tension

o

Low blood flow in exercise m uscles of patients with fibrom yalgia



Muscle biopsies from tender points have shown no reproducible abnorm alities.

Genetics Genetic predisposition m ay play role when sym ptom s triggered by

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exposure to environm ental stressors.

Etiology Mechanism 

Unknown



May involve neuroendocrine system or com bination of peripheral and central m echanism s, such as: o

Physiologic im balance in hypothalam ic-pituitaryadrenal axis with decreased free cortisol production

o

Low serum levels of insulin growth factor

o

Elevated levels of substance P (enhances pain perception) in cerebrospinal fluid (CSF)

o

Reduced serotonin levels

o

Sleep disturbance of norm al stage 3 and 4 phases (non-REM): 

Results in nonrestorative sleep and im m unologic dysfunction



Psychologic distress



Central hyperexcitability of nociceptive system

Diagnosis Signs and Symptoms History 

Generalized m usculoskeletal pain and m orning stiffness



Weakness and fatigue



Sleep disturbance



Tension or m igraine headaches



GI com plaints (e.g., irritable bowel syndrom e)



Genitourinary (GU) com plaints (e.g., interstitial cystitis)



Mood disturbances (e.g., depression, anxiety)

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

Paresthesias



Sensation of swollen hands and joints



Skinfold tenderness



Postexertional pain



Cold intolerance

Physical Exam Derm atographism

Essential Workup 

History and characteristic physical findings are key to m aking diagnosis.



Use classification criteria established by Am erican College of Rheum atology (ACR) for fibrom yalgia: o

Absence or less than num ber of required tender points does not exclude syndrom e.

o

Widespread pain present for at least 3 m onths on both left and right side of body: 

Pain above and below waist



Axial skeletal pain m ust be present (cervical or anterior chest or thoracic spine or low back pain).

o

Eleven of 18 specific tender points on digital palpation with force of 4 kg/cm (am ount of pressure required to blanch thum bnail)

o

The nine paired (bilateral) tender points are located at the: 

Occiput: suboccipital m uscle insertions



Low cervical: anterior aspects of C-5, C-7 intertransverse spaces



Trapezius: m idpoint of upper border



Supraspinatus: above m edial border of scapular spine

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

Second rib: second costochondral junction about 3 cm lateral to sternal border



Lateral epicondyle: about 2 cm below bony prom inence



Gluteal: upper outer quadrant of buttocks



Greater trochanter: posterior to trochanteric prom inence



Knee: m edial fat pad proxim al to joint line

Tests Lab 



Evaluate for alternative diagnoses: o

CBC

o

Blood chem istries

o

Erythrocyte sedim entation rate (ESR)

o

Muscle enzym es

o

Thyroid function tests

No specific laboratory abnorm alities are characteristic of fibrom yalgia.

Imaging No specific radiographic abnorm alities are characteristic.

Differential Diagnosis 

Myofascial pain syndrom e (trigger points present, not tender points)



Chronic fatigue syndrom e



Major depression



Polym yalgia rheum atica



Lym e disease



Hypothyroidism



Collagen vascular disease



Electrolyte im balance

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

Myopathies (m etabolic and drug induced)



Osteom alacia



Psychogenic rheum atism



Eosinophilia-m yalgia syndrom e

P.413

Treatment ED Treatment 

Patient education and reassurance: o

Em phasize that fibrom yalgia is not life threatening and does not reduce life expectancy.

o

Disorder is chronic but not crippling or deform ing.

o

Goal is to m anage pain and im prove functional disability.



Patients with poor coping skills m ay require psychiatric intervention.

Pharmacologic Therapy 

Pharm acotherapy for im proving pain, relaxing m uscles, and im proving sleep quality has been m ost successful with CNS agents.



Com binations of m edications (e.g., am itriptyline and fluoxetine or am itriptyline and cyclobenzaprine) m ay be m ore beneficial than either m edication alone.



Tricyclic antidepressants (TCAs; am itriptyline, nortriptyline)



Muscle relaxants (cyclobenzaprine)



Selective serotonin reuptake inhibitors (fluoxetine)

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

Serotonin norepinephrine reuptake inhibitors (duloxetine, m ilnacipran)



Tram adol with or without acetam inophen



Anticonvulsants (pregabalin)



Benzodiazepines (clonazepam ) are of no benefit other than their role in sleep disturbances.



Nonsteroidal anti-inflam m atory drugs (NSAIDs) and corticosteroids have not been shown to be effective.



Steroids or local anesthetic (lidocaine) injection into tender points is controversial: o



No studies available to prove efficacy

Opioids: no data showing benefit in long term

Medication (Drugs) 

Am itriptyline: 10â€“50 m g PO at bedtim e



Clonazepam : 0.5 m g PO at bedtim e



Cyclobenzaprine: 10â€“30 m g/d PO at bedtim e



Duloxetine: 60 m g PO b.i.d



Fluoxetine: 20â€“80 m g PO daily



Pregabalin: 450 m g PO daily



Tram adol: 200â€“300 m g PO daily

Lifestyle Modifications 

Physical exercise should be encouraged: o

Exercise program should be gradual to avoid overexertion and discouragem ent.

o

Aerobic exercise is m ore beneficial than sim ple stretching.

o 

Efficacy not m aintained if exercise stops

Good sleep pattern should also be discussed: o

Establishing nightly ritual in preparation for sleep

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o

Avoiding caffeine-containing beverages or foods in afternoon or evenings



Encourage stress m anagem ent and coping strategies.



Participation in educational program s (e.g., cognitive-behavioral therapy): o

Im provem ent is often sustained for m onths.

Follow-Up Disposition Admission Criteria 

Patients with serious underlying disease, intractable pain, or im m unocom prom ised



Patients with suicidal ideation

Discharge Criteria Patients with uncom plicated fibrom yalgia can be m anaged as outpatients.

References 1. Arnold LM, et al. A double-blind, m ulticenter trial com paring duloxetine with placebo in the treatm ent of fibrom yalgia patients with or without m ajor depressive disorder. Arthritis Rheum . 2004;50:2974â€“2984. 2. Arthritis Foundation. Prim er on the Rheum atic Diseases. 12th ed. Atlanta, GA; 2001:188â€“193. 3. Crofford LJ, et al. Pregabalin for the treatm ent of fibrom yalgia syndrom e: results of a random ized, double-blind, placebo-controlled trial. Arthritis Rheum . 2005;52:1264â€“1263. 4. Desm eules JA, et al. Neurophysiologic evidence for a central sensitization in patients with fibrom yalgia. Arthritis Rheum .

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2003;48:1420â€“1429. 5. Goldenberg DL, et al. Managem ent of fibrom yalgia syndrom e. JAMA. 2004;292:2388â€“2395.

Codes ICD9-CM 729.1

ICD10 M79.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F lail C hest

Flail Chest

Gregory W. Lampe

Basics Description 

Free floating segm ent of chest wall: o

Three or m ore adjacent ribs are fractured in two or m ore places.

o

Rib fractures in conjunction with sternal fractures or costochondral separations



The free-floating segm ent of chest wall paradoxically m oves inward during inspiration and outward during expiration.



The principle pathology associated with flail chest is the associated pulm onary contusion: o

Not alteration in ventilatory m echanics owing to the free-floating segm ent

Etiology 

Blunt thoracic traum a



Fall from a height



Motor vehicle accident



Assault



Missile injury



Ribs usually break at the point of im pact or posterior

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angle: o 

Weakest region structurally

Transfer of kinetic energy to the lung parenchym a adjacent to the injury: o

Disruption of the alveolocapillary m em brane and developm ent of pulm onary contusion

o

Arteriovenous shunting

o

Ventilation/perfusion m ism atch

o

Hypoxem ia

o

Respiratory failure m ay result

Pediatric Considerations Relatively elastic chest wall m akes rib fractures less com m on in children.

Diagnosis Signs and Symptoms History 

Blunt thoracic traum a by any m echanism



Mechanism as described by patient, parent or prehospital personnel:



o

Seat belt usage

o

Steering wheel dam age

o

Air bag deploym ent

Localized chest wall pain increases with deep inspiration, coughing, m oving



Pleuritic chest pain



Dyspnea



Hem optysis

Physical Exam

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

Flail chest paradoxically m oves inward during inspiration and outward during expiration: o

Initially this m ay not be seen because of m uscle spasm and splinting respirations.

o

Inspection under tangential light m ay m agnify paradoxical m otion of the chest wall.



Multiple rib fractures: o

Bony stepoffs

o

Ecchym osis

o

Crepitus

o

Edem a

o

Erythem a and tenderness associated with



Splinting respirations



Intercostal m uscle spasm



Dyspnea, tachypnea: o

Onset m ay be insidious, increasing over tim e.



Cyanosis, tachycardia, hypotension



Auscultation with initially norm al breath sounds progressing to wet rales or absent breath sounds.

Essential Workup Diagnosis is initially m ade on clinical grounds.

Tests Lab Arterial blood gas analysis: 

May reveal hypoxem ia



Elevated alveolar-arterial gradient

Imaging 

Chest radiograph aids diagnosis, revealing m ultiple rib fractures: o

May reveal associated intrathoracic pathology:

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o



Pneum othorax, hem othorax



Pneum om ediastinum



Pulm onary contusion



Widened m ediastinal silhouette

Pulm onary contusion appears within 6â€“12 hours after injury: 

Ranges from patchy alveolar infiltrates to frank consolidation



Thoracic CT is useful in detecting associated intrathoracic injuries not identified on chest radiograph.

Differential Diagnosis 

Chest wall contusion or intercostal m uscle strain



Costochondral separation



Sternal fracture and dislocation



Radiographic differential diagnosis includes: o

Acute respiratory distress syndrom e

o

Pulm onary laceration, infarction or em bolism

o

Congestive heart failure

o

Pneum onia, abscess, other infectious process

o

Noncardiogenic causes of pulm onary edem a

Treatment Pre Hospital 

Positioning the patient injured side down can stabilize the involved chest wall: o



Im prove ventilation in noninjured hem ithorax.

Thoracic traum a with significant m echanism or com bined with pre-existing pulm onary disease should be routed to the nearest traum a center.

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Initial Stabilization 

Manage airway and resuscitate as indicated



IV line, O 2 , continuous cardiac m onitoring and pulse oxim etry



Control airway: o

Endotracheal intubation

o

Indicated for patients with severe hypoxem ia (PaO 2 <60 m m Hg on room air, <80 m m Hg on 100% O 2 )

o

Significant underlying lung disease

o

Im pending respiratory failure

ED Treatment 

Maintain adequate oxygenation and ventilation.



Monitor O 2 saturation and respiratory rate.



In conscious and alert patients, O 2 adm inistration via face m ask is first-line therapy.



If patient cannot m aintain a PaO 2 >80 m m Hg on high-flow oxygen, consider continuous positive airway pressure via m ask or nasal bilevel positive airway pressure.



Early endotracheal intubation and m echanical ventilation if above fails: o



Physiologic internal fixation of the flail segm ent

External fixation or stabilization of the flail segm ent is not indicated.



Adequate pain control is critical to m aintaining adequate pulm onary function: o



Avoid splinting, atelectasis, and pneum onia.

Search for associated injuries and treat exacerbation of underlying lung disease.



Intercostal nerve blocks with 0.5% bupivacaine are safe and effective when perform ed properly: o

Provides 6â€“12 hours of pain relief

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o

Perform intercostal nerve block posteriorly, two to three fingerbreadths from the vertebral m idline.

o

Inject 0.5â€“1 m L just under the inferior surface of the rib where the neurovascular bundle is located.

o

Aspirate first to be certain the intercostal vessels have not been punctured.



Prophylactic antibiotics are not indicated.

Alert 

Avoid overhydration: o

In the setting of pulm onary contusion the need for IV crystalloid resuscitation m ust be weighed against the risk of increasing interstitial pulm onary edem a.

P.415

Medication (Drugs) 

Multiple acetam inophen/narcotic analgesic com binations are available, see alert below:



Acetam inophen: 300 m g/codeine 30 m g (peds: 0.5â€“1 m g/kg codeine) PO q4hâ€“q6h



Acetam inophen: 500 m g/hydrocodone 5 m g PO q4hâ€“q6h



Acetam inophen: 750 m g/hydrocodone 7.5 m g PO q4hâ€“q6h



Acetam inophen: 325 m g/hydrocodone 10 m g PO q4hâ€“q6h



Acetam inophen: 325 m g/oxycodone 5 m g PO q6h



Bupivacaine: 0.5% 0.5â€“1 m L per injection for intercostal nerve blocks



Hydrom orphone: 2â€“8 m g (peds: 0.03â€“0.08 m g/kg) PO

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4hâ€“q6h 

Hydrom orphone: 1â€“4 m g (peds: 0.015 m g/kg) IV/IM/SC q4hâ€“q6h



Morphine sulfate: 0.05â€“0.1 m g/kg IV/IM/SC q2hâ€“q6h



Patient-controlled analgesia using hydrom orphone or m orphine sulfate is effective.

Alert 

Consider thoracic epidural analgesia for patients with intractable pain, oversedation, or hypoventilation secondary to narcotic analgesics.



Avoid NSAIDs due to the risk of gastrointestinal bleeding.



The dose of acetam inophen/narcotic analgesic com binations is lim ited by the hepatic toxicity of acetam inophen.



The m axim um acetam inophen dose is 1 g per dose and 4 g per day (peds: 15 m g/kg/dose).

Follow-Up Disposition Admission Criteria All patients with flail chest are adm itted to a critical care setting for close m onitoring and adequate pain control.

Discharge Criteria Patients found to have flail chest, with or without pulm onary contusion, should not be discharged.

References 1. Gunduz M, Unlugenc H, Ozalevli M, Inanoglu K, Akm an H. A com parative study of continuous positive airway pressure (CPAP) and

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interm ittent positive pressure ventilation (IPPV) in patients with flail chest. Em erg Med J. 2005;22(5):325â€“329. 2. Wanek S, Mayberry JC. Blunt thoracic traum a: flail chest, pulm onary contusion, and blast injury. Crit Care Clin. 2004;20(1):71â€“81. 3. Eckstein M, Henderson S. Thoracic traum a. In: Marx J, Hockberger R, Walls R, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 6th ed. St. Louis, MO: Mosby; 2005, in press.

Codes ICD9-CM 807.4 Flail chest

ICD10 S22.5

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o o t F racture

Foot Fracture

Colleen Campbell

Basics Description Injury to tarsal bones or m etatarsals including calcaneus, talus, navicular, cuboid, cuneiform , and m etatarsals

Etiology 

Most com m on foot injuries are of the m etatarsals and phalanges.



The calcaneus is the m ost com m only fractured of the tarsal bones.



Calcaneus fractures: com pression injury from sudden high-velocity im pact to heel: o

Seventy-five percent are intra-articular; 50% have associated injuries:





10% spine fractures



25% with associated lower extrem ity traum a



5% bilateral, 5% open

Metatarsal fractures: divided into stress fractures, twisting injuries, or direct traum a: o

First m etatarsal: direct applied force

o

Second and third m etatarsals are m ost often involved in stress fractures and twisting injuries.

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o

Fifth m etatarsal: Avulsion fracture (dancer's fracture) of proxim al apophysis is m ost com m on injury.

o

Jones fracture: transverse fracture of the m etaphyseal-diaphyseal junction of fifth m etatarsal; results from twisting while foot inverted



Talus: caused by dorsiflexion with axial load, com m on snowboarder's injury



Navicular: results from axial com pression or stress fractures



Cuboid and cuneiform fractures are rare and occur in conjunction with other injuries, often with tarsal-m etatarsal injuries.



Tarsal-m etatarsal injuries (Lisfranc injuries): high-energy injuries: o

Axial load on plantar-flexed foot, or hindfoot fixed with forced foot eversion

o

Unstable forefoot on hindfoot

o

20% go undiagnosed on initial visit.

Pediatric Considerations 

Metatarsal fractures account for 90% of foot fractures in children: o

Avulsion fractures of the fifth m etatarsal are m ost com m on.

o

Physeal injury m ay occur with proxim al first m etatarsal fractures.



Other com m on injuries include phalangeal fractures (17%) and navicular fractures (5%).

Diagnosis

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Signs and Symptoms History 

History of preceding traum a m ost com m on



Stress fractures m ay present with increasing pain in setting of repetitive activities

Physical Exam 

Ecchym osis, pain, swelling, or deform ity of foot



Pain with weight bearing



Joint instability

Essential Workup 

Physical exam of extrem ity is necessary to assess neurovascular status, skin integrity, gross swelling, deform ity, or loss of function.



Exam ination of spine is also essential in suspected calcaneus fractures, as there is a 10% incidence of coexistent injury.



Anterior-posterior/lateral and oblique views are necessary for all foot fractures.



Com plications: o

Com partm ent syndrom e m ost com m only presents as severe pain in a swollen foot: 

Pressures >35 m m Hg require opening of all m ajor foot com partm ents.

o

Nonunion and avascular necrosis are com m on com plications with talar neck fractures owing to distal blood supply.

o

Calcaneus fractures m ay be accom panied by sural nerve injury; test sensation along lateral aspect of foot.

Tests

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Imaging Special views m ay be needed for som e fractures: 

Lisfranc fractures m ay require stress views with weight bearing.



Talar fractures m ay require a 45-degree internal oblique view.



Midfoot fractures m ay require an external oblique foot view.



Calcaneus fractures require an axial view and m ay require CT: o

Boehler angle <20 degrees suggests a com pression fracture of calcaneus.

o

Lum bosacral spine film s are necessary in all patients with calcaneus fractures.



Stress fractures m ay require 2 weeks to appear on plain film s; bone scan or CT m ay be used to elucidate suspected fractures.

Differential Diagnosis 

Anterior effects of calcaneus and talar dom e fractures can be m isdiagnosed as ankle sprains.



Foot contusions

Treatment Pre Hospital 

Ice bag should be placed on affected foot and foot and ankle im m obilized.



All patients suspected of calcaneus fracture should have spinal im m obilization; often, m echanism is fall from height >6 feet.

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Initial Stabilization Manage coexisting traum a as indicated. P.417

ED Treatment 

Airway, breathing, and circulation m anagem ent



Assess for neurovascular com prom ise distal to fracture site.



Dislocations m ust be reduced as quickly as possible with assessm ent of neurovascular status before and after procedure: o



Procedural sedation usually required

Im m obilize, ice, and elevate in a bulky splint: o

Application of circum ferential cast should be delayed until swelling subsides.



Crutches



Pain m anagem ent: o

If large am ount of swelling and pain with toe m ovem ent, suspect com partm ent syndrom e.



Orthopedic consult indicated early for displaced fractures: o

Many injuries require repair within 6 hours of injury to prevent delay of open reduction with internal fixation for 6â€“10 days owing to swelling.

Medication (Drugs) 

Cefazolin: 1 g IV/IM (peds: 25 m g/kg IV/IM)



Diprivan: 40 m g IV q10s until sedation



Etom idate: 0.1â€“0.2 m g/kg IV



Fentanyl: 50â€“250 Âµg IV titrated (peds: 2 Âµg/kg IV)

Pa ge 1 9 0



Ibuprofen: 800 m g PO (peds: 10 m g/kg PO)



Meperidine: 25â€“100 m g IV/IM titrated (peds: 1â€“1.75 m g/kg IV/IM)



Methohexital: 1.0â€“1.5 m g/kg IV



Morphine: 2â€“10 m g IV/IM titrated (peds: 0.1 m g/kg IV)

Follow-Up Disposition Admission Criteria 

Open fracture



Evidence of com partm ent syndrom e or neurovascular injury



Open reduction internal fixation required im m ediately

Discharge Criteria Most patients with m etatarsal fractures can be discharged with orthopedic follow-up.

Issues for Referral All open fractures, as well as all m idfoot/Lisfranc injuries and displaced fractures that are not successfully reduced, should be seen in ED by an orthopedic specialist.

References 1. Ribbans WJ, Natarajan R, Alavala S. Pediatric foot fractures. Clin Orthop Relat Res. 2005;432:107â€“115. 2. Steele PM, Bush-Joseph C, Bach B Jr. Managem ent of acute fractures around the knee, ankle, and foot. Clin Fam Pract. 2000;2(3):661â€“705. 3. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am .

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2000;18(1):85â€“113.

Codes ICD9-CM 825 Fracture of one or m ore tarsal and m etatarsal bones

ICD10 S92.9 Fracture of foot, unspecified

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o rearm F racture, Shaft/Distal

Forearm

Fracture, Shaft/Distal Trevor J. Mills Peter DeBlieux

Basics Description 

Shaft fractures (single and paired) often displaced by contraction of m uscles of arm ; som etim es associated with dislocations o

Galeazzi fracture: 

Distal radius fracture with distal radioulnar dislocation

o

Monteggia fracture: 

Proxim al ulnar fracture with dislocation of radial head



Distal fractures include extension, flexion, and intra-articular classifications: o

Colles fracture: 

Hyperextension fracture of distal radius



Distal fragm ent displaced dorsally



Radial deviation



May also involve ulnar styloid and distal

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radioulnar joint o

o

Sm ith fracture: 

Hyperflexion fracture of distal radius



Distal fragm ent displaced volarly

Barton fracture: 

Intra-articular fracture of dorsal rim of distal radius

 o

Often associated with dislocation of carpal bones

Hutchinson fracture: 

Intra-articular fracture of radial styloid

Pediatric Considerations 

Shaft fractures: o

Torus fracture: 

Com pression (buckling) of cortex on one or both sides

o

Greenstick fracture: 

Distraction of one side of cortex with opposite side intact

o

Plastic deform ity: 

Bowing of radius or ulna without apparent disruption of cortex

 

Multiple m icrofractures

Distal fractures: o

Salter-Harrisâ€“type fractures (see Salter-Harris classification)

Etiology 

Direct blow to forearm



Longitudinal com pression load:



o

Fall on outstretched hand (FOOSH)

o

Horizontal force

Excessive pronation, supination, hyperextension, or

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hyperflexion

Diagnosis Signs and Symptoms History 

Associated events and concurrent injuries



Past history of bone disease or old fractures



History of repetitive stress of forearm m ovem ent



Occupation



Hand dom inance

Physical Exam 

Physical exam with special attention to skin integrity, deform ity, and neurovascular status



Forearm pain, crepitus, tenderness to palpation, deform ity, shortening of forearm



Forearm edem a, ecchym osis, elbow or wrist joint effusions



Abnorm al m obility or loss of function at elbow/wrist/hand



Neurologic abnorm alities



Vascular com prom ise

Essential Workup Suspected forearm fractures require anteroposterior (AP) and lateral radiographs, including wrist and elbow.

Tests 

Com partm ent pressures should be m easured for suspected com partm ent syndrom e.



Som e intra-articular fractures m ay require CT im aging.

Differential Diagnosis 

Upper extrem ity m uscle, ligam entous injury

Pa ge 1 9 0



Elbow or wrist dislocations, including pediatric nursem aid's elbow



Forearm contusions, hem atom as



Cellulitis, abscesses, soft tissue m asses



Forearm osteogenic tum ors



Osteom yelitis



Upper extrem ity vascular or neurologic injuries



Elbow or wrist arthritis, joint effusions



Pediatric growth plates, nutrient vessels m ay be m istaken for fractures

Treatment Pre Hospital 

All suspected forearm fractures should be elevated, splinted, and im m obilized, including elbow and wrist joints.



All open fractures should be wrapped with sterile dressing before im m obilization: o

Do not reduce open fractures back under skin in the field.

o

In patients with isolated extrem ity traum a, analgesia m ay be adm inistered.

ED Treatment 



Shaft fractures, nondisplaced: o

Long-arm splint

o

Orthopedic referral

Shaft fractures, displaced: o

Orthopedic consultation

o

Often require open reduction, internal fixation

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



Distal fractures, nondisplaced o

Forearm sugar-tong or AP splint

o

Orthopedic referral

Distal fractures: Colles/Sm ith: o

Sim ple, noncom m inuted, extra-articular Colles and Sm ith fractures m ay be reduced in ED:

o



Splint (long-arm sugar-tong splint)



Sling



Referred to orthopedics

Com plicated Colles and Sm ith fractures require orthopedic consultation.



Distal fractures: Barton/Hutchinson: o

o

Uncom plicated Barton and Hutchinson fractures 

Splint (AP or sugar-tong splint)



Place in sling



Referred to orthopedics

Com plicated fractures require orthopedic consultation.





Open fractures: o

Cover with sterile dressings.

o

IM/IV antibiotics

o

Tetanus im m unization (if indicated)

o

Splint

o

Im m ediate orthopedic consultation

Forearm fractures associated with com partm ent syndrom e or neurovascular com prom ise require im m ediate orthopedic consultation.

P.419

Pediatric Considerations 

Torus and Greenstick fractures with <10Â° of angulation

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m ay be treated with long-arm splint, sling, and orthopedic referral. 

Plastic deform ities require orthopedic consultation: o

Som e m inim ally displaced plastic deform ities m ay be placed in long-arm splint and sling.



Salter-Harrisâ€“type fractures require orthopedic consultation.

Medication (Drugs) 

Acetam inophen: 325â€“1,000 m g PO q4h (peds: 10â€“15 m g/kg q4h PO)



Antibiotics: o

Open fractures require IM/IV antibiotics.

o

Cefazolin: 1â€“2 g IM/IV or equivalent first-generation cephalosporin; if contam inated, add an am inoglycoside



Codeine: 15â€“60 m g PO/IM q4h (peds: older than 2 years, 0.5â€“1.0 m g/kg q4h PO/IM)



Hydrocodone: 5â€“10 m g PO q4h



Ibuprofen: 200â€“800 m g q4hâ€“q8h (peds: older than 6 m onths, 5â€“10 m g/kg per dose q6h)



Morphine sulfate: 2â€“10 m g IV/IM; titrate to pain (peds: 0.1 m g/kg per dose IV/IM)



Tetanus (Td): 0.5 m L IM every 10 years

Follow-Up Disposition Admission Criteria

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

Open fractures



Fractures with com partm ent syndrom e or neurovascular com prom ise



Fractures needing im m ediate operative m anagem ent or general anesthesia for reduction



Suspected child abuse

Discharge Criteria 

Appropriate reduction and im m obilization



Arranged orthopedic follow-up



Adequate pain control m easures



Cast/splint care discharge instructions provided and understood by patient



Docum entation of intact neurovascular function after ED treatm ent

Issues for Referral All fractures (or suspected fractures) discharged from ED should be referred to orthopedic surgeon for close follow-up.

References 1. Dicke TE, Nunley JA. Distal forearm fractures in children: com plications and surgical indications. Orthop Clin North Am . 1993;24(2):333. 2. Patzakis MJ, Wilkens J. Factors influencing infection rate in open fracture wounds. Clin Orthop. 1988;243:36. 3. Perron AD. Evaluation and m anagem ent of the high-risk orthopedic em ergency. Em erg Med Clin North Am . 2003;21(1):159â€“204. 4. Price CT. Injuries to the shafts of the radius and ulna. In: Rockwood CA, Wilkins KE, Beaty JH, eds. Fractures in Children. Vol 3. 4th ed. Philadelphia: JB Lippincott; 1996:449â€“586. 5. Richards RR, Corley FG. Fractures of the shafts of the radius and ulna. In: Rockwood CA, Green DP, Bucholz RW, et al., eds. Fractures in Adults. Vol 1. 4th ed. Philadelphia: JB Lippincott; 1996: 869â€“929.

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6. Szabo RM. Extra-articular fractures of the distal radius. Orthop Clin North Am . 1993;24(2):229. 7. Wilkins KE, O'Brien E. Fractures of the distal radius and ulna. In: Rockwood CA, Wilkins KE, Beaty JH, eds. Fractures in Children. Vol 3. 4th ed. Philadelphia: JB Lippincott; 1996:586â€“653.

Codes ICD9-CM 813.20 813.40

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o reign Bo dy, Ear

Foreign Body, Ear

Kathleen Nasci Charles V. Pollack Jr.

Basics Description 

Foreign bodies lodged in the external auditory canal



Typical foreign bodies in children:





o

Stones

o

Sm all beads

o

Paper

o

Toys

o

Seeds and popcorn kernels

o

Beans and other food and organic m aterials

Typical foreign bodies in com petent adults: o

Cotton-swab tips

o

Earplugs

o

Insects

Inanim ate foreign objects are often associated with delayed presentations.



Most objects tend to becom e trapped in outer two-thirds of external auditory canal.



Children and psychiatric patients m ay insert anything sufficiently sm all to enter the external auditory canal.

Pa ge 1 9 1



Ear foreign bodies are m ost com m on in children younger than 8 years.



Com plications: o

Canal laceration

o

Perforation of tym panic m em brane, which is m ore likely to result from rem oval procedure

o 

Otitis externa

Sym ptom s usually resolve within a few days after foreign body rem oval.

Diagnosis Signs and Symptoms 

Decreased hearing



Unilateral ear pain



Fullness



Loud noises



Buzzing sound (with live insects)



Nausea



Dizziness



Ipsilateral tearing



Purulent discharge from the external ear



Itching



Bleeding

Essential Workup 

Always seek to identify the nature of the foreign body before trying to rem ove it: o

Live insect

o

Vegetable

o

Inanim ate object

Pa ge 1 9 1



Careful otoscopic exam ination: o

Minim ize pain.

o

Gain the patient's trust.

o

Achieve optim al visualization by having an assistant exert gentle, steady traction on the patient's lobule.

o

Perform a bilateral exam ination; especially im portant in children and psychiatric patients, and prevents overlooking a quiescent foreign body in the contralateral ear.

o

Repeat exam after rem oval to assess possible traum a of external canal or tym panic m em brane.

Tests Imaging 

Operating m icroscope: o



Use if em ergency departm ent rem oval fails

Radiographs are not indicated.

Differential Diagnosis 

Cerum en im paction



Granulom a



Hem atom a



Injury



Otitis externa



Perforated tym panic m em brane



Residual otitis externa after self-extraction of the foreign body



Tum or

Treatment

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Pre Hospital 

Cautions: o

Severe ear pain, sensation of m ovem ent, and loud, buzzing sound: 

Typical signs of a live insect in external auditory canal



Instill warm lidocaine or m ineral oil into affected ear to kill insect.



Controversies: o

Attem pts at rem oval in the field are not indicated: 

Lack of appropriate equipm ent



Prior failed attem pts m ay m ake future attem pts m ore difficult.

Initial Stabilization For a patient in distress because of a live insect: 

Drown or im m obilize insect before any rem oval attem pts.



Instill warm solution into the external auditory canal:



o

Mineral oil

o

Viscous lidocaine

o

Ether

o

2% lidocaine

o

Microscope im m ersion oil

Cold fluids should not be used so as to avoid a caloric response.

ED Treatment 

Appropriate instrum ents: o

Otoscope

o

Alligator forceps

o

Cupped forceps: num bers 3, 5, and 7 suction tips, preferably with Frazier suction cups

o

A wire loop

Pa ge 1 9 1

o

Ear curettes

o

A right-angled blunt hook



Achieve proper head im m obilization



Vegetable m atter rem oval: o

Visualize

o

Attem pt rem oval with forceps.

o

Be certain to delineate clearly between foreign body and inflam ed external auditory canal tissue.

o

Do not irrigate the external auditory canal if the foreign body is of such a nature that it m ight swell.



Nonvegetable inanim ate foreign body rem oval: o

Visualize

o

If easily grasped, attem pt rem oval with forceps.

o

If not accessible, attem pt rem oval with irrigation.

o

Perform careful visualization.

o

Place an Angiocath catheter adjacent to, or preferably distal to, the foreign body.

o

Inject warm water or sterile saline through catheter via a syringe.

o

Backwash the foreign body out.

o

Never attem pt rem oval by irrigation when the foreign body is a button battery.

P.421



Polished or sm ooth object extraction: o

Visualize

o

Direct suction

o

Blunt right-angled probe: pass beyond the foreign body; rotate 90Â°; rem ove it with the foreign body

o

Fogarty catheter: carefully pass beyond the foreign body and inflate and withdraw; this approach puts

Pa ge 1 9 1

the tym panic m em brane at particular risk of inadvertent injury o

Cyanoacrylate glue (superglue): place on the tip of a blunt probe, place on the foreign body for 10 seconds, and then pull; quick bonding m ay allow foreign body rem oval with the probe



Insect rem oval: o

Once killed, rem ove with forceps or by irrigation

o

Re-exam ine to ensure that all insect parts are rem oved



Sharp objects: o

Rem ove with operating m icroscope

o

Consider otolaryngologic referral if there is evidence of traum a or if patient is uncooperative,



Anesthesia or analgesia: o

None needed in adults for sim ple foreign body rem oval

o

Four-quadrant local anesthetic block

o

1â€“2% lidocaine, with or without epinephrine

o

Infiltrate around the external auditory canal.

o

Procedural sedation

o

Indicated for children and uncooperative adults

o

Use before attem pts, as unsuccessful efforts m ay produce bleeding, edem a, or injury to the tym panic m em brane

o

Ketam ine for children

o

Benzodiazepines for older patients

o

Consider fentanyl if analgesia is indicated during rem oval.

Medication (Drugs)

Pa ge 1 9 1



Fentanyl: 1 Âµg/kg



Ketam ine: 1â€“2 m g/kg IV or 4 m g/kg IM



Midazolam : 1 m g IV slowly every 2â€“3 m inutes up to 5 m g (peds: 6 m onths to 5 years, 0.05â€“0.1 m g/kg, titrate to m axim um of 0.6 m g/kg; 6â€“12 years, 0.025â€“0.05 m g/kg, titrate to m ax. of 0.4 m g/kg)

Follow-Up Disposition Admission Criteria Hospital adm ission is usually not necessary.

Discharge Criteria 

Patient should be instructed not to place any objects in ear.



A short course of analgesics after traum atic foreign body rem oval



Otitis externa: o



Topical antim icrobial such as Cortisporin suspension

Im m unocom prom ised patients m ay require oral antibiotics.





Perforated tym panic m em brane: o

Prophylaxis with antibiotics

o

Follow-up with ear/nose/throat specialist

Avoid subm ersion in water until follow-up if traum a or infection present.

References 1. Ansley JF, Cunningham MJ. Treatm ent of aural foreign bodies in children. Pediatrics. 1998;101:638â€“641.

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2. Balbani AP, Sanchez TG, Butugan O, et al. Ear and nose foreign body rem oval in children. Int J Pediatr Otorhinolaryngol. 1998;46:37â€“42. 3. Bressler K, Shelton C. Ear foreign body rem oval: a review of 98 consecutive cases. Laryngoscope. 1993;103:367â€“370. 4. Brown L, Denm ark TK, Wittlake WA, Vargas EJ, Watson T, Crabb JW. Procedural sedation use in the ED: m anagem ent of pediatric ear and nose foreign bodies. Am J Em erg Med. 2004;22(4):310â€“314. 5. Davies PH, Benger JR. Foreign bodies in the nose and ear: a review of techniques for rem oval in the em ergency departm ent. J Accid Em erg Med. 2000;17:91â€“94. 6. Kum ar S, Kum ar M, Lesser T, Banhegyi G. Foreign bodies in the ear: a sim ple technique for rem oval analysed in vitro. Em erg Med J. 2005;22(4):266â€“268.

Codes ICD9-CM 931 Foreign body in ear

ICD10 T16 Foreign body in ear

Pa ge 1 9 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o reign Bo dy, Eso phageal

Foreign Body,

Esophageal Jason J. Prystowsky

Basics Description 

Esophageal foreign bodies typically lodge at three sites of physiologic constriction: o

Cricopharyngeal m uscleâ€”63%, m ost com m on (C6)

o

Gastroesophageal junctionâ€”20% (T11)

o

Aortic archâ€”10% (T4)



90% of ingested foreign bodies pass spontaneously.



10â€“20% are rem oved endoscopically, and 1% or less require surgery.

Etiology 

Most com m on adult and adolescent foreign bodies are food boluses and bones: o

Esophageal pathology alm ost always underlies food im pactions.

o

Esophageal stricture, esophageal spasm , achalasia, esophageal m otor disorder



Increased risk: o

Edentulous adults

Pa ge 1 9 2

o

Intoxicated patients

o

Patients with underlying esophageal disease

Pediatric Considerations 

Eighty percent of foreign body ingestions occur in pediatric age group, particularly younger than 2 years.



Coins: o



Most com m on: 80% of esophageal foreign bodies

Predisposing factor: esophageal strictures

Diagnosis Signs and Symptoms 



Acute ingestion: o

Dysphagia

o

Odynophagia

o

Drooling

o

Vom iting

o

Choking

o

Gagging

o

Blood-stained saliva

Chronically retained foreign body: o

Respiratory sym ptom s predom inate (paraesophageal tissue swelling com prom ises adjacent trachea): 

Cough



Stridor



Hoarseness

o

Chest pain

o

Site of foreign body sensation usually corresponds to esophageal level of foreign body

o

Esophageal perforation:

Pa ge 1 9 2

o



Redness



Swelling



Crepitus in the neck

Less than 20% asym ptom atic

Pediatric Considerations 

Infants: signs/sym ptom s: o

Refusal to eat

o

Stridor

o

Upper respiratory tract infection

o

Neck/throat pain

Essential Workup 

History about object ingested: type, when, and how



Physical exam focused by degree of distress exhibited: o

o

o

Esophagus for: 

Obstruction



Perforation



Hem orrhage

Oropharynx: 

Red, irritated throat



Palatal abrasions

Lung: 

o

Abdom en: 



Stridor and wheezing

Peritonitis or bowel obstruction

Direct or indirect laryngoscopy can be useful.

Tests Imaging 

Biplane chest radiograph including all of neck for foreign body localization: o

Need for additional radiographs dictated by clinical

Pa ge 1 9 2

situation o

Those with food bolus need no radiographs usually.

o

Esophageal foreign bodies usually align them selves in coronal plane.

o

Esophageal perforation is noted by air in retropharyngeal space, in soft tissues of neck, or by pneum om ediastinum .



Esophageal contrast studies for nonradiopaque foreign bodies: o

Radiolucent objects (sm all pieces of glass, bone fragm ents, alum inum , plastic, pieces of wood)

o

Thin barium esophagogram : changes in contour of barium colum n localize foreign body.

o

Passage of contrast solution into stom ach: partial versus com plete obstruction

o

Cautions: 

Oral contrast in high-grade esophageal obstructions can increase risk of aspiration, and barium m ay coat m ucosa, lim iting subsequent endoscopy.



Traditional water-soluble contrast can cause severe tissue reaction in perforations because of its hyperosm olality.



Metal detectors have been used in localizing ingested m etal, particularly coins in pediatric population.



Endoscopy: o

Method of choice for localizing and m anaging m ost esophageal foreign bodies

o

Ability to inspect surrounding esophageal m ucosa for pathology

o 

Both diagnostic and therapeutic

CT can often detect foreign bodies not identified by other

Pa ge 1 9 2

m eans, especially if use 3D reconstruction.

Differential Diagnosis 

Globus hystericus phenom enon (â€œlum p in throatâ€•)



Esophagitis



Croup



Epiglottitis



Upper respiratory tract infection



Retropharyngeal abscess

Treatment Pre Hospital Cautions: 

Airway m aintenance and prevention of aspiration param ount



Oxygen for patients in distress



Place patient in whatever position gives m ost com fort.



Ipecac and cathartics contraindicated

Initial Stabilization 

Airway, breathing, and circulation m anagem ent first priority



Prevent aspiration

ED Treatment 

Foreign bodies lodged in upper or m id-esophagus: o



Extraction required

Asym ptom atic patients with coins or sm ooth objects (not button batteries) in distal esophagus: o

Observe up to 24 hours after ingestion to see whether it will pass into stom ach.

Pa ge 1 9 2

o 

Danger of perforation increases after 24 hours.

Im pacted food bolus obstructing esophagus: o

Em ergent rem oval indicated

o

Digestion with proteolytic enzym es (papain) not recom m ended because of serious m orbidity including esophageal perforation, hypernatrem ia, and aspiration



Extricate sharp or pointed esophageal foreign bodies regardless of their location: o

Perforation incidence ranges from 15â€“35%

o

Objects m ost com m only associated with com plications are:

o



Chicken and fish bones



Straightened paper clips



Toothpicks



Needles



Bread bag clips



Dental bridgework

Direct laryngoscopy can be perform ed if above cricopharyngeus.

o

Objects that reach stom ach and are shorter than 5 cm and <2 cm in diam eter usually pass through GI tract without difficulty, but daily radiographs are still recom m ended.

P.423



Button batteries: o

Extract em ergently wherever they lodge in esophagus

o

Batteries frequently leak: potassium hydroxide and m ercuric oxide are m ost toxic constituents.

Pa ge 1 9 2

o

Alkali produced from external flow of current can cause liquefaction necrosis.

o

Full-thickness m ucosal burns can occur within 4â€“6 hours (com bination of chem ical, electrical, pressure injuries).

o

Battery in stom ach will usually pass without difficulty: 

Batteries rem aining in stom ach for >3â€“4 days should be rem oved.



Large-diam eter batteries (>20 m m ) should be rem oved from stom ach after 48 hours.

o

Once past duodenal sweep, 85% are passed within 72 hours.





Narcotic/am phetam ine packets: o

Body packing seen in regions of high drug traffic

o

Packets usually seen on radiographs

o

Rupture or leakage of contents can be fatal.

Rem oval techniques: o

Fluoroscopically guided Foley catheter extraction: 

Successful and safe in experienced hands



Foley catheter (10â€“16 French) placed nasally, passed into esophagus, tip and balloon pushed beyond foreign body under fluoroscopic control



Foley balloon inflated with contrast and catheter slowly withdrawn



Contraindicated in chronic ingestions, uncooperative patients, sharp-pointed objects

o

Foley catheters m ay also be used to push distal foreign body into stom ach.



Endoscopy: o

Preferred m ethod to rem ove acute or chronic foreign bodies

Pa ge 1 9 2

o

Always used with im pactions of long duration (>2â€“4 days) because of associated esophageal irritation/edem a

o

General endotracheal anesthesia needed in difficult cases: infants, psychiatric patients, difficult foreign body

o

Bougienage: using dilator to push foreign body into stom ach



IV glucagon: o

Decreases lower esophageal sphincter tone without interfering with esophageal contractions

o

Often perm its distal food boluses to pass into the stom ach

o 

For im pactions <24 hoursâ€™ duration

Gas-form ing agents: o

Useful in patients with esophageal food im pactions <24 hours

o

Com bining intravenous glucagon followed by oral gas-form ing agents has also been successful.

o

Method has been occasionally associated with perforation.



Surgical intervention: o

Reserved for patients in whom foreign body cannot be rem oved by other m ethods

o

Approxim ately 1â€“2% of all patients

o

Toothpicks and bones com m on objects

Medication (Drugs) 

E-Z Gas: 30 m L solution (NaHCO 3 , citric acid. and sim ethicone) orally



Glucagon: 1â€“2 m g IV push after test dose to determ ine

Pa ge 1 9 2

hypersensitivity

Follow-Up Disposition Admission Criteria 

Seriously ill patients and those with com plications such as esophageal perforation, m igration of foreign body through esophageal wall, significant bleeding



Airway com prom ise



Sym ptom atic patients in whom attem pts to rem ove foreign body are unsuccessful

Discharge Criteria 

Asym ptom atic patients in whom foreign body has been rem oved or passed distal to esophagus



Asym ptom atic patients with distal esophageal sm ooth foreign bodies need re-exam ination within 12â€“24 hours to ascertain whether spontaneous passage into stom ach has occurred.

References 1. Calkins CM, Christians KK, Sell LL. Cost analysis in the m anagem ent of esophageal coins: endoscopy vs. bougienage. J Pediatr Surg. 1999;34:412â€“414. 2. Eisen GM, Baron TH, Dom initz JA, et al. Guideline for the m anagem ent of ingested foreign bodies. Gastrointest Endosc. 2002;55:802â€“806. 3. Mosca S, Manes G, Martion R, et al. Endoscopic m anagem ent of foreign bodies in the upper gastrointestinal tract: report on a series of 414 adult patients. Endoscopy. 2001;33:692â€“696.

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4. Ruben C, Liacouras C. Evaluation and m anagem ent of foreign bodies in the upper gastrointestinal tract. Pediatr Case Rev. 2003;3:150â€“156. 5. Soprano JV, Mandl KD. Four strategies for the m anagem ent of esophageal coins in children. Pediatrics. 2000;105:1497â€“1501.

Codes ICD9-CM 935.1 Foreign body in esophagus

ICD10 T18.1 Foreign body in esophagus

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o reign Bo dy, Nasal

Foreign Body,

Nasal Paul Blackburn

Basics Description 

Types of foreign bodies: o

Lim ited only by nostril size and im agination, activity of the child

o

Food

o

Paper

o

Pieces of toys

o

Beads

o

Rocks

o

Button batteries: high risk of com plications com pared with other foreign bodies (tissue necrosis, septal perforation, saddle nose); require rapid rem oval

o

Magnets: 

Used to sim ulate nasal piercing



Often im bedded in tissue, leading to difficult rem oval

 

May cause intestinal perforation if swallowed

Sinusitis is the m ost com m on com plication.

Pa ge 1 9 3



Average patient age: 2â€“4 years



Age not associated with particular type of foreign body

Diagnosis Signs and Symptoms 

Most nasal foreign bodies are asym ptom atic.



Som eone witnesses child putting object into nose.



Foreign body noticed by parent or caretaker.



Nasal discharge: o

Acute or chronic

o

Unilateral

o

Foul sm elling

o

Halitosis



Sinus discom fort



Epistaxis



Local inflam m ation



Septal perforation



Ingestion or aspiration of foreign body

Essential Workup Visualization of the foreign body in the nostril: 

Always check both nostrils

Tests Imaging 

Fiberoptic visualization if foreign body cannot be visualized on rhinoscopy



Sinus film s if present for extended period: o

Sym ptom persistence despite rem oval of the foreign body and antibiotics

Pa ge 1 9 3

Differential Diagnosis 

Sinusitis



Epistaxis



Intranasal m ass



Swollen inferior turbinate: o

May be m istaken for a pink bead

Treatment Pre Hospital 

Cautions: o

Transport in sitting position. 

Avoid posterior displacem ent, possible aspiration of foreign body.



Avoid interventions that upset the child.

ED Treatment 

Topical vasoconstrictors: o

Presence of m ucosal edem a, or bleeding secondary to rem oval attem pts



o

Nebulized epinephrine

o

Cocaine: 4%

o

Oxym etazoline: 0.05%

o

Phenylephrine: 0.125â€“0.5%

Positive pressure: o

Occlude contralateral nostril.

o

Positive pressure applied to m outh only

o

Deliver brisk puff as child begins to inhale.

o

Parent m ay tell the child he or she will be given a â€œbig kiss.â€•

o

Placem ent of 4 Ã— 4 gauze pads on caregiver's cheek

Pa ge 1 9 3

o

Foreign body dislodges onto cheek of the provider or into room

o

Repeated as necessary

o

Alternatively, deliver puff with a bag-m ask over the m outh and O 2 at 10â€“15 L/m in.

o

Alternatively, into contralateral nostril m ale-m ale adapter on oxygen tubing, deliver wall oxygen at 10â€“15 L/m in.

o

Nasal wash with 7 m l saline via bulb syringe contralateral nostril described; controversial; aspiration risk?







Hooked probe, alligator forceps: o

Anterior foreign bodies that are easily grasped

o

Headlam p, nasal speculum facilitate use

o

Risk of further posterior displacem ent

Suction catheter: o

Best for round, sm ooth objects

o

Optim al retrieval with suction catheter

o

Suction tip placed against the object

o

Suction turned up to 100â€“140 m m Hg

o

Catheter and object withdrawn

Cyanoacrylate tissue glue: o

Film of glue applied to cut end of hollow plastic swab handle

o

Apply against object for 60 seconds, then withdraw.

o

Caution with nontissue cyanoacrylate glues; tissue irritation

P.425



Balloon catheters: o

Used prim arily when instrum entation fails

Pa ge 1 9 3

o

5F or 6F Foley or Fogarty balloon catheter lubricated with 2% lidocaine jelly

o

Advance catheter past object

o

Following inflation with 2â€“3 m L of air, gently withdraw catheter gently withdrawn



Magnet for rem oval of m etal foreign body described; lim ited experience

Medication (Drugs) 

Cocaine: 4% solution, 2 drops affected nares



Lidocaine: 4% solution, 2 drops affected nares



Oxym etazoline: 0.05%, 2â€“3 drops/sprays affected nares



Phenylephrine: 0.125â€“0.5%, 2â€“3 sprays affected nares



Procedural sedation m ay be of im m ense im portance

Follow-Up Disposition Admission Criteria Referral for am bulatory surgical rem oval: 

Foreign body cannot be recovered in ED



Rem oval under general anesthesia is required

Discharge Criteria 

Ensure that all foreign bodies are rem oved from both nares.



Return if bleeding, infection (nasal discharge)



If a button battery was rem oved: o

Mandatory follow-up with ear/nose/throat specialist

o

Monitor for delayed sequelae

Pa ge 1 9 3

o

Ischem ic m ucosa

o

Turbinate or septal dam age

o

Saddle-nose deform ity

References 1. Backlin SA. Positive-pressure technique for nasal foreign body rem oval in children. Ann Em erg Med. 1995;25(4):554â€“555. 2. Chan TC, Ufberg J, Harrigan RA, Vilke GM. Nasal Foreign Body Rem oval. J Em erg Med. 2004;26(4):441â€“445 3. Douglas SA, Mirza S, Stafford FW. Magnetic Rem oval of a Nasal Foreign Body. Int J Pediatr Otorhinolaryngol. 2002;62(2):165â€“167. 4. Kadish HA, Corneli HM. Rem oval of Nasal Foreign Bodies in the Pediatric Population. Am J Em erg Med. 1997;15(1):54â€“56. 5. Lichenstein R, Guidice EL. Nasal Wash Technique for Nasal Foreign Body Rem oval. Pediatr Em erg Care. 2000;16(1):59â€“60. 6. Lin VY, Daniel SJ, Papsin BC. Button Batteries in the Ear, Nose, and Upper Aerodigestive Tract. Int J Pediatr Otorhinolaryngol. 2004;68(4):473â€“479. 7. Navitsky RC, Beam sley A, McLaughlin S. Nasal Positive-Pressure Technique for Nasal Foreign Body Rem oval in Children. Am J Em erg Med. 2002;20(2):103â€“104.

Codes ICD9-CM 933.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o reign Bo dy, Rectal

Foreign Body,

Rectal Jason J. Prystowsky

Basics Description 









Self-insertion (autoeroticism ): o

Phallic substitutes inserted by patient or partner

o

Foreign bodies (FBs) used to aid in rem oval of feces

Ingested: o

Chicken bones

o

Fish bones

o

Toothpick

Iatrogenic: o

Therm om eter

o

Enem a tips

Assault: o

Knife or pipe forcibly inserted

o

Incidence of perforation is very high.

Concealm ent: o

Body packing, â€œm ulesâ€• illegally transporting drugs

Pa ge 1 9 3

Diagnosis Signs and Symptoms 

Com plaint of rectal foreign body (FB)



Rectal fullness



Rectal pain



Perirectal abscess (with im bedded bones/toothpick)



FB on rectal exam ination: o

High-lying foreign bodies are located proxim al to rectosigm oid junction and are not palpable on rectal exam .

o

Low-lying foreign bodies are usually located in rectal am pulla and are palpable on rectal exam .



Som e patients m ay not be forthcom ing with history.



Can present with vague sym ptom s of abdom inal pain or obstruction



Can present as bowel perforation with full peritonitis

Essential Workup 

Identify num ber, type, and duration of FBs and m echanism of insertion.



Physical exam with em phasis on abdom inal and rectal exam



Biplane radiographic film s to confirm num ber and size of FBs



For assaulted patients, workup as for blunt traum a to abdom en

Tests Lab 

CBC: o

For bleeding or peritonitis

Pa ge 1 9 3



Urinalysis: o



For urethral/bladder injuries

Radiograph: o

Consider doing kidneys, ureters, and bladder (KUB) radiograph prior to rectal exam to rule out objects harm ful to exam iner.

o

Define and locate FB.

o

Assess for com plications of retained FB including bowel perforation and obstruction.

o

May be used serially to follow descent of FB

Differential Diagnosis 

Pseudo-FB: o

Patients insist there is FB when radiograph, rectal exam s, and proctoscopy results are norm al.



Perirectal abscess



Hem orrhoid

Treatment Pre Hospital Cautions: 

Patient has usually tried to rem ove FB and failed.



Further attem pts at extraction will not work and could cause perforation.

Initial Stabilization 

Perforation with peritonitis and sepsis: o

0.9% norm al saline (NS) IV fluid 500 m L bolus

o

Broad-spectrum antibiotics (anaerobic and gram -negative aerobes): 

Cefoxitin, cefotetan, ticarcillin-clavulanate,

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am picillin-sulbactam , im ipenem , m eropenem , ertapenem or 

Metronidazole/clindam ycin plus am inoglycoside/third generation cephalosporin/fluoroquinolone/aztreonam

o 

Urgent surgical consult

Advanced traum a life support (ATLS) with evidence of other traum a

ED Treatment 

Use appropriate sedation and analgesia.



Low-lying sm all rectal foreign bodies that are not fragile or sharp: o

Can be rem oved transanally if object can be firm ly held

o

Rem ove with gentle but firm continuous traction to overcom e anal sphincter.

o

Colonic m ucosa tightly adherent to distal end of FB creates vacuum and im pedes withdrawal of object: 

Passage of Foley catheter beyond object with insufflation of air breaks vacuum and perm its retrieval.

o

Awake and cooperative patients can facilitate transanal extraction with Valsalva.

o

May use instrum ents to assist with extraction: obstetrical forceps, tenaculum , ring forceps, vacuum extractor

o

Can attem pt bim anual m anipulation if low-lying FB

o

Sixty percent of rectal FBs m ay be rem oved transanally in ER under proper sedation.

o

Following extraction, anorectum m ust be thoroughly evaluated to rule out occult injury.

o

High-lying rectal foreign bodies:

Pa ge 1 9 3



Not im m ediately accessible through rectum



Usually require surgical or GI consult



Attem pt m ay be m ade to position object into low-lying position.



Direct visualization with large operating anoscope (after blockage of sphincter and pudendal nerve with local anesthesia)



Bim anual m anipulation



Adm ission and observation for spontaneous descent (with serial radiographs)



Laparotom y m ay be necessary as last resort if other m ethods fail, or if patient has evidence of perforation.

o

Consider surgical or GI consult for other com plicated rectal foreign bodies: 

Larger objects



Objects that have rem ained >24 hours with resulting edem a



Objects with sharp edges



Proctoscopy/sigm oidoscopy after extraction to exam ine colonic m ucosa

P.427

Medication (Drugs) 

Am picillin-sulbactam (Unasyn): 3g IV q6h (peds: 100â€“200 m g/kg/d div. q6h)



Aztreonam (Azactam ): 0.5â€“2g IV q8hâ€“q12h (peds: 30 m g/kg IV q6hâ€“q8h, m ax. 120 m g/kg/d)



Cefoxitin (Mefoxin): 1â€“2 g (peds: 30â€“40 m g/kg) IV

Pa ge 1 9 4

q6h 

Cefotetan (Cefotan): 1â€“2 g (peds: 20â€“40 m g/kg) IV q12h



Cefriaxone (Rocephin): 1â€“2 g IV q12h (peds: 50â€“75 m g/kg IV daily)



Ciprofloxacin (Cipro): 400 m g IV q8hâ€“q12h



Clindam ycin: 600â€“900 m g (peds: 20â€“40 m g/kg/24h) IV q8h



Ertapenem (Invanz): 1 g IV q24h



Gentam ycin: 1 m g/kg (peds: 2â€“2.5 m g/kg) IV q8h



Im ipenem (Prim axin): 0.5â€“1 g (peds: 15â€“25 m g/kg) IV q6h



Levofloxacin (Levoquin): 500 m g IV q24h



Meropenem (Merrem ): 1 g (peds: 60 m g/kg/d) IV q8h



Metronidazole: 15 m g/kg IV once, then 7.5 m g/kg IV q6h



Piperacillin-tazobactam (Zosyn): 3.75 g IV q6h or 4.5 g IV q8h (peds: 240â€“400 m g/kg/d div. q6hâ€“q8h)



Ticarcillin-clavulanate (Tim entin): 3.1 g (peds: 200â€“300 m g/kg/d) IV q4hâ€“q6h

Pediatric Considerations 

Rem oval under general anesthesia for children who are too young to cooperate



It is probably child abuse if FB other than enem a tips or therm om eter is present.

Follow-Up Disposition Admission Criteria 

Failed extraction in ED requires surgical rem oval in OR.

Pa ge 1 9 4



Evidence of m ucosal tear on proctoscopy should be observed for 24 hours (no antibiotic indicated).



Sym ptom of rectal pain associated with rem oval of sharp FB indicates possibility of sm all perforation with developing abscess and requires exam ination under anesthesia.



Any invasive procedure with analgesia and sedation requires inpatient observation for 24 hours.

Discharge Criteria 

Reliable patient atraum atic insertion and rem oval of rectal FB



Instruct to return for rectal pain, abdom inal pain, fever, or m assive rectal bleeding.

References 1. Abcarian H. Colorectal foreign bodies. In: Mazier PW, et al., eds. Surgery of the Colon, Rectum , and Anus. Philadelphia: WB Saunders; 1995. 2. Eftaiha M, Ham brick E.Abcarian H. Principles and m anagem ent of colorectal foreign bodies. Dis Colon Rectum . 1977;112:691â€“695. 3. Hellinger M. Anal traum a and foreign bodies. Surg Clin North Am . 2002;1253â€“1260. 4. Janicke DM, Pundt MR. Anorectal disorders. Em erg Clin North Am . 1996;14:757â€“788.

Codes ICD9-CM 937

ICD10 T18.5

Pa ge 1 9 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o urnier G angrene

Fournier

Gangrene Gary M. Vilke

Basics Description 

Inadequate hygiene leads to skin m aceration and excoriation: o



Portal of entry for bacteria in tissue

Once skin barrier is broken, polym icrobial flora spread along fascial planes of perineum .



Colles fascia fuses with urogenital diaphragm , slowing propagation posteriorly and laterally.



Anteriorly, Buck and Scarpa fascia are continuous, allowing rapid extension to anterior abdom inal wall and laterally along fascia lata.



Testes and urethra are usually spared.



Three anatom ic origins account for m ost cases: o

Lower urinary tract (40%): urethral strictures, indwelling catheters

o

Penile or scrotal (30%): condom catheters, hydradenitis, and balanitis

o

Anorectal (30%): fistulas, perirectal infections, and

Pa ge 1 9 4

hem orrhoids 

Rarely, intra-abdom inal sources such as perforating appendicitis, diverticulitis, or pancreatitis have produced Fournier gangrene by dependent contiguous spread.

Etiology 

Infection by polym icrobial flora (m ixed aerobic and anaerobic organism s)



Mixed bacteria exert synergistic tissue-destructive effect.



End arterial throm bosis in subcutaneous tissues produces anaerobic environm ent.



Bacterial toxins and tissue necrosis factors m ay contribute to clinical presentation.



Risk factors: o

Traum a

o

Diabetes

o

Alcoholism

o

Other im m unocom prom ised states

o

Morbid obesity

o

Abdom inal surgery

Diagnosis Signs and Symptoms 

Rapidly progressive necrotizing infection of perineum involving subcutaneous and fascial tissues and often m uscle layers: o

Usually seen in diabetics or im m unocom prom ised patients



Patients are often toxic in appearance with nausea, vom iting, fever, chills, and pain.

Pa ge 1 9 4



Sources of infection m ay be flora from genitourinary, rectal, or penile/scrotal regions.





Skin findings: o

Bronze or violaceous discoloration of skin

o

Thin brown watery discharge

o

Ulceration, bullous vesicles

o

Crepitance, subcutaneous air

o

Frank necrosis and eschar form ation

Pain is out of proportion to exam ination in early phases, but eventually dead tissue becom es insensate.



Lethargy and inappropriate indifference to the illness are com m on.

Pediatric Considerations 

Though unusual in children, >50 cases have been described.



Most often are com plications of burns, circum cision, balanitis, severe diaper rashes, or insect bites



Organism s are m ore frequently Staphylococcus or Streptococcus.



Pediatric patients have m ore local disease and are less toxic.

Essential Workup 

Fournier gangrene is a clinical diagnosis.



History and physical exam with special attention to perineum



Evaluate for signs of sepsis.



Early surgical consultation for em ergent dÃ©bridem ent is essential.



Other workup directed toward relevant coâ€“m orbid factors such as diabetes or im m unocom prom ised status

Tests

Pa ge 1 9 4

Lab 

Other than Gram stain of tissue and associated drainage, there are no specific laboratory tests that are diagnostic of Fournier gangrene.



Urinalysis should be perform ed.



Leukocytosis, anem ia, electrolyte im balances, acidosis, and renal failure are com m on.



Dissem inated intravascular coagulation (DIC) m ay be present; PT, PTT, fibrin-split products, and fibrinogen levels help identify.



If patient is suspected of or known to have diabetes, glucose, electrolytes, and serum ketones to evaluate for diabetes and diabetic ketoacidosis (DKA)



Culture of blood, urine, and tissue (when available)

Imaging 

Plain film s of the pelvis m ay reveal subcutaneous em physem a and ileus.



CT scanning helps if intra-abdom inal or ischiorectal source is suspected.



Ultrasound (US) m ay be useful in differentiating from other causes of acute scrotum .



Retrograde urethrography, anoscopy, proctosigm oidoscopy, and barium enem as m ay be helpful to localize anatom ic sources of infection.

Differential Diagnosis 

Testicular torsion



Scrotal cellulitis



Epididym itis/orchitis



Tinea cruris



Scrotal abscess/inguinal abscess



Perirectal infections

Pa ge 1 9 4



Insect and hum an bites

P.429

Treatment Pre Hospital Cautions: 

Patients m ay be hypotensive from septic shock and require aggressive fluid resuscitation and pressor support.

Initial Stabilization 

Manage airway and resuscitate as indicated.



Central venous access, aggressive fluid resuscitation, and pressure support as indicated: o

Avoid fem oral access, fem oral venipuncture, and lower extrem ity venous access



Early goal-directed therapy if septic



Foley catheter placem ent or suprapubic access if indicated

ED Treatment 

Em piric broad-spectrum antibiotics



Early em ergent aggressive surgical dÃ©bridem ent



Adjunctive hyperbaric oxygen therapy coordinated with surgical care



Treat dehydration and correct electrolytes.



Blood products as needed for DIC or anem ia; oxygen debt can be m inim ized by keeping hem atocrit >30%



Tetanus prophylaxis as indicated

Pa ge 1 9 4

Medication (Drugs) 

Antibiotic regim ens: o

Multidrug regim en: 

Am picillin: 2 g IV q6h (peds: 50 m g/kg) and



Clindam ycin: 900 m g IV q8h (peds: 10 m g/kg) and

 o

Gentam icin: 5 m g/kg daily load IV q8h

Single-drug regim ens (peds: safety not established) 

Am picillin/sulbactam : 3 g IV initial ED dose



Im ipenem : 1 g IV initial ED dose



Piperacillin/tazobactam : 3.375 g IV initial ED dose



Ticarcillin/clavulanate: 3.1 g IV initial ED dose or



Blood products as indicated



Dopam ine or dobutam ine IV drips starting at 5 Âµg/kg/m in titrating to effect if hypotensive after aggressive hydration



Insulin adjusted to control glucose and acidosis

Pediatric Considerations 

More conservative surgical approach



Adequate staphylococcal coverage

Follow-Up Disposition Admission Criteria 

All patients with Fournier gangrene require adm ission and surgical ICU care.



Mortality estim ates of 3â€“38% em phasize need for early

Pa ge 1 9 4

aggressive care. 

Consider early transfer to facility capable of providing adjunctive hyperbaric oxygen therapy if stable for transport.

Discharge Criteria No patients with Fournier gangrene should be discharged.

References 1. Corm an JM, Moody JA, Aronson WJ. Fournier's gangrene in a m odern surgical setting: im proved survival with aggressive m anagem ent. Br J Urol. 1999;84:85â€“88. 2. Jallali N, Withy S, Butler PE. Hyperbaric oxygen as adjuvant therapy in the m anagem ent of necrotizing fasciitis. Am J Surg. 2005;189:462â€“466. 3. Morpurrgo E, Galandiuk S. Fournier's gangrene. Surg Clin N Am . 2002;82:1213â€“1224. 4. Norton KS, Johnson LW, Perry T, et al. Managem ent of Fournier's gangrene: an eleven year retrospective analysis of early recognition, diagnosis, and treatm ent. Am Surg. 2002;68:709â€“713.

Codes ICD9-CM 608.83

ICD10 N49.8

Pa ge 1 9 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F racture, Open

Fracture, Open

Christy Rosa Mohler

Basics Description 

Continuity between skin violation and fracture site, ranging from a puncture wound to grossly exposed bone



Surgical em ergency as delays in care increase risk of infection and rate of com plications



Predisposition to com plications in certain patients: o

Massive soft tissue dam age

o

Severe wound contam ination

o

Com prom ised vascularity

o

Fracture instability

o

Com prom ised host (diabetes, vascular disease)

Diagnosis Signs and Symptoms 

Deform ity with nearby violation in skin integrity



Neurovascular com prom ise m ay occur.



Other significant injuries m ay be present: o

Thirty percent of patients with open lower extrem ity

Pa ge 1 9 5

fractures are m ultiple-traum a victim s.

Essential Workup 

Com plete neurologic and vascular exam ination



Plain radiographs including joints above and below the affected area

Tests Lab 

CBC, chem istry panel, coagulation studies for large-bone (fem ur, pelvis) fractures or m ultiple-traum a victim s



Type and screen or type and cross-m atch for potential of significant blood loss.

Imaging Doppler or angiography if vascular dam age suspected: 

Posterior knee dislocation



Ischem ic extrem ity



Massive soft tissue injury in high-risk areas

Diagnostic Procedures/Surgery 

Measurem ent of com partm ent pressures if concern for com partm ent syndrom e



Consider arthrogram by intra-articular injection of saline or m ethylene blue if joint involvem ent suspected.



Angiography if noninvasive techniques inadequate for ruling out vascular com prom ise

Differential Diagnosis Noncontinuous laceration/abrasion

Treatment

Pa ge 1 9 5

Pre Hospital 

Sterile dressings over open wound



Im m obilize joints above and below fracture; splint lim b.



Longitudinal traction of involved extrem ity if distal pulses absent



Traction splint for pain control if prehospital tim e prolonged

Initial Stabilization 

Airway, breathing, and circulation m anagem ent



Reduction and im m obilization of fracture with steady, longitudinal traction

ED Treatment 

Intravenous access



Keep patient NPO for conscious sedation or OR



Tetanus vaccination, if needed



Parenteral antibiotics within 3 hours of injury



Minim ize num ber of tim es dressing is rem oved to avoid secondary contam ination.



Exam ine regularly for com partm ent syndrom e and neurovascular status.



Early orthopedic consultation for form al irrigation, dÃ©bridem ent, and operative fixation (if needed): o

Irrigation and treatm ent is optim ally perform ed within 6 hours to reduce likelihood of infection.



Vascular surgery consultation for injuries with vascular dam age

P.431

Pa ge 1 9 5

Medication (Drugs) 

Cefazolin: 1â€“2 g (peds: 20 m g/kg IM/IV)



Add gentam icin: 6 m g/kg IV, for m ore extensive injuries (peds: 2.5 m g/kg IV)



Add penicillin G: 4â€“5 m illion U IV, in farm yard injuries and wounds at risk of contam ination with Clostridium or with vascular injury (peds: 50,000 U/kg IV)



Tetanus booster: 0.5 m L IM



Tetanus im m unoglobulin: 250 IU IM if not previously im m unized against tetanus



Morphine sulfate: 2â€“10 m g (peds: 0.05â€“0.1 m g/kg per dose IV or equivalent analgesic)

Pediatric Considerations Diphtheria-pertussis-tetanus booster for children younger than 7 years

Follow-Up Disposition Admission Criteria Most patients will be adm itted for irrigation and IV antibiotics and possibly dÃ©bridem ent or operative fixation.

Discharge Criteria Sim ple open fractures m ay be washed out and im m obilized in the em ergency departm ent after consultation with an orthopaedic surgeon. The patient should be discharged with oral antibiotics and follow-up in 24 hours.

References 1. Behrens FF, Sirkin MS. Fractures with soft tissue injuries. In:

Pa ge 1 9 5

Browner BD, et al., eds. Skeletal Traum a: Basic Science, Managem ent and Reconstruction. 3rd ed. Philadelphia: WB Saunders; 2003:293â€“319. 2. Geiderm an JM. General principles of orthopaedic injuries. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosbyâ€“Year Book; 2002:467â€“492. 3. Menkes JS. Injuries to the bones, joints and soft tissues: initial evaluation and m anagem ent of orthopaedic injuries. In: Tintinalli JE, ed. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:1651â€“1665. 4. Zalavras CG, Patzakis MJ. Open fractures: evaluation and m anagem ent. J Am Acad Orthop Surg. 2003;11(3):212â€“219.

Codes ICD9-CM 829.1 Unspecified bone, open

Pa ge 1 9 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ractures, Pediatric

Fractures,

Pediatric Adam Z. Barkin

Basics Description 

Anatom y: o

Diaphysis: physis to physis; bone shaft

o

Epiphysis: cartilaginous center at or near end of bone that is site of bone growth

o

Physis (equals epiphyseal or m etaphyseal growth plate): radiolucent line between epiphysis and m etaphysis; cartilaginous

o

Metaphysis: region of rapidly growing trabecular bone underlying base of cartilaginous growth plate; between diaphysis and epiphysis



Bones are highly resilient, elastic, and springy



Allow for fractures not seen in adults: o

Greenstick fracture: 

Incom plete fracture through cortex on opposite side of im pact

o

Torus (buckle) fracture: 

Usually at junction of m etaphysic and diaphysis

Pa ge 1 9 5

 o

Plastic deform ity: 

o

Com pression of bone of one cortex

Bowing without disruption of cortex

Fractures involving the physis



Cartilaginous growth plates are potential areas of injury.



Ligam ents m ore resistant to injury than growth plates



Salter-Harris classification: o

Risk of growth disturbance increases from type I to type V.

o

Type I: 

Separation of epiphysis from m etaphysis without displacem ent or injury to the growth plate

o

o



Tenderness and pain at point of growth plate



Radiograph typically norm al



Growth disturbance is rare.

Type II: 

Metaphyseal fracture extending to physis



Most com m on



Growth disturbance is rare.

Type III: 

Intra-articular fracture extending through the epiphysis into the physis

o



Most com m on site is distal tibial epiphysis.



Growth disturbance possible

Type IV: 

Epiphyseal, physeal, and m etaphyseal fracture



Intra-articular



Lateral condyle of hum erus is m ost com m on site.

 o

Growth disturbance highly likely

Type V:

Pa ge 1 9 5



Crush injury to epiphyseal plate, producing growth arrest



Usually occurs in joints that m ove in only one plane such as knee or ankle



Fractures often accom pany dislocations.



Nonaccidental traum a (NAT) if history inconsistent with findings

Etiology 

Mechanism is useful in defining the potential and type of injury: o

Falls, m otor vehicle accidents, blunt traum a, NAT



Obesity and rapid growth spurts are risk factors.



Com m on fractures include lower forearm , clavicle, tibia or fibula, supracondylar fracture of hum erus.



Nonaccidental traum a (NAT): o

Any fracture in a child younger than 1 year of age in whom history is not consistent with injury

o

Metaphyseal â€œcornerâ€• fractures are pathognom onic.

o

Posterior rib fractures

o

Spiral fem ur fracture

o

Fractures at different stages of healing

o

Skull fractures crossing suture lines, especially in children younger than 1 year

o

Unusual behavior in child or parent

Diagnosis Signs and Symptoms 

Decreased lim b m ovem ent, unwilling to use

Pa ge 1 9 5



Swelling



Tenderness



Deform ity



Ecchym oses



Crepitus



Lim p



Abnorm al neurovascular status of extrem ity



Com partm ent syndrom e:



o

Severe pain, especially in forearm , calf, foot

o

Pain with passive stretching of fingers or toes

o

Sensory deficit in the distal extrem ity

Open fracture m ay be obvious or subtle (collection of blood with fat globules under skin)

History 

Mechanism of injury: o

Velocity of car, bike, and so on

o

Height of fall



Neurologic com prom ise



Events surrounding injury



Other injuries

Physical Exam 

Thorough secondary survey looking for deform ities, bruising, other injuries



Assess neurovascular status: o

Motor/sensation

o

Distal pulses

o

Capillary refill



Range of m otion of all joints involved



Exclude concurrent injuries



Ensure that history consistent with injury

Essential Workup

Pa ge 1 9 5



Prom pt im m obilization



Im aging as below

Tests Lab 

Required only if concom itant injuries, surgery anticipated, or m ultiple/m ajor bone involvem ent



CBC, erythrocyte sedim entation rate (ESR) if infection suspected

Imaging 

Anteroposterior (AP), lateral, and oblique radiographs as necessary, including the joint above and below the fracture



Com parison views m ay be useful if growth plates involved.



Follow-up radiographs at 7â€“10 days m ay be required to exclude avascular necrosis or Salter I fractures.



Bone scan/CT/MRI m ay be useful to exclude fractures if plain radiographs are unhelpful or to evaluate for infection.

Diagnostic Procedures/Surgery Arthrocentesis if infection is suspected

Differential Diagnosis 

Sprain or strain



Contusion



Infection



Tum or



Neurologic deficits



Subtle dislocations such as radial head subluxation (nursem aid's elbow)



NAT

Pa ge 1 9 5

Treatment Pre Hospital Im m obilization

Initial Stabilization 

Resuscitation for concurrent injuries



Im m obilization

ED Treatment 

Managem ent of life-threatening concurrent injuries



Pain control



Dislocations require im m ediate assessm ent and attention to neurovascular com prom ise: o

Mechanism helps in understanding the direction of the force required to reduce.



Alignm ent is essential, particularly when fracture involves a joint surface.



Open fractures: o

Require em ergent orthopedic consultation for irrigation and dÃ©bridem ent

o

IV antibiotic therapy

P.433



Appropriate reporting of NAT



Salter-Harris fractures: o

Type I and type II fractures require im m obilization and orthopedic follow-up.

o

Type II distal fem ur fractures, type III, and type IV require urgent orthopedic consultation for anatom ic reduction.

Pa ge 1 9 6

o

Type V fractures require im m obilization and consultation.

o

Anatom ic reduction does not elim inate possibility of growth disturbance.



Clavicle fracture: o

Figure-of-eight splint or sling for com fort

o

Distal third clavicle fractures should be referred with initial sling and swathe or shoulder im m obilizer.



Supracondylar hum erus fracture: o

May present with only posterior effusion on lateral radiograph

o

Orthopedic consultation because of potential neurovascular com plications

o

Brachial artery injury, m edian nerve injury possible

o

Volar com partm ent syndrom e of forearm (results in Volkm ann contracture)

o

Epiphyseal injury with long-term growth abnorm alities





Distal radius and ulna fractures: o

Rotational deform ities m ust be elim inated.

o

Reduce angulated fractures >15Â°

o

Im m obilize for 4â€“6 weeks.

Colles fracture: o

Reduce by traction in the line of deform ity to disim pact the fragm ents, followed by pressure on the dorsal aspect of the distal fragm ent and volar aspect of the proxim al fragm ent.

o

Correct radial deviation.

o

Im m obilize the hand in ulnar deviation, wrist in neutral, and forearm in full pronation.

o 

Orthopedic consultation

Torus fracture (incom plete fracture; buckling or angulation

Pa ge 1 9 6

on the com pression side of the bone only: o 

Most often in distal forearm

Greenstick fracture (incom plete fracture of diaphysis of long bone with fracture on tension side of cortex): o

Im m obilize in long-arm splint for 4â€“6 weeks.

o

Reduction if angulation >30Â° in infants, >15Â° in children



Tibia or fibula fracture: o

Isolated fibular fractures: short-leg walking cast

o

Nondisplaced tibial fracture: long-leg posterior splint, non-weight bearing

o

Displaced tibial fracture and com plex fractures require consultation.



Toddler's fractures: o

Nondisplaced, oblique, distal tibia fracture

o

May need tangential view radiograph or bone scan to diagnose

o

Splint if concern and repeat radiograph in 7â€“10 days.





Radial head subluxation (nursem aid's elbow): o

Infant or preschooler

o

Longitudinal traction on wrist or hand

o

Radiograph if bony tenderness

o

Reduce with supination and elbow flexion.

o

Follow-up in 24â€“72 hours.

Slipped capital fem oral epiphysis: o

Disruption though capital fem oral epiphysis

o

Overweight adolescent boys

o

May have referred pain to knee, thigh, or groin

o

Non-weight bearing with prom pt orthopedic follow-up

Pa ge 1 9 6

Medication (Drugs) 

Acetam inophen: 10â€“15 m g/kg PO/PR (per rectum ) q4hâ€“q6h



Hem atom a block: 1% lidocaine without epinephrine (m ax. 3â€“5 m g/kg)



Ibuprofen: 10 m g/kg PO q6hâ€“q8h



Morphine: 0.05â€“0.2 m g/kg SC/IM/IV q2hâ€“q4h

Follow-Up Disposition Admission Criteria 

NAT (or per social services)



Potential neurovascular com prom ise/com partm ent syndrom e: o

Condylar or supracondylar hum erus fracture

o

Fem oral shaft

o

Com plete patella

Discharge Criteria 

Uncom plicated fracture: no concurrent injury or neurovascular/com partm ent com prom ise



Follow-up arranged and parents understand injury and m anagem ent

Issues for Referral 

All Salter-Harris fractures should have orthopedic follow-up.

References 1. Chew FS. Skeletal Radiology: The Bare Bones. 2nd ed. Baltim ore, MD: William s & Wilkins; 1997.

Pa ge 1 9 6

2. Della-Giustina K, Della-Giustina DA. Em ergency departm ent evaluation and treatm ent of pediatric orthopedic injuries. Em erg Med Clin North Am . 1999;17:895â€“922. 3. Marx JA. Rosen's Em ergency Medicine Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 4. Musgrave DS, Mendelson SA. Pediatric orthopedic traum a: principles in m anagem ent. Crit Care Med. 2002;30:S431â€“443. 5. Rodriguez-Merchan EC. Pediatric skeletal traum a: a review and historical perspective. Clin Orthop Relat Res. 2005;432:8â€“13.

Miscellaneous SEE ALSO: Conscious Sedation; C-spine Fractures, Pediatric; Fractures, Open; Nursem aid's Elbow; Shoulder Dislocation; Slipped Capital Fem oral Epiphysis

Codes ICD9-CM 829.0

Pa ge 1 9 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ro stbite

Frostbite

Paul Arnold

Basics Description Tissue dam age caused by cold tem perature exposure

Mechanism 

Tissue dam age results from : o

Direct cell dam age: owing to intracellular ice crystal form ation

o

Indirect cell dam age: extracellular ice crystal form ation leads to intracellular dehydration through osm osis.

o

Microvascular stasis and throm bosis: erythrocyte sludging leads to hypoxia, then vasospasm , ischem ia, tissue necrosis.

o

Progressive derm al ischem ia: m ediated by throm boxane and prostaglandins in blisters

o

Reperfusion injury: occurs after thawing; is caused by edem a, then throm bosis, inflam m atory leukocyte infiltration, and necrosis

o

Therm al shock: direct cell death owing to the extrem e cold



Devitalized tissue dem arcates as the injury evolves over

Pa ge 1 9 6

weeks to m onths, hence the expectant m anagem ent of severe frostbite

Etiology 

Cold exposure



Vulnerability increased owing to: o

Extrem es of age

o

Poor self-care:

o



Intoxication



Altered m ental status



Im m obility

Poor circulatory status

Diagnosis Signs and Symptoms 

Extrem ities (fingers, toes) and head (ears, nose) m ost com m only affected



Initial appearance of an injury often fails to predict eventual depth or outcom e

Superficial Frostbite 

Only skin structures involved: o

No tissue loss



Frozen skin loses touch, pain, or tem perature sensation.



Stinging, num bness, burning



Appearance: o

Initially white/waxy/m ottled

o

Becom es hyperem ic and edem atous as warm ing progresses



Rewarm ing leads within 3 hours to hyperem ia, swelling, and pain, which resolve within 2â€“3 days.

Pa ge 1 9 6

Deep Frostbite 

Subcutaneous, m uscle, nerve, or bone involved: o



Tissue loss inevitable

Initially insensate, injuries develop severe pain/burning on rewarm ing.



Tissue feels hard, woody to the touch.



Postrewarm ing appearance:



o

Edem a within 3 hours and lasts 5 days

o

Large clear blebs within 6â€“24 hours

o

Sm all, hem orrhagic blebs form after 24 hours,

o

Eschar form s in 9â€“15 days,

o

Mum m ification in 3â€“6 weeks

Reduced m obility, persistent m ottling, anesthesia despite edem a after rewarm ing are unfavorable prognostic indicators.



Devitalized tissue dem arcates as the injury evolves over weeks to m onths.

Essential Workup 

Diagnosis is based on the clinical presentation.



Look for underlying factors contributing to cold exposure and co-m orbid conditions requiring em ergency m anagem ent: o

Intoxication

o

Head injury

o

Traum a

o

Hypoglycem ia

o

Cardiac or neurologic problem s

Tests Lab 

None indicated in m ild cases

Pa ge 1 9 6





For severe frostbite: o

CBC

o

Electrolytes, BUN/creatinine, glucose

o

Urinalysis for evidence for m yoglobinuria

Cultures and Gram stains from open areas when infection suspected

Imaging Technetium -99 scintigraphy: 

Helpful in early identification of unsalvageable bone



Perm its earlier decision about am putation



Perform 2â€“7 days after cold injury.

Differential Diagnosis 

Frostnip: o

Superficial, reversible ice crystal form ation without tissue destruction

o

Transient num bness and paresthesia resolve after rewarm ing.



Trench foot: o

Exposure to wet cold for prolonged periods

o

Neurovascular dam age without ice crystal form ation

o

Pallor, m ottling, paresthesias, pulselessness, paralysis, and num bness

o 

Hyperem ia with rewarm ing lasting up to 6 weeks

Chilblains: o

Chronic repeated exposure to dry cold

o

Localized erythem a, cyanosis, plaques, and vesicles

Treatment Pre Hospital

Pa ge 1 9 6



Protect and im m obilize frostbitten area during transport.



Rem ove restrictive or wet garm ents.



Avoid dry rewarm ing of the frostbitten lim b if there is a likelihood of refreezing of the injury during transport.



If evacuation will be delayed and suitable facilities are available, field rewarm ing in warm (40â€“42Â°C) water can be attem pted.



Rubbing, m anipulating the lim b, or applying snow while it is still frozen is contraindicated.

P.435

Alert 

Hypotherm ia: o

Com m on in frostbite victim s

o

In the severely hypotherm ic patient, avoid rough handling to m inim ize risk of cardiac dysrhythm ias.

Initial Stabilization 

Airway, breathing, and circulation (ABCs) m anagem ent



Identify and correct hypotherm ia.



IV fluid volum e expansion with 0.9% norm al saline (NS) for severe frostbite



Protect frostbitten areas from excessive handling or dry warm ing during resuscitation.

ED Treatment 

If the injury is <24 hours old and has not yet been rewarm ed: o

Initiate rapid thawing of the injured extrem ity for 10â€“30 m inutes in 40â€“42Â°C water.

o

Stop treatm ent when the lim b is warm , red, and pliable.

Pa ge 1 9 6

o

Monitor water tem perature closely to prevent therm al injury.



Analgesia



Nonsteroidal anti-inflam m atory drugs (NSAIDs; e.g., ibuprofen) to com bat the effects of prostaglandins on skin necrosis



Aloe vera topical cream : o

Recom m ended for all intact blisters

o

Com bats the arachidonic cascade

o

Avoid preparations containing alcohol, scent, salicylates, all of which interfere with aloe effectiveness.



Blister dÃ©bridem ent or aspiration: o

Indicated for clear blebs: 

o

Rem oves throm boxane and prostaglandins

Contraindicated for hem orrhagic blebs: 

Exposes deeper structures to dehydration and infection



Tetanus prophylaxis



Antibacterial prophylaxis: o

Consider during the hyperem ic recovery phase (at least 2â€“3 days) in severely frostbitten areas.

o

Against streptococci, staphylococci, and Pseudom onads species (cephalosporin, penicillinase-resistant penicillin, quinolone)

o

Topical antibacterial agents interfere with the use of aloe vera cream and should be considered a second-line approach.



Elevation and splinting of frostbitten area



Change dressing 2â€“4 tim es daily.



Avoid vasoconstrictive agents (including tobacco).



Adjunctive and controversial m easures include:

Pa ge 1 9 7

o

Oxpentifylline: 

Im proves perfusion by increasing red blood cell deform ability and vasodilation

o

Throm bolytic therapy

o

Hyperbaric oxygen

o

Sym pathectom y

o

Early dÃ©bridem ent and free tissue transfer

Medication (Drugs) 

Aloe vera: topical cream (70% concentration) q6h



Cephalexin (cephalosporin): 500 m g (peds: 25â€“50 m g/kg/24h q6h) PO q.i.d.



Ciprofloxacin (quinolone): 500 m g PO b.i.d.



Dicloxacillin (penicillinase-resistant penicillin): 500 m g (peds: 25â€“100 m g/kg/24h q6h) PO q.i.d.



Ibuprofen (NSAID): 800 m g (peds: 40 m g/kg/24h q6hâ€“q8h) PO t.i.d.



Morphine sulfate: 0.1â€“0.2 m g/kg (peds: 0.1 m g/kg) IV or IM PRN (titrate to patient response)

Follow-Up Disposition Admission Criteria 

All but the m ost superficial and painless cases should be adm itted for at least 24â€“48 hours after rewarm ing.



Lower adm ission threshold where risk of refreezing exists

Discharge Criteria Rewarm ed injury with evidence of only superficial injury and close

Pa ge 1 9 7

follow-up availability

References 1. Biem J, et al. Out of the cold: m anagem ent of hypotherm ia and frostbite. Can Med Assoc J. 2003;168(3):305â€“311. 2. Hayes DW Jr, et al. Pentoxifylline. Adjunctive therapy in the treatm ent of pedal frostbite. Clin Podiatr Med Surg. 2000;17(4):715â€“722. 3. Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO: Mosby; 2002. 4. Murphy JV, et al. Frostbite: pathogenesis and treatm ent. J Traum a . 2000;48(1):171â€“178.

Miscellaneous SEE ALSO: Hypotherm ia

Codes ICD9-CM 991.3

ICD10 T35.7

Pa ge 1 9 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G allsto ne Ileus

Gallstone Ileus

Edward A. Stettner

Basics Description 

Mechanical intestinal obstruction secondary to im paction of a gallstone within bowel lum en



Stone is usually larger than 2.5 cm



1â€“5% of all intestinal obstructions



Most cases occur in patients older than 65 years: o

25% of bowel obstructions in patients older than 65 years



5:1 fem ale to m ale predom inance



Mortality 15â€“18%

Etiology 

Chronic gallbladder inflam m ation causes adhesions between gallbladder and adjacent bowel wall.



Cholecystenteric fistula develops, perm itting stone passage into intestine: o

Duodenum is m ost com m on site of fistula form ation, followed by colon.

o 

Gastric fistulas are rare.

Site of im paction: o

Term inal ileum m ost com m on (54â€“65%):

Pa ge 1 9 7



Narrowest part of sm all intestine

o

Jejunum (27%)

o

Duodenum (1â€“3%): 

Gastric outlet obstruction caused by duodenal im paction referred to as Bouveret syndrom e

o 

Colonic obstruction is rare.

Stones spilled intraperitoneally during cholecystectom yâ€”open or laparoscopicâ€”m ay also lead to bowel obstruction: o

Can have recurrent obstruction from subsequent gallstones

Diagnosis Signs and Symptoms 

â€œTum blingâ€• abdom inal discom fort: o

Episodic abdom inal pain as stone lodges and dislodges throughout the intestines

o

Com plete im paction leads to severe, often acute abdom inal pain.



Nausea



Vom iting: o

Can be bilious or feculent



Obstipation



Abdom inal distention and tym pany



Abdom inal tenderness: o

Peritoneal findings late



Abnorm al bowel sounds



Occasional jaundice



Only 50â€“60% of patients have history of biliary colic or disease.

Pa ge 1 9 7

Essential Workup Evaluation for intestinal obstruction

Tests Lab 

Electrolytes, BUN/creatinine, glucose since decreased oral intake and vom iting leads to: o

Hypochlorem ia

o

Hypokalem ia

o

Hyponatrem ia

o

Alkalosis

o

Preâ€“renal azotem ia



Liver function panel and bilirubin m ay be elevated.



Am ylase: o



Elevated in late obstructions

CBC/hem atocrit: o

Hem oconcentration secondary to dehydration

o

Elevated WBC nonspecific

Imaging 

Flat and upright abdom inal radiographs: o

Multiple air fluid levels and distended bowel consistent with bowel obstruction

o

Rigler triad: 2 of 3 pathognom onic (present in 30â€“50%) 

Air in the biliary tree (pneum obilia)



Partial or com plete bowel obstruction



Ectopic stone visualized within the intestinal tract



Chest radiograph: o



Evaluate for pneum operitoneum

Abdom inal CT scan:

Pa ge 1 9 7

o

Increasing use in evaluating sm all bowel obstruction

o

Can directly visualize and localize stone within intestinal lum en



Abdom inal ultrasonography: o

Can identify pneum obilia and gallstones, but lower yield in locating obstructing stone

Differential Diagnosis 

Paralytic ileus



Extrinsic bowel obstruction: o

Adhesions

o

Volvulus

o

Hernia

o

Intussusception



Gastrointestinal m alignancy



Diverticulitis



Bezoar



Inflam m atory bowel disease



Pseudo-obstruction



Cholecystitis



Ascending cholangitis



Pancreatitis

P.437

Treatment Initial Stabilization IV fluid resuscitation

ED Treatment

Pa ge 1 9 7



Nasogastric suction to decom press the stom ach and intestine



Nothing PO



Electrolyte replacem ent



Monitor urine output.



Analgesics



Broad-spectrum antibiotics to cover bowel flora: o

Piperacillin/tazobactam

o

Am picillin/sulbactam

o

Ticarcillin/clavulanate

o

Alternatives include im ipenem , m eropenem , third-generation cephalosporins plus m etronidazole.



Surgical consultation

Medication (Drugs) 

Am picillin/sulbactam : 3 g (peds: 100â€“200 m g/kg/24h) IV q6h



Piperacillin/tazobactam : 3.375 g (peds: 240â€“400 m g/kg/24h) IV q6h



Ticarcillin/clavulanate: 3.1 g IV q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

Adm it all patients with gallstone ileus.



Surgical evaluation for em ergent operative intervention

Discharge Criteria None

Pa ge 1 9 7

References 1. Bennett G, Balthazar E. Ultrasound and CT evaluation of em ergent gallbladder pathology. Radiol Clin North Am . 2003;41:1203â€“1216. 2. Delabrousse E, Bartholom ot B, et al. Gallstone ileus: CT findings. Eur Radiol. 2000;10:938â€“940. 3. Lobo D, Jobling J, et al. Gallstone ileus: diagnostic pitfalls and therapeutic successes. J Clin Gastroenterol. 2000;30(1):72â€“76. 4. Marschall J, Hayton S. Bouveret's syndrom e. Am J Surg. 2004;187:547â€“548 5. Rosenberg M, Parsiak K. Vom iting gravel. Am J Em erg Med. 2004;22(2):131â€“132.

Codes ICD9-CM 560.31 Gallstone ileus

ICD10 K56.3 Gallstone ileus

Pa ge 1 9 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Î³-G HB, Po iso ning

Î³-GHB, Poisoning

Amy V. Kontrick Mark B. Mycyk

Basics Description 

Naturally occurring analog of Î³-am inobutyric acid (GABA)



Used m edically for narcolepsy



Nonm edical uses: o

Bodybuilding agent

o

Euphoric agent

o

Date-rape/predatory agent



Onset of activity: 15â€“30 m inutes after ingestion



Duration of effect: 2â€“6 hours

Etiology Deliberate or accidental ingestion of Î³-hydroxybutyrate (GHB)

Diagnosis Signs and Symptoms 

Central nervous system : o

CNS depression

Pa ge 1 9 7











o

Ataxia/dizziness

o

Im paired judgm ent

o

Aggressive behavior

o

Clonic m ovem ents of the extrem ities

o

Com a

o

Seizures

Pulm onary: o

Respiratory depression

o

Apnea

o

Laryngospasm (rare)

Gastrointestinal: o

Nausea

o

Vom iting

Cardiovascular: o

Bradycardia

o

Atrioventricular block

o

Hypotension

Other: o

Nystagm us

o

Hypotherm ia

Withdrawal sym ptom s: o

Hypertension

o

Tachycardia

o

Hypertherm ia

o

Agitation

o

Diaphoresis

o

Trem ors

o

Nausea, vom iting, and abdom inal cram ping

o

Hallucinations, delusions, and psychosis

Essential Workup 

Diagnosis based on clinical presentation and an accurate history

Pa ge 1 9 8



Exclude coingestants if signs and sym ptom s inconsistent with GHB intoxication.

Tests Lab 

Confirm atory GHB screen is typically a send-out lab and does not change ED m anagem ent.



Urine toxicology screen to exclude coingestants



Serum alcohol level



Urinalysis and creatine kinase (CPK) if suspected rhabdom yolysis from prolonged im m obilization or agitation

Imaging 



ECG: o

Sinus bradycardia

o

Atrioventricular block

Chest radiograph: o



Aspiration pneum onia

Head CT if suspected occult head traum a

Differential Diagnosis 

Alcohol intoxication



Barbiturate overdose



Benzodiazepine overdose



Neuroleptic overdose



Opiate overdose



Withdrawal: o

Alcohol withdrawal

o

Sedative-hypnotic withdrawal

Treatment

Pa ge 1 9 8

Pre Hospital 

Transport all pills/bottles and drug paraphernalia involved in overdose for identification in em ergency departm ent.



Î³-Hydroxybutyrate (GHB) precursors (Î³-butyrolactone [GBL], 1,4 butanediol [1,4-BD], GHV [Î³-hydroxyvalerate], and GVL) have sam e effects as Î³-hydroxybutyrate.

Initial Stabilization 



ABCs (airway, breathing, circulation): o

Airway control essential

o

Adm inister supplem ental oxygen.

o

Intubate if indicated.

Adm inister thiam ine, dextrose (or Accu-Chek), and naloxone for depressed m ental status.

ED Treatment 

Supportive care



Bradycardia:







o

Atropine

o

Tem porary pacing

Hypotension: o

0.9% norm al saline IV fluid bolus

o

Trendelenburg

o

Dopam ine titrated to pressure

Seizures: o

Treat initially with benzodiazepine.

o

Treat refractory seizures with phenobarbital.

Withdrawal: o

Treat aggressively with benzodiazepine.

o

Treat with phenobarbital or propofol if large doses of benzodiazepines unsuccessful.

P.451

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Medication (Drugs) 

Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 2 5 over 1 m inute) IV; repeat if necessary



Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV q10â€“15m in



Dopam ine: 2â€“20 Âµg/kg/m in with titration to effect



Lorazepam : 2â€“4 m g (peds: 0.03â€“0.05 m g/kg) IV q10â€“15m in



Naloxone: 0.4â€“2 m g (peds: 0.1 m g/kg; neonatal: 10â€“30 Âµg/kg) IV or IM



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Propofol: 0.5â€“1.0 m g/kg IV (loading dose), then 5â€“50 Âµg/kg/m in (m aintenance dose)



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Intubated patient



Patient with hypotherm ia or other hem odynam ic instability



Coingestion prolonging duration of intoxication

Discharge Criteria 

Asym ptom atic after 6 hours of observation



No clinical evidence of withdrawal syndrom e

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Issues for Referral Consider substance abuse referral for patients.

References 1. Caldicott DG, Chow FY, Burns BJ, et al. Fatalities associated with the use of gam m a- hydroxybutyrate and its analogues in Australasia. Med J Aust. 2004;181(6):310â€“313. 2. Dyer JE, Roth B, Hym a BA. Gam m a- hydroxybutyrate withdrawal syndrom e. Ann Em erg Med. 2001;37:147â€“153. 3. Gahlinger PM. Club drugs: MDMA, gam m a- hydroxybutyrate (GHB), Rohypnol, and ketam ine. Am Fam Physician. 2004;69(11):2619â€“2926. 4. Li J, Stokes SA, Wockener A. A tale of novel intoxication: a review of the effects of Î³-hydroxybutyric acid with recom m endations for m anagem ent. Ann Em erg Med. 1998;31:729â€“736. 5. Shannon M, Quang LS. Gam m a-hydroxybutyrate, gam m a-butyrolactone, and 1,4-butanediol: a case report and review of the literature. Pediatr Em erg Care. 2000;16:435â€“440.

Codes ICD9-CM 967.8 Poisoning by sedatives and hypnotics, other

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G angrene

Gangrene

Karen B. Van Hoesen

Basics Description 

Gas gangrene or clostridial m yonecrosis



An acute, rapidly progressive, gas-form ing necrotizing infection of m uscle and subcutaneous tissue



Can be seen in posttraum atic or postoperative situations

Etiology 

Clostridial organism s: o

Facultative anaerobic, spore-form ing, gram -positive bacillus

o

Produce a num ber of toxins; the m ost prevalent and lethal is Î±-toxin



Clostridium perfringens is the m ost com m on bacteria; found in 80â€“90% of wounds



Other clostridial bacteria include Clostridium novyi, Clostridium septicum , Clostridium histolyticum , Clostridium biferm entans and Clostridium fallax.



Two distinct m echanism s for introduction of clostridial organism s: o

Traum atic and postoperative

o

Nontraum atic associated with diabetes m ellitus,

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peripheral vascular disease, alcoholism , IV drug abuse, and m alignancies

Diagnosis Signs and Symptoms 

Sudden severe pain of extrem ity or involved area



Low-grade fever



Tachycardia out of proportion to fever



Bronzing of the skin over involved area



Crepitus



Form ation of blebs and bullae



Thin, serosanguineous exudate and sweet odor



Rapid local extension



Obtunded sensorium



System ic toxicity

Essential Workup 

History and physical exam with special attention to clinical evidence of crepitus in soft tissue



Soft tissue x-rays of involved area to detect gas dissecting along fascial planes: o

The absence of gas does not rule out significant disease.



Stat gram stain of wound exudate for gram -positive bacillus with paucity of leukocytes

Tests Lab 

CBC with differential, electrolytes, blood urea nitrate, and creatinine



Coagulation studies

Pa ge 1 9 8



Evaluate for hem olysis



Stat gram stain of wound exudate



Anaerobic cultures of wound or tissue biopsy

Imaging 

Radiographs m ay reveal soft tissue gas.



CT if area involves abdom en or flank

Diagnostic Procedures/Surgery All patients with gas gangrene m ust undergo surgical debridem ent.

Differential Diagnosis 

Cellulitis



Necrotizing fasciitis



Nonclostridial m yositis and m yonecrosis



Other causes of gas in tissues, as from dissection from respiratory or gastrointestinal tracts

Treatment Initial Stabilization Manage airway and resuscitate as indicated: 

Rapid sequence intubation as needed



Supplem ental oxygen: o

Cardiac and oxygen saturation m onitors should be placed



IV access; consider central venous pressure m onitoring



Aggressive volum e expansion, including crystalloid, plasm a, packed RBCs, and album in if septic shock

ED Treatment 

Parenteral antibiotic therapy: o

Prim ary: penicillin G plus clindam ycin

Pa ge 1 9 8

o

Alternative: ceftriaxone or erythrom ycin

o

If m ixed infection: penicillin plus clindam ycin, m etronidazole, or vancom ycin and gram -negative coverage with gentam icin



Surgical consultation: o

DÃ©bridem ent, am putation, or fasciotom y are required.



Hyperbaric oxygen as adjunctive therapy: o

Early transfer to hyperbaric facility m ay be life saving



Tetanus prophylaxis



Observe for m ajor com plications including acute respiratory distress syndrom e, renal failure, m yocardial irritability, and dissem inated intravascular coagulation



Polyvalent antitoxin is not m ade in the United States, and studies have not dem onstrated efficacy: o

Because of the unacceptable hypersensitivity reactions, it is not routinely recom m ended.

P.439

Medication (Drugs) 

Ceftriaxone: 2.0 g (peds: 100 m g/kg/24h m ax. 4 g) IV q24h



Clindam ycin: 900 m g (peds: 40 m g/kg/d q6h) IV q8h.



Gentam icin: 2.0 m g/kg (peds: 2.0 m g/kg IV q8h) IV q8h



Metronidazole: 500 m g (peds: safety not established) IV q8h



Penicillin G: 24 m illion IU/24 hours (peds: 250,000 IU/kg/24h) IV q4hâ€“q6h

Pa ge 1 9 8



Tetanus im m une globulin: 500 IU IM



Tetanus toxoid: 0.5 m g IM

Follow-Up Disposition Admission Criteria 

All patients with gas gangrene and evidence of m yonecrosis m ust be adm itted for surgical dÃ©bridem ent and IV antibiotics.



Use of hyperbaric oxygen therapy is an im portant adjunct.

Discharge Criteria No patient with acute gangrene should be discharged.

Issues for Referral After stabilization with antibiotics and surgical debridem ent, consider referral for hyperbaric oxygen treatm ent as an adjunct.

References 1. Brook I. Microbiology and m anagem ent of m yositis. Int Orthop. 2004;28(5):257â€“260. 2. Clark LA, Moon RE. Hyperbaric oxygen in the treatm ent of life-threatening soft-tissue infection. Respir Care Clin North Am . 1999;5(2):203â€“219. 3. Headley AJ. Necrotizing soft tissue infections: a primary care review. Am Fam Physician. 2003 15;68(2):323â€“328. 4. Langhan M, Arnold L. Clostridial m yonecrosis in an adolescent m ale. Pediatrics. 2005;116(5):e735â€“737. 5. Perry BN, Floyd WE 3rd. Gas gangrene and necrotizing fasciitis in the upper extrem ity. J Surg Orthop Adv. 2004;13(2):57â€“68.

Codes

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ICD9-CM 040.0

ICD10 R02

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astric Outlet Obstructio n

Gastric Outlet

Obstruction Jenny Lu

Basics Description 

Mechanical obstruction that im pedes gastric em ptying, resulting from any disease process



Benign and m alignant causes: o

Edem a, scarring, stricture or hyperplasia of pylorus or duodenum

o

Intrinsic or extrinsic m ass, causing com pression at pylorus or at proxim al duodenum

Etiology 

Peptic ulcer disease



Pyloric stenosis (m ost com m on in pediatric population)



Neoplasm s (pancreatic m ost com m on)



Inflam m ation/edem a



Strictures/webs



Caustic ingestions



Gallstone obstruction

Pa ge 1 9 9

Diagnosis Signs and Symptoms History 

Interm ittent sym ptom s until obstruction becom es com plete



Vom iting, usually nonbilious



Abdom inal pain variable



Early satiety and epigastric fullness



Epigastric discom fort relieved with em esis

Physical Exam 

Vital signs: o

Usually norm al

o

Tachycardia, hypotension with significant volum e depletion



Weight loss in chronic, and with m alignancy



Abdom inal exam ination:



o

Variable epigastric distention

o

Tym pany

o

Succession splash >4 hours after eating

Malnutrition in chronic or late obstruction

Pediatric Considerations 

Abdom inal pain, nausea/vom iting: very com m on in elderly patients with acute m yocardial infarctions o

Obtain ECG in elderly/at risk of coronary artery disease

Pediatric Considerations 



Pyloric stenosis: o

Most com m on cause in pediatric population

o

Early as first week up to age 3 m onths

Initially occasional nonprojectile postprandial vom iting,

Pa ge 1 9 9

progressing to projectile (nonbilious) vom iting 

Midepigastric peristaltic wave prior to vom iting m ay be seen.



Epigastric â€œoliveâ€• m ass palpable in 80% to 90% of patients

Essential Workup 

Careful history and physical exam



Abdom inal ultrasound (US) in pediatric patients: o

Reveals elongated hypertrophic pyloric sphincter

Tests Lab 



CBC: o

Anem ia if blood loss from ulcer

o

High hem atocrit indicates hem oconcentration.

Electrolytes, BUN/creatinine, glucose: o

Hypokalem ia

o

Hypochlorem ic m etabolic alkalosis

o

Hypoglycem ia

o

Prerenal azotem ia



Urinalysis



Am ylase/lipase



Liver function tests, if m alignancy suspected



Helicobacter pylori, if peptic ulcer disease (PUD) suspected

Imaging 



Plain abdom inal radiographs (obstructive series): o

Dilated stom ach

o

Absence of air in bowel distally

Abdom inal CT for detecting neoplastic causes of obstruction

P.441

Pa ge 1 9 9

Diagnostic Procedures/Surgery 

Upper GI: o



To dem onstrate site of obstruction

Upper endoscopy: o

To visualize gastric outlet

Differential Diagnosis 

Proxim al bowel obstruction



Exacerbation of peptic ulcer disease



Gastroenteritis



Cholelithiasis



Cholecystitis



Acute pancreatitis



Diabetic gastroparesis



Psychogenic vom iting

Treatment Initial Stabilization 

0.9% norm al saline (NS) IV fluid resuscitation for prolonged obstruction and significant volum e depletion:



o

Adults: 1 L bolus

o

Peds: 20 m L/kg bolus

Correct electrolyte abnorm alities, especially hypokalem ia.

ED Treatment 

Nasogastric tube (NGT)



Foley catheter to m onitor urine output



Surgical consultation/intervention:

Pa ge 1 9 9

o

Balloon dilatation of benign strictures

o

Enteral stent placem ent (m alignant causes)

o

Gastrojejunostom y (m alignant causes)

o

Vagotom y and antrectom y or pyloroplasty or gastrojejunostom y or other variation (benign causes)

Medication (Drugs) 

Fam otidine: adults: 20 m g (peds: 0.6â€“0.8 m g/kg/24h div. q6hâ€“q8h) IV q12h or



Ranitidine: adults: 50 m g (peds: 2â€“4 m g/kg/24h div. q6hâ€“q8h) IV q8h



Pantoprazole: adults: 40 m g IV daily (also H. pylori treatm ent as needed)

Follow-Up Disposition Admission Criteria All patients with gastric outlet obstruction require adm ission for fluid resuscitation and possible surgical intervention.

References 1. Castellanos, Andres E. Gastric Outlet Obstruction. Available at http://www.em edicine.com /m ed/topic2713.htm . Last updated July 27, 2005. 2. Feldm an M, Friedm an LS, Sleisenger MH, eds. Feldm an, Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders; 1998:666â€“668. 3. Lam Y, et al. Endoscopic balloon dilatation and Helicobacter pylori

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eradication in the treatm ent of gastric outlet obstruction. Gastrointest Endosc. 1997;46(4):379â€“380. 4. Marx, JA. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1243. 5. Shaffer H. Perforation and obstruction of the gastrointestinal tract. Radiol Clin North Am . 1992;30:405. 6. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865. 7. Thom as M. Enteral Stents for the Palliation of Gastroduodenal Obstruction. Available at http://www.uptodate.com . Last updated Novem ber 15, 2005.

Codes ICD9-CM 537.0

ICD10 K31.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astritis

Gastritis

Jason M. Lebwohl

Basics Description 

Inflam m atory response of gastric m ucosa to injury



Three lines of defense of gastric m ucosa: o

Mucous layer that form s protective pH gradient

o

Surface epithelial cells that can repair sm all defects

o

Postepithelial barrier that neutralizes any acid that has traversed first two layers



No definite link between histologic gastritis and dyspeptic sym ptom s

Etiology Acute Gastritis 

Stress (sepsis, burns, traum a): o

Decrease in splanchnic blood flow leading to decreased m ucus production, bicarbonate secretion, and prostaglandin synthesis

o 

Results in m ucosal erosions and hem orrhage

Alcohol: o

Induces production of leukotrienes that cause m icrovascular stasis, engorgem ent, and increased

Pa ge 1 9 9

vascular perm eability o 

Leads to hem orrhage

Nonsteroidal anti-inflam m atory drugs (NSAIDs), including aspirin: o

Interfere with prostaglandin synthesis, leading to sim ilar cascade as induced by alcohol

o 

Results in m ucosal erosions

Steroids

Chronic Gastritis 

Produced by Helicobacter pylori



Mechanism of H. pylori unclear: o

Gram -negative spiral bacteria found in gastric m ucous layer

o

Contains enzym e urease that allows it to change pH level (alkaline) of its m icroenvironm ent

Diagnosis Signs and Symptoms History 

Dyspepsia



Epigastric pain or discom fort (episodic and chronic)



Bloating, indigestion, eructation, flatulence, and heartburn



Anorexia, nausea/vom iting



Dehydration, tachycardia, and electrolyte disturbances (with vom iting)



Hem atem esis, m elena, pallor, and signs of volum e depletion (hem orrhagic gastritis)

Physical Exam 

Careful physical exam including stool Hem occult testing

Pa ge 1 9 9

and vital signs with orthostatics 

Nasogastric tube (NGT) when history of hem atem esis or unstable vital signs



Abdom inal exam nonspecific

Essential Workup 

Airway, breathing, and circulation m anagem ent (ABCs)



Hem atocrit determ ination



Evaluation for dehydration/shock

Tests Lab 

Norm al laboratory values in uncom plicated gastritis



CBC: o

Anem ia with acute hem orrhagic gastritis

o

Leukocytosis: infection



Electrolytes, BUN, creatinine, glucose



Am ylase/lipase for pancreatitis in differential



Urinalysis: o

Assess dehydration/ketosis (starvation)

o

Bilirubin present with hepatitis

Imaging No specific im aging studies

Diagnostic Procedures/Surgery 



ECG: o

For elderly patients

o

Myocardial ischem ia in differential

Endoscopy: o

Outpatient unless significant hem orrhage

o

Allows for visualization of bleeding sites, histologic confirm ation of m ucosal inflam m ation, and detection of H. pylori

Pa ge 1 9 9



Noninvasive H. pylori testing: o

13

C and

14

C urea breath tests

o

Stool antigen test

o

Serology to detect antibodies to H. pylori

Differential Diagnosis 

Peptic ulcer disease (PUD)



Nonulcer dyspepsia (sym ptom s without ulcer on endoscopy)



Gastroesophageal reflux



Biliary colic



Cholecystitis



Pancreatitis



Hepatitis



Abdom inal aortic aneurysm



Aortic dissection



Myocardial infarction

Treatment Pre Hospital 

ABCs



IV fluid resuscitation

Initial Stabilization 

ABCs with acute erosive or hem orrhagic gastritis that presents with hem odynam ic instability



IV fluid resuscitation with lactated Ringer solution or 0.9% norm al saline (NS) via two large-bore catheters



NGT for gastric decom pression and lavage



Foley catheterization to assess volum e replacem ent

P.443

Pa ge 2 0 0

ED Treatment Pain control with: 

Antacids



GI cocktail: o

30 m L antacids plus 10â€“20 m L viscous lidocaine



H 2 antagonists



Sucralfate



Avoid narcoticsâ€”m ay m ask serious illness

Acute Hemorrhagic Gastritis 

IV fluid resuscitation



Blood transfusion if low hem atocrit



Reverse causes (alcohol, sepsis, NSAIDs, or traum a)



Prevent acute or erosive gastritis in critically ill: o

Antacids hourly or IV proton pum p inhibitors (PPI) or H 2 antagonists

o

Goal is to keep pH level at >4.

Chronic Gastritis 

Treatm ent of H. pylori infection: o

Invasive or noninvasive testing to confirm infection

o

Oral (PO) eradication antibiotic therapy options: 

Most com m on regim en consists of PPI (om eprazole 20 m g or lansoprazole 30 m g) plus clarithrom ycin 500 m g and am oxicillin 1 g, all taken b.i.d. for 2 weeks.



For penicillin-allergic patients: PPI plus clarithrom ycin 500 m g b.i.d. plus m etronidazole 500 m g b.i.d. for 14 days



H 2 blocker, bism uth subsalicylate (Pepto-Bism ol) plus either am oxicillin 1,000 m g

Pa ge 2 0 0

b.i.d. or tetracycline 500 m g q.i.d. in com bination with either m etronidazole 250 m g q.i.d. or clarithrom ycin 500 m g b.i.d. for 14 days o

Resistance: 

Increasing antibiotic resistance to m etronidazole (30â€“48%), and clarithrom ycin (>10%)



Uncom m on resistance to am oxicillin and tetracycline

 

No resistance to bism uth

Treatm ent controversial for asym ptom atic or nonulcer dyspepsia gastritis



Vitam in B 1 2 supplem entation for atrophic gastritis

Medication (Drugs) 

Bism uth subsalicylate: 525-m g tabs 2 PO q.i.d.



Cim etidine (H 2 -blocker): 800 m g PO at bedtim e nightly (peds: 20â€“40 m g/kg/24h) for 6â€“8 weeks



Fam otidine (H 2 -blocker): 40 m g PO at bedtim e nightly (peds: 0.5â€“0.6 m g/kg q12h) for 6â€“8 weeks



Lansoprazole (PPI): 30 m g PO b.i.d. for 2 weeks



Maalox plus: 2 to 4 tablets PO q.i.d.



Misoprostol: 100â€“200 Âµg PO q.i.d.



Mylanta II: 2â€“4 tablets PO q.i.d.



Nizatidine (H 2 -blocker): 300 m g PO at bedtim e nightly for 6â€“8 weeks



Om eprazole (PPI): 20 m g PO b.i.d. (peds: 0.6â€“0.7 m g/kg q12hâ€“q24h) for 2 weeks



Pantoprazole (PPI): 40 m g PO/IV daily for 2 weeks



Ranitidine (H 2 -blocker): 300 m g PO at bedtim e nightly

Pa ge 2 0 0

(peds: 5â€“10 m g/kg/24h given q12h) for 6â€“8 weeks 

Sucralfate: 1 g PO q.i.d. for 6â€“8 weeks

Follow-Up Disposition Admission Criteria 

Acute hem orrhagic or erosive gastritis that presents with upper GI tract bleeding, tachycardia, and hypotension



Uncontrolled pain or vom iting



Coagulopathy from m edication or liver disease

Discharge Criteria 

Unrem arkable physical exam with norm al CBC and hem e-negative stools



If hem e-positive stools, discharge if stable vital signs, norm al hem atocrit, and negative NGT aspiration for upper GI tract hem orrhage: o

Outpatient evaluation for endoscopy

Issues for Referral Outpatient referral for endoscopy and H. pylori testing

References 1. Czinn SJ. Helicobacter pylori infection: detection, investigation, and m anagem ent. J Pediatr. 2005;146:S21â€“26. 2. Eswaran S, Roy MA. Medical m anagem ent of acid-peptic disorders of the stom ach. Surg Clin North Am . 2005;85:895â€“906. 3. Leung WK, et al. Ulcer and gastritis. Prim Care. 2001;28(3):487â€“503. 4. McGuirk TD, et al. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):530â€“533.

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5. Sm oot DT, Go MF, Cryer B. Peptic ulcer disease. Prim Care. 2001;33(1):8â€“15. 6. Sung JJ, Chung SC, et al. Antibacterial treatm ent of gastric ulcers associated with Helicobacter pylori. N Engl J Med. 1995;332:139â€“142.

Miscellaneous SEE ALSO: Gastrointestinal Bleeding; Gastroesophageal Reflux Disease; Peptic Ulcer Disease

Codes ICD9-CM 535.5

Pa ge 2 0 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro enteritis

Gastroenteritis

Isam Nasr Harminder Brar

Basics Description Inflam m ation of stom ach and intestines associated with diarrhea and vom iting; often result of infectious or toxin exposure

Etiology Infectious 

Viruses: o



50â€“70% of all cases

Invasive bacteria: o

Cam pylobacter: contam inated food or water, wilderness water, birds and anim als:

o



Most com m on cause



Gross or occult blood is found in 60â€“90%.

Salm onella: contam inated water, eggs, poultry, or dairy products: 

Typhoid fever (Salm onella typhi) characterized by unrem itting fever, abdom inal pain, rose spots, splenom egaly, and bradycardia



Im m unocom prom ised susceptible

Pa ge 2 0 0

o

Shigella: fecal-oral route

o

Vibrio parahaem olyticus: raw and undercooked seafood

o

Yersinia: contam inated food (pork), water, and m ilk: 

May present as m esenteric adenitis or m im ic appendicitis



Specific food-borne disease (food poisoning): o

o

o

Staphylococcus aureus: 

Most com m on toxin-related disease



Sym ptom s 1â€“6 hours after ingesting food

Bacillus cereus: 

Classic source is fried rice left on steam tables.



Sym ptom s within 1â€“36 hours

Cholera: profuse watery stools with m ucous (rice-water stools)

o

Ciguatera: 

Fish intoxication



Onset 5 m inutes to 30 hours (average 6 hours) after ingestion



Paresthesias, hypotension, peripheral m uscle weakness

 o

Am itriptyline m ay be therapeutic.

Scom broid: 

Caused by blood fish: tuna, albacore, m ackerel, and m ahi m ahi



Flushing, headache, erythem a, dizziness, blurred vision, and generalized burning sensation





Sym ptom s last <6 hours.



Treatm ent includes antihistam ines.

Protozoa: o

Giardia lam blia;

Pa ge 2 0 0



High-risk groups: travelers, day care children, hom osexual m en, and cam pers who drink untreated m ountain water

Noninfectious Causes 



Toxins: o

Zinc, copper, cadm ium

o

Organic chem icals: polyvinyl chlorides

o

Pesticides: organophosphates

o

Radioactive substances

o

Alkyl m ercury

Altered host response to food substance (tyram ine, m onosodium glutam ate, tryptam ine)

Pediatric Considerations 

Focus evaluation on state of hydration.



Most of viral origin and self-lim ited



Rotavirus accounts for up to 50%.



Shigella infections associated with seizures

Diagnosis Signs and Symptoms History 

Nausea, vom iting, diarrhea



Bloody/m ucous diarrhea



Abdom inal cram ps or pain



Fever



Malaise, m yalgias, headache, anorexia



Hypotension, lethargy, and dehydration (severe cases)

Physical Exam

Pa ge 2 0 0



Dry m ucous m em branes



Tachycardia



Abdom inal tenderness



Perianal inflam m ation, fissure, fistula

Essential Workup 

Digital rectal exam ination to determ ine presence of gross or occult blood



Fecal leukocyte determ ination: o

Present with invasive bacteria

o

Absent in protozoal infections, viral, toxin-induced food poisoning

Tests Lab 



CBC indications: o

Significant blood loss

o

System ic toxicity

Electrolytes, glucose, BUN, creatinine indications: o

Lethargy, significant dehydration, toxicity, or altered m ental status

o

Diuretic use, persistent diarrhea, chronic liver or renal disease



Stool culture indications: o

Presence of fecal leukocytes

o

Historical m arkers (im m unocom prom ised, travel, hom osexual)

o 

Public health (food handler, day/health care worker)

Blood cultures indications: o

Suspected bacterem ia or system ic infections

o

Ill patients requiring adm ission

o

Im m unocom prom ised

o

Elderly patients and infants

Pa ge 2 0 0

Imaging Abdom inal radiographs have no value unless obstruction or toxic m egacolon suspected.

Pediatric Considerations 

Laboratory studies not required in m ost cases



Rotazym e assay detects rotavirus: o

Rarely indicated in m anaging outpatients

o

Helpful to cohort and avoid cross-contam ination am ong inpatients



Stool cultures indication: o

Fecal leukocytes

o

Toxic

o

Infants

o

Im m unocom prom ised

Differential Diagnosis 

Gastritis/peptic ulcer disease



Milk and food allergies



Appendicitis



Irritable bowel syndrom e



Ulcerative colitis/Crohn disease



Malrotation with m idgut volvulus



Meckel diverticulum



Drugs and toxins: o

Mannitol

o

Sorbitol

o

Phenolphthalein

o

Magnesium -containing antacids

o

Quinidine

o

Colchicine

o

Mushroom s

o

Mercury poisoning

Pa ge 2 0 0

Treatment Pre Hospital 

Difficult IV access with severe dehydration



Avoid exposure to contam inated clothes or body substances.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



IV fluid with 0.9% norm al saline (NS) resuscitation for severely dehydrated

P.445

ED Treatment 

Oral fluids for m ild dehydration (Gatorade/Pedialyte)



IV fluids for: o

Hypotension, nausea and vom iting, obtundation, m etabolic acidosis, significant hypernatrem ia or hyponatrem ia

o

0.9% NS bolus (adults: 500 m Lâ€“1 L, peds: 20 m L/kg) for resuscitation, then 0.9% NS or D 5 0.45% peds: NS (peds: D 5 0.25% NS) to m aintain adequate urine output





Bism uth subsalicylate (Pepto-Bism ol): o

Antisecretory agent

o

Effective clinical relief without adverse effects

Kaolin-pectin (Kaopectate): o

Reduces fluidity of stools

o

Does not influence course of disease

Pa ge 2 0 1



Antim otility drugs (diphenoxylate [Lom otil], loperam ide [Im odium ], paregoric, and codeine): o

Appropriate in noninfectious diarrhea

o

Initial use of sparse am ounts to control sym ptom s in infectious diarrhea

o

Avoid prolonged use in infectious diarrheaâ€”m ay increase duration of fever, diarrhea, and bacterem ia and m ay precipitate toxic m egacolon.



Antibiotics for infectious pathogens: o

Cam pylobacter: quinolones or erythrom ycin

o

Salm onella: quinolones or trim ethoprim sulfam ethoxazole (TMP-SMX)

o

Typhoid fever: ceftriaxone

o

Shigella: quinolone, TMP-SMX, or am picillin

o

Vibrio parahaem olyticus: tetracycline or doxycycline

o

Clostridium difficile: vancom ycin

o

Escherichia coli: quinolones or TMP/SMX

o

Giardia lam blia: m etronidazole

Medication (Drugs) 

Am picillin: 500 m g (peds: 20 m g/kg/24h) PO or IV q6h



Bactrim DS (TMP-SMX): one tab (peds: 8â€“10 m g TMP/40â€“50 m g SMX/kg/24h) PO b.i.d.



Ceftriaxone: 1 gram (peds: 50â€“75 m g/kg/12h) IM or IV b.i.d.



Ciprofloxacin (quinolone): 500 m g PO or 400 m g IV b.i.d. (older than 18 years)



Doxycycline: 100 m g PO or 400 m g IV b.i.d.



Erythrom ycin: 500 m g (peds: 40â€“50 m g/kg/24h) PO q.i.d.



Iodoquinol: 650 m g (peds: 30â€“40 m g/kg/24h) PO t.i.d.

Pa ge 2 0 1



Metronidazole: 250 m g (peds: 35 m g/kg/24h) PO t.i.d. (older than 8 years)



Prochlorperazine (Com pazine): 5â€“10 m g IV q3hâ€“q4h; 10 m g PO q8h; 25 m g per rectum (PR) q12h



Prom ethazine (Phenergan): 25 m g IM/IV q4h; 25 m g PO/PR (peds: 0.25â€“1 m g/kg PO/PR/IM)



Tetracycline: 500 m g PO or IV q6h

Follow-Up Disposition Admission Criteria 

Hypotension unresponsive to IV fluids



Significant bleeding



Signs of sepsis/toxicity



Intractable vom iting or abdom inal pain



Severe electrolyte im balance



Metabolic acidosis



Altered m ental status



Children with >10â€“15% dehydration

Discharge Criteria 

Mild cases requiring oral hydration



Dehydration responsive to IV fluids

References 1. Bitterm an R. Acute gastroenteritides. In: Marx JA, Hockberger RS, Walls RM, et al. eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 1301â€“1325. 2. Blacklow NR, Greenberg HB. Viral gastroenteritis. N Engl J Med. 1991;325:252.

Pa ge 2 0 1

3. Dupont HL. What's new in enteric infectious diseases at hom e and abroad. Curr Opinion Infect Dis. 2005;18:407â€“412.

Miscellaneous SEE ALSO: Diarrhea, Adult; Diarrhea, Pediatric

Codes ICD9-CM 558.9

ICD10 A06

Pa ge 2 0 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro eso phageal Reflux Disease

Gastroesophageal Reflux Disease Jason M. Lebwohl

Basics Description 

Spectrum of pathology in which gastric reflux causes sym ptom s and dam age to esophageal m ucosa



Reflux esophagitis versus nonerosive reflux disease



Approxim ately 40% of general population experience sym ptom s m onthly.

Etiology 

Incom petent reflux barrier allowing increase in frequency and duration of gastric contents into esophagus



Transient lower esophageal sphincter relaxations (TLESRs): o

Occur with higher frequency in gastroesophageal reflux disease (GERD) patients

o

Exposed esophageal m ucosa becom es acidified and with tim e necroses.

o 

Main antireflux barrier

Lower esophageal sphincter (LES): o

Crural diaphragm attachm ent (diaphragm atic sphincter)

Pa ge 2 0 1

o

Contributes to pressure barrier at gastroesophageal junction

o

Esophageal acid clearance via peristalsis and esophageal m ucosal resistance are additional barriers.

o

Most healthy individuals have brief episodes of reflux without sym ptom s.



Decreased LES tone: o

Sm oking

o

Foods: alcohol, chocolate, onion, coffee, tea

o

Drugs: calcium channel blockers, m orphine, m eperidine, barbiturates, theophylline, nitrates



Delayed gastric em ptying, increased body m ass, and gastric distention contribute to reflux.



Hiatal hernias associated with GERD: o

Significance varies in any given individual

o

Most persons with hiatal hernias do not have clinically evident reflux disease.



Acid secretion is sam e in those with or without GERD.



Associated m edical conditions: pregnancy, chronic hiccups, cerebral palsy, Down syndrom e, autoim m une diseases, diabetes m ellitus (DM), hypothyroidism

Diagnosis Signs and Symptoms History 

Typical signs and sym ptom s: o

Heartburn (pyrosis): 

Retrosternal burning pain

Pa ge 2 0 1



Radiates from epigastrium through chest to neck and throat

o

Dysphagia: 

Dysphagia suggests esophageal spasm or stricture.

o

Odynophagia: 

Odynophagia suggests ulcerative esophagitis.

o

Regurgitation

o

Water brash

o

Belching

o

Esophageal strictures, bleeding

o

Barrett esophagus (esophageal carcinom a)

o

Early satiety, nausea, anorexia, weight loss

o

Sym ptom s worse with recum bence or bending over

o

Sym ptom s usually relieved with antacids, although tem porarily



Atypical signs and sym ptom s: o

Noncardiac chest pain

o

Asthm a

o

Persistent cough, hiccups

o

Hoarseness

o

Pharyngeal/laryngeal ulcers and carcinom a

o

Frequent throat clearing

o

Recurrent pneum onitis

o

Nocturnal choking

o

Upper GI tract bleeding

Physical Exam Nonspecific

Pediatric Considerations 

Regurgitation is com m on in infants: o

Incidence decreases from twice daily in 50% of those

Pa ge 2 0 1

age 2 m onths to 1% of 1-year-olds. 

Signs: o

Frequent vom iting, irritability, cough, crying, and m alaise

o

Arching the body (hyperextension) at feeding and refusals of feedings



Failure to thrive



Form ula intolerance



Sepsis

Essential Workup 

Differentiate GERD from m ore em ergent conditions such as ischem ic heart pain, esophageal perforation, or aortic pathology.



History: typical



Physical exam : vital signs, head, ears, eyes, nose, throat (HEENT), chest and abdom inal exam s

Tests No gold standard

Lab 

CBC: o



Chronic anem ia from esophagitis

Stool testing for occult bleeding

Imaging 

No routine Im aging



Chest radiograph: o

Evidence of esophageal perforation, hiatal hernia, aortic disease

Diagnostic Procedures/Surgery 

Diagnostic trial of antacid: o

Those with persistent sym ptom s should be referred

Pa ge 2 0 1

for endoscopy. o

90% of GERD patients respond to proton pum p inhibitor (PPI) therapy.



Barium esophagram for prom inent dysphagia



Esophageal pH m onitoring: o



Correlate sym ptom s to acid reflux,

Esophageal m anom etry (poor sensitivity): o

Evaluate LES resting pressure and esophageal peristaltic contractions.



Esophagogastroduodenoscopy (EGD)â€”detects reflux esophagitis and com plications (Barrett's esophagus, hiatal hernia, stricture, ulcers, m alignancy)

Differential Diagnosis 

Ischem ic heart disease



Asthm a



Peptic ulcer disease



Gastritis



Hepatitis/pancreatitis



Esophageal perforation



Esophageal foreign body



Esophageal infection



Cholecystitis/cholelithiasis



Mesenteric ischem ia

P.447

Treatment Pre Hospital

Pa ge 2 0 1



Esophageal pain m ay m im ic angina.



Airway m ay need active control secondary to vom iting.

Initial Stabilization 

Airway, breathing, and circulation (ABCs) need to be evaluated.



IV fluid resuscitation for blood loss or shock

ED Treatment 





Sym ptom atic relief: o

Antacids

o

Antacids with viscous lidocaine

o

Sublingual nitroglycerine for esophageal spasm

o

Analgesics

Lifestyle m odifications: o

Avoid late-night or heavy/fatty m eals.

o

Minim ize tim e in supine position after eating.

o

Elevation of head of bed

o

Weight loss

o

Elim inate sm oking and alcohol intake.

Avoid direct esophageal irritants such as citric juices and coffee



Avoid foods that decrease LES pressures such as fatty foods, chocolate, and coffee.



Avoid drugs that lower LES tone.



Antacids (Maalox, Mylanta, etc.): o

Treatm ent of m ild and infrequent reflux sym ptom s

o

Not effective for healing esophagitis

o

Alginic acid slurry floats on surface of gastric contents, providing m echanical barrier



Sucralfate: o

Binds to exposed proteins on surface of injured m ucosa to form protective barrier

Pa ge 2 0 1

o 



May also directly stim ulate m ucosal repair

Metoclopram ide (prokinetic drug): o

Im proves peristalsis

o

Accelerates gastric em ptying

o

Increases LES pressure

H 2 -blockers: o

Effective for m ild to m oderate disease

o

Severe disease requires greater dosage than that used for peptic ulcer disease



Proton pum p inhibitors: o

More potent long-acting inhibitors of gastric acid secretion

o

Faster healing than other drug therapies

o

More efficacious in severe GERD and frank esophagitis



Endoscopic therapy: o

Suturing (plication), therm al injury, chem ical injection



Antireflux surgery (goal: increase LES pressure): o

Chronic reflux, younger patients, nonhealing ulceration, severe bleeding

o

Fundoplication can be m ore effective than m edical therapy in selected cases

Pregnancy Considerations 

Pyrosis present in 30â€“50% of pregnancies



Increased intra-abdom inal pressure, horm onal fluctuations lead to increased TLESRs.



EGD reserved for severe presentations



H 2 -blockersâ€”first-line therapy (longer safety record)



PPIsâ€”lim ited safety history in pregnancy

Pa ge 2 0 2

Medication (Drugs) 

Antacids: 30 m L plus viscous lidocaine, 10 m L, PO q6h



Cim etidine: 400 m g PO b.i.d., 300 m g IM/IV q6hâ€“q8h



Esom eprazole: 20â€“40 m g PO daily



Fam otidine: 20 m g PO/IV b.i.d. (peds: 0.5â€“1.0 m g/kg/d div. q8hâ€“q12h, m ax. 40 m g/d)



Lansoprazole: 15â€“30 m g daily



Metoclopram ide: 10â€“15 m g PO/IV/IM q6h before m eals and nightly at bedtim e



Nizatidine: 150 m g PO b.i.d.



Om eprazole: 20â€“40 m g PO daily



Pantoprazole: 40 m g PO/IV daily



Rabeprazole: 20 m g PO daily



Ranitidine: 150 m g (peds: 5â€“10 m g/kg q12h) PO b.i.d. or 300 m g PO nightly at bedtim e



Sucralfate: 1 g PO 1 hour before m eals and nightly at bedtim e

Follow-Up Disposition Admission Criteria 

Seriously ill patients



Significant esophageal bleeding



Uncontrolled reactive asthm a



Dehydration



Starvation and failure to thrive

Discharge Criteria Uncom plicated GERD: Refer to patient's prim ary care physician (PCP)

Pa ge 2 0 2

or gastroenterologist for further evaluation.

Issues for Referral Extraesophageal m anifestations (asthm a, laryngitis, etc.)

References 1. Cappell, MS. Clinical presentation, diagnosis, and m anagem ent of gastroesophageal reflux disease. Med Clin North Am . 2005;89(2):243â€“291. 2. Klinkenberg-Knol EC, Nelis F, Dent J, et al. Long-term om eprazole treatm ent in resistant gastroesophageal reflux disease: efficacy, safety and influence on gastric m ucosa. Gastroenterology. 2000;118:661â€“669. 3. Lundell L, Miettinen P, Myrvold HE, et al. Long-term m anagem ent of gastro-esophageal reflux disease with om eprazole or open antireflux surgery: results of a prospective, random ized clinical trial. Eur J Gastroenterol Hepatol. 2000;12:879â€“887. 4. Spechler SJ, Lee E, Ahnen D, et al. Long-term outcom e of m edical and surgical therapies for gastroesophageal reflux disease. JAMA. 2001;205:2331â€“2338.

Miscellaneous SEE ALSO: Gastritis; Peptic Ulcer Disease

Codes ICD9-CM 530.81

Pa ge 2 0 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro intestinal Bleeding

Gastrointestinal Bleeding Adit A. Ginde

Basics Description 

Active or recent bleeding arising from the gastrointestinal (GI) tract



Two categories: o

o



Upper GI tract 

Proxim al to the ligam ent of Treitz



Arises from esophagus, stom ach, or duodenum

Lower GI tract: 

Distal to the ligam ent of Treitz



Arises from jejunum , ileum , colon, or rectum

Mortality rate: o

10% overall

o

Increases as age increases

o

Ranges from <5% in children to as high as 25% in adults older than 70 years

Etiology Upper Gastrointestinal Hemorrhage 

Ulcerative disease of the esophagus, stom ach, or

Pa ge 2 0 2

duodenum : o

Peptic ulcer disease (55% of upper gastrointestinal hem orrhage [UGIH]): 

Helicobacter pylori infection



Drug induced (NSAIDs, aspirin, potassium supplem ents, iron supplem ents)





Curling ulcers from severe dam age to the CNS



Idiopathic

o

Reflux esophagitis

o

Infectious esophagitis:

o

o



Alcohol abuse

Gastric or esophageal erosions:

o







Candida



Herpes sim plex



Cytom egalovirus

Pill-induced esophagitis: 

Tetracycline



Quinidine



KCl



Aspirin



NSAIDs

Gastritis and stress ulcerations: 

Toxic agents (NSAIDs, alcohol, bile acids)



Mucosal hypoxia (traum a, burns, sepsis)



Chem otherapy

Esophageal foreign body

Portal hypertension: o

Esophageal varices (14% of UGIH)

o

Gastric varices

o

Duodenal varices

o

Portal hypertensive gastropathy

Arteriovenous m alform ations (6% of UGIH):

Pa ge 2 0 2

o

Aortoenteric fistula: 

Secondary to reconstructive aortoiliac surgery

o

Idiopathic angiom as

o

Osler-Weber-Rendu syndrom e

o

Dieulafoy vascular m alform ations (1% of UGIH): 

Rare unusually large subm ucosal or m ucosal vessels in the gastric m ucosa

o

Waterm elon stom ach: 

Gastric antral vascular ectasia



Tortuous vessels radiating outward from the pylorus like the dark stripes on the surface of a waterm elon



Cause unknown



Mallory-Weiss tear (10% of UGIH)



Gastric and esophageal tum ors



Hem orrhage from a pancreatic source



Hem obilia

Lower Gastrointestinal Hemorrhage 

Diverticulosis (33% of lower gastrointestinal hem orrhage [LGIH])



Cancer or polyps (19% of LGIH)



Colitis (18% of LGIH):





o

Ischem ic

o

Inflam m atory

o

Infectious

Vascular: o

Angiodysplasia (8% of LGIH)

o

Radiation telangiectasia

o

Aortocolonic fistula

Inflam m atory bowel disease: o

Crohn disease

o

Ulcerative colitis

Pa ge 2 0 2



Postpolypectom y



Anorectal (4% of LGIH): o

Internal or external hem orrhoids

o

Anal fissures

o

Rectal ulcer

Pediatric Considerations 

Meckel diverticulum



Intussusception

Diagnosis Signs and Symptoms History 

Hem atem esis



Coffee ground em esis



Black, m elanotic stools



Bright red blood per rectum



Abdom inal pain



Fatigue



Weakness



Dyspnea on exertion



Confusion

Physical Exam 

Tachycardia



Hypotension



Orthostasis



Pale appearance/conjunctiva/nail beds



Altered m ental status



Melanotic, bloody, or Hem occult positive stools

Pa ge 2 0 2

Essential Workup 

Distinguish between hem optysis and GI hem orrhage o

o

Pulm onary source: 

Bright red blood



Frothy in appearance



Sputum m ixed with blood is likely pulm onary.



PH >7

GI source: 

Dark red or brown blood



Accom panied by gastric contents



Worsens in setting of nausea/vom iting



PH <7



Hem atocrit, platelets, and coagulation profile



Nasogastric aspiration and lavage for suspected upper GI bleeding: o

Most useful for determ ining presence of current or recent upper GI bleeding: 

False negative rate is 25% if bleeding from duodenal source.



Presence of bile in aspirate is helpful in lowering false negative rate.

o

Room tem perature saline lavage to dem onstrate active bleeding: 

Lavage at least 500 cc or until clear



Iced lavage is not useful to stop bleeding and can cause hypotherm ia.



Rectal exam ination: o

Inspect for external hem orrhoids or anal fissure

o

Exam ine stool for black, red, m aroon, or norm al color.

o

Hem occult testing: False-positive Hem occult result: 

Raw m eat

Pa ge 2 0 2

 o

Som e iron preparations

Agents causing black stools but negative Hem occult: 

Iron



Charcoal



Bism uth (i.e., Pepto-Bism ol)



Food dyes



Beets

Tests Lab 

CBC: o

Anem ia

o

Low m ean corpuscular volum e associated with chronic blood loss

o

Throm bocytopenia



Electrolytes, blood urea nitrogen, creatinine, glucose



Coagulation profile (PT/PTT/INR)



LFTs, if upper GI bleeding suspected



Type and cross for active bleeding or unstable vital signs

Imaging Upright chest radiograph, if signs of peritonitis P.449

Diagnostic Procedures/Surgery 

Anoscopy: o

For suspected internal hem orrhoids (painless, bright red blood per rectum )



Esophagogastroduodenoscopy (EGD): o



Diagnostic and possibly therapeutic

Colonoscopy:

Pa ge 2 0 2







o

Diagnostic only

o

Best if done after adequate bowel preparation

Angiography: o

Effective if large, active bleeding

o

Diagnostic and possibly therapeutic

Radionucleotide scans: o

Effective for slow, active bleeding

o

Diagnostic only

Bowel resection: o

Reserved for refractory bleeding, usually in an unstable patient

Differential Diagnosis 

Hem aturia



Vaginal bleeding



Hem optysis



Oral/pharyngeal bleeding



Acute abdom en



Visceral traum a

Treatment Pre Hospital 

Stabilize the airway: o

Place the patient on 100% oxygen via m ask

o

Intubate for m assive upper GI bleed if not protecting airway



Insert at least one large-bore IV line (14â€“16 gauge, if possible): o

Adm inister crystalloids to m aintain SBP >90 m m Hg.

o

Attem pt second IV line while transporting patient.

Pa ge 2 0 2

o

Do not rem ain at the scene for a second IV line.

Initial Stabilization 

Adm inister 100% oxygen



Control airway in patients with m assive GI bleeding with unstable vital signs and altered m ental status.



Place cardiac, pulse oxim etry, and noninvasive blood pressure m onitors.



Initiate two large-bore (at least 16 gauge) IV lines: o

Consider central venous cordis catheter if unable to establish adequate peripheral venous access.

o

Adm inister 1 L NS bolus (peds: 20 cc/kg). Repeat once if necessary.

o

Transfuse packed RBCs if still unstable after NS boluses. 

Crossm atched or type specific blood if available. Otherwise use O negative for prem enopausal wom en and O positive for others



Adm inister fresh frozen plasm a (FFP) and Vitam in K if coagulopathic.

ED Treatment Treatment for All GI Bleeding Patients 

Consult gastroenterology for any significant GI bleeding



Consider surgical consult and/or interventional radiology (if available) for m assive ongoing bleeding, unstable patient, or evidence of perforation.



Follow serial hem atocrits, as levels m ay take hours to reflect blood loss.



Place Foley catheter to m onitor urine output.



Blood transfusion for: o

Unstable vital signs despite crystalloid infusion

o

Ongoing chest pain or ischem ic ECG changes

Pa ge 2 0 3

o

Significant anem ia, especially with ongoing bleeding

Treatment for Upper GI Bleeding 

IV proton pum p inhibitor (i.e., pantoprazole)



Octreotide (som atostatin analog) for suspected variceal bleeding: o



Decreases portal and intravariceal pressures

Consider vasopressin for suspected variceal bleeding: o

Potent vasoconstrictor

o

Adm inister concurrently with IV nitroglycerin to prevent tissue necrosis/m yocardial ischem ia.



Em ergent endoscopy: o

Indications: 

Active bleeding that does not clear with saline lavage



Hem odynam ic instability in setting of liver disease

o

Therapeutic options: 

Cauterization of bleeding ulcers or vessels



Injection sclerosis of visible vessels



Endoscopic sclerotherapy for varices (m ost effective)

 

Balloon tam ponade for varices (if refractory)

Spontaneous resolution: o

60% from variceal bleeding

o

80% from other upper GI tract sources

Treatment for Lower GI Bleeding 

Consider angiography for m assive, active bleeding



Consider bowel resection for m assive, active bleeding that is refractory to m edical m anagem ent.



Spontaneous resolution: o

80% of the tim e

Pa ge 2 0 3

o

25% rate of rebleeding

Medication (Drugs) 

Nitroglycerin: 5â€“50 m cg/m in (peds: 0.25â€“1 m cg/kg/m in) IV



Octreotide: 50 m cg (peds: 1â€“2 m cg/kg) IV bolus, then 50 m cg/hr (peds: 1â€“2 m cg/kg/hr) IV



Pantoprazole (Protonix): 40â€“80 m g (peds: dosing not approved) IV q24h



Vasopressin: 0.2â€“0.4 IU/m in (peds: 2â€“5 m U/kg/m in) IV, titrate up as needed. When no bleeding for 12 hours, taper over 24â€“48 hours.



Vitam in K: 10 m g (peds: 1â€“5 m g) PO/SC q24h. IV use is controversial and m ust be given slowly.

Follow-Up Disposition Admission Criteria 

Unstable vital signs at any tim e



Decreased hem atocrit with recent GI bleeding



Coagulopathy



Advanced age/com orbid conditions



Active upper GI bleeding



Lower GI bleeding: o

Large am ount of initial blood loss

o

Significant, active bleeding

Discharge Criteria 

Resolution of upper GI bleeding with negative nasogastric

Pa ge 2 0 3

lavage and EGD 

Minor or resolved lower GI bleeding



Stable vital signs



Stable hem atocrit >30



Norm al coagulation



Otherwise healthy patient

Issues for Referral Consider referral to gastroenterologist for outpatient colonoscopy and/or EGD.

References 1. Barkun A, Bardou M, Marshall JK. Consensus recom m endations for m anaging patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2003;139:843. 2. Bounds BC, Friedm an LS. Lower gastrointestinal bleeding. Gastroenterol Clin North Am . Decem ber 2003;32(4):1107â€“1125. 3. D'Am ico G, Criscuoli V, Fili D, et al. Meta-analysis of trials for variceal bleeding. Hepatology. 2002;36:1023. 4. Jensen DM, Machicado GA, Jutabha R, et al. Urgent colonoscopy for the diagnosis and treatm ent of severe diverticular hem orrhage. N Engl J Med. 2000;342(2):78â€“82. 5. McGuirck TD, Coyle WJ. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):523â€“539. 6. Sharara AI, Rockey DC. Medical progress: gastroesophageal variceal hem orrhage. N Engl J Med. 2001;345(9):669â€“681. 7. Van Dam J, Brugge WR. Medical progress: endoscopy of the upper gastrointestinal tract. N Engl J Med. 1999;341(23):1738â€“1748. 8. Zuccaro, G. Managem ent of the adult patient with acute lower gastrointestinal bleeding. Am J Gastroenterol. 1998;93:1202.

Codes ICD9-CM

Pa ge 2 0 3

578.9

Pa ge 2 0 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G iardia

Giardia

Ann P. Nguyen

Basics Description 

Noninvasive diarrhea



Found worldwide



5% of all travelersâ€™ diarrhea



Most com m on intestinal parasite in the United States: o

Highest incidence in sum m er m onths

o

Highest incidence in children aged 1â€“9 years and adults aged 30â€“39 years



A Centers for Disease Control nationally reportable disease as of 2002



Fecal-oral transm ission: o

Hum ans are m ajor reservoir.

o

Zoonotic reservoir in dom estic (dogs, cats, sheep, cattle) and wild anim als (beavers, deer, rodents)

o 

Reservoir in contam inated surface water

Populations at risk: o

Travelers to endem ic areas (developing countries, wilderness areas of U.S.)

o

Children in day care centers and their close contacts

o

Institutionalized persons

Pa ge 2 0 3

o

Practitioners of anal sexual activity

Etiology 

Giardia lam blia: o

A protozoan flagellate



Also called Giardia intestinalis or Giardia duodenalis



Biphasic life cycle of Giardia: o

Ingested as cysts

o

As few as 10 cysts shown to produce infection

o

Cysts becom e trophozoites in the duodenum and attach to intestinal villi.

o

Trophozoites re-encyst in the ileum and cysts are shed in the feces.



Alters the intestinal brush-border enzym es, im pairing digestion of lactose and other saccharides



No toxin produced

Diagnosis Signs and Symptoms History 

Onset 1â€“2 weeks postexposure



Infection m ay be asym ptom atic (m ost com m on).



Diarrhea of acute onset (90% of sym ptom atic patients): o

Foul-sm elling stools

o

Steatorrhea

o

Nonbloody

o

Self-lim iting within 2â€“4 weeks

o

More severe in im m unocom prom ised patients and patients with underlying bowel disease



Flatulence and bloating (70â€“75%)

Pa ge 2 0 3



Abdom inal cram ping (70%)



Nausea (70%)



Vom iting (30%)



Malaise (86%)



Anorexia (66%)



Weight loss (60â€“70%)



Fever is rare (15%).



30â€“50% of acute cases progress to chronic giardiasis (>4 weeks): o

Fat m alabsorption

o

Severe m acrocytic anem ia secondary to folate deficiency

o

Secondary lactase deficiency (in 20â€“40% of patients)



Infection is m ore severe and harder to eradicate in im m unosuppressed patients.

Pediatric Considerations 

With acute infection: o



Severe dehydration

With chronic infection: o

Failure to thrive

o

Growth retardation and cognitive im pairm ent owing to nutrient m alabsorption

Physical Exam 

Abdom inal exam is benign.



Extraintestinal m anifestations (10% of patients): o

Polyarthritis

o

Urticaria

o

Aphthous ulcers

o

Maculopapular rash

o

Biliary tract disease

Pa ge 2 0 3

Essential Workup 



History: o

Possible sources of exposure

o

Mem bership in high-risk group

Physical exam : o

If gross or occult blood on digital rectal exam , unlikely to be Giardia

Tests Lab 

Stool sam ple for m icroscopy (ova and parasites): o

50â€“70% sensitive if one sam ple

o

85â€“90% sensitive if three sam ples taken at 2-day intervals (ideal)



o

100% specific

o

Ability to detect other parasites

Stool enzym e-linked im m unosorbent assay (ELISA) or im m unofluorescent antibody (IFA) assay for Giardia antigen:





o

95% sensitive, 95â€“100% specific

o

Unlike m icroscopy, cannot rule out other parasites

Stool polym erase chain reaction (PCR): o

100% sensitive and 100% specific

o

Not yet widely available

Fecal leukocytes and stool culture unnecessary unless enteroinvasive organism s suspected (fever, bloody stool)



Serology for antiGiardia antibodies not helpful in the ED setting



Electrolytes, BUN/Cr, glucose o



If prolonged diarrhea or evidence of dehydration

CBC: o

Macrocytic anem ia in chronic giardiasis

Pa ge 2 0 3

o

Nondiagnostic in acute giardiasis

Imaging Abdom inal radiographs or CT of no value

Diagnostic Procedures/Surgery 

Duodenal sam pling: o

Entero-Test (patient swallows a weighted string, which is later retrieved and exam ined for Giardia)



Endoscopy: o

Duodenal aspiration

o

Endoscopic duodenal biopsy

Differential Diagnosis 







Viral gastroenteritis: o

Norwalk virus

o

Rotavirus

o

Hepatitis A

Bacterial infections: o

Staphylococcus

o

E. coli

o

Shigella

o

Salm onella

o

Yersinia

o

Cam pylobacter

o

Clostridium difficile

o

Vibrio cholerae

Other protozoa: o

Cryptosporidium

o

Microsporidia

o

Cyclospora

o

Isospora

o

Entam oeba

Inflam m atory bowel disease

Pa ge 2 0 3



Irritable bowel syndrom e



Lactase deficiency



Tropical sprue



Drugs and toxins:





o

Antibiotics

o

Calcium channel blockers

o

Magnesium antacids

o

Caffeine

o

Alcohol

o

Sorbitol

o

Laxative abuse

o

Quinidine

o

Colchicine

o

Mercury poisoning

Endocrine: o

Addison disease

o

Thyroid disorders

Malignancy: o

Colorectal carcinom a

o

Medullary carcinom a of the thyroid

P.453

Treatment Initial Stabilization 

ABCs: airway, breathing, circulation



IV 0.9 norm al saline (NS) if signs of significant dehydration

Pediatric Considerations

Pa ge 2 0 4



For severe dehydration (>10%): o

IV bolus with 0.9% NS at 20 m L/kg

o

Cardiac m onitor

o

Blood glucose determ ination

ED Treatment 

Oral fluids for m ild dehydration



Correct any serum electrolyte im balances.



Stool sam ple for m icroscopy



If stool sam ple is positive for Giardia: o

Metronidazole is first-line antiparasitic drug in United States: 

o

80â€“95% cure rate

Albendazole or furazolidone if m etronidazole unsuccessful

o

Quinacrine and tinidazole highly effective but not available in United States



If stool sam ple negative for Giardia: o

Refer to gastroenterologist for further specialized testing.

o

Consider em piric course of m etronidazole if high suspicion for Giardia.



Im m unocom prom ised patients at risk for disease that is refractory to standard drug regim ens: o

Try drug of a different class or m etronidazole plus quinacrine for at least 2 weeks

Pediatric Considerations 

Metronidazole is first line therapy (80â€“95% efficacy)



Alternatives: o

Furazolidone (80â€“95% efficacy)

o

Nitazoxanide (60â€“80% efficacy)

Pregnancy Considerations

Pa ge 2 0 4



Metronidazole contraindicated in first trim ester: o

Parom om ycin (55â€“90% efficacy) or furazolidone instead

Medication (Drugs) 

Albendazole: 400 m g (peds: 10â€“15 m g/kg/24h) PO daily for 5â€“7 days



Furazolidone: 100 m g (peds: 6â€“8 m g/kg/24h) PO q6h for 7â€“10 days



Metronidazole: 250 m g (peds: 30â€“40 m g/kg/24h) PO q8h for 5â€“7 days



Nitazoxanide: 500 m g (peds: 100 m g for ages 2â€“3 years, 200 m g for ages 4â€“11 years) PO b.i.d. for 3 days



Parom om ycin: 500 m g (peds: 25â€“30 m g/kg/24h) PO q8h for 5â€“10 days



Quinacrine: 100 m g (peds: 6 m g/kg/24h) PO q8h for 5â€“7 days



Tinidazole: 2,000 m g (peds: 50â€“75 m g/kg) PO once

Follow-Up Disposition Admission Criteria 

Hypotension or tachycardia unresponsive to IV fluids



Severe electrolyte im balance



Children with >10% dehydration



Signs of sepsis/toxicity (rare in isolated giardiasis)



Patients unable to m aintain adequate oral hydration: o

Extrem es of age, cognitive im pairm ent, significant

Pa ge 2 0 4

co-m orbid illness

Discharge Criteria 

Able to m aintain adequate oral hydration



Dehydration responsive to IV fluids

Issues for Referral Gastroenterology referral for diagnostic endoscopy if sym ptom s persist for >4 weeks despite drug therapy

References 1. Ali SA, Hill DR. Giardia intestinalis. Curr Opin Infect Dis. 2003;16:453â€“460. 2. Bailey JM, Erram ouspe J. Nitazoxanide treatm ent for giardiasis and cryptosporidiosis in children. Ann Pharm acother. 2004;38:634â€“640. 3. Gardner TB, Hill DR. Treatm ent of giardiasis. Clin Microbiol Rev. 2001;14:114â€“128. 4. Hlavsa MC, Watson JC, Beach MJ. Giardiasis surveillanceâ€”United States, 1998â€“2002. MMWR Surveillance Sum m aries. 2005;54(SS01):9â€“16. 5. Katz DE, Taylor DN. Parasitic infections of the gastrointestinal tract. Gastroenterol Clin North Am . 2001;30:797â€“815. 6. Lebwohl B, Deckelbaum RJ, Green PHR. Giardiasis. Gastrointest Endosc. 2003;57:906â€“913. 7. Nash TE, Ohl CA, Thom as E, et al. Treatm ent of patients with refractory giardiasis. Clin Infect Dis. 2001;33:22â€“28. 8. Petri WA. Therapy of intestinal protozoa. Trends Parasitol. 2003;19:523â€“526. 9. Verweij JJ, Blange RA, Tem pleton K, et al. Sim ultaneous detection of Entam oeba histolytica, Giardia lam blia, and Cryptosporidium parvum in fecal sam ples by using m ultiplex real-tim e PCR. J Clin Microbiol. 2004;42:1220â€“1223.

Pa ge 2 0 4

Miscellaneous SEE ALSO: Am ebiasis; Diarrhea, Adult

Codes ICD9-CM 007.1

ICD10 A07.1

Pa ge 2 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G lauco m a

Glaucoma

Yasuharu Okuda

Basics Description Disease characterized by elevation of intraocular pressure, optic neuropathy, and progressive loss of vision

Etiology 

Prim ary glaucom a: o

Open-angle glaucom a: 

Norm al anterior cham ber angle



Insidious onset with persistent rise in intraocular pressure



Most com m on type accounting for 90% of glaucom as in United States



Leading cause of blindness in African Am ericans



Risk factors include: African Am erican, age >40, fam ily history, m yopia, diabetes, and HTN

o

Angle-closure glaucom a: 

Narrowing or closing of anterior cham ber angle precluding natural flow of aqueous hum or from posterior to anterior cham ber of eye and through its filtering portion of trabecular m eshwork

Pa ge 2 0 4



Usually abrupt onset with sudden increase in intraocular pressure



Risk factors include: Asians and Eskim os, hyperopia, fam ily history, increased age, and fem ale gender



Secondary glaucom a occurs from other diseases, including diseases of eye, traum a, and drugs: o

Can be either open or closed angle

o

Drugs: steroids

o

Diseases: neurofibrom atosis, uveitis, neovascularization, and intraocular tum ors

o

Traum a

Diagnosis Signs and Symptoms History 

Prim ary open-angle glaucom a: o

Gradual reduction in peripheral vision or night blindness



o

Typically bilateral

o

Painless

Prim ary angle-closure glaucom a: o

Severe deep eye pain and headache often associated with nausea and vom iting

o

Decrease in visual acuity often described as visual clouding with halos surrounding light sources

o

Associated abdom inal pain, which m ay m isdirect diagnosis

o

Concurrent exposure to dim ly lit environm ent such as

Pa ge 2 0 4

m ovie theater o

Use of precipitating m edications: 

Mydriatic agents: scopolam ine, atropine



Sym pathom im etics: pseudoephedrine, albuterol



Antihistam ines: Benadryl, Antivert



Antipsychotics: Haldol



Phenothiazines: Com pazine, Phenergan



Tricyclic antidepressants: Elavil

Physical Exam 

Prim ary open-angle glaucom a: o



Decreased visual acuity

Prim ary angle-closure glaucom a: o

Decreased visual acuity

o

Pupil is m iddilated and nonreactive.

o

Corneal edem a with hazy appearance

o

Conjunctival injection

o

Firm globe to palpation

Essential Workup 

Detailed ocular exam ination



Visual acuity



Tonom etry: o

Norm al pressures are between 10 and 21 m m Hg.

o

Prim ary open-angle glaucom a: 

Degree of elevation can vary, but 25% to 30% of patients m ay have norm al intraocular pressures.

o

Prim ary angle-closure glaucom a: 

Any elevation is abnorm al, but usually seen in ranges >40 m m Hg.



Slit-lam p exam : o

Evaluation of anterior cham ber angle

Pa ge 2 0 4

o

Used to elim inate other possibilities in differential including corneal abrasion and foreign body

Tests Lab Directed toward workup of differential

Imaging Directed toward workup of differential

Differential Diagnosis 

Cavernous sinus throm bosis



Acute Iritis and uveitis



Retinal artery or vein occlusion



Tem poral arteritis



Retinal detachm ent



Conjunctivitis



Corneal abrasion

P.455

Treatment Initial Stabilization Initiate steps to lower intraocular pressure in acute closed-angle glaucom a.

ED Treatment 

Prim ary open-angle glaucom a: o



Recognition and prom pt ophthalm ologic referral

Prim ary angle-closure glaucom a (ophthalm ologic

Pa ge 2 0 4

em ergency): o

Intraocular pressure reduction: 

Topical beta-blocker, tim olol m aleate, to decrease aqueous hum or production



Topical Î± 2 -agonist, apraclonidine, to decrease aqueous hum or production



Carbonic anhydrase inhibitor, acetazolam ide, for reduction of form ation of aqueous hum or



Hyperosm otic agent, m annitol, to draw aqueous hum or from vitreous cavity into blood. (Indicated for severe attacks)

o

Movem ent of iris away from trabecular m eshwork: 

Topical parasym pathom im etic, pilocarpine hydrochloride, to constrict pupil once intraocular pressure is <40 m m Hg

o

Reduction of inflam m ation: 

o

Topical corticosteroid, prednisolone acetate

Em ergent ophthalm ology consultation for possible definitive surgical treatm ent, laser iridectom y, if no im provem ent with m edical m anagem ent

o

Adequate narcotic analgesia and antiem etics as needed

Medication (Drugs) 

Acetazolam ide: 500 m g IV or PO



Apraclonidine 1.0% solution: 1 drop to affected eye b.i.d.â€“t.i.d.



Mannitol 20%: 1â€“2 g/kg IV over 30â€“60 m inutes



Pilocarpine hydrochloride 1â€“2% solution: 1 drop q15â€“30m in until pupillary constriction occurs, then 1 drop q2hâ€“q3h

Pa ge 2 0 4



Prednisolone acetate 1% solution: 1 drop q15â€“30m in for total of 4 doses



Tim olol m aleate 0.5% solution: 1 drop topically to affected eye b.i.d.

Follow-Up Disposition Admission Criteria 

Severe pain, nausea, or vom iting



Patients receiving parenteral m edications should be observed for side effects.



Patients without im provem ent of sym ptom s or intraocular pressures should be adm itted for continued m onitoring of intraocular pressure, m edical treatm ent, and possible definitive surgical m anagem ent.

Discharge Criteria Patients with m inor sym ptom s and significant im provem ent of intraocular pressure m ay be safely discharged once seen by ophthalm ology and with close <24-hour follow-up.

Issues for Referral If no ophthalm ologist is available, treatm ent should be initiated and patient transferred to nearest hospital with ophthalm ologic consultation.

References 1. Berkoff D, Sanchez L. An uncom m on presentation of acute angle closure glaucom a. J Em erg Med. 2005;29(1):43â€“44. 2. Marx JA, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Pa ge 2 0 5

3. Morgan A, Hem phill R. Acute visual change. Em erg Med Clin North Am . 1998;16:825â€“843. 4. Rho D. Acute angle-closure glaucom a after albuterol nebulizer treatm ent. Am J Ophthalm ol. 2000;130(1)123â€“124. 5. Tripathi R, Tripathi B, Haggerty C. Drug-induced glaucom as: m echanism and m anagem ent. Drug Saf. 2003;26:749â€“767.

Pa ge 2 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G lo be Rupture

Globe Rupture

Alexander T. Limkakeng Jr.

Basics Description 

A full-thickness corneal or scleral injury owing to traum a



Blunt traum a: o

Causes an abrupt rise in intraocular pressure diffusely

o

Subsequent rupture of the eye either opposite the point of im pact or at the weakest points:





Extraocular m uscle insertion



Corneoscleral junction

Penetrating injury: o

Occurs with sharp objects or projectiles injuring the sclera or anterior eye directly

o

Most com m only anteriorâ€”the bony orbit protects the globe laterally and posteriorly

o

Posterior injury can occur with fracture of the bony orbit or with penetrating injuries of the eyelid or eyebrow.



Prognosis worse with: o

Larger lacerations

o

Injury posterior to the rectus insertion

Pa ge 2 0 5

o

Blunt injury

o

Intraocular foreign body, especially if m ade of organic m aterial

o

Vitreous extrusion

o

Lens dam age

o

Hyphem a

o

Retinal Detachm ent

o

Poor visual acuity at presentation

o

Afferent pupillary defect

o

Increased tim e to OR

Etiology 

Falls, im pact injuries



Sport-related injuries (e.g., elbow, ball im pacts, arrows, etc.)



Indirect concussive injuries (explosions)



Sharp instrum ent/stabbing injuries, accidental or intentional



Projectile injuries (industrial, firearm s, BB pellets, blast explosion shrapnelâ€”glass, etc.)

Diagnosis Signs and Symptoms 

Pain



Localized ecchym osis and swelling



Scleral or corneal laceration



Extrusion of intraocular contents



Markedly decreased visual acuity



Lim ited extraocular m otion



Hyphem a

Pa ge 2 0 5



Severe subconjunctival hem orrhage and edem a, especially if circum ferential bloody chem osis



Abnorm ally deep or shallow anterior cham ber



Low intraocular pressure: o

Note: do not perform tonom etry if there is obvious rupture.



Irregular pupil (points toward lesion)



Subluxed lens



Com m otio retinaeâ€”gray-white discoloration of the retina

History 

Mechanism of injury: o

Assess for possibility of retained intraocular foreign body



History of previous eye surgery



Preinjury visual acuity



Assess tetanus status



Ascertain tim e of last PO intake

Physical Exam 

Penlight or slit-lam p exam ination observing for signs of globe rupture



If the diagnosis of ruptured globe is m ade, defer further ocular exam ination until the tim e of surgical repair: o

Prevents placing any undue pressure on the eye and risking extrusion of the intraocular contents



If no evidence of globe rupture on initial survey, proceed with thorough ophthalm ologic exam ination: o

Visual acuity

o

Slit-lam p exam ination: 

Cornea



Anterior cham ber



Iris

Pa ge 2 0 5

 o

Sclera

Fluorescein: 

Seidel test: observe if fluorescein m oves away as contents (which appear yellow-green) leak out at site of rupture.

o

Visualize fundus/retina.

o

Measure intraocular pressure: 

Perform only if globe rupture is definitely not present.

Tests Lab Preoperative labs: 

CBC



Electrolytes



Coagulation studies

Imaging 

Orbital radiograph (anteroposterior/lateral) for m etallic intraocular foreign body



CT scan of the orbits (axial and coronal views)



MRI scan of the orbits after retained m etallic foreign body is ruled out



B-scan ultrasound of the eye

Diagnostic Procedures/Surgery 

Slit-lam p



Fluorescein

Differential Diagnosis 

Intraocular foreign body



Hyphem a



Severe subconjunctival hem orrhage and chem osis



Partial corneal laceration

Pa ge 2 0 5



Partial scleral laceration

P.457

Treatment Pre Hospital 

Place a shield (not patch) over eye with no pressure on the globe.



Use a Styrofoam cup if no shield available.

Initial Stabilization 

Keep m anipulation of the eye to a m inim um if ruptured globe is suspected.



Try to prevent any activity that will cause an increase in intraocular pressure such as straining, coughing, or vom iting.

ED Treatment 

Em ergent ophthalm ologic consultation



Bed rest



No food or drink (NPO)



Adm inister antiem etic for nausea/vom iting: o

Prochlorperazine (Com pazine)



Update tetanus status.



Adm inister prophylactic antibiotics IV:



o

Cefazolin (Ancef)

o

Gentam icin or clindam ycin

Succinylcholine is relatively contraindicated: o

However, with a defasciculating dose of a nondepolarizing agent and sufficient anesthesia, it

Pa ge 2 0 5

m ay be used.

Pregnancy Considerations 

Because of risk of extrusion of intraocular contents, straining should be avoided.



If necessary, delivery by cesarean section or tocolysis should be considered in conjunction with obstetric consultation.

Medication (Drugs) 

Cefazolin (Ancef): 1 g (peds: 25â€“50 m g/kg/24h) IV q6hâ€“q8h



Clindam ycin: 450 m g (peds: 25â€“40 m g/kg/24h div. q6hâ€“q8h) IV q8h



Gentam icin: 1 m g/kg (peds: 2â€“2.5 m g/kg) IV q8h



Prochlorperazine (Com pazine): 5â€“10 m g IV/IM

Follow-Up Disposition Admission Criteria 

All patients with globe rupture/penetrating eye injuries



Early enucleation for severe injury

Discharge Criteria Globe penetration excluded

Issues for Referral 

Em ergent ophthalm ologic consultation in the ER m ay be needed to definitively rule out globe rupture owing to difficulty with exam and the desire to m inim ize

Pa ge 2 0 5

m anipulation of the eye. 

Speed is of the essence since the risk of infection increases with prolonged tim e to operative repair.



If appropriate, patient should be counseled on use of protective eyewear to prevent recurrence.

References 1. Anesthesia. In: Miller RD, ed. Anesthetic Agents. Philadelphia: Churchill Livingstone; 2000:473. 2. Dunya IM, Rubin PAD, Shore JW. Penetrating orbital traum a. Int Ophthalm ol Clin. 1994;34:25â€“36. 3. Klystra JA, Lam kin JC, Runyan DR. Clinical predictors of scleral rupture after blunt ocular traum a. Am J Ophthalm ol. 1993;115(4):530â€“535. 4. Linden JA, Renner GS. Traum a to the globe. Em erg Med Clin North Am . 1995;13(3):581â€“605. 5. Navon SE. Managem ent of the ruptured globe. Int Ophthalm ol Clin. 1994;34:71â€“91. 6. Sabaci G, Bayer A, Mutlu M, et al. Endophthalm itis after deadly-weapon-related open-globe injuries. Am J Ophthalm ol. 2002;133:62â€“69.

Miscellaneous SEE ALSO: Blowout Fracture; Corneal Abrasion; Corneal Foreign Body; Hyphem a; Retinal Detachm ent; Visual Loss

Codes ICD9-CM 871.0

ICD10 S05.3

Pa ge 2 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G lo m erulo nephritis

Glomerulonephritis Scott A. Miller

Basics Description 

Syndrom e characterized by: o

Hem aturia

o

Red blood cell casts

o

Proteinuria

o

Hypertension

o

Renal insufficiency



Accounts for 10â€“15% of End-Stage Renal Disease (ESRD)



Com m on pathway of m ultiple diseases resulting in intraglom erular inflam m ation and cellular proliferation



Contributing factors: o

Genetics

o

Antibody deposition: 

Antibody attaches to glom erular antigen (native or im planted).

 o

Circulating antigen-antibody com plex deposited

Influx and activation of inflam m atory m ediators: 

Leukocytes, com plem ent, cytokines



Cell-m ediated im m une m echanism s

Pa ge 2 0 5



Results in glom erular dysfunction



Persistent inflam m ation can lead to scarring and perm anent dam age.

Etiology 

Postinfectious: o

Poststreptococcal glom erulonephritis (PSGN) 

Occurs 7â€“21 days after streptococcal pharyngitis or skin infection



Most com m on in children and m en



Ranges from asym ptom atic hem aturia to oliguric renal failure

o

Can follow other bacterial, fungal, viral, or parasitic infections



IgA nephropathy: o

Most com m on in m en in the third and fourth decades of life

o

Possibly related to increased production of IgA after infection



Rapidly progressive glom erulonephritis (RPGN): o

Can destroy renal function in days

o

Crescentic deposits in glom eruli destroy function.

o

Pauci-im m une (sm all vessel vasculitides): 

Often antineutrophil cytoplasm ic antibody (ANCA)-positive

o



Can involve other areas (i.e., lungs, skin)



Wegener granulom atosis



Microscopic polyangiitis

Im m une com plex deposits: 

Postinfectious



System ic disease (i.e., system ic lupus erythem atosus [SLE], Henoch-SchÃ¶nlein purpura [HSP])

Pa ge 2 0 6

o

Antiglom erular basem ent m em brane deposits: 

Goodpasture disease with pulm onary involvem ent



Mem branoproliferative glom erulonephritis (MPGN): o

Com plem ent deposits in basem ent m em brane

o

Hepatitis C

Diagnosis Signs and Symptoms 



Cardinal signs: o

Hem aturia

o

Proteinuria

Edem a: o

Owing to renal salt and water retention

o

Periorbital

o

Ascites

o

Pleural effusion



Hypertension



Oliguria



Azotem ia



Congestive heart failure



Renal failure



Nonspecific m anifestations:



o

Fatigue

o

Weight loss

o

Abdom inal pain

o

Nausea/vom iting

Autoim m une disorders: o

Arthralgias

o

Arthritis

Pa ge 2 0 6

o

Rash

o

Fever

Essential Workup Urinalysis for: 

Hem aturia, proteinuria, and RBC casts

Tests Lab 



Electrolytes, BUN, Cr: o

Renal function

o

Hyperkalem ia

Album in, total protein: o

Varying degrees of hypoalbum inem ia depending on clinical process



CBC: o

Anem ia secondary to chronic renal disease, neoplasm , Goodpasture disease

o 

PT, PTT: o



With or without elevated WBC in infections

Coagulation factors consum ed in certain types of GN

Labs to be considered for consultants: o

Culturesâ€”throat, skin, blood

o

24-hour urine collectionâ€”protein, urine electrolytes

o

Streptozym e or antistreptolysin O titer

o

Com plem ent levels (C1, C3, C4, CH 5 0 )â€”reduced in PSGN, MPGN, SLE

o

ANA, rheum atoid factorâ€”connective tissue diseases

o

Antiâ€”glom erular basem ent m em brane (GBM)â€”Goodpasture

o

ANCAâ€”Wegener

Imaging

Pa ge 2 0 6



Renal ultrasound o

Kidney size predictor of potential reversibility of disease, alternative diagnosis (i.e., neoplasm , stone)



Chest radiograph (CXR): heart size, pulm onary edem a, or hem orrhage

Diagnostic Procedures/Surgery Renal biopsy: Discern prim ary glom erulopathies versus other causes. P.459

Differential Diagnosis 





Hem atologic: o

Sickle cell disease

o

Coagulopathy

Renal: o

Infectious

o

Malform ation

o

Neoplasm

o

Ischem ic

o

Traum a

o

Vasculitis

Postrenal: o

Mechanical (i.e., stones, reflux, obstruction, catheterization)

o

Inflam m atory (i.e., cystitis, prostatitis, epididym itis, endom etriosis, periurethritis)

o 

Neoplasm

Factitious: o

Food

o

Drugs

o

Pigm enturia (i.e., m yoglobin, porphyria, hem oglobin)

Pa ge 2 0 6

o

Vaginal bleeding

Treatment Initial Stabilization ABCs: airway, breathing, circulation

ED Treatment 

Treatm ent m ainly supportive care: o

o







Blood pressure control: 

Loop diuretics



ACE inhibitor for m aintenance



Treat hypertensive em ergencies.

Dialysis: 

Fluid overload



Hyperkalem ia



Urem ia

PSGN: o

Usually resolves spontaneously

o

No benefit to antibiotics

IgA Nephropathy: o

Supportive care

o

Im m unosuppressives if inflam m ation on biopsy

o

Variable course, but m ost recover

RPGN: o

Can irreversibly destroy renal function in days

o

Em ergently consult nephrologist to discuss starting potentially toxic therapies.

o

Im m unosuppressives and high-dose steroids: 

Methylprednisolone and prednisone



Cyclophospham ide

Pa ge 2 0 6

 

Plasm apheresis for anti-GBM antibody

MPGN: o

Treat underlying disease if known.

Medication (Drugs) 

Benazepril: 5â€“40 m g PO daily (or any other ACE inhibitor)



Cyclophospham ide: dose in conjunction with nephrology



Diazoxide: 1â€“3 m g/kg IV, m ax. 150 m g, repeat q15m in



Furosem ide: 20â€“80 m g IV; m ax. 2 m g/kg/d



Methylprednisolone: 30 m g/kg IV on alternative days for 3 doses, followed by oral prednisone (dose in conjunction with nephrology)



Nitroprusside: 0.3â€“10 Âµg/kg/m in IV



Prednisone: 0.5â€“2 m g/kg/d

Follow-Up Disposition Admission Criteria 

Unstable vital signs



Oliguria, anuria



Urem ia



Acute renal failure



Electrolyte abnorm ality



Hypertensive em ergency



Congestive heart failure



Infectious cause of GN

Discharge Criteria

Pa ge 2 0 6

Healthy patients with no com orbid illness who present with m ild hem aturia and proteinuria with: 

Stable vital signs



No signs of infection



Otherwise norm al lab work



Close follow-up recom m ended

Issues for Referral All patients with glom erulonephritis should follow up with nephrology.

References 1. Couser WG. Glom erulonephritis. Lancet. 1999;353(9163):1509â€“1515. 2. Glassock RJ. Managem ent of rapidly progressive glom erulonephritis. Hosp Pract. (office ed). 2000;35(2):59â€“62, 65â€“66, 69â€“70. 3. Hricik DE, Chung-Park M, Sedor JR. Glom erulonephritis. N Engl J Med. 1998;339(13):888â€“899. 4. Madaio MP, Harrington JT. The diagnosis of glom erular diseases: acute glom erulonephritis and the nephrotic syndrom e. Arch Intern Med. 2001;161(1):25â€“34. 5. Vinen CS, Oliveira DB. Acute glom erulonephritis. Postgrad Med J. 2003;79:206â€“213.

Miscellaneous SEE ALSO: Nephritic Syndrom e; Nephrotic Syndrom e; Renal Failure

Codes ICD9-CM 583.9

ICD10

Pa ge 2 0 6

N05

Pa ge 2 0 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G o no co ccal Disease

Gonococcal

Disease JiWon E. Lee

Basics Description 

Infection of upper genital tract



Second m ost com m on com m unicable disease in United States:



o

Often seen with chlam ydia

o

600,000 new cases per year

Major cause of urethritis in m en, cervicitis/PID in wom en: o

Rising resistance to penicillin (up to 25%)

o

Hum ans only known host

o

Increasing incidence in wom en and m en who have sex with m en (MSM): 

Extragenital infections (pharynx, rectum ) occur m ore com m only in MSM.

Etiology Neisseria gonorrhoeae: 

Gram -negative aerobic diplococci

Pa ge 2 0 6

Diagnosis Signs and Symptoms Female 



Cervicitis: o

Most com m on m ucosal site of infection

o

Fifty percent asym ptom atic rate

o

Vaginal pruritis, m ucopurulent discharge

o

Cervical edem a, congestion, friability: 

Abnorm al vaginal bleeding



Abdom inal pain, dysparenuria

Pelvic inflam m atory disease (PID): o

10â€“40% occurrence rate

o

Pelvic/abdom inal pain, abnorm al vaginal bleeding, and dysparenuria

o

Sym ptom s often occur at onset of m enses.

o

Fever (50%)

o

Uterine tenderness, bilateral adnexal or cervical m otion tenderness: 



Nausea/vom iting

Fitz-Hugh Curtis syndrom e: o

Ten percent occurrence rate

o

Perihepatitis

o

Right upper quadrant pain/tenderness



Vaginal itching



Dysuria



Thirty percent to 40% asym ptom atic carriers



Proctitis: o

May self-inoculate

Male 

Incubation period 3â€“7 days

Pa ge 2 0 6



Sym ptom s occur in 10â€“14 days



Urethritis: o

Penile discharge or dysuria

o

Yellow-white thick discharge: 

Indistinguishable from nongonococcal urethritis (chlam ydia)



Prostatitis



Epididym itis: o

Acute, unilateral testicular pain and swelling: 



Rule out torsion/traum a.

Proctitis: o

Often asym ptom atic

o

One percent to 2% with tenesm us, pruritis ani, rectal bleed



o

Only site of infection in 40% of MSM

o

Threefold increase in HIV infection risk

Urinary tract infection (UTI): o

Dysuria

Disseminated 

One percent to 3% occurrence rate



Com m on cause of polyarthralgias, polyarthritis, or oligoarthritis in young, healthy patients



Fem ale > Male, 3:1: o



1 week postm enses

Triad: tenosynovitis, derm atitis, polyarthralgias: o

Fever, chills, m alaise

o

Migratory tenosynovitis at wrist, fingers, ankles, toes: 

o

Flexor tendon sheath of wrist/Achilles tendon

Derm atitis, few painless lesions: 

Pustular or vesiculopustular



Hem orrhagic, necrotic pustules on

Pa ge 2 0 7

erythem atous base



Begin distally



Resem ble m eningococcus



Healing crust in 4 days

Purulent arthritis without skin lesions: o





Knees, wrists, and ankles: 

Asym m etric, polyarthritis



Swollen, warm joint effusion

Arthralgia: o

Usually fewer than three joints



Endocarditis



Meningitis



Osteom yelitis

Other Pharyngitis: 

Oropharyngeal exudates or cervical lym phadenitis



Conjunctival injection/irritation

Essential Workup 

Clinical diagnosis in m ale gonorrhea: o



Gram stain 95% sensitive

Cervical culture in fem ale gonorrhea

Tests Lab 

Cultures (gold standard): o

Thayer-Martin m edium : 



Urethral/cervical culture

Gram stain: o

Intracellular gram -negative diplococci 

Sixty percent sensitive in sym ptom atic wom en



Ninety-five percent sensitive in sym ptom atic

Pa ge 2 0 7

m en 

Enzym e im m unoassay (EIA): o





Cervical swab or urine specim en

DNA probe: o

FDA approved

o

Cervical swabs

DNA am plification techniques: o

Nucleic acid am plification tests (NAATs) 

DNA or RNA sequences using polym erase chain reaction (PCR)



Pharyngeal/rectal cultures for local sym ptom s in high-risk individuals



Dissem inated gonococcal infection (DGI): o

Synovial fluid analysis: 

Neutrophilic leukocytosis, >50,000 cells/m m 3



Positive cultures when >80,000 cells/m m 3

o

Two or m ore sets of blood cultures

o

Synovial, skin, urethral or cervical, and rectal cultures: 





Thayer-Martin m edia

PID/lower abdom inal pain in fem ale: o

CBC

o

Urinalysis

o

Pregnancy test

Rapid plasm a reagin (RPR) o

For associated syphilis

P.461

Differential Diagnosis 

Urethritis: o

Chlam ydia

Pa ge 2 0 7



o

Trichom onas

o

UTI

o

Syphilis

DGI: o

Bacterial arthritis: 

Meningococcus (rash)

o

Hepatitis B

o

Connective tissue disease:

o



Reiter syndrom e



Rheum atoid arthritis



Psoriatic arthritis

Acute rheum atic fever: 

Poststreptococcal arthritis

o

Infective endocarditis

o

Others: 

HIV



Secondary syphilis



Viral infection



Lym e disease (rash)



Gout (arthritis)

Treatment ED Treatment 

Hydration (0.9% NS) for nausea/vom iting



Cervical, urethral, and anorectal infection: o

Ceftriaxone 125 m g IM once

o

Cefixim e 400 m g PO once

o

Ciprofloxacin 500 m g PO once

o

Ofloxacin 400 m g PO once

o

Avoid quinolones in pregnancy, nursing, and age <18

Pa ge 2 0 7

years old. o



Treat also for chlam ydia: 

Azithrom ycin 1 g PO once or



Doxycycline 100 m g PO b.i.d. for 7 days

Salpingitis/PID: o

Outpatient: 

One dose of cefixim e 400 m g PO/ceftriaxone 250 m g IM/spectinom ycin (2 g IM) plus doxycycline 100 m g b.i.d. for 14 days

o

Inpatient: 



Cefoxitin 2 g IV plus doxycycline 100 m g IV

Pregnancy: o

One dose of ceftriaxone/spectinom ycin plus erythrom ycin 500 m g PO b.i.d. for 7 days



Treat sexual partner



Test for syphilis (RPR) and HIV



DGI: o

Ceftriaxone 1 g IV/IM daily

o

Cefotaxim e 1 g IV q8h

o

Spectinom ycin 2 g IM q12h (penicillin allergic)

o

After 24â€“48 hours of above therapy, additional 7 days with:





Cefixim e 400 m g PO b.i.d.



Ciprofloxacin 500 m g PO b.i.d.



Ofloxacin 400 m g PO b.i.d.

Conjunctivitis: o

Adults: 

o

Ceftriaxone 1 g IM once

Ophtham ia neonatorum : 

Penicillin G 100,000 IU/kg/24h q6h



Ceftriaxone 25â€“50 m g/kg/24h daily



Ceftriaxone 125 m g IM/IV

Pa ge 2 0 7





Pharyngitis: o

Ceftriaxone 125 m g IM once

o

Ciprofloxacin 500 m g PO once

o

Ofloxacin 400 m g PO once plus

o

Azithrom ycin or doxycycline for chlam ydia

Meningitis/endocarditis: o

Ceftriaxone 1â€“2 g IV q12h: 

10â€“14 days for m eningitis



4 weeks for endocarditis

Pediatric Considerations 

Gonococcal ophthalm ia neonatorum : o

Mother with genital tract infection

o

Bilateral conjunctivitis 2â€“5 days postpartum : 

If untreated, leads to globe perforation and blindness

Pregnancy Considerations 

Avoid fluoroquinolones when patient is pregnant or nursing: o

Gonorrhea: ceftriaxone/spectinom ycin

o

Chlam ydia: erythrom ycin

Follow-Up Disposition Admission Criteria 

Moderate to severe DGI: o



Arthritis of weight-bearing joints

PID with: o

Peritonitis

o

WBC >15,000/m m 3

Pa ge 2 0 7

o

Intractable nausea/vom iting

o

Conjunctivitis requiring IV antibiotics

Discharge Criteria 

Uncom plicated genital, pharyngeal, or conjunctival infection



Mild DGI in nontoxic patient: o

Without arthritis in weight-bearing joint

Issues for Referral 

Infertility



Recurrent infection despite m ultiple therapy

References 1. Cook RL, et al. System atic review: noninvasive testing for Chlam ydia trachom atis and Neisseria gonorrhoeae. Ann Int Med. 2005;142(11):914â€“925. 2. Fox KK. et al. Gonorrhea in the HIV era: a reversal in trends am ong m en who have sex with m en. Am J Public Health. 2001;91:959. 3. Hopkins RS, et al. Sum m ary of notifiable diseasesâ€”United States, 2003. MMWR Morb Mortal Wkly Rep. 2005;52(54):1â€“85. 4. Khan A, et al. The prevalence of chlam ydia, gonorrhea, and Trichom onas in sexual partnerships. Sex Transm Dis. 2005;32(4):260â€“264.

Miscellaneous SEE ALSO: Chlam ydia; Urethritis

Codes ICD9-CM 98.0

Pa ge 2 0 7

ICD10 A54.9

Pa ge 2 0 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G o ut/Pseudo go ut

Gout/Pseudogout

Delaram Ghadishah

Basics Description 

Uric acid deposition into tissues affecting m ainly m iddle-aged m en and postm enopausal wom en: o

Most com m on crystalline diseases

o

Four phases: 

Asym ptom atic hyperuricem ia (serum urate >7 m g/dL)

o



Acute gout



Intercritical gout: quiet intervening periods



Tophaceous gout (up to 45% of cases)

Risk factors: 

Age >40



Male/fem ale ratio 2:1 to 6:1 <65 years old; 1:1 â‰¥65 years old

o



Hypertension



Use of loop or thiazide diuretics



Alcohol intake



Obesity

Urologic deposition of uric acid calculi m ay cause renal dysfunction.

Pa ge 2 0 7

o

Associated with avascular necrosis and deform ing arthritis

o

Most frequent in previously dam aged joints, tissues: 

Synovium



Subchondral bone



Bursae (olecranon; infrapatellar; prepatellar)



Achilles tendon



Extensor surface of the forearm s, toes, fingers, ear

 

Rarely CNS or cardiac (valves)

Pseudogout: a disorder caused by calcium pyrophosphate crystal deposition: o

Most com m on cause of acute m onarthritis after age 60

o

Risk factors: 

Hypercalcem ia (e.g., hyperparathyroidism , fam ilial)



Hem ochrom atosis; hem osiderosis



Hypothyroidism and hyperthyroidism



Hypophosphatem ia, hypom agnesem ia



Am yloidosis



Gout

Etiology 

Deposition of m onosodium urate crystals in tissues from supersaturated extracellular fluid owing to: o

Underexcretion (m ost com m only) or excessive production of uric acid

o

Any rapid change in uric acid levels 

Initiation or cessation of diuretics



Alcohol, salicylates



Cyclosporine



Lead acetate poisoning

Pa ge 2 0 7

 

Uricosurics or allopurinol

Pseudogout occurs secondary to excess synovial accum ulation of calcium pyrophosphate crystals



Precipitants for both gout and pseudogout include m inor traum a and acute illnesses: o

Surgery, ischem ic heart disease

Diagnosis Signs and Symptoms 

Gout and pseudogout both present as acute m onoarticular or polyarticular arthritis: o

Increased warm th, erythem a, and joint swelling are present.

o

Early attacks subside spontaneously within 3â€“21 days, even without treatm ent.

o

Later attacks m ay last longer, cluster, be m ore severe, and be polyarticular.



Gout: o

Sym ptom s present m axim ally within 12â€“24 hours.

o

Tophi and joint desquam ation m ay be present.

o

Wom en predom inantly present after m enopause and have polyarticular predom inance (up to 70%).

o

Less dram atic presentations in im m unosuppressed and elderly

o

Most com m on: first m etatarsophalangeal joint (75%) > ankle; tarsal area; knee > hand; wrist



Pseudogout: o

Typically involves larger joints than with gout

o

Most com m on: knee > wrist > m etacarpals; shoulder; elbow; ankle > hip; tarsal joints

Pa ge 2 0 8

o

Monoarticular (25%)

o

Asym ptom atic (25%)

o

Pseudo-osteoarthritis (45%): progressive degeneration, often sym m etric

o

Pseudorheum atoid arthritis (in elderly): 

Polyarticular variant with fever and confusion

Essential Workup 

Arthrocentesis and aspiration of tophi: o

Exam ine aspirant for crystals, Gram stain, cultures, leukocyte count, and differential

o

Fluid is typically thick pasty white: 

Gout: 20,000â€“100,000 WBC/m m 3 ; poor string and m ucin clot; no bacteria



Pseudogout: up to 50,000 WBC/m m 3 ; no bacteria



Microscopic exam ination of crystals under polarized light: o

o

Gout: 

Needle shaped



Strong birefringence



Negative elongation

Pseudogout: 

Rhom boid



Weak birefringence



Positive elongation

Tests Lab 

CBC often shows leukocytosis.



Chem istry panel to assess for renal im pairm ent



Magnesium and calcium , thyroid-stim ulating horm one (TSH), and serum iron



Uric acid level has lim ited value.

Pa ge 2 0 8



If infectious arthritis is suspected: o

Blood and urine cultures

o

Urethral, cervical, rectal, or pharyngeal gonococcal cultures

Imaging 



Plain radiographs to assess the presence of: o

Effusion

o

Joint space narrowing

o

Baseline status of joint

o

Contiguous osteom yelitis

o

Fractures or foreign body

Acute gout: soft tissue swelling; norm al m ineralization; joint space preservation



Chronic gout: calcified tophi; asym m etric bony erosions; overhanging edges; bony shaft tapering



Pseudogout: chondrocalcinosis; subchondral sclerosis or cysts (wrist); radiopaque calcification of cartilage, tendons, and ligam ents; radiopaque osteophytes

Diagnostic Procedures/Surgery 

Arthrocentesis



Aspiration of tophi

P.463

Differential Diagnosis 

Infectious arthritis



Traum a



Osteoarthritis



Reactive arthritis



Miscellaneous crystalline arthritis



Aseptic necrosis

Pa ge 2 0 8



Rheum atoid arthritis



System ic lupus erythem atosus



Sickle cell



Osteom yelitis

Treatment Initial Stabilization 

Relieve pain.



Rule out infectious cause.

ED Treatment 

Nonsteroidal anti-inflam m atory drugs (NSAIDs) are first-line treatm ent.



If NSAIDS ineffective or contraindicated: o

Steroids (oral, intravascular, intram uscular, intra-articular)

o

Colchicine (lim ited by toxicity)



Joint aspiration



Avoid aspirin.



Reduction of hyperuricem ia and long-term m anagem ent of gout and pseudogout are not within usual scope of ED care. o

Careful withdrawal of gout-producing agent

o

Uricosurics (e.g., probenecid, sulfinpyrazone)

o

Allopurinol to reduce uric acid synthesis

o

Increased fluid intake and urine alkalization to prevent renal stones

o

Long-term colchicine or NSAIDs prophylactically

Pa ge 2 0 8

Medication (Drugs) 

Allopurinol: 50â€“100 m g PO daily, m ax. 200â€“300 m g daily:



o

Adjust for kidney disease.

o

Discontinue with rash or fever.

o

Treatm ent of choice with uric acid kidney stones

Colchicine: 0.5 m g/h PO up to pain relief, 8 m g total, or GI toxicity: o

Can cause bone m arrow suppression at high doses

o

Not dialyzable

o

Long-term use m ay cause m yopathy.

o

Adjust dose for liver or kidney disease.

o

Does not prevent m onosodium urate deposition or joint dam age of chronic gout



Corticosteroids: o

Corticotropin: 40 Units IM, q8h, up to 3 doses

o

Methylprednisolone: 40 m g (peds: 1â€“2 m g/kg) IM or IV daily for 3â€“4 days

o

Prednisone: 40 m g (peds: 1â€“2 m g/kg) PO daily for 3â€“4 days; taper over 7â€“14 days

o

Triam cinolone: 10â€“40 m g plus dexam ethasone 2â€“10 m g intra-articularly



NSAIDs in m axim al doses initially for 3 days, then taper over 4 days: o

Ibuprofen: 800 m g (peds: 10 m g/kg) PO q.i.d.

o

Indom ethacin: 25â€“50 m g PO t.i.d.â€“q.i.d. (peds: 2 m g/kg/d t.i.d.â€“q.i.d.; not for children younger than 14 years old)

o

Ketorolac: 15â€“30 m g IM/IV in ED, m ay repeat for 1 dose (peds: 1 m g/kg to m ax. 30 m g IM or 0.5 m g/kg to m ax. 15 m g IV) IM

o

Naproxen: 500 m g PO t.i.d. (peds: 5 m g/kg PO

Pa ge 2 0 8

b.i.d.) o 

Sulindac: 200 m g PO t.i.d.

Probenecid: 250â€“500 m g PO t.i.d., m ax. 3 g daily: o

Not effective or less effective with renal disease or aspirin or diuretic use

o

Relatively contraindicated with presence of uric acid kidney stones



Sulfinpyrazone: 50 m g t.i.d., m ax. 800 m g daily

Geriatric Considerations NSAIDs m ay worsen renal function, fluid retention, gastropathy, hepatotoxicity, and cognitive function, particularly in the elderly.

Pediatric Considerations Gout not usually seen in children although possible during chem otherapy treatm ent for cancer

Follow-Up Disposition Admission Criteria 

Suspected infectious arthritis



Acute renal failure



Intractable pain

Discharge Criteria 

No evidence of infection



Adequate pain relief

Issues for Referral 

Septic arthritis



Renal failure

Pa ge 2 0 8

References 1. Agudelo CA, Wise CM. Crystal-associated arthritis in the elderly. Rheum Dis Clin North Am . 2000;26(3):527â€“546. 2. Buckley TJ. Radiologic features of gout. Am Fam Physician. 1996;54(4):1232â€“1238. 3. Harris MD, Siegel LB, Alloway JA. Gout and hyperuricem ia. Am Fam Physician. 1999;59(4):925â€“934. 4. Joseph J, McGrath H. Gout or â€œpseudogoutâ€•: how to differentiate crystal-induced arthropathies. Geriatrics. 1995;50(4):33â€“39. 5. Rott KT, Agudelo CA. Gout. JAMA. 2003;289:2857â€“2860. 6. Terkeltaub RA. Gout. New Engl J Med. 2003: 349:1647â€“1655. 7. Winklerprins VJ, Vincent J, Weism antel AM. How effective is prophylactic therapy for gout in people with prior attacks? J Fam Pract. 2004: 53(10):837â€“838.

Codes ICD9-CM 274.9 275.49

ICD10 M10.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G ranulo cyto penia

Granulocytopenia

Elicia Sinor Kennedy

Basics Description 

Less than norm al num ber of polym orphonuclear leukocytes



Num ber of polym orphonuclear + bands <500/m m 3 : o

Patients with a count <1,000 that has recently or rapidly fallen are at greater risk for infection than those with a count <500 but rising.

o

Patients with m yelodysplastic syndrom es should be considered granulocytopenic with higher counts because of defective neutrophils.

Etiology 

Most com m on in patients undergoing m yelosuppressive drug therapy or radiation treatm ent for neoplasm s



Chem icals



Im m une-related: o



Bone m arrow infiltration

Infection: o

Bacterial, prim arily staphylococcal and gram -negative

o 

Fungal

Vitam in deficiency (B 1 2 /folate)

Pa ge 2 0 8



Adverse reaction to drugs: o

Antibacterials

o

Antiplatelet agents

o

Antithyroid drugs

o

Antipsychotics

o

Antiepileptic drugs

o

NSAIDs

Diagnosis Signs and Symptoms 

Fever



Localized erythem a or fluctuance



Signs of lung consolidation: o

Rales

o

Rhonchi

o

Dullness



Dysuria



Urinary retention, urgency, or frequency



Change in bowel habits



Mucosal lesions

Essential Workup Com plete physical exam ination: 

Detailed exam ination of oral m ucosa and perianal area



Palpation of skin



Location of fluctuance or tenderness



Careful lung exam ination



Rectal exam ination if sym ptom s suggest perirectal abscess

Tests Lab

Pa ge 2 0 8



Com plete blood chem istry with differential



Blood culture from two different sites, with one from IV catheter site if present



Urinalysis and urine culture: o

Urinalysis m ay be norm al

Imaging 

Chest radiography even in absence of lung findings



Cerebrospinal fluid analysis for altered m ental status/signs of m eningitis

Differential Diagnosis 



Infection: o

Bacterial

o

Fungal

o

Viral

o

Protozoal/parasitic

Im m une suppression: o

Cell m ediated

o

Antineoplastic agents

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent



Initiate IV line, O 2 , m onitor.



For hypotension: o

Adm inister 1 L 0.9% norm al saline IV fluid bolus (peds: 20 cc/kg).

o

Initiate pressors as needed to stabilize blood pressure if no response to IV fluids.

Pa ge 2 0 8

General Measures 

Strict isolation



Adm inister broad-spectrum com bination antibiotics after cultures for suspected or docum ented infection: o

Im ipenem /cilastatin or fluoroquinolone

o

Ceftazidim e alone or with am inoglycoside (am ikacin, tobram ycin, gentam icin)



Cefepim e alone



Am inoglycoside plus antipseudom onal Î²-lactam (m ezlocillin, piperacillin, or ticarcillin)



Vancom ycin if patient is at risk to be carrier of Staphylococcus aureus or has history of previous staphylococcal infections

P.465

Medication (Drugs) 

Am ikacin: 15 m g/kg per 24 hours (peds: 15â€“30 m g/kg per 24 hours) div. q8hâ€“q12h IV



Cefepim e: 0.5â€“2 g q12h



Ceftazidim e: 1â€“2 g (peds: 30â€“50 m g/kg q8h) q8hâ€“q12h IV



Gentam icin: 1 m g/kg (peds: 2â€“2.5 m g/kg) q8h or 5 m g/kg q24h



Im ipenem /cilastatin: 250â€“1,000 m g q6hâ€“q8h



Levofloxacin: 500 m g IV q.i.d.



Mezlocillin: 3 g q4h over 30 m inutes



Piperacillin: 3 g q4h over 30 m inutes



Ticarcillin: 3 g (peds: 200â€“300 m g/kg per 24 hours) q4h

Pa ge 2 0 9

over 30 m inutes 

Tobram ycin: 1 m g/kg q8h IV (peds: 2â€“2.5 m g/kg q8h IV)



Vancom ycin: 1â€“2 m g/kg q8hâ€“q12h IV

Follow-Up Disposition Admission Criteria 

Signs of infection



Unreliable patient



Close follow-up unavailable

Discharge Criteria 

Previously diagnosed granulocytopenia



Com pletely asym ptom atic



Close follow-up ensured



Reliable patient

References 1. Avery RK, Longworth DL. Evolving concepts in the m anagem ent of patients with neutropenia and fever. Cleve Clin J Med. 1999;66:173â€“180. 2. Andres E, Noel E, Kurtz JE. Life-threatening idiosyncratic drud-induced agranulocytosis in elderly patients. Drugs and Aging. 2004;21(7):427â€“435. 3. Bagby GC. Disorders of neutrophil production. In: Bennett JC, et al., eds. Cecil's Textbook of Medicine. Philadelphia, Pa: WB Saunders; 1996: 908â€“915. 4. Calandra T. Spectrum and treatm ent of bacterial infections in cancer patients with granulocytopenia. Recent Results Cancer Res.

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1991;121:329â€“336. 5. Kaufm an DW, Kelly JP, Levy M, et al. The drug etiologies of agranulocytosis and aplastic anem ia. New York: Oxford University Press, 1991. 6. Schim pff SC. Infections in the cancer patientâ€” diagnosis, prevention, and treatm ent. In: Mandel G, et al., eds. Mandel, Douglas and Benne's Principles and Practice of Infectious Disease. New York, NY: Churchill Livingstone; 1995:2666â€“2684. 7. Vogelzang NJ, Flaherty JP. Fever and granulocytopenia: a viewpoint from an academ ic setting. Recent Results Cancer Res. 1993;132:79â€“88.

Codes ICD9-CM 288.0 Agranulocytosis

ICD10 D70 Agranulocytosis

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > G uillain-BarrÃ© Syndro m e

Guillain-BarrÃ© Syndrome Angela Loh

Basics Description 

Group of autoim m une conditions involving dem yelination and acute axonal degeneration of peripheral nerves



Usually preceded by triggering event, e.g., infection



Leading cause of acute, flaccid paralysis in Western countries



All ages, but rare in infancy



Weakness reaches nadir at 2â€“4 weeks.



Spontaneous resolution occurs over weeks to m onths.



Acute inflam m atory dem yelinating polyradiculoneuropathy (AIDP): o

Most com m on form of Guillain-BarrÃ© syndrom e (GBS; 90%); form erly synonym ous with GBS

o

Triggered by antecedent bacterial/viral infection

o

Dem yelination som etim es accom panied by axonal loss

o

Usually com plete recovery: 

85% with full recovery in 1 year



7â€“15% have perm anent neurologic sequelae.

Pa ge 2 0 9



Other form s of GBS: o

o

Acute m otor axonal neuropathy (AMAN): 

Pure m otor axonal involvem ent



67% seropositive for cam pylobacteriosis



Recovery often rapid



Often pediatric patients

Acute m otor sensory axonal neuropathy (AMSAN): 

Degeneration of m yelinated m otor and sensory nerves, but without significant inflam m ation or dem yelination



Sim ilar to AMAN, but also involves sensory nerves

o

Miller-Fisher syndrom e: 

Rare



Rapidly evolving ataxia, areflexia, ophthalm oplegia, m ild lim b weakness



Dem yelination and inflam m ation of cranial nerves II and VI, spinal ganglia, and peripheral nerves

 o

Resolves in 1â€“3 m onths

Acute panautonom ic neuropathy: 

Very rare



Involves sym pathetic and parasym pathetic nerves



Postural hypotension, dysrhythm ias, tachycardia, hypertension



Blurry vision, dry eyes, anhydrosis



Recovery gradual, often incom plete

Etiology 

Postinfectious: o

Two thirds with antecedent illness, usually respiratory or gastrointestinal

Pa ge 2 0 9

o

1â€“3 weeks between prodrom al illness and neurologic sym ptom s

o

Cam pylobacter jejuni m ost com m on antecedent infection

o 

Cytom egalovirus m ost com m on viral infection

Relationship to vaccines (oral polio, influenza) questionable

Diagnosis Signs and Symptoms History 

Rapidly evolving, sym m etric, ascending paralysis



Absent or m ild sensory sym ptom s (e.g., paresthesias of fingertips or toes)



Pain, com m only of pelvis, shoulder girdles, posterior thighs



Cranial nerve involvem ent m ay affect swallowing, facial m uscles, eye m ovem ents.



Preceding bacterial or viral infection

Physical Exam 

Sym m etric weakness; proxim al m uscles, legs m ore affected than arm s



Loss of deep tendon reflexes



Look for cranial nerve involvem ent.



Norm al sensory exam : o

Autonom ic dysfunction: 

Hypertension



Orthostatic hypotension



Ileus

Pa ge 2 0 9

o



Dysrhythm ias



Urinary retention

Miller-Fisher syndrom e: 

Ataxia, areflexia, ophthalm oplegia, m ild lim b weakness



Other subtypes described above



Features that suggest alternative diagnosis: o

Fever

o

Norm al reflexes

o

Upper m otor neuron signs

o

Asym m etric neurologic deficits

o

Sharply dem arcated sensory level

Tests Clinical diagnosis

Lab Electrolytes: 

Lum bar puncture: o

Increased protein 55â€“250 (m ay be present only after 7â€“10 days)

o

Few or no WBCs

o

Norm al opening pressure

Imaging CT or MRI to rule out cord com pression

Diagnostic Procedures/Surgery Electrophysiologic studies will be abnorm al.

Differential Diagnosis 

Cord com pression



Lym e disease



Tick paralysis



Transverse m yelitis

Pa ge 2 0 9



Botulism



Myasthenia gravis



Neoplastic m eningitis



Acute periodic paralysis



Poliom yelitis



Diphtheria



Eaton-Lam bert syndrom e



Acute interm ittent porphyria



Chronic heavy m etal poisoning



Tetrodotoxin poisoning



Psychogenic, m alingering

P.467

Treatment Pre Hospital Attention to airway m anagem ent

Initial Stabilization Airway assessm ent and m anagem ent: 

Progression to respiratory failure can be rapid.

ED Treatment 

Airway m anagem ent: o

About 30% will need ventilatory support.

o

May need intubation within 24â€“28 hours of onset

o

Frequent m onitoring of respiratory param eters: 

Forced vital capacity helpful



ICU adm ission if forced vital capacity (FVC) <20 m L/kg

Pa ge 2 0 9



Intubation recom m ended if FVC <15 m L/kg



Watch for autonom ic dysfunction.



Supportive therapy



Early neurology consult



Steroids not beneficial

Medication (Drugs) Plasm apheresis or intravenous im m unoglobulin, in conjunction with neurologic consultation

Follow-Up Disposition Admission Criteria 

All patients with GBS or suspected GBS warrant adm ission for close observation.



ICU adm ission for those with signs of respiratory com prom ise or autonom ic dysfunction

Discharge Criteria Patients should be considered for discharge only in consultation with neurologist.

References 1. Brody AJ, Sternbach G, Varon J. Octave Landry: Guillain-BarrÃ© syndrom e. J Em erg Med. 1994;12:833â€“837. 2. Hahn A. Guillain-BarrÃ© syndrom e. Lancet. 1998;352:635â€“641. 3. Jones HR. Childhood Guillain-BarrÃ© syndrom e: clinical presentation, diagnosis, and therapy. J Child Neurol. 1996;11(1):41â€“42.

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4. Lindenbaum Y, Kissel JT, Mendell JR. Treatm ent approaches for Guillain-BarrÃ© syndrom e and chronic inflam m atory dem yelinating polyradiculoneuropathy. Neurol Clin. 2001;19(1):187â€“204. 5. Newswanger DL, Warren CR. Guillain-BarrÃ© syndrom e. Am Fam Physician. 2004;69:2405â€“2410.

Codes ICD9-CM 357.0

Pa ge 2 0 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hallucino gen Po iso ning

Hallucinogen

Poisoning Brandon K. Wills

Basics Description 

Predom inantly alters perception, cognition, and m ood



All hallucinogens potentiate neurotransm itter release or bind directly to receptors: o

Serotonin (5-hydroxytryptam ine; 5-HT): Many hallucinogens are agonists or antagonists at 5-HT receptor subtypes.

o

Norepinephrine, N-m ethyl-D-aspartate (NMDA), dopam ine

Etiology 

Most exposures are intentional.



Com m on hallucinogens: o

Indoleam ine: 

Lysergic acid diethylam ide (LSD) (duration 6â€“12 hours)

 o

Morning glory (Ipom oea spp.)

Tryptam ines: 

Psilocybin (Psilocybe m ushroom s); frequently

Pa ge 2 1 0

adulterated with LSD 

N,N-dim ethyltryptam ine (DMT); 5-MeO-DMT (â€œfoxy-m ethoxyâ€•), and other tryptam ine congeners

o

Phenylethylam ines (hallucinogenic am phetam ines): 

Methylenedioxyam phetam ine (MDA)



Methylenedioxyetham phetam ine (MDEA)



Methylenedioxym etham phetam ine (MDMA; â€œecstasyâ€•; duration 8â€“12 hours)



Param ethoxyam phetam ine



Dim ethoxyam phetam ine



Mescaline (peyote cactus); frequently adulterated with LSD (duration 6â€“12 hours)

o

o

o

Arylcycloalkylam ines: 

Phencyclidine (PCP)



Ketam ine

Anticholinergic: 

Deadly nightshade (Atropa belladonna)



Jim sonweed (Datura stram onium )

Other: 

Piperazines: benzyl piperazine (BZP) and trifluorom ethylphenylpiperazine (TFMPP)



Dextrom ethorphan (DXM)



Marijuana

Diagnosis Signs and Symptoms 

Considerable individual variation; effects m ay last 4â€“12 hours depending on agent/dose.



Sym ptom s characterized by sym pathetic arousal

Pa ge 2 1 0



Usually oriented and able to give history of exposure, even while having delusions



Initial sym ptom s: o



Nausea, flushing, chills, trem or

Neurologic sym ptom s: o

Restlessness and dizziness early after ingestion

o

Affective lability

o

Desire to laugh (especially with Psilocybe m ushroom s)

o

Anxiety, despair, helplessness, dread

o

Intensified perceptions, visual distortions/intensification

o

Tactile distortions (especially with m escaline)

o

Synesthesia (blending of sensory m odalities, e.g., seeing sounds)



o

Religious or m ystical experiences

o

Sleep disruption

Neurologic signs: o

Unusual/bizarre behavior

o

Speech disruption

o

Mydriasis

o

Piloerection

o

Hyperreflexia

o

Com a with m assive exposure

o

Convulsions: 

Hallucinogenic am phetam ines



Children who becom e hyperpyrexic after Psilocybe m ushroom ingestion





Pulm onary: o

Mild tachypnea

o

Respiratory arrest (with m assive exposure)

Cardiovascular:

Pa ge 2 1 0

o

Tachycardia

o

Hypertension (with hallucinogenic am phetam ines)

o

Dysrhythm ia (with hallucinogenic am phetam ines)

o

Intracerebral hem orrhage (with hallucinogenic am phetam ines)



Gastrointestinal: o



Nausea/vom iting (especially with m escaline)

Metabolic: o

Hyperpyrexia: 

Especially with MDMA use at â€œraveâ€• clubs



Hepatic failure, renal failure, and dissem inated intravascular coagulopathy m ay follow.

 o 

May be lethal

Hyponatrem ia: has been reported with MDMA use

Hem atopoietic: o

Coagulopathies and hem orrhage at high doses owing to disruption of platelet serotonin function

Essential Workup 

Core tem perature m easurem ent



Determ ination of risk of rhabdom yolysis: o

Creatine kinase level

o

Urine dip or m yoglobin level

Tests Lab 

Electrolytes, blood urea nitrogen, creatinine, glucose levels



Urine toxicology screen: o

Rarely indicated

o

Distinguishing between hallucinogens is of little value.

o

Most hallucinogenic substances are not tested for on

Pa ge 2 1 0

routine drug screens. o

Am phetam ine screen is frequently negative for hallucinogenic am phetam ines (e.g., MDMA).

Differential Diagnosis 

Meningitis



Intracranial bleeds or lesions



Withdrawal (ethanol, sedative-hypnotic, baclofen)



Serotonin syndrom e (especially with concom itant serotonergic agents involved)



Psychiatric illnesses: o

LSD associated with prolonged psychoses resem bling schizoaffective disorders



o

Chronic am phetam ine/cocaine abuse

o

Steroids

Infectious/febrile seizures in hyperpyretic child

Pediatric Considerations Assess parent-child relationships for possibility of neglect or abuse.

Treatment Pre Hospital 

Controversies: o

Sedation with benzodiazepines versus haloperidol versus physical restraints: 

Benzodiazepines are generally preferred.



Sedation m asks sym ptom s and m ay lim it history.



Cautions: o

Sedate or restrain patient to ensure safe transport.

o

For hypertherm ic patient:

Pa ge 2 1 0



Sedation rather than physical restraint



Begin cooling m easures.

P.469

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Aggressive cooling if hypertherm ic



Intravenous access/rehydration with isotonic fluids for significant fluid loss or evidence of rhabdom yolysis



Naloxone, Accu-Chek, dextrose, and thiam ine if patient has altered m ental status

ED Treatment 

Cooling m easures: o

Cool m ist and fans

o

Benzodiazapines, if agitated

o

Paralytics with intubation, if needed (generally not succinylcholine)





Sedate for agitation or autonom ic signs: o

Benzodiazapines

o

Rarely neuroleptics: 

May intensify hallucinogenic experience



Possibly lower seizure threshold

Activated charcoal (AC) is not expected to be helpful for m ost agents owing to rapid absorption and delayed patient presentation: o

Consider AC for oral ingestions within 2â€“3 hours in patients with intact protective airway reflexes; especially for anticholinergics or seeds owing to delayed GI m otility/absorption.



Place in a quiet, calm environm ent.

Pa ge 2 1 0



Maintain urine output of 2â€“3 m L/kg/h and consider urine alkalinization for treatm ent of rhabdom yolysis.

Medication (Drugs) 

Dextrose D 5 0 W for hypoglycem ia: 1 am pule: 25 g/50 m L (peds: D 2 5 W, 0.5â€“1 g/kg or 2â€“4 m L/kg) IV



Benzodiazepine (Diazepam ): 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Haloperidol (Haldol): 2.5â€“5 m g IV or IM; not recom m ended for children



Naloxone (Narcan): initial dose: 2 m g (peds: 0.01â€“0.1 m g/kg) IV or IM



Sodium bicarbonate drip for rhabdom yolysis: 3 am pules in 1 L of D 5 W; infuse at 1.5â€“2 tim es m aintenance rates (keep urine pH >7.5)



Thiam ine (vitam in B 1 ): 100 m g (peds: 25 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Severely intoxicated



Atypical presentation



Prolonged sym ptom s (>12 hours after exposure)



Prolonged periods of agitation and hypertherm ia: o

Risk of rhabdom yolysis or organ dam age

Discharge Criteria Most patients can be discharged after receiving supportive therapy and observation once they are asym ptom atic.

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Pediatric Considerations Suspected cases of child abuse or neglect require referral to child protective services.

References 1. Abraham HD, Aldridge AM, Gogia P. The psychopharm acology of hallucinogens. Neuropsychopharm acology. 1996;14:285â€“298. 2. Acute reactions to drugs of abuse. Med Lett Drugs Ther. 2002;44:21â€“24. 3. Graem e KA. New drugs of abuse. Em erg Med Clin North Am . 2000;18:625â€“636. 4. Kalant H. The pharm acology and toxicology of â€œecstasyâ€• (MDMA) and related drugs. Can Med Assoc J. 2001;165:917â€“928. 5. Wilson JM, McGeorge F, Sm olinske S, et al. A foxy intoxication. Forensic Sci Int. 2005;148(1):31â€“36.

Codes ICD9-CM 969.6 Psychodysleptics (hallucinogens)

ICD10 T40.9 Other and unspecified psychodysleptics (hallucinogens)

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hand Infectio n

Hand Infection

Chet Shermer

Basics Description 

Hand infections are com m only seen in the ED.



The range of pathology is broad and m ay include acute and chronic conditions.

Alert Hand infections are potential liability issues and m ust be handled with extrem e caution. Referral to hand surgeon is alm ost always indicated.

Etiology 

Bacterial infection of the hand is associated with skin pathogens:



o

Staphylococcus or Streptococcus species

o

History of a puncture wound

Anaerobes are identified in 75% of paronychia in children owing to thum b sucking and nail biting.



Chronic paronychia m ay be caused by Candida albicans.



Herpetic whitlow is caused by type 1â€“2 herpes sim plex virus.



Clenched fist injuries involve a variety of pathogens,

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including anaerobic Streptococcus and Eikenella sp.

Diagnosis Signs and Symptoms 

Paronychia: o

Localized edem a, erythem a, and pain in proxim al portion of lateral nail fold

o

Fluctuance m ay be present and m ay extend beneath the nail m argin.

o

System ic signs and sym ptom s are usually not present.



Felon: o

Erythem a and tense swelling of the distal pulp space that does not extend proxim al to the proxim al interphalangeal (PIP) joint



o

Aching pain early, severe throbbing pain late

o

System ic signs are usually not present.

Herpetic whitlow: o

Distal pulp space is swollen, but rem ains soft.

o

Lateral nail folds m ay be affected.

o

Throbbing pain of the distal pulp space

o

Vesicles containing nonpurulent fluid are present and m ay form bullae.

o



System ic sym ptom s m ay be present: 

Fever



Lym phadenopathy



Constitutional sym ptom s

Flexor tenosynovitis: o

Kanavel signs: 

Severe pain and sym m etric edem a of the digit

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

Tenderness over the course of tendon sheath



Flexed position of the finger at rest



Pain on passive extension of the fingerâ€”m ay be the only finding in early infection



Clenched fist injury: o

Laceration over the m etacarpophalangeal (MCP) joint from striking an object with a clenched fist

o

Any laceration over the MCP m ust be assum ed to be a hum an bite wound until proven otherwise.



Web space abscess: o

Pain and edem a of the affected web space and adjacent palm

o 

Fingers are held abducted.

Palm ar space infections: o

Thenar space infection: 

Pain, tenderness, tense edem a of thenar em inence



Dorsal edem a without tenderness



Thum b is held abducted and flexed, and passive adduction is painful.

o

Midpalm ar space infection: 

Pain, edem a, and tenderness of the m idpalm ar space

o



Dorsal edem a without tenderness



Motion of m iddle and ring fingers is painful.

Hypothenar space infection: 

Pain and fullness over hypothenar em inence



No lim itation of finger m ovem ent

Essential Workup Most hand infections are diagnosed by history and physical exam ination with special attention to neurovascular status.

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Tests Lab 

Although usually not necessary, herpetic whitlow m ay be confirm ed by Tzanck test.



Gram stain and culture m ay guide antibiotic choice in felons.



Blood cultures, CBC are not routinely indicated.

Imaging 

Radiographs are usually not helpful unless there has been traum a or a suspected foreign body.



With felon, flexor tenosynovitis, and palm ar space infection, radiograph m ay identify osteom yelitis or foreign body.



Radiographs in clenched fist injury m ay reveal a fracture.

Differential Diagnosis 

Paronychia should be differentiated from herpetic whitlow and felon.



The differential for palm ar space infection includes flexor tenosynovitis, cellulitis, and web space infection.

Treatment 

Paronychia: o

Early paronychia/sim ple cellulitis without purulence present m ay be m anaged with oral antibiotics and rest: 

Cephalexin, dicloxacillin



Clindam ycin or erythrom ycin if associated with nail biting or oral contact

Pa ge 2 1 1

o

Superficial infections are drained by inserting a No. 11 blade between nail and eponychium and lifting the eponychium from the nail.

o

If necessary, the lateral nail fold m ay be incised tangential to the curvature of the nail.

o

When pus is present under the adjacent nail, one fourth of the nail should be rem oved.

o

When pus is present under the dorsal roof of the proxim al nail, rem ove one third of the proxim al nail.

P.471



Felon: o

A lateral incision avoiding the neurovascular bundle is preferred.

o

More extensive felons are drained through a unilateral longitudinal incision that does not cross the distal interphalangeal (DIP) flexor crease.

o

Disruption of fibrous septa is no longer recom m ended:

o



Results in an unstable fingertip



Loculations m ay need to be broken up.

Give oral antibiotics to cover skin pathogens, place a drain, and recheck in 48 hours: 



Cephalexin, dicloxacillin

Herpetic whitlow: o

Usually self-lim ited; do not incise and drain.

o

Oral acyclovir m ay be given to patients with system ic involvem ent.



Flexor tenosynovitis, web space abscess, palm ar space infection: o

Elevation, IV antibiotics, and pain control:

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

Am picillin/sulbactam , cefoxitin, ticarcillin/clavulanate

o

All of these infections require im m ediate consultation with a hand surgeon.



Clenched fist injury: o

Elevation, IV antibiotics, tetanus prophylaxis, and pain control in the ED: 

Am picillin/sulbactam , cefoxitin, ticarcillin/clavulanate

o

All bite wounds with evidence of infection or joint involvem ent require em ergent consultation with a hand surgeon.

o

If there are no signs of infection and no joint penetration, patients m ay be considered for outpatient treatm ent with oral antibiotics after appropriate irrigation and wound care: 

Am picillin/clavulanate or penicillin V plus cephalexin or dicloxacillin



Do not prim arily close lacerations associated with a hum an bite; delayed prim ary closure or healing by secondary intention is appropriate.

Medication (Drugs) 

Acyclovir: 400 m g PO t.i.d. for 10 days (peds: not recom m ended for herpetic whitlow)



Am picillin/clavulanate: 875/125 m g PO b.i.d. (peds: 40 m g/kg/d PO div. q6h)



Am picillin/sulbactam : 1.5â€“3.0 g IV q6h (peds: safety not established)



Cefoxitin: 2 g IV q8h (peds: 80â€“160 m g/kg/d IV or IM div. q6h)

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

Cephalexin: 500 g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO div. q6h)



Clindam ycin: 300 m g PO q.i.d. for 7 days (peds: 20â€“40 m g/kg/d div. q6h PO IV or IM)



Dicloxacillin: 500 m g PO q.i.d. for 7 days (peds: 12.5â€“50 m g/kg/d PO div. q6h)



Erythrom ycin: 500 m g PO q.i.d. for 7 days (peds: 40 m g/kg/d div. q6h PO)



Penicillin V: 250 m g PO q.i.d. (peds: 40 m g/kg/d PO div. q6h)



Ticarcillin/clavulanate: 3.1 g IV q4hâ€“q6h (peds: safety not established)

Follow-Up Disposition Admission Criteria 

Flexor tenosynovitis, web space abscess, palm ar space infections: o

All these infections require adm ission for IV antibiotics and drainage.



Clenched fist injury with signs of infection: o

Requires adm ission for surgical dÃ©bridem ent and IV antim icrobials

Discharge Criteria 

Paronychia and felons: o

Patients with uncom plicated paronychia or felon m ay be discharged from the ED with a recheck and drain rem oval in 48 hours.



Herpetic whitlow:

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o

Patients with herpetic whitlow m ay be discharged from the ED with appropriate follow-up.



Clenched fist injury without infection: o

May be discharged on oral antibiotics with follow-up in 24 hours

References 1. Antosia RE, Lyn E. The hand. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1997;1998:625â€“668. 2. Hausm an MR, Lisser SP. Hand infections. Orthop Clin North Am . 1992;23(1):171â€“185. 3. Tintinalli JE, Kelen GD, Stapcynski JS, eds. Em ergency m edicine: a com prehensive study guide. Hand Infect. 1999;277â€“280.

Codes ICD9-CM 136.9

ICD10 L08.9 L70.8 M70.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Haz m at

Hazmat

Moses S. Lee

Basics Description Hazm at refers to exposure to hazardous m aterials causing local or system ic toxicity.

Pathophysiology 

Acids cause coagulation necrosis with eschar, usually lim iting penetration to deeper tissue.



Alkalis cause liquefaction necrosis and soluble com plexes that penetrate into deep tissues.



Dam age also occurs through oxidation, protein denaturation, cellular dehydration, local ischem ia, and by m etabolic com petition/inhibition.

Etiology Hazardous m aterials are encountered in household, industry, agriculture, and transportation accidents and in crim inal/terrorist activities.

Associated Conditions Related to toxic agent and its effects

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Diagnosis Signs and Symptoms 



Skin: o

Chem ical burns; m ay appear deceptively m ild at first

o

Visible liquid or powder on skin

o

Absorption through skin m ay cause system ic toxicity.

Mucous m em branes (eyes, nasopharynx; see Corneal Burn): o

Ranges from subjective irritation to serious m ucosal burns

o 



Potential airway com prom ise

Pulm onary: o

Cough

o

Pleuritic chest pain

o

Bronchospasm

o

Dyspnea

o

Pulm onary edem a (im m ediate or delayed)

System ic (after skin or pulm onary absorption): o

Altered m ental status

o

Seizures

o

Tachy/brady dysrhythm ias

o

Hypotension/hypertension

o

Gastrointestinal sym ptom s

o

Electrolyte disturbances

o

Carboxyhem oglobinem ias and m ethem oglobinem ias

o

Cholinergic syndrom e (see Chem ical Weapons Poisoning, Nerve Agents)

Essential Workup 

Attem pt to identify substance using prehospital providers,

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Material Safety Data Sheet, and Chem trec (Chem ical Tr ansportation Em ergency Center). 

Material Safety Data Sheet (MSDS): o

Identifies chem icals

o

Differentiates vapor versus skin hazard

o

Determ ines need for decontam ination

o

Lim ited treatm ent data



Determ ine route and duration of exposure.



Inhalation injury m ore likely in an enclosed space



Determ ine toxicity using poison control, com puterized databases such as POISINDEX or TOXNET, or standard toxicology text.



Observe as needed for system ic toxicity.

Tests Lab 

Depends on substance



Electrolytes, BUN, creatinine, and glucose levels



Liver function tests



Calcium level



Magnesium level



Phosphorus level



Arterial blood gases: o

Metabolic acidosis

o

Carboxyhem oglobinem ias and m ethem oglobinem ias

o

Respiratory failure

Imaging Chest radiograph for pulm onary edem a

Differential Diagnosis 

Skin: o

Hypersensitivity reaction

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o 



Therm al burns

Pulm onary: o

Pneum onia

o

Pulm onary em bolism

o

Anaphylaxis

System ic: o

Status epilepticus

o

Overdose

o

Psychiatric illness

o

Myocardial infarction

Treatment Pre Hospital 



Recognize a Hazm at situation: o

Accident at industrial/agricultural site

o

Accident involving transport of hazardous m aterials

o

Suspected terrorist m ass casualty incident

o

Cholinergic syndrom e

o

Irritant m ucous m em brane sym ptom s

o

Chem ical burns

Protect yourself: o

Approach from upwind.

o

Do not enter scene until safety of m aterial is determ ined.

o

Use level A protective gear if safety not established

o

Anyone able to walk and talk is m inim ally contam inated.



Personal chem ical protective equipm ent: o

Level A: positive-pressure self-contained breathing apparatus (SCBA), fully encapsulated

Pa ge 2 1 1

chem ical-resistant suit, double chem ical-resistant gloves, chem ical-resistant boots, and airtight seals between suit, gloves, boots o

Level B: SCBA, nonencapsulated chem ical suit, double gloves, boots



o

Level C: air-purification device, suit, gloves, boots

o

Level D: Com m on work clothes

Identify substance: o

Departm ent of Transportation (DOT) placard, Material Safety Data Sheet (MSDS), shipping papers, hazard labels

o

If unsuccessful, call Chem ical Transportation Em ergency Center (Chem trec: 1[800] 424-9300) to determ ine substance and toxicity.

o 



Determ ine toxicity and need for decontam ination: o

Poison control

o

Chem trec

Decontam inate: o



Hazm at team s can do chem ical testing.

Hazm at team

Treat: o

Provide basic life support and advanced life support care as indicated.

o

Generally basic list support only in a â€œhot zoneâ€ •

o

Irrigate skin and ocular burns im m ediately and continue until arrival at hospital.

P.473

Initial Stabilization 

Protect em ergency departm ent personnel:

Pa ge 2 1 2

o

Secondary contam ination can occur from derm al contact or through inhalation of volatile gases/particles.



Keep patients outside in designated hot zones until decontam inated.



When in doubt, decontam inate.



Expect contam inated patients to arrive via em ergency m edical services or private vehicle.



If treatm ent is required before/during decontam ination: o

Use m inim um necessary staff in appropriate personal protection gear.

o 

Focus on life- and lim b-saving care only.

Decontam ination: o

Security to enforce hot zone

o

Rem ove, label, and double-bag clothing (including contact lens).

o

Copious irrigation with soap and water for 10â€“15 m inutes with special attention to obviously contam inated areas, wounds, and exposed eyes

o

Recapture water to prevent contam ination of the sewer and downstream areas: 

In an em ergency or m ass casualty situation, it is acceptable to let water drain into sewer.

o

Hydrotherapy: 

Mainstay of therapy for chem ical burns



Contraindicated only for elem ental m etals (sodium and potassium )

o

Allow patient to decontam inate him self or herself or use trained decontam ination team .

o

Decontam inate children, dependent elderly, m entally/physically challenged and their appliances (e.g., wheelchairs) with caregivers.

Pa ge 2 1 2

o

Gloves, m asks, goggles, and disposable gowns provide som e protection.

o

Rem ove/replace bandages, tourniquets, airway adjuncts, intravenous sets.

o

Retriage after decontam ination.

ED Treatment 

Provide supportive care as needed.



Determ ine if antidotal treatm ent would be effective and available.



Hazm at incidents provoke extrem e fear: o

Expect casualties suffering from collective hysteria.

o

Knowledge of toxicologic profile can exclude contam ination in these patients.



Em ergency departm ent staff m ay becom e sym ptom atic even if chem ical concentrations in the air are below toxic levels and m ay need to be escorted to fresh air.



Chem ical burns: o

Irrigation should be started as soon as possible and, if owing to a strong alkali, m ay need to be continued for hours.

o

Aggressive fluid resuscitation 2â€“4 m L/kg lactated Ringer solution per total burn surface area (TBSA) percent over 24 hours with one half given over the first 8 hours

o 

Pain control

Pulm onary sym ptom s: o

Bronchodilators, oxygen, intubation, and m echanical ventilation



Selected special treatm ents: o

Hydrofluoric acid burns: 

Calcium gluconate via topical cutaneous gel, subcutaneous or intra-arterial

Pa ge 2 1 2



For system ic toxicity: intravenous calcium gluconate and m agnesium

o

Phenol burns: 

Rem ove phenol from skin with polyethylene glycol 300 or 400 or with isopropyl alcohol.

o

Nitrates: 

Ingested or extensive burns m ay cause m ethem oglobinem ia.



Treat levels >30% with high-flow oxygen and intravenous m ethylene blue.

o

Elem ental m etals (sodium /potassium ): 

Water lavage is contraindicated and dangerous.



Cover with oil until substance can be dÃ©brided from skin.

o

Organophosphates/carbam ate insecticides (see: Chem ical Weapons Poisoning)

Medication (Drugs) 

Albuterol: 2.5â€“5.0 m g nebulized



Calcium gluconate: 10 m L of 10% solution



Magnesium : 2 g IV over 20 m in



Methylene blue: 1â€“2 m g/kg slow IV (peds: not recom m ended for <6 years old; >6 years old: 1 m g/kg IV/IM over 5 m in)

Follow-Up Disposition Admission Criteria

Pa ge 2 1 2



Airway com prom ise, respiratory difficulty (hypoxia)



Significant system ic sym ptom s



Adm it patients with chem ical burns to burn center.

Discharge Criteria 

Patients who are well after a period of observation and consultation with poison control



Superficial chem ical burns owing to a toxin without potential for system ic toxicity (weak acid/alkali)

References 1. Burgess JL, Kirk M, Borron SW, et al. Em ergency departm ent hazardous m aterials protocol for contam inated patients. Ann Em erg Med. 1999;34:205â€“212. 2. Goldfrank LR, Flom enbaum NE, Lewin NE. Goldrank's Toxicologic Em ergencies. 6th ed. New York: McGraw-Hill; 1998. 3. Greenberg MI, Cone DC, Roberts JR. Material Safety Data Sheet: a useful resource for the em ergency physician. Ann Em erg Med. 1996;27:347â€“352. 4. Waeckerle JF. Dom estic preparedness for events involving weapons of m ass destruction. JAMA. 2000;283:252â€“254. 5. Yeung R. Em ergency departm ent Hazm at decontam ination contingency plan. J Prehospital Med. Disaster Med. 2001;16.

Miscellaneous SEE ALSO: Chem ical Weapons Poisoning; Radiation Injury

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Head Traum a, Blunt

Head Trauma,

Blunt Gary M. Vilke

Basics Description Blunt traum a to head resulting in a variety of injuries ranging from closed head injury to death

Etiology Blunt traum a to head m ay cause several types of closed head injuries: 

Concussion: transient loss of consciousness or am nesia with norm al head CT



Subdural hem atom a: tearing of subdural bridging veins and bleeding into the subdural space



Epidural hem atom a: dural arterial injury, especially the m iddle m eningeal artery often associated with a skull fracture: o

Classically, transient loss of consciousness followed by a lucid interval, then rapid dem ise



Subarachnoid hem orrhage: bleeding into the subarachnoid space following traum a



Cerebral contusion: focal injuries to the brain

Pa ge 2 1 2

characterized as coup (beneath area of im pact) or contrecoup (area rem ote from im pact) 

Intracerebral hem orrhage: m ass intracranial lesion with bleeding into the brain parenchym a



Diffuse axonal injury: m icroscopic injuries scattered throughout the brain in a patient in deep com a

Diagnosis Signs and Symptoms 

Evidence of traum a to head includes: o

Scalp laceration, cephalohem atom a, or ecchym osis

o

Raccoon eyes: bilateral ecchym osis of orbits associated with basilar skull fractures

o

Battle sign: ecchym osis behind the ear at m astoid process associated with basilar skull fracture



o

Hem otym panum

o

Cerebral spinal fluid rhinorrhea or otorrhea

Evidence of increasing intracranial pressure includes: o

Decreasing level of consciousness, falling Glasgow com a scale score

o

Cushing response, bradycardia, hypertension, and dim inished respiratory rate

o

Dilated pupils associated with decorticate or decerebrate posturing

Tests Lab 

Rapid check of blood glucose level



Com plete blood count, platelet count, and coagulation param eters

Pa ge 2 1 2



Type and cross-m atch for surgical candidates.



Baseline electrolytes, blood urea nitrogen, and creatinine levels



Blood alcohol level if indicated

Imaging 

Cervical spine radiographs or helical CT when indicated



Head CT should be perform ed in patients with any of the following:



o

Loss of consciousness or am nesia of events

o

Progressive headache

o

Alcohol or drug intoxication

o

Unreliable history or dangerous m echanism

o

Posttraum atic seizure

o

Repeated vom iting

o

Signs of basilar skull fracture

o

Possible skull penetration or depressed skull fracture

o

Glasgow com a scale score <15

o

Focal neurologic findings

Patients on Coum adin or heparin or those with a history of bleeding dyscrasias m ust undergo im aging.



Older patients (>age 60â€“65 years) and alcoholics are at higher risk of intracranial hem orrhage: o

Have a low threshold for obtaining CT scan

Differential Diagnosis 

Penetrating head traum a



Any condition that alters m ental status that m ay have produced a fall and caused external evidence of head traum a (e.g., hypoglycem ic episode, seizure)

Pa ge 2 1 2

Treatment Pre Hospital 

Blunt head traum a patients with risk for intracranial lesion m ust go to a traum a center: o

High-risk patients include those with depressed consciousness, focal neurologic signs, m ultiple traum a, or palpable depressed skull fractures.



Moderate-risk patients should go to a hospital with availability of prom pt neurosurgical consultation: o

Moderate-risk patients include those with progressive headache, alcohol or drug intoxication, unreliable history, posttraum atic seizure, repeated vom iting, posttraum atic am nesia, signs of basilar skull fracture.



Protect and m anage the airway including intubation: o

Routine hyperventilation without signs of cerebral herniation should be avoided.



If evidence of cerebral herniation (see Signs and Sym ptom s) or progressive neurologic deterioration, then initiate m easures to decrease intracranial pressure: o

o 

Mild hyperventilation to keep PaCO 2 about 35: 

16â€“20 breaths per m inute in adults



20â€“24 breaths per m inute in children



24â€“26 breaths per m inute in infants

Elevating head of bed 20â€“30Â°

Cervical spine precautions m ust be m aintained in all patients.



Cautions: o

Avoid hypotension (systolic blood pressure <90 m m Hg); use intravenous crystalloid solutions to m aintain blood pressure.

Pa ge 2 1 2

o

Avoid hypoxia (oxygen saturation <90%); adm inister 100% oxygen.

o

Check blood glucose level.

Initial Stabilization Airway, breathing, and circulation m anagem ent: 

Control airway as needed: o

Rapid-sequence intubation if Glasgow com a scale score <8, unable to protect airway, or evidence of hypoxia

o

Norm alize PCO 2 , avoid hyperventilation and hypoventilation.

P.475



Treatm ent with etom idate or fentanyl as induction agent, succinylcholine (pretreat with m inidose paralytic), rocuronium , or vecuronium ; m orphine for ongoing sedation



Caution with fentanyl in hem odynam ically labile patients



Intravenous catheter placem ent with crystalloid solution as needed to avoid hypotension (keep systolic blood pressure >90 m m Hg)



Cervical spine precautions

ED Treatment 

Early neurosurgical consultation



If patient has evidence of cerebral herniation (see Signs and Sym ptom s), initiate m easures to decrease intracranial pressure: o

Mild hyperventilation: 16â€“20 breaths per m inute in adults, 20â€“24 breaths per m inute in children, and 24â€“26 breaths per m inute in infants to keep PaCO 2

Pa ge 2 1 2

about 35, which correlates to an end tidal CO 2 of 32â€“35 m m Hg o

Elevating head of bed 20â€“30Â°

o

Mannitol boluses intravenously: Do not adm inister m annitol unless systolic blood pressure >100 m m Hg and patient is adequately fluid resuscitated.



Phenytoin to prevent early posttraum atic seizures



The use of glucocorticoids is not recom m ended to lower intracranial pressure in head traum a patients.



Barbiturates are not recom m ended in the initial em ergency departm ent treatm ent of head-injured patients.



If definitive neurosurgical care is not im m ediately available, a single burr hole m ay preserve life until neurosurgical intervention can be obtained: o

Perform only in com atose patients with decerebrate or decorticate posturing on the side of a known m ass lesion who have not responded to hyperventilation and m annitol.



Transfuse as needed to keep hem atocrit >30%.



Avoid hypotherm ia, which will increase risks of coagulopathy during surgery.



Maintain NPO status.



Surgery: o

Surgical procedure based on findings of CT scan and neurosurgical consultation

Medication (Drugs) 

Etom idate: 0.2â€“0.3 m g/kg IV



Fentanyl: 3â€“5 Âµg/kg IV if systolic blood pressure >100 m m Hg

Pa ge 2 1 3



Mannitol: 0.25â€“1 g/kg IV bolus



Morphine sulfate: 2â€“20 m g IV (peds: 0.1 m g/kg IV up to adult doses)



Phenytoin: 15â€“20 m g/kg IV up to 1,000 m g



Rocuronium : 0.6 m g/kg IV



Succinylcholine: 1â€“2 m g/kg IV



Vecuronium brom ide: 0.1 m g/kg IV; m inidose pretreatm ent: 0.01 m g/kg IV

Follow-Up Disposition Admission Criteria 

Patients with m ass lesion associated with head traum a m ust be adm itted to the intensive care unit or undergo surgery.



Patients with subarachnoid hem orrhage and diffuse axonal injury should be initially adm itted to the intensive care unit.



Patients with ongoing sym ptom s including repetitive questioning, anterograde am nesia, or disorientation should be adm itted to a m onitored unit for neurologic evaluation.

Discharge Criteria 

Patients with resolved sym ptom s, negative findings on head CT, and no other co-m orbid factors (e.g., intoxication, additional traum a needing treatm ent) m ay be discharged.



Patients with m inor head traum a, no loss of consciousness or am nesia, and norm al neurologic exam findings m ay be discharged hom e with a friend or fam ily m em ber and head

Pa ge 2 1 3

injury instructions.

Pediatric Considerations Cases of suspected nonaccidental traum a m ust be reported to the appropriate legal agency.

References 1. Brain Traum a Foundation. Guidelines for Prehospital Managem ent of Traum atic Brain Injury. New York: Brain Traum a Foundation; 1999. 2. Brain Traum a Foundation. Managem ent and Prognosis of Severe Traum atic Brain Injury. New York: Brain Traum a Foundation; 2000. 3. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determ ining outcom e from severe head injury. J Traum a. 1993;34:216â€“222. 4. Com m ittee on Traum a. Head traum a: Advanced Traum a Life Support. 7th ed. Chicago: Am erican College of Surgeons; 2002. 5. King BS, Gupta R, Narayan RK. The early assessm ent and intensive care unit m anagem ent of patients with severe traum atic brain and spinal cord injuries. Surg Clin North Am . 2000;80(3):855â€“870.

Codes ICD9-CM 959.01 Head injury, unspecified

ICD10 S09.90 Unspecified injury of head

Pa ge 2 1 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Head Traum a, Penetrating

Head Trauma,

Penetrating Gary M. Vilke

Basics Description Penetrating injury to intracranial contents: 

High-velocity penetration: usually bullets, which cause traum a directly to brain tissue, but also have a â€œshock waveâ€• injury to local surrounding brain



Low-velocity penetration: usually knives, picks, or other sharp objects, with direct local traum a to brain tissue

Etiology 

Direct penetration of the skull into the intracranial cavity by foreign object: o

Direct or local dam age to brain tissue

o

Intracranial hem orrhage, including subdural, epidural, and intraparenchym al bleeds



A bullet that hits the skull, ricochets off, and does not fracture the skull can still cause significant traum a to the underlying brain tissue.

Pa ge 2 1 3

Diagnosis Signs and Symptoms 

Alteration in level of consciousness and neurologic exam varies based on object and location.



Evidence of increasing intracranial pressure: o

Decreasing level of consciousness

o

Falling Glasgow com a scale score

o

Cushing response: bradycardia, hypertension, and dim inished respiratory rate

o

Blown pupil associated with decorticate or decerebrate posturing



Evidence of penetrating injury to head or basilar skull fracture, or object still rem aining in head: o

Raccoon eyes: bilateral ecchym osis of orbits associated with basilar skull fractures

o

Battle sign: ecchym osis behind the ear at m astoid process associated with basilar skull fracture

o

Hem otym panum

o

Cerebral spinal fluid rhinorrhea or otorrhea

Essential Workup 

Determ ine the weapon type or caliber of weapon at scene.



Thorough exam to assess extent of injuries



Neurologic exam : o

Alteration in level of consciousness and neurologic exam varies based on object and location.

o

Evidence of penetrating injury to head

Tests Lab 

Com plete blood count



Platelet count

Pa ge 2 1 3



Coagulation perim eters



Type and cross-m atch.



Electrolytes, blood urea nitrogen, and creatinine baseline levels

Imaging 

CT of head depicts location of lesion and extent of dam age.



Skull radiographs m ay reveal depth of im palem ent, location of bone fragm ents, and presence of fragm ents within the cranium .



Cervical spine evaluation (when indicated): o

Helical CT scanning or anteroposterior, lateral, and odontoid views plain radiographs

Differential Diagnosis 

Blunt head traum a



Basilar skull fracture



Any condition that alters m ental status that m ay have induced a fall and caused secondary penetrating traum a

Treatment Pre Hospital 

Stabilize, but do not rem ove, foreign object (e.g., knife).



Determ ine the weapon type or caliber of weapon at scene.



Protect and m anage the airway to avoid hypoxem ia.



Avoid hyperventilation.



Maintain cervical spine precautions.



Transport to traum a center.



Avoid hypoxia (oxygen saturation <90%): o

100% oxygen

Pa ge 2 1 3



Avoid hypotension (systolic blood pressure<90 m m Hg): o

Intravenous crystalloid solutions

Initial Stabilization 

Airway, breathing, and circulation m anagem ent



Rapid-sequence intubation: o

For Glasgow com a scale <8, inability to protect airway, hypoxia or cerebral herniation

o

Medications include etom idate or fentanyl as induction agent, succinylcholine (pretreat with m inidose paralytic), rocuronium , or vecuronium ; and m orphine sulfate for ongoing sedation

o

Caution with fentanyl in the hem odynam ically labile patient

o

Norm alize PCO 2 . Avoid hyperventilation or hypoventilation.



Intravenous catheter placem ent



Crystalloid solution to m aintain systolic blood pressure >90 m m Hg



Address other sources of associated traum a.



Cervical spine precautions should be m aintained.

P.477

ED Treatment 

Early neurosurgical consultation



If patient has evidence of cerebral herniation (see Signs and Sym ptom s), initiate m easures to decrease intracranial pressure: o

Mild hyperventilation: 16â€“20 breaths per m inute in adults, 20â€“24 breaths per m inute in children, and 24â€“26 breaths per m inute in infants to keep PaCO 2

Pa ge 2 1 3

about 35, which correlates to an end tidal CO 2 of 32â€“35 m m Hg o

Elevating head of bed 20â€“30Â°

o

Mannitol boluses intravenously: Do not adm inister m annitol unless systolic blood pressure >100 m m Hg and patient is adequately fluid resuscitated.



Phenytoin intravenously to prevent early posttraum atic seizures



Glucocorticoids are not recom m ended to lower intracranial pressure in head traum a patients.



Barbiturates are not recom m ended in the initial em ergency departm ent treatm ent.



Transfuse as needed to keep hem atocrit >30%.



If definitive neurosurgical care is not im m ediately available, a single burr hole m ay preserve life until neurosurgical intervention can be attained: o

Perform only in com atose patients with decerebrate or decorticate posturing on the side of a known m ass lesion/hem atom a who have not responded to initial treatm ent.



Avoid hypotherm ia, which will increase risks of coagulopathy during surgery.



Maintain NPO status.



Surgery: o

Based on clinical and radiologic findings and neurosurgical consultation

Medication (Drugs) 

Etom idate: 0.2â€“0.3 m g/kg IV



Fentanyl: 3â€“5 Âµg/kg IV: o

If systolic blood pressure >100 m m Hg

Pa ge 2 1 3



Mannitol: 0.25â€“1 g/kg IV bolus



Morphine sulfate: 2â€“20 m g IV (peds: 0.1 m g/kg up to adult doses)



Phenytoin: 15â€“20 m g/kg IV up to 1,000 m g



Rocuronium : 0.6 m g/kg IV



Succinylcholine: 1â€“2 m g/kg IV



Vecuronium brom ide: 0.1 m g/kg IV: o

Pretreatm ent m inidose: 0.01 m g/kg IV

Follow-Up Disposition Admission Criteria Adm it all patients to intensive care unit or transport directly to surgery.

Discharge Criteria Do not discharge.

References 1. Brain Traum a Foundation. Guidelines for Prehospital Managem ent of Traum atic Brain Injury. New York: Brain Traum a Foundation; 1999. 2. Brain Traum a Foundation. Managem ent and Prognosis of Severe Traum atic Brain Injury. New York: Brain Traum a Foundation; 2000. 3. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determ ining outcom e from severe head injury. J Traum a. 1993;34:216â€“222. 4. Com m ittee on Traum a. Head traum a: Advanced Traum a Life Support. 7th ed. Chicago: Am erican College of Surgeons; 2002. 5. King BS, Gupta R, Narayan RK. The early assessm ent and

Pa ge 2 1 3

intensive care unit m anagem ent of patients with severe traum atic brain and spinal cord injuries. Surg Clin North Am . 2000;80(3):855â€“870.

Codes ICD9-CM 959.01 Head injury, unspecified

ICD10 S01.9 Open wound of head, part unspecified

Pa ge 2 1 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache, C luster

Headache, Cluster

Gary Johnson

Basics Description 

Not clearly understood, but m ay be result of vasoactive substances released from m ast cells



May have m any clinical and pathophysiologic sim ilarities with m igraine and variants

Etiology 

Cause is unclear at present.



Affects 0.1% of the population

Diagnosis Signs and Symptoms History 

Occurs predom inantly in m iddle-aged m en



Episodes are often nocturnal and are m ore com m on in spring and fall.



Headaches occur in clusters, several tim es per day for weeks or m onths at a tim e.

Pa ge 2 1 4



Attacks are m ore likely after ingestion of alcohol, nitroglycerine, or histam ine-containing com pounds.



More likely in tim es of stress, prolonged strain, overwork, and upsetting em otional experiences



No prodrom e or aura



Unilateral, excruciating, nonthrobbing, incapacitating headache



Pain is ocular or retrobulbar



Rarely lasts longer than 2 hours; often lasts a few m inutes

Physical Exam 

Com plete neurologic exam



Nasal congestion, lacrim ation, rhinorrhea, conjunctival injection, or facial flushing on the sam e side as headache



Horner syndrom e m ay be seen.

Essential Workup 

An accurate history and physical exam ination should confirm the diagnosis.



Life-threatening alternatives need to be ruled out.

Tests Lab 

Lum bar puncture (if m eningitis or subarachnoid hem orrhage is suspected)



Erythrocyte sedim entation rate (ESR; if tem poral arteritis is suspected)

Imaging CT scan/MRI (to rule out hem orrhage, tum or)

Differential Diagnosis 

Migraine headache



Trigem inal neuralgia



Meningitis

Pa ge 2 1 4



Tem poral arteritis



Intracerebral m ass lesion



Herpes zoster



Intracerebral bleed



Dental causes



Orbital/ocular disease (acute glaucom a)



Tem poral m andibular joint syndrom e

Treatment Pre Hospital 

Recognize m ore severe life-threatening causes of headache.



Adm inistration of oxygen by face m ask m ay alleviate sym ptom s.

Initial Stabilization 

Rule out life-threatening causes of headache.



Adm inistration of supplem ental oxygen

Medication (Drugs) 

Ergots: DHE 1 m L IV; repeat in 1 hour if necessary



Fentanyl: 2â€“3 Âµg/kg IV



Meperidine: 50â€“75 m g IM or IV



Morphine: 2â€“4 m g IV or IM, m ay repeat q10m in



Nonsteroidal anti-inflam m atory drugs (NSAIDs): ketorolac 15â€“30 m g IM or IV



Oxygen: 100% via face m ask



Prochlorperazine: 10 m g IM or IV



Sum atriptan: 6 m g SC, m ay repeat in 1 hour (m ax. of 2

Pa ge 2 1 4

doses in 24 hours) P.481

Follow-Up Disposition Admission Criteria 

Persistent headache unresponsive to usual m easures



Unclear headache diagnosis

Discharge Criteria 

Patients with m oderate to com plete pain relief, a norm al neurologic exam , and with a confident diagnosis of cluster headache

Issues for Referral Follow-up with a neurologist should be arranged.

References 1. Diener HC. Advances in the field of headache 2003/2004. Curr Opinion Neurol. 2004;17(3):271â€“273. 2. Diam ond S. The m anagem ent of m igraine and cluster headaches. Com pr Ther. 1995;21(9):492â€“498. 3. Kum ar KL. Recent advances in the acute m anagem ent of m igraine and cluster headaches. J Gen Intern Med. 1994;9(6):339â€“348.

Codes ICD9-CM 346.20

Pa ge 2 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache, M igraine

Headache,

Migraine Gary Johnson

Basics Description 

Poorly understood. May involve vasoconstriction, cortical excitation, or both



May begin with intracranial artery vasoconstriction: o

Results in reduced cerebral blood flow and aura; type of which is dependent on the area of reduced flow

o

Followed by rebound vasodilation of arteries during which headache occurs

o 

Arterial dilation, plasm a leak m ay cause pain.

Trigem inal nerve activation m ay account for headache.

Pediatric Considerations Migraines do present in the pediatric age group, but are less com m on.

Etiology 

Idiopathic



May be precipitated by chocolate, cheese, nuts, alcohol, sulfites, m onosodium glutam ate (MSG), stress, or puberty.

Pa ge 2 1 4



Fam ily history of m igraines in 60% of cases



Affects 5â€“15% of the population: o

Wom en 3 tim es m ore than m en

Diagnosis Signs and Symptoms History 

Com m on m igraine: o

Headache is recurrent, throbbing, and frequently unilateral.

o

Usually associated with photophobia, phonophobia, nausea, and vom iting



Classic m igraine: o

Sim ilar to com m on m igraine except it is preceded by a prodrom e; often visual sym ptom s such as bright lights, selective field defects, or jagged lines



Com plex m igraine: o

Migraine headache with associated focal neurologic sym ptom s such as num bness, weakness, paralysis, or aphasia

Essential Workup 

An accurate history and physical exam should confirm the diagnosis.



Patients with new onset of headache syndrom e need an objective evaluation to rule out m ore serious causes of severe headaches: o

Com plete neurologic exam ination

o

Im aging m ay be appropriate in ED.

Tests

Pa ge 2 1 4



Not needed for classic m igraine or established m igraines with typical sym ptom s



Lum bar puncture (LP) if m eningitis, subarachnoid hem orrhage, or pseudotum or cerebri is suspected



Erythrocyte sedim entation rate (ESR) if tem poral arteritis is suspected



Carbon m onoxide (CO) level if there is history or suspicion of CO exposure



Intraocular pressure m easurem ents if suspect glaucom a

Imaging CT or MRI of the head

Diagnostic Procedures/Surgery Lum bar puncture (LP)

Differential Diagnosis 

Meningitis/encephalitis



Subarachnoid/intracranial hem orrhage



Cerebral ischem ia (if com plex m igraine)



Hypertension



Brain tum or



Carbon m onoxide intoxication



Tem poral m andibular joint (TMJ) syndrom e



Glaucom a



Pseudotum or cerebri



Tem poral arteritis

P.483

Treatment

Pa ge 2 1 4

Pre Hospital 

It is im portant to recognize life-threatening causes of headache and transport rapidly: o

Sudden onset of sym ptom s, altered m ental status, neck stiffness, fever, or neurologic deficit is a useful sign that suggests a m ore serious cause of headache.

o

Prior history of sim ilar headache, absence of above sym ptom s, or strong fam ily history is m ore suggestive of m igraine.



Allow patients with m igraine headache to be in a calm , dark environm ent.

Initial Stabilization Patients with convincing evidence of increased intracranial pressure m ay need rapid-sequence intubation and controlled ventilation.

ED Treatment 

Abortive therapy and pain m anagem ent are the prim ary issues for patients in whom life-threatening causes of headache have been ruled out.



Generally, abortive therapy options should be attem pted first.



Narcotic pain m edications m ay be adm inistered as rescue therapy.



Intravenous saline hydration is often a helpful adjunct for m igraine headaches.

Medication (Drugs) 

Abortive therapy in ED: o

Sum atriptan: 6 m g SC or nasally; m ay repeat in 1 hour (m ax. 2 doses per 24 hours). Newer triptans

Pa ge 2 1 4

have also shown efficacy. o

Ergot alkaloids: DHE 1 m g IM or IV, then repeat in 1 hour if necessary.



o

Droperidol (if ECG norm al): 0.625â€“2.5 m g IM/IV

o

Metoclopram ide: 10 m g IV

o

Prochlorperazine: 10 m g IV

o

Valproic acid: 250â€“1000 m g IV

Rescue pain m edication: o

Hydrom orphone: 1â€“2 m g IM/IV per dose

o

Morphine: 2â€“10 m g IM/IV per dose

o

Nonsteroidal anti-inflam m atory drugs (NSAIDs): ketorolac 15â€“30 m g IM/IV



Prophylactic therapy: o

Beta-blockers: propranolol 40 m g PO b.i.d.

o

Ca 2 + channel blockers: verapam il 40 m g PO t.i.d.

o

Cyclic antidepressants: am itriptyline 25 m g PO t.i.d.

o

Topiram ate: 50â€“200 m g PO daily

Follow-Up Disposition Admission Criteria 

Severe intractable headache pain



Intractable vom iting, electrolyte im balance, or inability to take oral food or fluid



Unresolved com plex m igraines

Discharge Criteria Patients with m oderate to com plete pain relief, a norm al neurologic exam , and a confident diagnosis of m igraine

Issues for Referral

Pa ge 2 1 4

Rapidly evolving therapeutic options suggest neurologic follow-up is im portant.

References 1. Diener HC. Advances in the field of headache 2003/2004. Curr Opinion Neurol. 2004;17(3):271â€“273. 2. Green MW. The em ergency m anagem ent of headaches. Neurologist . 2003;9(2):93â€“98.

Codes ICD9-CM 346.90

Pa ge 2 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache

Headache

Richard Wolfe Jonathan A. Edlow

Basics Description 

Prolonged pain in the cranial vault, orbits, or nape of the neck



Intracranial and extracranial pain-sensitive structures project pain to the cranial surface. o

o

Intracranial: 

Circle of Willis blood vessels



Medium -size arteries and m ajor branches



Large veins



Dura



Meninges

Extracranial: 

Skin, scalp, fascia, m uscles



Mucosal linings of the sinuses



Arteries



Tem porom andibular joints



Teeth



Pain is transm itted via the 5th cranial nerve.



Pain m ay be caused by a num ber of m echanism s:

Pa ge 2 1 5

o

Nerve irritation

o

Traction on pain-sensitive vessels

o

Vasodilatation of pain-sensitive vessels: 

Hypoxia, hypercapnia, fever, histam ine injection, nitroglycerin ingestion, or a sudden rise in blood pressure



o

Prolonged contraction of cranial m uscles

o

Inflam m ation of pain-sensitive structures

o

Nonorganic pain

2â€“4% of all ED visits have a chief com plaint of headache o

95% have a benign etiology

o

Life-threatening etiologies are rare but difficult to diagnose and often m issed.

Etiology 

Vascular: o

Intra/extracranial vasodilatation and constriction of pain-sensitive blood vessels

o

Severe, throbbing headache

o

Divided into m igraine (the m ajority) and vascular nonm igrainous

o

Triggered by stress, horm one fluctuations, lack of sleep, certain foods



Tension: o

Unknown (possibly serotonin im balance, decreased endorphins)

o

Most com m on type of chronic recurring headache

o

Secondary to sustained contraction of head and neck m uscles

o

Triggered by poor posture, stress, anxiety, depression, cervical osteoarthritis



Cluster headaches: o

Triggered by alcohol, certain foods, altered sleep

Pa ge 2 1 5

habits, strong em otions 

Intracranial (traction): o

Mass lesions inside the calvarium stretching arteries and other pain-sensitive structures



Extracranial: o

Pathology from an extracranial site causing pain in a peripheral nerve of the head and neck





Unassociated with a structural lesion: o

Idiopathic stabbing headache

o

Cold stim ulus headache

o

Benign cough headache

o

Benign exertional headache

Other headaches: o

Multiple etiologies depending on cause (see differential diagnosis)

Diagnosis Signs and Symptoms History 

Attributes of the painâ€”PQRST: o

Provocative and palliative features: 

Position of the head, effect of coughing, straining, and m ovem ent

o

Quality: 

Throbbing or continuous



Deep or superficial



Change com pared with any prior headaches

o

Region

o

Severity:

Pa ge 2 1 5

 o

Tim ing: 





Is this the worst headache of the patient's life?

Is the onset sudden or gradual?

Associated findings: o

Visual sym ptom s

o

Dizziness

o

Nausea or vom iting

Historical factors indicating testing beyond the history and physical exam ination: o

o

New onset: 

Over the age of 50 years



In an HIV patient



In a cancer patient

Severe headache or â€œworst headache of m y lifeâ€ •

o 

Persistent vom iting

Risk factors for cerebral sinus throm bosis: o

Malignancy

o

Pregnancy

o

Protein S or C deficiency

o

Oral contraceptive

o

Ulcerative colitis

o

BehÃ§et syndrom e

Physical Exam 

Factors indicating testing beyond the history and physical exam ination: o

Abnorm al vital signs: 

Diastolic blood pressure >130 m m Hg



Fever

o

Altered level of consciousness

o

Papilledem a

o

Abnorm al neurologic findings or m eningism us

Pa ge 2 1 5



Tension: o

Most com m on recurrent pain syndrom e: 



o

Bilateral

o

Nonpulsatile

o

Bandlike

o

Mild to m oderate intensity

o

4- to 13-hour duration

Cluster: o



Requires 10 or m ore attacks of a specific nature

See Headache, Cluster

Migraine: o

See Headache, Migraine

Essential Workup 

Detailed history and CNS, head, eyes, ears, nose, and throat and neck exam ination



Dependent on the clinical differential diagnosis

Tests Lab 

Lab tests should be ordered only when the history or physical exam ination suggests threatening etiologies.



Erythrocyte sedim entation rate: o

If tem poral arteritis or other inflam m atory disorders suspected 

See Tem poral Arteritis

Imaging 

Head CT scan: o

Indications: 

Unclear diagnosis based on history and physical exam ination



Signs of increased intracranial pressure

Pa ge 2 1 5



Worst or first headache



Abrupt onset



Focal neurologic abnorm alities



Papilledem a



Recurrent m orning headache



Persistent vom iting



Headache associated with fever, rash, and nausea without system ic illness



Head traum a with loss of consciousness, focal neurologic findings, or lethargy

 o

Altered m ental status, m eningism us

> 95% sensitive for subarachnoid hem orrhage (SAH) <24 hours old (but sensitivity falls rapidly with tim e and is 50% at 7 days out)

o

Must do lum bar puncture (LP) if SAH suspected and CT is negative



Sinus im aging



Vascular assessm ent with angiogram or m agnetic resonance angiography (MRA): o

May be indicated if nonm igrainous vascular cause suspected



MRI o

Indicated to assess for etiologies that are m issed by CT scan and LP: 

Posterior fossa lesion (not im aged well on CT)



Pituitary apoplexy (this m ay be visualized with newer generation CT scanners)

 

Cerebral sinus throm bosis

MRA: o

Indicated if subarachnoid hem orrhage suspected, CT is negative, and unable to perform LP

o

Also for suspicion of carotid or vertebral dissection

Pa ge 2 1 5

P.479

Diagnostic Procedures/Surgery LP: 

Perform CT first if any of the following are present: o

New focal neurological finding

o

Papilledem a

o

Abnorm al m ental status

o

HIV positive



Intracranial infections



Detect blood not evident on CT scan



Note that there is no specific threshold num ber of red cells below which SAH is excluded and that the RBC count is a function of tim e from onset of headache.



Measure opening pressure to help diagnose pseudotum or cerebri and cerebral venous throm bosis and to help distinguish traum atic tap versus true hem orrhage.



Xanthochrom ia: o

Should be visible by spectrom etry 12 hours after onset of a subarachnoid hem orrhage

o

Spectrophotom etry has a high false-positive rate.

o

Visual inspection is the m ost com m only used m ethod in North Am erica.

Differential Diagnosis Acute Single Headache 

Single episode presenting within hours of onset



Subarachnoid hem orrhage



Meningitis: o

Bacterial

o

Viral

Pa ge 2 1 5

o 

Malaria

Vascular: o

Acute intracerebral hem orrhage

o

Hypertension

o

Cranial artery dissection

o

Cerebral venous sinus throm bosis

Ocular 

Acute narrow-angle glaucom a



Pituitary apoplexy



Tem poral neuritis



Traum atic: o

Intracranial hem orrhage

o

Postdural puncture headache

o

Acute posttraum atic headache



Acute sinusitis



Metabolic:



o

Fever

o

Hypoglycem ia

o

High-altitude disease

Toxic: o



Carbon m onoxide poisoning

Withdrawal: o

Narcotics

o

Benzodiazepines

o

Alcohol

Acute Recurrent Headache 

Presenting within days to weeks of onset



Cerebral sinus throm bosis



Pseudotum or cerebri



Tem poral arteritis



Subarachnoid hem orrhage (rebleed)

Pa ge 2 1 5



Migraine



Cluster



Tension



Hypoxic: o

Sleep apnea

o

Anem ia



Trigem inal neuralgia



Postherpetic neuralgia



Coital and exertional headache

Subacute Headache 

Presenting within weeks to m onths of onset



Chronic subdural hem atom a



Brain tum or



Brain abscess



Chronic sinusitis



Tem perom andibular joint syndrom e



Chronic posttraum atic headache



Pseudotum or cerebri (idiopathic intracranial hypertension)



Tem poral arteritis



HIV

Chronic Headache 

Presenting within m onths to years of onset



Chronic tension headache



Transform ational m igraine



Analgesic abuse/rebound



Depression



Extracranial: o

Trigem inal neuralgia: transient, shock-like facial pain

o

Tem poral arteritis: elderly, severe, scalp artery tenderness/swelling

o

Metabolic: severe anem ia

Pa ge 2 1 5

o

Acute glaucom a: nausea/vom iting, eye pain, conjunctival injection, increased intraocular pressure

o

Cervical: spondylosis, traum a, arthritis

o

Tem porom andibular joint syndrom e

Treatment Initial Stabilization 

ABCs if altered m ental status.



Em piric antibiotics if bacterial m eningitis is suspected.

ED Treatment 

Tension: o

Aspirin

o

Acetam inophen

o

NSAID

o

Nonpharm acologic (m editation, m assage, biofeedback)



For other etiologies see relevant chapters

Medication (Drugs) 

Chlorprom azine: 25â€“50 m g IM/IV (peds: 0.5â€“1 m g/kg/dose IM/IV/PO) q4hâ€“q6h



Dihydroergotam ine: 1 m g IM/IV, repeat q1h; m ax. 3 m g



Ergotam ine: 2 m g PO/SL at onset, then 1 m g PO q30 m inutes; m ax. 10 m g/week



Ketorolac: 30â€“60 m g IM; 15â€“30 m g IV once, then 15â€“30 m g q6h (peds: 1 m g/kg IV q6h)



Lidocaine 4%: 1 m L intranasal on sam e side as sym ptom s



Metoclopram ide: 5â€“10 m g PO/IV/IM q6hâ€“q8h

Pa ge 2 1 5



Morphine: 2.5â€“20 m g (peds: 0.1â€“0.2 m g/kg/dose) IM/IV/SC q2hâ€“q6h



Prochlorperazine: 5â€“10 m g IV/PO/IM t.i.d.â€“q.i.d.; m ax. 40 m g/d



Sum atriptan: 6 m g SC, repeat in 1 hour, up to 12 m g/24h

Follow-Up Disposition Admission Criteria 

Headache secondary to suspected organic disease



Chronic daily headache, pain refractory to outpatient m anagem ent



Persistent m igraine with intractable vom iting and dehydration



Headache com plicated by significant surgical or m edical history



Intracranial infection



Intracranial hem orrhage

Discharge Criteria 

Most m igraine, cluster, and tension headaches after pain relief



Local or m inor system ic infections

References 1. Edlow JA. Headache. In: Harwood-Nussâ€™ Clinical practice of em ergency m edicine. 4th ed. Philadelphia: 2005:94â€“100. 2. Perkins AT, Ondo W. When to worry about headache: head pain as a clue to intracranial disease. Postgrad Med. 1995;98(2):197â€“208. 3. Edlow JA. Diagnosis of subarachnoid hem orrhage in the em ergency

Pa ge 2 1 6

departm ent. Em erg Med Clin North Am . 2003;21(1):73â€“87

Codes ICD9-CM ICD9: 784.0 ICD10: R51

Pa ge 2 1 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Heart M urm ur

Heart Murmur

Leon D. Sanchez Jennifer De La Pena

Basics Description Abnorm al heart caused by functional or structural defect of the heart

Genetics Congenital defects of cardiac structures

Pathophysiology 

Stenotic lesions lead to pressure overload in the cham ber preceding the valve.



Pressure overload leads to hypertrophy of the cham ber in an attem pt to overcom e the increased resistance.



Regurgitant lesions lead to volum e overload of the cham ber preceding the valve.



Volum e overload leads to cham ber dilatation in an attem pt to accom m odate the regurgitant blood volum e.

Etiology 

Aortic stenosis: o

Rheum atic heart disease

o

Congenital bicuspid valve

o

Calcification of valve from aging

Pa ge 2 1 6

o 



Aortic regurgitation: o

Rheum atic heart disease

o

Endocarditis

o

Aortic dissection

o

Prosthetic valve

Idiopathic hypertrophic subaortic stenosis: o



Prosthetic valve

Congenital

Mitral stenosis: o

Rheum atic heart disease

o

Rheum atologic disorders (system ic lupus erythem atosus)









o

Calcification

o

Cardiac tum ors (atrial m yxom a)

o

Congenital

o

Prosthetic valve

Mitral regurgitation, acute: o

Endocarditis

o

Papillary m uscle dysfunction

o

Rupture of papillary m uscle

o

Rupture of chordae tendineae

o

Prosthetic valve

Mitral regurgitation, chronic: o

Rheum atic heart disease

o

Mitral valve prolapse

o

Connective tissue disease (Marfan disease)

Mitral valve prolapse: o

Congenital

o

Connective tissue disease

Tricuspid stenosis: o



Rheum atic heart disease

Tricuspid regurgitation:

Pa ge 2 1 6



o

Rheum atic heart disease

o

Endocarditis

o

Pulm onary hypertension

Patent ductus arteriosus: o



Congenital

Pericardial friction rub: o

Pericarditis

o

Pericardial effusion

Diagnosis Signs and Symptoms 

Aortic stenosis: o

Systolic crescendo-decrescendo m urm ur radiating to carotids

o

Carotid pulse is described as parvus and tardus (dim inished intensity and late upstroke).



o

Angina

o

Dyspnea on exertion

o

Exertional syncope

Aortic regurgitation: o

Diastolic blowing m urm ur at left sternal border

o

Austin Flint m urm ur is a diastolic rum ble from exposure of the m itral valve to the aortic regurgitant flow.

o

Pulm onary edem a

o

Dyspnea

o

Tachycardia

o

Chest pain

o

Pulse pressure m ay be widened.

o

Corrigan pulse or water ham m er pulse, a rapid

Pa ge 2 1 6

upstroke and downstroke of the carotid pulse



o

Quincke pulse, pulsations seen at the nail beds

o

Musse sign: bobbing with carotid pulse

Idiopathic hypertrophic subaortic stenosis: o

Systolic, harsh, crescendo-decrescendo m urm ur heard at left sternal border

o

Increases in volum e of the left ventricle at end diastole will decrease the intensity of the m urm ur.





o

Dyspnea

o

Chest pain

o

Exertional syncope

o

Sudden death

Mitral stenosis: o

Diastolic, rum bling m urm ur heard at the apex

o

Loud S 1 with an opening snap

o

Dyspnea

o

Orthopnea

o

Hem optysis

o

Pulm onary edem a

o

Em boli to system ic circulation

o

Atrial fibrillation

Mitral regurgitation, acute: o

Systolic, harsh, crescendo-decrescendo m urm ur heard at the base

o 

Pulm onary edem a

Mitral regurgitation, chronic: o

Holosystolic m urm ur heard at the apex radiating to the axilla



o

Dyspnea on exertion

o

Fatigue

o

Atrial fibrillation is com m on.

Mitral valve prolapse:

Pa ge 2 1 6

o

Early to m idsystolic click often followed by systolic m urm ur





o

Palpitations

o

Chest pain

Tricuspid stenosis: o

Diastolic, high-pitched m urm ur

o

Peripheral edem a

o

Hepatosplenom egaly

o

Ascites

o

Fatigue

o

Atrial fibrillation is com m on.

o

Large A wave in the jugular venous pulse

Tricuspid regurgitation: o

Holosystolic, blowing m urm ur best heard along the left sternal m argin





o

Peripheral edem a

o

Hepatosplenom egaly

o

Ascites

o

Atrial fibrillation is com m on.

o

Large V wave in the jugular venous pulse

Patent ductus arteriosus: o

Continuous m achinery m urm ur

o

Congestive heart failure

Pericardial friction rub: o

Interm ittent m urm ur

o

May have systolic and/or diastolic com ponent

o

Sym ptom s owing to pericarditis or pericardial effusion

Essential Workup For m ore details, see Valvular Heart Disease, Mitral Valve Prolapse, Congenital Heart Disease, Patent Ductus Arteriosus, Pericarditis, and Pericardial Effusion/Tam ponade.

Pa ge 2 1 6

P.485

Tests Lab 

Serum : o



CBC

Urine

Imaging 

Electrocardiogram



Chest radiograph



Echocardiogram : o



Evaluate valves, cham bers, flow.

Com puted tom ography o

Rule out aortic dissection.

Diagnostic Procedures/Surgery Acute regurgitant lesions: 

Cardiac catheterization

Differential Diagnosis See Etiology

Treatment Pre Hospital 

IV fluids: o

Patients with critical aortic stenosis are very sensitive to fluid shifts.



Oxygen as appropriate

Pa ge 2 1 6

Initial Stabilization 

Oxygen



IV access



Cardiac m onitor



Treat sym ptom s (congestive heart failure, dysrhythm ias).



Exercise care with fluids and m edications in aortic stenosis.

ED Treatment 

For m ore details, see Valvular Heart Disease, Mitral Valve Prolapse, Congenital Heart Disease, Patent Ductus Arteriosus, Pericarditis, and Pericardial Effusion/Tam ponade.



Intra-aortic balloon pum p m ay be a useful tem porizing m easure.



Antibiotics for endocarditis



Treat pulm onary edem a and dysrhythm ias as appropriate.



Avoid diuretics and inotropes in idiopathic hypertrophic subaortic stenosis.



Anticoagulation as necessary for atrial fibrillation

Medication (Drugs) 

Digoxin: 0.5 m g IV, then 0.25 m g IV 6 and 12 hours later



Diltiazem (Cardizem ): o

0.25 m g/kg (17.5 m g for 70-kg person) IV over 2 m inutes



o

May rebolus after 15 m inutes with 0.35 m g/kg IV

o

Start drip at 5â€“15 m g per hour.

Furosem ide (Lasix): o

20â€“80 m g IV; m ay increase dose if necessary

o

Max. of 600 m g per 24 hours

Pa ge 2 1 6





Heparin: o

80-U/kg bolus IV, then drip at 18 U/kg per hour

o

Monitor partial throm boplastin tim e.

Metoprolol (Lopressor): 5 m g IV q5â€“15m in for 3 doses, as tolerated







Nitroglycerin: o

10â€“20 Âµg per m inute IV

o

Titrate to effect.

o

Max. 300 Âµg per m inute

Nitroprusside: o

0.3 Âµg/kg per m inute IV

o

Titrate to effect

o

Max. 10 Âµg/kg per m inute

o

Protect bag from light

o

Thiocyanate toxicity from prolonged use

Propranolol (Inderal): 1 m g IV q2m in

Surgery 

As indicated



Acute m itral and aortic regurgitation m ay require em ergency surgery.



Critical aortic stenosis requires surgery to im prove m ortality.

Follow-Up Disposition Admission Criteria 

Signs of cardiac ischem ia



Syncope or near syncope



Pulm onary edem a

Pa ge 2 1 6



Hem odynam ic instability



Endocarditis



Arrhythm ia

Discharge Criteria 

Asym ptom atic



Hem odynam ically stable

References 1. Carabello BA, Crawford FA. Valvular heart disease. N Engl J Med. 1997;337:32â€“41. 2. Dunm ire SM. Infective endocarditis and acquired valvular heart disease. In: Rosen P, Barkin R, Danzl DF, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1998:1745â€“1754. 3. http://www.blaufuss.org/tutorial/ 4. http://www.sprojects.m m ip.m cgill.ca/MVS/MVSTETH.HTM

Codes ICD9-CM 785.2 Undiagnosed cardiac m urm urs

ICD10 R01.1 Cardiac m urm ur, unspecified

Pa ge 2 1 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > HELLP Syndro m e

HELLP Syndrome

Michael J. Bono

Basics Description 

HELLP syndrom e: hem olysis, elevated liver enzym es, and l ow platelets



Signs/sym ptom s of hem olysis, abnorm al liver function tests, and throm bocytopenia were recognized 100 years ago.



Weinstein coined the term HELLP syndrom e in 1982.



Liver involvem ent is hallm ark: o



Other organs m ay be involved (e.g., brain, kidneys).

HELLP syndrom e recently divided into three groups, representing severity of the disease; severity is directly related to the platelet count: o

Class 1: m ost severe form ; platelet nadir <50,000 cells/ÂµL

o

Class 2: less severe; platelet nadir between 50,000 and 100,000 cells/ÂµL

o

Class 3: least severe; platelet nadir between 100,000 and 150,000 cells/ÂµL



Most m aternal deaths occur with class 1.



Increased m ortality rate is associated with hem orrhage in

Pa ge 2 1 7

the hepatic or central nervous system s or vascular insult to the cardiopulm onary or renal system s.

Pediatric Considerations Perinatal m ortality is greater in infants of wom en with HELLP.

Epidemiology Incidence 0.3% of all pregnancies

Risk Factors 

Frequently white, m ultiparous, older pregnant wom en: o



Second trim ester

Pre-eclam psia/eclam psia: o

Twenty percent of wom en with pre-eclam psia/eclam psia will develop HELLP.

Etiology 

Unclear



Vasospasm is the basis: o

Vascular constriction causes resistance to blood flow and hypertension.

o

Vasospasm probably dam ages vessels directly.

o

Angiotensin II causes endothelial cells to contract.

o

Endothelial cell dam age and interendothelial cell leaks are the result.



Sm all-vessel leaks: o

Platelets and fibrinogen get deposited subendothelially.

o 

Fibrin deposition develops in severe cases.

Vascular changes and local tissue hypoxia lead to hem orrhage, necrosis, and end organ dam age.

Pa ge 2 1 7

Diagnosis Signs and Symptoms 

Nausea



Vom iting



Moderate to severe epigastric or right upper quadrant pain: o

Epigastric pain and nausea increase as the severity of HELLP worsens.



Headache



Possible visual changes



May present with flulike sym ptom s such as fatigue or m alaise



Continuum with severe pre-eclam psia; m ost patients will be hypertensive: o



May not have systolic or diastolic hypertension

Sym ptom s of significant m orbidity: o

Cardiogenic/noncardiogenic pulm onary edem a

o

Cardiac or pulm onary arrest

o

Pulm onary em bolus

o

Chest pain with m yocardial ischem ia

o

Hypertensive encephalopathy

o

Cerebral edem a with change in m ental status

o

Seizures, blindness

o

Hem orrhagic cerebrovascular accident

o

Peripheral edem a

o

Ascites

o

Hem aturia

o

Renal failure

Essential Workup 

History and physical exam with attention to sym ptom s of abdom inal pain, nausea, vom iting, and headache

Pa ge 2 1 7



Vital signs with attention to blood pressure (>140/90 is abnorm al)



Im m ediate com plete blood count with platelet count and sm ear, blood urea nitrogen, creatinine, liver function tests, coagulation profile, and m agnesium level



Urinalysis for protein; screen for urinary tract infections.



Obstetric history:



o

Parity

o

Deliveries

o

Outcom es

Weigh patient to determ ine recent weight gain.

Tests Lab 

Com plete blood count: o

Anem ia

o

Throm bocytopenia

o

Peripheral sm ear dem onstrates m icroangiopathic hem olytic anem ia (burr cells or schistocytes).

o

Other hem olysis m arkers are elevated lactate dehydrogenase (LDH) levels, increased reticulocyte count, and elevated bilirubin levels.



Platelet count and sm ear: o

Less than 100,000 cells per ÂµL



Dissem inated intravascular coagulation screen



Coagulation profile: o

Prothrom bin tim e

o

Partial throm boplastin tim e



Blood urea nitrogen, creatinine, and m agnesium levels



Liver function tests to assess hem olysis m arkers and hepatic dysfunction: o

Elevated aspartate am inotransferase level: >40 IU/L

Pa ge 2 1 7

o

Elevated alanine am inotransferase level: >40 IU/L

o

Elevated lactate dehydrogenase: >600 IU/L

Imaging 

Chest radiograph: o



CT of head: o



Suspected pulm onary edem a

Mental status changes (cerebral edem a)

Ultrasound of the pelvis (transabdom inal or transvaginal): o

Im age fetus and placenta

Alert Determ ination of gestational age and fetal viability is critical in HELLP.

Differential Diagnosis 





Gastrointestinal: o

Cholecystitis

o

Cholelithiasis

o

Biliary colic

o

Pancreatitis

o

Hepatitis

o

Ulcer disease

o

Acute fatty liver of pregnancy

o

Acute gastritis

o

Hiatal hernia

o

Severe gastroesophageal reflux

Hem atologic: o

Pre-eclam psia-associated throm bocytopenia

o

Gestational throm bocytopenia

o

Idiopathic throm bocytopenic purpura

o

Throm botic throm bocytopenic purpura

o

Hem olytic urem ic syndrom e

Neurologic:

Pa ge 2 1 7



o

Epilepsy

o

Encephalitis

o

Meningitis

o

Encephalopathy

o

Brain tum or

o

Intracranial hem orrhage

Other: o

Drug abuse

o

Pyelonephritis

o

Sepsis

P.487

Treatment Pre Hospital Cautions: 

Transport patient in left lateral decubitus position to prevent inferior vena cava syndrom e.



Venous access for anticipated seizure activity



Routine seizure m anagem ent (preferably with m agnesium sulfate) if the patient seizes

Alert Transport to a facility capable of providing high-risk obstetric care.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent



Left lateral decubitus position to prevent inferior vena cava syndrom e



One hundred percent oxygen via face m ask

Pa ge 2 1 7





Maternal m onitoring: o

Cardiac

o

Pulse oxim etry

o

Tocography

Fetal m onitoring

ED Treatment 

Control hypertension with antihypertensives (see Medications): o

Avoid angiotensin-converting enzym e inhibitors because of fetal side effects.



Heparin should be avoided because of bleeding com plications.



Treat pre-eclam psia or eclam psia with intravenous m agnesium sulfate: o

Magnesium sulfate is not given to treat hypertension.



Order type and screen for possible transfusion.



Call for em ergent obstetric consult, consider neonatology consult: o

Consider em ergent delivery.

o

Early plasm a exchange therapy has shown prom ise in postpartum patients with severe disease.



Discuss adm inistration of glucocorticoid with consultant: o

Helps fetal lung m aturity

o

Intravenous dexam ethasone m ore effective than intram uscular betam ethasone



o

Depends on gestational age of fetus

o

Does not reduce disease severity or duration

Lim it intravenous fluid adm inistration unless clinical evidence of dehydration: o

Excess fluids prom ote further capillary leak

o

Lactated Ringer or norm al saline at 60 m L per hour (no m ore than 125 m L per hour)

Pa ge 2 1 7

o

Monitor urine output with Foley catheter.

General Measures Diet As indicated

Activity Com plete bed rest

Special Therapy Blood products: 

Correct throm bocytopenia by platelet transfusion in wom en with platelet counts <20,000 cells/ÂµL, even without active bleeding, as risk of postpartum bleeding is significantly increased.



Platelet counts >40,000 cells/ÂµL are safe for vaginal delivery.



Correct throm bocytopenia to platelet counts >50,000 cells/ÂµL if cesarian delivery planned.



If coagulation dysfunction is present, transfusion with fresh frozen plasm a and packed red blood cells in consultation with obstetrics



Transfusion with packed red blood cells for hem oglobin <10 g/dL

Medication (Drugs) 

Hydralazine: 2.5 m g IV, then 5â€“10 m g q15â€“20 m in: o

Up to 40 m g total dose, to keep diastolic blood pressure <110 m m Hg

o 

Intravenous drip 5â€“10 m g/h titrated

Labetalol: 10 m g IV, then 20â€“80 m g IV q10m in: o

Up to 300 m g total dose

Pa ge 2 1 7

o 



IV drip 1â€“2 m g/m in titrated

Nitroprusside: 0.25 Âµg/kg/m in as a drip: o

Increase 0.25 Âµg/kg/m in q5m in.

o

Use only if no response to hydralazine or labetalol.

Magnesium sulfate: 4â€“6 g in 100 m L IV over 15â€“20 m inutes as loading dose: o

Maintenance drip starting at 2 g/h

o

Titrate to clinical effect

o

Watch for toxicity (antidote is calcium gluconate 10%, 10 m L IV over 3 m inutes).

o

Measure m agnesium sulfate level at 4â€“6 hours; adjust drip to achieve levels between 4 and 7 m Eq/L.

Follow-Up Disposition Admission Criteria 

Adm it all patients to obstetric service for continuous m onitoring of m other and fetus.



After stabilization in the em ergency departm ent, transfer to facility capable of m anaging high-risk obstetric conditions unless delivery is im m inent.



Intensive care unit adm ission: o

Pulm onary edem a

o

Respiratory failure

o

Cerebral edem a

o

Gastrointestinal bleeding with hem odynam ic instability

References 1. Audibert F, Friedm an SA, Frangieh AY, et al. Clinical utility of strict

Pa ge 2 1 7

diagnostic criteria for the HELLP (hem olysis, elevated liver enzym es, and low platelets) syndrom e. Am J Obstet Gynecol. 1996;175:460â€“464. 2. Detti L, Mecacci F, Piccioli A, et al. Postpartum heparin therapy for patients with the syndrom e of hem olysis, elevated liver enzym es, and low platelets (HELLP) is associated with significant hem orrhagic com plications. J Perinatol. 2005;25(4):236â€“240. 3. Eser B, Guven M, Unal A, et al. The role of plasm a exchange in HELLP syndrom e. Clin Appl Throm b Hem ost. 2005;11(2):211â€“217. 4. Helewa M. Hypertensive disorders in pregnancy. In: Cunningham FG, Gant N, Leveno K, et al., eds. William sâ€™ Obstetrics. 21st ed. New York: McGraw-Hill; 2001:567â€“618. 5. Houry D, Abbott J. Acute com plications of pregnancy. In: Marx J, Hockberger R, Walls R, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:2413â€“2433. 6. Isler CM. A prospective, random ized trial com paring the efficacy of dexam ethasone and betam ethasone for the treatm ent of antepartum HELLP (hem olysis, elevated liver enzym es, and low platelet count) syndrom e. Am J Obstet Gynecol. 2001;184:1332â€“1137. 7. Martin JN, Thigpen BD, Moore RC, et al. Stroke and severe preeclam psia and eclam psia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol. 2005;105(2):237â€“238.

Codes ICD9-CM 642.50 Hypertension in pregnancy, childbirth, or the puerperium , not specified as pre-existing, with either album inuria or edem a, or both; specified as severe

ICD10 O14.0 Moderate pre-eclam psia

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem aturia/Pro teinuria

Hematuria/Proteinuria Edward Ullman

Basics Description 

Microscopic hem aturia: three or m ore red blood cells per high-power field in two of three properly collected urine specim ens



Gross hem aturia: visible blood in properly collected urine specim en



Proteinuria: urinary protein excretion of >150 m g per day

Risk Factors 



Risk factors for disease in asym ptom atic proteinuria: o

Diabetes

o

Hypertension

o

NSAID abuse

o

Heroin use

Risk factors for disease in asym ptom atic hem aturia: o

Tobacco use

o

Occupational exposure to benzenes, arom atic am ines, and dyes

o

History of gross hem aturia

o

Age >40 years old

Pa ge 2 1 8

o

History of urologic disorder or disease

o

History of painful voiding

o

History of urinary tract infections (UTI)

o

Analgesic abuse

o

History of pelvic irradiation

Diagnosis Signs and Symptoms 

Dysuria



Blood in urine



Fever



Flank pain



Flank ecchym osis



Initial hem aturia (anterior urethral lesion)



Term inal hem aturia (posterior urethra, bladder, neck, trigone)



Cyclic hem aturia (endom etriosis or urinary tract)



Previous upper respiratory tract infection (10â€“21 days prior)



Previous skin infection (10â€“21 days prior)



Deafness (Alport syndrom e)



Peripheral edem a



Congestive heart failure



Hem optysis (Goodpasture disease)



Concurrent m enstruation



Testicular, epididym al, and prostatic tenderness or traum a



Term inal urethral lesion



Enlarged prostate



Penile/scrotal hem atom a



Atrial fibrillation:

Pa ge 2 1 8

o

Renal artery em bolus or throm bus



Organom egaly, flank m ass



Pregnancy consideration



Headache



Hypertension (greater than 140/90 m m Hg



Right upper quadrant pain

Essential Workup 

Urine dipstick



Urinalysis with m icroscopic analysis



Blood urea nitrogen level



Serum creatinine level



CBC



Pregnancy consideration



Liver function test



Platelet count

Tests Lab 



Urine: o

Culture

o

Cytology

o

Twenty-four-hour urine protein and creatinine levels

o

Spot ratio of urine protein to creatinine

o

Spot ratio of urine protein to osm olality

o

Protein electrophoresis

Serum : o

Coagulation studies

o

Protein electrophoresis

Imaging 

Helical CT scan



Renal ultrasound

Pa ge 2 1 8

Diagnostic Procedures/Surgery 

Cystourethroscopy



Urethrogram



Cystogram



Retrograde pyelogram



Intravenous pyelogram

Differential Diagnosis 



Glom erular hem aturia: o

IgA nephropathy (Berger disease)

o

Postinfectious glom erulonephritis

o

Mem branoproliferative glom erulonephritis

o

Focal glom erular sclerosis

o

Lupus nephritis

o

Wegener granulom atosis

o

Polyarteritis nodosa

o

Henoch-SchÃ¶nlein syndrom e

o

Throm botic throm bocytopenic purpura

o

Hem olytic urem ic syndrom e

o

Alport syndrom e

o

Goodpasture disease

Nonglom erular hem aturia: o

Infection (pyelonephritis, tuberculosis, schistosom iasis)

o

Inflam m ation (drug induced, radiation induced)

o

Renal and extrarenal tum or

o

Interstitial nephritis

o

Papillary necrosis

o

Polycystic kidney disease

o

Medullary sponge disease

o

Renal artery em bolism /throm bosis

o

Renal vein throm bosis

Pa ge 2 1 8

o

Sickle cell disease

o

Malignant hypertension

o

Hypercalcuria

o

Hyperuricosuria

o

Urolithiasis

o

Strictures

o

Endom etriosis

o

Foreign bodies

o

Benign prostatic hypertrophy

o

Coagulopathy/bleeding disorders

o

Traum a (renal pedicle injuries, urethral disruptions, bladder rupture)



o

Recent instrum entation

o

Frequent or interrupted coitus

o

Factitious

Glom erular proteinuria (>2 g per day): o

Minim al-change disease

o

Mem branous glom erulonephritis

o

Focal segm ental glom erulonephritis

o

Mem branoproliferative glom erulonephritis

o

Diabetes m ellitus

o

Collagen vascular diseases

o

Am yloidosis

o

Pre-eclam psia

o

Infection (HIV, hepatitis B, hepatitis C, poststreptococcal infection, syphilis)



o

Lym phom a

o

Chronic renal transplant rejection

o

Heroin use

o

Penicillam ine

Tubular proteinuria: o

Hypertensive nephrosclerosis

Pa ge 2 1 8





o

Uric acid nephropathy

o

Acute hypersensitivity interstitial nephritis

o

Fanconi syndrom e

o

Sickle cell disease

Overflow proteinuria: o

Monoclonal gam m opathy

o

Leukem ia

Proteinuria, other: o

Dehydration

o

Stress

o

Fever

o

Heat injury

o

Inflam m atory process

o

Orthostatic proteinuria

P.489

Treatment Pre Hospital 

Airway, breathing, and circulation m anagem ent



Control other traum a, if present.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent



Treat hem odynam ically unstable injuries first, if present.



Obtain initial labs (urinalysis with m icroscopic analysis, blood urea nitrogen, serum creatinine).



Pregnancy consideration, preeclam psia



Aggressive blood pressure control

Pa ge 2 1 8



Magnesium



Prom pt OB/GYN consultation

ED Treatment 

Uncom plicated UTIs: o







Antibiotics

Pyelonephritis: o

Antibiotics

o

Analgesics

o

Antipyretics

Rapidly progressing glom erulonephropathy: o

Steroid therapy

o

Urologic/nephrology consultation

Acute renal failure: o

Hem odialysis

o

Renal ultrasound

o

Urine electrolytes

o

Nephrology consultation



Renal colic



IV fluids



Analgesics



If initial presentation noncontrast helical cat scan



Gross hem aturia: o

Insertion of three-way Foley catheter with bladder irrigation to clear blood clots that m ay cause urinary retention from bladder obstruction

Medication (Drugs) 

Uncom plicated UTI: o

3 or 5-day treatm ent

o

Trim ethoprim /sulfam ethoxazole as first-line therapy

Pa ge 2 1 8

o

Ciprofloxacin or levofloxacin when the patient is allergic to sulfa or after failure of trim ethoprim /sulfam ethoxazole 

Ciprofloxacin: 250 m g PO b.i.d. (Do not use in pediatric/pregnant patients)



Levofloxacin: 250 m g PO daily (do not use in pediatric and pregnant patients)



Nitrofurantoin: 2 m g/kg PO daily



Trim ethoprim /sulfam ethoxazole DS: PO b.i.d. for 3 days (peds: 2 m g trim ethoprim /10 m g sulfam ethoxazole per kilogram PO daily)



Am oxicillin (peds) 30â€“50 m g/kg PO t.i.d. for 7â€“10 days



Outpatient pyelonephritis: o

Outpatient treatm ent with 7 days of ciprofloxacin or levofloxacin or 14 days of am oxicillin/clavulanate 

Am oxicillin/clavulanate: 500/125 m g PO t.i.d. for 14 days



Ciprofloxacin: 500 m g PO b.i.d. for 7 days



Levofloxacin: 250 m g PO daily for 7 days



Trim ethoprim /sulfam ethoxazole DS: PO b.i.d. for 14 days

Follow-Up Disposition Admission Criteria 

Intractable pain



Intolerance of oral fluids and m edications



Hem odynam ic instability

Pa ge 2 1 8



Hem aturia with traum atic injuries



Obstructing ureteral stones with evidence of system ic infection or renal failure



Hypertensive em ergency



Acute renal failure: azotem ia/urem ia/hyperkalem ia



Oliguria/anuria



Pregnant with pre-eclam psia, pyelonephritis, obstructing nephrolithiasis

Discharge Criteria 

Hem odynam ically stable without life-threatening issues



Infected ureteral stones without renal failure or obstruction

References 1. Ahm ed Z, Lee J. Asym ptom atic urinary abnorm alities. Med Clin North Am . 1997;81:641â€“652. 2. Grossfeld GD, Wolf JS, Litwin MS, et al. Asym ptom atic m icroscopic hem aturia in adults: sum m ary of the AUA best practice policy recom m endations. Am Fam Physician. 2001;63:1145â€“1154. 3. Sokolosky MC. Hem aturia. Em erg Med Clin North Am . 2001;19:621â€“632.

Codes ICD9-CM 599.7 Hem aturia 791.0 Proteinuria

ICD10 R31 Unspecified hem aturia R80 Isolated proteinuria

Pa ge 2 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o philia

Hemophilia

Steven H. Bowman

Basics Description 

Caused by deficiency of factor VIII or factor IX



Absence of factors causes partial inactivation of coagulation cascade and im paired hem ostasis.



Two types: o

Hem ophilia A: factor VIII deficiency

o

Hem ophilia B (Christm as disease): factor IX deficiency



Severity varies am ong different individuals reflecting available natural factor activity: o



Seventy percent of type A hem ophiliacs are severe.

Sym ptom s dependent on factor availability: o

5â€“30% factor activity (m ild hem ophilia): 

o

1â€“5% factor activity: 

o

Bleeding alm ost exclusively with traum a:

Occasional spontaneous hem orrhages

Less than 1%: 

Frequent spontaneous hem orrhages

Genetics 

Sex-linked recessive occurring in m ales

Pa ge 2 1 9



Rare disease: o

Hem ophilia A occurs in approxim ately 1 in 10,000 m ales.

o

Hem ophilia B occurs in approxim ately 1 in 30,000 m ales

Diagnosis Signs and Symptoms Bleeding: 

Hem arthrosis (m ost com m on): o

Knee (m ost com m on) > elbow > ankle > shoulder > wrist (least com m on)



Muscle hem orrhage



Postextraction or oral m ucosal bleeding



Epistaxis (only in severe disease)



Hem aturia



Sustained from m inor traum a



Intracranial hem orrhage



Gastrointestinal bleeding



Pseudotum ors (blood cysts)

Essential Workup 

Thorough physical exam ination



Factor-specific assays (see below)

Tests Lab 

CBC



Platelet count: norm al



PT/PTT: o

PT: norm al

Pa ge 2 1 9

o

PTT: increased



Bleeding tim e: norm al



Urinalysis: o



Asym ptom atic hem aturia is com m on finding.

Specific factor assays: o

Factor VIII:Ag (m easures factor VIII quantity): decreased

o

Factor VIII:c (m easures factor VIII activity): decreased

o

vWF (m easures von Willebrand factor activity): norm al

o

vWF:Ag (m easures von Willebrand factor quantity): norm al

Imaging Radiographic studies m ay be required in certain circum stances: 

Head CT to evaluate or exclude intracranial bleed



Renal ultrasound/intravenous pyelograph (US/IVP) to evaluate excessive hem aturia or renal traum a



Abdom inal CT to evaluate or exclude retroperitoneal bleeding

Differential Diagnosis 

Von Willebrand disease



Anticoagulant drugs



Antiplatelet agents



Throm bocytopenia



Hepatic dysfunction

Treatment Initial Stabilization

Pa ge 2 1 9



Control bleeding.



Establish IV access.

ED Treatment General 

Abort current bleeding episode by raising factor level.



Prevent additional m orbidity.



Coordinate ED care with prim ary provider (hem atologist).



Patients generally have excellent understanding of their disease.



Determ ine desired factor level based on risk of bleeding and location/system : o

Factor VIII required (in units) = wt (kg) Ã— 0.5 Ã— (% factor activity desired).

o

One IU factor VIII/kg raises activity approxim ately 2%.

o

Factor IX required (in units) = wt (kg) Ã— 1.0 Ã— (% factor activity desired).

o

One IU factor IX/kg raises activity approxim ately 1%.



May need to increase dose if inhibitors (antibodies to factor) are present or use special factor replacem ent



Patient/prim ary care provider or hem atologist usually has this inform ation.

Alert 

Avoid all IM injections.



Avoid aspirin and aspirin-containing products.

Approach to Factor Replacement 

Low to m oderate risk of bleeding: o

Soft tissue injury

o

Joint or m uscle bleeding

Pa ge 2 1 9

o

Desired hem ostatic factor level: 

o

Thirty percent to 50%

Em pirical factor VIII therapy: 

25â€“50 IU/kg

P.491



Moderate to severe risk of bleeding: o

GI or genitourinary (GU) bleeding

o

Desired hem ostatic factor level: 

o

Em pirical factor VIII therapy: 



50â€“100%

25â€“50 IU/kg

Severe risk of bleeding: o

CNS injury

o

Major traum a

o

Desired hem ostatic factor level: 

o

100%

Em pirical factor VIII therapy: 

50 IU/kg

Factor Replacement Options 

Cryoprecipitates: o

Obtained from fresh frozen plasm a (FFP) after thawing at 4Â°C

o

Contains m ultiple proteins but high in VIII, vWF, and fibrinogen





o

Use only if purified factor not available.

o

Not useful in hem ophilia B; does not contain factor IX

Factor VIII concentrates: o

Mainstay of m odern hem ophilia therapy

o

Choice based on patient's profile, prior agents, cost

Interm ediate-purity products:

Pa ge 2 1 9

o

Low factor VIII specific activity

o

Contain fibronectin, fibrinogen, other proteins

o

Viruses killed by solvent detergent extraction or pasteurization

o

Indicated for older hem ophiliacs, patients with prior exposure to blood products

o 



Exam ples: Hum ate-P, Profilate

High-purity products: o

High factor VIII specific activity

o

Contain fewer plasm a proteins

o

Exam ple: Alphanate

Very high purity products: o

Highest factor VIII specific activity

o

Contain no plasm a proteins

o

Either plasm a derived and m onoclonal antibody purified or produced using recom binant DNA technology

o

Indications: pediatric patients; those with lim ited prior exposure to blood products



o

Very expensive

o

Exam ple: Monoclate-P

Factor IX concentrates: o



Fewer options

Low-purity products also known as prothrom bin com plex concentrates (PCCs): o

Plasm a derived; contain factors VII, X, and prothrom bin

o

May be activated, i.e., able to initiate coagulation cascade (APCCs)

o

If adm inistered at frequent or prolonged intervals, m ay cause dissem inated intravascular coagulation (DIC) or throm bosis

Pa ge 2 1 9

o 

Exam ples: Profilnine (PCC); Autoplex (APCC)

High-purity concentrates o

Plasm a derived; purified either using chrom atography or im m unoaffinity



o

Expensive

o

Exam ple: Alphanine

Adjuncts o

DDAVP: 

Synthetic analogue of the antidiuretic horm one L-arginine vasopressin



Raises factor VIII level two to four tim es in patients with activity >5%



Not useful in patients with hem ophilia B



Maxim al effect occurs 15â€“30 m inutes after infusion.



Side effects: m ild flushing, headache, tachycardia, hypotension, hyponatrem ia



Dose 0.3 Âµg/kg of DDVAP diluted in 50 m L 0.9% norm al saline (NS) given over 15â€“30 m inutes

o

Am icar: 

Only for m ucosal bleeding



Do not use in children.



Do not use in hem arthrosis or hem aturia.

Specific Management Considerations 



Hem arthrosis: o

Replace factor prom ptly.

o

Splint

o

Ace, ice

o

Avoid aspirin.

o

Arthrocentesis rarely indicated

Muscle hem orrhage:

Pa ge 2 1 9

o

Replace factor prom ptly.

o

Forearm /calfâ€”consider com partm ent syndrom e.

o

Avoid cylindrical casts.

o

Psoas hem atom aâ€”groin pain, fem oral nerve paresthesias







Postextraction or oral m ucosal bleeding: o

Treat locally with Avitene or m icrofibrillar collagen.

o

Replace factor if severe.

o

Am icar m ay be useful.

Hem aturia: o

Generally m ild

o

Replace factor if sym ptom s >2 days (50â€“100%)

o

Hydrate.

o

Avoid Am icar and cryoprecipitate.

Intracranial hem orrhage: o

All head injuries should be considered significant, especially in children.



o

Do not delay therapy for diagnostic testing.

o

Replace factor to 100%.

o

CT scan aggressively.

Gastrointestinal bleeding: o

Secondary to ulcers, polyps, hem orrhoids

o

Replace factor prom ptly (50â€“100%).

o

Replace factor prior to endoscopy.

Follow-Up Disposition Admission Criteria 

Low threshold for adm ission

Pa ge 2 1 9



Generally observe 23 hours for resolution of bleeding.



Bleeding episodes m ay require m ultiple infusions.



Severe com plications



Head traum a

Discharge Criteria 

Minor bleeding with resolution



If subjective sym ptom s only

References 1. Cohen AJ, Kessler CM. Treatm ent of inherited coagulation disorders. Am J Med. 1995;99:675. 2. DiMichele D. Hem ophilia 1996: new approach to an old disease. Pediatr Clin North Am . 1996;43:709. 3. Friedm an K, et al. Inherited coagulation disorders. In: Lee G, et al., eds. Wintrobe's Clinical Hem atology. 11th ed. Philadelphia: Lippincott William s & Wilkins; 2004:1619â€“1667. 4. Furie B, Lim entani SA, Rosenfield C. A practical guide to the evaluation and treatm ent of hem ophilia. Blood. 1994;843. 5. Roberts HR, et al. Hem ophilia A and Hem ophilia B. In: Beutler E, et al., eds. William sâ€™ Hem atology. 6th ed. New York: McGraw-Hill; 2001:1639â€“1657.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o ptysis

Hemoptysis

Christian Young Peter Pang

Basics Description 

Expectoration of blood, originating from the tracheobronchial tree



Mortality: o

If bleeding rate >1000 m L/24 hours, m ortality increases significantly: 58% (80% if m alignancy present).

o

If bleeding rate <1000 m L/24 hours, m ortality is <10% (60% if m alignancy present).

o

The m ost com m on causes of hem optysis carry a very low (<1%) m ortality rate.



Source of bleeding is typically from bronchial arteries (95%) or pulm onary arteries (5%).



Massive hem optysis defined as 100â€“600 m L/24h (>8 m L/kg/d in children)

Etiology 

Adult: o

Acute and chronic bronchitis (50%)

o

Bronchiectasis

Pa ge 2 1 9

o

Bronchogenic carcinom a

o

Tuberculosis (TB) is the m ost com m on cause of hem optysis worldwide



Pediatric: o

Cystic fibrosis

o

Vascular anom alies

o

Aspiration of foreign bodies

o

Bronchial adenom as: 

>50% of bronchogenic neoplasm s in children are bronchial adenom as.

Diagnosis Signs and Symptoms History 

Chest pain (PE, pulm onary Infarct, pulm onary artery aneurysm )



Dyspnea (m oderate to severe pulm onary hem orrhage, hypoxem ia, m itral stenosis)



Fever (infectious etiology, vasculitis, neoplasm )



General m alaise or chronic constitutional sym ptom s (TB or m alignancy): o



Weakness, fatigue, night sweats, weight loss

Im portant historical points: o

Prior lung, renal, or valvular heart disease

o

History of cigarette sm oking

o

Chem ical, asbestos, or infectious exposure

o

Travel history (consider parasitic or fungal infectious etiology)

o

Aspirin, NSAID, or anticoagulant use

Pa ge 2 2 0

o

Consider Goodpasture syndrom e if hem aturia is present.

o

Recurrent or chronic hem optysis raises suspicion of arteriovenous m alform ations, bronchiectasis, and cystic fibrosis.

Physical Exam 

Clubbing of the fingers (chronic inflam m atory lung diseases)



Cutaneous ecchym osis (blood dyscrasia or anticoagulants)



Aphthous ulcers (BehÃ§et disease)



Nasal septal perforation (Wegener granulom atosis)



Hem aturia (Goodpasture syndrom e)



Unilateral lower extrem ity edem a m ay indicate DVT.



Suggestive of pseudohem optysis: o

Sinusitis, epistaxis, rhinorrhea, pharyngitis, upper respiratory infection, aspiration

Pediatric Considerations 

Thorough head, eyes, ears, nose, and throat exam to exclude nonpulm onary source of bleeding



Pulm onary exam is often norm al.



Wheezing m ay suggest obstruction (e.g., foreign body)



Crackles m ay indicate an underlying pulm onary etiology (e.g., pneum onia, hem othorax, heart failure).



Digital clubbing suggests chronic lung disease, cancer, or congenital heart disease.



Telangiectasias or hem angiom as raise suspicion of arteriovenous m alform ations.

Essential Workup Differentiate between hem optysis and pseudohem optysis: 

Note any precipitating factors, duration of sym ptom s, quantity, and quality of blood

Pa ge 2 2 0





Pulm onary source: o

Bright red blood

o

Frothy in appearance

o

Sputum m ixed with blood is likely pulm onary

o

PH >7

Gastrointestinal (GI) source: o

Dark red or brown blood

o

Accom panied by gastric contents

o

Worsens in setting of nausea/vom iting

o

PH <7

o

Gastric lavage m ay be used to rule out GI source of bleeding.

Tests Lab 

CBC with differential



PT/INR, PTT



Urinalysis (e.g., hem aturia suggests Goodpasture or pulm onary-renal syndrom e)



Febrile patient or suspected infectious etiology: o

Blood culture

o

Sputum culture and gram /acid fast/potassium hydroxide stain with cytology



Hypotensive patient (criteria for m assive hem optysis): o

Type and cross

o

Electrolytes

o

Com plete m etabolic (liver and renal function) panel

o

Coagulation profile 

Fibrin and fibrinogen degradation products (FDP) or Antithrom bin III if dissem inated intravenous coagulation suspected



Hypoxem ic patient:

Pa ge 2 2 0

o 

Arterial blood gas

Pediatric patient: o

Consider sweat-chloride test if cystic fibrosis is suspected.

Imaging 

Chest radiograph: o

Characterizes pathology (e.g., tum or, cavity, effusion, infiltrate, pneum othorax)

o

Early pulm onary hem orrhage m ay present as infiltrate.

o 

Approxim ately 20% will be norm al.

CT: o

High resolution CT has becom e gold standard for diagnosing bronchiectasis.

o

Ideal study for stable patients with hem optysis and a norm al chest radiograph

o

Can predict active TB by detecting cavitary lesions and acinar nodules

o

Higher sensitivity for peripheral tum ors that m ay not be apparent on bronchoscopy



Ventilation-perfusion or pulm onary arteriography if PE is suspected

Diagnostic Procedures/Surgery Bronchoscopy: 

Allows direct visualization of tum ors, foreign bodies, granulom as and infiltration



Valuable for collecting bronchial secretions for cytology and histology



Lim ited diagnostic yield in lesions outside the bronchial wall or distal to bronchial stenosis or occlusion

Differential Diagnosis

Pa ge 2 2 0

Pseudohemoptysis Expectorated blood that originates in the nasopharynx, oropharynx, or GI tract.

Infectious Acute or chronic bronchitis: 

Pneum onia: o

Staphylococcus, Klebsiella, Legionella, Pneum ococcus



Tuberculosis



Viral (Influenza, Varicella)



Fungal (Aspergillus, Coccidioides, Histoplasm a, Blastom yces)



Parasitic: o

Ascariasis, Am ebiasis, and Paragonim iasis.

P.493

Neoplastic 

Squam ous cell, sm all cell, carcinoid



Bronchial adenom a



Metastatic disease

Pulmonary 

Bronchiectasis



Pulm onary em bolism



Pulm onary infarction



Cystic fibrosis



Bronchopleural fistula

Cardiac 

Mitral stenosis



Tricuspid endocarditis



CHF

Pa ge 2 2 0



Any left-sided obstructive lesion

Systemic Disease 

Goodpasture syndrom e



System ic lupus erythem atosus



Vasculitis (Wegener granulom atosis, Henoch-SchÃ¶nlein purpura, BehÃ§et disease)

Hematologic 

Coagulopathy



Throm bocytopenia



Platelet dysfunction



DIC

Vascular 

Pulm onary hypertension



Arteriovenous m alform ation



Aortic aneurysm



Pulm onary artery aneurysm



Aortobronchial fistula

Drugs/Toxins 

Aspirin/antiplatelet therapy



Anticoagulants



Penicillam ine



Cocaine (â€œcrackâ€•) lung



Solvents (organic solvents, trim ellitic anhydride)

Trauma 

Tracheobronchial rupture



Fat em bolism



Pulm onary contusion

Iatrogenic 

Bronchoscopy/lung biopsy



Pulm onary artery or central venous catheterization

Pa ge 2 2 0



Transtracheal aspirate



Lym phangiography

Miscellaneous 

Foreign body aspiration



Catam enial hem optysis (pulm onary endom etriosis)



Am yloidosis



Idiopathic or cryptogenic (as high as 30% of cases)

Treatment Pre Hospital 

Respiratory and contact precautions



Airway m anagem ent o

Oxygen

o

Suctioning as needed

o

Endotracheal intubation if airway com prom ised, severe respiratory distress, or hypoxem ia



Dual large-bore IV access



Volum e resuscitation as needed



Continuous pulse oxim etry, close hem odynam ic and cardiac m onitoring

Initial Stabilization 

Airway and Breathing o

Endotracheal intubation for im pending respiratory failure

o

>8 Fr endotracheal tube to facilitate suctioning and subsequent bronchoscopy

o

Selective intubation of non-bleeding lung with single

Pa ge 2 2 0

or double lum en endotracheal tubes m ay be required



o

Supplem ental oxygen as needed

o

Continuous pulse oxim etry and cardiac m onitoring

Massive Hem optysis o

Principle risk to life is asphyxiation, not exsanguination

o

Maintain dual large-bore IV access

o

Volum e resuscitation with crystalloid or type specific blood as needed

ED Treatment 

Respiratory and droplet precautions for ED staff



Antibiotic therapy if infiltrate present on chest radiograph



Correct hypoxem ia and/or coagulopathy



If m assive hem optysis o

Large bore IV or central access with volum e resuscitation as needed

o

Early involvem ent of pulm onary, anesthesiology, interventional radiology and/or thoracic surgery

o

Pt should be positioned upright, or with side of hem orrhage in m ost dependent position

o

Adm inister blood products as needed

o

Intubation for airway protection, im pending respiratory failure, or to facilitate bronchoscopic evaluation

o

Endobronchial tam ponade with Foley or Fogarty (<4 Fr) catheter, or double lum en endotracheal tube

o

Bronchial artery em bolization (success rates reported as high as 98%). Rebleeding presents in 20% of cases

o

Surgery 

Lobectom y or pneum onectom y if unsuccessful em bolization or in presence of thoracic

Pa ge 2 2 0

aneurysm , traum a or arteriovenous m alform ation. 

Surgical resection is m ost effective for patients with localized lesions and adequate cardiopulm onary reserve

Follow-Up Disposition Admission Criteria 



ICU o

Intubation/positive pressure ventilation

o

Massive hem optysis

o

Hem odynam ic instability

o

Hypovolem ic shock

o

Severe or refractory hypoxem ia

o

Im pending respiratory failure

o

Im pending airway com prom ise

General: o

Mild hem optysis

o

TB

o

Stable foreign body

o

Lung abscess

o

Cavitary lung disease

Discharge Criteria 

Mild hem optysis due to tracheobronchitis



No coagulopathy



No supplem ental oxygen requirem ent



History of chronic stable hem optysis



Discharge with cough suppressants (Benzonatate, codeine)

Pa ge 2 2 0



Close follow-up

References 1. Cahill B, Ingbar D. Massive hem optysis: assessm ent and m anagem ent. Clin Chest Med. 1994;15(1):147â€“167. 2. Coss-Bu JA, Sachdeva RC. Hem optysis: A 10-Year Retrospective Study. Pediatrics. 1997;100(3):7eâ€“7. 3. Jean-Baptiste E. Clinical assessm ent and m anagem ent of m assive hem optysis. Crit Care Med. 2000;28:1642â€“1647. 4. Set PA, Flower CD, Sm ith IE, et al. Hem optysis: com parative study of the role of CT and fiberoptic bronchoscopy. Radiology. 1993;189:677â€“680. 5. Weinbergeer S. Etiology and evaluation of hem optysis. http://www.uptodate.com 1999.

Codes ICD9-CM 786.3

ICD10 R04.2

Pa ge 2 2 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o rrhagic F evers

Hemorrhagic

Fevers David Tanen

Basics Description Hem orrhagic fevers are a group of illnesses that are caused by several distinct fam ilies of viruses. Viral hem orrhagic fever is used to describe a severe m ultisystem syndrom e.

Risk Factors 

Travel in endem ic region



Biologic warfare



Exposure to pathogens via anim al or insect bite or ingestion

Pathophysiology 

Viral hem orrhagic fevers cause endothelial dam age and increase vascular perm eability, hem orrhage, and hypovolem ic shock.



Dissem inated intravascular coagulation (DIC) appears to be regular feature of Marburg and Crim ean-Congo hem orrhagic fever but is less frequent with Arenavirus infections.

Pa ge 2 2 1



Dengue hem orrhagic fever is thought to be im m une m ediated and is usually result of secondary infection.

Etiology 

Infection with RNA viruses that have zoonotic life cycles in specific geographic areas



Short incubation period (<10â€“21 days)



Exam ples of viral hem orrhagic fevers include the following: o

o

Filoviruses: unknown reservoir and vector: 

Ebola



Marburg

Arenaviruses: rodent reservoir, transm itted via inhalation of aerosolized virus in rodent excreta:

o



Lassa



South Am erican hem orrhagic fevers

Flaviviruses: hum an reservoir, transm itted via m osquito:

o



Dengue hem orrhagic fever



Yellow fever

Bunyaviridae: sm all m am m al reservoir, transm itted via m osquitoes or ticks:

o



Rift Valley fever



Crim ean-Congo hem orrhagic fever

Hantavirus: rodent reservoir, transm itted via inhalation of aerosolized virus in rodent excreta: 

Hem orrhagic fever with renal syndrom e

Alert 

These viruses represent a potential biowarfare threat: o

Highly infectious by aerosol (with exception of dengue)

o

Associated with high m orbidity and in som e cases

Pa ge 2 2 1

high m ortality o

Replicate well in cell culture, which perm its weaponization

Diagnosis Signs and Symptoms 





Most com m on (>50%) sym ptom s: o

Acute febrile illness

o

Malaise

o

Headache

o

Nausea/vom iting

o

Flushing

o

Diarrhea (nonbloody)

o

Abdom inal pain

o

Myalgias

Less com m on (<30%) sym ptom s: o

Gingival hem orrhage

o

Conjunctival injection/hem orrhage

o

Petechia

o

Hem atem esis

o

Melena

o

Epistaxis

Delayed presentations (>3 days into disease): o

As above with hem orrhagic sym ptom s becom ing m ore prom inent



Bleeding from gum s, nose, lungs, gastrointestinal tract, or uterus: o



Exanthem s

Marburg and Ebola: nonpruritic centripetal, papular, erythem atous eruption appearing between days 5 and 7,

Pa ge 2 2 1

which then coalesce into well-dem arcated m acules that m ay be hem orrhagic 

Yellow fever: jaundice



Dengue: bright m aculopapular truncal erythroderm a that blanches dram atically under light pressure: o

Shock

o

Seizures

o

Com a

Essential Workup 

Focus on differentiating from other acute febrile illnesses, especially in returned traveler.



Recognize possible biologic attack when unusual num ber of patients present with sim ilar and/or unusual findings.



History to identify potential pathogen: o

Include recent travel, illnesses, or other sources of exposure.

Tests Lab 

CBC: o

May see leukocytosis or leukopenia, throm bocytopenia



Electrolytes, BUN, creatinine, and glucose levels: o



Look for renal failure.

Liver function tests: o

Hepatic involvem ent is com m on, but jaundice occurs m ainly with yellow fever.



Prothrom bin tim e, partial throm boplastin tim e, and D-dim er tests: o

Look for coagulopathy and DIC (seen in Crim ean-Congo hem orrhagic fever, Ebola, and Marburg).

Pa ge 2 2 1

Special Lab Test In specialized laboratories (biohazard level 4), definitive diagnosis can be m ade by viral isolation, polym erase chain reaction, and im m unohistochem istry techniques: 

Coordinated with Centers for Disease Control and Prevention (CDC)



Thick and thin sm ears to help differentiate from m alaria

Differential Diagnosis 

Malaria: o



Dengue fever: o









A concern for traveler with fever

Com m on source of fever in traveler

Rickettsial: o

Rocky Mountain spotted fever

o

Typhus

Bacterial: o

Meningococcem ia

o

Sepsis

System ic disease: o

Leukem ia

o

Throm botic throm bocytopenic purpura

Pit viper envenom ation

P.495

Treatment Pre Hospital

Pa ge 2 2 1

Alert 

Any place in the world can now be reached within significantly shorter tim e than incubation period of alm ost all infectious diseases.



Early detection of viral hem orrhagic fever, natural or biologic attack, is key to control outbreak.



Most cases will derive from patients who traveled to or had contact with persons from parts of the world where the viruses are endem ic.

Initial Stabilization Protection of health care workers: 

Universal blood and body precautions



Isolation of patient



Use of protective clothing plus HEPA-filtered respirators to m inim ize exposure to aerosols for those involved in procedures such as suctioning, catheter placem ent, and wound dressing

ED Treatment 

Supportive therapy



Em piric therapy with antim alarial regim ens until definitive diagnosis is obtained



Aggressive treatm ent of secondary infections



Bleeding is usually m ild, and life-threatening loss of blood is rare: o

If indicated, hem orrhage can be m anaged by replacem ent of blood, platelets, and clotting factors.



Pulm onary artery catheter to m anage shock: o

Patients are often hypovolem ic because of third spacing and hem orrhage, but m ay readily develop pulm onary edem a with crystalloid infusion.



Ribavirinâ€”a synthetic nucleoside:

Pa ge 2 2 1

o

Useful for Lassa, South Am erican hem orrhagic fever, Crim ean-Congo hem orrhagic fever, and hem orrhagic fever with renal syndrom e; ineffective against filoviruses

o 

Causes a reversible hem olytic anem ia

Transfusion of im m une plasm a (convalescent plasm a therapy) for South Am erican hem orrhagic fever within first week of sym ptom s

Medication (Drugs) 

Ribavirin: o

IV loading dose of 33 m g/kg followed by 16 m g/kg q6h for 4 days, then 8 m g/kg q8h for 3 days

o 

Prophylactic 500 m g by m outh q6h for 7 days

Vaccines: o

Yellow fever is widely available.

o

South Am erican hem orrhagic fever, Rift Valley fever, and Hantavirus are under developm ent.



Other m edications under investigation: o

Nucleoside analog inhibitors of S -adenosylhom ocysteine hydrolase inhibit Ebola replication in m ice.

o

Zidam pidineâ€”a derivative of AZTâ€”increases survival of m ice infected with Lassa virus

Follow-Up Disposition Admission Criteria

Pa ge 2 2 1

Suspected cases of viral hem orrhagic fever: 

Isolation precautions



Intensive care unit for signs of shock or m ultiorgan system failure

Issues for Referral Notify Centers for Disease Control and Prevention at (770) 488-7100 or (800) 311-3435 for all suspected cases.

References 1. Centers for Disease Control and Prevention (CDC). Managem ent of patients with suspected viral hem orrhagic fever. MMWR Morb Mortal Wkly Rep. 1988;37(suppl 3):1â€“16. 2. Centers for Disease Control and Prevention (CDC). Update: m anagem ent of patients with suspected viral hem orrhagic feverâ€“United States. MMWR Morb Mortal Wkly Rep. 1995;44:475â€“479. 3. Boyle TJ, Bryan RT, Peters CJ. Em erging infectious diseases: viral hem orrhagic fevers and Hantavirus infections in the Am ericas. Infect Dis Clin North Am . 1998;12:95â€“110. 4. Franz DR, Jahrling PB, Friedlander AM, et al. Clinical recognition and m anagem ent of patients exposed to biological warfare agents. JAMA. 1997;278:399â€“411. 5. Mahanty S, Bray M. Pathogenesis of filoviral haem orrhagic fevers. Lancet. 2004;4:487â€“498.

Codes ICD9-CM 065 Arthropod-borne hem orrhagic fever A94 Unspecified arthropod-borne viral fever

ICD10 A-90â€“A-99 Athropod-borne viral fevers and viral hemorrhagic fevers

Pa ge 2 2 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o rrhagic Sho ck

Hemorrhagic

Shock Theodore C. Chan

Basics Description 

Loss of effective circulating blood volum e resulting in inadequate organ perfusion



Com pensated shock: o

Patient's physiologic reserve prevents significant alteration in vital signs.



Decom pensated shock: o

Loss of circulating volum e overcom es patient's physiologic reserve, resulting in signification alteration in vital signs.



Blood loss estim ate: o

Multiply 70 m L/kg (adult blood volum e) tim es body weight (kg) tim es percentage loss as determ ined by class of hem orrhage.

Risk Factors 

Traum a



Chronic or acute illness



Physical anom alies

Pa ge 2 2 1

Genetics 

Arteriovenous m alform ations



Other genetic anom alies

Pathophysiology In hem orrhagic shock, blood loss exceeds the body's ability to com pensate and provide adequate tissue and organ perfusion. At the tissue level, hypoperfusion leads to inadequate oxygenation, anaerobic m etabolism , cellular injury, and death.

Etiology 

Traum aâ€”penetrating and blunt: o

o

o

Abdom inal: 

Splenic injury (40% of abdom inal hem orrhage)



Liver injury (20% of abdom inal hem orrhage)

Chest: 

Hem othorax



Aorta or great vessel injury

Pelvis: 

Pelvic fracture with vascular injury



Abortion: com plete, partial, or inevitable



Aneurysm s m ay lead to thoracic, retroperitoneal, or intraperitoneal bleeding: o

Abdom inal aortic aneurysm m ost com m on

o

Mycotic aneurysm secondary to endocarditis



Aortogastric fistula



Arteriovenous m alform ations m ay lead to thoracic, retroperitoneal, or intraperitoneal bleeding.



Ectopic pregnancy



Epistaxis



Fractures (especially pelvis and long bones)



Gastrointestinal (GI) bleeding



Hem optysis

Pa ge 2 2 1



Malignancies



Mallory-Weiss tear



Placenta previa



Postpartum hem orrhage



Retroperitoneal bleeds



Splenic rupture



Vascular injuries

Associated Conditions Dependent on cause of hem orrhage

Diagnosis Signs and Symptoms 

Class I hem orrhage: loss of up to 15% of blood volum e (up to 750 m L in 70-kg adult):



o

Heart rate (HR) <100

o

Blood pressure (BP) norm al

o

Respiratory Rate (RR) 14â€“20

o

Increased or norm al pulse pressure

o

Slight anxiety

Class II hem orrhage: loss of 15â€“30% of blood volum e (750â€“1,500 m L):



o

HR >100

o

BP norm al

o

RR 20â€“30

o

Decreased pulse pressure

o

Mild anxiety

o

Sm all decrease in urine output

Class III hem orrhage: loss of 30â€“40% of blood volum e (1,500â€“2,000 m L)

Pa ge 2 2 2

o

HR >120

o

BP decreased

o

RR 30â€“40

o

Decreased pulse pressure

o

Significant change in m ental status: anxiety or confusion

o 

Marked decrease in urine output

Class IV hem orrhage: loss of >40% of blood volum e (m ore than 2,000 m L): o

HR >140

o

BP decreased

o

RR >35

o

Very narrow pulse pressure

o

Depressed m ental status: confusion, lethargy, loss of consciousness

o

Negligible urine output

o

Cold and pale skin

Pediatric Considerations 

Children often have greater physiologic reserve than adults and can preserve norm al vital signs longer.



System ic responses to blood loss in the pediatric patient include: o

Volum e loss <25%: weak, thready pulse and tachycardia; lethargy, irritability, and confusion; cool, clam m y skin; decreased urine output with increased urine specific gravity

o

Volum e loss 25â€“40%: tachycardia; m arked change in consciousness; dulled response to pain; cyanotic, cold extrem ities with decreased capillary refill; m inim al urine output

o

Volum e loss >40%: hypotension, tachycardia, or bradycardia; com atose; pale, cold skin; no urine

Pa ge 2 2 2

output

Pregnancy Considerations Physiologic m aternal hypervolem ia requires greater blood loss to m anifest m aternal perfusion abnorm alities which m ay result in decreased fetal perfusion.

Geriatric Considerations Underlying disease and m edications m ay alter responses to hem orrhage and blood loss.

Essential Workup 

Thorough health history



Description of events preceding and/or causing onset of sym ptom s



Com plete physical exam , including rectal exam , to determ ine shock category



Nasogastric tube: o

For undifferentiated hypovolem ic shock to rule out GI hem orrhage



Blood type and cross-m atch



Hem oglobin and hem atocrit levels



Insert Foley catheter: o



Monitor urine output.

Measure urine specific gravity.

Tests Lab 



Coagulation studies: o

Prothrom bin tim e

o

Partial throm boplastin tim e

o

International norm alized ratio

Other m easures of shock and tissue hypoperfusion: o

Arterial blood gas

Pa ge 2 2 2

o

Base deficit

o

Serum lactate level

o

Serum electrolytes

Imaging 

Chest radiograph: o





Blunt chest injuries



Thoracic arteriovenous m alform ation

Pelvic radiograph: o



Hem othorax:

Pelvic fracture

Focused Abdom inal Sonography for Traum a (FAST exam ): o

Abdom inal traum a

o

Possible abdom inal aortic aneurysm : Perform bedside evaluation.

o

Nontraum atic intraperitoneal hem orrhage

o

Fluid in Morison's pouch im plies significant hem orrhage or ascites.

o

Negative findings do not rule out intraperitoneal hem orrhage.





Endovaginal ultrasound: o

Positive pregnancy test

o

Fluid in the cul-de-sac

o

Ectopic pregnancy

Abdom inal CT scan: o

Detects both intraperitoneal and retroperitoneal hem orrhage

o

Perform ed once the patient has been stabilized

o

Abdom inal aortic aneurysm

P.497

Pa ge 2 2 2

Diagnostic Procedures/Surgery 

Diagnostic peritoneal lavage: o

For unstable traum a patients when ultrasound fails to show intraperitoneal hem orrhage

o

Detects intraperitoneal bleeding only

o

Aspiration of 10 m L of blood defines the need for em ergent laparotom y in unstable patients.



Endoscopy: o





In the setting of upper or lower GI bleeding

Angiography: o

Pelvic fracture

o

Retroperitoneal hem orrhage

o

Lower GI bleeding

Em bolization therapy for bleeding from arterial sources can be perform ed.

Pathologic Findings Dependent on causative factor

Differential Diagnosis See Shock

Treatment Pre Hospital 

Rapid assessm ent and transport to appropriate care center



IV access and fluid resuscitation are standard, but controversial.



Overaggressive fluid resuscitation to norm alize in field hypotension associated with increased m ortality in penetrating traum a

Pa ge 2 2 2

Initial Stabilization 

Airway and breathing: o

Intubation as indicated by patient's respiratory and m ental status

o 

100% oxygen via face m ask should be adm inistered.

Circulation: o

Two large-bore peripheral intravenous lines (16-gauge or larger)

o

Venous cutdown (saphenous) m ay be necessary.

o

Aggressive crystalloid resuscitation

o

Three-to-one rule: For one unit volum e of blood loss, give three volum es of crystalloid.



Early blood transfusion with evidence of class III or IV hem orrhage: o

Type-specific and cross-m atched blood is preferred when tim e perm its, often 1 hour.

o

Type-specific blood is usually available within 10â€“15 m inutes.



Type O blood can be used in im m ediate, life-threatening situations (type O Rh-negative blood only for wom en of child-bearing age).

ED Treatment 

Control hem orrhage (direct pressure, pelvic fixation/stabilization, etc.).



Place patient on continuous m onitor.



Central venous access m ay be indicated for central vena cava m onitoring, but placem ent of such lines should not interfere with resuscitation m easures.



Continually reassess patient for clinical response or deterioration: o

Monitor vital signs, m ental status, and urine output.

Pa ge 2 2 2

o

Follow serial blood gas, lactate level, and hem oglobin/hem atocrit m easurem ents.

o 

Maintain urine output at 50 m L per hour.

Response to initial fluid resuscitation is the key to determ ining subsequent therapy: o

Rapid response to fluid adm inistration indicates m inim al (less than 20%) blood loss.

o

Transient response to volum e resuscitation indicates ongoing hem orrhage or inadequate resuscitation; continue fluid and blood adm inistration and rapidly obtain necessary studies and consultations.

o

Minim al or no response to volum e resuscitation indicates ongoing severe blood loss; im m ediate angiography or surgical intervention is warranted.



Use fluids warm ed (approxim ately 39Â°C [102.2Â°F]) by m icrowave ovens, warm -water baths, or fluid warm ers.



Transfuse platelets and coagulation factors as indicated.



Consider autotransfusion devices with tube thoracostom y treatm ent and decom pression of large hem othoraces

Pediatric Considerations 

Access m ay be obtained by intraosseous route after one or two unsuccessful attem pts at peripheral access.



Maintain urine output at 1 m L/kg per hour for children and 2 m L/kg per hour for infants.

Pregnancy Considerations Optim izing perfusion and treatm ent of the m other is treatm ent of choice for fetus

General Measures Diet Nothing by m outh

Pa ge 2 2 2

Activity Strict bed rest

Special Therapy 

Blood products: cross-m atched, type-specific, O-positive or O-negative: o

O-negative should be reserved for wom en of child-bearing age

o

Adult: Initiate with four to six units of packed red blood cells.

o 

Pediatric: 10 m L/kg of packed red blood cells

Other blood products: o

Platelets

o

Coagulation factors, such as fresh frozen plasm a (large transfusions of packed red blood cells as opposed to whole blood m ay lead to significant dilution of platelet and coagulation factors)



Hem oglobin substitutes: o

Under study, but of no proven benefit

IV Fluids 

Crystalloids: norm al saline or lactated Ringer IV



Adults: 1- to 2-L bolus: o



Reassess for perfusion.

Pediatric: 20 m L/kg bolus

Surgery As indicated for causative factor after patient is stabilized

Follow-Up Disposition

Pa ge 2 2 2

Admission Criteria All patients with hem orrhage should be adm itted to the appropriate service.

Discharge Criteria Do not discharge.

References 1. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons, 2004. 2. Bickell WH, Wall MJ Jr, Pepe PE, et al: Im m ediate versus delayed fluid resuscitation for hypotensive patients. New Eng J Med. 1994;331:2205â€“2209. 3. Kline JA. Shock. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2001: 33â€“47. 4. Stainsby D, MacLennan S, Ham ilton PJ. Managem ent of m assive blood loss: a tem plate guideline. Br J Anaesth. 2000;85:487â€“491. 5. Wilson M, Davis DP, Coim bra R: Diagnosis and m onitoring of hem orrhagic shock during the initial resuscitation. J Em erg Med. 2003;24:413â€“422.

Codes ICD9-CM 958.4 Traum atic shock 785.59 Shock without m ention of traum a, other

ICD10 R57.1 Hypovolem ic shock

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o rrho id

Hemorrhoid

Julia Sone

Basics Description 

No precise definition exists.



Abnorm al vascular cushions of anal canal



Do not cause pain unless throm bosed/strangulated



Discrete m asses of thick subm ucosa contain: o

Blood vessels

o

Sm ooth m uscle

o

Elastic and connective tissue



Sliding down of part of anal canal lining



External hem orrhoids:



o

Vessels situated below dentate line

o

Covered by skin/anoderm

o

Drain to internal iliac veins

Internal hem orrhoids: o

Subm ucosal vessels above dentate line

o

Drain to portal system

o

Usually at left lateral, right posterolateral, and right anterolateral positions

o

Grade 1: painless, bleeding

o

Grade 2: prolapse with bowel m ovem ent (BM),

Pa ge 2 2 2

spontaneously reduce o

Grade 3: prolapse with BM, require m anual reduction

o

Grade 4: chronically prolapsed, not reducible

Etiology 

Exact cause unknown



Associated with straining and irregular bowel habits: o

Hard, bulky stools or diarrhea cause tenesm us/straining.

o

Push anal cushions out of anal canal

o

Weaken subm ucosal tissue



Higher resting anal pressures



Erect posture



Heredity: o





Absence of valves in veins

Increased intra-abdom inal pressure: o

Ascites

o

Pregnancy

Portal hypertension

Diagnosis Signs and Symptoms 

Painless, rectal bleeding with defecation



Blood on stool or toilet paper



Blood drips into toilet bowel



Severe pain if: o

Internal hem orrhoids prolapse and strangulate.

o

External hem orrhoids throm bose.



Pruritus ani



May also have fissure

Pa ge 2 2 3

History 



Length of bleeding: o

Pain?

o

Duration?

Any new lum ps or m asses by rectum ?

Physical Exam 

Exam ination of perianal area: o

Gently spread buttocks.

o

Discrete, dark blue, tender m ass covered with skin: throm bosed external hem orrhoid: 

o

Can have internal com ponent

Purplish, tender m ucosal covered m ass: prolapsed, strangulated internal hem orrhoid: 

Usually associated with enlarged, throm bosed external hem orrhoid

o

Have patient bear down to check for prolapsing hem orrhoids.

o 

Digital rectal exam m andatory to rule out cancer

Anoscopy to visualize anal canal: o

Identify bleeding internal hem orrhoids.

Tests Lab 

Hem atocrit (Hct) if history of significant blood loss



Platelets and PT/PTT/INR if patient on anticoagulants or severe coâ€“m orbid condition

Differential Diagnosis 

Rectal prolapse



Anal fissure



Perirectal abscess

Pa ge 2 2 3

Treatment Initial Stabilization Direct digital pressure to control bleeding

ED Treatment 

Conservative therapy for all: o

Hot sitz baths for 15 m inutes t.i.d. and after each bowel m ovem ent

o



High-fiber dietâ€”30 g/d: 

Eat m ore fresh fruits and vegetables.



Increase bran intake.

o

10â€“12 glasses of water per day

o

Stool softeners

o

Bulk-form ing laxatives

Excise throm bosed external hem orrhoid if severe pain and if the hem orrhoid is <5 days old: o

Follow with conservative therapy.

o

Place patient in prone jackknife position or left lateral decubitus.

o

Infiltrate surrounding skin and underneath clot using 27-gauge needle with lidocaine-containing epinephrine.

o

Make an elliptical incision to excise clot/skin.

o

Place a sm all piece of Gelfoam and/or gauze onto the wound and tape.

o

Rem ove dressing at tim e of first sitz bath in about 6 hours.

o

Give analgesics: 

Nonsteroidal anti-inflam m atory drugs (NSAIDs)



Acetam inophen

Pa ge 2 2 3



0.2% topical nitroglycerin ointm ent to anusâ€”decreases pain by inhibiting sphincter spasm



Manually reduce nonthrom bosed, prolapsed internal hem orrhoids: o

Follow with conservative therapy.

o

May need topical anesthetic or anal sphincter block with local anesthesia

o

Can sclerose bleeding internal hem orrhoids

o

Can rubber band ligate one or two internal hem orrhoids



Nonreducible internal hem orrhoids: o

Nonstrangulated: conservative m anagem ent and surgical referral

o

Strangulated: im m ediate surgical referral for excision

P.499

Medication (Drugs) 

Acetam inophen: 325â€“650 m g (peds: 15 m g/kg) with codeine 15â€“30 m g (peds: 0.5 m g/kg) PO q4h PRN



Bran/fiber: 20 g PO daily



Docusate sodium (Colace): 50â€“200 m g (peds: <3 years, 10â€“40 m g/d; 3â€“6 years, 20â€“60 m g/d; >6â€“12 years, 40â€“150 m g/d) PO q12h



ELA-Max 5 (5% lidocaine anorectal cream ): apply to perianal area q4h PRN pain (peds: not for <12 years of age).



Ibuprofen (Motrin): 400â€“600 m g (peds: 40 m g/kg/d) PO q6h

Pa ge 2 2 3



Psyllium seeds: 1â€“2 tsp (peds: 0.25â€“1 tsp/d) PO q24h

Follow-Up Disposition Admission Criteria 

Strangulated grade 4 hem orrhoids: o

Surgical consult for prolapsed, throm bosed internal hem orrhoids



Severe anem ia with bleeding hem orrhoids

Discharge Criteria Most patients will go hom e.

Issues for Referral Surgical referral for: 

Grade 3 or 4 internal hem orrhoids



Suspected anorectal or colonic tum ors, inflam m atory bowel disease, coagulopathy, pregnancy, or im m unocom prom ised

References 1. Janicke DM, Pundt MR. Anorectal disorders. Em erg Med Clin North Am . 1994;14:757â€“788. 2. Pfenninger JL, Surrell J. Nonsurgical treatm ent options for internal hem orrhoids. Am Fam Physician. 1995;52:821â€“834.

Codes ICD9-CM 455.6

ICD10 184.9

Pa ge 2 2 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o tho rax

Hemothorax

Thomas C. Lee

Basics Description 

Accum ulation of blood in the intrapleural space after blunt or penetrating chest traum a causing lung com pression: o

Results in decreased vital capacity, hypoxia, and respiratory com prom ise

o

Com m only associated with pneum othorax (25% of cases) as well as extrathoracic injuries (73% of cases)



Hem othorax can cause increased intrathoracic pressure resulting in com prom ised venous return and decreased cardiac output.



Loss of large intravascular volum e results in hem odynam ic instability.



Large hem othoraces cause the release of substances that can act as anticoagulants and contribute to continued intrathoracic bleeding.

Etiology 

Traum atic injuries to m ajor vessels: o

Laceration of m ajor blood vessels, including pulm onary artery, pulm onary vein, intercostal

Pa ge 2 2 3

artery, internal m am m ary artery, aorta, vena cava, and heart are associated with hem orrhage into the thoracic cavity. 

Traum atic lung parenchym al injuries: o

Often stops spontaneously owing to low pulm onary pressures and high concentrations of throm boplastin in lung



Nontraum atic spontaneous hem othoraces: o

Very rare

o

Coagulation disorder, m alignancy, prim ary vascular event (such as aortic dissection), infection

o

Com plication of spontaneous pneum othoraces

Diagnosis Signs and Symptoms 

Sm all am ount of blood in thorax (<400 m L): little or no change in patient's appearance, vital signs, or physical findings



Large am ount of blood (>1,000 m L): restlessness, anxiety, pallor, pleuritic pain, hem optysis, dyspnea, or air hunger



Tachycardia, tachypnea, hypotension



Chest inspection: asym m etric expansion, paradoxical wall m ovem ent, abrasion, contusion



Chest wall palpation: tenderness or crepitus over ribs, clavicles, scapulae, or the sternum ; subcutaneous em physem a, dullness to percussion



Auscultation: ipsilateral decreased breath sounds

Essential Workup

Pa ge 2 2 3



Chest radiography is the single best diagnostic tool; fluid collections >200â€“300 m L can usually be seen on upright, decubitus chest radiograph: o

In the supine position, up to 1,000 m L of blood m ay not be readily apparent.

o

Hem othorax appears as a slight haziness over the involved hem ithorax on the anteroposterior (AP) radiograph.

o

In the hem odynam ically stable patient, the optim al technique is an upright posteroanterior (PA) projection at full inspiration.



Pulse oxim etry, arterial blood gas

Tests Lab 

Hem atocrit m ay be helpful if it shows a drop or changes on serial evaluations.



Type and cross-m atch.

Imaging 

Ultrasound diagnostic im aging is a valuable tool in the evaluation of intrapleural fluid collection.



CT is useful in detecting sm all am ounts of intrapleural fluid not visible on the chest radiograph.

Differential Diagnosis 

Hem opneum othorax



Pneum othorax



Pulm onary contusion

Treatment

Pa ge 2 2 3

Pre Hospital Cautions: 

Difficult to differentiate hem othoraces from pneum othoraces clinically: o

All m ay present with dyspnea, pleuritic chest pain, decreased breath sounds, and hem odynam ic instability.

o

Certain clues aid in m aking the diagnosis such as subcutaneous em physem a for pneum othorax and dullness to percussion for hem othorax



Perform needle thoracostom y for potential tension pneum othorax if the patient hem odynam ically unstable.

Initial Stabilization Manage airway, breathing, circulation: 

Control airway as needed; endotracheal intubation for patients with im pending respiratory failure



Supplem ental oxygen



Intravenous access to restore circulating blood volum e



Needle thoracostom y should be perform ed in patients with hem odynam ic instability unless chest tube kit is im m ediately available.

ED Treatment 

Hem othorax is treated by evacuating accum ulated blood in the intrapleural space.



Tube thoracostom y evacuates blood; allows for re-expansion of the lung as well as constant m onitoring of blood loss.



Tube thoracostom y: o

Use a large-bore chest tube (36â€“40 French).

o

Insert in the fourth or fifth intercostal space at the m idaxillary line aim ing posteriorly and superiorly.

Pa ge 2 2 3

o

Tube is then connected to underwater-seal drainage and suction (20â€“30 m L H 2 O)

P.501



Autotransfusion should be used if available to replace blood loss.



Indications for thoracotom y: o

Initial tube drainage >20 m L/kg of blood (or 1,000 m L of blood for adults from the pleural cavity)

o

Persistent bleeding at a rate >7 m L/kg/h (or 200 m L/h for 4 hours)

o

Increasing hem othorax seen on chest radiography

o

Patient rem ains hypotensive despite adequate blood replacem ent and other sites of blood loss have been ruled out.

o

Patient decom pensates after initial response to resuscitation.



Indications for ED thoracotom y: o

Penetrating traum a: 

Traum atic arrest at any point with initial signs of life in the field



Blood pressure <50 m m Hg systolic after fluid resuscitation



Severe shock with clinical signs of cardiac tam ponade

o

Blunt traum a: traum atic arrest in the ED

Medication (Drugs) 

Local anesthetics for cutaneous anesthesia prior to tube thoracostom y in awake, conscious patients

Pa ge 2 2 3



Conscious sedation (m idazolam ) and analgesia (fentanyl) should be used for stable, awake patients prior to tube thoracostom y: o

Fentanyl: adult/peds: 2â€“5 Âµg/kg per dose

o

Midazolam : adult/peds: 0.02â€“0.04 m g/kg per dose

Follow-Up Disposition Admission Criteria Patients with hem othoraces large enough to require tube thoracostom ies should be adm itted for m onitoring and thoracostom y tube m anagem ent.

Discharge Criteria Patients with isolated sm all hem othoraces (detected incidentally on ultrasound or CT im aging) m ay be considered for discharge after 4â€“6 hours of observation if there is no evidence of continued bleeding and the patient is not hypoxic.

References 1. Eddy CA, Carrico CJ, Rusch VW. Injury to the lung and pleura. In: Moore EE, Mattox KL, Feliciano DV, eds. Traum a. 2nd ed. East Norwalk, CT: Appleton & Lange; 1991. 2. Meredith JW. Chest wall injury. In: Trunkey D, Lewis FR Jr, eds. Current Therapy of Traum a. 3rd ed. Philadelphia: BC Decker; 1991:216â€“219. 3. Parry GW, Morgan WE, Salam a FD. Managem ent of haem othorax. Ann R Coll Surg Engl. 1996;78(4):325â€“326. 4. Vukich DJ, Markovchick V. Thoracic traum a. In: Rosen P, et al., eds. Em ergency Medicine: Concept and Clinical Practice. 5th ed. St.

Pa ge 2 2 4

Louis, MO: Mosby; 2001:391â€“392.

Codes ICD9-CM 511.8

ICD10 J94.2

Pa ge 2 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Heno ch SchÃ¶ nlein Purpura

Henoch

SchÃ¶nlein Purpura Mark A. Hostetler

Basics Description Vasculitis

Etiology Mechanism 



Increased serum IgA: o

Circulating IgA com plexes

o

Glom erular m esangial deposition of IgA

Although cause is undefined, there are m any associated conditions: o

Infections

o

Group A strep

o

Mycoplasm a

o

Viral: varicella, Epstein-Barr (EB)

o

Drugs: penicillin, tetracycline, aspirin, sulfonam ides, erythrom ycin

o 

Allergens: insect bites, chocolate, m ilk, wheat

Peak incidence: school-aged children and young adults

Pa ge 2 2 4



More com m on in whites



Males > Fem ales



Occurs m ore often in winter/spring



Multisystem involvem ent can lead to life-threatening or long-term com plications: o

Intussusception

o

Proliferative glom erulonephritis

o

Chronic renal failure: 

More com m on in older children and adults (13â€“14%)

o

Intracranial hem orrhage

Diagnosis Signs and Symptoms 

General: o

Well-appearing child, despite nature and extent of rash

o

Recent or current upper respiratory tract infection

o

Malaise

o

Low-grade fever

o

Hypertension, if associated renal failure

o

Children <3 m onths m ay have only skin m anifestations.



Skin: o

Purpuric rash: 

Presenting sign in 50% of patients



One hundred percent of patients develop purpura



First appears as pink rounded papules that blanch

Pa ge 2 2 4



Progresses to 2â€“3 cm circular palpable purpura within 24 hours; m ay be discrete, or confluent



Rash begins in gravity-dependent areas of legs and buttocks.



Sym m etric distribution



May involve lower back



Rarely involves the face



Rash recurs in up to 40% of patients (within 6 weeks).



Abdom inal: o

Abdom inal pain: 

Seventy percent to 80% of cases



Colicky to severe



Abdom inal findings m ay precede the rash by 4 weeks.

o



GI bleeding: 

75% of cases



Occult to severe blood loss



Intussusception (ileo-ileal or ileocolic)

Renal-genitourinary: o

Asym ptom atic hem aturia: 



Occurs in 80% of cases

o

Scrotal pain

o

Testicular swelling

o

Renal failure

Extrem ities: o

Arthritis: 

70â€“80% of cases



Migratory periarticular pain



Most frequent in knees and ankles



Angioedem a

Pa ge 2 2 4



Neurologic: o

Headache

o

Seizure

o

Focal deficits

Essential Workup Exclude life-threatening causes of purpura, severe abdom inal pain, hem aturia, and CNS findings, if appropriate.

Tests Lab 



CBC: o

Platelet count norm al

o

WBC often elevated

PT, PTT (if bleeding or in shock; or if unsure of diagnosis and concerned about possibility of coagulopathy)



Electrolytes (if hypertension or urinalysis abnorm al)



BUN, creatinine (if hypertension or urinalysis abnorm al): o

May be elevated in cases with serious renal com plications





Urinalysis: o

Hem aturia is com m on

o

Proteinuria is suggestive of glom erulonephritis

Cultures to exclude com m on infections

Imaging 

Abdom inal im aging studies: o

Indicated if abdom inal pain or GI bleeding

o

Flat and upright abdom inal film s of lim ited use

o

Abdom inal ultrasound, barium enem a, or CT scan m ay be necessary to rule out intussusception.



Testicular ultrasound: o

Indicated in patients with testicular pain and swelling

Pa ge 2 2 4



Head CT: o

Indicated if CNS findings to exclude bleed

P.503

Differential Diagnosis 





Abdom inal pain: o

Gastroenteritis

o

Appendicitis

o

Inflam m atory bowel disease

o

Intussusception

o

Meckel diverticulum

Arthralgias: o

Acute rheum atic fever

o

Polyarthritis nodosa

o

Juvenile rheum atoid arthritis

o

System ic lupus erythem atosus

Rash: o



Infection: 

Meningococcem ia



Bacterial sepsis: streptococcal or staphylococcal



Rocky Mountain spotted fever



Infectious m ononucleosis



Bacterial endocarditis



Viral exanthem

o

Traum a/child abuse

o

Functional platelet disorders

o

Throm bocytopenia

o

Vasculitis

o

Erythem a nodosum

o

Drugs/toxins

Renal disease:

Pa ge 2 2 4

o 

Acute glom erulonephritis

Testicular swelling: o

Incarcerated hernia

o

Orchitis

o

Testicular torsion

Treatment Initial Stabilization 

Intravenous fluids for shock



Packed red blood cells for m assive GI hem orrhage

ED Treatment 

Em ergent intervention for life-threatening conditions, if any



Nonsteroidal anti-inflam m atory drugs (NSAIDs; ibuprofen): o



Arthralgias

Prednisone: o

Severe abdom inal pain once life-threatening pathology excluded



o

Painful subcutaneous edem a or arthritis

o

Renal disease (high-dose pulse therapy required)

o

Central nervous system involvem ent

Polyclonal im m unoglobulin therapy: o

Severe, life-threatening disease (controversial)

Medication (Drugs) 

Ibuprofen: 600 m g (5â€“10 m g/kg per dose) PO q6h



Prednisone: 60 m g (1â€“2 m g/kg/24h) PO daily for 5â€“7

Pa ge 2 2 4

days

Follow-Up Disposition Admission Criteria 

Severe abdom inal pain



CNS findings



Gastrointestinal bleeding



Intussusception



Evidence of renal failure

Discharge Criteria 

Norm al platelet count



Norm al renal function



Minim al or no abdom inal pain



If steroids started, follow up within 24 hours.

References 1. Causey AL, Woodall BN, Wahl NG, et al. Henoch-SchÃ¶nlein purpura: four cases and a review. J Em erg Med. 1994;12(3):331â€“341. 2. Durbin DR, Liacouras CA. Gastrointestinal em ergencies. In: Fleisher GR, Ludwig S, ed. Textbook of Pediatric Em ergency Medicine . 4th ed. Philadelphia: Lippincott William s & Wilkins; 2000: 1017â€“1041. 3. Hurwitz S. Clinical Pediatric Derm atology. 2nd ed. Philadelphia: WB Saunders; 1993:539â€“541. 4. Robson W, Leung A. Henoch-SchÃ¶nlein purpura. Adv Pediatr. 1994;41:163. 5. Rostoker G, et al. High-dose im m unoglobulin therapy for severe

Pa ge 2 2 4

IGA nephropathy and Henoch-SchÃ¶nlein purpura. Ann Intern Med. 1994;120:476. 6. Rostoker G. SchÃ¶nlein-Henoch purpura in children and adults. Diagnosis, pathophysiology and m anagem ent. Biodrug. 2001;15(2):99â€“138. 7. Szer IS. Henoch-SchÃ¶nlein purpura: when and how to treat. J Rheum atol. 1996;23(9):1661â€“1665.

Codes ICD9-CM 287.0

ICD10 D69.0

Pa ge 2 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hepatic Encephalo pathy

Hepatic

Encephalopathy Matthew N. Graber

Basics Description 

Changes in behavior and consciousness associated with hepatic insufficiency and the accum ulation of substances norm ally m etabolized by the liver. This accum ulation occurs when the liver is unable to perform its norm al m etabolic activity secondary to either hepatocellular dysfunction or portal system ic shunting: o

Accum ulation of am m onia from : 

Protein degradation by colonic bacteria



Deam ination of glutam ine in sm all bowel



Accum ulated am m onia crosses bloodâ€“brain barrier and allows for form ation of elevated levels of cerebrospinal fluid (CSF) glutam ine.



Am m onia levels correlate poorly with degree of hepatic encephalopathy (HE).

o

Other neurotoxins 

Short-chain fatty acids



Phenols

Pa ge 2 2 5









Mercaptans



Am ino acids such as tryptophan

Increased levels of inhibitory neurotransm itters: o

Benzodiazepines

o

Î³-Am inobutyric acid (GABA)

o

Serotonin

Decreased levels of excitatory neurotransm itters: o

Glutam ate

o

Dopam ine

o

Aspartate

o

Catecholam ines

Other contributing factors to HE: o

CSF glutam ine levels correlate closely with degree of HE.

o

Decreased cerebral blood flow and oxygen

o

Increased glucose consum ption and possible hypoglycem ia

o

Zinc deficiency

Genetics Inherited errors of the urea cycle

Etiology 

Advanced cirrhosis or fulm inant hepatic failure with hepatocellular dysfunction often in association with portal hypertension



Precipitating events: o

GI bleeding (m ore com m on in elderly)

o

Hypokalem ia

o

Alkalosis

o

Sepsis (e.g., spontaneous bacterial peritonitis)

o

Constipation

o

Noncom pliance with treatm ent regim en in chronic

Pa ge 2 2 5

liver failure o

High-protein diet

o

Hypoglycem ia

o

Hypovolem ia (e.g., post-large-volum e paracentesis)

o

Azotem ia (e.g., diuretic induced)

o

Narcotics or sedatives, including alcohol

o

Zinc deficiency as m ultiple urea cycle enzym es are zinc dependent

o

Hepatocellular injury

o

Viral- or drug-induced hepatitis

o

Post portosystem ic shunt placem ent

o

Recurrent encephalopathy can occur without precipitating factors.

Diagnosis Signs and Symptoms 

Wide range of m ental status changes affecting behavioral, intellectual, neurom uscular function and level of consciousness



Signs and sym ptom s of associated chronic liver disease, portal hypertension, or fulm inant hepatic failure (FHF): o

Ascites

o

Spider angiom ata

o

Testicular atrophy

o

Muscle wasting

o

Easy bruising

o

Palm ar erythem a

o

Gynecom astia



Asterixis with m ild to m oderate encephalopathy



Fetor hepaticusâ€”peculiar sweet odor associated with

Pa ge 2 2 5

severe HE

Grading (West Haven Criteria) 

Stage 0: o

No apparent clinical changes

o

Abnorm al neurophysiologic and neuropsychologic tests



Stage I: o

Personality changes, irritability, depression or euphoria







o

Reversal of norm al sleep pattern

o

Im pairm ent of writing, drawing, addition, subtraction

Stage II: o

Significant behavioral changes, often inappropriate

o

Lethargy

o

Slow responses

o

Asterixis

o

Slurred speech

o

Ataxia

Stage III: o

Disorientation to tim e and place

o

Am nesia

o

Paranoia

o

Nystagm us

o

Hypoactive reflexes

o

Positive Babinski reflex

o

Sem istupor to stupor

Stage IV: o

Dilated pupils

o

Stupor or com a

Essential Workup 

Elicit history of liver disease and prior episodes of HE.

Pa ge 2 2 5



Clinical diagnosisâ€”altered m ental status with evidence of liver failure or portal hypertension



Search for precipitating cause (particularly GI bleeding and infection).



Check for electrolyte abnorm alities: o

Even m inim al abnorm alities m ay m anifest as significant clinical changes.

Tests Lab 

Blood am m onia level: o

Increased in HE

o

Level correlates poorly with the degree of HE.

o

Helpful in detecting HE in cases of altered m ental status of unknown cause

o

Norm al am m onia level with suspected HE warrants search for other causes of altered m ental status.

o



Level affected by: 

Dehydration/hypovolem ia



Infusion of am ino acid solution



Massive tissue breakdown

Hem occult testing and nasogastric lavage to rule out GI bleeding



CBC to search for anem ia



Cultures of blood, urine, and ascitic fluid to search for infectious cause



Electrolytes, BUN, creatinine, glucose



PT/INR with elevations suggesting significant liver failure



Liver profile/liver enzym es



Urinalysis



Toxicology screen for alternate cause of altered level of consciousness:

Pa ge 2 2 5

o 

Acetam inophen and alcohol level as necessary

Additional labs as clinical scenario dictates: o

Thyroid-stim ulating horm one (TSH)

o

Arterial blood gas (ABG)

o

Magnesium

o

Zinc level

o

Viral serology

Diagnostic Procedures/Surgery 

Chest radiograph for pneum onia and signs of congestive heart failure (CHF)



ECG for arrhythm ia and electrolyte im balance



Head CT scan: o

For new-onset altered m ental status, focal neurologic deficit, or suspected traum a

o 



Cerebral edem a and atrophy associated with HE

CSF exam ination: o

For new-onset or unexplained worsening of HE

o

CSF glutam ine level correlates with severity of HE.

Paracentesis for spontaneous bacterial peritonitis (SBP) workup and culture of ascitic fluid



EEG is usually abnorm al, m ost com m only with generalized slowing and other nonspecific changes.

P.505

Differential Diagnosis 

Alcohol withdrawal syndrom es including delirium trem ens



Asterixis seen in other m etabolic encephalopathies: o

Urem ia

o

CO 2 narcosis

o

CHF

Pa ge 2 2 5

o

Sedative overdose

o

Toxic confusional states secondary to: 

Medications



Illicit drugs (e.g., am phetam ines, cocaine, etc.)

o

Metabolic encephalopathy

o

Hypokalem ia

o

Hypocalcem ia and hypercalcem ia



Urem ia



Hypoglycem ia



Sedative use including alcohol intoxication



Head traum a with concussion or intracranial bleed



Cerebrovascular accident and neuropsychiatric disorders



Meningitis or encephalitis

Pediatric Considerations 

Consider Reye syndrom e early (m ost com m on cause of FHF in children) even if PT is only m ildly prolonged.



Consider fatty acid Î²-oxidation disorder: o

Freeze serum and urine sam ple for subsequent testing.

Treatment Initial Stabilization For advanced stages of HE: 

Oxygen and airway protection



Cardiac m onitor



Fluid resuscitation



Usual initial altered m ental status treatm ent of naloxone, D 5 0 W (or bedside glucose) and thiam ine

ED Treatment

Pa ge 2 2 5

Identification and rem oval of precipitating factors is key and m ay im prove clinical picture alone.

Alert 

Liver failure predisposes patients to both hypoglycem ia and HE, and these can be additive to the clinical picture; therefore, frequent glucose checks are of absolute im portance.





Treatm ent of com plicating conditions: o

Acute GI bleeding

o

Sepsis

o

Electrolyte abnorm alities

o

Coagulopathy

o

Renal and electrolyte disturbances

Avoid sedative/narcotics if possible: o

If necessary, use agents not m etabolized by the liver.



Increase nitrogen elim ination: o

Bowel cleansing with laxatives and nonabsorbable sugars (i.e., lactulose, sorbitol PO or per rectum [PR])



Decrease am m onia-producing intestinal flora (in com bination with lactulose): o

Neom ycin (nephrotoxic and ototoxic)

o

Metronidazole



Correct zinc deficiency with zinc acetate or sulfate.



Short-term restriction of protein intake in diet



Flum azenil in patients who have received benzodiazepines m ay provide m oderate, short-term im provem ent.

Alert 

Avoid flum azenil unless you are sure that the patient is not a chronic alcoholic or benzodiazepine user as resultant

Pa ge 2 2 5

seizures m ay occur. 

Precautions to prevent bodily harm to the confused patient with HE



Liver transplantation provides cure for severe, spontaneous, or recurrent HE.



Possibly of benefit: o

L-carnitine

o

Album in dialysis

o

Brom ocriptine

o

Broad-spectrum antibiotic coverage

o

N-acetylcysteine

o

Lactobacillus acidophilus supplem entation

o

Ornithine aspartate

o

Benzoate

o

Branched-chain am ino-acid supplem entation

o

Chelation of m anganese with edatate calcium disodium

Medication (Drugs) 

Dextrose: 1 am p (25 g) of 50% dextrose 1â€“2 m L/kg (child: 2 m L/kg D 2 5 W) IV



Lactulose: 30 m L (peds: 0.3 m L/kg) PO or via nasogastric (NG) tube q6h titrated to produce 2 or 3 soft stools per day and stool pH <5



Metronidazole: 250 m g (peds: 10â€“30 m g/kg/d) q8h for 2 weeks



Narcan: 2 m g (peds: 0.1 m g/kg) IV/IM initial dose



Neom ycin: 1â€“3 g (peds: 50â€“100 m g/kg/d) PO q6h



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV/IM



Zinc acetate or sulfate: 220 m g PO q8h

Pa ge 2 2 5

Follow-Up Disposition Admission Criteria 

HE stage II, III, or IV or inadequate social support



Advanced stages of HE to ICU with urgent GI consult



Associated com plicating condition (GI bleeding and sepsis)



Uncertainty about cause of altered m ental status

Discharge Criteria 

Known chronic or interm ittent HE



Grades 0 or I with rem ediable cause



Adequate supervision at hom e



Close follow-up



Those appropriate for discharge should go hom e with: o

Low-protein diet

o

Lactulose prescription

Issues for Referral Refer to prim ary physician or GI for consideration of m edication or diet changes if recurrent early stage HE episodes.

References 1. Fraser C, Arieff AI. Hepatic encephalopathy. Med Clin N Am . 1985;73:793. 2. Riordan SM, William s R. Treatm ent of hepatic encephalopathy. New Engl J Med. 1997;337(7):473â€“479. 3. Vaquero J, et al. Infection and the progression of hepatic encephalopathy in acute liver failure. Gastroenterology. 2003;125(3):755â€“764.

Codes

Pa ge 2 2 5

ICD9-CM 572.2 Hepatic com a

Pa ge 2 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hepatic Injury

Hepatic Injury

Saul Levine

Basics Description 

The size of the liver places it at significant risk for injury: o

The liver is the solid organ m ost frequently injured in penetrating traum a.

o

Highly susceptible to blunt injuries, by direct blow or deceleration forces



Mechanism of injury and description of forces are im portant factors in evaluating patients for possible hepatic injury: o

Blunt traum a: 

Obtain inform ation about the forces and direction (horizontal or vertical) of any deceleration or com pressive forces.

o



Penetrating traum a: 

Type and caliber of the weapon



Distance from the weapon



Variety and length of knife or im paling object

Hepatic injuries are graded by severity, ranging from subcapsular hem atom a and lacerations to severe hepatic fragm entation.

Pa ge 2 2 6



Associated conditions include rib fractures and injuries to the spleen, diaphragm , kidney, lung, gallbladder, pancreas and blood vessels.



Overall m ortality of hepatic injury is reported at 8â€“10%.

Pediatric Considerations 

Poorly developed m usculature and relatively sm aller anteroposterior diam eter increase the vulnerability of liver to com pressive forces in children.



Nonoperative m anagem ent of isolated blunt hepatic traum a is increasingly com m on in pediatric traum a.

Etiology 

Traum a: o

o

Blunt m echanism : 

Deceleration



Acceleration



Com pression

Penetrating m echanism : 

Stab wound



Gunshot wound



Im paled object

Diagnosis Signs and Symptoms History History of traum a usually available from patient or prehospital providers

Physical Exam 

Neither sensitive nor specific for hepatic injury

Pa ge 2 2 6





System ic signs related to acute blood loss: o

May present with dizziness and weakness

o

Signs of shock including tachycardia and hypotension

Local signs: o

Right upper quadrant tenderness

o

Guarding

o

Abdom inal distention

o

Rigidity

o

Rebound

o

Tenderness

o

Contusions/abrasions

o

Penetrating wounds to the right chest, flank, or abdom en

Essential Workup 

Physical exam is unreliable.



Objective evaluation includes im aging of the abdom en or surgical exploration.

Tests Lab 

No hem atologic laboratory studies are specific for diagnosis of injury to the liver.



Obtain baseline hem oglobin level.



Liver function tests are not helpful in the acute setting.

Imaging 

Plain abdom inal radiographs: o



Little value

Bedside ultrasound: o

Screening tool for both blunt and penetrating abdom inal traum a

o

Procedure of choice in unstable patient

Pa ge 2 2 6

o

May identify intra-abdom inal fluid in the hepatorenal (Morison) pouch or parenchym al injuries

o

Suggests intra-abdom inal hem orrhage in patient with blunt, m ultiple-organ traum a



CT scan with intravenous contrast: o

Best depicts extent of hepatic injury and injuries to adjacent organs

o

Requires patient to be hem odynam ically stable

o

Extravasation of intravenous contrast during arterial phase of CT injection indicative of vascular or high-grade liver injury requiring surgical intervention

Diagnostic Procedures/Surgery 

Diagnostic peritoneal lavage (DPL): o

Usually done in conjunction with traum a surgeon

o

Sensitive for presence of hem operitoneum

o

Nonspecific for source of bleeding

o

Surgery and exploratory laparotom y if positive

o

Operative m anagem ent m ay be necessary for unstable patients and those with high-grade lesions.



Lower-grade injuries have been increasingly m anaged successfully without surgery.

Differential Diagnosis 

Other causes of intraperitoneal injury



Retroperitoneal injury



Thoracic injury



Diaphragm atic injury



Splenic injury

Treatment

Pa ge 2 2 6

Pre Hospital 

Obtain details of m echanism of injury.



Initiate large-bore intravenous access: o



Hem orrhage m ay be rapid and life threatening.

Moist saline dressings over penetrating wounds or evisceration



Direct pressure to control active bleeding



Full spinal im m obilization except in isolated penetrating traum a

Initial Stabilization Airway, breathing, and circulation m anagem ent: 

Control airway as needed; m ay have associated injuries including head injury.



Supplem ental oxygen, cardiac m onitor, pulse oxim etry



Adequate intravenous access, including central line, intraosseous line, and cutdown as dictated by the patient's status



Fluid resuscitation, initially with 2 L of crystalloid (norm al saline or Ringer lactate), followed by blood products as needed

P.507

ED Treatment 

Im m ediate laparotom y m ay be appropriate in the acutely injured patient with the following conditions: o

Hem odynam ic instability

o

Gunshot wounds to the anterior abdom en

o

Frank signs of intraperitoneal hem orrhage

o

Indications based on diagnostic procedures, such as diagnostic peritoneal lavage

Pa ge 2 2 6

o 

Failure of nonoperative m anagem ent

Stab wounds can be m anaged by local wound exploration followed by ultrasound or diagnostic peritoneal lavage when intraperitoneal penetration is not dem onstrated or equivocal.



Consider nonoperative m anagem ent for the following patients: o

Hem odynam ically stable with norm al m ental status

o

No evidence of other intra-abdom inal injury

o

Isolated low-grade (1â€“3) hepatic injury confirm ed by im aging study

o

Transfusion requirem ents â‰¤2 units of packed red blood cells



High-grade liver injuries (4 and 5) have less successful nonoperative rates.



Diet: nothing per m outh (NPO)



Activity: strict bedrest



Special therapy: o

Angiography with em bolization: selective use in patients with persistent bleeding m ay decrease the need for operative m anagem ent and blood transfusions.

Follow-Up Disposition Admission Criteria 

All patients with hepatic injury require hospitalization for definitive laparotom y or close hem odynam ic observation with serial exam inations or CT scans as well as hem atocrit

Pa ge 2 2 6

m easurem ents. 

Intensive care unit adm ission is usually indicated in the first 48 hours after injury.

Discharge Criteria Patients with proven or suspected hepatic injuries should not be discharged.

Issues for Referral Report all gunshot and stab wounds to appropriate local authorities.

References 1. Jacobs IA. Nonoperative m anagem ent of blunt splenic and hepatic traum a in the pediatric population. Am Surg. 2001;67:149â€“154. 2. Leone RT Jr. Nonoperative m anagem ent of pediatric blunt hepatic traum a. Am Surg. 2001;67:138â€“142. 3. Malhotra AK, Fabian TC, Croce MA, et al. Hepatic injury: a paradigm shift from operative to nonoperative m anagem ent in the 1990s. Ann Surg. 2000;231:804â€“813. 4. Marx J. Abdom inal traum a. In: Marx J, Hockberger R, Walls R, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:415â€“436. 5. Ochsner MG, Jaffin JH, Golocovsky M, et al. Major hepatic traum a. Surg Clin North Am . 1993;73:337â€“352. 6. Townsend CM. Abdom inal traum a. In: Townsend CM, Beaucham p DR, Evers MB, et al., eds. Sabiston Textbook of Surgery. 17th ed. Philadelphia: WB Saunders; 2004:521â€“523. 7. Trunkey DD. Hepatic traum a: contem porary m anagem ent. Surg Clin North Am . 2004;84:437â€“450.

Miscellaneous SEE ALSO: Abdom inal Traum a, Blunt; Abdom inal Traum a,

Pa ge 2 2 6

Penetrating; Abdom inal Traum a, Im aging; Colon Traum a; Diaphragm atic Traum a; Pancreatic Traum a; Renal Injury; Sm all Bowel Injury; Traum a, Multiple

Codes ICD9-CM 864.00 Injury to liver

ICD10 S36-1 Injury of liver or gallbladder

Pa ge 2 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hepatitis

Hepatitis

Michael Schmidt Amer Aldeen

Basics Description 

Inflam m ation of the liver owing to infectious, toxic, and autoim m une disorders



Infectious causes are the m ost com m on: o

Of infectious causes, hepatitis A is the cause of 40%, hepatitis B 30%, hepatitis C 20%

Etiology Mechanism 



Hepatitis A (HAV): o

Mean incubation: 1 m onth

o

Transm ission: enteric > sexual

o

No chronic disease

o

Fulm inant hepatic failure (FHF) in 0.1%

Hepatitis B (HBV): o

Mean incubation: 2 m onths

o

Transm ission: enteric, blood, sexual

o

10% progress to chronic disease: 

Risk increases with earlier age of initial

Pa ge 2 2 6

infection  o 



FHF in 1%

Risk of cirrhosis and hepatocellular carcinom a

Hepatitis C (HCV): o

Mean incubation: 1.5 m onths

o

Transm ission: blood > sexual

o

Eighty percent progress to chronic disease.

o

FHF extrem ely rare

o

Risk of cirrhosis and hepatocellular carcinom a

Hepatitis D (HDV): o

Mean incubation: 1 m onth

o

Superinfection of HBV, augm ents all pathologic actions of HBV





o

Sam e transm ission as HBV

o

FHF in 3%

Hepatitis E (HEV): o

Mean incubation: 1 m onth

o

Transm ission: enteric > blood

o

FHF in 1%

Secondary hepatitis viruses: cytom egalovirus, Epstein-Barr virus, herpes virus, HIV





Toxin-induced: o

Acetam inophen (m ost com m on)

o

Ethanol

o

Isoniazid

o

Ecstasy (MDMA)

o

Industrial solvents and cleaning solutions

o

Iron (hem ochrom atosis)

Auto-im m une hepatitis

Pediatric Considerations 

Vast m ajority of cases are caused by HAV.



Perinatal HBV infection develops into chronic disease 90%

Pa ge 2 2 7

of the tim e.

Pregnancy Considerations 

FHF occurs in 20% of pregnant wom en with HEV for unknown reasons.



Acute fatty liver of pregnancy and HELLP syndrom e (h em olysis, elevated liver enzym es, and low platelets) are pregnancy-specific causes of hepatitis.



All form s of im m unoprophylaxis are safe during pregnancy.

Diagnosis Signs and Symptoms 

Often asym ptom atic



Often m isdiagnosed as a nonspecific viral syndrom e or gastroenteritis







Preicteric phase: o

Flulike illness with fever, chills, m alaise

o

Nausea, vom iting, anorexia

o

Aversion to sm oking or certain foods

Icteric phase: o

Present in 70% of HAV, 30% of HBV, and 20% of HCV

o

Jaundice

o

Dark urine, light stools, pruritus

o

Right upper quadrant (RUQ) pain

o

Tender hepatom egaly

HAV and HEV are clinically indistinguishable, but HEV is found only in developing countries.

Essential Workup 

Detailed history for risk factors for hepatitis, including

Pa ge 2 2 7

toxic exposure and drug use 

Viral serologies are the m ainstay of diagnosis of viral causes.

Tests Lab 

CBC with diff



Electrolytes, BUN, creatinine, glucose





o

Azotem ia with hepatorenal syndrom e

o

Hypoglycem ia with severe liver dam age

Liver function tests (LFTs): o

Elevation in transam inases reflects injury

o

Degree of elevation does not correlate with severity.

Alkaline phosphatase: o

If very elevated, consider prim ary cholestatic process rather than viral hepatitis.



Bilirubin: o

Mild to m oderate elevation of conjugated bilirubin



Am ylase, lipase



PT/PTT/INR: o



Am m onia level: o



Prolonged PT/INR reflects m ore severe injury.

For patients with altered m ental status

Viral serologies: o

o

HAV: 

Anti-HAV IgM: acute infection



Anti-HAV IgG: previous exposure and im m unity

HBV: 

HBsAg m ay or m ay not be positive in acute infection.



Anti-HBc IgM: acute infection



Anti-HBs IgG: im m unity

Pa ge 2 2 7

o

Chronic HBV: 

HBsAg positive



HBeAg: active viral replication and high infectivity

o

HCV: 

Anti-HCV: confirm atory within 10 weeks of infection





Viral PCR: m ost specific test

o

HDV: anti-HDV or viral RNA

o

HEV: anti-HEV or viral RNA

Î±-fetoprotein for chronic HBV or HCV to evaluate for hepatocellular carcinom a



Monospot: for EBV



Urinalysis

P.509

Imaging 

Head CT to evaluate hepatic encephalopathy



RUQ ultrasound to evaluate for biliary obstruction

Differential Diagnosis 

Alcohol hepatitis



Autoim m une hepatitis



Nonalcoholic fatty liver disease



Toxic hepatitis



Hem ochrom atosis



Cholecystitis



Cholangitis



Liver abscess



Wilson disease



Infectious m ononucleosis

Pa ge 2 2 7



Heat stroke



HELLP syndrom e



Fitz-Hugh and Curtis syndrom e

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs) for FHF and severe hepatic encephalopathy

ED Treatment 

Treat hypovolem ia aggressively with isotonic fluids.



Correct electrolyte im balance.



Treat vom iting with m etoclopram ide.



Avoid hepatotoxic agents: acetam inophen, alcohol, phenothiazines.



Correct coagulopathy if active bleeding.



Ursodeoxycholic acid or cholestyram ine for cholestasis-induced itching



Evaluate for the differential diagnoses and treat accordingly.

Contact Immunoprophylaxis 

HAV: o

HAV IG 0.02 m L/kg IM within 2 weeks of exposure

o

HAV vaccine 1 m L (peds: 0.5 m L) IM at 0 and 6 m onths (com plete 2 weeks before exposure)



HBV: o

HBV IG 0.06 m L/kg IM within 10 days of exposure

o

HBV vaccine 1 m L (peds: 0.5 m L) IM at 0, 1, and 6 m onths



No effective im m unoprophylaxis for HCV, HDV, or HEV

Pa ge 2 2 7

Medication (Drugs) 

Cholestyram ine: 4 g PO 1â€“6 tim es per day



Dextrose D 5 0 W: 1 am p or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Metoclopram ide: 10 m g IV/IM q6hâ€“q8h, 10â€“30 m g PO q.i.d.



Naloxone: 2 m g (peds: 0.1 m g/kg) IV/IM



Thiam ine: 100 m g (peds: 50 m g) IV/IM



Ursodeoxycholic acid: 3 m g/kg t.i.d.

Follow-Up Disposition 

Most patients will be discharged hom e with close gastroenterology or infectious disease follow-up for further serologic testing.

Admission Criteria 

Intractable vom iting, dehydration, or electrolyte im balance not responding to ED treatm ent



Acute hepatitis with evidence of significant liver dysfunction: o

PT >3 seconds above control or INR >1.5

o

Bilirubin >20 m g/dL

o

Hypoglycem ia

o

Album in <2.5 g/dL



ICU adm ission for FHF



Hepatic encephalopathy



Pregnancy, im m unocom prom ised host, or possibility of

Pa ge 2 2 7

toxic hepatitis

Discharge Criteria 

Strict personal hygiene instructions



Avoid acetam inophen and alcohol.

References 1. Buggs AM. Hepatitis. http://www.em edicine.com , Aug 24, 2004. Last accessed 4/4/05. 2. Em erson SU, Purcell RH. Running like waterâ€”the om nipresence of hepatitis E. N Engl J Med. 2004;351:23â€“67. 3. Liang TJ, Reherm ann B, Seeff LB, et al. Pathogenesis, natural history, treatm ent, and prevention of hepatitis C. Ann Intern Med. 2000;132:296. 4. Liaw YF, Tsai SL, Sheen IS, et al. Clinical and virological course of chronic hepatitis B virus infection with hepatitis C and D m arkers. Am J Gastroenterol. 1998;93:354. 5. Tong MJ, el-Farra NS, Grew MI. Clinical m anifestations of hepatitis A: recent experience in a com m unity teaching hospital. J Infect Dis. 1995;171(suppl 1):S15.

Miscellaneous SEE ALSO: Hepatic Encephalopathy; Cholecystitis

Codes ICD9-CM 573.3

ICD10 K75.9

Pa ge 2 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hepato renal Syndro m e

Hepatorenal

Syndrome Anwer Hussain

Basics Description 

Renal failure (RF) in patients with acute or chronic liver disease with no other identifiable cause of renal pathology



Hepatorenal syndrom e (HRS) represents significant decline in renal perfusion due to severe liver disease: o

Type I hepatorenal syndrom e: 

Acute form with spontaneous RF in patients with liver disease



Rapidly progressive



Decrease in creatinine clearance (CrCl) by 50% or doubling of Cr in 2 weeks (>2.5)



80% m ortality within 2 weeks



Seen with acute liver failure or alcoholic hepatitis

 o

Oliguric or anuric

Type II hepatorenal syndrom e: 

Slow course of RF



Seen in patients with diuretic resistant ascites

Pa ge 2 2 7

 

Lower m ortality rate than type I HRS

Hallm arks of HRS: o

Prerenal disease

o

Reversible renal vasoconstriction and m ild system ic hypotension

o

Kidneys have norm al histology and structure.

o

Lack of im provem ent in renal function after volum e expansion



Liver disease causes system ic vasodilation with decrease in arterial blood volum e: o

Reflex activation of sym pathetic nervous system

o

Activation of renin-angiotensinâ€“aldosterone system (RAAS)

o



Stim ulation of num erous vasoactive substances: 

Nitric oxide



Prostacyclin



Atrial natriuretic peptide (ANP)



Arachidonic acid m etabolites



Platelet-activating factor



Endothelins



Catecholam ines



Angiotensin II



Throm boxane

Action of vasoconstrictors prevails over vasodilator effects: o

Renal hypoperfusion ensues due to renal cortical vasoconstriction.

o

Decrease in renal blood flow and glom erular filtration rates



Decreased urine sodium excretion (U Na <10 m Eq/d)



Incidence of HRS: o

18% at first year, 39% at 5 years

Pa ge 2 2 7



Hyponatrem ia and high plasm a renin levels are risk factors.

Etiology 

Chronic liver disease, especially alcohol related (cirrhosis, severe alcoholic hepatitis)



Fulm inant hepatic failure



Precipitating factors: o

o

o

Decreased effective blood volum e: 

GI bleeding



Vigorous diuresis



Large-volum e paracentesis

Use of nephrotoxic agent: 

Nonsteroidal anti-inflam m atory drugs (NSAIDs)



Am inoglycoside

Sepsis

Signs and Symptoms Signs of acute or chronic liver disease: 

Signs of portal hypertension



Ascites, often tense



Progressive oliguria



Jaundice or hepatic encephalopathy



Coagulopathy



Tachycardia



Hypotension



Dyspnea, tachypnea due to tense ascites

History Acute or chronic hepatic disease with advanced hepatic failure and portal hypertension

Physical Exam Consistent with severe hepatic disease

Pa ge 2 2 7

Essential Workup 

Azotem ia in setting of liver disease



Identify any precipitating factors.

Tests Lab 

CBC: o



Anem ia due to GI bleed

Electrolytes: o

Hyperkalem ia

o

Acidosis



Glucose



Elevated BUN, creatinine (Cr): o

Norm al Cr found with low glom erular filtration rate (GFR) in association with m uscle wasting, poor nutrition, and ascites

o

Cr increased by som e m edications (cim etidine, trim ethoprim , and spironolactone) due to inhibition of tubular secretion of creatinine

o

Hyperbilirubinem ia can artifactually lower serum creatinine.



PT, PTT



Urinalysis o

Absence of casts distinguishes HRS from acute tubular necrosis (ATN).

o 

Check for urinary tract infection (UTI).

Spot urine sodium and creatinine, and serum and urine osm olality: o

Spot urine Na + <10 m Eq/L

o

Fractional excretion of Na + <1%

o

Urine/plasm a creatinine >30:1

o

Hyperosm olar urine

Pa ge 2 2 8



24 hour urine output (low in absence of diuretics)



24 hour urine creatinine clearance: o

Accurately assess GFR



Blood, ascitic fluid, and urine culture as indicated



Urinary excretion of Î² 2 -m icroglobulinâ€”useful m arker of acute tubular dam age

Imaging 

CXR for signs of congestive heart failure (CHF) or fluid overload



ECG for dysrhythm ia or signs of hyperkalem ia



Renal ultrasound: rule out obstruction



Central venous pressure (CVP) m easurem ents: o



Differentiates prerenal (low) from HRS (elevated)

Duplex Doppler ultrasonography can be used to assess degree of renal vasoconstriction.

P.511

Differential Diagnosis 

HRS is diagnosis of exclusion.



ATN:



o

Urine sodium >30 m Eq/L

o

Urine osm olality equals plasm a osm olality.

o

Urine casts and cellular debris

Prerenal azotem ia: o

Urine output im proves following correction of hypovolem ia.



Obstruction



Interstitial nephritis



Postâ€“liver transplant renal dysfunction due to: o

HRS due to failure of transplanted liver

Pa ge 2 2 8

o

Medications, e.g., cyclosporine

o

Pre-existing renal disease

o

Perioperative hypovolem ia

Treatment Pre Hospital Attention to hypotension, active GI bleeding, respiratory distress

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Aggressive correction of hypovolem ia with: o

0.9% norm al saline (NS) IV fluid

o

Colloid volum e expanders: 100 g album in in 500 m L of norm al saline



o

Closely m onitor clinical status including use of CVP

o

Urine output should im prove with prerenal azotem ia

Manage life-threatening em ergencies of renal failure: o

Hyperkalem ia

o

Severe acidosis

o

Hypoxem ia

ED Treatment 

Exclude reversible or treatable causes of HRS.



Supportive care until hepatic function recovers



Do no harm â€”discontinue potentially nephrotoxic agents: o

NSAIDs

o

Am inoglycosides

o

Dem eclocycline



Treat prim ary disease



Search for and treat coexisting renal disease



Correct electrolyte im balances

Pa ge 2 2 8



Treat any associated cardiopulm onary disorder and hypoxia



Initiate broad-spectrum antibiotics if sepsis suspected



Correct liver associated com plications:



o

Obstructive jaundice

o

Hepatic encephalopathy

o

Hypoglycem ia

o

Peritonitis

Large-volum e paracentesis with IV album in replacem ent (to relieve tense ascites):



o

Increases renal blood flow

o

May briefly im prove HRS

Dialysis: o

Useful in correcting fluid, electrolytes, acid-base im balances, pulm onary edem a

o

Indicated for patients who have likelihood of hepatic regeneration, hepatic recovery, or liver transplantation



Liver transplant: o

Only available cure

Medication (Drugs) 



Dopam ine (renal dose): 2â€“5 Âµg/kg/m in: o

May im prove renal function

o

Not curative

Midodrine (7.5â€“12.5 m g PO t.i.d.) and octreotide (100â€“200 Âµg SC t.i.d.):



o

Octreotide is analog of som atostatin.

o

Midodrine is sym pathom im etic drug.

Misoprostol: 0.4 m g PO q.i.d. o

Synthetic analog of prostaglandin E 1

Pa ge 2 2 8





Ornipressin: 2-hour infusion at 6 IU/h: o

Vasopressin analog

o

Increases renal perfusion pressure and function

o

Not available in United States

Terlipressin: 2 m g/d for 2 days o

Synthetic analog of vasopressin

o

Intrinsic vasoconstrictor activity

o

Not available in United States

Follow-Up Disposition Admission Criteria 

All suspected HRS with GI and nephrology consults



ICU adm ission for associated cardiopulm onary disease, hepatic encephalopathy, m arked electrolyte im balances

Discharge Criteria None

References 1. Arroyo V, Guevara M, Gines P. Hepatorenal syndrom e in cirrhosis. Gastroenterology. 2002;122:1658â€“1676. 2. Dagher L, Moore K. The hepatorenal syndrom e. Gut. 2001;49:729â€“737. 3. Gentilini P, Vizzutti F, et al. Ascites and hepatorenal syndrom e. Eur J Gastroenterol Hepatol. 2001;13:313â€“316. 4. Gines P, Guevara M, Arroyo V, et al. Hepatorenal syndrom e. Lancet. 2003;362:1819â€“27. 5. Roberts LR, Kam ath PS. Ascites and hepatorenal syndrom e: pathophysiology and m anagem ent. Mayo Clin Proc. 1996;71:874.

Pa ge 2 2 8

6. Wong F, Blendis L. New challenge of hepatorenal syndrom e: prevention and treatm ent. Hepatology. 2001;34:1242â€“1251

Miscellaneous SEE ALSO: Hepatic Encephalopathy; Hepatitis

Codes ICD9-CM 572.4

ICD10 K76.7

Pa ge 2 2 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hernia

Hernia

Jenny Lu

Basics Description 

Abnorm al protrusion of peritoneal contents through defect in abdom inal wall



Incarceration: o

Contents in hernial sac cannot be m anipulated back into abdom en.



Strangulation: o

Com prom ise of vascular supply to entrapped bowel contained in hernia leading to ischem ia and gangrene

o

Tender, unreducible hernia with signs and sym ptom s of bowel obstruction (nausea/vom iting, fever, leukocytosis)

Etiology 

Indirect inguinal hernia: o

Results from persistent process vaginalis

o

Herniation of peritoneal contents through internal ring

o 

Right side m ore com m on than left

Direct inguinal hernia: o

Owing to defect or weakness in transversalis area in

Pa ge 2 2 8

Hesselbach triangle:







Inguinal ligam ent inferiorly



Inferior epigastric vessels laterally



Lateral border of rectus abdom inus m edially



Herniation through Hesselbach triangle

Incisional hernia: o

Resultant breakdown of surgical fascial closure

o

Herniation through surgical fascia (incisional)

Fem oral hernia: o

Peritoneum herniates into fem oral canal beneath inguinal ligam ent.

o

Frequently incarcerates due to protrusion through sm all orifice



Obturator hernia: o

Passes through obturator m em brane and exits beneath pectineal m uscle



Um bilical hernia: o

Failure of um bilical ring to close, congenitally

o

Protrusion through fibrom uscular um bilical ring/um bilicus

o

20â€“45% recurrence rate

Diagnosis Signs and Symptoms History 

Pain/swelling: o



Localized to region of hernia

Constant pain, vom iting, fever m ay indicate: o

Incarceration

Pa ge 2 2 8

o

Strangulation

o

Obstruction

Physical Exam Vital signs: 

Usually norm al



Tachycardia, hypotension with strangulation/sepsis

Inguinal Hernia 



Pain o

Localized to inguinal region

o

Exacerbated by straining/positional changes

o

Relieved by rest

Swelling: o

Males: interm ittent bulge in scrotum

o

Fem ales: bulge im m ediately inferior to inguinal ligam ent or in labia



Swelling of sperm atic cord, scrotum , or testes



Valsalva m aneuver done while finger directed toward internal ringâ€”m ay allow hernia sac to descend against finger

Femoral Hernia Pain/swelling: 

Localized to fem oral orifice inferior to inguinal ligam ent

Incisional Hernia Pain/swelling: 

Localized to previous incision/scar

Obturator Hernia 

Nonspecific abdom inal pain



Interm ittent intestinal obstruction



Weight loss



Pain:

Pa ge 2 2 8

o

Owing to pressure on obturator nerve from hernia (Howship-Rom berg sign)

o

Along m edial thigh

o

Radiating to hip

o

Relieved with thigh flexion

o

Exacerbated by hip extension, adduction, or external rotation

Spigelian Hernia 

Abdom inal pain/m ass along anterior abdom inal wall



Increased pain with m aneuvers increasing intra-abdom inal pressure



Interm ittent bowel obstruction



Palpable m ass along spigelian line: o

Convex line extending from costal arch to pubic tubercle along lateral edge of rectus m uscle

Pediatric Considerations 

Diagnosis difficult: o

Parents com plain of bulge in inguinal area often no longer present at tim e of exam .

o

Incarcerated hernias m ay present with irritability, abdom inal pain, or interm ittent vom iting.



Incidence of incarceration/strangulation is 10â€“20%: o

Greater than 50% in patients younger than 6 m onths of age

o 

Incidence of incarceration higher in girls than boys

Um bilical hernias: o

Strangulation and incarceration rare

o

Most close spontaneously.

o

Most surgeons will delay closure until 4 years of age.

Essential Workup Careful history and physical exam :

Pa ge 2 2 8



Palpate inguinal/fem oral area for tenderness/m asses.



Repeat exam ination while patient is standing/straining.

P.513

Tests Lab 

CBC: o



Electrolytes, BUN/creatinine, glucose: o



Leukocytosis with strangulation

If vom iting/dehydration

Urinalysis: o

For identifying genitourinary (GU) causes of groin pain

Imaging 

Plain abdom inal radiographs: o

Obstructive bowel pattern with incarceration or strangulation



Ultrasound: o



For identifying m asses in groin or abdom inal wall

CT: o

To diagnose obturator or spigelian hernia

o

Inability to obtain good exam owing to body habitus

Differential Diagnosis 

Hydrocele



Varicocele



Lym phadenitis



Testicular torsion



Testicular tum or



Undescended testis

Pa ge 2 2 9



Lym phogranulom a venereum

Treatment Initial Stabilization 0.9% norm al saline (NS) IV fluid resuscitation for bowel strangulation, obstruction, or sepsis: 

Adults: 1 L bolus



Peds: 20 m L/kg bolus

ED Treatment 



Incarcerated, unreducible, or strangulated hernias: o

Intravenous fluids (IVFs)

o

Nasogastric tube (NGT)

o

Surgical consultation

o

Preoperative antibiotics for strangulated hernia

Hernia reduction m ethod: o

Intravenous sedation (benzodiazepine) and analgesia (opiate) if necessary

o

Place in Trendelenburg.

o

Allow 20â€“30 m inutes for spontaneous reduction of hernia.

o

Manual reduction: 

Place constant, gentle pressure on hernia.



For inguinal hernias, achieve reduction by putting fingers of one hand on internal ring while gently pulling then pressing on hernia distal to external ring.

o

Obtain surgical consultation if reduction is unsuccessful after one or two attem pts.

o

Contraindications to reduction include:

Pa ge 2 2 9

o



Fever



Leukocytosis

Com plications: 

Introduction of strangulated bowel into abdom en



Further ischem ia/necrosis occurs with no clinical im provem ent.

o

Reduction in girls m ay be m ore difficult if ovary encased within hernia.

Medication (Drugs) Antibiotics (Controversial) 

Cefoxitin: 1â€“2 g (peds: 0â€“7 days: 40 m g/kg/24h q12h; >7 days: 80â€“160 m g/kg/24h div. q4hâ€“q6h) IV q6hâ€“q8h



Cefazolin: 1â€“1.5 g (peds: 25â€“50 m g/kg/d div. q6hâ€“q8h) IV q6hâ€“q8h

Analgesics 

Fentanyl: 1â€“4 Âµg/kg (peds: 1â€“4 Âµg/kg IV PRN) IV PRN



Cefazolin:1â€“1.5 g (peds: 25â€“50 m g/kg/d div. q6â€“8h) IV q6â€“8h

Sedatives 

Midazolam : 2.5â€“5 m g (peds: 0.07 m g/kg) IV PRN



Morphine sulfate: 2.5â€“10 m g per dose (peds: 0.1â€“0.2 m g/kg IV/IM/SC q2hâ€“q4h) IV/IM/SC q2hâ€“q6h PRN

Follow-Up

Pa ge 2 2 9

Disposition Admission Criteria 

Strangulated hernias require im m ediate surgical intervention.



Incarcerated hernias require adm ission for urgent surgical intervention.



Intestinal obstruction



Peritonitis



Vom iting/dehydration



Severe pain

Discharge Criteria 

After successful reduction has been achieved



Scheduled re-evaluation in 24 hours and referral to surgery

Issues for Referral As above

References 1. Brooks DC. Abdom inal Wall Hernias. Available at http://www.uptodate.com . Last updated: May 19, 2006. 2. Brooks DC. Treatm ent of Groin Hernias. Available at http://www.uptodate.com . Last updated: May 18, 2006. 3. Celdran A. Antibiotic use for hernia repair, J. Am Coll Surg. 2006;203(1):138â€“9. 4. Manthey D. Hernias. Available at http://www.em edicine.com /em erg/topic251.htm . Last accessed October 2004. 5. Mensching JJ, Musielewicz AJ. Abdom inal wall hernias. Em erg Med Clin North Am . 1996;14:739â€“756. 6. Miller PA, Mezwa DG, Feczko PJ, et al. Im aging of abdom inal hernias. Radiographics. 1995;15(2):333â€“347.

Pa ge 2 2 9

7. Perez AR. A random ized double-blind, placebo-controlled trial to determ ine the effectiveness of antibiotic prophylaxis for tension-free m esh herniorraphy, J. Am Coll Surg. 2005;200(3):393â€“7: discussion 397â€“8. 8. Ram sook C, Endom EE. Overview of inguinal hernia in children. Available at http://www.uptodate.com . Last accessed April 2006. 9. Townsend CM. Sabiston Textbook of Surgery. 17th ed. Philadelphia: WB Saunders; 2004.

Codes ICD9-CM 553.9

ICD10 K46.9

Pa ge 2 2 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Herpes Sim plex

Herpes Simplex

Joanne Davis Mark Richmond

Basics Description 

Viral disease characterized by recurrent painful vesicular lesions of m ucocutaneous area



Lips, genitalia, rectum , hands, and eyes m ost com m only involved



Characterized by latency in sensory ganglia and reactivation



Incubation period is approxim ately 4 days from exposure.



Viral shedding occurs from 7â€“10 days (up to 23 days) in prim ary infection and 3â€“4 days in recurrent infections.



Neonatal infections can occur in utero, intrapartum (m ost com m on), or postnatal; occur in 1/3,500 births per year in the United States



Hum an-to-hum an transm ission; 60â€“90% of population is infected with HSV-1 or HSV-2.



More com m on in blacks than whites in ages <40



Fem ales affected m ore than m ales

Etiology 

Herpes sim plex type 1 (HSV-1) or type 2 (HSV-2) are DNA

Pa ge 2 2 9

viruses of the Herpesviridae fam ily. 

Viral transm ission occurs through m ucosa or abraded skin by direct contact with infected secretions: o

Recurrent m ucosal shedding of HSV m ay transm it the virus.



Both viruses infect oral or genital m ucosa: o

Predilection of HSV-1 with orofacial infection

o

HSV-2 with genital infection

o

Com m on for HSV-1 to cause genital infections and HSV-2 to cause orofacial infections

Diagnosis Signs and Symptoms 

Prim ary infection m ay be unrecognized.



Classically presents with grouped 1- to 2-m m vesicles on an erythem atous base



Vesicles m ay be filled with clear or cloudy fluid or m ay appear as frank pustules.



Orofacial infection: o

Prim ary infection:

o

Gingivostom atitis or pharyngitis: 

Ulcerative exanthem involving gingival and m ucous m em branes



Fever, m alaise, irritability, headache, and m yalgias

o

Cervical adenopathy: 

Inability to eat owing to pain



Recurrent infection (recrudescence)



Usually involves lips, specifically the verm illion border

Pa ge 2 2 9



Com m only incited by sunlight, heat, stress, traum a, or im m unosuppression



Prodrom e of itching, tingling, throbbing, or burning followed by erythem a, papule/vesicle, ulcer, crust, and healing



Skin: o

History of exposure to HSV-1 or HSV-2

o

Abrupt onset of fever, edem a, erythem a, and localized tenderness

o

Herpetic whitlow: 

HSV-2 > HSV-1



Infection of pulp and lateral aspect of finger with single or m ultiple vesicles



May occur from autoinoculation with prim ary oral or genital infection or from direct inoculation from occupational exposure

o



Can last 3â€“4 weeks



Recurrence possible

Traum atic herpes: 

Can occur following cosm etic procedures of face, surgical and dental interventions, sun exposure or burns

o

Herpes gladiatorum : 

Mucocutaneous infection of chest, face, and hands in wrestlers transm itted through traum atized skin

o

Eczem a herpeticum : 

HSV-1 > HSV-2



Occurs in children and young adults with atopic derm atitis



Higher risk if on steroids or infected with HIV



Varicelliform eruption with spread to

Pa ge 2 2 9

surrounding skin





Fever, headache, and fatigue



HSV-associated erythem a m ultiform e



Usually presents on palm s and soles



Lasts 2â€“3 weeks

Eye: o

Most com m on cause of corneal blindness

o

Caused by extension of facial lesions or direct inoculation

o

Acute onset of pain and photophobia

o

Periauricular adenopathy, blurry vision, chem osis, and conjunctivitis

o

May be unilateral or bilateral

o

Dendritic lesions of cornea noted on fluorescein exam

o

Different from herpes varicella zoster as derm atom e not involved



CNS/encephalitis: o

Most com m on cause of severe sporadic encephalitis in the western world

o

Usually from HSV-1 reactivation disease

History May or m ay not have known history of exposure to HSV-1 or HSV-2

Physical Exam Vesiculoulcerative lesions in orofacial or genital area

Pediatric Considerations 

Up to 60â€“80% of babies who develop neonatal HSV are born to m others without history of genital herpes.



Vesicular skin lesions m ay or m ay not be present on initial exam .



Prim ary genital disease of the m other increases risk of transm itting virus to fetus.

Pa ge 2 2 9



Most prim ary infections occur during childhood; sym ptom atic in only 5â€“10% of children



Orofacial disease is m ost likely to present as gingivostom atitis in children younger than 5 years of age.



Whitlow m ay be caused by thum b-sucking children with oral herpes.

Tests 

Orofacial: o

Presum ptive diagnosis m ade by history and exam

o

If definitive diagnosis is necessary (e.g., system ic disease, child abuse): 

Viral culture of vesicles



Fluorescent antibody detection of antigen; serum antibody studies



Scrapings for Tzanck sm ear or Papanicolaou stain

 

Skin biopsy if hyperkeratotic or lichenoid lesions

Eye: o

Dendritic corneal lesions by fluorescein exam

o

Swab of affected area for viral culture or fluorescent antibody detection



CNS/encephalitis: o

Lum bar puncture with cerebrospinal fluid (CSF) pleocytosis and negative bacterial antigens

o

CSF polym erase chain reaction (PCR) test

o

MRI/CT

o

EEG diagnostic if spike and waves in tem poral region

Lab 

Lesion scrapings



Virus isolation by tissue culture of fluorescent antibody provides isolate that can be typed, but has lim ited

Pa ge 2 2 9

reliability depending on lab. 

Tzanck sm ear dem onstrating m ultinucleated giant cells, atypical keratinocytes, and large nuclei



Serum testing has lim ited ED use.



Enzym e-linked im m unosorbent assay (ELISA) testing m ay dem onstrate HSV antibodies, determ ining past exposure only.



Requires from 2 weeks to >3 m onths to detect seroconversion

P.517

Differential Diagnosis 



Orofacial and skin: o

Bacterial pharyngitis

o

Mycoplasm a pneum oniae pharyngitis

o

Stevens-Johnson syndrom e

o

Herpes zoster

o

Varicella

o

Pem phigus

o

Contact or chem ical derm atitis

o

Im petigo

Eye: o

Conjunctivitis: viral, bacterial, or allergic

o

Herpes zoster ophthalm icus

o

Scleritis/episcleritis

o

Angle-closure glaucom a

Treatment

Pa ge 2 3 0

Pre Hospital 

Maintain universal precautions.



Pain control

Initial Stabilization Protect airway in com atose or obtunded patients with suspected CNS disease.

ED Treatment 

Orofacial/gingivostom atitis: o

Prim ary disease in healthy children is generally not treated.

o

Prim ary disease in norm al host with m ild disease

o

Supportive treatm ent with hydration and topical anesthetics (viscous lidocaine, diphenhydram ine elixir)

o

Oral acyclovir: 

Severe disease or im m unocom prom ised patients: IV or oral acyclovir, valacyclovir, or fam ciclovir



If recurrent disease, oral acyclovir m ost helpful if started with prodrom e or at first sign of lesion



Reduces lesions and sym ptom s by 1â€“2 days



Topical antivirals generally ineffective for prophylaxis



Consider prophylaxis in patients with m ore than six episodes per year; history of herpes associated erythem a m ultiform e or herpes gladiatorum ; upcom ing intense sun exposure or stress; perioral/intraoral surgery; cosm etic facial procedures



Reduces frequency and severity of herpes labialis and m ay help decrease asym ptom atic

Pa ge 2 3 0

shedding, leading to decreased transm ission 

Does not cure or term inate the disease



When prophylaxis stopped, m ost patients have recurrences



Skin (other than orofacial or genital): o

May be treated with oral acyclovir

o

Antibiotics if secondary bacterial infection

o

Do not incise and drain: m ay lead to spread of infection.



Eye: o

Topical antiviral therapy with trifluridine or vidarabine

o

Vidarabine ointm ent for children

o

Do not treat with steroids: m ay cause increased viral replication

o

Suppressive therapy with oral acyclovir

o

Ophthalm ology consult

Pregnancy Considerations Acyclovir has been used to suppress genital herpes near end of pregnancy and appears safe, but is not FDA approved.

Medication (Drugs) 

Acyclovir: o

Orofacial 400 m g PO t.i.d. for 10â€“24 days or 5 m g/kg IV (5â€“10 m g/kg) q8h for 7â€“14 days

o

Peds: prim ary infection: 15 m g/kg PO 5 tim es per day for 7 days

o

Skin (not orofacial or genital): 400 m g (20 m g/kg) PO t.i.d. for 10 days

o

Eyes for suppression therapy: 400 m g PO b.i.d.

Pa ge 2 3 0

o

Encephalitis: 10â€“15 m g/kg (20 m g/kg) IV q8h for 14â€“21 days



Fam ciclovir: o

Orofacial/im m unocom prom ised host: 250â€“500 m g PO t.i.d. for 5 days



Fluocinonide: o



Adults: topical 0.05% gel q8h for 5 days

Penciclovir: o

Adults and unapproved peds: topical 1% cream applied q2h while awake for 4 days



Trifluridine: o

Adults and peds older than 6 years: one drop of 1% ophthalm ic ointm ent to eye q2h while awake (m ax. nine drops per day) for 14â€“21 days



Valacyclovir: o

Adults: 500â€“1,000 m g PO b.i.d. for 7 days (not FDA approved)



Vidarabine: o

Adults or peds older than 2 years: topical 0.5-inch ribbon of 3% ophthalm ic ointm ent to eye 5 tim es per day





Suppressive therapy: o

Acyclovir: 200 m g PO 5 tim es per day for 5 days

o

Fam ciclovir: 125 m g PO daily for 3â€“5 days

o

Valacyclovir: 500 m g PO b.i.d. for 3â€“5 days

Long-term prophylaxis: o

Acyclovi: 400 m g PO b.i.d.

o

Valacyclovir: 500â€“1,000 m g PO daily

o

Fam ciclovir: 250 m g PO b.i.d.

Alert Antiviral dosing m ay need adjustm ent for renal failure.

Pa ge 2 3 0

Follow-Up Disposition Admission Criteria 

Encephalitis, dissem inated disease, dehydration



Severe local or dissem inated disease in im m unocom prom ised host



Neonatal HSV



ICU versus ward based on toxicity and need for airway support

Discharge Criteria Uncom plicated local disease

Issues for Referral 

Neonatal herpes infection



Suppressive treatm ent options



Herpes infection during pregnancy

References 1. Brady RC, Bernstein DI. Treatm ent of herpes sim plex virus infections. Antiviral Res. 2004;61:81â€“94. 2. Nikkels AF, Pierard GE. Treatm ent of m ucocutaneous presentations of herpes sim plex virus infections. Am J Clin Derm atol. 2002;3:475â€“487. 3. Spruance SL, Kriesel JD. Treatm ent of herpes sim plex labialis. Herpes. 2002;9:64â€“69. 4. Waggoner-Fountain LA, Grossm an LB. Herpes sim plex virus. Pediatr Rev. 2004;25:86â€“93.

Miscellaneous

Pa ge 2 3 0

SEE ALSO: Genital Herpes

Codes ICD9-CM 054.2 Herpetic gingivostom atitis 054.3 Herpes encephalitis/m eningitis 054.42 Herpes keratitis 054.6 Herpetic whitlow 054.9 Herpes labialis 646.8 Herpes gestationis 771.2 Congenital herpes

Pa ge 2 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Herpes Zo ster

Herpes Zoster

Michelle E. Pyka Mark G. Richmond

Basics Description 

Com m only known as shingles or derm atom al zoster



Most com m on in patients with decreased cell- m ediated im m unity:



o

Older than 50 years of age

o

Neoplastic diseases (lym phoproliferative cancers)

o

Im m unosuppressive drugs

Dissem inates in 1â€“2% of norm al hosts and frequently in im m unocom prom ised hosts



Ram say Hunt syndrom e is characterized by zoster oticus, peripheral facial palsy, regional adenopathy, vertigo, and anesthesia of anterior two thirds of hem itongue: o



From 7th and 8th cranial nerve involvem ent

Postherpetic neuralgia (PHN) is a com plication of zoster: o

Described as pain that persists at site of zoster lesions for >1 to 3 m onths after cutaneous disease has healed

o

10â€“70% of patients will have pain after resolution of lesions.

Pa ge 2 3 0

o

Incidence increases with age older than 50 years, severe rash, and severe pain.



Syndrom e of herpes zoster occurring without rash is called zoster sine herpete.

Etiology 

Caused by varicella-zoster virus (VZV), a DNA virus in the Herpesviridae fam ily



Mostly in individuals who previously had chickenpox and very rarely in vaccinated individuals



Reactivation of a virus that lies dorm ant in dorsal root ganglia

Pregnancy Considerations Extrem ely low rate of fetal com plications; no need to consider term ination

Pediatric Considerations Childhood zoster is m ost com m on when varicella occurred in utero or within 6 m onths of life.

Diagnosis Signs and Symptoms 

Prodrom e of pain and paresthesias in derm atom al distribution: o

Character of pain m ay be sharp, dull, tingling, burning, or intense pruritus.

o

Pain precedes rash by 1â€“10 days.

o

Prodrom e less likely in young patients

o

Classical rash is grouped vesicles on erythem atous base.

o

Initially are patches of erythem a and then vesicles

Pa ge 2 3 0

o

Progress to scab and crust form ation over 10â€“12 days

o

Crusts fall off in 2â€“3 weeks.

o

Lesions evolve synchronously.

o

One derm atom e typically affected, rarely crosses m idline

o

Most com m on nerve distributions are thoracic and lum bar, followed by trigem inal and cervical.



Ocular involvem ent occurs in half of cases involving ophthalm ic division of trigem inal nerve: o

Closely associated with disease occurring at tip of nose (Hutchinson sign)

o

Corneal involvem ent begins as punctate keratitis, which m ay coalesce to form pseudodendritic or stellate pattern.



Dissem inated disease m ay cause signs and sym ptom s of m eningoencephalitis, m yelitis, peripheral neuropathy, hepatitis, and pneum onitis.



Im m unosuppressed patients are m ore likely to have severe disease and visceral involvem ent.

Essential Workup 

Clinical presentation is sufficient for diagnosis in m ost patients.



If definitive diagnosis is necessary, tissue culture is recom m ended.



Herpes zoster ophthalm icus (HZO) is diagnosed by slit-lam p exam : o

The pseudodendrites of HZO are elevated and plaquelike, sitting on top of epithelium , and stain brighter with rose bengal.

o

Is less ulcerative than HSV and stains less brightly with fluorescein

Pa ge 2 3 0

Tests Lab 

Cell yields are highest if base of vesicular lesions are scraped.



Num erous rapid im m unofluorescence assays exist to detect VZV in vesicular fluid and are preferred m ethod: o



Can distinguish between HSV and VZV

Tzanck sm ear dem onstrates giant cells and intranuclear inclusions.



IgM and IgG are m ost com m only m easured by enzym e-linked im m unosorbent assay (ELISA): o



Antibody titers rise 2 weeks after acute infection.

Polym erase chain reaction (PCR) m ay be useful in cerebrospinal fluid (CSF) analysis or verrucous lesions in which cultures are otherwise negative.

Differential Diagnosis 

Zosteriform herpes sim plex



Varicella



Herpes sim plex (HSV)



Nonherpetic conjunctivitis



Enteroviral infections (e.g., hand-foot-and-m outh disease)



Insect bites



Bullous im petigo



Molluscum contagiosum

Treatment Pre Hospital 

Zoster is potentially contagious and m ay cause varicella in

Pa ge 2 3 0

nonim m une health care workers: o 

Lesions should be covered.

Maintain universal precautions.

Initial Stabilization 

Rarely necessary



IV access to adm inister fluids and antiviral therapy



Dissem inated disease to CNS or lungs m ay require airway support.

P.519

ED Treatment 

Goal of treatm ent is to treat acute viral infection, decrease pain, and prevent postherpetic neuralgia.



Acyclovir, valacyclovir, or fam ciclovir is recom m ended: o

Should be instituted within 72 hours of rash form ation

o

Valacyclovir and fam ciclovir are recom m ended over acyclovir in prevention of PHN.



Foscarnet recom m ended for acyclovir-resistant VZV in im m unocom prom ised patients



Ocular involvem ent: o

Necessitates ophthalm ologic consultation

o

Oral (norm al host) or intravenous (im m unocom prom ised host) acyclovir is best started within 72 hours; m ay be beneficial up to 1 week after sym ptom onset.



Oral corticosteroids in acute zoster are controversial: o

May reduce pain

o

Do not help prevent PHN

o

If not contraindicated, recom m ended in patients >50 years old, severe disease (>21 lesions), or severe

Pa ge 2 3 1

pain 

Long-acting narcotics and topical lidocaine patches are recom m ended for m oderate to severe pain.



Over-the-counter analgesia for m ild pain



Postherpetic neuralgia (PHN) is difficult to m anage: o

Early use of antiviral drugs m ay prevent it.

o

Lidocaine patch or lidocaine and prilocaine cream provides short-term relief.

o

Topical capsaicin is controversial and should not be initiated in ED.

o

Sustained-release oxycodone useful for analgesia

o

Tricyclic antidepressants recom m ended: 

Nortriptyline and desipram ine have fewer side effects than am itriptyline.

o

Gabapentin is safe and effective.

Medication (Drugs) 

Acyclovir: adults: 800 m g PO 5 tim es per day for 7â€“10 days; im m unocom prom ised with severe disease 10â€“12 m g/kg IV infused over 1 hour q8h (peds: 20 m g/kg PO q.i.d. for 5 days, 10 m g/kg IV q8h)



Fam ciclovir: adults: 500 m g PO t.i.d. for 7 days (peds: not approved)



Foscarnet: 40 m g/kg IV q8h for 14â€“26 days



Gabapentin: 100â€“300 m g nightly at bedtim e increasing 100â€“300 m g every 3 days until adequate response or m ax. 3,600 m g/d div. t.i.d.



Lidocaine patch 5%: apply up to 3 patches for <12 hours within a 24-hour period.



Nortriptyline: 10â€“25 m g PO nightly at bedtim e; increase by 25 m g every 2â€“4 weeks until adequate response;

Pa ge 2 3 1

m ax. 125 m g/d 

Prednisone: 30 m g PO b.i.d. days 1â€“7, 15 m g PO b.i.d. days 8â€“14, and 7.5 m g b.i.d. days 15â€“21



Valacyclovir: 1,000 m g PO t.i.d. for 7 days (peds: not approved)



Varicella-zoster im m une globulin (VZIG): adults and peds: specialized dosing)

Pediatric Considerations Aspirin should be avoided because of risk of Reye syndrom e.

Follow-Up Disposition Admission Criteria 

Dissem inated disease



Im m unocom prom ised patients with any of the following: o

Involvem ent of trigem inal nerve

o

Herpes zoster ophthalm icus

o

Ram say Hunt syndrom e

o

Involvem ent of m ore than two derm atom es

o

Visceral involvem ent



Intractable pain



ICU versus ward depends on severity of disease.

Pediatric Considerations Zoster in the neonate requires adm ission and treatm ent with IV acyclovir.

Discharge Criteria 

Most are m anaged as outpatients.



Patients should be instructed that lesions m ay heal with

Pa ge 2 3 1

scarring or leave depigm ented areas. 

Recom m end isolation from steroid-dependent, pregnant, or im m unocom prom ised persons until lesions are crusted: o

VZIG recom m ended within 72 hours for exposed im m unocom prom ised contacts



Neonates born to seronegative m others exposed to zoster should receive VZIG within 24 hours.

Issues for Referral 

Recom m end referral of patients older than 60 years to prim ary care physician for vaccination therapy: o

Recent published data support Oka/Merck VZV vaccine; was found to be beneficial in reducing incidence of herpes zoster as well as PHN.



PHN m ay require long-term follow-up; referral to pain specialist m ay be required.

References 1. Chen TM, George S, et al. Clinical m anifestations of varicella-zoster virus infection. Derm atol Clin. 2002;20(2):267â€“282. 2. Dubinsky RM, Ali H, et al. Practice param eter: treatm ent of postherpetic neuralgia. Neurology. 2004: 63:959â€“965. 3. Gnann JW, Whitley RJ. Herpes zoster. N Engl J Med. 2002;347:340â€“346. 4. Jung BF, Johnson RW, et al. Risk factors for postherpetic neuralgia in patients with herpes zoster. Neurology. 2004;62:1545â€“1551. 5. Oxm an MN, Levin MJ, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med. 2005;352:2271â€“2284. 6. Starr CE, Pavan-Langston D. Varicella-zoster virus: m echanism s of pathogenicity and corneal disease. Ophthalm ol Clin North Am . 2002;15(1):7â€“15, v.

Pa ge 2 3 1

Codes ICD9-CM 053.9

ICD10 B02.9

Pa ge 2 3 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Herpes, G enital

Herpes, Genital

Wender Hwang Mark Richmond

Basics Description 

Genital herpes is a lifelong recurrent infection.



Approxim ately 1 in 4 Am ericans older than age 30 are seropositive for HSV-2: o



Most are asym ptom atic.

First episode/prim ary HSV infection: o

2â€“12-day incubation

o

Sym ptom s peak 8â€“10 days after onset.

o

Lesions heal in 3 weeks.

o

Prim ary infection m ay have m ore prom inent clinical syndrom e and com plications (e.g., encephalitis, m eningitis).

o

Prim ary infection m ay also go unnoticed: 

Greater than 50% of first recognized signs and sym ptom s are not prim ary infection.



Recurrent HSV infection: o

Average patient has three or four recurrences per year.

o

Virus reactivated from dorsal root ganglia

Pa ge 2 3 1

o

Triggered by local traum a, em otional stress, fever, sunlight, cold or heat, m enstruation, infection, and so on

o

Milder clinical syndrom e and fewer lesions that usually heal within 10 days



Asym ptom atic HSV infection: o

Virus is shed interm ittently and often transm itted by persons who are without lesions or sym ptom s.

o

Asym ptom atic viral shedding is detectable by polym erase chain reaction (PCR) test on 9â€“26% of days.

Etiology 

70â€“90% caused by a DNA virus herpes sim plex virus, type 2 (HSV-2): o

Rem ainder caused by herpes sim plex virus type 1 (HSV-1)



Increasing prevalence of genital HSV-1 infection: o

Higher rates of oral sex

o

Falling incidence of childhood (nonsexual) transm ission owing to im proved social conditions resulting in a larger pool of susceptible adolescents and adults



Prim ary genital infection by HSV-1 is sim ilar to HSV-2 in sym ptom s and duration, but recurs m uch less frequently.



Acquisition of HSV-2 in patients with pre-existing HSV-1 infection is less com m only associated with system ic sym ptom s: o

Acquisition of HSV-1 in persons with pre-existing HSV-2 infection is rare.



HSV vaccines currently in early clinical trials



High association with HIV and other sexually transm itted diseases (STDs)

Pa ge 2 3 1

Alert 

Contact isolation and universal precautions should be m aintained.



Patients with HIV coinfection have higher HIV viral levels in the blood and skin lesions during HSV recurrence.

Diagnosis Signs and Symptoms 

Local pain and itching



Herpetic cervicitis, vaginitis, or urethritis m ay present with dysuria, urinary hesitance or retention, vaginal discharge, or pelvic pain.



Herpetic pharyngitis or gingivostom atitis m ay occur with oral acquisition.



System ic sym ptom s like fever, headache, m alaise, photophobia, anorexia, m yalgias, and lym phadenopathy are m ore com m on with prim ary infection.

History 

1 to 2-day prodrom e of local tingling, burning, itching, or pain prior to eruption (can m im ic sciatica)



Classically, lesions are noted on day 2 as m acules and papules, then progress to vesicles, pustules, and then ulcerate by day 5.



Skin lesions crust over; m ucosal m em brane lesions heal without crusting.

Physical Exam 

Lesions on vulva, vagina, cervix, perineum , buttocks; penile shaft or glans



Grouped vesicles on an erythem atous base

Pa ge 2 3 1



On m oist m ucosal surfaces, ulcers m ay predom inate.



Atypical features m ay include localized edem a, erythem a, crusts, or fissures.

Pediatric Considerations 

Neonatal infections are often dissem inated or involve the CNS with high m orbidity and m ortality.



Congenital HSV in the neonate without vesicles m ay m im ic rubella, cytom egalovirus (CMV), or toxoplasm osis.



Consider sexual abuse in children with genital HSV; culture lesions and test for other STDs in suspected cases.

Essential Workup Diagnosis based on typical history and physical exam ination

Tests Lab 

Viral load in lesions of prim ary infection >> recurrence



Tzanck preparation and staining of fluid from lesions is insensitive and nonspecific.



Viral culture of vesicle fluid or ulcer base positive in 80â€“95% of cases, decreasing sensitivity as lesions crust and heal



PCR 1.5â€“4 tim es m ore sensitive than viral culture; test of choice for cerebrospinal fluid (CSF) analysis in suspected CNS infection



Serologic tests not helpful in acute disease: o

Highly sensitive and specific; detect anti-gG1 and anti-gG2 antibodies

o

Require from 2 weeks to >3 m onths to detect seroconversion

o

Cannot distinguish acute from chronic disease

o

HerpeSelect HSV-1/HSV-2 enzym e-linked

Pa ge 2 3 1

im m unosorbent assay (ELISA) assay, hours to days in lab o

POCkit HSV2, bedside results in 10 m inutes

Differential Diagnosis 

Syphilis (T. pallidum )



Chancroid (H. ducreyi)



Lym phogranulom a venereum (LGV)



Granulom a inguinale (C. granulom atis)



Candidiasis



BehÃ§et syndrom e

Treatment Initial Stabilization Rarely required unless associated with system ic sym ptom s requiring hospitalization: 

Dissem inated infection



Hepatitis



Pneum onitis



CNS involvem ent

ED Treatment 

Treatm ent partially controls sym ptom s and lesions; does not eradicate latent virus nor affect recurrences after drug is discontinued.



Episodic treatm ent of recurrences m ay shorten duration of lesions or am eliorate recurrences.



Daily suppressive therapy in patients with frequent recurrences (six or m ore per year) reduces frequency of recurrences by 75%.



Acyclovir interferes with viral DNA polym erase; equally

Pa ge 2 3 1

effective m edications with less frequent dosing regim ens are fam ciclovir and valacyclovir. 

Resistance to acyclovir in im m unocom prom ised individuals is 5â€“10%: o



Foscarnet 40 m g/kg IV t.i.d. m ay be effective.

Consider testing for concom itant STDs.

Pregnancy Considerations 

Wom en with prim ary HSV infection during pregnancy should receive antiviral therapy.



Asym ptom atic antiviral therapy after 36 weeks associated with decreased incidence of lesions at delivery: o

Decreased cesarean delivery rates

o

Unknown effect on transm ission because neither control nor therapy arm s had cases of neonatal herpes

P.515

Medication (Drugs) 

System ic or severe infection requiring hospitalization: o

Acyclovir: 5â€“10 m g/kg IV t.i.d., until clinical im provem ent: 



Neonate: 20 m g/kg IV t.i.d.

First episode (7- to 10-day therapy; extend if not healed in 10 days) o

Acyclovir: 400 m g PO t.i.d. or 200 m g PO 5 tim es per day 

o

Peds: 20 m g/kg PO t.i.d. or 5 m g/kg IV t.i.d.)

Fam ciclovir: 250 m g PO t.i.d.

Pa ge 2 3 2

o 

Valacyclovir: 1,000 m g PO b.i.d.

Recurrent infection (5-day therapy): o

Acyclovir: 800 m g PO b.i.d. or 400 m g PO t.i.d. or 200 m g PO 5 tim es per day





o

Fam ciclovir: 125 m g PO b.i.d.

o

Valacyclovir: 500â€“1,000 m g PO b.i.d.

Suppressive therapy (daily) o

Acyclovir: 400 m g PO b.i.d.

o

Fam ciclovir: 250 m g PO b.i.d.

o

Valacyclovir: 500â€“1,000 m g PO daily

Treatm ent of patients with HIV coinfection: o

Recurrent infection: use the non-HIV first-episode regim en above.

o

Suppressive therapy: use the non-HIV recurrent-infection regim en.

Follow-Up Disposition Admission Criteria 

System ic involvem ent (encephalitis, m eningitis), significant dissem ination



Severe local sym ptom s (pain, urinary retention)



Severely im m unocom prom ised patient

Discharge Criteria 

Im m unocom petent patient without system ic involvem ent



Discharge counseling: o

Avoid sexual contact during prodrom e until healed

o

Practice safe sex techniques even if there are no lesions.

Pa ge 2 3 2

o

Expect future recurrences; consider suppressive therapy if frequent.

o

Analgesics and antipruritics as needed

o

Dysuria and urinary retention m ay be relieved with sitz baths or pouring warm water over lesions during urination.

Issues for Referral 

Neonatal herpes infection



Sexual abuse in children



Herpes infection during pregnancy

References 1. Donovan B. Sexually transm issible infections other than HIV. Lancet. 2004;363:545â€“556. 2. Kim berlin DW, Rouse DJ. Clinical practice: genital herpes. N Engl J Med. 2004;350:1970â€“1977. 3. Sexually transm itted diseases treatm ent guidelines 2002. Centers for Disease Control and Prevention. MMWR Recom m Rep. 2002;51(RR-6):1â€“78. Available at http://www.cdc.gov/STD/treatm ent/2-2002TG.htm #GenitalHerpes. 4. Sheffield JS, et al. Acyclovir prophylaxis to prevent herpes sim plex virus recurrence at delivery: a system atic review. Obstet Gynecol. 2003;102:1396â€“1403.

Miscellaneous SEE ALSO: Herpes Sim plex

Codes ICD9-CM 054.1 Genital herpes 054.10 Genital herpes, unspecified

Pa ge 2 3 2

054.11 Herpetic vulvovaginitis 054.12 Herpetic ulceration of vulva 054.13 Herpetic infection of penis 054.19 Other

Pa ge 2 3 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hiccups

Hiccups

Carrie Tibbles James L. Smith Jr.

Basics Description 

Sudden, involuntary, contraction of the diaphragm (usually unilateral) and other inspiratory m uscles term inated by abrupt closure of the glottis.



Usually occur with a frequency of 4â€“60 per m inute



Occurs as a result of stim ulation of one or m ore lim bs of the hiccup reflex arc: o

Involves irritation of the vagus and phrenic nerves

o

The â€œhiccup centerâ€• is located in the upper spinal cord.



Male-to-fem ale ratio is 4:1: o

In m en, m ore than 90% of cases have an organic basis.

o

In wom en, a psychogenic cause is m ore likely.

Etiology 

Idiopathic



Gastrointestinal: o

Gastric distention

o

Esophageal lesions

Pa ge 2 3 2





o

Reflux esophagitis

o

Achalasia

o

Candida esophagitis

o

Carcinom a

o

Obstruction

o

Gastric lesions

o

Ulcer

o

Cancer

o

Hepatic lesions

o

Hepatitis

o

Hepatom a

o

Pancreatic lesions

o

Pancreatitis

o

Pseudocysts

o

Cancer

o

Inflam m atory bowel disease

o

Cholelithiasis

o

Cholecystitis

o

Appendicitis

o

Abdom inal aortic aneurysm

o

Postoperative, abdom inal procedure

Diaphragm atic irritation: o

Hiatal hernia

o

Tum ors

o

Pericarditis

o

Eventration

o

Splenom egaly

o

Hepatom egaly

o

Peritonitis

CNS lesions: o

Encephalitis

o

Ventriculoperitoneal shunt

Pa ge 2 3 2











o

Stroke

o

Subarachnoid hem orrhage

o

Arteriovenous m alform ations

o

Parkinson disease

o

Multiple sclerosis

Mediastinal and other thoracic lesions: o

Pneum onia

o

Aortic aneurysm

o

Tuberculosis

o

Myocardial infarction

o

Lung cancer

o

Mediastinal adenopathy

Metabolic causes: o

Urem ia

o

Hyponatrem ia

o

Gout

o

Hypocalcem ia

o

Diabetes

Toxic/drug-induced: o

Î±-Methyldopa

o

Benzodiazepines

o

Steroids

o

Barbiturates

o

General anesthesia

Psychogenic causes: o

Stress/excitem ent

o

Grief

o

Malingering

o

Conversion disorder

Head and neck: o

Otic foreign body irritating the tym panic m em brane

o

Pharyngitis

Pa ge 2 3 2

o

Laryngitis

o

Goiter

o

Retropharyngeal/peritonsillar abscess

Diagnosis Signs and Symptoms 

Characteristic sound abruptly ending an inspiratory effort



Attacks usually occur at brief intervals and last only a few seconds or m inutes.



Attacks lasting m ore than 48 hours or persisting during sleep suggest an underlying disorder.



Described as persistent if duration longer than 48 hours; intractable if greater than 1 m onth

Essential Workup 

Targeted history and review of system s to determ ine likelihood of potential underlying etiology:



o

Severity and duration of current episode

o

History of previous episodes and treatm ent attem pts

Careful physical exam ination in search of an underlying cause



Consider further diagnostic testing, dictated by history and physical, if hiccups are persistent or chronic

Tests Lab 

CBC with differential



Electrolytes, blood urea nitrogen, creatinine

Imaging 

Chest radiography

Pa ge 2 3 2



Further im aging m ay be indicated depending on clinical suspicion of a particular etiology; this can often be perform ed on an outpatient basis.

Differential Diagnosis Eructation P.521

Treatment ED Treatment 





Treat specific causes when identified: o

Rem ove foreign bodies from the ear

o

Relieve gastric distention with a nasogastric tube

Nonpharm acologic m aneuvers: o

Catheter stim ulation of the posterior pharynx

o

Direct stim ulation of the uvula with a cotton swab

o

Supraorbital pressure

o

Carotid sinus m assage

o

Digital rectal m assage

Pharm acologic treatm ent: o

Chlorprom azine

o

Haloperidol

o

Baclofen

o

Nebulized lidocaine

o

Am itriptyline

o

Phenytoin

o

Metoclopram ide

Pa ge 2 3 2

Medication (Drugs) 

Am itriptyline: 10 m g PO t.i.d.



Baclofen: 10 m g PO t.i.d.



Chlorprom azine: 25â€“50 m g IV/IM, 25â€“50 m g PO t.i.d.



Haloperidol: 2â€“5 m g IM



Lidocaine (4%): 3 m L nebulized, repeat if necessary



Metoclopram ide: 10 m g IV/IM, 10â€“20 m g PO q.i.d.



Phenytoin: 200 m g IV

Follow-Up Disposition Admission Criteria Adm ission is not indicated for uncom plicated cases of hiccups.

Discharge Criteria Rem edies that can be tried at hom e in case of recurrence: 

Swallowing a spoonful of sugar



Sucking on a hard candy or swallowing peanut butter



Breath holding/Valsalva m aneuver



Tongue traction



Lifting the uvula with a cold spoon



Drinking from the far side of a glass



Inducing fright



Sm elling salts



Rebreathing into a paper bag

Issues for Referral Referral in cases of intractable hiccups for investigation into underlying cause and m ore definitive therapeutic m easures:

Pa ge 2 3 2



Phrenic nerve block of dom inant diaphragm



Phrenic nerve crush or transection



Psychiatric interventions



Hypnosis



Behavioral m odification

References 1. Kolodzik PW, Eilers MA. Hiccups (singultus): review and approach to m anagem ent. Ann Em erg Med. 1991;20:565â€“573. 2. Launois S. Hiccup in adults: an overview European Respiratory Journal. 1993;Apr;6(4):563â€“575. 3. Lewis JH. Hiccups: reasons and rem edies. In: Lewis JH, ed. A pharm acologic approach to gastrointestinal disorders. Baltim ore: William s & Wilkins, 1994:116. 4. Rosseau P. Hiccups. South Med J. 1995;88(2):175â€“181.

Codes ICD9-CM 786.8

ICD10 R06.6

Pa ge 2 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > High Altitude Illness

High Altitude

Illness Christopher B. Colwell

Basics Description 



Incidence dependent on: o

Rate of ascent

o

Final altitude

o

Sleeping altitude

o

Duration at altitude

Acute m ountain sickness (AMS) incidence: o

Up to 67% incidence with rapid ascent (1â€“2 days) to >14,000 feet

o

Twenty-two percent incidence for skiers visiting resorts and sleeping at 7,000â€“9,000 feet, 40% at 10,000 feet





AMS risk factors: o

Previous history of high altitude illness

o

Exertion

o

Younger persons (<50)

o

Physical fitness not protective

High-altitude pulm onary edem a (HAPE) incidence:

Pa ge 2 3 3



o

Less than 1â€“2%

o

Varies with rate of ascent

High-altitude cerebral edem a (HACE) incidence <1%

Pregnancy Considerations 

Relationship between pregnancy and high-altitude illness is not clearly established.



Pregnancy-induced hypertension, proteinuria, and peripheral edem a are m ore com m on at high altitude, which m ay be related to m aternal hypoxem ia.



No evidence of increase in spontaneous abortions, placental abruption, or placenta previa at high altitudes



Travel by pregnant wom en with norm al pregnancies to m oderate altitudes appears safe, although caution should be exercised when traveling above 13,000 feet and for wom en with com plicated pregnancies.

Geriatric Considerations Although elderly persons are m ore likely to have underlying health problem s that m ay be affected by altitude, such as hypertension, chronic obstructive pulm onary disease (COPD), and coronary artery disease, the risk of developm ent of AMS is less in those older than age 55 than in other age groups.

Etiology 

Rapid ascent above 8,000 feet without proper acclim atization is the m ost com m on cause of high-altitudeâ€“related illness.



Rapidity of ascent, final altitude reached, sleeping altitude, and individual susceptibility all play a role in developm ent of high-altitude illness as well.

Pa ge 2 3 3

Diagnosis Signs and Symptoms History N/A

Acute Mountain Sickness (AMS) 

Headache plus at least one of the following: o

Nausea/vom iting

o

Fatigue/lassitude

o

Dizziness

o

Difficulty sleeping



Onset 4â€“12 hours after ascent



Generally benign and self-lim ited



Sym ptom s m ay becom e debilitating.

High-Altitude Pulmonary Edema (HAPE) 

Onset 2â€“4 days after ascent, m ost com m only on second night



Cough (dry at first, then productive)



Dyspnea at rest

High-Altitude Cerebral Edema (HACE) 

Life threatening



Occurs in presence of HAPE and/or AMS: o



Seen rarely as isolated entity

Onset: o

May occur 12 hours after onset of AMS

o

Usually requires 2â€“4 days for developm ent



Altered m ental status



Severe headache



Nausea/vom iting

Pediatric Considerations

Pa ge 2 3 3





AMS in infants and young children m anifested by: o

Increased fussiness

o

Decreased playfulness

o

Decreased appetite

o

Vom iting

o

Sleep disturbances

Incidence of HAPE greater in younger individuals (<20 years) than adults



No cases of HAPE or HACE reported in children <4 years old

Physical Exam N/A

AMS Without presence of high-altitude pulm onary or cerebral edem a, the physical exam will often be within norm al lim its: 

More m ild stages of AMS often m isdiagnosed as viral syndrom es or hangovers from alcohol ingestions

HAPE 

Tachypnea



Rales



Cyanosis



Fever m ay be present.



Severe respiratory distress and death m ay occur.

HACE 

Ataxia



Papilledem a, retinal hem orrhages



Altered m ental status/global encephalopathy o

Focal neurologic deficit less com m on: 

o

Seizure (rare)

Com a

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Essential Workup Clinical diagnosis in setting of recent altitude gain

AMS 

Diagnosis m ade with history of headache plus at least one of the following:



o

Nausea/vom iting

o

Lassitude/fatigue

o

Dizziness

o

Insom nia

No diagnostic laboratory or im aging studies

HAPE 

Dyspnea on exertionâ€”universal finding at altitude



Dyspnea at restâ€”sym ptom of HAPE, worse at night



Rales, cyanosis, or cough support diagnosis.



Tachycardia, tachypnea correlate with severity.

HACE 

Cerebellar ataxia with or without other sym ptom s of AMS



Papilledem a, retinal hem orrhages are associated findings.

Tests Lab Arterial blood gas (ABG) for HAPE: 

Reveals hypoxem ia (pO 2 30â€“50) and respiratory alkalosis, not acidosis

Imaging 

Chest radiograph in HAPE: o

Reveals patchy alveolar infiltrates with areas of clearing between patches

o

Unilateral or bilateral infiltrates (right m idlung field being m ost com m on)

Pa ge 2 3 3

o

Cardiom egaly, â€œbatwingâ€• distribution of infiltrates, and Kerley B lines (typical of cardiogenic pulm onary edem a)â€”absent in HAPE





ECG in HAPE: o

Tachycardia

o

Evidence of right-heart strain

CT and MRI scans in HACE: o

Vasogenic edem a of white m atter

P.523

Differential Diagnosis AMS 

Viral syndrom e



Exhaustion



Alcohol hangover



Carbon m onoxide poisoning



Meningitis



Encephalitis

HAPE 

Pneum onia



High-altitude bronchitis and pharyngitis



Pulm onary em bolism : o

More rapid onset

o

Pleuritic chest pain

HACE Cerebrovascular accidents/transient ischem ic attacks: 

Focal neurologic signs suggest vascular lesion.

Pa ge 2 3 3

Treatment Pre Hospital 

Severe cases require im m ediate evacuation to lower altitude.



Do not proceed to higher altitude in presence of sym ptom s.



Oxygen delivery or sim ulated descent in portable hyperbaric cham ber (Gam ow bag) can be lifesaving tem porary m easure m aking self-rescue possible.

Initial Stabilization HAPE and HACE 

Airway, breathing, and circulation m anagem ent (ABCs): o

Endotracheal intubation for im pending respiratory failure, hyperventilation, or airway protection



Establish IV access.



Supplem ental oxygen and m onitoring



Continuous positive airway pressure (CPAP) for HAPE

ED Treatment AMS 

Mild cases usually self-lim ited: o

Sym ptom atic treatm ent

o

Halt ascent until sym ptom s resolve



Acetazolam ide for m oderate to severe sym ptom s



Ibuprofen or acetam inophen for headache



Prom ethazine for nausea



Supplem ental oxygen in severe cases



Descent for severe or persistent sym ptom s



Acetazolam ide for AMS prophylaxis: o

In high-risk individual with planned rapid ascent

Pa ge 2 3 3

HAPE 

Im m ediate descent for m oderate/severe sym ptom s



Mild cases m ay be m anaged without descent if: o

Adequate oxygen supplies available

o

Serial m edical exam inations possible

o

Im m ediate descent for any deterioration in clinical status



Bed rest to avoid exercise-induced pulm onary hypertension



Supplem ental oxygen o

High flow rates (6â€“8 L/m in) until im provem ent, then continue with lower flow rates



Nifedipine when other interventions are unavailable



Î²-agonist inhalers m ay be helpful.

HACE 

Im m ediate evacuation to lower altitude



Oxygen



Dexam ethasone



Bed rest with elevation of head at 30Â° and in severe cases aggressive m anagem ent of elevated intracranial pressure

Medication (Drugs) 

Acetazolam ide: o

AMS treatm ent: 250â€“500 m g (peds: 5 m g/kg) PO b.i.d.

o

AMS prophylaxis: 250 m g PO b.i.d. (peds: 5 m g/kg) PO b.i.d.; start 24 hours before ascent



Dexam ethasone: 8 m g IV, then 4 m g PO/IV q.i.d.



Ibuprofen: 800 m g (peds: 5â€“10 m g/kg) PO t.i.d.

Pa ge 2 3 3



Nifedipine: 10 m g PO, then 30 m g sustained release (SR) PO b.i.d.



Prom ethazine: 12.5â€“25 m g (peds: 0.25â€“1 m g/kg) PO/PR (per rectum )/IM q4hâ€“q6h

Follow-Up Disposition Descent to a lower facility m andatory in severe cases

Admission Criteria 

Persistent sym ptom s after observation in lower altitude ED require adm ission.



HAPE



HACE

Discharge Criteria Once clinical im provem ent seen and oxygen saturation >95% on room air

Issues for Referral Offer prophylactic therapy for future ascents in patients with recurrent AMS (acetazolam ide) or HAPE (nifedipine).

References 1. Grissom CK, Roach RC, Sarnquist FH, et al. Acetazolam ide in the treatm ent of acute m ountain sickness: clinical efficacy and effect on gas exchange. Ann Intern Med. 1992;116(6):461â€“465. 2. Hackett PH, Roach RC. High-altitude illness. N Engl J Med. 2001;345:107â€“14. 3. Hackett PH, Roach RC. High altitude m edicine. In: Auerbach PS, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001:2â€“43. 4. Roach RC, et al. How well do older persons tolerate m oderate

Pa ge 2 3 3

altitude? West J Med. 1995;162:32â€“36. 5. Yaron M, Honigm an B. High altitude m edicine. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:2035â€“2050.

Codes ICD9-CM 993.2

ICD10 T70.2

Pa ge 2 3 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hip Injury

Hip Injury

Colleen Buono

Basics Description Hip Fracture 

Fracture of proxim al fem ur



Classified by: o

Location

o

Displacem ent/angulation

o

Open/closed

o

Com m inution

o

Fracture lines

o

Neurovascular state

Femoral Head/Neck Fracture (Intracapsular) 

Minor m echanism in eldery, high-energy m echanism in young



Patient m ay or m ay not be am bulatory.



Associated with hip dislocations (anterior > posterior)



Nondisplaced head/neck fractures difficult to visualize; increased m orbidity when fracture goes from nondisplaced to displaced



Fem oral neck is occasional site of stress fracture in

Pa ge 2 3 4

runners and m ilitary recruits (repetitive activity)

Intertrochanteric Fracture (Extracapsular) 

Often due to fall in elderly patients



Nonam bulatory with significant pain



Extrem ity often shortened, externally rotated



Can be site of significant blood loss

Subtrochanteric Fracture 

Usually due to direct, significant traum a in young patients or lesser traum a in elderly



Com m on site for pathologic fracture



Extrem ity shortened, displacem ent of proxim al fragm ent



Can be site of significant blood loss

Greater/Lesser Trochanter Fractures In young patients; usually apophyseal avulsion

Hip Dislocation 

Disarticulation of fem oral head



Posterior dislocation (m ost com m on): o

Often from m otor vehicle accident (MVA) in which knees strike dashboard

o 

Ten percent associated with sciatic nerve injury

Anterior dislocation: o

Often due to traum a with sudden abduction of thigh

o

Associated fem oral head fractures, fem oral nerve injury



Central dislocation with acetabular fracture: o

Usually from direct im pact to greater trochanter

o

Associated significant blood loss, sciatic nerve injury

Pediatric Considerations 

Usually have posterior hip dislocation: o

Trivial force required for posterior hip locations in

Pa ge 2 3 4

children <6 years old 

Fracture usually requires high-im pact traum a.



Must suspect non-accidental traum a (NAT)



Consider pathologic fracture with m inor traum a.

Etiology See individual injuries above.

Diagnosis Signs and Symptoms History 

Groin, hip, thigh, m edial knee pain, pain with am bulation/weight bearing in the setting of traum a



Minor traum a in the elderly due to osteoporosis; high-im pact traum a in young adults

Physical Exam 

Obvious signs of traum a: o

Deform ity or angulation, swelling, open fracture, or m issile entrance wound

o

Lower extrem ity held in position of com fort



Hip fracture: flexion, abduction, external rotation



Posterior hip dislocation: flexion, adduction, internal rotation of hip, flexion of knee, hip im m obile



Anterior hip dislocation: flexion, abduction, external rotation of hip, thigh shortening, hip im m obile

Pediatric Considerations 

Pediatric fracture patterns different due to developing cartilaginous com ponents: o

Assess for dislocation of the fem oral capital

Pa ge 2 3 4

epiphysis. 

Fracture classification and m anagem ent are also different.



Suspect NAT without obvious m echanism of injury.



Consider hip pain due to a separate process (lim b-length discrepancy, neurom uscular disorders, neoplastic invasion of bone).

Essential Workup 

Assess distal pulses, palpate com partm ents, evaluate sensation and m otor function.



If pulses are not equal or palpable, bedside Doppler or angiography m ay be necessary.





Search for associated injuries: o

Neurologic deficits

o

Vascular injury

o

Pelvic fractures

o

Spinal fractures

o

Blunt abdom inal traum a

Radiographs as outlined below: o

Rem ove splints and clothing when taking film s.

o

Positive exam plus negative standard film s indicates hip fracture until proven otherwise; further im aging (CT or MRI scan) is indicated.



In suspected child abuse, obtain appropriate radiographs to evaluate for other injuries.

Pediatric Considerations 

Assess m arkers for nonaccidental traum a: o

Delay in presentation; history of m echanism inconsistent with injury

o

Isolated traum a to the thigh, associated burns, bruises, linear abrasions

Tests

Pa ge 2 3 4

Lab CBC, type and crossm atch

Imaging 

Standard film s: AP pelvis and true lateral of hip



Fem oral neck fracture: anteroposterior (AP) pelvis with hip internally rotated 15â€“20Â°



Pubic ram i and acetabular fractures: pelvic inlet and outlet views



Acetabular fractures: Judet views (oblique views of hip)



High suspicion with negative plain film s: CT, MRI, or bone scan

Diagnostic Procedures/Surgery 

Joint aspiration with or without arthrogram under fluoroscope if suspect a septic joint, foreign body, or hem arthrosis, especially in gun shot wounds to hip



Operative repair or wash out

Differential Diagnosis 

Pubic ram us fracture



Acetabular fracture



Septic joint



Thigh, knee, ankle, or foot injury



Trochanteric bursitis



Iliotibial band tendinitis



Hip contusion

Treatment Pre Hospital 

Neurovascular exam is essential.

Pa ge 2 3 4



Im m obilize extrem ity in position of com fort for patient.

Initial Stabilization 

Airway, head, chest, or abdom inal injuries take precedence in m ultiple traum a.



Maintain pelvis and hip stability.



Monitor blood pressure continuously.



Cautions: o

DO NOT apply traction.

o

Monitor closely for developm ent of hem orrhagic shock as thigh can contain 4â€“6 units of blood.

P.525

ED Treatment 

Maintain pelvis and hip stability.



Rem ove splint and clothing.



Pain control: o

Isolated hip injuries: parenteral analgesia

o

Multitraum a or pediatric patients: fem oral nerve block



Orthopedic consultation: o

Necessary for all hip fractures and dislocations

o

Em ergent if neurovascular com prom ise

o

Open fractures m ust go directly to the OR for irrigation and dÃ©bridem ent.



Fractures requiring surgery: o



Cefazolin IV

Open fractures with lacerations, extensive soft tissue dam age, or contam ination: o



Add gentam icin/tobram ycin, tetanus.

If highly contam inated wound: Add penicillin G to cover

Pa ge 2 3 4

Clostridial species. 

Gunshot wounds: o

Culture m issile track, iodine dressing

Hip Dislocation 

A true orthopedic em ergency



Incidence of avascular necrosis and degenerative joint disease increases linearly with tim e to reduction: o

Perform reduction in ED, ideally <6 hours from onset.

o

Allis or Stim son m aneuvers

o

Also described: With patient in lateral decubitus position, m ove hip from flexed and adducted position to full external rotation with tibia perpendicular to floor.



Procedural sedation with etom idate, ketam ine, or m ethohexital plus m idazolam , propofol plus fentanyl



Look for fractures on postreduction im aging (plain film , CT).



Patients with prior hip arthroplasty m ay be reduced in the ED with procedural sedation and appropriate m onitoring.

Medication (Drugs) Antibiotics 

Cefazolin: 1 g IM/IV q6hâ€“q8h (peds: 25â€“50 m g/kg IM/IV div. q6hâ€“q8h m ax. 1 g)



Gentam icin/tobram ycin: 3â€“5 m g/kg/d IV/IM div. q8h (peds: 2â€“2.5 m g/kg q8h)



Penicillin G: 2 m illion IU IV q4h (peds: 100,000â€“400,000 IU/kg/d IV div. q4hâ€“q6h to m ax. 24 m illion IU in 24h)

Pa ge 2 3 4

Moderate Sedation 

Etom idate: 0.1â€“0.3 m g/kg IV once (not recom m ended for younger than 12 years of age)



Fentanyl: 50â€“100 m cg IV over 1â€“2 m inutes once (peds: >6 m onths 1â€“2 m cg/kg IV once)



Ketam ine: not recom m ended in adults owing to em ergence reaction (peds: 1.0â€“2 m g/kg IV, 4 m g/kg IM once)



Methohexital 1â€“1.5 m g/kg IV once (peds: not recom m ended)



Midazolam : 0.07 m g/kg IM or 1 m g slowly q2â€“3m in up to 5 m g m ax. (peds: 0.25â€“1.0 m g/kg PO once to a m ax. of 20 m g PO; 6 m o to 5 yr: 0.05â€“0.1 m g/kg IV titrate to m ax. 0.6 m g/kg 6â€“12 yr: 0.025â€“0.05 m g/kg IV titrate to m ax. 0.4 m g/kg



Propofol: 40 m g IV q10sec until induction; 5â€“10 m cg/kg/m in IV continuous infusion

Pain Control 

Hydrom orphone: 0.5â€“2.0 m g IM/SC/slow IV q4hâ€“q6h PRN; titrate for pain control (peds: 0.015 m g/kg/m in per dose IV q4hâ€“q6h PRN)



Morphine: 2â€“10 m g IV q4h, titrate for pain control (peds: 0.1 m g/kg IV q4h, titrate for pain control to m ax. 15 m g/dose)

Follow-Up Disposition Admission Criteria 

All hip fractures



Septic joint

Pa ge 2 3 4



Suspicion of occult fracture



Suspicion of nonaccidental traum a in children

Discharge Criteria 

Hip pain attributable to other cause



Fracture ruled out (negative radiographs plus negative clinical exam )



Patient with successful reduction of dislocated hip arthroplasty m ay be considered for discharge in consultation with orthopedics and with appropriate follow-up.

References 1. Dursteler B, Wightm an J. Etom idate-facilitated hip reduction in the em ergency departm ent. Am J Em erg Med. 2000;18: 204â€“208. 2. The Harriet Lane Handbook, Fifteenth Edition. 2000. Mosby, Inc. Saint Louis, Mo. 3. Hughes L, Beaty J. Fractures of the head and neck of the fem ur in children. J Bone Joint Surg. 1994;76A(2):283â€“292. 4. Kutty S, et al. Traum atic posterior hip location of hip in children. Pediatr Em erg Care. 2001;17:32â€“35. 5. Long W, et al. Managem ent of civilian gunshot injuries to the hip. Orthop Clin North Am . 1995;26(1):123â€“131. 6. McMurty A, Quaile A. Closed reduction of the traum atically dislocated hip: a new technique. Injury. 2001;32:162â€“164. 7. Rudm an N, McIlm ail D. Em ergency departm ent evaluation and treatm ent of hip and thigh injuries. Em erg Med Clin North Am . 2000;18:29â€“66. 8. Tarascon Pocket Pharm acopoeia 2006 Edition. Tarascon Publishing, Lom poc, CA. â€“ 9. Ward K, Yealy D. System ic analgesia and sedation in m anaging orthopedic em ergencies. Em erg Med Clin North Am . 2000;18:141â€“166.

Pa ge 2 3 4

10. Zuckerm an J. Hip fracture. N Engl J Med. 1996;334(23):1519â€“1525.

Miscellaneous SEE ALSO: Fem ur Fracture

Codes ICD9-CM 959.6

Core Content Code 18.4.13.1.8

Pa ge 2 3 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hirschsprung Disease

Hirschsprung

Disease Andrea Bracikowski Sally Santen

Basics Description 

Congenital aganglionosis m egacolon



1:5,000 live births

Genetics 

Mutations of the ret proto-oncogene found in both fam ilial and sporadic form s



Male-to-fem ale ratio 4:1



8% have positive fam ily history; 5â€“12% of siblings.



Associated chrom osom al abnorm ality (12%); m ost com m only Down syndrom e



Other congenital anom alies (GI, cardiac, craniofacial, cleft palate; 18%)

Etiology 

Absence of enteric ganglia in the distal bowel



Creates functional obstruction to passage of stool



Failure of neural crest cells to m igrate into

Pa ge 2 3 5

parasym pathetic Meissner (subm ucosal) and Auerbach (m yenteric) ganglions 

Begins at the internal anal sphincter and involves the rectosigm oid colon (75% of cases)



May extend entire length of gastrointestinal tract (often fatal)



Aganglionic segm ent chronically contracts, form ing an obstruction to the passage of stool.



Proxim al colon distends to hold stool that has not passed.



Stim ulation of the anus allows passage of stool.



Toxic m egacolon m ay develop.

Diagnosis Signs and Symptoms Three presentations, varying with age: 





Neonatal: o

Abdom inal distention

o

Delayed passage of m econium in first 48 hours

o

Vom iting

o

Neonatal enterocolitis

o

Sepsis

Infancy: o

Severe constipation

o

Chronic abdom inal distention

o

Vom iting

o

Failure to thrive

Later childhood and adulthood: o

Chronic constipation with obstruction

o

Enterocolitis at any age

o

Enterocolitis

Pa ge 2 3 5

o

Fever

o

Lethargy or toxic-appearing child

o

Abdom inal distention

o

Bloody, foul-sm elling diarrhea

o

Malnutrition

o

Reversible urinary tract infection (hydronephrosis, hydroureter, recurrent urinary tract infections [UTIs])

o

Acute appendicitis

o

Septicem ia

History 

Bowel m ovem ents frequently require rectal stim ulation or enem as.



Narrow caliber stools



Encopresis and diarrhea are uncom m on.



Absence of inciting factors associated with functional constipation (i.e., fissures, toilet training, diet)

Physical Exam 

Possible palpable colon on the left



Occult blood possibly owing to enterocolitis or anal fissures (constipation)

Essential Workup Abdom inal radiographs: 

Distended sm all bowel and proxim al colon with an em pty rectum are com m on findings.



Transition zone into a narrowed rectosigm oid segm ent



In neonates, film s will com m only show a distal obstructive pattern.



In children, with chronic constipation film s m ay show only large am ounts of stool.



In children with enterocolitis, bowel wall edem a or

Pa ge 2 3 5

pneum atosis intestinalis m ay be present.

Tests Lab CBC, electrolytes, glucose, urinalysis, blood culture if toxic

Imaging Barium enem a: 

Obtain after stabilization.



Dilated colon proxim al to the contracted aganglionic colon with uncoordinated peristalsis



Delayed barium evacuation

P.527

Diagnostic Procedures/Surgery 

Rectal m anom etry m ay assist in diagnosis, but is often abnorm al in long-standing constipation.



Full-thickness rectal biopsy confirm s diagnosis by the lack of ganglion cells.

Differential Diagnosis 



Infants: o

Meconium ileus or m econium plug from systic fibrosis

o

Congenital disorder

o

Intestinal or anal atresia or hypoplasia

o

Malrotation or duplication with volvulus

o

Necrotizing enterocolitis

Functional constipation o



Children: o



Sepsis

Functional constipation

Toxic

Pa ge 2 3 5

o 

Opiates, anticholinergics

Infectious o

Botulism

o

Trypanosom a cruzi



Acquired aganglionic colon



Metabolic or endocrine o

Hypothyroid/parathyroid, adrenal insufficiency, electrolyte abnorm ality



Structural



Spinal cord defects, abdom inal m asses

Treatment Initial Stabilization 

Ill-appearing children



Airway, breathing, and circulation m anagem ent (ABCs) with m onitoring



Initial bolus 0.9% IV fluids (20 m L/kg) for shock, dehydration, sepsis

ED Treatment 

Infants should be m anaged for bowel obstruction.



Consultation with a pediatric surgeon and pediatric gastroenterology



Unstable patient m ay require decom pression by loop colostom y; stom a m ust contain norm al bowel.



Stable children



Workup m ay be done as outpatient.



Definitive treatm ent is resection of the aganglionic section of bowel; staging unnecessary in relatively well child.



Return to norm al bowel function is the usual result.

Pa ge 2 3 5



Enterocolitis m ay occur at any tim e.



Ultim ate surgical goal is to place norm al ganglion containing bowel within 1 cm of the anal opening.

Medication (Drugs) 

When a child is toxic or has enterocolitis, use triple IV antibiotic coverage.



Am picillin: 50 m g/kg q8hâ€“q12h



Flagyl: 7.5 m g/kg q12hâ€“q48h



Gentam icin: 2.5 m g/kg qhâ€“q12h

Follow-Up Disposition Admission Criteria 

Infants and neonates presenting with bowel obstruction



Enterocolitis



Ill-appearing infants should be adm itted to a pediatric/neonatal intensive care unit (PICU/NICU).



If pediatric surgery is not available, transfer to a pediatric tertiary care center.

Discharge Criteria 

Older children with constipation



Well hydrated and taking oral fluid



Responsible parents



Close follow-up with prim ary care provider

Issues for Referral Care should be supervised by pediatric gastroenterologist/pediatric

Pa ge 2 3 5

surgeon.

References 1. Am iel J, Lyonnet S. Hirschsprung disease, associated syndrom es, and genetics: a review. J Med Genet. 2001;38:729â€“739. 2. Kays DW. Surgical conditions of the neonatal intestinal tract. Clin Perinatol. 1996;23:353â€“375. 3. Rudolph C, Benaroch L. Hirschsprung disease. Pediatr Rev. 1995;16:5â€“11. 4. Skinner MA. Hirschsprung disease. Curr Prob Surg. 1996;16:399â€“460. 5. Sullivan PB. Hirschsprung's disease. Arch Dis Child. 1996;74:5.

Pa ge 2 3 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > HIV/AIDS

HIV/AIDS

Mercedes Torres Amal Mattu

Basics Description 

Opportunistic diseases occurring with decreasing CD4 counts: o

o

o

CD <500 cells/m m 3 : 

Oroesophageal candidiasis



Pneum ococcal infection



Hairy leukoplakia



Im m une throm bocytopenic purpura

CD4 <200 cells/m m 3 : 

Pneum ocystis jiroveci pneum onia



Cryptococcal infection



Dissem inated tuberculosis



Cryptosporidiosis



Isosporiasis



Toxoplasm osis



Histoplasm osis

CD4 <50 cells/m m 3 : 

CNS lym phom a



Cryptococcosis

Pa ge 2 3 5





Mycobacterium avium com plex (MAC)



Tuberculosis (TB) pericarditis or m eningitis



Cytom egalovirus (CMV)



Cholangiopathy

Com m on m edication com plications: o

Hypersensitivity reaction: 

o

o

o

Pancreatitis: 

Dideoxyinosine



Dideoxycytidine



Lam ivudine



Cotrim oxazole



Pentam idine



Ritonavir



Stavudine



Zalcitabine

Peripheral neuropathy: 

Didanosine



Isoniazid



Linezolid



Stavudine



Zalcitabine

Kidney stones: 

o

o

Abacavir

Indinavir

Stevens-Johnson syndrom e: 

Nevirapine



Efavirenz



Cotrim oxazole

Dapsone (used for treatm ent of TB) can cause hem olytic anem ia.

o

Pentam idine can cause hypoglycem ia.

o

Many of the antiretroviral m edications can cause

Pa ge 2 3 5

som e hem atologic effects (e.g., anem ia or bone m arrow suppression), gastrointestinal upset, and rash.

Etiology 

The HIV retrovirus im pedes the im m une system by destroying the CD4 lym phocytes.



Risk factors: o

Sexual prom iscuity, m ultiple sexual partners

o

IV drug abuse

o

Hom osexuality

o

Blood transfusions prior to 1985

o

Unprotected sex with at-risk partners

o

Children of wom en who engage in high-risk behavior

Diagnosis Signs and Symptoms 

Prim ary HIV infection: o

Fever

o

Malaise

o

Rash on face and trunk

o

Flu-like syndrom e with lym phadenopathy and hepatosplenom egaly

o

Com m only described as â€œm ononucleosis-likeâ€•

o

Asym ptom atic period averaging 8 or m ore years after initial infection



Advanced disease (CD4 <200): o

Fatigue

o

Fevers

o

Night sweats

Pa ge 2 3 6

o

Weight loss/wasting

o

Alopecia

o

Chronic diarrhea with severe dehydration and electrolyte abnorm alities

o

Cough

o

Dyspnea

o

Hem optysis

o

Chronic low-grade headache

o

Altered m ental status

o

Seizures

o

Dem entia

o

Neuropathy

o

Painless visual loss

o

Skin lesions

History 

Recent CD4 count and viral load, lowest CD4 count



History of or current use of antiretroviral m edications



Medication com pliance



Length of diagnosis/illness



History of opportunistic infections



Previous hospitalizations or intensive care unit adm issions



Risk factors

Physical Exam Patients with a history of HIV/AIDS or possible undiagnosed HIV/AIDS need a thorough physical exam ination with particular attention paid to signs of opportunistic infection or advanced disease.

Essential Workup 

HIV serologic tests as noted below: o

There is a window of 6 m onths between prim ary infection and seroconversion, during which tests m ay be negative.

Pa ge 2 3 6



Respiratory sym ptom s: o

Chest radiograph

o

ABG

o

Induced sputum for gram stain, silver stain, acid-fast bacillus (AFB), and culture



o

Serum LDH

o

Blood cultures

Cardiac sym ptom s o

Serum cardiac m arkers, electrolytes

o

Chest radiograph

o

Electrocardiogram

o

Echocardiogram in cases of suspected pericarditis, effusion, or tam ponade



o

Blood cultures if endocarditis is suspected

o

Drug screen for cocaine and am phetam ines

Neurologic sym ptom s: o

Head CT with and without contrast

o

Lum bar puncture with opening pressure

o

Cerebrospinal fluid for glucose, protein, Gram stain and culture, cell count with differential, AFB sm ear, India ink stain, cryptococcus titer, and venereal disease research laboratory (VDRL).



Gastrointestinal sym ptom s: o

Stool for ova and parasites, Gram stain, culture, and Clostridium difficile assay

o

Urine analysis

o

For wom en: urine hcg, pelvic exam with wet m ount, and gonorrhea/chlam ydia testing

o

Liver functions tests, am ylase and lipase

o

Hepatitis serologies

o

Low threshold for CT abdom en/pelvis

o

Ultrasound if biliary sym ptom s present

Pa ge 2 3 6

o

Liberal indications for surgical consult, as HIV patients m ay not present with classic acute abdom en



Fever workup: o

Include aerobic/anaerobic, fungal, AFB, and Mycobacterium avium com plex blood cultures



Ocular sym ptom s: o

Fluorescein staining with slit lam p exam ination

Tests Lab 



Enzym e-linked im m unosorbent assay (ELISA) o

Detects IgG antibody against HIV

o

Sensitivity and specificity are approxim ately 99%.

o

Can be negative during the window period

Western blot: o

Detects IgG antibody against HIV proteins p24, gp120, gp 41

o

More specific than ELISA

o

Used to confirm a positive ELISA

o

The p24 antigen assay and PCR and viral cultures for HIV

o

Able to detect HIV during the 6-m onth seroconversion period



Rapid HIV testing: o

Results available in 5â€“20 m inutes

o

Four types of tests currently available

o

Sam ples include oral swabs, whole blood, serum , or plasm a

o

All reactive tests require confirm atory testing with western blot or ELISA

o 

>99% specific and sensitive

Absolute lym phocyte count (ALC):

Pa ge 2 3 6

o

Estim ate CD4 count

o

Multiply WBC Ã— percent lym phocytes

o

If ALC >2000, likely CD4 >200, if ALC <1000, likely CD4 <200

P.529

Imaging 

Chest radiograph: o

Bilateral interstitial infiltrates or pneum othorax: 

o

Reticulonodular infiltrates: 

o

TB

Lobar consolidation: 

o

TB, KS, or fungal pneum onia

Hilar lym phadenopathy with infiltrate: 

o

Pneum ocystis pneum onia

Bacterial pneum onia

Cavitation: 

TB, necrotizing bacterial pneum onia, coccidioidom ycosis

o

Enlarged cardiac silhouette: 

o

Pericarditis, dilated cardiom yopathy

Norm al: 

Does not rule out Pneum ocystis jiroveci pneum onia or TB



Head CT with and without IV contrast: o

Multiple ring-enhancing lesions with edem a in basal ganglia or cortex: 

o

Toxoplasm osis

Weakly enhancing periventricular lesions with edem a: 

CNS lym phom a

Pa ge 2 3 6

o

Multiple subcortical nonenhancing lesions: 



Progressive m ultifocal leukoencephalopathy

Abdom inal/pelvic CT: o

Splenom egaly: 

o

CMV, TB

Intestinal perforation or bowel obstruction: 

CMV colitis, lym phom a, histoplasm osis, MAC, appendicitis, ulcer disease, KS

o

Cholecystitis or cholangitis: 

o

Cryptosporidium , m icrosporidium , CMV

Pancreatitis: 

Medication-related, neoplasm , infectious

Differential Diagnosis 

Mononucleosis



Hepatitis



Syphilis



Rubella



Dissem inated gonococcal infection



Pulm onary em boli



TB



Pneum onia



Pulm onary m alignancies



Lym phocytic interstitial pneum onitis



Neurosyphilis



CMV encephalitis



CNS lym phom a



Coccidioidal m eningitis



Subarachnoid hem orrhage



Cerebral infarction



Cerebral edem a

Pa ge 2 3 6

Treatment Initial Stabilization 

ABCs



Supplem ental oxygen or intubation as necessary



Identify code status prior to intubation

ED Treatment 

Patients who appear to have bacterial infections, appear toxic, or have rapidly progressive sym ptom s should receive their first dose of antibiotics in the ED.



Prim ary HIV infection and m aintenance: o

Triple therapy (HAART): 

One nonnucleoside reverse transcriptase inhibitors (NNRTI) and two nucleoside reverse transcriptase inhibitors (NRTI)





One PI and two NRTIs



Triple NRTI

Toxoplasm osis: o

Pyrim etham ine: <60 kg: 50 m g, â‰¥60 kg: 75 m g PO daily (peds: 1 m g/kg PO b.i.d. Ã— 3 days, then 0.5 m g/kg PO b.i.d. Ã— 4 weeks)

o

Sulfadiazine: <60 kg: 1000 m g, â‰¥60 kg: 150 m g (peds: load 75 m g/kg, then 30 m g/kg) PO q6h



o

Leucovorin: 10â€“20 m g PO daily

o

Treat for at least 6 weeks

Cryptococcal m eningitis: o

Am photericin B: 6 m g/kg (peds: 3â€“4 m g/kg) IV daily

o

Flucytosine: 25 m g PO q.i.d.

o

Treat with above for 2 weeks, then fluconazole 100

Pa ge 2 3 6

m g (peds: 6 m g/kg) PO daily for 8 weeks 

Esophageal candidiasis: o



Fluconazole (dose above) for 14â€“21 days

MAC: o

Clarithrom ycin: 500 m g (peds: 15 m g/kg) PO b.i.d.

o

Etham butol: 15 m g/kg PO daily

o

May add rifabutin 300 m g PO daily if severe im m unosuppression



PCP: o

Trim ethoprim /sulfam ethoxazole: 20 m g/kg (peds: 15â€“20 m g/kg) daily div. q.i.d.

o

Pentam idine 4 m g/kg IV daily for sulfa-allergic patients

o

If PaO 2 <70 m m Hg or A-a gradient >35 m m Hg, add prednisone 40 m g PO b.i.d. for 5 days, then taper

Medication (Drugs) 

NRTIs: o

Abacavir: 300 m g (peds: 8 m g/kg) PO b.i.d. or 600 m g PO daily

o

Didanosine: <60 kg: 250 m g PO daily; â‰¥60 kg: 400 m g PO daily (peds: 120 m g/m 2 body surface area [BSA] PO q12h)

o

Em tricitabine: 200 m g (peds: unapproved) PO daily

o

Lam ivudine: 150 m g (peds: 4 m g/kg) PO b.i.d. or 300 m g PO daily

o

Stavudine: <60 kg: 30 m g PO bi.d.; â‰¥60 kg: 40 m g (peds: 1 m g/kg) PO b.i.d.

o

Zalcitabine: 0.75 m g (peds: unapproved) PO t.i.d.

o

Zidovudine: 300 m g PO b.i.d. (peds: 160 m g/m 2 BSA PO q8h)

Pa ge 2 3 6

o 

Tenofovir: 300 m g (peds: unapproved) PO daily

Protease inhibitors (PI) o

Am prenavir: 1400 m g (peds: 20 m g/kg) PO b.i.d.

o

Indinavir: 800 m g (peds: unapproved) PO q8h

o

Lopinavir/ritonavir: 400 m g/100 m g (peds:<40 kg: 10â€“12 m g/kg LPV, 2.5â€“3 m g/kg RTV) PO b.i.d.

o

Nelfinavir: 750 m g (peds: 25â€“35 m g/kg) PO t.i.d. or 1250 m g (peds: 45â€“55 m g/kg) PO b.i.d.

o

Ritonavir: 600 m g (peds: 400 m g/m 2 BSA) PO b.i.d.

o

Saquinavir: (m ust take with ritonavir 100 m g PO b.i.d.) 1000 m g PO b.i.d. (peds: unapproved)



NNRTIs: o

Delavirdine: 400 m g (peds: unapproved) PO t.i.d.

o

Efavirenz: 600 m g PO daily

o

Nevirapine: 200 m g (peds: 120 m g/m 2 BSA) PO daily for 14 days, then 200 m g (peds: 120 m g/m 2 BSA) PO b.i.d.



Fusion inhibitors: o

Enfuvirtide: 90 m g (peds >6 years old: 2 m g/kg) subcutaneously b.i.d.

Follow-Up Disposition Admission Criteria 

Unexplained fever with CNS involvem ent or suspected endocarditis



Severe hypoxem ia (PaO 2 <70 m m Hg)



Cardiac sym ptom s suggestive of acute coronary syndrom e



Pericardial effusion

Pa ge 2 3 6



Suspected bacterial pneum onia or TB



A change in neurologic status



New-onset seizures



Inability to am bulate



Inability to tolerate oral intake



Intractable diarrhea with dehydration

Discharge Criteria The patient can m aintain adequate oral intake, provide self-care, and am bulate.

Issues for Referral Patient should be referred to a prim ary HIV care provider for initiation of HAART therapy regim en and ongoing care.

References 1. Barbaro G, Fisher SD, Giancaspro G, et al. HIV-associated cardiovascular com plications: a new challenge for em ergency physicians. Am J Em erg Med. 2001;19(7):566â€“574. 2. Belleza WG, Browne B. Pulm onary Considerations in the Im m unocom prom ised Patient. Em ergency Medicine Clinics of North Am erica. 2003;21(2):499â€“531. 3. Guidelines for the Use of Antiretroviral Agents in HIV-1 Infected Adults and Adolescents. Panel on Clinical Practices for Treatm ent of HIV Infection. Departm ent of Health and Hum an Services, Centers for Disease Control. October 29, 2004, http://www.AIDSinfo.nih.gov. 4. Hovanessian HC. New developm ents in the treatm ent of HIV disease: an overview. Ann Em erg Med. 1999;33(5):546â€“555. 5. Moran GJ, House HR. HIV-related illnesses: the challenge of ED m anagem ent. Em erg Med Pract. 2002;4(1):128. 6. Slaven EM, Lopez F, Weintraub SL, et al. The AIDS Patient With Abdom inal Pain: A New Challenge for the Em ergency Physician. Em ergency Medicine Clinics of North Am erica. 2003;21(4):987â€“1015.

Pa ge 2 3 6

Codes ICD9-CM 042

ICD10 B24

Pa ge 2 3 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ho rdeo lum and C halaz io n

Hordeolum and

Chalazion Shari Schabowski

Basics Description Result from inflam m atory processes involving the glands of the eyelid along the lash line: 

Hordeolum â€”acute glandular obstruction resulting in inflam m ation



Chalazionâ€”end result of a chronic granulom atous inflam m ation

Hordeolum 

Develops owing to outflow obstruction in one or m ore of the glands of the eyelid



The eyelid has m any secretory glands: o

o

External hordeolum : 

Glands of Zeisâ€”superficial sebaceous glands



Glands of Mollâ€”superficial sweat glands

Internal hordeolum : 

Meibom ian glandsâ€”deeper m odified sebaceous glands



May evolve into chalazion

Pa ge 2 3 7



Obstructed glands m ay becom e secondarily infected.



May progress to localized abscess form ation or cellulitis

Chalazion Chronic granulom atous inflam m ation in the m eibom ian gland: 

Originates from inspissated secretions



Blockage of the gland's duct at the eyelid m argin m ay result in release of the contents of the gland into the surrounding eyelid soft tissue.



A lipogranulom atous reaction ensues.



Occasionally, chalazia becom e secondarily infected.



May evolve from incom pletely drained internal hordeolum

Etiology Hordeolum May becom e secondarily infected: 

Staphylococcus aureus m ost com m only

Diagnosis Signs and Symptoms Hordeolum 

Develops acutely when glandular outflow is obstructed



Red, tender, painful, swollen m ass within the distal eyelid m argin



Typically solitary, but m ay be m ultiple



Nontoxic-appearing patient



Presentation depends on which gland is affected: o

External hordeolum : 

Originates from obstruction of the superficial sebaceous or sweat glands whose ducts are

Pa ge 2 3 7

located between the eye lashes 

Exquisitely tender sm all m ass that points anteriorly

o

Internal hordeolum : 

Originates from obstruction of the sebaceous glands whose ducts are located on the inner aspect of the lid m argin



Painful sm all m ass that is palpable through the eyelid



May cause a foreign body sensation in the eye



Typically m ore inflam ed, larger, and m ore painful



Most com m only drains through the conjunctival surface after 1 week of treatm ent, but m ay drain through the skin



Associated with localized inflam m ation in the surrounding tissue: o



May lead to preseptal cellulitis

Tender preauricular lym ph nodes m ay be present.

Chalazion 

Firm , circum scribed, nontender, or m inim ally tender nodule



Noninflam ed



Typically long-standing



Sym ptom s m ost com m only owing to physical properties: o

Disrupts natural contour of eye

o

Obstructs visual field/peripheral vision

o

Pressure on globe

Essential Workup Com plete ophthalm ologic exam ination

Hordeolum

Pa ge 2 3 7



Identify the origin of the abscess.



Determ ine extent of surrounding inflam m ation/cellulitis.

Chalazion Determ ine whether physical properties of chalazion result in corneal exposure and injury.

Differential Diagnosis 

Hordeolum



Chalazion



Blepharitis



Dacryocystitis



Dacryoadenitis



Preseptal cellulitis



Pyogenic granulom a



Sebaceous cell carcinom a

P.531

Treatment ED Treatment Hordeolum 

Relieve obstruction and prevent abscess form ation: o

Warm com presses for 15 m inutes 4â€“6 tim es per day

o

Gently m assage the nodule to express obstructed m aterial.

o

Rarely, in severe cases, incision and drainage of internal hordeolum m ay be necessary:

Pa ge 2 3 7



Typically done by ophthalm ologist



If pointed toward the conjunctiva, vertical incision is m ade to avoid injury to the m eibom ian glands.

o

Prophylactic topical antistaphylococcal antibiotic ointm ent is applied in the cul-de-sac and m assaged along the lid m argin to stim ulate duct and prevent secondary conjunctivitis.

Chalazion For chalazion, com plaints typically reflect nonem ergent aesthetic and cum bersom e physical properties of the m ass: 

Referral to ophthalm ology for incision and curettage or steroid injection



Lubricating eyedrops m ay provide sym ptom atic relief

Medication (Drugs) 

Lacri-Lube ophthalm ologic drops: as needed for com fort



Sulfacetam ide ophthalm ologic ointm ent: applied every 2â€“4 hours until 24 hours after sym ptom s resolve com pletely



Gentam icin ophthalm ologic ointm ent: applied every 2â€“4 hours until 24 hours after sym ptom s resolve com pletely

Follow-Up Disposition Admission Criteria Secondary cellulitis or deep tissue infection develops

Pa ge 2 3 7

Discharge Criteria 

All uncom plicated cases m ay be discharged.



If incision and drainage is necessary, follow-up with ophthalm ology within 1â€“2 days



Sym ptom s are expected to resolve com pletely within 3â€“4 weeks; m ore typically com plete resolution is seen within 7â€“10 days.

References 1. Cullom R. The Will's Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. Philadelphia: Lippincottâ€“Raven Publishers; 1998. 2. Kanski JJ. Clinical Ophthalm ology. London: Butterworth-Heinem ann; 1994:24. 3. Lederm an C, Miller M. Disorders of the lacrim al system apparatus. Hordeola and chalazia. Pediatr Rev. 1999;20(8):283â€“284. 4. Prochazka MD, MSc, Allan V. Diagnosis and treatm ent of red eye. Prim ary Care Case Rev. 2001;4(1)23â€“31. 5. Rubin S, Hallagan L. Lids, lacrim als and lashes. Em erg Clin North Am . 1995;13(3):631â€“647.

Codes ICD9-CM 373.2 373.11

ICD10 H00.1 H00.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ho rner Syndro m e

Horner Syndrome

Richard S. Krause

Basics Description Unilateral sym pathetic denervation produces signs of Horner syndrom e: 

Relaxation of retracting m uscles in upper and lower lids: o



Loss of pupillary dilator innervation: o



Ptosis

Miosis (unopposed pupillary constriction)

Loss of sym pathetic stim ulation of sweat glands: o

Anhidrosis

Etiology 

Tum ors of lung or m etastases to cervical nodes: o

May interrupt preganglionic sym pathetic fibers (between thoracic sym pathetic trunk and superior cervical ganglion)



Traum a: penetrating neck wounds



Pneum othorax: o

Tension pneum othorax m ay cause traction on sym pathetic fibers owing to shift of m ediastinal structures.



Infiltration or infection of cervical nodes:

Pa ge 2 3 7

o 

Sarcoidosis, tuberculosis

Vascular disorders: o

Migraine or cluster headaches, carotid artery dissection

Pediatric Considerations 



Hereditary Horner syndrom e: o

Blue iris (or irregular coloration) on affected side

o

Brown on unaffected side (heterochrom ia iridis)

Birth traum a: o

May cause dam age to sym pathetic chain

Diagnosis Signs and Symptoms 

Horner syndrom e is characterized by: o

Ptosis: drooping of eyelid on affected side, usually slight

o

Miosis: decrease in pupillary size on involved side (pupillary asym m etry = 1 m m )

o 

Anhidrosis: lack of sweating on involved side of face

The im portance of Horner syndrom e is its association with certain disease states.

Essential Workup 

History and physical exam focused on neurologic findings



Chest radiograph to screen for tum or or pneum othorax

Tests Provocative Testing 

Pharm acologic (cocaine) testing confirm s diagnosis of sym pathetic ocular lesion:

Pa ge 2 3 7

o

One drop of 5% ocular cocaine solution is instilled into each eye.

o

Failure of pupil on involved side to dilate as m uch as other pupil (increase in am ount of anisocoria) in 1 hour is confirm atory (positive test).

Imaging 

CT or MRI of head, neck, or chest m ay be indicated depending on signs and sym ptom s.

Other 

Ocular tonom etry for suspected glaucom a



Carotid Doppler ultrasound (US) m ay be indicated to evaluate for carotid dissection (usually painful)

Differential Diagnosis 

Increased intracranial pressure (ICP): alm ost always associated with altered level of consciousness (LOC), headache



Sim ple anisocoria (pseudo-Horner syndrom e): 15â€“20% of the population have anisocoria and 3â€“4% also have m iosis and ptosis. o

Cocaine test is negative (both pupils dilate equally).

o

Inspect photo ID for pre-existing anisocoria.



Topical m edications or exposures



Migraine or cluster headache



Glaucom a, inflam m atory ocular diseases, or ocular traum a

Pediatric Considerations 

Birth traum a in newborns



Hereditary Horner syndrom e

P.533

Pa ge 2 3 7

Treatment Pre Hospital Cautions: 

The im portance of Horner syndrom e is its association with m ore serious underlying conditions.



Patients with increased ICP or tension pneum othorax m ust be recognized im m ediately.

Initial Stabilization 

If increased ICP is suspected, initiate m easures to control ICP: o



Intubation, osm otic diuretics

Tension pneum othorax: o

Needle thoracostom y followed by chest tube

ED Treatment Horner syndrom e per se requires no ED treatm ent.

Medication (Drugs) Cocaine: 5% (adult), 2.5% (peds:) ophthalm ic solution: One drop in each eye is diagnostic.

Follow-Up Disposition Admission Criteria Adm ission for isolated Horner syndrom e is not needed:

Pa ge 2 3 8



Adm ission m ay be needed for underlying condition.

Discharge Criteria Patients with isolated Horner syndrom e m ay be discharged with appropriate follow-up arranged for continued workup as outpatient.

References 1. Arcasoy S, Jett J. Current concepts: superior pulm onary sulcus tum ors and Pancoast's syndrom e. New Engl J Med. 1997;337:1370â€“1376. 2. Fields C, Barker F. Review of Horner's syndrom e and a case report. Optom Vis Sci. 1992;69(6):481â€“485. 3. Thanvi B, et al. Carotid and vertebral artery dissection syndrom es. Postgrad Med. 2005;81:383â€“388. 4. Wilheim H, et al. Horner's syndrom e: a retrospective analysis of 90 cases and recom m endations for clinical handling. Ger J Ophthalm ol. 1992;1(2):96â€“102.

Codes ICD9-CM 337.9

ICD10 G90.2

Pa ge 2 3 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hum erus F racture

Humerus Fracture

Julie Marmon

Basics Description 

Proxim al hum erus fractures involve: o

Hum eral head

o

Lesser tuberosity

o

Greater tuberosity

o

Bicipital groove

o

Account for 5% of all fractures

o

Typically seen in adults over the age of 45 years and the elderly

o

>70% of patients with a proxim al hum erus fracture are 60 years and older

o

Neer classification: A system that identifies the num ber of fragm ents and their location 

Fractures consist of 2- to 4-part fractures, and the locations include the anatom ic neck, the surgical neck, the greater and lesser tuberosity.



Fracture-dislocation and hum eral head splitting also part of Neer classification



Hum eral shaft fractures o

Hum eral shaft fractures are of three types:

Pa ge 2 3 8



Nondisplaced,



Displaced or angulated



Severely displaced or associated with neurovascular com prom ise

o

Hum eral shaft fractures account for 3% of all fractures

Etiology 

Most often a history of a fall



Fall onto an outstretched hand



High-energy direct traum a



Excessive rotation of the arm in the abducted position



Electrical shock or seizure



Pathologic fracture from m etastatic disease



Ball throwing

Pregnancy Considerations Discuss need for operative treatm ent with orthopaedics and weigh benefits against possible risks to fetus.

Diagnosis Signs and Symptoms 

Pain, swelling, and tenderness



Difficulty in initiating active m otion



Arm often closely held against the chest



Crepitus m ay be present



Ecchym osis within 24 to 48 hours at area of fracture



Dim inished peripheral pulses



Decreased sensation over the deltoid m uscle (axillary nerve), or forearm /first web space (radial nerve)

Essential Workup

Pa ge 2 3 8

Assessm ent of neurovascular status: 

Assess individual nerves: o

Radial (radial nerve palsy m ost com m on with m iddle and m iddle-distal transverse and spiral fractures)

o

Median

o

Ulnar

o

Axillary (sensation to the lateral aspect of the shoulder)

o

Musculocutaneous nerve (sensation to the extensor aspect of the forearm )



Presence of radial, ulnar, and brachial pulses, and good capillary refill in all digits



Diagnosis is confirm ed by x-ray.

Pediatric Considerations 

Salter-Harris I fractures are seen in children <5 years.



Neonatal fractures occur from obstetric traum a: o



Pseudoparalysis often seen

Physeal separation in the infant m ay also be the result of physical abuse



Children 5â€“10 years: o

Metaphyseal fractures due to rapid growth and thinning of the m etaphyseal cortex

o 

Most fractures are transverse or short oblique.

Salter Harris II fractures are seen in children â‰¥11 years.



Always consider nonaccidental traum a (NAT), especially with spiral fractures of the hum erus o

Im plies a rotational com ponent to the injury (especially age <3 years)

Tests Imaging

Pa ge 2 3 8



Proxim al hum erus fractures: o

Anteroposterior (AP), lateral views

o

Axillary, transthoracic, or â€œyâ€• view: 

Axillary view to assess tuberosity displacem ent, glenoid articular surface, and relationship of the hum eral head to the glenoid

o

CT scan can be useful in evaluating articular surfaces of glenoid and hum eral head.



Hum eral shaft fractures: o

AP and lateral views of entire hum erus are m andatory.

o

Include shoulder and elbow views to exclude associated joint involvem ent.

Differential Diagnosis 

Acute hem orrhagic bursitis



Traum atic rotator cuff tear



Dislocation



Acrom ioclavicular separation



Calcific tendinitis



Contusion



Tendon rupture



Neuropraxia



Pathologic fracture

Treatment Pre Hospital Cautions: 

Excessive m ovem ent of the arm m ay produce further neurovascular injury.

Pa ge 2 3 8



Im m obilization with sling and swath and transport



Rapid transport in presence of neurologic or vascular deficits

Initial Stabilization 

Prim ary and secondary survey for associated injuries



Airway m anagem ent and resuscitate as indicated



Im m ediate im m obilization to prevent further fracture displacem ent or neurovascular injury



Sling with arm supported at the side or in the Velpeau position



Axillary pad m ay also be used for com fort.



After im m obilization, perform another neurovascular exam .



Pain control with NSAIDs or narcotic analgesics



Application of ice to lim it swelling



Open hum erus fractures require covering with a sterile dressing, tetanus prophylaxis, and parenteral prophylactic antibiotics.

P.535

ED Treatment 

Orthopaedic consultation: o

Operative versus nonoperative treatm ent is decided in conjunction with orthopaedics



o

Pain m anagem ent

o

NSAIDs

o

Narcotics

Proxim al hum erus fractures: o

In general, the higher the num ber of fragm ents in the fracture and the greater the degree of

Pa ge 2 3 8

displacem ent, the m ore difficult it is to m anage the patient with a closed reduction. o

15â€“20% of proxim al hum erus fractures will have displaced fragm ents.



Nonoperative treatm ent: o

Initial im m obilization and early m otion succeeds in m any cases, as m ost proxim al hum eral fractures are m inim ally displaced.

o

Use a sling, swath, and axillary pad to im m obilize.

o

Closed reduction and orthopaedic consultation

o

Conscious sedation for all closed reductions

o

1-part and 2-part fractures often successfully treated with closed reduction

o

3-part and 4-part fractures are unstable and m ay need ORIF



Hum eral shaft fractures: o

Usually don't require elaborate reduction or im m obilization

o

Most hum eral shaft fractures can be m anaged nonoperatively, with expected union rates approaching 100%.

o

20Â° of anterior angulation and 30Â° of varus angulation are well tolerated by the m usculature around the hum erus.

o

Hum erus can tolerate up to 3 cm of shortening as a result of overriding fracture fragm ents with little functional deficit.

o

Nondisplaced fractures can be treated with a sugar-tong splint of the upper extrem ity.

o

Grossly displaced or com m inuted fractures require im m obilization with a light hanging cast. 

Contraindicated with a transverse fracture

Pa ge 2 3 8

o

Open fractures or fractures associated with neurovascular com prom ise require im m ediate orthopaedic consultation.

Pediatric Considerations In children nearing skeletal m aturity, determ ining the degree of displacem ent or separation of the proxim al hum eral epiphysis is essential as exact reduction is im portant to prevent later growth disturbance.

Medication (Drugs) 



Pain m edications: o

NSAIDs

o

Narcotics

Conscious sedation with closed reductions (see Conscious Sedation)

Follow-Up Disposition Admission Criteria 

Open fractures for operative m anagem ent and parenteral antibiotic therapy



Fractures associated with neurovascular com prom ise



Displaced fractures that cannot be treated through closed reduction



Significant associated injuries that require adm ission and observation

Discharge Criteria

Pa ge 2 3 8

Nondisplaced fracture or a fracture that is successfully treated with closed reduction and no associated injuries

Pediatric Considerations 

Pediatric patients are often less com pliant with im m obilization and less able to verbalize com plaints and m ay benefit from adm ission.



Assess safety of environm ent in cases suspicious of NAT.

References 1. Bucholz RW, Heckm an JD. Rockwood and Green's fractures in adults. 5th ed. Philadelphia, Pa.: Lippincott William s & Wilkins, 2002. 2. Gregory PR. Fractures of the shaft of the hum erus. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's fractures in adults. 5th ed. Philadelphia, Pa.: Lippincott William s & Wilkins, 2002. 3. Morrissy RT, Weinstein SL. Lovell and Winter's pediatric orthopaedics, vol 2. 5th ed. Philadelphia, Pa.: Lippincott William s & Wilkins, 2001. 4. Neer CS. Displaced proxim al hum eral fractures: I. Classification and evaluation. J Bone Joint Surg. 1970;52A:1077â€“1089. 5. Palvenen M, et al. Update in the epidem iology of hum erus fractures. Clinical Orthopaedics and Related Research. 2006;442:87â€“92. 6. Schem itsch E, Bhandari M. Fractures of the hum eral shaft. In: Browner: Skeletal Traum a: Basic Science, Managem ent, and Reconstruction, 3rd ed. Saunders, an im print of Elsevier, 2003. 7. Sim on R, Koenigskhecht S. Em ergency orthopaedics, the extrem ities, 3rd ed. Norwalk, CT: Appleton & Lange, 1993. 8. Willim as R, Hardcastle N. Hum eral fractures and nonaccidental injury in children. Em er Med J. 2005;22:124â€“125.

Miscellaneous

Pa ge 2 3 8

SEE ALSO: Conscious Sedation

Codes ICD9-CM 812.0 812.1 812.2 812.3 812.4 812.5

ICD10 S422 S423 S424

Pa ge 2 3 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydatidifo rm M o le

Hydatidiform Mole

Emi Latham

Basics Description Complete Mole 

Fetal tissue not present



Diffuse chorionic villi swelling



Diffuse trophoblastic hyperplasia



Can occur twinned to a norm al fetus

Partial Mole 

Fetal or em bryonic tissue m ay be present.



Focal chorionic villi swelling



Focal trophoblastic hyperplasia



Can also occur with twinning

Gestational Trophoblastic Tumor (GTT) 

Risk factors: o

Marked trophoblastic proliferation: 

Elevated hum an chorionic gonadatropin (hCG) levels

o



Excessive uterine enlargem ent



Prom inent theca lutein ovarian cysts

Older age

Pa ge 2 3 9

o 

Repetitive m olar pregnancies

Persistent disease possibility 20% in com plete and 2â€“4% in partial m oles



High-risk patients have a higher incidence of local invasion (31% versus 3.4%) and m etastatic disease (8.8% versus 0.6%) than low-risk patients.

Genetics 

Com plete m ole: o

Karotype: 46, XX (90%); 46, XY (10%)

o

Enucleate egg fertilized by two sperm or by a haploid sperm that duplicates

o 

Paternal DNA

Partial m ole: o

Karyotype: triploid 69XXX (90%); 69XXY (10%)

o

Haploid ovum duplicates and is fertilized by norm al sperm , or haploid ovum fertilized by two sperm .

o

Maternal and paternal DNA

Etiology 

Largely unknown



Advanced m aternal age is the best estim ated risk factor:



o

>40 years old carries five- to tenfold risk

o

Disease also noted in <20 years old

Frequency m ultiple tim es greater in Asian countries: o

One per 1,500 live births in the United States and Western Europe

o

Up to one per 120 live births in the Far East 

Increased risk not estim ated to persist when m other m oves to United States



Lower socioeconom ic status



Deficiency in anim al fat and vitam in A



Previous m olar pregnancy carries 1â€“2% risk in future

Pa ge 2 3 9

pregnancies 

Finding in one of 600 therapeutic abortions

Diagnosis Signs and Symptoms Usually Exaggerated Subjective Symptoms of Pregnancy 

Vaginal bleeding, m ost com m on (97%): o

Late first trim ester or early second trim ester

o

Usually painless and like â€œprune juiceâ€•

o

May also have tissue passage



Hyperem esis gravidarum



Pelvic pressure

Complete Mole 







Spontaneous abortion: o

Often described as grapelike vesicles

o

Usually occurs in second trim ester <20 weeks

Toxem ia (27%): o

Visual changes

o

Hypertension

o

Proteinuria

o

Hyperreflexia

o

Possibly convulsions

Hyperthyroidism (7%): o

Marked tachycardia, trem or

o

Due to Î²-hCG stim ulating thyrotropin receptors

Acute respiratory distress (2%): o

Tachypnea, diffuse rales, tachycardia, m ental status changes

Pa ge 2 3 9

o

Possibly em bolism of trophoblastic tissue

o

May also be due to cardiopulm onary changes from toxem ia, hyperthyroidism , or iatrogenic fluid replacem ent

Partial Mole 

Usually does not exhibit dram atic clinical features of com plete m ole



Frequently presents with sym ptom s sim ilar to patients with threatened or spontaneous abortion



Often presents at m ore advanced gestational age



May have fetal heart tones

Physical Exam 

Uterine size/date discrepancy (50â€“66%): o

Com plete m ole usually larger than dates would indicate

o 

Partial m ole can be sm aller than dating suggests

Ovarian m asses: o

Multiple bilateral theca lutein cysts due to high levels of Î²-hCG

Essential Workup hCG and Free Subunits 



Com plete m ole: o

Usually Î²-hCG >100,000 m IU/m L

o

Mean ratio of Î²-hCG to Î±-hCG is 20:9.

o

Higher serum level percentage of free Î²-hCG

Partial m ole: o

Mean ratio of Î²-hCG to Î±-hCG is 2:4.

o

Higher serum level percentage of free Î±-hCG



Can be followed as indicator of persistent disease



Î²-hCG >40,000 m IU/m L carries poor prognosis

Pa ge 2 3 9

Ultrasonography 

Original technology m ost accurate in 2nd trim ester: o

Com plete m ole produces characteristic â€œsnowstorm â€• vesicular sonographic pattern from absence of fetal tissue and swelling of chorionic villi with anechoic spaces.

o

Partial m ole produces â€œswiss-cheeseâ€• appearance from cystic changes in placenta with scalloping of villa and in shape of gestational sac.



Newer high-resolution ultrasound allows for diagnosis within the first trim ester: o



Com plex intrauterine m ass with m any sm all cysts

Theca lutein cysts: o

Bilateral, m ultiloculated

o

Large at 6â€“12 cm

Tests Lab 

Î²-hCG



Blood type, Rh and crossm atch



CBC to assess for anem ia and throm bocytopenia



Coagulation profile to assess for dissem inated intravascular coagulation



Electrolytes with blood urea nitrogen and creatinine



Liver function tests



TSH and thyroxin (free T4) if hyperthyroidism suspected



Urinanalysis to evaluate for protein if toxem ia suspected

Chest Radiograph 

To assess for pulm onary edem a in acute respiratory distress



To check for m etastatic disease

Pa ge 2 3 9



For baseline study

Pathology 

All conception products should be evaluated.



Products m ay be the only way to diagnose a partial m olar pregnancy.

Differential Diagnosis 

Threatened abortion



Missed abortion



Incom plete abortion



Ectopic pregnancy

P.537

Treatment Pre Hospital 

Ensure patent airway, provide oxygen.



IV access



Treat convulsions appropriately with benzodiazepine.



Save passed tissue for histological evaluation.

Initial Stabilization 

IV access



Cardiac m onitoring



Type and cross-m atch for blood, especially if patient requires uterine extraction.

ED Treatment 

Acute respiratory distress: o

Intubation and m echanical ventilation

Pa ge 2 3 9

o 

Chest x-ray (CXR)

Hyperthyroidism : o

Î²-adrenergic blockers 

Adm inister before m olar evacuation.



Stress of anesthesia or surgery m ay precipitate thyroid storm .



Preeclam psia/Eclam psia: o

Convulsions 

Adm inister benzodiazepine (Valium ) or m agnesium sulfate.

o

Hypertension: 



Coagulopathy: o



Adm inister Hydralazine or Labetalol

Transfuse with blood products as needed.

Suction Curettage: o

Done by obstetrician, possibly in ED

o

Curative in 80% of cases

o

Method of choice in wom en wishing to preserve fertility

o

Oxytocin infusion to induce m yom etrial tone, m ay require other uterotonic form ulations



Chem oprophylaxis: o

Very controversial

o

Prescribed by obstetritrician only for patients with follow-up

o

Usually used in high-risk com plete m ole or if horm onal m onitoring is unavailable



Hysterectom y: o

Patients in older age group

o

Patients not interested in keeping fertility

o

High-risk disease

o

Does not prevent possible m etastasis of GTT

Pa ge 2 3 9

Medication (Drugs) 

Diazepam : 0.2â€“0.4 m g/kg IV, or 0.3â€“0.5 m g PR, up to 5â€“10 m g, for m ax. 30 m g



Hydralazine: 5â€“10 m g IV q20m in, up to 60 m g



Labetalol: 20 m g IV with doubled dosing q10m in for m ax. 300 m g



Magnesium Sulfate: 4â€“6 g IV over 15â€“20 m inutes then m aintenance 1â€“2 g/h



Oxytocin: Postpartum bleeding, 10 units IM



Propranolol: 1 m g IV increm ents q2m in



Rhogam : 300 m cg within 72 hours

Follow-Up Disposition Admission Criteria 

Enlargem ent of uterus beyond 16 weeks of gestation size: o

The larger the uterus, the greater the risk for uterine perforation during suction curettage, hem orrhage and pulm onary com plications.



Clinical evidence of preeclam psia, hyperthyroidism , respiratory distress



Hysterectom y



Partial m olar pregnancy



Hem odynam ic instability

Discharge Criteria 

Uncom plicated dilation and curettage of low-risk and sm all-size m ole in reliable patient

Pa ge 2 3 9



Stress im portance of follow-up due to risk of persistent GTT: o

Î²-hCG tested at 48 hours after evacuation, then weekly for 3 weeks, then m onthly for 6 m onths

o

Î²-hCG should always decline; if it elevates, recheck CXR and uterine ultrasound.

Issues for Referral 

Pelvic rest for 4â€“6 weeks after uterine evacuation



Recom m end no pregnancies for 12 m onths



Future pregnancies should have early sonographic evaluation due to increased risk in future pregnancies.

References 1. Berkowitz RS, Goldstein DP. Managem ent of m olar pregnancy and gestational trophoblastic tum ors. In: Knapp RC, Berkowitz RS, eds. Gynecologic oncology. 2nd ed. New York, NY:Mc Graw-Hill; 1993: 328â€“338. 2. Bloss J, Miller D: Gestational trophoblastic disease. In: Hankins GDV, Clark SL, Cunningham FG, Gilstrap LC, eds. Operative obstetrics. Norwalk, CT: Appleton and Lange; 1995:695. 3. Goldstein DP, Berkowitz RS. Current m anagem ent of com plete and partial m olar pregnancy. J Reprod Med. 1994;39:139â€“146. 4. Kim DS, et al. Effects of prophylactic chem otherapy on persistent trophoblastic disease in patient with com plete hydatidiform m ole. Obstet Gynecol. 1986;67:690â€“694. 5. Soper JT, et al. Diagnosis and treatm ent of gestational trophoblastic disease: ACOG practice bulletin #53. Gynecol Oncol. 2004 Jun;93(3):575â€“585.

Codes ICD9-CM 630

Pa ge 2 3 9

ICD10 O01.0 O0.1 O01.9

Pa ge 2 4 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydro carbo n Po iso ning

Hydrocarbon

Poisoning James W. Rhee

Basics Description 

Main com plication from hydrocarbon exposure is aspiration: o

Hydrocarbon aspiration prim arily affects central nervous and respiratory system s.



Physical properties determ ine type and extent of toxicity: o

Viscosity (resistance to flow): 

Higher aspiration risk from products with lower viscosity

o

Volatility (ability of a substance to vaporize): 

Hypoxia from arom atic hydrocarbons displacing alveolar air

o

Surface tension (ability to adhere to itself at liquid's surface): 

Low surface tension allows easy spread from oropharynx to trachea, prom oting aspiration (e.g., m ineral oil, seal oil).



Volatile substance abuse:

Pa ge 2 4 0

o

Com m on solvents abused: 

Typewriter correction fluid



Adhesive



Gasoline



Cigarette-lighter fluid

o

Sniffing: product inhaled directly from container

o

Huffing: product inhaled through a soaked rag held to face

o

Bagging: product poured into bag and m ultiple inhalations taken from bag



Major classes of hydrocarbons: o

Aliphatics: 

Include kerosene, m ineral oil, seal oil, gasoline, solvents, and paint thinners



Pulm onary toxicity via aspiration



Asphyxiation from gaseous m ethane and butane by displacem ent of alveolar oxygen

o

o

Halogenated hydrocarbons: 

Include carbon tetrachloride and trichloroethane



Found in industrial settings as solvents



Well absorbed by lungs and gut



High toxicity



Liver and renal failure associated with ingestion

Cyclics or arom atic com pounds include toluene and xylene: 

Highly volatile and well absorbed from gut



Death from benzene reported with 15-m L ingestion

o

Terpenes or wood distillates include turpentine and pine oil: 

Significant gastrointestinal tract absorption



Significant central nervous system depression

Pa ge 2 4 0

Etiology 

Accidental exposures typical in young children



Inhalation abuse of volatile hydrocarbons



Suicide attem pts in adolescents and adults

Diagnosis Signs and Symptoms 

Often asym ptom atic at presentation



Odor of hydrocarbons on breath



Early: euphoria: o





Disinhibition

Late: dysphoria: o

Ataxia

o

Confusion

o

Hallucination

Sudden sniffing death: o

Cardiac arrest in volatile substance abusers secondary to hypersensitization of m yocardium leading to m alignant dysrhythm ias on adrenergic stim ulation





Pulm onary: o

Mild to severe respiratory distress

o

Cyanosis

o

Aspiration (prim ary com plication)

Central nervous system : o

Intoxication

o

Euphoria

o

Slurred speech

o

Lethargy

Pa ge 2 4 0

o 





Com a

Gastrointestinal tract: o

Local m ucosal irritation

o

Gastritis

o

Diarrhea

Cardiac: o

Tachycardia

o

Dysrhythm ias (volatile substance abuse)

Derm al: o

Local erythem a

o

Maculopapular or vesicular eruptions

o

Defatting derm atitis from chronic skin exposure

o

Huffer face rash in chronic abusers

Essential Workup Obtain inform ation on the following: 

Product: exact nam e on label, m anufacturer, and ingredients



Nature of ingestion or exposure: accidental or intentional



Estim ated am ount ingested



In industrial settings, Material Safety Data Sheets (MSDSs)

Tests ECG for intoxicated volatile substance abusers

Lab 

Pulse oxim etry: o



If abnorm al, follow with arterial blood gases.

Electrolytes; BUN, creatinine, and glucose levels; and liver function tests: o

For halogenated and arom atic hydrocarbon exposure

o

Metabolic acidosis

o

Hypokalem ia

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

Carboxyhem oglobin levels for m ethylene chloride exposure: o

Methylene chloride m etabolized to carbon m onoxide in vivo

Imaging Chest radiograph: 

Abnorm alities visible 20 m inutes to 24 hours after exposure



Increased bronchovascular m arking and bibasilar and perihilar infiltrates (typical)



Lobar consolidation (uncom m on)



Pneum othorax, pneum om ediastinum , and pleural effusion (rare)



Pneum atoceles resolve over weeks.

Differential Diagnosis 

Caustic, pesticide, or toxic alcohol ingestions



Accidental versus intentional: o



Psychiatric evaluation for all intentional ingestions

Child neglect: o

Poor supervision or unsafe hom e environm ent

P.539

Treatment Pre Hospital 

Decontam inate clothes, skin, and hair of any hydrocarbon exposure



Do not induce em esis.

Pa ge 2 4 0



Ipecac contraindicated owing to increased risk of aspiration



Keep volatile-substance abusers calm and avoid interventions that cause anxiety or distress.



Managem ent of accidental hydrocarbon exposures at hom e controversial: o

Fewer than 1% require physician intervention.

o

For asym ptom atic or quickly asym ptom atic after ingestion with reliable observer available

o

Applies only when exact product and its com ponents are known and there is no indication for gastric decontam ination or possibility for delayed organ toxicity

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Intravenous access and fluid resuscitation if hypotensive or ongoing fluid losses



Oxygen



Cardiac m onitor



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status

ED Treatment 

Supportive care



Treat respiratory sym ptom s: o

Oxygen

o

Nebulized Î² 2 -agonist for bronchospasm (albuterol)

o

Endotracheal intubation and m echanical ventilation for respiratory failure

o

Steroids not indicated for bronchospasm

o

Avoid using epinephrine in volatile substance abusers as it m ay precipitate dysrhythm ias

Pa ge 2 4 0



Gastric evacuation not indicated for vast m ajority of hydrocarbon ingestions: o

Aspiration risk higher than risk of system ic absorption for aliphatic hydrocarbon m ixtures, which account for m ost ingestions

o

Contraindicated if spontaneous em esis has occurred

o

Sm all-bore nasogastric tube aspiration of stom ach contents m ay be indicated for som e hydrocarbon (CHAMP) ingestions that have system ic toxicity: 

CHAMP: cam phor, halogenated hydrocarbons, a rom atic hydrocarbons, m etals (e.g., lead, m ercury), pesticides



Only for very recent ingestions



Benefit of doing this procedure needs to be weighed heavily against risk of aspiration and subsequent pneum onitis.



Cuffed-tube endotracheal intubation for airway protection during lavage if no gag reflex or altered m ental status



Activated charcoal not indicated except for significant coingestants



Cathartics not indicated: o

Diarrhea com m on with hydrocarbon

Medication (Drugs) 

Dextrose: D 5 0 W 1 am pule of 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

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Follow-Up Disposition Admission Criteria 

Sym ptom atic patients



Patients with potential delayed organ toxicity (carbon tetrachloride or other toxic additives)

Discharge Criteria 

Observe for 6 hours, then discharge: o

Asym ptom atic patients with norm al chest radiograph and pulse oxim etry findings

o

Asym ptom atic patients with abnorm al chest radiograph and norm al oxygenation and respiratory rate m ay be discharged if reliable follow-up is ensured.

o

Sym ptom atic patients on presentation who quickly becom e asym ptom atic



Observe volatile-substance abusers until m ental status clears.

Issues for Referral Psychiatry consult as needed

References 1. Anas N, Nam asonthi V, Ginsburg C. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA. 1981;246:840â€“843. 2. Dice WH, Ward G, Kelly J, et al. Pulm onary toxicity following gastrointestinal ingestion of kerosene. Ann Em erg Med. 1982;11:138â€“142. 3. Esm ail A, Meyer L, Pottier A, et al. Deaths from volatile substance

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abuse in those under 18 years: results from a national epidem iological study. Arch Dis Child. 1993;69:356â€“360. 4. Klein BL, Sim on JE. Hydrocarbon poisonings. Pediatr Clin North Am . 1986;33:411. 5. Machado B, Cross K, Snodgrass WR. Accidental hydrocarbon ingestion cases telephoned to a regional poison center. Ann Em erg Med. 1988;17:804â€“807.

Codes ICD9-CM 987.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydro cele

Hydrocele

Sean O. Henderson

Basics Description 

Com m unicating hydrocele: o

Patent processus vaginalis

o

Scrotum fills and em pties with peritoneal fluid depending on body position



Noncom m unicating hydrocele is owing to production of serous fluid by a disease process

Etiology 

Im balance between production and resorption of fluid within space between tunica vaginalis and tunica albuginea



Disease processes causing adult noncom m unicating hydrocele include: o

Epididym itis

o

Hypoalbum inem ia

o

Tuberculosis

o

Traum a

o

Mum ps

o

Sperm atic vein ligation

o

In Third World, hydrocele is prim arily caused by infections such as Wuchereria bancrofti or Loa Loa.

Pa ge 2 4 1

o

Rarely m alignancy (first-degree testicular neoplasm or lym phom a)



Rare etiology is the abdom inoscrotal hydrocele that m ay cause hydroureter or unilateral lim b edem a owing to com pression: o

Ultrasound reveals single sac extending from scrotum into abdom inal cavity via the deep inguinal ring

Pediatric Considerations 

Congenital in 6% of newborn boys



Usually diagnosed in newborn nursery



Caused by patent processus vaginalis, a structure that rem ains patent in 85% of newborns



May vary in size owing to position or crying: o

Patients m ay present with history of scrotal m ass that has resolved.



Most close by age of 2 years

Diagnosis Essential Workup 

History and exam ination with special attention to identifying torsion of testicle



Initial diagnostic test is transillum ination of affected side: o

This is rapidly being replaced as diagnostic test of choice by bedside ultrasound.

o

Bedside ultrasound: 

Allows visualization of hydrocele as well as of testicle



Especially in cases of m assive fluid collection, bedside ultrasound should be diagnostic test of

Pa ge 2 4 1

choice. 

Because of possibility in adults that a hydrocele m ay be owing to a prim ary neoplasm , the testicle m ust be palpated in its entirety.

Tests Lab No specific laboratory testing is indicated unless underlying cause dem ands it.

Imaging Ultrasound is diagnostic and allows visualization of testicular anatom y: 

Appears as large fluid-filled space surrounding the testicle

Differential Diagnosis 

Testicular neoplasm



Testicular torsion



Epididym itis



Orchitis



Indirect inguinal hernia

Treatment Initial Stabilization Stabilization should focus on underlying cause (e.g., trauma).

ED Treatment Appropriate exam ination of testicle to exclude prim ary neoplasm and referral P.541

Pa ge 2 4 1

Medication (Drugs) Treat underlying cause.

Pediatric Considerations See Disposition below.

Follow-Up Disposition Admission Criteria Patients with secondary hydrocele m ay need adm ission for further evaluation of underlying pathology (e.g., neoplasm , traum a).

Discharge Criteria 

Otherwise healthy patients without co-m orbid illness m ay be referred for further evaluation to urologist.



Hydrocele is usually repaired if cosm esis is a factor or in cases where it causes discom fort.



Repair can be: o

Surgical: 

Aspiration or sclerotherapy are alternatives to open hydrocelectom y.

o

Medical: 

Aspiration of hydrocele contents and sclerotherapy to prevent recurrence

Pediatric Considerations 

Most hydroceles in infant population will spontaneously resolve by 12 m onths of age:

Pa ge 2 4 1

o

Referral and observation are appropriate once diagnosis is m ade.



After age of 12â€“18 m onths, refer for surgical repair as com m unicating hydroceles usually have hernia that needs repair.

References 1. Akin EA, Khati NJ, Hill MC. Ultrasound of the scrotum . Ultrasound Q. 2004;20:181â€“200. 2. Beiko DT, Kim D, Morales A. Aspiration and sclerotherapy versus hydrocelectom y for treatm ent of hydroceles. Urology. 2003;61:708â€“712. 3. Kaplan GW. Scrotal swelling in children. Pediatr Rev. 2000;21:311â€“314. 4. Lau MW, Taylor PM, Payne SR. The indications for scrotal ultrasound. Br J Radiol. 1999;72:833â€“837. 5. Rabinowitz R, Hulbert WC. Acute scrotal swelling. Urol Clin North Am . 1995;22:101â€“105. 6. Rubenstein RA, Dogra VS, Seftel AD, et al. Benign intrascrotal lesions. J Urol. 2004;171:1765â€“1772.

Codes ICD9-CM 603.9

ICD10 N43.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydro cephalus

Hydrocephalus

Richard S. Krause

Basics Description 

Increased fluid in cranium



Obstructive hydrocephalus is m ost com m on form : o

Obstruction is within ventricular system or in subarachnoid space.



Acute obstructive hydrocephalus m ay cause rapid rise in intracranial pressure (ICP), rapidly leading to death or perm anent cerebral dam age.



Nonobstructive hydrocephalus causes subacute sym ptom s and is a potentially treatable form of dem entia.

Etiology 

Obstructive hydrocephalus: o

Obstruction of: 

Foram en of Monro



Third ventricle, fourth ventricle



Aqueduct of Sylvius



Foram ina of Luschka and Magendie (tum or or other m asses)



Subarachnoid space around brainstem (postinfectious or postsubarachnoid hem orrhage

Pa ge 2 4 1

[post-SAH]) o

Acute presentations usually secondary to cerebrospinal fluid (CSF) shunt blockage, SAH, or severe head traum a



Nonobstructive hydrocephalus: o

Norm al pressure hydrocephalus: 

Increased intracranial volum e without intracranial hypertension

o 

Increased ventricular size on CT

Pediatric hydrocephalus: o

Congenital hydrocephalus owing to neonatal hem orrhages, congenital m alform ations, or acquired postm eningitis secondary to subarachnoid scarring around brainstem

Diagnosis Signs and Symptoms Obstructive (Noncommunicating) Hydrocephalus 

Headache



Nausea and vom iting



Decreased level of consciousness



Urinary incontinence



Ocular palsies



Papilledem a, decreased vision



Pupillary dilation



Cushing response: o



Raised systolic pressure and bradycardia

Pediatric patients:

Pa ge 2 4 1

o 

Full fontanelle, irritability, and lethargy

May present like nonobstructive hydrocephalus if obstruction develops slowly

Nonobstructing (Communicating) Hydrocephalus 

Progressive dem entia, som nolence



Gait disturbance



Urinary incontinence



Im paired upward gaze



Generalized weakness and lethargy



Dem entia is often insidious with subacute onset of progressive intellectual deterioration.



No headache or papilledem a



Pediatric patients increase CSF volum e slowly: o

Craniom egaly

o

Retardation

o

Prom inent scalp veins

o

Im paired upward gaze (setting sun sign)

Essential Workup CT scan of the head will allow assessm ent of ventricular size and sym m etry: 

Aid in diagnosis of cerebral edem a, m ass lesions, and hem orrhage

Tests Lab Lum bar puncture (LP) is typically perform ed after head CT (for nonobstructive causes): 

Opening pressure on LP will reflect increased ICP in nonobstructive hydrocephalus.



CSF should be sent for routine tests if infection is

Pa ge 2 4 1

suspected. o

Gram stain, culture, protein, and glucose

Imaging MRI of brain reveals ventricular size and sym m etry and m ay allow for better visualization of m asses than CT.

Differential Diagnosis 

Acute cerebral infarction or hem orrhage



Intracranial infection



Mass effect from fast-growing tum or or hem atom a



Dem entia or delirium of other cause



Toxic or m etabolic encephalopathies

Pediatric Considerations 

Suspect hydrocephalus in infant whose head circum ference is increasing excessively.







Congenital anom alies: o

Constitutional m acrocrania

o

Megalencephaly

o

Dandy-Walker m alform ation

o

Arnold-Chiari m alform ation

o

Meningom yelocele

o

Choroid plexus papillom a

o

Hypoplasia/dysfunction of arachnoid villi

Infections: o

Rubella

o

Cytom egalovirus (CMV)

o

Toxoplasm osis

o

Syphilis

o

Bacterial m eningitis

o

Reye syndrom e

Tum ors, especially posterior fossa tum ors: o

Medulloblastom a, astrocytom a, ependym om a

Pa ge 2 4 1



Hem orrhage: o

Intraventricular bleed and fibrosis, subarachnoid bleed

P.543

Treatment Pre Hospital Cautions: 

Elevated ICP cannot be definitively diagnosed in the field.



When it is suspected, supplem ental O 2 and aggressive airway m anagem ent are indicated.



If not contraindicated, patients should be transported with head elevated at 30Â°.

Initial Stabilization 

Signs of im pending herniation: o

Rapid-sequence intubation (RSI) 

Thiopental or etom idate for induction



Paralytic choice is controversial.



Depolarizing agents (succinylcholine) m ay increase ICP, although this effect m ay not be clinically significant.



Nondepolarizing agents (rocuronium , vecuronium ) m ay be preferable.

o

Controlled ventilation to m aintain PaCO 2 at approxim ately 35 m m Hg

o

Maintain systolic blood pressure (BP) >100 m m Hg (adult) with fluids or pressors.

Pa ge 2 4 1

o 

Mannitol

If a CSF shunt is present and there are signs of im pending herniation: o

Forced pum ping of shunt cham ber: 

Flush device with 1 m L saline to rem ove distal obstruction.



Slow drainage of CSF from reservoir to achieve pressure <20 cm H 2 O.



IV m annitol to lower ICP

ED Treatment 

When signs of im pending herniation or acute shunt m alfunction are absent, hydrocephalus does not require ED treatm ent.



Definitive treatm ent involves either placem ent (or revision) of shunting device or treatm ent of underlying cause (e.g., tum or).



Increased ICP refractory to other treatm ents m ay respond to controlled lum bar drainage.



Neurologic sym ptom s (gait disturbance) or severe headache associated with norm al pressure hydrocephalus m ay respond to rem oval of 25â€“30 m L of CSF.

Medication (Drugs) 

Atropine: 0.02 m g/kg IV (m ax. 0.1 m g)



Etom idate: 0.2â€“0.3 m g/kg



Lidocaine: 1 m g/kg IV



Mannitol: 0.5â€“1 m g/kg



Rocuronium : 0.6 m g/kg IV



Succinylcholine: 1â€“1.5 m g/kg IV



Vecuronium : 0.1 m g/kg

Pa ge 2 4 2

Follow-Up Disposition Admission Criteria Evidence of increased ICP or shunt m alfunction requires adm ission.

Discharge Criteria Patients with presum ed norm al pressure hydrocephalus m ay be discharged for follow-up.

References 1. Black P. Hydrocephalus in adults. In: Youm ans JR, ed. Neurological Surgery. Philadelphia: WB Saunders; 1996:927â€“944. 2. Bret P, Guyotat J, Chazal J. Is norm al pressure hydrocephalus a valid concept in 2002? A reappraisal in five questions and proposal for a new designation of the syndrom e as â€œchronic hydrocephalusâ€•. J Neurol Neurosurg Psych. 2002;73(1):9â€“12. 3. Hebb A, Cusim ano M. Idiopathic norm al pressure hydrocephalus: a system atic review of diagnosis and outcom e. Neurosurgery. 2001;49:1166â€“1186. 4. Ledin T, Bynke O, Odkvist LM. Influence of cerebrospinal fluid tapping on dynam ic equilibrium in suspected hydrocephalus. Acta Otolaryngol. 1995;52(pt 2 suppl):317â€“319. 5. Mayer S, Chong J. Critical care m anagem ent of increased intracranial pressure. J Intensive Care Med. 2002;17(2):55â€“67. 6. Sainte-Rose C, Hydrocephalus in childhood. In: Youm ans JR, ed. Neurological Surgery. Philadelphia: WB Saunders; 1996:890â€“926.

Codes ICD9-CM 331.4

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ICD10 G91.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperbaric Oxygen Therapy

Hyperbaric

Oxygen Therapy Trevonne M. Thompson

Basics Description 

Adm inistration of 100% oxygen at greater than 1 atm ospheric pressure (typically 2â€“3 atm s)



Mechanism s of action: o

Increases oxygen availability at the cellular level: 

Breathing 100% oxygen at 3 atm s supplies enough dissolved oxygen to support life without hem oglobin.

o

Com presses form ed gas bubbles (in cases of air em bolism or decom pression sickness)



Two types of hyperbaric oxygen cham bers: o

o

Monoplace: 

Accom m odates one supine patient



Technician outside the cham ber for m onitoring



Com pressed with 100% oxygen

Multiplace: 

Holds m ultiple patients



Holds attendants who â€œdiveâ€• with the

Pa ge 2 4 2

patients 

Airlocks available for m edication/equipm ent transfer outside of the cham ber



Com pressed with airâ€”patients breath oxygen by face m ask, endotracheal tube, or face hood.

Diagnosis Signs and Symptoms Indications for hyperbaric oxygen therapy: 

Arterial gas em bolism



Decom pression sickness



Carbon m onoxide toxicity



Soft tissue infections:



o

Clostridial m yonecrosis

o

Necrotizing fasciitis

o

Refractory osteom yelitis

o

Chronic nonhealing wounds

Wound care: o

Radiation-induced tissue injury

o

Crush injuries

o

Therm al burns

o

Com prom ised skin grafts and flaps

Alert The em ergency physician should focus on arterial em bolism , decom pression sickness, and carbon m onoxide toxicity as uses for hyperbaric oxygen.

Essential Workup 

Determ ine need for hyperbaric oxygen therapy as described above.

Pa ge 2 4 2



Perform a com prehensive physical exam ination to screen for contraindications to therapy and to establish a pretreatm ent baseline exam ination.



Contraindications to therapy: o

Untreated pneum othorax is the absolute contraindication: 

o

May convert to a tension pneum othorax

Cardiovascular instability: 

Unstable patient cannot be treated in a m onoplace cham ber.



May be treated in m ultiplace cham ber when benefit outweighs risk

Tests Lab Arterial blood gas: 

To evaluate for hypoxia in appropriate cases

Imaging Chest radiography: 

To evaluate for occult pneum othorax

P.545

Treatment Initial Stabilization 

Evaluate and m anage airway, breathing, and circulation (ABCs).



Establish IV access.

Pa ge 2 4 2



One hundred percent oxygen



Cardiac m onitor (when appropriate)

ED Treatment 

Determ ine need for hyperbaric oxygen therapy.



Fill any devices with balloons (Foley catheters, endotracheal tubes) with fluid to avoid rupture during therapy.



Pretreat patients with any sinus com plaints with decongestants.



Place m yringotom y tubes in obtunded or m echanically ventilated patients or in patients with m iddle ear pathology (e.g., otitis m edia).

Alert 

Com plications of hyperbaric oxygen therapy: o

Sinus/ear pain

o

Barotraum a:

o



Ruptured tym panic m em branes



Tension pneum othorax

Seizures: 

o

Decom pression sickness: 

o

May be a result of oxygen toxicity

When decom pression is too rapid

Inability to access an unstable patient: 

When using a m onoplace cham ber

Medication (Drugs) Pseudoephedrine: 60 m g (peds: 2â€“5 years old, 15 m g; 6â€“12 years old, 30 m g) PO every q4hâ€“q6h

Pa ge 2 4 2

Follow-Up Disposition Admission Criteria 

Arterial gas em bolism



Decom pression sickness



Significant carbon m onoxide toxicity

Issues for Referral 

May need to transfer to a facility that has a hyperbaric oxygen cham ber



Evaluate risks and benefits when considering the transfer of a potentially unstable patient.



Divers Alert Network: o

Stationed at Duke University Medical Center, North Carolina

o

24-hour em ergency hotline for consultation of dive-related injuries

o

Referral source for hyperbaric oxygen cham bers

o

Telephone num bers:

o



(919) 684-8111



(800) 446-2671

Website: 

http://www.diversalertnetwork.org

References 1. Sheridan RL, Shank ES. Hyperbaric oxygen treatm ent: a brief overview of a controversial topic. J Traum a. 1999;47(2):426â€“435. 2. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. N Engl J Med. 1996;334(20):1642â€“1648.

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Miscellaneous SEE ALSO: Carbon Monoxide Toxicity; Decom pression Sickness

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypercalcem ia

Hypercalcemia

Jeffrey King

Basics Description 

Severity depends on level of serum calcium and rate of its rise



0.1â€“1% of patients on routine screening



Most cases m ild (<12 m g/dL) and asym ptom atic



Hypercalcem ic crisis, usually >14 m g/dL, associated with serious signs and sym ptom s





Calcium in bloodstream in three form s: o

Ionized: 45%

o

Bound to protein (prim arily album in): 40%

o

Bound to other anions: 15%

Ionized calcium â€”only physiologically active form

Etiology 

Prim ary hyperparathyroidism



Malignancy



Miscellaneous

Diagnosis

Pa ge 2 4 2

Signs and Symptoms History 



Neurologic: o

Headache

o

Fatigue

o

Weakness

o

Difficulty concentrating

o

Confusion

Renal: o

Polyuria, polydipsia

o

Com plaints related to oliguric renal failure

o

Chronically: com plaints related to renal calculi, nephrocalcinosis, interstitial nephritis



Gastrointestinal: o

Anorexia

o

Nausea

o

Vom iting

o

Abdom inal pain

o

Constipation

o

Com plaints related to intestinal ileus

o

Chronically: com plaints related to increased risk of peptic ulcer disease and pancreatitis



Derm atologic: o

Pruritus

Pediatric Considerations 

Failure to thrive



Slow developm ent



Mental retardation m ay ensue

Physical Exam 

Neurologic:

Pa ge 2 4 3



o

Irritability

o

Lethargy

o

Stupor

o

Com a

o

Hyporeflexia

Cardiovascular: o

Hypotension, if severely volum e depleted, or hypertension

o

Sinus bradycardia, cardiac arrest with severe hypercalcem ia (rare)



Renal: o



Signs of dehydration

Derm atologic: o

Band keratopathy

o

Ectopic calcification

Pediatric Considerations 

Characteristic facies: pug nose, fat nasal bridge, â€œcupid's bowâ€• upper lip



Hypotonia

Essential Workup 

Ionized and total serum calcium levels, album in levels: o

Norm al total calcium level is <10.5 m g/dL

o

Must correct for calcium that is protein bound, prim arily to album in

o

Corrected total calcium (m g/dL) = m easured total calcium (m g/dL) + 0.8 Ã— [4.0 â€“ album in concentration (g/dL)]



Electrolytes, BUN/creatinine, glucose o



Possible oliguric renal failure

ECG: o

Shortening of QT interval

Pa ge 2 4 3

o

Prolongation of PR interval

o

QRS widening

o

Accentuated side effects of digoxin

o

Sinus bradycardia, bundle branch block, AV block, cardiac arrest with severe hypercalcem ia (rare)

o

Can cause Osborn J wave at end of QRS com plex that is usually associated with hypotherm ia

Tests Lab 

Phosphate



Protein



Urinalysis



Parathyroid horm one level



Vitam in D level, if suspected



Digoxin level, if taking



Thyroid function tests

Imaging 

CT head, if altered m ental status



Workup for occult m alignancy, if no other cause

Diagnostic Procedures/Surgery Parathyroidectom y: 

For prim ary hyperparathyroidism resulting in sym ptom atic or severe hypercalcem ia



Som e patients require urgent parathyroidectom y.

Differential Diagnosis 

Prim ary hyperparathyroidism : o

Most com m on cause in outpatients

o

Most com m on cause of prim ary hypothyroidism is parathyroid adenom a.

o

Usually m ild, <11.2 m g/dL

Pa ge 2 4 3

o

Increased bone resorption, relative decrease in calcium excretion, increased intestinal calcium absorption



Malignancy: o

Most com m on cause in hospitalized patients

o

Most com m on paraneoplastic com plication of cancer

o

Most com m only from production of parathyroid horm one-related protein with sim ilar actions

o

May result from production of other bone-resorbing substances by tum or

o

May result from local effects of osteolytic skeletal m etastasis



Miscellaneous: o

Hypercalcem ia associated with granulom atous diseases

o

Excessive calcium supplem ents

o

Thiazide diuretics increase renal reabsorption.

o

Granulom atous disorders m ay lead to activation of vitam in D.

o

Acute vitam in A intoxication

o

Increased exogenous vitam in D intake

o

Milk-alkali syndrom e from excessive ingestion of calcium and nonabsorbable antacids such as m ilk or calcium carbonate

o

Long-term lithium therapy

o

Renal transplantation

o

Hyperthyroidism

o

Acute tubular necrosis

P.547

Pediatric Considerations

Pa ge 2 4 3



Differential diagnosis: differences from adults o

Prim ary hyperparathyroidism : 

o

Less com m on than in adults

Infantile hypercalcem ia: 

Uncertain cause



Possibly hypersensitivity and in utero excessive exposure to vitam in D

o

Im m obilization hypercalcem ia: 

Typically adolescent who is growing rapidly



Prolonged im m obilization, especially in traction, leads to hypercalciuria and then hypercalcem ia.



Presum ably from increased bone resorption with decreased or arrested bone m ineralization

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs), intravenous access, oxygen, cardiac m onitor



0.9% norm al saline (NS) 1 L bolus (20 m L/kg) for hypotension or severe dehydration



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) for altered m ental status

ED Treatment 

General: o

Im m ediate therapy for severe hypercalcem ia (corrected total >14 m g/dL) regardless of sym ptom s, and for sym ptom atic hypercalcem ia

o

Asym ptom atic, m ild hypercalcem ia does not require em ergency treatm ent.

Pa ge 2 4 3



Fluid adm inistration: o

Isotonic saline for restoration of intravascular volum e

o

Often need 2â€“5 L/d

o

Bedside vigilance necessary to prevent fluid overload

o

Correct other electrolyte abnorm alities.

o

Cardiovascular status of patient m ay necessitate central venous pressure m onitoring to adjust fluid adm inistration rates.



Renal elim ination: o

After volum e expansion and if needed to avoid overload, adm inister loop diuretics like furosem ide.

o

Avoid thiazide diuretics.

o

May need peritoneal or hem odialysis against a low calcium dialysate in renal failure



Inhibition of osteoclastic activity: o

Reduce m obilization of calcium from bone

o

Adm inister drug therapy when corrected calcium level >14 m g/dL or signs or sym ptom s

o

First-line drug therapy: 

Bisphosphonates: pam idronate (m ore potent and possibly less toxic), etidronate



Calcitonin: rapid onset but m odest decrease in levels

o

Other potential drug therapy: 

Plicam ycin: efficacious but num erous side effects



Hydrocortisone: especially useful with m alignancies, granulom atous disorders, or vitam in D intoxication

o 

Encourage am bulation in appropriate patients.

Underlying disorder: o

Prepare to treat underlying cause.

Pa ge 2 4 3

o

Parathyroidectom y for prim ary hyperparathyroidism resulting in sym ptom atic or severe hypercalcem ia

o

Treat tum or for m alignancy.

o

Discontinue m edication if cause.

Medication (Drugs) 

Calcitonin: 4 IU/kg IM/SC q12h



Etidronate: 7.5 m g/kg over 4 hours daily for 3â€“7 days IV



Furosem ide: 10â€“40 m g q6hâ€“q8h (peds: 1â€“2 m g/kg) IV



Gallium nitrate: continuous infusion of 200 m g/m 2 /d for 5 days IV



Hydrocortisone: 200â€“400 m g/d IV for 3â€“5 days (peds: consult pediatrician)



Pam idronate: single 24-hr infusion of 60â€“90 m g IV (peds: consult pediatrician)



Plicam ycin: 25 Âµg/kg/d over 4â€“6 hours IV for 3â€“8 doses

Follow-Up Disposition Admission Criteria 

Corrected total calcium level >13.0 m g/dL



Signs or sym ptom s attributed to hypercalcem ia



Monitored bed or ICU for corrected level >14 or serious signs and sym ptom s

Discharge Criteria Corrected calcium level <13.0 m g/dL and no signs or sym ptom s of

Pa ge 2 4 3

hypercalcem ia

Issues for Referral 

Rapid follow-up arranged to determ ine cause and long-term therapy



Consultation with endocrinologist should be considered.

References 1. Ariyan EA, Sosa JA. Assessm ent and m anagem ent of patients with abnorm al calcium . Crit Care Med. 2004;32(4 suppl.):S146â€“S154. 2. Carroll ME, Schaide DS. A practical approach to hypercalcem ia. Am Fam Physician. 2003;67(9):1959â€“1966. 3. Inzucchi SE. Managem ent of hypercalcem ia. Postgrad Med. 2004;115(5):27â€“36

Codes ICD9-CM 275.4

Pa ge 2 4 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperem esis G ravidarum

Hyperemesis

Gravidarum David Della-Giustina John Pease

Basics Description Hyperem esis gravidarum , also known as pernicious vom iting of pregnancy, is the m ost severe form along continuum of nausea and vom iting of pregnancy.

Etiology Exact cause unknown; however, possible causes include the following: 

Elevated gestational associated horm one levels



Thyrotoxicosis



Upper GI m otility dysfunction



Hepatic abnorm alities



Autonom ic nervous system dysfunction



Psychologic factors



Helicobacter pylori infection

Pa ge 2 4 3

Diagnosis Signs and Symptoms 

Nausea and vom iting during pregnancy affects between 50% and 90%.



Onset of sym ptom s by the 4thâ€“10th week of pregnancy with resolution by the 20th: o

Sym ptom s after the 20th week should raise one's suspicion of another process.



Hyperem esis gravidarum is a clinical diagnosis.



Hyperem esis is defined by the following: o

Persistent, severe nausea and vom iting

o

Dehydration

o

Weight loss of >5% of total body weight

o

Laboratory findings: increased urine specific gravity, ketonuria, electrolyte disturbances, ketonem ia

Essential Workup 

History and physical exam ination with special attention to state of hydration and abdom inal exam for other diagnoses associated with vom iting (appendicitis, cholecystitis, etc.)



The only m andated test is an uncontam inated urinalysis.



If patient has unrem itting vom iting for >24 hours, obtain a CBC, electrolytes, renal function, liver enzym es, bilirubin, and lipase.

Tests Lab 

Urinalysis: o

Increased specific gravity and ketonuria

o

Presence of glucose m andates checking serum glucose to rule out diabetes.

Pa ge 2 4 3

o

Presence of bilirubin m andates a search to rule out hepatobiliary cause for the vom iting.



CBC: o

May have an elevated hem atocrit owing to dehydration

o 

White blood cell count is usually norm al.

Electrolytes: o

Elevated blood urea nitrogen indicating volum e depletion

o

Hyponatrem ia, hypokalem ia, hypochlorem ia, and m etabolic alkalosis from loss of HCl in em esis



Liver function tests: o

Mild increases in bilirubin m ay occur, but should be <4 m g/dL.

o

AST and ALT m ay also be m ildly elevated, but not >100 IU/L



Am ylase/lipase: o

In one study, am ylase was elevated in 24% of patients with hyperem esis gravidarum ; however, the am ylase was not pancreatic in origin; thus, use lipase rather than am ylase to evaluate for pancreatitis.

Differential Diagnosis 

Pyelonephritis; m ost com m only m issed



Gastroenteritis



Hepatobiliary disease; hepatitis, cholecystitis, fatty liver of pregnancy



Pancreatitis



Appendicitis



Diabetic ketoacidosis



Hyperthyroidism



Urem ia; persistent nausea and vom iting are seen with severe renal dysfunction.

Pa ge 2 4 4

Treatment Initial Stabilization IV hydration using a crystalloid with dextrose (D 5 LR or D 5 NS)

ED Treatment 

IV hydration using up to 3 L of D 5 LR or D 5 NS



Dextrose is added to help break cycle of ketosis.



Treat until patient is no longer sym ptom atic from hypovolem ia.



Antiem etics adm inistered IV are given to break vom iting cycle. P.549



Most com m only used m edications: o

Phenothiazines (prom ethazine and prochlorperazine): 

Both Food and Drug Adm inistration (FDA) category C, m eaning have not been adequately studied

o

Metoclopram ide: 

o

Selective 5-HT3 receptor antagonist (ondansetron): 

o

FDA category B

FDA category B

These m edications have been used extensively in pregnancy, and there is little or no evidence that these antiem etics are associated with an increased risk of congenital anom alies.

o

Parenteral antiem etics are preferable to the risk of prolonged ketosis and the associated hypovolem ia.

Pa ge 2 4 4



Oral rehydration in the ED after the initial fluid resuscitation and antiem etics are given



Thiam ine 100 m g IV or IM in the patient who has a protracted course of sym ptom s: o

There are case reports of patients developing Wernicke encephalopathy owing to hyperem esis gravidarum .



Methylprednisolone m ay be effective for patients with hyperem esis gravidarum : o

Two studies dem onstrated relief in sym ptom s and decreased need for adm ission for hyperem esis.

Medication (Drugs) 

Methylprednisolone (category C): 48 m g IV or PO



Metoclopram ide (category B): 10â€“20 m g IV



Ondansetron (category B): 8 m g IV



Prochlorperazine (category C): 5â€“10 m g IV not to exceed 40 m g/d



Prom ethazine (category C): 12.5â€“25 m g IV



Discharge m edications: o

Use first-line m edications and elevate to the second-line agents for repeated visits.

o

Meclizine (category B): 25 m g PO q6h PRN, first line

o

Metoclopram ide (category B): 10 m g PO q6hâ€“q8h PRN, second line

o

Prochlorperazine (category C): 5â€“10 m g PO q6h or 25 m g PR q12h PRN, second line

o

Prom ethazine (category C): 12.5â€“25 m g PO or PR q4hâ€“q6h PRN, second line

o

Pyridoxine (vitam in B 6 ; category A): 25 m g PO t.i.d., first line (over-the-counter)

Pa ge 2 4 4

Follow-Up Disposition Admission Criteria 

Inability to tolerate oral intake after treatm ent



Inability to control the em esis despite treatm ent



Severe electrolyte or m etabolic disturbances

Discharge Criteria 

Most patients can be discharged as long as they are able to tolerate oral intake and have adequate follow-up.



Correction of dehydration and associated sym ptom s



Decreased ketonuria



Patients should be reassured that their sym ptom s are com m on and alm ost always self-lim ited.



Patients should be counseled to eat frequent, sm all m eals: o

Meals should contain sim ple carbohydrates and be low in fats.

o 

Avoid irritant or spicy foods.

Hom e IV therapy can be arranged if indicated.

References 1. Broussard C, Richter J. Nausea and vom iting of pregnancy. Gastroenterol Clin North Am . 1998;27:123â€“151. 2. Einarson A, Maltepe C, et al. The safety of ondansetron for nausea and vom iting of pregnancy: a prospective com parative study. Br J Obstet Gynaecol. 2004;111(9):940â€“943. 3. Eliakim R, Abulafia O, Sherer D. Hyperem esis gravidarum : a current review. Am J Perinatol. 2000;17(4):207â€“218. 4. Goodwin T. Hyperem esis gravidarum . Clin Obstet Gynecol.

Pa ge 2 4 4

1998;41(3):597â€“605. 5. Safari H, Alsulym an O, Gherm an R, et al. Experience with oral m ethylprednisolone in the treatm ent of refractory hyperem esis gravidarum . Am J Obstet Gynecol. 1998;178(5):1054â€“1058.

Codes ICD9-CM 643.00

ICD10 O21

Pa ge 2 4 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperkalem ia

Hyperkalemia

Christopher B. Colwell

Basics Description 





Potassium distribution: o

Extracellular space: 2%

o

Intracellular space: 98%

Potassium excretion: o

Renal: 90%

o

GI: 10%

Renal and extrarenal m echanism s m aintain norm al plasm a concentration between 3.5 and 5.0 m m ol/L.





Renal excretion of potassium affected by: o

Dietary intake

o

Distal renal tubular function

o

Acid-base balance

o

Mineralocorticoids

Regulation between intracellular and extracellular potassium balance affected by: o

Acid-base balance

o

Insulin

o

Mineralocorticoids

o

Catecholam ines

Pa ge 2 4 4

o

Osm olarity

o

Drugs

Etiology Decreased Potassium Excretion 

Most com m on cause: renal failure (acute or chronic)



Distal tubular diseases:





o

Acute interstitial nephritis

o

Renal transplant rejection

o

Sickle cell nephropathy

o

Renal tubular acidosis (diabetes)

Mineralocorticoid deficiency: o

Addison disease

o

Hypoaldosteronism

Drugs: o

Angiotensin-converting enzym e (ACE) inhibitors/angiotensin receptor blockers

o

Beta-blockers

o

Potassium -sparing diuretics

o

Nonsteroidal anti-inflam m atory drugs (NSAIDs)

o

Cyclosporine

o

High-dose trim ethoprim

o

Lithium toxicity

Intracellular to Extracellular Potassium Shifts 

Metabolic acidosis: o

Serum K + rises 0.2â€“1.7 m m ol/L for each 0.1 unit fall in arterial pH.



Hyperosm olar states



Insulin deficiency



Cell necrosis



Rhabdom yolysis



Hem olysis

Pa ge 2 4 4



Chem otherapy



Drugs:



o

Digitalis toxicity

o

Depolarizing m uscle relaxants (e.g., succinylcholine)

o

Beta-blockers

o

Î±-Agonists

Hyperkalem ic periodic paralysis

Excess Exogenous Potassium Load 

Cellular breakdown: o

Traum a

o

Tum or lysis



Salt substitutes



Oral potassium



Potassium penicillin G



Rapid transfusions of banked blood

Pseudohyperkalemia 

Traum atic venipuncture with hem olysis



Postvenipuncture release of potassium can occur in setting of:



o

Throm bocytosis (platelets >800,000/m m 3 )

o

Extrem e leukocytosis (WBC >100,000/m m 3 )

Prolonged tourniquet tim e

Diagnosis Signs and Symptoms History 

Neurom uscular sym ptom s, predom inantly weakness, which can progress to paralysis



Dyspnea owing to respiratory m uscle weakness

Pa ge 2 4 4



Cardiac dysrhythm ias can be initial m anifestation, so patients could also present with chest pain, palpitations, or syncope.

Physical Exam 

Muscular weakness (rare except in severe cases)



Cardiac dysrhythm ias (see ECG Changes)

Essential Workup 

Serum potassium >5.0 m m ol/L



Collect in heparinized tube if pseudohyperkalem ia suspected.

Tests Lab 

Electrolytes, BUN, creatinine, glucose: o

Elevated BUN, creatinine in renal failure

o

Hyponatrem ia with m ineralocorticoid deficiency

o

Mild m etabolic acidosis with type IV renal tubular acidosis



Arterial blood gases: o

Assess acid-base status



Creatinine kinase



Ca 2 +



For hyperkalem ia in face of norm al renal function, calculate transtubular potassium gradient (TTKG): o

TTKG = urine K Ã— Posm /Plasm a K Ã— Uosm

o

Posm , plasm a osm olality; Uosm , urine osm olality

o

TTKG >8 suggests extrarenal cause; TTKG <6 indicates renal excretory defect.

Imaging 

ECG: Changes correlate with degree of hyperkalem ia: o

Greater than 5.0â€“6.5: peaking of T waves;

Pa ge 2 4 4

shortening of QT c interval o

Greater than 6.5â€“8.0: PR prolongation; loss of P waves; widening of QRS com plexes

o

Greater than 8.0: intraventricular blocks; bundle branch blocks; QRS axis shifts; sine wave com plex



Serum potassium cannot be reliably predicted by ECG: o

Som e patients (particularly those with chronic renal failure) will tolerate higher potassium levels than others.

o

Potassium effects (as seen on ECG) m ore im portant than potassium level

Differential Diagnosis Pseudohyperkalem ia

Alert Most com m on cause of hyperkalem ia reported by lab is pseudohyperkalem ia owing to hem olysis.

Treatment Pre Hospital 

Treatm ent of hyperkalem ic-induced dysrhythm ias/cardiac arrest involves different drugs from usual advanced cardiac life support (ACLS) m easures (see Treatm ent, below): o

Inhaled albuterol can lower potassium tem porarily by 1 m m ol/L.

o 

Sodium bicarbonate can be effective.

Diagnosis suggested by prehospital rhythm strip or in at-risk populations (renal failure)

P.551

Pa ge 2 4 4

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



IV access



Cardiac m onitor

ED Treatment Hyperkalemia with ECG Changes (Widened QRS Complexes): Antagonize Potassium-Mediated Cardiotoxicity 

Adm inister calcium gluconate (in awake patient) or calcium chloride (in patient without pulse): o

Onset 1â€“3 m inutes

o

30â€“60-m inute duration

o

No effect on total serum potassium levels

Severe (>7.0) or Moderate (6.0â€“7.0) with ECG Changes (Heightened T waves or loss of P wave): Shift Potassium Intracellularly 





Adm inister com bination of insulin and glucose: o

Onset 20â€“30 m inutes

o

2â€“4-hour duration

IV sodium bicarbonate: o

Much m ore effective in patient who is acidotic

o

Onset 20 m inutes

o

2-hour duration

o

Caution in patients at risk for volum e overload

o

Worsens concom itant hypocalcem ia

Inhaled albuterol: o

Onset within 30 m inutes

Pa ge 2 4 5

o

2â€“4-hour duration

Enhanced Excretion for K + >6.0 without ECG Changes Adm inister cation exchange resin: 

Calcium or sodium polystyrene sulfonate PO or per rectum (PR)



Avoid in patients with suspected ileus or bowel obstruction.

All Patients 

Lim it exogenous potassium and potassium -sparing drugs.



Treat underlying cause.

Special Situations 

Renal failure: o

Arrange for dialysis.

o

Hem odialysis im m ediately effective at rem oving potassium





Furosem ide: o

Effective in absence of oliguric renal failure

o

Causes potassium -losing diuresis

Cardiac arrest: o

Adm inister CaCl 2 and NaHCO 3 with known or suspected hyperkalem ia.



Digoxin toxicity: o

Avoid calcium : 

When necessary, adm inister sm all doses extrem ely slowly.

o 

Consider Digibind for K + >5.5 m m ol/L.

Mineralocorticoid deficiency: o

Hydrocortisone

Pa ge 2 4 5

Medication (Drugs) 

Albuterol: 10â€“20 m g (peds: 2.5 m g if <25 kg; 5.0 m g if â‰¥25 kg) nebulized over 10 m inutes



Calcium chloride 10%: 10-m L am p (peds: 0.2 m L/kg per dose) IV over 2â€“5 m inutes



Calcium gluconate 10%: 20-m L am p (peds: 0.6â€“1.0 m L/kg) IV over 2â€“5 m inutes



Furosem ide: 40â€“80 m g (peds: 1.0 m g/kg) IVâ€”m odify dose to achieve appropriate diuresis



Hydrocortisone: 100 m g (peds: 1â€“2 m g/kg) IV



Insulin and glucose: 10 IU (peds: 0.1 IU/kg) regular insulin plus 50 m L 50% (peds: 0.5â€“1 g/kg) dextrose IV



Sodium bicarbonate: One to three am ps (44 m Eq per am p) IV over 20â€“30 m inutes (peds: 1.0â€“2.0 m Eq/kg per dose)



Sodium polystyrene sulfonate (Kayexalate) or calcium polystyrene sulfonate (preferred with volum e overload): o

Oral: 15 g m ixed with water or 50 m L of sorbitol q2h to total of 5 doses

o

Rectal enem a: 50 g in 200 m L of sorbitol q4hâ€“q6h

o

Peds: 1.0 g/kg orally or rectally

Follow-Up Disposition Admission Criteria Adm it m ost cases: 

Process of potassium rem oval is relatively slow.



Most potassium is intracellular and therefore not m easured on serum electrolytes.

Pa ge 2 4 5



Significant changes in levels will take tim e.



Levels m ay continue to rise.

Discharge Criteria Mild hyperkalem ia (<6.0 m m ol/L) provided that: 

Response to treatm ent has been dem onstrated



Known correctable cause



Further rises in serum potassium not anticipated



Early follow-up possible

References 1. Halperin M, Kam el K. Potassium . Lancet. 1998;352:135â€“140. 2. Mahoney B, Sm ith W, Lo D, et al. Em ergency interventions for hyperkalem ia. Cochrane Database Syst Rev. 2005;18(2):CD003235. 3. Mattu A, Brady W, Robinson D. Electrocardiographic m anifestations of hyperkalem ia. Am J Em erg Med. 2000;18:721â€“728. 4. Rastegar A, Soleim ani M. Hypokalaem ia and hyperkalaem ia. Postgrad Med J. 2001;77:759â€“764. 5. RodrÃguez-Soriano J. Potassium hom eostasis and its disturbances in children. Pediatr Nephrol. 1995;9(3):364â€“374.

Miscellaneous SEE ALSO: Renal Failure; Dialysis Com plications

Codes ICD9-CM 276.7

ICD10 E87.5

Pa ge 2 4 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypernatrem ia

Hypernatremia

Linda Mueller

Basics Description Hypernatrem ia definition: sodium >145 m Eq/L: 

Mild hypernatrem ia: serum sodium 146â€“155 m Eq/L



Severe hypernatrem ia: serum sodium >155 m Eq/L

Etiology Divided into 3 categories

Hypovolemic Hypernatremia 

Most com m on



Loss or deficiency of water and sodium with water losses being greater than sodium losses



Exam ples: o

Diuretics

o

Glucosuria

o

Mannitol

o

Renal failure

o

High-protein feedings

o

Lactulose

o

Excess sweating

o

Respiratory loss

Pa ge 2 4 5

o

Defective thirst m echanism

o

Lack of access to water

o

Diarrhea/vom iting

Isovolemic Hypernatremia 

Water deficiency without sodium loss; free water loss



Exam ples: o

Fever

o

Hypothalam ic diabetes insipidus: 

Head traum a



Tum or



Infection (tuberculosis [TB], syphilis, m ycoses, toxoplasm osis, encephalitis)

o



Granulom atous disease (sarcoid, Wegner)



Cerebrovascular accident



Aneurysm

Nephrogenic diabetes insipidus: 

Congenital



Drugs (lithium , am photericin B, foscarnet, dem eclocycline)



Obstructive uropathy



Chronic tubulointerstitial disease (sickle cell nephropathy, m ultiple m yelom a, am yloidosis, sarcoidosis, system ic lupus erythem atosus, polycystic kidney)



Electrolyte disorders (hypercalcem ia, potassium depletion)

Hypervolemic Hypernatremia 

Gain of water and sodium , with sodium gain greater than water gain



Exam ples: o

Iatrogenicâ€”m ost com m on cause:

Pa ge 2 4 5



Sodium bicarbonate adm inistration



NaCl tablets



Hypertonic parenteral hyperalim ent



Hypertonic intravenous fluid (IVF)



Hypertonic dialysis

o

Cushing disease

o

Adrenal hyperplasia

o

Prim ary aldosteronism

Pediatric Considerations 

More prone to iatrogenic causes



More likely to die or to have perm anent neurologic sequela



Morbidity ranges from 25â€“50%.



May present with high-pitched cry, lethargy, irritability, m uscle weakness

Diagnosis Signs and Symptoms General 

Most sym ptom s attributed to underlying cause (dehydration)



More m arked with acute changes



Death likely to occur with sodium of â‰¥185 m Eq/L



May see the following sym ptom s, usually at levels â‰¥160 m Eq/L: o

Neurologic 

Headache



Trem ulousness



Irritability



Ataxia

Pa ge 2 4 5

o

o



Mental confusion



Delirium



Seizures



Com a



Hyperreflexia



Asterixis



Chorea

Musculoskeletal 

Spasticity



Muscle weakness

Other 

Anorexia



Tachypnea



Poor Skin turgor



Nausea/vom iting

Hypovolemic Hypernatremia 

Tachycardia



Orthostasis



Dry m ucous m em branes



Oliguria



Azotem ia

Hypervolemic Hypernatremia 

Pulm onary edem a



Peripheral edem a

Essential Workup Serum Na + level

Tests Lab 

Electrolytes, BUN/creatinine, glucose



CBC

Pa ge 2 4 5



Urinalysis: o

Specific gravity

o

Urine/serum osm olality

o

Urine Na +

Imaging 



Chest radiograph: o

For infection/aspiration

o

Pulm onary edem a with hypervolem ic hypernatrem ia

CT brain: o

For altered m ental status

o

Venous sinus throm bosis

o

Subarachnoid hem orrhages

o

Subdural hem atom a

Differential Diagnosis 

Diabetic ketoacidosis



Hyperosm olar com a



Prim ary CNS lesions

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) IV bolus for severe hypotension



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) for altered m ental status

P.553

ED Treatment

Pa ge 2 4 5

General 

Calculate water deficit: o

Water deficit = 0.6 (weight in kg) Ã— (actual Na + â€“ desired Na + )/(actual Na + )



Do not rapidly correct hypertonicity to norm al serum osm olality: o

Rapid correction m ay cause seizures.

o

Reduce serum sodium level by <0.5â€“0.7 m Eq/L/h.

Hypovolemic Hypernatremia 

Replace volum e contraction with 0.9% NS IV bolus.



Change to D 5 W or hypotonic saline once volum e replenished and hem odynam ically stable

Isovolemic Hypernatremia 

Calculate water deficit.



Correct water deficit with D 5 W or hypotonic saline: o

Replace half of deficit in first 24 hours, then rem ainder over 1â€“2 days.

Hypervolemic Hypernatremia 

Rem ove excess water with diuretics or dialysis.



When euvolem ic, replace water deficit with D 5 W.



Avoid hypotonic saline solutions because patient already has excess of total body sodium .

Diabetes Insipidus (DI) Hypernatremia 

Sodium restriction



Desm opressin:



o

Aqueous vasopressin (DDAVP)

o

Best therapeutic agent

Chlorpropam ide (Diabinese) enhances effect of vasopressin at renal tubule.



Carbam azepine causes release of vasopressin.

Pa ge 2 4 5



Hydrochlorothiazide enhances sodium excretion.



Discontinue DI-inducing drugs.

Medication (Drugs) 

Chlorpropam ide (Diabinese): 100â€“500 m g/d



Vasopressin (DDAVP): 1â€“2 Âµg IV/SC q12h or 5â€“20 Âµg intranasally

Follow-Up Disposition Admission Criteria 

Newly diagnosed sodium >150 m Eq/L for m onitoring and treatm ent



Adm it sodium >160 m Eq/L or sym ptom atic patients to ICU.

Discharge Criteria 

Sodium <150 m Eq/L in asym ptom atic patient



Sodium >150 m Eq/L in patients with history of chronically elevated sodium who are at their baseline and asym ptom atic

References 1. Adrogue HS, Madias NE. Hypernatrem ia. N Engl J Med. 2000;342:1493â€“1499. 2. Ellison D. Disorders of sodium and water. Am J Kidney Dis. 2004;46(2):356â€“361. 3. Fall P. Hyponatrem ia and hypernatrem ia. A system atic approach to causes and their correction. Postgrad Med. 2000;107(5):75â€“82.

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4. Fried LF, Palevsky PM. Hyponatrem ia and hypernatrem ia. Med Clin North Am . 1997;81(3):585â€“609. 5. Lin M, Lu S, Lim I. Disorders of water im balance. Em erg Med Clin North Am . 2005;23:749â€“770, ix.

Codes ICD9-CM 276.0

ICD10 E87.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypero sm o lar Syndro m e

Hyperosmolar

Syndrome Matthew Robinson

Basics Description 

Results from a relative insulin deficiency in the undiagnosed or untreated diabetic



Sustained hyperglycem ia creates an osm otic diuresis and dehydration: o

Extracellular space m aintained by the osm otic gradient at the expense of the intracellular space

o

Eventually profound intracellular dehydration occurs.



Total body deficits of H 2 O, Na + , Cl - , K + , PO 4 - , Ca 2 + and Mg 2 +



In contrast to diabetic ketoacidosis (DKA), significant ketoacidosis does not occur: o

Circulating insulin levels are higher.

o

The elevation of insulin counterregulatory horm ones is less m arked.

o

The hyperosm olar state itself inhibits lipolysis (the release of free fatty acids) and subsequent generation of ketoacids.

Geriatric Considerations

Pa ge 2 4 6



Most com m only seen in elderly type II diabetics who experience a stressful illness that precipitates worsening hyperglycem ia and reduced renal function



In the elderly, 30â€“40% of cases are associated with the initial presentation of diabetes.

Pediatric Considerations Hyperosm olar syndrom e (HHS) rare in pediatric patients

Etiology 



Hyperosm olar state precipitated by factors that: o

Im pair peripheral insulin action

o

Increase endogenous or exogenous glucose

o

Decrease patient's ability to replace fluid loss

Infection is m ost com m on precipitating factor in 32â€“60% of cases.



Other precipitating causes include: o

Inadequate diabetes therapy

o

Medication om ission

o

Diet indiscretion

o

Infections

o

Pneum onia

o

Urinary tract infection

o

Sepsis

o

Medications/drugs

o

Diuretics

o

Beta-blockers

o

Calcium channel blockers

o

Phenytoin

o

Cim etidine

o

Am phetam ines

o

Ethanol

o

Coexisting illness

Pa ge 2 4 6

o

Myocardial infarction

o

Stroke

o

Renal failure

o

Heat stroke

o

Pancreatitis

o

Intestinal obstruction

o

Endocrine disorders

o

Burns

o

Heat stroke

Diagnosis Signs and Symptoms History 

Progression of signs and sym ptom s occurs over days to weeks.



Polyuria/polydipsia/weight loss



Dizziness/weakness/fatigue



Blurred vision



Leg cram ps

Physical Exam 

Dehydration



Tachycardia



Sunken eyes



Hypotension



Orthostasis



Dry m ucous m em branes



Decreased skin turgor



Collapsed neck veins



Com a/lethargy/drowsiness

Pa ge 2 4 6



Urinary output m aintained until late



Seizures/focal neurologic deficits



Concurrent precipitating m edical illness

Essential Workup 

Diagnostic criteria: o

Serum glucose â‰¥600 m g/dL (usually >1,000 m g/dL)

o

Minim al ketosis

o

pH â‰¥7.30, HCO 3 â‰¥15 m Eq/L

o

Effective serum osm olality >320 m Osm /kg: 

Effective serum osm olality = 2 Ã— Na + + glucose/18



Blood urea nitrogen not included because it is freely perm eable between fluid com partm ents

Tests Lab 

Broad testing indicated to evaluate hyperosm olar syndrom e and for precipitating causes



Electrolytes: o

K + m ay be elevated even in presence of total body deficit owing to shift from intracellular space to extracellular space.

o

Mild anion gap m etabolic acidosis owing to lactic acid, Î²-hydroxybutyric acid, or renal insufficiency

o

Increased sodium â€”Correct for hyperglycem ia: Corrected [Na + ] = [Na + ] + 1.6 Ã— [(glucose in m g/dL) â€“ 100]/100



BUN, creatinine: o

Azotem ia with elevated BUN/creatinine ratio owing to prerenal and intrarenal causes



Venous blood gas (VBG) or arterial blood gas (ABG) to

Pa ge 2 4 6

rapidly determ ine pH: o 

ABG necessary to evaluate m ixed acid base disorders

Serum ketones, Î²-hydroxybutyrate, and lactate level if pH < 7.3 or significantly elevated anion gap to evaluate m ixed acid-base disorder



Serum osm olarity



CBC: o

Leukocytosis owing to infection, stress, or hem oconcentration

o

Increased hem oglobin and hem atocrit owing to hem oconcentration



Lipase and am ylase: o

Pancreatitis com m on

o

Elevated am ylase and lipase with no evidence of pancreatitis com m on

o

May be owing to increased salivary secretion, hem oconcentration, or decreased renal clearance



Urinalysis: o

Check for ketones/glucose.

o

Assess for urinary tract infection (UTI).



Magnesium , calcium , phosphate



Blood cultures in sepsis



Creatine kinase for rhabdom yolysis: o

Incidence as high as 17%



Urine pregnancy test in fem ales of childbearing years



Cardiac enzym es and troponin for m yocardial infarction

Diagnostic Procedures/Surgery 

ECG



Chest radiograph



Head CT: indicated if com atose or with a focal neurologic deficit

Pa ge 2 4 6

Differential Diagnosis Differentiate from DKA: 

If acidosis or significant anion gap present, m ust determ ine cause (i.e., ketosis, [DKA], lactic acidosis, [hypoperfusion, sepsis, or postictal], or other cause of m etabolic acidosis



Mixed disorder of HHS and DKA present in up to 33% of patients

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

Secure airway in com atose patients.



Cardiac m onitor and 18-gauge IV



Naloxone, thiam ine, and blood glucose for com a of unknown cause



Restore hem odynam ic stability with IV fluids.



0.9% norm al saline (NS) 1â€“2 L over the first hour



Larger volum es of fluid m ay be needed to norm alize the vital signs and establish urine output.

P.555

ED Treatment 

General strategy: o

Frequent reassessm ent of volum e and m ental status

o

Electrolyte assessm ent difficult 

Serum levels of Na + , K + , PO 4 - do not accurately reflect the total body solute deficits or the

Pa ge 2 4 6

intracellular environm ent.  o 

Repeat electrolyte and glucose levels hourly.

Search for a precipitating illness.

Fluids: o

Begin resuscitation with 0.9% saline 1â€“2 L over 1â€“2 hours to restore intravascular volum e and achieve hem odynam ic stability.

o

Use 0.45% saline after initial resuscitation

o

Calculate total body water (TBW) deficit using corrected serum sodium : 

TBW deficit = 0.6 Ã— weight (Kg) Ã— (1 140/corrected Na + )

o

Average fluid deficit is 9 L.

o

Replace 50% of the fluid deficit over the next 12 hours.

o

Add D 5 to intravenous fluids when serum glucose <250 m g/dL.



Potassium : o

Anticipate hypokalem ia: 

Total body deficit of approxim ately 5â€“10 m Eq/kg body weight (replace over 3 days)

o

Begin potassium repletion after urine output is established. Do not start in anuric patients or if initial K + level is >5.5 m Eq/L. 

If the initial K + is norm al (3.5â€“5.5 m Eq/L), give 20â€“30 m Eq KCl in the first liter of fluids, then give 20 m Eq/h.



If the initial K + is low (<3.3 m Eq/L), begin 40 m Eq KCl/h and avoid insulin.

o

Follow repeat serum K + levels q1hâ€“q2h and adjust treatm ent accordingly.



Insulin:

Pa ge 2 4 6

o

Som e patients will not require insulin.

o

Use insulin as sole therapy in patients with fluid overload (i.e., acute renal failure [ARF]).

o

Begin only after achieving hem odynam ic stability and evaluating for hypokalem ia.

o

Earlier use of insulin m ay cause rapid correction of hyperglycem ia with collapse of the intravascular space, hypotension, and shock or hypokalem ia and dysrrhythm ias.

o

SQ or IM insulin not recom m ended owing to erratic absorption

o

Titrate drip to decrease serum glucose by 75â€“150 m g/dL/h.

o

Decrease drip rate by half when serum glucose <250 m g/dL.



Phosphate: o

Routine replacem ent not recom m ended

o

Supplem entation in severely hypophosphatem ic patients (<1.5 m Eq/L) with norm al serum calcium levels and norm al renal function

o

Potassium phosphate if concom itant potassium depletion



Magnesium : o

0.35 m Eq/kg m agnesium in fluids for first 3â€“4 hours (2.5â€“3.0 g MgSO 4 in 70-kg patient)

o 

Caution in acute renal failure

Anticoagulation: o

Arterial throm bosis m ay com plicate hyperosm olar state. 

o

Consider SQ heparin as prophylaxis.

Rem ain vigilant to detect throm botic com plications, e.g., m yocardial infarction, pulm onary em bolus,

Pa ge 2 4 6

m esenteric ischem ia. 

Pitfalls: o

Failure to look for precipitating event or cause

o

Too rapid correction of glucoseâ€”m ay lead to hypotension

o

Continuing isotonic fluids after volum e resuscitationâ€”m ay lead to hypernatrem ia

o

Continuing hypotonic fluids without frequent electrolytesâ€”m ay lead to cellular edem a, cerebral edem a

o

Failure to prevent hypokalem ia: respiratory depression, dysrhythm ias

o

Avoid dilantin in the event of seizure activity: 

Inhibits the endogenous release of insulin

Medication (Drugs) 

Insulin: Begin with 0.05â€“0.1 U/kg/h; m odify after assessing clinical response.



MgSO 4 (m agnesium sulfate): 50% (5 g/10 m L; dilute to at least 20% before IV use)



Naloxone: 2 m g (peds: 0.1 m g/kg) IV push (IVP)



Potassium phosphate IV: phosphates 3 m m ol/m L and potassium 4.4 m Eq/m L



Potassium phosphate PO: phosphorus 250 m g per tablet and potassium 1.1 m Eq per tablet



Thiam ine: 100 m g (peds: 10â€“25 m g) IVP

Follow-Up

Pa ge 2 4 7

Disposition Admission Criteria 

All but the m ildest cases should be adm itted to ICU: o

Frequent serial labs for the first 24 hours

o

Rapid shifts in fluids and electrolytes and the potential for deterioration in m ental status and arrhythm ias m andate close m onitoring.



Mild cases m ay be m anaged in an observation unit over 12â€“24 hours.

Discharge Criteria 

Patients m eeting the diagnostic criteria for hyperosm olar syndrom e should not be discharged.



Mild hyperglycem ia patients with m ild volum e deficits and norm al serum osm olarity can be discharged after hydration and correction of hyperglycem ia.

References 1. Chiasson JL, et al. Diagnosis and treatm ent of diabetic ketoacidosis and the hyperglycem ic hyperosm olar state. Can Med Assoc J. 2003;168:859. 2. Dace, et al. Hyperglycem ic crisis in diabetes m ellitus type 2. Endocrinol Metab Clin North Am . 2001;30(4):817. 3. Gaglia JL, et al. Acute hyperglycem ic crisis in the elderly. Med Clin N Am . 2004;88:1063. 4. Magee MF, Bhatt BA. Managem ent of decom pensated diabetes. Diabetic ketoacidosis and hyperglycem ic hyperosm olar syndrom e. Crit Care Clin. 2001;17(1):75â€“106.

Codes ICD9-CM 250.2 Diabetes with hyperosm olar com a

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperparathyro idism

Hyperparathyroidism Hugh Schuckman

Basics Description 

Parathyroid horm one (PTH) excess with sym ptom s owing to PTH actions: o

Decreases urinary Ca 2 + loss

o

Increases urinary PO 4 - 2 loss

o

Stim ulates vitam in D conversion from 25(OH)-D to 1,25(OH)-D in kidney

o 

Liberates Ca 2 + and PO 4 - 2 from bone

Hypercalciuria produces increased m agnesium losses in urine.



Magnesium (negative feedback to prevent hypercalcem ia): o

Cofactor in production of PTH

o

Essential for action of PTH in target tissues

Genetics 

Associated with m ultiple endocrine neoplasia type I: o

Hyperparathyroidism

o

Pancreatic islet disease (secrete any com bination of gastrin, insulin, pancreatic polypeptide, vasoactive polypeptide, or glucagons)

Pa ge 2 4 7

o

Pituitary disease: 

Hypersecretion of ACTH, prolactin, or growth horm one

 o

Pituitary failure owing to m ass effect

Foregut carcinoid tum or that m ay secrete corticotrophin-releasing horm one



Associated with m ultiple endocrine neoplasia type 2a: o

Hyperparathyroidism

o

Medullary carcinom a of the thyroid

o

Pheochrom ocytom a

Etiology Excess secretion of PTH owing to: 

Prim ary hyperparathyroidism (adenom a 85%, hyperplasia 14%, carcinom a <1%)



Secondary hyperparathyroidism : (response to vitam in D deficiency or chronic renal failure with hyperphosphatem ia): o

Calcium is low or norm al, but PTH levels are elevated.

Diagnosis Stones, bones, abdom inal groans, and psychic m oans

Alert 

Hypercalcem ic crisis: o

Anorexia, nausea, vom iting

o

Mental obtundation

Signs and Symptoms History 

Depend on the severity and rapidity of hypercalcem ia

Pa ge 2 4 7



Usually either an incidental finding or a secondary m anifestation such as renal calculi, peptic ulcer disease, pancreatitis, pseudo gout, gout, and so on

Pediatric Considerations 





Neonate: o

Hypotonia, weakness, and listlessness

o

Following delivery to hypoparathyroid m others

Hypercalcem ic infants: o

Broad forehead

o

Epicanthal folds

o

Underdeveloped nasal bridge

o

Prom inent upper lip

o

Mental retardation

Midteensâ€”nonspecific sym ptom s of hypercalcem ia

Physical Exam 

Dehydration



Cardiac: o

Hypertension (even in the face of dehydration)

o

Cardiac conduction abnorm alities (not proportional to degree of hypercalcem ia)

o

Bradydysrhythm ia

o

Bundle branch blocks

o

Com plete heart block

o

Asystole

o

Short QT interval (shortening of ST segm ent)

o

Potentiation of digitalis effects (Hypercalcem ia plus digoxin equals digitalis toxicity)



Neurologic: o

Headaches

o

Decreased reflexes

o

Proxim al m uscle weakness

Pa ge 2 4 7











o

Dem entia

o

Lethargy

o

Com a

Psychiatric: o

Personality changes

o

Depression

o

Inability to concentrate

o

Anxiety

o

Psychosis

GI: o

Anorexia, nausea, vom iting

o

Constipation

o

Peptic ulcer disease

o

Pancreatitis

General: o

Fatigue

o

Weight loss

o

Polyuria and polydipsia

Musculoskeletal: o

Gout/pseudogout

o

Bone pain, bone cysts (osteitis cystica)

o

Arthralgias

o

Chondrocalcinosis

Renal: o

Kidney stones

o

Nephrocalcinosis

o

Decreased renal concentrating ability

Essential Workup 

Calcium level



Album in: o

Elevated album inâ€”falsely elevated calcium level

o

Low album inâ€”falsely lowered calcium level

Pa ge 2 4 7



Evaluate for sym ptom s of hypercalcem ia, especially im pending parathyroid storm (hypercalcem ic crisisâ€”anorexia, nausea, vom iting, obtundation progressing to com a).



Review history for m edication ingestion (see Differential Diagnosis below).





No further ED workup if: o

Asym ptom atic

o

Norm al ECG

o

Calcium level <14 m g/dL when corrected for album in

If sym ptom atic with Ca 2 + <14 m g/dL or any patient with Ca 2 + â‰¥14 m g/dL, check: o

Ionized calcium

o

Chest radiograph (for congestive heart failure [CHF]/m alignancy)

o

Phosphorus

o

Electrolytes, BUN, creatinine

o

Sed rate

o

Alkaline phosphatase

o

Magnesium

o

Thyroid-stim ulating horm one (TSH)

o

CBC

P.557

Tests Lab 

Calcium correction for album in: o

Corrected Ca 2 + (m g/dL) = m easured Ca 2 + (m g/dL) + 0.8 [4.0 - album in (g/dL)]

o

Acidosis:

Pa ge 2 4 7



Shifts binding to album inâ€”increases ionized (m etabolically active) Ca 2 +



Decrease of 0.1 pH unit increases the ionized Ca 2+







by 3â€“8%

Phosphorus: o

Low in prim ary hyperparathyroidism

o

Usually high in secondary hyperparathyroidism

o

Norm al or high in m alignancy-related hypercalcem ia

Chloride/PO 4 - 2 ratio: o

>33â€”hyperparathyroidism

o

<30â€”m alignancy

Alkaline phosphatase: o

Increased in 50% of patients with hyperparathyroidism

o 





Erythrocyte sedim entation rate (ESR): o

Norm al in hyperparathyroidism

o

Elevated in m alignancy or granulom atous diseases

Anem ia: o

Present with m alignancy or granulom atous disease

o

Absent in hyperparathyroidism

Magnesium : o



Norm al with vitam in D excess

Low or low norm al

Parathyroid horm one (PTH): o

Elevated in prim ary and secondary hyperparathyroidism



PTH-related peptide: o

Secreted by squam ous cell carcinom as of lung, head, neck; renal carcinom as, bladder carcinom as, adenocarcinom as, and lym phom as

Imaging Chest radiograph:

Pa ge 2 4 7



To assess CHF risk during IV hydration



Granulom atous disease or m alignancy if cause of hypercalcem ia is uncertain

Diagnostic Procedures/Surgery Parathyroidectom y to treat and establish cause of hyperparathyroidism

Differential Diagnosis 



PTH related: o

Prim ary or secondary hyperparathyroidism

o

Fam ilial hypocalciuric hypercalcem ia

Malignancy related: o

PTH-related peptide or Ca 2 + release from osteolytic tum or



Vitam in D-related excess vitam in D intake or vitam in D production by granulom as



Im m obilizationâ€”associated with Paget disease



Drug induced: o

Thiazide diuretics

o

Lithium

o

Alum inum -containing antacids

o

Tam oxifen

o

Estrogens

o

Androgens

o

Vitam in A

Treatment Pre Hospital May present as a prim arily psychiatric disorder

Pa ge 2 4 7

Initial Stabilization 

Cardiac m onitor if: o

Sym ptom atic hypercalcem ia

o

Ca 2 + level >14 m g/dL



Hydrate with IV 0.9% norm al saline (NS).



Correct acidosis.

ED Treatment 

Treat hypercalcem ia: o

Vigorous hydration with 0.9% NS at m inim um of 250 m L/h unless CHF:

o



Lowers calcium 1.5â€“2.0 m g/dL in 24 hours



Achieve urine output 100 m L/h

Adm inister furosem ide or other loop diuretic (calciuric) after adequate volum e replacem ent or in presence of CHF: 

Com m on error: adm inistration of furosem ide before adequate hydration



If urinary sodium losses exceed replacem ent sodium , then renal conservation m easures retard calcium excretion.

o

Avoid thiazide diuretics (retard calcium excretion).

o

Consider glucocorticoid adm inistration (decreases gut absorption and increases renal excretion of Ca 2 + ); m ost effective with vitam in D intoxication or granulom atous diseases.

o

Start bisphosphonates (pam idronate or etidronate) in conjunction with prim ary physician (inhibits calcium m obilization from bone).



Treat cardiac dysrhythm ias in standard fashion: o



Correct acidosis.

Determ ine the cause of the hypercalcem ia.

Pa ge 2 4 7



Stop all m edications that m ay contribute to hypercalcem ia.



Exercise extrem e caution in use of digoxin.



Anticipate CHF and electrolyte im balance with frequent reassessm ent of patient and m onitoring of serum electrolytes and m agnesium levels.



Calcitonin if unable to use hydration



Em ergent dialysis with renal failure

Medication (Drugs) 

Calcitonin: 4â€“8 IU/kg SC q6h



Etidronate: 7.5 m g/kg in 500 m L NS over 3 hours (pregnancy category C/used, but safety not established in peds)



Furosem ide: 40 m g IV q6h after assurance of adequate hydration



Hydrocortisone: 100 m g (peds: 1â€“2 m g/kg) IV



Pam idronate: 60â€“90 m g IV in 1 L NS over 4â€“24 hours (pregnancy category C/used, but safety not established in peds)



Prednisone: 40â€“80 m g PO

Follow-Up Disposition Admission Criteria 

Corrected calcium >14 m g/dL



Sym ptom atic hypercalcem ia



Evidence of abnorm al cardiac rhythm or conduction

Pa ge 2 4 8

Discharge Criteria 

Not m eeting adm ission criteria



Able to m aintain adequate hydration

Issues for Referral If diagnosis is suspected, referral to check PTH levels and response to therapy

References 1. Goldm an L, Bennett JC, eds. Cecil's Textbook of Medicine. 22nd ed. Philadelphia: WB Saunders; 2000. 2. Greenspan FS, Gardner DG. Basic and Clinical Endocrinology. 7th ed.: Lange Publishers; 2003. 3. Tintinalli JE, Kelen GD, Stapczynski JS. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. McGraw-Hill; 2004. 4. Wallach J, ed. Interpretation of Diagnostic Tests. 7th ed. Boston: Little, Brown and Com pany; 2000.

Codes ICD9-CM 252.0 259.3 588.8

ICD10 E21.3

Pa ge 2 4 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypertensive Em ergencies

Hypertensive

Emergencies David F. M. Brown Megan Fix

Basics Description 

Hypertensive em ergency: o

Uncontrolled hypertension associated with acute end-organ dam age



Increase in circulating vasoconstrictors: o

Norepinephrine

o

Antiotensin II



Arteriolar fibrinoid necrosis



Endothelial dam age



Platelet and fibrin deposition



Loss of autoregulation of blood flow



End organ ischem ia:



o

Prom pts the renewed release of vasoconstrictors

o

Triggers a vicious cycle

2% of hypertensive patients will have a hypertensive em ergency.



Malignant hypertension:

Pa ge 2 4 8

o

Young African Am erican m en

o

Underlying renal disease

o

Flam e-shaped hem orrhages, soft exudates, papilledem a on funduscopic exam



Hypertensive encephalopathy: o

Severe hypertension

o

Altered m ental status

o

Papilledem a

o

CT shows characteristic posterior leukoencephalopathy.

Etiology 







CNS abnorm alities: o

Subarachnoid hem orrhage

o

Intracranial hem orrhage

o

Throm botic infarction

o

Encephalopathy

o

Head traum a

o

Transient ischem ic attacks

Cardiovascular abnorm alities: o

Acute coronary insufficiency

o

Acute aortic dissection

o

Accelerated hypertension

o

Acute heart failure

o

Myocardial infarction

o

Unstable angina

Renal system abnorm alities: o

Acute renal insufficiency

o

Acute glom erulonephritis

o

Renal artery stenosis

Excessive catecholam ine states: o

Pheochrom ocytom a

o

Adrenocortical tum ors

Pa ge 2 4 8

o

Monoam ine oxidase inhibitor interactions



Antihypertensive m edication withdrawal



Pregnancy-induced hypertension



Pre-eclam psia



Autonom ic hyperreactivity:



o

Guillain-BarrÃ© syndrom e

o

Acute interm ittent porphyria

Drugs: o

Cocaine

o

Am phetam ines

o

Oral contraceptives

o

Corticosteroids

o

Toxins

o

Heavy m etals

Diagnosis Signs and Symptoms 

Elevation of blood pressure



Assess signs of end-organ com prom ise: o

Chest pain (m yocardial ischem ia)

o

Back pain (aortic dissection)

o

Dyspnea (congestive heart failure [CHF])

o

Neurological sym ptom s

o

Seizures

o

Altered m ental status

o

Headache

o

Confusion

o

Visual disturbance

History

Pa ge 2 4 8



Duration and severity of preexisting hypertension



Previous end-organ com prom ise:



o

Renal

o

Cerebrovascular

o

Cardiovascular

o

Great vessels

Details of antihypertensive therapy: o



Com pliance

Illicit drug use

Physical Exam 

Blood pressure (BP) m easurem ent both arm s



Assess for end-organ com prom ise: o

o

Neurologic: 

Level of consciousness



Visual fields



Focal m otor/sensory deficits

Ophthalm ologic: 

Funduscopic exam ination (retinal hem orrhages, papilledem a)



Cardiac: o

Elevated JVP

o

Crackles

o

S3

Tests 

IV access



12-lead ECG



Standard hospital protocols for chest pain, CHF

Lab 

Blood urea nitrogen creatinine: o



Acute elevation if renal dam age

Electrolytes

Pa ge 2 4 8



Urinalysis: o



Plasm a rennin activity and aldosterone: o



Proteinuria and casts

If renovascular disease or hypercortisolism suspected

Urine toxicology screen: o

Indicated if illicit drug use suspected

o

Cocaine, am phetam ines

Imaging 

ECG: o



Assess for m yocardial ischem ia

Head CT: o

Exclude subarachnoid and intracerebral hem orrhage.

Diagnostic Procedures/Surgery 

Intra-arterial line: o



Continuous BP m onitoring

Lum bar puncture: o

Exclude subarachnoid hem orrhage.

Differential Diagnosis 

Subarachnoid hem orrhage



Intracerebral hem orrhage



Cerebral infarction



Acute m yocardial ischem ia



Acute m yocardial infarction



Acute pulm onary edem a



Aortic dissection



Pre-eclam psia/eclam psia



Withdrawal syndrom es:



o

Beta-blockers

o

Central-acting antihypertensive agents (clonidine)

States of catecholam ine excess: o

Pheochrom ocytom a

Pa ge 2 4 8

o

Cocaine/sym pathom im etic drug intoxication

o

Tyram ine ingestion when on MAOIs

Treatment Initial Stabilization 

ABCs



Cardiac m onitoring



Pulse oxim etry



Oxygen adm inistration



IV access



Antiischem ic therapy: o

With signs of acute m yocardial ischem ia or infarction

ED Treatment 

Treat end-organ dam age, not absolute BP.



Reduce the m ean arterial pressure by no m ore than 20â€“25%.



Decrease the diastolic BP to 100â€“110 m m Hg.



The reduction should occur over several m inutes to hours. P.559





More gradual reduction recom m ended in: o

Long history of poorly controlled hypertension

o

Acute ongoing injury to CNS

o

Cardiac involvem ent

Am erican Hospital Association guidelines for CVA recom m end decreasing BP only when the MAP is greater than 130 m m Hg or the SBP is greater than 220 m m Hg: o

Further BP reduction should be avoided in ED.

Pa ge 2 4 8

o

Goal is rapid onset, rapid m axim al effect, and rapid offset for easy titration.



Nitroprusside: o

Short-acting arterial and venous dilator

o

Im m ediate onset

o

Brief (2â€“3 m inutes) duration of action

o

Com plications:

o



Hypotension



Nausea



Reflex tachycardia



Thiocyanate toxicity



Degraded by light

Contraindication: 





Pregnancy

Labetalol: o

Com bined alpha and beta-blocker

o

Onset 5â€“10 m inutes

o

3- to 6-hour duration

o

Does not cause reflex tachycardia

o

Easy conversion to oral therapy

Fenoldopam : o

Selective postsynaptic dopam inergic receptor agonist (DA1)

o

Onset 3â€“4 m inutes

o

Duration 8â€“10 m inutes

o

Does not cause reflex tachycardia

o

Com plications: 

Flushing



Headache



Dizziness



Tachy/Bradycardia



ECG changes

Pa ge 2 4 8

 o

Contraindication: 



Glaucom a (relative)

Diazoxide: o

Sm ooth-m uscle relaxant

o

Indications:

o



Hypertensive encephalopathy



Malignant hypertension



Pregnancy-induced hypertension



Pre-eclam psia/eclam psia

Com plications: 

o



Increased intra-ocular pressure

Reflex sym pathetic stim ulation

Contraindications: 

Aortic dissection



Acute m yocardial ischem ia

Phentolam ine: o

Alpha-blocker

o

Agent of choice in states of catecholam ine excess

o

Indications:

o



Pheochrom ocytom a



MAOI reactions



Stim ulant abuse



Antihypertensive drug withdrawal states

Caution: 

Beta-blockers should be avoided in states of catecholam ine excess.





Only give after alpha-blockade



Only for tachydysrhythm ias

Use caution with oral agents in true hypertensive em ergency: o

Can cause a precipitous decrease in BP that is difficult to reverse and titrate

Pa ge 2 4 8

Specific Treatment Strategies 

Accelerated-m alignant hypertension: o



Nitroprusside

Cerebrovascular em ergencies: o

Treat only when MAP >130 m m Hg or SBP >220 m m Hg.

o

Esm olol and labetalol are appropriate (easily titrated and m inim al effect on cerebral vasculature).

o

Avoid calcium channel blockers which have been associated with increase in intracranial pressure.



Cardiovascular em ergencies (CHF, ACS, aortic aneurysm ): o

CHF: 

Nitroprusside to carefully reduce blood pressure for sym ptom relief

o



ACE inhibitor for CHF



Furosem ide



Nesiritide

ACS: 

Nitroglycerine (potent coronary vasodilator and reduces preload and afterload)

 o

o

Goal to reduce BP to norm al levels.

Aortic dissection: 

Goal is to reduce pulse pressure (dp/dt).



Avoid reflex tachycardia



Beta-blockers

Recreational drugs: 

Sym pathom im etics (cocaine, phenylephrine, m etham phetam ine, tyram ine in MAOI use)

o



Benzodiazepines



Avoid beta-blockers.

Pheochrom ocytom a: 

Phentolam ine (pure alpha-blockade)

Pa ge 2 4 9

Pregnancy Considerations 

Pre-eclam psia: o

Wom en who are pregnant for the first tim e

o

Between 20 weeks gestation and 2 weeks postpartum

o

Hypertension, peripheral edem a, proteinuria

o

Can progress to eclam psia

o

Treatm ent: 

Magnesium



Hydralazine



Diazoxide (second line)



Beta-blockers (second line)

Medication (Drugs) 

Diazoxide: 50â€“100 m g IV bolus repeated or 15â€“30 m g/m in IV infusion



Enalaprilat: 1.25â€“5 m g q6hr IV



Esm olol: 250â€“500 Âµg/kg/m in for 1 m inute, then 50â€“100 Âµg/kg/m inute for 4 m inute; m ay repeat



Fenoldopam : 0.1â€“0.3 Âµg/kg/m in as IV infusion



Hydralazine: 10â€“20 m g IV; 10â€“50 m g IM



Labetalol: 20â€“80 m g IV bolus q10m in; 0.5â€“2.0 m g/m in IV infusion



Nicardipine: 5â€“15 m g/hr IV



Nitroglycerin: 5â€“100 Âµg/m in IV infusion



Nitroprusside: 0.25â€“10 Âµg/kg/m in as IV infusion



Phentolam ine: 5â€“15 m g IV

Follow-Up

Pa ge 2 4 9

Disposition Admission Criteria 

All patients with hypertensive em ergencies



Signs of end-organ dam age



Intensive care unit for cardiac and BP m onitoring

Discharge Criteria Hypertensive urgencies: 

Absence of cerebral, ocular, cardiac, or renal dam age



Likely to be com pliant with prim ary care



Known to have hypertension



Reversible precipitating cause (m edication noncom pliance)



Able to resum e previous m edication regim en



Can be seen in follow up within 7 days: o

Return with chest pain or headache

References 1. Shayne PH, Pitts SR. Severely Increased Blood Pressure in the Em ergency Departm ent. Ann Em erg Med. 2003:41:513â€“529. 2. Vaughan Carl j, Delanty N. Hypertensive Em ergencies. Lancet. 2000;356:411â€“417.

Miscellaneous SEE ALSO: Aortic Dissection; Acute Coronary Syndrom e; Acute Stroke; Subarachnoid Hem orrhage; Congestive Heart Failure

Codes ICD9-CM 401.0 Essential hypertension, m alignant 401.1 Essential hypertension, benign 401.9 Essential hypertension, unspecified

Pa ge 2 4 9

ICD10 I110 Essential (prim ary) hypertension I111 Hypertensive heart disease I112 Hypertensive renal disease

Pa ge 2 4 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypertherm ia

Hyperthermia

Michelle Canham

Basics Description 

Continuum of increasingly severe illnesses secondary to overwhelm ing heat stress



Begins with dehydration and electrolyte abnorm alities and progresses to therm oregulatory dysfunction and m ultisystem organ failure



Body tem perature is m aintained within a narrow range by balancing heat load with heat dissipation.



Tem perature elevation is accom panied by an increase in oxygen consum ption and m etabolic rate.



Oxidative phosphorylation becom es uncoupled and a variety of enzym es cease to function above 42Â°C (108Â°F).

Heat Stroke 

Core body tem p >105Â°F (40.5Â°C)



Loss of therm oregulatory function, severe CNS dysfunction, and m ultisystem organ failure



Classic heat stroke (nonexertional): o

Occurs in those with com prom ised therm oregulation or an inability to rem ove them selves from a hot

Pa ge 2 4 9

environm ent (extrem es of age, debilitated)



o

Develops over days to weeks

o

Severe dehydration, skin warm and dry

Exertional heat stroke: o

Occurs in younger, athletic individuals with a com bined environm ental and exertional heat stress

o

Develops over hours

o

Internal heat production overwhelm s dissipating m echanism s.

o

May be sweating

Heat Exhaustion 

Core tem p: <104Â°F (40Â°C)



Fluid and electrolyte depletion



Therm oregulatory function is m aintained.



CNS function is preserved.

Heat Cramps Secondary to excessive sweating and sodium loss

Prickly Heat Blockage of sweat glands leading to rash

Etiology 

Pre-existing conditions that hinder the body's ability to dissipate heat: o

Age extrem es

o

Dehydration

o

Cardiovascular disease

o

Obesity

o

Hyperthyroidism

o

Febrile illness

o

Skin diseases that hinder sweating (psoriasis, eczem a)

Pa ge 2 4 9





Pharm acologic contributors: o

Sym pathom im etics

o

LSD/PCP

o

MAO inhibitors

o

Anticholinergics

o

Antihistam ines

o

Beta-blockers

o

Diuretics

o

Laxatives

o

Drug or alcohol withdrawal

Physical/environm ental factors: o

Prolonged exertion

o

Lack of m obility

o

Lack of air conditioning

o

Excessive hum idity

o

Lack of acclim atization

Pediatric Considerations Children are at increased risk of heat illness owing to increased body surface area to m ass ratio.

Diagnosis Signs and Symptoms Heat Stroke 

Classic triad: hypertherm ia, CNS dysfunction, anhydrosis: o

Perspiration is often present in early stages.



Core tem p: >105Â°F (40.5Â°C)



CNS: o

Severe confusion

o

Lethargy

Pa ge 2 4 9









o

Com a

o

Seizure

o

Ataxia

Cardiovascular (CV): o

Tachycardia

o

Hypotension

o

Wide pulse pressure

o

Conduction disturbances

Pulm onary: o

Tachypnea

o

Rales owing to noncardiac pulm onary edem a

GI: o

Nausea

o

Vom iting

o

Diarrhea

Skin: o

Cutaneous vasodilation

o

Dry and hot if severe dehydration

o

Sweating m ay be present if patient is not dehydrated.



Acute oliguric renal failure owing to rhabdom yolysis, dehydration



Hepatic failure



Acute bleeding owing to dissem inated intravascular coagulation (DIC)

Heat Exhaustion 

Core tem p: <104Â°F (40Â°C)



CNS: o

Headache

o

Fatigue

o

Malaise

o

Agitation

Pa ge 2 4 9





CV: o

Mild tachycardia

o

Dehydration

Pulm onary: o





Tachypnea

GI: o

Nausea

o

Vom iting

Skin: o

Perspiration present, often profuse

Heat Cramps 

Cram ps in heavily exercised m uscles



During or after exercise



Prim arily in lower extrem ities

Heat Tetany Carpal-pedal spasm â€”secondary to hyperventilation

Heat Edema 

Swelling of dependent areas of body



Resolves after acclim atization

Prickly Heat Pruritic m aculopapular rash over clothed areas

Essential Workup 

Accurate core tem perature



History of heat exposure



Heat exhaustionâ€”diagnosis of exclusion



Core tem perature >105Â°F (40.5Â°C) and CNS dysfunction required to m ake diagnosis of heat stroke

Tests Lab

Pa ge 2 4 9

Heat Stroke and Heat Exhaustion 

CBC: o



Leukocytosis, hem oconcentration often present

Electrolytes, BUN, creatinine, glucose o

Hypernatrem ia with severe dehydration

o

Hyponatrem ia can occur if drinking copious free water.

o 

Acute renal failure

Urinalysis (UA): o

Myoglobin present in rhabdom yolysis



Blood and urine cultures to rule out infection



Toxicology screen



Serum creatinine kinase to rule out rhabdom yolysis

P.561

Heat Stroke 

Liver function tests: o

Hepatic necrosis presents with elevated transam inases.



PT/PTT/DIC panel: o



Coagulopathy, DIC

Consider lum bar puncture.

Imaging 

ECG indicated in elderly or at cardiac risk



CT head for altered m ental status



Chest radiograph for adult respiratory distress syndrom e (ARDS), aspiration pneum onia

Differential Diagnosis 

Febrile illness/sepsis



Thyroid storm

Pa ge 2 4 9



Pheochrom ocytom a



Malignant hypertherm ia



Cocaine/PCP



Anticholinergics



MAO inhibitors



Meningitis/encephalitis



Cerebral falciparum m alaria



Delirium trem ens



Neuroleptic m alignant syndrom e

Treatment Pre Hospital Institute cooling m easures for severe heat illness: 

Rem ove from heat stress



Disrobe patient



Cover body with wet sheet

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Continuous core tem perature m onitoring with a rectal or esophageal probe



Im m ediate/rapid cooling if tem perature >104Â°F (40Â°C)



IV 0.9% norm al saline (NS) 500 m L fluid bolus if hypotensive



If altered m ental status, adm inister glucose (or Accu-Chek), thiam ine, naloxone

ED Treatment Cooling Measures 

Initiate for body tem perature >104Â°F (40Â°C).

Pa ge 2 5 0



Evaporative cooling: o

Extrem ely effective (0.05â€“0.3Â°C/m in)

o

Spray disrobed patient with fine m ist of warm water (prevents shivering).

o 

Airflow with fans blowing over patient

Conductive cooling: o

Ice packs to groin/axillaâ€”com bine with evaporative cooling treatm ent above.

o

Iced or cold water im m ersionâ€”effective but im practical



Iced peritoneal lavage and cardiopulm onary bypass for refractory cases



To avoid hypotherm ia, stop cooling therapy at 102Â°F (39Â°C)



Antipyretic agents are not helpfulâ€”underlying m echanism does not involve a change in the hypothalam us set point.



Avoid alcohol sponge bathsâ€”toxicity can occur owing to dilated cutaneous vessels.

Supportive Measures 

Rehydration for heat stroke/heat exhaustion: o

Initial rehydration with 0.5â€“1.0 L 0.9% NS

o

Avoid overhydrationâ€”m ay contribute to developm ent of ARDS

o

Peds: 20 m L/kg bolus

o

Place Foley catheter to m onitor urine output for heat stroke victim s.



Benzodiazepines for seizures or shivering



For heat cram ps: o

Adm inister analgesics and oral or IV hydration with electrolyte-containing fluid.



For hyperventilation heat tetany: o

Provide reassurance/calm ing m easures/rebreathing

Pa ge 2 5 0

in closed system (bag or nonrebreather without oxygen). 

For heat edem a: o

Lower extrem ity elevation

o

Rem ove from heat stress.

Medication (Drugs) 

Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 2 5 W over 1 m in) IV push (IVP)



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.4 m g/kg) IVP



Lorazepam : 1â€“2 m g (peds: 0.05â€“0.1 m g/kg) IVP



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IVP

Follow-Up Disposition Admission Criteria 

Heat strokeâ€”adm it to the ICU.



Heat exhaustionâ€”adm it to general or m onitored floor: o

Severe electrolyte abnorm alities

o

Renal failure/evidence of rhabdom yolysis

o

Elderly

Discharge Criteria All patients except those with heat stroke or severe heat exhaustion m ay be discharged.

References 1. Khosla R, Guntapalli KK. Heat-related illness. Crit Care Clin.

Pa ge 2 5 0

1999;15:251. 2. Lee-Chiong TL, Stitt JT. Heat stroke and other heat-related illnesses. Postgrad Med. 1995;98(1):26â€“36. 3. Walker JS, Barnes SB. Heat em ergencies. In: Tintinalli JE, ed. Em ergency Medicine: A Com prehensive Study Guide. 5th ed. New York: McGraw-Hill; 2000:1237â€“1242.

Codes ICD9-CM 780.6

ICD10 R50.9

Pa ge 2 5 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperthyro idism

Hyperthyroidism

Rita Cydulka Danielle A. Hoover

Basics Description 

Excessive thyroid horm one production results in a continuum of disease: o

Mild hyperthyroidism

o

Thyrotoxicosis

o

Thyroid storm or thyrotoxic crisis with life-threatening m anifestations



1â€“2% of patients with hyperthyroidism progress to thyroid storm .

Genetics 

Interplay between genetics and environm ent is likely.



Graves disease is associated with HLA-B8 and HLA-DR3.



Autosom al dom inant inheritance seen in som e fam ilies with nontoxic goiter: o

Chrom osom e 14q, MNG1, and

o

Chrom osom e Xp22, MNG2

Etiology 

Toxic diffuse goiter (Graves disease)

Pa ge 2 5 0



Toxic m ultinodular or uninodular goiter



T 3 toxicosis



Hashim oto thyroiditis



Malignancy



Hypothalam ic hyperthyroidism



Thyroid-stim ulating horm one (TSH)â€“producing pituitary tum or



Postpartum thyroiditis



Radiation thyroiditis



Ingestion of excessive iodine (Jodbasedow disease)



Drug induced: o

Am iodarone

o

Lithium

o

Iodine

o

Excessive thyroid horm one (factitious thyrotoxicosis)

Diagnosis Alert 

Thyroid storm is a life-threatening condition which m ay be precipitated by: o

Infection

o

Traum a

o

Diabetic ketoacidosis

o

Myocardial infarction

o

Cerebrovascular accident

o

Abrupt withdrawal or acute ingestion ofthyroid m edication



Thyroid storm s involves exaggerated signs and sym ptom s of thyrotoxicosis: o

Hyperpyrexia

Pa ge 2 5 0



o

Extrem e tachycardia/dysrhythm ias

o

Congestive heart failure

o

Shock

o

Disorientation/m ental status changes

Signs and sym ptom s reflect end organ responsiveness to thyroid horm one: o

o

Signs: 

Fever



Tachycardia disproportional to fever



Hyperhidrosis



Wide pulse pressure



Congestive heart failure (CHF)



Shock



Trem or



Disorientation/psychosis



Com a



Goiter



Thyrotoxic stare/exophthalm os



Thyrom egaly



Jaundice/tender liver

Sym ptom s: 

Weight loss



Dysphagia or difficulty breathing secondary to obstruction by a goiter



Rash/pruritus/hyperhidrosis



Palpitations/chest pain



Dyspnea



Abdom inal pain



Diarrhea/hyperdefecation



Myalgias



Weakness



Nervousness/anxiety

Pa ge 2 5 0



Menstrual irregularities



Heat intolerance



Insom nia

Geriatric Considerations 

Apathetic hyperthyroidism : o

Seen in the elderly

o

Owing to m ultinodular goiter

o

Subtle clinical findings: 

Often reflecting single-organ dysfunction (CHF)



Weight loss



Depressed m entation



Trem or



Hyperactivity

Signs and Symptoms History Gradual onset of aforem entioned signs and sym ptom s

Physical Exam 

Vital signs: o

Fever

o

Tachycardia

o

Elevation of systolic blood pressure

o

Tachypnea/hypoxia



Alopecia



Exophthalm os



Thyrom egaly or goiter



Thyroid bruit



Fine, thin, diaphoretic skin



Irregularly irregular heartbeat



Lung rales (CHF)



Abdom inal/right upper quadrant (RUQ)

Pa ge 2 5 0

tenderness/jaundice 

Muscular atrophy/weakness



Trem or



Mental status changes/com a

Essential Workup 

Search for the underlying cause.



Plasm a thyroid-stim ulating horm one (TSH) assay is the initial test of choice in the ED: o

Norm al level usually excludes hyperthyroidism .

o

If TSH levels are not available, strong clinical picture should prom pt initiation of therapy.

Tests Lab 

Thyroid function tests for: o

Sym ptom s of hyperthyroidism

o

Elderly patient with new-onset CHF

o

New atrial fibrillation/supraventricular tachycardia (AFib/SVT)



TSH (usually decreased)



Free T 4 (usually elevated) o



CBC: o



If free T 4 is unavailable, total T 4 and resin T 3 uptake

Anem ia

Electrolytes, BUN, creatinine, glucose: o

Elevated BUN, creatinine, secondary dehydration

o

Hypokalem ia



Calcium



Liver function tests



Urinalysis



Arterial blood gases for hypoxem ia



Cardiac m arkers

Pa ge 2 5 0



ECG: o

Tachydysrhythm ias

o

Atrial fibrillation

Imaging Chest radiograph (in CHF)

Differential Diagnosis 

Pheochrom ocytom a



Sepsis



Sym pathom im etic ingestion (e.g., cocaine, am phetam ines)



Psychosis



Heat stroke



Delirium trem ens



Malignant hypertherm ia



Neuroleptic m alignant syndrom e



Hypothalam ic stroke



Hypothyroidsim (m ay m im ic apathetic hyperthyroidism )



Factitious thyrotoxicosis

P.563

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Cardiac m onitor



Supplem ental oxygen to m eet m etabolic needs



Initiate cooling m easures: o

Acetam inophen for fever: 

Avoid aspirin (aspirin displaces thyroid horm one

Pa ge 2 5 0

from thyroglobulin). o

Cooling blanket

ED Treatment 

Identify and treat the precipitating event.



For thyroid storm , initiate treatm ent sequence outlined below.



Inhibit horm one synthesis using thioam ides: o

Propylthiouracil (PTU): 

Drug of choice



Decreases horm one synthesis and reduces peripheral conversion of T 4

o 

Methim azole

Block horm one release: o

Potassium iodide, or

o

Oral Lugol solutions, or

o

Sodium iodide

o

Adm inister iodine therapy at least 1 hour after thioam ides to prevent organification of the iodine.





Prevent peripheral conversion of T 4 â€“T 3 : o

PTU or

o

Dexam ethasone

Block the peripheral effects of thyroid horm one: o

Beta-blockade: 

Contraindicated/caution advised with CHF, diabetes m ellitus, and reactive airway disease

o





Propranolol



Esm olol

When beta-blocker is contraindicated, use: 

Reserpine



Guanethidine

Treatm ent of thyrotoxicosis, secondary thyroiditis: o

Beta-blockade

Pa ge 2 5 1

o 

Anti-inflam m atory m edications

General support: o

Acetam inophen for hyperpyrexia

o

Control congestive heart failure with digitalis and diuretics.

o

Manage dehydration

o

Hydrocortisone

Medication (Drugs) 

Dexam ethasone: 2 m g IV q6h (peds: 0.15 m g/kg)



Esm olol: 500 Âµg/kg IV over 1 m inute followed by m aintenance dose of 50 Âµg/kg/m in IV; titrate to effect



Guanethidine: 30â€“40 m g PO q6h



Hydrocortisone: 100 m g IV q8h



Lugol solutions: 8â€“10 drops PO q6h



Methim azole: 40 m g PO initially, then 25 m g PO q6h



Potassium iodide (SSKI): 5 drops PO q6h



Propranolol: 1â€“2 m g IV, repeated q10â€“15m in as needed



Propylthiouracil (PTU): 600â€“1000 m g initially, then 200â€“250 m g PO q4h (peds: 5â€“7 m g/kg/24h)



Reserpine: 1â€“5 m g IM q4hâ€“q6h, up to 15 m g/24h



Sodium iodide: 1 g IV q8hâ€“q12h

Pregnancy Considerations 

Physiologic changes associated with pregnancy m ay resem ble m any sym ptom s of hyperthyroidism , thus causing a delay in diagnosis.



Poorly controlled hyperthyroidism during pregnancy m ay result in: o

Prem ature labor

Pa ge 2 5 1



o

Pre-eclam psia

o

Low birth weight

o

Spontaneous abortion

o

Stillbirth

Thyroid storm often precipitated by stress, including infection or birth



Treatm ent: o

Initial stabilization as in the nonpregnant patient (ABCs, supportive m easures)

o

PTU considered the safest drug in inhibiting horm one synthesis

o

Propranolol m ay be safely used to treat the peripheral effects of excess thyroid horm one.

o

Radioactive iodine absolutely contraindicated during pregnancy or while nursing



Postpartum thyroiditis: o

Occurs in 5â€“10% of patients within 6 m onths of delivery

o

May require antithyroid m edications tem porarily

o

Half of those affected becom e euthyroid within 1 year

o

Transient hypothyroidism m ay follow; however, 40% of those affected go on to develop thyroid failure.

Follow-Up Disposition Admission Criteria 

Thyroid storm



Requiring IV m edications to control heart rate (HR)



Sym ptom atic patients (tachycardia, fever)

Pa ge 2 5 1

Discharge Criteria Minim ally sym ptom atic individuals who respond well to oral therapy

References 1. Larsen R, et al. William sâ€™ Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003. 2. Mestm an J. Hyperthyroidism in pregnancy. Clin Obstet Gynecol. 1997;40:45. 3. Tietgens ST, Leinung MC. Thyroid storm . Med Clin North Am . 1995;79:169â€“184. 4. Wogan JM. Selected endocrine disorders. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2001.

Codes ICD9-CM 242.9

ICD10 E05.9

Pa ge 2 5 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperventilatio n

Hyperventilation

Robert F. McCormack

Basics Description 

Hyperventilation syndrom e describes a constellation of sym ptom s (m ost com m only: dyspnea, chest pain, lightheadedness, and paresthesias) produced by a nonphysiologic increase in m inute ventilation. Minute ventilation m ay be increased by increasing respiratory rate or tidal volum e (sighs).



Pathologic or physiologic causes of hyperventilation m ust be excluded before the diagnosis of hyperventilation syndrom e can be assigned.

Prevalence 

10â€“15% in the general population



More com m on in wom en (m ay be related to progesterone)

Etiology 

Usually a response to psychological stressors



Etiology of sym ptom s is unclear; sym ptom s m ay be related to hypocapnia, hypophosphatem ia, or hypocalcem ia, but significant controversy exists in the literature.

Pa ge 2 5 1

Diagnosis Signs and Symptoms 









Cardiac: o

Chest pain

o

Dyspnea

o

â€œAir hungerâ€•

o

Palpitations

Neurologic: o

Dizziness

o

Light-headedness

o

Syncope

o

Paresthesias

o

Headache

o

Carpopedal spasm

o

Tetany

Psychiatric: o

Intense fear, anxiety

o

Giddiness

o

Feeling of unreality

General: o

Fatigue

o

Weakness

o

Malaise

Clinical signs are rare and varied: o

Tachypnea m ost com m on

o

However, tachypnea m ay not be present. Patient m ay increase tidal volum e rather than respiratory rate.



Carpopedal spasm :

Pa ge 2 5 1

o

May be dram atic

o

Chvostek sign m ay be present.

Essential Workup 

Diagnosis of exclusion: o

Prim ary pathologic or physiologic causes of hyperventilation m ust be investigated and excluded.



Clinical diagnosis based on the history and physical exam



Vital signs including pulse oxim etry



Hyperventilation syndrom e will not result in hypoxia.

Tests 

Hyperventilation provocation test after resolution of sym ptom s: o

Forced overbreathing for 3 m inutes m ay be attem pted to reproduce the sym ptom s.

o

Diagnostic accuracy is controversial.

o

Reproducibility of the sym ptom s m ay help the patient understand the role of overbreathing and help m anage future attacks.



ECG if chest pain present

Lab 

Consider an arterial blood gas in any hypoxic patient.



Electrolytes, blood urea nitrogen, creatinine, and glucose levels for suspected acidosis/diabetic ketoacidosis

Imaging Chest radiograph of any patient with hypoxia or focal findings on lung exam ination

Differential Diagnosis 

Pathologic



Hypoxia: o

Asthm a

Pa ge 2 5 1

o

Congestive heart failure

o

Pulm onary em bolus

o

Pneum onia



Severe pain



CNS lesions



Acidosis (DKA)



Pulm onary hypertension



Pulm onary em bolus



Hypoglycem ia



Mild asthm a



Drugs: o

Aspirin intoxication

o

Withdrawal syndrom e (e.g., alcohol, benzodiazepines)



Physiologic



Pregnancy



Pyrexia



Altitude

P.565

Treatment Pre Hospital 

Patients with abnorm al vital signs require IV access and pulse oxim etry.



Supplem ental oxygen if hypoxic

Initial Stabilization 

Patients with abnorm al vital signs require IV access and

Pa ge 2 5 1

pulse oxim etry 

Initiate therapy for pathologic or physiologic cause of hyperventilation.

ED Treatment 

Initiate treatm ent of hyperventilation syndrom e for the following:



Initial workup does not support a pathologic or physiologic cause.



History and physical exam findings suggest the diagnosis of hyperventilation syndrom e.



Reassurance, calm ing, and explanation of the voluntary com ponent of the patient's sym ptom s often have im m ediate dram atic results.



Do not use paper bag rebreathing to increase the PCO 2 . This has not been supported in the literature.



It m ay be dangerous in patients with hypoxia or a pathologic or physiologic cause for hyperventilation.



Clarification of the psychologic stressors helps the patient avoid further attacks.



Assess for need of psychiatric evaluation (i.e., suicidal ideation)



Anxiolytics



Short course of anxiolytics m ay benefit patients with definable tem porary stressors.

Medication (Drugs) 

ED treatm ent: o

Benzodiazepine if sym ptom s persist to break the cycle of anxiety and hyperventilation

o

Lorazepam : 1â€“2 m g PO or IV

Pa ge 2 5 1

o 

Valium : 2â€“5 m g PO or IV

Outpatient treatm ent: o

Buspirone: 5 m g PO t.i.d.

o

Valium : 2â€“5 m g PO or IV

Follow-Up Disposition Admission Criteria Hyperventilation syndrom e does not require adm ission.

Discharge Criteria 

Exclusion or successful treatm ent of prim ary pathologic or physiologic causes of hyperventilation



No acute psychiatric issues



Adequate follow-up with a prim ary care physician

References 1. Saisch S, Wessely S, William N. Patients with Acute Hyperventilation Presenting to an Innerâ€“City Em ergency Departm ent. Chest. 1996;110(4):952â€“957. 2. Gardner W. The pathophysiology of hyperventilation disorders. Chest. 1996;109:516â€“534. 3. Block M, Szidon P. Hyperventilation syndrom es. Com pr Ther. 1994;20:306â€“311. 4. Hanashiro PK. Hyperventilation: benign sym ptom or harbinger of catastrophe? Postgrad Med. 1990;88:191â€“193. 5. Gardner WN, Bass C. Hyperventilation in clinical practice. Br J Hosp Med. 1989;41:73â€“81. 6. Callaham M. Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients. Ann Em erg Med. 1989;18:622â€“628.

Pa ge 2 5 1

Codes ICD9-CM 306.1

ICD10 R06.4

Pa ge 2 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypervisco sity Syndro m e

Hyperviscosity

Syndrome Matthew B. Mostofi

Basics Description 

Clinical consequences of increased blood viscosity



Viscosity is the resistance a m aterial has to change in form .



The higher the blood viscosity, the m ore internal resistance to blood flows.



Increased cardiac output is required to provide adequate perfusion of hyper viscous blood.



Oxygen delivery is im paired as transit through the m icrocirculatory system slows.

Etiology 

The m ost com m on cause (85â€“90%) of hyperviscosity is increased concentration of gam m a globulins: o

Monoclonal gam m opathies: in m alignant diseases like Waldenstrom m acroglobulinem ia and m ultiple m yelom a

o

Polyclonal gam m opathies: usually rheum atic diseases (very rare)

Pa ge 2 5 2



Increased num bers of red blood cells, as in polycythem ia vera



Increased concentration (>100,000) of WBC, as in acute and chronic leukem ia

Diagnosis Signs and Symptoms 





Classic triad: o

Mucosal bleeding

o

Visual disturbances

o

Neurological

Hem atological: o

Bleeding is the m ost com m on m anifestation.

o

Epistaxis

o

Gingival, rectal, uterine bleeding

o

Prolonged postprocedural bleeding

o

Blood dyscrasias

o

Pruritus owing to red cell breakdown products

o

Splenic enlargem ent

Ocular: o

o

Change in visual acuity 

Blurring



Diplopia



Visual loss

Characteristic â€œlink-sausage effectâ€• on funduscopy

o

Alternating bulges and constrictions within the retinal veins

o

Retinal hem orrhage, detachm ent

o

Exudate, m icroaneurysm form ation

Pa ge 2 5 2

o 







Papilledem a

Renal: o

Nephritic or nephrotic syndrom e

o

Hem aturia

o

Sterile pyuria

Neurological: o

Headache

o

Ataxia

o

Mental status changes/com a

o

Dizziness/vertigo

o

Nystagm us

o

Tinnitus, hearing loss

o

Paresthesia, peripheral neuropathy

o

Seizure

Cardiovascular: o

Angina or m yocardial infarction

o

Dysrhythm ias

o

Congestive heart failure

Derm atologic: o

Raynaud phenom enon

o

Livedo reticularis

o

Palpable purpura

o

Eruptive spider nevuslike lesions

o

Digital infarcts

o

Peripheral gangrene

Essential Workup 

Evaluate end-organ ischem ia and bleeding.



Measure serum or whole blood viscosity.



Suspect diagnosis if the laboratory evaluation is ham pered by serum stasis and increased viscosity causing analyzer blockage

Pa ge 2 5 2

Tests Lab 

CBC with WBC differential: o

Anem ia or erythrocytosis can be seen in hyperviscosity syndrom e.

o

Anem ia usually norm ocytic and norm ochrom ic

o

Rouleaux of erythrocytes on the peripheral sm ear im portant diagnostic clue

o 

WBC for leukem ia

Electrolyte, blood urea nitrogen, creatinine, and glucose levels: o

Renal dysfunction is com m only noted in hyperviscosity syndrom e.

o

Hypercalcem ia and pseudohyponatrem ia in m ultiple m yelom a



Urinalysis: o

Proteinuria

o

Hem aturia

o

Sterile pyuria



Coagulation profile



Serum and urine protein electrophoresis



Measurem ent of serum viscosity (not routinely available in ED setting): o

Ostwald viscosim eter

o

Norm al range for the serum viscosity relative to water is 1.4â€“1.8.

o

Minim al viscosity at which sym ptom s develop is 4.0 centipoise (cp).



Elevated leukocyte alkaline phosphatase, lactate dehydrogenase, and serum vitam in B 1 2 levels

Differential Diagnosis

Pa ge 2 5 2

Bleeding and clotting disorders: 

Platelet disorders (qualitative and quantitative)



Hereditary factor deficiencies



Acquired disorders (vitam in K deficiency, liver disease)



Dissem inated intravascular coagulation

P.567

Treatment Pre Hospital IV fluid resuscitation with hem orrhage

Initial Stabilization 

Rehydrate with 0.9% norm al saline IV fluid.



Bleeding or end-organ ischem ia m ay not be controlled by any treatm ent except plasm apheresis.



In patients with anem ia and a leukem ic picture, avoid blood transfusion until pheresis is perform ed to avoid exacerbation of hyperviscosity syndrom e.

ED Treatment 

Plasm apheresis/leukapheresis: o

In stable patients: 40 m L/kg of body weight

o

In critical patients: 60 m L/kg of body weight

o

Side effects include hypocalcem ia with use of a citrate-containing anticoagulant and dysrhythm ia (rare).



Phlebotom y: o

Useful in acute severe cases if plasm apheresis not readily available

Pa ge 2 5 2

o

Blood (100â€“200 m L) can be withdrawn and replaced with isotonic saline.

Special Therapy Plasm apheresis: 

Many patients require m ore than one plasm apheresis.

Follow-Up Disposition Admission Criteria 

Evidence of end-organ ischem ia or hem orrhage



Intensive care unit adm ission for the following: o

Hem orrhage

o

Altered m ental status

o

Acute m yocardial infarction

Discharge Criteria Discharge after definitive treatm ent of the underlying disorder.

References 1. Forconi S, Pieragalli D, Guerrini M, et al. Prim ary and secondary blood hyperviscosity syndrom es and syndrom es associated with blood hyperviscosity. Drug. 1987;33(suppl 2):19â€“26. 2. Geraci JM, Hansen RM, Kueck BD. Plasm a cell leukem ia and hyperviscosity syndrom e. South Med J. 1990;83:800â€“805. 3. Gertz MA. Hyperviscosity Syndrom e. J Intensive Care Med. 1995;10:128â€“141. 4. Pim entel L. Medical com plications of oncologic disease. Em erg Med Clin North Am . 1993;22:407â€“419. 5. Som er T, Meiselm an HJ. Disorders of blood viscosity. Ann Med. 1993;25:31â€“39.

Pa ge 2 5 2

6. Stolz JF, Donner M, Larcan A. Introduction to hem orheology: theoretical aspects and hyperviscosity syndrom es. Int Angiol. 1987;6:119â€“132.

Codes ICD9-CM 273.3

ICD10 C88.0

Pa ge 2 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyphem a

Hyphema

Jamil D. Bayram Sami H. Uwaydat

Basics Description 

Blood in anterior cham ber (AC) of eye (between iris and cornea)



Hyphem a: grossly visible layering of blood



Microhyphem a: suspended RBCs visible by slit-lam p only

Genetics Genetic predisposition is related to hereditary blood dyscrasias (see below).

Etiology 

Blunt traum a: m ost com m on (70â€“80%).



Anteroposterior com pression of globe with sim ultaneous equatorial globe expansion causing rupture of iris strom al/ciliary body vessels



Penetrating traum a: direct injury to strom al vessels or sudden ocular decom pression



Spontaneous: less com m on, lower incidence of com plications: o

Tum ors:

Pa ge 2 5 2

o



Melanom a



Retinoblastom a



Xanthogranulom a



Metastatic tum ors

Blood dyscrasias: 

Hem ophilia



Leukem ia



Throm bocytopenia



Von Willebrand disease

o

Blood thinners: aspirin, Coum adin, heparin

o

Neovascularization of iris: in proliferative diabetic retinopathy, retinal vein occlusion, carotid stenosis

o

Postsurgical: cataract extraction, trabeculectom y, pars plana vitrectom y

Alert In children with no history of traum a, suspect child abuse.

Diagnosis Signs and Symptoms 

Photophobia



Blurring of vision



Decreased visual acuity



Ocular pain



Nausea/vom iting

History 

Previous visual acuity



Prior eye surgery



Prior glaucom a treatm ent



Past m edical history (blood disorders including sickle cell

Pa ge 2 5 2

disease) 

Mechanism of traum a



Exact tim e of injury and of visual loss



History of excessive tearing after injury

Alert History of excessive tearing m ay indicate open globe injury.

Physical Exam 

General physical exam with em phasis on associated bodily injuries



Periorbital ecchym osis



Eyelid lacerations



Enophthalm os (depression of the globe within the orbit)



Lim ited ocular m ovem ent with diplopia (m ay indicate orbital floor fracture)



Proptosis (m ay indicate retro-orbital hem orrhage)



Ocular exam o

Visual acuity

o

Rule out open globe (positive Seidel sign, corneal laceration, prolapse of intra-ocular structures)

o

Pupillary reaction to light (check for afferent pupillary defect prior to using dilating drops)

o

Tonom etry for intraocular pressure (IOP) m easurem ent

Alert 

Exclude globe perforation before m easuring intraocular pressure (IOP); low pressure can indicate globe perforation.



Slit-lam p exam ; look for layer of blood in AC: o

Four grades of hyphem a depending on percentage of anterior cham ber occlusion by blood: 

Grade I: less than one third

Pa ge 2 5 3



Grade II: one third to one half



Grade III: greater than one half



Grade IV: total (called 8-ball hyphem a; blood is dark and filling 100% of AC)

o

High-grade hyphem as are: 

More likely to rebleed (25% of grade I com pared with 67% of grade III)



More likely to develop glaucom a and corneal staining

 o

Less likely to recover visual acuity

Dilated fundus exam (avoid pressure on globe)

Tests Lab 

Laboratory tests should be individualized depending on case.



Platelet count, PT/PTT, bleeding tim e if bleeding disorder is suspected



BUN, creatinine, and pregnancy test if am inocaproic acid is to be used (see below)



Factor VIII assay if fam ily history of hem ophilia



Sickle cell screen especially in African Am ericans and Mediterranean descent

Imaging 

CT orbits (1-m m cuts) if open globe injury, intraocular foreign body, or orbital wall fracture are suspected



Ultrasound biom icroscopy (B scan) if total hyphem a and intraocular structures cannot be visualized

Alert Do not perform B scan if open globe injury is suspected (pressure applied during this procedure m ay cause extrusion of intraocular

Pa ge 2 5 3

contents).

Differential Diagnosis 

Uveitis



Endophthalm itis

Treatment Pre Hospital Place eye shield in case of corneal perforation.

Initial Stabilization 

Keep head upright to allow blood in AC to settle down.



Lim it activity, avoid bending, straining or exertion.



Place m etal or plastic shield over involved eye until integrity of globe is confirm ed.



Do not patch affected eye (if eye is patched, patient cannot notice sudden loss of vision).



Note that m etal and plastic shields have holes that let patient see through whereas patch com pletely blocks patient's vision.

ED Treatment 

Mild analgesics (avoid nonsteroidal anti-inflam m atory drugs [NSAIDs] because of antiplatelet effect)



Antiem etics (associated N/V m ay worsen hyphem a by increasing IOP)



Cycloplegics decrease pain from iritis: o

Atropine 1% eyedrops 2â€“3 tim es per day until hyphem a resolves



Topical steroids m ay decrease inflam m ation from iritis: o

Prednisolone acetate 1% eyedrops (or equivalent)

Pa ge 2 5 3

4â€“8 tim es per day until hyphem a resolves (usually 7â€“10 days) 

Am inocaproic acid (antifibrinolytic): o

Use in consultation with ophthalm ologist: 

Not com m only used because of frequent system ic side effects

o

Stabilizes fibrin clot in AC and decreases incidence of rebleed, but has no effect on final visual outcom e

o

50 m g/kg PO q4h for total of 5 days (do not exceed 30 g/d). Dose should be adjusted in renal failure.

o

May cause postural hypotension, nausea, vom iting, diarrhea

o

New topical form is not yet FDA approved.

o

Do not use in pregnant wom en or in patients prone to throm bosis. It can also cause acute renal failure in patients with hem ophilia.

P.569



Prednisone: o

o

Indications: 

Hem ophilia



Uncooperative children



Total hyphem a



History ofthrom botic disease

Dose: 0.6â€“0.75 m g/kg/24h in div. doses, up to 60 m g/d for 5 days



For increased IOP: o

For non-sickle cell patients, treat if IOP >30 m m Hg.

o

For sickle cell patients, treat if IOP >24 m m Hg.

o

Treat until IOP is controlled as indicated above.

o

Always start with one m edication. Add another if

Pa ge 2 5 3

unsuccessful in controlling pressure. 

B-blockersâ€”drug of choice: tim olol or levobunolol 0.5% b.i.d.



Alpha agonist: apraclonidine 0.5% or brim onidine 0.2% t.i.d.



Topical carbonic anhydrase inhibitors (CAI): dorzolam ide 2% or brinzolam ide 1% t.i.d.



Oral CAI: acetazolam ide 500 m g PO q12h (peds: 8â€“30 m g/kg/24h q6hâ€“q8h) or m ethazolam ide 50 m g q8h



Mannitol (1â€“2 m g/kg IV over 45 m inutes q24h) when all other eyedrops fail to lower IOP to acceptable level



Avoid CAI and m annitol in sickle cell patients, as they m ay cause acidosis and induce sickling.

o

Allow 25â€“30 m inutes for each eyedrop to work. If after using all the drops and m annitol, IOP is still high, then surgical evacuation of blood clot is warranted (AC tap or washout).



Drugs to avoid: o

Pilocarpine: constricts pupil and prevents visualization of lens and retina

o

Prostaglandin eyedrops (e.g., latanoprost): increase inflam m atory response

Follow-Up Disposition 

Discharge patient on atropine, prednisolone, and any appropriate IOP-lowering m edications.



Continue am inocaproic acid if decision was m ade to start it

Pa ge 2 5 3

in em ergency departm ent. 

Antiem etics if needed



Stool softeners to m inim ize straining during bowel m ovem ents



Arrange for follow-up with ophthalm ologist: o

Daily slit-lam p exam daily for 3 days after initial traum a, to m onitor for rebleeding, corneal staining, and increased IOP

o

Follow-up exam will determ ine length of treatm ent with atropine, prednisone acetate, and IOP-lowering eyedrops.



Note that hyphem a size is not criterion for discharge or adm ission; IOP control is m ost im portant.

Admission Criteria 

Medically uncontrolled IOP requiring surgical intervention



Ruptured globe



Noncom pliant patients



Associated ocular or orbital injuries



Children <7 years of age: o

Age group is usually at risk of am blyopia (also called lazy eye, which is irreversible visual loss secondary to visual deprivation in early childhood)



Patients at risk of com plications (sickle cell disease, hem ophilia)

Discharge Criteria 

Absence of any adm ission criteria with IOP <30 m m Hg for nonâ€“sickle patients and <24 m m Hg for patients with sickle cell disease/trait

Issues for Referral Below are patients who require im m ediate consultation with ophthalm ologist in em ergency departm ent. If this is not possible,

Pa ge 2 5 3

consultation should be arranged within 24 hours: 

Visual acuity worse than 20/200 at presentation



Sickle cell disease/trait with high IOP



Large hyphem a (filling greater than one third of AC)



Medically uncontrolled IOP

References 1. Berke S. Post-Traum atic Glaucom a. In: Yanoff M, Duker J, eds. Ophthalm ology. 2nd ed. St. Louis, MO: Mosby; 2004:1518â€“1521. 2. Crouch ER Jr, Crouch ER. Managem ent of traum atic hyphem a: therapeutic options. J Pediatr Ophthalm ol Strabism us. 1999;35(5):238â€“250. 3. Ham ill MB. Current concepts in the treatm ent of traum atic injury to the anterior segm ent. Ophthalm ol Clin North Am . 1999;12(3):457â€“464. 4. Hyphem a and m icrohyphem a. In: Rhee DJ, Pyfer MF, eds. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 1999:32â€“37. 5. Sankar PS, Chen TC, Grosskrentz CL. Traum atic hyphem a. Int Ophthalm ol Clin. 2002;42(3):57â€“68. 6. Walton W, Von Hagen S, Grigorian R. Managem ent of traum atic hyphem a. Survey Ophthalm ol. 2002;47(4):297â€“334.

Miscellaneous SEE ALSO: Endophthalm itis; Globe Rupture; Uveitis

Codes ICD9-CM 364.41

ICD10

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H21.0. Excludes traum atic hyphem a S05.1

Pa ge 2 5 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo calcem ia

Hypocalcemia

Michelle Canham

Basics Description 

Hypocalcem ia is defined as a total plasm a calcium level <8.7 m g/dL: o

Ionized calcium m ay be norm al and therefore have no clinical m anifestations occurring.



Norm al total serum calcium concentrations are 8.7â€“10.5 m g/dL: o

Under norm al conditions, the ionized calcium is approxim ately half of the total calcium level.

Etiology Incidence in the general population is 0.6%.

Mechanism 

From either increased loss of calcium from the circulation or decreased entry into the circulation



Intravascular calcium circulates in three form s: o

Bound to proteins (m ainly album in): 45â€“50%

o

Bound to com plexing ions (citrate, phosphate, carbonate): 5â€“10%

o

Ionized (free) calcium (physiologically active form ):

Pa ge 2 5 3

45â€“50% 

Serum levels of calcium are prim arily controlled by three horm ones: o

Parathyroid horm one (PTH): 

Decrease in calcium levels leads to an increase in PTH secretion (increasing bone resorption, renal absorption, intestinal absorption, and urinary phosphate excretion).

o

Vitam in D (1,25-dihydroxyvitam in D): 

Decrease in calcium level activates vitam in D (increasing bone resorption and intestinal absorption).

o

Calcitonin: 

Causes a direct inhibition of bone resorption with increased calcium levels



Hypoalbum inem ia is m ost com m on cause of hypocalcem ia: o

Each g/dL decrease in serum album in decreases protein-bound serum calcium by 0.8 m g/dL.

o

Will not change ionized (free) calcium

Pediatric Considerations 

Children have higher values of norm al calcium (9.2â€“11 m g/dL).



Neonatal hypocalcem ia: total serum calcium concentrations <7.0 m g/dL or serum -ionized calcium levels <4.4 m g/dL



Sym ptom s of hypocalcem ia in infancy: o

Hyperactivity, jitteriness

o

Tachypnea

o

Apneic spells with cyanosis

o

Vom iting

Pa ge 2 5 3

Diagnosis Signs and Symptoms 

Occur when ionized calcium <3.2 m g/dL



Depends on both the absolute and the rate of fall in calcium concentration

Neuromuscular 

Paresthesias



Hyperreflexia



Muscle spasm



Tetany: o

Neurom uscular irritability

o

Uncom m on unless ionized calcium <4.3 m g/dL



Latent tetany (Chvostek and Trousseau signs)



Laryngeal stridor



Seizures



Choreoathetosis

Cardiovascular 

Dysrhythm ias: o

Torsades de pointes

o

Heart block



Hypotension



Im paired contractility (congestive heart failure [CHF])



ECG changes: o

QT and ST prolongation

o

T-wave abnorm alities

Psychiatric 

Irritability/anxiety



Psychosis



Depression

Pa ge 2 5 4



Confusion



Delusions



Chorea



Parkinsonism s

Ocular 

Papilledem a



Cataracts



May occur in patients with acute onset hypocalcem ia

Essential Workup Serum -ionized calcium level confirm s the diagnosis

Tests Lab 

Arterial blood gas: o

Change from norm al pH of 0.1 units equals a reciprocal change in ionized calcium of approxim ately 1.7 m g/dL.



Serum album in



Electrolytes, BUN/creatinine, glucose



Magnesium



Phosphate: o

Increase in phosphate associated with hypoparathyroidism

o

Decrease in phosphate associated with vitam in D deficiency



PTH: o

Very high levels of PTH associated with pseudohypoparathyroidism

o

High levels of PTH associated with vitam in D deficiency

o

Low levels of PTH associated with

Pa ge 2 5 4

hypoparathyroidism 

Serum calcidiol or calcitriol

Imaging ECG: 

Prolonged QT interval



Heart block

Differential Diagnosis 

Im paired PTH action or secretion: o

Parathyroid or thyroid surgery or radical neck surgery and/or irradiation for head and neck cancer







o

Autoim m une disease (typically presents in childhood)

o

Congenital hypoparathyroidism

o

Neonatal secondary to m aternal hyperparathyroidism

o

Pseudohypoparathyroidism (resistance to PTH)

o

Infiltrative (am yloidosis, sarcoidosis)

Im paired vitam in D synthesis or action: o

Nutritional m alabsorption or poor intake

o

Renal or liver disease

o

Rickets disease

o

Pronounced hypophosphatem ia

Sepsis or severe burns: o

Im paired secretion of PTH and calcitriol

o

End organ resistance to the action of PTH

Calcium com plex form ation or sequestration: o

Hyperphosphatem ia

o

Ethylene glycol, ethylenediam inetetraacetic acid (EDTA), citrate (from transfusion)



o

Pancreatitis, rhabdom yolysis

o

Alkalosis (i.e., hyperventilation)

Hypom agnesem ia: o

Causes end organ PTH resistance

Pa ge 2 5 4



o

Decreased PTH secretion

o

Seen in chronic and/or critical illness

o

Must give m agnesium to correct hypocalcem ia

Medications: o

Mithram ycin, plicam ycin, phosphate, calcitonin, bisphosphonates





o

Phenobarbital, Dilantin

o

Cisplatin

o

Cadm ium , colchicine

o

Fluoride, citrate

Malignancies: o

Prostate cancer

o

Breast cancer

o

Lung cancer

o

Chondrosarcom a

â€œHungry bone syndrom eâ€•: o

After parathyroid rem oval

o

Rapid accretion of calcium as bone is rem ineralized

P.571

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

Establish intravenous catheter access.



Cardiac m onitor

ED Treatment Acute Management

Pa ge 2 5 4



Treat sym ptom atic hypocalcem ia as a m edical em ergency with parenteral calcium adm inistration.



Calcium IV bolus: o

Adm inister 100â€“300 m g of elem ental calcium over 10â€“20 m inutes (adult): 

10-m L am pule of 10% calcium chloride contain 272 m g of elem ental calcium .



10-m L am pule of 10% calcium gluconate contain 90 m g of elem ental calcium (less likely to induce tissue necrosis).

o

o

Faster IV rates: 

Can cause cardiac dysrhythm ias



Calcium salts are irritating to veins.

Intram uscular calcium gluceptate or calcium gluconate if IV access not available

o

Bolus doses increase ionized calcium for only 1â€“2 hoursâ€”m ust be followed by an infusion.



Calcium infusion: o

Calcium infusion rate: 0.5â€“1.5 m g/kg/h

o

Do not m ix calcium with bicarbonate or phosphate: 

o

Adm inister cautiously in patients taking digitalis: 



Precipitation of salts m ay form .

May initiate and exacerbate digitalis toxicity

Response to therapy: o

Individual responses vary.

o

Monitor calcium concentrations q1hâ€“q4h during therapy.

o

Titrate treatm ent to sym ptom s or ECG changes.

o

Consider hypom agnesem ia if the patient fails to respond to calcium therapy: 

Correct hypom agnesem ia with m agnesium 2 g intravenous piggyback (IVPB) 10% solution over

Pa ge 2 5 4

10 m inutes. o

In setting of acidosis, correct calcium first; alkalosis will further reduce ionized calcium .

o

Side effects of IV calcium : 

Nausea, vom iting



Hypotension



Dysrhythm ias

Chronic Management 

Oral calcium supplem entation



1â€“4 g/d of elem ental calcium in div. doses



Vitam in D: o

Enhances intestinal absorption

o

Initiate with calcium supplem entationâ€”alone not sufficient to restore calcium levels.

o

o 

Dose: 

200 IU for ages 19â€“50 years



400 IU for ages 51â€“70 years



600â€“800 for ages >70 years

Multivitam in contains 400 IU of vitam in D.

Vitam in D preparations: o

Ergocalciferol: 125 Âµg/d

o

Dihydrotachysterol: 100â€“400 Âµg/d

o

Calcifediol: 50â€“200 Âµg/d

o

Calcitriol 0.25â€“0.2 Âµg/d: 

Rapid onset (preferred)



Most active m etabolite of vitam in D

Pregnancy Considerations Calcitriol requirem ents m ay double or triple toward the end of pregnancy.

Pa ge 2 5 4

Medication (Drugs) 

IV Calcium : o

Calcium chloride: 1 g in 10 m L (1 g = 360 m g [13.6 m Eq] elem ental calcium )

o

Calcium gluceptate (IV/IM): 1 g in 5 m L (1 g = 90 m g [4.5 m Eq] elem ental calcium )

o

Calcium gluconate: 1 g in 10 m L (1 g = 90 m g [4.5 m Eq] elem ental calcium )



Oral calcium : o

Calcium carbonate: 350- to 1,500-m g tablets(1 g = 400 m g)

o

Calcium citrate: 950-m g tablets (1 g = 211 m g elem ental calcium )

o

Calcium glubionate: 18 g/5 m L of syrup (1 g = 65 m g elem ental calcium )

o

Calcium gluconate: 500- to 1,000-m g tablets (1 g = 90 m g elem ental calcium )

o

Calcium lactate: 350- to 1,000-m g tablets (1 g = 130 m g elem ental calcium )

Pediatric Considerations 

Initial calcium bolus with 10% calcium gluconate should be 9â€“18 m g of elem ental calcium /kg or 1â€“2 m L/kg not to exceed 5 m L in prem ature infants or 10 m L in term infants.



Calcitriol dose in children ranges from 0.1â€“3 Âµg/d.

Miscellaneous Calcium content of com m on foods: 

Milk or yogurt, 8 oz = 300 m g



Cheddar cheese, 1 oz = 200 m g

Pa ge 2 5 4



Calcium -fortified cereal, 1 cup = 300 m g



Calcium -fortified orange juice, 1 cup = 270 m g



Shrim p, 3 oz = 50 m g



Peanuts = 130 m g



Orange = 50 m g

Follow-Up Disposition Admission Criteria 

Sym ptom atic or severe ionized hypocalcem ia (<3.2 m g/dL)



Continuous IV calcium preparations necessary to m aintain calcium levels

Discharge Criteria 

Asym ptom atic hypocalcem ia



Ionized calcium >3.2 m g/dL in healthy patients with no coâ€“m orbid illness

References 1. Horak HA, Poum and R. Endocrine m yopathies. Neurol Clin. 2000;18(1):203â€“213. 2. Kapoor M, Chan Z. Fluid and electrolyte abnorm alities. Crit Care Clin. 2001;17(3):503â€“529. 3. Riggs JE. Neurologic m anifestations of electrolyte disturbances. Neurol Clin. 2002;20(1):227â€“239, vii. 4. Thom as MK, Dem ay MB. Vitam in D deficiency and disorders of vitam in D m etabolism . Endocrinol Metab Clin North Am . 2000;29(3):611â€“627, viii.

Codes

Pa ge 2 5 4

ICD9-CM 275.4

ICD10 E83.5

Pa ge 2 5 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo G lycem ia

HypoGlycemia

Matthew N. Graber

Basics Description 

Deficiency in counterregulatory horm ones (glucagon, epinephrine, cortisol, growth horm one) or excessive insulin response



Serum glucose <50 m g/dL

Genetics 

Congenital m etabolic and endocrine disorders that decrease gluconeogenic ability (e.g., hereditary fructose intolerance)



Congenital hyperinsulinism



Neonatal diabetes m ellitus (often a m utation effecting an ATP-dependent potassium channel)

Etiology 

Increased insulin levels: o

Overdose of oral hypoglycem ic agent or insulin

o

Oral antihyperglycem ics (i.e., Î±-glucosidase inhibitors, biguanides, and thiazolidinediones) do not cause hypoglycem ia alone, but m ay enhance the risk when used with insulin or sulfonylureas.

Pa ge 2 5 4

o

Sepsis

o

Insulinom a

o

Autoim m une hypoglycem ia

o

Alim entary hyperinsulinism

o

Renal failure (partially responsible for insulin m etabolism )

o

Liver cirrhosis (responsible for significant insulin m etabolism )



Underproduction of glucose: o

Alcohol (inhibitory effect on glycogen storage and gluconeogenesis)

o

Drugs

o

Salicylates

o

Beta-blockers (including eyedrops)

o

Selective serotonin reuptake inhibitors (SSRIs)

o

Som e antibiotics (e.g., sulfonylureas, pentam idine)

o

Adrenal insufficiency

o

Liver disease

o

Malnutrition

o

Dehydration



Cerebral edem a



Extrem es of age



Congestive heart failure



Renal failure



Counterregulatory horm one deficiency



Hypothyroidism or hyperthyroidism

Pregnancy Considerations 

Third-trim ester pregnant patients risk relative substrate deficiencyâ€“induced hypoglycem ia.



The fetus is less likely to becom e hypoglycem ic during m other's hypoglycem ic episode secondary to active glucose transport across placenta

Pa ge 2 5 5

o

Oral hypoglycem ic use in pregnancy m ay lead to profound and prolonged neonatal hypoglycem ia.

Diagnosis Signs and Symptoms 

Adrenergic: caused by excessive counterregulatory horm ones (i.e., epinephrine):







o

Diaphoresis

o

Anxiety

o

Tachycardia

o

Hunger

Neuroglycopenic: o

Dizziness

o

Confusion

Hyperactive or psychotic behavior: o

Slurred speech

o

Cranial nerve palsies

o

Seizures

o

Hem iplegia

o

Decerebrate posturing

Neonatal presentation: o

Asym ptom atic

o

Lim p

o

Bradycardia

o

Irritable

o

Trem ulous

o

Seizures

Alert Patients with hypoglycem ia unawareness m ay present with few if any

Pa ge 2 5 5

of the above signs and sym ptom s and instead m ay present with only late findings such as seizure, focal neurologic findings, altered m ental status, and com a.

Essential Workup 

Diagnosis requires: o

Dem onstration of neuroglycopenic signs and sym ptom s as defined above

o

Lab evidence of hypoglycem ia (Accu-Chek/Dextrostix)



Clearing of sym ptom s following glucose adm inistration

Tests Lab 

Blood glucose (initial and posttreatm ent)



Electrolytes, BUN, creatinine: o

Order if m ental status does not im prove post-glucose adm inistration or sepsis considered.



CBC



Urinalysis

Imaging Chest radiograph for: 

Possible aspiration



Pneum onia as source of sepsis

Diagnostic Procedures/Surgery ECG if suspect MI/ischem ia owing to hypoglycem ia or as cause of hypoglycem ia

Differential Diagnosis 

Neurologic: o

Cerebral vascular accident/transient ischem ic attack (CVA/TIA)

o

Seizure disorder

Pa ge 2 5 5



Drug or alcohol intoxication



Psychosis or depression

Pediatric Considerations 

Salicylate ingestion



Reye syndrom e



Growth horm one deficiency



Ketotic hypoglycem ia



Inborn errors of m etabolism

Treatment Pre Hospital 

Diagnosis with finger stick glucose (Accu-Chek)



Oral glucoseâ€“containing fluids or IV dextrose for hypoglycem ia



Adm inister thiam ine along with dextrose IV to prevent precipitation of Wernicke encephalopathy.

Initial Stabilization 

Glucose: o

Dextrose IV push (IVP)

o

Oral glucose in awake patient (with no IV) without risk of aspiration

o 

Glucagon IM if unable to establish IV access

Airway, breathing, and circulation m anagem ent (ABCs) with aspiration and seizure precautions

P.573

ED Treatment

Pa ge 2 5 5



Adm inister D 5 0 W 50 m L for decreased level of consciousness: o

Second or third am pule m ay be necessary

o

Com plications include volum e overload and hypokalem ia.



Initiate continuous IV infusion of 5â€“20% glucose solution for persistent m ild hypoglycem ia or if patient cannot eat.



Adm inister glucagon: o

If hypoglycem ia refractory to glucose

o

If IV access delayed

o

Ineffective in alcohol-induced hypoglycem ia and significant liver disease

o

May repeat twice q20â€“30m in

o

Adm inister hydrocortisone with glucagon for adrenal insufficiency.

o 



Effective in 10â€“20 m inutes

Adm inister octreotide: o

If hypoglycem ia refractory to glucose adm inistration

o

If hypoglycem ia secondary to sulfonylureas

Monitor blood glucose q2hâ€“q3h and prior to discharge.

Medication (Drugs) 

D 5 0 W: 1 am p (25 g) of 50% dextrose 1â€“2 m L/kg (child: 2 m L/kg D 2 5 W; infants: 5 m L/kg D 1 0 W) IVP



Glucagon: 0.5â€“2 m g IV/IM/SC: o

Child: 0.03â€“0.1 m g/kg IV/IM/SC

o

Infant: 0.3 m g/kg IV/IM/SC; m ay repeat in 4 hours



Hydrocortisone: 100 m g (peds: 1â€“2 m g/kg) IV



Oral glucose: 20 g orally equals approxim ately 12-oz nondiet fruit juice, 14-oz nondiet cola, 2.5-oz chocolate



Octreotide: 50 Âµg q12h SC/IV

Pa ge 2 5 5

Follow-Up Disposition Admission Criteria 

Overdoses of oral hypoglycem ic agent (i.e., sulfonylureas) or long-acting insulin m andate observation for at least 24 hours.



Failure of neuroglycopenic sym ptom s to im prove with glucose adm inistration suggests neurologic injury, pre-existing neurologic condition, or another cause for these sym ptom s.



Recurrent hypoglycem ic state in ED



Patients unable to tolerate oral fluids or food



Suicidal intentions



Older patients m ay require several days for com plete recovery from severe or prolonged hypoglycem ia.

Discharge Criteria 

Discharge m ild unintentional insulin overusage or failure to take oral calories if blood glucose norm al, sym ptom s resolved, tolerating oral intake, and can be observed.



Fam ilies of patient with recurrent hypoglycem ia should be instructed in IM glucagon adm inistration.

Issues for Referral Refer to prim ary physician for consideration of m edication or diet changes if recurrent hypoglycem ic episodes.

References 1. Com i RJ. Approach to acute hypoglycem ia. Endocrinol Metab Clin North Am . 1993;22(2):247â€“262.

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2. Service FJ. Hypoglycem ia. Med Clin North Am . 1995;79(1):16. 3. Service FJ. Medical progress: hypoglycem ic disorders. N Engl J Med. 1995;332:1144â€“1152. 4. Stanley CA, Baker L. The causes of neonatal hypoglycem ia. N Engl J Med. 1999;340:1200â€“1201.

Codes ICD9-CM 250.82 Diabetes with other specified m anifestations 251 Other disorders of pancreatic internal secretion 251.2 Hypoglycem ia, unspecified 775.6 Neonatal hypoglycem ia 962.3 Poisoning by insulin and antidiabetic agents

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo glycem ic Po iso ning

Hypoglycemic

Poisoning Mark B. Mycyk

Basics Description 

Oral or parenteral agents that m ay cause hypoglycem ia or other m etabolic im balances



Hypoglycem ic poisoning m ay be intentional or unintentional (accidental).

Etiology 

Insulin: o

Enhances glucose uptake into cells

o

Lim its glucose availability to the brain (m ost sensitive to hypoglycem ia)

o 

Influences potassium redistribution

Sulfonylurea agents: o

Enhance insulin release from Î² cells, reduce hepatic glucose production, and increase peripheral insulin sensitivity

o

Hypoglycem ic effect enhanced by polypharm acy, alcohol use, hepatic dysfunction, and renal insufficiency

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

Biguanide agents (m etform in): o

Antihyperglycem ic agents

o

Decrease elevated serum glucose concentrations, but generally do not cause hypoglycem ia on their own

o

In the presence of insulin, biguanides do the following: 

Increase glucose uptake into cells



Lim it glucose availability to the brain (m ost sensitive to hypoglycem ia)



Influence potassium redistribution



Decrease gastrointestinal glucose absorption



Decrease hepatic gluconeogenesis



Metabolize glucose to lactate in intestinal cells, which m ay accum ulate and lead to lactic acidosis



Thiazolidinediones: o

In the presence of insulin, thiazolidinediones increase glucose uptake and use and decrease gluconeogenesis



Î±-Glucosidase inhibitors: o

Lower system ic glucose by decreasing gastrointestinal absorption of carbohydrates

Diagnosis Signs and Symptoms 

Insulin or sulfonylureas: o

Overdose causes hypoglycem ia.

o

Sym ptom s m ost often occur when glucose <40â€“60 m g/dL (m ay occur at higher levels in diabetics).

o

Sym ptom s blunted by Î²-antagonists.

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o

Facial flushing, diaphoresis, pallor, piloerection

o

Hunger, nausea, abdom inal cram ping

o

Labored respirations, apnea

o

Headache, blurred vision

o

Paresthesias, weakness, incoordination, trem or

o

Anxiety, irritability, bizarre behavior, confusion, stupor, com a, seizures



o

Palpitations, tachycardia, bradycardia (late)

o

Hypertension

o

Hypotherm ia

Biguanides: o

Toxicity prim arily owing to lactic acid accum ulation

o

Nausea, vom iting, abdom inal pain

o

Agitation, confusion, lethargy, com a

o

Kussm aul respirations

o

Hypotension, tachycardia

Pediatric Considerations 

Neonatal hypoglycem ia m ay occur after m aternal use of sulfonylureas during labor.



Ingestion of one sulfonylurea tablet m ay cause hypoglycem ia in a child.



Onset of sym ptom atic hypoglycem ia m ay be delayed up to 8 hours.

Essential Workup 

Diagnosis based on clinical presentation and an accurate history



Monitor serum glucose concentration.



Monitor vital signs and neurologic status.



Obtain serum electrolytes and lactate for biguanide ingestion.



Obtain liver function tests for thiazolidinedione ingestion.

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Tests Lab 

Serum glucose before and after treatm ent



Electrolytes:



o

Check for hypokalem ia

o

Anion gap acidosis

BUN, creatinine: o

May reveal renal insufficiency, causing drug accum ulation



CBC



Ethanol level



Lactate level



Liver function tests



Arterial blood gas



Assays for im m unoreactive insulin and C-peptide levels: o

Confirm surreptitious self-adm inistration of exogenous insulin if insulin level is high and C-peptide is low in the setting of hypoglycem ia

o

Do not correlate with severity of clinical sym ptom s

Imaging 

ECG: sinus tachycardia, prem ature ventricular contractions (PVCs), atrial dysrhythm ias



EEG: diffuse slowing without focal abnorm alities



CT scan: cerebral edem a if prolonged hypoglycem ia



Chest radiograph: aspiration pneum onia or pulm onary edem a

Differential Diagnosis 

Addison disease



Panhypopituitarism



Sepsis

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

Insulinom a



Neuroendocrine tum ors



Cirrhosis



Chronic ethanol abuse



Ethanol ingestion



Salicylate ingestion



Î²-antagonist ingestion



Ackee fruit poisoning

P.575

Treatment Pre Hospital Transport all pills/pill bottles involved in overdose for identification in ED.

Initial Stabilization 



Airway, breathing, and circulation m anagem ent (ABCs): o

Airway control essential

o

Adm inister supplem ental oxygen.

o

IV access

o

Cardiac m onitor and pulse oxim etry

Naloxone, thiam ine, D 5 0 (or Accu-Chek) if altered m ental status

ED Treatment 

Hypoglycem ia: o

D 5 0 bolus, then 

IV infusion D 5 W or D 1 0 W to m aintain euglycem ia or m ild hyperglycem ia

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 

Food

Neuroglycopenia: o

May persist shortly after serum glucose corrected

o

Persistent sym ptom s require further dextrose adm inistration.



Decontam ination: o

Adm inister activated charcoal for recent or large ingestion of oral agent (sulfonylurea or biguanide).



Supportive care



Hypotension: o

0.9% norm al saline (NS) IV fluid bolus

o

Trendelenburg position

o

Dopam ine titrated to pressure

o

Pressors m ay increase lactate production; use cautiously with biguanide-induced lactic acidosis.



Adm inister sodium bicarbonate for biguanide-induced lactic acidosis if pH <7.0.



Adm inister benzodiazepines for seizures.



Inhibit insulin secretion for sulfonylurea overdose with recurrent hypoglycem ia with:



o

Octreotide

o

Diazoxide (watch for hypotension)

Early hem odialysis m ay be beneficial in cases of biguanide-induced lactic acidosis: o

Corrects acid/base abnorm alities

o

Enhances elim ination of the drug

Medication (Drugs) 

Activated charcoal: 1 m g/kg PO



Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 2 5 over 1 m inute) IV; repeat if necessary

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

Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV q10â€“15m in



Diazoxide: 200 m g PO or 1â€“3 m g/kg IV (infant: 8â€“15 m g/kg/24h q8hâ€“q12h PO/IV; child: 3â€“8 m g/kg/24h q8h PO/IV)



Glucagon: 1â€“2 m g (peds: 0.03â€“0.1 m g/kg) IM/SC/IV



Lorazepam : 2â€“4 m g (peds: 0.03â€“0.05 m g/kg) IV q10â€“15m in



Octreotide: 50â€“100 Âµg q8hâ€“q12h SC/IV



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Hypoglycem ia owing to sulfonylurea agents (m ay require several days of m onitoring) or long-acting insulin preparations



Intentional overdose or self-injection of insulin warrants adm ission for 24 hoursâ€™ glucose m onitoring.



All children with accidental ingestion of sulfonylureas



Metabolic alterations owing to biguanide ingestion or accum ulation

Discharge Criteria 

Accidental hypoglycem ia owing to short-acting insulin injection in the setting of dietary insufficiency



Discharge after glucose correction and a 4-hour period of observation.

Issues for Referral 

Patients with unintentional (accidental) poisoning require

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poison prevention counseling. 

Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.

References 1. Green RS, Palatnick W. Effectiveness of octreotide in a case of refractory sulfonylurea-induced hypoglycem ia. J Em erg Med. 2003;25(3):283â€“287. 2. Kruse JA. Metform in-associated lactic acidosis. J Em erg Med. 2001;20(3):267â€“272. 3. McLaughlin SA, Crandall CS, McKinney PE. Octreotide: an antidote for sulfonylurea-induced hypoglycem ia. Ann Em erg Med. 2000;36(2):133â€“138. 4. Spiller HA. Managem ent of antidiabetic m edications in overdose. Drug Safety. 1998;19(5):411â€“424. 5. Wolf LR, Sm eeks F, Policastro M. Oral hypoglycem ic agents. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:423â€“432.

Codes ICD9-CM 977.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo kalem ia

Hypokalemia

David N. Zull

Basics Description 



Defined as a serum potassium level <3.5 m Eq/L: o

Mild to m oderate 2.5â€“3.5 m Eq/L

o

Moderate to severe <2.5 m Eq/L

Frequency: o

Up to 20% of inpatients have docum ented hypokalem ia (5% have levels <3.0 m Eq/L).

o

Up to 14% of outpatients are m ildly hypokalem ic (m ost are related to diuretics or GI loss).

o 

5% of geriatric patients have K <3.0 m Eq/L.

Potassium is the m ajor intracellular cation: o

Gradient is m aintained by Na-K ATPase activity (enhanced by insulin and Î²-agonists) and m ineralocorticoids.



Total potassium stores in a 70-kg person are approxim ately 3,500 m Eq.



Electrophysiologic effects of hypokalem ia: o

Increase in the norm al intracellular to extracellular potassium gradient: 

Alters the depolarization threshold for m uscles

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and nerves  o

Inhibits the term ination of action potentials

Alterations in intracellular potassium directly affect cellular function.

Etiology 

Renal losses: o

Diuretics (thiazides, loop diuretics, carbonic anhydrase inhibitors), usually associated with loss of other cations (Mg 2 + , Ca 2 + , P 3 + , Na + )

o

Renal tubular dam age

o

Prim ary renal tubular disorders (RTA type I and II)

o

Interstitial nephritis, analgesic nephropathy, drug toxicity (am photericin, gentam icin, toluene), m yelom a kidney

o

Hyperaldosteronism : 

Prim ary (prim ary hyperaldosteronism , Cushing, pituitary tum or-producing ACTH, congenital adrenal hyperplasia)



Secondary (volum e depletion, congestive heart failure [CHF], cirrhosis, nephrotic)





Exogenous (licorice ingestion, steroids)

o

Hypom agnesem ia

o

Osm otic diuresis (m annitol, hyperglycem ia)

Congenital disorders: o

Bartter and Gitelm an syndrom esâ€”hypokalem ic m etabolic alkalosis and low blood pressure: 

Liddle syndrom e is the sam e but with hypertension.



Delivery of negatively charged ions to the collecting duct (bicarbonate, som e penicillins)



GI losses: o

Diarrhea:

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

Proportional to volum e and duration

o

Villous adenom as (K losses are m ore severe)

o

Laxative abuse

o

Vom iting and nasogastric suction result in volum e depletion and m etabolic alkalosis, which increases renal losses of potassium from bicarbonaturia and hyperaldosteronism .

o

Ureterosigm oidostom y

o

Intestinal fistulae, ileostom y

o

Cystic fibrosis



Intracellular shift of potassium



Alkalosis



Insulin



Adrenergic excess: o

Severe stress (traum a, m yocardial infarction, sepsis)

o

Treatm ent of asthm a (frequent Î²-agonists and theophylline toxicity)

o 

Cocaine, am phetam ines

Hypokalem ic periodic paralysis: o

Fam ilial

o

Thyrotoxic

o

Refeeding in prolonged starvation

o

B 1 2 adm inistration in severely deficient patient

o

Barium poisoning



Poor Intake (rare as a sole cause)



Nutritional (poverty, pica, dem entia)



Eating disorders



Dental problem s/oral lesions



Esophageal disease

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Diagnosis Signs and Symptoms History 

Neurom uscular: o

Severe weakness (K <2.5 m Eq/L)

o

May progress to paralysis if K <2.0 m Eq/L and rapid developm ent

o

Muscle cram ps

o

Muscle tenderness

o

Paresthesias

o

Generalized fatigue and m alaise



Constipation/Ileus



Cardiovascular: o

Ventricular and atrial dysrhythm ias (especially if underlying heart disease)



o

Potentiation of digoxin toxicity

o

Cardiac arrest

Polyuria (hypokalem ic nephropathy): o

Diabetes control worsened by hypokalem ia (inhibiting insulin release)

Physical Exam 

Hypertensionâ€”diuretic treatm ent, renal artery stenosis, prim ary hyperaldosteronism , licorice, congenital adrenal hyperplasia, Liddle syndrom e



Hypotensionâ€”GI losses, overdiuresis, Bartter and Gitelm an syndrom es



Neurom uscularâ€”m uscle weakness, decreased reflexes, m uscle tenderness if rhabdom yolysis

Tests Lab

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

Electrolytes, BUN, creatinine, glucose: o

High HCO 3 suggests diuretic abuse, vom iting, m ineralocorticoid excess, Bartter, Gitelm an.

o 

Low HCO 3 suggests renal tubular disease.

Urine K (spot sam ple): o

Less than 20 m Eq/L suggests GI loss, potassium shift into cells, poor intake.

o

More than 40 m Eq/L suggests renal loss.

o

Twenty to 40 m Eq/Lâ€”calculate transtubular potassium gradient (TTPG) = (urine K Ã— serum osm )/(serum K Ã— urine osm ): >7 suggests renal loss; <3 GI loss, poor intake; 3â€“7, m ixed



Urine Na: o

< 20 m Eq/L with elevated urine K suggests secondary hyperaldosteronism .



Plasm a renin if hypertensive: o

High renin: secondary hyperaldosteronism , renal artery stenosis

o

Low renin: prim ary hyperaldosteronism

Imaging ECG findings: 

Low-voltage T waves



Sagging of the ST segm ents



U waves: o

In severe hypokalem ia, the T disappears and the U wave predom inates, giving the illusion of dram atic QT prolongation.



Dim inutive P waves (som etim es m isread as a nodal rhythm )



Atrial (prem ature atrial contractions [PACs], atrial fibrillation [A fib]) and ventricular dysrhythm ias (prem ature ventricular contractions [PVCs], ventricular

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tachycardia [VT], torsade), o

Especially in patients with underlying cardiom yopathy or digoxin toxic

Differential Diagnosis 

Intrinsic cardiac disease with dysrhythm ias



Causes of m uscular weakness: o

Neurom uscular junction disease (m yasthenia gravis, organophosphate poisoning, botulism )



Spinal cord disease



Polyneuropathies



Prim ary acute m yopathies



Cataplexy

P.577

Treatment Initial Stabilization 

Volum e resuscitation



Airway, breathing, and circulation m anagem ent (ABCs)

ED Treatment 

Total body deficit is 200â€“300 m Eq per 1 m Eq/L decrem ent in serum potassium level.



Rate of replacem ent and route dependent on presence of sym ptom s, severity of hypokalem ia, and com orbidities



Com plete replacem ent over several days



Oral potassium preferable to IV therapy whenever possible

Oral Potassium

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

Potassium chloride: o

Preferred replacem ent in alm ost all cases

o

Liquid (or powder dissolved in water or juice) is m ore bioavailable, but nausea m ay occur.

o

10â€“40 m Eq per dose

o

Rapid rise in K, but will drop after 4 hours from transcellular shift

o

Tablets (wax m atrix and m icroencapsulated) are m ore palatable, m ore sustained effect, but slowly absorbed and have potential for sm all bowel ulceration.



Potassium gluconate or citrate: o

Use in acidotic patients.

o

Ineffective if accom panying m etabolic alkalosis unless saline given concom itantly

o

Gradual oral repletion effective

o

Greater than 120 m Eq over 24 hours is not well tolerated.

Intravenous Potassium 

Recom m ended if neurom uscular sym ptom s, cardiac arrhythm ias, ongoing GI losses, or severe hypokalem ia



Potassium chloride is the preferred replacem ent: o

Potassium phosphate is used only if accom panying severe hypophosphatem ia.



Adm inistration: o

A potassium rider at 10 m Eq/h piggybacked into m aintenance 0.9 norm al saline (NS) is safest and best tolerated (peds: 0.1â€“0.2 m Eq/kg/h)

o

15â€“20 m Eq/h are feasible by peripheral vein but not recom m ended: 

Higher rates of infusion are associated with pain and phlebitis.

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o

If K is added to m aintenance fluids, the concentration should not be >40 m Eq/L.

o

If sustained life-threatening dysrhythm ias, up to 40 m Eq/h by central line or two peripheral lines can be considered.

o

Frequent m onitoring of serum potassium is critical when large am ounts of K are used.



Hypokalem ic periodic paralysis and other situations in which there is significant transcellular K shifts (adrenergic excess): o

Sm all am ounts of K are effective (20 m Eq IV).

o

More zealous adm inistration m ay lead to rebound hyperkalem ia.

Electrolyte Corrections 

Magnesium : o

Consider if hypokalem ia is resistant to K replacem ent.

o 

Slow IV infusion of 2 g

Chloride: o

Hypokalem ia with alkalosis is resistant to replacem ent unless volum e depletion and hypochlorem ia is corrected by saline adm inistration.

Follow-Up Disposition Admission Criteria 

Need of IV potassium repletion



Cardiac dysrhythm ias



Profound m uscle weakness

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

Ongoing K losses



Serum potassium <2.5 m Eq/L



Associated with significant hypotension or severe hypertension



Significant com orbidities or geriatric

Discharge Criteria 

Asym ptom atic



Able to replete deficiency with oral potassium



Early follow-up available and reliable patient

Issues for Referral Nephrology referral or consult if suspicion of renal wasting

References 1. Lederer E, Erbeck K, Ouseph R. Hypokalem ia. Available at http://www.em edicine.com , Medicine, 2004. 2. Lin SH, Chiu JS, Hsu CW, et al. A sim ple and rapid approach to hypokalem ic paralysis. Am J Em erg Med. 2003;21:487â€“491. 3. Rastegar A, Soleim ani M. Hypokalem ia and hyperkalem ia. Postgrad Med J. 2001;77:759â€“764. 4. Riggs J. Neurologic m anifestations of neurologic disease: neurologic m anifestations of electrolyte disturbances. Neurol Clin. 2002;20:1â€“10. 5. Weiss-Guillet EM, Takala J, Jakob SM. Diagnosis and m anagem ent of electrolyte em ergencies. Best Pract Res Clin Endocrinol Metab. 2003;17:623â€“651.

Codes ICD9-CM 276.8

ICD10 E87.6

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo natrem ia

Hyponatremia

Linda Mueller

Basics Description 

Sodium <130 m Eq/L



Most com m on electrolyte disturbance (1â€“4% of hospitalized patients)

Etiology Pseudohyponatremia 

Low-m easured serum sodium but norm al m easured serum osm olarity



Occurs secondary to the displacem ent of sodium to aqueous phase of serum



Seen with elevated lipids or proteins



Disease exam ples include: o

Multiple m yelom a

o

Hyperlipidem ia

Hyponatremia with Normal Osmolarity and Fluid Overload 

Inappropriate retention of water



Disease exam ples include:

Pa ge 2 5 7

o

Congestive heart failure

o

Cirrhosis

o

Renal failure

o

Nephrotic syndrom e

Hyponatremia with Normal Osmolarity and Euvolemia 

Patients tend to have increased total body water without m arked edem a



Purest form of dilutional hyponatrem ia



Disease exam ples include: o

o

Endocrine abnorm alities: 

Hypothyroid



Stress



Sydrom e of inappropriate ADH (SIADH)

Diseases that cause SIADH: 

Pulm onary disease (tuberculosis, Legionella, Aspergillosis, chronic obstructive pulm onary disease)

o



CNS disorders (bleeding, m alignancy, traum a)



Cancer (sm all cell lung, pancreas, duodenum )



HIV infection

Water intoxication (3â€“7% of institutionalized psychotic patients), can also occur in m arathon runners

o

Mineralocorticoid abnorm alities

o

Postoperative hyponatrem ia (particularly after transurethral prostatectom y)

Hyponatremia with Normal Osmolarity and Hypovolemia 

Deficits in total body water and total body sodium

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

Sodium deficits exceed water deficits



Possible etiologies include: o

Gastrointestinal losses

o

Sweating

o

Burns

o

Cystic fibrosis

o

Salt-wasting nephropathies

o

Diuretics

Drug-induced 

Drugs m ay stim ulate antidiuretic horm one (ADH) and cause hyponatrem ia:



o

Clofibrate

o

Cyclophospham ide

o

Carbam azepine

o

Vincristine, vinblastine

o

Oxytocin

o

Brom ocriptine

o

Barbiturates

o

Opiates

Drugs m ay increase sensitivity to ADH and cause hyponatrem ia:



o

Chlorpropam ide

o

NSAIDs

Drugs m ay stim ulate thirst and cause hyponatrem ia: o

Thiothixene

o

Am itriptyline

o

Fluphenazine

o

Ecstasy

o

Fluoxetine

o

Sertraline

o

Haloperidol

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Hyponatremia with Hyperosmolarity 

Due to excessive osm otically active substances



Possible etiologies include: o

Elevated glucose (m ost com m on cause of hyponatrem ia)

o

Corrected Na + = 0.016 Ã— (m easured glucose â€“ to 100) + m easured sodium

o

Mannitol infusion

o

Maltose and glycine

Pediatric Considerations 

More prone to water intoxication



High incidence of iatrogenic hyponatrem ia

Diagnosis Signs and Symptoms Mild: Na + >120 mEq/L 

Headache



Nausea



Vom iting



Weakness



Anorexia



Muscle cram ps



Rhabdom yolysis

Moderate: Na + between 110 and 120 mEq/L 

Im paired response to verbal stim uli



Decreased response to painful stim uli



Visual/Auditory hallucinations



Bizarre behavior

Pa ge 2 5 7



Incontinence



Hyperventilation



Gait disturbance

Severe: Na + <110 mEq/L 

Signs of herniation: o

Decorticate/Decerebrate posturing



Bradycardia



Hypertension



Altered tem perature regulation



Dilated pupils



Seizure activity



Respiratory arrest



Com a/Unresponsive

Chronic May be asym ptom atic

Essential Workup 

Serum sodium level: o

Recheck sodium to verify.



Review patient m edication list.



Obtain good m edical history for possible etiologies.

Tests Lab 

Electrolytes, blood urea nitrogen (BUN)/creatinine



Glucose: o

Correct sodium value accordingly if severe hyperglycem ia.



Calculate osm olality: o

Plasm a osm olality = [2 Ã— NA(m Eq L) + Glucose/18 + BUN/2.8]



Urine sodium

Pa ge 2 5 7

Differential Diagnosis Pseudohyponatrem ia due to: 

Hyperglycem ia



Hyperlipidem ia



Hyperproteinem ia

P.579

Treatment Initial Stabilization 

ABCs



Initiate IV fluid with 0.9% NS.



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) for altered m ental status

ED Treatment Depends on severity and chronicity of hyponatrem ia and underlying etiology

Acute Hyponatremia with Severe CNS Symptoms 

Goal: o

Raise serum sodium by 10 m Eq/L or to level >120â€“125 m Eq/L over 6 hours with adm inistration of hypertonic saline



Calculate sodium deficit: o



Na + deficit = 0.6 (weight in kg)(140 â€“ Na + )

250 m L of 3% or 5% saline solution in adult over 4â€“6 hours will raise serum sodium by 10â€“15 m Eq/L

Pa ge 2 5 7

o 

OR m ay dose 1â€“2 m L/kg/h of 3% saline solution

Sodium contents: o

1 L 0.9% NS = 154 m Eq of sodium

o

1 L 3% saline = 513 m Eq of sodium

Hypovolemic Hyponatremia 

Correct underlying cause.



Replete volum e with 0.9% NS IV.



Prim ary goals to restore: o

Extracellular fluid

o

Cardiac output

o

Organ perfusion

Hypervolemic/Euvolemic Hyponatremia 

Water restriction to less than 1 L per day with high dietary salt intake



For faster correction of sodium : o

Adm inister IV 0.9% NS with loop diuretic (furosem ide).



Maxim um rate of correction = 0.5 m Eq/L/h

Medication (Drugs) 

Furosem ide: 20â€“40 m g IV push



Sodium replacem ent: o

Calculate Na + deficit

o

Replace no m ore than half of requirem ent over 8â€“12 hours

Follow-Up Disposition

Pa ge 2 5 8

Admission Criteria 

Sym ptom atic hyponatrem ia



Sodium <120 m Eq/L



Asym ptom atic, m ild hyponatrem ia (Na + 120â€“127 m Eq/L), with com orbid factors

Discharge Criteria 

Sodium greater than 130 m Eq/L and asym ptom atic



Known chronic history of hyponatrem ia with no acute changes



Asym ptom atic, m ild hyponatrem ia (Na + 120â€“129 m Eq/L) with no com orbid factors; however, m ust have close outpatient follow-up

References 1. Fall PJ. Hyponatrem ia and hypernatrem ia: a system atic approach to causes and their correction. Postgrad Med. 2000;107(5):75â€“82. 2. Fried LF, Palevsky PM. Hyponatrem ia and hypernatrem ia. Med Clin North Am . 1997;81(3):585â€“609. 3. Kum ar S, Berl T. Sodium . Lancet. 1998;352:220â€“228. 4. Lin M, Liu S, Lim I. Disorders of water im balance. Em erg Med Clin North Am . 2005;23(3):749â€“770, ix. 5. Mulloy AL, Caruana RJ. Hyponatrem ic em ergencies. Med Clin North Am . 1995;79:155â€“167. 6. Oh M. Pathogenesis and diagnosis of hyponatrem ia. Nephron. 2002;(Suppl 1):2â€“8. 7. Palm er B, Gates J, Lader M. Causes and m anagem ent of hyponatrem ia. Ann Pham acother. 2003;37:1644â€“1702

Codes ICD9-CM 276.1

Pa ge 2 5 8

ICD10 E87.1

Pa ge 2 5 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo parathyro idism

Hypoparathyroidism Hugh Schuckman

Basics Description 

Hypoparathyroidism is owing to a deficiency in parathyroid horm one (PTH).



Pseudohypoparathyroidism is owing to end organ unresponsiveness to PTH.



Parathyroid horm one (PTH): o

Decreases urinary Ca 2 + loss

o

Increases urinary PO 4 loss

o

Stim ulates vitam in D conversion from 25(OH)-D to 1,25(OH) 2 -D in kidney

o 

Liberates Ca 2 + and PO 4 from bone

Calcitonin: o

Prom otes deposition of Ca 2 + and PO 4 into bone (produced prim arily in C cells in thyroid)





Magnesium : o

Cofactor in production of PTH

o

Essential for action of PTH in target tissues

Hypoparathyroidism : o

Prim ary failure of the parathyroid gland (m ay have

Pa ge 2 5 8

associated Addison disease) 

Pseudohypoparathyroidism : o

Tissue unresponsiveness with elevated PTH levels

o

Associated with hypothyroidism and hypogonadism

Genetics 

Congenital absence



DiGeorge syndrom e:



o

Hypoparathyroidism

o

Thym ic dysplasia

o

Severe im m unodeficiency

Wilson disease: o





Destruction of gland owing to copper deposition

Autoim m une polyglandular syndrom e type I: o

Hypoparathyroidism

o

Adrenal insufficiency

o

Mucocutaneous candidiasis

Albright syndrom e (hereditary osteodystrophy): o

Short stature

o

Obesity

o

Round face

o

Short neck

o

Short 4th and 5th m etacarpals and m etatarsals (type I pseudohypoparathyroidism )

Etiology 

Failure of parathyroid gland: o

Autoim m une destruction

o

Surgical interruption of blood supply or gland rem oval



o

Radiation dam age

o

Hypom agnesem ia as PTH cofactor

End organ unresponsiveness to PTH

Pa ge 2 5 8

Diagnosis Alert The m ost com m on sym ptom atic presentation is postop for parathyroidectom y.

Pediatric Considerations 

Neonates/infants: o

Transient hypoparathyroidism in first year of life

o

Subnorm al intelligence proportional to duration of hypocalcem ia

o

Dental hypoplasia

Signs and Symptoms Physical Exam 

Related to severity, rapidity of onset, and duration of hypocalcem ia





General: o

Weakness

o

Malaise

Neurom uscular: o

Paresthesias (especially circum oral and extrem ities)

o

Carpal pedal spasm

o

Latent spasm elicited by: 

Chvostek sign (twitching of circum oral m uscles after tapping facial nerve in front of the tragus)



Trousseau sign (spasm after inflating blood pressure cuff 20 m m above patient's systolic blood pressure [BP] for 3 m inutes)

o

Laryngospasm /bronchospasm

o

Blepharospasm

Pa ge 2 5 8

o

Muscle cram ps

o

Tetany

o

Seizures (presenting sym ptom of one third with hypoparathyroidism )

o

Increased intracranial pressure (ICP) with papilledem a

o

Parkinson syndrom e and other extrapyram idal disorders

o 

Myelopathy

Cardiovascular: o

Prolonged QT interval (owing to ST segm ent prolongation)







o

Heart block

o

Congestive heart failure (CHF)

o

Ventricular fibrillation (VFib)

o

Vasoconstriction

Psychiatric: o

Im paired m em ory

o

Confusion

o

Hallucinations

o

Dem entia

Derm atologic: o

Brittle hair and nails

o

Psoriasis

Hyperpigm entation: o

Lenticular cataracts

Essential Workup 

If no hypocalcem ic sym ptom s with hypocalcem ia, check album in level: o

If still low after correcting for hypoalbum inem ia, check ionized Ca 2 + .



If hypocalcem ic sym ptom s with norm al total Ca 2 + , check

Pa ge 2 5 8

pH for alkalosis: o

If not alkalotic, check ionized Ca 2 + (active form ).

o

Metabolic or respiratory alkalosis increases the binding to album in reducing the ionized Ca 2 + .



If hypocalcem ic sym ptom s with low ionized Ca 2 + , check a PTH level: o

Low in prim ary hypoparathyroidism and in vitam in D deficiency

o

Elevated in pseudohypoparathyroidism and hypocalcem ia from renal failure

Tests Lab 

Calcium : Correct for album in using form ula: o

Corrected Ca 2 + (m g/dL) = m easured Ca 2 + (m g/dL) + 0.8[4.0 - album in (g/dL)]



Ionized Ca 2 + if sym ptom atic with low total calcium



Electrolytes, BUN, creatinine, glucose



Magnesium



Arterial blood gas (ABG) if sym ptom atic with norm al total Ca 2 + : o

Elevation of 0.1 pH unit decreases the ionized Ca 2 + by 3â€“8%.



Phosphorus: o

Elevated except when hypocalcem ia caused by vitam in D deficiency

o

Metastatic calcification can cause hypocalcem ia by tissue deposition when the calcium /phosphorus product is >60.

Imaging Tooth roots m ay be absent.

Pa ge 2 5 8

Diagnostic Procedures/Surgery ECG: 

Prolonged QT interval: o

Owing to ST-segm ent prolongation from hypocalcem ia

Differential Diagnosis 

Must differentiate from variety of causes of hypocalcem ia



Lab artifact: o

Low total calcium that is norm al when corrected for album in level with no sym ptom s of hypocalcem ia



Alkalosis: o

Sym ptom atic hypocalcem ia with a norm al total calcium



Hypom agnesem ia (needed for PTH secretion)



PTH resistance (congenital)



PTH suppression by ethanol, chem otherapeutics, or cim etidine P.581



Vitam in D deficiency (low Ca 2 + + low PO 4 ): o

Anticonvulsant use (decreased vitam in D absorption)

o

Liver disease

o

Resistance to vitam in D

o

Malabsorption or dietary deficiency



Gram -negative sepsis



Renal failure or nephrotic syndrom e



Chelation: o

Pancreatitis (fatty acids chelate calcium )

o

Am m onium bifluoride (tire cleaner spray)

o

Hydrofluoric acid

Pa ge 2 5 8

o

Citrated blood

o

Acute hyperphosphatem ia: 

Fleet enem as



Rhabdom yolysis



Acute renal failure

Treatment Pre Hospital 

Adm inister calcium in refractory VFib or status epilepticus in addition to usual m edications if known hypoparathyroidism or suspected hypocalcem ia.



Stridor m ay herald laryngospasm .

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o



Manage airway if laryngospasm .

Adm inister IV calcium bolus (chloride or gluconate) if unstable cardiac rhythm or tetany: o

Slow infusion m uch safer unless patient m arkedly sym ptom atic



Prepare for ventricular dysrhythm ias including ventricular fibrillation.



Seizure precautions

ED Treatment 

Calcium replacem ent: o

Ten percent calcium chloride (27.2 m g elem ental Ca 2+

/m L) 

For life-threatening conditions: 1 am p (10 m L) over 3â€“5 m in IV or 10%

o

Calcium gluconate (9 m g elem ental Ca 2 + /m L)

Pa ge 2 5 8



For life-threatening conditions: 1â€“3 am p (10 m L/am p) over 5â€“10 m in/am p

o

For non-life-threatening conditions, adm inister calcium via slow infusion of 500â€“1,000 m g elem ental Ca 2 + over 6â€“24 hours (peds: 100 m g elem ental Ca 2 + /kg/24h)

o

Continuous cardiac m onitoring

o

Stop infusion if bradycardia develops.

o

Perform frequent checks of serum Ca 2 + levels.

o

Calcium adm inistration m ay precipitate digitalis toxicity.

o

Supplem ent to lowest possible Ca 2 + level keeping the patient asym ptom atic, then switch to oral replacem ent. 

Soft tissue calcification m ay occur with calcium /phosphorus product of 60 (Ca Ã— PO 4 ).



Replace m agnesium if low.



Bind phosphorus: o

Alum inum hydroxideâ€“containing antacids (Maalox, Mylanta, or Gelusil) if creatinine <2

o

Calcium acetate (Phos-lo) or calcium carbonate when concurrent renal failure if creatinine >2



Vitam in D supplem entation



Avoid carbonated beverages (high in phosphorus).



Assess for associated endocrinopathies.

Medication (Drugs) 

Calcium acetate (Phos-lo 167 m g elem ental Ca): 1 or 2 tabs with m eals



Calcium carbonate 500 m g (elem ental Ca): 1 or 2 tabs q.i.d. (2â€“4 g/d) (peds: 45â€“65 m g/kg/d)

Pa ge 2 5 9



Calcium chloride 10% (27.2 m g elem ental Ca 2 + /m L): one am p over 3â€“5 m in IV if life-threatening condition; otherwise, slow infusion



Calcium gluconate 10% (9 m g elem ental Ca 2 + /m L): 1â€“3 am p over 5â€“10 m in per am p if life-threatening condition; otherwise, slow infusion



Magnesium oxide 400 m g: 1 or 2 tabs daily



Magnesium sulfate: 2 g IV (peds: 25â€“50 m g/kg up to 2 g) over 2 hoursâ€”if severe, 6 g over 6 hours



Vitam in D: 400 IU/d

Follow-Up Disposition Admission Criteria 

Sym ptom atic hypocalcem ia



Abnorm al ECG



Inability to take vitam in D or calcium orally



Corrected calcium <5 m g/dL

Discharge Criteria 

Asym ptom atic hypocalcem ia



Not m eeting any adm ission criteria

Issues for Referral Any patient requiring therapy or needing follow-up laboratory studies

References 1. Goldm an L, Bennett JC, eds. Cecil's Textbook of Medicine. 22nd ed. Philadelphia: WB Saunders; 2000. 2. Greenspan FS, Gardner DG. Basic and Clinical Endocrinology. 7th ed. Lange Publishers; 2003.

Pa ge 2 5 9

3. Tintinalli JE, Kelen GD, Stapczynski JS. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004. 4. Wallach J, ed. Interpretation of Diagnostic Tests. 7th ed. Boston: Little, Brown and Com pany; 2000.

Codes ICD9-CM 252.1

ICD10 E20.9

Pa ge 2 5 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo therm ia

Hypothermia

Jordan Moskoff

Basics Description Body tem perature <35Â°C

Risk Factors Poor tem perature tegulation: 

Very young



Advanced age



Co-m orbid condition



Intoxication

Pathophysiology 



Loss of heat: o

Radiationâ€”m ost rapid, 50% of heat loss

o

Conduction

o

Convection

o

Evaporation

o

Respiration

Heat production: o

Shivering

o

Nonshivering therm ogenesis

o

Increased thyroxine

Pa ge 2 5 9

o

Increased epinephrine

Etiology 















Derm al disease: o

Burn

o

Exfoliative dem atitis

o

Severe psoriasis

Drug induced o

Ethanol

o

Phenothiazines

o

Sedative-hypnotics

Environm ental: o

Im m ersion

o

Nonim m ersion

Iatrogenic: o

Aggressive fluid replacem ent

o

Heat stroke treatm ent

Metabolic: o

Hypoadrenalism

o

Hypopituitarism

o

Hypothyroidism

Neurologic: o

Acute Spinal cord transection

o

Head traum a

o

Stroke

o

Tum or

o

Wernicke disease

Neurom uscular inefficiency: o

Age extrem e

o

Im paired shivering

o

Lack of acclim atization

Sepsis

Pa ge 2 5 9

Pediatric Considerations Infants have a large body surface to m ass ratio.

Diagnosis Signs and Symptoms 

Mild 35â€“32.2Â°C (95â€“90Â°F): o

o

Initial excitation phase to com bat cold: 

Hypertension



Shivering



Tachycardia



Early tachycardia followed by bradycardia



Tachypnea



Vasoconstriction

Over tim e with onset of fatigue: 

Apathy



Ataxia



Cold diuresis



Defect in distal tubular reabsorption of sodium and water

 

Im paired judgm ent

Moderate 32.2â€“28Â°C (90â€“82.4Â°F): o

Atrial dysrhythm ias

o

Bradycardia: 

Decreased spontaneous depolarization of pacem aker cells



Refractory to atropine

o

Decreased level of consciousness

o

Decreased respiratory rate: 

Progressive respiratory depression with CO 2

Pa ge 2 5 9

retention



o

Dilated pupils

o

Dim inished gag reflex

o

Extinction of shivering

o

Hyporeflexia

o

Hypotension

o

J-wave (Osborn wave) on ECG

Severe <28Â°C (82.4Â°F): o

Apnea

o

Com a

o

Decreased or no activity on EEG (electroencephalography)

o

Nonreactive pupils

o

Oliguria: 

Renal blood flow depressed 50%

o

Pulm onary edem a

o

Ventricular dysrhythm ias/asystole: 

Cardiac cycle lengthens, resulting in increased intervals

Essential Workup 

Accurate core tem perature confirm s diagnosis.



Low-reading therm om eter

Tests Lab 

Arterial blood gas (ABG): o



Tem perature correction not needed

CBC: o

Hem atocrit rises owing to decreased plasm a volum e.

o

Leukopenia does not im ply absence of infection: 

High-risk groups, e.g., neonate, im m unocom prom ised should receive em piric

Pa ge 2 5 9

antibiotics. 

Electrolytes, BUN, creatinine: o

Vary during rewarm ing; recheck frequentlyâ€”especially creatine phosphokinase (CPK) and potassium (K + )



PT, PTT, and platelets: o



Prolonged clotting tim es, throm bocytopenia com m on

Toxicology screen: o

Alcohol/drug ingestion com m on

Imaging 

Chest radiograph: o



Pneum onia com m on com plication

ECG: o

Tachycardia to bradycardia

o

Atrial fibrillation with slow response

o

Ventricular fibrillation

o

Asystole

o

Prolonged PR, QRS, QT intervals

o

J Osborn Waves

o

ST elevation m im icking acute coronary syndrom e

Differential Diagnosis 

Environm ental



Sepsis



Prim ary CNS disorder

Treatment Pre Hospital 

Controversies: o

Cardiopulm onary resuscitation (CPR) not

Pa ge 2 5 9

recom m ended if: 

Electrical rhythm present without palpable pulse or blood pressure with short transport tim e



Cautions: o

Prolonged palpation/auscultation for cardiac activityâ€”30â€“45 seconds

o

Apparent cardiovascular collapse m ay be depressed cardiac output, often sufficient to m eet m etabolic dem ands.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Supplem ental oxygen

o

Oral and nasotracheal intubation are safe.

o

Place nasogastric (NG) tube postintubation.

o

Cardiac m onitor

o

Warm ed D5.9 norm al saline (NS) preferred over lactated Ringer: 



Shivering depletes glycogen.

Rem ove wet clothing and begin passive external rewarm ing.



Adm inister Narcan, D 5 0 W (or Accu-Chek), and thiam ine to a patient with altered m ental status.



Stress dose steroids (Solucortef 100 m g IV) for known adrenal insufficiency or treatm ent failure



Obtain accurate core tem peratures using rectal therm om eter.

P.583

ED Treatment Cardiac Arrest Resuscitation

Pa ge 2 5 9



Most dysrhythm ias correct with rewarm ing alone.



Ventricular fibrillation induction occurs with rough handling, chest com pressions, hypoxia, and acid-base changes.



CPR is less effective owing to decreased chest wall elasticity.



Defibrillation is rarely successful at tem peratures <28â€“30Â°C o

Defibrillate one to three tim es and then again post rewarm ing.

o

Once >30Â°C, if ventricular fibrillation persists use am iodarone.

o

Direct current results in m yocardial dam age.

Dysrhythmia Management 



Atrial fibrillation: o

Com m on <32Â°C

o

Usually converts spontaneously

Malignant ventricular dysrhythm ias: o

Am iodarone drug of choice

o

Avoid lidocaine and procainam ideâ€”m ay increase ventricular fibrillation.

Rewarming Techniques 

Faster rewarm ing rates (1â€“2Â°C/h) generally have better prognosis than slower rewarm ing rates (<0.5Â°C/h).



Active rewarm ing is necessary at core tem perature of <32Â°C: o

Internal therm ogenesis insufficient to increase body tem perature

o

Shivering extinguished

Passive External Rewarming

Pa ge 2 5 9



Ideal technique for m ost healthy patients with m ild hypotherm ia



Must have intact therm oregulatory m echanism s, norm al endocrine function, and adequate energy stores



Cover the patient with dry insulating m aterial.



Endogenous therm ogenesis m ust generate an acceptable rate of rewarm ing.



Disadvantageâ€”core rises very slowly.

Active External Rewarming 

Delivers heat directly to the skin



Safe in previously healthy young acutely hypotherm ic victim s



Requires intact circulation to rem ove peripherally rewarm ed blood to core



Associated with core tem perature after drop



Rewarm ing shockâ€”venous pooling in warm ed extrem ities secondary to vasodilatation



Cover trunk preferentially



Bair Hugger device provides forced warm airâ€”prevents shock or after drop.

Active Core Rewarming Techniques 

Airway rewarm ing (com plete hum idification at 40â€“45Â°C): o





Adm inister to all patients.

Heated IV (40â€“42Â°C) D5.9NS: o

Adm inister to all patients.

o

High flow rates m ust be m aintained.

o

Use blood warm er or calibrated m icrowave.

Heated gastric irrigation via nasogastric or orogastric tubes: o

Not recom m ended

Pa ge 2 6 0



o

Low am ount of surface area

o

Aspiration risk if airway not secured

Pleural irrigation (0.9 NS at 30â€“42Â°C): o

Use in severe hypotherm ia without cardiac activity.

o

1 or 2 chest tubesâ€”m idaxillary and m idclavicular bilaterally

o

Contraindicated in patients with cardiac rhythm because the chest tube m ay induce ventricular fibrillation



Heated peritoneal lavage (0.9 NS at 40â€“45Â°C): o

Use in unstable hypotherm ic patients or stable patients with severe hypotherm ia whose rewarm ing rates are <1Â°C/h.

o

1 or 2 catheters

o

Advantageous in patients with overdose or rhabdom yolysis

Extracorporeal Rewarming 

Most effective rewarm ing m ethod



Hem odialysis: o

Initiate for patients with drug overdoses or severe electrolyte disturbances.



Continuous arteriovenous rewarm ing: o

Blood pressure m ust be >60 m m Hg.

o

Blood circulated through warm er from percutaneously inserted fem oral arterial and contralateral venous catheters



Extracorporeal venovenous rewarm ing: o

Blood is rem oved via central venous catheter, heated to 40Â°C, and returned via second central or large peripheral venous catheter.



Cardiopulm onary bypass: o

Treatm ent of choice in severe hypotherm ia with

Pa ge 2 6 0

cardiac arrest o

Com plications include: 

Hem olysis



Arterial injury



Air em bolism



Those associated with system ic heparinization

Additional Therapy 

Methylprednisolone or hydrocortisone for suspicion of adrenocortical insufficiency or steroid dependence



Em piric treatm ent with levothyroxine only for m yxedem atous patients

Medication (Drugs) 

Am iodarone: 300 m g IV push (IVP) for ventricular fibrillation followed by 1 m g/kg infusion



Dextrose: D 5 0 W one am pâ€”50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Hydrocortisone: 250 m g IVP



Levothyroxine: 50â€“500 Âµg IV over several m inutes



Methylprednisolone: 30 m g/kg IVP



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Moderate to severe hypotherm ia (<32Â°C)

Pa ge 2 6 0



Young, healthy patients with no co-m orbid illness who have m ild accidental hypotherm ia (>32Â°C) that responds well to warm ing: o

Adm it to an observation area.

o

Discharge if asym ptom atic after 8â€“12 hours and they rem ain asym ptom atic.

Discharge Criteria 

Young, healthy patients with no co-m orbid illness



Very m ild accidental hypotherm ia (>35Â°C) that responds well to warm ing



Safe, warm environm ent to go to after discharge

References 1. Cheng D. The EKG of hypotherm ia. J Em erg Med. 2002;22(1):87â€“91. 2. Daniel F, Danzl DF. Accidental hypotherm ia. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1979â€“1996. 3. Hanania NA, Zim m erm an JL. Accidental hypotherm ia. Crit Care Clin. 1999;15(2):235â€“249. 4. Mccullough L. Diagnosis and treatm ent of hypotherm ia. Am Fam Physician. 2004;70:2325â€“2332.

Codes ICD9-CM 991.6

ICD10 T68

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypo thyro idism

Hypothyroidism

Rita Cydulka Jessica R. Goldstein

Basics Description 

Decreased levels of effective circulating thyroid horm one and sensitivity to catecholam ines lead to decreased m etabolic rate, com pensatory vasoconstriction, reduced blood volum e, heart rate, and cardiac output.



Myxedem a com a is a rare extrem e form of hypothyroidism characterized by altered m ental status and defective therm oregulation triggered by a precipitating event or illness.



Results from a deficiency of thyroid horm one



Prim arily owing to thyroid disease caused by: o

Autoim m une process, e.g., Hashim oto thyroiditis, postpartum thyroiditis

o

Iatrogenic failure, e.g., radiation, thyroidectom y, drugs



Pituitary disease or secondary failure accounts for less than 4% of cases.



Usually follows an indolent course with decom pensation after specific stress factors

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

Myxedem a com a caused by further stress on patient with hypothyroidism , which results in failure of com pensatory m echanism s. Stressors include: o

Hypoxia

o

Hypotherm ia

o

Hypotension

o

Hypoglycem ia

o

Hyponatrem ia

o

Adrenal insufficiency

o

Sedative hypnotic drugs

Etiology 

Prim ary: o

Congenital

o

Autoim m une: 

Thyroiditis



Hashim oto disease

o

Idiopathic

o

Iatrogenic:

o



Postsurgical



External radiation



Radioiodine therapy



Antithyroid drugs (iodides, lithium )

Inherited defect: 

Aplasia



Hypoplasia



Enzym atic defect



Treatm ent of m aternal hyperthyroidism

o

Ingestion of drugs or goitrogens during pregnancy

o

Neoplasm : prim ary (carcinom a) or secondary (infiltration)

o

Infection: viral (rarely aerobic or anaerobic bacteria)

o

Traum a: neck injury

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

Secondary: o

Pituitary tum or

o

Infiltrative disease (sarcoid) or tum or

o

Traum a

Diagnosis Signs and Symptoms History 

Weakness/fatigue/drowsiness



Cold intolerance



Headaches



Myalgias



Menorrhagia



Constipation



Weight gain



Em otional lability



Mental status changes

Physical Exam 

Puffy eyelids



Sparse pubic, axillary hair



Absent lateral one-third eyebrows



Prolonged relaxation phase deep tendon reflexes (DTRs)



Yellow tinged/dry skin



Pallor



Goiter



Myxedem aâ€”dry, waxy swelling of skin/subcutaneous tissues



Swelling of hands/feet



Huskiness of voice

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

Galactorrhea

Myxedema Coma 

Extrem e form of hypothyroidism (see above) triggered by stress or illness



Hypotherm ia



Bradycardia



Hypotension



Altered m ental status

Geriatric Considerations Suspect m yxedem a com a in decom pensated elderly wom en with history of chronic or untreated hypothyroidism .

Pregnancy Considerations 

Postpartum thyroiditis occurs in up to 5% of wom en.



Usually occurs 3â€“6 m onths postpartum



Com plain of depression, weakness, fatigue

Pediatric Considerations 

Neonatal Graves disease occurs in about 10% of wom en with Graves during pregnancy regardless of treatm ent.



Thyroid-stim ulating horm one (TSH) antibodies and propylthiouracil (PTU) cross placenta.



PTU excreted in sm all quantities in breast m ilk

Essential Workup Laboratory confirm ation of the diagnosis of hypothyroidism /m yxedem a com a is usually not possible in the ED.

Tests Search for the underlying cause of m yxedem a com a.

Lab 

Thyroid function studies: o

Free T 4 (low)

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o

High-sensitivity TSH (increased)

o

If free T 4 unavailableâ€”total T 4 (decreased) and resin T 3 uptake (increased)



CBC: o





Anem ia

Electrolytes, BUN, creatinine, glucose: o

Hyponatrem ia

o

Hypoglycem ia

AST, lactate dehydrogenase (LDH), creatine phosphokinase (CPK)



Arterial blood gases: o

Hypoxem ia/hypercapnia

o

Acidosis

Imaging ECG: 

Profound bradycardia

Differential Diagnosis 

Nephrotic syndrom e



Chronic nephritis



Hypoalbum inem ia



Chronic renal disease



Sepsis



Depression



Congestive heart failure (CHF)

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Intubation and ventilation m ay be necessary.

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

Cardiac m onitor



Blood pressure support



Supplem ental oxygen to m eet m etabolic needs



Correct hypotherm ia: o

Initiate passive warm ing m easures.

o

Aggressive rewarm ing m ay precipitate hypotension from vasodilation.

P.585

ED Treatment Mild hypothyroidism â€”refer for oral thyroid replacem ent as an outpatient.

Myxedema Coma 

Life-threatening condition



Initiate thyroid horm one replacem ent therapy if a high index of suspicion: o

Prom pt IV replacem ent im proves survival.

o

L-thyroxine (LT 4 ) or liothyronine (LT 3 ): 

Som e experts advocate LT 4 over LT 3

o

Reassess 4 hours after initial dose.

o

Use sm aller doses of thyroid horm one in the elderly or patients with cardiac disease.



Hydrocortisone to prevent Addisonian crisis



Dextrose for hypoglycem ia



IV fluid bolus for hypotension: o

Avoid pressors, if possible, as they m ay precipitate dysrhythm ias.

o

Response to pressors is poor until thyroid replacem ent initiated.

o

Thyroid horm one augm ents action of pressors.

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

Correct the underlying precipitant.

Medication (Drugs) 

Dextrose: 50â€“100 m L D 5 0 (peds: 2 m L/kg of D 1 0 over 1 m in) IV



Hydrocortisone: 100 m g (peds: 4 m g/kg) IV q6hâ€“q8h



L-thyroxine (LT 4 ): 300â€“600 Âµg load IV followed by 50â€“100 Âµg IV daily



Liothyronine (LT 3 ): 10â€“20 Âµg load IV followed by 10 Âµg IV q4h for 24h, then 10 ÂµgIV q6h for 24â€“48h.

Follow-Up Disposition Admission Criteria ICU adm ission for m yxedem a com a

Discharge Criteria Hypothyroid patients should be referred to a prim ary caretaker for initiation of oral thyroid horm one replacem ent therapy.

References 1. Fliers E, Wiersinga WM. Myxedem a com a. Rev Endocr Metab Disord. 2003;4:137â€“141. 2. Holm es L, Lakshm anan M. The patient with chronic endocrine disease. In: Herr RD, Cydulka RK, eds. Em ergency Care of the Com prom ised Patient. Philadelphia: Lippincottâ€“Raven Publishers; 1994:123â€“133. 3. Jordan RM. Myxedem a com a. Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am . 1995;79:185â€“194.

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4. Larson R, Davies TF, Hay ID. The thyroid. In: Wilson JD, ed. William sâ€™ Textbook of Endocrinology. 9th ed. Philadelphia, PA: WB Saunders; 2001:389â€“516. 5. Pim entel L, Hansen KN. Thyroid disease in the em ergency departm ent: a clinical and laboratory review. J Em erg Med. 2005;28(2):201â€“209. 6. Sarlis NJ, Gourgiotis L. Thyroid em ergencies. Rev Endocr Metab Disord. 2003;4(2):129â€“136. 7. Wogan JM. Endocrine disorders. In: Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO. Mosby; 2002.

Codes ICD9-CM 244.9

ICD10 E03.9

Pa ge 2 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Idio pathic Thro m bo cyto penic Purpura

Idiopathic

Thrombocytopenic Purpura Michael Schmidt Amer Aldeen

Basics Description 

Idiopathic throm bocytopenic purpura (ITP) is throm bocytopenia without apparent cause or abnorm alities in other cell lines.



Incidence is approxim ately 10/100,000 per yearâ€”m ay be an underestim ate owing to subclinical cases of throm bocytopenia.



Acute ITP: o

Half of cases involve children.

o

90% of children recover within 8 weeks with or without therapy.

o

Adult recovery is delayed and requires specific therapy to achieve rem ission.



Chronic ITP: o

Occurs m ostly in adults

o

Young wom en are m ost susceptible

o

Characterized by variable response to corticosteroids

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and other im m une suppressants

Genetics ITP appears to run in fam ilies, as do variations in response to corticosteroids for treatm ent.

Etiology 

Autoantibodies cause im m une-m ediated destruction of circulating platelets, prim arily in the spleen.



Som e patients do not possess autoantibodies, suggesting a role for T-cell-m ediated cytotoxicity.



Eradication of H. pylori can som etim es be associated with platelet recovery (unclear m echanism ).

Diagnosis Signs and Symptoms History 

Up to 28% of patients are asym ptom atic and diagnosed on routine CBC.



Bleeding is the m ost com m on com plaint: o

Com m on: 

Mucous m em brane: gingiva, epistaxis, conjunctival, m enorrhagia

o

Rare (m ore com m on in coagulopathies): 

GI bleeding, hem arthrosis, hem aturia, and hem atom as



84% of pediatric cases of ITP follow recovery from a viral illness.

Physical Exam 

Petechiae

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

Nonpalpable nature of purpura distinguishes ITP from Henoch-SchÃ¶nlein purpura (HSP).



Neurologic deficits from intracranial hem orrhage (ICH): o

ICH is the m ost com m on cause of death in ITP.

o

Risk of ICH in ITP increases with age: 

Age <40 years: 2%



Age >60 years: 48%

Essential Workup Diagnosis of exclusionâ€”other causes of throm bocytopenia m ust be ruled out.

Tests Lab 

CBC with differential and peripheral sm ear: o

Throm bocytopenia

o

Norm al platelet size

o

Norm al WBC and RBC m orphology and size



HIV testing



Electrolytes, BUN, creatinine: to evaluate kidney function for TTP/HUS (hem olytic urem ic syndrom e)

Imaging CT head to evaluate for ICH

Diagnostic Procedures/Surgery Bone m arrow biopsy: 

All adults >60 years



Atypical sym ptom s



Patients considering splenectom y



Children with persistent throm bocytopenia >6 m onths



Children unresponsive to intravenous im m unoglobulin (IVIG)



Children before steroids to evaluate for acute leukem ia

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Differential Diagnosis 







Im paired bone m arrow production: o

Bone m arrow fibrosis

o

Bone m arrow infiltration owing to m alignancy

o

Cytotoxic drugs used in chem otherapy

o

Congenital/acquired bone m arrow abnorm alities

Splenic sequestration: o

Portal hypertension

o

Neoplastic infiltration

o

Sickle cell disease

Accelerated destruction of platelets: o

Vasculitis

o

TTP/HUS

o

Dissem inated intravascular coagulation (DIC)

o

Cardiac valvular disease

Drug induced: o

o

Decreased platelet production: 

Chem otherapy



Thiazide diuretics



Ethanol



Estrogen

Increased destruction of platelets: 

Aspirin



Heparin



Chlorpropam ide



Chloroquine



Gold salts



Sulfonam ides



Insecticides

P.587

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Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Stabilize life-threatening bleeding: o

o

Intracranial hem orrhage: 

Airway control



Cautious hyperventilation or m annitol



Neurosurgery consultation

Hem orrhagic shock: 

Two large-bore IVs



Direct pressure for hem ostasis



Blood transfusions



Platelet transfusions: 2â€“3 tim es the norm al am ount

o



IV glucocorticoids



IVIG

Mucous m em brane bleeding: 

Apply topical collagen sponge.

ED Treatment 

Initial treatm ent options for ITP are based on: o

Degree of throm bocytopenia

o

Severity of illness

o

Duration of sym ptom s

o

Age

o

Risk factors for bleeding (hypertension, peptic ulcer disease, vigorous lifestyle)

o 

Hem atologist preference

Efficacy of treatm ent is dem onstrated in term s of platelet

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recovery tim e and not m orbidity or m ortality. 

Specific treatm ent options: o

Observation is recom m ended for children without bleeding com plications or profound throm bocytopenia (<20 K)

o

Profound throm bocytopenia (<20 K) 

High-dose corticosteroids: 75% response



IVIG: 80% response



Anti-D IG: 70% response (used only in Rh + patients)

o

Splenectom y: 

Second-line therapy if inadequate response to a course of glucocorticoid therapy



Two thirds of adult patients respond, three fourths of pediatric patients respond.



No specific indications for em ergent splenectom y

Pregnancy Considerations 

Differential diagnosis of throm bocytopenia during pregnancy: o

o

Gestational throm bocytopenia (75%): 

Usually of no clinical significance



Does not cause neonatal throm bocytopenia

HELLP syndrom e (hem olysis, elevated liver enzym es, and low platelets)

o

ITP (15%) 

Maternal platelet count does not correlate to neonatal throm bocytopenia.



Treatm ent with steroids or IVIG does not alter incidence of neonatal throm bocytopenia.



Degree of throm bocytopenia should not alter decision of vaginal birth versus C-section.

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

Measure neonatal CBC and check brain ultrasound for ICH.



Treat neonatal throm bocytopenia with IVIG and steroids.

Medication (Drugs) 

Anti-D IG: 50 Âµg/kg/24h IV



Collagen absorbable hem ostat sponges: Apply directly to bleeding surface with pressure 1â€²â€² Ã— 2â€²â€² and 3â€²â€² Ã— 4â€²â€² sponges.



Dexam ethasone: 40 m g PO daily



IVIG: 1â€“2 g/kg IV for 1 dose



Methylprednisolone: 1g IV q8h (peds: 30 m g/kg/24h)



Prednisone: 1 m g/kg/24h PO (peds: 2 m g/kg/24h)

Follow-Up Disposition Admission Criteria 

Life-threatening bleeding regardless of platelet count



Any bleeding with platelet count <20 K



Asym ptom atic patient with platelet count <20 K with issues of noncom pliance or poor follow-up

Discharge Criteria 

Asym ptom atic patients



Patients with m inor bleeding and platelets >30 K

Issues for Referral Hem atology referral is indicated in all cases (either outpatient or

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inpatient consultation).

References 1. Cines D, Blanchette V. Im m une throm bocytopenic purpura. N Engl J Med. 2002;346:13. 2. George J, Woolf S, Raskob G, et al. Idiopathic throm bocytopenic purpura: a practice guideline developed by explicit m ethods for the Am erican Society of Hem atology. Blood. 1996;88:3. 3. Provan D, Norfolk D, Bolton-Maggs P. Guidelines for the investigation and m anagem ent of idiopathic throm bocytopenic purpura in adults, children and in pregnancy. Br J Haem atol. 2003;120:574.

Miscellaneous SEE ALSO: HELLP Syndrom e; Throm botic Throm bocytopenic Purpura

Codes ICD9-CM 287.2

ICD10 D69.3

Pa ge 2 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Im m uniz atio ns

Immunizations

Ghazala Q. Sharieff

Basics Description 

Enhances or initiates resistance to infectious diseases.



Passive im m unization occurs by adm inistration of antibody or through placental antibody transm ission from the m other to the fetus: o

The transplacental antibodies can protect the newborn for the first few m onths of life.



Active im m unization results in stim ulation of the im m une system : o

Antibody response is seen after 7â€“10 days.

o

IgM followed by IgG response

o

The IgG antibodies (which confer resistance) peak between 2 and 6 weeks.

o

The route of vaccine adm inistration is im portant in im m une response: Im proper adm inistration m ay result in decreased im m unity.



Parenteral vaccines, unlike oral vaccines, m ay not induce m ucosal secretory IgA antibodies, which prevent organism absorption in the intestines

Etiology

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

Five types of vaccines are currently available: o

Attenuated (weakened) live virus used in m easles, m um ps, and rubella (MMR) vaccine and varicella (chicken pox) vaccine 

May cause serious infections in people with com prom ised im m une system sâ€”killed (inactivated) viruses or bacteria are used in som e vaccines.



Polio, pertussis, and influenza vaccines use killed virusâ€”vaccines are safe, even in people with com prom ised im m une system s.

o

Acellular pertussis vaccine causes fewer local and system ic reactions than whole cell pertussis vaccine.

o

Toxoid vaccines contain a toxin produced by the bacterium or virus (diphtheria and tetanus).

o

Hepatitis B vaccine is m ade with recom binant DNA technology.

o

Biosynthetic vaccines contain synthetic substances conjugated with an im m unogenic carrier protein, which appear to be antigens to the im m une system (Hibâ€“Haem ophilus influenzae type B and pneum ococcal vaccines).



Menjugate group C conjugate is another new vaccine for active im m unization of children older than 2 years of age, adolescents, and adults for the prevention of Neisseria m eningitis serogroup C.



Several com bination vaccines are also available, but m ay not be routinely adm inistered owing to the increased cost: o

Pediarix (diphtheria and tetanus toxoids and acellular pertussis adsorbed, hepatitis B [recom binant], and inactivated poliovirus vaccine com bined) is a com bination vaccine providing protection against five

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serious diseases sim ultaneously, thereby reducing the total num ber of shots infants receive by up to six. o

Com vaxâ€”com bines the hepatitis B and Hib vaccine into one shot

o

TriHIBitâ€”com bines Hib and DTaP: Unfortunately, this vaccine is licensed only for use as the fourth dose of the vaccination series at age 15â€“18 m onths.

o

Twinrixâ€”com bines hepatitis A and hepatitis B into one shot and is given as a three-dose series

Epidemiology 

Incidence of several life-threatening illnesses has been m arkedly reduced with widespread im m unization use.



Polio caused by wild-type viruses has been elim inated from the Western Hem isphere.



Hib, diphtheria, and tetanus vaccines have nearly elim inated these invasive diseases am ong children.



Incidence of m easles, rubella, and varicella has also declined, rubella is very uncom m on at present.



Seven-valent conjugate vaccine (PnCRM-7) (Prevnar; Wyeth Vaccines, Pearl River, New York), which contains serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F: o

PnCRM-7 is 80â€“100% effective against vaccine-type invasive disease and 50â€“60% effective against vaccine-type pneum ococcal otitis m edia.



Two new vaccines providing passive im m unity to respiratory syncytial virus (RespiGam [RSV-IG] and Palivizum ab) are already in use for infants younger than 24 m onths of age with a history of prem aturity <35 weeks gestation, chronic lung disease (bronchopulm onary dysplasia), severe congenital heart disease, or severe im m unodeficiencies.

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

Tdap is now recom m ended for children >7 years, adolescents, and adults.



A new rodavirus vaccine (Rotateq) is now available.

Diagnosis Signs and Symptoms Review prior im m unization reactions: 

The m ost com m on events associated with vaccination are m ild febrile and local reactions.

Hib Sterile abscesses m ay occur at the site of an intram uscular injection. Nerve and vascular injuries are uncom m on. Specific side effects to routine vaccinations are listed below.

Diphtheria-Tetanus-Pertussis 

Historically, m any of the significant reactions were associated with DTP rather than DTaP.



Mild local reactions (redness, induration, and tenderness at the injection site): o

Constitutional sym ptom s (fever <40.5Â°C, fussiness, drowsiness, crying)



Brief, generalized seizures m ay occur after adm inistration of DTaP. o

Usually seen in febrile children after the third or fourth dose of the vaccine series



Hypotonic-hyporesponsive episodes (collapse or shocklike state) are less com m on after DTaP vaccination.



Episodes of persistent, inconsolable crying for 3 or m ore hours have been observed following DTP injection and rarely after DTaP.

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

Encephalopathy



Guillain-BarrÃ© syndrom e (GBS) within 6 weeks of vaccination

Hepatitis B Prem ature infants with birth weights of <2 kg m ay have a decreased response to vaccination: 

Current recom m endations advise that preterm low-birth-weight infants receive hepatitis B vaccine at 1 m onth chronologic age.

Influenza 

Febrile reactions occur in children younger than 2 years of age between 6 and 24 hours following injection.



Slight increase in cases of GBS in adults.

Polio 

Several cases of oral vaccineâ€“associated paralytic polio (VAPP) had been reported in the United States annually using attenuated vaccine.



Inactivated poliovirus vaccine (IPV), which does not carry a risk of paralysis, was introduced into the routine im m unization schedule in 2000.



IPV contains three types of poliovirus inactivated with form aldehyde. Im m unity postvaccination is expected to be lifelong.

Measles-Mumps-Rubella 

Transient rash or fever â‰¥39Â°C from 6â€“12 days after vaccination



Transient throm bocytopenia within 2 m onths of vaccination. Other precautions to future im m unization include the recent adm inistration of im m une globulin and active tuberculosis.

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Varicella 

A few children m ay develop a m ild varicella-like illness with the developm ent of fewer lesions (either vesicular or m aculopapular) and lower rates of fever than unim m unized children with varicella disease.



Children who develop a postvaccination rash m ay rarely transm it the virus to others.

Essential Workup 

Take an im m unization history of status of im m unizations: o

If incom plete, take a good history as to the reason why im m unizations have not been adm inistered.



Reasons to defer vaccine adm inistration: o

All patients who are acutely ill with or without fever >38.5Â°C

o

Defer pertussis for 3 weeks after a convulsion.

o

Recent adm inistration of im m une globulin is a precaution to im m unization.

o

True contraindications to vaccination

o

Anaphylactic reaction to a previous dose of the vaccine: 

Anaphylaxis to baker's yeast contraindicates im m unization with hepatitis B vaccine.



Anaphylaxis to chicken or egg protein contraindicates influenza vaccination.



Anaphylaxis to neom ycin or gelatin contraindicates MMR im m unization.

P.589

o

Specific reactions within 48 hours of vaccine of a previous vaccine:

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

Severe, inconsolable scream ing for 3 hours



Distinctive high-pitched cry



Hyporesponsive episode



Tem perature >40.5Â°C unexplained by other cause



Severe local reaction involving the circum ference of the injected lim b unless owing to inadvertent subcutaneous injection

o

Encephalopathy within 7 days of vaccine: 

severe acute neurologic illness with prolonged seizures and/or unconsciousness and/or focal signs

o

Progressive neurologic disease excluding epilepsy

o

Im m unocom prom ised hosts should not receive the varicella vaccine.

o

Severely im m unocom prom ised patients (non-HIV related) should not receive the MMR vaccine.

o

Pregnant patients should not receive the varicella vaccine, and the hepatitis A vaccine should be used with caution. Live virus vaccines are not routinely recom m ended during pregnancy.



Vaccines m ay be given with the following: o

Mild acute illness with or without fever

o

Mild to m oderate local reaction (i.e., swelling, redness, soreness), low-grade or m oderate fever after previous dose

o

Lack of previous physical exam ination in well-appearing person

o

Current antim icrobial therapy

o

Convalescent phase of illness

o

Prem ature birth (hepatitis B vaccine is an exception)

o

Recent exposure to an infectious disease

Pa ge 2 6 2

o

History of penicillin allergy, other nonvaccine allergies, relative with allergies, receiving allergen extract im m unotherapy

o

HIV-infected children who are either asym ptom atic or not severely im m unocom prom ised should be vaccinated.



Review the tim ing of the patient's im m unizations and determ ine if catch-up im m unizations are necessary.



Specific discussion with the parents is required to review the risks and benefits of tetanus, particularly given the frequent occurrence of traum a and the need to provide both passive and active im m unity at that tim e: o

Generally, an inform ed consent is required or at a m inim um , docum entation in the chart that the risks and benefits have been thoroughly discussed.

o

In addition, The National Childhood Vaccine Injury Act requires that all health care providers provide parents or patients with copies of Vaccine Inform ation Statem ents before adm inistering each dose of the vaccines listed in the schedule.

Treatment 

Route and tim ing of vaccine adm inistration: See Reference 1.



Prophylaxis with acetam inophen at the tim e of injection and again at 4 and 8 hours postvaccination m ay reduce the incidence of fever and local reactions:



Children who receive varicella vaccine should avoid salicylates for 6 weeks postvaccination because of the association of varicella infection and salicylates to Reye

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syndrom e.

Follow-Up Disposition Admission Criteria 

Patients with serious adverse reactions following im m unization should be adm itted.



Patients with anaphylaxis and encephalopathy m ay require adm ission to a pediatric intensive care unit.



Unexpected adverse events should be reported to the Vaccine Adverse Event Reporting System (VAERS).

Discharge Criteria Patients m ay be discharged hom e after routine im m unizations unless an im m ediate adverse reaction occurs.

References 1. Advisory Com m ittee on Im m unization Practices of the CDC: Available at http://www.cdc.gov/nip. 2. Am erican Academ y of pediatrics (http://www.aap.org). 3. Am erican Academ y of Pediatrics. Red Book 2003: Report of the Com m ittee on Infectious Diseases. 26 th ed. Elk Grove Village, IL: Author; 2003. 4. Am erican Academ y of Pediatrics. Thim erosal in vaccinesâ€“Joint statem ent of the Am erican Academ y of Fam ily Physicians, The Am erican Academ y of Pediatrics, The Advisory Com m ittee on Im m unization Practices, and the United States Public Health Service. Available at: http://www.aap.org/policy/jointthim .htm l. 5. Black S, Shinefield H, Firem an B, et al. Efficacy, safety, and im m unogenicity of heptavalent pneum ococcal vaccine in children.

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Pediatr Infect Dis J. 2000;19:187â€“195. 6. Black SB, Shinefield HR, Hansen J, et al. Postlicensure evaluation of the effectiveness of seven valent pneum ococcal conjugate vaccine. Pediatr Infect Dis J. 2001;20:1105â€“1107. 7. Halsey NA, Hym an SL. Measles-m um ps-rubella vaccine and autistic spectrum disorder: report from the New Challenges in Im m unization Conference. Pediatrics. 2001;107:e84. 8. National im m unization hotline ([800] 232-2522). 9. Recom m ended Childhood and Adolsecent Im m unization Schedule, by Vaccine and Ageâ€”United States, 2006. Available at http://www.cdc.gov/nip/recs/child-schedule.htm

Miscellaneous SEE ALSO: Anaphylaxis; Encephalitis; Hepatitis; Influenza; Measles; Mum ps; Pertussis; Polio; Seizure, Adult; Seizure, Pediatric; Tetanus; Varicella

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Im m uno suppressio n

Immunosuppression Lara K. Kulchycki Larry A. Nathanson

Basics Description Deficiency in the ability to fight infection: 

Antibody (B cell)



Cellular (T cell)



Phagocytic dysfunction



Com plem ent deficiency



Breach of skin/m ucosal barriers



Congenital versus acquired

Etiology 

Aging: o

Im m unosenescence

o

Poor circulation and wound healing

o

Nosocom ial infections:

o



Recent or frequent hospitalizations



Nursing hom e residents

Blunted fever and inflam m atory responses



IV drug abuse



HIV infection:

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o

CD4 count determ ines susceptibility to particular pathogens









Diabetes: o

Hyperglycem ia im pairs im m une system

o

Large and sm all vessel vascular disease

o

Decreased sensation from peripheral neuropathy

Malnutrition: o

Poverty and hom elessness

o

Alcoholism

Asplenia: o

Functional asplenia (sickle cell disease)

o

Surgical rem oval of the spleen

Organ transplant recipients: o

Im m unosuppressive m edications

o

At risk for viral infections with cytom egalovirus, Epstein Barr virus, and hum an herpes viruses



Cancer and cytotoxic chem otherapy: o

Neutropenia defined as absolute neutrophil count (ANC) <500/m m 3 or <1,000/m m 3 with anticipated drop to <500 within 24â€“48 hours

o

Length and severity of neutropenia predicts the likelihood of infection.

o

In the United States, gram -positive organism s are the leading etiology of infection (60â€“70%).

o

Gram -negative infections are less com m on, but m ore dangerous.

o

Multiple organism s are com m on.

o

Anaerobic isolates are relatively rare.

o

Fungal pathogens are m ore likely with prolonged neutropenia (>1 week).

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Diagnosis Signs and Symptoms History: 

Fever m ay be the only sym ptom of a life-threatening infection.



One fifth of patients with neutrophil counts <100/m m 3 are bacterem ic.



Frequent lack of localizing sym ptom s



Use of prophylactic m edicines, such as trim ethoprim /sulfam ethoxazole or fluconazole, will alter the spectrum of likely pathogens and their resistance patterns.

Physical Exam 

Exam ine the patient from head to toe.



Evidence of inflam m ation m ay be absent: o

Surgical abdom en without peritoneal signs

o

Meningitis without m eningeal signs

o

Infected wounds or indwelling lines without induration, erythem a, or purulent discharge

Tests 

Labs: o

Choice of studies m ust be tailored to the patient and the presenting com plaint.

o

Interpretation is m ore difficult given im paired inflam m atory response: 

Pulm onary infections without infiltrates



Urinary tract infections without pyuria



Meningitis without cerebrospinal fluid (CSF) pleocytosis

o

CBC count with differential

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o

Blood cultures: 

Two sets of bacterial cultures



Draw one culture from an indwelling line, if present.



Fungal cultures if there is clinical suspicion of fungal pathogen

o

Urinalysis/Urine culture

o

Arterial blood gas: 

Can be useful in determ ining the need for em piric steroids in patients with suspected Pneum ocystis carinii (PCP)



Im aging: o

Chest radiograph recom m ended if patient is neutropenic, hypoxic, or has pulm onary sym ptom s/signs.

o

Further im aging can be tailored to the patient, such as CT or MRI scans.

Diagnostic Procedures/Surgery Lum bar puncture (LP) should be perform ed if there is a clinical suspicion for m eningitis: 

Check platelet counts and coagulation studies.



Consider sending cryptococcal antigen even in the absence of CSF pleocytosis.

Differential Diagnosis 

Infection: o

Oropharynx

o

Sinuses

o

Lung

o

Gastrointestinal tract

o

Perineum /Anus

o

Urinary tract

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

o

Skin/soft tissue

o

Indwelling catheters

Noninfectious etiology of fever: o

Drug fever

o

Certain cancers

o

Vasculitis

o

Pulm onary em bolism

Treatment Pre Hospital 

Establish IV access



IV fluid bolus

Initial Stabilization 

Aggressive fluid resuscitation for patients with hypovolem ia



Goal-directed therapy for patients with septic physiology



Consider central access with central venous pressure m onitoring to gauge fluid status.



Cardiac ultrasound can be used to evaluate for suspected m alignant pericardial tam ponade.



Adm inister pressors for hypotension that fails to respond to IV fluids: o

Dopam ine 5â€“20 m cg/kg/m in IV

o

Norepinephrine 2â€“12 m cg/m in IV

ED Treatment 

Rapidly collect appropriate cultures and adm inister broad-spectrum antibiotics.



Low-risk patients m ay be candidates for oral antibiotic regim ens and possibly even outpatient treatm ent for their

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fever. P.591



Low risk: o

Age <60 years

o

Outpatient status at tim e of fever

o

ANC >100 cells/m m 3

o

Tem perature <39Â°C

o

Duration of neutropenia <7 days

o

Expected resolution of neutropenia <10 days

o

Well appearing

o

Malignancy in rem ission

o

No history of fungal infections

o

Norm al chest radiograph

o

No change in m ental status

o

Lack of com orbid conditions: 

Shock



Hypoxia/tachypnea



Dehydration



Chronic pulm onary disease



Diabetes

Medication (Drugs) 

Oral regim ens: o

Com parable results in low-risk adults

o

Ciprofloxacin: 750 m g PO b.i.d. plus am oxicillin-clavulanate 500 m g PO 3 tim es daily



Parenteral m onotherapy: o

Ceftazidim e: 2 g IV q8h (peds: 150 m g/kg/d IV div. q8h)

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o

Cefepim e: 2 g IV q8h (peds: 150 m g/kg IV div. q8h)

o

Im ipenem -cilastatin: 0.5 g IV q6hâ€“q8h (peds: dose based on age/weight)

o

Meropenem : 1 g IV q8h (peds: dose based on location of infection)

o

Piperacillin-tazobactam (less well studied in neutropenia): 3.375 g IV q6h (peds: dose based on age)



For high-risk patients, consider adding an am inoglycoside (AG) for synergism : o

Gentam icin: 2â€“5 m g/kg IV q8hâ€“812h (peds: dose based on age)

o

Added AG increases risk of adverse events, including acute renal failure.



Em pirical vancom ycin is usually not indicated: o

Consider adding if suspected line sepsis or history of penicillin-resistant pneum ococci or m ethicillin resistant S. aures (MRSA)

o

Vancom ycin: I g IV q12h (peds: dose age- and weight-based)



Anaerobic coverage m ay be added if there is concern for oral or abdom inal/perianal infections: o

Clindam ycin: 600â€“900 m g IV q6â€“q12h (peds: 40â€“60 m g/kd/d IV div. q6h)

Follow-Up Disposition Admission Criteria 

Neutropenic precautions bed if needed

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

Adm it hem odynam ically unstable patients to the intensive care unit.



Maintain lower adm ission criteria for: o

Elderly

o

Diabetics

o

IV drug users

o

Children

Discharge Criteria 

Low-risk patients that are well appearing and tolerating oral antibiotics and fluids



24 hours follow up m ust be available in order to clinically reassess the patient and m onitor culture results.



Discuss the disposition with the responsible hem atology/oncology, infectious disease, or transplant physician prior to discharge.

References 1. Fishm an JA, Rubin RH. Infection in organ-transplant recipients. N Engl J Med. 1998;338(24):1741â€“1751. 2. Freifeld A, et al. A double-blind com parison of em pirical oral and intravenous antibiotic therapy for low-risk febrile patients with neutropenia during cancer chem otherapy. N Engl J Med. 1999;341(5):305â€“311. 3. Hidalgo M, et al. Outpatient therapy with oral ofloxacin for patients with low risk neutropenia and fever: a prospective, random ized clinical trial. Cancer. 1999;85(1):213â€“219. 4. Hughes WT, et al. 2002 guidelines for the use of antim icrobial agents in neutropenic patients with cancer. Clin Infect Dis. 2002;34(6):730â€“751. 5. Kern WV, et al. Oral versus intravenous em pirical antim icrobial therapy for fever in patients with granulocytopenia who are receiving cancer chem otherapy. International Antim icrobial Therapy

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Cooperative Group of the European Organization for Research and Treatm ent of Cancer. N Engl J Med. 1999;341(5):312â€“318. 6. Klastersky J, et al. The Multinational Association for Supportive Care in Cancer risk index: A m ultinational scoring system for identifying low-risk febrile neutropenic cancer patients. J Clin Oncol. 2000;18(16):3038â€“3051. 7. Malik IA, et al. Feasibility of outpatient m anagem ent of fever in cancer patients with low-risk neutropenia: results of a prospective random ized trial. Am J Med. 1995;98(3):224â€“231. 8. Mullen CA, et al. Outpatient treatm ent of fever and neutropenia for low risk pediatric cancer patients. Cancer. 1999;86(1):126â€“134. 9. Paul M, Soares-Weiser K, and Leibovici L, Beta lactam m onotherapy versus beta lactam -am inoglycoside com bination therapy for fever with neutropenia: system atic review and m eta-analysis. Bm j. 2003;326(7399):1111. 10. Pizzo PA. Fever in im m unocom prom ised patients. N Engl J Med. 1999;341(12):893â€“900. 11. Rolston KV. New trends in patient m anagem ent: risk-based therapy for febrile patients with neutropenia. Clin Infect Dis. 1999;29(3):515â€“521. 12. Talcott JA, et al. Risk assessm ent in cancer patients with fever and neutropenia: a prospective, two-center validation of a prediction rule. J Clin Oncol. 1992;10(2):316â€“322. 13. Wingard JR. Em pirical antifungal therapy in treating febrile neutropenic patients. Clin Infect Dis. 2004;39(Suppl 1):S38â€“S43.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Im petigo

Impetigo

Irving Jacoby

Basics Etiology 

Classic im petigo: o

The result of bacteria entering through traum atic skin portal from scratch, abrasion, or insect bite

o

Caused by Staphylococcus aureus, group A Î²-hem olytic streptococci, or both

o

More prevalent in warm clim ates and warm seasons

o

Often associated with poor hygiene

o

Coverage for both streptococci and S. aureus is given.



Bullous im petigo: o

Caused by S. aureus, phage group II

o

Epiderm al cleavage is caused by two staphylococcal exfoliative toxins: exfoliatins or exfoliative toxins A and B

Diagnosis Signs and Symptoms

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

Classic (nonbullous) im petigo: o

Begins as a single 2- to 4-m m erythem atous m acule or papule that m ay evolve into a vesicle or pustule, on a red base

o

Rupture of the vesicle, usually within 24 hours, leaves a honey-colored, dark brown, or reddish-black exudative crust.

o

Highly contagious

o

Often pruritic, m ay be spread from the original site of infection by scratching

o

Mild lym phadenopathy m ay be seen, usually not lym phadenitis.

o

System ic m anifestations are rare.

o

Rheum atic fever does not occur following streptococcal skin infection.

o

Skin infection with nephritogenic strains of group A streptococci are m ajor antecedents of poststreptococcal glom erulonephritis around the world.



Bullous im petigo: o

Occurs m ost com m only in the neonate, but can occur at any age

o

Lesions begin as vesicles that turn into flaccid bullae with clear yellow fluid.

o

Nikolsky sign is absent.

o

Large, fragile bullae rupture quickly, leaving only a shiny, erythem atous base with peeling edges.

History Fever and constitutional sym ptom s are uncom m on.

Physical Exam The diagnosis is m ade based on observation of the classic exam

Pa ge 2 6 4

findings, especially appearance, and distribution.

Essential Workup Cultures of fluid from bullae or pustules m ay be considered in those cases refractory to traditional therapy or if m ethicillin-resistant S. aureus (MRSA) is of particular concern during an outbreak.

Tests Lab 

Anti-streptolysin O titer after streptococcal im petigo is scant



Anti-DNase B response readily occurs; 90% of patients with nephritis com plicating streptococcal skin infections have elevated titers.

Differential Diagnosis 

Herpes sim plex



Varicella



Atopic derm atitis



Contact derm atitis



Derm atophytosis



Erysipelas



Candidiasis



Scabies



Pediculosis



Pem phigus vulgaris



Bullous pem phigoid



Therm al burns



Stevens-Johnson syndrom e



Bullous erythem a m ultiform e



Staphylococcal scalded skin syndrom e (SSSS; caused by system ic spread of exfoliatin in susceptible individuals)



Pem phigus neonatorum (Ritters Disease), or SSSS in the

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newborn 

Toxic epiderm al necrolysis (TEN)



Cutaneous anthrax

Treatment Pre Hospital 

Apply dressings to cover for transport.



Gloves m ust be worn, as agents can be transm itted person to person.



Cautions: o

Maintain universal precautions.

o

Siblings of affected children in sam e household should be checked for lesions.

Initial Stabilization In healthy children or adults, classic or bullous im petigo is not a life-threatening condition and does not require resuscitative m easures,

ED Treatment 

Sm all lesions m ay be treated with topical therapy alone using m upirocin or in conjunction with system ic therapy.



Larger, widespread lesions should be treated with system ic therapy.



Treatm ent should include a Î²-lactam aseâ€“resistant penicillin, cephalosporin, or m acrolide antim icrobial for 10 days: o

If no response, check for MRSA and switch antibiotic to cover for MRSA.



System ic antibiotic advisable during epidem ics of acute poststreptococcal glom erulonephritis

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

Local care should include cleansing, rem oval of crusts, and application of wet dressings to the affected areas.

P.593

Medication (Drugs) 

All treatm ent regim ens are 10 days.



Avoid use of erythrom ycin if high incidence of erythrom ycin resistance of streptococci or staphylococci in the com m unity.

Oral 

Am picillin/clavulanic acid: 250 m g PO q8h (peds: 20 m g/kg/d PO in div. doses q8h)



Azithrom ycin: 500 m g PO on day 1; 250 m g PO days 2â€“5 (peds: 10 m g/kg PO on day 1; 5 m g/kg PO days 2â€“5)



Cephalexin: 500 m g PO q.i.d. (peds: 25â€“50 m g/kg/d PO in div. doses q8hâ€“q12h)



Clarithrom ycin: 250 m g PO q12h (peds: 15 m g/kg in div. doses q12h)



Clindam ycin: 150 m g PO t.i.d. (peds: 5 m g/kg t.i.d.)



Dicloxacillin: 250 m g PO q6h (peds: 25â€“50 m g/kg/d PO in div. doses q6h)



Erythrom ycin ethylsuccinate: 250 m g PO q6h (peds: 40 m g/kg/d PO in div. doses q6h)



Linezolid: 600 m g PO b.i.d.â€”extrem ely expensive, used only for m ultiallergic patients or MRSA (peds: not approved for children)

Topical Mupirocin (2% ointm ent): adult and peds: Apply topically to affected

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area t.i.d. (non-bullous im petigo only).

Follow-Up Disposition Admission Criteria 

Adm ission for im petigo alone is rarely necessary.



Patients with disease that is widespread, especially widespread bullae, or refractory to outpatient therapy



Toxic, ill-appearing, or im m unocom prom ised patients require adm ission.



Nephritis m ay already be present at tim e patients present for care if presentation delayed m ore than 4â€“5 days.



More typically nephritis, if seen, occurs 2â€“4 weeks after a streptococcal skin infection.

Discharge Criteria 

Patients should not be toxic appearing.



Patients should be able to com ply with the recom m ended treatm ent regim en.



Follow-up for re-evaluation

Issues for Referral Periorbital edem a, leg swelling, or hem aturia or proteinuria should suggest poststreptococcal glom erulonephritis (PSGN).

References 1. Hirschm ann JV. Im petigo: etiology and therapy. In: Rem ington JS, Swartz M, eds. Current Clinical Topics in Infectious Diseases. Vol 22. Malden, MA: Blackwell; 2002:42â€“51. 2. Yun HJ, et al. Prevalence and m echanism s of low- and high-level m upirocin resistance in staphylococci isolated from a Korean

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hospital. J Antim icrob Chem other. 2003;51:619â€“623.

Codes ICD9-CM 684

ICD10 L01.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Inbo rn Erro rs o f M etabo lism

Inborn Errors

of Metabolism David A. Perlstein

Basics Description 

Defect in the type, am ount, and toxicity of m etabolites that accum ulate owing to an inherited abnorm al pathway in children; results in a variety of clinical findings. More than 400 hum an diseases caused by inborn errors of m etabolism



Epidem iology: o

Incidence: 

Variable: 1:10,000â€“1:200,000 births

Genetics Com m on inherited m etabolic diseases: 

Urea cycle defects



Organic acidem ias



Disorders of am ino acid m etabolism



Defects in fatty-acid oxidation



Mitochondrial disorders



Carbohydrate disorders



Mucopolysaccharidoses

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

Sphingolipidoses



Peroxisom al disorders

Pathophysiology Related to defect in m etabolic pathway

Etiology Diverse group of disorders involving genetic deficiency of an enzym e of an interm ediary m etabolite or a m em brane transport system

Diagnosis Signs and Symptoms 

Rapid decom pensation m ay occur.



Neonates, initial presentation: o

Asym ptom atic

o

Hypotherm ia (m itochondrial defects)

o

Hypotonia/hypertonia (peroxisom al disorders)

o

Apnea (urea cycle defects, organic acidosis)

o

Seizures (peroxisom al disorders, glucose transporter defects)

o

Com a (num erous)

o

Vom iting (num erous)

o

Poor feeding, growth (num erous)

o

Jaundice (galactosem ia, Niem ann-Pick C)

o

Hypoglycem ia (galactosem ia, m aple syrup urine

o

Dysm orphic features (lysosom al storage disorders, congenital adrenal hyperplasia, Sm ith-Lem li-Opitz)



Older children, untreated: o

Failure to thrive (urea cycle defects)

o

Dehydration (organic acidosis)

o

Vom iting (urea cycle defects and others)

Pa ge 2 6 4

o

Diarrhea (num erous)

o

Food intolerance (lipid defects, am ino acid defects)

o

Lethargy (urea cycle defects)

o

Ataxia (urea cycle defects)

o

Seizures (num erous)

o

Mental retardation (phenylketonuria [PKU] and others)

History Com plete history of current and concom itant illness: 

Newborn screening



Dietary



Fam ily



Consanguinity



Other

Physical Exam 

Abnorm al odor



Altered m ental status



Tachypnea



Abnorm al facies



Cataract



Cardiom yopathy



Hepatom egaly



Splenom egaly



Derm atitis



Jaundice

Essential Workup Key is to consider in differential diagnosis: 

Deteriorating neurologic status



Unexplained failure to thrive with dehydration, persistent vom iting, or acidosis



Shock unresponsive to conventional resuscitative

Pa ge 2 6 4

m easures

Tests Lab 

Bedside glucose determ ination



Electrolytes, BUN/creatinine, glucose



CBC with differential



Calcium level



Liver function tests, fractionated bilirubin, prothrombin tim e



Arterial or venous blood gas



Uric acid



Urinalysis



Chem istries, as indicated:



o

Am m onia level

o

Quantitative serum am ino acids

o

Urine organic and am ino acids

o

Lactate and pyruvate levels

Cultures: o

Blood

o

Cerebrospinal fluid

Imaging 

CT scan of head for altered m ental status



Chest radiograph

Diagnostic Procedures/Surgery Spinal tap

Differential Diagnosis 

Often m isdiagnosed as sepsis, dehydration, failure to thrive, toxic ingestion, or nonaccidental traum a



Infection: o

Sepsis

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



o

Meningitis

o

Encephalitis

Metabolic: o

Reye syndrom e

o

Hepatic encephalopathy

o

Hyperinsulinem ia

o

Horm onal abnorm ality

Renal: o

Renal failure

o

Renal tubular acidosis



Toxic ingestion



Central nervous system m ass lesions



Nonaccidental traum a

Treatment Pre Hospital Alert 

Careful assessm ent of airway, breathing, circulation



Bedside glucose, if possible



Intravenous glucose infusion takes precedence over fluid boluses unless patient in shock. Correction can occur concurrently.



Avoid lactated Ringer solution.



Keep child NPO.

Initial Stabilization For altered m ental status, adm inister Narcan, glucose (ideally after Accu-Chek and thiam ine.) P.595

Pa ge 2 6 5

ED Treatment 

Initiate IV glucose at rate of 8â€“10 m g/kg/m in to prevent catabolism : o

Corresponds to D 1 0 at 1.5 tim es m aintenance

o

Do not delay glucose infusion to give a â€œbolusâ€• of isotonic saline; m ay be given concurrently in a child in shock.

o

If patient is severely hypoglycem ic, give IV glucose bolus of D 2 5 .



Rehydrate if patient is hypoglycem ic: o



Restore norm al acid-base balance.

Adm inister bicarbonate if pH is <7.0. o

Initiate dialysis if severe acidosis does not im prove quickly.



Increase urine output to help in rem oval of som e toxins.



Initially, stop all oral intake; am ino acid m etabolites m ay be neurotoxic.



Treat severe hyperam m onem ia with dialysis or with am m onia-trapping drugs such as: o

Arginine hydrochloride

o

Sodium benzoate

o

Sodium phenylacetate

o

Sodium phenylbutyrate

o

Dosages vary with disease; consult m etabolic physician before use.



Identify and treat intercurrent or precipitating infection/illness.



Consult m etabolic physician when any child presents with suspected inherited m etabolic disease.

Pa ge 2 6 5

Medication (Drugs) 

D 2 5 : 2â€“4 m L/kg IV



Sodium bicarbonate: 1â€“2 m Eq/kg IV



Other disease-specific drugs including: pyridoxine and levocarnitine as indicated

Follow-Up Disposition Admission Criteria 

Infants and children presenting with new onset of suspected inherited m etabolic disease



Significant urinary ketones or not tolerating oral intake



Intensive care unit:



o

Significant altered m ental status

o

Severe or persistent acidosis

o

Unresponsive hypoglycem ia

o

Hyperam m onem ia

Transfer to specialized pediatric center m ay be indicated.

Discharge Criteria 

Norm al m ental status



Norm al hydration with unrem arkable labs



No evidence of significant intercurrent illness



Close follow-up arranged with prim ary care physician

References 1. Barness LA. An approach to the diagnosis of m etabolic diseases. Fetal Pediatr Pathol. 2004;23:3â€“10. 2. Behrm an RE, Kliegm an RM, Jenson HB. Nelson Textbook of Pediatrics. 17th ed. Philadelphia: WB Saunders; 2004.

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3. D'Agata ID, Balistreri WF. Evaluation of liver disease in the pediatric patient. Pediatr Rev. 1999;20:376â€“390. 4. Goodm an SI, Green CL. Metabolic disorders of the newborn. Pediatr Rev. 1994;15:359â€“365. 5. Korson MS. Advances in newborn screening for m etabolic disorders: what the pediatrician needs to know. Pediatr Ann. 2000;29:294â€“301. 6. Leonard JV. Inborn errors of m etabolism around tim e of birth. Lancet. 2000;356:583â€“587. 7. Thoene JG. Treatm ent of urea cycle disorders. J Pediatr. 1999;134:255â€“256. 8. Wolf AD, Lavine JE. Hepatom egaly in neonates and children. Pediatr Rev. 2000;21:303â€“310.

Codes ICD9-CM 270-279 Other m etabolic and im m unity disorders 277.9 Unspecified disorder of m etabolism

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Inflam m ato ry Bo w el Disease

Inflammatory

Bowel Disease Shayle Miller

Basics Description 

Idiopathic, chronic inflam m atory diseases of intestines, which can involve extraintestinal sites as well.



Differentiation between ulcerative colitis (UC) and Crohn's not always clear; interm ediate form s of inflam m atory bowel disease (IBD) exist.



May present as initial onset of disease or exacerbation of existing disease.



Maintain high index of suspicion owing to frequent, subtle presentation of Crohn's disease





Pediatric considerations: o

Can occur in first few years of life.

o

Extraintestinal m anifestations m ay predom inate.

Differences between Crohn's and UC: o

Rectum is alm ost always involved in UC with continuous inflam m ation proxim ally in colon.

o

Sm all intestine is not involved in UC.

o

Crohn's can occur anywhere from m outh to anus,

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often with norm al GI tract segm ents between affected areas. o

Crohn's involves transm ural inflam m ation, whereas UC is confined to subm ucosa.



Sim ilarities between Crohn's and UC: o

Higher rate of colon cancer with disease >10 years

o

Pain of exacerbation rem ission

o

Bim odal age distribution with early peak between teens and early 30s and second peak about age 60





Crohn's disease clinical pattern: o

Ileocecal: approxim ately 40%

o

Sm all bowel: approxim ately 30%

o

Colon: approxim ately 25%

o

Other: approxim ately 5%

UC clinical pattern on presentation: o

Pancolitis: 30%: 

o

Proctitis or proctosigm oiditis: 30%: 

o

Most severe clinical course

Relatively m ild clinical course

Left-sided colitis (up to splenic flexure): 40%: 

Between two above in severity

Etiology 

Unknown



Two diseasesâ€”these are separate entities with com m on genetic predisposition.



A positive fam ily history very com m on.



Multifactorial origin involving interplay am ong following factors:



o

Genetic

o

Environm ental

o

Im m une

Pathogenesis:

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o

Gut wall becom es unable to downregulate its im m une responses, ultim ately resulting in chronic inflam m ation.



There is no definitive evidence for etiologic role of infectious agent



Psychogenic factors m ay play role in som e sym ptom atic exacerbations.

Diagnosis Signs and Symptoms 

Crohn's disease can present with any clinical correlates of chronic inflam m atory, fibrostenotic, or fistualizing illness.



Ulcerative colitis m ay begin subtly or as catastrophic illness.



Constitutional, gastrointestinal, and extraintestinal m anifestations are com m on with both Crohn's and UC.

History 

Constitutional: o

o



Crohn's: 

Low-grade fever



Night sweats



Weight loss



Fatigue

UC: 

Fever usually only in fulm inant disease



Weight loss



Fatigue

Gastrointestinal: o

Abdom inal pain/tendernessâ€”Crohn's disease:

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

Episodic



Perium bilical; m ay localize to right lower quadrant (RLQ) with ileal disease



Generalized with m ore diffuse intestinal involvem ent



Can localize to area of intra-abdom inal abscesses or fistulous involvem ent



Tenderness and distension suggest obstruction or toxic m egacolon

o

Abdom inal pain/tendernessâ€”UC: 

More generalized than Crohn's disease



Often lim ited to predefecatory period



Tenderness with distensionâ€”suspect toxic dilation



Stool: o

o

Crohn's disease: 

Mild loose stool



Rarely m ore than four or five per day



About 50% bloody

UC: 

Diarrhea variable, can be severe



Vast m ajority are bloody, som etim es with severe hem orrhage





Mucus



Tenesm us and urgency com m on

Nausea/vom iting: o

Crohn's disease: 

o



Obstruction com m on with ileocolonic disease

UC: 

Obstruction rare



Dim inished bowel sounds with toxic dilation

Liver:

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



o

Sclerosing cholangitis can be seen.

o

Cholelithiasis can be seen in 35â€“60% of Crohn's.

Renal: o

Nephrolithiasis

o

Obstructive hydronephrosis

Musculoskeletal: o

Peripheral arthritis/arthralgiasâ€”follows disease activity

o

May be confused with juvenile rheum atoid arthritis, idiopathic growth failure, anorexia nervosa

Physical Exam 

Perianal: o

Crohn's disease: 

Perianal abscesses



Fissuresâ€”characteristically painless



Fistulasâ€”seen in up to half of patients with colonic disease

 o

May present prior to other m anifestations

UC: 

No perianal involvem ent



RLQ pain/m ass often m istaken for appendicitis



Extraintestinal: o

o

Eye: 

Uveitis



Episcleritis



Keratitis

Oral: 

o

Aphthous stom atitis

Derm atologic: 

Erythem a nodosum



Pyoderm a gangrenosum

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Essential Workup 

It m ay present as initial onset of disease or exacerbation of existing disease.



Maintain high index of suspicion because of subtle presentation of Crohn's disease.

Tests Lab 

Nothing diagnostic



CBC: o

Anem ia secondary to chronic or acute blood loss



Electrolytes, BUN/creatinine, glucose



Stool exam : o

Occult blood

o

Clostridium difficile

o

Fecal leukocytes m ay be present.

o

O & P and culture to rule out infectious cause of enteritis



Erythrocyte sedim entation rate (ESR) is always elevated.



Newer, investigational, serologic tests m ay have use as adjunctive diagnostic aides, screening testing, or predictors in therapy.

Imaging 

Upright chest and abdom inal radiographs for: o

Toxic m egacolon (>6 cm dilation)

o

Obstruction

o

Air in wall of colon (m ay indicate im pending perforation)

o

Perforationâ€”subdiaphragm atic air or free air outlining liver or gall bladder



CT abdom en:

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o

Distinguish abscess from localized inflam m atory m ass in Crohn's

P.597



Colonoscopy with biopsy can confirm diagnosis of UC or Crohn's: o

Can be withheld with severe sym ptom s owing to perforation risk.



Contrast im aging of sm all bowel, especially term inal ileum , m ay confirm diagnosis of Crohn's.

Differential Diagnosis 

Infectious enteritis



Pseudom em branous colitis (C. difficile)



Appendicitis



Diverticulitis



Diverticulosis



Functional bowel disease



Lym phom a involving bowel



Ischem ic colitis



Gonococcal or chlam ydial proctitis



HIV



Colon cancer



Vasculitis



Am yloidosis

Treatment Initial Stabilization 

IV 0.9% norm al saline (NS) volum e replacem ent if

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dehydrated 

Transfusion if significant blood loss

ED Treatment General Measures 

Nasogastric (NG) suction if obstruction or toxic dilation suspected



Broad-spectrum antibiotics for fulm inant UC or suspected perforation



Consider steroid replacem ent if stress doses required for those recently on oral steroids



Surgical evaluation indications: o

Free perforation

o

Intestinal obstruction

o

Massive, unresponsive hem orrhage

o

Toxic dilation: 

Not an absolute indication for surgical intervention



Intensive m edical m anagem ent with sm all bowel decom pression and close radiographic m onitoring and surgical consultation





Walled off perforation with abscess: o

Usually not indication for em ergent surgery

o

Careful observation for peritonitis

Medical therapy: o

Treatm ent is usually not initiated unless diagnosis already established.

o

Refill or restart m edications in patient with known disease.

o

ED prescribed m edical regim en should be individualized, and consultation with gastroenterologist strongly recom m ended:

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

Am inosalicylate (sulfasalazine m esalam ine) is used for m ild to m oderate disease.



Antidiarrheal agent (diphenoxylate) is usedâ€”but withhold if severe disease or suspect toxic m egacolon.



Steroid (prednisone, budesonide or hydrocortisone enem a, ACTH) is used for m oderate to severe disease.



Antibiotics (m etronidazole and/or ciprofloxacin) aid in treatm ent of Crohn's with colon/perineal involvem ent.



Im m unosuppressive agents (azathioprine, m ethotrexate) are used in severe disease.



Monoclonal antibodies neutralize cytokine tum or necrosis factor (TNF)-alpha and inhibit binding to TNF-alpha receptors (inflixim ab [Rem icade]). Used as parenteral therapy in disease unresponsive to other m odalities. Not ED drug, but be aware of potential severe adverse reactions, infusion reactions, autoim m une diseases and infections.

Pediatric Considerations If nonaccidental traum a is suspected, prom pt referral to appropriate child protective agencies is required along with m edical treatm ent.

Medication (Drugs) 

ACTH: 80â€“120 IU/24h IM or IV



Ciprofloxacin: 500 m g PO q12h



Hydrocortisone enem a: 60 m g



Mesalam ine enem as: 1â€“4 g retention enem aâ€”retain

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overnight 

Mesalam ine suppository: 500 m g per rectum (PR) b.i.d.



Mesalam ine tablets (Asacol sustained release 400 m g; Pentasa 250 m g): 800 m g PO t.i.d; 1,000 m g PO q.i.d.



Metronidazole: 250â€“500 m g (peds: 30 m g/kg/24h) PO t.i.d.



Prednisone: 40â€“60 m g PO daily



Sulfasalazine (Azulfidine): 500 m g PO q.i.d.

Follow-Up Disposition Admission Criteria 



Surgical indication: o

Massive, unresponsive hem orrhage

o

Perforation

o

Toxic dilation

o

Obstruction

Severe flare-up: o

Electrolyte im balance

o

Severe dehydration

o

Severe pain

o

High fever

o

Significant bleeding

Discharge Criteria 

Initial presentation of diarrhea, m ild pain, without toxicity, with close follow-up



Mild to m oderate exacerbation of known disease without obstruction, severe bleeding, severe pain, dehydration, with close follow-up, on renewed therapy or with addition

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of steroid

References 1. Chang JC, Cohen RD. Medical m anagem ent of severe ulcerative colitis. Gastroenterol Clin North Am . 2004;33(2):235â€“250, viii. 2. Lim WC, Hanauer SB. Controversies with am inosalicylates in inflam m atory bowel disease. Rev Gastroenterol Disord. 2004;4(3):104â€“117. 3. Sanborn WJ. New concepts in anti-tum or necrosis factor therapy for inflam m atory bowel disease. Rev Gastroenterol Disord. 2005;5(1):10â€“18. 4. Sanborn WJ. Serologic m arkers in inflam m atory bowel disease. Rev Gastroenterol Disord. 2004;4(4):167â€“174.

Codes ICD9-CM 555.9 556.9

ICD10 K50.9 K51.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Influenz a

Influenza

Philip Shayne

Basics Description 

Acute, usually self-lim ited, viral infection



Transm ission: by dispersion in sm all-particle aerosols created by sneezing, cough, and talking



Virus deposited on respiratory tract epithelium and absorbed



Incubation period: 1â€“2 days



Duration: 3 days: o

Severity of sym ptom s in proportion to height of the fever



Outbreaks usually occur during winter m onths.



Com plications: o

Prim ary influenza viral pneum onia

o

Secondary bacterial pneum onia

o

Exacerbations of chronic obstructive pulm onary disease (COPD)

o

Rare com plications: m yositis, m yocarditis, pericarditis, and aseptic m eningitis



Key features: o

Epidem ic nature of the disease

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o

Mortality results largely from pulm onary com plications.

Pediatric Considerations 

Children exhibit m ore lower-respiratory involvem ent (croup, bronchitis, bronchiolitis, pneum onitis) and higher tem peratures than adults.



Myalgias in the calf m uscle



Febrile convulsions occur in approxim ately 10% of children younger than 5 years of age with influenza infection.



Reye syndrom e: o

Influenza m ay be predisposing factor.

o

Rare and severe com plication

o

Characterized by fatty degeneration of the liver and cerebral edem a

o

o

Sym ptom s: 

Nausea



Vom iting



Stupor

Strong correlation with salicylates: Avoid aspirin products in children with influenza.

Etiology 

Most caused by three genera of the Orthom yxoviridae fam ily: influenza virus types A, B, and C



Epidem ics: o

Every 1â€“3 years

o

Caused by antigenic driftâ€”new variants from m inor changes in surface protein



o

Most cases occur in 2â€“3 weeks.

o

Duration of the epidem ic <6 weeks

Pandem ics: o

Every 10 years

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o

Caused by new strains created by antigenic shift â€”m ajor changes in virus structure



Waterfowl reservoir of influenza virus

Diagnosis Signs and Symptoms History 

Abrupt onset of high fever



Chills, shivering



Myalgias



Headache



Malaise



Anorexia

Physical Exam 

Fever: 38â€“40Â°C (100â€“104Â°F)



Nasal discharge



Conjunctivitis



Pharyngitis



Dry cough

Geriatric Considerations Elderly m ay present with high fever, lassitude, and confusion without pulm onary com plications.

Essential Workup Clinical diagnosis based on the signs and sym ptom s of influenza during the winter m onths in the setting of a known outbreak

Tests Lab

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

CBC (optional): o



WBC: norm al to m ildly decreased

Pulse oxim etry/arterial blood gas (ABG) for significant pulm onary sym ptom s

Imaging Chest radiograph for prom inent lower respiratory sym ptom s 

Norm al (50â€“90%)



Bilateral interstitial infiltration

Diagnostic Procedures/Surgery 

Culture of nasopharyngeal swab or aspirate is useful for population testing (to know what is prevalent in your com m unity)



Rapid enzym e-linked im m unosorbent assay (ELISA) antigen test: o

Can distinguish types A and B

o

Sensitivity about 75%, specificity 90%, within 2 days of sym ptom onset

o

Nasal swab better than throat

Differential Diagnosis 

Indistinguishable from m ost viral infections (upper respiratory tract infections [URIs])



Bronchitis



Atypical pneum onia



Epstein-Barr infection (infectious m ononucleosis)



Distinguishing features from anthrax: o

Influenza is m uch m ore likely to include a sore throat and rhinorrhea.

o

Anthrax is m uch m ore likely to include dyspnea and nausea.

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Treatment Initial Stabilization Aggressive fluid resuscitation, supplem ental oxygen, and positive-pressure ventilation as clinical circum stances dictate

ED Treatment 

Supportive and sym ptom atic: o

Antipyretics (acetam inophen or nonsteroidal anti-inflam m atory drugs [NSAIDs])â€”avoid aspirin



o

Cough suppressants

o

Rehydration

Antivirals effective if given within 48 hours of sym ptom onset: o

Am antadine and rim antadine effective against influenza A

o

Zanam ivir and oseltam ivir have activity against types A and B.

o

Reduce sym ptom duration by 1 day

o

Costly, except for am antadine

o

Accelerate functional recovery

o

Recom m ended for: 

Pneum onia



Patient with severe disease



Im m unocom prom ised



Patients at high risk for com plications

P.599

Prevention 

Inactivated, polyvalent influenza vaccine recom m ended

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annually for: o

Adults >65 years

o

Residents of nursing hom es and long-term care facilities

o

Children age 6â€“23 m onths

o

Children 6 m onths to 18 years old on chronic aspirin therapy

o

High-risk individuals (COPD, cardiovascular disease, im m unocom prom ised, diabetics)



o

Health care workers

o

Caretakers of children <6 m onths old

o

Wom en who will be pregnant during influenza season

Attenuated-live intranasal vaccine (FluMist) currently approved for healthy people. o

Contraindicated for: 

Pregnant wom en



Close contacts and health care workers for severely im m unocom prom ised patients



Chem oprophylaxis in the following settings: o

Short-term prophylaxis during outbreak of influenza A in high-risk patients who did not receive vaccine

o

In conjunction with vaccine in high-risk patients (including those with HIV infections) expected to respond poorly to vaccine

o

In lieu of vaccine when vaccine is contraindicated in high-risk individuals

o

In individuals providing care for high-risk persons

o

Zanam ivir not FDA approved for prophylaxis 

Could interfere with live-virus vaccine



Should not be started for at least 2 weeks after inoculation



Should be stopped 48 hours before

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adm inistration

Pregnancy Considerations 

Inactivated vaccine is recom m ended for wom en expected to be pregnant during influenza season.



Live-attenuated virus contraindicated in pregnancy

Medication (Drugs) 

Am antadine: o

200 m g PO initially, then 100 m g PO b.i.d. for 3â€“5 days

o

For patients >65 years old, decrease am antadine dosage to 100 m g/d



Oseltam ivir: 75 m g PO b.i.d. for 3â€“4 days



Rim antadine: 200 m g PO initially, then 100 m g PO b.i.d. for 3â€“5 days



Zanam ivir: 10 m g nasal insufflation b.i.d. for 3â€“5 days

Follow-Up Disposition Admission Criteria 

Hypoxia (pneum onia)



Severe dehydration



Alteration in m ental status

Discharge Criteria Most patients will have a short, self-lim ited course provided they are able to tolerate fluids and antipyretics.

References

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1. Antiviral drugs for prophylaxis and treatm ent of influenza. Med Lett. 2004;46(1194):85â€“86. 2. Arruda E, Hayden FG. Update on therapy of influenza and rhinovirus infections. Adv Exp Med Biol. 1996;394:174â€“187. 3. Call SA, Vollenweider MA, et al. Does this patient have influenza? JAMA. 2005;293:987â€“997. 4. CDC. Notice to readers: considerations for distinguishing influenza-like illness from inhalational anthrax. MMWR Morb Mortal Wkly Rep. 2001;50(44):984â€“986. 5. Flem ing DM. Managing influenza: am antadine, rim antadine and beyond. Int J Clin Pract. 2001;55(3):189â€“195. 6. Influenza vaccine 2004â€“2005. Med Lett. 2004;46(1193):83â€“84. 7. Mossad SB. Prophylactic and sym ptom atic treatm ent of influenza. Current and developing options. Postgrad Med. 2001;109(1):97â€“105.

Miscellaneous SEE ALSO: Anthrax

Codes ICD9-CM 487

ICD10 J11.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Intracerebral Hem o rrhage

Intracerebral

Hemorrhage Atul Gupta Rebecca Smith-Coggins

Basics Description Hem orrhage into brain parenchym a: 

Com pression of brain tissues



Secondary injury results from cerebral edem a, increased intracranial pressure, and the possibility of brain herniation.

Etiology Intracerebral hem orrhage can occur spontaneously or from traum a: 

Uncontrolled or acute hypertension (m ost com m on)



Vascular m alform ations: o

Arteriovenous m alform ation

o

Venous angiom as

o

Ruptured cerebral aneurysm s



Neoplasm (particularly m elanom a and gliom a)



Anticoagulant therapy (Coum adin, heparin)



Throm bolytic agents



Illicit drugs (cocaine, am phetam ines)

Pa ge 2 6 7



Bleeding disorders (hem ophilia)



Cerebral am yloid angiopathy



Traum atic hem orrhage secondary to blunt or penetrating injury

Diagnosis Signs and Symptoms History 

Severe headache, typically sudden in onset



Hypertension



Seizures



Evidence of head injury



Meningism us



Vom iting



Altered level of consciousness (m ay be com atose): o

Altered m ental status m ay occur as late as 24â€“48 hours after head injury.

Physical Exam Variable neurologic deficits depending on site of intracerebral hem orrhage: 

Putam en hem orrhage (35%): contralateral hem iparesis and hem isensory loss, with occasional dysphagia or neglect



Lobar hem orrhage (30%): variable signs depending on involved area



Cerebellar hem orrhage (15%): vom iting, ataxia, and nystagm us



Thalam ic hem orrhage (10%): sim ilar to putam en, but m ay also have eye m ovem ent abnorm alities

Pa ge 2 6 7



Caudate hem orrhage (5%): confusion, m em ory loss, hem iparesis, gaze paresis



Pontine hem orrhage (5%): quadriplegia, pinpoint pupils, ataxia, sensorim otor loss

Essential Workup Im m ediate noncontrast head CT: 

Acute hem orrhage appears as high-density lesion.

Tests Lab Check coagulation studies (PT/PTT, INR, platelets).

Imaging 

CT as above



New-generation MRI m ay be useful but currently not as available or rapid as CT.

Differential Diagnosis 

Seizure



CNS infection



CNS m ass



Electrolyte or acid-base abnorm ality



Intoxication/Wernicke encephalitis



Migraine headache



Transient ischem ic attack (TIA):



o

Todd paralysis

o

Air em bolism

Differential diagnosis once bleed is seen on CT: o

Spontaneous hem orrhage (hypertensive, arteriovenous m alform ation [AVM], neoplasm , etc.)

o

Traum atic hem orrhage

o

Subarachnoid hem orrhage

o

Subdural hem atom a

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o

Epidural hem atom a

Pediatric Considerations 

Additional differential diagnoses include: o

Moyam oya disease

o

Acute infantile hem iplegia

P.601

Treatment Pre Hospital 

C-spine precautions if head or neck injury is suspected



Elevation of head with C-spine control



Initial prehospital responder m ust ascertain neurologic defect to be able to note progression of sym ptom s.

Initial Stabilization 

Manage airway and resuscitate as needed: o

Patients with depressed level of consciousness should be intubated im m ediately for controlled ventilation.



Early neurosurgical consultation

ED Treatment Blood pressure (BP) m anagem ent: 

Must use caution in blood pressure control because acute lowering of BP to norm al in setting of increased intracranial pressure (ICP) could reduce cerebral perfusion to ischem ic levels



Use nitroprusside, esm olol, or labetalol to slowly lower diastolic blood pressure initially by 10%.

Pa ge 2 6 7



Norm otensive levels should be achieved over 12â€“24 hours.



May use hydralazine as an alternative



Treatm ent of elevated intracranial pressure



Controlled ventilation to PaCO 2 of 35 torr



Fluid restriction; elevate head of bed 30Â°



Mannitolâ€”osm otic diuresis



Use furosem ide as an alternative.



Correct coagulopathies if present.



Consider anticonvulsants: phenytoin.

Medication (Drugs) 

Esm olol: 0.5â€“1 m g/kg initial bolus IV, followed by 50â€“150 Âµg/kg/m in infusion



Furosem ide: 20â€“40 m g (peds: 0.5â€“1.0 m g/kg per dose) IV; m ay repeat as necessary



Hydralazine: 10â€“40 m g (peds: 0.1â€“0.2 m g/kg per dose) IV; m ay repeat as necessary



Labetalol: 20 m g (peds: 0.3â€“1.0 m g/kg per dose) IV; m ay give additional 40â€“80 m g IV q10m in to m ax. 300 mg



Mannitol: 1 g/kg IV



Nitroprusside: 0.5 Âµg/kg/m in IV initially and titrate to effect



Phenytoin: 15â€“20 m g/kg per dose (peds: 0.5â€“1.0 m g/kg/m in) at rate of 40â€“50 m g/h

Follow-Up

Pa ge 2 6 7

Disposition Admission Criteria 

To OR if surgical intervention is indicated



To ICU if intubated; altered level of consciousness; or on IV infusion for blood pressure control



Adm it to neurologic observation unit if norm al neurologic exam without evidence of progression of bleed, and hem odynam ically stable

Discharge Criteria All patients with intracerebral hem orrhage should be adm itted.

References 1. Broderick JP, Adam s HP Jr, Barsan W. Guidelines for the m anagem ent of spontaneous intracerebral hem orrhage: a statem ent for healthcare professionals from a special writing group of the stroke council, Am erican Heart Association. Stroke. 1999;30:905â€“915. 2. Diringer MH. Intracerebral hem orrhage: pathophysiology and m anagem ent. Crit Care Med. 1993;21:1591â€“1603. 3. Heiskanen O. Treatm ent of spontaneous intracerebral and intracerebellar hem orrhages. Stroke. 1993;24(12 suppl):I94â€“95. 4. MacKenzie JM. Intracerebral hem orrhage. J Clin Pathol. 1996;49(5):360â€“364. 5. Ojem ann RG, Heros RC. Spontaneous brain hem orrhage. Stroke. 1983;14:468â€“475. 6. Panagos PD. Intracerebral hem orrhage. Em erg Med Clin North Am . 2002;20:631â€“655.

Codes ICD9-CM 431

Pa ge 2 6 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Intussusceptio n

Intussusception

Roger Barkin

Basics Description 

The proxim al bowel invaginates into the distal bowel, producing infarction and gangrene of the inner bowel: o



Greater than 80% involve the ileocecal region.

Often occurs with a pathologic lead point in children >2 years: o

Hypertrophied lym phoid patches m ay be present in infants.

o

Children >2 years, one third of patients have pathologic lead point.

o

Children >6 years, lym phom a is the m ost com m on lead point.

o 

Adults usually have a pathologic lead point.

The m ost com m on cause of intestinal obstruction within the first 2 years of life



Epidem iology in the United States: o

Most frequently between 5 and 9 m onths of age

o

The incidence is 2.4 cases per 1,000 live births.

o

Male > fem ale predom inance of 2:1

o

Mortality is <1%.

Pa ge 2 6 7



Morbidity increases with delayed diagnosis.

Alert Patients, particularly those in the pediatric age group, with a picture of potential intestinal obstruction, especially with Hem atest positive stool or altered m ental status, need to have intussusception considered.

Etiology 

Most cases (85%) have no apparent underlying pathology.



Predisposing conditions that create a lead point for invagination: o

o

Masses/tum ors: 

Lym phom a



Lipom a



Polyp



Hypertrophied lym phoid patches



Meckel diverticulum

Infection: 

Adenovirus or rotavirus infection



Parasites

o

Foreign body

o

Henoch-SchÃ¶nlein purpura

o

Celiac disease and cystic fibrosis (sm all intestine intussusception)

Diagnosis Signs and Symptoms History 

Classic triad (present in <50% of patients): o

Abdom inal pain

Pa ge 2 6 8

o

Vom iting, often bilious

o

Stools have blood and m ucus (â€œcurrant jellyâ€• stools)



Recurrent painful episodes accom panied by pallor and drawing up of the legs; interm ittent fits of sudden intense pain with scream ing and flexion of legs: o



Occur in 5- to 20-m inute intervals

Mental status changes: o

Irritability

o

Lethargy or listlessness; child can be lim p or have a rag doll appearance

o 

May precede abdom inal findings

Stool variable: o

Hem e-positive (occult), bloody, or â€œcurrant jellyâ€•



Preceding illness several days or weeks prior to the onset of abdom inal pain:



o

Diarrhea

o

Viral syndrom e

o

Henoch-SchÃ¶nlein purpura

Recurrent intussusception occurs in <10% of patients.

Physical Exam 

Fever



Abdom en distended and swollen: o

A â€œsausageâ€• m ass m ay be palpated in the right upper quadrant.

o

May have absent cecum in right iliac fossa

o

Peristaltic wave m ay be present.

o

Rectal exam ination m ay reveal bloody stool and palpable m ass.



Dependent on the tim e from onset to diagnosis; perforation with peritonitis and sepsis m ay be present.

Pa ge 2 6 8

Essential Workup 

The diagnosis is suggested by the history and is proven radiographically.



A hem e-positive stool m ay aid in the diagnosis, particularly in the presence of lethargy or listlessness.

Tests Lab 

CBC



Serum electrolytes, BUN



Type and cross-m atch,

Imaging 

Abdom inal radiograph: o

Abnorm al in 35â€“40% of patients

o

Decreased bowel gas and fecal m aterial in the right colon

o

Abdom inal m ass

o

Apex of intussusceptum outlined by gas

o

Sm all bowel distention and air-fluid levels secondary to m echanical obstruction

o 

May aid in excluding intestinal perforation

Enem a: o

Often both diagnostic and therapeutic. Reoccurrences do happen. 

Seventy-four percent successful if intussusception present â‰¤24 hours



Thirty-two percent effective when present >24 hours



The m ore distal the intussusception, the lower the ability to reduce it radiographically



Recurrent disease has sim ilar success to initial

Pa ge 2 6 8

episode. o

Com plications include bowel perforation, reduction of necrotic bowel, incom plete reduction with delay in surgery, and overlooking pathologic lead point.

o

o

o



Barium : 

Traditional standard for diagnosis and treatm ent



Characteristic coiled spring appearance

Air: 

Fluoroscopic guidance



Avoids peritoneal contam ination of perforation



Increasingly used for diagnosis and treatm ent

Contraindications: 

Peritonitis



Perforation



Unstable patients secondary to sepsis or shock

Ultrasound is highly accurate and m ay be useful as a screening technique; operator dependent: o

Typical appearance is a â€œdonutâ€• structure, with hyperechoic core surrounded by hypoechoic rim of hom ogeneous thickness.

Diagnostic Procedures/Surgery If enem a is unsuccessful in reducing, surgery is required on an em ergent basis. P.603

Differential Diagnosis 

Infection



Acute gastroenteritis



Appendicitis



Inflam m atory bowel disease

Pa ge 2 6 8



Infectious m ononucleosis



Pneum onia



Pharyngitis/group A streptococcal



Pyelonephritis



Colic



Intestinal obstruction/peritonitis



Strangulated hernia



Malrotation/volvulus



Hirschsprung disease



Traum a



Intestinal vascular/hem orrhagic disorder



Anal fissure/hem orrhoids



Ulcer disease



Vascular m alform ations



Henoch-SchÃ¶nlein purpura



Polyp



Protein-sensitive enterocolitis



Diabetes m ellitus



Coagulopathy

Treatment Pre Hospital 

Intravenous access



IV bolus of 20 m L/kg of 0.9% norm al saline (NS) if evidence of hypovolem ia, abdom inal distention, peritonitis, sepsis



Diagnosis rarely confirm ed in prehospital setting

Initial Stabilization 

Intravenous access and initiation of 0.9% NS at 20 m L/kg

Pa ge 2 6 8

bolus 

Nasogastric tube

ED Treatment 

Stabilize patient hem odynam ically.



Surgical consultation



Abdom inal radiograph film series



Interventional radiography for reduction if no contraindications: o

Enem as are 75â€“80% successful at reduction, reflecting duration of condition.

o 

Recurrences m ay also be reduced radiographically.

Antibiotics: o

Initiate if evidence of peritonitis, perforation, or sepsis.

o 

Am picillin, clindam ycin, and gentam icin

Laparotom y: o

o

Indications: 

Enem a is unsuccessful



Enem a contraindicated



Pathologic lead point



Multiple recurrences

Procedure: 

Gentle m ilking of the intussusceptum



Resection of any nonviable bowel as well as any lead points that are identified

Medication (Drugs) 

Am picillin: 100â€“200 m g/kg/d q4h IV



Clindam ycin: 30â€“40 m g/kg/d q6h IV



Gentam icin: 5.0â€“7.5 m g/kg/d q8h IV

Pa ge 2 6 8

Follow-Up Disposition Admission Criteria 

Patients undergoing successful enem a reduction should be observed for 24â€“48 hours for com plications or reoccurrence.



Patients undergoing surgery

Discharge Criteria May be considered after a very prolonged period of observation following successful enem a reduction: 

Stable patient with norm al m ental status



Sym ptom atic relief of abdom inal pain during the postreduction period

Issues for Referral Surgeon should be aware of patients with potential diagnosis of intussusception.

References 1. Bajaj L, Roback MG. Postreduction m anagem ent of intussusception in a children's hospital em ergency departm ent. Pediatrics. 2003;112:1302. 2. Danem an A, Alton DJ: Intussusception: issues and controversies in diagnosis and reduction. Radiol Clin North Am . 1996;34:743. 3. Fecteau A, Flageole H, Nguyen LT, et al. Recurrent intussusception: safe use of hydrostatic enem a. J Pediatr Surg. 1996;31(6):859â€“861. 4. McCabe JB, et al. Intussusception. A supplem ent to the m nem onic for com a. Pediatr Em erg Care. 1987;3:118.

Pa ge 2 6 8

5. Stein M, Alton DJ, Danem an A. Pneum atic reduction of intussusception: 5-year experience. Radiology. 1992;183:681. 6. Stringer MD, Pablot SM, Brererton RJ. Paediatric intussusception. Br J Surg. 1992;79:867â€“876. 7. Winslow BT, Westfall JM, Nicholas RA. Intussusception. Am Fam Physician. 1996;54(1):213â€“217.

Codes ICD9-CM 560.0

ICD10 K56.1

Pa ge 2 6 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Iritis

Iritis

Jessica Freedman

Basics Description 

Inflam m ation of anterior uveal tract



Iritis and anterior uveitis are synonym ous.



Uveitis secondary to traum a is also called traum atic iritis.

Etiology 

Most cases are idiopathic, but m ay be traum atic or associated with num erous infectious and noninfectious system ic diseases.



May be acute or chronic



Noninfectious system ic diseases include the following: o

Ankylosing spondylitis

o

Reiter syndrom e

o

Sarcoidosis

o

BehÃ§et disease

o

Inflam m atory bowel disease

o

Juvenile rheum atoid arthritis

o

Kawasaki syndrom e

o

Interstitial nephritis

o

IgA nephropathy

o

Drug reactions

Pa ge 2 6 8



o

SjÃ¶gren syndrom e

o

Psoriatic arthritis

Infectious conditions include the following: o

o

o 



Viral: 

Rubella



Measles



Adenovirus



Herpes sim plex virus



Herpes zoster virus



HIV



Mum ps



Varicella



Cytom egalovirus



West Nile virus

Bacterial: 

Tuberculosis



Syphilis



Pertussis



Brucellosis



Lym e disease



Chlam ydia



Rickettsia



Gonorrhea



Leprosy

Fungal

Malignancies include the following: o

Leukem ia

o

Lym phom a

o

Multiple sclerosis

o

Malignant m elanom a

Other causes include the following: o

Cocaine use

Pa ge 2 6 8

o

Exposure to pesticides

o

Corneal foreign body

o

Blunt traum a

Diagnosis Signs and Symptoms 



Acute presentation: o

Ocular pain, red eye

o

Photophobia (consensual)

o

Lacrim ation

o

Decreased visual acuity (usually m ild)

o

Cells and flare in anterior cham ber; hypopyon

o

Posterior synechiae (adhesions of iris to lens)

o

Miosis

o

Low intraocular pressure (occasionally m ay be high)

o

Injection of perilim bal vessels (ciliary flush)

Chronic presentation: o

Recurrent episodes

o

Few or no acute sym ptom s

Essential Workup 

History and review of system s: o



Up to 50% m ay be associated with system ic disease.

Slit-lam p exam : o

Inflam m atory cells (leukocytes) or â€œflareâ€• in the anterior cham ber are diagnostic.

o

Flare is a hom ogeneous fog secondary to protein leakage into aqueous hum or.

o

Use short, wide beam to best appreciate cells and flare.

Pa ge 2 6 9

o

Cellular deposits with m ore severe inflam m ation



Intraocular pressure



If topical anesthesia relieves pain, probably not iritis

Tests 

None usually indicated



Tailored outpatient workup if history, signs, and sym ptom s point strongly to a certain cause (with referral to ophthalm ology, rheum atology, or internal m edicine)

Lab 

Tuberculosis: o



Sarcoidosis: o







o

Erythrocyte sedim entation rate

o

HLA-B27

Inflam m atory bowel disease:

o

HLA-B27

o

Cultures of conjunctiva and urethra

Psoriatic arthritis:



HLA-B27

Lym e disease: o



HLA-B27

Reiter syndrom e:

o 

PPD

Ankylosing spondylitis:

o 

Purified protein derivative (PPD)

Im m unoassays

Juvenile rheum atoid arthritis: o

Antinuclear antibody

o

Rheum atoid factor

Sarcoidosis: o

Angiotensin-converting enzym e

o

Serum lysozym e level

Pa ge 2 6 9



Sexually transm itted disease: o

Rapid plasm a reagin or VDRL test

o

Fluorescent treponem al antibody absorption (FTA-ABS) test

o

Appropriate cultures

Imaging 

Ankylosing spondylitis: o



Sarcoidosis: o



Sacroiliac spine radiograph

Chest radiograph

Tuberculosis: o

Chest radiograph

Differential Diagnosis 

Conjunctivitis



Keratitis



Acute angle-closure glaucom a



Episcleritis



Corneal abrasion



Corneal foreign body



Intraocular foreign body



Posterior segm ent tum or

P.605

Treatment Initial Stabilization 

Goal: o

Reduce inflam m ation and prevent com plications

Pa ge 2 6 9



Cycloplegic agent (short-acting): o

Decreases pain, photophobia

o

Prevents developm ent of posterior synechiae

ED Treatment 

Cycloplegia



Topical steroids if indicated: o

Use with caution, in consultation with ophthalm ologist.

o

May cause significant com plications (i.e., progression of herpes sim plex virus keratitis)



Treat secondary glaucom a.



Supportive m easures:



o

Warm com presses

o

Dark glasses

o

Analgesia

Identification of cause: o







Ankylosing spondylitis: o

System ic anti-inflam m atory agents

o

Physical therapy

Inflam m atory bowel disease: o

System ic steroids

o

Sulfadiazine

o

Vitam in A

Reiter syndrom e: o



Treat urethritis (and sexual contacts).

BehÃ§et disease: o



Initiate appropriate m anagem ent.

System ic steroids or im m unosuppressive agents

Infectious causes: o

Appropriate m anagem ent of underlying infection

Pa ge 2 6 9

Medication (Drugs) 

Cycloplegic: o

Cyclopentolate 1â€“2% for m ild to m oderate inflam m ation: 1 drop t.i.d. for (lasts up to 24 hours)

o

Hom atropine 2 or 5% for m oderate inflam m ation: 1 drop t.i.d. (lasts up to 3 days)

o

Atropine 1% for m oderate to severe inflam m ation: 1 drop t.i.d. (lasts 7â€“14 days)



Topical steroid: o

Prednisolone acetate 1%: 1 drop q1hâ€“q6h, depending on severity



Analgesic: o

Tylenol or Tylenol with codeine

Pediatric Considerations 

Cycloplegics not recom m ended in children younger than 6 years: o

May cause system ic anticholinergic toxicity with blurred vision, flushing, tachycardia, hypotension, and hallucinations

Follow-Up Disposition Admission Criteria Not indicated unless significant system ic illness

Issues for Referral 

Iritis: o

Refer to ophthalm ologist within 24 hours for follow-up care and possible steroid therapy.

Pa ge 2 6 9



Inflam m atory bowel disease: o



Reiter syndrom e: o



Rheum atology consult

Psoriatic arthritis: o



Gastroenterology consult

Rheum atology consult

Juvenile rheum atoid arthritis: o

Rheum atology consult

References 1. Bertolini J, Pelucio M. The red eye. Em erg Med Clin North Am . 1995;13:561â€“579. 2. Kunim oto D, Kanitkar K, Makar M. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Diseases. 4th ed. Philadelphia: Lippincott William s & Wilkins; 2004. 3. Leibowitz HM. The red eye. New Engl J Med. 2000;343:345. 4. Weinberg RS. Uveitis. Ophthalm ol Clin North Am . 1999;12:71â€“79.

Codes ICD9-CM 364.3

ICD10 H20.9

Pa ge 2 6 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Iro n Po iso ning

Iron Poisoning

Sean Bryant

Basics Description 

Peak concentrations are 2â€“4 hours postingestion.



Serum concentrations not reliable if obtained m ore than 4â€“6 hours after ingestion: o

Enteric coated or sustained releaseâ€”erratic and m ay warrant serial levels



Postabsorption: Iron redistributes into tissues and fall in serum iron occurs as free iron then causes dam age at cellular level.



Injury patterns: o

Corrosive injury to intestinal m ucosa results in profound fluid loss (shock), hem orrhage, and perforations.

o

Liver receives largest load of iron because of portal venous circulationâ€”has highest injury (hem orrhagic periportal necrosis)



Free iron: o

Concentrates in m itochondria, disrupting oxidative phosphorylation; catalyzes lipid peroxidation and free radical form ation, resulting in cell death, and

Pa ge 2 6 9

increases anaerobic m etabolism and acidosis o

Causes m yocardial depression, venodilation, and cerebral edem a



Hydration of ferric form yields three protons, resulting in acidem ia.

Etiology 

Elem ental iron ingestion: o

Nontoxic <20 m g/kg

o

Moderate to severe >40 m g/kg

o

Lethality possible >60 m g/kg

o

Elem ental iron equivalents:

o



Ferrous sulfateâ€”20% (325 m g = 65 m g Fe)



Ferrous gluconateâ€”12%



Ferrous fum arateâ€”33%

Prenatal vitam ins vary from 60â€“90 m g elem ental iron per tablet.

o

Children's vitam ins m ay contain 5â€“18 m g elem ental iron per tablet.

Pediatric Considerations 

Historically highest m ortality rate am ong pediatric accidental exposures (adult iron products)



Children's chewable iron products have been shown to be safe.

Diagnosis Signs and Symptoms 

Classically divided into five stages: o

Stage 1: gastrointestinal (0.5â€“6 hours): 

Abdom inal pain

Pa ge 2 6 9

o

o

o

o



Vom iting



Diarrhea



Hem atem esis



Hem atochezia

Stage 2: latent/quiescent (6â€“24 hours): 

Resolution of GI sym ptom s



Deceptive phase



Possible hypotension and acidosis

Stage 3: shock and organ failure (6â€“72 hours): 

Hypoperfusion



Metabolic acidosis



Com a



Coagulopathy

Stage 4: hepatic failure (2â€“3 days): 

Coagulopathy



Hypoglycem ia



Jaundice



Elevated liver function tests (LFTs) and bilirubin

Stage 5: obstruction (2â€“4 weeks): 

Gastric outlet and sm all bowel obstruction



Abdom inal pain, vom iting



Patient m ay present in or skip any of the five stages.



If onset of stage 1 does not occur within 6 hours, likely not significant ingestion

Essential Workup Acute iron poisoning is clinical diagnosis, regardless of laboratory results.

Tests Lab 

Serum iron levels (Âµg/dL) o

Peak absorption between 2 and 6 hours

Pa ge 2 6 9





o

Four hours m ost com m on tim e for peak level

o

Delayed peak with enteric coated/sustained release

Electrolytes, BUN/creatinine, glucose: o

Anion gap m etabolic acidosis

o

Hyperglycem ia early

o

Hypoglycem ia late

Arterial blood gas (ABG): o



Metabolic acidosis

CBC: o

Anem ia with significant hem orrhage

o

Leukocytosis



Liver function



Coagulation profile



Lactate level



Type and screen if hem orrhage



Total iron-binding capacity (TIBC) is not useful.

Imaging Abdom inal radiograph check for: 

Tablets (children's chewables rarely visible)



Absence of pill fragm ent interpretation: o

Patient did not ingest iron.

o

Iron was in solution or has already dissolved.

o

Patient ingested pediatric m ultivitam in product.

o

Absence of radiopacities does not rule out significant or lethal ingestion.



Perforation

Differential Diagnosis 

Sepsis



Acetam inophen toxicity



Toxic ingestions causing anion gap acidosis: o

Salicylate

Pa ge 2 6 9

o

Cyanide

o

Methanol

o

Ethylene glycol



Mushroom s



Heavy m etals



Theophylline toxicity



GI bleed from other causes (alcoholic liver disease)

P.607

Treatment Initial Stabilization 



Airway, breathing, and circulation m anagem ent (ABCs): o

Airway if needed

o

Venous access and fluids for hypotension

o

Cardiac m onitor and pulse oxim etry

Narcan, thiam ine, dextrose (or Accu-Chek) as needed for altered m ental status

ED Treatment Decontamination 

Iron is poorly adsorbed to activated charcoal.



Gastric lavage has not been shown to change outcom e.



NaHCO 3 , phospho soda, and oral deferoxam ine are not recom m ended.



If pill fragm ents are visualized or history of significant ingestion: o

Adm inister whole bowel irrigation (WBI) with adm inistration of Go-Lytely (peds: 10â€“15 m L/kg/h;

Pa ge 2 7 0

adult: 1â€“2 L/h) while m onitoring progression with kidneys, ureters, and bladder (KUBs) radiograph. o 

Caution with GI bleed

Endoscopy or gastrotom y can rem ove bezoar form ation after m assive ingestions (>240 m g/kg).

Chelation with Deferoxamine (DFO) 

DFO is highly specific chelator of parenteral iron.



IV infusion results in m ore constant DFO levels and is route of choice: o



Must be given as soon as possible (<24 hours)

Adm inistration techniques: o

Increase IV infusion rate to 15 m g/kg/h over 20 m inutes, m onitoring for hypotension.

o

Decrease infusion rate if hypotension occurs.

o

Infusion rates as high as 45 m g/kg/h have been used and tolerated.

o

Disregard m anufacturer's recom m endation of m axim um daily doses of 6 g in serious iron exposures.



IM DFO challenge test is not advocated.



Indication for adm inistration: o

Sustained GI sym ptom s

o

Altered m ental status

o

Hypotension, lethargy, m etabolic acidosis, or shock

o

Serum iron >500 Âµg/dL

o

Serum iron >350 Âµg/dL and pills seen on KUB

o

Rising serum iron levels

o

Interpret serum levels cautiouslyâ€”tim e since ingestion m ust be considered: 

Treatm ent m ay be indicated in patient who presents late, after distribution stage (>8 hours postingestion), with serum iron level <350

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Âµg/dL o

If serum iron levels not readily available, base treatm ent decisions on clinical course.



Length of infusion (controversial): o

DFOâ€“iron com plex causes urine to turn vin rose colorâ€”this suggests continuing infusion until urine returns to norm al.

o

Resolution of signs and sym ptom s of significant toxicity is criteria for discontinuing DFO.

o

Prolonged DFO therapy longer than 24â€“48 hours m ay precipitate adult respiratory distress syndrom e (ARDS).

o

In severe cases with continued signs and sym ptom s, infusion m ay be continued cautiously at lower dose.



Controversies: o

Safety of DFO infusions given for >24 hours

o

Maxim al infusion rates and total am ount of DFO given

o

What serum iron concentration warrants treatm ent

o

End point of treatm ent (best end point is resolution of poisoning, i.e., acidem ia)

o 

Role of extracorporeal elim ination

Contact regional poison center for m oderate to severe iron exposures.

Follow-Up Disposition Admission Criteria 

GI sym ptom s or dehydration



Patients treated with deferoxam ine

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

ICU adm ission for com a, shock, m etabolic acidosis, or iron levels >1,000 Âµg/dL

Discharge Criteria 

Asym ptom atic with negative radiograph



Minim al to no sym ptom s after 6-hour observation



Mild GI sym ptom s that have resolved without evidence of m etabolic acidosis and serum iron <350 Âµg/dL

References 1. Anderson BD, Turchen SG, Manoguerra AS, et al. Prospective analysis of ingestions of iron containing products in the United States: are there differences between chewable vitam ins and adult preparations? J Em erg Med. 2000;19:255â€“258. 2. Bryant SM, Leikin J. Iron. In: Brent J, Wallace KL, Burkhart KK, et al., eds. Critical Care Toxicology. St. Louis, MO: Mosby; 2005. 3. Leikin J, Paloucek F. Iron. In: Poisoning and Toxicology Handbook. Hudson, OH: Lexi-Com p; 2002. 4. Mills KD, Curry SC. Acute iron poisoning. Em erg Med Clin North Am . 1994;12(2):397â€“413. 5. Perrone J. Iron. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. New York: McGraw-Hill; 2002. 6. Tenenbein M. Benefits of parenteral deferoxam ine for acute iron poisoning. J Toxicol Clin Toxicol. 1996;34(5):485â€“489. 7. Tenenbein M. Iron. In: Ford MD, Delaney KA, Ling LJ, et al., eds. I. Philadelphia: WB Saunders; 2001.

Codes ICD9-CM 964.0

ICD10 T45.4

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Irritable Bo w el

Irritable Bowel

Scott A. Miller

Basics Description 

Syndrom e of abdom inal pain and altered bowel habits with no m echanical, biochem ical, or inflam m atory conditions explaining sym ptom s



Prevalence estim ated to be 12%



Sym ptom -based diagnosis

Genetics There is a fam ilial aggregation of irritable bowel syndrom e (IBS), but it is unclear if this represents a genetic link or learned illness behavior.

Etiology 

Multiple possible pathophysiologic factors



Altered gastrointestinal m otility: o

Increased m otility associated with diarrhea (D-IBS)

o

Decreased m otility associated with constipation (C-IBS)



Increased gut sensitivity (visceral hyperalgesia): o



Exaggerated response to norm al GI physiology

Mucosal inflam m ation:

Pa ge 2 7 0

o

Increased incidence of IBS sym ptom s after bacterial enteritis



Em otional stress: o

Increased incidence of anxiety, som atoform disorders, or history of abuse in patients who seek care

o

No evidence of increased psychiatric illness in those who do not seek care

Diagnosis Signs and Symptoms History 

Rom e II criteria: At least 12 weeks (which need not be consecutive) in the preceding 12 m onths of abdom inal pain or discom fort with two of the following three features: o

Relieved with defecation and/or

o

Onset associated with a change in the frequency of stool and/or

o

Onset associated with a change in form (appearance) of stool



Manning and Rom e I criteria exist with differing sensitivities and specificities.



Other sym ptom s consistent with IBS: o

Abdom inal distention or bloating

o

Passage of m ucus in stools

o

Altered stool passage (straining, urgency, or feeling of incom plete evacuation)

o

Postprandial upper abdom inal discom fort

o

Sym ptom s of gastroesophageal reflux

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o 

Flatulence

Fem ale:m ale ratio of 2:1 overall, m uch higher in those who seek care



Alarm features (suspect m ore serious etiology): o

Onset of sym ptom s past age 50 years

o

Unexplained weight loss

o

Progressive or unrelenting abdom inal pain

o

Sym ptom s awaken patient at night.

o

Fam ily history of colon cancer

o

Large-volum e diarrhea

o

Hem atochezia

Physical Exam 

Usually well appearing



Norm al physical exam



May have tender sigm oid or palpable sigm oid cord

Essential Workup Clinical diagnosis, so careful history crucial

Tests Lab 

Typically no abnorm alities found



Labs directed at excluding other serious pathology



CBC



Electrolytes, BUN, creatinine, glucose



Liver function tests



Stool studies



Thyroid studies



Antigliadin antibodyâ€”celiac disease, can be done by prim ary m edical doctor (PMD)

Imaging 

To exclude serious pathology

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

Plain abdom inal film s if concerned about obstruction



Abdom inal CT if concerned about other surgical pathology



Gallbladder ultrasonography

Diagnostic Procedures/Surgery 

Colonoscopy with biopsy



Hydrogen breath testâ€”lactose intolerance



Upper GI endoscopy

Differential Diagnosis 

Celiac disease



Inflam m atory bowel disease o

Ulcerative colitis/proctitis

o

Crohn disease



Infectious enteritis



Sm all intestinal bacterial overgrowth



Lactose intolerance



Colorectal cancer



Diverticular disease



Biliary disease



Diabetes



Pancreatitis



Hypothyroidism or hyperthyroidism



Obstruction



Peptic ulcer disease



Acute interm ittent porphyria

P.609

Treatment

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Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



IV fluid for dehydration

ED Treatment 

Em pathetic approach and therapeutic physicianâ€“patient relationship





Exercise: o

Im proves gastric em ptying

o

Im proves constipation

Diet: o

Avoid dietary excesses, caffeine, or any triggers

o

Moderation of fat intake

o

Avoidance of beans, cabbage, uncooked broccoli, other flatulent foods if sym ptom atic









5HT4 receptor agonist tegaserod: o

Stim ulates peristalsis

o

Helpful in C-IBS

Constipation sym ptom s: o

High-fiber diet, fiber supplem ents

o

Osm otic laxatives: 

Magnesium hydroxide



Magnesium citrate



Polyethylene glycol



Lactulose



Sorbitol

Diarrhea sym ptom s: o

Bowel training

o

Loperam ide

o

Diphenoxylate-atropine

Abdom inal pain: o

Avoid narcotics.

Pa ge 2 7 0

o

o

o

Antispasm odics/anticholinergics: 

Dicyclom ine



Hyoscyam ine



Warn of anticholinergic side effects.

Nonnarcotic analgesics: 

Acetam inophen



Nonsteroidal anti-inflam m atory drugs (NSAIDs)



Tram adol



Gabapentin

Tricyclic antidepressants: 



Raise threshold for and tolerance of pain

Psychotherapy and selective serotonin reuptake inhibitors (SSRIs): o

More psychopathology am ong those who seek treatm ent for IBS, so m ay be useful

Medication (Drugs) 

Am itriptyline: 25 m g PO at bedtim e



Dicyclom ine: 10â€“20 m g PO q.i.d.



Diphenoxylate-atropine: 5 m g PO q.i.d.



Gabapentin: Start at 100 m g PO daily.



Hyoscyam ine: 0.125â€“0.25 m g PO or sublingual



Lactulose: Start at 10 g PO daily.



Loperam ide: 2 m g PO q4h PRN



Magnesium citrate: 150â€“300 m L (1.745 g/30 m L solution) once, m ay repeat



Magnesium hydroxide: 650 m g to 1.3 g PO q.i.d.



Polyethylene glycol: 17 g PO daily



Sorbitol: 1 g/kg PO daily



Tegaserod: 6 m g PO b.i.d.



Tram adol: 50 m g PO b.i.d.

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Follow-Up Disposition Admission Criteria 

Suspicion of an em ergent abdom inal condition



Severe sym ptom s with associated psychiatric disorder



Uncertainty about the diagnosis

Discharge Criteria Alm ost all patients can be m anaged as outpatients.

Issues for Referral 

All patients need to follow up with prim ary care physician.



Som e m ay benefit from GI or psychiatric referral.

References 1. Cash BD, Chey WD. Diagnosis of irritable bowel syndrom e. Gastroenterol Clin North Am . 2005;34(2):205â€“220. 2. Lacy BE. Irritable bowel syndrom e: a prim er on m anagem ent. Rev Gastroenterol Disord. 2003;3(3):S32â€“S42. 3. Lesbros-Pantoflickova D, Michetti P, et al. Meta-analysis: the treatm ent of irritable bowel syndrom e. Alim ent Pharm acol Ther. 2004;20:1253â€“1269. 4. Mertz HR. Irritable Bowel Syndrom e. N Engl J Med. 2003;349:2136â€“2146. 5. Schoenfeld, P. Efficacy of current drug therapies in irritable bowel syndrom e: what works and does not work. Gastroenterol Clin North Am . 2005;34(2):319â€“335.

Miscellaneous

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SEE ALSO: Inflam m atory Bowel Disease; Gastroenteritis

Codes ICD9-CM 564.1

ICD10 K58.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Irritable Infant

Irritable Infant

Stacey A. Suecoff David H. Rubin

Basics Description 

Most children have som e period of the day when they are m ost irritable, usually toward the evening: o

Norm al infant crying ranges from 1â€“4 hours by 6 weeks of age.



Irritability based on a com parison with the child's norm al pattern



Colic is the m ost com m on cause of inconsolable crying in infants, occurring in as m any as 25% of healthy children: o

Episodes of scream ing accom panied by drawing up knees and passage of flatus

o

Usually begins at 2â€“3 weeks and m ay continue through 12 weeks

o

Diagnosis of exclusion

Etiology 

Infection/inflam m ation: o

Minor acute infections (upper respiratory infection, otitis m edia, thrush, gingivostom atitis)

o

Urinary tract infection

Pa ge 2 7 1

o

Meningitis

o

Osteom yelitis

o

Pneum onia

o

Gastroenteritis

o

Gastroesophageal reflux, esophagitis



Colic



Teething



Constipation



Parental anxiety



Traum a: o

Foreign body, fracture, tourniquet (hair around digit or penis)

o

Hem atom aâ€”subdural, epidural

o

Corneal abrasion

o

Child abuse

o

Diaper pin

o

Splinter

o

Anal fissure



Sickle cell crisis



Incarcerated hernia, testicular torsion



Intussusception



Medications: o

Diphtheria, pertussis, and tetanus (DPT) vaccine reaction





o

New prescription

o

Hom e rem edy

o

Vitam in use/overdose

Deficiency: o

Malnutrition

o

Iron deficiency/anem ia

Hypoxiaâ€”cardiopulm onary disorder: o

Supraventricular tachycardia

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o 

Endocrine/m etabolic: o



Congestive heart failure

Hypoglycem ia

Vascular

Diagnosis Signs and Symptoms History Obtain com plete history (including neonatal history) and inform ation regarding routine feeding, crying.

Physical Exam 

Assess vital signs including rectal tem perature and pulse oxim etry.



Measure and plot for percentiles: height, weight, and head circum ference.



Perform a thorough physical exam with infant com pletely undressed.

Tests Lab 

CBC, urinalysis, chem istries, and cultures as indicated by history and physical exam ination



Stat blood glucose at bedside if indicated.

Imaging 

Fluorescein eye exam



Chest radiograph to exclude cardiopulm onary disease



ECG



CT scan of the head



Contrast radiograph studies such as barium enem a for

Pa ge 2 7 1

specific indications

Diagnostic Procedures/Surgery 

Skeletal survey



Stool hem occult test

Differential Diagnosis See Etiology above. P.611

Treatment Initial Stabilization 

Manage underlying conditions; stabilize airway, breathing, and circulation (ABCs).



Im m ediate rem oval of hair tourniquets, splinters, and so on.

ED Treatment 

Initial evaluation of the child focusing on parentâ€“child interaction and then on potential underlying conditions



Colic responds to soothing, rhythm ic activities, avoiding stim ulants (coffee, cola), m inim izing daytim e sleep: o

Soy or hydrolyzed casein form ula m ay be transiently beneficial.

o

Parents m ust reduce stress:

o

No proven pharm acologic therapy



Support, em pathy, close follow-up



Prolonged observation of the child is usually appropriate.

Pa ge 2 7 1

Medication (Drugs) Dependent on the underlying condition

Follow-Up Disposition Admission Criteria 

Life-threatening underlying condition



Significant parental stress secondary to crying infant

Discharge Criteria 

No serious condition



Functional and supportive fam ily



Excellent follow-up is essential; parents m ust feel that their observations and concerns are not being ignored; close follow-up and ongoing observation will occur.

References 1. Barnett RM. Psychiatric and behavioral disorders. In: Barkin RM, ed. Pediatric Em ergency Medicine. 2nd ed. St. Louis, MO: Mosby; 1997:1042â€“1055. 2. Barr RG. Colic and crying syndrom es in infants. Pediatrics. 1998;102(5 suppl E):1282â€“1286. 3. Chalabi R, Matre WM, Greene MK. Infant with irritability, feeding problem s, and progressive developm ent abnorm alities presenting repeatedly to a pediatric em ergency departm ent. Pediatr Em erg Care . 1997;13(2):123â€“126. 4. Garrison MM, Christakis DA. A system atic review of treatm ents for infant colic. Pediatrics. 2000;106(1 pt 2):184â€“190. 5. Hiscock H, Jordan B. 1. Problem crying in infancy. Med J Aust.

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2004;181(9):507â€“512. 6. Hyam s JS. Functional gastrointestinal disorders. Curr Opin Pediatr. 1999;11(5):375â€“378. 7. Ruiz-Contreras J, Urquia L, Bastero R. Persistent crying as predom inant m anifestation of sepsis in infants and newborns. Pediatr Em erg Care. 1999;15(2):113â€“115. 8. Swischuk LE. Irritable infant and left lower extrem ity pain. Pediatr Em erg Care. 1997;13(2):123â€“126. 9. Trocinski DR, Pearigen PD. The crying infant. Em erg Med Clin North Am . 1998;16:895â€“910.

Codes ICD9-CM 799.2

ICD10 R68.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Irritant G as Expo sure

Irritant Gas

Exposure Sean Bryant

Basics Description 

An irritant is any noncorrosive substance that on im m ediate, prolonged, or repeated contact with respiratory m ucosa will induce a local inflam m atory reaction.



Respiratory irritants are inhaled as gases, fum es, particles, or liquid aerosols.



Inhaled irritants: o

Pulm onary toxicity determ ined prim arily by its water solubility



Inhalation accidents frequently involve a m ixture of irritant gases as well as chem ical asphyxiants: o

Carbon m onoxide

o

Hydrogen cyanide

o

Hydrogen sulfide

o

Oxides of nitrogen

Risk Factors Exposure to potential irritants:

Pa ge 2 7 1



Occupational



Leisure



Intentional



Accidental

Pathophysiology Cellular injury through interaction with respiratory m ucosal water with subsequent form ation of acids, alkalis, and free radicals

Etiology 

Settings: o

Industrial: chem ical m anufacturing, m ining, plastics, and petroleum industries



o

Hom e: im proper use or storage of cleaning chem icals

o

Fires: Com bustion yields toxic gases.

Im m ediate onset of upper airway inflam m ation with highly water-soluble irritant gases or with aerodynam ic diam eter >5 Âµm : o

Am m onia (fertilizers, refrigerants, dyes, plastics, synthetic fibers, cleaning agents): 

Im m ediate sym ptom s range from m ild edem a and erythem a to full-thickness burns and airway obstruction.

o

Sulfur dioxide (fum igants used on produce, bleaching, tanning, brewing, wine m aking, com bustion of coal, and sm elting of sulfide-containing ores): 

o

Com bines with water, form ing sulfuric acid

Hydrogen chloride (form ed during com bustion of chlorinated hydrocarbons such as polyvinyl chloride): 

o

Com bines with water, form ing hydrochloric acid

Chloram ine (generated when am m onia and bleach are m ixed): 

When exposed to m oist surfaces, releases

Pa ge 2 7 1

hydrochlorous acid o

Acrolein (production of plastics, pharm aceuticals, synthetic fibers; form ed during com bustion of petroleum products, cellulose, wood, paper): 

May cause protein dam age via free radical production and sulfhydryl binding

o

Form aldehyde (production of plywood, particle board, insulation; com bustion product of gas stoves and heaters): 

Com bines with water to form sulfuric acid and form ic acid

o

Hydrogen fluoride (com bustion of fluorinated hydrocarbons): 



Depletes calcium stores, resulting in cell death

Latent period of m inutes to hours before onset of sym ptom s with irritant gases of interm ediate water solubility or aerodynam ic diam eter of 1â€“5 Âµm : o

Chlorine (product of chlorinated chem icals; bleaching agent): 

Upper and lower airway dam age after reacting with water to form hydrochloric and hydrochlorous acids



Delayed onset of sym ptom s up to 24 hours after inhalation with irritant gases of poor water solubility or aerodynam ic diam eter <1 Âµm (with little or no warning of exposure): o

Oxides of nitrogen produced: 

In m anufacture of dyes and fertilizers



By electric arc welding and gas blowing



By ferm entation of nitrogen-rich silage (silo-filler's disease)

 o

In com bustion of nitrocellulose and polyam ides

Phosgene/carbonyl chloride (arc welding and

Pa ge 2 7 2

pesticide production: com bustion of chlorinated hydrocarbons and solvents) o

Ozone (produced during arc welding)

o

Cadm ium oxide (oxyacetylene welding and electroplating)

Diagnosis Signs and Symptoms 

Dependent on water solubility



Highly water-soluble gases:





o

Eye, nose, throat burning

o

Shortness of breath

o

Wheezing

o

Cough

o

Hoarseness

o

Stridor

o

Obstruction

Interm ediate water solubility: o

Upper and lower tract involvem ent

o

Mucosal irritation

o

Bronchospasm

o

Dyspnea

o

Wheezing

o

Cough

o

Rales

o

Possible delayed pulm onary edem a

Other: o

Derm al irritation

o

Headache

o

Nausea

Pa ge 2 7 2

o

Vom iting

o

Confusion

o

Seizures

o

Syncope

Essential Workup History of exposure to irritant gases in addition to noted sym ptom s confirm s diagnosis.

Tests ECG in the following patients: 

Elderly



Cardiac history



Evidence of significant pulm onary sym ptom s

P.613

Lab 



Arterial blood gas: o

Assess oxygenation, ventilation status, and pH.

o

Pulse oxim etry is unreliable.

Carbon m onoxide level: o

If sm oke inhalation with concom itant irritant gas inhalation (see Carbon Monoxide Poisoning)



Methem oglobin level: o



Serum calcium level: o



If oxides of nitrogen are suspected

If hydrogen fluoride is suspected

Lactate: o

Elevation m ay indicate cellular poisoning from carbon m onoxide or cyanide.



Pregnancy test in all fem ales of childbearing age



Rapid dextrose

Pa ge 2 7 2



Cardiac enzym e levels if acute coronary syndrom e suspected

Imaging Chest radiograph: 

Frequently norm al on presentation



May take up to 24 hours to reveal pulm onary edem a or evidence of diffuse injury

Diagnostic Procedures/Surgery 

Spirom etry: o

Assess evidence suggesting airway narrowing and bronchoconstriction.



Direct laryngoscopy: o



Assess evidence of upper airway edem a.

Corneal fluorescein: o

Assess evidence of corneal burns/injury.

Differential Diagnosis 

Asthm a exacerbation



Allergic stim uli (pollen)



Physical stim uli (cold air)



Bronchitis



Pneum onia



Occupational asthm a



Hypersensitivity pneum onitis



Congestive heart failure

Treatment Pre Hospital Rescuer's goal is to prevent self-contam ination with use of protective

Pa ge 2 7 2

clothing or equipm ent (self-contained breathing apparatus).

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

One hundred percent oxygen through a tight-fitting, nonrebreathing face m ask

o

Early intubation m ay be necessary to protect airway from edem a.

o

Mechanical ventilation

o

Continuous positive airway pressure or positive end expiratory pressure m ay enhance oxygenation.



Decontam inate by rem oving clothes and irrigating skin and ocular tissues.

ED Treatment 

Inhaled nebulized Î² 2 -adrenergic agonists (albuterol) for bronchoconstriction



Inhaled/IV/PO corticosteroids: beclom ethasone, m ethylprednisolone, prednisone: o

Controversial

o

No controlled trials that docum ent benefit of acute corticosteroids after irritant gas inhalation



Nebulized sodium bicarbonate (3.75% solution) after chlorine gas exposure: o

Reported to im prove oxygenation in several case reports/series



Nebulized calcium gluconate after acute hydrogen fluoride inhalation: o



Reported, but with no proven benefit

Cyanide antidote kit if hydrogen cyanide is suspected (see Cyanide Poisoning)



Oxygen or hyperbaric oxygen therapy if carbon m onoxide poisoning docum ented

Pa ge 2 7 2

Medication (Drugs) 

Albuterol: 0.5 m L (peds: 0.03 m L or 0.15 m g/kg per dose) of 0.5% solution diluted in norm al saline to 3 m L aerosolized



Calcium gluconate: nebulized (2.5â€“3% solution) prepared by adding 0.15 g of calcium gluconate to 6 m L of norm al saline



Metaproterenol: 0.3 m L (peds: 0.1â€“0.3 m L) of 5% solution diluted in norm al saline to 3 m L aerosolized



Sodium bicarbonate: nebulized (3 m L of 8.4% sodium bicarbonate m ixed with 2 m L of norm al saline to prepare 5 m L of 5% solution): o

Repeat as needed.

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission: o

Intubated patients

o

Significant respiratory insufficiency or potential upper airway obstruction



Persistently sym ptom atic with bronchospasm or oxygen requirem ent



Exposure to irritant gases that affect peripheral airways: o

Delayed pulm onary edem a and respiratory failure m ay occur.



Conservative treatm ent for children, pregnant fem ales,

Pa ge 2 7 2

elderly patients, or those with pre-existing chronic obstructive pulm onary or coronary disease

Discharge Criteria 

Mild exposures that respond well to supportive care and have no oxygen requirem ent or bronchospasm after a 4to 6-hour observation period



Follow-up chest radiograph during observation and prior to discharge, especially if any sym ptom s are present or clinically worsening

References 1. Bosse GM. Nebulized sodium bicarbonate in the treatm ent of chlorine gas inhalation. J Toxicol Clin Toxicol. 1994;32:233â€“241. 2. Newm an-Taylor AJ. Respiratory irritants encountered at work. Thorax. 1996;51:541â€“545. 3. Rorison DG, McPherson SJ. Acute toxic inhalations. Em erg Med Clin North Am . 1992;10:409â€“435. 4. Vinsel PJ. Treatm ent of acute chlorine gas inhalation with nebulized sodium bicarbonate. J Em erg Med. 1990;8:327â€“329. 5. Weiner AL, Bayer MJ. Inhalation: gases with im m ediate toxicity. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 6. Weiss SM, Lakshm inarayan S. Acute inhalation injury. Clin Chest Med. 1994;15:103â€“116.

Miscellaneous SEE ALSO: Carbon Monoxide Poisoning; Cyanide Poisoning

Codes ICD9-CM 987.9

Pa ge 2 7 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Iso niaz id Po iso ning

Isoniazid

Poisoning Sean Bryant

Basics Description 

Com plexes with and inactivates pyridoxal-5 phosphate, the active form of pyridoxine (vitam in B 6 )



Com plexes with pyridoxine, which is then renally elim inated



Inhibits pyridoxine phosphokinase, hindering the conversion of pyridoxine to its active form



Interfering with pyridoxine levels yields a net decrease in gam m a-am inobutyric acid (GAMA) production



Depressed GABA causes cerebral excitability and seizures.



Inhibits lactate dehydrogenase, decreasing the conversion of lactate to pyruvate: o



Contributes to the profound anion gap acidosis

Chronic toxicity: o

Interferes with synthesis of nicotinic acid (niacin)

o

Causes syndrom e indistinguishable from pellagra after m onths of therapy (niacin deficiency)



Som e actions sim ilar to the m ono am ine oxidase

Pa ge 2 7 2

inhibitors: o

Reports of a tyram inelike reaction to isoniazid

o

Rare cases of m ania, diaphoresis, depression, obsessive-com pulsive disorder, and psychosis

Pharmacokinetics 

Rapidly absorbed reaching peak levels within 1â€“2 hours



Volum e of distribution 0.6 L/kg and 10% protein binding



Renally excreted within 24 hours after acetylation in the liver



Half life <1 hour in fast acetylators, and 2â€“4 hours in slow-acetylating individuals

Etiology 

High risk includes im m igrants, hom eless, HIV infected, alcoholics, and lower socioeconom ic status populations



Slow acetylators (60% of African Am ericans and whites com pared to 20% of Asians) are m ore prone to chronic effects/toxicity.



LD50 in hum ans estim ated to be 80â€“150 m g/kg



Ingestions less than 1.5 g lead to m ild toxicity, and those of 10 g or m ore often result in fatality

Diagnosis Signs and Symptoms Acute Toxicity 

Neurologic: o

Altered m ental status

o

Seizures refractory to traditional m ethods of control

o

Agitation

o

Com a

Pa ge 2 7 2









o

Dizziness

o

Ataxia

o

Hyperreflexia

o

Slurred speech

o

Hallucinations

o

Psychosis

Gastrointestinal (GI): o

Nausea

o

Vom iting

Renal: o

Anuria

o

Oliguria

Cardiovascular: o

Hypotension

o

Tachycardia

o

Shock

o

Cyanosis

Metabolic: o

Profound anion gap m etabolic acidosis (elevated lactate)

o

Hypertherm ia

Chronic Toxicity 



Neurologic: o

Peripheral neuropathy

o

Optic neuritis, optic atrophy

o

Psychosis

o

Insom nia

o

Vertigo

o

Pellagra

GI hepatitis o

Liver failure, hepatitis

o

Nausea, vom iting, constipation

Pa ge 2 7 2

o

Anorexia

Essential Workup Without specific history of ingestion, initiate general workup for: 

Altered m ental status



Seizures



Metabolic acidosis

Tests Lab 

ABG: o





Profound m etabolic acidosis

Electrolytes, blood urea nitrogen/creatinine, glucose: o

Elevated anion gap acidosis

o

Hyperglycem ia

CBC: o

o

Acute toxicity: 

Leukocytosis



Eosinophilia

Chronic toxicity: 

Agranulocytosis



Eosinophilia



Hem olysis



Anem ia

Imaging 

Chest radiograph: o

Evidence of tuberculosis increases suspicion for toxicity

o 

Evaluate for aspiration pneum onia

CT/lum bar puncture if indicated and questionable history

Differential Diagnosis 

Toxins:

Pa ge 2 7 3



o

Tricyclic antidepressants

o

Salicylates (aspirin)

o

Theophylline

o

Methanol/ethylene glycol

o

Paraldehyde

o

Lithium

o

Carbon m onoxide

o

Cocaine

o

Agents that cause m etabolic acidosis

CNS: o

Cerebrovascular accident

o

Intracranial hem orrhage/m ass/traum a/abscess



Hypoglycem ia



Urem ia



Thyrotoxicosis

P.615

Treatment Initial Stabilization 



ABCs: o

Supplem ental oxygen

o

Intubate if necessary for airway protection

o

Cardiac m onitor

o

0.9% NS access

Narcan, thiam ine, D 5 0 W (Accu-Chek) if altered m ental status

ED Treatment

Pa ge 2 7 3



Vitam in B 6 (pyridoxine): o

Specific antidotal treatm ent for INH toxicity

o

Goal: 1 g of pyridoxine for each gram of INH ingested (1 g q2â€“3m in)

o

Adm inister 5 g for unknown am ount ingested.

o

May repeat in 20 m inutes for refractory seizures or persistent com a

o

If insufficient quantity of pyridoxine available, contact other hospital pharm acies and your regional poison control center to obtain m ore.

o

If no parenteral pyridoxine available, crush tablets and adm inister as a slurry.





Seizure control: o

Pyridoxine restores deficiency in GABA

o

Benzodiazepines are synergistic with pyridoxine

o

Phenytoin has no role

Gastric decontam ination after stabilization: o

Consider gastric lavage only in life-threatening ingestions presenting within 1 hour with a protected airway (being aware of potential seizure activity and obtundation)

o 



Activated charcoal dosed at 10:1 ratio (AC: drug)

Hem odialysis: o

Persistent sym ptom s despite adequate therapy

o

Renal insufficiency in sym ptom atic patients

Sodium bicarbonate: o

For severe m etabolic acidosis

o

Acidosis usually resolves spontaneously after elim ination of seizures.

Medication (Drugs)

Pa ge 2 7 3



Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Lorazepam (benzodiazepine): 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV/IM initial dose



Pyridoxine (vitam in B 6 ): 1 g IV for each gram of INH ingested (see above)



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV/IM

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission for refractory seizures, severe acidosis, com a, altered m ental status



Uncontrolled nausea/vom iting, unclear history of ingestion, or suicidal

Discharge Criteria 

Sym ptom s are usually observed within 45 m inutes of an acute overdose but m ay be delayed for 2 hours or longer



Discharge if asym ptom atic after 6 hours

References 1. Boyer EW. Antituberculous agents. In: Goldfrank LR, ed. Goldfrank's toxicologic em ergencies. McGraw-Hill, 2002. 2. Brent J, Vo N, Kulig K, et al. Reversal of prolonged isoniazid-induced com a by pyridoxine. Arch Intern Med.

Pa ge 2 7 3

1990;150:1751â€“1753. 3. Henry GC, Haynes S. Isoniazid and other antituberculous drugs. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical toxicology. Philadelphia, PA: WB Saunders, 2001. 4. Leikin J, Paloucek F. Isoniazid. In: Poisoning and toxicology handbook. Hudson, OH: Lexi-com p, 2002. 5. Mcfee RB, Mofenson HC, Carracio TR. Isoniazid poisoning. Em erg Med. 2000;32:57â€“58.

Miscellaneous SEE ALSO: Seizures

Codes ICD9-CM 961.8

ICD10 T37.1

Pa ge 2 7 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Iso pro pano l Po iso ning

Isopropanol

Poisoning Paul Kolecki

Basics Description 

CNS depressant effect of isopropanol is two to three tim es as potent as ethanol.



Many products that contain isopropanol also contain m ethanol, ethylene glycol, and ethanol.



Rapidly absorbed following oral ingestion



Ketogenic, but does not cause significant acidosis



Metabolized by alcohol dehydrogenase to acetone (a CNS depressant): o

Concom itant ethanol ingestion doubles half-life of isopropanol but not acetone.

o 

Acetone elim inated by lung and kidney

Half-life: o

Isopropanol: 3â€“16 hours

o

Acetone: 7.5â€“26 hours

Etiology 

Isopropanol (isopropyl alcohol): clear, colorless, volatile liquid with faint odor of acetone and bitter taste

Pa ge 2 7 3



Available as 70% rubbing alcohol solution: o

May contain blue dye that was added to inhibit its abuse (â€œblue heavenâ€•)





Found in: o

Various toiletries

o

Disinfectants

o

Window-cleaning solutions

o

Paint rem over

o

Solvents

o

Jewelry cleaners

o

Detergents

o

Antifreeze

Typical adult patient: chronic alcoholic who has been on drinking binge and recently depleted his or her ethanol supply



Derm al and rectal adm inistration can cause system ic toxicity.

Diagnosis Signs and Symptoms 

Usually occur within 30â€“60 m inutes of ingestion



Neurologic: o

Lethargy

o

Weakness

o

Headache

o

Inebriation

o

Vertigo

o

Ataxia

o

Apnea

o

Com a

Pa ge 2 7 3

o

Initial excitation phase seen with ethanol ingestion is absent.











Gastrointestinal: o

Nausea/vom iting

o

Abdom inal pain

o

Gastritis

o

Hem atem esis

Cardiovascular: o

Hypotension

o

Tachycardia

o

Myocardial depression

o

Peripheral vascular dilatation

Pulm onary: o

Respiratory depression

o

Hem orrhagic tracheobronchitis

Derm atologic: o

Skin irritation

o

Burns

Ocular: o

Irritation

o

Lacrim ation

Pediatric Considerations 

Accidental ingestions com m on <6 years old



Rubbing alcohol sponge baths m ay cause inhalational toxicity.

Essential Workup 

History of ingestion



Odor of isopropanol or acetone on patient's breath

Tests Lab

Pa ge 2 7 3



Electrolytes, BUN, creatinine (Cr), glucose: o

Hypoglycem ia occurs.

o

Does not produce significant acidosis unless accom panied by end organ hypoperfusion

o

Acetone can produce false elevation of serum Cr: 

When acetone level >40 m g/dL, Cr values rise at approxim ately 1 m g Cr/100 m g/dL acetone.



Cr returns to baseline following acetone m etabolism .



CBC: o

Decreased hem atocrit with significant hem orrhagic gastritis



Arterial blood gas (ABG): o

Acidosis rare unless owing to hypoperfusion or coingestant



Urinalysis: o

Ketones present



Serum ketones present



Isopropanol level: o



Com a with level >150 m g/dL

Serum osm olarity: o

Osm olar gapâ€”difference between m easured and calculated osm olarity

o

Calculated osm olarity = 2 Na + BUN/2.8 + glucose/18 + ethanol/4.3.

o

Osm olar gap present if m easured m inus calculated osm olality >10

o

Gap increases by 1 m Osm /kg for each 5.9 m g/dL of isopropanol and 5.5 m g/dL of acetone.

Imaging 

Chest radiograph: for aspiration pneum onia with altered m eatal status (AMS) and vom iting

Pa ge 2 7 3



CT head: concom itant head injury occurs.

Differential Diagnosis For CNS depression and elevated osm olar gap includes: 

Ethanol



Ethylene glycol



Methanol



Glycerol



Mannitol

Pediatric Considerations Prone to hypoglycem ia following exposure P.617

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs) o



Maintain airway and assist in ventilation if necessary.

Hypotension: o

Treat initially with 0.9% norm al saline (NS) IV fluid bolus.

o

Initiate dopam ine or norepinephrine infusion if hypotension persists.

o

Packed red blood cells with significant hem orrhagic gastritis



Naloxone, thiam ine, dextrose (or Accu-Chek) if altered m ental status

ED Treatment

Pa ge 2 7 3



Prim arily supportive therapyâ€”no specific antidote



Irrigate skin/eyes for derm al or ocular exposure.



Consider activated charcoal: o

For coingestants

o

Large doses can absorb significant am ounts of isopropanol.



Do not treat with ethanol infusion or 4-m ethylpyrazole.



Hem odialysis: o

Effectively rem oves isopropanol and acetone

o

Most m anaged with supportive care alone

o

Indications: 

Hem odynam ic instability despite fluid replacem ent and use of pressors



Levels >400 m g/dL (associated with severe hypotension and prolonged com a)

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Dopam ine: 2â€“20 Âµg/kg/m in IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sorbitol: 1â€“2 g/kg to m ax. 150 g (peds >1 year old: 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurry



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up

Pa ge 2 7 4

Disposition Admission Criteria Moderate to severe isopropanol toxicity (altered m ental status, hypotension)

Discharge Criteria 

Observe asym ptom atic patients following ingestion for 2â€“4 hours before discharge.



Mild intoxication that resolves over 4â€“6 hours

References 1. Burkhart KK, Kulig K. The other alcohols. Methanol, ethylene glycol, and isopropanol. Em erg Med Clin North Am . 1990;8:913â€“928. 2. Sharm a AN. Toxic Alcohols. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:980â€“990.

Codes ICD9-CM 980.2

ICD10 T55.2

Pa ge 2 7 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Jaundice

Jaundice

Andrew Chang

Basics Description Yellow pigm entation of tissues and body fluids due to elevated serum bilirubin

Etiology 

Unconjugated hyperbilirubinem ia: Unconjugated bilirubin is the direct breakdown product of hem e, water insoluble, and m easured as indirect bilirubin: o

Hem olytic: 

o

o

Hepatic: 

Decreased conjugation of bilirubin



Gilbert syndrom e

Decreased uptake: 



Excessive production of unconjugated bilirubin

Physiologic jaundice

Conjugated hyperbilirubinem ia: o

Conjugated bilirubin is water soluble and m easured as direct bilirubin.

o

In conjugated hyperbilirubinem ia, bilirubin is returned to the bloodstream after conjugation in the liver instead of draining into the bile ducts.

Pa ge 2 7 4

o

Hepatocellular dysfunction: 

Hepatitis



Cirrhosis



Tum or invasion



Toxic injury

o

Intrahepatic (nonobstructive) cholestasis

o

Extrahepatic (obstructive) cholestasis

Diagnosis Signs and Symptoms History 





Cholestasis: o

Pruritus

o

Pale stools

o

Dark urine

Malignancy: o

Anorexia

o

Weight loss

o

Malaise

Abdom inal pain

Physical Exam 

Right upper quadrant tenderness: o

Courvoisier's rule: 

Painless jaundice and a palpable, nontender gallbladder represent m alignant com m on duct obstruction.



Stigm ata of cirrhosis: o

Abdom inal collateral circulation including caput m edusae, hepatosplenom egaly, or hepatic atrophy

Pa ge 2 7 4

o

Ascites

o

Spider telangiectasis

o

Palm ar erythem a

o

Dupuytren contractures



Palpable gallbladder



Hepatom egaly



Splenom egaly



Abdom inal m ass



Evidence of cachexia



Kayser-Fleischer rings: o

Wilson disease

Essential Workup 

History and physical exam ination, together with routine laboratory tests, will suggest the diagnosis in about 80% of patients with jaundice.



Bilirubin levelâ€”severity m ay suggest cause of obstruction: o

Malignancy causes highest levels (10â€“30 m g/dL).

o

Choledocholithiasis rarely exceeds 15 m g/dL.

Tests Lab 

Alkaline phosphatase: o

If no bone disease and not pregnant, then elevation suggests im paired biliary tract function.

o

2Ã—: hepatitis and cirrhosis

o

3Ã—: extrahepatic biliary obstruction (i.e., choledocholithiasis) and intrahepatic cholestasis (i.e., drug-induced and biliary cirrhosis)



Am inotransferasesâ€”provide evidence of hepatocellular dam age: o

Alanine am inotransferase (ALT, SGPT): prim arily in

Pa ge 2 7 4

the liver o

Aspartate am inotransferase (AST, SGOT): liver, heart, kidney, skeletal m uscle, and brain



GGTP (Î³-glutam yl transpeptidase)â€”throughout hepatobiliary system , pancreas, heart, kidneys, and lungs: o

May be the m ost sensitive indicator of biliary tract disease



5â€²-Nucleotidaseâ€”widespread tissue distribution: o

Confirm s hepatic origin of an elevated alkaline phosphatase level



Album in: decreased with severe liver disease



Prothrom bin tim e: Prolonged level is an im portant prognostic indicator in patients with acute hepatitis.

Imaging 

Ultrasound: m ost effective initial im aging technique: o

More than 90% effective in identifying cholelithiasis

o

Ductal dilation is a reliable indicator of extrahepatic obstruction: 

A dilated com m on bile duct (CBD) and gallbladder suggest distal obstruction, whereas dilation of the intrahepatic ducts (without CBD dilation) suggests proxim al obstruction.

o

Tum ors of the liver and head of pancreas usually well visualized

o 

Distinguishes solid liver tum ors from cystic structures

Plain radiographs: o

May show evidence of hepatic and splenic enlargem ent or biliary calcifications



Hepatic nuclear scan (HIDA): o

Accurate m ethod of diagnosing acute cholecystitis or cystic duct obstruction

o

Tim e consum ing (usually several hours)

Pa ge 2 7 4



CT: o

Superior to ultrasound in detecting pancreatic and intra-abdom inal tum ors

o

Can help differentiate fluid-containing structures

Diagnostic Procedures/Surgery Endoscopic retrograde cholangiopancreatography (ERCP): 



Diagnostic: o

Stones seen as filling defects within bile duct lum en.

o

Malignancies seen as strictures

Therapeutic: o

Extraction of com m on bile duct stones and insertion of stents to bypass m alignant obstructions

o

Biopsy under direct vision.

Differential Diagnosis 

Prehepatic: o

Hem olysis (sickle cell, other hem oglobinopathies)

o

Ineffective erythropoiesis

o

Drugs

o

Gilbert syndrom e: usually benign inherited form of unconjugated hyperbilirubinem ia



o

Crigler-Najjar syndrom e

o

Prolonged fasting

Hepatocellular: o

Hepatitis (infectious, alcoholic, autoim m une, toxin, drug induced)

o

Cirrhosis

o

Postischem ia

o

Hem ochrom atosis

P.619

Pa ge 2 7 4





Intrahepatic cholestasis: o

Pregnancy

o

Drugs

o

Dubin-Johnson syndrom e

o

Rotor syndrom e

o

Benign recurrent cholestasia

o

Fam ilial syndrom es

o

Sepsis

o

Postoperative jaundice

o

Lym phom a

Extrahepatic obstruction: o

Com m on duct stone

o

Biliary stricture

o

Bacterial cholangitis

o

Sclerosing cholangitis

o

Carcinom a (am pulla, gallbladder, pancreas), cholangiosarcom a

o

Pancreatitis, pancreatic pseudocyst

o

Hem obilia

o

Duodenal diverticula

o

Ascariasis

o

Postâ€“laparoscopic cholecystectom y com plications

o

Congenital biliary atresia

o

Congenital choledochal cyst

Pediatric Considerations 

Intrahepatic cholestasis: o

Cardiovascular (congenital heart disease, congestive heart failure, shock, asphyxia)

o

Metabolic or genetic (Î± l -antitrypsin deficiency, trisom y 18 and 21, cystic fibrosis, Gaucher's disease, Niem ann-Pick disease, glycogen storage disease type IV)

Pa ge 2 7 4

o

Infectious (bacterial sepsis, cytom egalovirus [CMV], enterovirus, herpes sim plex virus [HSV], rubella, syphilis, tuberculosis, varicella, viral hepatitis)

o

Hem atologic (severe isoim m une hem olytic disease)

Treatment Initial Stabilization 

Isotonic IV fluid therapy if dehydrated



Toxic-appearing patients: o

Supplem ental oxygen, cardiac m onitoring

o

Nasogastric suction and bladder catheterization

ED Treatment 

For bacterial cholangitis/sepsis, obtain blood cultures and adm inister parenteral antibiotics:



o

Am picillin, gentam icin, and m etronidazole or

o

Ticarcillin, or piperacillin, and m etronidazole or

o

Cefoxitin and tobram ycin

Obstructive extrahepatic jaundice: o



Surgical consult

Choledocholithiasis: o

ERCP papillotom y, balloon or basket retrieval, or open surgery



Obstructive intrahepatic or nonobstructive jaundice: o

Medical m anagem ent: 

Withdraw causative drug, ethanol



Interferon for chronic hepatitis B and C



Penicillam ine and phlebotom y for Wilson disease and hem ochrom atosis



Corticosteroids for chronic hepatitis of

Pa ge 2 7 4

autoim m une origin

Pediatric Considerations 

Exchange transfusion: o

Em ergent treatm ent of m arkedly elevated bilirubin (>20 m g/dL in full-term infants) and for correction of anem ia caused by isoim m une hem olytic disease



Phototherapyâ€”for neonatal jaundice when bilirubin = 17 m g/dL: o

Measure bilirubin once to twice daily and stop when bilirubin has been reduced by about 4â€“5 m g/dL



Phenobarbital: in sepsis and drug-induced causes; decreases conjugated bilirubin



Metalloporphyrins: investigational inhibitors of hem e oxygenase

Medication (Drugs) 

Am picillin: 2 g IV q6h (peds: 25 m g/kg IV q6hâ€“q8h)



Cefoxitin: 2 g IV q6h (peds: 40â€“160 m g/kg/d div. q6hâ€“q12h)



Gentam icin: 2â€“5 m g/kg IV q8h (peds: sam e)



Metronidazole: 1 g IV q12h (peds: 30 m g/kg/d div. q12h)



Piperacillin/TZ: 3 g IV q6h (peds: 300 m g/kg/d div. q6h [>2 m onths of age])



Ticarcillin/CL: 3 g IV q6h (peds: 75â€“100 m g/kg/d div. q6h)



Tobram ycin: 2â€“5 m g/kg IV q6h (peds: sam e)

Follow-Up

Pa ge 2 7 4

Disposition Admission Criteria 

Bacterial cholangitis



Intractable pain



Intractable em esis



Associated pancreatitis



Elevated prothrom bin tim e

Discharge Criteria 

No evidence of infection (evaluate as outpatient)



Tolerating liquids

References 1. Dennery PA, Seidm an DS, Stevenson DK. Neonatal hyperbilirubinem ia. N Engl J Med. 2001;344:581â€“590. 2. Faust TW, Reddy KR. Postoperative jaundice. Clin Liver Dis. 2004;8:151â€“166. 3. Frank BB. Clinical evaluation of jaundice: a guideline of the Patient Care Com m ittee of the Am erican Gastroenterological Association. JAMA. 1989;262(21):3031â€“3034. 4. Gartner LM, Herschel M. Jaundice and breastfeeding. Pediatr Clin North Am . 2001;48:389â€“399. 5. Roche SP, Kobos R. Jaundice in the adult patient. Am Fam Physician. 2004;69:299â€“304. 6. Rossi RL, Traverso LW, Pim entel F. Malignant obstructive jaundice. Surg Clin North Am . 1996;76:63â€“70. 7. Stevenson DK, Wong RJ, DeSandre GH, et al. A prim er on neonatal jaundice. Adv Pediatr. 2004;51:263â€“288.

Codes ICD9-CM 782.4

Pa ge 2 7 5

ICD10 R17

Pa ge 2 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Kapo si Sarco m a

Kaposi Sarcoma

Adam Wos

Basics Description 

A m esenchym al tum or involving blood and lym phatic vessels



Associated with hum an herpesvirus 8 (HHV-8) also known as Kaposi sarcom a herpesvirus (KSHV)



Lesions are typically found on the skin, m ucous m em branes, GI and respiratory tracts, lym phatic system , and visceral organs.



Tum ors consist of spindle-shaped cells between collagen bundles, neovascular spaces, extravasated erythrocytes, and an infiltrate of lym phocytes.



Staging based on AIDS Clinical Trials Group (ACTG) classification o



Characterizes patients as good or poor based on: 

Tum or burden



Im m une function



Presence or absence of system ic illness

Four epidem iologic m anifestations: o

Classic Kaposi sarcom a (KS): 

Initially described in 1872 in m ales in

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Mediterranean region and Eastern Europe 

Prim arily cutaneous disease, occurring after sixth decade of life, with a typically indolent course

o

Endem ic African KS: 

High prevalence up to 12% in sub-Saharan Africa



Clinical pattern ranges from benign cutaneous disease to fulm inant lym phadenopathic disease.

o

Iatrogenic im m unosuppressive KS: 

Occurring in organ transplant recipients or patients receiving chronic im m unosuppressive therapy

o

AIDS-related KS: 

The m ost com m on HIV-associated m alignancy



Incidence has declined significantly in the United States in the era of highly active antiretroviral therapy (HAART)



Decreased incidence as an AIDS-defining illness



Unpredictable clinical course, even in patients with well-controlled HIV disease

Etiology Mechanism 

HHV-8 is found in all KS lesions, yet not all those infected with HHV-8 have KS: o

HHV-8 is felt to be necessary but not sufficient by itself to cause KS.



Host genetic factors likely contribute.



HHV-8 genom e codes for viral cyclins, cytokines, and antiapoptotic factors: o

Thought to disrupt m itosis, interrupt apoptosis, and

Pa ge 2 7 5

increase angiogenesis 

Spindle cells thought to originate from peripheral blood hem atopoietic precursors: o

First invade derm is and progress from m acular to plaque to tum or stage



Risk of developing KS increases with degree of im m unosuppression: o

Measured by lower CD4 counts and higher HHV-8 and HIV viral loads



AIDS-KS lesions tend to flare during opportunistic infections.



Survival for patients with HIV-related KS is influenced m ore heavily by the depth of im m unosuppression and the control of the underlying HIV disease than by tum or burden.



Modes of transm ission of HHV-8: o

Sexual contact, especially am ong hom osexual m ales, who have m uch higher risk of KS than other HIV patients

o

Vertical transm ission from m other to child

o

Saliva appears to be m ost frequent form of transm ission in endem ic African form .

o

Blood products

o

Donated transplanted organs

Diagnosis Signs and Symptoms 

Cutaneous: o

Lesions m ay arise quickly within a few days.

o

Red, pink, purple, or brown m acular lesions with

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occasional yellow halos o

Irregularly shaped, ranging from several m illim eters to few centim eters in size

o

Frequently lesions are sym m etric and arranged along lines of skin tension.

o

Painless and nonpruritic

o

Com m on sites include face, especially adnexal structures of eyes and nose, trunk, and lower extrem ities.

o

Lym phatic obstruction can lead to severe edem a, pain, and ulceration, especially in lower extrem ities, groin, and periorbital areas.



Oral: o

Most com m on site of initial involvem ent

o

Purplish lesions on palate and gingiva

o

Can be easily traum atized from norm al chewing, causing bleeding, ulceration, and secondary infection



Visceral: o

Gastrointestinal: 

Com m on, but usually asym ptom atic



Does not typically affect prognosis



Can occur anywhere in GI tract but m ost com m only in stom ach



Lesions begin as m acular and subm ucosal.



Lesions m ay progress to becom e nodular and bulky with central ulceration.



Advanced disease m ay present with pain, obstipation, and bleeding.

o

Respiratory: 

Found in about one third of KS patients



Lesions in tracheobronchial tree, pulm onary parenchym a, or pleura

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

Presents at the lower range of CD4 counts



Eighty-five percent of patients have evidence of cutaneous disease.



Frequently presents concom itantly with opportunistic infections



Sym ptom s: dyspnea, nonproductive cough



Chest pain, fever, and hem optysis are less com m on.



Sym ptom s m ay persist for weeks, then progress rapidly to pulm onary failure.



Lung sounds often clear, but m ay have crackles, wheezes, or signs of pleural effusion



System ic: o

Lym phatic obstruction is m ost com m on cause of m orbidity; can occur in absence of cutaneous involvem ent.

o

Solid organs such as liver, spleen, heart, bone m arrow, and urogenital tract are less com m only affected.

Essential Workup 

History should focus on sym ptom s by system , and exam iner should assess degree of im m une com prom ise.



Physical exam ination: o

Careful exam ination of skin, oral m ucosa for lesions

o

Fecal occult blood in patients with suspected GI bleed

o

Lung exam for signs of crackles or dullness to percussion that m ay suggest a pleural effusion

Tests Lab 

Punch biopsy of skin lesions with histologic exam ination is the gold standard of diagnosis:

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o

Not usually perform ed in ED

o

Dem onstrates angioproliferation with spindle cells, cleftlike spaces, and extravasation of RBCs



CBC m ay show leukopenia, throm bocytopenia from AIDS, anem ia in setting of GI bleed.



Arterial blood gas (ABG) in setting of respiratory distress m ay dem onstrate hypoxem ia or respiratory alkalosis.



Electrolytes, liver panel, blood cultures, sputum sm ear and culture, lactate dehydrogenase (LDH) in setting of fever and respiratory sym ptom s to rule out other causes



Thoracentesis in setting of pleural effusion typically exudative, or frankly bloody

P.621

Imaging 



Chest radiograph: o

Bilateral opacities in a central or perihilar distribution

o

Nodular densities

o

Pleural effusions

o

Intrathoracic adenopathy

Thallium /gallium scan: o

KS lesions are thallium avid and gallium negative.

o

Opposite pattern of opportunistic infections and non-Hodgkin lym phom a



Chest CT can guide biopsy of extrabronchial lesions.



Kidneys, ureters, and bladder (KUB) radiograph or CT of abdom en to look for sm all bowel obstruction if suspected

Diagnostic Procedures/Surgery 

Bronchoscopy with lesional biopsy: o

Gold standard for diagnosis of pulm onary KS

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o 

Dem onstrates cherry red nodules

GI endoscopy to evaluate source of bleeding or upper GI obstruction

Differential Diagnosis 

Cutaneous disease: o

Bacillary angiom atosis (Bartonella species infection of the skin)





o

Purpura

o

Hem atom a

o

Hem angiom a

o

Arteriovenous m alform ation

o

Angiosarcom a

o

Derm atofibrom a

o

Nevi

Gastrointestinal disease: o

Peptic ulcer disease

o

Pancreatitis

o

Hepatobiliary tract disease

o

Carcinoid tum or

o

Stom ach cancer

o

Variceal disease

Pulm onary disease: o

Com m unity acquired pneum onia

o

Active tuberculosis

o

Opportunistic infections such as Pneum ocystis carinii, aspergillosis, Coccidioides

o

Lung carcinom a

o

Non-Hodgkin or Hodgkin lym phom a

Treatment

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Pre Hospital Determ ination of the existence of any advanced directives for patients with advanced AIDS

Initial Stabilization 

Protection for health care workers: o

Universal precautions



Adm inister oxygen.



Place on cardiac m onitor and m easure pulse oxim etry.



Establish IV access with 0.9% norm al saline.



Endotracheal intubation and m echanical ventilation if respiratory failure evident



Resuscitation with intravenous crystalloid, blood products as needed if hypotensive from GI bleed

ED Treatment 

Care of KS m ust take into account type of KS, extent of tum or, and organs involved.



ED care focused on stabilizing acute m anifestations of disease and appropriate referral for m anagem ent of nonem ergent lesions





Goal of treatm ent for AIDS-KS is palliation of sym ptom s: o

Cosm etically disfiguring lesions

o

Problem atic oral lesions

o

Pain and edem a from lym phadenopathy

Intensification of HAART m edications is first line of treatm ent in AIDS-KS.



Local therapy of cutaneous lesions: o

Cryotherapy

o

Radiation therapy

o

Laser therapy

o

Local excision surgery for troublesom e lesions at carefully selected sites

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o

Topical treatm ent with alitretinoin gel

o

Intralesional chem otherapy with vinblastine or vincristine



System ic therapy: o

Liposom al anthracyclines (pegylated liposom al doxorubicin): 

First-line therapy for advanced KS



Higher response rates with fewer adverse events than previous standard of bleom ycin and vincristine

o

Paclitaxel: 

High response rate in patients who have failed anthracyclines

o

Interferon alpha: 

Indicated for HIV-related KS if CD4 count is >400 and KS in early stages

o

Experim ental: 

Thalidom ide



Angiogenesis inhibitors



Anti-HHV-8 therapy with ganciclovir, cidofovir, or foscarnet

Medication (Drugs) 

Vinblastine: 0.1â€“0.5 m g/cm 2 of lesion intralesional, up to 2 m g; repeat once in 3 weeks



Interferon alpha: 30 m illion U/m 2 body area SC three tim es weekly



Pegylated liposom al doxorubicin: 20 m g/m 2 body area IV every 3 weeks



Paclitaxel: 100 m g/m 2 body area IV every 2 weeks



Thalidom ide: 100 m g PO daily for 8 weeks

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Follow-Up Disposition Admission Criteria 

Respiratory failure



Unstable GI bleed



Bowel obstruction



Secondary infection of lesion or sepsis

Discharge Criteria Patients with uncom plicated KS lesions m ay be discharged with referral to a hem atologist/oncologist or HIV specialist.

Issues for Referral Uncom plicated m ucocutaneous lesions for local therapy as indicated for palliation

References 1. Belleza WG, Browne B. Pulm onary considerations in the im m unocom prom ised patient. Em erg Med Clin North Am . 2003;21(2):499â€“531, xâ€“xi. 2. Hengge UR, et al. Update on Kaposi's sarcom a and other HHV8 associated diseases. Part 1: epidem iology, environm ental predispositions, clinical m anifestations, and therapy. Lancet Infect Dis. 2002;2(5):281â€“292 3. Huang L, Stansell JD. Pulm onary com plications of hum an im m unodeficiency virus infection. In: Murray J, Nadel J, eds. Textbook of Respiratory Medicine. 3rd ed Philadelphia: WB Saunders; 2000:2204â€“2206. 4. Levine AM, Hancock BW, MacPhail P, et al. The treatm ent of AIDS-related cancer. Lancet Oncol. 2003;4(9):576â€“581.

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5. Mbulaiteye SM, Parkin DM, Rabkin CS. Epidem iology of AIDS-related m alignancies: an international perspective. Hem atol Oncol Clin North Am . 2003;17(3):673â€“696. 6. VonRoenn JH. Clinical presentations and standard therapy of AIDS-associated Kaposi's sarcom a. Hem atol Oncol Clin North Am . 2003;17(3):747â€“762.

Codes ICD9-CM 176.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Kaw asaki Disease

Kawasaki Disease

Adam Z. Barkin

Basics Description 

Acute inflam m atory process involving m ultiple organs



Vasculitis m ost severe in m edium -sized arteries, including coronary arteries



Stages: o

Acute (lasts 1â€“2 weeks): 

Fever, oral m ucosal erythem a, conjunctival injection, erythem a and edem a of hands and feet, cervical adenopathy, aseptic m eningitis, hepatic dysfunction, diarrhea



Myocarditis, pericardial effusion, no aneurysm s by echocardiography

o

Subacute (when fever, rash, and lym phadenopathy resolve until about 4 weeks): 

Anorexia, irritability, desquam ation of hands and feet, throm bocytosis



Coronary artery aneurysm s visible on echocardiography

 o

Risk for sudden death is highest.

Convalescent phase (about 6â€“8 weeks):

Pa ge 2 7 6



Clinical signs are absent.



Erythrocyte sedim entation rate (ESR) norm alizes.



Epidem iology: o

Eighty percent of cases occur in children <4 years old; peak at 1â€“2 years; rare in infants <3 m onths old.

o

Adult cases have been reported.

o

Asians are at highest risk.

o

Males > Fem ales 1.5:1.

Genetics Possible genetic predisposition

Etiology Unknownâ€”thought to be infectious based on m anifestations of disease, epidem ics, and increased num bers of cases in winter and early spring

Diagnosis Signs and Symptoms History 

Tem perature >38.5Â°C (often spiking) for at least 5 days: o





Begins abruptly and m ay last >2 weeks

Cardiac: o

Shortness of breath

o

Chest pain

HEENT: o

Eyes: 

Conjunctivitis



Photophobia

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o

Mouth: 

Erythem a, dry and fissured lips, strawberry tongue, pharyngeal erythem a



Skin rash



Musculoskeletal: o



Neurologic: o



Arthralgia, arthritis

Extrem e irritability

Gastrointestinal: o

Diarrhea

o

Vom iting

o

Abdom inal pain

Physical Exam 



Cardiac: o

Evidence of congestive heart failure

o

Evidence of pericarditis

o

Rub

o

Myocarditis

o

Evidence of valvular disease

o

Murm ur

HEENT: o

Eyes: 

Bilateral conjunctival injection without exudates



Bulbar conjunctiva is m ore frequently involved than palpebral conjunctiva.



Usually within 2 days of onset of fever and lasting 1â€“2 weeks

 o

Photophobia, uveitis, iritis

Mouth: 

Erythem a, dry and fissured lips, strawberry tongue, pharyngeal erythem a

o

Lym ph:

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

Cervical lym phadenopathy (node diam eter >1.5 cm )





Neurologic: o

Irritability

o

Meningism us

Skin: o

Rash, prim arily on the trunk

o

May be m aculopapular, scarlatiniform , or erythem a m ultiform eâ€“like; erythroderm a

o

Changes in the hands or feetâ€”erythem a, edem a (acute phase); unwilling to bear weight

o

Desquam ation (subacute phase) of the tips of fingers and toes 2â€“3 weeks after onset of illness





Genitourinary: o

Urethritis

o

Meatitis

Gastrointestinal: o

Hydrops of the gallbladder

Essential Workup 

Diagnostic criteria: o

Fever for 5 days plus four of the five following criteria:

o

Bilateral conjunctival injection

o

Changes in oral m ucosa

o

Polym orphous erythem atous rash

o

Changes in hands or feetâ€”edem a, erythem a, desquam ation

o 

Cervical lym phadenopathy >1.5 cm

Atypical cases can be seen without m eeting diagnostic criteria.



Experienced clinicians can m ake the diagnosis before 5 days of fever.

Pa ge 2 7 6

P.623

Tests Lab 

CBC: o

WBCâ€”norm ally elevated with shift to left in acute phase

o

Norm ocytic anem ia

o

Throm bocytopenia if m yocardial infarction or severe coronary disease

o 



Throm bocytosis usually in second to third week

Urinalysis: o

Sterile pyuria

o

Proteinuria

Erythrocyte sedim entation rate (ESR) elevated from first week until 4â€“6 weeks



Increased C-reactive protein



Cerebrospinal fluid (CSF) pleocytosis



Cultures: negative blood, urine, CSF, throat



Increased transam inases and bilirubin

Imaging 



Echocardiogram : o

Acute phase (baseline)

o

2â€“3 weeks

o

6â€“8 weeks

Chest radiograph

Diagnostic Procedures/Surgery 

ECG if concern about m yocardial infarction or pericarditis



Slit-lam p exam â€”uveitis

Pa ge 2 7 6

Differential Diagnosis 



Viral infections: o

Adenovirus

o

Enterovirus

o

Measles

o

Epstein-Barr virus

o

Rubella

o

Rubeola

Bacterial infection: o

Scarlet fever (responds rapidly to penicillin)

o

Staphylococcal scalded skin syndrom e

o

Rickettsial disease, including Rocky Mountain spotted fever and leptospirosis



Drug reaction: o

Stevens-Johnson syndrom e

o

Erythem a m ultiform e

Treatment Pre Hospital 

Airway, breathing, and circulation m anagem ent (ABCs)



Oxygen

Initial Stabilization ABCs with focus on cardiovascular system

ED Treatment 

Initiate intravenous gam m aglobulin (IVIG) and aspirin therapy: o

Do not generally need to m onitor salicylate levels because decreased absorption and increased

Pa ge 2 7 6

clearance 

Treatm ent within the first 10 days of illness reduces cardiac sequelae from range of 20â€“25% to range of 2â€“4%



Cardiology consultation



Treatm ent of m yocardial infarctions as in adults



Corticosteroids are controversial.

Medication (Drugs) 

IVIG: 2 g/kg IV over 10â€“12 hours; retreatm ent m ay be required for persistent (>48â€“72 hours) or recrudescent fever



Aspirin: 80â€“100 m g/kg/d PO q6h until about day 14 when fever has resolved; then 3â€“5 m g/kg/d PO daily for 6â€“8 weeks

Follow-Up Disposition Admission Criteria 

Adm it all patients who fulfill diagnostic criteria for Kawasaki disease.



Adm it toxic-appearing patients who do not yet m eet the criteria for Kawasaki disease.

Discharge Criteria 

Nontoxic children who do not fulfill diagnostic criteria



Close follow-up is required.

Issues for Referral

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Cardiology consultation for all patients

References 1. Burns JC. Kawasaki disease. Adv Pediatr. 2001;48:157â€“177. 2. Muta H, Ishii M, Egam i K, et al. Early intravenous gam m a-globulin treatm ent for Kawasaki disease: the nationwide surveys in Japan. Pediatrics. 2004;114:751â€“754. 3. Newburger JN, Takahashi M, Gerber MA, et al. Diagnosis, treatm ent, and long-term m anagem ent of Kawasaki disease: a statem ent for health professionals from the Com m ittee on Rheum atic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, Am erican Heart Association. Pediatrics. 2004;114:1708â€“1733. 4. Yam am oto LG. Kawasaki disease. Pediatr Em erg Care. 2003;19:422â€“424.

Codes ICD9-CM 446.1

ICD10 M30.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Knee Dislo catio n

Knee Dislocation

Kelly Anne Foley

Basics Description 

Defined by the position of the tibia in relation to the distal fem ur: o

Anterior dislocation: 

Most com m on dislocation, accounts for 60%



Hyperextension of the knee



Rupture of the posterior capsule at 30Â°



Rupture of the posterior cruciate ligam ent (PCL) and popliteal artery (PA) occurs at 50Â°

o

Posterior dislocation

o

Direct blow to the anterior tibia with the knee flexed at 90Â°, â€œdashboard injuryâ€• 

Anterior cruciate ligam ent (ACL) is usually spared.

o

Medial dislocation: 

Varus stress causing tear to the ACL, PCL, and lateral collateral ligam ent (LCL)

o

Lateral dislocation: 

Valgus stress causing tear to the ACL, PCL and m edial collateral ligam ent (LCL)

Pa ge 2 7 7



Associated injuries: o

Popliteal artery (PA) injury 

PA occurs in 35% of dislocations.



Failure to revascularize within 6â€“8 hours: Am putation rate approaches 90%.



Anterior dislocations place traction on PA and cause contusion or intim al injury, which m ay result in delayed throm bosis.



Posterior dislocations cause direct intim al fracture and transection of the artery with im m ediate throm bosis.

o

Peroneal nerve injury: 

Less com m on than PA injury



If present, m ust rule out concom itant arterial insult



Hypesthesia of first web space, inability to dorsiflex foot



Poor prognosis for recovery



Medial dislocation causes injury by traction of the nerve.



Rotary injuries have a high incidence of traction and transection.

Etiology High-energy injuries such as m otor vehicle crashes, autoâ€“pedestrian accidents, and athletic injuries (football m ost com m on)

Diagnosis Signs and Symptoms

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

Grossly deform ed knee



Grossly unstable knee in AP plane or on varus/valgus stress



Lack of distal pulse: o



Popliteal artery injury is prim ary concern.

Signs of distal ischem ia: o

Pallor, paresthesias, pain, paralysis

Essential Workup 

History of m echanism of injury



Com plete and careful physical exam : o

Pulsesâ€”palpation, Doppler, ankle-brachial index (ABI), and cap refill

o

Neurologicâ€”sensation to first web space and great toe, m ovem ent of toes, dorsiflexion of foot



AP and lateral knee radiographs



Docum ented repeat exam if any closed reduction is attem pted

Tests Imaging 

AP/lateral radiograph of knee



MRI within 1 week of injury to define ligam entous injury

P.625

Diagnostic Procedures/Surgery 

ABIâ€”likelihood of significant arterial injury requiring surgery low if â‰¥0.9



Peripheral vascular ultrasonography



Arteriogram should be considered: o

High suspicion of PA injury

Pa ge 2 7 7

o

Poor pulses or distal perfusion after reduction

o

Peroneal nerve injury

o

Ischem ic sym ptom s despite norm al pulses

Differential Diagnosis 

Tibial plateau fracture



Supracondylar fem oral fracture



Ligam entous/tendonous avulsion fracture

Treatment Pre Hospital 

Airway, breathing, and circulation m anagem ent (ABCs)



Docum entation of pulses and m otor response essential



Splint knee in slight flexion to prevent PA traction or com pression.

Initial Stabilization 

ABCs especially when m otor vehicle crash or autoâ€“pedestrian accident



Fluid resuscitation, hypotension m ay alter distal pulses and perfusion.



Closed reduction im m ediately for any lim b ischem ia



Early surgical consult in an open injury or high suspicion or arterial injury

ED Treatment 

Closed reduction by longitudinal traction and lifting fem ur into norm al alignm ent without placing pressure on popliteal fossa



Posterior leg splint/knee im m obilizer with knee in 15â€“20Â° flexion

Pa ge 2 7 7



Repeat neurovascular exam after m anipulation and frequent intervals.



IV analgesia for patient com fort



Surgical consult: open injury, PA injury, or unable to reduce

Follow-Up Disposition Admission Criteria All patients require adm ission for observation of lim b perfusion and PA repair if necessary.

Discharge Criteria All patients should be adm itted.

Issues for Referral Eventual repair of ligam entous injuries: 

Usually at 3 weeks



Arthroscopic surgery contraindicated for 2 weeks after injury to prevent com partm ent syndrom e

References 1. Browner, ed. Skeletal Traum a: Basic Science, Managem ent, and Reconstruction. 3rd ed.: Elsevier; 2003:Chapter 55. 2. Green JR, Cam bize S, Owens BD, et al. Knee dislocation. Em ed J [serial online]. 2005. Available at http://www.em edicine.com /orthoped/topic409.htm . 3. Mills JW. The value of ankle-brachial index for diagnosing arterial injury after knee dislocation: a prospective study. J Traum a. 2004;56(6):1261â€“1265. 4. Miranda, FE. Confirm ation of the safety and accuracy of physical

Pa ge 2 7 7

exam in the evaluation of knee dislocation for injury of the popliteal artery: a prospective study. J Traum a. 2002;52(2):247251.

Codes ICD9-CM 836.50

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Labo r

Labor

James Walker

Basics Labor denotes the sequence of physiologic occurences that result in a fetus being transported from the uterus through the birth canal.

Description 

Labor brings about changes in cervix to allow passage of fetus through birth canal



Synchronous, coordinated contractions of uterus



Contractions progress in m agnitude, duration, and frequency to produce dilation of cervix and ultim ate delivery.



Labor is divided into three stages: o

Stage 1: From onset of uterine contractions to full dilation of cervix

o

Stage 1 is further divided into latent and active phases: 

In latent phase; uterine contraction with little change in cervical dilation or effacem ent; contractions are m ild, short (<45 seconds), and irregular.



This is followed by active phase, which begins around tim e of cervical dilation of 3â€“4 cm ;

Pa ge 2 7 7

contractions are strong, regular (every 2â€“3 m inutes), and last longer (>45 seconds). o

Stage 2: From onset of com plete cervical dilation to tim e of delivery of infant

o

Stage 3: From tim e of delivery of baby to tim e of placental delivery



Total duration of labor varies with each wom an.



Generally, lengths of first and second stages of labor are significantly longer for nulliparous wom an: o

Nulliparous: Mean length for first stage of labor is 14.4 hours and 1.0 hours for second stage of labor.

o

Parous: Mean length of first stage of labor is 7.7 hours and 0.2 hours for second stage of labor.



Length of second stage of labor is greatly influenced by â€œthree Psâ€•:



o

Passenger (infant size and presentation)

o

Passageway (size of bony pelvis and soft tissues)

o

Powers (uterine contractions)

Problem s with any of these three Ps can cause abnorm al progression of labor: o

Fetal m alposition, uterine dysfunction, cephalopelvic disproportion



False labor (Braxton-Hicks contractions): o

Irregular, nonsynchronous contractions of uterus several weeks to days before onset of true labor, and does not cause cervical dilation

Etiology 

Prem ature labor occurs in 8â€“10% of pregnancies.



About 30â€“40% of prem ature labor is caused by uterine, cervical, or urinary tract infections.



Prem ature rupture of m em branes is defined as rupture of am niotic/chorionic m em branes at least 2 hours before

Pa ge 2 7 7

onset of labor in patient before 37 weeksâ€™ gestation. o

This occurs in only 3% of pregnancies, but accounts for 30â€“40% of all prem ature births.

Diagnosis Signs and Symptoms 

Sym ptom s of labor: o

Interm ittent low abdom inal pain with or without low back pain



o

Occurring regularly at least every 5 m inutes

o

Lasting 30â€“60 seconds

Preterm labor is of sufficient frequency and intensity to bring about changes in dilation or effacem ent of cervix before 37 weeks.



Labor is not associated with vaginal bleeding: o

Patients with third-trim ester abdom inal pain or vaginal bleeding should raise suspicion of placenta previa or placental abruption.



Sudden release of clear fluid from vagina or feeling of constant perineal wetness can represent rupture of m em branes: o

This is not always associated with labor, but often leads to onset of labor.

Essential Workup 

All patients presenting in possible labor should have im m ediate sterile pelvic exam to assess dilation, effacem ent of cervix, and possibility of im m inent delivery.



Bim anual pelvic exam should not be done in third-trim ester patient with vaginal bleeding until

Pa ge 2 7 7

ultrasound can be done to assess for placenta previa or placental abruption. 

Patients with suspected rupture of m em branes should have sterile speculum exam with visual exam ination of cervix and collection of fluid from vaginal area.



Suggestive of rupture of m em branes: o

Presence of ferning when fluid is allowed to dry on a slide



o

Presence of pooling of fluid in vagina

o

Change of color of litm us paper from yellow to blue

Patients with preterm labor and with cervical changes should have urinalysis with culture and cervical cultures.



Fetal m onitoring should be initiated.

Tests Lab 

If patient is in labor, CBC, type, and screen should be sent.



Urinalysis for proteinuria



In patients with no prenatal care, obtain Rh factor and antibody screen.



Cervical cultures and urine culture in patients with preterm labor

Imaging 

Not generally needed



Third-trim ester patients with abdom inal pain and vaginal bleeding should have em ergent ultrasound to evaluate for placenta previa or abruption.

Differential Diagnosis 

Braxton-Hicks contractions are irregular uterine contractions without associated cervical changes.

Pa ge 2 7 8



Round uterine ligam ent pain, m usculoskeletal back pain



Other com m on causes of abdom inal pain, such as appendicitis

P.627

Treatment Pre Hospital 

Em ergency m edical services (EMS) personnel should place patients in labor on oxygen and in left lateral recum bent position to m axim ize delivery of oxygen to uterus.



Maternal transport of high-risk obstetric patients before delivery results in im proved outcom es instead of transfer of neonate after delivery.



Air transport of high-risk obstetric patients has been shown to be beneficial and cost effective.



Patients in labor who are transported by aircraft should have high-flow oxygen available in the event of cabin decom pression at high altitudes.

Initial Stabilization If delivery is im m inent (presenting part visible), prepare for im m ediate vaginal delivery in ED (see Delivery, Uncom plicated).

ED Treatment 

Unless delivery is im m inent, patient should be sent directly to labor and delivery unit.



If transport to labor and delivery will be delayed, or if transfer to another facility is necessary, these steps should be taken:

Pa ge 2 7 8

o

IV hydration with 1 L of norm al saline or D-5-LR over 30â€“60 m inutes

o

Maternal m onitoring and, if available, fetal m onitoring

o

If labor needs to be arrested (prem ature fetus), begin tocolytic such as Î²-agonist terbutaline or MgSO 4 . 

Magnesium toxicity is suggested by loss of deep tendon reflexes.



High doses of m agnesium can cause cardiac dysrhythm ias and respiratory depression.

Medication (Drugs) 

Magnesium sulfate: 4â€“6 g IV over 30 m inutes, followed by 2â€“6 g/h



Terbutaline: 0.25 m g SC; m ay repeat sam e dose in 30 m inutes

Follow-Up Disposition Admission Criteria 

All patients in labor who are not at risk for im m inent delivery should be adm itted to labor and delivery departm ent.



Preterm patients in labor dem and im m ediate obstetric consultation and should be adm itted to labor and delivery departm ent for further treatm ent.

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References 1. Gianopoulos JG. Em ergency com plications of labor and delivery. Em erg Med Clin North Am . 1994;12:201â€“217. 2. Liao JB, Buhim schi CS, Norwitz ER. Norm al labor: m echanism s and duration. Obstet Gynecol Clin North Am . 2005;32:145â€“164.

Codes ICD9-CM 650.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Labyrinthitis

Labyrinthitis

Paul A. Andrulonis Charles V. Pollack

Basics Description 

An inflam m ation that decreases afferent firing from the labyrinth



The CNS interprets this decreased signal as head rotation away from the diseased labyrinth.



The resulting im balance in firing from the labyrinth results in spontaneous nystagm us with the fast phase away from the pathologic side.



The three m ost com m on causes of peripheral vertigo are: o

Benign paroxysm al positional vertigo (BPPV)

o

MÃ©niÃ¨re disease

o

Labyrinthitis

Etiology 



Labyrinthitis: o

Serousâ€”viral or bacterial

o

Suppurativeâ€”bacterial

o

Chronic

BPPV: o

Dislodgem ent of otoconia debris:

Pa ge 2 7 8

o

Idiopathicâ€”49%

o

Posttraum aticâ€”18%

o

Sequela of labyrinthitisâ€”15%

o

Sequela of ischem ic insult

Pediatric Considerations 

Suppurative and serous labyrinthitis: o

Usually secondary to acute otitis m edia, m astoiditis, or m eningitis



BPPV: o

Onset between 1 and 5 years of age

o

Sym ptom s: abrupt onset of crying, nystagm us, diaphoresis, em esis, ataxia

o

Recurrences for up to 3 years

o

Migraineâ€“BPPV com plex is the m ost com m on etiology of pediatric vertigo.



MÃ©niÃ¨re disease: o

Rare before 10 years of age

Diagnosis Signs and Symptoms History 

Sensation of m ovem ent or spinning



Nausea and vom iting



No auditory com plaints

Physical Exam 

Pallor



Diaphoresis



Nystagm us: o

Augm ented by head m ovem ent or rapid head shaking

Pa ge 2 7 8



o

Acute onset

o

Positional

o

Horizontal, frequently with rotational com ponent

o

Direction is constant.

o

Attenuates with fixation

o

Fatigable

Caloric testing: o

Irrigate external ear canal with cold water for 20 seconds.

o

Norm al response causes horizontal nystagm us with the fast phase away from the irrigated ear.

o

Labyrinthitis produces partial or com plete loss of response.



Dix-Hallpike m aneuver o

Tests for evidence of BPPV.

o

The patient's head is rotated 45Â°.

o

The patient is then brought from a sitting position to a supine position with the head extending 20Â° below the exam table.

o

Observe for 5â€“15 second latent torsional nystagm us directed at the downward ear.

o

Clockwise torsional nystagm us with the left ear down

o

Counterclockwise torsional nystagm us with the right ear down

o

The m aneuver is then repeated with the head turned to the opposite side.

o

Reverse nystagm us m ay occur when patient returns to sitting position.

o 

Fatigable with repeat testing

Labyrinthitis: o

No consensus on definition

o

Peripheral vertigo

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o

Single episode of prolonged vertigo lasting days to weeks

o

Peak onset 30â€“60 years old

o

Recent upper respiratory tract infection in 50% of patients

o

Sym ptom s predom inantly with head m ovem ent but also persist at rest

o 

Recovery phase gradual over weeks to m onths

BPPV: o

Positional peripheral vertigo

o

Precipitated by directional specific head m ovem ents (e.g., rolling over in bed, looking up, sham pooing in beauty saloon basin)

o

Recurrent episodes usually last less than 5 m inutes.

o

May take m onths to resolve com pletely

o

Recurrence is not uncom m on.

Essential Workup 

Careful neurologic exam to exclude focal findings



Exclude underlying infections: o

Acute otitis m edia

o

Meningitis

o

Ram say Hunt syndrom e (herpetic lesions on the tym panic m em brane)



Orthostatics



Auditory evaluation

Tests 

Indicated only if evaluating patients for central vertigo or m ore unusual etiologies of peripheral vertigo



Rarely helpful in the routine em ergency evaluation of labyrinthitis



Once perform ed, ensure appropriate follow-up for delayed

Pa ge 2 7 8

lab results, such as syphilis screening.

Lab 

Finger-stick glucose



Syphilis screening



Rheum atoid factor

Pediatric Considerations Lum bar puncture if clinical suspicion of m eningitis

Imaging 

Indications: o

Findings suggestive of central nystagm us



Acute or gradual onset



Not positional but m ay be exacerbated by head m ovem ents



Pure directionâ€”vertical, horizontal, or torsional



Direction m ay change



Nonfatigable



Minim al effect with fixation:



o

High cardiovascular risk factors

o

Focal neurologic findings

Head CT: o



Fine cuts through the cerebellum

MRI and MRA o

Evaluates the posterior fossa, the eighth cranial nerve and the vestibulobasilar circulation

o

Im aging study of choice in patients suspected of central vertigo

Alert Consider brain im aging in patients older than 45 years, children, and patients with cardiovascular risk factors. P.629

Pa ge 2 7 8

Differential Diagnosis 

Peripheral vertigo: o

Acoustic neurom a

o

Autoim m une inner-ear disease

o

BPPV

o

Cholesteatom a

o

MÃ©niÃ¨re disease (associated tinnitus, â€œfullnessâ€• or hearing loss)

o

Otosyphilis

o

Ototoxic drugs (loop diuretics, am inoglycosides, streptom ycin, salicylates, ethanol)

o

Perforated tym panic m em brane

o

Perilym ph fistula (sym ptom s accentuated with valsalvae)



o

Posttraum atic vestibular concussion

o

Suppurative labyrinthitis (toxic appearance)

o

Tem poral bone fracture

Central vertigoâ€”often presents with sym ptom s indistinguishable from peripheral vertigo because the labyrinth has a m onosynaptic connection to the brainstem : o

Brainstem ischem ia

o

Cerebellar hem orrhage (high risk of herniation requires intensive care unit [ICU] adm ission)

o

Inferior cerebellar ischem ia (high risk of herniation requires ICU adm ission)

o

Multiple sclerosis (paresthesias, optic neuritis)

o

Partial seizures of tem poral lobe

o

Vestibular-m asseter syndrom e (associated m asseter m uscle weakness)

o

Vestibular m igraine (30% have vertigo independent

Pa ge 2 7 8

of headaches) o

Wallenberg syndrom e (associated Horner syndrom e, crossed sensory signs)



Cardiac arrhythm ia (presyncopal sym ptom s)



Hypoglycem ia (gradual onset, not positional)



Hypotension (exacerbated with standing)



Cervicogenic disease (onset with rotational neck m ovem ent)



Hypothyroidism

Treatment Pre Hospital 

Antiem etics for nausea and vom iting



IV fluids for dehydration



Fall precautions



Assessm ent for acute stroke



Telem etry for arrhythm ia



Finger-stick glucose to exclude hypoglycem ia



Blood pressure check for hypotension

ED Treatment 

Medications are m inim ally beneficial for BPPV.



Avoid chronic use to encourage developm ent of vestibular com pensation.



Medications for sym ptom atic relief: o

Vestibular suppressants: diazepam , m eclizine, scopolam ine



o

Antiem etics: prochlorperazine, prom ethazine

o

Corticosteroids: poor evidence for efficacy

Debris repositioning is prim ary therapy for BPPV. Effective

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relief in 50â€“80% of patients. 

Epley m aneuver: o

While sitting, turn head 45Â° to the left.

o

Lie back quickly with shoulders on a pillow and head reclined onto the bed.

o

Wait for 30 seconds.

o

Turn head 90Â° to the right (without raising it) and wait again for 30 seconds.

o

Turn body and head another 90Â° to the right and wait for another 30 seconds.

o 

Sit up on the right side.

Sem ont m aneuver: o

From a sitting position, the patient is quickly forced to lie down on the affected side.

o

The patient should rem ain in position for 4 m inutes.

o

Then turn to the other side, always keeping the ear downwards.

o

The patient is again m aintained in the position for 4 m inutes.



Brand-Daroff exercises



Vestibular enhancem ent exercises



Surgery for failed m edical and physical therapy: o

Posterior canal plugging to occlude canal

o

Nerve section

Medication (Drugs) 

Diazepam (benzodiazepine): 2â€“10 m g IV; 5â€“10 m g (0.1â€“0.3 m g/kg/24h) PO q6hâ€“q12h



Meclizine (antihistam ine): 25 m g (50 m g/24h older than 12 years) PO q6h



Prochlorperazine: 5â€“10 m g (0.3 m g/kg/24h IM or PO

Pa ge 2 7 9

over 2 years old) IV, IM, or PO q6hâ€“q8h 

Prom ethazine: 12.5â€“25 m g (1.5â€“2.0 m g/kg/24h) IV or PO q4hâ€“q6h



Scopolam ine (anticholinergic, not approved in pediatrics): 0.6 m g PO q4hâ€“q6h; 1.5 m g transderm al patch q3d

Pediatric Considerations 

Dim enhydrinate: 5 m g/kg/24h PO, IM, IV, or PR



Bacterial labyrinthitis: o

Antibiotics IV

o

Surgical dÃ©bridem ent

Pregnancy Considerations Class D m edication: Diazepam

Follow-Up Disposition Admission Criteria 

Intractable nausea and vom iting



Severe dehydration



Unsteady gait



Sym ptom s concerning for an acute stroke or central etiology of vertigo

Discharge Criteria 

Tolerate oral fluids



Steady gait



Norm al neurological exam



Avoid driving, heights, and operating dangerous equipm ent.



Fall precautions

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

Arrange neurology or otolaryngology follow-up.



For BPPV, patient should perform Epley m aneuver three tim es/day

Issues for Referral 

Recurrent sym ptom s



Concern for cholesteatom a

References 1. Baloh RW. Vestibular neuritis. N Engl J Med. 2003;348:1027â€“1032. 2. Goebel JA. Managem ent options for acute versus chronic vertigo. Otolaryngol Clin North Am . 2000;33(3):483â€“493. 3. Hilton M, Pinder D. The Epley m anoeuvre for benign paroxysm al positional vertigo. Cochrane Database Syst Rev. 2004;(3):CD003162. 4. Korres SG, Balatsouras DG. Diagnostic, pathophysiologic, and therapeutic aspects of benign paroxysm al positional vertigo. Otolaryngologyâ€”Head and Neck Surgery. 2004;131(4):438â€“444. 5. Teach SJ. Dizziness. In: Fleisher GR, Ludwig S, eds. Pediatric em ergency m edicine. 4th ed. Philadelphia, Pa.: Lippincott William s & Wilkins. 2000;217â€“222. 6. Tusa RJ. Vertigo. Neurol Clin. 2001;19(1):23â€“55.

Miscellaneous SEE ALSO: Dizziness; Vertigo

Codes ICD9-CM 386.30

ICD10 H83.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Laceratio n M anagem ent

Laceration

Management Gordon Chew

Basics Description 

A laceration is a disruption in skin integrity m ost often resulting from traum a.



May be single or m ultiple layered

Diagnosis Signs and Symptoms Lacerations m ay be accom panied by: 

Bleeding



Tissue foreign bodies



Hem atom a



Pain or num bness



Loss of m otor function



Dim inished pulses, delayed capillary refill

History 

Mechanism and circum stances of injury

Pa ge 2 7 9



Tim e of injury



History of foreign body (glass, splinter, teeth)



Tetanus im m unization



Co-m orbid condition that m ay im pede wound healing

Physical Exam 

Evaluate nerve and m otor function.



Docum ent associated neurovascular injury.



Assess presence of devitalized tissue, debris from foreign m aterials, bone or joint violation, tendon injury: o

Avoid digital exploration if the object is believed to be sharp.

Essential Workup 

Consider repair in operating room if unable to be perform ed safely within the em ergency departm ent, especially for children requiring deep sedation.



Consider surgical consultation for com plex lacerations, especially involving eyes, face.

Pediatric Considerations Assess for possible nonaccidental traum a.

Tests Imaging 

Evaluation for possible foreign bodies



Plain radiography: o

Soft tissue views m ay aid in visualization.

o

Objects with the sam e density as soft tissue m ay not be seen (wood, plants).



Ultrasonography



CT scan



MRI with m etal precautions

Differential Diagnosis

Pa ge 2 7 9



Skin avulsion



Contusion



Abrasion

Treatment Pre Hospital 

Obtain hem ostasis, or control of bleeding with direct pressure.



Straighten any flaps of skin whose blood supply m ay be strangulated.



Application of splint if needed



Universal precautions

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Control of hem ostasis

ED Treatment 

Tim e of onset: o

Lacerations m ay be closed prim arily â‰¤8 hours old in areas of poorer circulation.

o

Lacerations m ay be closed â‰¤12 hours old in areas of norm al circulation.

o

On face, lacerations m ay be closed â‰¤24 hours if clean and well irrigated.

o

If not closed, wound m ay heal by secondary intention or by delayed prim ary closure (DPC) in 3â€“5 days.



Analgesia and conscious sedation: o

Adequate analgesia is crucial for good wound m anagem ent.

o

Conscious sedation m ay be required (see Conscious

Pa ge 2 7 9

Sedation). 

Local anesthetics: o

o

Topical: 

TAC (tetracaine, adrenaline, cocaine)



EMLA (eutectic m ixture, lidocaine, prilocaine)

Local/regional: 

Lidocaine, bupivacaine



Epinephrine will cause vasoconstriction and im prove duration of action of anesthetic.



Avoid epinephrine in the penis, digits, toes, ears, eyelids, tip of nose, skin flaps (necrosis), and severely contam inated wounds (im pairs defense).



For patient com fort, inject slowly with sm all-gauge needle; buffer every 9 m L of 1% lidocaine with 1 m L 8.4% sodium bicarbonate.



Consider a 1% diphenhydram ine solution in the lidocaine-allergic patient.



Exploration and rem oval of foreign body: o

Indications for rem oval of a foreign body include: 

Potential or actual injury to tendons, nerves, vasculature





Toxic substance or reactive agent



Continued pain

Irrigation and dÃ©bridem ent: o

Surrounding intact skin m ay be cleaned with an antiseptic solution (povidone-iodine). 

Do not use antiseptic solution within the wound itself because it m ay im pair healing.

o

Scrub with a fine-pore sponge only if significant contam ination or particulate m atter.

o

Irrigation with 200 m L or m ore of norm al saline

Pa ge 2 7 9

(NS): 

Optim al pressure (5â€“8 psi) generated with 30-m L syringe through 18- to 20-gauge needle

 

DÃ©bride devitalized and contam inated tissue.

Wound repair: o

Universal precautions

o

Wounds that cannot be cleaned adequately should heal by secondary intention or DPC.

o

Reapproxim ate all anatom ic borders carefully (e.g., skinâ€“verm ilion border of lip)

o

Consider tissue adhesive for wounds with clean borders, low tension.



Single-layered closure: o

Sim ple interrupted sutures: 

o

Avoid in lacerations under tension.

Horizontal m attress sutures (running or interrupted): 

Edem atous finger and hand wounds



Ideal in skin flaps where edges at risk for necrosis

o

Vertical m attress: 



For wounds under greater tension

Multiple-layered closure: o

Closes deep tissue dead space

o

Lessens tension at the epiderm al level, im proves cosm etic result

o

Buried interrupted absorbable suture, sim ple or running nonabsorbable sutures for epiderm is



Dressing: o

Dress wound with antibiotic ointm ent and nonadherent sem iporous dressing.

o

Inform patient about scarring and risk for infection, use of sunscreen.

Pa ge 2 7 9

o 

Apply splint if needed.

Antim icrobial agents: o

Uncom plicated lacerations do not need prophylactic antibiotics.

o

If antibiotics are used, initiate before wound m anipulation or as early as possible.

o

Lacerations with high likelihood of infection: 

Anim al, hum an bites, especially to hand (see Hand Infection)

 o

Contam inated with dirt, bodily fluids, feces

Tetanus im m unization

P.631

Medication (Drugs) 

See Conscious Sedation.



Tetanus (Td adults, DT peds): 0.5 m L IM



Local anesthetics: o

Topical, applied directly to wound with cotton, gauze: 

EMLA (eutectic m ixture, 5% lidocaine, and prilocaine): apply for 60 m inutes.



TAC (0.5% tetracaine, 1:2,000 adrenaline, 11.8% cocaine): Apply for 20â€“30 m inutes.

o

Injected: 

Bupivacaine (m ax.: 2 m g/kg; duration 3â€“10 hours)



Lidocaine (m ax.: 4.5 m g/kg; duration 1.5â€“3.5 h)

Suture Materials

Pa ge 2 7 9



Absorbable: o

For use in m ucous m em branes and buried m uscle/fascial layer closures: 

Naturalâ€”dissolve <1 week, poor tensile strength, local inflam m ation



Plain catgut



Chrom ic



Fast-absorbing gut for certain facial lacerations where cosm esis is im portant



Synthetic braidedâ€”tensile strength dim inishing over 1 m onth, m ild inflam m ation



Polyglycolic acid (Dexon)



Polyglactin 910 (Vicryl)



Synthetic m onofilam entâ€”tensile strength 70% at 1 m onth, inflam m ation degree unknown





Polydioxanone (PDS)



Polyglyconate (Maxon)

Nonabsorbable: o

Greatest tensile strength

o

Monofilam ent: 

Nylon (Ethilon, Derm alon)



Polypropylene (Prolene)



Polybutester (Novofil): can stretch with wound edem a

 o



Polyethylene, stainless steel

Multifilam ent: 

Cotton



Silk (local inflam m ation)

Needle types: o

Cutting (cuticular and plastic) types are m ost often used in outpatient wound repair.



Staples:

Pa ge 2 8 0



o

For linear lacerations of scalp, torso, extrem ities

o

Avoid in hands, face, and areas requiring CT or MRI.

Adhesive tapes (Steri-Strips): o

For lacerations that are clean, sm all, and under m inim al tension

o

Avoid in wounds that have potential to becom e very swollen.

o

Pretreat wound edges with tincture of benzoin to im prove adhesion.



Tissue adhesives: o

Good cosm etic results have been achieved in sim ple lacerations with low skin tension.

o

An alternative to sutures/staples, especially in children

Follow-Up Disposition Admission Criteria 

Few lacerations by them selves necessitate adm ission unless they require significant dÃ©bridem ent or ongoing intravenous antibiotics, or are com plicated by extensive wound care issues or co-m orbid processes (head injury, abdom inal traum a).



It is unsafe for a child to return hom e when nonaccidental traum a is suspected.

Discharge Criteria 

Wounds at risk for infection or poor healing require a wound check within 48 hours



Tim e of suture rem oval dependent on location and

Pa ge 2 8 0

peripheral perfusion: o

Scalp: 7â€“10 days

o

Face: 3â€“5 days

o

Oral: 7 days

o

Neck: 4â€“6 days

o

Abdom en, back, chest, hands, feet: 7â€“10 days

o

Upper extrem ity: 7â€“10 days

o

Lower extrem ity: 10â€“14 days

o

Overlying joints: 10â€“14 days

Issues for Referral 

Com plicated lacerations (tendon involvem ent) m ay require further repair in the outpatient surgical office.



Be sure to discuss tem porary skin closure and splinting with your surgical consultant.



Specific follow-up should be arranged prior to patient discharge.

References 1. Chisolm C, Howell JM. Soft tissue em ergencies. Em erg Med Clin North Am . 1992;10(4):665â€“705. 2. Hollander JE, Singer AJ. Laceration m anagem ent. Ann Em erg Med. 1999;34(3):356â€“367. 3. Roberts PA, Lam acraft G. Techniques to reduce the discom fort of pediatric laceration repair. MJA 1996;164(1):32â€“35. 4. Stone S, Carter WA. Wound preparation. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill, 2004:41.

Miscellaneous SEE ALSO: Hand Infection

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Codes ICD9-CM 998.2

Pa ge 2 8 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Laryngitis

Laryngitis

Yi-Mei Chng

Basics Description 

Inflam m ation of the m ucosa of the larynx



Peaks parallel epidem ics of individual viruses



Most com m on during late fall, winter, early spring

Etiology 



Viral upper respiratory infections m ost com m on: o

Influenza A and B

o

Parainfluenza types 1 and 2

o

Adenovirus

o

Coronavirus

o

Coxsackie virus

o

Respiratory syncytial virus

o

Measles

o

Rhinovirus

Bacterial infections in 10% of cases: o

Î²-Hem olytic streptococcus

o

Streptococcus pneum oniae

o

Haem ophilus influenzae

o

Moraxella catarrhalis

o

Bordetella pertussis

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

o

Diphtheria

o

Tuberculosis

o

Syphilis

o

Leprosy

Fungal infections: o

Histoplasm osis

o

Blastom ycosis

o

Candidiasis

o

Actinom ycosis



Allergic



Voice abuse or m isuse



Inhalation of caustic substances or other airborne irritants



Autoim m une (rheum atoid arthritis, relapsing polychondritis, Wegener granulom atosis, or sarcoidosis)



Gastroesophageal reflux disease



Idiopathic

Pediatric Considerations Acute spasm odic laryngitis (spasm odic croup)

Diagnosis Signs and Symptoms History 

Hoarseness



Abnorm al sounding voice



Throat tickling



Feeling of throat rawness



Constant urge to clear the throat



Cough



Fever

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

Malaise



Dysphagia

Physical Exam 

Regional lym phadenopathy



Stridor in infants



Hoarse voice

Essential Workup 

Acute laryngitis: o

In m ost cases, the history and inspection of the throat suffice to distinguish between viral and bacterial laryngitis.



Chronic laryngitis (>3 weeks): o

The workup should be directed toward chronic infections, gastroesophageal reflux, neurologic disorders, and tum ors.

o

Visualization of the larynx should be perform ed.

o

The patient should be referred to an ear-nose-throat specialist for biopsy.

o

Visualization of nodules indicate the need to adm it to rule out TB.

Tests Lab 

Blood tests are not generally indicated: o

An elevated WBC count is not a reliable way to distinguish between bacterial and viral illness.



Throat culture: o

Indicated when throat inspection suggests a bacterial infection

Imaging Soft-tissue neck film s:

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

Rarely indicated because direct laryngoscopy provides a m ore com prehensive assessm ent

Diagnostic Procedures/Surgery Direct laryngoscopy: 

Red, inflam ed vocal cords, with rounded edges



Occasionally hem orrhage or exudates



Dem onstration of laryngeal pseudom em brane to distinguishing diphtheria from other infectious form s of laryngitis



This procedure is m ainly used to rule out epiglottitis.

Differential Diagnosis 

Asthm a



Epiglottitis



Esophageal reflux



Vocal nodules



Laryngeal or thyroid m alignancy



Croup/Laryngotracheobronchitis



Foreign body inhalation or other traum a

Treatment Pre Hospital Supportive care and am bulance transport are not generally indicated.

Alert 

If there are signs of respiratory distress, epiglottitis should be suspected: o

Transport sitting up.

o

Provide supplem ental oxygen.

o

Intubation m ay be difficult or im possible and should

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only be attem pted in patients in extrem is.

Initial Stabilization Stabilization is only required if the patient shows signs of respiratory distress: 

The patient should be m anaged for epiglottitis.



Supplem ental oxygen via a nonrebreathing m ask



Orotracheal intubation when tim e perm its in the OR



The neck should be prepped and the equipm ent ready for a surgical airway.

P.633

ED Treatment 

Antibiotics should be adm inistered only for bacterial infection:



o

Oral penicillin for streptococcal infections

o

Erythrom ycin for M. catarrhalis

Steroids m ay aid in decreasing the tim e to resolution of sym ptom s.

Medication (Drugs) 

Erythrom ycin: 250 m g (peds: 30â€“50 m g/kg/d div. q.i.d.) q.i.d. PO



Proton pum p inhibitors: o

Nexium 20â€“40 m g (peds: no dose available) PO per day



Penicillin V: 250 m g (ped: 25â€“50 m g/kg/d div. b.i.d.â€“q.i.d.) q.i.d. PO

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Follow-Up Disposition Admission Criteria 

Tuberculous laryngitis: o



Highly contagious requiring isolation

Signs of epiglottitis, respiratory distress, neck traum a, or anaphylaxis

Discharge Criteria 

Voice restâ€”whispering not recom m ended because it puts further strain on inflam ed vocal cords



Steam inhalations or cool-m ist hum idifier



Increase fluid intake.



Analgesics



Avoid sm oking.



Sym ptom s usually resolve in 10â€“14 days, if viral cause.

Issues for Referral Refer patients with chronic laryngitis to otolaryngologist.

References 1. Ballenger JI, Snow JB, eds. Ballenger's Otorhinolaryngology head and neck surgery. 16th ed. BC Decker, 2002. 2. Behrm an RE, Kliegm an R, Jenson H, eds. Nelson textbook of pediatrics. 16th ed. Philadelphia, Pa.: WB Saunders, 2002. 3. Lynch JS, Roberti CG. Acute laryngitis. Lippincott's Prim ary Care Practice: Ear, Nose, and Throat Problem s. Philadelphia, Pa.: WB Saunders, 2000;4(5):534â€“538. 4. Mehanna HM, Kuo T, Chaplin J, et al. Fungal Laryngitis in Im m unocom petent patients. J Laryngol Otol. 2004;118(May 5):379â€“381.

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Miscellaneous SEE ALSO: Epiglottitis

Codes ICD9-CM 464.0 476.0

ICD10 J04.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Larynx F racture

Larynx Fracture

Diane Devita David Della-Giustina

Basics Description Disruption of any of the cartilaginous structures between the pharynx and trachea: 

Epiglottis, thyroid, arytenoid, cricoid, corniculate, and cuneiform cartilages

Etiology 

Rare injury, incidence appears to be decreasing.



Blunt traum a to the anterior neck associated with m otor vehicle or m otorcycle crash, assault, or recreational activities



Typical m echanism is hyperextension of neck with a direct blow to the exposed anterior neck.



â€œClotheslineâ€• injury is a classic m echanism (victim struck in neck by cord, wire, or branch hung across path of travel).

Pediatric Considerations 

Bicycle handlebars: o

Extended neck hits the bar, com pressing structures

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between the bar and vertebral colum n.

Diagnosis Signs and Symptoms 

May be subtle or delayed for hours



Neck tenderness



Bruising or abrasions over the anterior neck



Hoarseness or voice changes



Hem optysis



Dysphonia



Stridor



Subcutaneous em physem a



Dyspnea



Loss of norm al cartilaginous landm arks of neck

Essential Workup 

Cervical spine radiograph: o

Exam ine for concom itant spinal injury as well as soft-tissue swelling and subcutaneous em physem a.



Chest radiograph: o

Identify pneum othorax, pneum om ediastinum , and subcutaneous em physem a.



CT scan of larynx: o

Â¾Recom m ended unless the patient is going directly to surgery

o

Useful even in cases of apparently less severe sym ptom s and m inor abnorm alities on indirect laryngoscopy



Pulse oxim etry

Tests

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Lab Arterial blood gas if the patient is having respiratory difficulty: 

Identifies hypoxia, hypercarbia

Diagnostic Procedures/Surgery 

Fiberoptic laryngoscopy: o

Allows visualization of injuries involving the airway, vocal cords



Arteriography: o

Only when concerned with possible vascular injuries



Fiberoptic bronchoscopy and esophagoscopy



Surgical exploration



Surgery: o

As indicated by severity of injury

o

Em ergent surgical repair if necessary

Differential Diagnosis Associated injuries: 

Hyoid fracture



Thyroid cartilage disruption



Recurrent laryngeal nerve disruption



Carotid artery injury



Phrenic nerve injury



Cervical spine injury



Hypoxic cerebral injury



Airway edem a



Aspiration pneum onitis



Air em bolism

Pediatric Considerations 

Pediatric larynx located higher in the neck, m ore cartilaginous and m obile than adults; thus, pediatric patients are m ore resistant to laryngeal fractures.

Pa ge 2 8 1



Loosely attached subm ucosal tissue allows for greater soft tissue traum a, m assive edem a, and hem atom a form ation: o

With sm aller airway diam eters, rapid airway com prom ise can occur.



Neck tenderness is a m ore com m on com plaint than dysphagia or dyspnea.

Treatment Pre Hospital 

Cautions: o

Aggressive airway m anagem ent is necessary: oxygen, suction.

o

Cervical spine im m obilization

o

Injury m ay be overlooked if intubated prehospital for other injuries owing to loss of subjective com plaints.



Controversies: o

Elective intubation not advocated

Initial Stabilization Airway m anagem ent is of prim ary concern: 

Severe injuries m ay require operative m anagem ent.



Early intubation to preclude respiratory em barrassm ent



Form al tracheostom y under local m ay be required rather than endotracheal intubation when m ore severe neck injury is present.



Avoid repeated intubation attem pts: o



Proceed to surgical airway.

Cricothyrotom y for severe m axillofacial injuries and injury is superior to cricothyroid cartilage.



Avoid cricothyrotom y if hem atom a present over the

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cricothyroid m em brane or evidence of cricotracheal disruption. 

Em ergent tracheostom y m ay be the only option to secure an airway.

P.635

Pediatric Considerations 

Elective intubation is potentially dangerous.



Mandatory flexible fiberoptic laryngoscopy



CT scan if m anagem ent course in doubt

ED Treatment 

Supplem ental hum idified oxygen



Elevate head of bed to decrease cerebral and neck soft tissue edem a.



Intravenous access



Consult otolaryngologist for surgical evaluation.



Positive end expiratory pressure and volum e-controlled ventilation for severe pulm onary injury associated with acute respiratory distress syndrom e or aspiration pneum onitis

Medication (Drugs) 

For laryngeal injury with subcutaneous em physem a: o

Assum e that the m ucosa of the upper airway has com m unicated with the deep tissue of the neck: 

Am picillin/sulbactam : 1.5â€“3.0 g (peds: 50 m g/kg) IV q6h



Clindam ycin: 600â€“900 m g IV q8h (peds: 25â€“40 m g/kg/24h IV)

Pa ge 2 8 1



Histam ine 2 blockers to prevent irritation to m ucosal injuries (e.g., ranitidine 150â€“300 m g IV; peds: 2â€“4 m g/kg/d div. q6h IV)



For laryngeal edem a, the following m ay be used: o

Steroids: 

Controversial, but m ay be used for m assive edem a. If used, m ost effective within a few hours of injury



Dexam ethasone: 4 m g (peds: 0.15â€“0.6 m g/kg per dose) IV

Pediatric Considerations If stridor present, consider nebulized racem ic epinephrine: 2.25% 0.25â€“0.5 m L in 2.5 m L norm al saline (NS).

Follow-Up Disposition Admission Criteria 

Patients with true laryngeal injuries m ust be adm itted to a m onitored setting for observation and airway m anagem ent; prepare for em ergent surgical repair of laryngeal defect.



Patients with suspected laryngeal injury or highly suspicious m echanism m ust be adm itted to a m onitored setting for observation and serial flexible fiberoptic laryngoscopic exam inations.

Pediatric Considerations Mandatory adm ission recom m ended in all patients for oxim etry, oxygen, and serial fiberoptic laryngoscopy exam inations

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Discharge Criteria Patients without evidence of serious laryngeal injury, airway edema, or com prom ise after an appropriate period of observation in the em ergency departm ent (usually 6 hours): 

Patients can appear deceptively norm al for several hours after injury; if there is any doubt, adm it to a m onitored setting.

References 1. Atkins Z, Abbate S, Fisher S, et al. Current m anagem ent of laryngotracheal traum a: case report and literature review. J Traum a. 2004;56:185â€“190. 2. Francis S, Gaspard D, Rogers N, et al. Diagnosis and m anagem ent of laryngotracheal traum a. J Natl Med Assoc. 2002;94:21â€“24. 3. Gold SM, Gerber ME, Hott SR, et al. Blunt laryngotracheal traum a in children. Arch Otolaryngol Head Neck Surg. 1997;123:83â€“87. 4. Ikram M, Naviwala S. Case report: acute m anagem ent of external laryngeal traum a. Ear Nose Throat J. 2000;79:802â€“804. 5. Kleinsasser NH, Priem er FG, Schulze W, et al. External traum a to the larynx: classification, diagnosis, therapy. Eur Arch Otorhinolaryngol. 2000;257:439â€“444. 6. Muniz A, Foster R, Ram iah V. Laryngeal traum a m im icking croup. J Traum a. 2001;51:565â€“567. 7. O'Mara W, Hebert AF. External laryngeal traum a. J La State Med Soc. 2000;152:218â€“222.

Codes ICD9-CM 959.09

ICD10 S12.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lead Po iso ning

Lead Poisoning

Gerald Maloney Jr.

Basics Description 

Lead has m ultiple m echanism s: o

Binds sulfhydryl groups and affects m ultiple enzym atic processes

o

Resem bles Ca ++ and therefore can interfere with Ca ++ -dependent processes, including cell signaling

o

Mutagenic potentialâ€”not known to be a hum an carcinogen



Distribution: o

Up to 99% of lead is bound to erythrocytes after initial absorption.

o

o

Ultim ately redistributed into bone 

Ninety-five percent of total body lead in adults



Seventy percent of total body lead in children

High lead levels in the serum will com prom ise the bloodâ€“brain barrier and result in lead entry into the CNS and neurotoxicity.



Often coexists with iron deficiency; this allows for increased lead absorption in the gut.



Im pairs hem e synthesis, leading to elevated erythrocyte

Pa ge 2 8 1

protoporphyrin; this com plexes with zinc, causing elevated zinc protoporphyrin (ZPP).

Etiology 

Acute toxicity: o

Most often owing to environm ental exposure or ingestion of substance containing high lead levels



o

Pottery glaze

o

Certain folk rem edies

o

Jewelry

o

Weights

o

Hom e-distilled alcoholic beverages

Chronic toxicity: o

o

Occupational exposures: 

Most com m on via inhalation route



Sm elting



Deleading



Bridge painting

Hom e exposures: 

Lead paint ingestion by children

o

Contam ination of drinking water or food

o

Use of folk rem edies containing high lead concentrations



In the United States, lead intoxication is prim arily owing to ingestion of leaded paints and m ost frequently affects children age 1â€“6 years.



May also be seen when a retained bullet enters synovium or other body cavity where it is system ically absorbed

Diagnosis

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Signs and Symptoms 

Neurologic: o

Seizures (m ay be prolonged and refractory)

o

Encephalopathy

o

Learning disabilities/decreased intelligence

o

Cerebral edem a

o

Peripheral neuropathy (wrist drop), classic (but rarely seen) finding with chronic toxicity



Gastrointestinal: o

Colicky abdom inal pain (lead colic)

o

Ileus

o

Nausea/vom iting

o

Lead lines in gum s (Burton lines) appear as bluish tint to gingival line

o 





Hepatitis/pancreatitis

Cardiovascular: o

Hypertension (generally secondary to renal failure)

o

Myocarditis and conduction defects

Renal: o

Chronic renal insufficiency with long-term exposure

o

Saturnine gout

Hem atologic: o

Anem ia (owing to interference with globin chain synthesis)



o

Elevated ZPP

o

Increases RBC fragility so decreased RBC life span

Musculoskeletal: o

Lead lines from increased Ca ++ deposition (not actually lead itself)

o

May lead to decreased bone strength and growth

Essential Workup

Pa ge 2 8 2

Lead level

Tests Lab 

Whole blood lead level: o

Norm al <10 Âµg/dL

o

100 Âµg/dLâ€”severe encephalopathy; cognitive effects increase with rising levels.

o

Expect that lead levels m ay rise again after treatm ent is com pleted as lead redistributes into the serum again.

o

Levels correlate poorly with sym ptom s. 

Acute exposures m ay be sym ptom atic with levels of 40â€“50 Âµg/dL.



Chronic exposures m ay have m inim al findings at levels of 70 Âµg/dL.





CBC: o

For presence of anem ia

o

RBC indices

Electrolytes, BUN, creatinine, glucose: o

For renal insufficiency



Transam inases, liver function tests



Iron studies



Zinc protoporphyrin (ZPP)

Imaging 

Plain abdom inal radiographs to look for radio-opaque foreign body



Long bone series to look for lead lines (specifically in children)



Cranial CT/other studies as indicated by patient's condition

Differential Diagnosis

Pa ge 2 8 2



Heavy m etal intoxications



Cyclic antidepressants/other seizure-inducing toxins



Encephalopathy/m eningitis/encephalitis



Causes of increased intracranial pressure



Reye syndrom e



Status epilepticus



Bowel obstruction



Guillain-BarrÃ© syndrom e



Addison disease



Cholera



Peripheral neuropathies

Treatment Pre Hospital Alert 

If possible to do so safely, bring containers in suspected overdose/poisoning.



Decontam inate skin



Support airway/breathing and circulation.



Cardiac m onitoring



Seizure m anagem ent

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Cardiac m onitor

o

Isotonic crystalloids as needed for hypotension; vasopressors for refractory hypotension



Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status P.637

Pa ge 2 8 2





Cardiovascular: o

Isotonic crystalloids to support blood pressure

o

Vasopressors for refractory hypotension (rare)

Neurologic: o

Treat seizures with benzodiazepines.

o

Assist ventilation as needed for respiratory insufficiency owing to neurom uscular weakness.



Renal: o

Hem odialysis for renal failure

ED Treatment 

Decontam ination: o

If opacities seen on upright abdom inal film , institute whole bowel irrigation at 1â€“2 L/h of polyethylene glycol until abdom inal film s are clear.

o 



Activated charcoal is not effective.

Evaluate need for chelation therapy; based on: o

Levels

o

Acuity of exposure

o

Sym ptom s

o

Consultation with a m edical toxicologist (advised)

All sym ptom atic patients need chelation: o

Begin with British antilewisite (BAL) and continue for 5 days. 

Stop BAL at 3 days if lead level is <50 Âµg/dL and clinically im proved.

o

Start CaNa 2 EDTA (calcium disodium ethylenediam ine tetra-acetate) after second dose of BAL.



Asym ptom atic patients with lead levels >70 Âµg/dL should be chelated in a fashion sim ilar to sym ptom atic patients.



Asym ptom atic patients with levels <70 Âµg/dL m ay be

Pa ge 2 8 2

treated with an oral chelating agent (dim ercaptosuccinic acid [DMSA]). 

Som e experts recom m end using CaNa 2 EDTA for chelation if levels >50 Âµg/dL.



Som e controversy as to when to begin chelation if levels <45 Âµg/dL and asym ptom atic

Pediatric Considerations 

Currently, lead levels >10 Âµg/dL are considered the action level: o

Level at which investigation into the cause of the exposure and m onitoring m ust occur



Much controversy as to long-term cognitive effects of lead and at which level to chelate asym ptom atic children with elevated lead levels

Pregnancy Considerations 

Much controversy about fetal lead toxicity



Consultation with m aternal-fetal m edicine and m edical toxicology recom m ended in pregnant patients with elevated lead levels

Medication (Drugs) 

Calcium disodium EDTA: o

Multiple regim ens; for acute encephalopathy, 50 m g/kg/d as continuous IV infusion (adults and peds) or 1 g/m 2 q12h

o 

Treat for 5 days

Dextrose 50%: 25 g (50 m L; peds: 0.5 g/kg D 2 5 W) IV for hypoglycem ia



Diazepam : 5â€“10 m g (peds: 0.1 m g/kg) IV for seizure control

Pa ge 2 8 2



Dim ercaprol (British antilewisite [BAL]): o

3 m g/kg IM q4h for 3â€“5 days if m ild to m oderate sym ptom s; 4 m g/kg IM q4h for 5 days for severe sym ptom s (seizure, encephalopathy)

o 

Caution: cannot use if patient has peanut allergy

DMSA (succim er): 10 m g/kg PO q8h for 5 days, then q12h for 14 days (adults and peds)



Lorazepam : 2â€“4 m g IV or IM



Naloxone: 0.4â€“2.0 m g (peds: 0.1 m g/kg) IV



Thiam ine: 100 m g (peds: 1 m g/kg) IM or IV

Follow-Up Disposition Admission Criteria 

Sym ptom atic lead intoxications



Children at high risk for re-exposure in their current environm ent



Pregnant patients with elevated lead levelsâ€”consult obstetrical and toxicology.

Discharge Criteria 

Asym ptom atic patients not requiring parenteral chelation (generally <50 Âµg/dL)



Patients with suspected chronic intoxications who do not require adm ission should be referred for outpatient evaluation.



Ensure that hom e environm ent is safe for patient prior to discharge.

References

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1. Henretig F. Lead. In: Goldfranks Toxicologic Em ergencies. 7th ed. 2002. 2. Morgan BW, Todd K. Elevated lead levels in urban m oonshine drinkers. Ann Em erg Med. 2001;37(1):51â€“54. 3. Needlem an H. Lead poisoning. Ann Rev Med. 2004;55:209â€“222. 4. Shannon M. Severe lead poisoning in pregnancy. Am bul Pediatr. 2003;3(1):37â€“39.

Codes ICD9-CM 984.0 984.1 984.8 984.9

Pa ge 2 8 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Legg-C alvÃ©-Perthes Disease

Legg-CalvÃ©-Perthes Disease Brandon H. Backlund

Basics Description Avascular necrosis of all or part of fem oral head in children

Genetics Association with factor V Leiden m utation and anticardiolipin antibodies

Etiology 

Multiple episodes of infarction causing characteristic findings



Disruption of vascular supply to fem oral head with exact underlying cause unknown



Growing evidence im plicating hypercoagulable states; m ay be m ultifactorial



Risk factors include growth horm one therapy, exposure to secondhand sm oke, and low birth weight



Progression through four stages of disease: o

Synovitis: brief duration (weeks), reaction to ischem ia

o

Necrosis and collapse of fem oral head

Pa ge 2 8 2

o

Fragm entation: resorption of avascular bone; deform ation of fem oral head often occurs at this stage.

o

Reconstitution: form ation of new bone



More com m on in boys with m ale-to-fem ale ratio of 4:1



Most com m only occurs between ages of 3 and 9 years: o

Range, 2â€“18 years of age



Bilateral in 10â€“15% of cases



Associated with short stature and delayed skeletal m aturation

Diagnosis Signs and Symptoms History 

Frequently insidious onset



Lim p often presenting com plaint



Pain: o

Aching in hip, groin, anterom edial thigh, or anterom edial knee

o

May be m ild

o

Aggravated by activity, relieved by rest

o

Muscle spasm com m on com plaint early in course of disease

Physical Exam 

Tenderness over anterior aspect of hip joint



Joint stiffness:



o

Lim itation of internal rotation seen earliest

o

Lim ited abduction

Muscle atrophy and shortening of leg on affected side late

Pa ge 2 8 2

findings 

Otherwise well-appearing and afebrile



May be asym ptom atic

Essential Workup 

Radiographs of hip m ost im portant study for diagnosis in em ergency room



Consider and exclude septic arthritis (usually an acute febrile illness).

Tests Lab CBC, erythrocyte sedim entation rate (ESR) if septic arthritis a concern

Imaging 

Hip radiographs: o

Anteroposterior and frog-leg views of hip

o

Early findings: 

Coxa m agna: cartilaginous overgrowth of fem oral head, m ay see joint space widening or lateral shift of fem oral head in acetabulum



Subchondral fracture (Caffey sign): crescentic subchondral radiolucency



Minim al joint effusion, prom inence of soft tissues over capsule

o

Over subsequent weeks: 

Increased opacity of fem oral head



Fragm entation of fem oral head



May see m etaphyseal â€œcystsâ€• (also known as physeal bridge): radiolucent areas in m etaphysis representing ingrowth of cartilage from growth plate

Pa ge 2 8 2

 

Flattening of fem oral head (coxa plana)

Ultrasound: o

Evaluate for effusion.

o

Evaluate articular cartilage for thickening and enlargem ent.

o 

Evaluate deform ity and containm ent of fem oral head.

Technetium -99m bone scan: o

Detects changes in fem oral head earlier than plain radiographs

o

Shows decreased uptake in fem oral head on affected side



Magnetic resonance im aging: o

Shows decreased signal in fem oral head

P.639

Diagnostic Procedures/Surgery Hip joint aspiration if concern for septic arthritis; m ay need orthopedic consultation

Differential Diagnosis 

Unilateral involvem ent: o

Transient (or toxic) synovitis

o

Septic arthritis

o

Osteom yelitis

o

Juvenile rheum atoid arthritis

o

Rheum atic fever

o

Traum a:

o



Fem oral neck fracture



Hip dislocation



Slipped capital fem oral epiphysis

Tuberculosis:

Pa ge 2 8 3

o 

Tum or

Bilateral involvem ent: o

Hypothyroidism

o

Epiphyseal dysplasia

o

Gaucher disease

Treatment ED Treatment 

Pain control m ain ED intervention



May need crutches to avoid weight bearing

Medication (Drugs) 

Diazepam : 0.1â€“0.2 m g/kg per dose (m ax. 5 m g) PO q6hâ€“q8h PRN m uscle spasm



Ibuprofen: 10 m g/kg per dose PO q6hâ€“q8h PRN pain

Follow-Up Orthopedic consultation to determ ine m anagem ent; m ay be outpatient

Disposition Admission Criteria Need for adm ission rare, indicated for: 

Severe pain or m uscle spasm not controlled by oral m edications



Social considerations; bedrest/care at hom e not possible

Pa ge 2 8 3

Discharge Criteria 

Adequate pain control with oral m edications



Orthopedic follow-up arranged

Issues for Referral 

Very young or m inim al involvem ent usually good outcom e with m inim al intervention



For m ore severe disease, range of treatm ent options including conservative treatm ent, orthotics, traction, and surgical osteotom y, determ ined by consulting orthopedist

References 1. Balasa V, et al. Legg-Calve-Perthes disease and throm bophilia. J Bone Joint Surg Am . 2004;86-A(12):2642â€“2647. 2. Docquier P, et al. Orthopaedic concerns in children with growth horm one therapy. Acta Orthop Belg. 2004;70(4):299â€“305. 3. Gordon JE. et al. Sm oking and socio-econom ic status in the etiology and severity of Legg-Calve-Perthesâ€™ disease. J Pediatr Orthop B. 2004;13(6):367â€“370. 4. Lappin K, et al. Does low birthweight predispose to Perthesâ€™ disease? Perthesâ€™ disease in twins. J Pediatr Orthop B. 2003;12(5):307â€“10. 5. Staheli L. Practice of Pediatric Orthopedics. Philadelphia: Lippincott William s & Wilkins; 2001:146â€“151. 6. Szepesi K, et al. The m ost severe form s of Perthesâ€™ disease associated with the hom ozygous factor V Leiden m utation. J Bone Joint Surg Br. 2004;86(3):426â€“429. 7. Tachdijan M. Clinical Pediatric Orthopedics. Norwalk, CT: Appleton & Lange; 1997:210â€“223. 8. Wall E. Legg-Calve-Perthes disease. Curr Opin Pediatr. 1999;11(1):76â€“9. 9. Yilm az D, et al. Evaluation of anticoagulant system in Turkish children with Perthes disease. Pediatr Int. 2005;47(1):43â€“48.

Pa ge 2 8 3

Codes ICD9-CM 732.1

ICD10 M91.1

Pa ge 2 8 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Leukem ia

Leukemia

Linda Mueller

Basics Description 

Neoplasm s of white blood cells (WBCs) that have undergone a m alignant transform ation



Hyperleukocytosis: o

Occurs with WBC >100,000/m m 3

o

Leads to occlusions of sm all vessels prim arily in brain or lungs

o

Present with confusion, stupor, or shortness of breath

Chronic Myelogenous Leukemia (CML) 

Overproduction of granulocytic WBCs (neutrophils): o

Neutrophil function preserved



Throm bocytosis



Basophilia



Philadelphia chrom osom e present in bone m arrow of >95%

Chronic Lymphocytic Leukemia (CLL) 

Most com m on leukem ia in adults



Overproduction of m onoclonal lym phocytes



Cells accum ulate in lym ph nodes, bone m arrow, liver,

Pa ge 2 8 3

spleen 

Particularly prone to herpes virus infections

Acute Leukemias 

Proliferation of undifferentiated im m ature cells: o

Acute m yelogenous leukem ia (AML)â€”im m ature m yeloid cells

o

Acute lym phocytic leukem ia (ALL)â€”im m ature lym phoid cells (blasts)



Rapidly fatal

Etiology 

Cause unknown



Fam ilial clustering in CLL



Increased incidence of AML, ALL, and CML with ionizing radiation

Pediatric Considerations 

Usually have ALL: o



Most com m on pediatric cancer

Sixty percent to 80% rem ission in those who are standard risk



Better overall prognosis, except if younger than 1 year of age



May develop leukostasis at lower levels

Diagnosis Signs and Symptoms Chronic Myelogenous Leukemia 

Asym ptom atic



Fatigue

Pa ge 2 8 3



Weight loss



Left upper quadrant pain, tenderness



Abdom inal fullness



Splenom egaly (m ost com m on)



Later stage: o

Headaches

o

Bone pain

o

Arthralgias

o

Fever

o

Leukotactic sym ptom s: 

Dyspnea



Drowsiness



Confusion

Chronic Lymphocytic Leukemia 

Asym ptom atic



Fatigue



Lethargy



Weight loss



Lym phadenopathy



Splenom egaly



Hepatom egaly

Acute Lymphocytic Leukemia (ALL); Acute Myelogenous Leukemia (AML) 

Fever



Fatigue



Pallor



Headache



Angina



Congestive heart failure, dyspnea on exertion



Bone pain



Granulocytic sarcom a (isolated m ass of leukem ic blasts)

Pa ge 2 8 3



Easy bleeding (throm bocytopenia): o

Petechiae

o

Ecchym osis

o

Epistaxis

o

Hem orrhage



Infections (granulocytopenic)



Organ involvem ent with advanced ALL: o

Lym phadenopathy

o

Hepatom egaly

o

Splenom egaly

o

Leukem ic m eningitis: 

Headache



Nausea



Seizures

Essential Workup CBC/platelets: 





CML: o

WBC range, 10,000â€“1 m illion/m m 3

o

Neutrophils predom inate.

o

Throm bocytosis in 50%

CLL: o

Absolute lym phocytosis >5,000

o

WBC range, 40,000â€“150,000/m m 3

Acute leukem ia (AML/ALL): o

Anem ia

o

Throm bocytopenia

o

Elevation/depression of WBC

Tests Lab 

Electrolytes, BUN, creatinine, glucose, calcium



Uric acid level:

Pa ge 2 8 3

o 

Lactate dehydrogenase: o



Frequently elevated, especially in ALL

Increased in acute leukem ias

Coagulation profile: o

Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), fibrinogen, fibrin-split products

o

If dissem inated, suspect intravascular coagulation.



Blood/urine cultures if fever



Arterial blood gases/pulse oxim etry for shortness of breath

Imaging 

Bone m arrow biopsy: o

Required to m ake diagnosis

o

CMLâ€”hypercellular with m yeloid hyperplasia

o

CLLâ€”lym phocytosis (30â€“100%)

o

Acute leukem iaâ€”hypercellular with blast cells, which replace norm al m arrow



Leukocyte alkaline phosphatase test: o

Decreased in neutrophils in CML



Ph1 chrom osom e present in CML



Chest radiograph

P.641

Differential Diagnosis 



CML: o

Lym phom a

o

Myeloproliferative syndrom es

o

System ic lupus erythem atosus

o

Infectionâ€”bacterial, fungal, m ycobacterial

CLL: o

Pertussis

Pa ge 2 8 3



o

Infectious lym phocytosis

o

Cytom egalovirus

o

Epstein-Barr virus/m ononucleosis

o

Hepatitis

o

Rubella

Acute leukem ia: o

Aplastic anem ia

o

Leukem oid reactions to infections

Treatment Initial Stabilization 

One hundred percent oxygen for hypoxia/shortness of breath



IV access with 0.9% norm al saline (NS)



Initiate platelet transfusion for severe bleeding from throm bocytopenia.



Begin broad-spectrum antibiotics for fever and granulocytopenia.



Treat dissem inated intravascular coagulation (see Dissem inated Intravascular Coagulation).

ED Treatment 

Treat leukostasis: o

Rehydrate with 500-m L bolus (20 m L/kg) IV 0.9% NS

o

Adm inister acetazolam ide to alkalinize urine.

o

Initiate allopurinol.

o

Arrange for leukapheresis.

o

Whole-brain radiation for CNS effects

o

Adm inister hydroxyurea for CML: 20â€“30 m g/kg single dose daily

Pa ge 2 8 3



Transfuse packed RBCs for sym ptom atic anem ia: o

May require irradiated, filtered, and HLA-type specific blood

Post ED Treatment 

CLL: o

Chem otherapy

o

Prednisone for im m une-m ediated throm bocytopenia

o

Radiation to localized nodular m asses/enlarged spleen





CML: o

Interferon therapy

o

Chem otherapy

o

Bone m arrow transplantation

ALL: o

Chem otherapy

o

CNS prophylaxis with intrathecal m ethotrexate/cranial radiation

o 

Bone m arrow transplantation

AML: o

Chem otherapy

o

Bone m arrow transplantation

Follow-Up Disposition Admission Criteria 

Newly diagnosed leukem ia with: o

Sym ptom atic anem ia

o

WBC >30,000

o

Throm bocytopenia

Pa ge 2 8 4



ICU adm ission for unstable patients with dissem inated intravascular coagulation, blast crisis, or bleeding

Discharge Criteria Asym ptom atic patients without significant laboratory abnorm alities

References 1. Abram son N. Leukocytosis: basics of clinical assessm ent. Am Fam Physician. 2000;62:2053â€“2060. 2. Lowenberg B. Acute m yeloid leukem ia. N Engl J Med. 1999;341:1051â€“1062. 3. Pui C. Acute lym phoblastic leukem ia. N Engl J Med. 1998;339:605â€“614. 4. Sawyers C. Chronic m yeloid leukem ia. N Engl J Med. 1999;340:1330â€“1340. 5. Tsiodras S. Infection and im m unity in chronic lym phocytic leukem ia. Mayo Clin Proc. 2000;75:1039â€“1054.

Codes ICD9-CM 208.9

ICD10 C95.9

Pa ge 2 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lightning Injuries

Lightning Injuries

Paul Arnold

Basics Description Constellation of problem s caused by lightning strikes

Mechanism 

Lightning is a stream of negative current that proceeds downward from cloud to ground.



Because of the brief duration (1â€“100 m illiseconds) of lightning: o

Current tends to pass over the skin rather than through the body (flashover).

o 

Deep tissue injuries are rare.

Mechanism s of injuryâ€”electrical: o

Direct strike

o

Side splash injury: 

Current jum ps from another object to the victim .

o

Contact strike: 

Current passes to victim through an object he or she is touching.

o

Ground strike: 

Current m oves through ground surface and m ay

Pa ge 2 8 4

injure m ultiple victim s. o

Hypothetically, an upward stream er of positive current from the ground can also cause injury.



Mechanism s of injuryâ€”other: o

Blunt injury owing to atm ospheric shock wave, or fall

o

Therm al burning

Etiology Exposure to lightning: 

Usually during outdoor activity



Lightning can strike indoor victim s who are handling ungrounded electrical equipm ent or telephones.

Diagnosis Signs and Symptoms History 

Consider lightning strike in unwitnessed falls, cardiac arrests, or unexplained com a in an outdoor setting.



Conscious patients m ay report: o

Pain

o

Neurologic deficits including: 

Num bness or paraesthesias



Weakness



Visual disturbance



Headache



Confusion

o

Chest pain

o

Respiratory distress

Physical Exam 

Cardiorespiratory injuries:

Pa ge 2 8 4

o

Cardiac asystole: 

Due to direct current injury



May resolve spontaneously as the heart's intrinsic autom aticity resum es

o

Respiratory arrest 

Caused by paralysis of m edullary respiratory center



May persist longer than cardiac asystole and lead to hypoxia-induced ventricular fibrillation

o

Acute m yocardial infarction (rare)

o

Shock:

o





Neurogenic (spinal injury)



Hypovolem ic (traum a)

Mottled or cold extrem ities: 

Caused by autonom ic vasom otor instability



Usually resolves spontaneously in a few hours

Neurologic injuries: o

Confusion, cognitive or m em ory defects

o

Altered level of consciousness (>70% of cases)

o

Flaccid m otor paralysis

o

Seizures

o

Fixed dilated pupils owing to either serious head injury or autonom ic dysfunction



Traum atic injuries: o

Blunt traum a: 

To the head or spine



Fractures, dislocations, m uscle tears, and com partm ent syndrom es

o

Ruptured tym panic m em brane with ossicular disruption (up to 50%)

o

Burns: 

Discrete entrance and exit wounds uncom m on

Pa ge 2 8 4



Direct therm al injury is uncom m on owing to the brevity of electrical currents.



Therm al burns can arise from evaporation of water on skin, ignited clothing, heated m etal objects (buckles/jewelry).

o

Feathering pattern of fernlike â€œburnsâ€•: 

Cutaneous im prints from electron showers that track over skin





Pathognom onic of lightning injury



Resolve within 24 hours

Ophthalm ologic injuries: o

Cataracts occur days to years after injury

o

Corneal lesions

o

Intraocular hem orrhages

o

Retinal detachm ent

Essential Workup Confirm atory history from bystanders or rescuers of the circum stances of the injury

Tests Lab 

CBC for baseline hem atocrit



Urinalysis for m yoglobin



Electrolytes for acidosis



BUN, creatinine for renal function



Troponin, creatine kinase (CK), and cardiac enzym es for m uscle/cardiac dam age

Imaging 

Chest radiograph



Cervical spine radiograph



Head CT for altered m ental status or significant head

Pa ge 2 8 4

traum a 

Relevant im aging for specific injuries

Diagnostic Procedures/Surgery ECG: 

Nonspecific ST changes com m on



Acute m yocardial infarction rare

Differential Diagnosis Other causes of com a, cardiac dysrhythm ia, or traum a: 

Hypoglycem ia



Intoxication



Drug overdose



Cardiovascular disease



Cerebrovascular accident (CVA)

Treatment Pre Hospital 

Field triage should rapidly focus on providing ventilatory support to unconscious victim s or those in cardiopulm onary arrest: o

Prevents reversible asystolic cardiac arrest from degenerating into hypoxia-induced ventricular fibrillation

o

Conscious victim s are at lower risk for im m inent dem ise.





Spine im m obilization for: o

Cardiopulm onary arrest (suspected traum a)

o

Significant m echanical traum a

o

Suspected loss of consciousness at any tim e

Cover superficial burns with sterile saline dressings.

Pa ge 2 8 4



Im m obilize injured extrem ities.



Rapid extrication to decrease risk for repeat lightning strikes

P.643

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Standard advanced cardiac life support (ACLS) m easures for cardiac arrest



Diligent prim ary and secondary survey for traum atic injuries and other causes of collapse/injury: o



Maintain cervical spine precautions until cleared.

Treat altered m ental status with glucose, naloxone, or thiam ine as indicated.



Hypotension requires volum e expansion and pressor agents.

ED Treatment 

IV access for m edication adm inistration



Clean and dress burns.



Tetanus prophylaxis



Treat m yoglobinuria if present:



o

Diuretics, such as furosem ide or m annitol

o

Alkalinize urine to a pH of 7.45

o

Maintain urine output with IV fluid adm inistration.

Volum e expansion: o

Do not follow burn treatm ent form ulas because flashover burns are rarely the cause of fluid loss.

o

Occult deep burn injury is rare when com pared with other types of electrical current injury.

o

Titrate volum e adm inistration to urine output:

Pa ge 2 8 4



Fluid loading m ay be dangerous if patient also has head injury.



Com partm ent syndrom e: o

Must be distinguished from vasospasm , autonom ic dysfunction, and paralysis, which are usually self-lim ited phenom ena

o

Delay fasciotom y if possible because it will rarely be necessary.



Nonsteroidal anti-inflam m atory drugs (NSAIDs) and high-dose steroids have been proposed to reduce long-term neurologic and corneal dam age.

Medication (Drugs) 

Furosem ide: 1 m g/kg IV slow bolus q6h



Mannitol: 0.5 m g/kg IV, repeat PRN



Sodium bicarbonate: 1 am p IV push (peds: 1 m Eq/kg) followed by 2â€“3 am ps/L D 5 W IV fluid

Follow-Up Disposition Admission Criteria 

Seriously injured and postcardiac arrest victim s



History of change in m ental status/altered level of consciousness



Myoglobinuria



Acidosis



History of dysrhythm ias or ECG changes: o

May not resolve spontaneously

Pa ge 2 8 4

o

24- to 48-hour observation period to identify potentially unstable cases

Discharge Criteria 

Asym ptom atic patients with no injuries



Close follow-up required owing to the risk for delayed sequelae: o

Neurologic

o

Ophthalm ologic

o

Psychologic

References 1. Cooper MA. A fifth m echanism of lightning injury. Acad Em erg Med. 2002;9(2):172â€“174. 2. Cooper MA. Lightning injuries. In: Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. Philadelphia: Mosby; 2002. 3. O'Keefe Gatewood M, Zane RD. Lightning injuries. Em erg Med Clin North Am . 2004;22(2):369â€“403.

Miscellaneous SEE ALSO: Electrical Injury

Codes ICD9-CM 994.0

ICD10 T75.0

Pa ge 2 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lithium Po iso ning

Lithium Poisoning

Sean Bryant

Basics Description 

GI absorption is rapid: o

Regular release: peak serum levels 2â€“4 hours

o

Sustained release: peak serum levels 4â€“12 hours



Half-life 24 hours



Slow distribution



Volum e of distribution (V d ): 0.6â€“0.9 L/kg



Elim ination: o

Not m etabolized

o

Excreted renally unchanged

o

Reabsorbed in the proxim al tubules by sodium transport m echanism

o

Elim ination half-life (therapeutic) is 20â€“24 hours and prolonged in chronic users.



Therapeutic and toxic indices: o

Therapeutic and toxic effects occur only when lithium is intracellular.

o

Narrow toxic-to-therapeutic ratio

o

Therapeutic level 0.6â€“1.2 m Eq/L (after intracellular/extracellular equilibration)

Pa ge 2 8 5

o

Because of its size, renal handling sim ilar to sodium , potassium , and m agnesium

Risk Factors 





Acute conditions increasing risk of toxicity: o

Dehydration (greater percent reabsorbed)

o

Overdose

Chronic conditions increasing risk of toxicity: o

Hypertension

o

Diabetes m ellitus

o

Renal failure

o

Congestive heart failure

o

Advanced age

o

Dose change

o

Drug interactions

o

Lithium therapy

o

Low-salt diet

The following increase serum lithium levels owing to decreased renal clearance or exacerbated effects: o

Nonsteroidal anti-inflam m atory drugs

o

Thiazides

o

Angiotensin-converting enzym e inhibitors

o

Dilantin

o

Tricyclic antidepressants

o

Phenothiazines

Etiology 

Acute or chronic conditions affecting lithium clearance



Overdose

Diagnosis

Pa ge 2 8 5

Signs and Symptoms Acute Toxicity 

Less com m on and less serious than chronic toxicity



Neurologic (m ild):









o

Weakness

o

Fine trem or

o

Light-headedness

Neurologic (m oderate): o

Ataxia

o

Slurred speech

o

Blurred vision

o

Tinnitus

o

Profound weakness

o

Coarse trem or

o

Fasciculations

o

Hyperreflexia

o

Apathy

Neurologic (severe): o

Confusion

o

Com a

o

Clonus

o

Extrapyram idal sym ptom s

o

Seizure

Gastrointestinal: o

Very com m on

o

Nausea/vom iting

o

Diarrhea

o

Abdom inal pain

Cardiac: o

Prolonged QT, ST depression

o

T-wave flattening m ost com m on ECG abnorm ality

Pa ge 2 8 5

o

U waves

o

Serious arrhythm ia (rare)

Chronic Toxicity 

Neurologic: o

Most com m on

o

Sam e sym ptom s as acute

o

Severe toxicity includes Parkinson-type sym ptom s, psychosis, and m em ory deficits.







Renal: o

Nephrogenic diabetes insipidus

o

Interstitial nephritis

o

Distal tubular acidosis

o

Direct cellular dam age

Derm atologic: o

Derm atitis

o

Ulcers

o

Localized edem a

Endocrine: o



Hypothyroidism

Hem atologic: o

Leukocytosis

o

Aplastic anem ia

Essential Workup 

Lithium level: o

Obtain history of tim e of ingestion or last dose.

o

Because of prolonged distribution, repeat every 2 hours to detect trend.



Stratify patient into one of three categories of toxicity to interpret level and predict toxicity: acute, acute on chronic, chronic: o

Acute toxicity:

Pa ge 2 8 5



Intentional overdose in patient not previously taking lithium



Poor correlation between lithium level and sym ptom s because intracellular distribution has not yet occurred



Toxic levels m ay appear in asym ptom atic patients.



Lithium level >4 m Eq/L is toxic because clearance is slow and com plications are possible.

o

Acute on chronic toxicity: 

Intentional or accidental overdose in patient on lithium therapy



Lithium level >3 m Eq/L usually associated with sym ptom s.

o

Chronic toxicity: 

Patients on lithium therapy who progressively develop toxicity secondary to factors other than acute ingestion



Stronger correlation between lithium level and sym ptom s



Lithium level >1.5 m Eq/L m ay be toxic.

Tests Lab 

Electrolytes, BUN, creatinine, and glucose levels to determ ine electrolyte disturbances/renal function



Aspirin and/or acetam inophen levels as indicated



Urinalysis: o

Specific gravity

Differential Diagnosis 

Consider lithium toxicity with altered m ental status and

Pa ge 2 8 5

fasciculations. 

Endocrine: o



Hypoglycem ia

Toxicologic: o

Organophosphates

o

Cholinergic substances

o

Heavy-m etal poisoning

o

Neuroleptic overdose

o

Black widow/scorpion envenom ation

o

Strychnine poisoning

P.645

Treatment Pre Hospital 

Transport all appropriate pill bottles to hospital.



Intravenous access, oxygen, and cardiac m onitoring

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Secure intravenous access with 0.9% norm al saline.



Cardiac m onitor



Naloxone, thiam ine, dextrose (or Accu-Chek) if altered m ental status



Benzodiazepine (diazepam ) for seizures

ED Treatment 

Prevent absorption: o

Consider gastric lavage only if patient presents within 1 hour of acute life-threatening ingestion and has

Pa ge 2 8 5

protected airway. o

Activated charcoal: 

Lithium not absorbed by charcoal



Consider one dose of activated charcoal if possible coingestants

o

Whole-bowel irrigation: 

Polyethylene glycol solution (PEG/GoLytely)



Indicated with sustained-release products



Flushes lithium through gut



Adm inister (2 L/h per nasogastric [NG] tube) until rectal effluent is clear.



Contraindications include bowel obstruction or perforation, ileus or hypotension, and unprotected airway in obtunded or seizing patient.



Enhance elim ination: o

Intravenous fluids: 

Rapidly correct any pre-existing fluid deficit with 0.9% norm al saline at 150â€“300 m L/h.



Saline hydration im proves glom erular filtration and decreases proxim al tubule reabsorption of lithium .



Maintain urine output between 1 and 2 m L/kg/h.



Lim ited value once glom erular filtration rate m axim ized



Sodium bicarbonate offers no additional advantage.

o

Loop, thiazide, and osm otic diuretics not recom m ended: 

Dehydration m ay result in worsening toxicity.



No direct effect on renal reabsorption, because lithium is reabsorbed in proxim al tubules

Pa ge 2 8 5

o

Kayexalate (sodium polystyrene sulfonate): 

Anim al studies indicate reduced lithium levels.



Only very large doses studied



Com plications m ay include hypokalem ia, hyperkalem ia, fluid overload, and dysrhythm ias.



Dialysis: o

Peritoneal dialysis not recom m ended

o

Hem odialysis recom m ended for augm enting elim ination (below)

General Measures 

Correct electrolyte abnorm alities.



Continuous cardiac m onitoring



Maintain well-hydrated state.



Observe for neurologic changes.

Special Therapy 

Hem odialysis recom m ended for severe cases or acute ingestions with high levels indicating im m inent toxicity



Controversial indications (valid criteria not established): o

Severe and progressive neurologic abnorm alities

o

Renal failure

o

Altered m ental status

o

Ventricular arrhythm ia/cardiogenic shock

o

History of congestive heart failure or pulm onary edem a

o

Acute ingestions with levels >4 m Eq/L

o

Chronic ingestions with levels >2.5 m Eq/L



Standard end point is lithium level <1 m Eq/L.



Repeat lithium level 6 hours after dialysis checking for evidence of redistribution.



May need to repeat dialysis owing to rebound effect

Pa ge 2 8 5

(redistribution of intracellular lithium ). 

May reduce the potential for developing perm anent neurologic sequelae with chronic toxicity

Medication (Drugs) 

Dextrose: D 5 0 1 am pule: 25 g (peds: D 2 5 W 4 m L/kg) IV



Diazepam : 5 m g (peds: 0.2â€“0.4 m g/kg) IV q5m in until seizures controlled



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or via endotracheal tube



Polyethylene glycol: 2 L/h (peds: 2 m L/kg/h) via nasogastric tube



Thiam ine: 100 m g IV

Follow-Up Disposition Admission Criteria 

Sym ptom atic



Requiring hem odialysis



Lithium level unchanged, increased, or >2 m Eq/L despite em ergency departm ent intervention



Moderate to severe sym ptom s with chronic levels >4 m Eq/L warrant adm ission to intensive care unit.



Intentional ingestion

Discharge Criteria Decreasing lithium levels every 2â€“4 hours in asym ptom atic patient and serum lithium level <2 m Eq/L

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Issues for Referral Intentional overdose: 

Psychiatry consultation

References 1. Bailey B, McGuigan M. Com parisons of patients hem odialyzed for lithium poisoning and those for whom dialysis was recom m ended by PCC but not done: what lesson can we learn? Clin Neurol. 2000;54:388â€“392. 2. Belanger DR, Tierney MG, Dickinson G. Effect of sodium polystyrene sulfonate on lithium bioavailability. Ann Em erg Med. 1992;21:1312â€“1315. 3. Bosse GM, Arnold TC. Overdose with sustained release lithium preparation. J Em erg Med. 1992;10:719â€“721. 4. Henry GC. Lithium . In: Goldfrank LR. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002. 5. Leikin J, Paloucek F. Lithium : Poisoning and Toxicology Handbook. Hudson, Ohio: Lexi-Com p, 2002. 6. Osborn HH, Malkevich D. Lithium . In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 7. Scharm an EJ. Methods used to decrease lithium absorption or enhance elim ination. Clin Toxicol. 1997;35:601â€“608.

Codes ICD9-CM 985.8

ICD10 T56.5

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ludw ig's Angina

Ludwig's Angina

Paul Blackburn

Basics Description 

A life-threatening infection of the floor of the m outh



Rapidly spreading gangrenous cellulitis, necrotizing fasciitis of subm axillary, sublingual, subm andibular spaces



First described by von Ludwig in 1836



Mortality exceeded 50% in preantibiotic era.



Most deaths due to respiratory obstruction



Im proved dental care, antibiotics reduce incidence



Four cardinal aspects: o

Bilateral involvem ent of m ore than one deep-tissue space

o

Gangrene with serosanguineous, putrid infiltration; little or no frank pus

o

Involvem ent of connective tissue, fasciae, and m uscles; not glandular structures

o 

Spread by fascial space continuity, not lym phatics

Brawny, painful induration of suprahyoid neck results in woody edem a of the floor of the m outh; tongue, soft tissues forced superiorly, posteriorly.



Rapid respiratory obstruction (asphyxia) can occur.

Pa ge 2 8 6

Etiology 





Odontogenicâ€”50â€“90% of reported cases: o

Most com m only second, third m andibular m olars

o

Children less likely to have an odontogenic source

Less com m only: o

IV drug injections into neck veins

o

Mandibular fractures

o

Oral lacerations

o

Sialadenitis

o

Peritonsillar abscess

o

Tongue piercing

Invariably polym icrobial, oral flora: o

Most com m on pathogens Strep viridans, Staph aureus, Staph epiderm idis

o

Anaerobes: m ost com m only Bacteroides species

Diagnosis Signs and Symptoms 

Subm andibular pain



Tongue elevation, protrusion



Trism us: o

Difficult to exam ine m outh, pharynx



Dysphonia



Odynophagia



Stridor



Anxiety



Salivary incontinence



Fever



Tachypneic, tachycardic

Pa ge 2 8 6



Patient will prefer sitting/â€œsniffingâ€• position.



Subm andibular area hard, â€œwoody,â€• painful

Essential Workup Diagnosis apparent from the history, physical exam ination

Tests Lab 

WBC count



Blood cultures

Imaging 

Soft tissue film s of neck: o



Edem a, presence of gas

CT, MRI detects severe cellulitis, abscesses, intrathoracic extension.



Panorex detects odontogenic abscesses.



Chest radiograph: o



Intrathoracic extension

Ultrasound detects abscesses.

Differential Diagnosis 

Cellulitis



Peritonsillar abscess



Salivary gland abscess



Lym phadenitis



Angioneurotic edem a



Lingual carcinom a



Sublingual hem atom a secondary to anticoagulation

Treatment

Pa ge 2 8 6

Pre Hospital 

Transport in sitting position: o



Supplem ental oxygen, suction secretions as needed

Early, aggressive airway protection

Initial Stabilization 

Airway com prom ise is the prim ary concern



Expect difficulty: altered anatom y, swollen tissue, trism us



Rapid-sequence intubation m ay result in loss of supporting structures; loss of visualization, patent airway



Sedation-assisted orotracheal intubation is preferred: o



Short-acting agents (etom idate, thiopental)

Awake, fiberoptic laryngoscopic intubation is recom m ended as a first-line approach



Avoid blind nasotracheal intubation: o

Distorted anatom y

o

Risk of inducing bleeding or perforating an abscess



Cricothyrotom y, jet ventilation m ay be difficult.



Tracheostom y is the â€œgold standardâ€• m anagem ent: o

Risk of secondary intrathoracic spread

ED Treatment 

Initiate broad spectrum antibiotics: o

Aerobic/anaerobic/polym icrobial infection

o

Clindam ycin or penicillin G + m etronidazole; also cefoxitin, ticarcillin/clavulanate, piperacillin/tazobactam , am picillin/sulbactam



Steroids of no proven benefit



Hyperbaric oxygen if m ediastinitis, necrotizing fasciitis of the chest wall

P.647

Pa ge 2 8 6

Medication (Drugs) 

Antibiotics: o

Am picillin/SB: 3 g IV q6h

o

Cefoxitin: 2 g IV q8h

o

Clindam ycin: 900 m g IV q8h

o

Metronidazole: 500 m g IV q6h

o

Penicillin G: 4 m IU IV q4hâ€“q6h Piperacillin/TZ: 3.375 g IV q6h

o 

Ticarcillin/CL: 3.1 g IV q4hâ€“q6h

General anesthetics: o

Etom idate: 0.2â€“0.3 m g/kg IV

o

Thiopental: 3â€“5 m g/kg IV

Follow-Up Disposition Admission Criteria 

All are adm itted



Intensive care unit or m onitored setting; airway com prom ise can be precipitous

References 1. Barakate MS, Jensen MJ, Hem li JM, et al. Ludwig's angina: report of a case and review of m anagem ent issues. Ann Otol Rhinol Laryngol . 2001;110(5 Pt 1):453â€“456. 2. Britt JC, Josephson GD, Gross CW. Ludwig's angina in the pediatric population: report of a case and review of the literature. Int J Pediatr Otorhinolaryngol. 2000;52(1):79â€“87.

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3. Busch RF, Shah D. Ludwig's angina: im proved treatm ent. Otolaryngolâ€”Head Neck Surg. 1997;117(6):S172â€“S175. 4. Chandradeva K, Palin C, Ghosh SM, Pinches SC. Percutaneous transtracheal jet ventilation as a guide to tracheal intubation in severe upper airway obstruction from supraglottic oedem a. Br J Anaesth. 2005;May;94(5):683â€“686. 5. Ovassapian A, Tuncbilek M, Weitzel EK, Joshi CW. Airway m anagem ent in adult patients with deep neck infections: a case series and review of the literature. Anesth Analg. 2005;Feb100(2):582â€“589. 6. Spitalnic SJ, Sucov A. Ludwig's angina: case report and review. J Em erg Med. 1995;13(4):499â€“503.

Codes ICD9-CM 528.3 Cellulitis and abscess

ICD10 K12.2 Cellulitis and abscess of m outh M72.6 Necrotizing fasciitis

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lunate Dislo catio n

Lunate Dislocation

Mary Anne Fuchs Alec Tuan Huynh

Basics Description 

Dislocation of the lunate relative to the radius and distal row of m etacarpals, either dorsally or volarly



In perilunate dislocation, relationship of lunate to radius is m aintained and lunate is dislocated relative to capitate.



Usually from high-energy hyperextension with ulnar deviation of the wrist

Etiology 

Im plies disruption of all four perilunate ligam ents and radiocarpal ligam ent



In volar dislocations, m edian nerve injury occurs in the carpal tunnel.



Associated fractures of the radial styloid, scaphoid, capitate, and triquetrum are com m on and, if present, should raise suspicion of an occult perilunate ligam entous injury.

Pa ge 2 8 6

Diagnosis Signs and Symptoms Frequently m issed injury

History 

Often from fall or m otor vehicle accident



Pain and tenderness in the wrist

Physical Exam 

Mass or swelling in the wrist, either dorsally or volarly depending on direction of dislocation



Gross deform ity often m asked by swelling



May display signs of m edian nerve injury

Essential Workup 

Clinical exam is frequently not diagnostic.



Assess skin integrity and neurovascular status, including two-point discrim ination.



Radiographs as outlined below

Tests Imaging 

Radiographic im aging to include three views of the wrist



Lateral view m ost useful: o

Disruption of the norm al im aginary longitudinal line through the centers of the radius, lunate, and capitate indicates dislocation or subluxation.

o

In volar dislocations, the lunate is frequently tilted with the opening of the â€œcupâ€• toward the palm (spilled teacup sign)



Posteroanterior (PA) view: o

The dislocated lunate has a triangular (as opposed to the usual quadrangular) appearance.

Pa ge 2 8 6

o

Disruption of a sm ooth and continuous arc form ed by the radiocarpal row suggests lunate dislocation.

Pediatric Considerations Radiograph can be difficult to interpret unless full ossification is present. P.649

Geriatric Considerations Other fractures are com m on.

Differential Diagnosis 

Lunate fracture



Perilunate dislocation



Scapholunate dissociation



Scaphoid fracture

Treatment Pre Hospital 

Dress open wounds.



Im m obilize in neutral position.

Initial Stabilization Im m obilize in position of com fort with a volar or â€œsugar tongsâ€• splint.

ED Treatment 

Identify m ultiple traum a or other injuries.



Contact a hand surgeon for im m ediate reduction and possible operative intervention.

Pa ge 2 8 6



Closed reduction can be difficult or unstable



Open reduction and internal fixation are frequently required.

Pediatric Considerations Although serious injury is unusual, children with wrist pain should be splinted and referred for ongoing evaluation of possible occult fractures.

Follow-Up Disposition Admission Criteria 

Adm ission is often necessary for definitive care.



Open fracture, presence of m ultiple traum a, or other m ore serious injuries m andates adm ission.

Discharge Criteria Patients with closed dislocations or fractures that have been adequately reduced and im m obilized in the ED m ay be discharged with orthopedic follow-up.

References 1. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990:637â€“649. 2. Eisenhauer MA. Forearm and wrist. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby-Year Book; 2002:535â€“542. 3. Mital RC. The wrist and forearm . In: Schwartz D, et al. Em ergency Radiology. New York: McGraw-Hill; 2000:48â€“63. 4. Perron AD. Orthopedic pitfalls in the ED: lunate and perilunate

Pa ge 2 8 6

injuries. Am J Em erg Med. 2001;19(2):157â€“162. 5. Sim on RR, Koenigsknecht SJ, eds. Em ergency Orthopedics: The Extrem ities. 4th ed. New York: McGraw-Hill; 2001:176â€“180. 6. Uehara DT. The hand in em ergency m edicine. Em erg Clin North Am . 1993;11(3):781â€“796.

Codes ICD9-CM 833.00

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym e Disease

Lyme Disease

Moses S. Lee

Basics Description 

Most com m on tickborne illness in North Am erica



Endem ic in northeastern, upper m idwestern, and northwestern California

Etiology 

Peak between April and Novem ber; 80â€“90% in sum m er m onths



Spirochete Borrelia burgdorferi introduced by Ixodes tick: o

Ixodes dam m ini (deer tick) m ost com m on



Fewer than 50% of patients recall tick bite.



Pathogenesisâ€”com bination of:



o

Organism -induced local inflam m ation

o

Cytokine release

o

Autoim m unity

No person-to-person transm ission

Diagnosis

Pa ge 2 8 7

Signs and Symptoms Stage I (Early) 

Onset few days to m onth after tick bite (arthropod transm ission)



30â€“50% of patients recall tick bite.



Erythem a chronicum m igrans (ECM): o

Pathognom onic finding: 

o

Bull's-eye rash

Maculopapular, irregular expanding annular lesion: 

Single or m ultiple



Central clearing with red outer border



Diam eter >5 cm



Regional adenopathy



Low-grade, interm ittent fever



Headache



Myalgia



Arthralgias



Fatigue



Malaise

Stage II (Secondary, Disseminated) 

Days to weeks after tick bite



Interm ittent and fluctuating sym ptom s with eventual disappearance



Triad of aseptic m eningitis, cranial neuritis, and radiculoneuritis:



o

Facial (Bell) palsy m ost com m on cranial neuritis

o

May present without rash

o

Prognosis generally good

Cardiac: o

Tachycardia

o

Bradycardia

Pa ge 2 8 7

o

Atrioventricular block

o

Myopericarditis

Stage III (Tertiary, Late) 

Onset >1 year after disease onset



Acroderm atitis chronica atrophicans: o

Extensor surfaces of extrem ities, especially lower leg

o

Initial edem atous infiltration evolving to atrophic lesions

o 

Resem bles scleroderm a

Arthritis: o

Brief arthritis attacks

o

Monoarthritis

o

Oligoarthritis

o

Occasionally m igratory

o

Most com m on joints (descending order): 

Knee



Shoulder



Elbow

Other 





Gastrointestinal: o

Hepatitis

o

Right upper quadrant pain

Ocular: o

Keratitis

o

Uveitis

o

Iritis

o

Optic neuritis

Jarisch-Herxheim er reaction: o

Worsening of sym ptom s a few hours after treatm ent initiated

o

More com m on in patients with m ultiple ECM lesions

Pa ge 2 8 7



Babesiosis occurs sim ultaneously in endem ic areas.

Persistent Lyme Disease Articular and neurologic sym ptom s despite treatm ent: 

Chronic axonal polyneuropathy or encephalopathy

Recurrent Lyme Disease 

Relapse despite treatm ent



Second episodes less severe

Pediatric Considerations 

More likely than adults to be febrile



Only 50% of children with arthralgias have history of ECM.



Facial palsy accom panied by aseptic m eningitis in one third



Asym ptom atic cardiac involvem ent with abnorm al ECGs



Appropriately treated children have excellent prognosis for unim paired cognitive functioning.



Untreated children m ay have keratitis, joint pain, or chronic encephalopathy.

Essential Workup 

Clinical diagnosis: o

Presence of ECM obviates serologic tests.



Careful search for tick



Lum bar puncture when m eningeal signs



Arthrocentesis for acute arthritis



ECG

Tests Lab 



CBC: o

Leukocytosis

o

Anem ia

o

Throm bocytopenia

Erythrocyte sedim entation rate (ESR):

Pa ge 2 8 7

o

Greater than 30 m m /h

o

Most com m on laboratory abnorm ality



Electrolytes, BUN, creatinine, glucose



Liver function tests: o

Elevated liver enzym es (gam m a-glutam yl transferase [GGT] m ost com m on)





Culture: o

Low yield

o

Not indicated

Cerebrospinal fluid (CSF): o

Pleocytosis

o

Elevated protein

o

Obtain CSF spirochete antibodies.

P.651

Special Tests 

Serology: o

Obtain enzym e-linked im m unosorbent assay (ELISA), im m unofluorescence assay (IFA), and Western blot when disease suggested without ECM lesion.

o

Antibodies m ay persist for m onths to years.

o

Positive serology or previous Lym e disease does not ensure protective im m unity.





Polym erase chain reaction assay: o

Highly specific and sensitive

o

Not available for routine use

Joint fluid: o



Cryoglobulin increased fivefold com pared with serum

Joint film s m ay show soft tissue, cartilaginous, osseous changes.

Pa ge 2 8 7

Differential Diagnosis 

Other tickborne illnesses: o

Deer tick usually larger (1 cm ) than ixodid ticks (1â€“2 m m )



o

Rocky Mountain spotted fever

o

Tularem ia

o

Relapsing fever

o

Colorado tick fever

o

Tick-bite paralysis

Rheum atic fever: o

Rash of erythem a m arginatum

o

Tem porom andibular joint arthritis m ore com m on than in Lym e disease

o

Valvular involvem ent rather than heart block

o

Chorea m ay be isolated finding.



Viral m eningitis



Syphilis



Septic arthritis



Parvovirus B19 infectionâ€”polyarticular arthritis



Infectious endocarditis



Juvenile rheum atoid arthritis



Reiter syndrom e



Brown recluse spider bite



Fibrom yalgia



Chronic fatigue syndrom e

Treatment Initial Stabilization 

500 m L (20 m L/kg) 0.9% norm al saline (NS) IV fluid bolus

Pa ge 2 8 7

fluids for dehydration 

IV access for neurologic and cardiac involvem ent



Cardiac m onitoring



Tem porary pacem aker for heart block

ED Treatment 

Rem ove tick: o

Disinfect site.

o

With blunt instrum ent, grasp tick close to skin and pull upward with gentle pressure.



Adm inister: o

Aspirin as adjunctive therapy for cardiac involvem ent

o

Nonsteroidal anti-inflam m atory drugs (NSAIDs) for arthritis and arthralgias



Vaccine (LYMErix) for prevention of disease: o

A recom binant surface protein

o

For persons in high/m oderate risk areas

o

For travelers to endem ic areas

o

Three doses (0 to 1 m onth to 12 m onths)

Stage I 

Am oxicillin, doxycycline, or cefuroxim e (21 days)



Azithrom ycin (14â€“21 days)



Parenteral therapy in pregnant patients

Stage II 

Oral therapy for isolated Bell palsy and m ild involvem ent: o

Am oxicillin with probenecid (30 days) or doxycycline (avoid if pregnant or <9 years old; 10â€“21 days)



Parenteral therapy for m ore severe involvem ent (m eningitis, carditis, severe arthritis): o

Ceftriaxone, cefotaxim e (14â€“21 days), or penicillin G (14â€“28 days)

Pa ge 2 8 7

Stage III Parenteral therapy: 

Penicillin G, cefotaxim e (14â€“21 days), or ceftriaxone (14â€“28 days)

Medication (Drugs) 

Am oxicillin: 500 m g (peds: 40 m g/kg/24h) PO t.i.d.



Aspirin: 80â€“100 m g/kg/d (peds: 50â€“100 m g/kg/d in six divided doses) PO



Azithrom ycin: 500 m g PO daily



Cefotaxim e: 2 g (peds: 100â€“150 m g/kg/24h) IV q8h



Ceftriaxone: 2 g (peds: 100 m g/kg/24h) IV daily



Doxycycline: 200 m g PO b.i.d. for 3 days, then 100 m g PO b.i.d. for 21â€“28 days



Penicillin G: 20â€“24 m IU IV div. q4hâ€“q6h



Probenecid: 500 m g PO t.i.d.

Follow-Up Disposition Admission Criteria 

Meningoencephalitis



Telem etry/ICU adm ission for carditis

Discharge Criteria Patients treated with oral therapy

References 1. Asch ES, Bujak DI, Weiss M, et al. Lym e disease: an infectious and post-infectious syndrom e. J Rheum atol. 1994;121:157â€“162.

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2. Preboth M. Infectious Diseases Society of Am erica guidelines on the treatm ent of Lym e disease. Am Fam Physician. 2001;63:2065â€“2067. 3. Sigal LH. Current recom m endations for the treatm ent of Lym e disease. Drugs. 1992;43:683â€“699. 4. Steere AC. Lym e disease. N Engl J Med. 2001;345:115â€“125.

Codes ICD9-CM 88.81

ICD10 A69.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym phadenitis

Lymphadenitis

John Mahoney Dolores Gonthier

Basics Description 

Lym ph nodes m ay be swollen and tender as part of the system ic response to infection: o

Becom e engorged with lym phocytes and m acrophages

o

May be prim arily infected

o

Infection in distal extrem ity m ay result in painful tender adenopathy proxim ally.



Acute suppurative lym phadenitis m ay occur after pharyngeal or skin infection.

Etiology 

Most frequently caused by bacterial infection



Most com m on organism s in pyogenic lym phadenitis: o

Group A Î²-hem olytic streptococcus

o

Staphylococcus aureusâ€”including resistant strains (see below)

o

Cervical location owing to pharyngeal or periodontal process: streptococcus and anaerobes



Axillary lym phadenitis:

Pa ge 2 8 8

o

Streptococcus pyogenes (Group A Î²-hem olytic streptococcus)



Nosocom ial m ethicillin-resistant S. aureus: o

Risk factors: recent hospital or long-term care adm ission, surgery, injection drug use, vascular catheter, dialysis, recent antibiotic use, unresponsive infection.

o 

Resistant to m ost antibiotics (see Treatm ent)

Com m unity-acquired m ethicillin-resistant S. aureus (CA-MRSA): o

No single identified risk factor

o

Different antibiotic susceptibility than nosocom ial MRSA; trim ethoprim -sulfam ethoxazole (TMP/SMX) and clindam ycin m ay be effective.

o

Variable, rising local prevalence should be considered when starting em piric antibiotic therapy.

o

Suspect in unresponsive infections, m ultiple or recurrent abscesses.

Pediatric Considerations 

Acute unilateral cervical suppurative lym phadenitis: o

Most com m on younger than age 6 years

o

Group A streptococcus, S. aureus, and anaerobes are m ost com m on causes.

Diagnosis Signs and Symptoms 

Painful swelling, inflam m ation/infection of lym ph nodes



Com m only presents sim ultaneously with acute cellulitis or abscess if pyogenic cause

Pa ge 2 8 8



Axillary lym phadenitis: o

Fever, axillary pain, and acute lym phedem a of arm s and chest, without features of cellulitis or lym phangitis; ipsilateral pleural effusion m ay be present.

History 

Occupation



Exposure to pets



Sexual behavior



Drug use



Travel history



Associated sym ptom s:



o

Sore throat, cough

o

Fever

o

Night sweats

o

Fatigue

o

Weight loss

o

Pain in nodes

Duration of lym phadenopathy

Physical Exam 

Extent of lym phadenopathy (localized or generalized)



Size of nodes: o

Abnorm al size by site: 

Generalâ€”>1 cm



Epitrochlearâ€”>0.5 cm



Inguinalâ€”>1.5 cm



Presence or absence of nodal tenderness



Signs of inflam m ation over node



Skin lesions



Splenom egaly



Enlargem ent of supraclavicular or scalene nodes is always

Pa ge 2 8 8

abnorm al.

Essential Workup 

Acute regional lym phadenitis is clinical diagnosis, often part of larger syndrom e (cellulitis).



History and physical exam ination to reveal infectious source

Tests Lab 

White blood count is not essential: o



Possible leukocytosis with left shift or norm al

Com plete blood count, Epstein-Barr virus (EBV), cytom egalovirus (CMV), HIV, and other serologies based on clinical findings

Imaging Ultrasound or CT in patients who do not im prove or progress to suppuration

Diagnostic Procedures/Surgery Consider percutaneous needle aspiration or surgical drainage in patients who do not im prove or progress to suppuration.

Differential Diagnosis 



Com m on infections: o

Adenovirus

o

Scarlet fever

o

Catscratch disease

o

Fungal

o

Herpes zoster

Unusual infections: o

Sporotrichosis (rose thorns)

o

Diphtheria

o

West Nile fever

Pa ge 2 8 8





o

Plague

o

Anthrax

o

Typhoid

o

Rubella

Venereal infections: o

Syphilis

o

Genital herpes

o

Chancroid

o

Lym phogranulom a venereum

Other system atic infections causing generalized lym phadenitis:



o

HIV

o

Infectious m ononucleosis (EBV or CMV)

o

Toxoplasm osis

o

Tuberculosis

o

Infectious hepatitis

o

Dengue

Drug reaction: o

Phenytoin

o

Allopurinol



Silicone im plants



Malignancy



Rheum atologic disorders



System ic lupus erythem atosus



Sarcoidosis



Am yloidosis



Serum sickness

Pediatric Considerations 

Kawasaki disease



PFAPA syndrom e (periodic fever, aphthous stom atitis, pharyngitis, cervical adenitis)

P.653

Pa ge 2 8 8

Treatment Initial Stabilization Ensure airway, breathing, and circulation m anagem ent (ABCs) and hem odynam ic stability.

ED Treatment 

General principles: o

Antibiotics based on involved prim ary organ/suspected pathogen (see also Cellulitis)

o

Consider local prevalence of MRSA and other resistant pathogens in addition to usual causes.



o

Usual outpatient treatm ent: 7â€“10 days

o

Elevation

o

Application of m oist heat

o

Analgesics

Drainage of abscesses if present: o

Obtain culture if drainage perform ed, especially to help identify resistant pathogens.



Skin origin: o

Outpatient: oral dicloxacillin; alternatives: oral m acrolide or cephalexin

o 

Inpatient: IV nafcillin or equivalent

Pharyngeal or periodontal origin: o

Outpatient: oral penicillin VK; alternatives: oral clindam ycin or am oxicillin/clavulanate

o

Inpatient: IV penicillin G (aqueous) and IV m etronidazole; alternatives: IV am picillin/sulbactam

Pa ge 2 8 8

or IV clindam ycin 

Axillary lym phadenitis: o

Outpatient: oral penicillin VK; alternatives: oral m acrolide or am oxicillin/clavulanate

o

Inpatient: IV penicillin G (aqueous); alternatives: IV am picillin/sulbactam



Acute unilateral cervical suppurative lym phadenitis: o

Outpatient: oral penicillin VK; alternatives: oral clindam ycin or am oxicillin/clavulanate



Methicillin-resistant S. aureus: o

Nosocom ial MRSA: IV vancom ycin or oral or IV linezolid

o

Com m unity-acquired MRSA: 

Add oral TMP/SMX to em piric treatm ent or use oral clindam ycin alone.



Oral doxycycline or com bination of oral TMP/SMX and rifam pin m ay be effective for cases not responding to above.



More severe: IV clindam ycin or IV vancom ycin

Medication (Drugs) 

Am oxicillin/clavulanate: 500â€“875 m g (peds: 45 m g/kg/24h) PO b.i.d. or 250â€“500 m g (peds: 40 m g/kg/24h) PO t.i.d.



Am picillin/sulbactam : 1.5â€“3 g (peds: 100â€“300 m g/kg/24h up to 40 kg; over 40 kg, give adult dose) IV q6h



Cephalexin: 500 m g (peds: 50â€“100 m g/kg/24h) PO q.i.d.



Clindam ycin: 450â€“900 m g (peds: 20â€“40 m g/kg/24h) PO or IV q8h



Dicloxacillin: 125â€“500 m g (peds: 12.5â€“25 m g/kg/24h)

Pa ge 2 8 8

PO q6h 

Doxycycline: 100 m g PO b.i.d. for adults



Erythrom ycin base: (adult) 250â€“500 m g PO q.i.d.



Linezolid: 600 m g PO or IV q12h (peds: 30 m g/kg/d div. q8h)



Metronidazole: (adult) 15 m g/kg IV once, followed by 7.5 m g/kg IV q6h



Nafcillin: 1â€“2 g IV q4h (peds: 50â€“100 m g/kg/24h divided q6h); m ax. 12 g/24h



Penicillin VK: 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q6h



Penicillin G (aqueous): 4 m IU (peds: 100,000â€“400,000 U/kg/24h) IV q4h



Rifam pin: 600 m g PO b.i.d. for adults



Trim ethoprim /sulfam ethoxazole (TMP/SMX): 1 DS tab PO q12h (peds: 6â€“10 m g/kg/24h TMP div. q12h)



Vancom ycin: 1 g IV q12h (peds: 10 m g/kg IV q6h, dosing adjustm ents required under age 5 years); check serum levels.

Follow-Up Disposition Admission Criteria 

Toxic appearing



History of im m une suppression



Concurrent chronic m edical illnesses



Unable to take oral m edications



Unreliable patients

Discharge Criteria

Pa ge 2 8 8



Mild infection in a nonâ€“toxic-appearing patient



Able to take oral antibiotics



No history of im m une suppression or concurrent m edical problem s



Has adequate follow-up within 24â€“48 hours

Issues for Referral 

If not found in context of acute infection, and not quick to resolve with course of antibiotics, evaluate for m ore serious underlying causes (e.g., m alignancy).



Lym ph node biopsy m ay be helpful in the following circum stances: o

Clinical findings indicate likely m alignancy.

o

Lym ph node size >1 cm

o

Supraclavicular location

References 1. Boyce JM. Severe streptococcal axillary lym phadenitis. N Engl J Med. 1990;323:655â€“658. 2. Henry PH, Longo DL. Enlargem ent of the lym ph nodes and spleen. In: Braunwald E, Fauci AS, Hauser SL, et al., eds. Harrison's Principles of Internal Medicine. 16th ed. New York: McGraw-Hill; 2005:343â€“348. 3. Moran GJ, Talan DA. Com m unity-acquired m ethicillin-resistant Staphylococcus aureus: is it in your com m unity and should it change practice? Ann Em erg Med. 2005;45:321â€“322. 4. Padm anabhan R, Fraser T. The em ergence of m ethicillin-resistant Staphylococcus aureus in the com m unity. Cleve Clin J Med. 2005;72(3):235â€“241. 5. Swartz MN, Pasternack MS. Lym phadenitis and lym phangitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:1204â€“1214.

Pa ge 2 8 8

6. Thom as KT, Feder HM, Lawton AR, et al. Periodic fever syndrom e in children. J Pediatr. 1999;135(1):15â€“21. 7. Lym ph node enlargem ent and fever. In: Gorbach SL, Falagas M, eds. The 5-Minute Infectious Diseases Consult. Philadelphia: Lippincott William s & Wilkins; 2001:.

Miscellaneous SEE ALSO: Cellulitis; Lym phangitis

Codes ICD9-CM 683

ICD10 I88.9

Pa ge 2 8 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym phangitis

Lymphangitis

John Mahoney

Basics Description 

Lym phangitis is infection of lym phatics that drain focus of inflam m ation.



Histologically, lym phatic vessels are dilated and filled with lym phocytes and histiocytes: o

Inflam m ation frequently extends into perilym phatic tissues and m ay lead to cellulitis or abscess form ation.

Etiology 

Acute lym phangitis: o

Likely caused by bacterial infection

o

Most com m only group A Î²-hem olytic streptococcus

o

Less com m only owing to other strep groups, and occasionally Staphylococcus aureus

o

Other organism s: 

Pasteurella m ultocida (cat or dog bite)



Spirillum m inus (rat-bite fever)



Wuchereria bancrofti (filariasis): 

Consider in im m igrants from Africa, Southeast Asia/Pacific, and tropical South

Pa ge 2 8 9

Am erica

o



Mosquitoborne



Usually involves lower extrem ities

Com m unity-acquired m ethicillin-resistant S. aureus (CA-MRSA): 

No single identified risk factor



Different antibiotic susceptibility than nosocom ial MRSA; trim ethoprim -sulfam ethoxazole (TMP/SMX) and clindam ycin m ay be effective.



Variable, rising local prevalence should be considered when starting em piric antibiotic therapy.



Suspect in unresponsive infections, m ultiple or recurrent abscesses.



Chronic lym phangitis: o

Usually caused by m ycotic, m ycobacterial, and filarial infections

o

Sporothrix schenckii (m ost com m on cause of chronic lym phangitis in U.S.) 

Inoculation occurs while gardening or farm ing (rose thorn).



Organism is present on som e plants and in sphagnum m oss.



Multiple subcutaneous nodules appear along course of lym phatic vessels.



Typical antibiotics and local treatm ent fail to cure lesion.

o

Mycobacterium m arinum : 

Atypical m ycobacterium



Grows optim ally at 25â€“32Â°C in fish tanks and swim m ing pools

Pa ge 2 8 9



May produce a chronic nodular, single wartlike or ulcerative lesion at site of abrasion



Additional lesions m ay appear in distribution sim ilar to sporotrichosis.

o

Nocardia brasiliensis

o

Mycobacterium kansasii

o

Wuchereria bancrofti

Diagnosis Signs and Symptoms 

Acute lym phangitis: o

Warm , tender erythem atous streaks develop and extend proxim ally from source of infection.

o

Regional lym ph nodes often becom e enlarged and tender (lym phadenitis).



o

Peripheral edem a of involved extrem ity

o

System ic m anifestations: 

Fever



Rigors



Tachycardia



Headache

Chronic (nodular) lym phangitis: o

Erythem atous nodule, chancriform ulcer, or wartlike lesion develops in subcutaneous tissue at inoculation site.

o

Often presents without pain or evidence of system ic infection

o

Multiple lesions possible along lym phatic chain

History

Pa ge 2 8 9

History and physical directed at discovering source of infection

Physical Exam 

Fever



Erythem atous streaks from source of infection proceeding toward regional lym ph nodes

Essential Workup Lym phangitis is clinical diagnosis.

Tests Lab 

White blood count unnecessary but often elevated



Gram stain and culture of initial lesion to focus antim icrobial selection and reveal resistant pathogens (MRSA): o

Aspirate point of m axim al inflam m ation or punch biopsy.

o 

Essential if treatm ent failure

If sporotrichosis or M. m arinum infection is suspected, diagnosis should be confirm ed by culture of organism from wound.



Blood culture m ay reveal organism .

Imaging 

Im aging not com m only perform ed



Plain radiographs m ay reveal abscess form ation, subcutaneous gas, or foreign bodies if these are suspected.



Extrem ity vascular im aging (Doppler ultrasound) can help rule out deep venous throm bosis.

Differential Diagnosis 

Throm bophlebitis; deep venous and superficial: o

Differentiation from lym phangitis:

Pa ge 2 8 9



Absence of initial traum atic or infectious focus



No regional lym phadenopathy



Intravenous line infiltration



Sm allpox vaccination, norm al variant of usual reaction to vaccination



Phytophotoderm atitis: o

Linear inflam m atory reaction, m im ics lym phangitis

o

Lim e rind, lim e juice, and certain plants can act as photosensitizing agents.

P.655

Treatment Initial Stabilization If patient septic, m anage airway and resuscitate as indicated.

ED Treatment 

Antim icrobial therapy should be initiated with first dose in ED.



General principles: o

Consider local prevalence of MRSA and other resistant pathogens in addition to usual causes.



o

Usual outpatient treatm ent: 7â€“10 days

o

Elevation

o

Application of m oist heat

Acute lym phangitis, em piric coverage: o

Outpatient: oral dicloxacillin or cephalexin; alternatives: oral m acrolide or levofloxacin

o

Inpatient: IV nafcillin or equivalent

Pa ge 2 8 9



Lym phangitis after dog or cat bite: IV am picillin/sulbactam



Methicillin-resistant S. aureus: o

Nosocom ial MRSA: IV vancom ycin or oral or IV linezolid

o

Com m unity-acquired MRSA: 

Add oral TMP/SMX to em piric treatm ent or use oral clindam ycin alone.



Oral doxycycline or com bination of oral TMP/SMX and rifam pin m ay be effective for cases not responding to above.

 

More severe: IV clindam ycin or IV vancom ycin

Sporotrichosis: o

Itraconazole or saturated solution of potassium iodide (SSKI)



Mycobacterium m arinum : o

Localized granulom as are usually excised.

o

Antim icrobial therapy is usually reserved for m ore severe infections: 

Lim ited data on what com bination of agents should be used



Rifam pin and etham butol m ay be best choice.

Medication (Drugs) 

Am picillin/sulbactam : 1.5â€“3 g (peds: 100â€“300 m g/kg/24h up to 40 kg; >40 kg, give adult dose) IV q6h



Cephalexin: 500 m g (peds: 50â€“100 m g/kg/24h) PO q.i.d.



Clindam ycin: 450â€“900 m g (peds: 20â€“40 m g/kg/24h) PO or IV q8h



Dicloxacillin: 125â€“500 m g (peds: 12.5â€“25 m g/kg/24h) PO q6h



Doxycycline: 100 m g PO b.i.d. for adults

Pa ge 2 8 9



Erythrom ycin base: (adult) 250â€“500 m g PO q.i.d.



Itraconazole (adult): 100â€“200 m g PO daily, continue until lesions resolve (6â€“12 weeks); peds: not approved for use



Levofloxacin: (adult only) 500â€“750 m g PO or IV daily



Linezolid: 600 m g PO or IV q12h (peds: 30 m g/kg/24h div. q8h)



Nafcillin: 1â€“2 g IV q4h (peds: 50â€“100 m g/kg/24h div. q6h); m ax. 12 g/24h



Rifam pin: 600 m g PO b.i.d. for adults



Saturated solution of potassium iodide (SSKI): 5â€“10 drops, increase to 40â€“50 drops (peds: 5â€“10 drops, increase to 25â€“40) PO t.i.d. Take in m ilk, juice, or carbonated beverage to avoid bitter taste.



Trim ethoprim /sulfam ethoxazole (TMP/SMX): 1 DS tab PO q12h (peds: 6â€“10 m g/kg/24h TMP div. q12h)



Vancom ycin: 1 g IV q12h (peds: 10 m g/kg IV q6h, dosing adjustm ents required under age 5 years); check serum levels.

Follow-Up Disposition Admission Criteria 

Toxic appearing



History of im m une suppression



Concurrent chronic m edical illnesses



Unable to take oral m edications



Unreliable patients

Discharge Criteria

Pa ge 2 8 9



Mild infection in a nonâ€“toxic-appearing patient



Able to take oral antibiotics



No history of im m une suppression or concurrent m edical problem s



Adequate follow-up within 24â€“48 hours

References 1. Rex JH, Okhuysen PC. Sporothrix schenckii. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:2984â€“2988. 2. Sm ego RA, Castiglia M, Asperilla MO. Lym phocutaneous syndrom e: a review of non-sporothrix causes. Medicine. 1999;78(1):38â€“63. 3. Swartz MN, Pasternack MS. Lym phadenitis and lym phangitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:1204â€“1214.

Miscellaneous SEE ALSO: Cellulitis; Lym phadenitis

Codes ICD9-CM 457.2 682.9

ICD10 I89.1

Pa ge 2 8 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym pho granulo m a Venereum

Lymphogranuloma Venereum Joel Kravitz

Basics Description Also known as strum a, tropical bubo, Nicolas-Favre-Durand disease

Etiology Chlam ydia trachom atisâ€”serotypes L1, L2, and L3

Diagnosis Signs and Symptoms History Prim ary genital lesions: 

Incubation: 3â€“30 days after sexual exposure to Chlam ydia trachom atis



Painless genital chancre lasts 2â€“3 days (rarely, a papule or vesicle) o

Initial lesion is rarely noticed.

Physical Exam 

Inguinal adenopathy:

Pa ge 2 8 9

o

Occurs 1â€“3 weeks after initial inoculation

o

Adenopathy is unilateral in two thirds of cases.

o

Buboes (large inguinal lym ph nodes) form in inguinal and fem oral chains.

o

Groove sign: scarred or coalescent buboes above and below inguinal ligam ent give a linear depression parallel to the inguinal ligam ent (seen in 30%).

o

Anal-receptive patients m ay develop hem orrhagic proctocolitis.

o

Perirectal lym phatic inflam m ation causes fistulae and strictures.

o

System ic sym ptom s (absent with chancroid) m ay include fever, m yalgias, headache, erythem a nodosum , nausea, and vom iting: 



Meningoencephalitis is rare

Chronic com plications: o

Genital strictures, perineal and perianal fistulae, and elephantiasis of the ipsilateral leg

Tests Lab 

Standard chlam ydia DNA probes do not test for lym phogranulom a venereum (LGV) strain.



False-positive VDRL in 20%



Serologic testing and culture are the standard.



Com plem ent fixation titers >1:64 are consistent with LGV infection.

Diagnostic Procedures/Surgery Bubo aspirationâ€”specific but expensive and im practical

Differential Diagnosis 

Genital herpes (ulcers usually not seen in LGV)

Pa ge 2 8 9



Syphilisâ€”nodes are nontender, longer incubation.



Chancroidâ€”m ultiple ulcers, no system ic sym ptom s



Granulom a inguinaleâ€”lesions are painless and bleed easily.

P.657

Treatment Initial Stabilization No field or ED stabilization required

Medication (Drugs) Antibiotics: 

First lineâ€”doxycycline: 100 m g PO b.i.d. for 3 weeks



Alternativeâ€”erythrom ycin: 500 m g PO q.i.d. for 3 weeks

Pregnancy Considerations Pregnant patients receive erythrom ycin.

Follow-Up Disposition Admission Criteria Hospitalization rarely needed (i.e., severe system ic sym ptom s)

Discharge Criteria Im m unocom petent patient without system ic involvem ent

Pa ge 2 9 0

Issues for Referral 

Outpatient follow-up required to confirm diagnosis and cure



Rectal infection m ay require retreatm ent.

References 1. Borchardt KA, Noble MA. Sexually Transm itted Diseases. Boca Raton, FL: CRC Press; 1997. 2. Centers for Disease Control and Prevention: 2002 guidelines for treatm ent of sexually transm itted diseases. MMWR. 2002;47:RR. 3. Ernst AA, Marvez-Valls E, Martin DH. Incision and drainage versus aspiration of fluctuant buboes in the em ergency departm ent during an epidem ic of chancroid. Sex Transm Dis. 1995;22(4):217â€“220. 4. Goens JL, Schwartz RA, DeWolf K. Mucocutaneous m anifestations of chancroid, lym phogranulom a venereum and granulom a inguinale. Am Fam Physician. 1994;49(2):415.

Codes ICD9-CM 099.1

Pa ge 2 9 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M alaria

Malaria

Jordan Moskoff

Basics Description 

Protozoan infection transm itted through the anopheles m osquito



Incubation period 8â€“16 days



Periodicity of disease owing to life cycle of protozoan: o

Exoerythrocytic phase: Im m ature sporozoites m igrate to liver where they rapidly m ultiply into m ature parasites (m erozoites)

o

Erythrocytic phase: m ature parasites released into circulation and invade RBC

o

Replication within RBC followed 48â€“72 hours later by RBC lysis and release of m erozoites into circulation, repeating cycle

o

Fever corresponds to RBC lysis.

Plasmodium Falciparum 

Most cases and alm ost all deaths



Usually presents as an acute, overwhelm ing infection



Able to infect red cells of all ages: o



Results in greater degree of hem olysis and anem ia

Causes widespread capillary obstruction:

Pa ge 2 9 0

o 

Results in end organ hypoxia and dysfunction

More m oderate infection in people who are on or who have recently stopped prophylaxis with an agent to which the falciparum is resistant



Posttraum atic im m unosuppression m ay cause relapse of m alaria in patients who have lived in endem ic areas.

Plasmodium Vivax and Ovale 

May present with an acute febrile illness



Dorm ant liver stages (hypnozoites) that m ay cause relapse 6â€“11 m onths after the initial infection

Plasmodium Malariae May persist in the bloodstream at low levels up to 30 years

Etiology 

Transm ission usually occurs from the bite of infected fem ale anopheles m osquito.



North Am erican transm ission possible: o

Anopheles m osquitoes on the east and west coasts of the United States

o

Transm ission m ay also occur through infected blood products and shared needles.

Pediatric Considerations 

Sickle cell trait protective



Cerebral m alaria m ore com m on in children



In highly endem ic areas with m inim al lab capability, all children presenting with febrile illness m ay be treated.

Pregnancy Considerations Pregnant patients especially prim igravid at higher risk

Pa ge 2 9 0

Diagnosis Signs and Symptoms Timing 

P. falciparum â€”exhibits within 8 weeks of return



P. vivaxâ€”delayed several m onths



Most sym ptom atic within 1 year

General 

Malaise



Chills



Feverâ€”usually >38Â°C: o

Classic m alaria paroxysm : 

Fifteen m inutes to 1 hour of chills



Followed by 2â€“6 hours of nondiaphoretic fever â‰¤39â€“42Â°C



Profuse diaphoresis followed by defervescence



Pattern every 48 hours (vivax and ovale) or every 72 hours (falciparum )

o

Fever pattern m ay be variedâ€”rare to have classical fever.



Orthostatic hypotension



Myalgias/arthralgias

Hematology 

Hem olysis: o

Blackwater feverâ€”nam ed from the dark color of the urine partially owing to hem olysis in overwhelm ing falciparum infections



Jaundice



Splenom egaly: o

More com m on in chronic infections

o

May cause splenic rupture

Pa ge 2 9 0

CNSâ€”Cerebral Malaria 

Headache



Focal neurologic findings



Mental status changes



Com a



Seizures

GI 

Em esis



Diarrhea



Abdom inal pain

Pulmonary 

Shortness of breath



Rales



Pulm onary edem a

Severe Malaria One or m ore of the following: 

Greater than 20% m ortality even with optim al m anagem ent



Prostrationâ€”unable to sit up by oneself



Im paired consciousness



Respiratory distress or pulm onary edem a



Seizure



Circulatory collapse



Abnorm al bleeding



Jaundice



Hem oglobinuria



Severe anem ia

Essential Workup Oil em ersion light m icroscopy of a thick-sm ear Giem sa stain: 

Dem onstrates intraerythrocytic m alaria parasites

Pa ge 2 9 0



Cannot exclude diagnosis without three negative sm ears in 48 hours



Only high degrees of parasitem ia will be evident on a standard CBC sm ear.

Tests Lab 



CBC: o

Anem iaâ€”25%

o

Throm bocytopeniaâ€”70% <150

o

Leukocytopenia

Electrolytes, BUN, creatinine, glucose: o

Renal failure

o

Hypoglycem ia (rare)

o

Lactic acidosis

o

Hyponatrem ia



Urinalysis



Liver function tests: o

Increased in 25%

o

Increased bilirubin, lactate dehydrogenase (LDH) signs of hem olysis

Imaging 

Chest radiographâ€”for pulm onary edem a

Diagnostic Procedures/Surgery 

Im m unofluorescence assay (IFA), enzym e-linked im m unosorbent assay (ELISA), or DNA probes:



o

Differentiates the type of plasm odium present

o

Five percent to 7% will have m ixed infections.

Lum bar puncture/cerebrospinal fluid (CSF) analysis: o

Perform ed to distinguish cerebral m alaria from m eningitis

Pa ge 2 9 0

o

CSF lactate/protein elevated with m alaria

o

CSF pleocytosis/hypoglycem ia absent with m alaria

Differential Diagnosis 

Meningitis



Encephalitis



Stroke



Acute renal failure



Acute hem olytic anem ia



Sepsis



Hepatitis



Viral diarrheal illness



Hypoglycem ic com a



Heat stroke

P.659

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) fluid bolus for hypotension



Im m ediate cooling if tem perature >40Â°C



Acetam inophen



Mist/cool-air fans



Naloxone, D 5 0 W (or Accu-Chek), and thiam ine if altered m ental status

ED Treatment 

Dependent on identifying the type of m alaria present and geographic area of acquisition

Pa ge 2 9 0



Assum e drug resistant until proven otherwise.



Plasm odium vivax, Plasm odium ovale, Plasm odium m alariae, and nonâ€“chloroquine-resistant P. falciparum : o

Treated with oral chloroquine in both adults and children: 

o

Chloroquineâ€”safe in pregnant wom en

Chloroquine-sensitive for falciparum , including Central Am erica, Caribbean, and Middle East

o

Eradicate persistent hypnozoites in vivax and ovale with prim aquine beginning after com pletion of course of chloroquine.



Chloroquine-resistant falciparum infectionâ€”PO treatm ent options: o

Quinine, plus 

Doxycycline (avoid in pregnant wom en and children <8 years old)



Clindam ycin (use in pregnant wom en and children <8 years old)





o

Mefloquineâ€”safety unproved in pregnancy

o

Atovaquoneâ€”proguanil

Chloroquine-resistant P. vivax infection: o



Pyrim etham ine-sulfadoxine

Atovaquoneâ€”proguanil plus prim aquine

Severe falciparum â€”IV treatm ent: o

Chloroquine if known susceptible

o

If chloroquine resistant: 

Quinidine (rotary isom er of quinine) or quinine plus doxycycline or clindam ycin



Quinine not readily available in the United States and is a known abortifacient



Exchange transfusions: o

Rapidly rem oves parasitic RBCs, toxins, and red cell

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debris, replacing them with fresh plasm a and RBCs o

Efficacy not proved in random ized trials

o

Consider in seriously ill with P. falciparum parasitem ias >10%



Steroids not recom m ended for cerebral m alaria: o

Dexam ethasone worsens both duration of com a and prognosis.



Supportive therapy for com plications

P. Falciparum Antibiotic Resistance 

Chloroquine sensitive in the Caribbean, Central Am erica, and the Middle East



Pyrim etham ine-sulfadoxine resistance in South Am erica, Africa, southern and southeast Asia, and Indonesia



Mefloquine resistance in Southeast Asia

Chemoprophylaxis 

Chloroquine: o

Drug of choice for travel to areas without chloroquine resistance

o

300 m g PO weekly

o

Begin 2 weeks prior to departure and continue for 4 weeks after return.



Mefloquine: o

For chloroquine-resistant areas

o

250 m g PO weekly

o

Begin 2 weeks before departure and continue for 4 weeks after return.



Doxycycline: o

For chloroquine/m efloquine-resistant areas

o

100 m g PO daily

o

1 day prior to entering area

o

Continue for 4 weeks after return

Pa ge 2 9 0





Prim aquine: o

30 m g PO every day

o

1 day prior to entering area

o

Continue 1 week after return.

Vaccine not currently available, but several in field trial

Medication (Drugs) 

Acetam inophen: 1 g (peds: 15â€“20 m g/kg) PO



Chloroquine: 600-m g base initially (1,000 m g of chloroquine phosphate) followed by an additional 300 m g (500 m g salt) 6 hours later and again on days 2 and 3 (peds: 10 m g/kg base PO, followed by 5 m g/kg base 6 hours later and on days 2 and 3)



Clindam ycin: 300 m g (peds: 5 m g/kg/8h) PO t.i.d. for 5â€“7 days beginning on the third day of quinine therapy



Dextrose: D 5 0 W 1 am pâ€”50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Doxycycline: 100 m g PO b.i.d. for 7 days; >8 years only, 1.5â€“2 m g/kg (m ax. 100 m g) b.i.d. for 5â€“7 days



Malarone (atovaquone/proguanil): o

Prophylaxis: 250 m g/100 m g PO per day

o

Treatm ent: 1,000 m g/400 m g (4 tablets) PO per day for 3 days



Mefloquine: 1250-m g single dose (peds: 25-m g/kg single dose)



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Prim aquine phosphate: 15-m g base (peds: 0.3-m g base/kg/24h) PO for 14 days



Pyrim etham ine-sulfadoxine (Fansidar): three tablets PO on last day of quinine treatm ent

Pa ge 2 9 1



Quinidine gluconate: 10 m g/kg loading dose (m ax. 600 m g) in norm al saline infused slowly over 1â€“2 hours, followed by continuous infusion of 0.02 m g/kg/m in until patient is able to begin oral therapy



Quinine: 650 m g PO t.i.d. for 3â€“7 days



Quinine dihydrochloride: 20 m g salt/kg loading dose in 5% dextrose over 4 hours, followed by 10 m g salt/kg over 2â€“4 hours q8h (m ax. 1,800 m g/d) until patient is able to begin oral treatm ent



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

ICU adm ission for severe P. falciparum infection



Suspected acute P. falciparum infection



Severe dehydration



Inability to tolerate oral solution/m edication



More than 3% of RBC containing parasites

Discharge Criteria 

Nonâ€“P. falciparum infection



Able to tolerate oral m edications

References 1. Stanley J. Malaria. Em erg Med Clin North Am . 1997;15:113â€“155. 2. Suh K. Malaria. Can Med Assoc J. 2004;170(4):1693â€“1702. 3. White NJ. The treatm ent of m alaria. N Engl J Med. 1996;335:800â€“806.

Codes

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ICD9-CM 84.6

ICD10 B54

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M algaigne F racture

Malgaigne

Fracture Theodore Chan

Basics Description 

Am ong m ost unstable pelvic fractures: o

Displacem ent or potential displacem ent of entire hem ipelvis



Vertical shear forces result in anterior and posterior disruption of hem ipelvis.



Malgaigne fracture indicates that significant forces were applied to pelvic bones.



Fractures often occur from vehicular traum a, pedestrian struck by autom obile, or falls from heights.

Incidence As m any as 20% of all vehicular traum a fatalities have associated Malgaigne fracture.

Etiology 

Involves at least two breaks in continuity of pelvic ring



Tile type C pelvic fracture: o

Resulting in rotational and vertical instability in

Pa ge 2 9 1

pelvic ring (see Pelvic Fracture) 

Both anterior and posterior disruption with real or potential displacem ent of intervening fragm ents or hem ipelvis o

Anterior disruption of sym physis pubis; 2â€“4 pubic ram i fractures



Posterior displacem ent and instability through sacrum , sacroiliac joint, or ileum

Pediatric Considerations 

Children can have proportionately greater blood loss with pelvic fractures.



Nonaccidental traum a should always be considered.

Associated Conditions Pelvic hem orrhage and hem orrhagic shock: 

Intra-abdom inal



Genitourinary and urinary tracts



Gynecologic, including uterine and vaginal



Neurologic



Major vessel

Diagnosis Signs and Symptoms 

Gross pelvic instability, often with anterior iliac crest displaced or m obile



Shortening of legs from m igration of hem ipelvis



Ecchym oses, swelling, abrasions, and open wounds involving hips, groin, buttocks, perineum , pelvis



Severe pain on pelvic m ovem ent, tilt, and com pression



Often presents in setting of m ultiple traum a

Pa ge 2 9 1



Evidence of perineal, urethral, rectal, and vaginal injuries



In hem orrhagic shock: o

Tachycardia, hypotension, narrowed pulse pressure

o

Altered m ental status

o

Cool and pale extrem ities

Essential Workup 

Pelvic radiography is m ost valuable initial diagnostic test.



Single anteroposterior (AP) view of pelvis should be done early for any m ajor traum a victim in whom pelvic fracture is suspected: o

Most m algaigne fractures will be seen on AP view of pelvis.



Inlet projection (30Â° caudal angulation) allows visualization of posterior pelvis: o



May aid in assessm ent of posterior displacem ent

Other radiographic signs suggesting presence of Malgaigne fracture include the following: o

Pubic sym physis disruption with diastasis >15 m m

o

Sym physis disruption associated with overlapping of pubis

o

Sym physis disruption associated with unilateral fracture of both ram i

o

Bilateral breaks of both pelvic ram i or m arkedly displaced unilateral fractures of both ram i

o

Vertical fracture of sacrum (these fractures rarely occur as isolated pelvic fractures)

o

Asym m etry of iliac wings

o

Avulsion of ischial spine or L-5 transverse process associated with hem ipelvis m igration

Tests Lab

Pa ge 2 9 1



Type and cross-m atch.



Hem oglobin/hem atocrit, platelet count, and coagulation studies (PT/PTT)

Imaging 

Com puted tom ography scan: o

To delineate Malgaigne fracture and retroperitoneal hem atom a



Magnetic resonance im aging m ay be indicated with evidence of neurologic injury.



Abdom inal ultrasound and diagnostic peritoneal lavage are rapid bedside evaluations for intraperitoneal hem orrhage: o

Avoid false-positive results (higher m ortality rate in victim s with pelvic fractures who undergo negative laparotom y)

Diagnostic Procedures/Surgery 

Diagnostic peritoneal lavage: o

Supraum bilical open approach for diagnostic peritoneal lavage for Malgaigne fracture



Surgery as indicated

Differential Diagnosis 



Other pelvic fractures: o

Straddle fracture

o

Open-book fracture

o

Severe m ultiple pelvic fractures; see Pelvic Fracture

Intra-abdom inal injury and hem orrhage

Treatment Pre Hospital

Pa ge 2 9 1



Controversy: o

Pneum atic antishock garm ent (PASG) as alternative in victim s suspected of having pelvic fracture: 

Particularly when faced with prolonged transport tim e or hem odynam ic instability



Caution: o

Aggressive fluid resuscitation m ust occur before deflation of PASG abdom inal com partm ent if it has been used.

P.661

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs) of traum a care: 

Avoid using lower extrem ity IV sites.



Aggressive resuscitation with blood or crystalloid: o

O-negative or type-specific blood if hem odynam ically unstable



Im m obilize pelvis to prevent further injury and decrease bleeding.



PASG: Use in ED is controversial, but allows rapid pelvic im m obilization and pelvic com pression to slow bleeding.



External fixator requires m ore tim e to place than PASG, but â€œsplintsâ€• pelvis in sim ilar m anner. o

Contraindicated in severely com m inuted Malgaigne fracture



Placem ent of stabilization device should not interfere with further workup and care (e.g., ultrasound [US], diagnostic peritoneal lavage [DPL]).

Diagnostic Procedures/Surgery

Pa ge 2 9 1

Pelvic hem orrhage: 

Angiography and selective vessel em bolization: o



Particularly for sm all-vessel arterial bleeding

Direct operative control of pelvic bleeding; m ost likely necessary for large vessels

ED Treatment 

Im m ediate traum a surgery and orthopedics consultation



Nothing by m outh



Prioritization of studies: com puted tom ography, angiography, or surgery: o

In hem odynam ically unstable patient, rapidly perform ed US or DPL can determ ine treatm ent course.

o

If US or DPL aspirate is positive for bleeding, patient should undergo celiotom y with external pelvic fixation followed by selective angiography.

o

If DPL or US is negative, patient should undergo external fixation as appropriate, followed by selective angiography.

o

Hem odynam ically stable patient m ay undergo com puted tom ography evaluation of abdom en, pelvis, and retroperitoneum with external fixation as appropriate.

Special Therapy Blood products: 

Cross-m atched, type specific, or O-negative



Four to 6 IU (peds: 10 m L/kg initial transfusion)

IV Fluids Crystalloid fluids, norm al saline, or lactated Ringer solution: 

2-L IV bolus (peds: 20 m L/kg bolus)

Pa ge 2 9 1

Surgery 

As indicated on basis of clinical findings and orthopedic/surgical consult



Pelvic hem orrhage: o

Direct operative control of pelvic bleeding; m ost likely necessary for large vessels

o

Angiography and selective vessel em bolization, particularly for sm all-vessel arterial bleeding

Follow-Up Disposition Admission Criteria 

All patients with Malgaigne fractures because of the m agnitude of the insult, instability of fracture, and likelihood of hem orrhage and concom itant injury.



Adm it to intensive care unit or m onitored setting.

Discharge Criteria Stable patients without Malgaigne fracture

References 1. Allen CF, Goslar PW, Barry M, et al. Managem ent guidelines for hypotensive pelvic fracture patients. Am Surg. 2000;66:735â€“738. 2. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons; 2004. 3. Coppola PT, Coppola M. Em ergency departm ent evaluation and treatm ent of pelvic fractures. Em erg Med Clin North Am . 2000;18:127. 4. Lashutka MK, Bahner D, Werm an H. Adult pelvic fractures. Traum a

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Rep. 2002;3:1â€“12

Miscellaneous SEE ALSO: Hem orrhagic Shock; Pelvic Fracture

Codes ICD9-CM 808.43 808.8

ICD10 S32.7

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M allo ry-Weiss Syndro m e

Mallory-Weiss

Syndrome Robert C. Montana

Basics Description 

Partial-thickness intralum inal longitudinal m ucosal tear of distal esophagus or proxim al stom ach



Sudden increase in intra-abdom inal and/or transgastric pressure causes: o

Mild to m oderate subm ucosal arterial and/or venous bleeding: 

May be related to underlying pathology



â€œMushroom ingâ€• of stom ach into esophagus during retching has been observed endoscopically.

Etiology 

Associated with: o

Seizures

o

Forceful coughing/laughing

o

Lifting

o

Straining

o

Blunt abdom inal traum a

Pa ge 2 9 2



o

Childbirth

o

Cardiopulm onary resuscitation

Risk factors: o

Alcoholics: 



Especially after recent binge

o

Patients with hiatal hernia

o

Hyperem esis gravidarum

Greater bleeding associated with: o

Portal hypertension

o

Esophageal varices

o

Coagulopathy

Diagnosis Signs and Symptoms History 

Multiple bouts of nonbloody vom iting and/or retching followed by hem atem esis: o

Most bleeding is sm all and resolves spontaneously.

o

Massive life-threatening hem orrhage can occur.



Epigastric pain



Back pain



Dehydration: o

Dizzy, light-headed; syncope

Physical Exam 

Hem atem esis



Melena



Postural hypotension



Shock

Essential Workup

Pa ge 2 9 2



CBC



Rectal exam for occult blood

Tests Lab 

Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), INR



Electrolytes, BUN, creatinine, glucose



Am ylase/lipase if abdom inal pain



Type and cross-m atch: o

At least four units of packed red blood cells (PRBCs) if bleeding is severe



ECG if elderly or with cardiac history

Imaging 

Upright chest radiograph for free air from esophageal or gastric perforation



Upper endoscopy (esophagogastroscopy): o

Procedure of choice to locate, identify, and treat source of bleeding

Differential Diagnosis 

Nasopharyngeal bleeding



Hem optysis



Esophageal rupture (Boerhaave syndrom e)



Esophagitis



Gastritis



Gastroenteritis



Duodenitis



Ulcer disease



Varices



Carcinom a



Vascular-enteric fistula

Pa ge 2 9 2



Hem angiom a

Treatment Pre Hospital 

Airway control: o

One hundred percent oxygen or intubate if unresponsive or airway patency in jeopardy



If hem odynam ically unstable or m assive hem orrhage: o

Initiate two large-bore IV catheters.

o

One-liter bolus (20 m L/kg) lactated Ringer (LR) solution or 0.9% norm al saline (NS)

o

Trendelenburg position

P.663

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Intravenous access with at least one large-bore catheter; m ore if unstable

o

Central catheter placem ent if unstable for m ore efficient delivery of fluids and m onitoring of central venous pressure

o

IV fluids of either 0.9% NS (or LR) at 250 m L/h if stable; wide open if hem odynam ically unstable

o

Dopam ine for persistent hypotension unresponsive to aggressive fluid resuscitation



Large-bore Ewald tube placem ent with evidence of large am ount of bleeding: o

Safe

Pa ge 2 9 2

o

Will not aggravate Mallory-Weiss tear

o

Lavage blood from stom ach with water while patient is on side in Trendelenburg position.



Nasogastric (NG) tube placem ent to check for active bleeding



Transfuse O-negative red blood cells im m ediately if hypotensive and not responsive to 2 L of crystalloid.



Most bleeding stops spontaneously with conservative therapy.

ED Treatment 

NPO



Transfuse PRBCs if unstable or lowering hem atocrit with continued hem orrhage.



Bladder catheter to m onitor urine output



Monitor fluid status closely.



With continuing hem orrhage, arrange for im m ediate endoscopy: o



Control bleeding endoscopically via: 

Electrocoagulation



Injection therapy (epinephrine)



Band ligation



Hem oclips



Application of blood-clotting agents

Intravenous vasopressin in m assive bleeding and unavailable endoscopy



In persistent/unresponsive hem orrhage, angiographic infusion of vasopressin



Surgeryâ€”last but definitive treatm ent m odality using techniques to oversew bleeding site or perform gastrectom y



Failure of above m ay require gastric arterial em bolization in patients of poor surgical risk.

Pa ge 2 9 2



Avoid Sengstaken-Blakem ore tubes (especially in presence of hiatal hernia).



Antiem etics, antacids, and H 2 blockers are helpful.

Medication (Drugs) 

Dopam ine: 2â€“20 Âµg/kg/m in IV piggyback (IVPB)



Vasopressin: 0.1â€“0.5 IU/m in IVPB titrating up to 0.9 IU/m in as necessary

Follow-Up Disposition Admission Criteria 



ICU adm ission for: o

Continued or m assive hem orrhage

o

Hem odynam ic instability

o

Extrem e age

o

Poor underlying m edical condition

o

Com plications

General floor adm ission if never unstable and m inim al bleed that has since cleared

Discharge Criteria 

History of m inim al bleed that has stopped



Hem odynam ically stable



Norm al/stable hem atocrit



Negative or trace hem e-positive stool



Negative or trace gastric aspirate

References

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1. Hastings PR, et al. Mallory-Weiss syndrom e: review of 69 cases. Am J Surg. 1981;142(5);560â€“562. 2. Michel L, et al. Mallory-Weiss syndrom e: evolution of diagnostic and therapeutic patterns over two decades. Ann Surg. 1980;192:716â€“721. 3. Sugawa C, et al. Mallory-Weiss syndrom e: a study of 224 patients. Am J Surg. 1983;145(1):30â€“33. 4. Younes Z, et al. The spectrum of spontaneous and iatrogenic esophageal injury: perforations, Mallory-Weiss tears, and hem atom as. J Clin Gastroenterol. 1999;29(4):306â€“317.

Miscellaneous SEE ALSO: Gastrointestinal Bleeding

Codes ICD9-CM 530.7

ICD10 K22.6

Pa ge 2 9 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M alro tatio n

Malrotation

Andrea Bracikowski Sally Santen

Basics Description 

Incom plete rotation and fixation of intestine during em bryogenesis during transition from extracolonic position during 10th week of gestation



Risk factor: o



Congenital defect

Associated conditions: o

o

Gastrointestinal anom alies: 

Duodenal stenosis/atresia/web



Meckel diverticulum



Intussusception



Gastroesophageal reflux



Om phalocele or gastroschisis



Congenital diaphragm atic hernia



Hirschsprung disease

Metabolic acidosis

Etiology 

Duodenojejunal junction rem ains right of m idline.



Cecum rem ains in the upper left abdom en with abnorm al

Pa ge 2 9 2

m esenteric attachm ents. 

Abnorm al anatom y predisposes to obstruction and other conditions.



Usually found in com bination with other congenital anom alies (70%): cardiac, esophageal, urinary, anal

Epidemiology 

1 in 500 live births



Incidence: o

In neonates, m ale-to-fem ale ratio 2:1

o

40% of patients present within first year

o

50% diagnosed by age 1 m onth

o

75% diagnosed by age 1 year of life

Diagnosis Signs and Symptoms 



Neonates: o

Bilious em esis

o

Abdom inal distention

o

Bloody stools

o

Constipation/obstipation

o

Difficulty feeding

o

Poor weight gain

Older than 1 year: abdom inal pain followed by bilious em esis



Older children and adolescents: o

Chronic vom iting

o

Interm ittent colicky abdom inal pain

o

Diarrhea

o

Hem atem esis

Pa ge 2 9 2

o

Constipation

o

May not exhibit abnorm al physical findings at tim e of presentation (50â€“75%)



Adults: sym ptom s vague and nonspecific



General: o

Dehydration, acidosis

o

Peritonitis

o

Ischem ic bowel

o

Sepsis, shock

History 

Bilious vom iting is hallm ark.



Other pertinent historyâ€”acute or chronic abdom inal pain, poor feeding, lethargy

Physical Exam 

Abdom inal exam ination



Evaluate for congenital anom alies.

Essential Workup Diagnosis is suggested by history and physical exam findings and is delineated by contrast radiography.

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose; hypoglycem ia in infants with poor feeding and em esis



Urinalysis

Imaging 

Plain abdom inal radiographs: o

Diagnostic in <30%

o

Volvulus likely if accom panied by: 

Duodenal obstruction (requiring no further

Pa ge 2 9 3

studies) 

Gastric distention with paucity of intralum inal gas distally

 o

Generalized distention of sm all-bowel loops

Upright film s in neonate to dem onstrate obstruction of duodenum 

Triangular gas shadows in right upper quadrant from liver edge overlying air-filled duodenum



Upper GI contrast studies: o

Ninety-five percent sensitive and 86% accurate

o

Findings: 

Absence of ligam ent of Treitz



Dilation of proxim al duodenum with term ination in conical or beak shape



Spiral or corkscrew appearance of duodenum



Proxim al jejunum on right side of abdom en (although readily displaced in neonates)

 

Thickening of sm all-bowel folds

Contrast enem a: o

If obstruction equivocal

o

Evaluates position of cecum in m idline of upper abdom en or to left of m idline

o 

More than 20% false-negative results

Adjuncts: o

Ultrasound

o

CT

o

MRI

o

Angiogram (barber pole sign)

P.665

Differential Diagnosis

Pa ge 2 9 3







Early life: o

Midgut volvulus

o

Hirschsprung disease

o

Necrotizing enterocolitis

Children with acute abdom inal pain and peritoneal signs: o

Appendicitis

o

Intussusception

o

Overwhelm ing sepsis

Older children and adults with vague abdom inal pain: o

Irritable bowel syndrom e

o

Peptic ulcer disease

o

Biliary and pancreatic disease

o

Psychiatric disorders

Treatment Alert Midgut volvulus m ay result in need for rapid volum e and electrolyte replacem ent/resuscitation to correct severe hypovolem ia and m etabolic acidosis.

Initial Stabilization 

Airway, breathing, circulation



Norm al saline (0.9%) intravenous fluid bolus (20 m L/kg) for shock, sepsis, or dehydration



Initiate antibiotics for signs of sepsis or peritonitis.

ED Treatment 

Em ergent surgical correction. May require transfer to facility with pediatric surgical expertise when associated with m idgut volvulus for: o

Detorsion of volvulus

Pa ge 2 9 3

o

Restoration of intestinal perfusion

o

Resection of obviously necrotic areas

o

Replacem ent of long segm ents with questionable vascular integrity back into abdom inal cavity for return evaluation and possible celiotom y in 36 hours



Diet; o

Nothing by m outh

Medication (Drugs) 

Am picillin: 100â€“200 m g/kg/d IV q4h



Clindam ycin: 30â€“40 m g/kg/d IV q6h



Gentam icin: 5.0â€“7.5 m g/kg/d IV q8h

Follow-Up Disposition Admission Criteria 

Acute abdom en



Surgical intervention



Significant dehydration



Acidosis



Sepsis



Shock

Discharge Criteria Stable, m inim ally sym ptom atic, without associated conditions (unusual): 

Surgical evaluation prior to discharge

References

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1. Ford EG, Senac MO, Srikanth MS, et al. Malrotation of the intestine in children. Ann Surg. 1992;215:172â€“178. 2. Kam al I. Defusing the intra-abdom inal ticking bom b: intestinal m alrotation in children. Can Med Assoc J. 2000;162:1315â€“1317. 3. Maxson RT, Franklin PA, Wagner CW. Malrotation in the older child: surgical m anagem ent, treatm ent, and outcom e. Am Surg. 1995;61:135â€“138. 4. Messineo A, MacMillan JH, Palder SB, et al. Clinical factors affecting m ortality in children with m alrotation of the intestine. J Pediatr Surg. 1992;27:1343â€“1345.

Codes ICD9-CM 751.4 Anom alies of intestinal fixation

ICD10 Q43.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M andibular F ractures

Mandibular

Fractures David W. Munter

Basics Description 

Typically owing to a direct force



The m ost com m on area fractured is the angle, followed by the condyle, m olar, and m ental regions.



Because of its thickness, the m andibular sym physis is rarely fractured.



Multiple fractures are seen in >50% of cases owing to the ringlike structure of the m andible.



Bilateral m andibular fractures m ost com m only result from m otor vehicle accidents (MVAs).



Open fractures are com m on, including lacerations of the gum overlying a fracture.

Etiology 

The m andible is the third m ost com m on facial fracture following nasal and zygom atic fractures.



MVAs, personal violence, contact sports, or industrial accidents



Patients are often intoxicated and unable to give a clear

Pa ge 2 9 3

history of events. 

Facial and head lacerations and facial fractures are the m ost com m only associated injuries.

Pediatric Considerations 

Mandibular fractures are uncom m on in children <6 years of age; when they do occur, they are usually greenstick fractures and can be m anaged with soft diet alone.



Inform parents that because any fracture of the m andible m ay dam age perm anent teeth, follow-up with a specialty consultant is advisable.

Diagnosis Signs and Symptoms 

Mandibular pain



Facial asym m etry, deform ity, and dysphagia



Malocclusion, decreased range of m otion of the tem porom andibular joint (TMJ), trism us, or a grating sound conducted to the ear

History 

Mechanism of injury



Malocclusion, dental pain, associated injuries

Physical Exam 

Inspect m axillofacial area for deform ity, including ecchym osis or swelling.



Malocclusion, trism us, or facial asym m etry



Loose, fractured, or m issing teeth; gross m alalignm ent of teeth; separation of tooth interspaces, bleeding at the base of teeth; gum lacerations between teeth; and ecchym osis or hem atom a of the floor of the m outh

Pa ge 2 9 3



Step-off, bony disruption, or point tenderness with palpation along the entire length of the m andible



Protrusion or lateral excursion of the jaw



Interference with norm al m andibular function, including decreased range of m otion or deviation of the m andible with opening: o

The exam iner should be able to insert three fingers between the m andible and m axilla.

o

Inability of the patient to hold a tongue depressor laterally between teeth when pulled by the exam iner, or attem pted to be broken by twisting (positive tongue blade test)



Paresthesia of the lower lip or gum s indicates secondary dam age to the inferior alveolar nerve.



Inability to note m otion of the m andibular condyles when palpated through the external ear canals suggests m andible fracture.



Tenderness of the condyle at the TMJ

Tests Imaging 

Plain film s or dental panoram ic views should be obtained.



Plain film s including an anteroposterior (AP), bilateral obliques, and Towne view should be obtained: o

Mandibular views are best for evaluating the condyles and neck of m andible (m ore com m on site of fracture).



Dental panoram ic view m ay be obtained: o

Panorex best evaluates the sym physis and body (less com m on fracture site).



If condylar fracture is still suspected and not noted on initial radiographs, obtain CT of the condyles in the

Pa ge 2 9 3

coronal plane. 

Missing teeth that cannot be found m andate a chest radiograph to rule out aspiration.



Obtain cervical spine film s if the neck cannot be cleared clinically.

Differential Diagnosis 

Contusions



Dislocation of the m andible: o

If a single condyle is dislocated, the jaw will deviate away from the side of the dislocation.

o

If fractured, the jaw will deviate toward the fractured side.



Isolated dental traum a

Treatment Pre Hospital Cautions: 

Protect the airway.



Protect the cervical spine.



Preserve any avulsed teeth.

P.667

Initial Stabilization 

20â€“40% of patients with m andibular fractures have associated injuries: o

Â¾Treatm ent is directed toward im m ediate, potentially lethal injuries such as airway obstruction, aspiration, m ajor hem orrhage, cervical spine injury,

Pa ge 2 9 3

and intracranial injury. 

Airway m ust be protected.



Cervical spine precautions



If oral intubation cannot be perform ed, nasotracheal intubation should be perform ed unless associated facial injuries are present, in which case cricothyrotom y m ay be indicated.

ED Treatment 

With the exception of condylar fractures, m any m andibular fractures are associated with m ucosal, gingival, or tooth socket disruption and should be considered open fractures: o

Antibiotics such as penicillin, clindam ycin, or erythrom ycin to cover intraoral anaerobic pathogens



Tetanus prophylaxis



Definitive care usually consists of reduction and fixation by wiring upper and lower teeth in occlusion for 4â€“6 weeks: o

Linear, nondisplaced, or greenstick fractures m ay be treated with soft diet without wiring.



If m andible dislocation is present, while the jaw is open apply bilateral downward pressure on the occlusal surface of the posterior lower teeth while grasping the m andible: o

The goal is to free the condyle from its anterior position to the em inence.

o

Reduction is facilitated by m uscle relaxants (diazepam or m idazolam ) or anesthetic injection of m astication m uscles.

o

A bite block should be used, or the exam iner's fingers should be wrapped in gauze to prevent injury.

Medication (Drugs)

Pa ge 2 9 3



Acetam inophen: 650 m g (peds: 10â€“15 m g/kg) PO q4h



Clindam ycin: 150â€“450 m g PO q.i.d. (peds: 10â€“20 m g/kg/24h)



Diazepam : 5â€“10 m g (peds: 0.1â€“0.2 m g/kg) IV



Erythrom ycin: 250â€“500 m g (peds: 30â€“50 m g/kg/24h) PO q.i.d.



Ibuprofen: 600â€“800 m g (peds: 20â€“40 m g/kg/24h) PO t.i.d.â€“q.i.d.



Midazolam : 2â€“5 m g (peds: safety not established, but 0.02â€“0.05 m g/kg per dose has been used) IV



Penicillin: 250â€“500 m g (peds: 25â€“50 m g/kg/24h) PO q.i.d.

Follow-Up Disposition Admission Criteria 

Significant displacem ent or associated dental traum aâ€”open fractures require urgent specialty consultation for possible adm ission.



The severity of associated traum a m ay indicate adm ission.



Any patient with the potential for airway com prom ise should be adm itted.



An unreliable patient with nondisplaced fractures should be adm itted for definitive fixation.



In the pediatric population, if the m echanism of injury is not appropriate to the injuries seen, pediatric or child protective services consultation should be obtained.

Discharge Criteria 

Patients with nondisplaced, closed fractures m ay be

Pa ge 2 9 4

discharged on analgesics and a soft diet. 

Patients should be referred to an otorhinolaryngologist or an oral m axillofacial surgeon in a tim ely fashion.

References 1. Alonso LL, Purcell TB. Accuracy of the tongue blade test in patients with suspected m andibular fracture. J Em erg Med. 1995;13:297â€“304. 2. Luyk NH, Ferguson JW. The diagnosis and initial m anagem ent of the fractured m andible. Am J Em erg Med. 1991;9:352â€“359. 3. Newm an J. Medical im aging of facial and m andibular fractures. Radiol Technol. 1998;69:417â€“435. 4. Ogundare BO, Bonnick A, Bayley N. Pattern of m andibular fractures in an urban m ajor traum a center. J Oral Maxillofac Surg. 2003;61(6):713â€“718. 5. Schwab RA, Genners K, Robinson WA. Clinical predictors of m andibular fractures. Am J Em erg Med. 1998;16:304â€“305.

Miscellaneous SEE ALSO: Dental Traum a; Facial Fractures

Codes ICD9-CM 802.20

ICD10 S02.6

Pa ge 2 9 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M arine Enveno m atio n

Marine

Envenomation Adam Black Timothy Erickson

Basics Description 

Marine envenom ation refers to poisoning caused by sting or bite from m arine species.



Sponges: o

Contain sharp spicules with irritants that cause pruritic derm atitis



Coelenterates (Cnidaria jellyfish): o

Contain stinging cells known as nem atocysts on their tentacles

o

Fluid-filled cysts eject sharp, hollow thread-tube on contact.

o

Thread-tube penetrates skin and envenom ates victim .

o 

Starfish: o



Box jellyfish can kill within 60 seconds.

Sharp, rigid spines are coated with slim y venom .

Sea urchins:

Pa ge 2 9 4

o 

Sea cucum bers: o



Hollow, sharp spines filled with various toxins

Hollow tentacles secrete holothurin, a liquid toxin.

Cone shells: o

Venom injected through dartlike, detachable tooth

o

Active peptides interfere with neurom uscular transm ission.

o 

Presents with puncture wounds sim ilar to wasp stings

Stingrays: o

Most com m on cause of hum an m arine envenom ations

o

Tapered spines attached to tail inject venom into victim .





Scorpion fish: o

Lionfish usually m ild; stonefish can be life threat.

o

Sharp spines along dorsum and pelvis of fish

o

Often stepped on inadvertently

o

Neurotoxic venom

Catfish: o



Dorsal and pectoral spines contain venom glands.

Sea snakes: o

Hollow fangs with associated venom glands

o

Highly neurotoxic venom blocks neurom uscular transm ission.

Diagnosis Signs and Symptoms 

Sponges: o

Itching and burning a few hours after contact

o

Local joint swelling and soft tissue edem a

o

Fever

Pa ge 2 9 4

o

Malaise

o

Dizziness

o

Nausea

o

Muscle cram ps

o

In severe cases, desquam ation in 10 days to 2 m onths



Coelenterates (Cnidaria jellyfish): o

o

Mild envenom ation: 

Im m ediate stinging sensation



Pruritus



Paresthesia, burning sensation



Throbbing



Blistering/local edem a/wheal form ation

Moderate/severe: 

Neurologic: ataxia, paralysis, delirium , seizures



Cardiovascular: anaphylaxis, hem olysis, hypotension, dysrhythm ias



Respiratory: bronchospasm , laryngeal edem a, pulm onary edem a, respiratory failure



Musculoskeletal: m uscle cram ps or spasm , arthralgias



Gastrointestinal: nausea, vom iting, diarrhea, dysphagia, hypersalivation/thirst



Ophthalm ologic: conjunctivitis, corneal ulcers, elevated intraocular pressure



Echinoderm ata: o

o

Starfish: 

Im m ediate pain



Bleeding



Mild edem a



Paresthesias/nausea/vom iting if severe

Sea urchins:

Pa ge 2 9 4



Intense pain and severe local m uscle aches



Nausea, vom iting



Paresthesias, hypotension, or respiratory distress with m ultiple stings

o

Sea cucum bers: 

Mild contact derm atitis



Corneal and conjunctival involvem ent: Severe reactions can lead to blindness.



Mollusks: o

Cone shells: 

Puncture wounds sim ilar to wasp stings



Sharp burning and stinging



Paresthesias indicate severe envenom ation.



Can evolve into m uscular paralysis and respiratory failure, dysphagia, syncope, dissem inated intravascular coagulation



Stingrays: o

Puncture wounds or jagged lacerations

o

Local, intense pain, edem a, bleeding; necrosis if severe



o

Nausea, vom iting, diarrhea

o

Diaphoresis

o

Headache

o

Tachycardia

o

Seizures

o

Paralysis

o

Hypotension

o

Dysrhythm ias

Scorpion fish: o

Intense local pain for 6â€“12 hours

o

Erythem a m ay progress to cellulitis.

o

Headache

Pa ge 2 9 4



o

Nausea, vom iting, diarrhea

o

Pallor

o

Delirium

o

Seizures

o

Fever

o

Hypertension

Catfish: o

Local pain, ischem ic appearance progressing to erythem a



o

Swelling, bleeding, and edem a

o

Local m uscle spasm s

o

Diaphoresis

o

Neuropathy/fasciculations/weakness/syncope

Sea snakes: o

Bite initially causes very little pain.

o

Pinlike pairs of fang m arks

o

Onset from 5 m inutes to 6 hours

o

Muscle pain, lower extrem ity paralysis, arthralgias

o

Trism us, blurred vision, dysphagia, drowsiness

o

Severe signs include:

o



Ascending paralysis



Aspiration



Com a



Renal and liver failure

If untreated, 25% m ortality

Essential Workup 

Careful history/repeated evaluation of wound sites



Soft tissue radiographs to detect foreign body

Tests Lab 

CBC

Pa ge 2 9 4



Electrolytes, blood urea nitrogen, creatinine, and glucose levels



Liver function test



Urinalysis



Arterial blood gases if severe sym ptom s

Differential Diagnosis 

Allergic reaction



Cellulitis



Gastroenteritis



Aspiration pneum onia

P.669

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Establish intravenous access with 0.9% norm al saline.

ED Treatment 

General: o

Prepare for anaphylactic reactions (epinephrine/steroids).

o

Prepare for intubation if needed.

o

Benadryl for itch/burn/hives

o

Tetanus prophylaxis

o

Corticosteroids for severe local reactions

o

Narcotic analgesia: 

o

Most m arine envenom ations cause severe pain.

Antibiotic prophylaxis for the following:

Pa ge 2 9 4

o



Large lacerations or burns



Deep puncture wounds



Grossly contam inated wounds



Elderly or chronically ill

Antibiotic choices: 

Trim ethoprim /sulfam ethoxazole (TMP-SMX; Bactrim )





Tetracycline



Ciprofloxacin



Third-generation cephalosporin

Sponges: o

Gently dry skin and rem ove spicule: 

o

Adhesive tape m ay aid in rem oval.

Five percent vinegar (or 40â€“70% isopropyl alcohol) soaks q.i.d. for 10â€“30 m inutes



Coelenterates (Cnidaria jellyfish): o

Rinse wound with saltwater or seawater: 

Hypotonic solutions trigger m ore nem atocysts.

o

Do not rub skin to avoid release of nem atocysts.

o

Inactivate toxin with 30-m inute soak of 5% acetic acid (vinegar)

o

Rem ove rem aining nem atocysts with razor.

o

Apply topical anesthetics once nem atocysts rem oved.

o

Sea Safe jellyfish sun block products available

o

Box-jellyfish stings (Australia) em ergent cases: 

Adm inister Chironex antivenin: one am pule (20,000 units) intravenously diluted 1:5 with crystalloid.

o 

Corticosteroids for severe reactions

Starfish: o

Im m erse in nonscalding hot water for pain relief.

o

Irrigate and explore all puncture wounds.

Pa ge 2 9 4

o 







Prophylactic antibiotics for significant wounds

Sea urchins: o

Im m erse in nonscalding hot water for pain relief.

o

Rem ove any rem aining spines.

o

Prophylactic antibiotics for significant wounds

Sea cucum bers: o

Im m erse in nonscalding hot water for pain relief.

o

Five percent acetic acid soaks

o

Ocular involvem ent: 

Proparacaine for pain



Copious irrigation with norm al saline



Careful slit-lam p exam

Cone shells: o

Hot water im m ersion for pain relief

o

Be prepared for cardiac or respiratory support.

Stingrays: o

Copious irrigation with rem oval of any visible spines

o

Local suction is controversial.

o

Hot water soaks for pain relief

o

Narcotics for pain control

o

High incidence of bacterial infection: 

Adm inister prophylactic antibiotics for significant wounds.



Scorpion fish: o

Hot water soaks for pain relief and venom inactivation

o

Copious irrigation, rem oval of any visible spines

o

Local lidocaine or regional block for severe pain

o

Surgical exploration for deep penetration/foreign bodies

o

Stonefish antivenin for severe envenom ations: 

May cause serum sickness

Pa ge 2 9 4



One 2-m L am pule diluted in 50-m L saline intravenously slow



Catfish: o

Hot water soaks for pain relief and venom inactivation

o

Copious irrigation, rem oval of any visible spines

o

Consider local lidocaine, regional block, or narcotics for severe pain.

o

Surgical exploration for deep penetration/foreign bodies

o

Leave puncture wounds open to heal.

o

Consider prophylactic antibiotics for hand, foot, or deep wounds.



Sea snakes: o

Im m obilize bitten extrem ity.

o

Apply pressure bandage for venous occlusion (prehospital).

o

Keep victim warm and still.

o

Polyvalent sea snake antivenin reduces m ortality to 3%: 

May require 3â€“10 am pules (1,000 U each)



Prepare early for assisted ventilation.

Medication (Drugs) 

Cefixim e: 400 m g (peds: 8 m g/kg/24h) PO daily



Ciprofloxacin: 500 m g PO b.i.d.



Epinephrine: 0.3â€“0.5 m L SC 1:1,000 (peds: 0.01 m L/kg)



Tetracycline: 500 m g PO q.i.d.



Trim ethoprim /sulfam ethoxazole (Bactrim DS): one tablet (peds: 5 m g liquid (40/200/5 m L)/10 kg per dose) PO b.i.d.

Pa ge 2 9 5

Follow-Up Disposition Admission Criteria Significant signs of system ic involvem ent

Discharge Criteria 

No signs of system ic illness after 8 hours of observation



Wound check within 48 hours

References 1. Aldred B, Erickson T, Lipscom b J. Lionfish envenom ations in an urban wilderness. Wilderness Environ Med. 1996;4:291â€“296. 2. Auerbach P. Envenom ations by aquatic anim als. In: Auerbach PS, ed: Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001: 1450â€“1487. 3. Erickson T, Auerbach P. Marine envenom ations and seafood poisoning. In Erickson T, Ahrens W, Aks SE, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2005: 524â€“532. 4. Lee JY, Teoh LC, Leo SP. Stonefish envenom ations of the handâ€”a local m arine hazard: a series of 8 cases and review of the literature. Ann Acad Med Singapore. 2004;33(4):515â€“520. 5. McKinistry DM. Catfish stings in the United States: case report and review. J Wilderness Med. 1993;4:293. 6. Nim orakiotakis B, Winkel KD: Marine envenom ations. Aust Fam Physician. 2003;32:969â€“979. 7. Perkins RA, Morgan SS. Poisoning, envenom ation, and traum a from m arine creatures. Am Fam Physician. 2004;69:885â€“890. 8. Tom aszewski C. Aquatic envenom ations. In: Ford M, DeLaney K, Ling L, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders;

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2001: 970â€“984. 9. Watters MR, Stom m el EW. Marine neurotoxins: envenom ations and contact toxins. Curr Treat Options Neurol. 2004;6(2):115â€“123.

Codes ICD9-CM 989.5

ICD10 T63.6

Pa ge 2 9 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M astitis

Mastitis

Marco Coppola Timothy Stallard

Basics Etiology 

Staphylococcus aureus m ost com m on



Coagulase-negative Staphylococcus, Streptococcus species, Escherichia coli, Haem ophilus influenzae

Diagnosis Signs and Symptoms 

Fever usually >39Â°C



Chills, rigors, m alaise



Tachycardia



Breast pain, induration, erythem a, warm th; usually unilateral



Onset typically 2â€“3 weeks to m onths postpartum while breast-feeding



Rare during first postpartum week



More com m on in advanced m aternal age and patients with diabetes

Pa ge 2 9 5

Essential Workup Physical exam ination with special attention to detecting abscess: 

Abscess is frequently difficult to detect, but is m ore com m on in periareolar area.



Purulent nipple discharge with palpation

Tests Lab Breast m ilk culture usually not required

Imaging Consider breast ultrasound if abscess is suspected: 

Mam m ography is not indicated acutely.

Differential Diagnosis 

Breast engorgem ent: o

Transient fever <39Â°C of 4â€“16 hoursâ€™ duration

o

Appearing 48â€“72 hours postpartum

o

Bilateral nonerythem atous engorgem ent



Carcinom a (inflam m atory)



Cyst, tum or



Abscess form ation

Treatment Initial Stabilization No specific stabilization

ED Treatment 

Outpatient oral antibiotics for 10 days: o

Î²-Lactam aseâ€“resistant penicillin, e.g., dicloxacillin (Dynapen)

Pa ge 2 9 5

o

First-generation cephalosporin, e.g., cephalexin (Keflex)

o 

Erythrom ycin if penicillin allergic

Surgical consultation if evidence of abscess

P.671

Medication (Drugs) 

Cephalexin: 500 m g q6h PO for 10 days



Clindam ycin: 300 m g q6h PO for 10 days



Dicloxacillin: 250 m g q6h PO for 10 days



Erythrom ycin: 500 m g q6h PO for 10 days

Follow-Up Disposition Admission Criteria 

Incision and drainage under general anesthesia m ay be necessary and require adm ission.



Im m unocom prom ised or evidence of septicem ia



Patients with diabetes m ay account for one third of m astitis cases: o

Make sure their diabetes is not out of control.

Discharge Criteria 

Most patients m ay be m anaged in outpatient setting.



Most sym ptom s resolve within 48 hours of therapy.



In sim ple m astitis, breast-feeding m ay be continued, including using affected breast:

Pa ge 2 9 5



o

Gently m assage to enhance drainage.

o

Counsel that this will not harm baby.

Breast support, warm com presses, and analgesia for com fort



In frank abscess, discontinue breast-feeding until purulent discharge resolves.



Follow-up should be arranged to exclude diagnosis of inflam m atory carcinom a.

References 1. Calhoun BC, Brost B. Em ergency m anagem ent of sudden puerperal fever. Obstet Gynecol Clin North Am . 1995;22(2):357â€“367. 2. Gilbert DN, et al., eds. The Sanford Guide to Antim icrobial Therapy . 22nd ed. Hyde Park, VT: Antim icrobial Therapy, Inc.; 2002. 3. Terregino CA, Greenm an RA. Breast disorders. In: Tintinalli J, et al., eds. Em ergency Medicine: A Com prehensive Study Guide. 5th ed. New York: McGraw-Hill; 2000.

Codes ICD9-CM 611.0

ICD10 N61

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M asto iditis

Mastoiditis

Jonathan Fisher

Basics Description 

Inflam m ation, infection, and destruction of the m astoid air cells caused by acute purulent otitis m edia



Middle ear and m astoid air cells are contiguous via the aditus ad antrum .



Fluid accum ulation from closure of channel due to otitis m edia creates opportunity for infection.



Manifestation ranges from clinically insignificant inflam m ation of m astoid air cells to infection and destruction of the bone.



Acute m astoiditis: o

Occurs to som e degree in all cases of otitis m edia

o

Inflam m atory changes of the m astoid

o

Early signs and sym ptom s are those of acute otitis m edia.

o

Usually secondary to contam ination with infectious m aterial trapped in the m astoid by inflam m atory obstruction of the channel between m iddle ear and m astoid air cells



Acute m astoiditis with periostitis:

Pa ge 2 9 5

o

As infection progresses, periosteum of the m astoid bone is involved, causing periostitis.

o 

Subperiosteal abscess m ay be present.

Acute m astoid ostitis (also called coalescent m astoiditis): o

Progression of the infection within the m astoid air cells leads to destruction of the m astoid trabeculae causing coalescence of bony trabeculae.

o

Mastoid em pyem a or a draining fistula m ay be present.

o

May progress to severe head and neck com plications if untreated



Masked m astoiditis: o

Mastoid infection, which lingers after an acute otitis m edia has been treated

o 

Chronic m astoiditis: o





May progress to acute or coalescent m astoiditis

Infection lasting m ore than 3 m onths

Mastoiditis can be a com plication of a prim ary disorder: o

Leukem ia

o

Mononucleosis

o

Sarcom a of the tem poral bone

o

HIV

o

Kawasaki disease

Prevalence is equal in m ales and fem ales.

Etiology 

Distribution of organism s in acute m astoiditis can differ from that in acute otitis m edia:



o

Streptococcus pneum oniae

o

Group A streptococcus

o

Staphylococcus aureus

o

Haem ophilus influenzae

Gram -negative enteric bacteria m ost com m on with chronic

Pa ge 2 9 5

m astoiditis:



o

Pseudom onas aeruginosa

o

Escherichia coli

o

Proteus m irabilis

o

Bacteroides species

Other less com m on causes: o

Mycobacterium tuberculosis

o

Aspergillus species in im m unocom prom ised states

Complications 

Bezold abscess: o

Extension of infection to soft tissue below pinna or behind the sternocleidom astoid m uscle of neck after erosion through the m astoid tip



Petrositis: o

Spread of the infection to the petrous air cells



Osteom yelitis of the calvarium



Gradenigo syndrom e: o

Erosion of the m edial tem poral bone causing otorrhea, retroorbital pain, and cranial nerve VI paralysis



Intracranial com plications: o

Subperiosteal abscess

o

Subdural em pyem a: 

Extension of infection to CNS with em pyem a around the tentorium

o

Sinus throm boses

Pediatric Considerations 

More frequently seen in the pediatric population due to strong association with otitis m edia



S. pneum oniae m ost com m on cause in children

Pa ge 2 9 5

Diagnosis Signs and Symptoms History 

Ear pain



Otorrhea



Mild to severe hearing loss



Fever



Headache



History of irritability in a child



History of recurrent otitis m edia

Physical Exam 

Tenderness, edem a, and erythem a over the m astoid



Lateral and inferior displacem ent of the auricle



Loss of the postauricular crease



Swelling of the posterior and superior ear canal wall



Tym panic m em brane abnorm alities consistent with severe otitis m edia



Purulent fluid drainage



Bulging tym panic m em brane

Tests Lab 

CBC count: o



Leukocytosis

Cultures of drainage im portant owing to diversity of organism s: o

If spontaneous drainage present or after surgical drainage



Blood cultures

Pa ge 2 9 6

Imaging 

Mastoid plain radiographs: o

Early stage of disease m ay show hazy or cloudy but intact m astoid.

o

May reveal opacification or coalescence of the m astoid air cells or coalescence as disease progresses

o

Low sensitivity since m ay be negative

P.673



CT scan: o

More useful, especially if abscess form ation present

o

Can determ ine presence and extent of destruction of trabeculae as well as evaluate for the com plications of m astoiditis



MRI: o

If intracranial involvem ent suspected but not confirm ed by CT

Diagnostic Procedures/Surgery Lum bar puncture 

Cerebrospinal fluid evaluation for signs of m eningitis

Differential Diagnosis 

Otitis m edia



Cellulitis



External otitis m edia



Scalp infection with inflam m ation of posterior auricular nodes



Rubellaâ€”posterior auricular node enlargem ent



Traum a to pinna or postauricular area

Pa ge 2 9 6

Treatment Initial Stabilization 

ABCs



Airway m anagem ent for signs of airway com prom ise



0.9% NS IV fluid bolus for hypotension/volum e depletion

ED Treatment 

Otolaryngologist consult for surgical drainage: o

Drainage is the definitive therapy for acute or coalescent m astoiditis.

o

Em ergent drainage if the patient is toxic appearing

o

Types of surgical procedures: 

Myringotom y drainage and tym panostom y tube placem ent



Mastoidectom y and drainage for severe extension (needed in about 50% of cases)



Initiate IV antibiotics: o

Sem isynthetic penicillins (Unasyn, Tim entin) with chloram phenicol

o

Third-generation cephalosporins (ceftriaxone, cefotaxim e)

o

Im ipenem

o

Given increasing proportion of S. aureus as causative organism , consider including antistaphylococcal agent before culture results.

o

Parenteral antibiotics can be switched to oral after patient afebrile for 36â€“48 hours



Adm inister pain m edications: o

NSAIDs

o

Oral or parenteral narcotics

Pa ge 2 9 6

Medication (Drugs) 

Am picillin sulbactam (Unasyn): 1.5â€“3 g IV q6h



Cefotaxim e: 1â€“2 g (peds: 50â€“180 m g/kg/24h) IV q4hâ€“q6h



Ceftriaxone: 1â€“2 g (peds: 50â€“75 m g/kg/24h) IV q12hâ€“q24h



Chloram phenicol: 50â€“100 m g/kg/24h IV or PO q6h



Im ipenem : 250 m gâ€“1 g IV q6hâ€“q8h



Ticarcillin clavulanate (Tim entin): 3.1 g IV q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

Clinical suspicion of acute or coalescent m astoiditis



Subperiosteal abscess



Toxic appearing

Discharge Criteria Patients with acute or coalescent m astoiditis should not be discharged.

Issues for Referral Otolaryngologist consult for surgical drainage

References 1. Bitar CN, Kluka EA, Steele RW. Mastoiditis in children. Clin Pediatr . 1996;35(8):391â€“395. 2. Luntz M, Brodsky A, Nusem S, et al. Acute m astoiditis the antibiotic era: a m ulticenter study. Int J Pediatr Otorhinolaryngol.

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2001;57(1):1â€“9. 3. Pfaff JA, Moore GP. Otolaryngology In: Marx JA et al. Rosen's Em ergency Medicine Concepts and Clinical Practice. 5th ed. St. Louis, Mo.: Mosby, 2002;928â€“938 4. Wang N, Ewen, Burg J. Mastoiditis: a case-based review. Pediatr Em erg Care. 1998;14:290â€“293.

Codes ICD9-CM 383.00 383.9 383.1

ICD10 H70.9

Pa ge 2 9 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M DM A Po iso ning

MDMA Poisoning

Mark B. Mycyk

Basics Description 

MDMA: 3,4-m ethylenedioxym etham phetam ine (â€œecstasyâ€•)



Schedule I drug m anufactured illegally



Used recreationally: o

Rave parties

o

Dance clubs

o

College cam puses



Onset of effects: 15â€“30 m inutes after ingestion



Duration of effects: 2â€“6 hours



Pills com m only contain contam inants: o

Caffeine

o

Ephedrine

o

Dextrom ethorphan

o

Ketam ine

o

Related m ethylated am phetam ines (MDA, MDEA, MDBA, PMA)

Pathophysiology 

Am phetam inelike structure stim ulates catecholam ine release.

Pa ge 2 9 6



Mescalinelike ring structure enhances serotonergic and dopam inergic activity.

Etiology Deliberate or accidental ingestion of MDMA

Diagnosis Signs and Symptoms 







Overdose: o

Altered m ental status

o

Severe sym pathom im etic sym ptom s

Central nervous system : o

Excitation

o

Com a

o

Seizures

o

Cerebral edem a

o

Brainstem herniation

Cardiovascular: o

Hypertension (early)

o

Hypotension (late)

o

Palpitations

o

Ventricular tachycardia and ectopy

Pulm onary: o





Pulm onary edem a

Metabolic: o

Hyponatrem ia

o

Hypoglycem ia

o

Syndrom e of inappropriate antidiuretic horm one

Musculoskeletal: o

Bruxism

Pa ge 2 9 6



o

Restlessness

o

Rigidity

Renal: o





Hepatic: o

Jaundice

o

Hepatitis

Hem atologic: o







Rhabdom yolysis

Dissem inated intravascular coagulation

Gastrointestinal: o

Vom iting

o

Diarrhea

o

Abdom inal cram ping

Psychiatric: o

Euphoria

o

Flight of ideas

o

Delirium /hallucinations

Other: o

Hypertherm ia

o

Mydriasis

o

Nystagm us

Essential Workup 

Diagnosis based on clinical presentation and an accurate history



Obtain core tem perature.



Exclude toxic coingestants or contam inants.

Tests ECG: 

Sinus tachycardia (m ost com m on)



Dysrhythm ias, conduction disturbances

Lab

Pa ge 2 9 6



Electrolytes, BUN, creatinine, and glucose levels



PT/PTT/INR



Urine dip for blood and m yoglobin



Urine toxicology screen to exclude coingestants: o

May cause positive am phetam ine and m etham phetam ine screen



Quantitative MDMA levels rarely helpful



Creatine phosphokinase (CPK) level if rhabdom yolysis suspected



Liver function tests for significant overdose or suspected hepatitis

Imaging 

Chest radiograph if suspected aspiration pneum onia



Head CT if suspected intracranial hem orrhage

Differential Diagnosis 

Cocaine overdose



Am phetam ine overdose



Anticholinergic overdose



Serotonin syndrom e



Occult head injury



Sepsis



Thyroid storm



Pheochrom ocytom a

Treatment Pre Hospital 

Transport all pills/pill bottles involved in overdose for identification in em ergency departm ent.



Watch for MDMA paraphernalia:

Pa ge 2 9 6

o

Pacifiers

o

Glow sticks

o

Surgical m asks

P.675

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

Airway control essential



Adm inister supplem ental oxygen.



Intubate if indicated.



IV access



Naloxone, thiam ine, dextrose (or Accu-Chek), if altered m ental status

ED Treatment 

Supportive care



Monitor core tem perature and cardiac rhythm for at least 6 hours.



Hydrate with 0.9% norm al saline IV.



Hypertension:





o

Nitroprusside

o

Phentolam ine

o

Esm olol

Hypotension: o

0.9% norm al saline intravenous bolus

o

Trendelenburg position

o

Pressors titrated to blood pressure

Anxiety/restlessness/agitation: o



Diazepam or lorazepam as needed

Seizures: o

Treat initially with benzodiazepines.

Pa ge 2 9 6

o 

Phenobarbital for persistent seizures

Rhabdom yolysis: o

Hydrate aggressively with 0.9% norm al saline intravenously



o

Consider sodium bicarbonate adm inistration.

o

Hem odialysis if renal failure

Hypertherm ia: o

Standard cooling m easures

o

Treat agitation with benzodiazepines.

o

Consider dantrolene in refractory cases.

Medication (Drugs) 

Dantrolene: 1â€“2 m g/kg to m ax. 10 m g/kg IV



Diazepam : 5â€“10m g (peds: 0.2â€“0.5 m g/kg) IV q10â€“15m in



Esm olol: 500 Âµg/kg IV bolus, then 50 Âµg/kg/m in IV



Lorazepam : 2â€“6 m g (peds: 0.05â€“0.1 m g/kg) IV q10â€“15m in



Naloxone: 0.4â€“2 m g (peds: 0.1 m g/kg; neonatal: 10â€“30 Âµg/kg IV or IM



Nitroprusside: 0.3 Âµg/kg/m in to m ax. 10 Âµg/kg/m in



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Phentolam ine: 1â€“5 m g (peds: 0.02â€“0.1 m g/kg) IV bolus q5â€“10m in



Propofol: 0.5â€“1.0 m g/kg IV (loading dose), then 5â€“50 Âµg/kg/m in (m aintenance dose)

Follow-Up

Pa ge 2 9 7

Disposition Admission Criteria 

Seizures



Persistent cardiovascular instability



Rhabdom yolysis



Loss of behavioral control



Depressed m ental status



Dissem inated intravascular coagulation

Discharge Criteria Asym ptom atic 6 hours after oral overdose

Issues for Referral Consider substance abuse referral for patients.

References 1. Ben-Abraham R, Szold O, Rudick V, Weinbroum AA. â€˜Ecstasyâ€™ intoxication: life-threatening m anifestations and resuscitative m easures in the intensive care setting. Eur J Em erg Med . 2003;10(4):309â€“313. 2. Gahlinger PM. Club drugs: MDMA, gam m a- hydroxybutyrate (GHB), Rohypnol, and ketam ine. Am Fam Physician. 2004;69:2619â€“2626. 3. Kalant H. The pharm acology and toxicity of â€œecstasyâ€• (MDMA) and related drugs. Can Med Assoc J. 2001;165:917â€“928. 4. Patel MM, Wright DW, Ratcliff JJ, et al. Shedding new light on the â€œsafeâ€• club drug: m ethylenedioxym etham phetam ine (ecstasy)related fatalities. Acad Em erg Med. 2004;11(2):208â€“210. 5. Schwartz RH, Miller NS. MDMA (ecstasy) and the rave: a review. Pediatrics. 1997;100:705â€“708. 6. Shannon MW. Methylenedioxym etham phetam ine (MDMA, â€œecstasyâ€•). Pediatr Em erg Care. 2000;16:377â€“380.

Codes

Pa ge 2 9 7

ICD9-CM 969.7

ICD10 T43.6

Pa ge 2 9 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M easles

Measles

Austen Chai

Basics Etiology 

Negative-strand param yxovirus



Hum ans are only known reservoir.



Highly contagious; outbreaks seen in nonim m unized or underim m unized

Diagnosis Signs and Symptoms Incubation (8â€“14 days) 

Transm ission via direct contact or inhalation of infectious droplet

Prodrome (2â€“8 days) 

Mild respiratory illness



Koplik spots: o

Sm all white to grayish-blue specks on buccal m ucosa

o

Pathognom onic for rubeola

o

Transient and disappear within 48 hours after onset

Pa ge 2 9 7

of rash

Active Disease 

Cough, coryza, conjunctivitis with fever and rash



Rash begins on head and neck and spreads centrifugally downward: o

Initially pale, then discrete and m aculopapular, and ultim ately, confluent

o

Clinical im provem ent seen in 48 hours of appearance of rash

o

Rash clears in 3â€“4 days and m ay desquam ate as rash fades.

Complications 

Respiratory: o

Cough m ay persist for 1â€“2 weeks after m easles infection.

o

Pneum onia seen m ost com m only in im m unocom prom ised



o

Most com m on cause of fatality

o

Laryngotracheobronchitis in patients <2 years old

CNS: o

o

Encephalom yelitis: 

Usually 1â€“14 days after onset of rash



Fever, headache, vom iting, and stiff neck



Lethargy, stupor, and seizure followed by com a



More than half will have perm anent residuals.

Subacute sclerosing panencephalitis (SSPE): 

Develops weeks to years after infection



Insidiously progressive degeneration of CNS functions



Personality change, intellectual deterioration, m otor and visual deficits, com a, and death

Pa ge 2 9 7



Cardiovascular: o

Transient m yocarditis, pericarditis, and conduction defects

o

Rarely clinically significant

o

Congestive heart failure in elderly patients



Throm bocytopenic purpura



Otitis m edia



Sinusitis

Essential Workup 

Diagnosis is based on clinical findings.



Cough, coryza, and conjunctivitis with fever and subsequent rash

Tests Lab 

Cerebrospinal fluid (CSF) analysis for suspected encephalitis



Viral cultures and antibody testing generally im practical

Imaging Chest radiograph for suspected pneum onia

Differential Diagnosis 

Rubella; o

Milder course, postauricular nodes, pinker rash, no conjunctivitis



Scarlet fever: o

Sandpaper-textured rash, strawberry tongue, sore throat



Infectious m ononucleosis: o



Serologic test available

Roseola: o

Rash appears after tem perature falls.

Pa ge 2 9 7





Erythem a infectiosum (Fifth disease): o

No prodrom e and without fever

o

Red flushed cheeks with lacelike rash when fading

Enterovirus: o



No respiratory com plaints

Kawasaki disease: o

Rash on palm and soles



Secondary syphilis



Toxic shock syndrom e



Drug reactions: o

Usually without fever and upper respiratory infection sym ptom s

P.677

Treatment Pre Hospital 

Nonim m unized prehospital care personnel should be advised of potential risks described above.



Risk for spontaneous abortion and prem ature birth in nonim m unized pregnant prehospital personnel if infected

ED Treatment 

Prevention with vaccination is cornerstone of therapy: o

Two doses of m easles vaccine given as m easles, m um ps, and rubella (MMR)

o

First dose at 12â€“15 m onths and second dose typically before school entry



Antipyretics

Pa ge 2 9 7



IV rehydration as needed



Isolate suspected cases.



Postexposure prophylaxis for the nonim m une: o

Give MMR if <72 hours after exposure: 

o

Avoid if pregnant, im m unocom prom ised.

Im m une globulin 100â€“400 m g/kg IV or 0.25 m L/kg IM to 15 m L (m ax.) 

If given <6 days after exposure, will prevent or m odify m easles



Oxygenation and airway protection for: o

Pneum onia

o

Encephalitis

Follow-Up Disposition Admission Criteria 

Severe pneum onia



Dehydration



Encephalitis



SSPE



Im m unocom prom ised patients:



o

AIDS

o

Im m unosuppressive therapy

Elderly patients with coâ€“m orbid conditions

Discharge Criteria Duration of infectivity inform ation: 

Four days before sym ptom s and up to 4 days after onset of rash



Im m unocom prom ised are contagious for duration of

Pa ge 2 9 7

illness.

References 1. Am erican Academ y of Pediatrics. Measles. In: Pickering LK, ed. Red Book 2003: The Report of the Com m ittee on Infectious Diseases. 23rd ed. Elk Grove Village, IL: Am erican Academ y of Pediatrics; 2003:419. 2. Centers for Disease Control and Prevention. Measles, m um ps and rubella: vaccine use and strategy for elim ination of m easles, rubella, and congenital rubella syndrom e and control of m um ps. Recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 1998;47(RR-8):157. 3. Gable EK. Pediatric exanthem s. Prim ary Care. 2000;27(2):353â€“369. 4. Goldm an L, ed. Cecil Textbook of Medicine. 21st ed. Philadelphia: WB Saunders; 2000:1802â€“1805.

Codes ICD9-CM 55.9

ICD10 B05.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M eckel Diverticulum

Meckel

Diverticulum John Bailitz

Basics Description 

Most com m on congenital abnorm ality of the gastrointestinal tract



Ileal true diverticula: o

50% contain norm al ileal m ucosa.

o

50% contain either gastric (m ost com m on), pancreatic, duodenal, colonic, endom etrial, or hepatobiliary m ucosa.



Rule of two: o

2% prevalence in general population

o

2% lifetim e risk for com plications decreasing with age

o

45% of sym ptom atic patients younger than 2 years old



o

Male-to-fem ale ratio of 2:1

o

Average length 2 inches

o

About 2 feet from the ileocecal valve

Com plications:

Pa ge 2 9 7



o

Obstruction and diverticulitis in adults

o

Hem orrhage and obstruction in children

o

Mean age 10 years

Obstruction: o

Diverticulum attached to the um bilicus, abdom inal wall, other viscera, or is free and unattached leading to: 

Intussusception: diverticulum is the leading edge.



Volvulus: persistent fibrous band leads to bowel rotation.



Diverticulitis: o

Opening obstructed

o

Bacterial infection follows

o

Presents like appendicitis (m ost com m on preoperative diagnosis with Meckel diverticulum )

Pediatric Considerations 

Most com m on cause of significant lower GI bleeding in children



Present younger than age 5 with episodic painless, brisk, and bright red rectal bleeding



Ectopic gastric tissue with secretions leading to erosions and bleeding

Etiology Rem nant of the om phalom esenteric duct that typically regresses by the seventh week of gestation

Diagnosis Signs and Symptoms

Pa ge 2 9 8





General: o

Fever

o

Malaise

o

Weakness

o

Fatigue

Gastrointestinal: o



Abdom inal pain: 

Location depends on cause



Appendicitislike

o

Vom iting

o

Changes in bowel m ovem ents

o

Hem atochezia

o

Melena

o

Peritonitis and septic shock (late com plications)

Cardiovascular: o

Tachycardia (owing to pain or blood loss)

o

Hypotension and shock (owing to bleeding)

Essential Workup 

May cause a variety of signs and sym ptom s: o

Fewer than 10% diagnosed preoperatively

o

Consider in patient with recurrent nonspecific abdom inal pain, nausea and vom iting, or rectal bleeding.



History/physical exam narrow diagnosis, but will not give specific findings for Meckel diverticulum .



Rectal exam m andatory



Nasogastric (NG) tube placem ent: o

Most com m on cause of lower GI bleeding is upper GI bleeding.

Tests Lab

Pa ge 2 9 8



CBC: o

Decreased hem atocrit owing to bleeding

o

Rarely a cause of chronic anem ia

o

Leukocytosis with diverticulitis/gangrene/perforation



Electrolytes, BUN, creatinine, glucose



Type and screen when significant GI bleeding.

Imaging 

Abdom inal radiographs: o

No value in diagnosing Meckel diverticulum

o

Elim inates other causes of abdom inal pain or GI bleeding



Technetium -99m pertechnetate radioisotope scan: o

Noninvasive scan that identifies Meckel diverticulum containing heterotopic gastric m ucosa

o

Ninety percent accurate in children

o

Forty-five percent accurate in adults

P.679



Sm all bowel enteroclysis: o

75% accuracy

o

Barium /m ethyl cellulose introduced through NG tube into distal duodenum or proxim al jejunum

o

Increases the ability to detect Meckel diverticulum in adults

o

Diverticulum m ay be short and wide-m outhed, m aking diagnosis difficult.





Barium enem a: o

Introduces fluid into distal sm all bowel

o

Look for diverticulum .

Angiogram for further evaluation of Meckel diverticulum if radioisotope scan and enteroclysis norm al:

Pa ge 2 9 8

o

Blood supply is not always abnorm al.



Ultrasound m ay be useful in nonbleeding presentations.



Laparoscopic evaluation m ay provide both diagnosis and definitive treatm ent.



ECG: o

Elim inate m yocardial ischem ia as cause of abdom inal pain.

o

With significant blood loss

Differential Diagnosis 



Adults: o

Appendicitis

o

Volvulus

o

Bowel obstruction

o

Diverticulitis

o

Adhesions

o

Internal hernias

o

Upper GI bleeding

o

Hem orrhoids

o

Inflam m atory bowel disease

o

Pseudom em branous colitis

o

Polyps

o

Intussusception

Pediatric: o

Intussusception

o

Volvulus

o

Atresia

o

Strictures

o

Malrotation

o

Adhesions

o

Milk allergy

o

Gastroenteritis

o

Henoch-SchÃ¶nlein purpura

Pa ge 2 9 8

o

Hem olytic-urem ic syndrom e

o

Anal fissures

o

Polyps

Treatment Initial Stabilization 

Stabilization followed by early surgical evaluation



Hypotension: o

Aggressive fluid resuscitation

o

Packed RBC transfusion with brisk rectal bleeding (m ore com m on in children)

o

Pressors for septic shock



NG tube



Foley



Preoperative antibiotics



NPO

Medication (Drugs) 

Am picillin sulbactam (Unasyn): 3 g (peds: 100â€“200 m g am picillin/kg/24h) q8h IV



Cefoxitin (Mefoxin): 1â€“2 g (peds: 100â€“160 m g/kg/24h) IV q6h



Dopam ine: 2â€“20 Âµg/kg/m in IV

Follow-Up Disposition

Pa ge 2 9 8

Admission Criteria Presum ptive diagnosis of Meckel diverticulum with diverticulitis, obstruction, intussusception, hem orrhage, or volvulus requires adm ission and surgical evaluation.

Discharge Criteria None

References 1. D'Agostino J. Com m on abdom inal em ergencies in children. Em erg Med Clin North Am . 2002;20:139â€“153. 2. Ham oui N, Docherty SD. Gastrointestinal hem orrhage: is the surgeon obsolete? Em erg Med Clin North Am . 2003;21:1017â€“1056. 3. McCollough M, Sharieff GQ. Abdom inal surgical em ergencies in infants and young children. Em erg Med Clin North Am . 2003;21:909â€“935.

Codes ICD10 Q43.0

Pa ge 2 9 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M edial C o llateral Ligam ent Strain

Medial

Collateral Ligament Strain Richard A. Craven

Basics Description Most com m only injured knee ligam ent

Etiology 

Direct traum a to lateral knee



Most com m on: valgus stress with external rotary com ponent on flexed knee:



o

From catching a ski tip

o

Side tackle (football)

When accom panied by other ligam ent injury: o

Hyperextension with external rotation (anterior cruciate ligam ent [ACL] and posterior cruciate ligam ent [PCL] injured first)

o

Anterior stress (ACL injured first)

Pediatric Considerations 

Medial collateral ligam ent (MCL) attaches distal to tibial epiphysis and proxim al to fem oral epiphysis.



Isolated MCL injury infrequent before growth plate closure

Pa ge 2 9 8

(<14 years old) 

MCL injury m ay accom pany underlying fracture.



Most injuries owing to direct traum a producing valgus stress (sports, autoâ€“pedestrian)

Diagnosis Signs and Symptoms 

Tearing sensation and im m ediate pain in m edial aspect of knee: o

Medial pain and tenderness m ay be m ore pronounced with partial tears than with com plete tears.



Localized swelling: o

Hem arthrosis signifies tear of capsular portion of MCL or cruciate injury.



Variable ability to bear weight: o

May be able to bear weight with com plete tear

o

Patients often describe buckling sensation on weight bearing.

o

Additional findings with involvem ent of other ligam ents

History 

Mechanism of injury



Weight bearing or rotational forces increase likelihood of m eniscal injury.



Valgus strain stresses MCL.

Physical Exam N/A

Complete Knee Examination 

Palpate m edial fem oral condyle (m ost com m on site for

Pa ge 2 9 8

MCL tear). 

Valgus stress testing: o

In flexion: Grasp lateral aspect of knee and abduct while externally rotating at ankle with knee in 30Â° of flexion.



o

In extension: sam e as above but with knee extended

o

Joint laxity

Classification of ligam ent injuries (sprains): o

Grade 1: stretched fibers without tear; firm end point on stress testing

o

Grade 2: extracapsular fibers tear without com plete rupture; m ild instability but firm end point on stress testing; inability to extend knee fully

o

Grade 3: com plete rupture; no fixed end point on stress testing; hem arthrosis

o

Check function of deep peroneal nerve.

o

First dorsal web space sensation

o

Ankle and toe dorsiflexion

Alert 

Underlying fracture should be ruled out before stress test.



Exam ine ipsilateral hip and ankle.



Re-exam in >24 hours m ay be necessary if severe m uscle spasm and pain present.



Intra-articular instillation of anesthetic and analgesic m ay be required to perform adequate exam .

Essential Workup 

Com plete knee exam ination



Check for concom itant neurovascular injuries.

Tests Imaging

Pa ge 2 9 8



Standard radiographs give no clues to MCL tears, but can reveal fractures, effusions, tendon calcifications, osteophytes, and foreign bodies:



o

Views: AP, lateral, oblique, notch view

o

Fatâ€“fluid level is pathognom onic of fracture.

MRI accurately detects collateral ligam ent injuries and other intra-articular structures and disorders (m enisci, ACL, PCL, osteonecrosis, occult fractures).



Arteriogram s to evaluate vascular integrity for severe associated injuries (e.g., knee dislocation)



Ultrasound useful to diagnose cysts and popliteal artery aneurysm s

Diagnostic Procedures/Surgery 

Aspiration of joint effusion m ay be therapeutic (relieve pain) and diagnostic (hem arthrosis with cruciate tears, fat globules with fractures).



Arthroscopy used by consultant for diagnosis and repair of m eniscal and cruciate injuries

Differential Diagnosis 

Meniscal, other ligam ent injuries, and fractures m ay be concom itant.



Hip injury m ay present with knee pain.



Arthritis (rheum atoid, osteoid, septic), cellulitis, bursitis

Pediatric Considerations 

Exam ine hip and obtain radiograph if any concern for hip pathology (especially slipped capital fem oral epiphysis).



Epiphyseal plate tenderness m ay signify nondisplaced Salter I fracture.

P.681

Pa ge 2 9 8

Treatment Pre Hospital Im m obilize in slight flexion.

Alert 

Evaluate for knee dislocation.



Docum ent neurovascular status.



MCL injury m ay be overlooked in the m ultiple traum a victim .

Initial Stabilization Maintain joint im m obilization in neutral position or position of com fort by prehospital personnel.

ED Treatment 

Grade 1 or 2: interm ittent ice, elevation, rest, crutches, com pression (splint or knee im m obilizer)



Grade 3: as grade 1 or 2, but requires definitive orthopedic referral



Joint aspiration of large hem arthrosis m ay help relieve pain.

Medication (Drugs) 

Nonsteroidal anti-inflam m atory drugs (NSAIDs) recom m ended



Narcotic analgesics as needed



Joint installation of anesthetic (e.g., bupivacaine 0.25%, 5 m L) with an analgesic (e.g., m orphine 1â€“5 m g diluted to 30 m L) m ay be required for severe pain.

Pa ge 2 9 9

Follow-Up Disposition Admission Criteria To m anage severe associated injuries

Discharge Criteria 

Absence of associated injuries requiring adm ission



Ensure com pliance with splinting and adequate follow-up.

Issues for Referral 

Grade 1 or 2 sprain: prim ary care physician or orthopedic physician within 2â€“4 weeks



Grade 3 sprain: orthopedic physician urgent referral

References 1. Casazza BA, Young JL, Rossner KK. Musculoskeletal disorders of the lower lim bs. In: Braddom RL, Buschbacher RM, eds. Physical Medicine and Rehabilitation. 2nd ed. Philadelphia: WB Saunders; 2000:840â€“841. 2. Gray SD, Kaplan PA, Dussault RG. Im aging of the knee: current status. Orthop Clin North Am . 1997;28(4):643â€“658. 3. Sherk HH. Injuries of the knee. In: Fleisher GR, Ludwig, eds. Textbook of Pediatric Em ergency Medicine. 4th ed. Philadelphia: Lippincott William s & Wilkins; 2000. 4. Sim on R, Koenigsknecht SJ. Soft tissue injuries and disorders of the knee. In: Em ergency Orthopedics: The Extrem ities. 4th ed. New York: McGraw-Hill; 2001:453â€“461. 5. Sm ith BW, Green GA. Acute knee injuries. Part II: diagnosis and treatm ent. Am Fam Physician. 1995;51:799â€“806. 6. Stewart C. Knee injuries: diagnosis and repair. Em erg Med Rep.

Pa ge 2 9 9

1997;18(1):112.

Codes ICD9-CM 844.1

ICD10 S83.7

Pa ge 2 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M edial M eniscus Injury

Medial Meniscus

Injury Charles S. Graffeo

Basics Description 

Am ong m ost com m on adult knee injuries



Medial m eniscus injury 10 tim es m ore com m on than lateral



Sudden rotary m otion of knee associated with squatting, pivoting, turning, and bending.



Com m on in those sports with low stance positions: o

Wrestling and football

o

Occupations such as carpet installers and plum bers

Etiology 

Medial m eniscus is m ore firm ly attached to the joint capsule: o

Less m obile than the lateral m eniscus

o

Predisposing it to injury when tensile/com pressive forces are applied



Tears are the result of tensile or com pressive forces between the fem oral and tibial condyles: o

With knee flexion, the fem ur rotates internally on the

Pa ge 2 9 9

flexed tibia, displacing the m edial m eniscus toward the center of the joint. o

With rapid forceful extension, the m eniscus m ay be trapped centrally, resulting in peripheral segm ent stretching or tear.

o

Extension of the tear m ay result in a free segm ent that m ay becom e displaced into the joint, resulting in a true locked joint.

Diagnosis Signs and Symptoms 

Usually present within 24 hours of acute injury



May report hearing a pop, feeling a tear, catch, lock, or a click



Usually occurs with rotational force, often when knee is flexed

History 

Patient m ay recall the knee â€œgiving way.â€•



Inability to fully extend knee is com m on.



Effusion found in 50% and usually occurs over 6â€“12 hours



Pain often interm ittent/localized to the joint line



Unlike ligam entous injury, patients often report com pletion of activities at tim e of injury.

Physical Exam 

Physical exam ination with special attention to joint line tenderness: o

High predictive value of 75â€“85% and neurovascular system

Pa ge 2 9 9



Effusion is found in 50% and is typically delayed in onset.



Inability to extend the joint at 20â€“45Â° secondary to true or pseudo locking is a com m on finding.

Essential Workup 

Lim itation of extension owing to severe pain from m uscle spasm /effusion suggests pseudo locked joint



True locked joint from torn fragm ent within the joint occurs in only 30%.



Provocative testing should be deferred until severe pain resolves: o



McMurray, Apley, Steinm ann, Childress, and Helfet

Recent system atic review concludes that physical diagnostic tests have low diagnostic accuracy.

Tests Lab If arthrocentesis perform ed, send joint fluid for cell count, protein and glucose, gram stain, culture, and crystals, as indicated.

Imaging 

Plain radiograph m ay dem onstrate effusion or associated bony abnorm alities.



MRI has replaced arthrography: o

Diagnostic accuracy greater than 90â€“98%, depending on type of injury

Diagnostic Procedures/Surgery 

Arthroscopy the standard for diagnostic accuracy



Arthrocentesis: o

May afford significant sym ptom atic relief when effusion is present

o

Aspiration of bloody fluid suggests cruciate ligam ent tear or injury to peripheral vascular part of

Pa ge 2 9 9

m eniscus.

Differential Diagnosis 

Osteochondral fractures



Osteochondritis dessicans



Patellofem oral joint syndrom es



Anterior and posterior cruciate ligam ent injury



Medial/lateral collateral ligam ent injury



Iliotibial band syndrom e



Lum bar radiculopathy



Gout and other inflam m atory arthropathies

P.683

Treatment Pre Hospital 

Application of ice packs



Im m obilization in a position of com fort



Careful neurovascular exam ination



Assess for dislocations and associated injuries.

Initial Stabilization Assess for significant associated injuries.

ED Treatment 

Arthrocentesis m ay afford relief with large effusions and assist in reducing locked joint.



Arthrocentesis should be followed by application of com pressive dressing.



Reduction of locked joint should be perform ed within first

Pa ge 2 9 9

24 hours after injury: o

With patient seated, hang extrem ity off edge of exam ination table at 90Â°. 

o

This alone m ay reduce locked joint.

Applying gentle traction and rotation of tibia usually result in reduction of the locked joint.



Nonsteroidal anti-inflam m atory drugs, both parenteral and oral



Weight bearing and range of m otion are perm itted as tolerated.



Individuals unable to bear weight or those with severe restriction of range of m otion m ay be placed in a knee im m obilizer or crutches as needed.



Definitive treatm ent by orthopedic consultant: o

Operative vs. nonoperative treatm ent is dependent on m ultiple factors.

Medication (Drugs) 

Nonsteroidal anti-inflam m atory m edications



Supplem ent with narcotic analgesia for breakthrough pain

Follow-Up Disposition Admission Criteria 

Intractable pain is suggestive of true locked joint and m ay require em ergent orthopedic consult.



Evidence of potential for neurovascular com prom ise



High-risk elderly patients unable to m anage splinting

Pa ge 2 9 9

devices

Discharge Criteria 

Patients capable of following a structured discharge plan



No com orbid conditions likely to negatively im pact outcom e

Issues for Referral Refer all patients for close orthopedic follow-up

References 1. Antosia RE, Lyn E, Marx J. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 2. Koski JA. Meniscal injury and repair: clinical status [Review]. Orthop Clin North Am . 2000;31:419â€“436. 3. Sim on RR, Koenigsknecht SJ, Em ergency Orthopedics the Extrem ities. 4th ed. McGraw-Hill2001. 4. Scholten RJ. The accuracy of physical diagnostic tests for assessing m eniscal lesions of the knee: a m eta-analysis. J Fam Pract. 2001;50:938â€“944. 5. Solom on DH. The rational clinical exam ination: does this patient have a torn m eniscus or ligam ent of the knee? JAMA. 2001;286:1610â€“1620.

Codes ICD9-CM 959.7

Pa ge 2 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M Ã©niÃ¨ re Disease

MÃ©niÃ¨re

Disease Charles V. Pollack Jr.

Basics Description 

Episodic vertigo, hearing loss, tinnitus, and aural fullness sensation, although all sym ptom s m ay not be present sim ultaneously



Estim ated to affect about 0.1% of United States. population



Affects m en and wom en equally



Fam ily history in greater than 7%



May develop at any age: o



Peak incidence between the ages of 20 and 50 years

Classically unilateral, but m ay be bilateral in up to 40% of cases



Characterized by recurrent, interm ittent attacks or rotatory vertigo, decreased hearing, tinnitus, and sensation of aural pressure



Attacks occur with little or no warning



Persists from 5 m inutes to several hours



Close clustering of attacks m ay occur

Pa ge 2 9 9



Hearing loss is progressive over tim e, sensorineural in nature, and initially involves lower frequencies.

Etiology 

Endolym phatic hydrops: o

Progressive dilation of the endolym phatic space

o

Thought to be overproduction or reduced absorption of endolym phatic fluid

o

Long-term therapy directed at decreasing production or enhancing drainage of endolym ph



Im m une m echanism : o

Im m une com plex deposition in endolym phatic sac in patients with MÃ©niÃ¨re disease

o

Autoantibodies directed against endolym phatic sac in sera of MÃ©niÃ¨re patients

Diagnosis A diagnosis of exclusion

Signs and Symptoms History 

Unilateral ear fullness and pressure



Decreased hearing



Tinnitus



Vertigo: o

Intense and whirling in nature

o

Reaching m axim um intensity within m inutes, slowly subsides over hours



Horizontal nystagm us, often with a rotational com ponent



Nausea and vom iting

Physical Exam

Pa ge 3 0 0



Patient typically lies with the affected ear up and avoids looking toward the norm al side because doing so exaggerates the nystagm us and dizziness.



Must exclude central CNS lesion, peripheral pathology in ear (ruptured TM, cholesteatom a, cerum en im paction, etc)

Essential Workup 

Com plete history and neurologic exam



Patients with central vertigo or focal neurologic findings require neuroim aging



Focal findings include new unilateral hearing loss, usually with tinnitus

Tests Lab None routinely helpful

Imaging CT or MRI of brain: 

Indicated for any patient with focal neurologic findings or central vertigo



The m ost im portant diagnosis to exclude is acoustic neurom a

Diagnostic Procedures/Surgery Patients with MÃ©niÃ¨re disease require audiom etry and electronystagm ography (ENG) testing, but these tests are not necessary to the ED evaluation.

Differential Diagnosis 

Otologic: o

Chronic suppurative otitis m edia

o

Benign positional vertigo

o

Acoustic neurom a

o

Vestibular neuronitis

Pa ge 3 0 0



o

Otosclerosis

o

Otic capsule dysplasia

System ic: o

Vertebrobasilar insufficiency or stroke

o

Basilar m igraine

o

Epilepsy

o

Multiple sclerosis

o

Paget disease

o

Thyroid disease

o

Drugs/m edications

o

Autoim m une disorders

o

Syphilis

o

Head injury

o

CNS lesion

P.685

Treatment Pre Hospital 

Vertigo and neurologic sym ptom s can represent a stroke: o

Rapid transport to ED



Protect patient from falling



Maintain in com fortable position



IV isotonic fluids for patients with vom iting



Monitor for dysrhythm ia

Initial Stabilization 

IV hydration with isotonic fluids



Benzodiazepines

Pa ge 3 0 0



Antiem etics, benzodiazepines

ED Treatment Supportive therapy

Medication (Drugs) 



Sym ptom atic: o

Diazepam : 5â€“10 m g PO, PR, or IV

o

Lorazepam : 0.5â€“2.0 m g PO, IV, or IM

o

Meclizine: 12.5â€“25 m g PO q8h

o

Metoclopram ide: 10 m g IV or IM

o

Prom ethazine: 10â€“25 m g PO, PR, IV or IM.

Therapeutic (patients with established diagnosis of MÃ©niÃ¨re disease): o

Acetazolam ide: 250 m g PO daily

o

Furosem ide: 20 m g PO daily

o

Hydrochlorothiazide (HCTZ): 25â€“50 m g PO daily

o

Triam terene: 100 m g PO daily

Follow-Up Disposition Admission Criteria 

Central cause of vertigo



Patients refractory to ED therapy

Discharge Criteria 

Patient with norm al neurologic exam ination



Sym ptom s adequately controlled in ED



Refer to neurology or ear-nose-throat clinic for outpatient

Pa ge 3 0 0

audiom etry and ENG testing. 

Recurrent attacks are typical.



Restrict sodium , tobacco, caffeine, and alcohol intake.



Avoid driving, operating dangerous equipm ent, and working at heights until attacks have resolved and sedating m edications have been withdrawn.

Issues for Referral 

Persistent sym ptom s



Concern for ear pathology

References 1. Jam es A: MÃ©niÃ¨re's disease. Clin Evid. 2004;11:664â€“672. 2. Kim HH. Trends in the diagnosis and m anagem ent of MÃ©niÃ¨re's disease. Otolaryngol Head Neck Surg. 2005;132:722â€“726. 3. Knox GW, McPherson A. MÃ©niÃ¨re's disease: differential diagnosis and treatm ent. Am Fam Physician. 1997;55:4:1185â€“1190. 4. Saeed SR. Diagnosis and treatm ent of MÃ©niÃ¨re's disease. Br Med J. 1998;316:368â€“372. 5. Thai-Van, et al. MÃ©niÃ¨re's disease pathophysiology and treatm ent. Drugs. 2001;61:8:1089â€“1102.

Miscellaneous SEE ALSO: Dizziness

Codes ICD9-CM 388.31 386.00 386.10 386.20

Pa ge 3 0 0

ICD10 H81.0

Pa ge 3 0 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M eningitis

Meningitis

Austen Chai Patricia Shipley

Basics Description CNS infection

Etiology 

Bacterial: o

Neonates: group B streptococcus, gram -negative bacilli, Listeria species infection

o

Children/adults: Streptococcus pneum oniae, Neisseria m eningitides, Haem ophilus influenzae (now rare owing to vaccination)

o

Elderly/alcoholic: S. pneum oniae, gram -negative bacilli, Listeria species infection

o

Neurosurgical patients: staphylococcus- and gram -negative organism s

o

Transplant recipients and dialysis patients: rising incidence of Listeria species infection

o

AIDS: as above, plus tuberculosis, syphilis



Viral



Fungal



Chem ical, drug, or toxin induced

Pa ge 3 0 0

Pediatric Considerations 

Pneum ococcus m ost com m on cause of bacterial m eningitis



Pneum ococcal vaccine now part of childhood im m unization schedule



Dexam ethasone reduces sensorineuronal hearing loss caused by H. influenzae.



Meningitis does not present as uncom plicated febrile seizure.

Diagnosis Signs and Symptoms General 

Fever



Meningism us: o

Kernig: flexed knee resists extension (bilateral).

o

Brudzinski: flexion of neck produces flexion at hips.



Confusion/altered m ental state



Headache



Photophobia



Papilledem a



Focal CNS abnorm alities



Seizures



Petechial rash (m eningococcal)



Associated infections: sinusitis, otitis, pneum onia

Infant/Pediatric 

Fever or hypotherm ia



Lethargy



Weak suck



Vom iting/dehydration

Pa ge 3 0 0



Respiratory distress



Irritability



Bulging fontanel



Meningism us: com m only absent when <12 m onths old

Elderly and Immunocompromised 

Confusion with or without fever



Less striking sym ptom s

Essential Workup 

Initiate treatm ent im m ediately based on clinical suspicion



Give antibiotic therapy if at all possible after blood cultures but before other diagnostic procedures.



Routine CT before lum bar puncture (LP) unnecessary, but indicated with:





o

Im m unodeficiency/HIV

o

History of CNS disease (abscess, bleed, m ass lesion)

o

History of seizure <7 days

o

Focal neurologic deficit

o

Dim inished consciousness/m entation/com atose

o

Older than 60 years

o

Papilledem a

LP: o

Do not delay antibiotics for LP

o

Do not delay LP unless: 

Risk for herniation (see above)



Unstable patient



Overlying soft tissue infection

Cerebrospinal fluid (CSF) analysis: o

Cell count and differential

o

Gram stain, culture and sensitivity

o

Protein and glucose

o

Opening pressure

Pa ge 3 0 0

o

Acid fast and fungal stains

o

Latex agglutination: 

Useful if patient with prior antibiotic treatm ent



Best if urine and blood also tested



Detects: m eningococcus, pneum ococcus, group B streptococcus, H. influenzae, E. coli, cryptococcus

o

Polym erase chain reaction: 

Useful for virus and bacteria



Highly sensitive and specific for herpes sim plex virus (HSV)

o

Repeat cell count as needed for traum atic tap.

o

Interpretation: 

Culture is diagnostic.



Greater than 5 WBC/m L is highly sensitive for m eningitis.



Cell count m ay be norm al in HIV/AIDS.



Neonatal considerations: up to 25 WBC/m L m ay be norm al, norm al protein up to 120â€“170 m g/dL

o

o

Typical bacterial m eningitis: 

WBC >100 (usually 1,000â€“20,000)



Differential >80% PMNs



Protein >200 m g/dL



Glucose <40% of serum

Typical viral m eningitis: 

WBC <2,000



Differential: initially polym orphonuclear neutrophils (PMNs), then after 24 hours, predom inantly lym phocytes



Protein <200 m g/dL



Glucoseâ€”norm al

Pa ge 3 0 0

o

o

Typical fungal m eningitis: 

WBC <500



Differentialâ€”lym phocytes



Protein >200 m g/dL



Glucoseâ€”low

Typical tuberculosis m eningitis: 

WBC range, 100â€“400



Differentialâ€”m ixed



Proteinâ€”variable



Glucoseâ€”variable

Tests Lab 

Blood and urine culture



Serum C-reactive protein: o

Useful for gram -negative m eningitis in pediatric patients

o

Elevated levels very suggestive of bacterial m eningitis



CBC



Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), and platelet: o

Obtain before LP in severe sepsis or dissem inated intravascular coagulation (DIC)



Electrolytes/glucose: o

Serum -to-CSF glucose ratio

o

Assess for m etabolic acidosis.



Toxicology studies as needed



Urinalysis



Chest radiograph: pneum onia, tuberculosis

Differential Diagnosis 

Encephalitis

Pa ge 3 0 1



Brain, spinal, epidural abscess



Febrile seizure



CNS/system ic lupus erythem atosus (SLE) cerebritis



Intracranial bleed



Prim ary or m etastatic CNS m alignancy



Stroke



Venous sinus throm bophlebitis



Traum a



Toxic/m etabolic

P.687

Treatment Pre Hospital Adm inister prophylactic antibiotics to any close personal contacts of patient diagnosed with m eningococcal m eningitis: 



Adults: o

Rifam pin: 600 m g PO b.i.d. for 2 days, or

o

Ciprofloxacin: 500 m g PO single dose, or

o

Ceftriaxone: 250 m g IM (if pregnant)

Children: o

Ceftriaxone: 125 m g IM, or

o

Rifam pin: 5 m g/kg if <1 m onth old and 10 m g/kg if >1 m onth old

Initial Stabilization 

Isolate patient.



Airway protection, oxygen as needed



0.9% norm al saline (NS) bolus to treat dehydration and

Pa ge 3 0 1

hypotension 

Consider dexam ethasone: o

Hydrocortisone for severe hypotension caused by Waterhouse-Friderichsen syndrom e (m eningococcem ia)



Antibiotics: o

Obtain blood cultures and adm inister antibiotics prom ptly.

o

Do not delay to obtain LP or CT unless absolutely necessary.

ED Treatment Empiric Antibiotic/Steroid Selection for Bacterial Infection 

Neonate: o

Am picillin plus (cefotaxim e or am inoglycoside) plus vancom ycin



Age 1â€“3 m onths: o

Am picillin plus ceftriaxone or cefotaxim e plus vancom ycin



Children >3 m onths: o



Adults: o



Ceftriaxone plus vancom ycin plus dexam ethasone

Ceftriaxone 2 g q12h plus vancom ycin 1 g q12h

Older than 50 years/alcoholism /im m une im paired: o

Ceftriaxone 2 g q12h plus vancom ycin 1 g q12h plus am picillin 2 g q4h



CNS surgery/shunt/traum a: o

Vancom ycin 1 g q6hâ€“q12h plus m eropenem 2 g q8h or ceftazidim e 2 g q8h

Other

Pa ge 3 0 1



Dexam ethasone: o

Give with or just before first antibiotic dose when possible.

o

Benefit shown for children and against H. influenzae

o

Reduces risk of death or persistent neurologic deficits in adults with bacterial m eningitis

o

Not effective, possibly toxic in patients without bacterial m eningitis

o

Give with antibiotics if patient has altered m ental status or with focal neurologic deficit.

o

Add if CSF is cloudy, has positive Gram stain, or >1,000 WBC/m m 3

o

Dosage: 10 m g IV q6h for 4 days (m ax. 16 doses) for adults

o

Discontinue when bacterial m eningitis has been excluded.



Vancom ycin: o

Add when concerned about penicillin-resistant pneum ococci.



Cefotaxim e m ay be used in place of ceftriaxone.



Meropenem : o

Alternative choice for children >3 m onths old and adults



Vancom ycin plus (aztreonam or chloram phenicol) plus Bactrim : o

Consider only for severe penicillin allergy (i.e., anaphylaxis).



o

Do not delay therapy for lesser allergy history.

o

Consult infectious disease specialist.

Aztreonam : o

May use in place of cephalosporins in patients allergic to penicillin

Pa ge 3 0 1

Medication (Drugs) 

Am ikacin: (peds: 7.5 m g/kg IV q8h)



Am picillin: 2 g (peds: 50â€“100 m g/kg q6hâ€“q8h) IV q4h



Aztreonam : 2 g (peds: 30 m g/kg) IV q6hâ€“q8h



Bactrim : 4â€“5 m g/kg TMP IV q12h



Cefotaxim e: 75 m g/kg IV q8h



Ceftazidim e: 2 g IV q8h



Ceftriaxone: 2 g (peds: 50â€“100 m g/kg) q12h



Chloram phenicol: 1 g (peds: 25 m g/kg) IV q6h



Dexam ethasone: 0.4 m g/kg IV q12h for 2 days



Gentam icin: (peds: 2.5 m g/kg IV q8h)



Hydrocortisone: 100â€“300 m g IV



Meropenem : 40 m g/kg q8h



Tobram ycin: (peds: 2.5 m g/kg IV q8h)



Vancom ycin: 1 g (peds: 15 m g/kg q6h) q6hâ€“q12h

Follow-Up Disposition Admission Criteria 

All known or suspected cases of bacterial infections



Im m unocom prom ised host



Any toxic-appearing patient

Discharge Criteria 

Clear viral infection with well-controlled sym ptom s



Thorough and specific discharge instructions



Careful follow-up plan discussed with prim ary care physician

Pa ge 3 0 1

References 1. De Gans J, van de Beek D. Dexam ethasone in adults with bacterial m eningitis. N Engl J Med. 2002;347:1549â€“1556. 2. Goldm an L, ed. Cecil Textbook of Medicine. 21st ed. Philadelphia: WB Saunders; 2000: 1645â€“1654. 3. Hasbun R, et al. Com puted tom ography of the head before lum bar puncture in adults with suspected m eningitis. N Engl J Med. 2001;345:1727â€“1733. 4. Pong A, Bradley JS. Bacterial m eningitis and the newborn infant. Infect Dis Clin North Am . 1999;13:711â€“733. 5. Preventing pneum ococcal disease am ong infants and young children. Recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Recom m Rep. 2000;49(RR-9):1â€“35. 6. Tunkel AR, et al. Practice guidelines for m anagem ent of bacterial m eningitis. Clin Infect Dis. 2004;39:1267â€“1284.

Codes ICD9-CM 320 047.9

ICD10 G03.9

Pa ge 3 0 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M eningo co ccem ia

Meningococcemia

Ann Buchanan

Basics Description 

Acquired from close contact with an infected individual or an asym ptom atic carrier by inhalation of airborne nasopharyngeal droplets carrying the bacteria



Bacteria attach to and enter nasopharyngeal epithelial cells.



Bacteria spread from the nasopharynx through the bloodstream via entry of vascular endothelium .



Most circulating m eningococci are elim inated by the spleenâ€”som e penetrate endothelial cells at other sites to cause infection (m eninges, synovium , conjunctivae).



Meningococci produce an endotoxin (lipooligosaccharide): o

involved in pathogenesis of the skin, adrenal m anifestations, and vascular collapse



Hum an oropharynx/nasopharynxâ€”only reservoir



Carrier usually has developed im m unity to serotype-specific antibody (not im m une to all serotypes): o

Age <5 years: 1% carrier rate

o

Age 20â€“40 years: 30â€“40% carrier rate

o

Lower rate of im m unity in children, which is reflected

Pa ge 3 0 1

by the higher rates of infection 

Most com m on in fall and spring



Increased incidence in m ilitary recruits/close living conditions



Epidem icsâ€”ages 5â€“9 years m ost/earliest affected

Etiology 

Neisseria m eningitidis: o

Serotypes A, B, C, D, H, I, K, L, X, Y, Z, 29E, and W135

o

Serotype B m ost com m on in United States

o

More than 95% of infections caused by A, B, C, Y, and W135



Available vaccines offer protection against serotypes A, C, Y, W135 (consider in epidem ics)

Pregnancy Considerations The safety of m eningococcal vaccine is unclear in pregnancy.

Diagnosis Signs and Symptoms â€œMildâ€• Meningococcemia 

Most com m on



Preceded by upper respiratory infection (URI)



Fever, chills, m yalgias/arthralgias, m alaise



Often self-lim ited, resolving in several days



Can progress to m eningitis (m ortality rate, 2â€“10%) or overwhelm ing sepsis without m eningitis

Overwhelming Meningococcal Sepsis 

Ten percent of overall m eningococcem ia cases

Pa ge 3 0 1



High m ortality rate (20â€“60%)



Most deaths occur in first 48 hours.



Sudden onset of illness and rapid progression of clinical course



Initial presentation m ay be m ild: o

Mild tachycardia

o

Mild tachypnea/respiratory sym ptom s

o

Mild hypotension



Fever, chills, vom iting, headache, rash, m uscle tenderness



Toxic appearing



Infants: lethargy, poor feeding, bulging fontanel



Rash: o

Com bination of purpura/ecchym osis: 

May later exhibit coalescence, necrosis/sloughing of the involved skin (purpura fulm inans)

o

Petechiae (over skin, m ucous m em branes, conjunctivae) seen in 50â€“60%

o

Macules

o

Papules (scrapings of papules dem onstrate the organism on Gram stain)



Deteriorate quickly over several hours: o

Hypotension/shock

o

Acidosis

o

Acute respiratory distress syndrom e (ARDS)

o

Dissem inated intravascular coagulation (DIC)



Meningitis m ay or m ay not be present.



Waterhouse-Friderichsen syndrom e:



o

Bilateral hem orrhagic destruction of adrenal glands

o

Vasom otor collapse

Acute renal failure: o

From prolonged hypotension (low renal perfusion

Pa ge 3 0 1

causing acute tubular necrosis)

Chronic Meningococcemia 

Uncom m on



Well appearing



Recurrent fevers, chills, arthralgias over weeks to m onths



Interm ittent rashâ€”alone or in com bination with: o

Purpura

o

Petechiae

o

Macules

o

Papules



Splenom egaly (20%)



Meningococcal m eningitis (25%): o

Headache

o

Fever

o

Neck stiffness

o

Confusion

o

Lethargy

o

Obtundation

Septic Arthritis 

Occurs during active m eningococcem ia



Multiple joints involved



Joint pain, redness, swelling, effusion, fever, chills



Extrem ely lim ited or no range of m otion

Other Meningococcal Infections 

Occur with m eningococcal infection elsewhere



Conjunctivitisâ€”m ay occur alone



Sinusitis



Panophthalm itis



Urethritis



Salpingitis



Prostatitis

Pa ge 3 0 1



Pneum onia



Myocarditis/pericarditis: o

Occurs late in onset

o

Usually associated with serogroup C

Essential Workup 

Do not allow workup (including delay in lum bar puncture) to postpone adm inistration of antibiotics in suspected cases of m eningococcem ia.



Suspect diagnosis in setting of dram atic clinical presentation.



Gram stain and culture of: o

Peripheral blood, cerebrospinal fluid (CSF), sputum , urine, joint aspirate, or petechial/papular scrapings

o

Gram stain: intracellular or extracellular gram -negative diplococci

Tests Lab 

CBC: o

Elevated WBC initially, later m ay be suppressed in severe disease

o

Decreased platelet count when large areas of purpura/petechiae or DIC



Electrolytes, BUN, creatinine, glucose



CSF: o

Gram stain, culture, protein and glucose, cell count with differential

o

Consistent with bacterial infection in m eningococcal m eningitis



Arterial blood gases for acidosis, hypoxia



Fibrinogen levels, fibrin degradation products, prothrom bin tim e (PT), partial throm boplastin tim e (PTT) if DIC

Pa ge 3 0 2

suspected 

Throat/nasopharyngeal swab o

Positive swab does not establish the diagnosis of m eningococcem ia.



Analysis of buffy-coat layer of peripheral blood for bacteria if sepsis is suspected



Blood culture: o

Often negative with chronic m eningococcem ia

o

Positive in m ild and overwhelm ing m eningococcem ia



Im m unoassays (beware false negatives)



Polym erase chain reaction (PCR), especially useful when antibiotics given before specim en collection

Imaging Chest radiograph: 

If pneum onia suspected



For the source of m eningococcal sepsis



To rule out ARDS

Diagnostic Procedures/Surgery Am putations and dÃ©bridem ent of necrotic tissue and/or extrem ities m ay be necessary. P.689

Differential Diagnosis 

Viral exanthem



Vasculitis



Mycoplasm a



Rocky Mountain spotted fever



Toxic shock syndrom e



Henoch-SchÃ¶nlein purpura



Idiopathic throm bocytopenic purpura (ITP)

Pa ge 3 0 2



Dengue fever



Dissem inated gonococcal infection



Influenza



Streptococcus group A and B



Throm botic throm bocytopenic purpura

Treatment Pre Hospital Postexposure prophylaxis needed for prehospital personnel in close contact with patient

Initial Stabilization 

Wear m ask and gloves, observe droplet precautions.



Notify Departm ent of Health.



Airway, breathing, and circulation m anagem ent (ABCs)â€”im m ediate endotracheal intubation for severe acidosis, hypoxia, or decreased m ental status: o

Hyperventilate to treat acidosis (target PCO 2 about 25)



Treat hypotension: o

0.9% norm al saline (NS) bolus of 20 m L/kg; cautious rehydration with ARDS, congestive heart failure

o

Begin dopam ine or norepinephrine (epinephrine if no response) if hypotensive after 2 L of IV fluids.



Naloxone, thiam ine, dextrose (Accu-Chek) for altered m ental status



Initiate IV antibiotics: o

First line: high-dose penicillin (proven m eningococcem ia) or third-generation cephalosporin (broader coverage pending definitive diagnosis)

Pa ge 3 0 2

o

Second line: am picillin

o

Third line: chloram phenicol (penicillin-allergic patients)

Overwhelming Meningococcal Sepsis 

Severe acidosis (pH <7.0â€“7.1 or serum HCO 3 <8â€“10) o

Adm inister IV NaHCO 3 along with hyperventilation.



Insert Foley catheter to m onitor urine output.



Place in respiratory isolation.



High-dose steroids: o

To protect against cranial nerve injury in the setting of ongoing infection (controversial)

o 

Adm inister with adrenal gland injury.

DIC treatm ent: o

Adm inister fresh frozen plasm a and platelet transfusions.

o

Heparin not indicated unless significant throm botic com plications evident clinically (e.g., cyanosis or cold digits, low urine output despite adequate volum e status, and blood pressure)

Mild Meningococcemia 

Initiate IV antibiotics im m ediately.



Adm ission in respiratory isolation

Prophylaxis Options for Close Contacts 

Ideally, prophylaxis should be given within first 24 hours.



Ten-day window of observation



Rifam pin: 600 m g (10 m g/kg) PO q12h for 4 doses



Single-dose ceftriaxone: o

125 m g IM for age <12 years

o

250 m g IM for age >12 years



Single-dose ciprofloxacin: 500 m g PO adults only



Serogroup-specific vaccine as adjunct only

Pa ge 3 0 2

Vaccine 

Vaccine recom m ended in m ilitary recruits, travelers to endem ic areas, com plem ent-deficient or asplenic patients, first-year college dorm itory residents



Vaccine against group C also recom m ended for groups of older children and adults in periods of group C m eningococcal outbreaks



Vaccine m ay be used in group A outbreaks for children as young as 3 m onths.

Medication (Drugs) 

Am picillin: 2â€“3 g (peds: 200â€“400 m g/kg/24h) IV q6h



Cefotaxim e: 2 g (peds: 200 m g/kg/24h) IV q6h



Ceftriaxone: 2 g (peds: 80â€“100 m g/kg/24h) IV q12h



Chloram phenicol: 50â€“100 m g/kg/24h IV q6h (m ax. 4 g/d)



Ciprofloxacin: 500 m g PO



Dexam ethasone: 0.15 m g/kg IV for pediatric m eningitis



Dopam ine: 5â€“20 Âµg/kg/m in IV titrate to blood pressure (BP)



Epinephrine: 2â€“10 Âµg/m in IV titrate to BP



Heparin: 3,000â€“5,000 IU (peds: 80 IU/kg) IV bolus followed by 600â€“1,000 IU/h (peds: 18 IU/kg/h) IV drip



Hydrocortisone (Solu-Cortef): 100 m g (peds: 2 m g/kg) bolus IV for adrenal insufficiency q8h



Norepinephrine: 0.5â€“30 Âµg/m in IV titrate to BP



Penicillin G: 24 m IU/d (peds: 250,000 IU/kg/24h) IV divided q4h: o

Prophylaxis: 250 m g (peds: 25â€“37.5 m g/kg) IM single dose

Pa ge 3 0 2



Rifam pin: 600 m g (peds: 5â€“10 m g/kg) PO b.i.d. for 2 days



Sodium bicarbonate: 2â€“5 m Eq/kg (peds: 0.5â€“1.0 m Eq/kg) IV over 30 m inutes to 4 hours

Follow-Up Disposition Admission Criteria 

ICU adm ission for overwhelm ing sepsis with respiratory isolation



Respiratory isolation adm ission for m ild m eningococcem ia

Discharge Criteria Prophylaxis for close patient contacts

References 1. Apicella M. Neisseria m eningitidis. In: Mandell GL, ed. Principles and Practice of Infectious Disease. 5th ed. New York: Churchill Livingstone; 2000. 2. Cartwright K. Early m anagem ent of m eningococcal disease. Infect Dis Clin North Am . 1999;13(3):661. 3. Centers for Disease Control and Prevention. Control and prevention of m eningococcal disease and control and prevention of serogroup C m eningococcal disease: evaluation and m anagem ent of suspected outbreaks: recom m endations of the Advisory Com m ittee on Investigation Practices (ACIP). MMWR Morb Mort Wkly Rep. 1997;46(RR-5). 4. Leclerc F, Leteurtre S, Crem er R, et al. Do new strategies in m eningococcem ia produce better outcom es? Crit Care Med. 2000;28(9 suppl): S60â€“63.

Pa ge 3 0 2

5. Mahm ud Javid. Meningococcem ia. 2005 Jan 6. Available at http://www.em edicine.com /m ed/topic1445.htm . Accessed 2005 April 15. 6. Rosenstein NE. Update on Haem ophilus influenzae serotype B and m eningococcal vaccines. Pediatr Clin North Am . 2000;47(2):337.

Miscellaneous SEE ALSO: Meningitis

Codes ICD9-CM 36.2

ICD10 A34.0

Pa ge 3 0 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ercury Po iso ning

Mercury Poisoning

Keri L. Carstairs David Tanen

Basics Description Mercury: 

Three form s: elem ental, inorganic salts, and organic



Reacts with sulfhydryl groups, causing enzym e inhibition and alterations in cellular m em branes



Binds to phosphoryl, carboxyl, am ide, and am ine groups of enzym es

Etiology 

Exposure usually thorough gastrointestinal tract and inhalation and less frequently derm al exposure



Exposure through m anufacturing of chlorine and caustic soda, diuretics, antibacterial agents, antiseptics, therm om eters, batteries, fossil fuels, plastics, paints, jewelry, lam ps, explosives, fireworks, vinyl chloride, and pigm ents



Exposure through taxiderm y, photography, dentistry, m ercury m ining



Contam inated seafood

Pa ge 3 0 2

Diagnosis Signs and Symptoms 

Naturally occurring m ercury is converted into three prim ary form s, each with its own toxicologic effects:



Elem ental m ercury: o

Usually inhalation exposure; subcutaneous and intravenous exposures are less com m on.

o

Considered nontoxic from oral ingestion

o

Sym ptom s from inhalation occur within hours: 

Cough and dyspnea, which m ay progress to pulm onary edem a



Metallic taste, salivation



Weakness, nausea, diarrhea, fever, headaches, visual disturbances

o

Subcutaneous deposits m ay present as granulom as or abscesses.

o

Intravenous exposure presents with sym ptom s consistent with pulm onary em bolization.

o

Subacute sym ptom s: 



Ataxia, weakness, and paresthesias

Inorganic salts: o

Owing to acute ingestion

o

Gastrointestinal caustic: 

Abdom inal pain with nausea, vom iting, and diarrhea



Metallic taste, sore throat



Hem orrhagic gastroenteritis with hem atochezia and hem atem esis

o

Acute tubular necrosis

o

Acrodynia (pink disease):

Pa ge 3 0 2

o 



Idiosyncratic, occurs m ainly in children



Painful extrem ities

Pink discoloration with desquam ation

Organic m ercury: o

Acute versus chronic ingestion

o

Historically, infants exposed in wom b are m ost severely affected (Minam ata Bay, Japan)

o

May see GI sym ptom s acutely

o

Delayed CNS toxicity predom inates and m ay take weeks to m onths to m anifest: 

Paresthesias



Ataxia



Paralysis



Visual field constriction



Dysarthria



Hearing loss



Mental deterioration



Death

Essential Workup Whole blood m ercury level: 

Norm al blood <10 ug/dL



Blood levels are useful in acute intoxications and organic m ercury exposures, but m ay be unreliable in chronic exposures or recent seafood ingestion.

Tests Lab 

Per patient com plaint and clinical condition



Abdom inal pain, gastrointestinal bleeding: o

CBC

o

Electrolytes, BUN, creatinine, glucose

o

PT/PTT/INR

Pa ge 3 0 2





Trem ors, neuropsychiatric effects: o

CBC with peripheral sm ear

o

Electrolytes, BUN, creatinine, glucose

o

Lum bar puncture

24-hour urine m ercury collection o

Norm al urine levels <20 ug/dL

o

Spot urines are not diagnostic.

Imaging 

Chest radiograph: o

For noncardiac pulm onary edem a

o

Evidence of intravenous m ercury in pulm onary vascular tree



Abdom inal radiograph: o

For presence of m ercury with intentional oral ingestion



Head CT: o

May detect cerebellar atrophy

Differential Diagnosis 

Multisystem involvem ent often confused with other heavy-m etal intoxications



Cerebrovascular accident



Senile dem entia/Alzheim er disease



Parkinson disease



Peptic ulcer disease



Gastrointestinal bleeding



Pancreatitis



Sepsis



Late inhalation: o

Em physem a

o

Pneum othorax

o

Acute respiratory distress syndrom e

Pa ge 3 0 3

P.691

Treatment Pre Hospital 

Rem ove from toxin exposure.



Decontam ination: o



Wash exposed skin

For altered m ental status: o

Dextrose

o

Thiam ine

o

Naloxone (Narcan)

o

Oxygen

Initial Stabilization 

Secure airway, breathing, and circulation (ABCs) and m onitoring.



0.9% norm al saline (NS) intravenous fluid resuscitation for hypotension: o

Blood transfusion for significant gastrointestinal hem orrhage



Naloxone, D 5 0 W, thiam ine for altered m ental status

ED Treatment 

Elem ental m ercury: o

For inhalation exposure, observe closely for several hours for developm ent of noncardiogenic pulm onary edem a.

o

Ingested elem ental m ercury passes through norm al intestinal tract with m inim al absorption.

Pa ge 3 0 3

o

Consider chelation for sym ptom atic patients with oral dim ercaptosuccinic acid (DMSA).

o 

Abscess drainage with incision and drainage

Inorganic salt ingestion: o

Adm inister activated charcoal.

o

Perform gastric lavage for recent ingestion as indicated.

o

Aggressive 0.9% NS intravenous fluid resuscitation/blood products for hypovolem ic shock: 

o

Hydrate and m aintain urine output (1 m L/kg/h).

Consider chelation with IM dim ercaprol (British antilewisite [BAL]): 

Early adm inistration m ay avert severe renal injury.

o

Oral DMSA efficacy lim ited secondary to severe gastrointestinal sym ptom s



Organic m ercury: o

Perform gastric lavage and adm inister activated charcoal.

o

Provide sym ptom atic care as needed.

o

Consider chelation with oral DMSA.

Medication (Drugs) 

Dextrose D 5 0 W: one am pule: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Dim ercaprol (BAL): 5 m g/kg IM once, then 2.5 m g/kg q8hâ€“q12h for 1 day, then 2.5 m g/kg q12hâ€“q24h for 7â€“10 days



Dim ercaptosuccinic acid (DMSA): 10 m g/kg PO q8h for 5 days, then q12h for 2 weeks



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV/IM initial

Pa ge 3 0 3

dose 

Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria Sym ptom atic patients

Discharge Criteria 

Asym ptom atic patients with history of ingestion of elem ental m ercury and intact intestinal tract



Patients with history of inhalation exposure to elem ental m ercury who rem ain asym ptom atic after 6 hours of observation

References 1. Clarkson TW, Magos L, Myers GJ. The toxicology of m ercuryâ€”current exposures and clinical m anifestations. N Eng J Med. 2003;349:1731â€“1737. 2. Graem e KA, Pollack CV. Heavy m etal toxicity. Part I: arsenic and m ercury. J Em erg Med. 1998;16:45â€“56. 3. Sue YJ. Mercury. In: Goldfrank LR, Flom enbaum NA, Lewin RG, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. Norwalk, Conn: Appleton & Lange; 2002:1239â€“1248.

Codes ICD9-CM 985.0

ICD10 T56.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M esenteric Ischem ia

Mesenteric

Ischemia Edward A. Stettner

Basics Description 

Decreased or occluded blood flow to the intestines through he m esenteric vessels leading to ischem ic or infracted bowel



Can be from arterial or venous blockage, or low flow state



1 in 1,000 of all hospital adm issions



1â€“2% of all adm issions for abdom inal pain: o

Most cases occur in patients older than age 50 years.

o

Mortality 60â€“70%

Etiology 

Acute m esenteric arterial em bolism : o

50% of cases of acute m esenteric ischem ia

o

Mean age 70 years

o

Em boli m ost com m only arise in left atria or ventricle, from a dysrhythm ia, valvular lesions, or ventricular throm bus from a prior m yocardial infarction

o

Typically lodge 3â€“10 cm distal to the origin of the superior m esenteric artery (SMA)

Pa ge 3 0 3



Preserves blood flow to proxim al sm all and large bowel

o

Risk factors include dysrhythm ia (especially atrial fibrillation), valvular heart disease, prior m yocardial infarction, aortic aneurysm , or dissection.



Mesenteric artery throm bus: o

SMA throm bus in 15% of cases of acute m esenteric ischem ia

o

Rare in other vessels

o

Develops from plaque rupture of m esenteric atherosclerotic disease

o

50â€“80% m ay have long-standing intestinal angina (chronic m esenteric ischem ia).

o

Risk factors include age, atherosclerotic disease, hypertension.



Mesenteric venous throm bosis: o

5â€“15% of cases of acutem esenteric ischem ia

o

Subacute/indolent presentation

o

20â€“40% m ortality

o

Typically occurs in younger patients with underlying hypercoagulable state

o

Risk factors include: 

Hypercoagulable state (lupus, protein C and S deficiency





Sickle cell disease



Antithrom bin III deficiency



Malignancy



Pregnancy



Sepsis



Estrogen therapy



Recent traum a or inflam m atory conditions

Nonocclusive m esenteric ischem ia:

Pa ge 3 0 3

o

20â€“30% of cases of acute m esenteric ischem ia

o

Occurs in low cardiac output states with decreased m esenteric blood flow

o

Risk factors include congestive heart failure, sepsis, diuretic use, volum e depletion, recent surgery (especially cardiac).



Chronic m esenteric ischem ia: o

â€œIntestinal anginaâ€• 

Postprandial, diffuse abdom inal pain occurring approxim ately 1 hour after eating, lasts 1â€“2 hours



Patients m ay develop food aversions and eat sm all m eals to avoid pain.



Uncom m on causes: o

Spontaneous m esenteric arterial dissection

o

Median arcuate ligam ent syndrom eâ€”com pression of the celiac axis or SMA by the arcuate ligam ent of the diaphragm

o

Extrinsic com pression from tum ors

o

Medications: 

Digitalis



Ergotam ine



Cocaine



Pseudoephedrine



Pitressin

Diagnosis Signs and Symptoms 

Sudden onset, severe diffuse abdom inal pain in acute ischem ia:

Pa ge 3 0 3

o

Pain out of proportion to exam : 

Patients m ay have relatively benign abdom inal exam despite severe pain.



Nausea



Vom iting



Diarrhea



Occult gastrointestinal bleeding



Late findings: o

Peritoneal signs owing to irreversible bowel ischem ia

o

Abdom inal distention

o

Hypoactive bowel sounds

Essential Workup Maintain a high level of suspicion in patients older than age 50 years with unexplained abdom inal pain.

Tests Lab 

Often nonspecific and nondiagnostic



CBC: o



Chem istry panel: o



Elevated white blood cell count (90% >15,000)

Approxim ately 50% have a m etabolic acidosis.

Am ylase: o

Hyperam ylasem ia found in 50% of cases



Creatine phosphokinase (CPK) m ay be elevated.



Lactate: o

Elevated in 90% of patients

o

High levels correlate with m ortality.

Imaging 

Flat and upright abdom inal radiographs: o

Often obtained to rule out acute obstruction

Pa ge 3 0 3

o

Frequently norm al

o

Late findings 

Thum bprinting from bowel wall edem a and hem orrhage



Pneum atosis intestinalis: air in bowel wall from tissue necrosis

 

Pneum obilia

Doppler ultrasonography: o

Can detect decreased blood flow in SMA but m ore helpful in chronic m esenteric ischem ia



Abdom inal CT scan: o

Can detect bowel wall edem a, pneum atosis

o

Newer helical and m ultidetector row CT scanners can directly visualize m esenteric vascular anatom y and m ay identify em boli.

o

CT angiography becom ing m ore frequent diagnostic strategy



MRI: o

Excellent im ages of m esenteric vasculature especially with MR angiography

o 

Acquisition tim e and availability lim its utility

Angiography: o

Gold standard diagnostic m odality

o

Allows for direct visualization of em boli and adm inistration of vasodilating or fibrinolytic agents

o

Invasive, tim e consum ing, and potentially nephrotoxic

Differential Diagnosis 

Bowel obstruction



Volvulus



Gastrointestinal m alignancy



Diverticulitis

Pa ge 3 0 3



Inflam m atory bowel disease



Peptic ulcer disease



Perforated viscus



Cholecystitis



Ascending cholangitis



Pancreatitis



Appendicitis



Abdom inal aortic aneurysm



Myocardial infarction



Renal stones

P.693

Treatment Pre Hospital Initiate fluid replacem ent for dehydrated or hypotensive patients.

Initial Stabilization Fluid resuscitation

ED Treatment 

Caution: o



Early diagnosis is critical to decrease m ortality.

General m easures: o

Airway, breathing, and circulation m anagem ent (ABCs) with fluid resuscitation as needed

o

Nasogastric suction to decom press the stom ach and intestine

o

NPO

o

Electrolyte replacem ent as needed

Pa ge 3 0 3

o

Cardiac m onitor for dysrhythm ia

o

Consider invasive cardiac m onitoring if patient is unstable.

o

Monitor urine output.

o

Analgesics

o

Broad-spectrum antibiotics to cover bowel flora (m ay need to adjust dose if concom itant renal failure) 

Piperacillin/tazobactam



Am picillin/sulbactam



Ticarcillin/clavulanate



Alternatives include im ipenum , m eropenem , third-generation cephalosporins plus m tronidazole

o

Anticoagulation with heparin

o

Stat surgical consultationâ€”all patients with peritoneal signs should have exploratory laparotom y.



Specific therapies: o

Papaverine 30â€“60 m g/h intra-arterial: 

Phosphodiesterase inhibitor causes m esenteric vasodilatation.





Adm inistered through angiography catheter

o

Intra-arterial throm bolytics can be used.

o

Surgical revascularization often indicated

Caution: o

Avoid vasoconstrictive m edications, which m ay worsen ischem ia. 

If vasopressors are needed, use lowest dose possible.

Medication (Drugs) 

Am picillin/sulbactam : 3 g (peds: 100â€“200 m g/kg/d) IV

Pa ge 3 0 4

q6h 

Heparin sulfate: 80 units/kg IV bolus followed by 18 units/kg/h infusion



Metronidazole: 1.0 g (peds: 12 m g/kg) load IV followed by 500 m g (peds: 7.5 m g/kg) IV q6h



Piperacillin/tazobactam : 3.375 g (peds: 240â€“400 m g/kg/d) IV q6h



Ticarcillin/clavulanate: 3.1 g IV q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

Adm it all patients with m esenteric ischem ia.



Aggressive pursuit of diagnosis is m andatory.



Surgical evaluation for em ergent operative intervention

Discharge Criteria 

None

References 1. Kim AY, Ha HK. Ultrasound evaluation of suspected m esenteric ischem ia: efficacy of radiologic studies. Radiol Clin North Am . 2003;41:327â€“342. 2. Krupski WC, Selzm an CH, Whitehall TA. Unusual causes of m esenteric ischem ia. Surg Clin North Am . 1997;77(2):471â€“499. 3. Martinez JP, Hogan GJ. Mesenteric ischem ia. Em erg Med Clin North Am . 2004;22:909â€“928. 4. McKinsey JF, Gewertz BL. Acute m esenteric ischem ia. Surg Clin North Am . 1997;77(2):307â€“317.

Codes

Pa ge 3 0 4

ICD9-CM 557.0 Acute vascular insufficiency of intestine 557.1 Chronic vascular insufficiency of intestine

ICD10 K55.0 Acute vascular disorders of intestine K55.1 Chronic vascular disorders of intestine

Pa ge 3 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M etacarpal Injuries

Metacarpal

Injuries David Palafox

Basics Description 

Most m etacarpal injuries are caused by crush injuries, a direct blow with hand versus object, orburn.



Most com m on fracture is boxer's fracture of distal fifth m etacarpal neck.

Diagnosis 

Pain or swelling at the site of injury



Deform ity at the site of injury



Malalignm ent of the distal tip of the finger on flexion indicates rotational deform ity.



Lines drawn down the longitudinal axis of each digit in flexion norm ally should converge on the scaphoid volarly.



Lim itation of m ovem ent secondary to pain and anatom ic deform ity

Alert

Pa ge 3 0 4



Have a high suspicion for â€œfight bite.â€• This injury is the direct blow of a closed fist against a hum an tooth: o

Concern is violation of the extensor sheath, m etacarpophalangeal (MCP) joint, or m etacarpal head by a tooth with subsequent infection by oral flora.

Signs and Symptoms History Not all patients are truthful as to cause of injury.

Essential Workup Exam ination should pay specific attention to skin integrity and alignm ent of the distal phalanges in flexion and extension.

Tests Imaging 

Hand radiographs when fracture suspected and/or to rule out opaque foreign body



Special radiographic views (CT) of the proxim al m etacarpals and the carpom etacarpal joints m ay be necessary for patients with a suggestive physical exam and no definite fracture on a standard three-view series.

Differential Diagnosis Fracture of the m etacarpal m ay be accom panied by dislocation of adjacent phalanges or carpal bones.

Treatment Pre Hospital 

Most do not require EMS transport solely for m etacarpal

Pa ge 3 0 4

injury. 

Cautions: o

Metacarpal injuries should be splinted in position of com fort.

Initial Stabilization 

Other, m ore serious injuries should be treated first.



Im m obilize hand pending evaluation.



Lacerations should be cleaned as soon as possible, and consideration should be given to the possibility of foreign body.



Therm al burns are treated with early analgesia.

ED Treatment 

Elevation, rest, and interm ittent application of ice for the first 24 hours are appropriate treatm ent for all hand injuries (RICE).



Boxer's fractures usually have som e volar flexion of the distal fragm ent: o

Reduction should be attem pted for volar angulation of 40Â° or m ore.

o

Fractures of the fourth and fifth m etacarpals that are stable and with no significant rotational com ponent can be treated with a padded ulnar gutter splint.



Fractures of the index and m iddle finger m etacarpals are m ore difficult to stabilize: o



Radial gutter splint and early orthopedic referral

Thum b m etacarpal fractures are uniform ly com plicated and should all be referred early to a hand surgeon or orthopedist: o



Place in thum b spica splint.

Dislocations should be reduced im m ediately and splinted; m etacarpal dislocations are rare and frequently need open

Pa ge 3 0 4

reduction and pinning. P.695



Appropriate splinting position for the MCP joint is the intrinsic plus, or â€œcobraâ€• position (20â€“30Â° wrist extension): o

MCP joint as close to 90Â° of flexion as possible

o

Proxim al interphalangeal (PIP) and distal interphalangeal (DIP) joints in extension



Antibiotics for oral flora should be started early for any open injury to the m etacarpals suspicious for injury against a tooth and m ay require curettage of the im paction site in the operating room .



Sim ple torus (buckle) fractures m ay be splinted and m ay be followed by a prim ary care physician.

Medication (Drugs) 

Check for tetanus status and vaccinate per im m unization schedule.



Silvadene cream or bacitracin ointm ent is appropriate for therm al burn injury.



Analgesics m ay be necessary; nonsteroidal anti-inflam m atory drug (NSAID) or hydrocodone is usually sufficient.



For hum an bites or dirty wounds, adm inister am oxicillin/clavulanate (Augm entin), or o

A cephalosporin or other penicillinase-resistant antibiotic given parenterally is appropriate.

Pa ge 3 0 4

Follow-Up Disposition Admission Criteria 

Open fractures or dislocations require urgent surgical intervention and should be adm itted.



All thum b m etacarpal fractures or dislocations should be seen by an orthopedist or hand surgeon because of the special im portance of the thum b in all activities of the hand.



Infection from a bite wound requires prom pt orthopedic consultation, adm ission for irrigation, dÃ©bridem ent, and intravenous antibiotics.

Discharge Criteria 

Patients with a stable transverse or oblique fracture in a good splint m ay be discharged for early orthopedic follow-up.



Metacarpal-carpal dislocations are usually unstable enough to require surgery even if reduction is achieved, but this m ay be sem iurgent rather than em ergent.



If a m etacarpal fracture produces im paired range of m otion or m isalignm ent of the finger, the patient will require surgical repair in the first several days after injury.

Pediatric Considerations Epiphyseal injuries m andate orthopedic referral.

References 1. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 3rd ed. New York: Churchill Livingstone; 1990.

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2. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990. 3. Am erican College of Radiology, Expert Panel on Musculoskeletal Im aging. Acute Hand and wrist traum a. 2001. 4. Harrison B, Holland P. Diagnosis and m anagem ent of hand injuries in the ED. Em erg Med Pract. 2005;7(2):.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ethano l Po iso ning

Methanol

Poisoning Kirk Cumpston

Basics Description 

Colorless, volatile liquid



Absorbed in 30â€“60 m inutes



Metabolized by liver



Half-life 4â€“8 hours



Mechanism : o

Inebriating

o

Nontoxic

o

Metabolites of form aldehyde and form ic acid produce toxic effects.

o 

Uncouples oxidative phosphorylation

Form ic acid level determ ines degree of acidosis, visual sym ptom s, and m ortality.



Form ic acidâ€”directly toxic to retinal and optic nerve tissue



Methanol m etabolism : o

Step 1: m ethanol converted to form aldehyde by liver enzym e alcohol dehydrogenase

Pa ge 3 0 4

o

Step 2: form aldehyde then rapidly converted by aldehyde dehydrogenase to form ic acid

o

Step 3: form ic acid is degraded to carbon dioxide and water by folate-dependent m echanism .

o

Steps 1 and 3 are rate-lim iting steps.

Etiology 



Com m on sources of m ethanol: o

Wood alcohol

o

Windshield washer fluid

o

Inhalational abuse of carburetor cleaners

Fuel antifreeze solutions: o

Form alin

o

Gasoline

o

Paint solvents

o

Household cleaners



Sterno cans



Moonshine

Diagnosis Signs and Symptoms 



GI: o

Anorexia

o

Nausea/vom iting

o

Abdom inal pain

CNS: o

Headache

o

Dizziness

o

Confusion

o

Inebriation

Pa ge 3 0 5



o

Com a

o

Seizures

Ophthalm ologic: o

Blurry vision

o

Photophobia

o

â€œSnow fieldsâ€•

o

Mydriasis

o

Blindness

o

Optic disc: 

Hyperem ia or pallor



Papilledem a

Essential Workup 

History of all substances ingested



Inquire about visual sym ptom s.



Funduscopic exam ination



Drawn sim ultaneously: o

Arterial blood gas (ABG)

o

Serum m ethanol, ethylene glycol, isopropyl alcohol, and ethanol levels

o

Electrolytes, BUN, creatinine, and glucose

o

Measured serum osm olality (by freezing-point depression is preferred)

Tests Lab 

Calculate anion gap = (Na + ) â€“ (Cl - + HCO 3 - ): o



Norm al = 8â€“12.

Determ ine serum osm ol gap: o

Osm ol gap = m easured osm olality - calculated osm olarity: 

Calculated osm olarity = 2(Na + ) + glucose/18 + BUN/2.8 + ethanol (in m g/dL)/4.6.

Pa ge 3 0 5



Traditionally an osm ol gap >10 is considered indication for ruling out occult m ethanol ingestion. However, potentially toxic serum concentrations of m ethanol can be present with osm ol gap <10.

o

Osm ol gap: 

Screens for m ethanol



Most sensitive early in poisoning and norm alizes as m ethanol is m etabolized



Serum m ethanol concentrations confirm m ethanol poisoning: o

However, if presentation is late after ingestion, no parent com pound m ay be detected and generally concom itant severe high anion gap m etabolic acidosis will be present.



Ethanol concentration: o

Determ ines am ount of ethanol bolus necessary to obtain therapeutic level

o

Ethanol concentration m ay have clinical im plications and is pertinent in interpreting laboratory tests.

Differential Diagnosis 

Increased osm ol gap: ME DIE A o

Methanol

o

Ethanol

o

Diuretics/Diluents (m annitol, glycerin, sorbitol, propylene glycol),



o

Isopropyl alcohol

o

Ethylene glycol

o

Acetone, am m onia

Elevated anion gap m etabolic acidosis: ACAT MUDPILES o

Alcoholic ketoacidosis

o

Cyanide, CO, H 2 S, others

Pa ge 3 0 5

o

Acetam inophen in fulm inant hepatic failure

o

Toluene

o

Methanol, m etform in

o

Urem ia

o

Diabetic ketoacidosis

o

Paraldehyde, phenform in, propylene glycol

o

Iron, INH

o

Lactic acidosis

o

Ethylene glycol

o

Salicylate, acetylsalicylic acid (ASA; aspirin), starvation ketosis

Treatment Pre Hospital Transport all substances that the patient m ay have ingested.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Dextrose, naloxone, and thiam ine for altered m ental status

Prevent Further Methanol Absorption 

Gastric lavage will likely not be helpful because of rapid absorption of m ethanol and delay in presentation >1 hour.



Ipecac-induced em esis not recom m ended



Activated charcoal: o

For potential coingestants

o

Poorly adsorbs m ethanol

Prevent Methanol Conversion to Toxic Metabolites

Pa ge 3 0 5



4-Methylpyrazole (4-MP, fom epizole, Antizol): o

Com petitive inhibitor of alcohol dehydrogenase

o

FDA approval for use in m ethanol poisoning

o

Indications for fom epizole therapy: 

Intentional m ethanol ingestion



Accidental m ethanol ingestion of m ore than a sip



Altered m ental status or visual sym ptom s associated with unexplained osm ol gap and/or elevated anion gap m etabolic acidosis

P.697

o

Initiate before serum m ethanol concentration returns if intentional ingestion or m ore than a sip.

o

Advantages: 

No need for continuous infusion



No inebriation/CNS depression



Ease of dosing



No hypoglycem ia, no hyponatrem ia, no hyperosm olality



No checking serum concentrations



Reduced nursing care and m onitoring



Occult m ethanol exposure can often be ruled out before second dose is needed.

 o



Class C in pregnancy

Disadvantages: 

Initial cost of product



Blurry vision



Transient elevation of LFTs

Ethanol therapy: o

Not FDA approved for treatm ent of m ethanol

Pa ge 3 0 5

o

Initiate before m ethanol level returns if potentially toxic ingestion is highly suspected or confirm ed by history.

o

Ethanol has greater affinity than m ethanol for alcohol dehydrogenase.

o

Slows m etabolism to form aldehyde and form ic acid by com petitive inhibition

o

Indications for ethanol therapy: 

Intentional m ethanol ingestion



Accidental m ethanol ingestion of m ore than a sip



Altered m ental status or visual sym ptom s associated with unexplained osm ol gap and or elevated anion gap m etabolic acidosis

o

Therapeutic range is 100â€“150 m g/dL.

o

Continue until m ethanol level is <25 m g/dL.

o

Advantages:

o



Cost of product



Easily accessible



Oral and IV routes

Disadvantages: 

CNS depression



Respiratory depression



Hyponatrem ia or hypernatrem ia



Hypoglycem ia



Hyperosm olarity



Continuous infusion



Frequent laboratory testing



Labor intensive



Contraindicated in pregnancy



Exacerbation of m edical conditions (e.g., GI ulcers, gastritis, hepatitis, pancreatitis, GI

Pa ge 3 0 5

bleeding) 

Drug interactions

Enhance Elimination of Methanol and Its Toxic Metabolites 

Hem odialysis: o

Decreases elim ination half-life of m ethanol

o

Rem oves form aldehyde and form ic acid

o

Indications: 

Ingestion of >1 m L/kg of 100% m ethanol



Ophthalm ologic m anifestations



Severe m etabolic acidosis unresponsive to bicarbonate therapy

o



Persistent electrolyte or fluid im balance



Renal insufficiency



Serum m ethanol level >25 m g/dL

Continue hem odialysis until m ethanol level approaches zero.



Folic acid and folinic acid (leucovorin): o

Folic acid: cofactor required for conversion of form ic acid to carbon dioxide and water

o

Folinic acid: activated form of folic acid, used only for initial dose

o

Supplem ental folate im portant in m alnourished individuals (alcoholics)

Correct Acid-Base Abnormalities Sodium bicarbonate for severe acidosis (pH <7.1)

Medication (Drugs) 

4-Methylpyrazole: o

Loading dose: 15 m g/kg slow infusion over 30

Pa ge 3 0 5

m inutes o

Maintenance dose: 10 m g/kg q12h for 4 doses, then 15 m g/kg q12h until m ethanol levels reduced <25 m g/dL

o

Dosing related to hem odialysis: 

Do not adm inister dose at beginning of dialysis if last dose was <6 hours previously.



Adm inister next dose if last dose was >6 hours previously.



Dose q4h during dialysis.



If tim e between last dose and end of dialysis was <1 hour from last dose, do not adm inister new dose.



If tim e between last dose and end of dialysis was 1â€“3 hours from last dose, adm inister one half of next scheduled dose.



If tim e between last dose and end of dialysis was >3 hours from last dose, adm inister next scheduled dose.



Ethanol: o

Oral: 50% ethanol solution (100-proof liquor) via nasogastric tube (NGT): 

Loading dose 2 m L/kg



Maintenance dose 0.5 m L/kg/h



Maintenance dose during hem odialysis 1 m L/kg/h

o

IV: 10% ethanol in D 5 W: 

Loading dose 8 m L/kg over 30â€“60 m inutes



Maintenance infusion 2 m L/kg/h



Maintenance infusion during hem odialysis 4 m L/kg/h

o

Folic acid: 50 m g IV q4h for 24 hours

Pa ge 3 0 5

o

Folinic acid: 1â€“2 m g/kg/IV

o

Sodium bicarbonate: 1â€“2 m Eq/kg in 1 L of D 5 W with 40 m Eq KCl at 250 m L/h

o

Thiam ine: 100 m g IV

Follow-Up Disposition Admission Criteria 

Significant historical m ethanol ingestion even if initially asym ptom atic



ICU adm ission for seriously ill patients



Transfer to another facility if hem odialysis or antidote is indicated but not readily available.

Discharge Criteria Asym ptom atic patient with isolated m ethanol ingestion if serum m ethanol level is <25 m g/dL; norm al acid/base status and electrolytes.

References 1. Brent J, McMartin K, Phillips S, et al. Fom epizole for the treatm ent of m ethanol poisoning. N Engl J Med. 2001;344:424â€“429. 2. Hovda KE, Froyshov S, Gudm undsdottir H, et al. Fom epizole m ay change indication for hem odialysis in m ethanol poisoning: prospective study in seven cases. Clin Nephrol. 2005;64(3):190â€“197. 3. Jacobsen D, McMartin KE. Antidotes for m ethanol and ethylene glycol poisonings. J Toxicol Clin Toxicol. 1997;35(2):127â€“143. 4. Leikin J, Paloucek F. Methanol. Fom epizole. Alcohol. In: Leikin JB, Paloucek F, eds. Leikin and Paloucek's Poisoning and Toxicology

Pa ge 3 0 5

Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:201â€“202, 599â€“600, 810â€“812. 5. Sham m a A. Toxic alcohols. In: Goldfrank Flom enbaum , Lewin, et al., eds. Goldfrank's Toxicological Em ergencies. 7th ed. New York: McGraw-Hill; 2002:980â€“990.

Codes ICD9-CM 980.1

ICD10 T51.1

Pa ge 3 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ethem o glo binem ia

Methemoglobinemia Gerald Maloney

Basics Description 

Iron m olecule in hem oglobin is oxidized from Fe 2 + to Fe 3 + , resulting in a form of hem oglobin that cannot transport oxygen.



Oxygen-carrying capacity of blood is reduced and cyanosis is generally present with significant levels.



Norm al m ethem oglobin levels are â‰¤1%; sym ptom s usually occur with levels >20%.



Methem oglobin: o

Oxidation of hem oglobin iron from ferrous (Fe 2 + ) to ferric (Fe 3 + ) state

o

Decreases total oxygen-carrying capacity (functional anem ia)

o

Shifts hem oglobin oxygen-dissociation curve to the left, im pairing 0 2 release to tissues

o

Maintained at physiologic level (1â€“2%) by nicotinam ide adenine dinucleotide (NADH)-m ethem oglobin (cytochrom e B 5 ) reductase in RBCs

Pa ge 3 0 6



Congenital m ethem oglobinem ia: o

NADH-m ethem oglobin (cytochrom e B 5 ) reductase deficiency (hom ozygous or heterozygous)

o

Heterozygous hem oglobin M and other abnorm al hem oglobins



Acquired m ethem oglobinem ia results from oxidant stress on RBCs: o

Som e m ethem oglobin-inducing agents are direct oxidants (e.g., nitrites)

o

Many substances produce oxidant injury via N -hydroxylam ine m etabolites.

o

Methem oglobinem ia m ay be delayed relative to initial substance exposure.



Many m ethem oglobin-inducing agents also cause Heinz body hem olytic anem ia (HA): o

Caused by oxidant injury of RBC proteins

o

Glucose-6-phosphate dehydrogenase (G6PD)â€“deficient patients have higher risk.

o

Patients with m ethem oglobinem ia should be worked up for HA.



Methem oglobinem ia m ay serve as m arker for genetic abnorm alities: o

Heterozygous NADH-m ethem oglobin (cytochrom e B 5 ) reductase deficiency

Etiology 

More serious with coexisting anem ia



Cyanide (CN) antidote kit: o

Induces m ethem oglobinem ia via am yl and sodium nitrite

o

CN will preferentially com plex with m ethem oglobin, which can then be chelated by sodium thiosulfate.



Nitrates/nitrites (m ost com m on):

Pa ge 3 0 6

o

Nitrites (NO 2 )

o

Nitrates (NO 3 ), e.g., nitroglycerine, via m etabolic conversion to nitrites

o 











Nitric oxide (NO)

Dyes: o

Aniline dyes

o

Methylene blue (excessive)

Antiparasitic drugs (high potential for MetHb form ation): o

Dapsone

o

Prim aquine

o

Chloroquine

Local anesthetics (high potential for MetHb form ation): o

Benzocaine

o

Lidocaine

o

Prilocaine

Analgesics: o

Phenazopyridine (Pyridium )

o

Phenacetin

Antibiotics: o

Nitrofurantoin

o

Sulfones

o

Sulfonam ides

Others: o

Metoclopram ide

o

Naphthalene (m othballs)

o

Paraquat (herbicide)

o

Arsine gas (AsH 3 )

o

Chlorates (ClO 4 )

o

Phenols (e.g., dinitrophenol, hydroquinone)

Pa ge 3 0 6

Diagnosis Signs and Symptoms 

Central cyanosis, refractory to oxygen adm inistration: o

Cyanosis evident at m ethem oglobin (MetHb) of 10% to 15% of total hem oglobin in nonanem ic patient (or 1.5 g m ethem oglobin/dL blood)



Dyspnea/tachypnea



Chest pain/dysrhythm ias



Syncope



Altered m ental status with levels >50%

Essential Workup 

Thorough history: o

Exposure to m ethem oglobin-inducing agent

o

All substances ingested and tim e(s) of ingestion

o

G6PD deficiency

o

Medical conditions vulnerable to im paired oxygen delivery (e.g., coronary artery disease)



Physical exam : o

Cyanosis

o

Em phasis on m ental status and cardiovascular findings

o

Icterus or dark-colored urine with accom panying hem olytic anem ia



Pulse oxim etry is inaccurate in m ethem oglobinem ia. o

MetHb interferes with pulse oxim etry m easurem ent of hem oglobin oxygen saturation.

o

Saturation decreases to approxim ately 85% with increasingly m ore severe m ethem oglobinem ia.

o 

Pulse oxim etry cannot be used to guide m anagem ent.

Arterial blood gas (ABG) for: o

Methem oglobin level

Pa ge 3 0 6



o

Carboxyhem oglobin level

o

PaO 2 and PaCO 2

ECG

Tests Lab 

Blood classically described as chocolate-colored



CBC with m anual differential count and sm ear analysis for evidence of hem olytic anem ia



Urinalysis for blood versus intact RBCs to detect presence of free hem oglobin in urine

P.699

Imaging 

Chest radiograph to rule out other pulm onary pathology



ECG

Differential Diagnosis 

Hypoxia: o

Congestive heart failure (CHF)

o

Chronic obstructive pulm onary disease (COPD)

o

Pulm onary em bolism



Irritant gas exposure



Blue discoloration: o

Hypoxia

o

Sulfhem oglobinem ia

o

Cyanide poisoning

o

Hydrogen sulfide poisoning

o

Excess m ethylene blue adm inistration

o

Tellurium toxicity

o

Skin contact/staining with blue dye

Pa ge 3 0 6

Treatment Pre Hospital 

Bring to hospital all substances patient m ay have ingested.



Question witnesses and observe scene for household products and other potential coingestants: o

Docum ent and relay findings to em ergency m edical staff.



Com m ercial or industrial sites: o

Obtain relevant Material Safety Data Sheets (MSDSs) if available to identify com m ercial or chem ical products.

o

Avoid derm al exposures.

Initial Stabilization 



Airway, breathing, and circulation m anagem ent (ABCs): o

Cardiac m onitor

o

Isotonic crystalloids as needed for hypotension

Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status



Supplem ental oxygen

ED Treatment 

Decontam inationL o

If owing to acute ingestion/overdose within previous 1â€“2 hours, and protective airway reflexes are intact, adm inister 75 g of activated charcoal PO.



Rem ove source of oxidant stress.



Methylene blue: o

Indications: 

Asym ptom atic with levels >30%

Pa ge 3 0 6



Sym ptom atic patients with levels >10â€“20%, especially if coâ€“m orbid diseases are present

o

Expect transient worsening of saturations on pulse oxim etry after m ethylene blue is adm inistered: 

o

No specific intervention required

Use with caution in patients with glucose-6 pyruvate decarboxylase deficiency: 



May cause hem olysis

If no im provem ent with m ethylene blue, consider that source of oxidant stress is not elim inated, or that sulfhem oglobinem ia is present: o

Sulfhem oglobin is sulfur m olecule bound to hem oglobin; presents sim ilar to m ethem oglobin, but is self-lim ited



RBC transfusion: o

May be necessary to increase blood oxygen-carrying capacity

o 

Exchange transfusion: o



Especially if hem olytic anem ia is present

Especially with neonates/infants

Hyperbaric oxygen therapy: o

Increases oxygen delivery to tissues by m ass effect, independent of hem oglobin

o

Use in life-threatening m ethem oglobinem ia if im m ediately available.

Pediatric Considerations 

Children m ay develop significant m ethem oglobinem ia from apparently m inor ingestions.



Sym ptom s delayed several hours after ingestion, so prolonged observation necessary



Neonates also at higher risk of m ethem oglobinem ia (owing to decreased stores of NADH m ethem oglobin reductase)

Pa ge 3 0 6

Medication (Drugs) 

Dextrose 50%: 25 g (50 m L) (peds: 0.5 g/kg D 2 5 W) IV for hypoglycem ia



Methylene blue: 1 m g/kg of 1% solution IV over 5 m inutes (adult and peds): o



May repeat if no im provem ent in 1 hour

Naloxone: 0.4â€“2.0 m g (peds: 0.1 m g/kg) IV, m ay repeat up to 10 m g for suspected opioid intoxication



Thiam ine: 100 m g (peds: 1 m g/kg) IM or IV

Follow-Up Disposition Admission Criteria 

Severely sym ptom atic patients



Patients requiring m ultiple doses of m ethylene blue



Dapsone m ay cause prolonged recurrent m ethem oglobinem ia

Discharge Criteria Methem oglobin levels <20% and falling with no sym ptom s or coâ€“m orbid disease

References 1. Bradberry SM, Aw TC, William s NR, et al. Occupational Methaem oglobinem ia. Occup Environ Med. 2001;58:611â€“615. 2. Price D. Methem oglobinem ia. In: Goldfrank, Flom enbaum , Lewin, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. 2002:. 3. Ward KE, McCarthy MW. Dapsone-induced m ethem oglobinem ia.

Pa ge 3 0 6

Ann Pharm acother. 1998;32(5):549â€“553. 4. Wright RO, Lewander WJ, Woolf AD. Methem oglobinem ia: etiology, pharm acology, and clinical m anagem ent. Ann Em erg Med. 1999;34:646â€“656.

Codes ICD9-CM 289.7

Pa ge 3 0 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M itral Valve Pro lapse

Mitral Valve

Prolapse Liudvikas Jagminas

Basics Description 

Clinical syndrom e resulting from diverse pathogenic m echanism s of one or m ore portions of the m itral valve apparatus



Occurs when the leaflet edges of the m itral valve do not coapt



Com m only due to abnorm al stretching of one of the m itral valve leaflets during systole: o

Myxom atous proliferation of the spongiosa layer within the valve causing focal interruption of the fibrosa layer

o

Excessive stretching of the chordae tendineae, leading to traction on papillary m uscles



Theoretical explanations for associated chest pain: o

Focal ischem ia from coronary m icroem bolism due to platelet aggregates and fibrin deposits in the angles between the leaflets

o

Coronary artery spasm

Pa ge 3 0 6



Produces a nonejection m id-to-late systolic click heard at the apex



Mitral regurgitation m ay occur in som e patients



Age of onset is 10â€“16 years.



Wom en-to-m en ratio 3:1



Can be identified by echocardiography in 2â€“4% of the general population and in 7% of autopsies



A variety of neuroendocrine and autonom ic disturbances occur in som e patients

Genetics 

Strong hereditary com ponent



Som etim es transm itted as an autosom al dom inant trait with varying penetrance

Etiology 

Marfan syndrom e



Relapsing polychondritis



Ehlers-Danlos syndrom e (i.e., types I, II, IV)



Osteogenesis im perfecta



Pseudoxanthom a elasticum



Stickler syndrom e



System ic lupus erythem atosus



Polyarteritis nodosa



Polycystic kidney disease



Von Willebrand syndrom e



Duchenne m uscular dystrophy

Diagnosis Signs and Symptoms History

Pa ge 3 0 7



Palpitations in up to 40% of cases: o

Usually ventricular prem ature beats or paroxysm al supraventricular tachycardia

o 

Up to 40% have sym ptom s of dysautonom ia

Chest pain occurs in 10%: o

Sharp, localized, of variable duration, and nonexertional

o

Rarely m ay respond to nitroglycerin



Panic attacks



Anxiety



Fatigue



Depression in up to 70%



Nervousness



Migraine headaches



Irritable bowel



Syncope/presyncope: o

Occurs in 0.9% of patients



Orthostasis



Dyspnea and fatigue relatively uncom m on

Physical Exam 

Mid to late systolic click at the cardiac apex: o

Standing or Valsalva m oves click closer to S1.

o

S1 m ay be accentuated when prolapse occurs early in systole.

o

Squatting m oves click closer to S2.



Late systolic m urm ur



Skeletal abnorm alities are observed in two thirds of patients: o

Height-to-weight ratio greater than norm al

o

Arm span greater than height (dolichostenom elia)

o

Scoliosis

o

Pectus excavatum

Pa ge 3 0 7

o

Arachnodactyly

o

Joint hyperm obility



Hypom astia



Cathedral palate

Pediatric Considerations Dysrhythm ias, sudden death, and bacterial endocarditis have been reported.

Essential Workup 

History and auscultation of a m idsystolic click are often sufficient to m ake the diagnosis.



Echocardiography confirm s the diagnosis when clinical inform ation is insufficient.

Tests Lab Not required to establish the diagnosis

Imaging 

ECG: o

Usually norm al

o

Occasionally ST-T wave depression and inversion in leads III and aVF

o 

Prem ature atrial and ventricular contractions

Chest radiograph: o

Typically norm al

o

If m itral regurgitation is present, m ay show both left atrial and ventricular enlargem ent

o

Calcification of the m itral annulus in patients with Marfan syndrom e



Ultrasound: o

Marked superior systolic displacem ent of m itral leaflets (â‰¥2 m m above annulus) with coaptation

Pa ge 3 0 7

point at or superior to annular plane o

Chordal rupture

o

Doppler m itral regurgitation

o

Annular dilation

o

Minor criteria: 

Isolated m ild to m oderate superior systolic displacem ent of the posterior m itral leaflet



Moderate superior systolic displacem ent of both m itral leaflets

Diagnostic Procedures/Surgery 

Cardiac studies m ay be indicated in patients with chest pain when the etiology is uncertain: o

Exercise stress test

o

Myocardial perfusion scintigraphy

o

Cardiac catheterization

o

Single-photon em ission CT m yocardial perfusion im aging



Electrophysiologic testing for patients with unexplained syncope or Wolff-Parkinson-White (WPW) syndrom e

P.701

Differential Diagnosis 

Myocardial infarction/ischem ia



Hypertrophic cardiom yopathy with obstruction



Idiopathic hypertrophic subaortic stenosis



Tachyarrhythm ias



Atrial fibrillation/flutter



Ventricular septal defect



Papillary m uscle dysfunction



Hypokalem ia

Pa ge 3 0 7



Hypom agnesem ia



Valvular heart disease



Pheochrom ocytom a



Anem ia



Thyrotoxicosis



Pregnancy



Toxicity from cocaine, am phetam ines, or other sym pathom im etics



Ventricular tachycardia



WPW syndrom e



Rheum atic endocarditis



Anxiety/Panic disorder



Stress



Menopause

Treatment Pre Hospital 

ABCs



IV access



Supplem ental oxygen



Cardiac m onitoring



Pulse oxim etry

Initial Stabilization 

Cardiac m onitoring



Supplem ental oxygen



IV catheter placem ent

ED Treatment 

Pulse oxim etry



Beta-blockers

Pa ge 3 0 7

o

Patients with tachycardia or severely sym ptom atic chest pain



Digoxin is an alternative for supraventricular tachycardia and prevention of chest pain and fatigue



Antibiotic prophylaxis: o

When perform ing surgical procedures (e.g., contam inated wound repair, abscess incision and drainage)

o

o

Indicated in the following settings: 

Presence of a m urm ur



Evidence of nontrivial MR on echocardiography



Men older than 45 years with valve thickening

Prophylaxis is not suggested for patients who have an isolated click without a m urm ur or for patients without evidence of MR on an echocardiogram .

Medication (Drugs) 

Am oxicillin: 2 g PO 1 hour before the procedure (peds: 50 m g/kg PO 1 hour before procedure)



Am picillin: 2 g IV/IM 30 m inutes before the procedure (peds: 50 m g/kg IV/IM 30 m inutes before the procedure)



Clindam ycin: 600 m g PO 1 hour before procedure (peds: 20 m g/kg PO 1 hour before procedure; not to exceed 600 m g)



Propranolol: 1â€“3 m g IV at 1m g/m in, 80â€“640 m g/d PO (peds: 1â€“4 m g/kg/d PO div. b.i.d./q.i.d.



Isoproterenol: 0.02â€“0.06 m g IV Ã— 1, 0.01â€“0.02 m g IV or 2â€“20 m g/m in infusion



Atenolol 0.3â€“2 m g/kg PO daily, m ax. 2 m g/kg/d



Digoxin: 0.5â€“1 m g IV/IM div. 50% initially then 25% Ã— 2 q6hâ€“q12h or 0.125â€“0.5 m g PO daily

Pa ge 3 0 7

Follow-Up Disposition Admission Criteria 

Severe m itral regurgitation



Severe chest pain with ischem ic sym ptom s



Syncope or near syncope



Life-threatening dysrhythm ias



Cerebral ischem ic events, including transient ischem ic attack

Discharge Criteria 

Asym ptom atic



No laboratory abnorm alities



No significant m itral regurgitation or dysrhythm ias

Issues for Referral 

Cardiology consultation warranted in cases of ventricular dysrhythm ia or risk of sudden death as well as when sym ptom s of severe m itral regurgitation (MR) are present



Cardiothoracic surgery follow up is recom m ended for patients with hem odynam ically significant MR



Pilots with m itral valve prolapse m ay develop MR under positive G force and be at risk for dysrhythm ia or syncope.

References 1. Avierinos JF, Gersh BJ, Melton LJ: Natural history of asym ptom atic m itral valve prolapse in the com m unity. Circulation. Septem ber 10, 2002;106(11):1355â€“1361. 2. Bobkowski W, SiwiÃ±ska A, Zachwieja J: A prospective study to determ ine the significance of ventricular late potentials in children

Pa ge 3 0 7

with m itral valvular prolapse. Cardiol Young. July 2002;12(4):333â€“338. 3. Bonow RO, Carabello B, de Leon AC, et al. ACC/AHA guidelines for the m anagem ent of patients with valvular heart disease. Executive sum m ary. A report of the Am erican College of Cardiology/Am erican Heart Association Task Force on Practice Guidelines (Com m ittee on Managem ent of Patients With Val. J Heart Valve Dis. 1998;7(6):672â€“707. 4. Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis. Recom m endations by the Am erican Heart Association. JAMA. June 11, 1997;277(22):1794â€“1801. 5. Freed LA, Levy D, Levine RA, et al: Prevalence and clinical outcom e of m itral-valve prolapse. N Engl J Med. July 1, 1999;341(1):1â€“7. 6. Freed LA, Benjam in EJ, Levy D: Mitral valve prolapse in the general population: the benign nature of echocardiographic features in the Fram ingham Heart Study. J Am Coll Cardiol. October 2, 2002;40(7):1298â€“1304. 7. Theal M, Sleik K, Anand S: Prevalence of m itral valve prolapse in ethnic groups. Can J Cardiol. April 2004;20(5):511â€“515.

Codes ICD9-CM 349.0

ICD10 I34.1

Pa ge 3 0 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M o lluscum C o ntagio sum

Molluscum

Contagiosum Guy Tarleton Jeffrey A. Bush

Basics Description 

Molluscum contagiosum (MC) is a generally benign hum an disease characterized by m ultiple sm all, painless, pearly lesions.



MC appears on epithelial surface, spreads through close contact or autoinoculation.

Etiology 

MC is caused by a double-stranded DNA poxvirus.



Transm ission in children is by direct skin-to-skin contact, fom ites, pool or bath water.



Transm ission in adults is m ost often by sexual contact; autoinoculation com m on at any age.

Diagnosis Signs and Symptoms

Pa ge 3 0 7

History 

Incubation period: 14â€“50 days



Patients usually asym ptom atic, with occasional pruritus or tenderness



10â€“25% of patients m ay have eczem atous reaction surrounding the lesions.



Untreated lesions in im m unocom petent hosts usually resolve within several m onths, but can last up to 5 years.

Physical Exam 

Lesions are sm ooth-surfaced, firm , spherical papules, 3â€“5 m m in diam eter.



May be flesh colored, white, translucent, or light yellow



Distinctive central um bilication in 25%



Distribution in children: face, trunk, and extrem ities; healthy adults: genitals and lower abdom en; occasionally perioral; rarely on palm s and soles



MC is com m only seen with HIV infection, causing atypical involvem ent of face, neck, and trunk, lesions to 1.5 cm , and a progressive course.



Occasional intraocular or periocular involvem ent presenting as trachom a or chronic follicular conjunctivitis

Essential Workup 

History and careful skin exam ination



Skin biopsy for confirm ation

Tests Lab If anogenital, consider testing for HIV, syphilis, hepatitis B.

Differential Diagnosis 

Basal cell carcinom a, histiocytom a, keratoacanthom a, intraderm al nevus

Pa ge 3 0 7



Darier disease, nevoxanthoendotheliom a, syringom a, epithelial nevi, sebaceous adenom a



Atopic derm atitis, derm atitis herpetiform is, m ycosis fungoides, Jessner lym phocytic infiltration

Treatment Pre Hospital Maintain universal precautions.

Initial Stabilization Not applicable in routine cases

ED Treatment 

Treatm ent is aim ed at destruction or rem oval of virus-infected epithelial cells and is indicated to prevent autoinoculation and transm ission: o

Avoid being overly aggressive: Lesions are self-lim ited in im m unocom petent hosts.



Physical treatm ent m odalities generally m ost effective: o

Curettage after local anesthesia with EMLA (eutectic m ixture, lidocaine, prilocaine) or ethyl chloride

o

Cryotherapy with liquid nitrogen

o

Podophyllin, trichloroacetic acid, cantharidin, and tretinoin applied topically are variably effective.



Griseofulvin and m ethisazone orally for extensive disease have given m ixed results.



Highly active antiretroviral therapy (HAART) has been effective in reducing incidence in HIV-infected patients.



Topical im iquim od has shown effectiveness in several sm all studies.



Exam ine sexual partners for MC and other sexually

Pa ge 3 0 8

transm itted diseases: o

Patients should avoid contact sports, swim m ing pools, shared baths and towels, scratching, and shaving until lesions have resolved.



Re-exam ine treated patients for recurrence every 2â€“4 weeks; two to four treatm ents often needed to clear lesions com pletely.

P.703

Medication (Drugs) 

Cantharidin 0.9% solution with equal parts acetone and flexible collodion: apply topically one to three treatm ents every 7 days or until resolution.



Podophyllin (podofilox 0.5%): apply topically q12h for 3 days, withhold for 4 days; repeat 1-week cycle up to four tim es until resolved.



Trichloroacetic acid (50â€“80%): apply and cover with bandage 5â€“6 days.



Tretinoin 0.1%: apply topically q12h for 10 days or until resolution of lesions.



Im iquim od 2%: apply topically b.i.d. for 3â€“5 consecutive days for 16 weeks.

Follow-Up Disposition Admission Criteria

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Widespread disease with extensive superinfection in an im m unocom prom ised host

Discharge Criteria Patients without extensive superinfection m ay be safely treated as outpatients.

References 1. Allen AL, Siegfried EC. Managem ent of warts and m olluscum in adolescents. Adolesc Med. 2001;12(2):vi, 229â€“242. 2. Lewis EJ, Lam M, Crutchfield CE 3rd. An update on m olluscum contagiosum . Cutis. 1997;60(1):29â€“34. 3. Ordoukhanian E, Carrington D. Warts and m olluscum contagiosum : beware of treatm ents worse than the disease. Postgrad Med. 1997;101(2):223â€“226, 229â€“232, 235. 4. Sladden MJ, Johnston GA. Com m on skin infections in children. Br Med J. 2004;329:403. 5. Sm ith KJ, Yeager J, Skelton H. Molluscum contagiosum : its clinical, histopathologic, and im m unohistochem ical spectrum . Int J Derm atol. 1999;38(9):664â€“672.

Codes ICD9-CM 078.0

ICD10 B08.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M o no am ine Oxidase Inhibito r, Po iso ning

Monoamine Oxidase Inhibitor, Poisoning James W. Rhee

Basics Description 

Monoam ine oxidase inhibitors (MAOI) are prescribed prim arily for depression.



Selegiline, a selective m onoam ine oxidase B inhibitor, is som etim es used to treat Parkinson disease.



MAOI pharm acologic actions: o

Disruption of equilibrium between endogenous m onoam ine synthesis and degradation resulting in:





Increased neural norepinephrine levels



Downregulation of several receptor types

o

Inhibition of irreversible (noncom petitive) enzym e

o

Inhibition of other B 6 -containing enzym es

Monoam ine oxidase (MAO): principal inactivator of neural bioactive am ines: o

MAO A: 

Present in the gut and liver



Protects against dietary bioactive am ines

Pa ge 3 0 8

o

MAO B: 

Present in neuron term inals and platelets



Sym pathom im etic am ines: type of bioactive am ines

Etiology 

MAOI overdose: o

Toxicopharm acology poorly understood

o

MAO inhibitors: am phetam inelike in structure: 

Early: indirect sym pathom im etic effect



Late: sym patholytic response (hypotension seen here)



MAOI hypertensive crisis syndrom e: o

Results from im paired norepinephrine degradation, com bined with m assive norepinephrine release precipitated by exposure to an indirect- or m ixed-acting sym pathom im etic agent

o

Com m on precipitants: tyram ine, cocaine, am phetam ines



Serotonin syndrom e: o

Com m only results from exposure to com binations of agents that affect serotonin m etabolism or action

o

Agents that increase serotonin synthesis: 

o

Tryptophan

Agents that increase serotonin release: 

Indirect- and m ixed-acting sym pathom im etic agents

 o

Dopam ine receptor agonists

Agents that decrease serotonin reuptake: 

Selective serotonin reuptake inhibitors (SSRI)



Tricyclic antidepressants



Newer antidepressants: trazodone, nefazodone, venlafaxine

Pa ge 3 0 8

 o

Meperidine, dextrom ethorphan, tram adol

Agents with direct serotonin receptor agonist: 

Buspirone, sum atriptan, lysergic acid diethylam ide (LSD)

o

Agents that decrease serotonin breakdown: 

o

MAOIs

Agents that increase nonspecific serotonin activity: 

Lithium

Diagnosis Signs and Symptoms 

MAOI overdose: o

Delayed onset (12 hours)

o

Initial hypertension with headache

o

Hyperadrenergic activity:

o



Tachycardia



Hypertension



Mydriasis



Agitation

Neurom uscular excitation: 

Nystagm us



Hyperreflexia



Trem or



Myoclonus



Rigidity



Seizures

o

Hypertherm ia

o

Associated com plications: 

Rhabdom yolysis



Renal failure

Pa ge 3 0 8





Dissem inated intravascular coagulation (DIC)



Acute respiratory distress syndrom e (ARDS)

MAOI hypertensive crisis syndrom e (MAOI interaction with drug or food):



o

Hypertension

o

Tachycardia or bradycardia

o

Hypertherm ia

o

Headache, usually occipital

o

Altered m ental status

o

Intracranial hem orrhage

o

Seizures

Serotonin syndrom e (SS): o

Increased neurom uscular activity

o

Increased deep tendon reflexes: 

Lower extrem ity m ay be greater than upper

o

Trem or

o

Myoclonus

o

Rigidity (when severe)

o

Autonom ic nervous system hyperactivity: 

o

Hypertherm ia

CNS: 

Agitation



Hallucinations



Delirium



Com a

o

Diarrhea

o

SS versus neuroleptic m alignant syndrom e (NMS): 

Both present along a spectrum of severity (m ild to severe)



Onset: several hours (SS) versus days (NMS)



Gastrointestinal sym ptom s: m ay be present (SS) versus absent (NMS)

Pa ge 3 0 8



Only drug/m edication history m ay differentiate in m any cases.

Essential Workup 

History of ingested substances



Rectal tem perature m onitoring as indicated



Blood pressure/cardiac m onitoring

Tests Lab 



Urinalysis: o

Blood

o

Myoglobin

Electrolytes, blood urea nitrogen/creatinine, glucose: o

Hypoglycem ia m ay contribute to altered m ental status.

o

Acidosis m ay accom pany severe toxicity.

o

Rhabdom yolysis m ay cause renal failure.

o

Hyperkalem iaâ€”life-threatening consequence of acute renal failure



Coagulation profile to m onitor for potential DIC: o

International norm alized ration, prothrom bin tim e test, partial throm boplastin tim e test, platelets



Creatinine Kinase (CPK): o



Markedly elevated in rhabdom yolysis

Urine toxicology screen: o

May be positive for am phetam ines given the structural sim ilarities between som e MAOIs and am phetam ines



Aspirin and acetam inophen levels if suicide attem pt a possibility



Arterial blood gas

Pa ge 3 0 8

Imaging 

Chest radiograph: o



ARDS

Head CT for: o

Significant headache

o

Altered m ental status

o

Focal neurologic signs

o

For subarachnoid hem orrhage, intracerebral bleed

Diagnostic Procedures/Surgery Lum bar puncture for: 

Suspected m eningitis (headache, altered m ental status, hyperpyrexia)



Suspected subarachnoid hem orrhage and CT norm al

Differential Diagnosis 



Hypertherm ia: o

Infection

o

Hyperthyroidism

o

Heat stroke

o

Anatom ic thalam ic dysfunction

o

Neuroleptic m alignant syndrom e

o

Malignant hypertherm ia

o

Malignant catatonia

o

Ethanol or drug withdrawal

o

Anticholinergic toxicity

o

Sym pathom im etic overdose

o

Cocaine-associated delirium /rhabdom yolysis

o

Salicylate toxicity

o

Theophylline toxicity

o

Nicotine toxicity

Hypertension: o

Hypoglycem ia

Pa ge 3 0 8

o

Carcinoid syndrom e

o

Pheochrom ocytom a

o

Accelerated renovascular hypertension

o

Ethanol or drug withdrawal

o

Sym pathom im etic toxicity

P.705

Treatment Pre Hospital 

Patient m ay be uncooperative or violent.



Secure IV access.



Protect from self-induced traum a.

Initial Stabilization 

ABCs



IV access and fluid resuscitation if hypotensive



Oxygen



Cardiac m onitor



Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status

ED Treatment 

Gastrointestinal decontam ination: o

Gastric lavage if within one hour of ingestion or if clinical condition m andates endotracheal intubation

o 

Adm inister activated charcoal.

Hypertherm ia: o

Benzodiazepines if agitated

o

Active cooling if tem perature >40Â°C

Pa ge 3 0 8

o



Tepid water m ist



Evaporate with fan

Paralysis: 

Indicated if m uscle rigidity and hyperactivity contributing to persistent hypertherm ia





Nondepolarizing agent (e.g., vecuronium )



Avoid succinylcholine



Intubation; m echanical ventilation

o

Adm inister acetam inophen.

o

Apply cooling blankets.

Severe, m alignant hypertension: o

Nitroprusside (for MAOI overdose)

o

Calcium -channel blocker or phentolam ine (for MAOI/food interaction)

o

Use short-acting IV agent that can be rapidly â€œturned off.â€•

o

Phentolam ine contraindicated in MAOI overdose (results in unopposed beta agonist)





Hypotension: o

Initially bolus with isotonic crystalloid solution

o

If no response, adm inister norepinephrine.

o

Dopam ine theoretically contraindicated

Dysrhythm ias (prem orbid sign in MAOI overdose): o





Treat with lidocaine or procainam ide.

Seizures: o

Benzodiazepines

o

Barbiturates if benzodiazepines unsuccessful

o

Pyridoxine for refractory seizures

Rigidity: o

Benzodiazepines

o

Paralysis with vecuronium , endotracheal intubation and m echanical ventilation

Pa ge 3 0 9



ARDS: o

Oxygen

o

Intubation and positive end-expiratory pressure (PEEP) as indicated







DIC: o

Fresh-frozen plasm a

o

Platelets

o

Whole-blood transfusions

Rhabdom yolysis: o

IV isotonic crystalloid solution

o

Maintain hydration.

o

Maintain adequate urine output.

Specific treatm ent for serotonin syndrom e: o

Hum an data lim ited to case reports and series

o

Mainstay: supportive care, discontinuation of offending agents

o

Nonselective serotonin antagonists: 

Cyproheptadine

Medication (Drugs) 

Activated charcoal: 1â€“2 g/kg PO



Cyproheptadine: 4â€“8 m g PO/per NGT q1hâ€“q4h until therapeutic response; m axim um daily dose: 0.5 m g/kg (peds: 0.25 m g/kg/d; m ax. 12 m g/d; safety not established age <2 years)



Dextrose: D 5 0 W 1â€“2 am p (50â€“100 m L or 25â€“50 g) (peds: D 2 5 W 2â€“4 m L/kg) IV push (IVP)



Diazepam : 5â€“10 m g (peds: 0.1 m g/kg slowly) increm ents IVP



Lidocaine: 1â€“1.5 m g/kg IV bolus at 25â€“50 m g/m in followed by infusion at 20â€“50 Âµg/kg/m in (peds: 1

Pa ge 3 0 9

m g/kg IV bolus at 25â€“50 m g/m in followed by infusion at 20â€“50 Âµg/kg/m in) 

Lorazepam : 1â€“2 m g increm ents IVP



Nitroprusside: 0.3â€“10 Âµg/kg/m in IV



Norepinephrine: 2â€“4 Âµg/m in peds: 0.05â€“0.1 Âµg/kg/m in) IV.



Phentolam ine: 5 m g (peds: 0.05â€“0.2 m g/kg/dose) increm ents IVP



Sodium bicarbonate: bolus: 1â€“2 m Eq/kg IVP; adult infusion: 3 am p sodium bicarbonate in 1,000 m L D 5 W at 2â€“3 m L/kg/h IV



Vecuronium : 0.1 m g/kg IVP

Follow-Up Disposition Admission Criteria 

All MAOI overdose patients require adm ission to a m onitored unit for 24 hours.



Intensive care unit adm ission for seriously ill patients

Discharge Criteria Resolved m ild hypertensive syndrom e or resolved m ild serotonin syndrom e: 

Discharge after several hours of ED observation.

Issues for Referral Following significant MAOI toxicity, m edications need to be reassessed to prevent future crises.

References 1. Blake AS, Wiley JF. Serotonin syndrom e: a new pediatric

Pa ge 3 0 9

intoxication. Pediatr Em erg Care. 1999;(6):440â€“443. 2. Boyer EW, Shannon M. The serotonin syndrom e. New Engl J Med. 2005;352:1112â€“1120. 3. Brent J. Monoam ine oxidase inhibitors and the serotonin syndrom e. In: Haddad LM, Shannon MW, Winchester JF, eds. Clinical m anagem ent of poisoning and drug overdose. 3rd ed. Philadelphia: WB Saunders,1998:452â€“464. 4. Graudins A, Stearm an A, Chan B. Treatm ent of the serotonin syndrom e with cyproheptadine. J Em erg Med. 1998;16:615â€“619. 5. Mills KC. Serotonin syndrom e: a clinical update. Crit Care Clin. 1997;13(4):763â€“783. 6. Oates JA, Sjoerdsm a A. Neurologic effects of tryptophan in patients receiving a m onoam ine oxidase inhibitor. Neurology. 1960;10:1076â€“1078. 7. Sternbach H. The serotonin syndrom e. Am J Psychiatry. 1991;148:705â€“713.

Codes ICD9-CM 969.0 (MAOI overdose) 333.99 (serotonin syndrom e)

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M o no nucleo sis

Mononucleosis

Ian Greenwald

Basics Description 

Results in m ost cases from infection with the Epstein-Barr virus (EBV): o

Non-EBV cases of infectious m ononucleosis (IM) caused by:





Adenovirus



Cytom egalovirus (CMV)



Group A Î²-hem olytic streptococci



Hepatitis A



Hum an herpes virus



HIV



Rubella



Toxoplasm a gondii

More than 90% of adults on serologic testing dem onstrate prior infection with EBV: o

Vast m ajority of people do not recollect specific IM syndrom e.



Mode of transm ission is contact with saliva (usually from an asym ptom atic individual) o

Nicknam e â€œkissing diseaseâ€•

Pa ge 3 0 9



Incubation period: 4â€“6 weeks



Viral shedding in pharyngeal secretions can persist for >1 year.



Im m unologic response: o

Recruitm ent and activation of cytotoxic T cells: 

T-cell response is largely responsible for an elevated absolute lym phocyte count.



Subtype of the T-cell lineage, cytotoxic CD8 cells (Downey cells), contain eccentrically placed and lobulated nuclei with vacuolated cytoplasm : the â€œatypical lym phocytesâ€• seen on differential.

o

B-cell response: 

B cells are transform ed into plasm acytoid cells that secrete im m unoglobulins.

o

IgM antibody secreted: the heterophile antibody

o

Clinically m anifested by an inflam m atory response in the posterior pharynx, regional adenopathy, and splenom egaly.





Mortality from IM is rare, but secondary to: o

Splenic rupture

o

Airway edem a

o

Secondary bacterial infection

o

Hepatic failure

o

Myocarditis

Com plications: o

Hepatitis: 

Most com m on com plication, and jaundice occurs in approxim ately 5% of patients.

o

Neurologic including: 

Encephalitis



Meningitis

Pa ge 3 0 9





Guillain-BarrÃ© syndrom e



Optic neuritis

EBV infection has also been strongly linked to African Burkitt lym phom a and nasopharyngeal carcinom a.

Pediatric Considerations 

In children younger than 4 years, infection with EBV is often asym ptom atic.



In children who do becom e sym ptom atic, there is propensity toward atypical presentations: o

Mesenteric lym phadenopathy and splenom egaly can cause the illness to present with abdom inal pain.

o

Infants and toddlers can present with only irritability and failure to thrive.



Children with splenom egaly should not return to contact sports until exam has norm alized.

Signs and Symptoms 

Insidious onset over several days to weeks



Prodrom al fatigue, m alaise, arthralgias, and m yalgias



Prom inent sore throat and fever



Periorbital edem a occurs in 15â€“35% of patients.



Headache



Significant abdom inal pain is uncom m on and should raise im m ediate concern for splenic rupture.

Physical Exam 

Exudative pharyngitis and tonsillitis (sim ilar appearance to streptococcal pharyngitis)



Fever



Sym m etric tender lym phadenopathy



Hepatom egaly occurs in 15â€“25% of patients.



Splenom egaly occurs in 5â€“60% of patients.



Nonspecific m aculopapular rash can develop.

Pa ge 3 0 9



Macular erythem atous rash can develop if the patient has been given am picillin: o

Typically develops 5â€“9 days after the onset of antibiotic therapy and should not be interpreted as a penicillinlike allergy



Petechia can occur on the skin or at the junction between the hard and soft palate.

Tests Lab 

WBC with differential: o

Modest elevation in total WBC between 10,000 and 20,000, which peaks during the second week of the illness



Lym phocyte countâ€”findings suggestive of IM: o

Greater than 50% lym phocytes on differential

o

Absolute lym phocyte count >4,500

o

Elevated lym phocyte count with >10% atypical lym phocytes.



Liver function tests: o

Elevated with transam inases up to three tim es norm al found in 80â€“85% of patients

o

Significant elevations in bilirubin to the point of causing clinical jaundice in approxim ately 5% of cases



Monospot test detects presence of heterophile antibodies: o

Most patients develop heterophile antibodies after about 1 week of illness.

o

Sm all percentage of patients never develop heterophile antibodies.

o

Heterophile antibodies peak at 2â€“5 weeks and m ay persist for several m onths.

Pa ge 3 0 9

o

Positive test relates to a titer >1:40.

o

Rare false-positives can be seen with CMV, leukem ia, lym phom a, rubella, hepatitis, or lupus.



Testing does exist for EBV-specific antibodies but is expensive, tim e consum ing, and rarely needed.

Imaging Focused abdom inal sonography for traum a (FAST)/CT scan of abdom en for significant abdom inal pain looking for evidence of splenic rupture

Differential Diagnosis 

Divided into infectious and noninfectious causes:



Infectious:



o

Adenovirus

o

CMV

o

Streptococcal pharyngitis

o

HIV

o

Hepatitis A, B, C

o

Diphtheria in nonim m unized populations

o

Mum ps

o

Toxoplasm osis

Noninfectious: o

Leukem ia

o

Lym phom a

o

Medication induced syndrom eâ€”phenytoin, sulfa drugs

P.707

Pa ge 3 0 9

Treatment Pre Hospital Alert 

Follow standard universal precautions.



Airway, breathing, and circulation m anagem ent



Initiate IV hydration with norm al saline if patient clinically dehydrated secondary to pharyngitis sym ptom s.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent



If possible, avoid placing patient in the sam e general area as posttransplant and other im m unocom prim ised patients.

ED Treatment General Measures 



Supportive therapy: o

Hydration with IV or PO fluids

o

Antipyretics for fever control

o

Analgesics for pain of sore throat

Steroids (m ethylprednisolone or prednisone) if there is significant pharyngeal/tonsillar edem a



Antiviral therapy has no effect on clinical course.



Antibiotics if concerned for bacterial super-infection: o



Avoid am picillin because of associated rash.

Counsel patient on athletic activity lim itations.

Pediatric Considerations Advise parents of athletic activity lim itations and the need to be cleared by pediatrician prior to returning to gym and contact sports.

Medication (Drugs)

Pa ge 3 0 9



Methylprednisolone: 125 m g IV (peds: 2 m g/kg IV)



Prednisone: 40 m g PO daily for 4 days (peds: 1 m g/kg)

Follow-Up Disposition Admission Criteria 

Significant airway edem a that represents any level of potential airway com prom ise



Neurologic or severe hem atologic/hepatic com plications



Inability to take PO

Discharge Criteria 

No airway com prom ise



Mild hem atologic com plications or m ild hepatitis



Ability to take PO fluids



Return to all sports for those patients without palpable splenom egaly 4 weeks after onset of illness



Patients with splenom egaly need close outpatient follow-up with several weeks of resolved splenom egaly before return to full activity.

References 1. Am erican Academ y of Pediatrics. Epstein-Barr virus infections. In: Am erican Academ y of Pediatrics Red Book: Report of the Com m ittee on Infectious Disease. 25th ed. Elk Grove Village, IL: Author; 2000. 2. Auwaerter PG. Infectious m ononucleosis: return to play. Clin Sports Med. 2004;23(3):485â€“497. 3. Ebell MH. Epstein-Barr virus infectious m ononucleosis. Am Fam Physician. 2004;70(7):1279â€“1287. 4. Fafi-Karem er S, Morand P, Brion JP, et al. Long-term shedding of

Pa ge 3 1 0

infectious Epstein-Barr virus after infectious m ononucleosis. J Infect Dis. 2005;191(6):985â€“989. 5. Hanna BC, McMullan R, Hall SJ. Corticosteroids and peritonsillar abscess form ation in infectious m ononucleosis. J Laryngol Otol. 2004;118(6):459â€“461. 6. Melio F. Pharyngitis. In: Rosen P, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Codes ICD9-CM O75

ICD10 B27.9

Pa ge 3 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ultiple M yelo m a

Multiple Myeloma

Maggie Ferng

Basics Description 

Norm al cells transform into m yelom a cells at the hem atopoietic stem cell level.



Pathologic derangem ents: o

Tum or cells within m arrow lead to bone destruction and cytopenia.

o

Im m unodeficiency develops secondary to suppression of norm al im m une functions.

o

Myelom a proteins lead to hyperviscosity and am yloidosis.

o 

Multifactorial renal failure

Plasm a cell secretions activate osteoclasts, leading to: o

Bone lysis, pathologic fractures, and neurologic im pairm ent

o

Hypercalcem ia (exacerbated by im paired renal function)



Anem ia owing to m arrow infiltration and renal insufficiency



Im m unocom prom ised owing to: o

Decrease in the num ber of norm al im m unoglobulins

o

Qualitative and quantitative defects in T- and B-cell

Pa ge 3 1 0

subsets



o

Granulocytopenia

o

Decreased cell-m ediated im m unity

Hyperviscosity secondary to protein accum ulation: o



Leads to high-output congestive heart failure

Myelom a light chains accum ulate in the renal epithelial cells and destroy the entire nephron.

Etiology 

Incidence: 4 cases per 100,000 population: o

1% of all cancers

o

15% of all hem atopoietic m alignancies

o

10,000 deaths per year



Mean age at diagnosis is 62 years



Slightly higher incidence in wom en and African Am ericans (reason unknown)

Pediatric Considerations 

Multiple m yelom a (MM) is rarely seen in children.



Less than 2% in patients younger than 40 years of age

Diagnosis Signs and Symptoms 

Bone pain predom inates (with secondary disuse or neurologic sequelae): o

Ribs/sternum

o

Spine

o

Clavicle

o

Skull

o

Shoulder

o

Hip

Pa ge 3 1 0

o 



Constitutional sym ptom s: o

Anem ia

o

Weakness

o

Fatigue

o

Recurrent infection

o

Weight loss

Asym ptom atic (20%): o



Back

MM found on follow-up of routine blood screening

Multiple bouts of sepsis secondary to the encapsulated organism s (Streptococcus pneum oniae, Haem ophilus influenzae, and Staphylococcus

Essential Workup 

Official diagnosis requires: o

Dem onstrating pathologic cells in the bonem arrow

o

Monoclonal gam m opathy on electrophoresis

o

Clinical signs such as anem ia, renal insufficiency, or lytic bone lesions



Com plications: o

Pathologic fractures

o

Hypercalcem ia

o

Renal failure

o

Recurrent infection

o

Anem ia

o

Spinal cord com pression (10% of all MM patients)

Tests Lab 

CBC: o

Norm ochrom ic, norm ocytic anem ia

o

Throm bocytopenia

o

Leukocytosis

Pa ge 3 1 0



Rouleaux form ation on peripheral blood sm ear



Electrolytes, BUN, creatinine, glucose: o



Serum calcium : o



Renal insufficiency

Hypercalcem ia owing to bone resorption

Urinalysis: o

Dipstick selects for album in and not light-chain proteinuria.

o

False-negative screening urinalysis for protein com m on



Elevated erythrocyte sedim entation rate (ESR)

P.709

Imaging 



Plain radiographs dem onstrate: o

Lytic bone lesions

o

Pathologic fractures

Urinary and serum electrophoresis: show a m onoclonal protein spike: o



Quantitative screening for light chain is diagnostic.

Technetium pyrophosphate bone scan: o

Lights up bone deposition

o

False-negative scan with MM owing to an uncoupling of bone absorption and deposition that results in a negative bone scan even when lytic lesions present



Bone m arrow biopsy: increase in plasm a cells



Cytogenetic screening m ay offer prognostic significance.

Differential Diagnosis 

Monoclonal gam m opathy



Chronic lym phocytic leukem ia

Pa ge 3 1 0



Non-Hodgkin lym phom a



WaldenstrÃ¶m m acroglobulinem ia



Bone m arrow plasm acytosis includes collagen vascular disease, cirrhosis, im m une com plex disease, viral illness, papular m ucinosis.

Treatment Pre Hospital Im m obilize appropriately patients with MM who present with back pain or neurologic sym ptom s: 

Presum e to have a pathologic spinal fracture

Initial Stabilization Recognition and treatm ent of: 

Hypercalcem ia



Renal failure



Sepsis



Spinal cord com pression



Anem ia

ED Treatment 

Analgesics m ainstay of therapy in ED



Splint pathologic fracture; im m obilize pathologic spine fractures.



Chem otherapyâ€”adm inister on inpatient/outpatient basis: o

Early or asym ptom atic stages do not need treatm ent.

o

Chem otherapy in early stage shows no benefit.

o

Melphalan and prednisone com bination chem otherapy the m ost com m on treatm ent: 

Sym ptom relief and decrease in M protein levels in up to 70% of patients

Pa ge 3 1 0

o

Alternative chem otherapy includes cyclophospham ide with or without prednisone or VAD (vincristine, doxorubicin [Adriam ycin], and dexam ethasone).



Prolonged m elphalan use m ay lead to a secondary leukem ia.



High-dose chem otherapy with stem cell transplantation has shown prom ise.



Thalidom ide is useful for salvage therapy.

Follow-Up Disposition Admission Criteria 

Refractory pain requiring system ic analgesics



Life-threatening com plications of MM, including acute renal failure, hypercalcem ia, sepsis, spinal cord com pression, hyperviscosity, neutropenia, and cardiac tam ponade

Discharge Criteria Pain controlled with oral analgesics

Miscellaneous SEE ALSO: Anem ia; Hypercalcem ia; Renal Failure; Sepsis

References 1. Altundag K, Altundag O, Gundeslioglu O, et al. Multiple m yelom a. N Engl J Med. 2005;352:840â€“841. 2. Bortezom ib com pared with dexam ethasone in treating patients with relapsed or refractory m ultiple m yelom a. Paper presented at: Annual Meeting of the Am erican Society of Clinical Oncology (ASCO);

Pa ge 3 1 0

June 5, 2004; New Orleans, LA. 3. Hideshim a T, Chauhan D, Podar K, et al. Novel therapies targeting the m yelom a cell and its bone m arrow m icroenvironm ent. Sem in Oncol. 2001;28:607â€“612. 4. Kyle RA, Rajkum ar SV. Multiple m yelom a. N Engl J Med. 2004;351:1860â€“1873.

Codes ICD9-CM 203.0

ICD10 C90.0

Pa ge 3 1 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ultiple Sclero sis

Multiple Sclerosis

Richard S. Krause

Basics Description 

Recurrent episodes of CNS dem yelinization: o



Signs and sym ptom s depend on location of lesions.

Multiple sclerosis (MS) occurs in distinct patterns: o

Relapsing recurring m ultiple sclerosis: two or m ore episodes lasting â‰¥24 hours separated by â‰¥1 m onth

o

Prim ary progressive m ultiple sclerosis: slow or stepwise progression over at least 6 m onths

o

Secondary progressive m ultiple sclerosis: initial exacerbations and rem issions followed by slow progression over at least 6 m onths

o

Stable m ultiple sclerosis: no progression (without treatm ent) over at least 18 m onths

Etiology 

MS is chronic dem yelinating disease of CNS: o

Etiology is not well understood.



Presum ed to be T-cellâ€“m ediated autoim m une disease



There is evidence for viral trigger.



Plaques in white m atter:

Pa ge 3 1 0

o

Characterized by infiltrate of T-cells and m acrophages



Persons of northern European origin m ost often affected (in United States)



Increased prevalence is seen m oving away from equator.

Diagnosis Signs and Symptoms 

Initial attacks of MS usually represent single lesion, are abrupt in onset, and are seen in characteristic patterns (in order of decreasing frequency): o

Optic neuritis: 

Eye pain exacerbated by m ovem ent progressing to visual loss

o

Paresthesias (or changed sensory level) in one lim b

o

Lim b (usually leg) weakness

o

Diplopia: 

Internuclear ophthalm oplegia from lesion of m edial longitudinal fasciculus



Results in unilateral or bilateral paralysis of adduction of eye on horizontal gaze

o

Trigem inal neuralgia

o

Urinary retention

o

Vertigo

o

Transverse m yelitis: 

Acute onset of m otor and sensory findings at specific spinal cord level



Often associated with bladder or bowel incontinence



Can be early m anifestation of MS

Pa ge 3 1 1



Sym ptom s typically develop abruptly (m inute to hours) and last 6â€“8 weeks.



Most com m on in young wom en of northern European descent:



o

Increased risk in first-degree relatives

o

Peak age: 30 years

o

Fem ale-to-m ale ratio, 2:1

Pain is uncom m on sym ptom in MS: o

Exceptions: trigem inal neuralgia, early optic neuritis

Essential Workup 

MS is suspected based on history and physical exam .



Definitive diagnosis is not m ade in ED and requires observation over tim e and confirm atory testing.



Physical exam : focused on â€œhardâ€• neurologic signs: o

Afferent pupillary defect

o

Internuclear ophthalm oplegia

o

Sensory level or sphincter disturbance (transverse m yelitis)

o

Physical exam should reveal objective evidence of neurologic dysfunction.



MRI is sensitive but not specific: o



May see plaques (m ay also see on CT)

Lum bar puncture m ay show â€œoligoclonal bandsâ€• on cerebrospinal fluid (CSF) electrophoresis.

Differential Diagnosis 

Signs and sym ptom s of MS usually focal; diffuse sym ptom s (seizures, syncope, and dem entia) seldom owing to MS



System ic lupus erythem atosus: o

CNS involvem ent usually in setting of known disease and usually nonfocal



Sarcoid:

Pa ge 3 1 1

o

CNS m anifestations usually with known disease and lung involvem ent and nonfocal



Lym e disease: o

May m im ic MS

o

Seek history of rash and tick exposure in geographic areas of high risk.

o

Lym e titers m ay aid in diagnosis.



Psychiatric illness is diagnosis of exclusion.



Postinfectious or postim m unization dem yelination m ay m im ic MS, usually in children.



MS unlikely in patients with: o

Norm al neurologic exam

o

Abrupt hem iparesis

o

Aphasia

o

Pain predom inating

o

Very brief sym ptom s (seconds to m inutes)

o

Age <10 or >50 years

P.711

Treatment Initial Stabilization Fever in MS patients should be treated aggressively because it can worsen neurologic m anifestations of MS.

ED Treatment 

Acute optic neuritis or transverse m yelitis: o

High-dose parenteral steroids possibly effective

o

Oral steroids contraindicated (oral prednisone has

Pa ge 3 1 1

been reported to exacerbate sym ptom s) 

Exacerbations: o

High-dose IV m ethylprednisolone (up to 1 g/d) or other parenteral corticosteroid regim en



Sym ptom atic treatm ent: o

Spasticity: baclofen

o

Trem or: clonazepam

o

Urinary sym ptom s: 

Treat infection.



Self-catheterization for increased postvoid residual (PVR)



Oxybutynin m ay prom ote continence between catheterizations.

o

Trigem inal neuralgia: carbam azepine

o

Fatigue, general weakness: no specific treatm ent

Medication (Drugs) 

Baclofen: 10 m g PO t.i.d. initially; m ay increase to 25 m g t.i.d.



Carbam azepine: 100 m g PO b.i.d.â€“200 m g q.i.d.



Clonazepam : 0.5 m g/d PO, increase in 0.5-m g increm ents and up to three tim es a day



Methylprednisolone: 1 g IV



Oxybutynin: 5 m g PO b.i.d. or t.i.d.

Follow-Up Disposition Admission Criteria

Pa ge 3 1 1



Acute exacerbation that requires IV therapy



Patients unable to care for them selves owing to severity of their illness or in whom another condition requiring inpatient treatm ent cannot be effectively ruled out

Discharge Criteria 

Suspected MS: Patients m ay be referred for outpatient evaluation if their general condition perm its and other serious conditions requiring adm ission have been effectively ruled out.



Com plication of known MS: Discharge if effective outpatient treatm ent available for condition.

References 1. Antel JP: Multiple sclerosisâ€”em erging concepts of disease pathogenesis. J Neuroim m unol. 1999;98(1):45â€“48. 2. Brod SA, Lindsey JW, Wolinsky JS. Multiple sclerosis: clinical presentation, diagnosis, and treatm ent. Am Fam Physician. 1996;54:1301â€“1311. 3. Leary S, Porter B, Thom pson A. Multiple sclerosis: diagnosis and the m anagem ent of acute relapses. Postgrad Med J. 2005;81:302â€“308. 4. Poser CM. The epidem iology of m ultiple sclerosis: a general overview. Annals of Neurology. 1994;36(suppl 2):S180â€“S199. 5. Rolak LA. The diagnosis of m ultiple sclerosis. Neurol Clin. 1996;14(2):27â€“43.

Codes ICD9-CM 340

ICD10 G35

Pa ge 3 1 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M um ps

Mumps

Austen Chai

Basics Etiology 

Param yxovirus, single-stranded RNA virus



Hum an reservoir

Pediatric Considerations 

May present as lower respiratory tract infection



System ic sym ptom s and serious com plications less com m on



Mum ps vaccine with m easles and rubella (MMR) should be adm inistered to all children on or after 12 m onths of age.



Adm itted patients should be isolated from unim m unized.

Diagnosis Signs and Symptoms Incubation (12â€“25 days) 

Viral transm ission via respiratory droplets and saliva



Replication in nasopharynx and regional lym ph nodes



Virem ia to m eninges and glands; salivary, pancreas,

Pa ge 3 1 1

testes, and ovaries

Active Illness (1 to 10 days) 

Nonspecific prodrom al sym ptom s



May include low-grade fever, headache, m alaise, m yalgia, anorexia, otalgia, jaw pain



Up to 20% of infections are asym ptom atic but still contagious.



Up to 50% of cases have nonspecific sym ptom s of upper respiratory tract infection, fever, m alaise, anorexia, and headache.



Contagious 3 days before and up to 6 days after sym ptom s end



Parotitis (30â€“40% of patients): o

Most com m on m anifestation of m um ps

o

Painful and tender unilateral or bilateral enlargem ent of parotid gland

o

May begin as earache or pain at angle of jaw

o

Any salivary gland m ay be affected

o

Skin overlying swollen gland is nonerythem atous.

o

Sym ptom s decrease after 1 week and resolve by 10th day.

o 

Contagious until swelling resolves

Orchitis (20â€“50% of postpubertal m ales): o

Most com m on com plication in postpubertal m ales

o

May occur alone, before, during, but m ost com m only, after parotitis

o

Unilateral or bilateral (up to 30%)

o

Abrupt, painful, tender swelling with nausea, vom iting, and fever

o

Pain and swelling resolve in 1 week.

o

Testicular atrophy in up to 50% of patients

o

Sterility rare

Pa ge 3 1 1





Oophoritis (5% of postpubertal fem ales): o

May m im ic appendicitis if right sided

o

Fertility not im paired

Pancreatitis (2â€“5%): o

May occur without any other m anifestations of m um ps

o

Fever, nausea, vom iting, and epigastric pain

o

May see transient hyperglycem ia

o

May be com plicated by pseudocyst form ation and shock



CNS involvem ent: o

Aseptic m eningitis (10â€“15% of patients)

o

Usually resolves without sequelae in 3â€“10 days

o

Encephalitis (very rare)

o

Deafness (80% unilateral) with perm anent hearing im pairm ent



Other: o

Myocarditis (rarely with sym ptom atic involvem ent)

o

Glom erulonephritis

o

Polyarthralgia and arthritis

o

Throm bocytopenic purpura

o

Ocular com plaints

Essential Workup Diagnosis based on clinical findings P.713

Tests Lab 

Laboratory tests as needed



Cerebrospinal fluid (CSF) for sym ptom atic CNS

Pa ge 3 1 1

involvem ent 

Hyperam ylasem ia usually owing to parotitis



Viral cultures: o

Provides definitive diagnosis

o

From blood, throat swab, salivary gland secretions, CSF, or urine

o

Not indicated unless need to confirm diagnosis in absence of parotitis



Enzym e im m unoassay: o

Rapid detection

o

Not indicated unless need to confirm diagnosis in absence of parotitis

Differential Diagnosis 



Bacterial parotitis: o

Com m only Staphylococcus aureus

o

Erythem atous and tender parotid gland

o

Usually in elderly or im m unocom prom ised

Calculus parotid: o

Stone m ay be palpable or be seen on sialogram .



Cervical adenitis



Tum ors: o

Older patients

o

History of indolent course



Testicular torsion



Bacterial epididym o-orchitis

Treatment Pre Hospital Nonim m unized prehospital care personnel exposed to m um ps should

Pa ge 3 1 1

be advised of potential risks.

Initial Stabilization IV fluids for vom iting/dehydration

ED Treatment 

Prevention with m um ps vaccination is cornerstone of therapy: o

MMR at 1 year of age

o

Second MMR at 4â€“6 years of age, no later than 12 years of age



Supportive and sym ptom atic: o

Antipyretics

o

Analgesia: 

Acetam inophen, nonsteroidal anti-inflam m atory drugs (NSAIDs), narcotics (for severe pain)

o

IV fluids for vom iting and dehydration

o

Ice pack

o

Scrotal support

Follow-Up Disposition Admission Criteria 

Seriously ill who m ay require supportive care



Severe vom iting and dehydration



Encephalitis



Severe pancreatitis



Isolate adm itted patients.

Discharge Criteria 

Virtually all patients

Pa ge 3 1 1



Contagious until about 9 days after onset of sym ptom s

References 1. Am erican Academ y of Pediatrics. Mum ps. In: Pickering LK, ed. 2000 Red Book: Report of the Com m ittee on Infectious Diseases. 25th ed. Elk Grove Village, IL: Author; 2000:405â€“408. 2. Centers for Disease Control and Prevention. Measles, m um ps, and rubella: vaccine use and strategy for elim ination of m easles, rubella, and congenital rubella syndrom e and control of m um ps. Recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Recom m Rep 1998;47(RR-8):1â€“57. 3. Goldm an L, ed. Cecil Textbook of Medicine, 21st ed. Philadelphia: WB Saunders; 2000:808â€“810. 4. Mandell GL, ed. Principles and Practice of Infectious Disease. 5th ed. Philadelphia: Churchill Livingstone; 2000:1776â€“1780.

Codes ICD9-CM 72.9

ICD10 B26.9

Pa ge 3 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M unchausen's Syndro m e

Munchausen's

Syndrome J. C. Huffman T. A. Stern

Basics Description Intentional production/feigning of physical sym ptom s m otivated by a need to assum e the sick role

Etiology 

No universal etiology



Patients often have a history of gaining support/attention via illness during childhood and of abusive or neglectful upbringing.

Diagnosis Difficult to m ake a definitive diagnosis but several com m on features exist

Signs and Symptoms 

Frequent visits to EDs for what appears to be an acute illness

Pa ge 3 1 2



Num erous hospital adm issions (often prolonged)



A plausible, but dram atic, case history



Escalating dem ands for diagnostic testing and therapeutic interventions



Hostility/bullying m anner and evasiveness regarding specifics



Arrival with num erous m edical reports, hospital cards, or insurance form s



Masochistic acceptance of painful procedures



Use of m edically sophisticated language



Em ploym ent in a m edically related field



A paucity of verifiable history



Pseudologia fantastica (the telling of wild, untrue stories)



Vast array of possible presenting m edical com plaints and signs

Social History 

Frequent hom elessness and significant wandering between cities and states



An absence of close interpersonal relationships



A history of sadistic and rejecting parents



A history of chronic childhood illness

Gastrointestinal 

Vom iting



Diarrhea



Abdom inal pain

Hematologic 

Dizziness



Weakness associated with bleeding



Anem ia (from self-phlebotom y or abuse of anticoagulants)

Neurologic

Pa ge 3 1 2



Feigned seizures



Loss of consciousness

Musculoskeletal 

Self-induced wounds



Multiple scars

Cardiac 

Com plaints of chest pain



Palpitations



Dysrhythm ias

Renal 

Renal colic



Dysuria



Hem aturia

Endocrine 

Hypoglycem ia (from self-adm inistration of insulin)



Hyperthyroidism :



o

Secondary to exogenous adm inistration of thyroxine

o

See Hyperthyroidism

Hyperdynam ic states (from use of epinephrine): o

Tachycardia

o

Hypertension

o

Diaphoresis

Infectious 

From injection of sputum or feces



Factitious fever from m anipulation of therm om eters

Pulmonary Shortness of breath

Pediatric Considerations 

Munchausen syndrom e by proxy

Pa ge 3 1 2



A form of child abuse



A parent provides a m isleading history or induces illness in their child to obtain m edical attention.

Essential Workup 

The diagnosis is suggested by inconsistencies in the history or the pattern of illness and by the recognition of the above patterns of behavior.



Diligent detective work, including obtaining records from other hospitals and calling on fam ily m em bers who can provide evidence of sim ilar prior presentations



Direct observation of the patient and a search of the patient's room /belongings that m ay reveal their m ethod of deception (e.g., insulin vials and syringes)



Critical to perform tests/workup that focus on objective findings of illness on exam

Tests Depend on organ system involved and on objective findings

Lab 

Testing stool for phenolphthalein m ay detect laxative abuse.



Testing blood for C3 peptide reveals exogenous insulin adm inistration.

Imaging Do not rely on im aging brought by the patient to m ake diagnoses or treatm ent plans. P.715

Diagnostic Procedures/Surgery Avoid unless clear objective findings indicate the necessity of a

Pa ge 3 1 2

procedure

Differential Diagnosis 

True prim ary physical illness: o

Munchausen patients often with co-m orbid prim ary m edical illness



True illness secondary to self-destructive acts or surgical interventions: o



Sm all bowel obstruction, infection, dehydration

Malingering: o

Also has intentional sym ptom production

o

In this case, a clear-cut secondary gain (e.g., m eals/room , disability benefits) is present.

o

The patient is usually m uch less willing to undergo painful procedures.





Conversion disorder: o

Sym ptom s not consciously/intentionally produced

o

Typically with neurologic sym ptom s

o

Blindness

o

Hem iparesis

o

Seizures

Som atization disorder o

Sym ptom s not consciously produced

o

Multiple som atic com plaints

o

Multiple organ system involvem ent

Treatment Initial Stabilization Treat obvious threats to life or lim b: 

Hypoglycem ia, bleeding, or wounds

Pa ge 3 1 2

ED Treatment 

Identify objective physical illness and treat as appropriate.



Docum ent history/findings suggestive of factitious illness.



Flag chart or create list to identify such patients.



Refer for psychiatric care if the patient accepts referral.



Report Munchausen syndrom e by proxy to child protective services.



Be aware of your em otional reaction to avoid inappropriate abandonm ent or treatm ent.

Follow-Up Disposition Admission Criteria 

Often requires m edical adm ission to treat or stabilize physical conditions



Psychiatric adm ission m ay be of benefit, but is rarely accepted by patient.

Discharge Criteria 

Medical stability



Not an active threat to harm self



Appropriate referral for m edical and psychiatric follow-up arranged

Issues for Referral 

May offer psychiatric referral as a m ethod of dealing with stress caused by illness



Psychiatric providers located directly in m edical settings (e.g., prim ary care physician office) m ay be m ore accepted.

Pa ge 3 1 2



Overall, this is a chronic illness with poor prognosis.

References 1. Feldm an MD, Ford CV. Factitious disorders. In: Sadock BJ, Sadock VA, eds. Kaplan and Sadock's Com prehensive Textbook of Psychiatry. 7th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2000:1533â€“1543. 2. Robertson MM, Cervilla JA. Munchausen's syndrom e. Br J Hosp Med . 1997;58(7):308â€“312. 3. Souid AK, Keith DV, Cunningham AS. Munchausen syndrom e by proxy. Clin Pediatr. 1998;37(8):497â€“503. 4. Stern TA. Munchausen's syndrom e revisited. Psychosom atics. 1980;21:329â€“336. 5. Walker EA. Dealing with patients who have m edically unexplained sym ptom s. Sem in Clin Neuropsychiatry. 2002;7:187â€“195.

Codes ICD9-CM 301.51

ICD10 F68.1

Pa ge 3 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ushro o m , Po iso ning

Mushroom,

Poisoning Adam Black Timothy Erickson

Basics Description Amanitin/Phalloidin 



Species: o

Am anita phalloides (â€œdeath capâ€•)

o

Am anita virosa/verna (â€œdestroying angelâ€•)

o

Galerina m arginata; Galerina venenata

Mechanism : o

Cyclopeptide toxins inhibit RNA polym erase 2, which kills GI epithelium , hepatocytes, nephrocytes

Gyromitrin 



Species: o

Gyrom itra esculenta (â€œfalse m orelsâ€•)

o

Other Gyrom itra species

Mechanism : o

Inhibits pyridoxal phosphate

o

Dam age to RBCs, hepatocytes, neurons

Pa ge 3 1 2

Muscarine 



Species: o

Inocybe (several species)

o

Clitocybe (several species)

Mechanism : o

Parasym pathom im etic

Coprine 

Species: o



Coprinus atram entarius (â€œinky capsâ€•)

Mechanism : o

Blocks acetaldehyde dehydrogenase 

Causes disulfiram like reaction if m ixed with alcohol

Ibotenic Acid/Muscimol 



Species: o

Am anita pantherina (â€œthe pantherâ€•)

o

Am anita m uscaria (â€œfly agaricâ€•)

Mechanism : o

GABA agonists

Psilocin/Psilocybin 

Species: o



Psilocybe and Panaeolus species as well as others

Mechanism : o

Sim ilar structure to lysergic acid diethylam ide (LSD)

Gastric Irritants Many various m ushroom s including those norm ally considered edible

Orellanine 

Species: o



Cortinarius (several species)

Mechanism :

Pa ge 3 1 2

o

Direct renal toxicity

Diagnosis Signs and Symptoms Amanitin/Phalloidin 

Nausea



Vom iting



Abdom inal cram ps



Bloody diarrhea



Clinical course: o

Onset of sym ptom s 6â€“36 hours

o

Transient latent phase m ay last 2 days (no pain)

o

Can progress to hepatic or renal failure and death in 4â€“7 days

o

Most lethal m ushroom toxins

Gyromitrin 



First 6 hours: o

Abdom inal cram ps

o

Vom iting

o

Watery diarrhea

Later sym ptom s: o

Weakness

o

Cyanosis

o

Confusion

o

Seizures

o

Com a

Muscarine 

Cholinergic sym ptom s include: o

Miosis

Pa ge 3 1 3



o

Salivation

o

Lacrim ation

o

Sweating

o

Diarrhea

o

Flushed skin

o

Nausea

o

Bradycardia

o

Bronchoconstriction

Onset usually within 1 hour (m ay be delayed)

Coprine 



Disulfiram like reaction when com bined with alcohol: o

Flushing

o

Sweating

o

Nausea

o

Vom iting

o

Palpitations

o

Chest pain

Begins m inutes after com bining this toxin with ethanol

Ibotenic Acid/Muscimol 



Anticholinergic sym ptom s include: o

Hallucinations

o

Dysarthria

o

Ataxia

o

Muscle cram ps

o

Vom iting

o

Seizures

o

Com a

Clinical course: o

Relatively rapid onset of 30â€“60 m inutes

Psilocin/Psilocybin 

Visual hallucinations

Pa ge 3 1 3



Alteration of perception



Nausea



Mydriasis



Tachycardia



Fever and seizures in children: o

Rarely fatal (case report of m yocardial infarction in 18 year old)

Gastric Irritants 

Group of toxins that cause nausea, vom iting, intestinal cram ps, and watery diarrhea



Onset 30 m inutes to 2 hours, usually resolved in 6â€“12 hours

Orellanine 

Nausea



Headache



Sweating



Chills



Low-back pain



Thirst



Clinical course o

May progress to oliguria and acute renal failure

o

Markedly delayed onset of sym ptom s (2â€“14 days)

Essential Workup 

Mushroom description: o

Fewer than 3% of cases result in an exact m ushroom identification.



Careful history and physical exam : o

Special detail to tim ing of sym ptom onset

Tests Lab

Pa ge 3 1 3



CBC



Prothrom bin tim e (PT), partial throm boplastin tim e (PTT)



Electrolytes, BUN, creatinine, glucose



Urinalysis



Liver function tests (LFTs), creatine phosphokinase (CPK)

Differential Diagnosis 

Sym ptom s with late onset (>6 hours) indicate m ore lethal toxins.



Always entertain possibility of m ultiple species ingestion.



Com bination with ETOH m ay suggest coprine (disulfiram reaction).



Consider other illicit drugs with visual hallucinations.



Fertilizers, insecticides, fungicides, if m ushroom s were found in a public place



Botulism if canned m ushroom s

Treatment Pre Hospital Bring any unconsum ed m ushroom s or m ushroom pieces to hospital to aid in diagnosis: 

Refrigerate specim ens if possible, place in brown paper bag.

P.717

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Establish IV 0.9% norm al saline (NS)



Monitor

Pa ge 3 1 3



Naloxone, D 5 0 W (or Accu-Chek) and thiam ine for altered m ental status

ED Treatment General 



Decontam ination: o

Activated charcoal (50â€“100 g)

o

Gastric decontam ination if early after ingestion and: 

Patients have not yet vom ited.



Norm al m ental and respiratory status



Not undergoing hallucinations

Fluid rehydration and electrolyte replacem ent as necessary



Call local poison control center and request m ycologistâ€”digital picture m ay be electronically sent for identification.



Obtain specim ens (vom itus if needed) for identification.

Toxin-Specific Therapy 

Am anitin/phalloidin: o

Ewald oral gastric tube aspiration of m ushroom fragm ents if 1â€“2 hours postingestion

o

Adm inister charcoal orally every 2â€“4 hours

o

Hypoglycem ia and elevated PT: 

Signs of liver failure



Adm inister fresh frozen plasm a and vitam in K for coagulation disorders with active bleeding.

o

Adm inister calcium in presence of hypocalcem ia.

o

Liver transplant for severe hepatic necrosis

o

Consider N-acetylcysteine, high-dose penicillin G, or silibinin if available (thioctic acid controversial)



Gyrom itrin: o

Adm inister pyridoxine (vitam in B 6 ) in severely

Pa ge 3 1 3

sym ptom atic patients. o

Treat seizure with benzodiazepines.

o

Treat liver dysfunctions as outlined for am anitin/phalloidin group.

o 

Muscarinic: o





Dialysis for renal failure

Adm inister atropine in severe cases.

Coprine: o

Self-lim ited toxicityâ€”supportive care

o

Avoid syrup of ipecac (contains alcohol).

o

Beta-blockers for cardiac dysrhythm ias

Ibotenic acid/m uscim ol: o

Usually self-lim ited toxicity

o

Provide supportive care.

o

Monitor for hypotension.

o

Treat m oderate anticholinergic sym ptom s with benzodiazepines, severe sym ptom s with physostigm ine.





Psylocin/psilocybin: o

Self-lim ited toxicity

o

Monitor if tachycardic.

o

Dark, quiet room and reassurance

o

No aggressive oral decontam ination if hallucinating

o

External cooling m easures if needed in children

GI Irritants: o



When poisoning from above groups not suspected: 

Adm inister fluids and antiem etics.



Supportive care

Orellanine and Am anita sm ithiana: o

Closely m onitor BUN, creatinine, electrolytes, and urine output.

o

Forced diuresis with Lasix contraindicated:

Pa ge 3 1 3

 o

Accelerates nephrotoxicity in rats

Diuresis with alkalinization of urine with NaHCO 3 if signs of rhabdom yolysis

o

Hem odialysis/renal transplantation m ay be needed.

o

Monitor LFTs in cases in which cyclopeptide-containing m ushroom s are suspected.

o

Monitor CPK, urine output: Tricholom a equestre (â€œm an on horseâ€•) m ushroom s can lead to acute rhabdom yolysis.

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 100 g PO



Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5â€“1.0 m g IV (peds: 0.04 m g/kg) q10m in if secretions recur, to m ax. 1 m g/kg in children and 2 m g/kg in adults



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Lorazepam (benzodiazepine): 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Physostigm ine: 0.5â€“2 m g IM or IV in adults



Propranolol: 1 m g (peds: 0.01â€“0.1 m g/kg) IV



Pyridoxine: 25 m g/kg over 30 m inutes



Sorbitol: 1â€“2 g/kg to m ax. of 150 g. Avoid in very young children (peds: >2 years: 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurry



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Pa ge 3 1 3

Follow-Up Disposition Admission Criteria 

All sym ptom atic patients: o

Protracted vom iting, dehydration, liver or renal toxicity, or seizures



Transfer to tertiary m edical center for early signs of renal or hepatic failure.



Sym ptom atic infants and young children found with m ushroom s: o



Assum e ingestion.

ICU adm ission for known ingestion of an am anitin-containing m ushroom : o

Early liver service consultation

Discharge Criteria Asym ptom atic during 6â€“8 hours with 24 hours of close hom e observation available

References 1. Bedry R, Baudrim ont I, Deffieux G, et al. Wild m ushroom intoxication as a cause of rhabdom yolysis. N Engl J Med. 2001;345:798â€“802. 2. Berger KJ, Guss DA. Mycotoxins revisited. Part I. J Em erg Med. 2005;28(1):53â€“62. 3. Berger KJ, Guss DA. Mycotoxins revisited. Part II. J Em erg Med. 2005;28(2):175â€“183. 4. Diaz JH. Evolving global epidem iology, syndrom ic classification, general m anagem ent, and prevention of unknown m ushroom ingestion. Crit Care Med. 2005;33(2):419â€“426.

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5. Fischbein C, Aks S, Mueller GM. Mushroom poisoning. In: Erickson T, Ahrens W, Aks S, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2005:533â€“540. 6. Fischbein C, Mueller G, Leacock P, et al. Digital im aging: a prom ising tool for m ushroom identification. Acad Em erg Med. 2003;10:808â€“811. 7. Ganzert M, Felgenhauer N, Zilker T. Indication of liver transplantation following am atoxin intoxication. J Hepatol. 2005;42(2):202â€“209. 8. Goldfrank LR. Mushroom s. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:. 9. McPartland JM, Vilgalys RJ, Cubeta MA. Mushroom poisoning. Am Fam Physician. 1997;55:1797â€“1800, 1805â€“1809. 10. O'Donnel M, Flem ing S. The renal pathology of m ushroom poisoning. Histopathology. 1997;30(3):280â€“282. 11. Satora L, Pach D, Butryn B, et al. Fly agaric (Am anita m uscaria) poisoning, case report and review. Toxicon. 205;45:941â€“943. 12. Warden CR, Benjam in DR. Acute renal failure associated with suspected Am anita sm ithiana m ushroom ingestions: a case series. Acad Em erg Med. 1998;8:808â€“812.

Codes ICD9-CM 988.1

ICD10 T62.0

Pa ge 3 1 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yasthenia G ravis

Myasthenia Gravis

Angela Loh

Basics Description 

Antibody-m ediated condition that results in painless, fatigable weakness



Bim odal distribution: o

One peak in second and third decades affecting m ostly wom en

o 

Second peak in sixth and seventh decades

Ocular or generalized: o

Ocular m uscle weakness: 

Most com m on initial sym ptom (60%)



Alm ost all patients with m yasthenia gravis will have ocular involvem ent within 2 years.

o

Generalized: 

Usually affects proxim al lim bs, axial m uscle groups such as neck, face, bulbar m uscles



Acute or subacute, with relapses and rem issions



Associated with thym om a in 20% and with thym ic hyperplasia in 70%



Myasthenic crisis: o

Respiratory failure resulting from m yasthenic

Pa ge 3 1 3

weakness o

Triggers: infection, surgery, traum a, m edication changes (e.g., rapid tapering of steroids)

o

Difficult to distinguish from cholinergic crisis resulting from excessive doses of acetylcholinesterase (AChE) inhibitors

Etiology 

Antibody-m ediated attack on nicotinic acetylcholine receptors



Som e patients m ay be acetylcholine receptor antibody (AChR Ab) negative



Medications that worsen m yasthenic weakness: o

Am inoglycosides, am picillin, ciprofloxacin, erythrom ycin

o

Local anesthetics

o

Antidysrhythm ics (propafenone, quinidine, procainam ide)

o

Beta-blockers

o

Phenytoin

o

Neurom uscular blocking agents

o

Penicillam ine can cause m yasthenia gravis as well as other autoim m une conditions.

Diagnosis Signs and Symptoms History 

Weakness worse with repeated or sustained m uscular activity



Im proves with rest

Pa ge 3 1 4







Ocular weakness: o

Diplopia

o

Ptosis while driving or reading

Bulbar and facial m uscle weakness: o

Trouble chewing, speaking, swallowing

o

Inability to keep jaw closed after chewing

o

Slurred, nasal speech

Lim b weakness: o

Difficulty clim bing stairs, rising from chair, reaching up with arm s

Physical Exam 



Ocular findings: o

Ptosis, diplopia

o

Inability to keep eyelid shut against resistance

o

No pupillary changes

Bulbar and facial findings: o

Ask patient to count to 100; look for changes in speech.



o

Decreased facial expression

o

Head droop

Lim b findings: o

Repetitively test proxim al m uscles or sm all m uscles of hand.

o

Reflex and sensory exam are norm al.

Essential Workup 

Search for secondary triggers.



Assess for respiratory com prom ise.

Tests Lab 

CBC

Pa ge 3 1 4



Electrolytes



Liver function tests



Thyroid function tests



Search for infectious source; consider chest radiograph



Anti-AChR Ab:



o

Positive in 90% with generalized disease

o

Positive in 50% with ocular disease

Other tests for initial diagnosis: o

Antistriated m uscle antibody

o

Antinuclear antibody (ANA)

o

Rheum atoid factor

o

Erythrocyte sedim entation rate (ESR)

Imaging 

Head CT or MRI to rule out com pressive lesions causing cranial nerve findings



Chest CT with contrast to look for associated thym om a

Diagnostic Procedures/Surgery 

Edrophonium (Tensilon) test: o

Short-acting acetylcholinesterase inhibitor

o

Produces rapid, short-lived (2 to 5 m inutes) im provem ent in strength



o

Positive in 90% of m yasthenia gravis patients

o

Keep patient on cardiac m onitor during test.

o

Atropine at bedside for possible bradycardia

Ice test: o

Place ice on eyelid for 2 m inutes.

o

Im provem ent in ptosis suggests m yasthenia gravis.

Differential Diagnosis 

Hyperthyroidism



Electrolyte abnorm alities



Graves disease

Pa ge 3 1 4



Botulism



Lam bert-Eaton syndrom e



Am yotrophic lateral sclerosis



Guillain-BarrÃ© syndrom e



Inflam m atory m uscle disorders



Multiple sclerosis



Periodic paralysis



Intracranial m ass lesions

P.719

Treatment Pre Hospital Attention to airway m anagem ent

Initial Stabilization 

Myasthenic crisis: o

Most im portant is early intubation and m echanical ventilation.

o

Though no single param eter can predict need for respiratory support; consider following forced vital capacity or m ean inspiratory pressure

o

Considerations regarding paralytics 

Decreased sensitivity to depolarizing agents m ay necessitate higher dose; consider doubling the usual dose of succinylcholine



Nondepolarizing agents can cause extended paralysis; consider halving the usual dose of vecuronium

Pa ge 3 1 4



Others recom m end m idazolam , etom idate, or thiopental instead.

ED Treatment 

Treat infections aggressively.



Search for and rem ove triggers.



Atropine for AChE inhibitor effects (bradycardia, GI sym ptom s, increased bronchial or oral secretions)



Myasthenic crisis m ay require plasm apheresis or intravenous gam m aglobulin.



Steroids and im m unosuppressive therapies are not used in acute m anagem ent.

Medication (Drugs) 

Atropine: 0.4â€“0.5 m g IV or IM



Edrophonium (Tensilon): 2 m g IV over 15â€“30 seconds; if no effect after 45 seconds, can give second dose of 8 m g IV slowly



Pyridostigm ine (Mestinon): for m yasthenic crisis, infusion at 1â€“2 m g/h



Other m edications that m ay be initiated by neurologist: o

Prednisone, azathioprine, m ycophenolate m ofetil, cyclosporine, tacrolim us, rituxim ab

Follow-Up Disposition Admission Criteria 

Myasthenic crisis or questionable respiratory status

Pa ge 3 1 4

m andates adm ission to intensive care unit (ICU). 

Myasthenic patients with worsening sym ptom s



New-onset m yasthenic sym ptom s



Diagnosis unclear, but m yasthenia a possibility

Discharge Criteria Myasthenic patients who are im proving can be considered for discharge in consultation with neurology.

References 1. Bedlack RS, Sanders DB. How to handle m yasthenic crisis. Postgrad Med. 2000;107(4):211â€“214. 2. Berrouschot J, Baum ann I, Kalischewski P, et al. Therapy of m yasthenic crisis. Crit Care Med. 1997;25:1228â€“1235. 3. Drachm an DB. Myasthenia gravis. N Engl J Med. 1994;330:1797â€“1810. 4. Kothari M. Myasthenia gravis. J Am Osteopath Assoc. 2004;104(9):377â€“384. 5. Sanders DC, Scoppetta CS. Treatm ent of patients with m yasthenia gravis. Neurol Clin North Am . 1994;12(2):343â€“365. 6. Thom as CE, et al. Myasthenic crisis: clinical features, m ortality, com plications, and risk factors of prolonged intubation. Neurology. 1997;48:1253â€“1260. 7. Vincent A, Palace J, Hilton-Jones D. Myasthenia gravis. Lancet. 2001;357:2122â€“2128.

Codes ICD9-CM 358.0

Pa ge 3 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yo cardial C o ntusio n

Myocardial

Contusion Robert S. Hamilton

Basics Description 

Pathologically characterized by discrete and well-dem arcated area of hem orrhage



Usually subendocardial



May extend in pyram idal transm ural fashion



Most com m only involves anterior wall of right ventricle or atrium

Etiology 

Blunt traum a to chest: o

High-speed deceleration accidents

o

May occur in accidents with speeds as low as 20â€“35 m ph



Autoâ€“pedestrian injuries



Falls



Prolonged closed-chest cardiac m assage



Heart m ay be com pressed between sternum and vertebrae.



Strike sternum during deceleration

Pa ge 3 1 4



Dam aged by abdom inal viscera upwardly displaced by force on abdom en

Associated Conditions 

Life-threatening dysrhythm ias



Cardiogenic shock/congestive heart failure



Hem opericardium with tam ponade



Valvular/m yocardial rupture



Intraventricular throm bi



Throm boem bolic phenom ena



Coronary artery occlusion from intim al tearing or adjacent hem orrhage and edem a m ay rarely occur.

Diagnosis Signs and Symptoms 



Clinical picture is varied and nonspecific: o

Excruciating chest pain

o

Cardiogenic shock

o

Subtle ECG changes without clinical sym ptom s

Most com m on sign is tachycardia out of proportion to degree of traum a or blood loss.



Friction rub m ay occur rarely.



Retrosternal chest pain unrelieved by nitroglycerin:



o

Often delayed up to 24 hours

o

May respond to oxygen

Evidence of significant thoracic traum a: o

Contusions, abrasions

o

Palpable crepitus

o

Sternal fracture

o

Visible flail segm ents

Pa ge 3 1 4



Other injuries m ay m ask signs and sym ptom s of m yocardial contusion.

Essential Workup 

No single diagnostic study (other than autopsy findings!) confirm s presence of m yocardial contusion.



Only abnorm al ECG and creatine phosphokinase (CPK)-MB have been shown to correlate directly with com plications requiring treatm ent.



ECG: o

Best initial screening tool

o

Most com m on rhythm is sinus tachycardia (70%).

o

Norm al ECG does not rule out m yocardial dam age.

o

ECG changes m ay be subtle or include nonspecific findings such as right bundle branch block.

o

At least one repeat ECG is recom m ended because changes m ay occur over tim e.

o

Serious dysrhythm ias m ay result in hem odynam ic instability:





Atrial fibrillation



Ventricular tachycardia



Ventricular fibrillation

Echocardiography should be perform ed on all patients with any ECG changes, elevated CPK-MB, or elevated troponin-I or troponin-T.

Tests Lab 



CPK-MB, troponin: o

Levels should be sent on all patients being adm itted.

o

Sensitivity varies from 11â€“85%.

o

Specificity decreased in m ultiple traum a.

Cardiac troponin and m yoglobin assays have not been as

Pa ge 3 1 4

well studied.

Imaging 



Radiographs, CT, MRI detect associated injuries: o

Pulm onary contusion

o

Rib or sternal fractures

o

Acute pulm onary edem a

o

No specific findings in cardiac contusion

Echocardiography: o

Generally regarded as best im aging study for detecting cardiac contusion

o

Detects wall-m otion abnorm alities and effusions

o

Allows direct visualization of cardiac cham bers and valves

o

May not visualize sm all (possibly clinically insignificant) contusions

o

Transesophageal echocardiography (TEE) m ay be used in patients with painful chest wall injuries.

o 

May also visualize great vessels

Radionuclide ventriculography: o

Has been largely abandoned owing to wide availability of echocardiography



Thallium -201 scintigraphy (single photon em ission com puted tom ography [SPECT]): o

Sensitive and specific to left ventricular injury

o

Unable to evaluate right ventricle, which is m ost com m only injured

Differential Diagnosis 

Cardiac rupture



Tam ponade



Valvular dam age



Other traum atic chest wall injury

Pa ge 3 1 4



Angina or m yocardial infarction

P.721

Treatment Pre Hospital Prehospital personnel should convey accurate inform ation to em ergency departm ent personnel: 

Mechanism of injury



Motor vehicle status



Steering wheel and dashboard dam age



Use of restraint devices



Vehicle speed



Patient position

Initial Stabilization Manage airway and resuscitate as indicated: 

Oxygen



Intravenous access



Cardiac m onitoring

ED Treatment 

Dysrhythm ias m ay be treated with sam e pharm acologic agents used for nontraum atic dysrhythm ias: o

Supraventricular tachycardia: 

Adenosine or calcium channel blocker if patient not hypovolem ic

o

Bradycardia: 

Atropine



Pacing

Pa ge 3 1 5

o

o

o

Ventricular dysrhythm ias: 

Electrical conversion



Am iodarone



Lidocaine



Procainam ide

Cardiac arrest: 

Epinephrine



Atropine



Other interventions as appropriate

Rapid atrial fibrillation or flutter: 

Diltiazem , or digoxin if patient not hypotensive



Prophylactic treatm ent of dysrhythm ias is not indicated.



Cardiogenic shock caused by m yocardial contusion: o

Judicious fluid adm inistration

o

Inotropic support (dopam ine or dobutam ine)

o

Intra-aortic balloon counterpulsation m ay be necessary.

Medication (Drugs) 

Medications used in cardiac contusion are supportive for dysrhythm ias or hem odynam ic com prom ise secondary to injury.



There is no prim ary therapy for cardiac contusion.



Adenosine: 6 m g rapid IVP (peds: 0.1â€“0.2 m g/kg rapid IVP), m ay repeat 12 m g q1â€“2m in twice if no response



Am iodarone: load 150 m g IV over 10 m inutes (peds: 5 m g/kg), then 1 m g/m in for 6 hours, then 0.5 m g/m in (peds: 5 Âµg/kg/m in)



Atropine: 0.5â€“1.0 m g (peds: 0.02 m g/kg per dose, m inim um 0.1 m g) IV or endotracheal tube (ET)



Digoxin: Load 0.5 m g (peds: 0.02 m g/kg) IV, then 0.25

Pa ge 3 1 5

m g (peds: 0.01 m g/kg) IV q6h for 2 m ore doses 

Diltiazem : 10â€“20 m g (peds: 0.25 m g/kg) IV over 2 m inutes, m ay rebolus 0.35 m g/kg (adult and peds) 15 m inutes later



Dobutam ine: 2â€“15 Âµg/kg/m in (adult and peds)



Dopam ine: 2â€“20 Âµg/kg/m in (adult and peds)



Epinephrine: 1 m g (peds: 0.01 m g/kg) IV or ET for cardiac arrest (1:10,000 solution)



Lidocaine: load 1 m g/kg IV, then 0.5 m g/kg q8â€“10m in to m ax. 3 m g/kg (adult and peds); infusion 1â€“4 m g (peds: 20â€“50 Âµg/kg) per m inute IV



Procainam ide: 100 m g (peds:15 m g/kg per dose) IV q10m in up to 17 m g/kg



Verapam il: 0.1â€“0.3 m g/kg up to 5â€“10 m g IV over 2 m inutes (not approved in children)

Follow-Up Disposition 

Adverse outcom es, particularly dysrhythm ias, are uncom m on but generally occur within first 24 hours.



No single test or com bination of tests will accurately predict which patients can be discharged safely from ED: o

All patients in whom diagnosis is seriously being entertained should be adm itted.

Admission Criteria 

ECG abnorm alities



Cardiac enzym e abnorm alities



Hem odynam ic instability



Other studies suggesting cardiac contusion

Pa ge 3 1 5



Adm it to m onitored unit for close observation.

Discharge Criteria Asym ptom atic patients with no ECG abnorm alities or dysrhythm ia and with norm al cardiac enzym es after 4- to 6-hour period m ay be discharged.

References 1. Chu WW, Dieter RS, Stone CK. Evolving clinical applications of cardiac m arkers: a review of the literature. WMJ. 2002;101(3):49â€“55. 2. Kaye P, O'Sullivan I. Myocardial contusion: em ergency investigation and diagnosis. Em erg Med J. 2002;19:8â€“10. 3. Maenza RL, Seaberg D, D'Am ico F. A m eta-analysis of blunt cardiac traum a: ending m yocardial confusion. Am J Em erg Med. 1996;14:237â€“241. 4. Roxburgh JC. Myocardial contusion. Injury. 1996;27:603â€“605. 5. Sybrandy KC, Cram er MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003;89(5):485â€“459.

Codes ICD9-CM 861.01

ICD10 S28.8

Pa ge 3 1 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yo carditis

Myocarditis

Liudvikas Jagminas

Basics Description 

An inflam m atory change in the heart m uscle which is characterized by m yocyte necrosis and subsequent m yocardial destruction



May result in a dilated cardiom yopathy



Direct cytotoxic effect of causative agent followed by a secondary im m une response o

Over 4â€“14 days m acrophage activation and cytokine expression

o

Surviving cells develop the classic histologically apparent infiltration of m ononuclear cells

o

Natural killer cells target m yocardium expressing viral RNA and continue m yocyte necrosis

o

T lym phocytes infiltrate the m yocardium with direct lysis of cardiocytes

o

Often results in cardiac dysfunction and heart failure

o

40â€“50% of patients report recent antecedent viral illness



True incidence is unknown because m any cases are asym ptom atic.

Pa ge 3 1 5



Autopsy studies have dem onstrated evidence of m yocarditis in 0.5â€“1% of cases



Male to Fem ale ratio is 1.5:1



Average age of patients with m yocarditis is 42 years

Etiology 





Viral: o

Enteroviruses (coxsackie B)

o

Adenovirus

o

Herpesvirus (including cytom egalovirus [CMV])

o

Hepatitis C

o

Influenza

o

Echovirus

o

Herpes sim plex virus

o

Varicella-zoster

o

Epstein-Barr virus

o

Cytom egalovirus

o

Mum ps

o

Rubeola

o

Variola/vaccinia

o

Yellow fever

o

Rabies

o

HIV

Bacteria: o

Diphtheria

o

Tuberculosis

o

Brucellosis

o

Psittacosis

o

Meningococcus

o

Mycoplasm a

o

Group A streptococcus

Protozoa: o

Leishm aniasis

Pa ge 3 1 5

o

Malaria

o

Toxoplasm osis in the im m unocom prom ised host

o

Treponem a cruzi (Chagas disease): 

Most com m on cause of heart failure and m yocarditis worldwide



20 m illion persons infected Central and South Am erica



o

Trichinosis

o

Trypanosom iasis

Spirochetes: o

Borrelia burgdorferi, the spirochete agent in Lym e disease

o 





Syphilis

Rickettsial: o

Scrub typhus

o

Rocky m ountain spotted fever

o

Q fever

Fungal: o

Candidiasis

o

Aspergillosis

o

Cryptococcosis

o

Histoplasm osis

o

Actinom ycosis

o

Helm inthic

o

Trichinosis

o

Echinococcosis

o

Schistosom iasis

o

Cysticercosis

Drugs: o

Acetam inophen

o

Am picillin

o

Chem otherapeutic agents (anthracyclines)

Pa ge 3 1 5



o

Cocaine

o

Hydrochlorothiazide

o

Lithium

o

Methyldopa

o

Penicillin

o

Sulfam ethoxazole

o

Sulfonam ides

o

Zidovudin

o

Radiation

o

Hypersensitivity

o

Heavy m etals

o

Hydrocarbons

o

Carbon m onoxide

o

Arsenic

Autoim m une disorders: o

System ic lupus erythem atosus (SLE)

o

Wegener granulom atosis

o

Kawasaki disease

o

Giant cell arteritis

o

Sarcoidosis



Peripartum cardiom yopathy



Bites/stings: o

Scorpion

o

Snake

o

Black widow venom

Diagnosis Signs and Symptoms History

Pa ge 3 1 5



Fatigue



Myalgias/arthralgias



Malaise



Fever



Chest pain: o

Reported in 35%

o

Most com m only pleuritic, sharp, stabbing, precordial



Dyspnea on exertion is com m on.



Orthopnea and shortness of breath if congestive heart failure (CHF) is present



Palpitations are com m on



Syncope: o

May signal high-grade aortic valve block or risk for sudden death

Physical Exam 

Fever



Tachypnea



Tachycardia: o

Often out of proportion to fever



Cyanosis



Hypotension: o

Due to left ventricular dysfunction

o

Uncom m on in the acute setting and indicates a poor prognosis when present



Bibasilar crackles



Rales



Jugular venous distention (JVD)



Peripheral edem a



Hepatom egaly



Ascites



S 3 or a sum m ation gallop if significant biventricular involvem ent

Pa ge 3 1 5



Intensity of S 1 m ay be dim inished



Murm urs of m itral or tricuspid



Pericardial and pleural friction rub

Pediatric Considerations 

Particularly infants, present with nonspecific sym ptom s: o

Fever

o

Respiratory distress

o

Poor feeding or, in cases with CHF, sweating while feeding

o

Cyanosis in severe cases

Essential Workup 

Physical exam ination



ECG



Chest radiograph

Tests Lab 

Cardiac enzym e levels: o

Levels are only elevated in a m inority of patients.

o

Norm ally there is a slow elevation and fall over a period of days.

o

More abrupt rise observed with acute m yocardial infarction.

o

Cardiac troponin I m ore sensitive because it is present for longer periods after m yocardial dam age



Erythrocyte sedim entation rate (ESR) is elevated in 60% during the acute phase.



Leukocytosis is present in 25%.



Viral titers; cultures rarely positive



Mycoplasm a, antistreptolysin titers



Hepatitis panels

Pa ge 3 1 5



Monospot testing



CMV serology



Blood cultures

P.723

Imaging 

ECG: o

Sinus tachycardia m ost frequent finding

o

Transient, nonspecific ST- and T-wave changes

o

Atrial and ventricular dysrhythm ias

o

Heart block and conduction defects com m on: 

20% have a conduction delay, including Mobitz I, Mobitz II, or com plete heart block

 

20% have a left bundle branch block

Chest radiograph: o

Norm al cardiac silhouette

o

Pericarditis or overt clinical CHF is associated with cardiom egaly



o

Pulm onary edem a

o

Vascular redistribution

o

Interstitial and alveolar edem a

o

Pleural effusion

Echocardiography: o

Im pairm ent of left ventricular systolic and diastolic function

o

Segm ental wall m otion abnorm alities

o

Im paired ejection fraction

o

Pericardial effusion

o

Ventricular throm bus has been identified in 15% of patients



Gallium -67- and indium -111-labeled antim yosin antibody

Pa ge 3 1 6

scans 

Gadolinium -enhanced MRI: o

Indicate cardiac inflam m ation and m yocyte necrosis

Diagnostic Procedures/Surgery 

Right ventricular endom yocardial biopsy: o

Appropriate in heart transplant recipients

o

Polym erase chain reaction am plification of viral genom e in endom yocardial tissue



Polym erase chain reaction (PCR) identification of a viral infection from pericardial fluid, or other body fluid sites

Differential Diagnosis 

Acute m yocardial infarction



Acute and chronic pulm onary em bolus



Aortic dissection



Adrenal insufficiency



Environm ental challenges



Esophageal perforation/rupture/tear



Hyperpyrexia



Hypotherm ia



Kawasaki Disease



Pericarditis



Pneum onia



Viral



Bacterial



Sepsis



Severe hypothyroidism and hyperthyroidism



Toxin-m ediated disease

Treatment

Pa ge 3 1 6

Alert 

Avoid sym pathom im etic and beta-blocker drugs because they increase the extent of m yocardial necrosis and m ortality.



Patients presenting with Mobitz II or com plete heart block require pacem aker placem ent.

Initial Stabilization 

ABCs



Supplem ental oxygen



Cardiac m onitor



Pulse oxim etry



IV access

ED Treatment 

Sam e as for acute CHF/pulm onary edem a (see Congestive Heart Failure)



Treat dysrhythm ias if present.



Transthoracic or transvenous pacing for sym ptom atic heart block



Supplem ental oxygen



ACE inhibitors (captopril)



Reduce afterload and inflam m ation.



Digoxin



CHF or atrial fibrillation



Diuretics (furosem ide, bum etanide)



Im m unosuppressive therapy (e.g., cyclosporine, prednisone) are of unproved benefit except in patients with im m une m ediated disease (e.g., SLE).



Hyperim m unoglobulin therapy im proves cardiac function in CMV-associated m yopericarditis.



NSAIDs contraindicated in early and acute-phase m yocarditis because they increase m yocardial dam age.

Pa ge 3 1 6



Heparin and warfarin decrease risk for throm boem bolic events in patients with depressed LV function or intracardiac throm bus

Pediatric Considerations 

IV im m unoglobulin is an effective treatm ent option in pediatric viral m yocarditis



Im proved LV function and trend toward better survival

Medication (Drugs) 

Captopril: o

Adult dose: initial dose 6.25 m g; can titrate to 50 m g/dose

o

Pediatric dose: 

Infants: 0.15â€“0.3 m g/kg/dose (m ax. 6 m g/kg)

 

Digoxin: o

Adult dose: 

o

o 

Children: 0.5â€“1.0 m g/kg/24h

0.125â€“0.375 m g PO per day

Pediatric dose: 

Infants: 12.5 to 20.0 m cg/kg IV or PO



2â€“10 years old: 7.5â€“15.0 m cg/kg IV or PO



5â€“10 years: 20â€“35 m cg/kg PO



>10 years: 10â€“15 m cg/kg PO

Maintenance dose: use 25â€“35% of PO loading dose

Furosem ide: o

Adult dose: 

20â€“80 m g/d PO/IV/IM; titrate up to 600 m g/d for severe edem atous states

o

Pediatric dose:

Pa ge 3 1 6



1â€“2 m g/kg PO; not to exceed 6 m g/kg; do not adm inister >q6h 1 m g/kg IV/IM slowly under close supervision; not to exceed 6 m g/kg



Im m une globulin IV (Gam im une, Gam m agard, Gam m ar-P, Sandoglobulin): o

Adult dose: 

o

2 g/kg IV over 2â€“5 d

Pediatric dose: 

Not established

Follow-Up Disposition Admission Criteria Sym ptom atic patients with m yocarditis: 

New-onset



CHF



Dysrhythm ia



Mobitz II or com plete heart block



Em bolic events



Cardiogenic shock

Discharge Criteria Asym ptom atic patient with no evidence of dysrhythm ia or cardiac dysfunction

References 1. Brady WJ, Ferguson JD, Ullm an EA, Perron AD: Myocarditis: em ergency departm ent recognition and m anagem ent. Em erg Med Clin North Am . 2004 Nov; 22(4):865â€“885. 2. D'Am brosio A, Patti G, Manzoli A. The fate of acute m yocarditis

Pa ge 3 1 6

between spontaneous im provem ent and evolution to dilated cardiom yopathy: a review. Heart. 2001;85:499â€“504. 3. Feldm an AM, McNam ara D. Myocarditis. N Engl J Med. 2000;343(19):1388â€“1398. 4. Fuse K, Kodam a M, Okura Y, et al. Predictors of disease course in patients with acute m yocarditis. Circulation. 2000;102(23):2829â€“2835. 5. Gajarski RJ, Towbin JA. Recent advances in the etiology, diagnosis and treatm ent of m yocarditis and cardiom yopathies in children. Curr Opin Pediatr. 1995;7(5):587â€“594. 6. Liu PP, Mason JW: Advances in the understanding of m yocarditis. Circulation. 2001 Aug 28;104(9):1076â€“1082. 7. Oakley CM. Myocarditis, pericarditis and other pericardial diseases. Heart. 2000;84(4):449â€“454.

Codes ICD9-CM 429.0

ICD10 109.0 151.4

Pa ge 3 1 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nasal F ractures

Nasal Fractures

David W. Munter

Basics Description 

Fractures of nasal skeleton are m ost com m on body fractures.



Most nasal fractures are result of blunt traum a, frequently from m otor vehicle crashes, sports injuries, and altercations.



Lateral forces are m ore likely to cause displacem ent than are straight-on blows.



Characteristics that suggest associated injuries: o

History of traum a with significant force

o

Loss of consciousness

o

Findings of facial bone injury

o

Frontal bone crepitus

o

Cerebrospinal fluid (CSF) leak

Etiology 

The vast m ajority of nasal fractures are from direct traum a



Altercations account for m ost nasal fractures in adults



Direct blows, especially sports, account for m ost nasal fractures in children

Pa ge 3 1 6

Diagnosis Signs and Symptoms 

Nasal deform ity, asym m etry, swelling, or ecchym osis



Epistaxis



Periorbital ecchym osis (â€œraccoon eyesâ€•) from dam age to branches of ethm oidal artery: o



May indicate nasofrontoethm oid com plex injury

Palpable sharp edges, depressions, or other irregularities suggest nasal fracture.



Crepitus or m obility of skeletal parts on palpation



Septal hem atom a:



o

Bluish fluid-filled sac overlying nasal septum

o

Critical to detect because it m ust be drained

Flattening of nasal root and widening of intercanthal distance (telecanthus): o

Indicative of serious nasofrontoethm oid com plex injury



Clear rhinorrhea indicates possible CSF leak: o

Rhinorrhea m ay be delayed.



Loss of sense of sm ell suggests significant injury.



Tear duct injuries m ay be present with abnorm al tearing.



Associated eye injuries: o

Subconjunctival hem orrhage

o

Hyphem a

o

Retinal detachm ents

History 

Direct blow



Associated injuries or sym ptom s

Pa ge 3 1 6



Presence of epistaxis



Changes in vision or sm ell

Physical Exam 

Physical exam ination with visual inspection and palpation is m ost im portant.



It is critical to identify a septal hem atom a: o





Bluish bulging m ass on nasal septum

Exam ine closely for telecanthus: o

Intercanthal width >30â€“35 m m

o

Wider than width of one eye

o

May indicate nasofrontoethm oid fracture

o

Usually associated with depressed nasal bridge

CSF rhinorrhea: o

Indicates m ore serious underlying facial bone or skull fracture

o

CSF m ixed with blood will cause double ring sign when placed on filter paper.

Essential Workup 

Evaluate nasolacrim al duct for patency: o

Instill fluorescein into eye and look for it in nasopharynx under inferior turbinate.

o 

Absence im plies duct injury.

Eyelash traction test: o

Grasp eyelashes on eyelid and pull laterally:

o

If eyelid m argin does not becom e taut or â€œbow string,â€• then m edial portion of tendon has been disrupted.

o

This test is perform ed on both upper and lower eyelids. 

Possible for only one portion of tendon to be selectively injured

Pa ge 3 1 6

Tests Imaging 

Nasal radiographs are rarely indicated: o

Norm ally do not alter initial or subsequent m anagem ent

o

Gross deform ities will need referral.

o

Fractures without deform ity will be treated conservatively regardless of radiographic findings.

o

Patients with associated facial bone deform ity, crepitus, or tenderness m ay require radiographs.



CT is test of choice if facial bone, nasofrontoethm oid, or depressed skull fractures are suspected.

Differential Diagnosis 

Other facial injuries such as orbital, frontal sinus, m axillary sinus, or cribriform plate fractures



Nasofrontoethm oid fracture

Treatment Pre Hospital 

Managem ent of airway takes precedence.



Nasotracheal intubation is contraindicated.



Consider orotracheal intubation or cricothyroidotom y if definitive airway control is needed.



Cervical spine precautions are indicated if there is associated traum a.



Epistaxis can norm ally be controlled with direct pressure; pinch nares together.

Initial Stabilization

Pa ge 3 1 6



Airway m anagem ent with orotracheal intubation or cricothyroidotom y: o

Nasotracheal intubation is contraindicated.



Cervical spine precautions



Other injuries take precedence.

P.725

ED Treatment 



Abrasions and lacerations: o

Proper cleansing of facial wounds is essential.

o

Lacerations m ay be sutured.

Epistaxis m ust be controlled if it does not stop spontaneously: o

Anesthetize/vasoconstrict with topical cocaine, lidocaine, or neosynephrine spray.

o

Identify bleeding source; cauterize anterior source if necessary.

o

Pack nares with petroleum jellyâ€“im pregnated gauze or any num ber of com m ercial packs.

o

Posterior packs are rarely needed.

o

Prophylactic antibiotics to prevent sinus infection are indicated if packed.

o

Displaced fractures do not need reduction in ED unless airway is com prom ised.

o

Generally recom m ended to let swelling go down and reduce fracture in 3â€“5 days



Septal hem atom a m ust be drained im m ediately in ED: o

Anesthetize with topical cocaine or lidocaine and vascular constriction with neosynephrine.

o

Attem pt to aspirate with 18- to 20-gauge needle on 3-m L syringe.

Pa ge 3 1 7

o

Rolling cotton swab down septum m ay facilitate drainage.

o

Holding m ucosa down against cartilage m ust be done to prevent reaccum ulation.

o

This can be done with petroleum jelly gauze packing.

o

Both nares should be packed to ensure adequate pressure: 

Packing is left in place for 3â€“5 days or until follow-up with ear, nose, and throat (ENT).

o

Prophylactic antibiotics are prescribed.

Medication (Drugs) 

Am oxicillin: 500 m g PO t.i.d. (peds: 40 m g/kg PO divided t.i.d.)



Am oxicillin/clavulanate: 500/125â€“875/125 m g PO b.i.d. (peds: 40 m g/kg/d of am oxicillin PO b.i.d.



Cocaine: topical 4%



Lidocaine: 1â€“2% without epinephrine



Neosynephrine nasal spray



Trim ethoprim -sulfam ethoxazole: double strength (DS) PO b.i.d. (peds: 40 m g/kg/d sulfam ethoxazole PO b.i.d.)

Follow-Up Disposition Admission Criteria 

Most nasal fractures do not require adm ission.



Adm it patients with nasoethm oid fractures or m ore significant craniofacial injuries.

Pa ge 3 1 7

Discharge Criteria 

No evidence of significant head, neck, or other injuries



Follow up with ENT, plastic surgery, or oral m axillofacial (OMF) surgeon in 3â€“5 days for m anagem ent: o

Patients with septal hem atom a should follow up in 24 hours for re-evaluation after drainage.



Return for signs of clear rhinorrhea, difficulty breathing, fever, or signs associated with head injury.

Pediatric Considerations 

Follow up with specialist sooner because fibrous union begins in only 3â€“4 days.



Consider contacting child protective services if any suspicion of nonaccidental traum a: o

History does not fit injury.

o

Always consider nonaccidental traum a as potential m echanism of injury.



Fractures are rare in children; nasal injuries in children are m ore likely to be cartilaginous.



Significant injuries in children are not always fully appreciated.

References 1. Cox AJ. Nasal fracturesâ€”the details. Facial Plast Surg. 2001;16:87â€“94. 2. Druelinger L, Guenther M, Marchand EG. Radiographic evaluation of the facial com plex. Em erg Med Clin North Am . 2000;18:393â€“410. 3. Ellis E, Scott K. Assessm ent of patients with facial fractures. Em erg Med Clin North Am . 2000;18:411â€“447. 4. Fedok FG. Com prehensive m anagem ent of naso-ethm oidorbital injuries. J Craniom axillofac Surg. 1995;1(4):36â€“48. 5. Hegtvedt AK, Larsen PE. Isolated nasal fractures. Atlas Oral Maxillofac Surg Clin North Am . 1994;2:1â€“18.

Pa ge 3 1 7

6. Kucik CJ, Clenney T, Phelan J. Managem ent of acute nasal fractures. Am Fam Physician. 2004;70:1315â€“1320. 7. Staffel JG. Optim izing treatm ent of nasal fractures. Laryngoscope. 2002;112:1709â€“1719.

Codes ICD9-CM 802.0

ICD10 S02.2

Pa ge 3 1 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Near Dro w ning

Near Drowning

Janet Poponick

Basics Description Definitions 



Drowning: o

Death by suffocation after subm ersion in a liquid

o

Death within 24 hours of the accident

Near drowning: o

Survival beyond 24 hours of subm ersion accident

Scenario of Drowning 

Unexpected subm ersion with struggle



Aspiration of sm all am ount of water



Laryngospasm



Hypoxia

Pathophysiology 

Aspiration: o

Sm all volum e of water

o

No significant electrolyte changes

o

Grossly contam inated water: risk for pulm onary infection



Hypoxem ia:

Pa ge 3 1 7

o

Metabolic lactic acidosis

o

Multisystem organ dysfunction

o

Myocardial dysfunction

o

Coagulation abnorm alities (dissem inated intravascular coagulation [DIC])

o

Renal failure

o

CNS dysfunction

Pediatric Considerations 



Hypotherm ia: o

More com m on in young children

o

Larger body surface-to-m ass ratio

o

Decreases the m etabolic rate

o

Survival with full recovery possible (neuroprotective)

Diving reflex: o

Young children m ore susceptible

o

Potentiated by fear

o

Triggered by subm ersion of face in cold water

o

Bradycardia ensues: redistribution of blood flow to the heart and brain

Diagnosis Signs and Symptoms 

Cardiopulm onary arrest



Cyanosis



Dyspnea



Copious pulm onary secretions



Loss of consciousness



Cerebral edem a/injury



Evidence of traum a:

Pa ge 3 1 7

o 

Cervical spine injury

Hypotherm ia

Essential Workup 

Inform ation from witnesses or em ergency m edical services (EMS) personnel at the scene



Rectal tem perature for hypotherm ia

Tests Lab 

Arterial blood gas



CBC



Electrolytes, BUN, creatinine, glucose:



o

Usually norm al

o

Hyperkalem ia

o

Hypernatrem ia or hyponatrem ia

Alcohol and toxicology screen

Imaging 

Chest radiograph: o

Diffuse or focal infiltrates

o

May be norm al initially



Cervical spine series



ECG: o

Long QT interval

Differential Diagnosis Consider reason for subm ersion 

Dysrhythm ia (long QT syndrom e)



Myocardial infarction



Seizure



Syncope



Traum a

Pediatric Considerations

Pa ge 3 1 7



Consider child abuse/neglect: o

Especially infants in bathtub near drowning

Treatment Pre Hospital 

Attention to airway, breathing, and circulation (ABCs): o

Avoid further aspiration.

o

Apply cricoid pressure during bag-to-m ask ventilation.

o

Secure airwayâ€”intubate.



Strict cervical spine precautions



Ninety percent survival with appropriate intervention

Controversies Abdom inal thrusts to rem ove water: 

Increases risk for aspiration



Useful if foreign body in airway

Initial Stabilization 

ABCs



Core tem perature: o

Initiate rewarm ing (see Hypotherm ia).

o

Rem ove wet clothing.

ED Treatment 

Correct hypoxem ia: o

Titrate to oxygen saturation.

o

Intubate and provide m echanical ventilation with positive end expiratory pressure.



Evaluate and treat traum atic injuries.



Correct acidosis:

Pa ge 3 1 7

o 

Adm inister sodium bicarbonate if pH <7.1.

Cardiopulm onary arrest: o

Initiate advanced cardiac life support (ACLS) m easures.

o

Continue rewarm ing efforts.

o

Continue resuscitation until core tem perature >32Â°C or until spontaneous pulse and respirations return.



Poor prognostic signs: o

Severe acidosis (pH â‰¤7.0)

o

Ventricular fibrillation

o

Low oxygen saturation

P.727

Medication (Drugs) 

Atropine: 1 m g (peds: 0.02 m g/kg) IV



Epinephrine: 1 m g (peds: 0.01 m g/kg) IV



Lidocaine: 1 m g/kg IV



Sodium bicarbonate: 1 m Eq/kg IV

Pediatric Considerations 

Hypotherm ia m ay be protective: o

Aggressive rewarm ing

o

Aggressive resuscitation



Evaluate for child abuse/neglect:



Fam ily history: sudden death, sim ilar episode: o



Long QT syndrom e

Prevention is key to treatm ent: o

Supervision around water

Pa ge 3 1 7

o

Em pty pails and buckets

Follow-Up Disposition Delayed sym ptom atology occurs: 

Pulm onary edem a (12 hours later)



Neurologic abnorm alities

Admission Criteria 

ICU: o

Patients who required cardiopulm onary resuscitation (CPR) or artificial ventilation



o

Abnorm al chest radiograph

o

Arterial blood gas abnorm alities

o

Glascow com a scale (GSC) <13

Adm it observation status: o

Subm ersion for >1 m inute

o

History of cyanosis or apnea

o

Patients who required brief assisted ventilation

o

GCS â‰¥13

Discharge Criteria 

Questionable history of subm ersion: o

Observe in ED for 6â€“8 hours

o

No respiratory distress

o

No neurologic im pairm ent



Discharge to reliable hom e.



Hom e-going instructions: o

Return for shortness of breath or m ental status changes.

Pa ge 3 1 7

References 1. Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncom plicated near-drowning. Am J Em erg Med. 2000;18:9â€“11. 2. Choi G, Kopplin LJ, Tester DJ, et al. Spectrum and frequency of cardiac channel defects in swim m ing-triggered arrhythm ia syndrom es. Circulation. 2004;1102:2119â€“2124. 3. Harries M. Near drowning. Br Med J. 2003;327:1336â€“1338. 4. Zuckerm an GB, Gregory PM, Santos-Dam iant SM. Predictors of death and neurologic im pairm ent in pediatric subm ersion injuries. Arch Pediatr Adolesc Med. 1998;152:134â€“140.

Codes ICD9-CM 994.1

ICD10 W74

Pa ge 3 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Injury by Strangulatio n/Hanging

Neck

Injury by Strangulation/Hanging Patrick Cline Holland David Della-Giustina

Basics Description 

Hanging: o

Com plete: victim 's entire body is suspended off the ground.

o

Incom plete: som e part of victim 's body contacts the ground.

o

Typical: the point of suspension is placed centrally over the occiput.

o

Atypical: the point of suspension is in any position other than over the central occiput.

o

Intentional: suicide, hom icide, autoerotic

o

Accidental: often children or clothing caught in m achinery



Strangulation: o

Ligature: m aterial used to com press structures of neck

o

Manual: physical force used to com press structures of

Pa ge 3 1 8

neck o

Postural: airway obstruction from body weight (over an object) or position (typically in infants)

Etiology 

Hanging or strangulation: o

External neck pressure causes cerebral hypoxia secondary to either arterial or venous obstruction or m ore likely a com bination of both.

o

Pressure on neck structures m ay cause airway, soft tissue, and vascular injuries.

o

Cervical spine injuries are rare except with judicial-type hanging.



Judicial: o

Victim is dropped a distance at least equal to his or her height:

o

Forceful distraction of head from torso results in a decapitation type of injury (fracture of cervical spine and transection of spinal cord).



Death: o

Secondary to m echanical closure of blood vessels or airway

o

Secondary to cardiac arrest from extrem e bradycardia secondary to increased vagal tone from carotid sinus pressure

o

Secondary to direct neurologic injury to the spinal cord

o

Secondary to cerebral hypoxia

Associated Conditions 

Larynx fracture



Hyoid fracture o

Most com m only seen in m anual strangulation

Pa ge 3 1 8



Thyroid cartilage disruption



Vascular disruption: o

Arterial or venous



Phrenic nerve injury



Cervical spine injury



Hypoxic cerebral injury



Airway edem a



Aspiration pneum onitis (m ay be late m anifestation)



Neurogenic pulm onary edem a (m ay be late m anifestation)



Air em bolism : o

Consider when subcutaneous air and vascular injuries are present.

Diagnosis Signs and Symptoms 





Airway disruption: o

Neck ecchym osis or em physem a

o

Dyspnea

o

Dysphonia or stridor

o

Loss of norm al cartilaginous landm arks

Neurologic injury: o

Hoarseness

o

Dysphagia

o

Altered m ental status

o

Neurologic deficit

Vascular injuries: o

Expanding hem atom a

o

Pulse deficits or bruits

o

Evidence of cerebral infarction

o

Subconjunctival or skin petechiae

Pa ge 3 1 8



Cervical spine injury: o

Respiratory arrest

o

Paralysis

Pediatric Considerations 

Structures of neck are m ore cartilaginous and m obile than in adults.



More resistant to crush injuries and fractures



Rapid airway com prom ise can occur with relatively little edem a of soft tissues secondary to sm aller airway diam eter.

Essential Workup 

Plain radiography: o

Cervical spine/soft tissue neck to evaluate for bony injuries as well as soft tissue swelling and subcutaneous em physem a

o

Chest to evaluate for subcutaneous em physem a as well as aspiration pneum onitis



Pulse oxim etry

Tests Lab 

Arterial blood gas: o

Evaluate for evidence of hypoxia or respiratory com prom ise.



Hem atocrit: o



Check for evidence of significant blood loss.

Type and cross-m atch: o

In anticipation of transfusion for vascular injuries

Imaging 

Arteriography: o

Definitive evaluation for potential vascular injuries

Pa ge 3 1 8



CT scan of neck: o

Further defines soft tissue injuries



Carotid duplex im aging with flow studies



CT scan of the brain for suspected cerebral injury or ischem ia

Diagnostic Procedures/Surgery 

Fiberoptic endoscopy: o

Allows direct visualization for evaluation of endolaryngeal injury

o 

May aid in intubation

Surgical exploration

P.729

Treatment Pre Hospital 

Early and aggressive airway m anagem ent: oxygen, suction, intubation



Cervical spine stabilization

Initial Stabilization 

Aggressive airway m anagem ent with cervical spine precautions is param ount: o

Early intubation to preclude respiratory com prom ise



Supplem ental hum idified oxygen



Control bleeding with application of direct pressure: o

Do not explore in the ED.



Em ergent tracheostom y m ay be required.



Cricothyrotom y if severe m axillofacial injuries are

Pa ge 3 1 8

present: o

Avoid if hem atom a over cricothyroid m em brane or evidence of cricotracheal disruption is seen.

o

Arrange for em ergent tracheostom y (see Larynx Fracture).

ED Treatment 

IV access



Consult otolaryngologist in m anagem ent of neck soft tissue injuries.



Elevate head of bed to decrease cerebral edem a.



Monitoring of intracranial pressure if evidence of severe hypoxic cerebral injury



Neck injury with subcutaneous em physem a: o

Assum e that m ucosa of upper airway com m unicates with deep tissues of neck.

o 

Adm inister antibiotics.

Laryngeal edem a: o

Consider steroids.

Medication (Drugs) 

Hypoxic brain injury: o

Mannitol: 0.25â€“1 g/kg IV (for cerebral edem a; not routinely used in pediatric cases)

o 

Phenytoin: 15 m g/kg IV as needed for seizures

Neck injury with subcutaneous em physem a: o

Am picillin/sulbactam : 3 g (peds: 100â€“400 m g/kg/d) IV q6h

o

Clindam ycin: 600 m g (peds: 25â€“40 m g/kg/d) IV q8h



Laryngeal edem a:

Pa ge 3 1 8

o

Dexam ethasone: 4 m g (peds: 0.25â€“0.5 m g/kg) IV q6h

Follow-Up Disposition Admission Criteria 

Adm it patients with strangulation or hanging-m echanism injuries to a m onitored setting: o

To observe for airway com prom ise (m ay have delayed onset)



Prepare for em ergent surgical correction of laryngeal injuries.



All patients with suspected suicidal or hom icidal strangulation injury should have psychiatric or social work consultation.

Discharge Criteria Only patients proven not to have strangulation or hanging injuries m ay be discharged after appropriate observation in the ED for the developm ent of any airway com prom ise or m ental status changes.

References 1. Iserson KV. Strangulation: a review of ligature, m anual and postural neck com pression injuries. Ann Em erg Med. 1984;13:179â€“185. 2. Kaki A, Crosby ET, Lui AC. Airway and respiratory m anagem ent following non-lethal hanging. Can J Anesth. 1997;44:445â€“450. 3. McClane GE, Strack GB, Hawley D. A review of 300 attempted strangulation cases. Part II: clinical evaluation of the surviving victim . J Em erg Med. 2001;21:311â€“315.

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4. Sabo RA, Hanigan WC, Flessner K, et al. Strangulation injuries in children. Part I: clinical analysis. J Traum a. 1996;40:68â€“72. 5. Wahlen BM, Thierbach AR. Near-hanging. Eur J Em erg Med. 2002;9:348â€“350.

Codes ICD9-CM 959.09 Injury of face and neck

ICD10 W84

Pa ge 3 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Traum a, Blunt, Anterio r

Neck Trauma,

Blunt, Anterior Tamaki Kimbro

Basics Description Blunt anterior neck traum a m ay result in various injuries: 

Vascular injuries: o

Carotid or vertebral artery injury

o

Intram ural hem atom a, intim al tear, throm bosis, and pseudoaneurysm

o 



Laryngotracheal injuries: o

Tracheal hem atom a or transection

o

Fracture of thyroid cartilage

o

Vocal cord disruption

Pharyngoesophageal injuries: o



Hem orrhage or neck hem atom a

Hem atom a or perforation of pharynx or esophagus

Nervous system injuries: o

Ischem ic or throm boem bolic events

o

Direct injury to recurrent laryngeal nerve or stellate ganglion resulting in Horner syndrom e



Cervical spine injury

Pa ge 3 1 8

Etiology 

Motor vehicle accidents: o

Unrestrained occupants involved in frontal collisions m ay strike neck on dashboard or steering wheel.

o

Shoulder harness can also cause shearing injury to anterior neck.



Assault: blows to anterior neck from fists, weapons, or other objects



â€œClothesline injuryâ€•: o

Motorcycle, snowm obile, or all-terrain vehicle

o

Drivers strike neck on cord or wire suspended between two objects.



Strangulation

Pediatric Considerations Head is proportionally larger in children, increasing risk of acceleration-deceleration injury to neck.

Diagnosis Signs and Symptoms 

Presentation varies depending on m echanism of injury and structures involved: o

o

Vascular injury: 

Hem orrhage, ecchym osis, edem a



Loss of character of lateral neck profile



Carotid bruit or thrill



Neurologic deficits (often delayed)

Laryngotracheal injury: 

Voice changes, hoarseness, aphonia



Dyspnea, inspiratory stridor, labored breathing

Pa ge 3 1 9



Subcutaneous em physem a, tenderness to palpation

o

o

Pharyngoesophageal injury: 

Dysphagia, odynophagia, hem atem esis



Tenderness to palpation



Infection, sepsis (delayed presentation)

Neurologic injury: 

Central or peripheral nervous system deficits

Physical Exam 

Ensure adequate airway.



Inspection of neck for hem orrhage, ecchym osis, edem a, or distortion of anatom y



Auscultation for carotid bruits



Palpation to detect tenderness or subcutaneous em physem a



Neurologic exam ination to detect evidence of ischem ic event, spinal cord injury, or peripheral nerve dam age

Tests Lab 

Type and cross-m atch.



Baseline CBC and chem istry panel

Imaging 

Cervical spine radiographs



Chest radiograph to rule out associated injury to thorax



Carotid duplex ultrasound is noninvasive, rapid screening test for arterial injury.



CT m ay be used in stable patient to evaluate laryngotracheal injury, cartilage disruption, or cervical spine injury.



Angiography is still considered standard for evaluation of

Pa ge 3 1 9

arterial injury. 

Indications for angiography: o

Presence of carotid bruit

o

Pulse deficit

o

Expanding hem atom a

o

Neurologic abnorm ality unexplained by intracranial injuries

Diagnostic Procedures/Surgery 

Unstable patients m ust go directly to surgery.



Endoscopy to detect internal soft tissue defects in larynx and trachea



Indications for esophagram or rigid esophagoscopy: o

Odynophagia

o

Hem atem esis

o

Subcutaneous em physem a

Differential Diagnosis 

Peripheral or central nervous system injury



Cervical spine injury



Associated head or thoracic traum a

P.731

Treatment Pre Hospital 

Airway m ust be vigilantly m onitored: o

Edem a or expanding hem atom a can progress to airway com prom ise.



Early oral intubation indicated for clinical signs of

Pa ge 3 1 9

respiratory distress:



o

Stridor

o

Air hunger

o

Labored breathing

o

Expanding neck hem atom a

Blind nasotracheal intubation should be avoided: o

Owing to anatom y distortion and risk of hem atom a rupture



Cervical spine m ust be stabilized.

Initial Stabilization Airway m anagem ent with cervical spine control: 

Im m ediate intubation indicated for patients with signs of airway com prom ise or im pending com prom ise



Orotracheal intubation initial m ethod of choice



Cricothyroidotom y or em ergent tracheostom y m ay be needed if oral intubation is unsuccessful.



Care should be taken to avoid puncturing neck hem atom a during invasive procedures.



Bleeding into pharynx can be reduced by packing throat with heavy gauze after airway is secured by intubation.



Unstable patients m ust go directly to OR.

General Measures 

Surgical consultation should be obtained for patients with suspicion of vascular, tracheal, or esophageal injury.



Im m ediate surgical repair required for sym ptom atic vascular injury, tracheal injury, pharyngeal or esophageal injury



Laryngeal injury m ay not require im m ediate surgical repair.



Once airway is secured, patient should be placed on voice rest, hum idified oxygen, and prophylactic antibiotics.

Pa ge 3 1 9

Medication (Drugs) Prophylactic antibiotics recom m ended in presence of laryngotracheal or pharyngoesophageal injury: 

Cefoxitin: 2 g (peds: 80â€“160 m g/kg/d div. q6h) IV q8h or



Clindam ycin: 600â€“900 m g (peds: 25â€“40 m g/kg/d div. q6hâ€“q8h) IV q8h or



Penicillin G: 24 m IU (peds: 150,000â€“250,000 IU/kg/d div. q4hâ€“q6h) IV per day div. q4hâ€“q6h plus



Metronidazole: 1 g load, then 500 m g (peds: 30 m g/kg/d div. q12h) IV q6h

Follow-Up Disposition Admission Criteria 

Patients who are sym ptom atic, have abnorm al studies, or have significant blunt traum a m echanism m ust be adm itted and observed for at least 24 hours.



Patients with suspicion of airway or vascular injury m ust be adm itted to ICU.

Discharge Criteria Only patients with m ost trivial injuries who have negative studies m ay be discharged from ED after thorough evaluation.

References 1. Fuhrm an GM, Stieg FH, Buerk CA. Blunt laryngeal traum a. J Traum a. 1990;30:87.

Pa ge 3 1 9

2. McKevitt EC, Kirkpatrick AW, Vertesi L, et al. Blunt vascular neck injuries: diagnosis and outcom es of extracranial vessel injury. J Traum a. 2002;53(3):472â€“476. 3. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic m odalities and outcom es. Ann Surg. 2002;236(3):386â€“393. 4. Newton K. Neck traum a. In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 371. 5. Sweeney TA, Marx JA. Blunt neck injury. Em erg Med Clin North Am . 1993;11:71â€“79.

Codes ICD9-CM 959.09 Injury of face and neck

ICD10 S19.8

Pa ge 3 1 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Traum a, Penetrating, Anterio r

Neck

Trauma, Penetrating, Anterior Tamaki Kimbro

Basics Description 

Wound that penetrates platysm a m uscle



Neck is divided into three zones based on superficial landm arks: o

Zone I lies below cricoid cartilage: 

Penetrating traum a in this zone carries highest m ortality owing to injury to thoracic structures.

o

Zone II lies between cricoid cartilage and angle of m andible: 

Zone II wounds have lower m ortality because hem orrhage can be controlled with direct pressure.



Structures m ore easily accessible for surgical exploration

o

Zone III lies above angle of m andible.

Pediatric Considerations Larynx is located higher in neck and receives better protection from m andible and hyoid bone.

Pa ge 3 1 9

Etiology 

Gunshot wounds



Stab wounds



Miscellaneous (e.g., glass shards, m etal fragm ents, anim al bites)

Diagnosis Signs and Symptoms 

Vary depending on specific structures injured



Vascular injury: o

Active hem orrhage or hem atom a

o

Tracheal deviation, loss of norm al anatom ic landm arks







o

Pulse deficits in upper extrem ities

o

Thrills or bruits in neck

Laryngotracheal injury: o

Respiratory distress

o

Hoarseness, voice changes

o

Hem optysis

o

Neck pain or tenderness

o

Crepitus

Pharyngoesophageal injury: o

Dysphagia

o

Odynophagia

o

Hem atem esis

Neurologic injury: o

Central or peripheral nervous system deficits

Physical Exam 

Careful exam ination of wound to determ ine extent of

Pa ge 3 1 9

injury and whether it penetrates platysm a 

Wounds should never be probed blindly: o

May result in uncontrolled hem orrhage

Essential Workup 

Lateral neck radiograph to evaluate soft tissue injury and detect foreign bodies



Chest radiograph to detect hem opneum othorax, m ediastinal air, or bleeding that extends into upper m ediastinum

Tests Lab 

Type and cross-m atch.



Baseline CBC and chem istry panel

Imaging 

Angiography: o

Considered standard for evaluating arterial injury

o

Indicated for penetrating wounds in zone I or zone III



CT angiography can be used in stable patients to screen for vascular, cervical spine, or laryngotracheal injury.



Color duplex ultrasound: noninvasive, rapid screening test for arterial injury



Esophagram with water soluble contrast or dilute barium : o

Low sensitivity

o

Com bine with esophagoscopy to exclude injury.

o

Indications: Wound approaches/crosses m idline, subcutaneous air.

Diagnostic Procedures/Surgery Bronchoscopy can be helpful in evaluating tracheal injury.

Differential Diagnosis

Pa ge 3 1 9



Peripheral or central nervous system injury



Cervical spine injury



Associated head or thoracic traum a

Treatment Pre Hospital 

Frequent suctioning to clear airway of blood, secretions, or vom itus



Lateral decubitus or prone positioning m ay be required to prevent aspiration.



Airway m ust be vigilantly m onitored, as edem a or expanding hem atom a can progress to airway com prom ise.



Indications for early oral intubation: o

Clinical signs of respiratory distress

o

Stridor

o

Air hunger

o

Labored breathing

o

Expanding neck hem atom a

Alert 



Nasotracheal intubation should be avoided: o

Potential rupture of expanding hem atom a

o

Distortion of anatom y.

Occlusive dressings should be applied to lacerations over m ajor veins to prevent air em bolism .

Initial Stabilization 

Airway m anagem ent with cervical spine control: o

Patients who are in respiratory distress or com atose require im m ediate intubation.

o

Patients who are stable without evidence of

Pa ge 3 1 9

respiratory distress m ay be m anaged aggressively with prophylactic intubation or observed closely with airway equipm ent at bedside. o

Orotracheal intubation with rapid-sequence induction is m ethod of choice for securing airway in penetrating neck traum a.

o

Blind nasotracheal intubation is contraindicated with apnea, severe facial injury, or airway distortion.

o

Endoscopic intubation is contraindicated with active bleeding that m ay obscure scope.

o

Percutaneous transtracheal ventilation m ay be useful when oral or nasotracheal intubation fails: 

This is contraindicated in cases of upper airway obstruction.



May cause barotraum a

P.733

o

Cricothyroidotom y, tracheostom y, or intubation via penetrating wound m ay be required in cases of severe facial injury, laryngotracheal injury, or uncontrolled upper-airway hem orrhage.



Breathing: o

Zone I injury can cause pneum othorax or subclavian vein injury and hem othorax: 

May require needle decom pression and tube thoracostom y



Circulation: o

External hem orrhage: 

Control with direct pressure.



Blind clam ping of vessels is contraindicated owing to risk of further neurovascular injury.

Pa ge 3 2 0

o

Uncontrolled bleeding or hem odynam ic instability: Send directly to OR.

o

After intubation, throat can be packed with heavy gauze to tam ponade bleeding.

o

Hem othorax: tube thoracostom y

General Measures 

Nasogastric tube should not be placed because of risk of rupturing pharyngeal hem atom a.



Prophylactic antibiotics are recom m ended (cefoxitin, clindam ycin, penicillin G plus m etronidazole).



Tetanus prophylaxis

Medication (Drugs) 

Cefoxitin: 2 g (peds: 80â€“160 m g/kg/d div. q6h) IV q8h or



Clindam ycin: 600â€“900 m g (peds: 25â€“40 m g/kg/d div. q6hâ€“q8h) IV q8h or



Penicillin G: 2.4 m IU (peds: 150,000â€“250,000 IU/kg/d div. q4hâ€“q6h) IV per day div. q4hâ€“q6h plus



Metronidazole: 1 g load, then 500 m g (peds: 30 m g/kg/d div. q12h) IV q6h

Surgery 

Surgical consult for all wounds that penetrate platysm a m uscle



Controversy exists regarding m andatory versus selective surgical exploration in stable patients: o

Mandatory approach: 

Surgical exploration is indicated in all cases of penetrating neck traum a because significant injury m ay not m anifest outward signs or

Pa ge 3 2 0

sym ptom s. o

Selective approach: 

Surgical exploration for specific indications



Expanding or pulsatile hem atom a



Active bleeding



Absence of peripheral pulses



Hem optysis



Horner syndrom e



Bruit



Subcutaneous em physem a



Respiratory distress



Air bubbling through wound

Follow-Up Disposition Admission Criteria 

All patients with penetrating neck traum a should be adm itted and observed for at least 24 hours.



Observation m ust take place in facility capable of providing definitive surgical care.



Patients with injuries suggesting airway or vascular injury m ust be adm itted to ICU.

Discharge Criteria Asym ptom atic patients who have negative studies m ay be discharged after 24 hours of observation.

References 1. Carducci B, Lowe RA, Dalsey W. Penetrating neck traum a: consensus and controversies. Ann Em erg Med. 1986;15:208.

Pa ge 3 2 0

2. Kendall JL, Anglin D, Dem etriades D. Penetrating neck traum a. Em erg Med Clin North Am . 1998;16:85â€“105. 3. Munera F, Cohn S, Rivas LA. Penetrating injuries of the neck: use of helical com puted tom ographic angiography. J Traum a. 2005;58(2):413â€“418. 4. Newton K. Neck traum a. In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 371. 5. Rathlev NK. Penetrating neck traum a: m andatory versus selective exploration. J Em erg Med. 1990;8:75â€“78.

Codes ICD9-CM 959.09 Injury of face and neck

ICD10 S19.8

Pa ge 3 2 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Necro tiz ing So ft Tissue Infectio ns

Necrotizing

Soft Tissue Infections Karen B. Van Hoesen

Basics Description 

Necrotizing soft-tissue infections are usually caused by toxin-producing, virulent bacteria.



Characterized by widespread fascial and m uscle necrosis with relative sparing of the skin



Crepitant anaerobic cellulitis: o

Necrotic soft-tissue infection with abundant connective tissue gas



Progressive bacterial gangrene: o

Slowly progressive erosion affecting the total thickness of skin but not involving deep fascia



Nonclostridial m yonecrosis (synergistic necrotizing cellulitis): o

Aggressive soft-tissue infection of skin, m uscle, subcutaneous tissue and fascia



Necrotizing fasciitis: o

Progressive, rapidly spreading infection with extensive dissection and necrosis of the superficial

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and deep fascia 

Fournier gangrene: o

Mixed aerobic-anaerobic soft-tissue necrotizing fasciitis of the skin of the scrotum and penis in m en and the vulvar and perianal skin in wom en

Etiology 

Conditions that lead to the developm ent of necrotizing soft-tissue infections: o

Local tissue traum a with bacterial invasion

o

Local ischem ia and reduced host defenses: 

More frequently in diabetics, alcoholics, im m unosuppressed patients, IV drug users, and patients with peripheral vascular disease



Polym icrobial etiology including: o

Group A Î²-hem olytic streptococcus (GABHS); group B streptococcus, staphylococci, enterococci, bacillus, pseudom onas, Enterobacter, Bacteroides, clostridia, and Vibrio species



Possible relationship between the use of NSAIDs and severe invasive GABHS infections has been suggested.

Diagnosis Signs and Symptoms 

Rapid progression of pain and swelling of involved area



Pain out of proportion to physical findings



In first 24 hours, rapid developm ent of local swelling, heat, erythem a, and tenderness



24â€“48 hours: purple and blue discoloration, blisters and bullae develop (often hem orrhagic)

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

Necrosis of fascia and fat produces a watery, thin, foul-sm elling fluid.



System ic toxicity with fever, tachycardia, and depressed m entation

Pediatric Considerations 

Neonates: Om phalitis and circum cision are predisposing factors



Children: surgery, traum a, varicella, and congenital and acquired im m unodeficiencies are m ajor factors for the developm ent of necrotizing fasciitis: o

GABHS necrotizing fasciitis as a com plication of varicella has been reported

Physical Exam 

Skin: erythem a, tense edem a, grayish or other discolored wound drainage, vesicles or bullae, necrosis, ulcers or crepitus



Pain that extends past m argin of infection



General: fever, tachycardia, diaphoresis, toxic delirium

Essential Workup 

Diagnosis can be difficult.



Careful exam ination for the aforem entioned signs and sym ptom s in high-risk patients



Necrotizing soft-tissue infections m ust be suspected in patients who appear very ill and have pain out of proportion to physical findings.



Diagnosis requires incision and probing of tissue.

Tests Lab 

CBC with differential, electrolytes, blood urea nitrogen, and creatinine, dissem inated intravascular coagulation

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panel 

Calcium level: hypocalcem ia can develop from extensive fat necrosis.



Gram stain and aerobic/anaerobic cultures of wound or tissue biopsy

Imaging 

X-rays to detect soft-tissue gas



CT scan or MRI can delineate extent of spread of the infection

Diagnostic Procedures/Surgery All patients with suspected necrotizing soft tissue infections m ust undergo surgical debridem ent.

Differential Diagnosis 

Cellulitis



Gas gangrene

Treatment Pre Hospital IV fluid resuscitation

Initial Stabilization Manage airway and resuscitate as indicated: 

Rapid sequence intubation as needed



Supplem ental oxygen, m onitor, evaluate for acid-base disturbances



IV access, CVP line m ay be needed



Aggressive volum e expansion including crystalloid, plasm a, packed RBCs, and album in

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ED Treatment 

Antibiotics: broad coverage of aerobic gram -positive and gram -negative organism s and anaerobes: o

Penicillin or cephalosporin, an am inoglycoside, and anaerobic coverage with either clindam ycin or m etronidazole

o

Penicillin G if strep or clostridia

o

Im ipenem cilastatin or m eropenem if polym icrobial

o

Am picillin-sulbactam (Unasyn)

o

Piperacillin-tazobactam (Zosyn)

P.735



Surgical consultation: o

Early dÃ©bridem ent of all necrotic tissue with fasciotom y and drainage of fascial planes is param ount



Hyperbaric oxygen as an adjunct: o

Early transfer to hyperbaric facility m ay result in greater tissue salvage



Observe for m ajor com plications including acute respiratory distress syndrom e, renal failure, m yocardial irritability, and DIC

Medication (Drugs) 

Am picillin-sulbactam (Unasyn): 1.5â€“3 g (peds: 100â€“400 m g/kg/d of am picillin div. q6h) IV q6h



Ceftriaxone: 2 g (peds: 100 m g/kg/24h; m ax. 4 g) IV q24h



Clindam ycin: 900 m g (peds: 40 m g/kg/d q6h) IV q8h



Gentam icin: 2.0 m g/kg (peds: 2.0 m g/kg IV q8h) IV q8h

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

Im ipenem -cilastatin: 250â€“1,000 m g IV q6hâ€“q8h



Meropenem 1 g (peds: 20â€“40 m g/kg up to 2 g/dose) IV q8h



Metronidazole: 500 m g (peds: safety not established) IV q8h



Penicillin G: 24 m IU/24 h (peds: 250,000 IU/kg/24h) IV q4hâ€“q6h



Piperacillin-tazobactam 3.375â€“4.5 g (peds: 240 m g/kg/d pf piperacillin div. q8h) IV q6h

Follow-Up Disposition Admission Criteria 

All patients with a necrotizing soft-tissue infection m ust be adm itted for surgical dÃ©bridem ent and IV antibiotics.



Early hyperbaric oxygen therapy is an im portant adjunct.

Discharge Criteria No patient with necrotizing soft tissue infection should be discharged.

Issues for Referral After stabilization with antibiotics and surgical dÃ©bridem ent, consider referral for hyperbaric oxygen treatm ent as an adjunct.

References 1. DiNubile MJ, Lipsky BA. Com plicated infections of skin and skin structures: when the infection is m ore than skin deep. J Antim icrob Chem other. 2004 Jun;53 Suppl 2:ii37â€“50. 2. Headley AJ. Necrotizing soft tissue infections: a primary care review. Am Fam Physician. 2003 Jul 15;68(2):323â€“328. 3. Legbo JN, Shehu BB. Necrotizing fasciitis: a com parative analysis

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of 56 cases. J Natl Med Assoc. 2005 Dec;97(12):1692â€“1697. 4. Perry BN, Floyd WE 3rd. Gas gangrene and necrotizing fasciitis in the upper extrem ity. J Surg Orthop Adv. 2004 Sum m er;13(2):57â€“68. 5. Wilkinson D, Doolette D. Hyperbaric oxygen treatm ent and survival from necrotizing soft tissue infection. Arch Surg. 2004 Dec;139(12):1339â€“1345.

Codes ICD9-CM 709.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Necro tiz ing Ulcerative G ingivitis

Necrotizing

Ulcerative Gingivitis Stephen K. Epstein Laura B. Glicksman

Basics Description 

Periodontal disease



Characterized by the â€œpunched outâ€• appearance of the gingival papillae



Synonym (s): o

Acute necrotizing ulcerative gingivitis

o

Trench m outh

o

Vincent disease

o

Fusospirochetal gingivitis



Not contagious



Occurs m ost often in children in developing nations.



Occurs m ost often in young adults in developed countries.



Males affected m ore than fem ales



Can progress to m ore advanced disease:



o

Necrotizing ulcerative periodontitis

o

Orofacial gangrene (nom a)

Mainly occurs in sub-Saharan Africa

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

Rare; seen m ostly in severely im m unocom prom ised patients

Etiology 

Caused by an overgrowth of oral flora



Prevotella interm edia



Spirochetes



Predisposing factors (not required for diagnosis): o

Em otional and physical stress

o

Poor oral hygiene/gingivitis

o

Sm oking

o

Im m unodeficiencies (e.g., HIV)

o

Im m unosuppression

o

Malnutrition

Diagnosis Signs and Symptoms Essential Clinical Features 

Painful gingival lesions



â€œPunched-out,â€• craterlike ulcers of the papillae



Ulcers bleed easily or spontaneously

Non-Essential Clinical Features 

â€œPseudom em braneâ€• of necrotic debris covering the ulcerated area



Foul breath



Fever/m alaise

History 

Acute, generalized oral pain



Bleeding gum s:

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o

Spontaneous or with m inim al m anipulation



Foul breath



Malaise



Low-grade fever

Physical Exam 

Loss of interdental papillae (key clinical feature)



â€œPunched-out,â€• craterlike ulcers of the papillae



Necrotic debris often present over ulcerated surfaces



â€œPseudom em braneâ€• of inflam m atory and necrotic cells



Covers ulcerative lesions



Leaves a bleeding surface when rem oved



Lym phadenopathy, particularly subm andibular



Foul breath



Low-grade fever

Essential Workup 



Consider system ic disease: o

Neutropenia

o

HIV

Other reasons for im m unosuppression or im m unocom prom ise



Rule out com plications: o

Progression to necrotizing ulcerative periodontitis

o

Lesions extending to periodontal ligam ent and alveolar bone

o

Alveolar bone destruction

o

Progression to orofacial gangrene (nom a)

Tests Lab Laboratory tests not clinically helpful

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Differential Diagnosis 

Other diseases rarely have the essential clinical feature of â€œpunched-outâ€• interdental papillae with ulcerations



Infectious diseases: o







Acute herpetic gingivostom atitis: 

Affects entire gingival, not just papillae



Low grade fever com m only present



Contagious

Viral: o

Viral infections: Epstein-Barr, Varicella Zoster virus

o

Thrush

o

Actinom ycosis

o

Streptococcal/gonococcal gingivitis/stom atitis

o

Secondary syphilis

o

Diphtheria

o

Vesiculobullous disease

o

Pem phigoid

o

Pem phigus

o

Oral lichen planus

o

System ic lupus erythem atosus

Traum a: o

Toothpicks

o

Vigorous toothbrushing/flossing

Im m unocom prom ise: o

Leukem ia

o

Agranulocytosis (m alignant neutropenia)

o

HIV

P.737

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Treatment Initial Stabilization IV fluids for dehydration

ED Treatment 



Adm inister system ic and topical pain m anagem ent: o

Narcotics rarely necessary

o

Viscous lidocaine

DÃ©bride pseudom em brane: o

Use gauze or cotton-tip applicator soaked in diluted H 2



O2 .

Antibiotics (penicillin/m etronidazole or clindam ycin) when indicated:



o

Fever

o

Lym phadenopathy

Institute outpatient therapy: o

Rem ove predisposing factors.

o

Dilute hydrogen peroxide rinses.

o

Chlorhexidine gluconate (Peridex)

o

Antibiotics if indicated

o

Avoid irritants (spicy foods, hot beverages).

o

Analgesics for pain control

o

Im prove oral hygiene with daily brushing and flossing of teeth.

Medication (Drugs) 

Oral rinses: o

Chlorhexidine gluconate (Peridex): 15 m L swish/spit b.i.d.

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o

Hydrogen peroxide (3% solution diluted in half): rinse up to 12 tim es daily



Metronidazole: 250â€“750 m g (peds: 30 m g/kg/q24h) PO q.i.d. Ã—7 days



Penicillin VK: 500 m g (peds: under age 12, 25â€“50 m g/kg q24h) PO q.i.d. Ã—10 days



Clindam ycin: 300 m g PO (peds: 6â€“8 m g/kg q24h) t.i.d.

Follow-Up Disposition Admission Criteria 

Extensive disease with system ic signs



Severe dehydration/inability to tolerate PO fluids



Evidence of orofacial gangrene (nom a): infection of m outh/face: o

70% m ortality with no treatm ent

Discharge Criteria Able to m aintain hydration

Issues for Referral Urgent referral to a dentist or periodontist for deep scaling and debridem ent

References 1. Am erican Academ y of Periodontology. Param eter on acute periodontal diseases. J Periodont. 2000;71(5 suppl):863â€“866. 2. Am erican Academ y of Periodontology. Treatm ent of Plaque-Induced Gingivits, Chronic Periodontitis, and Other Clinical Conditions. J Periodontol. 2001;72:1790â€“1800. 3. Am erican Academ y of Periodontology. Periodontal Diseases of

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Children and Adolescents. J Periodontol. 2003;74:1696â€“1704. 4. Corbet EF. Diagnosis of acute periodontal lesions. Periodontol. 2000. 2004;34:204â€“216. 5. Berm ejo-Fenoll A, Sanchez-Perez A. Necrotising periodontal diseases. Med Oral Patol Oral Cir Bucal. 2004;9(Suppl):S108â€“19. 6. Enwonwu CO, Falkler WA, Idigbe EO. Oro-facial gangrene (nom a/cancrum oris): pathogenetic m echanism s. Crit Rev Oral Biol Med. 2000;11(2):159â€“171. 7. Musa NJ, Kum ar V, Hum prheys L, et al. Oral Pem phigoid Masquerading as Necrotizing Ulcerative Gingivitis in a Child. J Periodontol. 2002;73:657â€“663. 8. Rowland RW. Necrotizing Ulcerative Gingivitis. Ann Periodontol. 1999;4:65â€“73. 9. Periodontal Em ergencies, in The Periodontic Syllabus (Fedi PF editor). Phildelphia: Lea & Febinger, 1985.

Codes ICD9-CM 523.0

ICD10 A69.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Needle Stick

Needle Stick

Gordon Chew

Basics Description Mechanism s of exposure to blood or body fluid: 

Percutaneous



Mucous m em brane



Skin

General Prevention 

Universal precautions



Avoid recapping of needles



Wear gloves: decreases am ount of blood exposure by 50%



Double gloving



Follow bodyâ€“substance isolation protocols.



Hepatitis B virus vaccination

Risk Factors 

Risk of seroconversion from a single needle-stick exposure without prior im m unization: o

Hepatitis B virus: 37â€“62% from HBsAg-positive and HBeAg-positive source, 23â€“37% from HBsAg-npositive and HBeAgnegative source

o

Hepatitis C virus: 1.8%

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o 

HIV: blood 0.3%, m ucous m em brane 0.09%

Infectiousness of various body fluids for HIV: o

Plasm a/serum : 10â€“5,000 ppm

o

Cerebrospinal fluid: 10â€“1,000 ppm

o

Sem en: 10â€“50 ppm

o

Vaginal secretions, urine, saliva, tears, breast m ilk: <1 ppm



Factors affecting risk: o

Viral load

o

Actual injection volum e

o

Type and size of needle

o

Portal of entry (depth of inoculation)

o

Duration of contact

o

Level of disease in source patient

o

Host susceptibility

o

Barriers (e.g., through gloves)

Diagnosis Signs and Symptoms History Exposure to blood or body fluid 

Date, tim e, circum stances, details of exposure, source



Im m unizations

Tests Fem ales with body-fluid exposure who are considering antiviral therapy m ust have serum or urine pregnancy testing.

Lab To be done with occupational health if possible: 

Baseline serology for HIV (enzym e im m unoassay, Western

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blot), hepatitis B virus, hepatitis C virus (anti-HCV), ALT 

Assess adequacy of hepatitis B virus vaccination.



Obtain consent from source patient for HIV (consider rapid HIV-antibody test), hepatitis B virus, hepatitis C virus (anti-HCV) testing.

Imaging 

Not applicable unless concerned for retained tissue foreign body

Differential Diagnosis Principally concerned with transm ission of hepatitis B virus, hepatitis C virus, and HIV

Treatment Pre Hospital Alert 

Prehospital personnel should always m aintain universal precautions to prevent needlestick or other body fluid exposure.



Patients with exposure should be evaluated for prophylactic therapy.

Initial Stabilization 

Copious cleaning, wound care



Direct and im m ediate referral to occupational health when available to ensure strictest confidentiality in laboratory testing and treatm ent



In the ED after hours, patients with needlestick exposure m ust be triaged with high priority, as tim e is im portant in the initiation of prophylactic therapy.

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ED Treatment General Measures 

If referral to occupational health unavailable, initiate prophylactic therapy in ED.



Tetanus prophylaxis if necessary



HIV: o

Begin basic versus expanded antiretroviral prophylaxis regim e after considering HIV status of source and severity of exposure. Som e organizations advocate only the expanded three-drug regim en. Treat for 28 days.

o

Basic regim en: 

Zidovudine (AZT) plus lam ivudine (3TC); also sold as com bination drug Com bivir; or

o



Lam ivudine (3TC) plus stavudine (d4T); or



Didanosine (ddI) plus stavudine (d4T)

Expanded regim en: basic regim en plus one of the following:

o



Indinavir



Nelfinavir



Efavirenz



Abacavir

Other retroviral agents are available, but should not be used routinely. Consider only after expert consultation. These include ritonavir, saquinavir, am prenavir, delavirdine, nevirapine, lopinavir/ritonavir (Kaletra).



o

Safer sex advice

o

Counseling

Hepatitis B virus: known HB s Ag-positive source: o

Com plete vaccination confirm ed by titer: no

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prescription o

Incom plete vaccination: hepatitis B virus vaccine booster

o

Unvaccinated: hepatitis B im m une globulin as soon as possible, begin hepatitis B virus vaccine series. P.739

o

Nonresponder to vaccine: hepatitis B im m une globulin as soon as possible, repeat in 30 days; consider revaccination with three-dose series.

o

Unknown responder to vaccine with inadequate titer: hepatitis B im m une globulin as soon as possible, vaccine booster





Hepatitis B virus: known HB s Ag-negative source: o

Vaccinated: no prescription

o

Unvaccinated: hepatitis B virus vaccine series

Hepatitis B virus: unknown source: o

Com plete vaccination confirm ed by titer: no prescription

o

Incom plete vaccination: hepatitis B virus vaccine booster

o

Unvaccinated: Begin vaccine series.

o

Nonresponder to vaccine: hepatitis B im m une globulin as soon as possible with revaccination three-dose series, repeat hepatitis B im m une globulin in 30 days if high-risk exposure.

o

Unknown responder to vaccine with inadequate titer: vaccine booster and recheck titer in 1â€“2 m onths



Hepatitis C virus: use of im m unoglobulins or antivirals (interferon, ribavirin) inconclusive as prophylaxis, but possibly beneficial if initiated early when infection evident

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Medication (Drugs) HIV: 

Zidovudine: o

300 m g PO b.i.d.

o

Side effects: gastrointestinal sym ptom s, headache, fatigue, m yalgias, m arrow suppression, seizure



Lam ivudine: o

150 m g PO b.i.d.

o

Side effects: gastrointestinal sym ptom s, headache, fatigue, neuropathy, congestion, cough (caution with trim ethoprim /sulfam ethoxazole)



Com bivir (com bination zidovudine plus lam ivudine): o

1 tablet PO b.i.d.

o

Side effects: See side effect profiles of zidovudine and lam ivudine



Didanosine: o

400 m g PO daily; or if wt <60 kg, then 125 m g PO b.i.d.

o

Side effects: pancreatitis, gastrointestinal sym ptom s, lactic acidosis, neuropathy



Stavudine: o

40 m g PO b.i.d.; or if wt <60 kg, then 30 m g PO b.i.d.

o

Side effects: peripheral neuropathy, gastrointestinal sym ptom s, headache, pancreatitis, elevated liver function tests, neutropenia, anem ia



Indinavir: o

800 m g PO q8h

o

Side effects: nephrolithiasis, hyperbilirubinem ia, gastrointestinal sym ptom s

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

Nelfinavir: o

1250 m g PO b.i.d.

o

Side effects: gastrointestinal sym ptom s, weakness, rash



Efavirenz: o

600 m g PO at bedtim e

o

Side effects: Stevens-Johnson syndrom e, rash, sleep disruption, dizziness, psychiatric



Abacavir: o

300 m g PO b.i.d.

o

Side effects: hypersensitivity reactions, gastrointestinal sym ptom s, headache, fatigue



For som e of the antiretroviral agents, the oncogenic and teratogenic effects are unknown.

Hepatitis B: 

Hepatitis B im m une globulin: 0.06 m L/kg IM



Hepatitis B virus booster: unit-dose vial

Follow-Up Disposition Admission Criteria Adm ission not necessary

Discharge Criteria Patients can be m anaged as outpatients with appropriate follow-up in occupational m edicine clinic.

References 1. Beltram i EM, William s IT, Shapiro CN, et al. Risk and m anagem ent of blood-borne infections in health care workers. Clin Microbiol Rev.

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2000;13:385â€“407. 2. Centers for Disease Control and Prevention. Updated U.S. Public Health Service guidelines for m anagem ent of occupational exposures to HBV, HCV, and HIV and recom m endations for postexposure prophylaxis. MMWR Recom m Rep. 2001;50(RR-11)1â€“42. 3. Henderson DK. Risk for exposures to and infection with HIV am ong health care providers in the em ergency departm ent. Em erg Med Clin North Am . 1995;13:199â€“211. 4. Lutwick L. Postexposure prophylaxis. Infect Dis Clin North Am . 1996;10:899â€“915.

Miscellaneous SEE ALSO: National Clinicians' Postexposure Prophylaxis Hotline: Phone (888) 448-4911; Internet: http://www.ucsf.edu/hivcntr. Accessed 11/15/05.; MMWR Recom m Rep. 2001;50(RR-11)

Codes ICD9-CM 998.2 Accidental puncture or laceration during a procedure

ICD10 T75.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neo natal Jaundice

Neonatal Jaundice

Michele Chetham

Basics Results from a transient im balance between rates of bilirubin production and bilirubin elim ination: 

Newborns have higher rates of bilirubin production than adults because of increased RBC m ass and shorter RBC life span.



Newborns, especially preterm infants, have rate lim itations in hepatic conjugation and biliary excretion of bilirubin, increased enterohepatic circulation, and dim inished bilirubin binding to album in- and bilirubin-binding protein.

Alert Although norm ally benign, significantly elevated bilirubin can cause significant injury and reflect a potentially life-threatening underlying condition.

Description 

In the vast m ajority of newborns, this represents physiologic jaundice and is not pathologic: o

Bilirubin norm ally increases from 1.5 m g/dL in cord blood to a m ean of 6.5 m g/dL on day 3, followed by a gradual decline to norm al adult levels of 1.5 m g/dL

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by day 10 or 12 of life: 

However, serum bilirubin levels m ay rise to dangerous levels exceeding neuroprotective defenses causing bilirubin toxicity to the basal ganglia, hippocam pus, brainstem nuclei and cerebellum .

o

Acute bilirubin encephalopathy (ABE) describes the acute m anifestations of bilirubin toxicity seen in the first weeks after birth.

o

Kernicterus is the chronic form of bilirubin encephalopathy, resulting in significant m ortality; survivors m ay have serious neurologic consequences including a choreoathetoid type of cerebral palsy, gaze abnorm alities, hearing loss, and dental dysplasia.

o

Bilirubin-induced neurologic dysfunction (BIND) refers to the wide spectrum of disorders caused by increasingly severe hyperbilirubinem ia from m ild dysfunction to ABE and kernicterus.

o

Rate of progression of BIND depends on rate of increase of bilirubin levels, duration of hyperbilirubinem ia, album in-binding reserves, unbound bilirubin level, host susceptibility, com orbidities.

o

Death is owing to respiratory failure and progressive com a, or intractable seizures.



Neurotoxic effects of hyperbilirubinem ia are seen m ore com m only with hem olytic disease, less com m only in healthy newborns.



Severe hyperbilirubinem ia m ay be caused by pathologic conditions.



Risk factors for hyperbilirubinem ia:

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o

Hem olytic disease

o

Gestation 35â€“38 weeks

o

Low birth weight

o

Large weight loss after birth

o

Breast-feeding

o

Ethnicity: Asian, Native Am erican, Greek Islander

o

Siblings with hyperbilirubinem ia

o

Fam ily history of G6PD deficiency or hereditary spherocytosis

o

Maternal diabetes

o

Perinatal factors: polycythem ia, birth traum a, infection



Early discharge of newborns has resulted in m ore problem atic jaundiced newborns owing to delayed diagnosis and increased breast-feeding.

Etiology Unconjugated Hyperbilirubinemia 

Physiologic jaundice



Jaundice in breast-fed infants: o

Breast-feeding jaundiceâ€”exaggeration of physiologic jaundice owing to inadequate ingestion of breast m ilk in the first week of life; prolongation up to 8 weeks m ay be caused by factors in breast m ilk that inhibit hepatic conjugation of bilirubin.



Specific hem olytic conditions: o

Blood group isoim m unization owing to ABO, Rh, and m inor blood group incom patibility; ABO is m ost com m on: Rh disease is unusual (RhoGAM prevents).



o

Red cell m em brane defects: hereditary spherocytosis

o

Red cell enzym e deficiencies: G6PD deficiency

Sepsis: bacterial, viral, or protozoal

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

Birth traum a: o

Increased hem e load from resolving cephalohem atom a or ecchym osis



Polycythem ia: o

Caused by m aternal-fetal transfusion

o

Fetal-fetal transfusion

o

Infants of diabetic m others



Congenital hypothyroidism



Defective hepatic conjugation: o

Gilbert syndrom e (fam ilial partial defect in glucuronyl transferase activity) is a com m on benign condition.

o

Crigler-Najjar syndrom e (congenital absence of glucuronyl transferase causes lifelong unconjugated hyperbilirubinem ia)

o

Lucy-Driscoll syndrom e (severe unconjugated hyperbilirubinem ia thought to be owing to inhibition of infant's glucuronyl transferase by unidentified m aternal serum factors)

Conjugated Hyperbilirubinemia 

Failure of hepatic excretion of conjugated bilirubin



Causes include neonatal hepatitis, congenital biliary atresia, extrahepatic biliary obstruction, shock liver from neonatal asphyxia, neonatal hem osiderosis

Diagnosis Signs and Symptoms History 

Sleepiness, poor intake, and inadequate urine output m ay be present.

Pa ge 3 2 2





Early phase of acute bilirubin encephalopathy (ABE): o

Feeding difficulties with poor suck

o

Fussiness and irritability

o

Lethargy with altered awake-sleep pattern

o

Hypotonia

Interm ediate Phase of ABE: o

High-pitched cry, irritability

o

Increased tone with backward arching of neck (retrocollis) and trunk (opisthotonos) alternating with hypotonia

o 

Fever

Signs of advanced ABE: o

Pronounced retrocollis-opisthotonos

o

Sem icom a, seizures

o

Bicycling m ovem ents

Physical Exam 

Yellowish discoloration of skin, tissues such as sclerae, and body fluids in the newborn infant



Indicates an elevated serum bilirubin level



Increasing levels of bilirubin affect skin color progressing from the face downward: o

Blanch skin with digital pressure to reveal underlying skin colorâ€”only approxim ates level



o

Faceâ€”bilirubin levels >6â€“8 m g/dL

o

Feetâ€”bilirubin levels >12â€“15 m g/dL

Physical exam clues to som e causes: o

Sepsis: lethargy, tem perature instability, poor feeding, vom iting, apnea or tachypnea

o

Hem olytic disease: pallor, hepatosplenom egaly

o

Extravascular hem olysis: birth traum a associated with cephalohem atom a or bruising

o

Polycythem ia: ruddy com plexion

Pa ge 3 2 3

o

Cholestatic jaundice: persistent jaundice for >3 weeks, dark urine, or light-colored stool



Visual diagnosis of jaundice is unreliable, especially in darkly pigm ented infants.

Essential Workup 

Clinical diagnosis



Total serum bilirubin (TSB) m andatory in any infant with suspected or obvious jaundice



Direct (conjugated) and indirect (unconjugated) bilirubin levels



Interpret TSB according to infant's age in hours, not days, to determ ine risk and need for treatm ent.



Determ ine if TSB level drawn prior to birth hospitalization discharge.



Transcutaneous m easurem ent of bilirubin (TcB) correlates well with TSB and is available in som e centers.



Further evaluation is recom m ended for these newborns with jaundice: o

Occurs in the first 24 hours of life

o

Persists beyond the first week of life

o

TSB levels reach level to initiate intensive phototherapy.

o

Bilirubin is >10% or >2 m g/dL conjugated.

o

Any signs of ABE

Tests Lab 

Serum album in, electrolytes, calcium



CBC with differential and sm ear for RBC m orphology



Reticulocyte count



Maternal and infant blood type



Direct Coom bs test on cord blood:

Pa ge 3 2 3

o

Hospital routines vary: Som e will test newborns from all type O m others.

o

If not available, direct Coom bs test on infant's blood



Further workup is directed at suspected cause.



Red cell enzym e assay



Liver function tests



Sepsis evaluation



Urine-reducing substance

P.741

Imaging Evaluation for obstructive liver disease (direct hyperbilirubinem ia): consultation and im aging studies

Differential Diagnosis 

See Etiology.



Essential to differential unconjugated from conjugated

Treatment Initial Stabilization 0.9% norm al saline (NS) 20 m L/kg, bolus if signs of dehydration

ED Treatment 

Treatm ent guidelines for infants â‰¥35 weeks gestation based on TSB plotted versus age in hours for infants at lower, m edium , or higher risk.



Higher risk are 35â€“37 6/7 weeks plus risk factors.



Medium risk are â‰¥38 weeks plus risk factors, or 35â€“37 6/7 weeks and well.

Pa ge 3 2 3



Lower risk are â‰¥38 weeks and well.



Risk factors: isoim m une hem olytic disease, G6PD deficiency, asphyxia, significant lethargy, tem perature instability, sepsis, acidosis, album in <3.0 g/dL



Hospitalization for intensive phototherapy is indicated when TSB (m g/dL) is above: o

o

o

o

o

o

o

12 hours: 

Higher risk 6.0



Medium risk 7.5



Lower risk 9.0

24 hours: 

Higher risk 7.5



Medium risk 9.5



Lower risk 11.5

36 hours: 

Higher risk 9.5



Medium risk 11.5



Lower risk 13

48 hours: 

Higher risk 11.0



Medium risk 13.0



Lower risk 15.0

60 hours: 

Higher risk 12.5



Medium risk 14.5



Lower risk 16.5

72 hours: 

Higher risk 13.5



Medium risk 15.0



Lower risk 18.0

96 hours: 

Higher risk 14.5

Pa ge 3 2 3

o





Medium risk 17.0



Lower risk 20.0

5â€“7 days: 

Higher risk 15.0



Medium risk 18.0



Lower risk 21.0

Intensive phototherapy should decrease TSB >0.5 m g/dL/h.



Indications for exchange transfusions are also determ ined by age in hours and risk stratification: o

For exam ple, at 48 hours, exchange transfusion recom m ended if higher risk with TSB â‰¥16 m g/dL, m edium risk with TSB â‰¥19 m g/dL, and low risk with TSB â‰¥22 m g/dL.



Im m ediate exchange transfusion is recom m ended regardless of TSB level if infant shows signs of acute bilirubin encephalopathy: o

Type and cross-m atch for 170 m L/kg of blood for double-volum e exchange transfusion.

o

Album in infusion 1 gm /kg if serum album in is low (<3.4 g/dL) prior to exchange transfusion



If isoim m une hem olytic disease, intravenous im m unoglobulin (IVIG) 0.5â€“1 g/kg over 2 hours if TSB level is nearing exchange criteria



Im m ediate consultation with neonatologist recom m ended to determ ine treatm ent



If any delay in adm ission/transfer, initiate intensive phototherapy in ED.



Intensive phototherapy im plies the use of high level of irradiance in the 430- to 490-nm band delivered to as m uch of infant's surface area as possible.



Encourage feeding with increased frequency, whether

Pa ge 3 2 3

breast-fed or bottle-fed; supplem ental dextrose-water is not useful. 

If not feeding well, initiate enteral feeds to decrease enterohepatic circulation and increase intestinal bilirubin clearance.



Treat coâ€“m orbid illness (sepsis, liver dysfunction, polycythem ia, hypothyroidism , and so on)



Breast-feeding and breast m ilk jaundice: o

Most infants can continue to breast-feed.

o

Encourage m others to nurse at least 8â€“12 tim es per day for first several days.

o

May need supplem ental IV hydration if dehydrated

o

2â€“3 day cessation of breast-feeding recom m ended for those infants with breast m ilk jaundice and levels not responding to phototherapy

o

Encourage m other to m aintain lactation by use of breast pum p or m anual expression during period of cessation.



Physiologic jaundice: reassurance and arrange appropriate follow-up

Medication (Drugs) Experim ental phase only: hem e-oxygenase inhibitor tin-m esoporphyrin

Follow-Up Disposition Admission Criteria

Pa ge 3 2 3



Infants requiring intensive phototherapy



NICU adm ission for infants requiring exchange transfusion



Evidence of significant anem ia, sepsis, dehydration, or evidence of obstructive liver disease that m ay require hospitalization for diagnostic evaluation



Rapid transport to NICU; transport phototherapy if transport tim e >30 m inutes

Discharge Criteria 

Stable infant with hyperbilirubinem ia not requiring phototherapy



Stable infant with uncom plicated nonhem olytic hyperbilirubinem ia not m eeting intensive phototherapy guidelines, m ay have hom e phototherapy arranged if appropriate follow-up can be ensured



Direct com m unication with prim ary care provider and often neonatal consultant is essential.



Frequently asked questions with answers for parents in English and Spanish available at http://www.aap.org/fam ily/jaundicefaq.htm . Accessed 11/15/05.

References 1. AAP Subcom m ittee on Hyperbilirubinem ia. Clinical Practice Guideline: Managem ent of hyperbilirubinem ia in the newborn infant 35 or m ore weeks of gestation. Pediatrics. 2004;114:297â€“316. 2. Bhutoni VK, Donn SM, Johnson LH. Risk m anagem ent of severe neonatal hyperbilirubinem ia to prevent kernicterus. Clin Perinatol. 2005;32:125â€“139. 3. Shapiro SM. Bilirubin toxicity in the developing nervous system . Pediatr Neurol. 2003;29:410â€“421.

Codes

Pa ge 3 2 3

ICD9-CM 774.6

ICD10 P59.9

Pa ge 3 2 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neo natal Sepsis

Neonatal Sepsis

Lazaro Lezcano

Basics Description 

Life-threatening infection of the newborn, rarely occurring as late as 3 m onths of age



Overwhelm ingly bacterial: o

Rarely viral or fungal infection

o

Organism s usually present in the m aternal perineal flora.



Occurs in 3â€“5 newborns per 1,000 live births



Risk factors: o

o

Perinatal: 

History of recent fever (>37.5Â°C)



Urinary tract infection



Chorioam nionitis



Prolonged rupture of m em branes (>18 hours)



Foul lochia



Uterine tenderness



Intrapartum asphyxia

Neonatal: 

Prem aturity



Fetal tachycardia (>180 beats/m in)

Pa ge 3 2 3



Male



Twinning (especially second twin)



Developm ental or congenital im m une defects



Adm inistration of intram uscular iron



Galactosem ia



Congenital anom aly (urinary tract, asplenia, m yelom eningocele, sinus tract)



Om phalitis

Etiology Sepsis 





Bacterial: o

Group B streptococcus

o

Escherichia coli

o

Listeria m onocytogenes

o

Coagulase-negative Staphylococcus

o

Treponem a pallidum

Viral: o

Herpes sim plex is a com m on viral cause

o

Enterovirus

o

Adenovirus

Fungi: o



Candida species

Protozoa: o

Malaria

o

Borrelia

Meningitis 

Bacterial: o

Group B streptococcus

o

E. coli type K1

o

L. m onocytogenes

o

Other streptococci

Pa ge 3 2 3

o

Nontypeable Haem ophilus influenzae

o

Coagulase-positive and coagulase-negative

o

Staphylococcus

o

Less com m only: Klebsiella, Enterobacter,

o

Pseudom onas, T. pallidum , and Mycobacterium tuberculosis

o

Citrobacter diversus (im portant cause of brain abscess)





o

Additional pathogens: Mycoplasm a hom inis and

o

Ureaplasm a urealyticum

Viral: o

Enteroviruses

o

Herpes sim plex virus (type 2 m ore com m only)

o

Cytom egaloviruses

o

Toxoplasm a gondii

o

Rubella

o

HIV

Fungi: o

Candida albicans and other fungi

Diagnosis Signs and Symptoms History 



Nonspecific history: o

â€œNot acting norm alâ€•

o

Feeding poorly

o

Irritable or lethargic

General: o

Toxic appearing

Pa ge 3 2 4

o

Altered m ental statusâ€”irritable or lethargic

o

Apnea or bradycardia

o

Mottled, ashen, cyanotic, or cool skin

Physical Exam 

Vital signs: o

Hypertherm ia/hypotherm ia

o

Tachypnea

o

Tachycardia

o

Prolonged capillary refill tim e



Abdom inal distention



Jaundice



Bruising or prolonged bleeding



Sepsis syndrom e in the neonate: o

Septic shock

o

Hypoglycem ia

o

Seizures

o

Dissem inated intravascular coagulation (DIC)

o

If untreated, cardiovascular collapse and death

Essential Workup 

Sepsis evaluation followed by em piric antibiotics and support



Determ ine a source for the infection.



Identify m etabolic abnorm alities.

Tests Lab 

Bedside glucose determ ination



CBC: o

WBCs elevated or suppressed

o

Shift to the left

o

Throm bocytopenia

Pa ge 3 2 4



Urinalysis



Cultures as soon as the diagnosis is entertained: o

Blood, cerebrospinal fluid (CSF), catheterized or suprapubic urine, stool



Lum bar puncture: o

May need to delay if hem odynam ically unstable

o

Cell count, protein, glucose, culture



Serum glucose needed to exclude hypoglycem ia



ABG and oxim etry: o





Metabolic acidosis is com m on.

Electrolytes and calcium : o

Hyponatrem ia

o

Hypocalcem ia

DIC panel: o

Coagulopathy is a late com plication.

o

Monitor PT, PTT, and fibrinogen-split products.

P.743

Imaging Chest radiograph to rule out pneum onia

Differential Diagnosis 





Heart disease: o

Hypoplastic left heart syndrom e

o

Myocarditis

Metabolic disorders: o

Hypoglycem ia

o

Adrenal insufficiency (congenital adrenal hyperplasia)

o

Organic acidoses

o

Urea cycle disorders

Intussusception

Pa ge 3 2 4



Child abuse



CNS: o

Intracranial hem orrhage

o

Perinatal asphyxia



Neonatal jaundice



Hem atologic em ergencies: o

Neonatal purpura fulm inans

o

Severe anem ia

o

Methem oglobinem ia

o

Malignancy (congenital leukem ia)

Treatment Pre Hospital Cautions: 

Ventilatory support if obtunded, apneic, or respiratory distress



IV access



Continuous m onitoring

Initial Stabilization 

Airway m anagem ent indicated if obtundation, apnea, or respiratory distress



IV access to adm inister fluids and pressors as needed



Continuous m onitoring

ED Treatment 

Im plem ent em piric treatm ent for neonatal sepsis if presentation at all consistent, particularly if any risk factors are present.



Adm inister antibiotics: o

Am picillin and gentam icin

Pa ge 3 2 4

o

Add vancom ycin if the patient's condition continues to deteriorate or any suggestion of Streptococcus pneum oniae.

o 

Cefotaxim e m ay be substituted for gentam icin.

Support for septic shock if present

Medication (Drugs) 

Am picillin: 200 m g/kg/d q6h IV/IM for infants >2 kg birth weight and older than 2 weeks; 150 m g/kg/d q8h if younger than 7 days



Cefotaxim e: 150 m g/kg/d q6h IV/IM for infants >2 kg birth weight and older than 1 week; 150 m g/kg/d q8h IV/IM if 8â€“28 days of age; 100 m g/kg/d IV/IM q12h if 0â€“7 days of age



Gentam icin: 2.5 m g/kg per dose q8h IV/IM if postconceptual age >37 weeks and older than 7 days; 2.5 m g/kg per dose q12h if younger than 7 days



Vancom ycin: 15 m g/kg per dose IV q8h if postconceptual age >37 weeks and older than 7 days; 15 m g/kg IV q12h if younger than 7 days

Follow-Up Disposition Admission Criteria All patients with suspected sepsis are adm itted to the hospital for supportive care, IV antibiotic therapy, and close m onitoring.

References

Pa ge 3 2 4

1. Anderson MR, Blum er JI. Advances in the therapy for sepsis in children. Pediatr Clin North Am . 1997;44:179â€“205. 2. Edwards MS. Postnatal bacterial infections. In: Fanaroff AA, Martin RJ, eds. Neonatal-Perinatal Medicine. Diseases of the Fetus and Infant. 7th ed. St. Louis, MO: Mosby; 2002:706â€“722. 3. Polin RA, Parravicini E, Regan JA, et al. Bacterial sepsis and m eningitis. In: Taesch HW, Ballard RA, Gleason CA. Avery's Diseases of the Newborn. 8th ed. Philadelphia: Elsevier Saunders, 2005: 551â€“568. 4. Shapiro NI, Zim m er GD, Barkin AZ. Sepsis syndrom e. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Codes ICD9-CM 771 790.7

ICD10 P36.9

Pa ge 3 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nephritic Syndro m e

Nephritic

Syndrome Anwer Hussain

Basics Description 

Acute glom erulonephritis (AGN) is acute inflam m atory dam age to glom erulus, associated with: o

Abrupt onset of hem aturia with or without RBC casts

o

Acute renal failure m anifested by edem a, hypertension, azotem ia



o

Variable proteinuria

o

Active urine sedim ent (RBC casts)

Exact m echanism of AGN unclear: o

Com bination of autoim m une reactivity to specific antigens at renal glom eruli

o

Glom erulonephritis com prises 25â€“30% of end-stage renal disease (ESRD)

Etiology Postinfectious Causes of Acute Nephritic Syndrome (PIGN) N/A

Pa ge 3 2 4

Poststreptococcal Glomerulonephritis (PSGN) 

Occurs between the ages of 3 and 15 years but can occur at any age



Due to group A Î²-hem olytic streptococci



Incidence of GN is 5â€“10% in pharyngitis and 25% in skin infections.



Consider PIGN in new onset proteinuria, RBC casts, and any recent infection.



Latent period between infection and onset of nephritis helps differentiate between PSGN and IgA nephropathy: o

1â€“3 weeks in pharyngeal infection

o

2â€“4 weeks in cutaneous infection



Renal biopsy usually not necessary for diagnosis.



Hum p-shaped subepithelial deposits due to antigen-antibody reaction



Low com plem ents for 6â€“8 weeks (C3, CH50)



Progresses to severe renal failure if infection persists



Treat with antibiotics



Prognosis: o

Excellent; >95% recover spontaneously with norm alization of renal function within 6â€“8 weeks, even with dialysis

o

Hem aturia usually resolves in 3â€“6 m onths

o

Transient nephrotic phase in 20% of patients during resolution of illness

o

ESRD occurs <5%.

o

Rapidly progressive GN (RPGN) is rare, occurring in <1% cases.

o

Most cases resolve spontaneously with no long-term sequelae.

Other Infectious Sources of GN

Pa ge 3 2 4



Sepsis, pneum onia, endocarditis, viral, HIV



Pulm onary, intraabdom inal, cutaneous



Syphilis, leprosy, schistosom iasis, and m alaria

Hepatitis Virusâ€“Related Glomerular Disease 

Can present with either nephritic or nephrotic sym ptom s



Causes m em branoproliferative GN



Com plem ents rem ain low indefinitely (com pared to PIGN): o

Nephrotic sym ptom s m ore typical

Infectious Endocarditis 

Risk groups: parenteral drug abusers and patients with prosthetic valves



Antibiotic treatm ent of infectious endocarditis (IE) results in resolution of GN.

Noninfectious Causes of GN 

System atic lupus erythem atosus, Henoch-SchÃ¶nlein purpura, vasculitis, Wegener granulom atosis



Goodpasture syndrom e

IgA Nephropathy 

Most com m on cause of AGN (>25%), worldwide



Antibody-Antigen causes im m une com plex deposition of IgA and C3.



Com plem ent levels are usually norm al.



IgA-N has different presentations: o

Gross hem aturia following upper respiratory infection (URI)

o

Microscopic hem aturia with proteinuria

o

Hem aturia occurs either during viral illness or after exercise.

o

Prognosis is related to serum creatinine, blood pressure, and proteinuria.

Pa ge 3 2 4

o

50% of patients with proteinuria m ay develop progressive renal disease.

o

Angiotensin converting enzym e inhibitor or angiotensin receptor blocker RBS m ay help

Rapidly Progressive Glomerulonephritis (RPGN) 

Certain patients with AGN m ay progress rapidly to renal failure.



Hallm arks are crescents on renal biopsy.

Diagnosis Signs and Symptoms 

Hem aturia: o

Abrupt onset with dysm orphic RBCs and RBC casts

o

Gross hem aturia in 30â€“40% (coffeeâ€“ or Coca Colaâ€“colored urine)



Hypertension



Edem a: o

Periorbital edem a

o

Generalized edem a m ore com m on in infants



Azotem ia



Infection source: upper respiratory tract or skin com m onâ€”for exam ple, PSGN



Congestive heart failure: o

40% occurrence in patients older than 60 years

o

Rare in children



Renal failure m ore com m on in elderly



Arthritis, arthralgias, and various skin rashes: PSGN, system ic disease

Pa ge 3 2 4



Nonspecific m anifestations: o

Malaise

o

Weakness

o

Anorexia

o

Nausea/vom iting

History Recent URI, skin or any other infection

Essential Workup Urinalysis to detect: 

Hem aturia, proteinuria, and RBC casts



RBC casts diagnostic of an active glom erular inflam m ation

Tests Lab 

CBC: o

Anem ia (seen in m ore chronic cases of GN or other system ic disease)

o 

Acute leukocytosis (indicates infectious process)

Electrolytes, blood urea nitrogen, creatinine, glucose: o

Baseline for renal function

o

Check for electrolyte abnorm alities.



Serum album in



Cultures (throat, skin, urine, blood): o

As clinically suspected for infection source

P.745

Imaging 

Renal ultrasound: kidney-size abnorm ality



Chest radiograph: cardiom egaly, pulm onary edem a, infection

Pa ge 3 2 5



Renal biopsy: o

Generally not done for PSGN, as sym ptom s typically resolve in
o

Recom m ended if atypical features of PSGN, persistent abnorm al com plem ent levels, persistent hypertension, and proteinuria >3 g/d

o

Facilitates diagnosis for other causes of nephritis

Diagnostic Procedures/Surgery 

Serum com plem ent level (C3, CH 5 0 ): decreased in IE, shunt nephritis and PSGN



Streptococcal antibodies: o

Antistreptolysin (ASO), antistreptokinase (ASK), antideoxyribonuclease B (ADNase B), anti-nicotinyl adenine dinucleotidase (ANADase), and antihyaluronidase (AH)

o

ASO m ore reactive in pharyngeal infections

o

ADNase B, ANADase, and AH m ore reactive in cutaneous infections

o

ASK elevated in recent hem olytic streptococcus infections

o 

Titers do not correlate with prognosis of disease.

24-hour urine protein collection: o

Proteinuria initially present in 5% of children, 20% adults with PSGN

Differential Diagnosis (See Glom erulonephritis, for further inform ation on types of GN) 

Renal: o



Prim ary glom erular disease

System ic: o

Goodpasture syndrom e

o

Vasculitis

Pa ge 3 2 5

o 

Henoch-SchÃ¶nlein purpura

Other (rare): o

Hem olytic-urem ic syndrom e

o

Throm botic throm bocytopenic purpura

o

Acute hypersensitivity interstitial nephritis

o

Guillain-BarrÃ©

o

DPT vaccine

o

Serum sickness

Treatment Initial Stabilization ABCs

ED Treatment 

Antibiotics for streptococcal infection: o

Penicillin (erythrom ycin if penicillin allergic)

o

Prophylactic antibiotics to siblings of PSGN patients



Restriction of salt and water intake



Adm inister loop diuretics (furosem ide).



Treat pulm onary edem a:



o

Oxygen

o

Morphine

o

Loop diuretics

BP stabilization to decrease proteinuria, retard progression of GN: o

ACE inhibitor

o

Hypertensive em ergency: nitroprusside or other antihypertensive m edication



Dialysis for: o

Severe hyperkalem ia

Pa ge 3 2 5

o

Fluid overload

o

Urem ia

o

Correct electrolyte abnorm alities

Medication (Drugs) 

ACE inhibitor, depends on m eds chosen



Erythrom ycin: 250â€“500 m g (peds: 30â€“50 m g/kg/24h) PO q6h for 7â€“10 days



Furosem ide: 20â€“80 m g qd/b.i.d. (peds: 1 m g/kg/dose)



Morphine sulfate: 2â€“4 m g (peds: 0.1 m g/kg/dose, m axim um 15 m g/dose) IV q5m in



Nitroprusside: 0.3â€“10 Âµg/kg/m in IV



Penicillin: o

Benzathine penicillin: 1.2 m illion units (peds: 0.6 m illion units for <30 kg) IM

o

Penicillin VK: 250â€“500 m g PO q6h for 7â€“10 days

Follow-Up Disposition Admission Criteria 

Evidence of infectious cause for GN



Oliguria, anuria



Urem ia



Elevated creatinine, BUN levels



Edem a



Electrolyte abnorm alities



Hypertension



CHF

Pa ge 3 2 5

Discharge Criteria Mild cases of clinical nephritis in healthy patients with: 

No com orbid illness



Strict supervision/m onitoring of sym ptom s, diet, urine output, and m edication



Close follow-up with PMD and nephrology referral

References 1. Couser W, Glom erulonephritis. Lancet. 1999;353:1509â€“1515. 2. Carithers RL. Hepatitis C and renal failure. Am J Med. 1999;107(6B):90Sâ€“94S. 3. Donadio J, rande J, IgA Nephropathy. N Engl J Med. Vol 347,10:738â€“748 4. Kirpal SC, Sakhuja V. Glom erulonephritis due to other infections. In: Massry SG, Glassock RJ, eds. Textbook of nephrology. 3rd ed. Baltim ore: William s & Wilkins,1995:703â€“710. 5. Korbet SM, Schwartz MM. Hum an im m unodeficiency virus infection and nephrotic syndrom e. Am J Kidney Dis. 1992;20:97â€“103. 6. Prakash U, Nephrology. Mayo clinic Internal Medicine Review. 2000â€“01. 7. Tejani A, Ingulli E. Poststreptococcal glom erulonephritis, Current clinical and pathologic concepts. Nephron. 1990;55:1.

Miscellaneous SEE ALSO: Glom erulonephritis; Nephrotic syndrom e; Renal failure

Codes ICD9-CM 583.9

ICD10

Pa ge 3 2 5

N05

Pa ge 3 2 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nephro tic Syndro m e

Nephrotic

Syndrome Anwer Hussain

Basics Description Diseases causing defect in glom erular filtration barrier, producing nephrotic urine: 

Proteinuria >3.5 g/d



Hypoalbum inem ia (serum album in < 3 g/dL)



Hypogam m aglobulinem ia



Peripheral edem a due to hypoalbum inem ia



Hyperlipidem ia (fasting cholesterol >200 m g/dL)



Urine fat (oval fat bodies, fatty/waxy casts)



Glom erular basem ent m em brane altered by: o

Im m une com plexes

o

Nephrotoxic antibodies

o

Nonim m une m echanism s

o

Result: increased filtration and excretion of album in and large protein

Pathophysiology 

Proteinuria due to protein loss



Edem a due to sodium retention and hypoalbum inem ia

Pa ge 3 2 5



Postural hypotension, syncope, and shock due to severe hypoalbum inem ia



Hyperlipidem ia due to hepatic lipoprotein synthesis stim ulated by decreased plasm a oncotic pressure



Cum ulative throm boem bolism risk increased if: o

Hypovolem ia

o

Low serum album in

o

High protein excretion

o

High fibrinogen levels

o

Low antithrom bin III levels

Etiology Due to prim ary renal or system ic diseases

Membranous Nephropathy 

Prim ary cause of nephrotic syndrom e in adults



Other causes include chronic infection (hepatitis B virus, hepatitis C virus, syphilis, drugs, solid tum ors, system atic lupus erythem atosus [SLE])



Renal biopsy shows involvem ent of all glom eruli.



Wom en have better prognosis.



30% m ay slowly progress to renal failure.



Renal vein throm bosis causes sudden loss of renal function.



Treat with steroids and cytotoxic agents in severe cases.

Minimal Change Disease 

Most com m on cause (90%) of nephrotic syndrom e in children



15â€“20% cause in idiopathic adult nephrotic syndrom e



Causes: idiopathic, NSAIDS, Hodgkin disease



Urine sedim ent shows m altese cross in polarized light



Best prognosis am ong all nephrotic syndrom es



Good response to steroids

Pa ge 3 2 5

Focal Segmental Glomerulosclerosis (FSGS) 

Young patients (15â€“30 years old) with nephrotic syndrom e



Presents with high blood pressure, renal insufficiency, proteinuria, m icroscopic or gross hem aturia



Causes include HIV, heroin abuse, obesity, hem atologic m alignancies



Prim ary FSGS respond to steroids



Secondary FSGS treated with ACEI



Poor prognosis if proteinuria >10 g/day



Collapsing FSGS usually seen in HIV patients

Membranoproliferative Glomerulonephritis (MPGN) 

May present with nephrotic, nonnephrotic or nephritic sedim ent



Com plem ents are persistently low.



Supportive care, steroids m ay be helpful in children.



ASA and dipyridam ole m ay slow progression.

MembranoproliferativeSecondary Etiology (30%) N/A

Diabetes Mellitus 

Most com m on secondary cause of nephrotic range proteinuria in adults



Microalbum inuria (30â€“300 m g/24hr) prim ary indicator of renal disease



Worsening of renal function in five to seven years



Does not cause rapid decline in renal function



Strict control of blood sugar and angiotensin converting enzym e inhibitor (ACEI) slows progression.

Pa ge 3 2 5

Monoclonal Gammopathies 

Am yloidosis, m ultiple m yelom a, and light chain nephropathy



Renal m anifestations include proteinuria, nephrotic syndrom e, nephritic syndrom e, acute renal failure.



Pseudohyponatrem ia, low anion gap, hypercalcem ia. Bence-Jones proteinuria



Congo red stain of am yloid shows apple green birefringence in polarized light.



Also seen in â€œskin popperâ€• drug addict



Supportive care: steroid and m elphalan have som e benefit

Systemic Lupus Erythematosus (SLE) 

Diseases can present initially as a nephritic process, with progression to nephrotic syndrom e



Rarer causes: o

Pre-eclam psia

o

Drug reaction (NSAIDs, heroin, gold, penicillam ine)

o

HIV

o

Hepatitis

HIV-Associated Nephropathy (HIV-AN) 

Focal segm ental glom erulosclerosis m ost com m on nephropathy



Collapsing glom erulopathy in seropositive HIV carriers with supernephrotic syndrom e result in end-stage renal failure in m onths.

Diagnosis Signs and Symptoms 

Many patients asym ptom atic

Pa ge 3 2 5



Proteinuria



Peripheral edem a: o

Mild pitting edem a to generalized anasarca with ascites



Hyperlipidem ia



Lipiduria (urine fatty casts and oval fat bodies)



Postural hypotension/syncope/shock



Hypertension



Hem aturia: o

Microscopic or gross hem aturia (secondary to renal vein throm bosis)



Renal Insufficiency to acute renal failure in som e cases



Tachypnea, tachycardia, with/without hypotension: o

Acute onset: suggests pulm onary em bolus (PE), secondary to renal or deep venous throm bosis due to hypercoagulable state

o

Up to 30% occurrence of PE in m em branous glom erulonephritis (GN)

o

Chronic or exertional tachypnea due to: 

Pulm onary edem a



Pleural effusions



Infection risk due to im m unosuppressive treatm ent and frequent exposure to infections such as Pneum ococcus

 

Ascites

Bone fractures (due to underlying osteom alacic bone disease)



Protein m alnutrition



Other com plications include accelerated atherosclerosis, susceptibility for infection and hypovolem ia

History System ic disease such as diabetes, SLE, HIV, use of NSAIDS or gold

Pa ge 3 2 6

or penicillam ine

Physical Exam Varies depending on degree of hypoalbum inem ia, hem odynam ic status, and the etiology of nephrotic syndrom e

Essential Workup Urinalysis: 

Dipstick protein largely positive: o

Urine specific gravity >1.025 lowers the diagnostic significance of proteinuria



Microscopic analysis for urinary casts and the presence of cellular elem ents: o

Oval fat bodies

o

Free lipid droplets

P.747

Tests Lab 



CBC plus differential: o

Anem ia com m on

o

Leukocytosis: infection

o

Leukopenia: neoplastic disease or sepsis

o

Throm bocytopenia: liver disease

PTT, PT, INR o

Coagulation profiles abnorm al with concurrent liver disease, for exam ple, hepatitis



D-dim er, fibrinogen, antithrom bin III o

Suspected throm boem bolic event: 

Often patients are asym ptom atic with PE or renal vein throm bosis, therefore need high

Pa ge 3 2 6

clinical suspicion 

24 hour urine protein, total protein to creatinine ratio



Serum album in: <3 g/dL



Serum total protein



Electrolytes, blood urea nitrogen, creatinine, glucose, Ca, Mg, P



Lipid profile: elevated total cholesterol, LDL, and VLDL



Additional lab tests m ay be necessary for system ic diseases



ANA, serum and urine protein electrophoresis, hepatitis profile, syphilis, cryoglobulins, com plem ent levels

Imaging 

Renal ultrasound: o

Not helpful

o

Used in suspected secondary causes of nephrotic syndrom e



Renal biopsy: o

Definitive test for patients who do not respond to a short course of corticosteroids

o

Helps discern prim ary versus secondary pathology and for specific therapy

Diagnostic Procedures/Surgery Renal angiography, CT scan, or MRI for suspected renal vein throm bosis

Differential Diagnosis Proteinuria Resulting from Other Causes 

Renal parenchym al disease: o

Chronic renal disease

o

Mechanical nephropathy (obstruction/reflux)

Pa ge 3 2 6



o

Orthostatic proteinuria

o

Acute pyelonephritis

o

Sickle cell disease

Other causes: o

Congestive heart failure

o

Essential hypertension

o

Acute febrile illness

o

Pregnancy (preeclam psia)

o

Severe obesity

Treatment Initial Stabilization ABCs: 

Supplem ental oxygen if respiratory distress



IV fluids: o

Slow rehydration for decreased blood pressure or orthostatic hypotension due to decreased intravascular volum e

o

Active rehydration in the presence of severe hypotension, shock

ED Treatment 

Control edem a: o

Restrict sodium intake (3 g NaCl)/day.

o

Loop diuretic (furosem ide):titrate dose until response seen.

o

Thiazides and potassium -sparing diuretics

o

Goal: slow diuresis: 

Aggressive diuresis can precipitate acute renal failure due to hypovolem ia and increase the risk

Pa ge 3 2 6

of throm boem bolic com plications 

Throm boem bolic prevention/treatm ent: o

Heparin: 80 IU/kg bolus followed by 18 IU/kg/h drip IV for throm boem bolic event



o

No prophylactic anticoagulation

o

Consider low-dose ASA 80 m g

o

Support stockings

Plasm apheresis, for severe cases

Post-ED Treatment 

Glucocorticosteroid: m ainstay of treatm ent for prim ary nephrotic syndrom e



ACEI/Angiotensin receptor blocker: decreases proteinuria, prevents worsening of renal function



Adverse effects of ACEI include renal failure and hyperkalem ia.



Cholesterol-lowering agents/dietary m anipulation (bile acid resin, statins)



Cytotoxic agents/cyclosporine



Recom binant erythropoietin for anem ia



Diet m anipulation: o

Protein-restricted diet: 

Not recom m ended



Associated risk of m alnutrition, which worsens prognosis of renal disease

o

Sodium -restricted diet, recom m ended to reduce hypertension and edem a

Medication (Drugs) 

Furosem ide: 20â€“100 m g PO b.i.d.â€“t.i.d. (peds: 1 m g/kg/dose) IV; m ax. 2 m g/kg/d

Pa ge 3 2 6



Heparin: 80 IU/kg bolus followed by 18 IU/kg/h drip IV



Metolazone (Zaroxolyn): 5â€“20 m g/d PO

Follow-Up Disposition Admission Criteria 

Moderate to severe heart failure, ascites, respiratory com prom ise



Signs of com orbid illness, such as undiagnosed m alignancy, poorly controlled diabetes, im m unocom prom ised host



Acute renal failure



Evidence of throm boem bolic event

Discharge Criteria 

Patients with no com orbid disease, norm al vital signs, and norm al blood work



Close follow-up with a nephrologist or general internist for further evaluation and treatm ent m andatory

References 1. Glassock RJ, Brenner BM. The m ajor glom erulopathies. In: Wilson et al, eds. Harrison's principles of internal m edicine. 13th ed. New York: McGraw-Hill,1995:1295â€“1313. 2. Glassock RJ, Cohen AH. The prim ary glom erulopathies. Dis Mon. 1996;42(6):329â€“383. 3. Kelepouris E, Agus Z, Overview of heavy proteinuria and the nephrotic syndrom e. Uptodate. 2005 4. Madaio MP, Harrington JT. The diagnosis of glom erular diseases: acute glom erulonephritis and the nephrotic syndrom e. Arch Intern

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Med. 2001;161(1):25â€“34. 5. Orth SR, Ritz E. The nephrotic syndrom e. N Engl J Med. 1998;338(17):1202â€“1211 6. Prakash U, Mayo clinic Internal Medicine review; 2000â€“01

Miscellaneous SEE ALSO: Glom erulonephritis; Nephritic syndrom e; Renal failure

Codes 581.9

ICD10 N04

Pa ge 3 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neuro leptic M alignant Syndro m e

Neuroleptic

Malignant Syndrome Gary Johnson

Basics Description 

May develop anytim e during therapy with neurolepticsâ€”from a few days to m any years



Muscular rigidity from dopam ine antagonism in the nigrostriatal pathway



Hypertherm ia owing to blockage of hypothalam ic therm oregulation



More likely in the setting of benzodiazepine withdrawal



May be indistinguishable from other causes of drug-induced hypertherm ia (m alignant hypertherm ia, serotonin syndrom e, anticholinergic toxins, or sym pathom im etic poisoning)

Etiology 

Rare com plication of treatm ent with neuroleptics: o



Phenothiazines, butyrophenones, and thiothixenes

Occurs in approxim ately 1% of patients treated with neuroleptics (especially haloperidol)



Has also been associated with withdrawal from dopam ine

Pa ge 3 2 6

agonists in Parkinson disease

Diagnosis Signs and Symptoms 

Life-threatening condition



Hallm arks of the disease: o

Hypertherm ia (tem perature m ay be as high as 106â€“107Â°F, 41Â°C)

o

Altered level of consciousness

o

Significant skeletal m uscle rigidityâ€”lead-pipe rigidity

o

Autonom ic instability (tachycardia, labile blood pressure [BP])

History 

Neuroleptic use



Discontinuation of antiparkinsonian drugs

Physical Exam 

Fever



Tachycardia, labile BP



Delirium



Muscle rigidity

Essential Workup 

An accurate history (especially current m edications) and physical exam confirm the diagnosis.



CPK, WBC determ ination, and liver function tests

Tests Lab Electrolytes, glucose, BUN, creatinine, PT/PTT, urinalysis, and urine

Pa ge 3 2 6

m yoglobin

Imaging CT scan, EEG if the cause of altered level of consciousness is unclear

Diagnostic Procedures/Surgery Lum bar puncture to rule out other causes of fever or altered mental status

Differential Diagnosis 

Meningitis, encephalitis, sepsis



Malignant hypertherm ia, severe dystonic reaction



Serotonin syndrom e



Anticholinergic poisoning



Sym pathom im etic poisoning



Tetanus



Heat stroke



Strychnine poisoning



Vascular CNS event



Thyrotoxicosis



Rabies

P.749

Treatment Pre Hospital 

Ventilation m ay be difficult because of chest wall rigidity.



Cool the patient, and treat seizures if they occur.



Check fingerstick glucose.

Initial Stabilization

Pa ge 3 2 6



Airway intervention and circulatory support as needed



IV, supplem ental O 2 , cardiac m onitor



Im m ediate IV benzodiazepines (diazepam , lorazepam ): o



May require repeated large doses

If sym ptom s are not controlled within a few m inutes, rapid-sequence intubation and neurom uscular blockade are necessary: o

Nondepolarizing neurom uscular blockers (vecuronium , rocuronium , pancuronium ) are preferable to succinylcholine



Measures to control hypertherm ia: o



Ice packs, m ist and fan, cooling blankets, and so on

Aggressive IV fluid therapy with lactated Ringer solution or norm al saline (NS)

ED Treatment 

Relief of m uscle rigidity



Benzodiazepines are the drug of choice: o

Brom ocriptine is a dopam ine agonist that m ay play a role in longer-term m anagem ent.

o

Dantrolene is a direct skeletal m uscle relaxant that m ay play a role in longer-term m anagem ent.

o

Neither brom ocriptine nor dantrolene has a rapid onset and neither has been dem onstrated to alter outcom e.



Discontinue neuroleptics.



Recognize com plications (rhabdom yolysis, respiratory failure, acute renal failure); m ortality can be as high as 20%

Medication (Drugs)

Pa ge 3 2 7



Diazepam : 5 m g IV q5m in



Lorazepam : 1 m g IV q5m in

Follow-Up Disposition Admission Criteria 

All patients with the diagnosis seriously considered should be adm itted.



Patients will often require intensive care.

References 1. Halloran LL, Bernard DW. Managem ent of drug-induced hypertherm ia. Curr Opinion in Pediatr. 2004;16(2):211â€“215. 2. Silva RR, Munoz DM, Alpert M, et al. Neuroleptic m alignant syndrom e in children and adolescents. J Am Acad Child Adolesc Psychiatry. 1999;38(2):187â€“194.

Codes ICD9-CM 333.92

Pa ge 3 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neuro leptic Po iso ning

Neuroleptic

Poisoning Mark B. Mycyk

Basics Description 

Neuroleptics (antipsychotics) used for m anagem ent of: o

Psychotic disorders

o

Depressive neurosis

o

Dem entia in the elderly

o

Behavioral problem s in children

o

Antiem etic



Peak plasm a levels within 4 hours



Dystonia occurs within hours to days of ingestion.



Akathisia occurs within days to weeks of increased dosing.

Etiology 

Typical neuroleptics (phenothiazines, butyrophenones) strongly antagonize dopam inergic receptors: o

Haloperidol (Haldol)

o

Chlorprom azine (Thorazine)

o

Thioridazine (Mellaril)

o

Fluphenazine (Prolixin)

o

Prom ethazine (Phenergan)

Pa ge 3 2 7

o 

Droperidol (Inapsine)

Atypical neuroleptics have weaker dopam inergic antagonism and m oderate serotonergic antagonism : o

Clozapine (Clozaril)

o

Risperidone (Risperdal)

o

Olanzapine (Zyprexa)

o

Quetiapine (Seroquel)

o

Ziprasidone (Geodon)



Both exhibit strong Î±-adrenergic antagonism .



Both exhibit anticholinergic activity.

Diagnosis Signs and Symptoms 







Overdose: o

Toxic effects are typically m ild to m oderate.

o

CNS sym ptom s predom inate.

Neurologic: o

Slurred speech

o

CNS depression

o

Agitation

o

Com a

o

Seizures

o

Extrapyram idal sym ptom s (dystonia, akathisia)

Cardiovascular: o

Hypotension

o

Tachycardia

o

Prolonged QRS or QTc

o

Torsades de pointes

Respiratory: o

Respiratory depression

Pa ge 3 2 7





Gastrointestinal: o

Constipation

o

Dry m outh

Genitourinary: o

Urinary retention



Hypertherm ia:



Ocular: m iosis or m ydriasis



Hem atologic: anem ia, agranulocytosis (clozapine)



Neuroleptic m alignant syndrom e (NMS): o

Hypertherm ia

o

Skeletal m uscle rigidity

o

Altered m ental status

o

Autonom ic dysfunction

Alert 

Chronic use: o

New-onset diabetes m ay occur with atypical neuroleptic use.

Essential Workup 

Monitor vital signs with significant ingestions.



Cardiac m onitor



Pulse oxim etry

Tests Lab 

Electrolytes, BUN, creatinine, glucose



CBC for clozapine overdose



Urinalysis: o



Dip for m yoglobin if rhabdom yolysis suspected

Creatine phosphokinase (CPK) levels if NMS suspected, agitation, or prolonged im m obilization



Urine toxicologic screen to exclude coingestants

Pa ge 3 2 7



Quantitative levels are rarely helpful.

Imaging ECG: 

QTc/QRS prolongation



Conduction disturbances

Differential Diagnosis 

Antidepressant overdose



Antihistam ine overdose



Cocaine overdose



Am phetam ine overdose



MDMA overdose



Opioid overdose



Occult head injury



Endocrine disorder



Sepsis

P.751

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs): 

Adm inister supplem ental oxygen.



Adm inister naloxone, thiam ine, D 5 0 (or Accu-Chek) for altered m ental status.



Intubate if respiratory depression.

ED Treatment 

Supportive care

Pa ge 3 2 7



Decontam ination: o

Adm inister single dose of activated charcoal if recent ingestion.



Hypotension: o

0.9% norm al saline (NS) IV fluid bolus

o

Trendelenburg

o

Treat resistant hypotension with norepinephrine or phenylephrine.

o 

Dopam ine m ay be ineffective.

Ventricular dysrhythm ias: o

Avoid class 1a antidysrhythm ics: potential exacerbation of neuroleptic cardiotoxicity.



o

Magnesium for prolonged QTc

o

Cardioversion if hem odynam ically unstable

Dystonic reactions: o

Adm inister diphenhydram ine or benztropine m esylate.





Hypertherm ia: o

Rapid cooling

o

Adm inister dantrolene and brom ocriptine.

Seizures: o

Treat initially with diazepam or lorazepam .

o

Phenobarbital for persistent seizures

Medication (Drugs) 

Activated charcoal: 1â€“2 g/kg PO



Benztropine m esylate: 1â€“2 m g IV or PO



Brom ocriptine: 2.5â€“10 m g q8h PO



Dantrolene: 1â€“2 m g/kg q10m in IV (10 m g/kg m ax.)



Diazepam : 5â€“10 m g IV q10â€“15m in (0.2â€“0.5 m g/kg)



Diphenhydram ine: 25â€“50 m g IV (1 m g/kg)

Pa ge 3 2 7



Lorazepam : 2â€“4 m g (peds: 0.03â€“0.05 m g/kg) IV q10â€“15m in



Magnesium sulfate: 1â€“2 g IV over 5â€“15 m inutes



Norepinephrine: 1â€“2 Âµg/kg/m in IV titrate to blood pressure (BP)



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Phenylephrine: 40â€“80 Âµg/m in IV titrate to BP

Disposition Admission Criteria 

Adm it overdose with CNS sedation, agitation, dysrhythm ias, or vital sign abnorm alities to m onitored bed.



Adm it if neuroleptic results in new-onset diabetes with severe hyperglycem ia and/or ketoacidosis.

Discharge Criteria 

Asym ptom atic after 6 hours of observation



Patients successfully treated for acute dystonia should be given 3-day course of diphenhydram ine to prevent recurrence.

Issues for Referral 

Patients with unintentional (accidental) poisoning require poison prevention counseling.



Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.



New-onset diabetes requires prim ary care/endocrine follow-up.

References 1. Burns MJ. The pharm acology and toxicology of atypical antipsychotic agents. J Toxicol Clin Toxicol. 2001;39(1):1â€“14. 2. De Roos FJ. Neuroleptics. In: Ford MD, Delaney KA, Ling LJ, et al.,

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eds. Clinical Toxicology. Philadelphia: WB Saunders, 2001:539â€“545. 3. Leslie DL, Rosenhek RA. Incidence of newly diagnosed diabetes attributable to atypical antipsychotic m edications. Am J Psychiatry. 2004;161:1709â€“1711. 4. Trenton A, Currier G, Zwem er F. Fatalities associated with therapeutic use and overdose of atypical antipsychotics. CNS Drugs. 2003;17(5):307â€“324.

Codes ICD9-CM E853.0

Pa ge 3 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > No ncardio genic Pulm o nary Edem a

Noncardiogenic Pulmonary Edema David Jerrard

Basics Description 

Functional disruption of the capillaryâ€“alveolar m em brane from a noncardiac source



Diffuse injury to either the alveolar epithelium or to the vascular endothelium



Pulm onary parenchym al changes m im ic congestive heart failure (CHF): o

Cephalad redistribution of blood flow, pulm onary effusions, and cardiom egaly do not develop.



Typically, onset of this edem a is within 1â€“2 hours of noxious insult.



First described by William Osler in 1889 in a patient â€œpoisonedâ€• by m orphine.



Approxim ately 250,000 cases occur each year in the United States.

Etiology 

Cause of capillary leak or alveolar m em brane dam age is uncertain.



Proposed m echanism s include hypoxia, im m unologic

Pa ge 3 2 7

effects, or direct toxic effects. 

Major causes: o

Sm oke inhalation

o

Salicylate intoxication

o

Toxic gas inhalation

o

Transfusion reaction

o

Near drowning

o

Dissem inated intravascular coagulation

o

High-altitude pulm onary edem a (HAPE)

o

Radiation pneum onitis

o

Narcotic abuse

o

Urem ia

o

Cardiopulm onary bypass

o

Major traum a

o

Aspiration

o

Bacterial pneum onia

Diagnosis Signs and Symptoms 

Fatigue



Weakness



Anxiety



Shortness of breath



Cough



Malaise

Physical Exam 

Tachycardia: o

Characteristically seen secondary to decreasing PO 2 levels

Pa ge 3 2 8



Scattered rhonchi and rales



Dyspnea



Tachypnea



Cyanosis



Pink, frothy sputum



The stigm as of left- and right-sided heart failure will not be found

Essential Workup 

History and physical to identify severity and determ ine underlying etiology



The chest radiograph is essential in confirm ing the diagnosis and in assessing severity.

Tests Lab 

General lab abnorm alities are not specific to noncardiogenic pulm onary edem a.



Serum protein levels: o

Hypoproteinem ia m ay be useful for differentiating perm eability-induced pulm onary edem a (noncardiogenic) from cardiogenic pulm onary edem a.



Interleukin-8 level in lung lavage washings: o

Rapid increase in the early stages of acute lung injury before full developm ent of acute respiratory distress syndrom e

Imaging Chest radiograph: 

Initially norm al



Classic butterfly pattern of pulm onary edem a



Unilateral patchy infiltrates resem bling pneum onia



Lack of cardiom egaly

Pa ge 3 2 8

Diagnostic Procedures/Surgery Pulm onary artery catheter: 

Pulm onary capillary wedge pressures norm al or near-norm al in contrast to elevated pressures with cardiogenic pulm onary edem a

Differential Diagnosis 

Cardiogenic pulm onary edem a



Chronic obstructive pulm onary disease exacerbation



Pulm onary em bolus



Restrictive lung disease



Pneum onia

P.753

Treatment Pre Hospital 

Patent airway



Adequate oxygenation

Cautions â€”Patients will not typically respond to usual m easures to treat CHF

Initial Stabilization 

Supplem ental oxygen (high-flow oxygen)



IV catheter



Continuous cardiac m onitor



Continuous pulse oxim etry

ED Treatment

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

The treatm ent of noncardiogenic pulm onary edem a (NCPE) is supportive



NCPE associated with drug overdose usually responds to high-flow O 2



Diuretics are not used



Rem oval of trigger that m ay have caused NCPE o

Noxious gas

o

Having patient descend from elevation in cases of HAPE



Noninvasive ventilatory support (BiPAP, CPAP) m ay be used if im m ediately available o

Measure blood gases frequently

o

If unable to provide adequate oxygenation or ventilation, intubation is required

o 

Useful in NCPE caused by drug overdose

Endotracheal intubation is often necessary o

Positive end-expiratory pressure (PEEP) of 5â€“10 cm H2O 

NCPE of a neurogenic etiology has a worsened prognosis when PEEP is em ployed

o

Im proved oxygenation

o

Decrease work of breathing

o

To reduce the likelihood of atelectasis, tidal volum es should be on order of 12â€“15 m L/kg

o

Initially place on 100% O 2 



Measure PO 2 and decrease FIO 2 accordingly

Steroids and cyclooxygenase inhibitors have not been proven effective

Follow-Up

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Disposition Admission Criteria All sym ptom atic patients should be adm itted to ICU 

Sym ptom s m ay worsen at any point for up to 3 days after noxious insult

Discharge Criteria Asym ptom atic patients (especially narcotic overdose, HAPE, or aspiration) 

Observe in ED for 6â€“12 hours and then discharge with close follow-up scheduled if no evidence of pulm onary edem a is present and adequate oxygenation is dem onstrated

References 1. Macias DJ, Brillm an JC. Adult respiratory distress syndrom e. In: Harwood-Nuss A, Linden C, Luten R, et al, eds. The clinical practice of em ergency m edicine. 2nd ed. Philadelphia: JB Lippincott Co, 1996:640â€“643. 2. McIntyre RC Jr. Thirty years of clinical trials in acute respiratory distress syndrom e. Crit Care Med. 2000;28(9):3314â€“3331. 3. Perina DG. Noncardiogenic pulm onary edem a. Em erg Med Clin North Am . 2003;21(2):385â€“393

Codes ICD9-CM 518.4

ICD10 J81

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > No nstero idal Anti-inflam m ato ry Po iso ning

Nonsteroidal Anti-inflammatory Poisoning Michele Zell-Kanter

Basics Description 

Inhibit cyclo-oxygenase (COX) that blocks the conversion of arachidonic acid to prostaglandin



Typically, ingestion of an nonsteroidal anti-inflam m atory drug (NSAID) is benign.



Fatalities reported with large ingestions



Greater potential for toxicity with underlying congestive heart failure (CHF) or renal failure: o

NSAIDs cause sodium and water retention and decrease renal blood flow

o

Very little overdose experience with the COX-2 inhibitors (celecoxib); treatm ent should be the sam e as for the traditional NSAIDs

o

Patients m ay ingest rofecoxib and valdecoxib from stored supplies even though both are no longer available.

Pa ge 3 2 8

Diagnosis Signs and Symptoms Gastrointestinal 

Nausea



Vom iting



Epigastric pain

CNS 

Drowsiness



Dizziness



Lethargy



Seizures

Cardiovascular 

Hypotension



Tachycardia

Pulmonary 

Eosinophilic pneum onia



Apnea



Hyperventilation

Renal 

Acute renal failure



Acute tubular necrosis



Acute interstitial nephritis

Liver 

Hepatocellular injury



Cholestatic jaundice

Metabolic Mild, short-lived m etabolic acidosis

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Hypersensitivity 

Aseptic m eningitis



Asthm a exacerbation

Essential Workup 

Generally, NSAID ingestion results in only m ild toxicity.



Exact identification of drug helpful: o

Subtle toxicologic differences am ong the NSAIDs

Tests Lab 

Electrolytes, BUN/creatinine, glucose: o

Baseline renal function

o

Check for m etabolic acidosis.



CBC



Arterial blood gas (ABG) for large overdoses



PT/PTT: o

False-positive bilirubin/ketone dipstick with etodolac ingestion



NSAID difficult to detect on toxicology screens

Differential Diagnosis Agents causing m etabolic acidosis, altered m ental status, and GI irritation: 

Salicylates



INH



Ethylene glycol



Methanol



Isopropanol

P.755

Pa ge 3 2 8

Treatment Pre Hospital Collect prescription bottles/m edications for identification in the ED.

Initial Stabilization 

ABCs



Naloxone, thiam ine, dextrose (or Accucheck) for altered m ental status

ED Treatment 

Supportive care and GI decontam ination



Gastric lavage: o

If the patient presents within 1 hour of ingestion with an intact gag reflex

o

If no gag reflex is present, protect airway with a cuffed endotracheal tube before lavage.



Avoid syrup of ipecac because NSAIDs m ay cause CNS depression and seizures in the overdose setting.



Adm inister activated charcoal and sorbitol early (after lavage com pletion).



Extracorporeal m ethods to enhance elim ination are not beneficial owing to high degree of plasm a protein binding.

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2â€“4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose

Pa ge 3 2 8



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sorbitol: 1â€“2 g/kg to a m ax. of 100 g (peds: older than 1 year, 1â€“1.5 g/kg as a 35% solution to a m ax. of 50 g) PO m ixed in the activated charcoal slurry; use only for first dose.



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Pediatric Considerations Piroxicam , naproxen, ketoprofen, and m efenam ic acid have caused seizures in children.

Follow-Up Disposition Admission Criteria 

Protracted vom iting, hem atem esis



CNS depression, seizure activity



Metabolic acidosis



CHF, hypotension, hypertension



Renal failure

Discharge Criteria Nontoxic ingestion in a patient who is asym ptom atic 6â€“8 hours after ingestion

References 1. Paloucek FP, Rynn KO. Nonsteroidal anti-inflam m atory drugs (NSAIDs). In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:281â€“284. 2. Seifert SA, Bronstein AC, McGuire TH. Massive ibuprofen ingestion with survival. J Toxicol Clin Toxicol. 2000;38:55â€“57.

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3. Zuckerm an GB, Uy CC. Shock, m etabolic acidosis, and com a following ibuprofen overdose in a child. Ann Pharm acother. 1995;29:869â€“871.

Codes ICD9-CM 965.6

ICD10 T39.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nursem aid's Elbo w

Nursemaid's

Elbow Daren D. Girard Daniel L. Savitt

Basics Description 

One of the m ost com m on injuries of the upper extrem ity in children younger than 5 years: o

Caused by longitudinal traction on an extended, pronated arm

o

Typical history is a sharp pull on the child's outstretched arm such as lifting the child by the wrist.

o 

Alternatively, caregiver m ay report history of a fall.

Subluxation of the radial head: o

Annular ligam ent slips or tears and becom es interposed between the radial head and the capitellum

Diagnosis

Pa ge 3 2 9

Signs and Symptoms 

Child refuses to use arm .



Elbow slightly flexed with forearm held close to trunk



Pain with flexion of the elbow



Pain with forearm supination or pronation



Absence of point tenderness



Minim al to no swelling

Essential Workup 

Clinical diagnosis: o

Classic history, passive position of arm , and physical exam are sufficient for diagnosis.



Radiographs: o

Not routinely indicated

o

Obtain to exclude or diagnose other injuries if any of the following are present: 

Point tenderness



Soft tissue swelling



Deform ity



Ecchym osis of the elbow



Failed reduction



Child continues to favor after reduction.

Differential Diagnosis 

Hum erus or radius fracture



Elbow dislocation



Joint infection



Osteom yelitis



Tum or

Treatment

Pa ge 3 2 9

Pre Hospital Cautions: 

Place ice on the injured elbow to reduce pain and swelling.



Im m obilize in a sling or splint to facilitate transport and prevent further injury.



Assess distal neurovascular status.

Initial Stabilization Assess distal m otor, sensory, and vascular function.

ED Treatment 

Two com m on reduction techniques



Supination/flexion technique: o

Grasp child's hand in handshake position.

o

Stabilize injured elbow with the other hand.

o

In a sm ooth, swift m otion, fully supinate the forearm and flex the elbow.



Hyperpronation technique: o

Grasp child's hand in handshake position.

o

Stabilize injured elbow with the other hand.

o

Hyperpronate and extend the forearm .

P.757



Palpable click m ay accom pany successful reduction, but is not essential.



Child m ay cry during the reduction, but is frequently pain free and using the arm shortly thereafter.



Second reduction attem pt if the child does not use arm 15 m inutes after first attem pt



Consider opposing technique for second reduction attem pt.



Radiographic studies indicated if the second reduction attem pt is unsuccessful

Pa ge 3 2 9



Perform postreduction neurovascular assessm ent.

Medication (Drugs) Acetam inophen: 15 m g/kg PO q4h: 

Ibuprofen 10 m g/kg PO q6hâ€“q8h

Follow-Up Disposition Admission Criteria None

Discharge Criteria 

Discharge to hom e after child regains full, unrestricted use of the arm .



Patient instructions: o

Inform parents not to pull or lift the child by the hand, wrist, or forearm .

o

Warn fam ily of increased incidence of recurrence until the child reaches 5â€“6 years of age.



Splint with prom pt orthopedic referral for any injury of the elbow with a radiographic abnorm ality; condylar, supracondylar, or displaced fractures need orthopedic evaluation expedited.



Posterior splint with orthopedic follow-up in 24â€“48 hours, if reduction attem pts fail and no radiographic abnorm alities can be identified



Warn fam ily to observe for neurovascular com prom ise.

References

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1. Kaufm an D. Evaluation of the patient with extrem ity pain: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):77â€“95. 2. Macias CG, Bothner J, Wiebe R. A com parison of supination/flexion to hyperpronation in the reduction of radial head subluxations. Pediatrics. 1998;102(1):e10. 3. Macias CG, Wiebe R, Bothner J. History and radiographic findings associated with clinically suspected radial head subluxations. Pediatr Em erg Care. 2000;16(1):22â€“25. 4. McDonald J, Whitelaw C, Goldsm ith LJ. Radial head subluxation: com paring two m ethods of reduction. Acad Em erg Med. 1999;6(7):715â€“718.

Codes ICD9-CM 832.0

ICD10 S59.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oculo m o to r Nerve Palsy

Oculomotor

Nerve Palsy James M. Leaming

Basics Description 

Com plete: o

Com pressive lesions such as aneurysm s or tum ors

o

Brainstem herniation with com pression of third cranial nerve 



Increased intracranial pressure

Incom plete: o

Vascular infarction of vasa nervorum of third cranial nerve

Etiology 

Intracranial or orbital tum or



Aneurysm (particularly posterior com m unicating artery)



Traum a



Intracranial hem orrhage



Diabetes m ellitus



Migraine headache



Infection, m eningitis



Arteriovenous m alform ation or fistula

Pa ge 3 2 9



Cavernous sinus throm bosis



Neuropathy (e.g., m yasthenia gravis, Guillain-BarrÃ©)



Collagen vascular diseases (e.g., sarcoidosis)

Pediatric Considerations 

Traum a is m ost com m on cause of acquired oculom otor nerve palsies.



Other causes less com m on than in adult population: o

Diabetes

o

Posterior com m unicating artery aneurysm s

o

Metastatic tum or

o

Pituitary lesions

Diagnosis Signs and Symptoms 

Diplopia, with involved eye deviated laterally and downward



Com plete: o



Mydriasis of involved eye

Incom plete: o

Reactive m idpoint pupil of involved eye

History History is of utm ost im portance in determ ining cause: 

History of long-standing diabetes m ellitus



Head traum a, either recent or distant



Unintentional weight loss



Recent infection involving the upper respiratory tract, eyes, or ears



Severe headache (classic thunderclap or chronic and worsening)

Pa ge 3 2 9



Constitutional sym ptom s: nausea, vom iting, fever

Physical Exam Ophthalm ologic exam ination: 

Extraocular m ovem ents



Exophthalm us



Funduscopic exam ination to dem onstrate papilledem a



Direct and consensual pupillary reaction

Essential Workup CT/MRI of brain, orbit, sinuses

Tests Lab 

CBC with differential



Erythrocyte sedim entation



Antinuclear antibodies, rheum atoid factor to evaluate for vasculitis



Lum bar puncture

Imaging 

Doppler im aging for arteriovenous m alform ations, dural sinus throm bosis



Cerebral arteriogram rarely useful as m ost aneurysm s are seen on CT or MRI

Differential Diagnosis 

Infection



Malignancy



Vasculitis

Pediatric Considerations Consider congenital oculom otor nerve palsy.

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Treatment Pre Hospital Without associated traum a, no specific prehospital care issues exist.

Initial Stabilization 

Initial stabilization of posttraum atic patient should concentrate on underlying traum atic condition.



Airway m anagem ent and resuscitation as indicated



Any patient with evidence of herniation should have the following m easures to control intracranial pressure: o

Intubation using rapid-sequence induction and controlled ventilation to a PCO 2 level of 35â€“40 m m Hg

o

Elevate head of bed 30Â°.

o

Mannitol

P.759

ED Treatment General Measures 

Crucial to differentiate between aneurysm and other com pressive lesions early in ED evaluation



Differentiation between incom plete and com plete oculom otor nerve palsy guides focus of ED treatm ent.



Medication regim en determ ined by cause: o

Aneurysm : 

Control severe hypertension with nitroprusside.



Decrease intracranial pressure with intubation.



Controlled ventilation



Elevation of head



Mannitol

Pa ge 3 2 9

o

Intracranial tum or: control increasing intracranial pressure as above.

o

Inflam m ation and edem a: decrease with intravenous steroids.

o

Meningitis: 

Rapid adm inistration of intravenous antibiotics



Intravenous steroids m ay be useful to decrease inflam m atory response and edem a.

o

Vasculitis and collagen vascular diseases: Decrease inflam m atory cell infiltration with intravenous steroids.

o

Neuropathy: m yasthenia gravisâ€”edrophonium chloride test

Medication (Drugs) 

Ceftriaxone: 1â€“2 g (peds: 50â€“100 m g/kg) IV



Dexam ethasone: 10 m g IV (peds: 0.15â€“0.5 m g/kg IV single dose in ED)



Edrophonium Cl: 5â€“8 m g IV (peds: 0.15 m g/kg IV; 1/10 test dose given first)



Mannitol: 1 g/kg IV (peds: not routinely recom m ended)



Methylprednisolone: adults/peds: 1â€“2 m g/kg IV single dose in ED

Follow-Up Disposition Admission Criteria 

Com plete oculom otor nerve palsy of any cause requires

Pa ge 3 3 0

adm ission and em ergency neurosurgical evaluation. 

Incom plete oculom otor nerve palsy with abnorm al CT or MRI, abnorm al laboratory studies, or other focal neurologic or constitutional sym ptom s

Discharge Criteria Incom plete oculom otor nerve palsy with negative CT or MRI, norm al laboratory studies, and no other sym ptom s can be referred for urgent outpatient neurologic evaluation.

References 1. Chen CC, Pai YM, Wang RF, et al. Isolated oculom otor nerve palsy from m inor head traum a. Br J Sports Med. 2005;39(8):e34. 2. Ing EB, Sullivan TJ, Clarke MP, et al. Oculom otor nerve palsies in children. J Pediatr Ophthalm ol Strabism us. 1992;29:331â€“336. 3. Kodsi SR, Younge BR. Acquired oculom otor, trochlear, and abducent cranial nerve palsies in pediatric patients. Am J Ophthalm ol . 1992;114:568â€“574. 4. Richards BW, Jones FR Jr, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the oculom otor, trochlear, and abducens cranial nerves. Am J Ophthalm ol. 1992;113:489â€“496. 5. Tiffin PA, MacEwen CJ, Craig EA, et al. Acquired palsy of the oculom otor, trochlear, and abducens nerves. Eye. 1996;10(pt 3):377â€“384.

Codes ICD9-CM 378.81 Palsy of conjugate gaze

ICD10 G58.8

Pa ge 3 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Opiate Po iso ning

Opiate Poisoning

Amy V. Kontrick Mark B. Mycyk

Basics Description 

Bind to Âµ, Îº, and Î´ opiate receptors in CNS and PNS



Physical and psychologic dependence occurs.



Peak plasm a levels: o

PO: 1â€“2 hours

o

Intram uscular: 0.5â€“1 hour

o

Intravenous or intranasal: seconds to m inutes

Etiology 

Overuse or abuse of oral prescription analgesics for m oderate to severe pain



Street preparations of narcotic analogs m ay contain adulterants: o

Cocaine

o

PCP

o

Strychnine

o

Dextrom ethorphan

o

Quinine

o

Scopolam ine

Pa ge 3 3 0

Diagnosis Signs and Symptoms 











CNS: o

CNS depression

o

Com a

o

Seizures

Gastrointestinal: o

Nausea

o

Vom iting

o

Constipation

Cardiovascular: o

Hypotension

o

Bradycardia

o

Palpitations

Pulm onary: o

Respiratory depression

o

Bronchospasm

o

Pulm onary edem a

o

Apnea

Other: o

Miosis

o

Hypotherm ia

Withdrawal: o

Hypertension

o

Tachycardia

o

Tachypnea

o

Abdom inal cram ps

o

Diarrhea

o

Piloerection

o

Yawning

Pa ge 3 3 0

Pediatric Considerations 



Neonatal withdrawal: o

Infants born to addicted m others

o

Onset: 12â€“72 hours after birth

o

Irritability, trem ors, poor feeding, and dehydration

Diphenoxylate (Lom otil): toxicity m ore severe in children than adults and m ay be fatal

Essential Workup Monitor vital signs and pulm onary status with significant exposure: 

Pulse oxim etry or arterial blood gases



Chest radiograph if persistent hypoxia or possible aspiration



Abdom inal radiograph if body packing suspected

Tests Lab 

Plasm a opiate levels not clinically useful: o

Treatm ent based on clinical presentation, not opiate level



Urine toxicity screen for opioids m ay not identify som e synthetic opioids (e.g., m ethadone).



Acetam inophen level for overuse or abuse of oral prescription analgesic products

Differential Diagnosis 

Clonidine overdose



Barbiturate overdose



Benzodiazepine overdose



Î³-Hydroxybutyrate (GHB) overdose



Neuroleptic overdose



Occult head injury

Pa ge 3 3 0

Treatment Pre Hospital 

Transport all pills/pill bottles involved in overdose for identification in ED.



Provide respiratory support.



Adm inister naloxone.

Initial Stabilization 



Check airway, breathing, and circulation (ABCs): o

Airway control essential

o

Adm inister supplem ental oxygen.

Adm inister naloxone: o

Reverses respiratory depression and com a in opiate overdoses

o

Intubate if naloxone does not reverse respiratory depression.

P.761

ED Treatment 

Naloxone adm inistration: o

Start with low doses for opiate-habituated patients.

o

High doses (10 m g) m ay be required to reverse the effects of propoxyphene, m ethadone, and fentanyl.

o

Adm inister repeated doses that reversed sym ptom s, as needed every 20â€“60 m inutes.

o

For long-acting opioids, consider an hourly infusion of two thirds the dose needed to reverse sym ptom s.



Decontam ination: o

Adm inister activated charcoal for oral ingestion.

Pa ge 3 3 0

o

Adm inister whole bowel irrigation with polyethylene glycol for asym ptom atic body packers.



Treat opiate withdrawal with clonidine or m ethadone.



Hypotension:



o

0.9% norm al saline IV fluid bolus

o

Trendelenburg test

o

Initiate dopam ine for resistant hypotension.

Seizures: o

Treat initially with diazepam .

o

Adm inister phenobarbital for persistent seizures.

Medication (Drugs) 

Activated charcoal: 1â€“2 g/kg PO



Clonidine: 0.1â€“0.3 m g PO b.i.d. for 10 days; 0.1â€“0.2 m g/kg/d transderm al patch



Diazepam : 5â€“10 m g IV (peds: 0.2â€“0.5 m g/kg IV) q10â€“15m in



Dopam ine: 2â€“20 Âµg/kg/m in; titrate to effect



Methadone: 15â€“40 m g/d



Naloxone: 0.4â€“2 m g (peds: 0.1 m g/kg; neonates: 10â€“30 Âµg/kg) IV or IM



Phenobarbital: 10â€“20 m g/kg IV (loading dose)



Polyethylene glycol: 2 L/h until clear rectal effluent and/or passage of packets

Follow-Up Disposition Admission Criteria

Pa ge 3 3 0



Sym ptom atic after oral overdose



Repeated naloxone dosing or infusion needed to reverse sym ptom s



Children younger than 5 years postdiphenoxylate ingestion should be observed for 24 hours.



Opiate body packers

Discharge Criteria 

Asym ptom atic 6 hours after oral overdose



Asym ptom atic 4 hours after naloxone adm inistration



Com plete elim ination of opiate packets

Issues for Referral Consider substance abuse referral for patients.

References 1. Dietze P, Jolley D, Cvetkovski S, et al. Characteristics of non-fatal opioid overdoses attended by am bulance services in Australia. Aust N Z J Public Health. 2004;28(6):569â€“575. 2. Kelly AM, Kerr D, Dietze P, et al. Random ised trial of intranasal versus intram uscular naloxone in prehospital treatm ent for suspected opioid overdose. Med J Aust. 2005;182(1):24â€“27. 3. Kleinschm idt KC, Wainscott M, Ford MD. Opioids. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:637â€“639. 4. Sporer KA. Acute heroin overdose. Ann Intern Med. 1999;130:584â€“590.

Codes ICD9-CM 850.0

ICD10 T460.6

Pa ge 3 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oppo rtunistic Infectio n

Opportunistic

Infection Elicia Sinor Kennedy

Basics Description Unusual infections that occur when host suffers a decrease in resistance against norm ally nonpathogenic organism s

Etiology 

Occurs in HIV patients when the CD4 T-lym phocyte count falls below 200 cells/m m 3 or less than 14% of the total lym phocyte count: o

Pneum ocystis jiroveci pneum onia

o

Cryptococcal infection

o

Dissem inated tuberculosis

o

Cryptosporidiosis

o

Isosporiasis

o

Toxoplasm osis

o

Histoplasm osis

o

Cryptococcosis

o

Mycobacterium avium com plex

o

Tuberculosis pericarditis or m eningitis

o

Cytom egalovirus

Pa ge 3 3 0





Cell-m ediated deficiency: o

Hem atologic m alignancies

o

Lym phom a

o

High-dose glucocorticoid therapy

o

Autoim m une disorders

o

Viral infections

o

Cytotoxic drugs/chem otherapy

o

Radiation therapy

o

Associated with: 

Legionella



Nocardia



Salm onella



Mycobacteria

Neutrophil im pairm ent/depletion: o

Cytotoxic drugs

o

Aplastic anem ia

o

Drug reactions: 

Dapsone

o

Neoplastic invasion of bone m arrow

o

Arsenic

o

Penicillin

o

Chloram phenicol

o

Procainam ide

o

Vitam in deficiencies

o

Associated with: 

Staphylococcus and Î±-hem olytic Streptococcus



Enteric organism s and anaerobes

Diagnosis Signs and Symptoms

Pa ge 3 3 0



New or worsening fatigue



Confusion



Tachypnea



Fever



Chills



Pulm onary source of infection:





o

Cough

o

Congestion

o

Rales

Genitourinary source of infection: o

Dysuria

o

Increased frequency

o

Urinary retention

Gastrointestinal (GI) source of infection: o

Vom iting

o

Diarrhea

o

Bleeding

Physical Exam 

Signs of system ic inflam m atory response syndrom e: o

Tem perature >38Â°C or <36Â°C

o

Heart rate >90 beats per/m inute

o

Respiratory rate >20 breaths per m inute or PCO 2 <32 m m Hg



Septic shock



New m urm ur



Inspect skin and m ucosa carefully for a portal of entry.



Exam ine oral m ucosa and perianal area for erythem a and palpate for tenderness or crepitus.

Essential Workup Full workup indicated owing to im paired im m unity: 

Signs of infection in the im m unocom prom ised patient m ay

Pa ge 3 3 1

not be present. 

Can present with subtle signs with rapid deterioration



Signs such as fever m ust lead to a full evaluation of patient.



Thorough physical exam critical to search for site of infection

Tests Lab 

CBC with differential for neutropenia or leukocytosis: o

WBC >12,000 is a criteria for the system ic inflam m atory response score

o

Neutropenia: 

Num ber of polym orphonuclear + bands <500/m m 3



Cultures (aerobic, anaerobic, fungal, viral as indicated): o

Urine

o

Blood

o

Wound

o

Fecal



CD4 count



Urinalysis for presence of WBC, nitrite, leukocyte esterase



Electrolytes, blood urea nitrogen/creatinine glucose; anion gap acidosis suggests severe infection.



Arterial blood gas for hypoxia/acidosis



Lactate level; elevated value suggests serious infection.



PT/PTT for evidence of dissem inated intravascular coagulation

Imaging 

Chest radiograph: o

Nonspecific for predicting a particular infectious etiology

Pa ge 3 3 1

o

o

Pneum onia: 

Segm ental or subsegm ental infiltrate



Air bronchogram s



Abscess



Cavitation



Em pyem a



Pleural effusion

Pneum ocystis carinii pneum onia: 

Classically reveals bilateral interstitial or central alveolar infiltrates

 

Radiograph norm al in up to 25% of patients

High-resolution chest CT: o

Early studies show high sensitivity for PCP in HIV-positive patients

o 

Reveals patchy ground-glass attenuation

Abdom inal CT with contrast: o

Indicated if a GI source of infection is suggested by the clinical exam ination

Diagnostic Procedures/Surgery Lum bar puncture: 

Cerebrospinal fluid analysis if signs of CNS infection

P.763

Treatment Initial Stabilization 

Check airway, breathing, and circulation



Initiate 0.9% norm al saline intravenous 500-m L bolus for

Pa ge 3 3 1

hypotension. 

Oxygen



Cardiac m onitor for unstable vital signs



Early initiation of antibiotic therapy

General Measures 

Strict isolation



Antibioticsâ€”com bination of expanded-spectrum penicillin (m ezlocillin, ticarcillin, piperacillin) and am inoglycoside (am ikacin, tobram ycin): o

Monotherapy with a third-generation cephalosporin (ceftazidim e, cefepim e), fluoroquinones (levofloxacin, gatifloxacin), or other broad-spectrum antim icrobials (im ipenem /cilastatin) m ay be considered if am inoglycosides contraindicated.

o

Vancom ycin is not recom m ended as part of initial therapy unless there is a high incidence of m ethicillin-resistant organism s in the area.

o

Antifungals (am photericin B, fluconazole) if patient is on adequate antibiotics for 1 week.

Medication (Drugs) 

Am photericin B: 025 m g/kg IV per day



Cefepim e: 1â€“2 q12h IV



Ceftazidim e: o

Adults: 1â€“2 g IV q8â€“12h

o

Pediatric: 100â€“150 m g/kg per 24 hours IV q8â€“12h



Fluconazole: 400 m g first dose, then 200â€“400 m g IV per day (peds: 3â€“6 m g/kg per 24 hours IV q12h)



Gatifloxacin: 400 m g IV per day

Pa ge 3 3 1



Im ipenem /cilastatin: 500â€“1,000 m g IV q6â€“8h, m ax. 50 m g/kg per day or 4,000 m g per day



Levofloxacin: 500 m g IV per day



Piperacillin: 3 g over 30 m inutes q4h



Ticarcillin: 3 g IV q4h over 30 m inutes (peds: 200â€“300 m g/kg per 24 hours IV over 30 m inutes q4h)



Vancom ycin: 1â€“2 g IV every 12 hours (peds: 10â€“50 m g/kg per 24 hours IV q6h

Follow-Up Disposition Admission Criteria Suspected or confirm ed system ic infection

Discharge Criteria System ic infection excluded

References 1. Daar ES, Meyer RD. Bacterial and fungal infections. Med Clin North Am . 1992;17:173â€“195. 2. Em m anouilides C, Glaspy J. Opportunistic infections in oncologic patients. Hem atol Oncol Clin North Am . 1996;10:841â€“860. 3. Giam arellou H. Em piric therapy for infections in the febrile, neutropenic, com prom ised host. Med Clin North Am . 1992;79:559â€“578. 4. Pizzo PA. The com prom ised host. In: Bennett JC, et al., eds. Cecil's Textbook of Medicine. Philadelphia: WB Saunders; 1996: 908â€“915. 5. Rubin ZA, Som ani J. New options in the treatm ent of invasive fungal infections. Sem inars in Oncology. 2004: 31(2 Suppl

Pa ge 3 3 1

4):91â€“98.

Pa ge 3 3 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Optic Artery Occlusio n

Optic Artery

Occlusion Yasuharu Okuda

Basics Description 

Obstruction of the central retinal artery associated with sudden painless loss of vision



Occurs in older population, 50â€“70 years of age



Risk factors include hypertension, sickle cell disease, vasculitis, valvular heart disease, lupus, traum a, and coronary artery disease.

Etiology 

Em bolic: o

Occlusion by intravascular m aterial from a proxim al source: 

Atherosclerotic disease (m ajority)



Valvular heart disease



Atrial m yxom a



Dissection of the ophthalm ic artery in the region of the cribriform plate (rare)



Throm botic: o

Obstruction of flow from the rupture of a pre-existing

Pa ge 3 3 1

intravascular atherosclerotic plaque 

Inflam m atory: o

Inflam m ation from diseases such as tem poral arteritis and lupus



Arterial spasm : o



Associated with m igraine headaches

Decreased perfusion o

Low flow conditions such as in severe hypotension or high pressure situations seen in acute angle closure glaucom a or retrobulbar hem orrhage.

Diagnosis Signs and Symptoms History 

Sudden, painless, m onocular loss of vision



Prior episodes of sudden visual loss: o

Lasts a few seconds to m inutes (am aurosis fugax)

o

Caused by transient em bolic phenom ena or decreased ocular blood flow



Partial field deficits: o

Only if branch of central retinal artery involved

Physical Exam 

Significantly decreased visual acuity with loss of afferent pupillary reflex



Retinal appearance: o

Em boli visualized within vascular tree of the retina 

Appears as glinting white or yellow flecks (Hollenhorst plaques) within the vessels

o

Ischem ic edem a visible within 15â€“20 m inutes of

Pa ge 3 3 1

occlusion o

Affected arteries em pty or showing dark red stationary or barely pulsatile segm ented rouleaux (â€œbox carringâ€•)

o

Within one to two hours: 

Opacification of the usually transparent infarcting retinal nerve layer occurs.



â€œCherry-red spotâ€• rem ains over the fovea (only area where there is very thin retina allowing the vascular choroids to show through).

Tests Visual acuity

Lab 

Directed towards evaluating underlying etiology of occlusion



CBC with differential and platelet count



Prothrom bin tim e/partial throm boplastin tim e test (PTT)



Electrolytes, blood urea nitrogen/creatinine, glucose



Electronic spin resonance for giant cell arteritis (in patients >55 years old)



ANA



Rheum atoid factor



Rapid plasm a reagin



Hem oglobin electrophoresis



Serum protein electrophoresis

Imaging 

Directed toward evaluating underlying etiology of occlusion



Carotid artery evaluation by ultrasound and Doppler



Cardiac evaluation: o

ECG

Pa ge 3 3 1



o

Echocardiography

o

Holter m onitoring

Fluorescein angiography or electroretinography to confirm the diagnosis

Differential Diagnosis 

Central retinal vein occlusion



Retinal detachm ent



Giant cell arteritis (tem poral arteritis)



Acute angle closure glaucom a



Optic neuritis

P.765

Treatment Initial Stabilization 

Initiate treatm ent im m ediately because irreversible visual loss occurs at 90 m inutes: o

Only im m ediate treatm ent m ay help to salvage or restore sight to the affected eye



Goals of therapy include dislodging or dissolving the em bolus, arterial dilation to im prove forward flow, and reduction of intra-ocular pressure to im prove the profusion gradient.

ED Treatment 

Im m ediate global m assage in an attem pt to dislodge the em bolus: o

Lay patient flat and apply digital global m assage bolus.

Pa ge 3 3 1

o

On closed eyelid, apply constant pressure for 15 seconds and rem ove for 15 seconds. Repeat for 5 cycles.



Increase PCO 2 to dilate retinal vessels: o

Have patient breath into paper bag for 10 m inutes each hour or use inhaled Carbogen.



Adm inister IV acetazolam ide to decrease intra-ocular pressure.



Apply topical tim olol m aleate to reduce intra-ocular pressure.



Adm inister aspirin and IV heparin for prevention of clot propagation.



Obtain em ergent ophthalm ology consultation for: o

Anterior cham ber paracentesis to help reduce intraocular pressure

o 

Possible intra-arterial fibrinolysis for clot lysis

Adm inister high dose system ic steroids in suspected cases of inflam m atory arteritis.

Medication (Drugs) 

Acetazolam ide: 500 m g IV or PO



Aspirin: 325 m g PO



Carbogen: inhalation of 95% oxygen and 5% carbon dioxide m ixture.



Heparin: 80 U/kg IV bolus then 18 U/kg/hr continuous infusions (rate adjusted based on PTT level)



Methylprednisolone: 250 m g IV in suspected cases of inflam m atory arteritis



Tim olol m aleate 0.5% solution: one drop topically to affected eye

Pa ge 3 3 2

Follow-Up Disposition Admission Criteria Acute central retinal artery occlusion for workup for source of em bolic phenom ena or throm bosis

Discharge Criteria Chronic retinal artery occlusion with no evidence of active disease can be worked up as an outpatient.

Issues for Referral All suspected cases warrant em ergent ophthalm ology consultation.

References 1. Arnold M, Koerner U, Rem onda L, et al. Com parison of intra-arterial throm bolysis with conventional treatm ent in patients with acute central retinal artery occlusion. J Neurol Neurosurg Psychiatry. Feb 2005;76(2):196â€“199. 2. Fraser S, Siriwardena D. Interventions for acute non-arteritic central retinal artery occlusion. Cochrane Database Syst Rev. 2002;(1):CD001989. 3. Morgan A, Hem phill R. Acute visual change. Em erg Med Clin North Am . Nov 1998;16(4):825â€“843.

Codes ICD9-CM 362.30

Pa ge 3 3 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Optic Neuritis

Optic Neuritis

Alexander T. Limkakeng Jr.

Basics Description 

Optic nerve dysfunction owing to an inflam m atory process, com m only associated with m yelin destruction



Grouped by site of inflam m ation: o

Papillitis: inflam m ation of the optic disk

o

Retrobulbar neuritis: inflam m ation of the optic nerve proxim al to the globe



Five-year risk for clinically definite m ultiple sclerosis following optic neuritis: o

Norm al MRIâ€”16%

o

More than 3 lesions on MRIâ€”51%

Genetics High prevalence of A23, B7, and DR2 HLA alleles in patients with optic neuritis: 

Especially those that progress to clinically definite m ultiple sclerosis

Etiology 

Idiopathic: o

Most com m on

Pa ge 3 3 2

o 

Multiple sclerosis (MS): o





Single isolated events

20â€“50% of patients with optic neuritis

Viral infections: o

Chicken pox

o

Measles

o

Mononucleosis

o

Herpes zoster

o

Encephalitis

Postviral optic neuritis: o

Usually occurs 4â€“6 weeks after a nonspecific viral illness



Granulom atous inflam m ation: o

Tuberculosis

o

Syphilis

o

Sarcoidosis

o

Cryptococcal infection



System ic lupus erythem atosus



HIV: o

Cytom egalovirus

o

Toxoplasm osis

o

Histoplasm osis

o

Cryptococcus



Lym e disease



Contiguous inflam m ation of m eninges, orbit, sinuses, and intraocular inflam m ation



Drug induced: o

Etham butol

o

Tam oxifen

Pa ge 3 3 2

Diagnosis Signs and Symptoms 



Visual loss occurring over days (rarely over hours): o

Adults usually unilateral

o

Bilateral visual loss m ore com m on in children

Retrobulbar pain: increased with m ovem ent of the affected eye



Light, color vision, and depth perception loss m ore pronounced than visual acuity loss



Afferent pupillary defect occurring in unilateral cases



Visual field defects: o



Central scotom a

Funduscopic exam usually reveals either swollen (papillitis) or norm al disk:



Uhthoff sign: o

Visual deficit occurring with exercise or increased body tem perature

o

Unusual sign seen occasionally

History 

Age (typically wom en age 18â€“45 years)



Pain on eye m ovem ent



Speed of onset of sym ptom s



Associated sym ptom s



Previous episodes



Fam ily history of optic neuritis, MS

Physical Exam 

Check blood pressure (BP)



Com plete ophthalm ologic and neurologic exam ination, especially assessm ent of: o

Pupillary function

Pa ge 3 3 2

o

Afferent pupillary defect

o

Visual field defect

o

Color vision (Ishihara color plates)

o

Evaluation of the vitreous body for cells

o

Dilated retinal exam (swollen optic disk)

Tests Lab 

CBC



Erythrocyte sedim entation rate (ESR)



RPR, FTAâ€“ABS



Lym e titer



Antinuclear antibody (ANA)



Purified protein derivative (PPD) testing



HIV testing

Imaging 

Chest radiograph for tuberculosis, sarcoid



CT scan or MRI of brain and orbits: o

Inflam m ation of the retrobulbar optic nerve during the acute phase m ay appear as enlargem ent, thus falsely raising the issue of an optic nerve m ass.

o

Visual field testing (preferably autom ated testing, such as Octopus or Hum phrey)

P.767

Differential Diagnosis 

Acute papilledem a



Ischem ic optic neuropathy



Severe system ic hypertension



Intracranial tum or com pressing the afferent visual

Pa ge 3 3 2

pathway 

Orbital m ass com pressing the optic nerve



Toxic or m etabolic neuropathy:



o

Heavy m etal poisoning

o

Anem ia

o

Malnutrition

o

Alcohol

o

Chloroquine

o

Etham butol

o

INH

Leber hereditary optic atrophy

Treatment ED Treatment 

Early ophthalm ologic and neurologic consultations



IV steroid pulse followed by oral steroids: o

Recom m ended for those with two or m ore dem yelinating lesions on MRI without a prior history of MS or optic neuritis

o

Decreases recurrence, progression to MS over 2 years, and shortens duration of visual im pairm ent, but does not affect rate of progression at 5 years or visual outcom e at 1 year.

o

Treatm ent should be individualized for those with one lesion on MRI.

Medication (Drugs) Methylprednisolone: 250 m g IV q6h for 3 days

Pa ge 3 3 2

Follow-Up Disposition Admission Criteria 

Bilateral vision loss



If other sources of acute vision loss cannot be ruled out



IV steroid pulse treatm ent needed

Discharge Criteria 

Unilateral visual im pairm ent



Good hom e support system s



Neurology and ophthalm ology follow-up arranged

Issues for Referral Referral for interferon beta 1a treatm ent as outpatient for those with two or m ore dem yelinating lesions on MRI: 

Reduces progression to MS

References 1. Balcer LJ, Galetta SL. Treatm ent of acute dem yelinating optic neuritis. Sem in Opthalm . 2002;17(1):4â€“10. 2. Beck RW, Cleary PA, Anderson MM, et al. Optic Neuritis Study Group. A random ized controlled trial of corticosteroids in the treatm ent of acute optic neuritis. N Eng J Med. 1992;326:581â€“588. 3. Beck RW, Cleary PA, Anderson MM, et al. Optic Neuritis Study Group. Visual function 5 years after optic neuritis: experience of the ONTT. Arch Opthalm . 1997;115(12):1545â€“1552. 4. Jacobs LD, Beck RW, Sim on JH, et al.CHAMPS Study Group. Interferon beta-1a for optic neuritis patients at high risk for m ultiple sclerosis. Am J Ophthalm . 2001;132:463â€“471. 5. Kunim oto DY, Kanitkark KD, Makar MS, eds. Wills Eye Manual. 4th

Pa ge 3 3 2

ed. Philadelphia: Lippincott William s & Wilkins; 2004.

Miscellaneous SEE ALSO: Visual Loss

Codes ICD9-CM 377.3

ICD10 H46

Pa ge 3 3 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Organo pho sphate Po iso ning

Organophosphate Poisoning Sean Bryant

Basics Description 

Organophosphates (pesticides and nerve agents) irreversibly bind to cholinesterases, causing deactivation of acetylcholinesterase.



Initial accum ulation of acetylcholine at neural synapse results in cholinergic overdrive (central and peripheral).



Predom inate effects (m uscarinic, nicotinic, CNS) m ay vary and can overlap.



Death usually secondary to respiratory failure resulting from weakness of respiratory m uscles, pulm onary edem a, and central depression of respiratory drive.

Pediatric Considerations 

Sym ptom s are difficult to differentiate in toddlers.



Com m on sym ptom s: m iosis, salivation, and m uscle weakness



Seizures found in 25% (3% of adults).

Etiology 

Exposure to insecticides (organophosphorus com pounds)

Pa ge 3 3 2



Exposure to chem ical nerve agents (Sarin, Som an, VX, Tabun)

Diagnosis Signs and Symptoms 

Classic presentationâ€”cholinergic toxidrom e: o



DUMBELS: 

Diarrhea/diaphoresis



Urination



Miosis/m uscle fasciculations



Bradycardia, bronchorrhea, bronchospasm



Em esis



Lacrim ation



Salivation

Chronic interm ittent exposure, nonspecific sym ptom s: o

Weakness

o

Fatigue

o

Malaise

o

Anorexia

Mild Exposure 



Visual: o

Miosis

o

Decreased visual acuity

CNS: o

Headache

o

Dizziness

o

Trem ors of tongue and eyelids

o

Anxiety

o

Weakness

Pa ge 3 3 3



Gastrointestinal (GI): o

Anorexia

Moderate Exposure 





CNS: o

Muscle fasciculation followed by flaccid paralysis

o

Respiratory m uscle weakness

o

Incoordination

GI: o

Nausea

o

Vom iting

o

Abdom inal cram ps

Exocrine glands: o

Salivation

o

Lacrim ation

Severe Exposure 

Visual: o









Pinpoint nonreactive pupils

Respiratory: o

Respiratory difficulty

o

Pulm onary edem a

Cardiovascular o

Bradycardia

o

Heart block

CNS: o

Convulsion

o

Com a

o

No sphincter tone

GI: o

Diarrhea

Muscarinic Manifestations 

Respiratory:

Pa ge 3 3 3



o

Bronchoconstriction

o

Wheezing

o

Dyspnea

o

Increased bronchial secretion

o

Cough

o

Pulm onary edem a

Cardiovascular: o

Bradycardia (tachycardia m ay follow pulm onary edem a and hypoxia)

o 





GI: o

Nausea, vom iting

o

Abdom inal pain

o

Diarrhea

o

Tenesm us

o

Fecal incontinence

Exocrine glands: o

Diaphoresis

o

Salivation

o

Lacrim ation

Pupils: o



Miosis, occasionally anisocoria

Ciliary body: o



Cyanosis

Blurred vision

Bladder: o

Frequency

o

Urinary incontinence

Nicotinic Manifestations 



Striated m uscle: o

Fasciculation

o

Weakness including respiratory m uscles

Sym pathetic ganglia:

Pa ge 3 3 3



o

Mydriasis

o

Tachycardia

o

Hypertension

o

Bronchodilation

CNS: o

Agitation

o

Restlessness

o

Trem ors

o

Confusion

o

Depression

o

Ataxia

o

Weakness

o

Com a

o

Seizures

o

Death

Essential Workup 

Inquire about possible exposure, occupation, recent insecticide in hom e, m islabeled, or poorly stored insecticides: o



Obtain original container if suicide attem pt.

Look for parasym pathetic and CNS signs with m uscle weakness or paralysis.

Tests Lab 

RBC and plasm a cholinesterase levels to confirm diagnosis: o

RBC (true) cholinesterase level is best reflection of synaptic inhibition (a send-out lab)

o

Plasm a (pseudo) cholinesterase level not as reliable but m ore tim ely

o

Cholinesterase levels

Pa ge 3 3 3

o



Latent exposure: >50% of norm al value



Mild exposure: 20â€“50% of norm al value



Moderate exposure: 10â€“20% of norm al value



Severe exposure: <10% of norm al value

Do not wait for cholinesterase results before adm inistering treatm ent



CBC



Electrolytes, glucose, blood urea nitrogen, creatinine



Arterial blood gas when respiratory sym ptom s

Imaging 

Chest radiograph if respiratory difficulty is present or suspect pulm onary edem a



ECG: o

Dysrhythm ias (atrial fibrillation, ventricular tachycardia, torsades de pointes, QT prolongation)



o

Bradycardia

o

Heart block

o

ST-Tâ€“wave abnorm alities

CT scan of head for altered m ental status when diagnosis is uncertain

P.769

Differential Diagnosis Mild to Moderate Exposure 

Gastroenteritis



Asthm a



Venom ous arthropods bite (black widow, scorpion)



Nonspecific viral syndrom e



Progressive peripheral neuropathy (Guillain-BarrÃ© syndrom e)

Pa ge 3 3 3



Carbon m onoxide

Severe Exposure 

Narcotic overdose



Com a and m iosis: o

PCP, m eprobam ate, phenothiazine, clonidine

o

Muscarinic-containing m ushroom sâ€”cholinergic crisis without nicotinic sym ptom s

o 



Nicotine poisoning

Metabolic and infectious: o

Ketoacidosis, sepsis, m eningitis, encephalitis

o

Hypoglycem ia

o

Reye syndrom e

Neurologic: o

Cerebrovascular accident

o

Subdural or epidural hem atom a

o

Postictal state

Treatment Pre Hospital 

Decontam ination is initial priority: o

DABC: decontam inate, airway, breathing, circulation

o

Rem ove all clothes and store as toxic waste (double bagged)



Protection of health care workers of utm ost im portance: o

Im penetrable gloves (neoprene, nitrile), gowns, eye protection



Decontam inate skin with soap and water: o

Shower or gentle scrubbing ideal if done before entrance into the ED

Pa ge 3 3 3



Maintain airway and oxygenate.



IV access and place on cardiac m onitor

Initial Stabilization 



Decontam inate ABCs: o

Decontam ination and protection of staff

o

Maintain airway and oxygenate

o

For unstable airway, intubate, and ventilate

o

IV access with D 5 W 0.9% NS

Altered m ental status: adm inister thiam ine, glucose, and naloxone (Narcan)

ED Treatment 

Atropine: o

Blocks acetylcholine at m uscarinic receptor sites

o

No effect on nicotinic receptors

o

Onset of action is 1â€“4 m inutes, peaks at 8 m inutes.

o

Goal of therapy/end point: 

o

Drying secretions of tracheobronchial tree

Adm inister test dose 1â€“2 m g IV/IM: 

No clinical response: double dose every 5 m inutes until m uscarinic findings subside

o

Dose: 1â€“4 m g IV q5m in (peds: 0.05â€“0.2 m g/kg)

o

Com m on pitfalls in therapy: 

Not giving enough atropine



Using pupillary findings (m ydriasis) as end point of atropine therapy



Dilated pupils or tachycardia are not contraindications to the adm inistration of atropine.



Pralidoxim e (2-PAM): o

Regenerates cholinesterase by reversing the phosphorylation of the enzym e

Pa ge 3 3 3

o

Synergistic with atropine and m uscarinic signs and sym ptom s will start to resolve within 10â€“40 m inutes.

o

Side effects include neurom uscular blockade with rapid infusion, respiratory arrest, hypertension, nausea/vom iting, dizziness, and blurred vision.

o

End point is resolution of m uscle weakness and fasciculations.

o

Effective only if given before enzym e aging occurs (point at which cholinesterase is perm anently inactivated)

o

Onset of aging varies between products

o

No restriction to its use even if 24â€“48 hours have passed



Supportive care: o

Derm al decontam ination: rem ove clothes and flush skin with water

o

Gastric lavage (considered in early presentation of life-threatening ingestion): 

Gastric em ptying should be done with continuous suction via a nasogastric tube.



Handle contents with care and avoid com ing in direct contact with it to prevent exposure.

o

Respiratory difficulty: 

Frequent respiratory secretion suction required



Treat bronchospasm with atropine and not bronchodilators.



Tachycardia m ay result from hypoxia induced by pulm onary secretions and bronchospasm .



Atropine will dry secretions and paradoxically lower the heart rate in light of m ore effective oxygenation:

Pa ge 3 3 3



Intubate and ventilate if necessary.

Medication (Drugs) 

Atropine: 1â€“4 m g (peds: 0.05â€“0.2 m g/kg) IV q5m in (see previous section for details)



Dextrose: D 5 0 W, 1 am p (25 g) of 50% dextrose (peds: 2â€“4 m L/kg D 2 5 W) IV push



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV/IM



Pralidoxim e: 1â€“2 g (peds: 20â€“40 m g/kg) dissolved in 0.9% NS over 30-m inute IV; repeat in one hour if necessary, then every 3â€“8 hours as needed: o

Som e propose a continuous infusion of 500 m g/h to obtain a necessary serum concentration of 4 m g/L

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission for m ild, m oderate, or severe exposure confirm ed with a response to atropine



Any sym ptom atic patient should be adm itted for m onitoring.



Avoid CNS-depressive effects of opioids, phenothiazines, and antihistam ines, as these m ay potentiate toxicity of organophosphates

Discharge Criteria 

Asym ptom atic for 6â€“12 hours after exposure



Ensure close reliable follow-up and specific instructions when to return for evaluation.

Pa ge 3 3 3

References 1. Clark RF. Insecticides: Organic Phosphorous Com pounds and Carbam ates. In Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. McGraw-Hill, 2002;1346â€“1365. 2. Minton NA, Murray SG. A review of organophosphate poisoning. Med Toxicol. 1988;3:350â€“375. 3. Tafuri J, Toberts J. Organophosphate poisoning. Ann Em erg Med. 1987;16:193â€“202. 4. William s JL, DeBisschop HC, Verstraete AG, et al. Cholinesterase reactivation in organophosphorus poisoned patients depends on the plasm a concentrations of the oxim e pralidoxim e m ethylsulphate and of the organophosphate. Arch Toxicol. 1993;67:79â€“84. 5. Zwiener RJ, Ginsburg CM. Organophosphate and carbam ate poisoning in infants and children. Pediatrics. 1988;81:121â€“126.

Codes ICD9-CM 989.3

ICD10 T60.0

Pa ge 3 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osgo o d-Schlatter Disease

Osgood-Schlatter Disease Raj J. Patel

Basics Description 

Inflam m ation at boneâ€“tendon junction of patellar tendon into ossification center of tibial tuberosity: o

Repetitive stress

o

Partial avulsion injuries

o

Fragm entation m ay lead to heterotopic ossification anterior to tibial tuberosity.



Fusion of tubercle to tibia norm ally occurs by 18 years of age: o

Elim inates any further sym ptom s

Etiology Active adolescent boys between 10 and 15 years of age and girls between 8 and 13 years of age: 

Two to three tim es m ore com m on in boys



Fivefold incidence in very athletic children

Diagnosis

Pa ge 3 3 4

Signs and Symptoms 

Pain and swelling over tibial tuberosity: o

Often bilateral, but unilateral cases m ore sym ptom atic



Pain exacerbated by running, jum ping, and kneeling activities



Increased pain while sitting with knees flexed

Essential Workup Clinical diagnosis: 

Typically pain, swelling, and tenderness localized over tibial tubercle



Exam ination of knee joint unrem arkable

Tests Imaging Knee radiographs in unilateral cases to exclude potentially serious pathology only if presentation not typical for Osgood-Schlatter disease

Differential Diagnosis 

Fracture



Legg-CalvÃ©-Perthes disease: o

Referred hip pain



Osteochondritis desiccans



Osteom yelitis



Patellofem oral syndrom e



Septic joint



Sinding-Larsen-Johansson syndrom e: o



Slipped-capital fem oral epiphysis: o



Apophyseal injury at inferior pole of patella

Referred hip pain

Stress fracture

Pa ge 3 3 4



Tendinitis or bursitis

P.771

Treatment Initial Stabilization 

Place leg in position of com fort.



Im m obilize if necessary to m inim ize pain.

ED Treatment 



Mainstay of therapy: o

Nonsteroidal anti-inflam m atory drugs (NSAIDs)

o

Lim ited activity for 2â€“4 m onths is recom m ended.

o

Ice to affected area after activity

o

Com press painful area with elastic bandage.

o

Elevate leg.

o

Avoid corticosteroid injections.

Mild cases: o

Avoid overuse until sym ptom atic im provem ent.

o

Apply protective padding.

o

Reassurance of benign, self-lim ited course

o

Stretching and strengthening exercises of quadriceps and ham strings



Severe cases: o

Surgical excision of prom inent tibial tubercle or ossicle under patellar tendon only after com plete skeletal m aturity

Pa ge 3 3 4

Medication (Drugs) Ibuprofen: 10 m g/kg PO q6h; m ax. 50 m g/kg/d

Follow-Up Disposition Discharge Criteria Discharge all patients.

Issues for Referral Repeat visits after reasonable conservative approach (pediatric orthopedics)

References 1. Bloom OJ, Mackler L, Barbee J. What is the best treatm ent for Osgood-Schlatter disease? J Fam Pract. 2004;53(2):153â€“156. 2. Greene WB, ed. Essentials of Musculoskeletal Care. 2nd ed. Rosem ont, IL: Am erican Academ y of Orthopedic Surgeons; 2001:684â€“685. 3. Morrissy RT, Weinstein SL, eds. Lovell and Winter's Pediatric Orthopaedics. 5th ed. Philadelphia: Lippincott William s & Wilkins; 2001:1280â€“1281. 4. Orava S, Malinen L, Karpakka J, et al. Results of surgical treatm ent of unresolved Osgood-Schlatter lesion. Ann Chir Gynaecol. 2000;89(4):298â€“302. 5. Peck DM. Apophyseal injuries in the young adult. Am Fam Physician. 1995;51:1891â€“1895.

Codes ICD9-CM 732.4

Pa ge 3 3 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo genesis Im perfecta

Osteogenesis

Imperfecta Daniel Davis

Basics Description 

Inherited abnorm ality of procollagen am ino acid sequence



Bone hypom ineralization and incom plete ossification result in brittle bones.



Abnorm al collagen affects all connective tissue to varying degrees.



Tim e course is variable: o

Most cases involve fractures during childhood followed by quiescence during adolescence and early adulthood.

Etiology 

Procollagen defects result in bone and connective tissue m atrix abnorm alities.



Defects in different sites on procollagen protein chain result in m ore severe form s.



Defects are inherited, either autosom al recessive (generally m ilder) or autosom al dom inant (m ore severe).



Lethal cases involve sporadic or new m utations.

Pa ge 3 3 4



Ehlers-Danlos syndrom e involves m utations of sam e procollagen protein in different location.

Pediatric Considerations 

Most cases involve pathologic fractures during childhood.



Multiple fractures often initiate evaluation for abuse, but possibility of pathologic fractures also should be considered.

Diagnosis Signs and Symptoms Multiple heritable defects that lead to brittle bones: 

Often associated with other connective tissue abnorm alities

Bones 

Multiple recurrent fractures (especially in long bones) are hallm ark of this disease.



Fractures m ay be present at birth or m ay recur in the elderly.



All bones are affected to som e extent (see Im aging/Special Tests).

Eyes 

Blue sclera are another hallm ark of this disease.



No visual changes are reported.

Ears 

Hearing loss usually begins in adolescence; >90% of patients have som e deficit by age 30 years.



Hearing loss is generally sensorineural, although som e m iddle ear abnorm alities have been dem onstrated.

Pa ge 3 3 4

Other 

Yellow-brown or blue-gray discoloration and abnorm al shape of teeth



Shares several features with Ehlers-Danlos syndrom e: o

Loose joints

o

Valve problem s

o

Vascular abnorm alities



Thyroid abnorm alities m ay be seen.



Extrem e cases m ay result in perinatal death.

Essential Workup 

Diagnosis is usually m ade as com bination of clinical and radiographic findings.



History of repeated fractures or fractures with unim pressive m echanism



Thorough search for other tender areas and evaluation of eyes, teeth, and joints is im portant for diagnosis.



Careful exam ination of neurovascular status distal to fracture

Tests Lab 

Evaluate for m etabolic derangem ents such as hyperparathyroidism , vitam in C or D deficiencies, and calcium /phosphate abnorm alities.



DNA studies m ay be indicated for fam ilial analysis, prenatal testing, and genetic counseling.



Tissue biopsy is controversial, but m ay help differentiate from tum ors.

Imaging 

Radiographs of fracture sites: o

May reveal osteopenia (usually m ild)

Pa ge 3 3 4

o

Crum pled long bones (â€œaccordion fem oraâ€•)

o

Incom plete ossification at physes



Skeletal survey is m andatory, especially in children.



Skull film s m ay show worm ian appearance of irregular ossification.



Popcornlike deposits on long-bone ends is poor prognostic finding.



Form al audiologic testing as outpatient is required in older patients.

P.773

Differential Diagnosis 

Nonaccidental traum a in children



Ehlers-Danlos syndrom e



Hypophosphatasia



Achondroplasia



Scurvy



Congenital syphilis



Celiac disease

Treatment Pre Hospital Personnel should obtain inform ation about m echanism or social factors that point toward pathologic fracture versus nonaccidental traum a.

Initial Stabilization 

Airway m anagem ent and resuscitation as indicated



Fracture im m obilization/splinting

Pa ge 3 3 4

ED Treatment 

Specific fracture m anagem ent dictated by type and location of injury



Orthopedic consultation regarding need for traction or operative fixation



No specific treatm ent for osteogenesis im perfecta exists at present.

Medication (Drugs) 

Pain m edications as indicated



Elderly wom en m ay benefit from calcium (1â€“1.5 g/d) and estrogen replacem ent (0.625 m g/d).

Follow-Up Disposition Admission Criteria 

Adm ission is determ ined by m ultiple traum a or operative needs for fracture repair.



Pediatric patients m ay need adm ission to investigate possibility of nonaccidental traum a.

Discharge Criteria 

Patients m ay be considered for outpatient m anagem ent if isolated fracture is present and appropriate hom e resources are available.



Most patients should be discharged with orthopedic and prim ary physician follow-up.

References

Pa ge 3 3 4

1. Chandrasom a P, Taylor CR. Concise Pathology. East Norwalk, CT: Appleton & Lange, 1991. 2. Cole WG. Advances in osteogenesis im perfecta. Clin Orthop Relat Res. 2002;(401):6â€“16. 3. McKusick VA. Heritable Disorders of Connective Tissue. 4th ed. St. Louis, MO: Mosby; 1972. 4. Prockop DJ. Heritable disorders of connective tissue. In: Wilson JD, et al., eds. Harrison's Principles of Internal Medicine. 12th ed. New York: McGraw-Hill; 1991:1860.

Codes ICD9-CM 756.51

ICD10 Q78.0

Pa ge 3 3 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo m yelitis

Osteomyelitis

Anthony J. Medak Irving Jacoby

Basics Description 

Osteom yelitis (OM): infection of bone with ongoing inflam m atory destruction



Usually bacterial, but fungal OM does occur.

Etiology Hematogenous OM 

Prim arily in children, elderly, IV drug abuse (IVDA) patients



Seeding of bacteria to bone from rem ote site of infection via bloodstream



Children have acute OM and adults subacute or chronic.



Hem atogenous OM of long bones rarely occurs in adults.



Most children with acute hem atogenous OM have no preceding illness.



One third have history of traum a to affected area.



Staphylococcus aureus is m ost com m on cause of OM in all ages.



Neonates: S. aureus, Enterobacteriaceae, group A and B

Pa ge 3 3 5

streptococci, and Escherichia coli 

Children: S. aureus, group A streptococci, Haem ophilus influenzae, Enterobacteriaceae



Salm onella: com m on in sickle cell disease



Adults: S. aureus, Enterobacteriaceae, Pseudom onas, gram -negative rods, Staphylococcus epiderm idis, gram -positive anaerobes, esp peptostreptococcus



Illicit drug users: Candida, Pseudom onas, Serratia m arcescens



Prolonged neutropenia: Candida, Aspergillus, Rhizopus, Blastom yces, Coccidioidom ycosis

Hematogenous Vertebral OM 

Uncom m on



Most prevalent in adults older than 45 years



Involves the disk and vertebra above and below



Often in setting of long-term urinary catheter placem ent, IVDA, cancer, hem odialysis, or diabetes



IVDA: OM of pubic sym physis, sternoclavicular, and sacroiliac (S-I) joints



Lum bar vertebrae m ost com m on, followed by thoracic, then cervical



Posterior extension leads to epidural/subdural abscess or m eningitis.



Anterior extension m ay lead to paravertebral, retropharyngeal, m ediastinal, subphrenic, retroperitoneal, or psoas abscess.

Direct or Contiguous OM 

Organism (s) directly seeded in bone due to traum a, esp following open fractures: o

Spread from adjacent site of infection or from surgery

Pa ge 3 3 5



More com m on in adults and adolescents



S. aureus, Enterobacteriaceae, Pseudom onas



Norm al vascularity o

S. aureus and S. epiderm idis, gram -negative bacilli, and anaerobic organism s



Vascular insufficiency/diabetes o

Sm all bones of feet are com m on sites.

o

Infection resulting from m inor traum a, infected nail beds, cellulitis, or skin ulceration

o

If ulcer size >2 cm 2 and >3 m m in depth, bone involvem ent is likely.



o

Polym icrobial including anaerobes

o

If bone palpated, high correlation with OM

Puncture wound through tennis shoe: S. aureus, Pseudom onas



Clavicular OM can occur as com plication of subclavian vein catheterization.

Chronic OM 

Osteom yelitis that persists or recurs



Distinguishing characteristic is necrotic bone (sequestrum ) that m ust be dÃ©brided.



S. epiderm idis, S. aureus, Pseudom onas aeruginosa, Serratia m arcescens, and E. coli

Diagnosis Signs and Symptoms Vary with duration of disease

History 

Pain: localized, deep, dull, and throbbing; occurs with and

Pa ge 3 3 5

without m ovem ent 

Fever and chills



Malaise, nausea, vom iting



Reluctance to use extrem ity



Consider OM as a cause of fracture nonunion

Physical Exam 

Tenderness to palpation, warm th, erythem a, edem a, decreased range of m otion



Drainage of sinus tract

Essential Workup 

CBC



ESR and C-reactive protein



Radiographs



Blood and wound cultures and sensitivities

Tests Lab 

CBC; WBC m ay be elevated but often norm al



ESR and C-reactive protein (usually elevated)



Blood cultures (positive in ~50% of cases)

Imaging 

Plays a central role in evaluation



Start with plain film s; other tests often required

Radiographs 

May be norm al for the first 2â€“3 weeks of sym ptom s



Earliest finding is periosteal elevation, followed by cortical erosions, then new bone form ation



40â€“50% of focal bone loss needed to detect lucency on radiograph; fewer than one third of cases have diagnostic findings at 10 days



Obtain chest radiograph if tuberculosis (TB) suspected

Pa ge 3 3 5

Bone scan 

Technetium -99m m ethylene diphosphonate ( 9 9 m Tc-MDP)



Measures increase in bone m etabolic activity



~95% sensitive but less specific than MRI



Bone scan abnorm al after 2â€“3 days of sym ptom s



Negative study 24 hours after onset of sym ptom s rules out acute OM

Leukocyte Scintigraphy 

Indium -111â€“labeled WBCs



More specific but less sensitive than bone scan



Difficult to distinguish bone inflam m ation from soft-tissue inflam m ation (i.e., cellulitis, tum ors, inflam m atory arthritis)



False negative in chronic infection

CT 

Reveals bone edem a, cortical destruction, periosteal reaction, sm all foci of gas or foreign bodies, joint surface dam age, and soft-tissue involvem ent when plain film s not helpful



Useful in vertebral OM

MRI 99m



As sensitive as

Tc-MDP scan but m ore specific



Reveals bone edem a, cortical destruction, periosteal reaction, joint surface dam age, and soft-tissue involvem ent before x-rays



Effective in early detection (diagnosis m ay be evident by MRI before scintigraphy)



Test of choice to identify vertebral OM and OM in diabetic foot ulcers



Occasional false-positive results in traum a, previous

Pa ge 3 3 5

surgical procedures, or neuropathic joint disease P.775

Ultrasound 

An em erging m odality for OM



Periosteal elevation or thickening, fluid collections adjacent to bone often seen



May show findings of OM days prior to plain film s

Diagnostic Procedures/Surgery 

Gold standard for diagnosis is open biopsy with histology and tissue gram stains, including culture and sensitivities



Needle aspiration has lower sensitivity than open biopsy



Culture of sinus or drainage from wound can be m isleading; correlates well with S. aureus, but not as reliable for other organism s.

Pediatric Considerations 

70â€“85% of children have fever higher than 38.5Â°C.



Neonates com m only afebrile



Only approxim ately one in three of children will have leukocytosis



Blood cultures positive in ~50%

Differential Diagnosis 

Cellulitis



Paronychia/felon



Bursitis, toxic synovitis, septic arthritis



Extrem ity fracture



Bone infarction in sickle cell patients



Acute leukem ia, m alignant bone tum ors



Mechanical back pain

Pa ge 3 3 5



Spinal epidural abscess



Brucellosis, esp in S-I joint



TB, m ore com m on in thoracic spine (Pott's disease)

Treatment Initial Stabilization Em ergent stabilization if septic or if neurologic deficits from spine involvem ent

ED Treatment 

Em piric antibiotic treatm ent in ED



Cultures should guide subsequent antibiotic regim en



Antibiotics: depend on patient's age and organism (see Medications section)



Orthopaedic and infectious disease consultation



Surgical intervention m ay be needed to optim ize treatm ent (e.g., infected fracture, bone necrosis)



Parenteral antibiotic treatm ent for 4â€“6 weeks

Medication (Drugs) 

Newborn to 4 m onths: penicillinase-resistant synthetic penicillin (e.g., nafcillin: 37 m g/kg IV q6h) plus a third-generation cephalosporin (e.g., ceftriaxone: 50â€“75 m g/kg IV per day); if suspect m ethicillin-resistant Staphylococcus aureus (MRSA) then vancom ycin (40â€“60 m g/kg IV q6h) plus a third-generation cephalosporin. (note: doses are based on age >28 days)



Children (>4 m onths): penicillinase-resistant synthetic penicillin (e.g., nafcillin: 37 m g/kg IV q6h to m ax. 8â€“12

Pa ge 3 3 5

g/d). If suspect MRSA, then vancom ycin (40â€“60 m g/kg IV q6h to m ax. 2â€“4 g/d). Add third-generation cephalosporin if suspicion for gram negative rods, or presence on gram stain noted (e.g., ceftriaxone: 50â€“75 m g/kg IV per day to m ax. 2â€“4 g/d) 

Adult: penicillinase-resistant synthetic penicillin (e.g., nafcillin: 2 g IV q4h); if suspect MRSA, vancom ycin (15 m g/kg IV q12h)



Sickle cell anem ia with OM: ciprofloxacin 400 m g IV q12h, or levofloxacin 750 m g IV q24h (not in children); alternative: third-generation cephalosporin



Postâ€“nail puncture through tennis shoe: ciprofloxacin 750 m g PO b.i.d. or levofloxacin 750 m g PO q24h; alternative: ceftazidim e 2 g IV q8h



Involving orthopaedic prosthesis or hardware: add rifam pin (10 m g/kg PO/IV per day to m axim um of 600 m g/d) to regim en for S. aureus. Hardware rem oval generally required.



Post-traum atic OM: vancom ycin and ceftazidim e



If vancom ycin resistant enterococcus present: linezolid 600 m g IV q12h Ã— 6 weeks

Pediatric Considerations Children with hem atogenous OM m ay undergo short-course IV antibiotics and then be changed to oral for additional 1â€“2 months.

Follow-Up Disposition Admission Criteria 

Patients with acute OM should be adm itted.

Pa ge 3 3 5



Patients with chronic osteom yelitis usually require adm ission for surgical procedures, debridem ent, and obtaining bone cultures and histology.

Discharge Criteria Subacute or chronic OM patients m ay be considered for outpatient m anagem ent if hom e IV antibiotics arranged, bone specim ens obtained, and necrotic bone dÃ©brided.

Issues for Referral 

Cases refractory to debridem ent and antibiotics benefit from hyperbaric oxygen as an adjunct to standard treatm ent.



Approxim ately two thirds of these cases will dem onstrate benefit.

References 1. Carek PJ, Dickerson LM, Sack JL. Diagnosis and m anagem ent of osteom yelitis. Am Fam Physician. 2001;63(12):2413â€“2420. 2. Ghiorzi T, Mackowiak P. Diagnosis of osteom yelitis. In: Rose BD, ed. UpToDate. Waltham , MA: UpToDate, 2005. 3. Lew DP, Waldvogel FA. Osteom yelitis. Lancet. 2004;364:369â€“379. 4. Santiago Restrepo C, Gim enez CR, McCarthy K. Im aging of osteom yelitis and m usculoskeletal soft tissue infections: current concepts. Rheum Dis Clin North Am . 2003;29(1):89â€“109. 5. Shuford JA, Steckelberg JM. Role of oral antim icrobial therapy in the m anagem ent of osteom yelitis. Curr Opin Infect Dis. 2003;16:515â€“519.

Codes ICD9-CM 730.20

Pa ge 3 3 5

ICD10 M86.9

Pa ge 3 3 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo po ro sis

Osteoporosis

Daniel Davis

Basics Description 

Overall decrease in skeletal m ass, generally diffuse



Trabecular bone (especially vertebrae and fem ur) affected m ore com m only and earlier



Disease begins in adolescence, but fractures do not usually m anifest until age 50 or older.



Fem ales affected m uch m ore com m only than m ales, especially postm enopause

Etiology 

Overall increase in resorption over form ation of new bone



Advanced age is m ost im portant risk factor.



Inadequate dietary calcium im portant factor, especially early in life



Sedentary lifestyle is risk factor (weight bearing on bone favors new bone form ation).



Decrease in estrogen with m enopause is key factor in wom en.



Other causes include long-term steroid use, alcoholism , m ethotrexate.



May be fam ilial or hereditary factor as well

Pa ge 3 3 6

Pediatric Considerations Although disease appears to start in adolescence, pediatric patients are asym ptom atic.

Diagnosis Signs and Symptoms 

Usually asym ptom atic until pathologic fractures occur



Fractures with insignificant m echanism or recurrent fractures are hallm ark.



Vertebral colum n m ost com m only involved



Multiple com pression fractures of vertebral colum n often lead to kyphosis and scoliosis.



Hip fractures (fem oral neck and intertrochanteric fractures) also com m on

Essential Workup 

Fracture without significant m echanism and identification of risk factors is m ost im portant.



Careful neurovascular exam ination distal to fem ur or other extrem ity fracture



Rectal tone and postvoid residual determ ination should be done in patients with vertebral fractures.



Radiographs of suspected fracture m ay show osteopenia (late finding in disease).



Spine film s m ay show old com pression fractures.



CT scan should be perform ed to better evaluate vertebral fractures: o

Retropulsion, spinal canal com prom ise is not always apparent on plain film s.

o

Make sure CT cuts extend full level above and below

Pa ge 3 3 6

injuries on spine radiographs.

Tests Lab Serum chem istries, such as calcium , parathyroid horm one, and alkaline phosphatase, m ay help differentiate between other illnesses.

Imaging 

Plain film s can identify fractures; however, age of each fracture m ay be difficult to determ ine.



Bone scan or CT help determ ine age of fractures, especially in spine.



Bone densitom etry can provide prognostic inform ation and help guide therapy.

Differential Diagnosis 

Multiple m yelom a or other m etastatic tum or



Osteogenesis im perfecta (usually apparent in childhood)



Hyperparathyroidism



Other dem ineralizing bone diseases

Treatment Pre Hospital Cautions: 

Obtain prehospital inform ation on m echanism to help diagnose pathologic fracture.



Avoid aggressive m anipulation or m ovem ent of patient, as this m ay exacerbate bony injury.

Initial Stabilization Im m obilize fractures

Pa ge 3 3 6

P.777

ED Treatment 

Fractures are treated with expectation of delayed or incom plete healing.



Prevention is far m ore effective than treatm ent.



Long-term therapy is beneficial (see Medications).



Use of orthotic back braces and vests should be arranged in conjunction with orthopedic spine consultation.



Exercise is also helpful.



Balance m ust be achieved between osteoporosis risk and steroid or m ethotrexate therapy.

Medication (Drugs) 

Alendronate: 10 m g/d



Calcitonin: 0.5 m g/d SC of hum an, 100 IU/d SC of salm on; alternative: nasal spray (100 IU) one spray per day in alternate nostrils



Calcium supplem entation (often with vitam in D): 1â€“1.5 g/d



Estrogen: 0.625 m g/d (with or without m edroxyprogesterone)



Etidronate: 400 m g/d for 2-week cycles every 15 weeks



Raloxifene (selective estrogen receptor m odulator): 60 m g PO daily



Sodium fluoride: 25 m g b.i.d. with calcium

Pediatric Considerations Ensure adequate calcium in diet from early age.

Pa ge 3 3 6

Follow-Up Disposition Admission Criteria 

Per norm al orthopedic protocols, with special considerations for age and social situation



Com pression fractures are generally stable, but possibility of burst fracture with cord com pression m ust be ruled out.



Any cervical fracture or fracture with neurologic sym ptom s requires adm ission with em ergent consultation with neurosurgery or orthopedics.



Adm ission m ay be necessary for pain control and because of decreased am bulation.

Discharge Criteria 

Per norm al orthopedic protocols with special considerations for age and social situation



Patients with m inim al injuries, able to care for them selves at hom e, or with appropriate assistance, and adequate postoperative pain control m ay be discharged with orthopedic follow-up

References 1. Chandrasom a P, Taylor CR. Concise Pathology. East Norwalk, CT: Appleton & Lange, 1991. 2. Krane SM, Holick MF. Metabolic bone disease. In: Wilson JD, et al., eds. Harrison's Principles of Internal Medicine. 12th ed. New York: McGraw-Hill; 1991:19â€“21. 3. North Am erican Menopause Society. Managem ent of postm enopausal osteoporosis: position statem ent. Menopause. 2002;9(2):84â€“101.

Pa ge 3 3 6

4. Papaioannou A, et al. Diagnosis and m anagem ent of vertebral fractures in elderly adults. Am J Med. 2002;113(3):220â€“228.

Codes ICD9-CM 733.00

ICD10 M81.9

Pa ge 3 3 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Otitis Externa

Otitis Externa

Assaad J. Sayah

Basics Description 

Inflam m ation or infection of the auricle, auditory canal, or external surface of the tym panic m em brane (TM): o



Spares the m iddle ear

Also called â€œswim m er's earâ€• due to the usual history of recent swim m ing: o



Occasional cases after norm al bathing

Necrotizing otitis externa: o

Infection starts at ear canal and progresses through periauricular tissue toward base of skull

o

Occurs in elderly, diabetic, or other im m unocom prom ised patients

o

Caused by Pseudom onas aeruginosa

o

Can lead to cellulitis and osteom yelitis

Etiology 

Often precipitated by an abrasion of the ear canal or m aceration of the skin from persisting water or excessive dryness



Predisposing factors include: o

History of ear surgery or TM perforation

Pa ge 3 3 6



o

Narrow or abnorm al canal

o

Hum idity

o

Allergy

o

Traum a

o

Abnorm al cerum en production

P. aeruginosa, Staphylococcus aureus, Streptococcal species, and rarely fungi.

Diagnosis Signs and Symptoms History 

Itching of the external ear canal is usually the first sym ptom



1â€“2 day history of progressive pain



Ear drainage



Decreased auditory acuity



Clogged sensation in ear

Physical Exam 

Pain in ear or with m otion of pinna/tragus



Swollen, erythem atous external ear canal



Ear drainage



Decreased auditory acuity



Pain/swelling in preauricular area

Necrotizing (Malignant) Otitis Externa 

Pain, tenderness, swelling in periauricular area



Headache



Otorrhea



Cranial nerve palsy o

Facial nerve m ost affected

Pa ge 3 3 6

Essential Workup Clinical diagnosis with typical signs/sym ptom s: 

Pain in ear or with m otion of pinna/tragus



Otoscopic exam ination



Swollen, erythem atous external ear canal



Ear drainage



Cheesy white or gray green exudate

Tests Lab 

None usually indicated except when possibility of necrotizing otitis externa: o

Signs of system ic toxicity or local spread of infection should be checked



WBC count



ESR



Glucose (check for diabetes)



Cultures

Imaging CT/MRI to exclude osteom yelitis if the patient has signs of toxicity or bony involvem ent

Diagnostic Procedures/Surgery 

Rem ove debris with a soft plastic curette or gentle irrigation with peroxide/water m ix.



Wick placem ent m ay be needed to facilitate m edication delivery.

Differential Diagnosis 

Necrotizing otitis externa



Otitis m edia



Folliculitis from obstruction of sebaceous glands



Otic foreign bodies

Pa ge 3 3 6



Herpes zoster infection of the geniculate ganglion



Parotitis



Periauricular adenitis



Mastoiditis



Dental abscess



Sinusitis



Tonsillitis



Pharyngitis



Tem porom andibular joint pain

Pediatric Considerations Consider ear canal foreign bodies in children with purulent drainage from edem atous, painful ear canals. P.779

Treatment ED Treatment 

Clean external ear canal: o

Rem ove the inflam m atory debris by gentle curettage with a cotton-tipped wire applicator.

o

Occasional suction with a Fraser suction tip m ay be necessary.



Insert a cotton or gauze wick 10â€“12 m m into the canal after cleansing, if the ear canal is very edem atous.

Medication (Drugs) 

Most cases respond well to topical treatm ent:

Pa ge 3 3 6

o

Antiseptic, anti-inflam m atory, and drying otic drops elim inate the pathogenic bacteria and allow for rapid healing of the canal.

o

Acetic acid solutions such as Dom eboro otic (2% acetic acid): 4â€“6 drops q4hâ€“q6h.

o

Corticosporin otic (hydrocortisone 1%, polym yxin + neom ycin) suspension: 4 drops to ear canal q.i.d. (use suspensions and not solutions with suspected tym panic m em brane perforation)

o

Ofloxacin: 5 drops b.i.d. (drug of choice in perforated tym panic m em brane)



Oral antibiotics: o

Adm inister to patients with cellulitis of the face or neck, severe edem a of the ear canal, concurrent otitis m edia, or when the tym panic m em brane cannot be visualized.

o

Treat diabetics and other im m unocom prom ised patients with oral ciprofloxacin and follow closely for sym ptom s of m alignant otitis externa.



o

Am oxicillin: 500 m g (peds: 40 m g/kg/d) PO t.i.d.

o

Ciprofloxacin: 500 m g PO b.i.d.

IV antibiotics for patients with necrotizing otitis externa, severe cellulitis, or septic looking



Prophylaxis: o

Apply rubbing alcohol or acetic acid (2%) to keep the external ear canal dry and prevent recurrence of infection

Follow-Up Disposition

Pa ge 3 3 7

Admission Criteria 

Necrotizing otitis externa



Significant involvem ent of the pinna



Signs of system ic illness

Discharge Criteria 

Most patients



Close follow-up for patients at risk of otitis externa



Ear-nose-throat follow-up for perforated tym panic m em brane, worsening of sym ptom s or failure of initial m anagem ent



Patient instructions: o

Avoid swim m ing and keep ears com pletely dry for 3â€“4 weeks.

o

Apply m edications as directed

o

Return if worse pain, fever, hearing loss develops, or there is any change in m ental or neurologic status.

o

Follow-up if sym ptom s are not im proved within 2â€“3 days

References 1. Beers SL, Abram o TJ. Otitis externa review. Pediatr Em erg Care. 2004;20(4):250â€“256. 2. Schapowal a. Otitis externa: a clinical overview. Ear Nose Throat J . 2002;81(8 Suppl 1):21â€“22. 3. Rutka J. Acute otitis externa: treatm ent perspectives. Ear Nose Throat J. 2004;83(9 Suppl 4):20â€“21; discussion 21â€“22. 4. Hughes E, Lee JH. Otitis externa. Pediatr Rev. 2001;22(6):191â€“197. 5. Sander R. Otitis externa: a practical guide to treatm ent and prevention. Am Fam Physician. 2001;61(5):927â€“936, 941â€“942.

Codes

Pa ge 3 3 7

ICD9-CM 380.10

ICD10 H60.9

Pa ge 3 3 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Otitis M edia

Otitis Media

Assaad J. Sayah

Basics Description 

Infection of the m iddle ear



Most com m only occurs in children 6â€“36 m onths of age

Etiology 

Usually associated with (or as a result of) upper respiratory tract infections





Viral: o

Parainfluenza

o

Respiratory syncytial virus

o

Influenza

o

Adenovirus

o

Rhinovirus

Bacterial: o

Staphylococcus pneum oniae

o

Moraxella catarrhalis

o

Haem ophilus influenzae

o

Streptococcus pyogenes

o

Mycoplasm a pneum oniae



Associated with blockage of eustachian tube



Predisposing factors:

Pa ge 3 3 7

o

Deficient m ucus, cilia, or antibodies

o

Intubation, especially nasotracheal

o

Am erican Indians, Eskim os

o

Down syndrom e

o

Cleft palate

Diagnosis Signs and Symptoms History 

Ear pain



Irritability



Rhinitis



Vom iting, diarrhea



Poor feeding



Fever



Sensation of plugged ear



Pulling at ear



Vertigo, tinnitus



Conjunctivitis

Physical Exam 

Tym panic m em brane inflam m ation, bulging and lim ited m obility



Decreased visibility of the landm arks of the m iddle ear

Essential Workup 

Exclude associated conditions.



Otoscopic exam ination for appearance and m obility of tym panic m em brane o

Full visualization essential

o

Increased vascularity, erythem a, purulence

Pa ge 3 3 7

o

Obscured landm arksâ€”bony, light reflex

o

Pneum atic otoscopyâ€”m obility, bulging, retracted

Tests Lab Cultures unhelpful unless done by tym panocentesis

Imaging CT scan if associated m astoiditis is suspected.

Diagnostic Procedures/Surgery 



Tym panocentesisâ€”indications: o

Severe pain or toxicity

o

Failure of antim icrobial therapy

o

Suspicion of suppurative com plication

o

Sick neonate

o

Im m unocom prom ised patient

Tym panom etry and acoustic otoscopy m ay be useful with difficult exam inations.

Differential Diagnosis 



Infection: o

Otitis externa

o

Mastoiditis

o

Dental abscess

o

Peritonsillar abscess

o

Sinusitis

o

Lym phadenitis

o

Parotitis

o

Meningitis

Traum a: o

Perforation of the tym panic m em brane

o

Foreign body in ear

o

Barotraum a

Pa ge 3 3 7

o

Instrum entation



Serous otitis m edia or eustachian tube dysfunction



Im pacted ear cerum en



Im pacted third m olar



Tem porom andibular joint dysfunction

P.781

Treatment ED Treatment 

Most m ild cases could resolve without antibiotics



Antibiotics are indicated for all infants younger than 6 m onths and older children with certain diagnosis or severe illness.



Considerations should include recurrent nature of otitis m edia, lack of clinical response, and resistance patterns in com m unity.



Parenteral antibiotics indicated in febrile toxic children younger than 1 year or with im m unocom prom ise.



Antihistam ines, decongestants, and steroids have no proven efficacy.



Antipyretics and analgesics are im portant (avoid local analgesics in perforated tym panic m em branes).

Medication (Drugs) 

Am oxicillin: 500 m g PO t.i.d (peds: 80 m g/kg/d PO t.i.d) for 7â€“10 days

Pa ge 3 3 7



Am oxicillin-clavulanic acid: 500 m g PO t.i.d. (peds: 80 m g/kg/d PO t.i.d) for 7â€“10 days



Azithrom ycin: 10 m g/kg PO day 1, then 5 m g/kg/d PO days 2â€“5



Cefuroxim e: 500 m g PO b.i.d. (peds: 30m g/kg PO b.i.d)



Trim ethoprim (TMP)-sulfam ethoxazole: 8 m g of TMP/kg/d PO b.i.d.

Follow-Up Disposition Admission Criteria Febrile toxic children who are: 

Younger than 1 year, im m unocom prom ised



Moderately or severely dehydrated



Unable to tolerate oral fluids or m edications



Suspected or proven associated significant infection



Suspected abuse



Unreliable caretaker

Discharge Criteria 

Children without any of the aforem entioned criteria



Follow-up in 10â€“14 days to ensure resolution



Indications for earlier follow-up: o

Child does not get better in 24â€“48 hours

o

Any progression of signs or sym ptom s

o

New problem s develop including a rash

o

Any concerns arise

Complications 

Recurrent otitis m edia: o

Three episodes within 6 m onths or 4 or m ore

Pa ge 3 3 7

episodes within 1 year 

Perforated tym panic m em brane



Serous otitis m edia



Conductive hearing loss



Facial nerve injury



Mastoiditis



Cholesteatom a



Meningitis



Subdural em pyem a



Venous sinus throm bosis

References 1. Rosenfeld RM, Lous J, Bluestone CD et al. Recent advances in otitis m edia. 9. Com plications and sequelae. Ann Otol Rhinol Laryngol. Suppl 2005; 194:140â€“160. 2. Jung TT, Hunter ll, Alper CM et al. Recent advances in otitis m edia.8. Treatm ent. Ann Otol Rhinol Laryngol. 2005;194(suppl):114â€“139 3. Bauchner H. Ear, ears, and m ore ears Arch Dis Child. 2001:84(2):185â€“186. 4. Am erican Academ y of Pediatrics: Diagnosis and m anagem ent of acute otitis m edia. Pediatrics. 2004;113(5):1451â€“65.

Codes ICD9-CM 382.9

ICD10 H66.9

Pa ge 3 3 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oto lo gic Traum a

Otologic Trauma

Shan Liu

Basics Description 

Ear cartilage has no blood supply and is nutritionally dependent on perichondrium .



Hem atom as often disrupt perichondrium and cartilage leading to ischem ia, possible perichondritis, necrosis, and cauliflower ear.



Penetrating injuries or anim al bites m ay lead to infection of cartilage.

Etiology 

Blunt traum a (often contact sports)



Penetrating traum a (e.g., tym panic m em brane perforation from cotton swabs)



Blast injury



Lightning injury; both tym panic-m em brane and ossicular disruption occur in 50% of lightning strikes.



Chem ical exposure



Therm al injury



Diving injuries: o

Inner-ear barotraum as

o

Tym panic m em brane rupture

Pa ge 3 3 7

Pediatric Considerations Consider nonaccidental traum a

Diagnosis Signs and Symptoms 

Severe ear pain



Bleeding



Auricular deform ity:



o

Edem a

o

Hem atom a

o

Laceration

o

Am putation

Decreased hearing: o

Partial loss suggests tym panic m em brane rupture.

o

Com plete hearing loss suggests additional injuries to ossicles or inner ear.



Hem otym panum



Purulent or bloody discharge from ear canal



Tinnitus



Vertigo: o

Inner ear injury

o

Tym panic m em brane perforation in water

History 

Mechanism



Associated injuries



Allergies



Medications



Past otologic history

Physical Exam

Pa ge 3 3 8

Search for concom itant injury; exam ine: 

Head



Cranial nerves



Vascular structures



Tem poral bone



Pinna



External ear canal



Tym panic m em brane



Hearing

Tests Lab Wound culture if signs of infection

Differential Diagnosis 

Infection



Hem angiom a



Foreign body in ear

Treatment Pre Hospital If auricle is am putated, wrap in m oist gauze and place in plastic bag.

Initial Stabilization 

Check airway, breathing, and circulation; full traum a evaluation; resuscitation as appropriate



Sterile dressing to injured site

General Measures 

All injury types: o

Anesthesia:

Pa ge 3 3 8



Local anesthesia via nerve block to auriculotem poral branch of m andibular nerve, lesser occipital nerve, greater auricular nerve, and auricular branch of vagus nerve; use 1% lidocaine or 0.25% m arcaine.



Alternative: inject ring of anesthetic around base of pinna.



Managem ent of tym panic m em brane perforation



Tetanus prophylaxis if necessary



For hum an and anim al bites, use both penicillin and Ceftazidim e or Augm entin.



Specific injury types: o

Hem atom a: drainage im perative to reapproxim ate perichondrium to cartilage to prevent cartilage necrosis, ideally within 72 hours. However, no clearly defined best treatm ent based on m eta-analysis. Treatm ent traditional is as follows: 

Antistaphylococcal antibiotics for 7â€“10 days



Aspiration: preferred alterative if clot not yet form ed. Use 18â€“20-gauge needle for aspiration; m ilk hem atom a until totally evacuated. P.783



Incision and drainage: m ore effective with larger and/or clotted hem atom as. Incise along curvature of pinna with no. 15 scalpel, evacuate, and irrigate; apply pressure dressing for 3â€“7 days to prevent reaccum ulation.



Vaseline gauze: place to fill crevices of pinna. Place over and behind pinna; wrap soft gauze

Pa ge 3 3 8

firm ly around head. 

Alternatively, suture dental rolls into place over incised area.



Therm oplastic splints, if available, can be used.



If patient presents again with reaccum ulation, reaspirate, consider wick placem ent.



Laceration: o

Prophylactic antibiotics are controversial.

o

Clean and dÃ©bride wound, anesthetize as necessary.

o

Superficial abrasions: clean, dress with antibiotic ointm ent.

o

Sim ple lacerations: 5.0 or 6.0 m onofilam ent nylon or polypropylene suture, then pressure dressing. May use absorbable suture on m edial skin lacerations to avoid having to bend ear for suture rem oval.

o

Exposed auricular cartilage: carefully dÃ©bride jagged edges; com pletely cover cartilage to prevent perichondritis. Can rem ove sm all am ount of cartilage to allow skin coverage. Approxim ate cartilage first with absorbable sutures at m ajor landm arks; include anterior and posterior perichondrium in stitch.

o

Avulsions: <2 cm total avulsions m ay be used as graft and survive; >2 cm : consult or urgently refer to otolaryngologist or plastic surgeon; save in subcutaneous pocket.

Medication (Drugs) 

Augm entin (am oxicillin-clavulanate): o

Adults: 875/125 m g PO t.i.d. (peds: 40 m g/kg per day PO t.i.d.

Pa ge 3 3 8



Dicloxacillin: 250 m g PO q.i.d.



Erythrom ycin: 250 m g PO q.i.d.



Penicillin VK: 250 m g PO q.i.d.

Follow-Up Disposition Admission Criteria 

Concom itant serious traum atic injuries



Need for IV antibiotics



Im m unosuppressed persons with serious infections, perichondritis, or chondritis

Discharge Criteria 

Able to tolerate oral antibiotics



Follow up wound suture repair.



Follow up hem atom as after 24 hours to determ ine whether re-accum ulation of fluid.

References 1. Cantrill ST. Facial traum a. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1998. 2. Henderson JM, Salam a AR, Blanchaert RH. Managem ent of Auricular Hem atom a Using a Therm oplastic Splint. Arch Otolaryngol Head Neck Surg. 2000;126(7):888â€“890. 3. Jones SEM, Mahendran S. Interventions for Acute Auricular Haem atom a. The Cochrane Database of System atic Reviews. 2005, Vol (2). 4. Lam m ers RL, Trott AT. Methods of wound closure. In: Rogers JR, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 3rd ed.

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Philadelphia: WB Saunders; 1998. 5. Manthey DE, Harrison BP. Otolaryngologic procedures. In: Rogers JR, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 3rd ed. Philadelphia: WB Saunders; 1998. 6. Spring PM, Am edee RG. Ear pain and drainage. In: Calhoun KH, ed. Expert Guide to Otolaryngology. Philadelphia: Am erican College of Physicians; 2001. 7. Turbiak TW. Ear traum a. Em erg Med Clin North Am . 1987;5:243â€“251.

Miscellaneous SEE ALSO: Tym panic Mem brane Perforation

Codes ICD9-CM 959.09 Injury of face and neck

ICD10 S09.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ovarian C yst/To rsio n

Ovarian

Cyst/Torsion Kyan J. Berger

Basics Description 

Ovarian cysts: o

Generally asym ptom atic until com plicated by hem orrhage, torsion, rupture, or infection

o

Follicular cysts: 

Most com m on



Occur from fetal life to m enopause



Unilocular; diam eter 3â€“8 cm



Thin wall predisposes to rupture, which usually causes m inim al or no bleeding.



Rupture during ovulation at m idcycle known as m ittelschm erz

o

Corpus luteal cysts: 

Most significant



Diam eter 3 cm



Rapid bleeding from intracystic hem orrhage causes rupture.



Rupture m ost com m on just before m enses

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begins 

Can cause severe intraperitoneal bleeding



Gradual bleeding into cyst or ovary distends capsule and m ay cause pain without rupture.



Adnexal torsion: o

Twisting of vascular pedicle of ovary, fallopian tube, or paratubal cyst

o

Causes adnexal ischem ia leading to necrosis

o

Occlusion of lym phatics and venous drainage lead to rapid enlargem ent of adnexa.

Risk Factors Adnexal torsion: 

Highest frequency in reproductive-age wom en, especially m id-20s



Ovarian cysts



Ovarian hyperstim ulation



Tum ors:



o

Serous cystadenom a m ost com m on

o

Teratom as

Pelvic surgery: o

Tubal ligation

o

Hysterectom y



Pregnancy



History of pelvic inflam m atory disease

Alert 

Anticoagulated patients at increased risk of: o

Hem orrhagic corpus luteal cyst

o

Significant bleed from ruptured cyst, including with ovulation

Etiology 

Ovarian cyst:

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o

Follicular, corpus luteal, theca lutein, cystic teratom a, endom etriom a (chocolate cyst)

o

Follicular cysts result from nonrupture of m ature follicle or failure of atresia of im m ature follicle.

o

Corpus luteal cysts result from norm al intracystic hem orrhage 2â€“4 days after ovulation.



Adnexal torsion: o

Right > left

o

Highest frequency in reproductive fem ales

Alert Cysts found in postm enopausal wom en suggests carcinom a.

Diagnosis Signs and Symptoms History 

Ovarian cyst: o

Lower-quadrant abdom inal pain: 

Sudden, sharp, unilateral



Onset often with exercise, intercourse, traum a, or pelvic exam



o

Dizziness, syncope

o

Fever rare

Adnexal torsion: o

Lower-quadrant abdom inal pain: 

Sudden, sharp, colicky



Unilateral



Radiation to back, flank, or groin



May be chronic or recurrent with torsion-detorsion

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o

Nausea, vom iting

o

Occasional signs/sym ptom s: 

Fever



Vaginal bleeding



Urinary tract infection sym ptom s

Physical Exam 

Ovarian cyst: o

Abdom inal tenderness (m ild to severe with peritonitis)



o

Adnexal tenderness

o

Pelvic m ass

o

Hem orrhagic shock possible: 

Usually from corpus luteal cyst rupture



Orthostasis, hypotension, tachycardia

Adnexal torsion: o

Abdom inal tenderness (m ild to severe)

o

Adnexal tenderness

o

Adnexal m ass

o

Leukocytosis (occasional)

Essential Workup 

Pregnancy test essential to rule out ectopic pregnancy



Rapid hem oglobin determ ination

Tests Lab 

Urine or serum hum an chorionic gonadotropin (HCG) determ ination



CBC



Urinalysis



If significant hem orrhage, type and cross packed red blood cells.

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Imaging 

Ultrasound, to reveal: o

Adnexal cysts and m asses: 

Cystic m asses <5 cm in prem enopausal wom en generally benign





Should be re-evaluated at end of m enstruation

o

Pelvic free fluid

o

Enlarged ovary (suggests torsion)

Doppler: o

May show decreased flow with torsion

o

Im portant to docum ent norm al blood flow on Doppler in ED, even though does not rule out recent torsion of ovary

P.785



MRI: o

Consider in pregnant patients with right lower quadrant (RLQ) pain and nondiagnostic ultrasound and Doppler



CT: o

May dem onstrate cysts, evidence of torsion, or suggest alternative diagnosis

Alert Ultrasound sensitivity for diagnosis of ovarian torsion is not well established; continue workup if high clinical suspicion.

Diagnostic Procedures/Surgery 

Culdocentesis: o

May yield serosanguineous fluid with ruptured cyst

o

Hem atocrit >15% suggests significant hem operitoneum .

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

Laparoscopy is gold standard for torsed adnexa and definitive diagnosis.

Differential Diagnosis 



For pelvic pain: o

Ectopic pregnancy

o

Pelvic inflam m atory disease

o

Round ligam ent pain

o

Endom etriosis

o

Neoplasm

o

Torsion of uterus

o

Appendicitis

o

Diverticulitis

o

Inflam m atory bowel disease

o

Renal colic

For adnexal m ass: o

Benign tum ors

o

Malignant tum ors

o

Polycystic ovaries

Treatment Pre Hospital Alert Patients m ay becom e hem odynam ically unstable, so intravenous access is im portant.

Initial Stabilization Airway m anagem ent and resuscitation as indicated: 

Provide supplem ental oxygen and intubation as needed for respiratory failure.

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

Intravenous access and volum e replacem ent with norm al saline or lactated Ringer solution or blood transfusion when indicated

ED Treatment 

Focus on stabilizing patient and providing analgesia.



Uncom plicated cyst rupture:



o

Analgesia

o

Observation

Unstable patients and patients with significant hem orrhage: o

Keep NPO.

o

Arrange im m ediate gynecologic consultation and adm ission.

o

Unstable patients and patients with torsion require im m ediate adm ission to OR.

Medication (Drugs) 

Acetam inophen: 325â€“650 m g PO/PR (peds: 15 m g/kg PO/PR, m ax. 650 m g) q4h



Ibuprofen: 400â€“600 m g (peds: 5â€“10 m g/kg) PO q6h



Morphine sulfate: 2â€“4 m g (peds: 0.1 m g/kg) IV/SC q5m in

Follow-Up Disposition Admission Criteria 

Significant hem orrhage ascertained by serial hem atocrits, orthostasis, culdocentesis, or evidence of shock

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

Culdocentesis fluid hem atocrit >15%



All patients with torsion

Discharge Criteria Stable patients with ruptured cyst and without coagulopathy or evidence of significant hem orrhage can be discharged with close follow-up with gynecologist.

References 1. Beaunoyer M, Chapdelaine J, Bouchard S, et al. Asynchronous bilateral ovarian torsion. J Pediatr Surg. 2004;39:746â€“749. 2. Copeland LJ, Jarrell JF. Textbook of Gynecology. 2nd ed. Philadelphia: WB Saunders; 2000. 3. Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann Em erg Med. 2001;38:156â€“159. 4. Pena JE, Ufberg D, Cooney N, et al. Usefulness of Doppler sonography in the diagnosis of ovarian torsion. Fertil Steril. 2000;73:1047â€“1050. 5. Tanos Scheaher JG. Ovarian cysts: a clinical dilem m a. Gynecol Endocrinol. 1994;8:59â€“67. 6. White M, Stella J. Ovarian torsion: 10-year perspective. Em erg Med Australas. 2005;17(3):231â€“237.

Codes ICD9-CM 620.2 Other and unspecified ovarian cyst 620.5 Torsion of ovary, ovarian pedicle, or fallopian tube

ICD10 N83.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paget's Disease

Paget's Disease

Daniel Davis

Basics Description 

Occurs in approxim ately 3% of patients older than 40 years



Starts with resorptive or osteolytic phase, during which osteoclasts rem ove healthy bone



Hypervascularity begins in resorptive phase: o



Predisposes to hem atom a and fracture

Resorbed bone is eventually replaced by irregular, dense, disorganized trabecular bone in sclerotic or osteoplastic phase.



Malignant transform ation is rare: o

Osteosarcom a is m alignancy of concern.

o

Usually m alignant transform ation occurs in 1%.

Etiology 

Unknown



May represent vascular hyperplasia with subsequent inflam m ation



Presence of nucleocapsids from m easles, canine distem per, or respiratory syncytial virus m ay im plicate viral cause.

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

Fam ilial or genetic com ponent

Pediatric Considerations 

Generally not seen in children

Diagnosis Signs and Symptoms 

Paget disease involves resorption of norm al bone and its replacem ent with fibrous and sclerotic tissue.



It is also known as osteitis deform ans.



Usually focal, bones m ost frequently involved include:



o

Pelvis

o

Fem ur

o

Skull

o

Tibia

o

Spine

o

Flat bones

Many patients are asym ptom atic, with disease discovered by incidental radiographs or elevated alkaline phosphatase levels.



Acute (resorptive/osteolytic) phase: o

Pathologic fractures

o

Pain from acute lysis, pathologic fracture, or resultant arthritis

o

Hypercalcem ia or renal stones

o

Hypervascularity m ay result in significant bleeding if affected bone is fractured.

o

Widespread disease: 

Increased vascularity and blood flow m ay result in high-output cardiac failure.

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

Secondary (sclerotic/osteoplastic) phase: o

Long-bone involvem ent m ay present with swelling or deform ity and gait abnorm ality.

o

Skull involvem ent m ay lead to headaches or abnorm al skull contours (change in hat size).

o

Severe skull or spine involvem ent m ay result in CNS com pression.

o

Hearing loss m ay result from nerve com pression or ossicle involvem ent.

o

Sarcom a occurs in <1% of patients.

Essential Workup 

Diagnosis usually suggested by radiographs



During resorptive phase, lytic lesions are often not seen, except in skull where lesions are well dem arcated (osteoporosis circum scripta).



Bowing of long bones m ay occur with resorption and strength loss.



New bone initially appears irregular and spotty and later becom es hom ogeneous and dense (â€œivory patternâ€•).



Excess bone m ay be deposited along stress lines, leading to cortical irregularities.



Thorough neurologic exam m ust be docum ented, especially with vertebral or pelvis involvem ent.

Tests Lab 

Alkaline phosphatase is m ost dram atic m arker of disease activity (especially resorptive phase).



Calcium and phosphate levels should be checked as well, but are usually norm al.



ECG if suspect hypercalcem ia and chest radiograph with evidence of high-output cardiac failure

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

Increased bone form ation m ay lead to elevations in urine hydroxyproline or serum osteocalcin or procollagen fragm ents.



Alterations in parathyroid horm one (PTH) levels occur as secondary changes during resorptive/osteolytic phase (low PTH) and sclerotic/osteoplastic phase (high PTH).

Imaging 

CT or MRI defines m argins and helps evaluate for neoplasm or hem atom a: o

Spiral CT to detect renal calculi



Bone scan is m ost sensitive for diagnosis of Paget disease.



Radionuclide scans (technetium -99m , gallium -67) m ay help guide therapy by assessing response to therapy.

Differential Diagnosis 

Prim ary hyperparathyroidism



Multiple m yelom a



Hodgkin variants



Acrom egaly



Osteosarcom a

P.787

Treatment Pre Hospital 

Pre hospital personnel should obtain inform ation about m echanism of injury or social factors that suggest pathologic fracture.



Adequate im m obilization can lim it excessive bleeding

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around fracture site.

Initial Stabilization 

Airway m anagem ent and resuscitation as indicated



High-output cardiac failure should be treated as outlined in Congestive Heart Failure chapter.



Prom pt im m obilization of fractures will lim it excessive bleeding around fracture site.

ED Treatment 

Analgesia for pain of lytic lesions, fractures, or arthritis includes nonsteroidal anti-inflam m atory drugs (NSAIDs) and narcotics.



High-dose prednisone can suppress disease.



Fracture treatm ent is often m ore conservative, owing to difficulties with bleeding during operative repair.



Orthopedic consultation for severe arthritis and definitive fracture m anagem ent



Hypercalcem ia m ay be treated with IV fluids, furosem ide (Lasix), calcitonin, inorganic phosphate, etidronate, m itram ycin.



Long-term chem otherapy m ay provide tem porary or prolonged rem ission.



CNS com pression requires em ergent neurosurgical consultation and possible decom pression.

Medication (Drugs) 

Alendronate: 40 m g/d for 6 m onths



Calcitonin: 0.5 m g/d SC of hum an, 100 IU/d SC of salm on



Chem otherapy with plicam ycin/m itram ycin, dactinom ycin, diphosphonate



Etidronate: 400 m g/d for 6-m onth cycles

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

Furosem ide (Lasix): 20â€“80 m g IV for hypercalcem ia



Inorganic phosphate

Follow-Up Disposition Admission Criteria 

Adm ission as indicated for m ajor traum a or injury, or excessive bleeding



Orthopedic procedures



Hypercalcem ia



CNS com pressive sym ptom s

Discharge Criteria 

No evidence of significant bleeding, neurologic com prom ise, or hypercalcem ia, and adequate pain control



Appropriate fracture im m obilization and orthopedic follow-up

References 1. Chandrasom a P, Taylor CR. Concise Pathology. East Norwalk, CT: Appleton & Lange; 1991. 2. Favus M. Prim er on the m etabolic bone diseases and disorders of m ineral m etabolism . Kelseyville CA: Am erican Society for Bone and Mineral Research; 1990. 3. Ryan WG. Parathyroid horm one, calcitonin, vitam in D, m inerals, and m etabolic bone diseases. In: Bone RC, Rosen RL, eds. Quick Reference to Internal Medicine. New York: Igaku-Shoin; 1994:13â€“29. 4. Schneider D, et al. Diagnosis and treatm ent of Paget's disease of bone. Am Fam Physician. 2002;65:2069â€“2072.

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Codes ICD9-CM 731.0

ICD10 M88.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pancreatic Pseudo cyst

Pancreatic

Pseudocyst Trevor Lewis

Basics Description 

Cystic collection of fluid with high content of pancreatic enzym es lacking true epithelial lining



Localized in parenchym a of pancreas or adjacent abdom inal spaces (lesser peritoneal sac)



Requires 4 or m ore weeks to form from onset of acute pancreatitis

Etiology 

Ethanol abuse accounts for 70â€“80% cases.



Other causes include traum a, biliary tract disease, hypertriglyceridem ia, and recent surgery.



Average age at diagnosis is 45 years.



Occurs m ore frequently in m en than in wom en



Com plication in 2% of acute pancreatitis; up to 10% of chronic pancreatitis

Pediatric Considerations 

Greater than 60% result from blunt traum a.

Pa ge 3 4 0



Usually can palpate a m ass

Signs and Symptoms Frequency: 

Abdom inal pain: 86%



Nausea/vom iting: 72%



Palpable m ass: 49%



Weight loss: 35%



Pleural effusion: 15%



Jaundice: 13%



Ascites: 11%



Internal hem orrhage: 7%

Gastrointestinal 

In chronic pancreatitis, pseudocyst heralded by change in typical pain pattern



Sym ptom s reflecting structural com pression by pseudocyst: o

Nausea, vom iting, weight lossâ€”duodenal or gastric outlet obstruction

o

Jaundiceâ€”com m on bile duct com pression

Respiratory Left lung pleural effusion com m on

Cardiac 

Com m only occurs with pseudocyst rupture or hem orrhage



Tachycardia



Hypotension



Shock (depending on fluid losses)

Infected Pseudocyst 

Fever



Chills



Leukocytosis

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Pseudocyst Hemorrhage 

Hypotension



Expanding abdom inal m ass



Usually erodes into splenic or gastroduodenal arteries

Ruptured Pseudocyst Abdom inal rigidity, severe pain: 

Occurs when cyst ruptures into peritoneal cavity

Essential Workup 

Laboratory tests not helpful in diagnosis



Useful to anticipate com plications

Tests Lab 

Am ylase: o





Norm al value in up to 50% of pseudocysts

CBC: o

Leukocytosis suggests infected pseudocyst

o

Low hem atocrit with pseudocyst hem orrhage

Electrolytes, BUN, creatinine, glucose: o

Hypocalcem ia

o

Hypokalem ia with extensive fluid losses

o

Hypom agnesem ia with underlying ethanol abuse

o

Hyperglycem ia

Imaging 



CT scan: o

Im aging test of choice

o

Indicated for all cases of newly suspected pseudocyst

Ultrasound: o

Useful for follow-up of previously diagnosed pseudocyst to assess pseudocyst dim ensions



Angiography:

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o

Helpful in cases of pseudocyst hem orrhage

o

Usually im practical owing to instability of patient

Differential Diagnosis 

Pancreatic abscess



Neoplastic pancreatic cysts



Perforated ulcer



Ruptured abdom inal aortic aneurysm (pseudocyst hem orrhage)



Myocardial infarction



Biliary colic



Intestinal obstruction

Treatment Pre Hospital 

Initiate IV access in cooperative patients.



Apply cardiac m onitor.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Supplem ental oxygen



Cardiac m onitor



IV fluids

P.789

ED Treatment 

Fluid resuscitation: o

Fluid losses m ay necessitate large fluid volum es.

o

Continuously assess vitals, urine output, and

Pa ge 3 4 0

electrolytes to ensure rapid and adequate replacem ent of intravascular volum e. 

Correct electrolytes abnorm alities (hypocalcem ia, hypokalem ia, hypom agnesem ia)



Blood products: o

Transfuse im m ediately in cases of pseudocyst hem orrhage pending definitive surgical treatm ent.



Analgesia (opiate analgesia drug of choice)



Nasogastric suction if intractable nausea/vom iting



Antiem etics (prom ethazine)

Geriatric Considerations Consider central venous pressure (CVP) m onitoring in elderly.

Medication (Drugs) 

Calcium gluconate 10%: 10 m L IV over 15â€“20 m inutes



Magnesium sulfate: 16 m Eq (2 g) in 50 m L D 5 W over 20 m inutes



Meperidine (Dem erol): 25â€“50 m g IV; 50â€“75 m g IM q3hâ€“q4h



Morphine: 2â€“4 m g IV



Potassium chloride: 10 m Eq/h IV



Prom ethazine: 12.5â€“25 m g PO/IM/IV or by rectum (PR)

Follow-Up Disposition Admission Criteria 

All newly diagnosed pseudocysts >6 cm



Pseudocysts <6 cm if sym ptom s of acute pancreatitis

Pa ge 3 4 0



Previously known pseudocysts if cyst is increasing in size com pared with old studies



Hem odynam ic instability



Severe abdom inal pain



Fever/infected pseudocyst

Discharge Criteria Refer stable, asym ptom atic patient with pseudocyst <6 cm for urgent surgical clinic follow-up.

Issues for Referral 

Surgical consultation: o

Em ergent surgical consultation m andatory in cases of suspected ruptured pseudocyst or pseudocyst hem orrhage as definitive treatm ent is em ergent laparotom y



Surgical treatm ent options (pseudocyst >6 cm or persists for >6 weeks): o

Observation (no acute intervention): 

o

Surgical excision: 

o

Used infrequently

External drainage: 

o

Usually reserved for asym ptom awtic patients

CT- or ultrasound-guided percutaneous drainage

Internal drainage: 

Open versus endoscopic technique

References 1. Aguilar M, Jones RS, Sanfey H. Pseudocysts of the pancreas: a review of 97 cases. Am Surg. 1994;60:661â€“668. 2. Baillie J. Pancreatic pseudocysts. Gastrointest Endosc. 2004;59:873â€“879. 3. Cooperm an AM. An overview of pancreatic pseudocysts: the em peror's new clothes revisited. Surg Clin North Am .

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2001;81:391â€“397. 4. Maule W, Reber H. Diagnosis and m anagem ent of pancreatic pseudocysts, pancreatic ascites, and pancreatic fistulas. In: Go V, et al., eds. The Pancreas. New York: Raven Press; 1993:71â€“78. 5. Werner J, Warshaw AL. Pseudocysts, postinflam m atory cystic fluid collections, and other non-neoplastic cysts. In: Trede M, et al., eds. Surgery of the Pancreas. New York: Churchill Livingstone; 1997:405â€“410.

Miscellaneous SEE ALSO: Pancreatitis

Codes ICD9-CM 577.2

ICD10 K86.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pancreatic Traum a

Pancreatic

Trauma Beth Anne Joseph

Basics Description 

Direct epigastric blow com pressing pancreas against vertebral colum n



Injury to pancreas from penetrating object

Pediatric Considerations 

Traum a affects proportionately larger areas leading to m ultisystem injuries.



Children have less protective m uscle and subcutaneous tissue.



Children will less often present with hypotension.

Etiology 

Penetrating traum a: m ost com m on m echanism



Blunt traum a: deep location of pancreas requires significant force to cause injury: o

Steering wheel or bicycle handlebars to abdom en

o

In children, evaluate for nonaccidental traum a

Associated Conditions

Pa ge 3 4 0

Ninety percent of pancreatic injuries associated with injuries to adjacent structures: 

Liver, stom ach



Major arteries and veins



Spleen, kidney



Duodenum , colon, sm all bowel



Com m on bile duct, gallbladder

Diagnosis Alert Extent of pancreatic injury m ay not be apparent on initial evaluation.

Signs and Symptoms 

Abdom inal pain: o

Diffuse or epigastric

o

Often out of proportion to physical exam and vital signs



Soft-tissue contusion in upper abdom en



Injury to lower ribs or costal cartilage



Acute abdom en, often associated with other intra-abdom inal injuries



Hypotension



Grey-Turner sign: o



Flank ecchym osis

Cullen sign: o

Perium bilical ecchym osis

History Concise; details of incident especially im portant for blunt traum a

Physical Exam 

Inspection for abrasions, contusions, penetrating wounds:

Pa ge 3 4 0

o

Must logroll patient for full inspection



Auscultation for presence or absence of bowel sounds



Palpation to determ ine location and severity of pain, presence of guarding, and rebound tenderness



Rectal exam for occult blood, vaginal exam , or penile exam



Serial physical exam inations and vital signs for unidentified injuries

Essential Workup 

Pace of workup dictated by patient condition and other injuries



Abdom inal CT with IV contrast essential to evaluate for pancreatic traum a

Tests Lab 

Blood type, screen, or cross-m atch



Hem atocrit, WBC with differential



Am ylase: o

Not a reliable indicator of pancreatic traum a

o

Serial levels m ay increase sensitivity, but specificity still poor.

o

Elevated am ylase m ay be early indicator of potential pancreatic injury.

o

Norm al am ylase does not rule out pancreatic injury.



Lipase



Urinalysis



Pregnancy test



Alcohol and drug screening if indicated



Prothrom bin tim e/partial throm boplastin tim e, blood urea nitrogen, and creatinine

Pa ge 3 4 1

Imaging Note that all im aging tests m ay m iss pancreatic injury: 

Cervical spine, chest radiograph film s, and pelvis film s as for all blunt traum a patients



Bedside ultrasound



CT scan with IV contrast, helical CT if available: o

Shows better contrast enhancem ent of pancreatic parenchym a than standard scanning



Endoscopic retrograde cholangiopancreatography: o

Useful for patients with persistent hyperam ylasem ia

o

Unexplained abdom inal sym ptom s

Diagnostic Procedures/Surgery Diagnostic peritoneal lavage to identify intraperitoneal injuries: 

Check fluid for am ylase level.



May still m iss significant pancreatic injury

Differential Diagnosis Other abdom inal traum atic injuries P.791

Treatment Pre Hospital Transport to closest traum a center.

Initial Stabilization 

Airway m anagem ent, resuscitation as indicated



Nasogastric-tube suction m ay be especially helpful in setting of pancreatic traum a.

Pa ge 3 4 1

General Measures 

Follow standard traum a treatm ent for blunt abdom inal traum a.



Penetrating traum a: o

Tetanus prophylaxis and broad spectrum antibiotic therapy.



Intra-abdom inal injury requiring operative intervention: o



Broad spectrum antibiotic therapy

Must cover for colonic bacteria: o

Aerobic: Escherichia coli, Enterobacter, Klebsiella, Enterococcus

o

Anaerobic: Bacteroides fragilis, Clostridium , Peptostreptococcus

Medication (Drugs) 



Adults: o

Cefotetan: 2g IV plus gentam icin 2 m g/kg IV or

o

Cefoxitin: 2 g IV plus gentam icin 2 m g/kg IV or

o

Ceftriaxone: 1â€“2 g IV plus Flagyl 15 m g/kg IV or

o

Clindam ycin: 600 m g IV plus gentam icin 2 m g/kg IV

Children: o

Cefotetan: 20 m g/kg IV plus gentam icin 2 m g/kg IV or

o

Cefoxitin: 40 m g/kg IV plus gentam icin 2 m g/kg IV or

o

Ceftriaxone: 50 m g/kg per dose IV plus Flagyl 15 m g/kg IV

Follow-Up

Pa ge 3 4 1

Disposition Admission Criteria 

All patients with pancreatic injuries m ust be adm itted.



Abdom inal pain after blunt traum a requires serial exam ination and observation for 24 hours.



Intoxicated traum a patient requires adm ission and serial exam inations for unidentified injury.

Discharge Criteria Only for very m inor traum a and with no evidence of pancreatic or any other intra-abdom inal injury

References 1. Beckingham IJ. ABC of diseases of liver, pancreas and biliary system : liver and pancreatic traum a. BMJ. 2001;322:783â€“785. 2. Bradley EL, Young PR, Chang MC, et al. Diagnosis and initial m anagem ent of blunt pancreatic traum a. Ann Surg. 1998;6:861â€“869. 3. Em m ick RH Jr, Peterson SR. Evaluation of pancreatic injury after blunt abdom inal traum a. Ann Em erg Med. 1996;27:658â€“661. 4. Jurkovich J. Injury to the duodenum and pancreas. In: Feliciano DV, Mattox KL, Moore EE, eds. Traum a. 3rd ed. Norwalk, CT: Appleton & Lange; 1996:473â€“494. 5. Novelline RA, Rhea JT, Bell T. Helical CT of abdom inal traum a. Radiol Clin North Am . 1999;37:591â€“612.

Codes ICD9-CM 863.84 Pancreas, m ultiple and unspecified sites

ICD10 S36.2

Pa ge 3 4 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pancreatitis

Pancreatitis

Trevor Lewis

Basics Description 

Inflam m ation of pancreas owing to activation, interstitial liberation, and digestion of gland by its own enzym es



Acute pancreatitis: o

Exocrine and endocrine function of gland im paired for weeks to m onths

o 

Glandular function will return to norm al.

Chronic pancreatitis: o

Exocrine and endocrine function progressively deteriorate with resultant steatorhea and m alabsorption.

o

Dysfunction progressive and irreversible

Etiology 

Gallstones and alcohol abuse m ost com m on causes of acute pancreatitis (75â€“80%)



Alcohol abuse accounts for 70â€“80% of chronic pancreatitis.



Acute: o

Biliary tract disease

o

Chronic alcoholism

Pa ge 3 4 1



o

Obstruction pancreatic duct

o

Ischem ia

o

Drugs

o

Infectious

o

Postoperative

o

Metabolic diseases

o

After renal transplant

o

Scorpion venom

o

Penetrating peptic ulcer

o

Hereditary

Chronic o

Chronic alcoholism

o

Obstruction pancreatic duct

o

Tropical

o

Hereditary

o

Shwachm an disease

o

Enzym e deficiency

o

Idiopathic

o

Hyperlipedem ia

Pediatric Considerations Cause m ainly viral, traum a, and drugs

Diagnosis Signs and Symptoms 

Frequency: o

Abdom inal pain: 95â€“100%

o

Epigastric tenderness: 95â€“100%

o

Nausea and vom iting: 70â€“90%

o

Low grade fever: 70â€“85%

Pa ge 3 4 1



o

Hypotension: 20â€“40%

o

Jaundice: 30%

o

Grey Turner/Cullen Sign: <5%

o

Subcutaneous fat necrosis: <1%

GI: o

Severe, persistent epigastric pain radiating to back: 

Colicky or rebound tenderness suggest nonpancreatic source.



Worse when supine

o

Bowel sounds usually decreased or absent

o

Significant GI bleed in patients with acute severe pancreatitis is uncom m on.

o

Cullen sign: 

Bluish discoloration at um bilicus secondary to hem orrhagic pancreatitis

o

Grey Turner sign: 

Bluish discoloration at flank secondary to hem orrhagic pancreatitis



Respiratory: o

Pleuritic chest pain

o

Dyspnea

o

Lung exam :

o 





Left pleural effusion (m ost com m on)



Atelectasis



Pulm onary edem a

Hypoxem ia (30%)

Cardiac: o

Tachycardia

o

Hypotension

o

Shock

Neurologic: o

Irritability

Pa ge 3 4 1

o

Confusion

o

Com a

o

Chvostek and Trousseau signs are rare despite laboratory evidence of hypocalcem ia.

Ranson Criteria 





Indicators of m orbidity and m ortality: o

0 to 2 criteria: 2% m ortality

o

3 or 4 criteria: 15% m ortality

o

5 or 6 criteria: 40% m ortality

o

7 or 8 criteria: 100% m ortality

Criteria on adm ission: o

Age older than 55 years

o

WBC count >16,000 m m 3

o

Blood glucose >200 m g/dL

o

Serum lactate dehydrogenase (LDH) >350 IU/L

o

AST >250 IU/L

Criteria during first 48 hours: o

Hem atocrit fall >10%

o

BUN increase > 5 m g/dL

o

Serum calcium <8 m g/dL

o

Arterial PO 2 <60 m m Hg

o

Base deficit >4 m Eq/L

o

Estim ated fluid sequestration >6 L

Essential Workup Laboratory tests confirm physical diagnosis.

Tests Lab 

Am ylase: o

Rise within 6 hours of pain onset

o

More than five tim es upper lim it is highly specific for

Pa ge 3 4 1

pancreatitis. o

More than 1,000 IU suggests biliary pancreatitis.

o

May be norm al during acute inflam m ation owing to significant pancreatic destruction

o 





Secreted from various sources

Lipase: o

Rise within 4â€“8 hours pain onset

o

More reliable indicator of pancreatitis than am ylase

Electrolyte, BUN, creatinine, glucose: o

Hypokalem ia occurs with extensive fluid losses.

o

Hyperglycem ia

CBC: o

Increased hem atocrit with fluid losses

o

Hem atocrit >47% at risk for pancreatic necrosis

o

Decreased hem atocrit with retroperitoneal hem orrhage

o

WBC count >12,000 unusual

P.793



Calcium /m agnesium : o

Hypocalcem ia indicates significant pancreatic injury.

o

Hypom agnesem ia occurs with underlying alcohol abuse.



Liver function tests: o

Useful for prognostic indicators if suspected biliary cause



Pregnancy test



Arterial blood gases (ABGs): o

Indicated if hypoxic (assess PO 2 ) or toxic appearing (assess base deficit)



ECG:

Pa ge 3 4 1

o

Assess electrolyte im balances, ischem ia.

Imaging 

Abdom inal series radiograph: o

Excludes free air

o

May visualize pancreatic calcifications

o

Most com m on finding is isolated dilated bowel loop (sentinel loop) near pancreas.





Chest radiograph: o

Pleural effusion

o

Atelectasis

o

Infiltrate

Ultrasound (US): o



Useful if gallstone pancreatitis suspected

Abdom inal CT indications: o

High-risk pancreatitis (>three Ranson criteria)

o

Hem orrhagic pancreatitis

o

Suspicion pseudocyst

o

Diagnosis in doubt

Diagnostic Procedures/Surgery Endoscopic retrograde cholangiopancreatography (ERCP): 

Indicated for severe pancreatitis with cholangitis or biliary obstruction

Differential Diagnosis 

Mesenteric ischem ia/infraction



Myocardial infarction



Biliary colic



Intestinal obstruction



Perforated ulcer



Pneum onia



Ruptured aortic aneurysm



Ectopic pregnancy

Pa ge 3 4 1

Treatment Pre Hospital 

Initiate IV access in cooperative patients.



Apply cardiac m onitor.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Supplem ental oxygen



Cardiac m onitor



IV fluids

ED Treatment 

Airway m anagem ent: o

Pulm onary com plaints necessitate supplem ental oxygen.

o

Endotracheal intubation for adult respiratory distress syndrom e (ARDS) or severe encephalopathy



Fluid resuscitation: o

Large fluid volum es (up to 5â€“6 L in first 24 hours) owinge to fluid losses

o

Continuously assess vitals, urine output, and electrolytes to ensure rapid and adequate replacem ent of intravascular volum e.



Geriatric considerations: o

Consider central venous pressure (CVP) m onitoring when fluid overload is concern.



Correct electrolyte abnorm alities if present: o

Hypocalcem ia (calcium gluconate)

o

Hypokalem ia occurs with extensive fluid losses.

o

Hypom agnesem ia occurs with underlying alcohol

Pa ge 3 4 2

abuse. 

Blood products: o

In hem orrhagic pancreatitis, transfuse to hem atocrit level of 30%.

o

Fresh frozen plasm a and platelets if coagulopathic and bleeding



Analgesia: o



Opiate analgesia is drug of choice.

Nasogastric suction: o

Not useful in cases of m ild pancreatitis

o

Beneficial in severe pancreatitis or intractable vom iting



Antiem etics



Antibiotics: o

Indicated it pancreatic necrosis >30% on abdom inal CT

Medication (Drugs) 

Calcium gluconate 10%: 10 m L IV over 15â€“20 m inutes



Meperidine (Dem erol): 25â€“50 m g IV, 50â€“75 IM q3hâ€“q4h



Morphine: 2â€“4 m gIV



Im ipenem : 500 m g IV q6h



Potassium chloride: 10 m Eq/h IV



Prom ethazine: 12.5â€“25 m g PO/IM/IV or by rectum (PR)

Follow-Up Disposition

Pa ge 3 4 2

Admission Criteria 

Acute pancreatitis with significant pain, nausea, vom iting



ICU adm ission for hem orrhagic/necrotizing pancreatitis

Discharge Criteria 

Mild acute pancreatitis without evidence of biliary tract disease and able to tolerate oral fluids



Chronic pancreatitis with m inim al abdom inal pain and able to tolerate oral fluids

Issues for Referral Surgical consultation for ERCP in severe pancreatitis with cholangitis or biliary obstruction

References 1. Banks PA. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 1997;92(3):377â€“386. 2. Go V, et al, eds. The Pancreas. New York: Raven Press; 1993:575â€“535. 3. Heinisch A, Scholm erich J, Leser H. Diagnostic approach to acute pancreatitis: diagnosis, assessm ent of etiology and prognosis. Hepatogastroenterology. 1993;40(6):531â€“537. 4. Mayerle J, et al. Medical treatm ent of acute pancreatitis. Gastroenterol Clin N Am . 2004;855â€“869. 5. Tenner S. Initial m anagem ent of acute pancreatitis: critical issues during the first 72 hours. Am J Gastoenterol. 2004;99:2489â€“2494.

Miscellaneous SEE ALSO: Pancreatic Pseudocyst

Codes ICD9-CM

Pa ge 3 4 2

577.0 577.1

ICD10 K85

Pa ge 3 4 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Panic Attack

Panic Attack

B. J. Beck

Basics Description 

Characteristic, acute episodes of physical sym ptom s and intense fear that rapidly peak within 10 m inutes and resolve in about 20 m inutes



There m ay be a nonfearful variant in m edical patients.

Panic Disorder 

Recurrent, unexpected panic attacks with one or m ore m onths of persistent: o

Concerns about having another attack

o

Worry about the im plications or consequences of the attacks

o

Behavioral change, such as phobic avoidance, related to the attacks



Episodic, recurrent, or chronic attacks



Frequently com orbid with depression, substance abuse, disability, suicidal tendency

Genetics Probably genetic: 

Fam ily history of panic or anxiety is com m on.

Pa ge 3 4 2

Etiology Mechanism Lim bic system , norepinephrine release, other neurotransm itters (e.g., serotonin) im plicated

Risk Factors 

Major life events in year preceding onset



Fam ily history of panic or anxiety



Childhood shyness or separation anxiety



May develop in the course of predisposing physical illness or cocaine abuse: o

May persist after the illness or substance use has resolved

Diagnosis Signs and Symptoms 

Multiple system s suggest autonom ic arousal



Cardiac:





o

Palpitations

o

Tachycardia

o

Chest pain

Respiratory: o

Shortness of breath

o

Sm othering

o

Choking

Neurologic: o

Trem or

o

Dizziness

o

Light-headedness

o

Feeling faint

Pa ge 3 4 2





o

Num bness

o

Tingling

o

Sweating

o

Chills

o

Flushing

o

Feelings of unreality or detachm ent

Gastrointestinal: o

Nausea

o

Cram ps

o

Abdom inal pain

Intense fears: o

Autom atic, stereotypic

o

Im m inent death

o

Having a heart attack

o

Hum iliation

o

Loss of controlâ€”â€œgoing crazyâ€•

History 

Known m edical conditions



All m edications, including over the counter



Herbal supplem ents



Recreational drugs/alcohol use



Caffeine consum ption



Age at onset



Fam ily history of panic, anxiety



Initiating life events



Childhood antecedents



Resultant avoidance



Response to previous m edication trials

Physical Exam 

Thorough physical and neurological exam



Guided by particular sym ptom s

Pa ge 3 4 2

Tests Lab 

Toxicology screen



CBC



Electrolytes, blood urea nitrogen/creatinine, glucose



Thyrotropin

Imaging ECG for suspected m itral valve prolapse (MVP)

Diagnostic Procedures/Surgery 



ECG o

Age >40 years

o

Cardiac sym ptom s

Sleep-deprived EEG if seizure suspected

Differential Diagnosis 

Consider organic causes if: o

Panic presents late in life (>50 years old)

o

No childhood antecedents or fam ily history

o

No initiating or m ajor life events

o

Without avoidance or significant fear

o

With a history of poor response to previous trials of antipanic or antidepressant m edication





Medications: o

Neuroleptics (akathisia)

o

Bronchodilators

o

Digitalis

o

Anticholinergic agents

o

Psychostim ulants

o

Diet pills

Respiratory: o

Chronic obstructive pulm onary disease

Pa ge 3 4 2

o 







Pulm onary em bolus

Cardiovascular: o

Angina

o

Arrhythm ia

o

Anem ia

o

MVP m ay be com orbid with panic.

Substances: o

Stim ulant abuse

o

Withdrawal (alcohol, sedative-hypnotics)

o

Excessive caffeine intake

Endocrine: o

Hyperthyroidism

o

Hypoglycem ia

o

Parathyroid disorders

o

Pheochrom ocytom a

Neurologic: o

Com plex partial, or lim bic seizures (fear, physical sym ptom s, perceptual distortions)

o 

Transient ischem ic attack

Psychiatric: o

Other anxiety, stress, or phobic disorders; for exam ple, obsessive-com pulsive disorder, posttraum atic stress disorder, or social phobia

P.795

Treatment Initial Stabilization 

Be calm and reassuring.

Pa ge 3 4 2



Most panic attacks resolve within 20â€“30 m inutes without any treatm ent.



Fear m ay trigger another panic attack.

ED Treatment 

High-potency benzodiazepines:



Drugs of choice o

Clonazepam : 

Slow for em ergency use



Long-acting without rapid onset/offset phenom ena



Best choice in this class for m aintenance therapy of recurrent panic attacks

o

Alprazolam : 

Rapid onset



Rebound anxiety occurs due to short duration and rapid offset.

 o

May lead to escalating doses with continued use

Lorazepam : 

Quick onset



Advantage of sublingual use



Longer effect and less abrupt offset than alprazolam





Avoid low-potency benzodiazepines: o

Diazepam

o

Chlordiazepoxide

Treat recurrent panic attacks and panic disorder with SSRI (or TCA) antidepressants, with or without clonazepam : o

Will not work im m ediately

o

Do not need to be started em ergently, especially if there is not clear, established access to follow-up m anagem ent



Prelim inary case reports on the efficacy of olanzapine for

Pa ge 3 4 2

treatm ent resistant panic disorder 

Discharge therapy: o

Several clonazepam tablets in case of repeated attacks: 

Do not prescribe alprazolam â€”withdrawal m ay trigger further attacks.

Medication (Drugs) 

Alprazolam : 0.5 m g PO



Clonazepam : 0.5 m g PO in the ED; 0.25â€“0.5 m g PO b.i.d. for initial outpatient therapy



Lorazepam : 1 m g PO or SL

Follow-Up Disposition Admission Criteria 

As m edically indicated to rule out organic cause



Meets criteria for psychiatric adm ission (suicidal, hom icidal)

Discharge Criteria Most panic attacks do not require inpatient level of care.

Issues for Referral 

Managed care m ental health carve-outs



Psychopharm acological and cognitive behavioral therapy evaluation for repeated attacks, or interepisode fear or avoidance



Stigm a

Pa ge 3 4 3



Prim ary care follow-up m ay be an acceptable alternative to specialty, m ental health/psychiatry referral.

References 1. Fleet RP, Martel J-P, Lavoie KL, et al. Non-fearful panic disorder: a variant of panic in m edical patients? Psychosom atics. 2000;41:311â€“320. 2. Huffm an JC, Pollack MH. Predicting panic disorder am ong patients with chest pain: an analysis of the literature. Psychosom atics. 2003;44:222â€“236. 3. Roy-Byrne PP, Clary CM, Miceli RJ, et al. The effect of selective serotonin reuptake inhibitor treatm ent of panic disorder on em ergency room and laboratory resource utilization. J Clin Psychiatry . 2001;62:678â€“682. 4. Wulsin L, Liu t, Storrow A, et al. A random ized, controlled trial of panic disorder treatm ent initiation in an em ergency departm ent chest pain center. Ann Em erg Med. 2002;39:139â€“143. 5. Khaldi S, Korreich C, Dan B, Pelc I. Usefulness of olanzapine in refractory panic attacks. J Clin Psychopharm . 2003;23:100â€“101. 6. Mago R, Berlin M. Olanzapine and panic attacks. Am J Psychiatry. 2000;157:659â€“660. 7. Rayburn NR, Otto MW. Cognitive-behavioral therapy for panic disorder: a review of treatm ent elem ents, strategies, and outcom es. CNS Spectr. 2003;8:356â€“362.

Codes ICD9-CM 300.01

ICD10 F41.0

Pa ge 3 4 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paraphim o sis

Paraphimosis

Daniel Firestone

Basics Description 

Paraphim osis is a urologic em ergency.



It is the entrapm ent of the retracted foreskin proxim al to the glans of the penis.



Leads to lym phatic congestion, venous obstruction, which m ay result in arterial com prom ise to the glans

Etiology 

A num ber of conditions of the foreskin m ay predispose to paraphim osis, including:



o

Phim osis

o

Inflam m ation

o

Traum a

Com m only iatrogenic, from failure to replace the foreskin after exam ination, catheterization, or cleaning

Diagnosis Signs and Symptoms

Pa ge 3 4 3



Retracted foreskin



Pain



Swollen, edem atous glans



Local cellulites



Necrosis of glans in untreated cases

Essential Workup 

Paraphim osis is a clinical diagnosis with the clinical findings described earlier.



Exam ination should include a search for constricting foreign bodies, constricting bands.



Treatm ent m ust not be delayed pending diagnostic laboratory or radiographic studies.

Tests Imaging If history suggests penile foreign body, radiographs m ay be obtained once the vascular com prom ise has been relieved.

Differential Diagnosis 

Foreign bodies constricting the penile shaft m ay m im ic paraphim osis; these include: o

Hair tourniquets

o

Wire, string, or other m aterial used for sexual enhancem ent or punishm ent



Balanoposthitis



Traum a (zipper injuries)



Acute idiopathic penile edem a

Treatment Pre Hospital

Pa ge 3 4 3



Patients should be transported prom ptly; do not attem pt reduction in the field.



Pre hospital personnel can be advised to apply an ice pack to the glans with adequate protection of the skin.

Initial Stabilization 

Ice can be applied to the glans while preparing to reduce the prepuce: o

Use the thum b of a glove as an ice-filled condom to aid in direct application.



The incarcerated foreskin m ust be released as soon as possible to prevent ischem ia and necrosis of the glans.



The pain associated with reduction techniques m ust be m anaged with som e com bination of conscious sedation, adequate analgesia, and local anesthesia.

P.797

ED Treatment 

The following sequence of procedures should be followed: o

Paraphim osis can m ost frequently be reduced using a penile block and com pressing the glans m anually while applying traction on the foreskin.

o

Penile block is perform ed by infiltrating 5 m L of 1% lidocaine without epinephrine in the angle between the inferior ram i of the sym physis pubis. 

Then use another 5 m L to infiltrate a wheel along the sides of the penis.

 o

This produces a block after 5 m inutes.

In children, conscious sedation will usually be required.

o

If m anual reduction is unsuccessful, then the

Pa ge 3 4 3

technique of m ultiple punctures m ay facilitate reduction: 

One m akes m ultiple holes in the swollen foreskin with a sm all sterile needle (26 g), allowing expression of edem a fluid.

o

If this fails to return the foreskin to its original position, it will be necessary to incise the constricting ring of tissue with a dorsal longitudinal slit in the foreskin after sterile preparation. 

If the incision has been on the long side, after reduction it m ay be necessary to suture the incision transversely with 3.0 absorbable sutures.



If a delay is likely before the paraphim osis can be treated (e.g., NPO status), then applying a gauze swab soaked in 50% dextrose will reduce edem a by osm osis and facilitate reduction.

Medication (Drugs) 

Appropriate analgesics or anesthetics as required



It appears that prophylactic antibiotics following the m ultiple puncture technique are not routinely indicated: o

Their role in paraphim osis reduction by incision is not well studied.

Follow-Up Disposition Admission Criteria

Pa ge 3 4 3

Necrosis or cellulitis of the penis

Discharge Criteria 

Successful reduction with relief of sym ptom s



Close urologic follow-up

Issues for Referral 

Urologic consultation is required.



Subsequent circum cision to prevent recurrence is an area of clinical debate; historically, it has been com m on practice.

References 1. Little B, White M. Treatm ent options for paraphim osis. Int J Clin Pract. 2005 May; 59(5):591â€“593. 2. Barone JG, Fleisher MH. Treatm ent of paraphim osis using the â€œpunctureâ€• technique. Pediatr Em erg Care. 1993;9(5):298â€“299. 3. O'Donnell JA II. Phim osis and paraphim osis. In: Barkin RM, et al, eds. Pediatric em ergency m edicine. 2nd ed. St. Louis, MO: Mosby, 1997:1152â€“1153. 4. Pontari MA. Phim osis and paraphim osis. In: Seidm an, Hanno PM, eds. Current urologic therapy. 3rd ed. Philadelphia, PA: WB Saunders, 1994:392â€“397. 5. Raveenthwan V. Reduction of paraphim osis: a technique based on pathophysiology. Br J Surg. 1996;83(9):1247.

Miscellaneous SEE ALSO: Phim osis

Codes ICD9-CM

Pa ge 3 4 3

605

Pa ge 3 4 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Parkinso n's Disease

Parkinson's

Disease James M. Leaming

Basics Description 

Gradually progressive disorder of m iddle or late life



Aggregates of m elanin-containing nerve cells in the brainstem : o

Substantia nigra locus ceruleus



Reactive gliosis with nerve cell loss



Lewy bodies: o

Eosinophilic intracytoplasm ic inclusions



Decreased dopam ine in the caudate nucleus and putam en



Accelerated cortical atrophy



Can begin unilaterally, but generalizes to sym m etric

Etiology 

Sporadic or idiopathic, degenerative



Type A Encephalitis of von Econom o



CNS viral infections



Vascular infarction



Intoxications: o

Phenothiazine

Pa ge 3 4 3

o

Butyrophenones

o

Metoclopram ide

o

Illicit drugs

o

Carbon m onoxide: 

o

Bilateral infarctions of the globus pallidus

Manganese

Diagnosis Signs and Symptoms 

â€œPill-rollingâ€• resting trem or



â€œCog-wheelâ€• rigidity due to increased m uscular tone



Stooped posture and instability of posture



Stiffness and slowness of m ovem ent



â€œMasked faceâ€• appearance



Depression and dem entia



Sudden change in baseline m otor function or m ental status: o

May be the only indication of system ic disease such as infection

Essential Workup 

History is of prim ary im portance: o



Diagnosis is m ade based on clinical findings.

Im portant historical inform ation includes: o

Onset of sym ptom , whether gradual or sudden

o

History of encephalitis, herpes virus infection, or carbon m onoxide exposure

o

Patients with established Parkinson disease: 

Sudden change in baseline m otor function



Change in m ental status

Pa ge 3 4 3



Should prom pt workup for infectious process such as urinary tract infection

Tests Lab 

No specific or recom m ended laboratory studies necessary to confirm the diagnosis



Nonidiopathic Parkinson disease m ay require directed laboratory studies.



Urinalysis, CBC, chest radiograph, and other appropriate workup for occult infection in patients with established disease

Imaging 

CT scan/MRI are not required to diagnose Parkinson disease but are often elem ents of evaluation for dem entia.



Chest radiograph m ay be indicated for any signs of respiratory tract infection.

Differential Diagnosis 

Benign fam ilial trem or



Major depression



Wilson disease



Huntington disease



Alzheim er disease



Creutzfeldt-Jacob disease



Carbon m onoxide poisoning



B 1 2 deficiency



Hydrocephalus



Multi-infarct dem entia



Essential trem or disorders

P.799

Pa ge 3 4 4

Treatment ED Treatment 

Treatm ent with anti-Parkinsonian m edications can be initiated in the ED to alleviate sym ptom s.



Consultation with neurology for recom m ended m edication regim ens and ongoing support and m onitoring is prudent.



For patients with m ild disease, no m edication m ay be required.



For m oderate disease anticholinergic m edications and dopam inergic m edications should be used.



Treat underlying infection, if present.

Medication (Drugs) 

Am antadine: 100 m g b.i.d.



Benztropine: 0.5â€“1 m g t.i.d.



Brom ocriptine: 15 m g every day



Levodopa/Dopa carboxylase inhibitor (carbidopa) com bination: 25/100 m g every day



Trihexyphenidyl: 1â€“2 m g q.i.d.

Follow-Up Disposition Admission Criteria

Pa ge 3 4 4



Patient with intercurrent infections, dehydration, or other m edical problem s



Depression with intent to do self-harm



Medication regim en adjustm ent

Discharge Criteria 

Mild to m oderate disease without m edications



Moderate to severe disease with m edications and urgent neurologic outpatient follow-up

References 1. Flint MB, Beal M, Richardson EP, et al. Parkinson's disease. In: Isselbacher KJ, et al, eds. Harrison's principles of internal m edicine. New York: McGraw-Hill, 1994. 2. Freidm an JH and Factor SA: Atypical antipsychotics in the treatm ent of drug-induced psychosis in Parkinson's disease. Mov Disord. 2000;15:201. 3. Lieberm an, A. Managing the neuropsychiatric sym ptom s of Parkinson's disease. Neurology. 1998;50[6 Suppl 6]:533â€“538. 4. Obeso JA, et al. Levodopa m otor com plications in Parkinson's disease. Trends Neurosci. 2000;23(Suppl):S2. 5. Rajput A, et al. Epidem iology of parkinsonism : Incidence, classification, and m ortality. Ann Neurol. 1984;16:178. 6. Richard IH and Nutt J. Worsening of m otor function in Parkinson's disease: A â€˜typicalâ€™ response to â€˜atypicalâ€™ antipsychotic m edications. Neurology. 2000;55:748. 7. Shulm an LM, et al. The use of dopam ine agonists in very elderly patients with Parkinson's disease. Mov Disord. 2000;15:664.

Codes ICD9-CM 332.0

ICD10

Pa ge 3 4 4

G20

Pa ge 3 4 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paro nychia

Paronychia

Gene Ma

Basics Description 

Disruption of the seal between the nail plate and the nail fold m ay allow entry of bacteria into the eponychial space.



Inflam m ation of the nail folds surrounding the nail plate

Etiology 

Acute paronychia: predom inantly Staphylococcus aureus but also streptococci, Pseudom onas, and anaerobes



Chronic paronychia: predom inantly Candida albicans, but m ay also be other fungi, atypical m ycobacteria; com m only coexisting with Staphylococcus species

Diagnosis Signs and Symptoms History 

Acute paronychia: nail biting, finger sucking, aggressive m anicuring or m anipulation, and traum a predispose to developm ent.

Pa ge 3 4 4



Chronic paronychia: occupations with persistent m oist hands; dish washers, bartenders; also increased in patients with peripheral vascular disease

Pediatric Considerations Frequently anaerobic m outh flora in children from nail biting

Physical Exam 

Begins as swelling, pain, and erythem a in the dorsolateral corner of the nail fold bulging out over the nail plate



Progresses to subcuticular abscess

Essential Workup 

History and physical exam with special attention to evaluating for concom itant infections such as felon or cellulitis



Assess tetanus status.

Tests Lab 

No specific tests are useful.



Cultures not routinely indicated

Imaging Soft tissue radiographs if foreign body is suspected; routine film s if osteom yelitis suspected

Differential Diagnosis 

Felon



Herpetic whitlow



Traum a or foreign body



Prim ary squam ous cell carcinom a



Metastatic carcinom a



Osteom yelitis

Pa ge 3 4 4

Treatment ED Treatment Acute Paronychia 

Early paronychia without purulence present m ay be m anaged with warm -water soaks four tim es a day with or without oral antibiotics.



Early superficial subcuticular abscess: o

Elevation of the eponychial fold by sliding the flat edge of a no. 11 blade (18-gauge needle or sm all clam ps m ay be used) gently between the proxim al nail fold and the nail plate near the point of m axim al tenderness

o

A digital nerve block or local anesthesia m ay be necessary.



Partial nail involvem ent: o

If the lesion extends beneath the nail, rem ove a longitudinal section of the nail.

o 

Vaseline or iodoform gauze packing for 24 hours

Runaround abscess: o

If the lesion extends beneath the base of the nail to the other side, rem ove one quarter to one third of the proxim al nail with two sm all incisions at the dorsolateral edges of the nail fold and pack eponychial fold with petroleum or iodoform gauze to prevent adherence.

P.801



Extensive subungual abscess:

Pa ge 3 4 4

o 

Rem ove entire nail.

Early paronychia without purulence present m ay be m anaged with warm soaks alone, but beyond that, antibiotics are recom m ended if there is any apparent cellulitis, abscess, or system ic signs of infection.



Cephalexin, dicloxacillin, and am oxicillin-clavulanate are appropriate first-line agents, with treatm ent regim ens ranging from 5â€“10 days, depending on severity.



Clindam ycin, erythrom ycin, or am oxicillin-clavulanate if associated with nail biting or oral contact or allergy

Chronic Paronychia 

Avoidance of predisposing exposures



Eponychial m arsupialization involving rem oval of a crescentic piece of skin just proxim al to the nail fold including all thickened tissue down to, but not including, germ inal m atrix: o

Topical steroids with a topical antifungal agent have been used with success.

o

Antistaphylococcal treatm ent should also be adm inistered.

o

Oral antifungal therapy is rarely necessary.

Medication (Drugs) 

Am oxicillin-clavulanate: 875 m g PO b.i.d. for 7 days (peds: 25 m g/kg/d PO q12h)



Cephalexin: 500 g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO q6h)



Clindam ycin: 300 m g PO q.i.d. for 7 days (peds: 20â€“40 m g/kg/d div. q6h PO, IV, IM)



Dicloxacillin: 500 m g PO q.i.d. for 7 days (peds: 12.5â€“50

Pa ge 3 4 4

m g/kg/d PO q6h) 

Erythrom ycin: 500 m g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO q6h)

Follow-Up Disposition Admission Criteria Adm ission is not needed for paronychia alone.

Discharge Criteria 

Patients with uncom plicated paronychias m ay be discharged with appropriate follow-up instructions.



Patients with packings should be re-evaluated in 24 hours.

Issues for Referral Chronic paronychias refractory to treatm ent

References 1. Canales FL, Newm eyer WL, Kilgore ES. The treatm ent of felons and paronychias. Hand Clin. 1989;5(4):515â€“523. 2. Hochm an LG. Paronychia: m ore than just an abscess. Int J Derm atol. 1995;34(6):385â€“386. 3. Jebson PJ. Infections of the fingertip. Paronychias and felons. Hand Clin. 1998;14:547â€“55, viii. 4. Moran GJ, Talan DA. Hand infections. Em erg Med Clin. 1993;11(3):601â€“619. 5. Rockwell PG. Acute and chronic paronychia. Am Fam Physician. 2001;63(6):1113â€“1116.

Codes ICD10

Pa ge 3 4 4

L03.0

Pa ge 3 4 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Patellar Injuries

Patellar Injuries

Francis L. Counselman

Basics Description Dislocation 

Usually caused by sudden flexion and external rotation of tibia on fem ur, with sim ultaneous contraction of quadriceps m uscles



Lateral dislocation of patella m ost com m on, with patella displaced over the lateral fem oral condyle



Uncom m on dislocations include superior, m edial, and rare intraarticular dislocation.



Direct traum a to patella

Fracture 

Direct traum a: o

Most com m on m echanism of injury

o

Secondary to direct blow or fall on patella

o

Usually results in com m inuted or m inim ally displaced fracture



Indirect forces: o

Avulsion injury secondary to contraction of the quadriceps tendon

Pa ge 3 4 5

o

Usually results in transverse or displaced fracture (often both)



Types of patellar fractures: o

Transverse: 50â€“80% (usually m iddle or lower third of patella)

o

Com m inuted (or stellate): 30â€“35%

o

Longitudinal: 25%

o

Osteochondral

Patellar Tendon Rupture 

Usually caused by forceful eccentric contraction on a flexed knee (e.g., jum p landing and weight lifting)



Often occurs in m iddle-aged athlete

Patellar Tendinitis Overuse syndrom e from repeated acceleration, deceleration, jum ping, landing

Etiology Dislocation 

Risk factors for patellar dislocation: o

Genu valgum (knock-knee)

o

Genu recurvatum (hyperextension of knee)

o

Shallow lateral fem oral condyle

o

Deficient vastus m edialis

o

Lateral insertion of patellar tendon

o

Shallow patellar groove

o

Patella alta (high-riding patella)

o

Deform ed patella

o

Pes planus (flatfoot)



Com m on injury in adolescents, especially girls



The younger the patient at tim e of initial dislocation, the greater the risk of recurrent dislocation.

Pa ge 3 4 5

Fracture 

Direct traum a



Indirect forces caused by forcible quadriceps tendon contraction



Male-to-fem ale ratio of 2:1



Highest incidence in 20- to 50-year-old age group

Patellar Tendon Rupture 

Peak incidence in third and fourth decades: o



Often athletically active individual

Risk factors: o

History of patellar tendinitis

o

History of diabetes m ellitus, previous steroid injections, rheum atoid arthritis, gout, system ic lupus erythem atosus

o

Previous m ajor knee surgery

Patellar Tendinitis 

Microtears of tendon m atrix from overuse



Seen in high jum pers, volleyball and basketball players, and runners

Diagnosis Signs and Symptoms Dislocation 

History of feeling knee â€œgo outâ€•; popping, ripping, or tearing sensation



Pain



Inability to bear weight



Obvious lateral deform ity of patella

Pa ge 3 4 5



Mild to m oderate swelling



Often reduced spontaneously before ED evaluation



Tenderness along patella



Positive apprehension or Fairbanks sign: o

Attem pts to push the patella laterally elicit patient apprehension.

Fracture 

Pain over anterior knee



Difficulty am bulating



Increased pain with m ovem ent of patella



Tenderness and swelling over patella



Difficulty or inability to extend knee



Palpable defect, crepitus, or joint effusion/hem arthrosis

Patellar Tendon Rupture 

Abrupt onset of severe pain



Decreased ability to bear weight



Occasionally hem arthrosis



Proxim ally displaced patella



Incom plete extensor function



Unable to m aintain knee extension against force

Patellar Tendinitis 

â€œJum per's kneeâ€•



Pain in area of patellar tendon



Pain worse from sitting to standing or going up stairs



Point tenderness at distal aspect of patella or proxim al patellar tendon

Essential Workup 

Radiographs essential: o

Anteroposterior (AP) and lateral views of knee should be obtained.

Pa ge 3 4 5

o

Postreduction radiographs should include AP, lateral, and sunrise (or skyline, axial) views to exclude osteochondral fracture (in patellar dislocations).

o

Bipartite patella (patella with accessory bony fragm ent connected to m ain body by cartilage) m ay be m istaken for fracture; com parison view m ay help differentiate.



For patellar tendon rupture, a high-riding patella (i.e., patella located superior to level of intercondylar notch) observed



For patellar tendinitis, radiographic findings unlikely with sym ptom s of <6 m onthsâ€™ duration

Differential Diagnosis 

Patellar subluxation



Fem oral or tibial fracture



Traum atic bursitis



Quadriceps tendon rupture

P.803

Treatment Pre Hospital Patient should be transported in supine position with knee flexed and supported.

Initial Stabilization Appropriate history and physical exam to identify any associated injuries (e.g., fem oral fracture, hip fracture, posterior hip dislocation) and to assess extensor m echanism

Pa ge 3 4 5

ED Treatment Dislocation 

For sim ple lateral patellar dislocation, reduce dislocation by extending the knee gently to 180Â°: o

Occasionally m ay need to apply sim ultaneous pressure over lateral aspect of patella in m edial direction



For other types of patellar dislocation (superior, m edial, intraarticular), do not attem pt reduction; obtain orthopedic consultation.



Aspiration of joint with sterile technique is necessary if reduction is difficult secondary to hem arthrosis.



If osteochondral fracture is present (28â€“50% of cases), obtain orthopedic consultation.



Although reduction is typically easy to accom plish, procedural sedation or parenteral analgesia m ay facilitate.

Fracture 

Orthopedic consultation when patellar fracture is confirm ed



Initial treatm ent often consists of long-leg bulky splint and subsequent operative repair.

Patellar Tendon Rupture 

Orthopedic consultation, with surgical repair within 2â€“6 weeks

Medication (Drugs) 

Fentanyl citrate: 1â€“2 Âµg/kg (peds: 0.5â€“1.0 Âµg/kg) IV



Midazolam HCL: 1â€“3 m g (peds: 0.05â€“0.1 m g/kg, m ax.

Pa ge 3 4 5

dose 2.5 m g) IV 

Morphine sulfate: 2â€“5 m g per dose (peds: 0.1â€“0.2 m g/kg per dose) IV



Meperidine: 50â€“150 m g (peds: 0.5â€“0.8 m g/lb) IM



Toradol: 60 m g IM; 30 m g IV (peds: 0.5â€“1 m g/kg IV, m ax. 15 m g dose if <50 kg; m ax. 30 m g dose if >50 kg, IV)

Follow-Up Disposition Admission Criteria 

Patients with superior, m edial, or intraarticular dislocation or inability to reduce lateral dislocation require orthopedic consultation in ED and possible adm ission.



Patellar dislocation associated with a fracture (osteochondral or lateral fem oral condyle) requires orthopedic consultation in ED.



Operative intervention indicated if fragm ents are displaced >4 m m , if patient unable to raise extended leg off bed, or if articular step-off >3 m m .



All open fractures require dÃ©bridem ent and irrigation and should be adm itted.



For patellar tendon rupture, discuss case with orthopedics.

Discharge Criteria 

Patients with successful reduction of lateral patellar dislocation and norm al postreduction radiographs m ay be discharged with knee im m obilization, crutches, and orthopedic follow-up.



Fracture is displaced <3 m m and patient has full active

Pa ge 3 4 5

knee extension: o

Knee im m obilizer, or bulky long-leg splint, partial to full weight bearing as tolerated with crutches, and orthopedic follow-up within a few days



For patellar tendonitis: rest, avoid inciting activity, heat, and nonsteroidal anti-inflam m atory drugs (NSAIDs)

References 1. Atkin DM, Fithian DC, Marangi KS, et al. Characteristics of patients with prim ary acute lateral patellar dislocation and their recovery within the first 6 m onths of injury. Am J Sports Med. 2000;28:472â€“479. 2. Cash JD, Hughston JC. Treatm ent of acute patellar dislocation. Am J Sports Med. 1988;16:244â€“249. 3. Enad JG. Patellar tendon ruptures. South Med J. 1999;92:563â€“566. 4. Sim on RR, Koenigsknecht SJ. Em ergency Orthopedics the Extrem ities. 4th ed. New York: McGraw-Hill; 2001.

Codes ICD9-CM 836.3 822.0

ICD10 S89.9

Pa ge 3 4 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Patent Ductus Arterio sus

Patent Ductus

Arteriosus Steven Lelyveld

Basics Description 

Patent vessel in the fetal heart connects the pulm onary trunk to the descending aorta.



Shortly after birth, changes norm ally provoke contraction, closure, and fibrosis.



Sudden increase in the partial pressure of oxygen



Changes in the synthesis and m etabolism of vasoactive eicosanoids

In the preterm infant, persistent patency of the ductus m ay be a norm al lifesaving response. 

The patent ductus usually has a norm al structural anatom y.



Patency results from hypoxia and im m aturity

In the full-term newborn, patency of the ductus is a congenital m alform ation. 

Deficiency of both the m ucoid endothelial layer and the m uscular m edia of the ductus



As pulm onary vascular resistance falls, aortic blood is

Pa ge 3 4 5

shunted into the pulm onary artery. 

Extent of the shunt reflects the size of the ductus and the ratio of the pulm onary to system ic vascular resistances.

Up to 70% of the left ventricular output m ay be shunted through the ductus to the pulm onarycirculation. Risk factors: 

Prem ature birth



Coexisting cardiac anom alies



Conditions resulting in hypoxia



High altitude



Maternal rubella infection



Fem ale-to-m ale ratio, 3:1

Etiology 

Prem aturity



Congenital anom aly



Hypoxia



Prostaglandins

Diagnosis Signs and Symptoms History 

Isolated patent ductus arteriosus, an unanticipated event



Patent ductus arteriosus, as part of a larger congenital cardiac anom aly, m ay be diagnosed by ultrasound during pregnancy.

Physical Exam 

Asym ptom atic when the patent ductus arteriosus is sm all



Congestive heart failure (CHF)



Wide pulse pressure



Prom inent apical im pulse

Pa ge 3 4 5



Thrill



Maxim al in the second left intercostal space



Radiates toward the left clavicle, down the left sternal border, or toward the apex



Systolic and continuous



Continuous m urm ur



Hum m ing top or rolling thunder



Begins soon after onset of the first sound, reaches m axim al intensity at the end of systole, and wanes in late diastole



Localized to the second left intercostal space or radiates down the left sternal border or to the left clavicle



Recurrent pulm onary infections



Retardation of physical growth

Essential Workup 

Establish the diagnosis with im aging studies.



Rule out com plications such as heart failure and endocarditis.

Tests Lab Unhelpful in m aking the diagnosis

Imaging 

Chest radiograph: o

Usually norm al in infants

o

In children and adults: 

Increased intrapulm onary m arkings



Calcifications



Left ventricle and left atrial enlargem ent



Dilated ascending aorta



Dilated pulm onary arteries

Pa ge 3 4 6



EKG: o

Abnorm al if the ductus is large 

Left ventricular hypertrophy



Right ventricular hypertrophy is a sign of severity.



Echocardiography: o

Norm al if the ductus is sm all

o

Left atrial enlargem ent

o

Size of the ductus can be determ ined by scanning from the suprasternal notch.

o

Doppler studies will determ ine aortic to pulm onary artery flow during diastole.



Cardiac catheterization: o

Norm al or increased right-sided pressure

o

Oxygenated blood in the pulm onary artery confirm s left-to-right shunting.

o

Injection of contrast into the ascending aorta shows opacification of the pulm onary arteries.

P.805

Differential Diagnosis 

Venous hum : o

Com m on insignificant bruit

o

Heard in the neck or anterior portion of the chest

o

Soft hum m ing sound in systole and diastole

o

Decreased by light com pression of the jugular venous system



Total anom alous pulm onary venous connection to the innom inate vein: o



Continuous m urm urlike venous hum

Aorticopulm onary septal defect:

Pa ge 3 4 6

o

Murm ur is often only systolic.

o

Heard at the right sternal border



Ruptured sinus of Valsalva



Coronary arteriovenous fistulas



Anom alous origin of left coronary artery from the pulm onary artery



Absence or atresia of pulm onary valve



Aortic insufficiency with ventricular septal defect



Peripheral pulm onary stenosis



Truncus arteriosus

Treatment Alert Supplem ental oxygen if CHF

Initial Stabilization 

Sm all, asym ptom atic shunts m ay not need closure.



Pulm onary support



Supplem ental oxygen

ED Treatment 

Sodium and fluid restriction



Correction of anem ia to hem atocrit >45%



Antibiotic prophylaxis for endocarditis



Preterm infants: o

Usually closes spontaneously

o

Varies with the m agnitude of shunting and severity of respiratory distress syndrom e

o

Pharm acologic inhibition of prostaglandin synthesis with indom ethacin during the first 2â€“7 days of life



Full-term infants and children:

Pa ge 3 4 6

o

Surgical closure is required, even in asym ptom atic patients, as spontaneous closure is rare

o

Ligation and division

o

Transfem oral catheter technique to occlude PDA with foam plastic plug or double um brella

Medication (Drugs) Indom ethacin: 0.2â€“0.25 m g/kg per dose; repeat q12hâ€“q24h for 3 doses

Follow-Up Disposition Admission Criteria 

Heart failure



Endocarditis



Pulm onary hypertension

Discharge Criteria 

Asym ptom atic



Prophylactic antibiotics



Close follow-up with plans for early surgical closure

Issues for Referral A pediatric cardiologist/neonatologist should be involved in all patients who have any evidence of heart failure, particularly if pharm acologic m anagem ent is being considered.

References 1. Bernstein D. The cardiovascular system . In: Behrm an RE, Kliegm an RM, eds. Nelson's Textbook of Pediatrics. 17th ed.

Pa ge 3 4 6

Philadelphia: WB Saunders; 2004:1510â€“1512. 2. Friedm an WF, Silverm an S. Congenital heart disease in infancy and childhood. In: Braunwald E, ed. Heart Disease. 6th ed. Philadelphia: WB Saunders; 2001:1533â€“1535. 3. Moore P, Brook MM, Heym ann MA. Patent ductus arteriosus. In: Allen HD, et al., eds. Moss and Adam sâ€™ Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adult. 6th ed. Philadelphia: Lippincott William s & Wilkins; 2001:652â€“669. 4. Park MK, Troxler RG. Pediatric Cardiology for Practioners. 4th ed. St. Louis, MO: Mosby; 2002: 141â€“144. 5. Young KD. Congenital heart disease. In: Strange GR, et al., eds. Pediatric Em ergency Medicine: A Com prehensive Study Guide. 2nd ed. New York: McGraw-Hill; 2002:235â€“245.

Codes ICD9-CM 747.0

ICD10 Q25.0

Pa ge 3 4 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pediatric Traum a

Pediatric Trauma

Grace Kim Lance Brown

Basics Description 

Pathophysiology and anatom y of adolescents and young adults are sim ilar.



Eighty percent of pediatric traum a is blunt; 80% of m ultisystem traum a includes head injury.



Traum a is the leading cause of death in children younger than 8 m onths of age in the United States.



Twenty-eight percent of traum a victim s younger than 3 m onths of age have been abused or neglected.

Etiology 

Most cases of pediatric traum a are single-system , m inor, blunt injuries.



Com m on m echanism s of injury include m otor vehicle accidents and falls.



Penetrating injuries are rare in younger children.



Risk factors include inadequate supervision, developm ental inadequacy of child to perform task, inadequate attention to task, showing off, risk taking, drugs, and alcohol.

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Diagnosis Signs and Symptoms History 

History is often straightforward and provided by the child, parents, witnesses, or param edics. If inconsistent with injury, consider child abuse.



Mechanism (s) of injury is relatively poor predictor of injury severity, but m ay suggest type of injury.



Variables that increase the likelihood of serious injuries include handlebar injuries, significant passenger space intrusion, and failure to use a car seat or seat belt during a m otor vehicle accident.



AMPLE history includes allergies, m edications, past m edical history, tim e of last m eal, and events leading up to injury.

Physical Exam 

Prim ary survey: o

For children who have altered m ental status, a traditional stepwise ABCDE evaluation based on assessing the airway, breathing, circulation, d isability, and exposure is appropriate.



Secondary survey: o

General: 

Mass-to-surface ratio m ay im pact insensible water loss and increase the risk of hypotherm ia.



Com pensatory m echanism s m ay delay signs of hypovolem ia. Few findings m ay be present until loss of 25â€“20% of blood volum e, at which

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tim e decom pensation abruptly occurs.  o

Sm aller total blood volum e (80 m L/kg)

Head: 

Note bulging fontanel, scalp hem atom as, m idface instability, auricular and septal hem atom as, lacerations, functional or cosm etic deform ities to the face, and pupillary abnorm alities.



Open sutures/fontanelles m ay delay the onset of other signs and sym ptom s of increased intracranial pressure (ICP).



Large head/occiput causes cervical spine flexion when patient is supine on adult backboard.

o

Eye/ENT (ears, nose, and throat) exam ination: 

Look for evidence blood, traum a, hem otym panum , hyphem a, and so on.



Large tongue and tonsillar hypertrophy m ay obstruct the airway.

o

Neck: 

Tracheal deviation and posterior neck step-offs are exceedingly unusual in children.



Shorter trachea increases risk of right m ainstem intubation.



Cricoid cartilage is narrowest portion of airway in children younger than 8 years of age.



Children with altered m ental status cannot have their cervical spine precautions cleared in the em ergency departm ent. These children should rem ain in a cervical collar (and be taken off the spinal board) while in the em ergency departm ent.



Pseudosubluxation (anterior displacem ent of C-2

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on C-3) occurs in 20% of patients. 

The term spinal cord injury without radiologic abnorm ality (SCIWORA) is controversial in the MRI era.

o

Chest: 

Note the overall work of breathing, grunting, asym m etric breath sounds, posterior abrasions, chest wall deform ities, and crepitus.



Flexible and com pliant chest walls m ake pulm onary contusions m ore likely than rib fractures in young children.

 o

o

Diaphragm atic breathing

Abdom en: 

Bruising, abrasions, and tenderness



Distention is usually caused by gastric air.



Liver and spleen relatively large



Rib cage covers less of abdom en.



Bladder is intra-abdom inal in children <2 years.

Extrem ities: 

Palpation and evaluation of jointsâ€™ stability and tenderness

o

o



Assess pulses and com partm ents.



Salter-Harris classification



Unique injuries: greenstick and buckle fractures

Neurological exam : 

Age-appropriate m ental status assessm ent



Assess m ovem ent of the extrem ities.

Skin: 

Assess for prolonged capillary refill and pallor.



Bruising of the ears, dorsa of the feet, or genitalia m ay suggest nonaccidental traum a.

o

Patterns of Injury:

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

Car versus pedestrian: Waddell triad (fem ur, torso, and head injuries)â€”uncom m on



Bicycle handlebar injuries m ay im pale child: pancreatic or sm all bowel injury.



Lap belt syndrom e: abdom inal ecchym oses and intestinal injury with or without lum bar spine fracture



Minor history with m ajor injury: child abuse

Essential Workup 

History and age-appropriate physical exam ination are the only essential com ponents to a workup for all children who present for an evaluation following traum a.



Standard radiographic and laboratory â€œtraum a panelsâ€ • are not evidence based.

Tests Lab 

Laboratory tests should generally be individualized, reflecting the patient's clinical presentation.



A fall in hem atocrit of >5% has a sensitivity of 5% for identifying intra-abdom inal injuries.



An initial hem atocrit of <30% has a sensitivity of 5% for identifying intra-abdom inal injuries.



Am ylase and lipase have reasonable test characteristics, but because of the low incidence of pancreatic injuries, the false-positive tests far outnum ber the true positives.



Aspartate am inotransferase (AST) and alanine am inotransferase (ALT) cannot be used as the sole determ inant in deciding which children should undergo com puted tom ographic (CT) scanning of the abdom en and pelvis.



Gross hem aturia is predictive of urinary tract injuries, but

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m icroscopic hem aturia is not. 

Blood bank specim en for typing, as appropriate



A pregnancy test indicated for teen fem ales who m ay be pregnant



Diagnostic peritoneal lavage (DPL) is rarely indicated with availability of im aging m odalities.

P.807

Imaging 

The traditional â€œc-spine, chest, pelvisâ€• set of radiographs is no longer universally accepted; selective approach m ay be m ore appropriate.



Forgo cervical spine radiographs in children who are awake, alert, cooperative, without neck pain, have no tenderness on palpation of the neck, are without pain on range of m otion testing, and are without distracting injury: o

An unconscious child will not be able to have his or her cervical spine cleared in the em ergency departm ent and often undergoes m agnetic resonance im aging (MRI) (less often CT scanning) as an inpatient.



Chest radiographs indicated for grunting respirations, hypoxia, asym m etric breath sounds, dyspnea, endotracheally intubation, and thoracostom y tube or central venous catheter placem ent in the internal jugular or subclavian veins



Pelvic radiographs are seldom indicated. Children with clinically significant pelvic pain typically undergo CT scanning of the abdom en and pelvis.



CT scanning of the head is indicated for abnorm al m ental status, prolonged loss of consciousness, persistent

Pa ge 3 4 7

headache, bulging fontanel, tem poral or parietal scalp hem atom a, and uncontrollable vom iting. 

CT scanning of the abdom en and pelvis typically indicated for children with altered m ental status, gross hem aturia, abdom inal bruising above the ileac crests, handlebar injuries, and abdom inal tenderness



Ultrasound has lim ited utility as the presence of free fluid (i.e., blood) does not indicate the need for laparotom y. The usefulness of the focused abdom inal sonography for traum a (FAST) exam ination in young children needs further study.

Differential Diagnosis Nonaccidental traum a should be considered when the history is inconsistent with the diagnosis.

Treatment Pre Hospital 

Rapid transport to a facility capable of m anaging the child's suspected injuries



Priorities include stabilization of airway (intubation by param edics in the prehospital setting is controversial), breathing, circulation.



Im m obilization of cervical spine and extrem ity fractures

Initial Stabilization 

Most traum atized children are stable throughout their em ergency departm ent course.



Stabilization m ay require: o

Aggressive fluid resuscitation with norm al saline, large-bore IVs; tachycardia m ay be only sign of fluid

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loss early in presentation. o

Laboratories and radiographs as indicated

o

Adm inistration of packed red blood cells

o

Endotracheal intubation: 

Tube size based on age in years or length-based tape



(16+ age in years) divided by 4



Initial estim ate of the depth of insertion is three tim es the size of endotracheal tube (ETT).



Must check placem ent by auscultation, chest rise, pulse oxim etry, and end tidal CO 2 , then chest radiograph

o

Cervical spine im m obilization using appropriately sized collar

o

Thoracostom y tube

o

Urinary catheter (look for blood at the m eatus)

o

Cardiorespiratory and pulse oxim etry m onitoring and oxygen adm inistration

o

Gastric decom pression with a nasogastric or orogastric tube

ED Treatment 

Risk stratify based on history and physical exam ination.



Acknowledge the lim itations of using the m echanism of injury to predict the severity of injuries.



Assess priorities; reassess frequently.



Provide analgesia; sedate as appropriate.



Clean wounds and splint fractures.



Tetanus im m unization if indicated



Allow parents at the bedside.

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Medication (Drugs) 

Norm al saline/lactated Ringer: 20 m L/kg boluses IV



Packed red blood cells: 10 m L/kg units IV



Etom idate: 0.3 m g/kg IV



Morphine sulfate: 0.1 m g/kg IV



Succinylcholine: 1.5 m g/kg IV



Lorazepam : 0.1 m g/kg IV



Propofol: 2 m g/kg IV



Ketam ine: 2 m g/kg IV (generally thought to raise intraocular and intracranial pressureâ€”usually avoided when head injury is suspected)

Follow-Up Disposition Admission Criteria 

Persistent altered m ental status, endotracheal intubation, thoracostom y tube placem ent, intra-abdom inal or intracranial injury identified on CT scanning, pulm onary contusion, fractures requiring operative m anagem ent, nonaccidental traum a



Hem odynam ic instability



Airway concerns



CT scan negative for intra-abdom inal injury, but persistent abdom inal pain as pancreatic or bowel injury is possible



Failure to identify an appropriate adult to be responsible for the child (e.g., both parents are adm itted to the hospital for their injuries)

Discharge Criteria

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

Most traum atized children with norm al m ental status and norm al radiographic tests (if obtained) can be discharged hom e to a reliable care giver.



Posttraum atic stress syndrom e m ay develop, and parents should be advised to seek appropriate counseling should concerns develop.

References 1. Davis DH, Localio AR, Stafford PW, et al. Trends in operative m anagem ent of pediatric splenic injury in a regional traum a system . Pediatrics. 2005;115:89â€“94. 2. Dowd MD, McAneney C, Lacher M, et al. Maxim izing the sensitivity and specificity of pediatric traum a team activation criteria. Acad Em erg Med. 2000;7:1119â€“1125. 3. Erez I, Lazar L, Guterm acher M, et al. Abdom inal injuries caused by bicycle handlebars. Eur J Surg. 2001;167:331â€“333. 4. Lee SL, Sena M, Greenholz SK, et al. A m ultidisciplinary approach to the developm ent of a cervical spine clearance protocol: process, rationale, and initial results. J Pediatr Surg. 2003;38:358â€“362. 5. Spady DW, Saunders DL, Schopflocher DP, et al. Patterns of injury in children: a population based approach. Pediatrics. 2004;113:522â€“529. 6. Vo NJ, Gash J, Browning J, et al. Pelvic im aging in the stable traum a patient: is the AP pelvic radiograph necessary when abdom inopelvic CT shows no acute injury? Em erg Rad. 2004;10:246â€“249.

Miscellaneous SEE ALSO: Abuse, Pediatric; Fractures, Pediatric; Traum a, Multiple

Codes

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ICD9-CM 850.0 Concussion without loss of consciousness 864.0 Injury to the liver, without m ention of open wound into cavity 865.0 Injury to spleen, without m ention of open wound into cavity 866.0 Injury to kidney, without m ention of open wound into cavity 869.0 Internal injury to unspecified or ill defined organs

Pa ge 3 4 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pediculo sis

Pediculosis

Danielle J. Douglas

Basics Etiology 

Infestation by Pediculus capitis (head louse), Pediculus corporis (body louse), or Pthirus pubis (pubic louse)



Bites are painless.



Signs and sym ptom s result from host response to saliva and anticoagulant injected during feeding.



Transm itted by direct contact and fom ites; pubic lice are transm itted by sexual contact, use of contam inated objects like com bs, clothing, bed linen, hats.



Obligate hum an parasites cannot survive away from hosts m ore than 7â€“10 days.

Diagnosis Signs and Symptoms 

Head lice: o

Scalp and posterior neck erythem a, scaling, and excoriated papules

o

Nits (egg casings) attached to hair shafts

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o

Excoriations m ay lead to pyoderm a, posterior cervical lym phadenopathy, and febrile episodes.





o

Most often found in postauricular and occipital areas

o

Not an indicator of poor hygiene

Body lice: o

Linear excoriations of neck and trunk

o

Pus or serum stains on clothing

o

Nits found in seam s of clothing

o

Often an indicator of poor hygiene

Pubic lice: o

Intense pruritus, particularly at night

o

Occasional urticaria with typical flare/wheal form ation

o

May infest eyelashes and scalp in children

o

Characteristic bluish m acules (m aculae caeruleae) appear infrequently on trunk and thighs.

o

Prefer the perineum and pubic areas

o

Inguinal adenopathy

Physical Exam 

Exam ine hair for adult lice and nits.



Nits are cem ented on hair shafts and are not easily rem oved.



Head lice and pubic lice infestation is confirm ed by differentiating nits from scales, hair casts, and other easily brushed-off artifacts.



Em pty nits are not diagnostic of active infection.



Body lice are observed only in very heavy infestation; infestation is confirm ed by finding nits in clothing seam s.

Tests Lab 

Nits m ay be visualized under low-power m icroscopy along

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hair shafts. They are <1 m m long: o

Fluorescent under Wood lam p



Mature lice are 3â€“4 m m long.



Pubic louse about 1 m m long but wider body than head or body louse

Differential Diagnosis 

Scabies



Contact or allergic derm atitis



Seborrheic derm atitis

Treatment Pre Hospital Cautions: 

Maintain universal precautions.

Initial Stabilization Not applicable for routine cases

ED Treatment 

Head lice: o

Topical pediculicidal agents: Perm ethrin 1% cream rinse (Nix) is the best first-line agent; it has low toxicity and is ovicidal; pyrethrin (Rid) also has low toxicity, but is less effective; lindane sham poo is effective, but m ay cause CNS toxicity and seizures if applied incorrectly or overused.

o

All agents require reapplication in 7â€“10 days if further adult lice or nits noted.

o

Rem ove nits with fine-toothed com b.

o

Exam ine all m em bers of household; treat infested

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individuals. o

Change clothing and m achine wash and dry (using hot cycles) all clothing, towels, linens, and headgear. 

Vacuum floors and furniture.



Wash com bs and brushes in hot water for 10â€“20 m inutes or coat with pediculicide for 15 m inutes and wash.

o

Tem perature >131Â°F (55Â°C) for >5 m inutes kills eggs, nym phs, and m ature lice.



Pubic lice: o

Topical pediculicide applied to hairy areas of chest, axilla, and groin

o

Rem ove nits with fine-toothed com b. P.809

o

Treat sexual contacts sim ultaneously.

o

Wash and dry bedding and clothing using hot cycles.

o

Treat eyelash involvem ent with topical petrolatum twice daily for 9 days.



Body lice: o

Wash and dry bedding and clothing using hot cycles.

o

Apply topical pediculicide cream or lotions from chin to toes.

o

Oral antihistam ines and topical steroids m ay help pruritic sym ptom s of all lice infestations.

Medication (Drugs) 

Antipruritics: o

Cetirizine (Zyrtec): age older than 12 years, 5â€“10 m g PO (peds: ages 6â€“11 years, 5â€“10 m g PO;

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ages 2â€“5 years, 2.5 m g PO) daily o

Diphenhydram ine (Benadryl): 25â€“50 m g PO (peds: 5 m g/kg/d) q6h

o

Hydroxyzine (Atarax): 25 m g PO q8h (peds: 12.5 m g per dose q6h)



Pediculicides: o

Lindane (Î³-benzene hexachloride) 1% sham poo: lather for 4 m inutes, then rinse; third-line agent after Perm ethrin or Rid given side effects. 

Lotion: apply chin to toes, wash off after 8 hours; avoid use in children, lactation, pregnancy, or seizure disorder.

o

Perm ethrin 1% cream rinse (Nix): apply to scalp and hair, rinse after 10 m inutes; reapply in 7â€“10 days if needed.

o

Pyrethrin/piperonyl butoxide (Rid): apply to scalp and hair, wash after 10 m inutes; repeat in 7â€“10 days; avoid in patients with ragweed allergies.

o

Mercuric oxide ophthalm ic ointm ent 1%: use for louse infestation of eyelids: apply q.i.d. for 14 days.

o

Trim ethoprim -sulfam ethoxazole: 8 m g/kg/d of TMP in divided doses is effective for head lice in patients who have previously failed treatm ent.

Follow-Up Disposition Admission Criteria Extensive bacterial superinfection; system ic hypersensitivity reaction with cardiorespiratory com prom ise

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Discharge Criteria 

Mild to m oderate infestation with absence of significant superinfection or hypersensitivity reaction



Children m ay return to school after initial treatm ent if repeat therapy is adm inistered in 7â€“10 days.



Pubic lice are often associated with sexually transm itted diseases; prudent screening is recom m ended. Pubic lice m ay also indicate sexual abuse in children.

References 1. Angel TA, Nigro J, Levy ML. Infestations in the pediatric patient. Pediatr Clin North Am . 2000;47(4):921â€“935, viii. 2. Chosidow O. Scabies and pediculosis. Lancet. 2000;355:819â€“826. 3. Elston DM. Controversies concerning the treatm ent of lice and scabies. J Am Acad Derm atol. 2002;46(5):794â€“796. 4. Potts J. Eradication of ectoparasites in children. How to treat infestations of lice, scabies, and chiggers. Postgrad Med. 2001;110(1):57â€“59, 63â€“64. 5. Roberts RJ. Head lice. N Engl J Med. 2002;346:1645.

Codes ICD9-CM 132.9

ICD10 B85.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pelvic F racture

Pelvic Fracture

Theodore C. Chan

Basics Description 

3% of all bony fractures



Pelvis is m ade up of sacrum and two innom inate bones: o

The innom inate bones consist of the ilium , ischium , and pubis.



Boney structures are stabilized by network of ligam ents, m usculature, and other soft tissues in the pelvic area.



Anterior stability and support are provided by the sym physis pubis and pubic ram i.



Posterior stability and support are provided by the sacroiliac com plex and pelvic floor.



Pelvis provides protection for lower urinary tract; gastrointestinal tract; gynecologic, vascular, and nervous structures contained in the region: o

Pelvic fractures have a high associated m ortality rate and require urgent diagnosis and therapy.

Etiology 

Sixty-five percent of pelvic fractures caused by vehicular traum a, including pedestrians struck by autom obiles



Ten percent caused by falls

Pa ge 3 4 8



Ten percent caused by crush injuries



The rem ainder caused by athletic, penetrating, or nontraum atic injuries





Mortality rate from pelvic fractures is 6â€“19%: o

Increases to 30% with open fractures

o

Increases to 50% with hem orrhagic shock

Significant pelvic hem orrhage can occur in unstable, high-energy pelvic fractures (Tile type B and C fractures): o

Bleeding m ost com m only from posterior injuries involving the venous plexuses

o

Retroperitoneal hem atom a that m ay tam ponade in the enclosed pelvic space

Tile Classification System 

Includes stable single bone and avulsion fractures as well as pelvic ring fractures



Predicts need for operative repair



Type A: stable pelvic ring injuries: o

A1: avulsion fractures of the innom inate bone (ischial tuberosity, iliac crest)

o

A2-1: iliac wing fractures

o

A2-2: isolated ram i fractures; m ost com m on pelvic fracture



o

A2-3: four-pillar anterior ring injuries

o

A3: transverse fractures of sacrum or coccyx

Type B: partially stable pelvic ring injury (rotationally unstable, but vertically stable): o

B1: unilateral open-book fracture

o

B2: lateral com pression injury 

B2-1: ipsilateral double ram i fractures and posterior injury



B2-2: contralateral double ram i fractures and posterior injury (bucket-handle fracture)

Pa ge 3 4 8

 

B2-3: bilateral type B injuries

Type C: unstable pelvic ring injuryâ€”rotationally and vertically unstable, Malgaigne fracture: o

Anterior disruption of sym physis pubis or two to four pubic ram i with posterior displacem ent and instability thru sacrum , SI joint, or ileum 

C1: unilateral vertical shear fracture



C2: unilateral vertical shear com bined with contralateral type B injury

 

C3: bilateral vertical shear fracture

Acetabular fractures (posterior lip, central/transverse, anterior colum n, or posterior colum n fractures)

Young Classification System 

Based on m echanism of injury



Only fractures that result in disruption of pelvic ring included; no single bone, avulsion, or acetabular fractures



Predicts chance of associated injuries and m ortality risk: o

LC: lateral com pression

o

APC: anteroposterior com pression

o

VS: vertical shear

o

CM: com bination of injury patterns

Pediatric Considerations 

Children can have proportionately greater hem orrhage.



Nonaccidental traum a is a concern.

Pregnancy Considerations Gravid uterus m ay be at risk for injury, including uterine rupture.

Diagnosis Signs and Symptoms

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

Localized pain, swelling, ecchym oses, tenderness over hips, groin, perineum , and lower back



Lower extrem ities m ay be shortened or rotated.



Pain on hip m ovem ent, am bulation, sitting, standing, defecation



Tenderness on lateral com pression of pelvis, palpation of sym physis pubis or sacroiliac (SI) joints



Often presents with other traum atic injuries including neurologic, intra-abdom inal, genitourinary, perineal, rectal, vaginal, and vascular injury



Gross pelvic instability, deform ity, asym m etry in lower extrem ity



Evidence of hem orrhagic shock



Inability to actively or passively perform range of m otion of involved hip

Essential Workup 

Pelvic radiograph is m ost valuable initial test.



A single AP view of the pelvis can confirm diagnosis in 90% of cases and should be obtained as early as possible when fracture suspected: o

Most significant unstable pelvic fractures will be seen on the single AP view.

o

Other views include: 

Inlet projection: 30-degree caudal view; allows visualization of posterior arch



Outlet projection: 30-degree cephalic angulation; allows visualization of sacrum



Judet oblique views: allow evaluation of acetabulum

Tests Lab

Pa ge 3 4 8



Type and cross-m atch.



Hem oglobin/hem atocrit, platelet count, and coagulation studies (PT/PTT)

Imaging 

CT scan m ay further delineate pelvic fracture(s), retroperitoneal hem atom a, visceral injuries.



MRI indicated with evidence of neurologic injury



Diagnostic peritoneal lavage (DPL) is a rapid bedside evaluation for intraperitoneal hem orrhage: o

In the setting of pelvic fracture, the supraum bilical open approach for DPL should be used.



Abdom inal ultrasound (US) m ay be used in place of DPL, but differentiation of intraperitoneal from extraperitoneal hem orrhage from pelvic fracture can be difficult.

Differential Diagnosis 

Norm al variants (i.e., os acetabuli epiphyseal line, can m im ic type I fracture on radiograph)



Ligam entous injury



Spinal injury



Intra-abdom inal injury and hem orrhage

P.811

Treatment Initial Stabilization Airway, breathing, and circulation (ABCs) of traum a care: 

Avoid using lower extrem ity IV sites.



Aggressive resuscitation with blood or crystalloid,

Pa ge 3 4 8

O-negative or type-specific blood if hem odynam ically unstable 

Im m obilize the pelvis to prevent further injury and decrease bleeding.



PASG: Use in ED is controversial, but allows rapid pelvic im m obilization and pelvic com pression to slow bleeding.



External fixator requires m ore tim e to place than PASG but â€œsplintsâ€• pelvis in a sim ilar m anner; contraindicated in severely com m inuted pelvic fracture.



Placem ent of a stabilization device should not interfere with further workup and care (e.g., US, DPL).

ED Treatment 

Determ ine which pelvic fractures are stable and which are unstable.



Type A fractures are generally stable.



Type B and C fractures are unstable.



Type A fractures: o

Treated conservatively with bed rest, analgesics, and com fort m easures; m anagem ent decisions m ay be m ade in conjunction with orthopedics.

o

For four-pillar anterior ring injuries, a CT scan should be obtained to evaluate the posterior pelvis.

o

Ensure that there are no other breaks in the pelvic ring.



Type B and C fractures: o

Im m ediate orthopedics consultation; patient should rem ain NPO.

o

May require ED pelvic stabilization m easures

o

Assess for pelvic hem orrhage (see Pelvic Hem orrhage).



Acetabular fractures: o

Im m ediate orthopedics consultation; patient should

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rem ain NPO. 

Pelvic hem orrhage: o

Mechanical stabilization of unstable pelvic fractures (usually by application of external pelvic fixation)



o

Angiography and selective vessel em bolization

o

Direct operative control of pelvic bleeding

Prioritization of studies: CT, angiography, or surgery: o

In the hem odynam ically unstable patient: 

Open B and C fractures: surgical exploration



Closed fractures: DPL or US can help determ ine m anagem ent in term s of need for surgical exploration or selective angiography.

o

In the hem odynam ically stable patient, the patient can go to CT scan for evaluation of the abdom en, pelvis, and retroperitoneum with external fixation as appropriate.

Medication (Drugs) 

Blood products: 4â€“6 U cross-m atched, type specific, or O negative (peds: 10 m L/kg)



Crystalloid fluids: 2-L IV bolus of norm al saline (NS) or lactated Ringer (peds: 20 m L/kg)

Follow-Up Disposition Admission Criteria 

Hem odynam ic instability, and pelvic hem orrhage to the ICU

Pa ge 3 4 8



Type B or C pelvic fracture



Acetabular fracture



Other related injuries (e.g., genitourinary, intra-abdom inal, neurologic)



Intractable pain

Discharge Criteria Type A pelvic fracture; hem odynam ically stable with no evidence of other injuries

References 1. Allen CF, Goslar PW, Barry M, et al. Managem ent guidelines for hypotensive pelvic fracture patients. Am Surg. 2000;66:735â€“738. 2. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons; 2004. 3. Coppola PT, Coppola M. Em ergency departm ent evaluation and treatm ent of pelvic fractures. Em erg Med Clin North Am . 2000;18(1):127. 4. Lashutka MK, Bahner D, Werm an H. Adult pelvic fractures. Traum a Rep. 2002;3:1â€“12.

Codes ICD9-CM 808.8

ICD10 S32.8

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pelvic Inflam m ato ry Disease

Pelvic

Inflammatory Disease Erich Salvacion

Basics Description 

Pelvic inflam m atory disease (PID) is an acute, com m unity-acquired, sexually transm itted infection of the upper genital tract, including the uterus, fallopian tubes, ovaries, or adjacent structures.



Most frequent gynecologic cause for ED visits (350,000 per year)



Represents a spectrum of infection: o

No single diagnostic gold standard

o

Requires low clinical threshold for considering the diagnosis and starting em piric antibiotic therapy



Progressive disease can lead to tubo-ovarian abscess (TOA)



Fitz-Hugh-Curtis syndrom e is a capsular inflam m ation of the liver associated with PID: o

Sharp right upper quadrant abdom inal pain

o

Worse with inspiration, m ovem ent, or coughing

Etiology

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



Risk factors: o

Age younger than 35 years

o

Multiple or sym ptom atic sexual partners

o

Previous episode of PID

o

Nonbarrier contraception

o

Oral contraception

o

African Am erican ethnicity

Most com m on causes of PID are Chlam ydia trachom atis and Neisseria gonorrhea.



Other organism s include groups A and B streptococci, staphylococci, gram -negative rods (com m only Klebsiella species, Escherichia coli, and Proteus species), and anaerobes.

Diagnosis Signs and Symptoms 

Lower abdom inal pain, usually bilateral



Vaginal discharge



Abnorm al uterine bleeding



Dysm enorrhea



Dysuria



Dyspareunia



Nausea and vom iting



Fever and chills



Proctitis



Lower abdom inal tenderness



Decreased bowel sounds



Bilateral adnexal tenderness



Cervical m otion tenderness



Purulent endocervical discharge

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

Adnexal m ass or fullness



Right upper quadrant tenderness

Essential Workup 

History and physical exam including pelvic exam ination



Pregnancy test to rule out ectopic pregnancy or com plications of an intrauterine pregnancy



Cervical culture for N. gonorrhea and C. trachom atis



Minim um criteria for clinical diagnosis:



o

Lower abdom inal tenderness or

o

Uterine/adnexal tenderness or

o

Cervical m otion tenderness

Supportive criteria for diagnosis: o

Fever >38.3Â°C (101Â°F)

o

Abnorm al cervical/vaginal discharge

o

Intracellular gram -negative diplococci on endocervical Gram stain

o

Leukocytosis >10,000/m m 3

o

Elevated erythrocyte sedim entation rate (ESR) or C-reactive protein

o

WBCs or bacteria in peritoneal fluid obtained by culdocentesis or laparoscopy

Tests Lab 

CBC



Gram stain of endocervix



Urine polym erase chain reaction (PCR)



Microscopic exam of vaginal discharge in saline



Liver enzym es m ay be elevated in Fitz-Hugh-Curtis syndrom e.



Positive urinalysis (UA) or occult blood in stool decrease the probability of PID.

Pa ge 3 4 9



ESR or C-reactive protein m ay be elevated, but not routinely recom m ended.

Imaging 

Patients with adnexal fullness or an adnexal m ass on exam should have im m ediate transvaginal ultrasound (US) to exclude a tubo-ovarian abscess.



Consider obtaining a pelvic US in patients who use an intrauterine device, fail outpatient antibiotic therapy for PID, or who have inadequate pelvic exam s due to pain or obesity.

Diagnostic Procedures/Surgery Laparoscopy m ay be useful in confirm ing PID in a patient with high suspicion of com peting diagnosis, or patients who have failed outpatient treatm ent for PID.

Differential Diagnosis 

Ectopic pregnancy (m ust be excluded with a pregnancy test in any wom an suspected of having PID)



Acute appendicitis



Adnexal torsion



Endom etriosis



Cystitis



Urolithiasis



Ovarian tum or



Adenom yosis uteri



Chronic pelvic pain



Benign ovarian cyst



Diverticulitis



Inflam m atory bowel disease



Mesenteric vascular disease



Irritable bowel syndrom e

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Treatment Pre Hospital 

No specific pre hospital considerations



Appropriate pain m anagem ent

Initial Stabilization 

Resuscitation rarely indicated



Pain control

ED Treatment 

Outpatient: o

Regim en A (for patients not sexually active): 

Ofloxacin or levofloxacin; with m etronidazole when anaerobes are a particular concern

o

Regim en B (for sexually active patients): 

Ceftriaxone or cefoxitin/probenecid plus doxycycline; with m etronidazole when anaerobes are a particular concern



Ceftriaxone or cefixim e plus azithrom ycin; single dose indicated for cervicitis only

o 

Must evaluate and treat sex partner as appropriate

Inpatient: o

Doxycycline plus cefoxitin or cefotetan

o

Alternatives include gentam icin plus clindam ycin; or m etronidazole plus levofloxacin or ofloxacin; or am picillin/sulbactam plus doxycycline.

o

Continue parenteral antibiotic adm inistration for 24 hours after clinical im provem ent, followed by oral doxycycline or clindam ycin for a total of 14 days.

o

TOAs m ay require drainage or surgical intervention in addition to antibiotics.

Pa ge 3 4 9

o

Laparoscopy can be used to lyse adhesions in the acute and chronic stages of Fitz-Hugh-Curtis syndrom e. 

Add m etronidazole when anaerobes are a particular concern.

P.813

Medication (Drugs) 

Am picillin/sulbactam : 3 g IV q6h



Azithrom ycin: 1 gPO single dose (cervicitis only)



Cefixim e: 400 m g PO single dose (cervicitis only)



Cefotetan: 2 g IV q12h



Cefoxitin: 2 g IM single dose (outpatient); 2 g IV q6h (inpatient)



Ceftriaxone: 250 m g IM single dose



Clindam ycin: 450 m g PO q.i.d. for 14 days (outpatient); 900 m g IV q8h (inpatient)



Doxycycline: 100 m g PO b.i.d. for 14 days (outpatient); 100 m g IV or PO q12h (inpatient)



Gentam icin: 2 m g/kg loading dose followed by 1.5 m g/kg IV q8h



Levofloxacin: 500 m g PO daily for 14 days (outpatient); 500 m g IV q24h (inpatient)



Metronidazole: 500 m g PO b.i.d. for 14 days (outpatient); 500 m g IV q8h (inpatient)



Ofloxacin: 400 m g PO b.i.d. for 14 days (outpatient); 400 m g IV q12h (inpatient)



Probenecid: 1 g PO single dose

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Follow-Up Disposition Admission Criteria 

Uncertain diagnosis and toxic appearance



Suspected pelvic abscess, including TOA



Pregnancy



Im m unodeficiency



Severe illness (e.g., vom iting or severe pain)



Failure of outpatient therapy



Probable noncom pliance with outpatient therapy (e.g., adolescents)



Consider adm ission if appropriate clinical follow-up cannot be arranged.

Discharge Criteria 

Patients who do not m eet adm ission criteria m ay be treated as outpatients.



Recent studies have shown that in wom en with m ild to m oderate PID, there was no difference in reproductive outcom es between wom en random ized to inpatient versus outpatient treatm ent.

References 1. Centers for Disease Control and Prevention. 2002 guidelines for treatm ent of sexually transm itted diseases. MMWR Morb Mortal Wkly Rep. 2002;51(RR-6):1. 2. Drugs for sexually transm itted infections. Treat Guidel Med Lett. 2004;2:67. 3. Grim es DA. Intrauterine device and upper-genital-tract infection. Lancet. 2000;356:1013.

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4. McCorm ack WM. Pelvic inflam m atory disease. N Engl J Med. 1994;330:115â€“119. 5. Ness RB, et al. Effectiveness of inpatient and outpatient treatm ent strategies for wom en with pelvic inflam m atory disease: results from the Pelvic inflam m atory disease Evaluation And Clinical Health (PEACH) random ized trial. Am J Obstet Gynecol. 2002;186(5):929â€“937. 6. Pastorek JG. Pelvic inflam m atory disease and tubo-ovarian abscess. Obstet Gynecol Clin North Am . 1989;16:347â€“361. 7. Peipert JF, Ness RB, Blum e J, et al. Clinical predictors of endom etritis in wom en with sym ptom s and signs of pelvic inflam m atory disease. Am J Obstet Gynecol. 2001;184:856. 8. Ross J. Pelvic inflam m atory disease. Br Med J. 2001;322:658â€“659.

Codes ICD9-CM 614.9

ICD10 N73.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pem phigus

Pemphigus

James T. Steen James T. Vandenberg Christopher S. Kang

Basics Description 

Autoantibody (IgG)-m ediated blistering disease of the skin and m ucous m em brane: o



Characterized by loss of cell-to-cell adhesion.

Acquired blistering diseases include those caused by drugs (e.g., toxic epiderm al necrolysis) and idiopathic (e.g., bullous diabeticorum ).



Pem phigoid: a term describing the group of syndrom es that cause a separation of the epiderm is from the derm is



If untreated, m ortality rates average >75% at 5 years.



Pem phigus is a rare disease with a worldwide incidence of 0.1â€“0.5 cases per 100,000.



Incidence equal for m ales and fem ales



Two m ajor subtypes exist: o

Vulgaris; m ore serious with deeper involvem ent: 

Affects m ost races in m iddle age and elderly Jewish patients

o

Foliaceus; m ilder and m ore superficial:

Pa ge 3 4 9



No preference for Jewish persons

o

Vulgaris accounts for 80% of all cases.

o

Seventy percent of patients with vulgaris present with oral lesions.

o

Superficial pem phigus (foliaceus) often lacks oral lesions and has better prognosis.



Pem phigus is m ost com m on in individuals 40â€“60 years old, but has been reported in people ranging from neonates to 89 years of age.

Pediatric Considerations 

Pem phigus is rare in children.



Neonates m ay develop the disease secondary to transplacental transfer of IgG.



Neonatal pem phigus spontaneously resolves in several weeks as the m aternal antibodies are catabolized.

Etiology/Genetics 

IgG autoantibodies are directed against pem phigus antigens found in all keratinocytes.



Autoantibodies cause acantholysis: o

Separation of the keratinocytes from each other and loss of cellâ€“cell adhesion

o 

Leads to blistering

Im m unogenetic predisposition secondary to higher frequencies of specific HLA haplotypes



Drugs m ay induce or trigger pem phigoid reactions: o

Penicillam ine, captopril, rifam pin, piroxicam , and phenobarbital



Pem phigoid reactions m ay occur in association with a neoplasm , usually lym phom a (paraneoplastic pem phigus).



Endem ic pem phigus foliaceus (fogo selvagem ) m ay be triggered or transm itted by bites from flying insects.

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Diagnosis Signs and Symptoms 

Generalized or focal flaccid bullae (blisters) of the skin and m ucosa



Painful skin erosions with shreds of detached epithelium



Painful nonhealing oral erosions



Crusting, partially healing skin erosions from ruptured bullae



Hypertrophic, hyperplastic erosive plaques with pustules in intertriginous areas (pem phigus vegetans)



Moist, edem atous, exfoliative erosions in seborrheic areas (pem phigus foliaceus)



Erythem atous, scaly, crusting skin lesions in a m alar distribution (pem phigus erythem atosus)

History 

Typically features m ucocutaneous blisters followed by erosions



Often appear first in m ucous m em branes and several m onths later appear cutaneously



Skin lesions are painful flaccid blisters that m ay appear anywhere.

Physical Exam Nikolsky sign (separation of the epiderm is with lateral pressure) is characteristic but not diagnostic.

Essential Workup 

Suspected based on clinical presentation



Biopsy with histologic and im m unofluorescence testing is essential for definitive diagnosis (arrange with a

Pa ge 3 5 0

derm atologist).

Tests Lab Serum antibody titers, detected by indirect im m unofluorescence, are often used as a m arker of disease activity; however, the ED physician usually does not order these titers.

Imaging No diagnostic im aging test exists.

Diagnostic Procedures/Surgery Biopsy

Differential Diagnosis 

Bullous pem phigoid



Derm atitis herpetiform is



Erythem a m ultiform e



Toxic epiderm al necrolysis



Epiderm olysis bullosa



Hand, foot, and m outh disease



System ic lupus erythem atosus



System ic vasculitis



Oral candidiasis



Herpes sim plex gingivostom atitis



Erosive lichen planus



Seborrheic derm atitis

P.815

Treatment

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Pre Hospital If severe disease, IV access, pulse oxim etry m onitor, and cardiac m onitor

Initial Stabilization 

If sym ptom s of hypotension or sepsis are present, IV fluid resuscitation should be guided by the Parkland burn form ula: o

4 m L of crystalloid/kg body weight per percentage of body surface area involved per 24 hours

o

Give half of the total calculated fluid over the course of the first 8 hours, the rem ainder over the next 16 hours.

o 

Adjust fluids to keep urine output >0.5 m L/kg/h

If signs or sym ptom s of sepsis are present, initiate broad-spectrum antibiotic coverage.



In steroid-dependent patients, adm inister stress-dose steroids.

ED Treatment 

System ic corticosteroids are the m ainstay of therapy.



Severe disease: conventional high-dose corticosteroids: o

If severe sym ptom s are unresponsive to high-dose PO corticosteroids, consider pulse IV corticosteroids and adm ission for plasm apheresis.



Mild to m oderate disease should receive PO prednisone, and intralesional triam cinolone acetonide m ay be used.



Adjuvant im m unosuppressive therapy m ay also be added to decrease the sym ptom s associated with high-dose system ic corticosteroids or in patients with contraindications to steroid therapy: o

Dapsone, gold, azathioprine, cyclophospham ide, cyclosporine, m ethotrexate, m ycophenolate, and IV

Pa ge 3 5 0

im m unoglobulins

Medication (Drugs) 

Hydrocortisone: 100â€“300 m g IV stress-dose steroids



Methylprednisolone (pulse IV therapy; adults): 1 g IV over 3 hours daily



Prednisone: 20â€“400 m g PO daily (adults); severe disease, 200â€“400 m g PO daily for 5â€“10 weeks, then taper; m ild to m oderate disease, 20â€“80 m g PO daily



Triam cinolone acetonide: 20 m g/m L 0.1-m L injection into each superficial lesion

Follow-Up Disposition Admission Criteria 

Adm it to the ICU or burn unit if any signs and sym ptom s of shock or sepsis are present, because aggressive fluid resuscitation, wound care, and m ultiple m edications will be required.



Adm it to a floor bed if pulse parenteral steroid therapy or plasm apheresis is indicated.



Adm it first-tim e presentations of disease to facilitate treatm ent and definitive diagnosis.

Discharge Criteria 

Discharge if m ild to m oderate disease will not require aggressive steroid m anagem ent or plasm apheresis.



A follow-up evaluation is essential to m onitor the course of the disease and to adjust treatm ent.

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References 1. Ahm ed AR. Intravenous im m unoglobulin therapy in the treatm ent of patients with pem phigus vulgaris unresponsive to conventional im m unosuppressive treatm ent. J Am Acad Derm atol. 2001;45(5):679â€“690. 2. Ahm ed AR, Sam i N. Intravenous im m unoglobulin therapy for patients with pem phigus foliaceus unresponsive to conventional therapy. J Am Acad Derm atol. 2002;46(1):42â€“49. 3. Bystryn JC, Steinm an NM. The adjuvant therapy of pem phigus. Arch Derm atol. 1996;132:203â€“212. 4. Cotell S, Robinson ND, Chan LS. Autoim m une blistering skin diseases. Am J Em erg Med. 2000;18(3):288â€“299. 5. Korm an NJ. New im m unom odulating drugs in autoim m une blistering diseases. Derm atol Clin. 2001;19(4):637â€“648. 6. Odom RB, Jam es WD, Berger TG, et al. Andrewsâ€™ Diseases of the Skin: Clinical Derm atology. Philadelphia: WB Saunders; 2000. 7. Udey MC, Stanley JR. Pem phigusâ€”diseases of antidesm osom al autoim m unity. JAMA. 1999;282(6):572â€“576. 8. Usatine RP, Sauret J. Rupturing bullae not responding to antibiotics. J Fam Pract. 2004;53(12):981â€“983.

Codes ICD9-CM 694.4

ICD10 L10.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Penile Shaft F racture

Penile Shaft

Fracture Ian R. Grover

Basics Description 

Traum atic rupture of the corpus cavernosum and the encom passing tunica albuginea



May involve the corpus spongiosum and urethra



Hem atom a form ation occurs at rupture site.



Injury is usually unilateral and transverse.



Most com m on fracture site is the proxim al shaft of the penis.



During erection, pressure within corpus cavernosum is m axim al, close to arterial pressure, increasing volum e in each corpus to m axim um , which thins tunica albuginea, m aking it susceptible to rupture.



Penile erection stretches spongiosum to the lim it, which will lim it m ovem ent vertically while still allowing lateral m ovem ents; this form s a bend at base of penis, m aking it vulnerable to lateral swing and rupture of corpus cavernosum .



Twenty-five percent to 30% have associated urethral

Pa ge 3 5 0

injury, which m ay be partial or com plete. 

Caused by blunt traum a to erect penis during: o

Sexual intercourse

o

Manipulation

o

Fall on erect penis

o

Entanglem ent in clothing

Etiology 

Peyronie's disease



Urethritis in past



Surgical procedure on corpus cavernosum or traum a to corpus cavernosum resulting in weak scar tissue

Diagnosis Signs and Symptoms History 

Sudden painful sensation in erect penis during sexual intercourse or soon after with loss of erection: o

May hear cracking or crunching sound at the tim e of traum a



May have dysuria, inability to void, or an increase in size of the swelling with voiding owing to extravasation of urine



Problem s with poor erections after the injury



Blood at the urethral m eatus after intercourse



Penile deviation with erection



Urinary retention or weak urinary stream

Physical Exam 

Swelling and blue-black discoloration at base of penis, usually on one side

Pa ge 3 5 0



Ecchym osis m ay also involve scrotum .



Penis flaccid and edem atous with angulation away from the side of tear



Defect in the penile shaft m ay be palpable at the site of the tear.



Blood at tip of penis or frank hem aturia suggests an associated urethral injury.

Tests Lab Urinalysis to evaluate urethral traum a: 

May have frank blood or m icroscopic hem aturia



PT/PTT if patient is on coum adin or has a history of bleeding disorder

Imaging 

Retrograde urethrographyâ€”recom m ended in all cases of suspected urethral traum a: o

Should be done with low pressure during injection, before urethral catheterization



Cavernosography and MRI of penis m ay be needed to confirm diagnosis and site of tear.



Ultrasonography m ay also be done to confirm a suspected tear.

Diagnostic Procedures/Surgery Diagnostic exploration of the penis is recom m ended when cavernosography is negative but clinical suspicion of a fracture is high.

Differential Diagnosis 

Cellulitis of penis



Contusion of penis



Lym phangitis of penis

Pa ge 3 5 0



Neoplasm of penis



Paraphim osis



Traum a because of constrictive ring or other structure



Urethral injury



Vasculature rupture, especially superficial or deep dorsal vein or dorsal artery

P.817

Treatment Pre Hospital 

Other injuries take precedence in the setting of m ultiple traum a.



Local treatm ent: ice packs locally to penis; splinting with tongue blade



Elevate the area to reduce swelling.

Initial Stabilization 

Pain control



Needle suprapubic cystotom y in patients with urethral traum a and full bladder to relieve patient discom fort

ED Treatment 

Com bined efforts of ED physician and urologist are aim ed toward restoration of norm al shape of penis and sexual and urinary functions.



ED treatm ent directed to reduce hem orrhage, prevent further com plications



Prophylactic antibiotic use is unnecessary.



Urethral catheterization in all cases after excluding

Pa ge 3 5 0

urethral traum a 

Urologic evaluation and early surgical treatm ent are essential to prevent com plications such as erectile dysfunction, im potence, penile deform ity, urethral stenosis.



All patients with suspected or definite diagnosis m ust have early urologic evaluation.

Medication (Drugs) 

Diazepam : 2â€“5 m g IV



Fentanyl: 0.05â€“0.2 m g IV



Hydrom orphone: 0.5â€“1.0 m g IV



Lorazepam : 0.5â€“1.0 m g IV



Morphine sulfate: 0.1 m g/kg IV

Follow-Up Disposition Admission Criteria All patients with penile fracture m ust be hospitalized for prom pt surgery.

Discharge Criteria N/A

Issues for Referral If im m ediate urologic consultation and treatm ent unavailable, patient m ay be transferred to a suitable hospital after initial stabilization and transfer criteria have been m et

References

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1. Asgari MA, et al. Penile fractures: evaluation, therapeutic approaches and long-term results. J Urol. 1996;155:148â€“149. 2. Eke N. Fracture of the penis. Br J Surg. 2002;89(5):555â€“565. 3. Ekwere PD, Al Rashid M. Trends in the incidence, clinical presentation, and m anagem ent of traum atic rupture of the corpus cavernosum . J Natl Med Assoc. 2004;96(2):229â€“233. 4. Fedel M, et al. The value of MRI in diagnosis of suspected penile fracture with atypical clinical findings. J Urol. 1996;155(6):1924â€“1927. 5. Haas CA, et al. Penile fracture and testicular rupture. World J Urol. 1999;17(2):101â€“106. 6. Kervancioglu S, et al. Color Doppler sonographic findings in penile fracture. J Clin Ultrasound. 2005;33(1):38â€“42. 7. Koifm an L, et al. Penile fracture experience in 56 cases. Int Braz J Urol. 2003;29(1):35â€“39. 8. Muentener M, et al. Long-term experience with surgical and conservative treatm ent of penile fracture. J Urol. 2004;172(2):576â€“579.

Codes ICD9-CM 959.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peptic Ulcer

Peptic Ulcer

Jason M. Lebwohl

Basics Description 

Produced by breakdown in gastric or duodenal m ucosal defenses



Im balance exists between production of acid and ability of m ucosa to prevent dam age.

Etiology 

Helicobacter pylori: o

Gram -negative spiral bacteria that live in m ucous layer

o

Responsible for 90â€“95% of duodenal ulcers and 80% of gastric ulcers

o

Increases antral gastrin production and decreases m ucosal integrity



NSAIDs: o

Interfere with prostaglandin synthesis

o

Lead to break in m ucosa



Aspirin



Cigarette sm oking



Alcohol

Pa ge 3 5 1

Diagnosis Signs and Symptoms 







Epigastric pain or tenderness (80â€“90%): o

Burning, gnawing, aching pain

o

Location: m idline, xiphoid, or um bilicus

Duodenal ulcers: o

Pain occurs 90 m inutes to 3 hours after m eals.

o

Usually awakens patient at night

o

Food and antacids relieve pain.

Gastric ulcers: o

Pain worsens after m eals.

o

Nausea and anorexia

Difficult to differentiate clinically between gastric and duodenal ulcers



Relief of pain with antacids



Hem e-positive stools



Com plications of peptic ulcer disease (PUD): o

o

Acute perforation: 

Rigid boardlike abdom en



Generalized rebound tenderness



Pain radiation to back or shoulder

Obstruction: 

Pain with vom iting



Succussion splash from retained gastric contents and abdom inal distention

o

Hem orrhage: 

Hem atem esis



Melena



Hypotension



Tachycardia

Pa ge 3 5 1



Skin pallor



Orthostatic changes

Essential Workup 

Careful physical exam ination including Hem occult testing and vital signs with orthostatics



For stable patients, oral GI cocktail typically relieves pain: o

Antacid: 30 m L

o

Viscous lidocaine: 10 m L

Tests Lab 

Norm al lab values in uncom plicated ulcer disease



CBC:



o

Low hem atocrit with bleeding

o

Leukocytosis with perforation/penetration

Am ylase/lipase: o

Elevated with perforation/penetration

o

Pancreatitis in differential diagnosis



Electrolytes, BUN/creatinine, glucose for critically ill



Type and cross-m atch: o

For significant blood loss

Imaging Chest radiograph/abdom inal series: 

Evaluate for perforations/obstructions

Diagnostic Procedures/Surgery 



ECG: o

For elderly patients

o

Myocardial ischem ia in differential diagnosis

Endoscopy: o

Procedure of choice

o

Outpatient unless significant hem orrhage

Pa ge 3 5 1

o

Allows for biopsies of gastric/duodenal ulcers for presence of H. pylori

o 



Detects m alignant gastric ulcers

Upper GI series: o

Single contrast barium diagnoses 70% to 80%.

o

Double contrast diagnoses 90%.

Gastrin level is elevated in Zollinger-Ellison syndrom e.

Differential Diagnosis 

Gastroesophageal reflux



Biliary colic



Cholecystitis



Pancreatitis



Gastritis



Abdom inal aortic aneurysm



Aortic dissection



Myocardial infarction



Subset with sym ptom s and no ulcer on endoscopy called nonulcer dyspepsia

Treatment Pre Hospital 

Airway, breathing, and circulation m anagem ent (ABCs)



IV fluid resuscitation for hypotensive/shock patients

Initial Stabilization 

ABCs



Identify ulcer com plications (hem orrhage, perforation, obstruction)



Treat hypotension with LR/norm al saline (NS) fluid bolus via two large-bore IVs

Pa ge 3 5 1



Type and cross early.



Nasogastric tube (NGT) for gastric decom pression/check for hem orrhage

P.819

ED Treatment 

Pain control with antacids (GI cocktail) or IV H 2 antagonists



Avoid narcoticsâ€”m ay m ask serious illness.



Prom otion of ulcer healing: o

Antacids

o

H 2 antagonists (cim etidine, fam otidine, ranitidine, nizatidine)

o

Sucralfate

o

Prostaglandin congers (m isoprostol)

o

Protease pum p inhibitors (PPIs; om eprazole, lansoprazole, or pantoprazole)









Gastric outlet obstruction: o

Decom press stom ach with NGT.

o

IV hydration

Gastric hem orrhage o

IV fluid resuscitation

o

Blood transfusion depending on loss/hem atocrit

o

Foley catheter to m onitor volum e status

o

GI consultation

Perforation: o

IV hydration

o

Foley catheter

o

Preoperative antibiotics

o

Em ergency surgical consultation

Treatm ent of H. pylori infection:

Pa ge 3 5 1

o

Invasive or noninvasive testing to confirm infection

o

Oral eradication antibiotic therapy options: 

Proton pum p inhibitor (om eprazole 20 m g b.i.d.) or lansoprazole 30 m g PO b.i.d. and two antibiotics (clarithrom ycin 500 m g b.i.d. plus m etronidazole 500 m g b.i.d.) for 14 days



H 2 blocker, bism uth subsalicylate (Pepto-Bism ol) plus either am oxicillin 1,000 m g b.i.d. or tetracycline 500 m g q.i.d. in com bination with either m etronidazole 250 m g q.i.d. or clarithrom ycin 500 m g b.i.d. for 14 days



Most com m on regim en: om eprazole 20 m g or lansoprazole 30 m g plus clarithrom ycin 500 m g and am oxicillin 1 g, all taken twice a day for 2 weeks

Medication (Drugs) 

Bism uth subsalicylate: two 525-m g tabs PO q.i.d.



Cim etidine (H 2 blocker): 800 m g PO nightly at bedtim e (peds: 20â€“40 m g/kg/24h) for 6â€“8 weeks



Fam otidine (H 2 blocker): 40 m g PO nightly at bedtim e (peds: 0.5â€“0.6 m g/kg q12h) for 6â€“8 weeks



Lansoprazole (PPI): 30 m g PO b.i.d. for 2 weeks



Maalox plus: 2â€“4 tablets PO q.i.d.



Misoprostol: 100â€“200 Âµg PO q.i.d.



Mylanta II: 2â€“4 tablets PO q.i.d.



Nizatidine (H 2 blocker): 300 m g PO nightly at bedtim e for 6â€“8 weeks: 20 m g PO b.i.d. (peds: 0.6â€“0.7 m g/kg q12hâ€“q24h) for 2 weeks



Pantoprazol (PPI): 40 m g PO daily for 2 weeks

Pa ge 3 5 1



Ranitidine (H 2 blocker): 300 m g PO nightly at bedtim e (peds: 5â€“10 m g/kg/24h given q12h) for 6â€“8 weeks



Sucralfate: 1 g PO q.i.d. for 6â€“8 weeks

Follow-Up Disposition Admission Criteria 

Gastric obstruction



Perforation



Active upper GI bleed



Melena



Uncontrolled pain



Anem ia

Discharge Criteria 

Unrem arkable physical exam ination with norm al CBC and hem e-negative stools



If hem e-positive stools, discharge if stable vital signs, norm al hem atocrit, and negative NGT aspiration for upper GI hem orrhage

Issues for Referral Outpatient GI evaluation and endoscopy

References 1. Louw JA, Marks IN. Peptic ulcer disease. Curr Opinion Gastroenterol. 2004,20(6);533â€“537. 2. McGuirk TD, et al. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):530â€“533. 3. Sm oot DT, et al. Peptic ulcer disease. Prim Care. 2001;28(3):487â€“503.

Pa ge 3 5 1

Miscellaneous SEE ALSO: Gastroesophageal Reflux Disease; Gastritis; Gastrointestinal Bleeding

Codes ICD9-CM 533.9

Pa ge 3 5 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perfo rated Visco us

Perforated

Viscous Ingrid D. Carter

Basics Description Perforation of viscous structure into peritoneal cavity: 

Inflam m ation



Ulceration



Shearing/crushing or bursting forces in traum a



Obstruction



Chem ical peritonitis occurs as result of disruption of gastric or intestinal lining into peritoneal cavity.

Etiology 

Peptic ulcer disease



Appendicitis



Inflam m atory bowel disease



Diverticular disease



Colon carcinom a



Foreign body ingestion



Traum a



Radiation enteritis

Pa ge 3 5 1

Pediatric Considerations 

Blunt traum a m ore com m on cause of bowel rupture than penetrating traum a



Jejunum is m ost com m on site of rupture.

Diagnosis Signs and Symptoms 

Sudden severe abdom inal pain: o

Initially local

o

Rapidly becom ing diffuse



Rigidity



Guarding



Rebound tenderness



Absent bowel sounds



Hypovolem ic shock: o

Tachycardia

o

Hypotension

Essential Workup Upright chest radiograph: 

Best dem onstrates pneum operitoneum



When in upright position for 5â€“10 m inutes, m ay detect as little as 1â€“2 m L of free air under diaphragm

Tests Lab 

CBC



Electrolytes, BUN/creatinine, glucose



Lipase



Urinalysis

Pa ge 3 5 2



Liver function test

Imaging 

Abdom inal radiographs: o

Left lateral decubitus film

o

Supine abdom en

o

Double wall

o

Air in intestinal lum en and peritoneal cavity allows for visualization of both serosal (not norm ally seen) and m ucosal surfaces of intestine.



Abdom inal CT: o

Detects sm all am ounts of free air from perforated viscous



ECG

Differential Diagnosis 

Intra-abdom inal abscess



Pneum om ediastinum with peritoneal extension



Pancreatitis



Peptic ulcer disease



Inferior wall m yocardial infarction



Cholecystitis

P.821

Treatment Initial Stabilization Treat hypotension/tachycardia with 0.9% norm al saline: 

Adults: 500 m L to 1 L bolus



Pediatric: 20 m L/kg bolus

Pa ge 3 5 2

ED Treatment 

Nasogastric tube



Foley catheter



Adm inister broad-spectrum antibiotics:



o

Cephalosporin

o

Am inoglycoside plus clindam ycin

Im m ediate surgical consultation for operative intervention

Medication (Drugs) 

Am ikacin: 15 m g/kg/24h IV q8h



Cefoxitin: 2 g (peds: <7 days: 20 m g/kg IVq12h; >1 week, 80â€“160 m g/kg IV q6h) IV q6h



Clindam ycin: 600â€“900 m g (peds: 20 to 40 m g/kg/24h) IV q8h



Morphine sulfate: 2â€“4 m g (peds: 0.1 m g/kg) IV q2hâ€“q3h

Follow-Up Disposition Admission Criteria Suspected or confirm ed perforation requires adm ission and im m ediate surgical consultation.

Discharge Criteria None

References 1. Graff LG, Robinson D. Abdom inal pain and em ergency departm ent evaluation. Em erg Med Clin North Am . 2001;19:123â€“136.

Pa ge 3 5 2

2. Shaffer H. Perforation and obstruction of the gastrointestinal tract. Radiol Clin North Am . 1992;30:405â€“426. 3. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865â€“877.

Codes ICD9-CM 799.8 K63.1

Pa ge 3 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pericardial Effusio n/Tam po nade

Pericardial

Effusion/Tamponade Sandra S. Yoon Teriggi J. Ciccone Carlo L. Rosen

Basics Description 



Pericardial effusion: o

Accum ulation of fluid in the pericardial sac

o

Occurs in 10% of cancer patients

Pericardial tam ponade: o

Accum ulation of pericardial fluid with elevation of pressure in the pericardial space that results in im pairm ent of ventricular filling and decreased cardiac output.

o

Potentially lethal

o

Rapid accum ulation of 50â€“200 m L of fluid in the pericardial sac causes hem odynam ic com prom ise and pericardial tam ponade.

o

Occurs in 15% of patients with idiopathic pericarditis

o

Occurs in 2% of patients with penetrating chest traum a

Pa ge 3 5 2

Etiology 

Medical causes: o

Idiopathic

o

Bacterial, viral, fungal, and parasitic infections

o

Tuberculosis

o

HIV

o

Malignancy

o

Urem ia, dialysis

o

Autoim m une/collagen vascular diseases

o

System ic lupus erythem atosus

o

Rheum atoid arthritis

o

Rheum atic fever

o

Scleroderm a

o

Radiation therapy

o

Myxedem a

o

Drug toxicity (isoniazid, doxorubicin, procainam ide, hydralazine, phenytoin)

o 

Postm yocardial infarction (Dressler syndrom e)

Surgical causes: o

Penetrating chest traum a

o

Blunt traum a rarely causes pericardial effusion

o

Thoracic aortic dissection

o

Iatrogenic (cardiac catheterization, postâ€“cardiac surgery, central line placem ent)

Diagnosis Signs and Symptoms 

Most are asym ptom atic



Pleuritic chest pain:

Pa ge 3 5 2

o

Relieved by sitting forward



Dyspnea



Cough



Fatigue



Malaise



Pericardial friction rub



Signs of shock or right heart failure



Fever >38Â°C is uncom m on; if present, consider purulent pericarditis



Pulsus paradoxus: o

Fall in systolic blood pressure >10 m m Hg with inspiration

o 



Sensitive but not specific

Dressler syndrom e: o

Fever

o

Chest pain

o

Pericardial friction rub

o

Seen several weeks after a m yocardial infarction

Beck triad: o

Classic presentation of cardiac tam ponade

o

Only present in one third of patients

o

Hypotension

o

Muffled heart sounds

o

Jugular venous distention (JVD): 

JVD m ay be absent in hypovolem ic patients

Essential Workup 

ECG: o

Low voltage:

o

Electrical alternans 

Alternating beat-to-beat variation of QRS am plitude



Rare in patients with traum atic pericardial

Pa ge 3 5 2

effusion or tam ponade 

Chest radiograph: o

Enlarged cardiac silhouette only in cases of pericardial effusion/tam ponade that develop over tim e



Echocardiography: o

Fluid in pericardial sac

o

Transthoracic echo is accurate for penetrating cardiac injury and effusions or tam ponade.

o

Right ventricular or atrial diastolic collapse-characteristic finding suggestive of tam ponade.

o

â€œSniffâ€• test: 

Inferior vena cava will not collapse in patients with tam ponade.



Suggestive of increased central venous pressure (CVP)

Tests Lab 

CBC



Electrolytes, blood urea nitrogen/creatinine, glucose for renal failure in suspected urem ic pericarditis



Cardiac enzym es m ay be elevated



Blood cultures if an infectious source is suspected

Imaging 

Chest CT for detecting hem opericardium



Transesophageal echocardiography



MRI with gadolinium

Diagnostic Procedures/Surgery 

Pericardiocentesis and fluid analysis:

Pa ge 3 5 2

o

Further work-up of m edical causes of pericardial effusion with determ ination of the etiology of the pericardial fluid



CVP determ ination: o

May be used in penetrating chest traum a patients

o

CVP >15 cm H 2 O suggests tam ponade, but m ay be norm al in the hypovolem ic patient.

Differential Diagnosis 

Other causes of shock



Myocardial infarction



Myocardial ischem ia



Congestive heart failure



Pulm onary em bolus



Sepsis



Tension pneum othorax



Hem othorax



Air em bolism



Aortic dissection



Gastrointestinal tract bleeding



Ruptured abdom inal aortic aneurysm

P.823

Treatment Pre Hospital Insert two large-bore IV lines in all cases of suspected cardiac tam ponade.

Initial Stabilization

Pa ge 3 5 2



IV fluid resuscitation with NS or blood



Pericardiocentesis for unstable patients to decom press the tam ponade



ED thoracotom y with pericardiotom y for patients in cardiac arrest after penetrating thoracic traum a or those who rem ain unstable after volum e replacem ent and pericardiocentesis

ED Treatment 

Bacterial pericardial effusion: o

Initiate antibiotic therapy to cover gram -negative and anaerobic organism s and Staphylococcus aureus.

o

May require partial surgical resection of the pericardium



Urem ic pericardial effusion: o



Dressler syndrom e and postirradiation pericardial effusion: o



Arrange urgent dialysis

Initiate NSAIDs

Medical causes of tam ponade in patients who are unstable: o

Perform pericardiocentesis with placem ent of an indwelling catheter for continued drainage





Traum atic pericardial tam ponade: o

Consult traum a surgeon im m ediately.

o

Definitive therapy is thoracotom y in the OR.

Aortic dissection: o

Im m ediate surgical consultation for operative repair

Medication (Drugs) 

Aspirin: 650 m g PO q4h



Ibuprofen: 800 m g PO q8h



Indom ethacin: 25â€“75 m g PO b.i.d.

Pa ge 3 5 2

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission for acute, sym ptom atic pericardial effusion/tam ponade



New pericardial effusion

Discharge Criteria Known sm all effusion in asym ptom atic stable patient

References 1. Braunwald E. Pericardial diseases. In: Fauci AS, Braunwald E, Isselbacher KJ, et al. eds. Harrison's principles of internal m edicine. 14th ed. New York: McGraw-Hill, 1998:1334â€“1341. 2. Ciccone TJ, Grossm an SA. Cardiac Ultrasound. Em er Med Clin of N Am erica. 2004;23(3):621â€“640. 3. Jouriles NJ. Pericardial and m yocardial disease. In: Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice, 5th ed. St. Louis, MO: Mosby, 2002:1130â€“1149. 4. Lange RA, Hillis LD. Acute Pericarditis. N Eng J Med. 2004;351:2195â€“2202. 5. Rosen CL, Wolfe RE. Blunt chest traum a. In: Ferrera PC, et al. eds. Traum a m anagem ent, an em ergency m edicine approach. St. Louis, MO: Mosby, 2001:232â€“258. 6. Soler-Soler J, Sagrista-Sauleda J, Perm anyer-Miralda G. Managem ent of pericardial effusion. Heart. 2001;86(2):235â€“240. 7. Tsang TSM, Oh JK, Seward JB. Diagnosis and m anagem ent of cardiac tam ponade in the era of echocardiography. Clin Cardiol. 1999;22:442â€“446.

Pa ge 3 5 3

Miscellaneous SEE ALSO: Cardiogenic Shock

Codes ICD9-CM 429.0

ICD10 131.3 131.9

Pa ge 3 5 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pericarditis

Pericarditis

Wende R. Reenstra

Basics Description 

Inflam m ation, infection, or infiltration of the pericardial sac, which surrounds the heart: o



Pericardial effusion m ay or m ay not be present

Acute pericarditis: o

Rapid in onset

o

Potentially com plicated by accum ulation of pericardial fluid leading to cardiac tam ponade



Constrictive pericarditis: o

Results from chronic inflam m ation causing thickening and adherence of the pericardium to the heart

Etiology 

Idiopathic (m ost com m on)



Viral: o

Echovirus

o

Coxsackie

o

Adenovirus

o

Varicella

o

Epstein-Barr virus

o

Cytom egalovirus

Pa ge 3 5 3









o

Hepatitis B

o

AIDS

Bacterial: o

Staphylococcus

o

Streptococcus

o

Haem ophilus

o

Salm onella

o

Legionella

o

Tuberculosis

Fungal: o

Candida

o

Aspergillus

o

Histoplasm osis

o

Coccidioidom ycosis

o

Blastom ycosis

o

Nocardia

Parasitic: o

Am ebiasis

o

Toxoplasm osis

o

Echinococcosis

Neoplastic: o

Lung

o

Breast

o

Lym phom a

o

Leukem ia

o

Melanom a



Urem ia



Myxedem a



Myocardial infarction: o



Dressler syndrom e

Connective tissue disease o

System ic lupus erythem atosus

Pa ge 3 5 3

o

Rheum atoid arthritis

o

Scleroderm a



Radiation



Chest traum a



Postpericardiotom y



Aortic dissection



Pancreatitis



Inflam m atory bowel disease



Am yloidosis



Drugs: o

Procainam ide

o

Crom olyn sodium

o

Hydralazine

o

Dantrolene

o

Methysergide

o

Mesalam ine

Diagnosis Signs and Symptoms History 



Chest pain: o

Retrosternal or precordial

o

Usually sharp

o

Pleuritic

o

Radiating to the shoulder or the trapezial ridge

o

Worsened with cough or inspiration

o

Increased with recum bency

o

Im proved with leaning forward

Fever

Pa ge 3 5 3



Mild dyspnea



Cough



Hoarseness



Nausea



Anorexia

Physical Exam 

Tachypnea



Tachycardia



Odynophagia



Friction rub: o

Heard best at lower left sternal border

o

Any of three com ponents:

o 





Presystolic



Systolic



Early diastolic

Interm ittent and exacerbated by leaning forward

Beck triad with the accum ulation of pericardial fluid: o

Muffled heart sounds

o

Increased venous pressure (distended neck veins)

o

Decreased system ic arterial pressure (hypotension)

Ewart sign: o

Dullness and bronchial breathing between the tip of the left scapula and the vertebral colum n



Pulsus paradoxus: o

Exaggerated decrease (>10 m m Hg) in systolic pressure with inspiration



Constrictive pericarditis: o

Signs of both right- and left-sided heart failure

o

Pulm onary and peripheral edem a

o

Ascites

o

Hepatic congestion

Pa ge 3 5 3

Essential Workup 

ECG: o

Stage: 1 

ST-segm ent elevation diffusely except aVR and V1



ST segm ents concave up



No reciprocal ST-segm ent depression in other leads (in contradistinction to the changes seen in acute m yocardial infarction)

o

o

Stage 2: 

ST segm ents return to norm al



T waves flatten



PR segm ents m ay becom e depressed

Stage 3: 

o

T-wave inversion

Stage 4: 

Eventual resolution of all changes



Differentiation from m yocardial infarction



No Q waves form ed



T-wave inversion occurs after the resolution of the ST-segm ent changes

P.825

Tests Lab 

CBC



Leukocytosis



Erythrocyte sedim entation rate m ay be elevated



Cardiac enzym es: o

Helpful in distinguishing pericarditis from m yocardial

Pa ge 3 5 3

infarction o

Reported elevated with the inflam m ation of pericarditis

Imaging 

Chest radiograph: o

Can be norm al

o

May show enlargem ent of the cardiac silhouette

o

No change in heart size until >250 m L of fluid has accum ulated in the pericardial sac



Echocardiography: o

Diagnostic m ethod of choice for the detection of pericardial fluid

o

Can detect as little as 15 m L of fluid in the pericardial sac



Chest CT: o

Useful for the detection of calcifications or thickening of the pericardium

Diagnostic Procedures/Surgery Pericardiocentesis: 

Indicated when a pericardial effusion is present and fluid is needed to determ ine the underlying etiology



Used to obtain fluid for protein, glucose, culture, cytology, gram and acid-fast stains, and fungal sm ears

Differential Diagnosis 

Acute m yocardial infarction



Pulm onary em bolism



Pneum othorax



Aortic dissection



Pneum onia



Em pyem a



Cholecystitis

Pa ge 3 5 3



Pancreatitis

Treatment Pre Hospital 

ABCs, IV access, O 2 , m onitor



Consider fluid bolus if no crackles.

Initial Stabilization 

ABCs



Pericardiocentesis: o

For hem odynam ic com prom ise secondary to cardiac tam ponade

o

Rem oval of even a sm all am ount of fluid can lead to a dram atic im provem ent.

o

Guided by ultrasound is the safest technique.

ED Treatment 

Treatm ent dependent on the underlying etiology



Idiopathic, viral, rheum atologic, and posttraum atic:



o

NSAID regim ens effective

o

Corticosteroids reserved for refractory cases

Bacterial: o

Aggressive treatm ent with IV antibiotics along with drainage of the pericardial space

o

Search for prim ary focus of infection.

o

Therapy guided by determ ination of pathogen from pericardial fluid tests



Neoplastic: o



Treat underlying m alignancy.

Urem ia: o

Intensive 2- to 6-week course of dialysis

Pa ge 3 5 3

o

Caution should be used if using nonsteroidal m edications.



Expected course/prognosis: o

Most patients will respond to treatm ent within 2 weeks.

o

Most have com plete resolution of sym ptom s: 

Few progress to recurrent bouts with eventual developm ent of constrictive pericarditis or cardiac tam ponade.

Medication (Drugs) 

Aspirin: 350â€“650 m g PO q3hâ€“q4h



Ibuprofen: 400â€“800 m g PO q6hâ€“q8h



Indom ethacin: 25â€“50 m g PO q6h

Follow-Up Disposition Admission Criteria Intensive care unit: 

Hem odynam ic instability



Cardiac tam ponade



Associated m alignant dysrhythm ia



Any suspicion of m yocardial infarction



Severe pain unresponsive to oral m edications



Suspicion of bacterial etiology



Patients having undergone pericardiocentesis due to the relatively high incidence of com plications

Discharge Criteria

Pa ge 3 5 3



Mild sym ptom s in patients without any hem odynam ic com prom ise



Close follow-up



Able to tolerate a regim en of oral m edication

References 1. Bessen HA and Byyny R, Acute Pericarditis and Cardiac Tam ponade. In: Wolfson AB et al eds. Harwood-Nussâ€™ Clinical Practice of Em ergency Medicine. 4th ed. Philadelphia: Lippincott William s and Wilkins 2005:294â€“297. 2. Jourilles NJ. Pericardial and m yocardial disease. In: Rosen P, et al. eds. Em ergency m edicine: Concepts and clinical practice, 5th ed. St. Louis, MO: Mosby YearBook, 2002:1130â€“1138. 3. Maisch B. The classification of pericardial disease in the age of m odern m edicine. Curr Cardiol Rep. 2002;4(1):1321. 4. Maisch B. Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology, new diagnostic im aging m ethods, and treatm ent. Curr Opin Cardiol. 1994;9:379â€“388. 5. Pankuweit S, Ristic AD, Seferovic PM, Maisch B. Bacterial pericarditis: diagnosis and m anagem ent. Am J Cardiovasc Drugs. 2005;5(2):103â€“112. 6. Ristic AD, Seferovic PM, Maisch B. Managem ent of pericardial effusion the role of echocardiography in establishing the indications and the selection of the approach for drainage. Herz. February 2005;30(2):144â€“150. 7. Yazdani K, Maraj S, Am anullah AM. Differentiating constrictive pericarditis from restrictive cardiom yopathy. Rev Cardiovasc Med. Spring 2005;6(2):61â€“71.

Miscellaneous SEE ALSO: Pericardia Effusion/Tam ponade

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Codes ICD9-CM 423.9

ICD10 I31.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perilunate Dislo catio n

Perilunate

Dislocation John MacKay

Basics Description Dislocation of carpal bones (usually capitate) volar or dorsal from lunate

Etiology 

Fall on outstretched hand usually dorsiflexed



Motor vehicle accidents bracing hands on steering wheel

Associated Conditions Scaphoid is frequently fractured with perilunate dislocation.

Diagnosis Signs and Symptoms 

Pain in wrist



Swelling or palpable deform ity in wrist

Physical Exam 

Diagnosis often m issed by clinical exam

Pa ge 3 5 4



Pay special attention to skin integrity and neurovascular status, including two-point discrim ination.

Essential Workup Im aging of wrist

Tests Imaging 

Radiographic im aging that includes three views of wrist



Perilunate dislocation visualized best on true lateral view: o

Distal carpal row, capitate seen dorsal or volar to lunate

o 

Lunate in its norm al relationship to radius

CT and MRI are not generally needed for diagnosis, but som e orthopedists m ay request them for preoperative planning.

Pediatric Considerations 

Wrists are rarely sprained in children, and radiograph is difficult to interpret.



Com parison view of other wrist m ay be helpful.

Differential Diagnosis 

Lunate fracture



Lunate dislocation: o



Dislocation occurs between lunate and distal radius.

Scapholunate dissociation and other sim ilar ligam entous disruptions

Pediatric Considerations Consider nonaccidental traum a

Pa ge 3 5 4

Treatment Alert 

Concern is for other, m ore serious, injuries.



Dress open wounds.



Im m obilize in neutral position.



Elevation, cold to reduce swelling



Age-appropriate social m anagem ent

Initial Stabilization 

Im m obilize, ice, elevate, pending definitive evaluation.



Identify other, m ore serious, associated injuries.

P.827

General Measures Reduction of dislocation: 

Operative fixation to reduce and m aintain fracture is frequently required.



Consultation with orthopedist before first attem pt at reduction recom m ended



Give patient appropriate procedural sedation.



Place hand in finger traps and use counterweights.



Place finger pressure at level of dislocation and gently exaggerate injury, then bring to appropriate position, m aintaining pressure over dislocated segm ent.



Im m obilize wrist using thum b-spica or sugar-tong splint in neutral position.



Pain control

Pediatric Considerations 

Wrists are rarely sprained in children, and radiograph is difficult to interpret.

Pa ge 3 5 4



Although perilunate dislocation is unusual in pediatric patients, children with wrist pain should be splinted and referred for ongoing evaluation: o

Wrist should be splinted with thum b-spica sugar tong splint.



Consider nonaccidental traum a.

Follow-Up Disposition Admission Criteria 

Open dislocation, presence of m ultiple traum a, or other, m ore serious, injuries



Inability to reduce dislocation or m aintain reduction



Preference of consulting orthopedist



Neurovascular com prom ise

Discharge Criteria 

Closed injuries



Adequate reduction



No neurovascular involvem ent



Orthopedic follow-up within 2 days

References 1. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990:637â€“649. 2. Eisenhauer MA. Wrist and forearm . In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, MO: Mosby; 2002:535â€“542. 3. Escarza R, Chin HW. Wrist injuries. In: Hart RG, Uehara DT,

Pa ge 3 5 4

Wagner MJ, eds. Em ergency and Prim ary Care of the Hand. Dallas, TX: Am erican College of Em ergency Physicians; 2001:139â€“160. 4. Uehara DT, Wolanyk D, Escarza RH. Wrist injuries. In: Am erican College of Em ergency Physicians. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004: 1675â€“1684.

Codes ICD9-CM 833.00

ICD10 S63.0

Pa ge 3 5 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perio do ntal Abscess

Periodontal

Abscess John Sullivan

Basics Description 



Collection of pus in supporting structures of teeth: o

Periodontal ligam ent

o

Alveolar bone

Periodontal pockets result from progression of periodontal disease and resultant bone loss: o

Food and debris accum ulate in periodontal pockets.

o

Coronal epithelial tissues can reattach to tooth while bacteria and food debris rem ain trapped in pocket, im pairing drainage.

o

Food and debris becom e secondarily infected in setting of im paired drainage.



Com plications: o

Osteom yelitis

o

Dentocutaneous fistula

o

Cavernous sinus throm bosis

o

Ludwig angina

o

Maxillary sinusitis

Pa ge 3 5 4

o

Tooth loss

Pediatric Considerations 

Periodontal abscess rare in children.



Periapical abscess com m on: o

Originates in pulp

o

Associated with caries

Etiology Anaerobic and Gram negative pathogens: 

Usually polym icrobial

Diagnosis Signs and Symptoms Periodontal abscess is a clinical diagnosis.

History 

Dental pain



Malaise



Fever

Physical Exam 

Focal swelling or fluctuance of gum s and or face



Tenderness to palpation



Increased tooth m obility



Parulis: o

Pim plelike lesion on gingival, representing term inal aspect of a sinus tract

o

May be seen in chronic abscess



Expression of pus from sinus tract



Heat sensitivity



Lym phadenopathy

Pa ge 3 5 4



Trism us generally absent, unless infection has spread to m uscles of m astication

History Necessary

Tests Ancillary testing not essential to m ake diagnosis

Lab Anaerobic culture of pus: 

Com plicated abscess



Im m unocom prom ised patients

Imaging Panoram ic, periapical, or occlusal radiographs: 

Not essential to m ake diagnosis



Can confirm and help define extent of abscess

Diagnostic Procedures/Surgery Electric pulp testing: 

Perform ed by dental consultant to verify viability of tooth

Differential Diagnosis 

Periapical abscess



Aphthous ulcers



Oral herpes



Salivary gland tum ors



Mum ps



Blocked salivary gland due to siladenitis or dehydration



Localized adenopathy due to oral infections



Facial cellulitis



Maxillary sinusitis



Acute otitis m edia



Peritonsillar abscess



Pediatric consideration: Periapical abscess

Pa ge 3 5 4



For asym ptom atic parulis: o

Fibrom a

o

Pyogenic or peripheral ossifying granulom a

o

Kaposi's sarcom a

Treatment Pre Hospital Rarely associated with airway em ergencies, but if any signs of airway com prom ise are present: 

Intubation equipm ent at bedside



Transport in sitting position



Supplem ental oxygen



Suction secretions as needed

Initial Stabilization 

Assess for airway patency.



Establish definitive airway via endotracheal intubation or cricothyrotom y/tracheostom y in presence of: o

Respiratory distress

o

Inability to handle secretions

o

Oropharyngeal tissue swelling that im pairs or threatens airway

ED Treatment 

Analgesia with NSAIDs or opiates m ay be required



Incision and drainage: o

Anesthetize gingiva superficially with 2% lidocaine with 1:100,000 epinephrine until blanching occurs.

o

Make a 1-cm stab incision using a scalpel blade toward alveolar bone.

o

Blunt dissection using m osquito hem ostat

Pa ge 3 5 5

o

Irrigate cavity with saline.

o

If abscess cavity sufficiently large, place one quarterâ€“inch iodoform gauze drain or fenestrated Penrose drain for 24â€“48 hours; to prevent its aspiration, secure gauze or drain with silk suture.



Antibiotics: o

Indicated if abscess extensive or if system ic signs present

o

Penicillin considered first-line em piric therapy

o

Erythrom ycin, azithrom ycin, clindam ycin for penicillin-allergic patients

o

Clindam ycin for penicillin-allergic patients or patients not responding to penicillin

o 

Am picillin/sulbactam for severe infections

Warm saltwater rinses hourly while awake for 24â€“48 hours.

P.829

Medication (Drugs) 

Penicillin G: 4 m illion Units (peds: 16â€“66 m U/kg) IM/IV q4h



Penicillin VK: 250â€“500 m g (peds: 6â€“12 m g/kg) PO q.i.d.



Am picillin/sulbactam IV: 1.5â€“3.0 g (peds: 15â€“30 m g/kg) IV/IM q6h



Azithrom ycin PO: 500 m g (peds: 10 m g/kg) PO first day then 250 m g (peds: 5 m g/kg) PO per day Ã— 4 days



Clindam ycin PO: 150â€“450 m g (peds: 2.5â€“7.5 m g/kg) PO q.i.d.

Pa ge 3 5 5



Clindam ycin IV: 300â€“900 m g (peds: 8.3â€“13.3 m g/kg) IV q8h



Erythrom ycin PO: 250â€“500 m g (peds: 10â€“17 m g) PO q6hâ€“q8h

Follow-Up Disposition Admission Criteria 

Severe infection or com plication requiring parenteral antibiotics



Necrosis or cellulitis involving areas with potential airway com prom ise



Cavernous sinus throm bosis



Osteom yelitis



Outpatient therapy failure



Im m unocom prom ised patients: o

Neutropenia

o

Uncontrolled diabetes

o

Advanced HIV

o

Cancer patients undergoing chem otherapy



Ludwig angina



System ic involvem ent with significant dehydration



Patients unable to handle secretions



Patients unable to m anage infection at hom e because of physical or m ental disability or psychosocial factors

Discharge Criteria 

Uncom plicated cases



Dental follow-up available in 24â€“48 hours

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References 1. Am sterdam JT. Oral Medicine. In: Marx ed. Rosen's Em ergency Medicine; Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby, 2002;892â€“908. 2. Benko K, Em ergency Dental Procedures. In: Roberts J, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 4th ed. Philadelphia: W.B. Saunders, 2004;1317â€“1340. 3. Clerehugh V, Tugnait A. Diagnosis and m anagem ent of periodontal diseases in children and adolescents. Periodontol 2000. 2001;26:146â€“168. 4. Douglas AB, Douglas JM. Com m on Dental Em ergencies. Am Fam Phys. 2003. 5. Herrera D, et al. The Periodontal Abscess, Short-term clinical and m icrobiological efficacy of 2 system ic antibiotic regim es. J. Clin. Periodontol 2000 Jun; 27(6):387â€“404. 6. McLeod DE, Lainson PA, Spivey JD. Tooth loss due to periodontal abscess: a retrospective study. J Periodontol. 1997 Oct: 68(10):963â€“966. 7. Mulut M, et al. Fatal Descending Necrotizing Mediastinitis. Em erg Med J. 2004 Jan; 21(1):122â€“123. 8. Pappa H, Jones DC. Mediastinitis from odontogenic infection: A case report. Br Dent J. May 14, 2005;198(9):547â€“548. 9. Robert A. Bacteria in the m outh. Dent Update. April 2005;32(3):134â€“136, 39â€“140, 142. 10. Sawalha W, Ahm ad M. Case Report: Bilat Pleural em pyem a following periodontal abscess. Eastern Med Health J. 2001;(7):846â€“851. 11. Van Winkelhoff AJ, Ram s TE, Slots J. System ic antibiotic therapy in periodontics. Periodontol 2000. 1996;10:45â€“78. 12. Wayne DB, Trajtenberg CP, Hym an DJ. Periodontal disease: a review for the prim ary care physician. South Med J. 2001;94:925â€“932.

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Miscellaneous SEE ALSO: Toothache

Codes ICD9-CM 523 Gingival and periodontal diseases

ICD10 K05.2

Pa ge 3 5 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perio rbital and Orbital C ellulitis

Periorbital

and Orbital Cellulitis Shari Schabowski

Basics Description Periorbital Cellulitis 

Periorbital cellulitis is anatom ically distinguished by its location isolated to the tissues anterior to the orbital septum : o

Orbital septum is the connective tissue extension of the orbital periosteum that is reflected into the upper and lower eyelids.

o

Extension into the tissues deep to the orbital septum is rare because the septum represents a nearly im penetrable barrier.



Most com m only presents as a com plication of upper respiratory tract infection (URTI) and sinusitis: o

Swelling owing to inflam m atory edem a from vascular and lym phatic congestion

o 

Not infected tissue

May occur as a com plication of a localized inflam m ation/infection in the eyelid or adjacent structures:

Pa ge 3 5 5

o

Blepharitis

o

Hordeolum

o

Dacryocystitis

o

Surrounding skin disruptions: 

Insect bites



Minor traum a



Im petigo or other derm atologic disorders

Orbital Cellulitis 

Inflam m atory process in the structures posterior to the orbital septum



Occurs secondary to extension from an adjacent structure: o

Sinusitis: 

Most com m only ethm oid

o

Dental abscess

o

Retained foreign body in the orbit

o

Puncture wounds

o

Orbital fracture

o

Postoperative infection

o

Hem atogenous spread from a rem ote source

o

Rare causeâ€”extension of periorbital cellulitis

Etiology Periorbital Cellulitis 

Streptococcus pneum oniae



Staphylococcus aureus



Streptococcus pyogenes



Moraxella catarrhalis



H. influenzae (children younger than 5 years)



Gonococcus: o



May extend from conjunctivitis or dacryoadenitis

Consider nonbacterial cause.

Pa ge 3 5 5

Orbital Cellulitis 

S. pneum oniae



S. pyogenes: o

Currently streptococcal infections are the m ost com m on cause.



S. aureus: o

Com m on in puncture wounds



S. pyogenes



Staphylococcus epiderm idis



Anaerobes



Bacteroides



Gram -negative: o



Associated with traum a

Fungal infectionâ€”cerebrorhino-orbital phycom ycosis (CROP): o

Life-threatening disease presenting with orbital cellulitis

o

Rapidly fatal in 75% of cases

o

Presentation: 

Eighty percent of cases occur in diabetic patients with a recent episode of diabetic ketoacidosis (DKA).



Predisposing factor: severe m etabolic acidosis



Toxic appearance



All age groups



More com m on in im m unocom prom ised patients



Begins in the paranasal sinuses



Proliferates in the blood vessels and causes throm bosis and necrosis



Bloody nasal discharge



Frequently presents with evidence of necrosis of the palate and/or nasal m ucosa

Pa ge 3 5 5

Pediatric Considerations 

In children younger than 2 years, H. influenzae is an im portant cause of bacterem ic periorbital cellulitis: o

Toxic appearance

o

Tem perature >39Â°C

o

Erythem atous and violaceous swollen eyelids

o

Dram atic decrease (80%) since Hib vaccine: 

Incidence decreases significantly after two im m unizations.

o

Preceded by upper respiratory infection

Diagnosis Signs and Symptoms Periorbital Cellulitis/Orbital Cellulitis 

Both will present with a unilateral, red, swollen eye.



Differences include: o

Anatom ic location

o

Extent of deep tissue involvem ent

o

Cause and m echanism of infection

o

Associated com plications

Periorbital Cellulitis 

Periorbital erythem a, warm th, tenderness, and swelling



Often preceded by URTI o

Typically unilateral and involving the upper or the lower lid, rarely involving both

o

Gradual onset

o

Swelling m ay becom e predom inant sym ptom leading to obscured vision in affected eye.

Pa ge 3 5 5

Orbital Cellulitis 



Orbital involvem ent: o

Blurred vision or diplopia

o

Photophobia

Typically involves upper and lower lid: o

About 95% unilateral



Swelling m ay obscure vision in the affected eye.



Headache

Periorbital Cellulitis 

Associated with low-grade fever usually <39Â°C



Typically nontoxic appearance



Painful, red, warm , swollen eye

Orbital Cellulitis 

Toxic appearance



Fever >39Â°C:



o

Restricted, painful extraocular m ovem ents

o

Afferent pupillary defect

o

Conjunctival injection

o

Chem osis

o

Proptosis

Meningism us

Essential Workup 

Physical exam to rule out orbital involvem ent: o

Orbital involvem ent m ay lead to serious com plications.

o

High level of suspicion: 

Patients who appear toxic



Orbital pain



Painful restriction of eye m ovem ent



Proptosis swelling of upper and lower lids

Pa ge 3 5 5



Com plete neurologic exam ination to rule out CNS involvem ent: o



High level of suspicion for CNS penetration: 

Altered m ental status



Meningism us



Visual loss

Identify com plicating m edical problem s: o

Im m unocom prom ise

o

Diabetes

Tests Lab 

Supportive but not diagnostic



CBC: o

WBC <15,000 for periorbital cellulitis

o

WBC >15,000 m ay suggest bacterem ic periorbital cellulitis.



Blood culture



Gram stain and culture of tissue aspirate or swab of draining purulent m aterial: o

Chocolate agar plate should be used when gonorrhea suspected.

P.831

Imaging CT scan orbits: 

Indicated if: o

Suspect orbital cellulitis or traum atic penetration of the orbital septum

o

Failure to respond to parenteral antim icrobial therapy

Pa ge 3 5 6



Dem onstrates extent: o

Orbital cellulitis

o

Sinusitis

o

Orbital em physem a

o

Subperiosteal abscess

o

Presence of foreign body

Diagnostic Procedures/Surgery Lum bar puncture: 

Rule out CNS involvem ent.



Consider in patients with: o

Signs or sym ptom s of m eningism us

o

Toxic appearance

o

Patients at risk of H. influenzae type B: younger than 4 years and nonâ€“Hib vaccinated

Differential Diagnosis Periorbital Cellulitis 

Lack of fever and leukocytosis suggests noninfectious cause: o

Insect bite

o

Allergy



Dacryoadenitis



Dacryocystitis



Hordeolum



Orbital cellulitis

Orbital Cellulitis 

Periorbital cellulitis



Contusion



Dacryoadenitis



Dacryocystitis



Hordeolum

Pa ge 3 5 6



Retrobulbar hem orrhage



Cavernous sinus throm bosis



Cranial nerve palsy



Inflam m atory orbital pseudotum or



Graves disease



Orbital rhabdosarcom a

Treatment Initial Stabilization 

IV fluids for vom iting/dehydration/sepsis



0.9% norm al saline (NS) 500-m L bolus (20 m L/kg children) for hydration and resuscitation

ED Treatment Periorbital Cellulitis 

Antibiotics: o

Typically responds to oral antibiotics unless appears bacterem ic or toxic

o 

IV antibiotics for severe infections/treatm ent failures

Antipyretics and pain m edication as needed

Orbital Cellulitis 

Antipyretics



Pain m edication



Early adm inistration of parenteral antibiotics



Ophthalm ologic consultation



If sinusitis is the source, consider ear, nose, and throat (ENT) consultation.



Em ergent surgical intervention m ay be necessary.



If Bacteroides is suspected organism :

Pa ge 3 5 6

o

Surgical dÃ©bridem ent

o

Vancom ycin



Tetanus toxoid when appropriate



If proptosis leaves the cornea exposed: o

Lubricating drops (Lacri-Lube: 2 drops q2hâ€“q4h PRN)



Suspect CROP: o

Am photericin B IV at highest tolerated dose

o

Topical am photericin B (1 m g/m L) irrigation or nasal packing

o

Local dÃ©bridem ent

Medication (Drugs) Periorbital Cellulitis 

Augm entin: 500 m g (peds: 45 m g/kg/24h) PO t.i.d.



Cephalexin: 500 m g (peds: 100 m g/kg/24h) PO q.i.d.



Cefazolin: 1 g (peds: 100 m g/kg/24h) IV q6hâ€“q8h



Cefotaxim e: 1â€“2 g (peds: 150 m g/kg/24h) IV q6hâ€“q8h



Clindam ycin: 600 m g (peds: 40 m g/kg/24h) IV q6h; 300 m g (peds: 20 m g/kg/24h) PO q.i.d.



Dicloxacillin: 500 m g (peds: 100 m g/kg/24h) PO q.i.d.



Vancom ycin: 500 m g (peds: 40 m g/kg/24h) IV q6h

Orbital Cellulitis 

Ceftriaxone: 1â€“2 g (peds: 100 m g/kg/24h) IV q12hâ€“q24h



Erythrom ycin ophthalm ologic ointm ent: applied q4h to lower cul-de-sac



Gentam icin: 5 m g/kg/24h IV



Metronidazole: 15 m g/kg IV load, then 7.5 m g/kg q6h



Nafcillin: 1â€“2 g (peds: 100 m g/kg/24h) IV q4h

Pa ge 3 5 6



Vancom ycin: 1 g (peds: 40 m g/kg/24h) q12h

Follow-Up Disposition Periorbital Cellulitis 

Toxicity



Progression of infection on oral antibiotics



Unable to arrange follow-up within 24â€“48 hours



High risk H. influenzae type B

Orbital Cellulitis 

IV antibiotics



Observation for progression: o



Without visual findings or restriction

Surgical incision and drainage

Periorbital Cellulitis 

Localized infection and inflam m ation



Tolerating oral antibiotics



Good follow-up

Orbital Cellulitis Adm it all: 

High risk of CNS penetration and ophthalm ologic com plications

References 1. Chang CH, et al. Antibiotic treatm ent of orbital cellulitis: an analysis of pathogenic bacteria and bacterial susceptibility. J Ocul Pharm acol Ther. 2000;16(1):75â€“79. 2. Danter EM, Jolly BT. Pediatric ophthalm ology. Em erg Med Clin North Am . 1995;13(3):669â€“680.

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3. Ghosh C. Periorbital and orbital cellulitis after H. influenzae B vaccination. Ophthalm ology. 2001;108:1514â€“1515. 4. Jain A, Rubin PA. Orbital cellulitis in children. Int Ophthalm ol Clin. 2001;41(4):71â€“86.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peripheral Neuro pathy

Peripheral

Neuropathy Minh V. Le

Basics Description Peripheral neuropathy is a general term for peripheral nerve disorders of any cause.

Diagnosis Signs and Symptoms 

Sensory nerve dysfunction: o

Num bness, localized tingling, paresthesias, dysesthesias

o

Vibration and position sensations decreased with large-fiber neuropathy

o

Pain and tem perature sensation decreased with sm all-fiber neuropathy

o

Deep tendon reflexes decreased secondary to decrease sensation of afferent lim b



Motor nerve dysfunction:

Pa ge 3 5 6

o

o

Weakness 

Distal greater than proxim al



Occasionally fasciculations

Muscle atrophy, dim inished tone with long-standing m otor nerve involvem ent

o

Loss of reflexes secondary to slowing of conduction along m otor nerve efferent lim b



Autonom ic nerve dysfunction: o

Orthostasis, constipation, urinary retention, or im potence

Essential Workup 

Studies based on acuteness, severity of neuropathy, and m ost likely diagnosis



Neurologic consult early if acute and severe sym ptom s

Tests Lab 

Basic m etabolic panel



CBC



Liver function tests



Urinalysis



Thyrotropin-stim ulating horm one



HIV, or vitam in B 1 2 based on individual presentations



ECG

Imaging Chest radiograph if indicated

Diagnostic Procedures/Surgery 

Electrom yographic studies, nerve conduction studies, and nerve biopsy per neurologic consult on adm ission or outpatient follow-up



Lum bar puncture as appropriate

Pa ge 3 5 6

Differential Diagnosis 





Focal: o

Entrapm ent

o

Com m on sites of com pression: 

Carpal, ulnar tunnel



Tarsal tunnel



Peroneal



Myxedem a



Rheum atoid arthritis



Am yloidosis



Acrom egaly

o

Com pressive neuropathies

o

Traum a

o

Ischem ic lesions

o

Diabetes m ellitus (DM), vasculitis

o

Leprosy

o

Sarcoidosis

o

Neoplastic infiltration or com pression

Multifocal (m ononeuropathy m ultiplex): o

DM

o

Vasculitis: 

Polyarteritis nodosa



System ic lupus erythem atosus



SjÃ¶gren syndrom e

o

Sarcoid

o

Leprosy

o

Malignancy related

o

HIV/AIDS

o

Hereditary predisposition to pressure palsies

Sym m etric: o

Endocrine: 

Most com m on is DM

Pa ge 3 5 6



Hypothyroidism

P.833

o

o

Medications: 

Isoniazid



Lithium



Metronidazole



Phenytoin



Cim etidine



Hydralazine



Am itriptyline



Am iodarone

Nutritional diseases: 

Alcoholism



B 1 2 /folate deficiency



Thiam ine

o

Critical illness neuropathy

o

Hypophosphatem ia

o

Guillain-BarrÃ© syndrom e

o

Toxic neuropathy:

o



Carbon m onoxide



Acrylam ide



Carbon disulfide



Ethylene oxide



Organophosphate esters



Lead

Myelopathy m im icking peripheral neuropathy: 

Back pain



Saddle anesthesia



Lower extrem ity weakness

Pa ge 3 5 6

Treatment Pre Hospital 

Pain control as needed



Airway protection as indicated

Initial Stabilization Establish airway protection with severe acute peripheral neuropathy, such as Guillain-BarrÃ© syndrom e.

ED Treatment Variable depending on acuity of sym ptom s

Medication (Drugs) 

Variable depending underlying diagnosis



Neurontin is often effective: 300 m g PO t.i.d. up to 1800 m g/d.

Follow-Up Disposition Admission Criteria 

Respiratory distress or acute gait disturbance



Intractable pain

Discharge Criteria Stable respiratory and gait status with outpatient follow-up

References 1. England JD, Asbury AK. Peripheral Neuropathy. Lancet.

Pa ge 3 5 7

2004;2151â€“2161. 2. Morgenlander JC. Recognizing peripheral neuropathy. Postgrad Med. 1997;102:71â€“80. 3. Pascuzzi RM, Fleck JD. Acute peripheral neuropathy in adults. Neurol Clin. 1997; 15(3):529â€“547. 4. Poncelelet AN. An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician. 1998;57:755â€“764.

Codes ICD9-CM 356.9

ICD10 G62.9

Pa ge 3 5 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peripheral Vascular Disease

Peripheral

Vascular Disease Sally Santen

Basics Description 

Peripheral arterial vascular disease (PAD) consists of three inter-related m anifestations:



o

Chronic arterial insufficiency

o

Acute arterial insufficiency

o

Atheroem bolism

Atherosclerosis causes PAD: o

Patients with PAD m ay also have coronary artery and cerebrovascular disease.



Chronic arterial insufficiency (CAI): o

Progressive obstructing atherosclerotic disease causing subacute ischem ia and pain (claudication). Fifteen percent develop critical leg ischem ia.

o

Risks factors: 

Age



Sm oking



Diabetes



Hyperlipidem ia

Pa ge 3 5 7

 o

Hypertension

Associated with m orbidity and m ortality of other form s of atherosclerosis (coronary artery disease, stroke)

o



Com plications: 

Aneurysm



Throm bosis



Ulceration



Lim b loss

Acute arterial insufficiency (AAI): o

Caused by either arterial throm bosis (50%) or em bolism

o

Causes acute lim b ischem ia with signs and sym ptom s of the 6 Ps



Atheroem bolism : o

Caused by rupture or partial disruption of an atherosclerotic plaque (aorta, fem oral, iliac)

o

Gives rise to cholesterol em boli showers and obstructing arteriolar networks

o

May be precipitated by invasive arterial procedures such as cardiac catheterization

Etiology 

Obstruction by atherosclerotic plaques (CAI)



Arterial throm bosis



Arterial em boli: o

Cardiac em boli from dysrhythm ias, valvular heart disease, or cardiom yopathy (80%)

o

Aneurysm s

o

Infection

o

Tum or

o

Vasculitides or foreign body

o

Throm bosis of plaques from preexisting CAI

Pa ge 3 5 7



Atheroem bolism

Diagnosis Signs and Symptoms Chronic Arterial Insufficiency 

Claudication: o

Aching pain in the calves (fem oropopliteal occlusion) or buttocks and thighs (aortoiliac region)

o

Occurs with activity and slowly relieved by rest

o

Classic claudication present in about half of patients with PVD



Severe disease presents with lim b pain at rest: o

Usually starting in the foot

o

Rapidly progressive claudication or ulceration

Physical Exam 

Absent or decreased peripheral pulses



Delayed capillary refill with cool skin



Increased venous filling tim e



Bruits



Pallor and dependent rubor of the leg



Muscle and skin atrophy



Thickened nails and loss of dorsal hair



Ulcerations (especially toes or heels) or gangrene with severe disease

Acute Arterial Insufficiency Sudden onset of pain and pallor in extrem ity

Physical Exam 

Six Ps:

Pa ge 3 5 7



o

Pain (first sym ptom )

o

Pallor

o

Pulselessness

o

Poikilotherm ic

o

Paresthesias (late finding)

o

Paralysis (late finding)

Identification of a source of a possible em bolic process is crucial (atrial fibrillation, cardiom egaly).

Atheroembolism 

Com plaint of cold and painful fingers or toes



Sm all atherosclerotic em boli m ay effect both extrem ities: o

Ischem ic and painful digits

o

â€œBlue toe syndrom eâ€•

o

Livedo reticularis

Essential Workup 

CAI: o

Ankle-brachial index (ankle systolic blood pressure [BP] divided by arm systolic BP)

o

Bedside test to determ ine whether CAI is present.

o

Ratio of <0.9 is abnorm al and <0.4 indicates severe disease.

o

Calcific arteries (diabetes) can have false negative ABI or elevated ABI (>1.3).



AAI: o

Physical diagnosis using the six Ps

o

Those with acute-on-chronic arterial insufficiency tolerate lim b ischem ia better than those without CAI due to well-developed collateral circulation.



Atheroem bolism : o

Clinical diagnosis with affected areas painful, tender, and m ay be either dusky or necrotic

Pa ge 3 5 7

Tests Lab 

CBC and platelets



Electrolytes, blood urea nitrogen, creatinine, glucose



Coagulation studies



Creatine phospokinase to evaluate for ischem ia



Special tests: o

Hold blood for special hem atologic studies if a hypercoagulable state suspected.

o

Sedim entation rate if vasculitis suspected

o

Blood cultures if endocarditis possible

Imaging 

Doppler ultrasound (US): o

Visualizes both venous and arterial system s

o

Identifies level of arterial occlusion, as well as throm bosis and aneurysm

o

Sensitivity and specificity >80â€“90% for occlusion of vessels proxim al to the popliteal vessels



Plethysm ography/Segm ental pressure m easurem ents: o

Uses m easurem ents of the volum e and character of blood flow to detect areas of CAI

o

Less widely available than US, therefore requires an experienced technician

o 

Approxim ates US in sensitivity and specificity

Angiography: o

Determ ines details about the anatom y, including the level of occlusion, stenosis, and collateral flow

o

Useful where the diagnosis of AAI is uncertain or before em ergent bypass grafting

o

Advantage is intervention (atherectom y, angioplasty, or intralum inal throm bolytics) can be done at the

Pa ge 3 5 7

tim e of diagnosis. 

CT angiogram : o

CT is useful for diagnosis of occlusive aortic disease or dissection.

o

Rapidly available and reliable

o

Many centers have m oved to CT angiogram as the first-line diagnostic tool. The decision for operative or angiographic intervention is based on the CT angiogram .

o

Requires contrast, therefore m ay not be first line for patients with renal insufficiency

P.835



MRI: o

MRI is sensitive for evaluation of CAI and dissection.

o

Disadvantages are that MRI is tim e consum ing and expensive.



Operative revascularization: o

Depending on the location of the lesion and severity of disease, peripheral arterial disease can be treated by angiographic intervention (atherectom y, angioplasty, or intralum inal throm bolytics) or by operative revascularization.

Differential Diagnosis 

Acute throm bosis or em boli



Arterial dissection



Deep venous throm bosis



Massive venous insufficiency



Com partm ent syndrom e



Buerger disease



Spinal stenosis

Pa ge 3 5 7



Neuropathy



Bursitis



Arthritis



Reflex sym pathetic dystrophy

Treatment Pre Hospital 

Maintain hem odynam ic stability with fluids.



Apply cardiac m onitor.



Place the ischem ic lim b at rest and in a dependent position.



Provide oxygen if low oxygen saturation or pulm onary sym ptom s.

Initial Stabilization 

IV fluid bolus for hypotension



ECG, m onitor, pulse oxim etry



Supplem ental oxygen

ED Treatment 

CAI: o

Antiplatelet and anticoagulant drugs m ay help but have not been definitively shown to prevent progression of CAI. 

o

Clopidogrel m ay be used as first-line treatm ent.

Given that other form s of atherosclerosis are com m only present in patients with CAI, other m edications for m edical m anagem ent of CAI are cilostazol and pentoxifylline

o

Invasive therapy depending on the severity of obstruction:

Pa ge 3 5 7

o





Atherectom y



Bypass grafting



Balloon angioplasty

Initiate m easures to prevent disease progression: 

Tobacco cessation



Aggressive m anagem ent of hyperlipidem ia



Exercise therapy

AAI: o

Lim it further clot propagation with heparin.

o

Do not anticoagulate patients suspected of having an aortic dissection or sym ptom atic aneurysm .

o

Em ergent consultation with a vascular surgeon: 

To determ ine which diagnostic study to best m ake the diagnosis



To begin arrangem ents for possible operative therapy or other intervention

o

Options for operative therapy include throm bectom y, em bolectom y, regional arterial throm bolysis, or bypass grafting.

o

Blood flow to the affected lim b m ust be re-established within 4â€“6 hours after onset of ischem ic sym ptom s.

o



Com plications of AAI include: 

Com partm ent syndrom e



Irreversible ischem ia requiring am putation



Rhabdom yolysis, renal failure



Electrolyte disturbances

Atheroem bolism : o

Treat conservatively if a lim ited am ount of tissue is involved and renal function is not significantly com prom ised.

o

No available therapy for the ischem ic digits besides

Pa ge 3 5 7

supportive wound care and analgesia o

Am putation for irreversibly necrotic toes

o

Vascular surgeon referral within 12â€“24 hours of ED visit

o

Prevent further em bolic events by a thorough investigation and correction of the source of atheroem boli.

Medication (Drugs) 

Aspirin: 81â€“325 m g/d



Cilostazol: 100 m g b.i.d.



Clopidogrel: 75 m g/d



Heparin: 80 U/kg bolus IV followed by 18 U/h IV



Pentoxifylline: 400 m g t.i.d.

Follow-Up Disposition Admission Criteria 

All patients with AAI are adm itted for evaluation and revascularization.



CAI: consider adm ission for rapidly progressive claudication or ischem ic pain at rest: o

To undergo heparinization and angiography to rule out an acute throm bosis



Atheroem bolism with large areas involved, significant pain, infection, or renal com prom ise

Discharge Criteria 

Atheroem bolism :

Pa ge 3 5 8

o

If they have sm all lesions, adequate pain controls, no evidence of renal com prom ise or superinfection, and follow-up within 24 hours.



CAI: o

No evidence of rapid progression, critical leg ischem ia, gangrene, or infection

Issues for Referral 

CAI will need urgent referral to vascular surgery.



Atheroem bolism , depending on the origin of the em boli, m ay need referral to vascular surgery or to cardiology.

References 1. Belch JJ, Topol EJ, Agnelli G, et al. Critical issues in peripheral arterial disease detection and m anagem ent. Arch Intern Med. 2003;163:884â€“892. 2. Dorm andy JA, Rutherford RB. Managem ent of peripheral arterial disease. J Vasc Surg. 2000;31:S1â€“S296. 3. Halperin JL. Evaluation of patients with peripheral vascular disease. Throm bosis Res. 2002;106:V303â€“311. 4. Hiatt WR. Drug therapy: m edical treatm ent of peripheral arterial disease and claudication. N Engl J Med. 2001;344:1608â€“1621. 5. Mukherjee D, Yadav JS. Update on peripheral vascular diseases: from sm oking cessation to stenting. Cleve Clin J Med. 2001;68:723â€“733.

Miscellaneous SEE ALSO: Arterial Occlusion

Codes ICD9-CM 414.0

Pa ge 3 5 8

ICD10 173.9

Pa ge 3 5 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perirectal Abscess

Perirectal Abscess

Scott A. Miller

Basics Description Localized infection and accum ulation of purulent m aterial adjacent to anus or rectum

Genetics No genetic link has been described.

Etiology 

Predom inant theory is anal crypt gland infection, with subsequent spread of infection to adjacent areas separated by m uscle and fascia: o

o

Perianal: 

Most com m on



Usually with red bulge near anus

Ischiorectal: 

Large potential space



May becom e very large before diagnosed



Can com m unicate posteriorly with other side form ing â€œhorseshoeâ€• abscess

o

Intersphincteric: 

Contained at prim ary site of origin between

Pa ge 3 5 8

internal and external sphincters  o

May be difficult to diagnose

Supralevator: 

Very deep above levator ani



Needs operative dÃ©bridem ent under general anesthesia



Often system ic sym ptom s before diagnosis is m ade



Rarely caused by surgery, episiotom ies, traum a, or hem orrhoids





Bacterial cause is typically a m ix of stool pathogens: o

Escherichia coli

o

Bacteroides species

o

Peptostreptococcus species

o

Streptococcal species

o

Staphylococcus species

Associated diseases: o

Diabetes

o

Inflam m atory bowel disease

o

Malignancy

o

Im m unocom prom ised host

Diagnosis Signs and Symptoms History 

Perianal pain: o

Constant

o

Aggravated by defecation, sitting, coughing, or sneezing

Pa ge 3 5 8

o

Perianal abscesses or ischiorectal abscesses that extend to perineum



Dull deep pelvic or rectal pain: o

More likely to have system ic toxicity owing to delayed diagnosis and spread of infection

o

Ischiorectal and supralevator abscesses



Rectal or perirectal drainage



Fever/chills



Constipation



Difficult urination

Physical Exam 

Perianal swelling, erythem a, induration, fluctuance, tenderness: o





Intra-anal and intrarectal swelling: o

Intersphincteric and supralevator abscesses

o

May be only clue to abscess

Pelvic exam : o



Perianal and large ischiorectal abscesses

Thickened rectovaginal septum or tenderness

Hypotension or signs of dehydration if system ic infection present



Local anesthesia insufficient for thorough rectal exam ination and determ ination of extent of abscess on all but sm all, superficial abscesses (m ostly perianal)

Essential Workup 

Careful history and physical param ount in m aking diagnosis



Have high index of suspicion for any constant perirectal pain.

Alert 

Factors associated with significant m orbidity and

Pa ge 3 5 8

m ortality: o

Delay in diagnosis or treatm ent: 

Hem orrhoid m ost com m on m isdiagnosis

o

Inadequate initial exam ination or treatm ent

o

Associated system ic disease

Tests No labs or im aging routinely indicated

Lab 

CBC: o



Wound culture: o



Leukocytosis with left shift

Consider if giving antibiotics.

Blood cultures: o

If concern for sepsis exists

Imaging 

CT



MRI



Ultrasound: o

May be helpful in diagnosis and delineating extent of abscess

Diagnostic Procedures/Surgery 

Incision and drainage is the definitive m anagem ent.



Barium enem a or anoscopy/proctoscopy m ay be helpful to diagnose supralevator or intersphincteric abscess bulging into rectum .

Differential Diagnosis 

Anal fissure



Sentinel pile in the posterior m idline or anterior m idline



Throm bosed or inflam ed hem orrhoids



Anal ulcer (i.e., HIV)

Pa ge 3 5 8



Proctitis (i.e., gonococcal)



Anorectal carcinom a

Pediatric Considerations Rectal duplication in children

Treatment Initial Stabilization 

IV fluids if septic or dehydrated



Pain m eds

P.837

ED Treatment 

Antibiotics alone without drainage is contraindicated: o

Infection m ay worsen, leading to extensive soft tissue destruction, sepsis, or death.

o

Adm inister prior to surgery with valvular heart disease.



Incision and drainage (I&D) for all abscesses



Bedside drainage under local anesthetic: o

Sm all visible abscess, nontoxic patient (m ostly perianal and sm all superficial ischiorectal abscesses)

o

May attem pt needle aspiration initially to localize, but I&D m ust be done.

o

Radial incision close to anal verge: 

Facilitates surgical excision of potential subsequent fistula

o

Elliptical or cruciate incision: 

Ensure ongoing adequate drainage.

Pa ge 3 5 8

o

Explore cavity breaking any loculations.

o

Pack with iodoform gauze: 

Rem ove/replace at 48-hour intervals.



Follow up with surgeon in 24â€“48 hours (evaluate for fistula).



Operative exam ination and dÃ©bridem ent under anesthesia: o

All supralevator and intersphincteric abscesses

o

Ischiorectal abscesses that are large or have extensive necrosis

o

Unable to drain under local anesthetic

o

Im m unosuppressed (i.e., HIV, diabetics, transplant recipients, patients on chem otherapy)



Antibiotic adm inistration: o

Rarely necessary: 

Marked cellulitis



Im m unosuppression



Valvular heart disease



System ic infection



Prosthetic device

o

If required, often need IV antibiotics and adm ission

o

Oral: 

o

Am oxicillin clavulanate or ofloxacin

Intravenous: 

Cefoxitin



Am picillin sulbactam



Com bination therapy with am picillin, gentam icin, and clindam ycin or m etronidazole



Postoperative care: o

Sitz baths t.i.d. 24 hours after I&D

o

High-fiber diet or bulking agent

o

Analgesic

Pa ge 3 5 8

Alert 

Large ischiorectal abscesses: o

Do not I&D if drainage already occurring inside the rectum .

o

I&D of draining abscess m ay result in high extrasphincteric fistula.

Medication (Drugs) 

Am picillin: 500 m g IV q6h



Am picillin sulbactam : 1.5â€“3 g IV q6h



Am oxicillin clavulanate: 875 m g PO q12h or 500 m g PO q8h



Cefoxitin: 1â€“2 g IV q6hâ€“q8h



Clindam ycin: 600 to 2,700 m g/d IV div. q6hâ€“q12h



Gentam icin: 3â€“6 m g/kg/d IV div. q8h



Metronidazole: 7.5 m g/kg IV q6h



Ofloxacin: 400 m g PO q12h

Follow-Up Disposition Admission Criteria 

Need for operative drainage



System ic toxicity/signs of sepsis

Discharge Criteria 

Adequate I&D with return of discernible pus



Ability to am bulate and care for wound

Issues for Referral

Pa ge 3 5 8

All should be referred to surgeon to evaluate for fistula: 

Fistulas develop in 25% to 50% of anorectal abscesses.

References 1. Billingham RP, Isler JT, et al. The diagnosis and m anagem ent of com m on anorectal disorders. Curr Probl Surg. 2004;41(7):586â€“645. 2. Janicke DM, Pundt MR. Anorectal disorders. Em erg Med Clin North Am . 1996;14:757â€“788. 3. Marcus RH, Stine RJ, Cohen, MA. Perirectal Abscess. Ann Em erg Med. 1995;25(5):597â€“603. 4. Nelson R. Anorectal abscess fistula: what do we know?. Surg Clin N Am . 2002;82:1139â€“1151.

Miscellaneous SEE ALSO: Abscess; Anal Fissure; Hem orrhoid

Codes ICD9-CM 566

ICD10 K61.0

Pa ge 3 5 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perito nsillar Abscess

Peritonsillar

Abscess Lee Shockley Kurt Whitaker

Basics Description 

Consists of suppuration outside the tonsillar capsule



Most com m on deep infection of the head and neck



Occurs in all ages, m ost frequently from 10â€“40 years of age



Peritonsillar abscess (PTA) m ay be life threatening.



Com plications o

Airway com prom ise (uncom m on)

o

Sepsis (uncom m on)

o

Recurrence (2â€“22%)

o

Extension to lateral neck or m ediastinum

o

Spontaneous perforation and aspiration

o

Jugular vein throm bosis (â€œLem ierre diseaseâ€•)

Etiology Two theories explain the developm ent of PTA: 

Direct bacterial invasion into deeper tissues in the patient with acute pharyngitis

Pa ge 3 5 9



Acute obstruction and bacterial infection of sm all salivary glands in the superior tonsil:



Most com m on pathogens o

Î±-hem olytic streptococcus

o

Î²-hem olytic streptococcus

o

Staphylococcal species

o

Anaerobes

o

Mixed organism s

Diagnosis Signs and Symptoms History 

Sore throat (100%)



Fever (26â€“97%)



Voice change



Dysphagia



Drooling



Headache



Pain radiating to the ear



Decreased PO intake



Malaise

Physical Exam 

Fever



Trism us (55â€“100%)



â€œHot potatoâ€• voice



Tonsils/soft palate erythem atous



Suppuration



Unilateral peritonsillar bulge on soft palate



Uvular deviation away from affected side

Pa ge 3 5 9



Halitosis

Tests 

Usually a clinical diagnosis m ade by visually exam ining oropharynx



May be difficult with severe trism us

Lab 

Throat culture and m onospot



CBC and culture of the abscess contents m ay be useful in som e cases.

Imaging 

Bedside intraoral ultrasound (US): o

High-frequency endocavity US transducer with a lubricated latex cover is used.

o

Can aid identification and localization of abscess in the hands of em ergency physicians

o

A cooperative patient can be instructed to place the transducer at the point of m axim al tenderness.



Soft tissue lateral neck: o

If suspicion for epiglotitis or retropharyngeal abscess exists



Chest radiograph o

With severe respiratory sym ptom s or draining abscess



CT scan of neck: o

If suspicion exists for other deep space infection of the neck, CT m ay be indicated.

Diagnostic Procedures/Surgery Needle aspiration is diagnostic and often curative.

Differential Diagnosis 

Peritonsillar cellulitis

Pa ge 3 5 9



Epiglottitis



Retropharyngeal abscess



Peripharyngeal abscess



Tracheitis



Meningitis



Retropharyngeal hem orrhage



Dystonic reactions



Cervical osteom yelitis



Cervical adenitis



Epidural abscess



Other deep space infection of the neck

Treatment Pre Hospital 

Rarely associated with airway em ergencies, but diagnosis is likely to be uncertain in transport, so suction and intubation equipm ent should be at the bedside,



Pulse oxim etry, supplem ental oxygen



Cardiac m onitor



IV access

Pediatric Considerations 

PTA occurs in children (younger than 18 years) in 24â€“39% of reported cases.



Young children m ay need sedation or general anesthesia if incision and drainage (I&D) or aspiration of the abscess is attem pted.



Obtain soft-tissue lateral neck radiograph before oral exam ination in young children with sym ptom s of upper airway obstruction.

Pa ge 3 5 9

Initial Stabilization 

Sam e as for pre hospital



Airway m anagem ent m ay be necessary.



Equipm ent for intubation and cricothyroidotom y should be available

ED Treatment 

Antibiotics should be adm inistered.



A single dose of steroids m ay im prove sym ptom s.



Adequate anesthesia prior to aspiration or I&D procedures is im portant.



No clear benefit has been found of one drainage technique over another: o

Needle drainage: 

Successful 87â€“93%



Should be perform ed by person experienced in drainage procedure and adept at advanced airway techniques

 

Less painful, less invasive than I&D

The internal carotid artery lies about 2.5 cm posterolaterally to the tonsil; sheathing the aspiration needle to prevent introduction of the needle to <0.5 cm is prudent.



The superior pole of the tonsil is the m ost com m on place for m axim al fluctuance (followed by the m iddle pole and then the inferior pole): o

Repeat aspiration is necessary in 10%

P.839



Incision and drainageo

Successful 90â€“92%

Pa ge 3 5 9

o

An 11- or 15-blade scalpel is used to incise the m ucosa for 1 cm from posterior to anterior in the area of m axim al fluctuance.

o

Avoid m ore than 0.5 cm depth.

o

Suction should be ready to rem ove purulent drainage and blood.

o

Packing is not used

Medication (Drugs) â€”Length of antibiotic treatm ent should be 7â€“10 days: 

Am oxicillin and sulbactam : 1.5â€“3 g IV q6h



Am oxicillin and clavulanate: 500 m g PO q12h (45 m g/kg/d div. q12h)



Clindam ycin 300 m g: PO Q6 hours (8â€“16 m g/kg/24h)



Cefoxitin (2 g IV q6h): 80â€“160 m g/kg/d div. q6h



Dexam ethasone: 10 m g IV/IM/PO single dose (0.6 m g/kg; not to exceed 10 m g)



Erythrom ycin: 250â€“500 m g/kg/d IV div. q6h (30â€“50 m g/kg/d PO div. q6hâ€“q8h):



Metronidazole 1 g IV over 1 hour then 500 m g IV/PO q6hâ€“q8h; not to exceed 4 g/d (15 m g/kg IV over 1 hour then 7.5 m g/kg IV/PO q6hâ€“q8h)



Penicillin is the antibiotic of first choice: o

Penicillin G benzathine: 1 m illion U IV q6h (12,500â€“25,000 U/kg q6h)

o

PCN VK 500 m g PO q6h (25â€“50 m g/kg/d divided q6hâ€“q8h)

o

The addition of m etronidazole to penicillin m ay increase the success rate.

Pa ge 3 5 9

Follow-Up Disposition Admission Criteria 

Airway com prom ise



Sepsis



Altered m ental status



Dehydration and inadequate PO intake

Discharge Criteria 

Most patients with PTA can be discharged hom e on oral antibiotics after abscess drainage.



Must be able to tolerate sufficient oral intake and antibiotics



Close follow-up recom m ended in 24â€“48 hours; treatm ent failures and recurrences are relatively com m on.

Issues for Referral 

Referral to an otolaryngologist or surgeon should be provided.



Tonsillectom y is recom m ended 6â€“8 weeks following treatm ent of the abscess.

References 1. Johnson RF, Stewart MG, Wright CC. An evidence-based review of the treatm ent of peritonsillar abscess. Otolaryngol Head Neck Surg. March 2003;128(3):332â€“343. 2. Johnson RF, Stewart MG. The contem porary approach to diagnosis and m anagem ent of peritonsillar abscess. Curr Opin Otolaryngol Head Neck Surg. June 2005;13(3);157â€“160. 3. Lyon M, Blaivas M. Intraoral ultrasound in the diagnosis and treatm ent of suspected peritonsillar abscess in the em ergency

Pa ge 3 5 9

departm ent. Acad Em erg Med. January 2005;12(1):85â€“88. 4. Ozbek C, Aygenc E, et al. Use of steroids in the treatm ent of peritonsillar abscess. J Laryngol Otol. June 2004;118(6):439â€“442.

Codes ICD9-CM 475

ICD10 J36

Pa ge 3 5 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pertussis

Pertussis

Roger Barkin

Basics Description 

Acute respiratory tract infection spread by sm all respiratory droplets



Bacteria (fim briae) attach to respiratory epithelial cells and proliferate, producing toxins: o

Ciliary dysfunction, accum ulation of cellular debris, increased m ucus production, lym phocytic and granulocytic infiltration



Bronchiolar congestion, obstruction, and necrosis



Obstruction of the airway due to m ucous plug, leading to hypoxia and hypoventilation



Increased intrathoracic or intracranial pressure



Secondary bacterial infection m ay exacerbate respiratory distress/failure.



CNS injury caused by encephalitis, increased intracranial pressure, and/or hypoxia



Uncom plicated cases last 6â€“10 weeks; half of cases last <6 weeks.



Mortality: o

Mortality greatest in those younger than 1 year (13

Pa ge 3 5 9

deaths in 2003)



o

1.3% for patients younger than 1 m onth

o

0.3% in children between 2 and 11 m onths

o

90% of deaths are secondary to bacterial pneum onia.

Epidem iology: o

Incubation period is 6 to 20 days, usually 7â€“10 days.

o

Mostly young children; 24% in children younger than 6 m onths

o

Increasing incidence in adolescents: 

Incidence in 2002 was 3.01 cases per 100,000 population (8,296 cases reported).

o

Adults are the prim ary reservoir

o

Peak incidenceâ€”late sum m er/fall

o

Preventable with diphtheria-tetanus-pertussis (DTP) vaccine

o

Newly introduced acellular vaccines have fewer side effects and equal efficacy to cellular vaccines.

Etiology Bordetella pertussis: 

A fastidious, gram -negative, pleom orphic bacillus

Diagnosis Signs and Symptoms 

Generally three recognized phases with progression: o



Infants m ay have indistinct stages.

Catarrhal stage: o

Approxim ately 1-week duration

o

Rhinorrhea

Pa ge 3 6 0



o

Mild cough

o

Minim al fever

Paroxysm al stage: o

Classic â€œwhoopingâ€• cough, increasing in severity

o

Coughing spasm that ends with a sudden inflow of airâ€”the whoop; unrem itting paroxysm s

o

Posttussive em esis

o

Cyanosis with respiratory distress/failure

o

Apnea (infants younger than 6 m onths)

o

Altered m ental status secondary to hypoxia or encephalitis





Convalescent stage: o

Waning cough

o

Im proving respiratory status

Atypical presentations: o

Often atypical in children younger than 6 m onths

o

Partially im m unized children have less severe disease.

o

Adult m anifestations are often only rhinorrhea, sore throat, persistent cough; often in fam ily m em bers.



Com plications: o

o

Head, eyes, ears, neck, throat 

Epistaxis



Subconjunctival hem orrhage

Respiratory: 

Acute respiratory arrest



Pneum onia caused by secondary infection



Pneum othorax



Subcutaneous or m ediastinal em physem a with crepitus



Bronchiectasis

Pa ge 3 6 0

o

o

GI: 

Hernia: inguinal or abdom inal



Rectal prolapse

Neurologic: 

Seizures



Encephalitis



Com a



Intracranial hem orrhage



Spinal epidural hem orrhage

Alert The child with pertussis m ay have significant respiratory distress or apnea.

Essential Workup 

The ED diagnosis should be m ade on clinical grounds.



Attem pt to establish a history of a contact.



Observe the paroxysm al cough with the characteristic whoop.



Use ancillary studies to further support the clinical diagnosis and exclude com plications.

Tests Lab 

WBC count: o

Leukocytosis (20,000â€“50,000 cells/m m 3 ) with m arked lym phocytosis

o

Elevation of WBC and lym phocytosis parallels severity of cough



Direct im m unofluorescence assay (DFA) of nasopharyngeal m ucus



False-positive results and negative results



Im m unofluorescent and enzym e im m unoassays to exclude

Pa ge 3 6 0

respiratory syncytial virus 

Done on either nasal wash or nasopharyngeal swab (Dacron)



Culture of nasopharynx or cough plate on a Bordet-Gengou m edium

Imaging 

Chest radiograph: o

Most often norm al

o

Perihilar infiltrates

o

Atelectasis

o

Occasionally characteristic â€œshaggyâ€• right heart border

o

Secondary bacterial pneum onia

P.841

Differential Diagnosis 

Infection: o

Parallel whooping cough syndrom e caused by Bordetella parapertussis, Chlam ydia trachom atis, Chlam ydia pneum oniae, Bordetella bronchiseptica, or adenovirus

o

Pneum onia: bacteria, m ycoplasm a, m ycobacterium

o

Bronchiolitis



Reactive airway disease



Foreign body



Cystic fibrosis

Treatment

Pa ge 3 6 0

Initial Stabilization 

Oxygen and respiratory support



Suction m ucous plugs.

ED Treatment 

Universal precautions: o

Specifically requires droplet precautions



Maintenance of adequate hydration



Monitor oxygenation during paroxysm s; supplem ent oxygen



Airway m anagem ent m ay be life saving in younger children.



Antibiotics: o

Effective in the catarrhal stage

o

Prevent further transm ission in the paroxysm al stage

o

Azithrom ycin is the first-line agent.

o

Alternatively, clarithrom ycin, erythrom ycin, or trim ethoprim -sulfam ethoxazole m ay be used, although the efficacy is unproven; useful if erythrom ycin is not tolerated.



Corticosteroids and albuterol m ay reduce paroxysm s of coughing, but further studies are required.

Medication (Drugs) 

Clarithrom ycin: 7.5 m g/kg PO b.i.d.



Erythrom ycin: 10 m g/kg PO q.i.d.



Azithrom ycin: 10 m g/kg PO every day (load), then 5 m g/kg PO daily for 5 days



Trim ethoprim -sulfam ethoxazole: 4/20 m g/kg PO b.i.d.

Pa ge 3 6 0

Follow-Up Disposition 

Adm ission Criteria



Patients younger than 1 year



Apnea



Cyanosis during paroxysm s of cough



Significant associated pneum onia



Encephalitis

Discharge Criteria 

Children without apnea, respiratory com prom ise, altered m ental status, or com plications and respiratory distress



Warm liquids to reduce coughing spasm



Rem ove thick secretions with bulb suction in infants.



Drink lots of fluids.



Avoid cough triggers: cigarette sm oke, pollutants, perfum es.



All exposed persons should seek chem oprophylaxis: o

Household and other close contacts should receive 10 days of erythrom ycin; those younger than 7 years who are unim m unized or received fewer than 4 doses of DTP vaccine should receive additional im m unizations.

o

Exposed children, especially incom pletely im m unized children, should be observed for 20 days and receive chem oprophylaxis and be vaccinated as m entioned.

o

Sym ptom atic children should be excluded from school or work; individuals with pertussis m ay return after 5 days of full treatm ent.

References

Pa ge 3 6 0

1. Cattaneo L, Edwards K. Bordetella pertussis (whooping cough). Sem in Pediatr Infect Dis. 1995;6(2):107â€“118. 2. Halperin SA, Bartoluss R, Langley JM, et al. Seven days of erythrom ycin estolate is as effective as fourteen days for the treatm ent of Bordetella pertussis infection. Pediatrics. 1997;100:65. 3. Langley JM, Halperin SA, Boucher FD, et al. Azithrom ycin is as effective as and better tolerated than erythrom ycin estolate for the treatm ent of pertussis. Pediatrics. 2004;114:e96â€“101. 4. Lebel MH, Mehra S. Efficacy and safety of clarithrom ycin versus erythrom ycin for the treatm ent of pertussis: a prospective, random ized, single blind trial. Pediatr Infect Dis J. 2001;20:1149â€“1154. 5. Pickering LK, et al. 2003 Red Book: Report of the Com m ittee on Infectious Diseases. 26th ed. Elk Grove Village, IL: Am erican Academ y of Pediatrics; 2003. 6. Yaari E, et al. Clinical m anifestations of Bordetella pertussis infection in im m unized children and young adults. Chest. 1999;115:1254.

Codes ICD9-CM 033.9

ICD10 A37.9

Pa ge 3 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phalangeal Injuries, F o o t

Phalangeal

Injuries, Foot Taylor Young Cardall

Basics Description 

The phalanges of the foot are prone to injury.



Fifth (or sm all) toe m ost com m only affected

Etiology 

Usually the result of direct traum a



Stubbing the toe, kicking a hard surface, or dropping a heavy object onto toes m ost com m on m echanism s of injury

Diagnosis Signs and Symptoms History History m ay predict the type of injury found and should include: 

Tim e of injury



Mechanism

Pa ge 3 6 0



History of previous traum a



Status of tetanus im m unization if laceration is present

Physical Exam 

Tenderness, swelling, crepitus, and ecchym osis of affected digit



Subungual hem atom as are often present.



Lacerations or crush-type wounds



Docum ent neurovascular status of the affected digit.

Essential Workup Radiographs of involved digit

Tests Imaging 

Radiographs of involved digit



Lateral view m ay be m ost sensitive.

Differential Diagnosis 

Fracture



Contusion



Abrasion/laceration



Dislocation

Treatment Pre Hospital 

Ice to affected digit



Direct pressure and dressing to any wounds

Initial Stabilization 

Ice to affected digit



Direct pressure and dressing to any wounds

Pa ge 3 6 0

ED Treatment 

Fractures involving the proxim al phalanx and interphalangeal (IP) joint of the hallux: o

Nondisplaced, nonintra-articular fractures m ay be placed in a short-leg walking cast with toe extension for com fort.

o

Displaced, nonintra-articular fractures: 

Closed reduction with digital block anesthesia



Longitudinal traction



Placem ent in short-leg walking cast with toe extension

o

Intra-articular fractures of the hallux m erit orthopedic consult: 

Frequently treated with open reduction and internal fixation



Fractures involving the proxim al phalanx and IP joint of the lesser toes: o

Rarely cause long-term disability

o

Nondisplaced fractures: 

Treat with splinting or buddy taping



Gauze padding between the taped toes to prevent skin breakdown

o



Displaced fractures: 

Closed reduction by digital block anesthesia



Longitudinal traction



Buddy taping or splinting

o

Hard-sole shoe, weight bearing as tolerated

o

Oral analgesics for pain

o

Pain usually resolved by two to three weeks

IP joint dislocations: o

Closed reduction by digital block anesthesia

o

Longitudinal traction with gentle downward pressure

Pa ge 3 6 0

on distal phalanx o

Buddy tape to adjacent toe

o

Unstable or unsuccessful reductions require orthopedic consultation

o 

Oral analgesics for pain

Distal tuft fractures: o

Subungual hem atom as should be drained.

o

Nail-bed laceration repair m ay be necessary. P.843



o

Buddy tape digit to adjacent toe.

o

Weight bearing as tolerated

o

Oral analgesics for pain

o

Pain usually resolved in two to three weeks

Open fractures: o

Orthopedic consultation

o

Prophylactic antibiotics

Medication (Drugs) 

NSAIDS are useful treating acute pain: o

Ibuprofen 800 m g (peds: 5â€“10 m g/kg) PO t.i.d.

Narcotic analgesics m ay be required for severe pain: 

Cephalexin: 1 g IM/IV in ED (peds: 50â€“100 m g/kg IM/IV in ED) for open fractures

Follow-Up Disposition

Pa ge 3 6 1

Admission Criteria 

Intra-articular fractures involving the proxim al phalanx of the great toe



Unstable or blocked dislocations



Open fractures require orthopedic consultation in the ED.

Discharge Criteria All other fractures m ay be discharged with orthopedic follow-up in 2â€“3 weeks to evaluate healing.

Issues for Referral Patient copies of any radiographs obtained m ay facilitate early follow-up.

References 1. Ho K, Abu-Laban RB. Ankle and foot. In: Marx JA, ed. Rosen's Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002:706â€“735. 2. Kensinger DR, Guille JT, Horn BD, et al. The stubbed great toe: im portance of early recognition and treatm ent of open fractures of the distal phalanx. J Pediatr Orthop. 2001;21:31â€“34. 3. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am . 2001;18:85â€“113.

Codes ICD9-CM 959.7

ICD10 S93.4

Pa ge 3 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phalangeal Injuries, Hand

Phalangeal

Injuries, Hand David Palafox

Basics Description 

The fingers are body part m ost frequently injured in athletic or occupational accidents.



Children usually present with crush injuries.



Hyperextension injuries m ost com m only cause ligam entous injury or chip fractures.



Hyperflexion injury to the tip of digits m ay cause m allet finger injury with avulsion fracture at the insertion of the extensor tendon on the distal phalanx.



Crush injuries m ost com m only cause fractures and diffuse soft tissue injury.

Alert 

Indications for reim plantation in am putation: o

Thum b

o

Single digit between proxim al interphalangeal (PIP) and distal interphalangeal (DIP) joint

o

Multiple digits

o

Am putation in child

Pa ge 3 6 1

Pediatric Considerations 

Injuries m ay be m ore difficult to diagnose in children who are unable to cooperate for a full exam ination.



Open epiphyses m ake radiographic interpretation less sensitive.



Careful repeated exam ination and protective splinting are necessary.

Etiology Accident

Diagnosis Signs and Symptoms 

Pain in the area of injury



Swelling and ecchym osis



Deform ity, laceration, burn, or am putation of the digit



Loss of m otion in the digit involved

Alert High-presure injection injury requires im m ediate consult to orthopedic hand surgeon.

Essential Workup 

Careful history and com plete physical: o

Explore all wounds fully to identify tendon injury or foreign body and perform two-point discrim ination testing.

o

Radiographic series of the affected hand if there is any suggestion of m ore than a m inor superficial injury



Special attention directed at assessing individual tendon

Pa ge 3 6 1

status, neurovascular integrity, and identifying rotational deform ity 

Exam ination conducted first to assess function, then under anesthesia, and finally with tourniquet if needed to allow a bloodless field for better exam ination of lacerated areas o

For distal digits, an elastic band can be used at the base of the digit.

Tests Imaging Plain radiography of involved digits including true lateral and oblique views

Differential Diagnosis 

Tendon laceration/rupture; partial/com plete



Com plicated open injuries m ay include several injuries, and the entire hand should be exam ined carefully.



Beware of lacerations over dorsal m etacarpal-phalangeal areas, which m ay be â€œfight bitesâ€• (hum an bites).

Pediatric Considerations Many fractures in children are torus (buckle) fractures of the phalanges.

Treatment 

Most phalangeal dislocations are dorsal or dorsolateral: o

These m ay be reduced under digital block.

o

Gentle distraction, hyperextension, and guiding the base of the dislocated phalanx into proper position with m ild pressure

o

Always check for stability postreduction by having

Pa ge 3 6 1

patient perform active range of m otion (ROM). 

Sim ple im pacted transverse or sm all corner fractures not exceeding 25% of a joint surface and dislocations: o

Treated with â€œbuddyâ€• splinting in functional position or padded splint in neutral position

o

Splint for several days, with arrangem ents for appropriate follow-up within a week.

P.845



Unstable fractures (rotational deform ity, oblique fractures, fractures involving larger portion of a joint, angulated fractures, or significant epiphyseal injuries): o



Splinted and referred for urgent orthopedic care

Subungual hem atom a: o

Blood released by using a heated paper clip, electric cautery, or a hole drilled in the nail with an 18-gauge needle

o

This injury does not have to be treated as open injury just because of subungual hem atom a.



Nail avulsions: o

Repair of nail bed lacerations

o

Splinting of the eponychium and germ inal m atrix to avoid adhesions

o

The avulsed nail can be used or a sm all piece of gauze or foil can be inserted in the area.



Many other lacerations can be left open with protective cover and allowed to heal secondarily.

Pre Hospital 

Most patients do not require em ergency m edical services (EMS) transport solely for phalangeal injury.



Cautions:

Pa ge 3 6 1

o

Prehospital personnel should not attem pt to reduce a phalangeal dislocation at the scene unless there will be an unusually long transport tim e or there is vascular or neurologic com prom ise: 

Reduction m ay be successful but prom pt the physician to m iss significant ligam entous injuries.

Alert 

Am putated digits or tissue should be placed in clean m oist saline gauze, placed in plastic bag, and then placed in a separate bag with ice. Do not place digit in direct contact with ice!



Bleeding should be treated with appropriate direct pressure dressings.

Initial Stabilization 

Assess for other, m ore serious injuries.



Rem ove all rings from injured hand.



Im m obilize the involved areas by proxim al-to-distal splinting.



Interm ittent ice pack application with constant elevation for the first 24 hours



Dislocations or severely deform ed fractures producing vascular com prom ise should be reduced im m ediately to a neutral position and im m obilized.

Medication (Drugs) 

Evaluate tetanus status and vaccinate per im m unization schedule.



Mild analgesics should be offered, with nonsteroidal anti-inflam m atory drugs (NSAIDs) or hydrocodone usually

Pa ge 3 6 1

sufficient. 

Antibiotics are not indicated for sim ple noncontam inated wounds: o

Indicated for high-risk wounds such as bite wounds or grossly contam inated injury

Follow-Up Disposition Patients with a stable fracture in an appropriate splint m ay be discharged for orthopedic follow-up.

Pediatric Considerations 

Sim ple fractures can be treated with splinting if no significant rotational deform ity.



Epiphyseal fractures (Salter-Harris injuries) m andate orthopedic referral

Admission Criteria 

Open joint injuries or fractures usually adm itted for irrigation, dÃ©bridem ent, and early repair



Closed injuries requiring surgical m anagem ent m ay be adm itted for early operative intervention: o

Acceptable to wait a day or two for sem ielective repair of clean injuries

References 1. Am erican College of Radiology, Expert Panel on Musculoskeletal Im aging. Acute Hand and wrist traum a. 2001. 2. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 3rd ed. New York: Churchill Livingstone; 1990. 3. Am erican Society for Surgery of the Hand. The Hand: Prim ary

Pa ge 3 6 1

Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990.

Codes ICD9-CM 959.5

ICD10 S60.9

Pa ge 3 6 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pharyngitis

Pharyngitis

David A. Vitberg Brian J. Browne

Basics Description 

Inflam m ation/infection of the pharynx



Third m ost com m on com plaint for physician visits



200 visits per 1,000 population annually in the United States



$300 m illion annually to diagnose and treat



Strep throat: o

15â€“30% childhood pharyngitis

o

5â€“10% adult pharyngitis

o

Unusual in children younger than 3 years

o

Peak ages 4â€“11 years

o

Peak m onths January through May; also start of school year

Etiology 

Viral: o

Most com m on cause of infectious pharyngitis

o

Rhinovirus (20%)

o

Coronavirus (>5%)

o

Adenovirus (5%)

Pa ge 3 6 1



o

Herpes sim plex virus (4%)

o

Parainfluenza virus (2%)

o

Influenza virus (2%)

o

Coxsackievirus (<1%)

o

Epstein-Barr virus (<1%)

o

Cytom egalovirus (<1%)

o

HIV-1 (<1%)

o

Acute retroviral syndrom e

Bacterial: o

Streptococcus pyogenes (group A Î²-hem olytic streptococci [GABHS]) (15â€“30%)

o

Group C Î²-hem olytic streptococci (5%)

o

Neisseria gonorrhoeae (gonococcal pharyngitis) (<1%)



o

Corynebacterium diphtheriae (<1%)

o

Arcanobacterium haem olyticum (<1%)

o

Chlam ydia pneum onia

o

Mycoplasm a pneum oniae (<1%)

o

Syphilis

o

Tuberculosis

Fungal: o

Candida (thrush)



Chem ical burns



Foreign bodies



Inhalants



Postnasal drip



Lym phom a

Diagnosis Signs and Symptoms

Pa ge 3 6 2



Sore throat



Pharyngeal erythem a and exudates



Odynophagia



Dysphagia



Fever



Cervical adenopathy



Dim inished oral intake



Fatigue



Soft palatal petechia



Viral:



o

Cough

o

Rhinorrhea

o

Lack of cervical adenopathy

GABHS: o

Sudden-onset sore throat

o

Odynophagia

o

Fever

o

Headache

o

Abdom inal pain

o

Nausea and vom iting

o

Uncharacteristic sym ptom s: 

Coryza



Hoarseness



Cough



Diarrhea

o

Tonsillopharyngeal erythem a

o

Tonsillopharyngeal exudates

o

Beefy red, swollen uvula

o

Anterior cervical lym phadenitis

o

Scarlatiniform rash

o

Uncharacteristic signs: 

Conjunctivitis

Pa ge 3 6 2





Anterior stom atitis



Discrete ulcerative lesions

Centor criteria for strep throat: o

Criteria: 

Tonsillar exudates



Tender anterior cervical lym phadenopathy



Fever by history



Absence of cough

o

The m ost widely used decision rule

o

If three or four criteria are present, the positive predictive value for GABHS infection is 40â€“60%.

o

The absence of 3 or 4 of the criteria has an 80% negative predictive value.

o

Patients with none or only one of these criteria should not be tested or treated.

o 

Following these criteria often leads to overtreatm ent.

Diphtheria: o

Airway-threatening gray pharyngeal m em brane

o

Myocarditis (two thirds of patients); clinically evident cardiac dysfunction (10â€“25%)

o 



Cranial and peripheral neuritis (5%)

Mononucleosis: o

Hepatosplenom egaly

o

Jaundice

o

Rash

Gonococcal pharyngitis: o

Always evaluate children for sexual abuse

o

Recurrent episodes of pharyngitis

Essential Workup 

Physical exam ination



Focused airway exam ination

Pa ge 3 6 2

Tests Lab 

Throat culture: o

Gold standard

o

24â€“48 hours for results, which delays treatm ent

o

Necessitates recontacting patient/fam ily

o

False-negative rate for GABHS is 10%.

o

False-positive rate for GABHS is 20%: 

Often related to GABHS carrier state with superim posed viral pharyngitis

o

Not cost effective and not routinely recom m ended for evaluation of adults

o

Neither throat culture nor rapid strep test (RST) can differentiate acutely infected patients from asym ptom atic carriers with intercurrent viral pharyngitis.

o

Throat culture should be collected when gonococcus is being considered.



RST: o

Results are available within 30 m inutes.

o

Sensitivity 85â€“95%

o

Specificity 96â€“99%

o

All patients with positive RST results should be treated.

o

Negative RST results in children and adolescents (not adults) should be confirm ed with a conventional throat culture.

o

Confirm atory culture is not recom m ended for adults.

o

Use of a high-sensitivity antigen test (e.g., RST) without (or in lieu of) a culture does not increase the risk of suppurative or nonsuppurative com plications

Pa ge 3 6 2

of GABHS infection. o

Use of a high-sensitivity antigen test (e.g., RST) without culture confirm ation of all negative results is the m ost cost-effective strategy in the treatm ent of pharyngitis.

o

The new optical im m unoassay is extrem ely accurate; negative results do not require confirm atory culture.



Monospot: o

Detects heterophil antibody for suspected m ononucleosis



o

90% sensitive in patients >5 years of age

o

75% sensitive in patients 2â€“4 years of age

o

<30% sensitive in patients <2 years of age

CBC with peripheral sm ear for suspected m ononucleosis: o



50% lym phocytes, 10% atypical lym phocytes

Loeffler m edia culture for diphtheria

Imaging 

Lateral neck radiograph for suspected epiglottitis, retropharyngeal abscess, or foreign body



Contrast-enhanced CT scan to identify and define the extent of com plications such as retropharyngeal abscess

P.847

Differential Diagnosis 

Epiglottitis



Peritonsillar/retropharyngeal abscess



Diphtheria



Mononucleosis



Ludwig's angina



Candida infection

Pa ge 3 6 2



Gonorrhea



HIV acute retroviral syndrom e



Acute leukem ia/lym phom a



Oropharyngeal cancer



Foreign body



Inhalants and chem ical burns



Postnasal drip

Treatment Pre Hospital 

Observe/m anage airway for respiratory distress



NS hydration for hypotension/dehydration

Initial Stabilization 

ABCs



Volum e resuscitation: o

1L (peds: 20 m L/kg) NS bolus for signs of volum e depletion or if patient is unable to tolerate oral solutions

ED Treatment Antipyretics/analgesics: 

Acetam inophen



Ibuprofen



Topical analgesics (Chloraseptic spray or lozenges)

GABHS Infection 

Without treatm ent, GABHS pharyngitis is often a m ild and self-lim ited infection.



When GABHS are present in the throat, antibiotic therapy accelerates sym ptom relief (fever and pain) by 1â€“2

Pa ge 3 6 2

days. 

Although sym ptom duration m ay be slightly shortened with antibiotics, the real goal of treatm ent is prevention of acute rheum atic fever (a com plication rarely seen in the United States).



Antibiotics: o

Penicillin V is the drug of choice for GABHS pharyngitis.

o

For patients who are allergic to penicillin and those who fail therapy with a Î²-lactam , the m acrolides are an acceptable alternative. Erythrom ycin therapy is often com plicated by gastrointestinal side effects. Azithrom ycin is favored for its once-daily adm inistration.

o

Antibiotics should be stopped prom ptly with a negative throat culture.

o

Delaying antibiotic treatm ent for 24â€“48 hours while awaiting culture results does not increase the risk of poststreptococcal com plications.

o

Im m ediate antibiotic therapy should be avoided, except for high-risk patients (those with severe infection or an im m unocom prom ised state) and in areas with a high incidence of rheum atic fever.

o

A â€œtreat-allâ€• strategy is not recom m ended because of the extrem ely low incidence of poststreptococcal sequelae and em ergence of antibiotic resistance.



Corticosteroids: o

Oral steroids are equally efficacious at relieving pain in patients with pharyngitis, as are equivalent dosages of IM steroids.

o

IM injections should be reserved for patients unable

Pa ge 3 6 2

to tolerate oral intake. o

Steroids should be avoided by patients with diabetes, im m une suppression, or suppurative infection.



Com plications: o

Acute rheum atic fever

o

Peritonsillar/retropharyngeal abscess

o

Poststreptococcal glom erulonephritis

o

Pediatric autoim m une neuropsychiatric disorder associated with streptococcal infection (PANDAS) 

A rare, and controversial, consequence of Streptococcus infection



Sudden onset of sym ptom s like those of obsessive-com pulsive disorder, caused by an autoim m une reaction that affects the basal ganglia



Treatm ent failure: o

A full 10-day course of penicillin is necessary to eradicate infection from the pharynx.

o

Docum ented in up to 35% of GABHS patients treated with penicillin V, particularly in children <6 years old. A likely m ajor factor is poor com pliance with the standard 10-day penicillin treatm ent regim en.

Diphtheria 

Goals of therapy: o

Prevent airway obstruction by pseudom em brane.

o

Treat the infection.

o

Counteract exotoxin-m ediated m yocarditis and neuritis.



Horse antitoxin: o

Dose is dictated by illness severity.



Penicillin or erythrom ycin



Com plications:

Pa ge 3 6 2

o

Myocarditis

o

Peripheral neuritis (cranial neuropathies)

o

Cardiac dysfunction

Gonococcal Pharyngitis 

Treat according to the usual sexually transm itted disease protocol



Third-generation cephalosporin (gonorrhea)



Always treat for chlam ydia (azithrom ycin)

Medication (Drugs) 

Penicillin: o

Unable to tolerate oral intake: 

<27 kg: penicillin G benzathine (Bicillin LA): 0.6 m illion U IM Ã— 1



>27 kg: penicillin G benzathine (Bicillin LA): 1.2 m illion U IM Ã— 1

o

o

Able to tolerate oral intake: 

<12 years: 250 m g PO b.i.d. Ã— 10 days



>12 years: 500 m g PO b.i.d. Ã— 10 days

Probability of relapse is 50% if penicillin is discontinued after 3 days of therapy.



Macrolides o

Penicillin hypersensitivity/allergy

o

Adults: erythrom ycin, 500 m g PO q.i.d. Ã— 10 days

o

Children: 

Erythrom ycin ethylsuccinate, 40 m g/kg/d PO div. q.i.d. Ã— 10 days



Azithrom ycin, 12 m g/kg once daily for 5 days or 20 m g/kg once daily for 3 days



Oral cephalosporins:

Pa ge 3 6 2

o

Reasonable to use in patients with penicillin allergy and inability to tolerate m acrolides



Steroids: o

Dexam ethasone: 0.6 m g/kg to a m ax. 10 m g IM Ã— 1

o

Prednisone: 40â€“60 m g PO Ã— 1

Follow-Up Disposition Admission Criteria 

Airway com prom ise



Severe dehydration



Suspected child abuse

Discharge Criteria Able to tolerate oral intake

References 1. Bisno AL. Acute pharyngitis. N Engl J Med. 2001;344(3):205â€“211. 2. Centor RM, Witherspoon JM, Dalton HP, Brody CE, Link K. The diagnosis of strep throat in adult in the em ergency room . Medical Decision Making. 1981;1(3):239â€“246. 3. Webb KH, Needham CA, Kurtz SR. Use of a high-sensitivity rapid strep test without culture confirm ation of negative results: 2 yearsâ€™ experience. J Fam Pract 2000;49(1):34â€“38. 4. Webb KH. Does culture confirm ation of high-sensitivity rapid streptococcal tests m ake sense? A m edical decision analysis. Pediatrics. 1998;101(2):E2. 5. Marvez-Valls EG, Stucky A, Ernst AA. A random ized clinical trial of oral versus intram uscular delivery of steroids in acute exudative

Pa ge 3 6 2

pharyngitis. Acad Em erg Med. 2002;9(1):9â€“14. 6. Mell LK, Davis RL, Dwens D. Association between streptococcal infection and obsessive-com pulsive disorder, Tourette's syndrom e, and tic disorder. Pediatrics 2005;116(1):56â€“60.

Codes ICD9-CM 462

ICD10 J02.9

Pa ge 3 6 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phencyclidine, Po iso ning

Phencyclidine,

Poisoning Steven Aks

Basics Description 

Dissociative anesthetic structurally related to ketam ine: o

Causes decreased perception of pain and agitation



Half-life of 21â€“24 hours, but m ay be longer in overdose



Enterohepatic recirculationâ€”recirculated into the stom ach

Etiology 

Drug of abuse: o

Frequently encountered as an adulterant of m arijuana



Street nam es for phencyclidine (PCP) include: o

Angel dust

o

Wicky stick

o

Wicky weed

o

Wacky weed

o

Wet

o

Illy

o

Em balm ing fluid

Pa ge 3 6 3

o

Sherm an

Pediatric Considerations Exposure in toddlers reported via passive exposure

Diagnosis Signs and Symptoms Central Nervous System 

Altered m ental status: o

Agitation

o

Bizarre/violent behavior

o

Belligerence



Com a



Seizures



Nystagm us (vertical, horizontal, or rotatory)

Cardiovascular 

Hypertension



Tachycardia

Musculoskeletal 

Traum atic injury (decreased pain perception)



Rhabdom yolysis (owing to vigorous m uscular contraction)

Vital Signs Hypertherm ia

Essential Workup 

Clinical diagnosis based on presentation supported by urine toxicology screen: o

Dextrom ethorphan and ketam ine m ay give false-positive.

Pa ge 3 6 3



Careful physical exam for occult traum a



Exclude other causes of altered m ental status.

Tests Lab 

CBC



Electrolytes, BUN/creatinine, glucose



Urinalysis: o



Dip for m yoglobin (rhabdom yolysis)

Creatine phosphokinase (CPK): o

If urine dip for blood is positive



Ethanol level



Serum osm olality to rule out toxic alcohol ingestion

Imaging 

Chest radiograph for aspiration pneum onia



Extrem ity/spine radiographs when there is associated traum a



CT scan of the head when there is head traum a/altered m ental status

Differential Diagnosis Drugs of Abuse 

Cocaine



Am phetam ines



Designer drugs: o

Methcathinone (Cat)

o

Ecstasy

o

ICE



Ketam ine



Other sym pathom im etics



Alcohols

Drugs That Cause Nystagmus

Pa ge 3 6 3



Lithium



Carbam azepine



Sedative-hypnotics



Alcohols



Phenothiazines



Dextrom ethorphan

Treatment Pre Hospital Cautions: 

Use restraints/additional personnel to control com bative patient.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



IV



Cardiac m onitor



Naloxone, thiam ine, glucose (or Accu-Chek) if altered m ental status



Protect patient/staff from injury

ED Treatment 

Maintain patient in a quiet place; avoid stim ulation.



Physical restraints for violent patient



Sedation: o

Benzodiazepines

o

Butyrophenones (haloperidol) theoretically can lower the seizure threshold.



Activated charcoal/sorbitol if oral coingestants



IV 0.9% norm al saline (NS) hydration/sodium bicarbonate/m annitol for rhabdom yolysis

Pa ge 3 6 3

P.849

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Ativan (lorazepam ): 2 m g IV increm ents



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam : 5 m g IV increm ents



Haloperidol: 5 m g IV increm ents



Mannitol: 25â€“50 g IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sodium bicarbonate: 2 am p diluted in 1 L of D 5 W, given at 125â€“250 m L/h (for rhabdom yolysis) to urine pH of 7.0



Sorbitol: 1â€“2 g/kg to a m ax. 100 g (peds: older than 1 year, 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurryâ€”use only for first dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Prolonged altered m ental status



Significant traum atic injuries



Rhabdom yolysis



Hypertherm ia

Pa ge 3 6 3

Discharge Criteria Becom e lucid after a period of observation (6 hours)

References 1. Hahn I-H. Phencyclidine and ketam ine. In: Erickson TB, Ahrens W, Aks SE, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2004: 297â€“302. 2. Moriarty AL. What's â€œnewâ€• in street drugs: â€œilly.â€• J Pediatr Health Care. 1996;10:41â€“42. 3. Patel R, Connor G. A review of thirty cases of rhabdom yolysis-associated acute renal failure am ong phencyclidine users. Clin Toxicol. 1986;23:547â€“556. 4. Shannon M. Recent ketam ine adm inistration can produce a urine toxic screen which is falsely positive for phencyclidine. Pediatr Em erg Care. 1998;14:180. 5. Silber TJ, Iosefsohn M, Hicks JM, et al. Prevalence of PCP use am ong adolescent m arijuana users. J Pediatr. 1988;112:827â€“829.

Codes ICD9-CM 968.3

ICD10 T41.1

Pa ge 3 6 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phenyto in, Po iso ning

Phenytoin,

Poisoning Michele Zell-Kanter

Basics Description 

Follows zero-order pharm acokinetics: o

Sm all increm ental increase in dose can result in a large increase in plasm a concentration.



Half-life in overdoseâ€”up to 70 hours



Cardiovascular toxicity from IV adm inistration owing to the diluent propylene glycol



Fosphenytoin, a prodrug for parenteral adm inistration, is m etabolized to its active m oiety.

Etiology 

Phenytoin intoxication results from acute, chronic, or acute on chronic ingestion.



If the cause of the intoxication is unclear in a patient on phenytoin, consider: o

Change in the brand of phenytoin

o

Change in dosage form

o

Drug interaction

Pa ge 3 6 3

Diagnosis Signs and Symptoms 







Levels 20â€“40 Âµg/m L: o

Nystagm us

o

Dizziness

o

Ataxia

o

Drowsiness

o

Nausea/vom iting

o

Diplopia

o

Slurred speech

Levels 40â€“90 Âµg/m L: o

Confusion

o

Disorientation

Level >90 Âµg/m L: o

Com a

o

Respiratory depression

o

Paradoxical seizures

Hypotension/bradycardia with rapid IV adm inistration: o

Fosphenytoin injection does not contain propylene glycol.

o 

Hypotension/dysrhythm ia unlikely with fosphenytoin

Hypersensitivity reaction following chronic use: o

Rash

o

Fever

o

Neutropenia

o

Agranulocytosis

o

Hepatitis

o

Cholangitis

Essential Workup

Pa ge 3 6 3



Determ ine the tim e and am ount of ingestion.



Phenytoin level: o

After oral overdose, the peak plasm a concentration m ay not be reached until 24 hours or m ore postâ€“acute ingestion.

o

Repeat levels every 4 hours until levels have peaked and are declining.

o

Once levels begin declining, check every 24 hours until <30 Âµg/m L.

Tests Lab 

Fosphenytoin level: o

Measured as phenytoin

o

Measure fosphenytoin after conversion to phenytoin is com plete (2 hours postâ€“IV infusion/4 hours postâ€“IM injection).

o

Prior to com plete conversion to phenytoin, im m unoanalytic techniques m ay overestim ate plasm a phenytoin concentrations owing to cross-reactivity with fosphenytoin.



Electrolytes, BUN, creatinine, glucose: o

Check for anion gap m etabolic acidosis owing to coingestant.

o

Determ ine glucose with altered m ental status.

Differential Diagnosis 

Intoxication with other CNS depressants



Guillain-BarrÃ© syndrom e



Botulism



Posterior fossa tum or



Acute cerebellitis

P.851

Pa ge 3 6 3

Treatment Pre Hospital 

Differentiate phenytoin-induced altered m ental status from other potentially serious causes: o



Head traum a com m on in seizure population

Collect/transport prescription bottles and m edications to aid in identification and quantification of ingestion.

Initial Stabilization 



Airway, breathing, and circulation m anagem ent (ABCs): o

IV access

o

Cardiac m onitor (with IV overdose)

Treat hypotension with IV fluids and Trendelenburg position: o

Dopam ine for refractory hypotension



Treat paradoxical seizures with diazepam .



Gastric lavage if within 1 hour of ingestion



Activated charcoal: o

Adm inister single dose.

o

Multiple-dose activated charcoal m ay increase the clearance of phenytoin; does not correlate with clinical im provem ent in patients with phenytoin toxicity.

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO

Pa ge 3 6 4



Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Dopam ine: 2â€“20 Âµg/kg/m in IV titrated to desired blood pressure



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sorbitol: 1â€“2 g/kg to m ax. 100 g (peds: >1 year old: 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurryâ€”use only for first dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Altered m ental status, severe ataxia, increasing phenytoin level



Level >25 Âµg/m L



ICU adm ission with intoxication from IV phenytoin

Discharge Criteria 

Level â‰¤25 Âµg/m L



Am bulatory without ataxia

References 1. Browne TR. Fosphenytoin (Cerebyx). Clin Neuropharm acol. 1997;20:112. 2. Glick TH, Workm an TP, Gaufberg SV. Preventing phenytoin intoxication: safer use of a fam iliar anticonvulsant. J Fam Pract. 2004;53:197â€“202. 3. Kawasaju C, Busgu R, Uekihara S, et al. Charcoal hem operfusion

Pa ge 3 6 4

in the treatm ent of phenytoin overdose. Am J Kidney Dis. 2000;35:323â€“326. 4. McKinney PE. Phenytoin. In: Ford MD, Delaney KA, Ling LJ, et al. eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:485â€“492.

Codes ICD9-CM 966.1

ICD10 T42.0

Pa ge 3 6 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pheo chro m o cyto m a

Pheochromocytoma David N. Zull

Basics Description 

Catecholam ine-producing tum or arising from the chrom affin tissues of the sym pathetic nervous system





Origin from the adrenal m edulla or sym pathetic ganglia: o

80% solitary adrenal (usually the right side)

o

10% bilateral (usually inherited form )

o

10% extra-adrenal in location

Location: o

Abdom inal, within m esenteric ganglia (86%)

o

Thorax (10%)

o

Neck (3%)

o

Urinary bladder (1%)

o

10% m alignant (usually inherited form )

Incidence 

Incidence ranges from 0.05â€“0.2% of hypertensive patients, but higher proportion of patients with severe hypertension.



2 per m illion population per year



Peaks in the 3rd to 5th decade, 10% in children

Pa ge 3 6 4



Male = Fem ale



In about half of cases, the diagnosis is m ade postm ortem .



Ten percent are asym ptom atic, found incidentally by CT scanning.

Genetics 

Inherited form in 25%



Autosom al dom inant trait with pheochrom ocytom a (Pheo) alone or in com bination with other endocrine tum ors



Usually associated with m ultiple endocrine neoplasia (MEN), less so with von Hippel-Lindau (VHL) disease: o

MEN 2A (m edullary thyroid carcinom a [CA], Pheo, and hyperparathyroidism )

o

MEN 2B (m edullary thyroid CA, Pheo, oral m ucosal neurom as, skeletal and bony abnorm alities)

o

VHL (hem angiom as of the retina, cerebellum , and brainstem , with renal tum ors)



Other associated diseases include neurofibrom atosis, tuberous sclerosis, Sturge-Weber syndrom e, and paragangliom as of the neck.

Etiology 

The tum or synthesizes and stores catecholam ines in the sam e m anner as the norm al adrenal m edulla.



Most secrete norepinephrine and epinephrine, but m ay secrete predom inantly one or the other.



Paroxysm al release of catecholam ines



Spontaneously owing to changes in blood flow or tum or necrosis



Direct pressure on the gland from external forces (traum a, exercise)



Precipitation of release (opiates, glucagons, m etoclopram ide, histam ine)

Pa ge 3 6 4



Augm entation of catecholam ine effect (tricyclic antidepressants [TCAs], beta-blockers, and sym pathom im etics)

Diagnosis Signs and Symptoms History 

Hypertensionâ€”m oderate to severe, refractory to treatm ent



40%â€”paroxysm s with norm al blood pressure (BP) between episodes



30%â€”sustained hypertension with paroxysm s



30%â€”sustained hypertension without paroxysm s



Classic features of paroxysm s: o

Sudden onset

o

Duration: m inutes to hours

o

Intervals: days to m onths

o

Increasing frequency, duration, and severity with tim e



Clinical characteristics: o

Hypertensive crisis or urgency

o

Headache

o

Tachycardia/palpitations

o

Profuse diaphoresis

o

Apprehension/anxiety

o

Precipitants (see Etiology)

o

Other clinical m anifestations

o

Hypotension (decreased plasm a volum e and blunted sym pathetic reflexes)

Pa ge 3 6 4



o

Orthostasis

o

Shock associated with traum a or surgery

Associated sym ptom s: o

Chest pain (m yocardial ischem ia, dissection)

o

Syncope (arrhythm ia, hypotension)

o

Abdom inal pain, vom iting (tum or necrosis, m esenteric ischem ia)

o

Trem ors, sweating, increased heart rate

o

Weight loss/fevers (increased m etabolic rate)

o

Diarrhea (if vasoactive intestinal peptide [VIP] producing tum or)

o

Flushing or pallor

o

Lethargy, confusion (hypertensive encephalopathy)

o

Focal neurologic findings (cerebral vascular accident [CVA])

o

Acute hem orrhagic tum or necrosis

o

Acute abdom en

o

Marked hypertension followed by declining BP leading to hypotensive shock

Physical Exam 

Moderate to severe hypertension, often with orthostatic changes



Tachycardic, diaphoretic, evidence of weight loss



No palpable m asses (tum ors tend to be sm all)

Essential Workup 

Accurate BP determ ination



ECG: o

Ischem ia

o

Dysrhythm ias

Tests

Pa ge 3 6 4

Lab 

CBC: o

Elevated hem oglobin owing to dim inished plasm a volum e

o 

Indicated when abdom inal pain/infection

Electrolytes, BUN, creatinine, glucose: o

Lactic acidosis

o

Renal failure secondary to hypertension/renal dam age

o

Hyperglycem ia owing to im paired response to insulin and effect of catecholam ines

o

Hypercalcem ia owing to excess parathyroid horm one (PTH)



Urinalysis: proteinuria and hem aturia

Diagnostic Studies 

Fractionated plasm a m etanephrine: o

Ninety-nine percent sensitive, 85% specificâ€”excellent screening, but false-positives

o 

Least likely to be interfered by m edications or stress

Clonidine suppression test if diagnosis uncertain (levels not suppressed if Pheo)



Provocative testing with glucagon is not recom m ended.



Twenty-four-hour urine collection for free catecholam ines, m etanephrine (total and fractionated), and vanillylm andelic acid test (VMA): o

Ninety-eight percent com bined specificity

o

Must include creatinine to verify adequate collection

o

Medications that interfere: levodopa, m ethyldopa, MAO inhibitors, labetalol, propanolol, radiographic contrast m edia, sym pathom im etics, benzodiazepines, TCAs, caffeine, nicotine

Pa ge 3 6 4

o

May require several collections

o

Should be done at the tim e of a paroxysm

Imaging 

CT scanning sensitive for adrenal m asses >1 cm



MRI or positron em ission tom ography (PET) scanning useful in identifying extra-adrenal tum ors



Metaiodobenzylguanidine scan (MIBG) radionuclear scintiscanâ€”high specificity for localization, but not sensitive enough to exclude Pheo



Chest radiograph for pulm onary edem a



CT head for CVA/intracranial bleed

Diagnostic Procedures/Surgery 

Fine-needle aspiration is contraindicated.



Laparoscopic resection is feasible in m any cases.

P.853

Differential Diagnosis 

Panic attack



Thyrotoxicosis



Cocaine or am phetam ine intoxication



MAO inhibitor reaction



Hypertensive crisis



Alcohol withdrawal



Severe m igraine

Treatment Initial Stabilization

Pa ge 3 6 4



IV access



Continuous cardiac/blood pressure m onitoring

ED Treatment 

Hypertensive crisis: o

Alpha-blockade with phentolam ineâ€”first-line agent

o

Nitroprusside for uncontrolled hypertension

o

Vigorous fluid resuscitation required as vasoconstriction is relieved



Beta-blockade (labetalol or esm olol): o

For further BP control

o

If tachycardia develops during induction of alpha-blockade

o

Never use alone: institution of beta-blockade without prior Î±-adrenergic blockade m ay exacerbate hypertension by antagonizing Î²-m ediated vasodilatation in sm ooth m uscle.



Ventricular tachydysrhythm ias: o

Beta-blockade

o

Am iodarone

o

Lidocaine

Medication (Drugs) Management of Hypertensive Paroxysm 

Phentolam ine: o

2.5â€“5.0 m g IV bolus at 1 m g/m in

o

Repeat bolus q5m in to response.

o

Infusion: 100 m g in 500 m L D 5 W (dose as for nitroprusside)



Nitroprusside: o

0.5â€“10 Âµg/kg/m in IV infusion

Pa ge 3 6 4



Beta-blockade: o

Esm olol: load 500 Âµg/kg over 1 m inute, followed by 50 Âµg/kg/m in for 4 m inutes; if adequate therapeutic effect not achieved within 5 m inutes, repeat loading dose and increase infusion to 100 Âµg/kg/m in; repeat loading dose and titrate infusion rate upward at 50 Âµg/kg/m in q4â€“q5m in as needed; om it further loading doses once nearing therapeutic target.

o

Labetalol: begin with 10â€“20 m g IV; BP falls within 5 m inutes, m ax. effect at 10 m inutes; can double IV dose q15â€“q30m in until target reached.

o

Metoprolol: 5 m g IV q15m in until response

Mild to Moderate Hypertension 

Doxazosin: 1â€“8 m g/d orally



Nicardipine: 5â€“15 m g IV over the first hour, then 3â€“5 m g/h infusion



Prophylaxis of hypertensive paroxysm (preoperative): o

Phenoxybenzam ineâ€”start at 10 m g b.i.d. orally, titrate up 10 m g every other day until desired effect

o

Beta-blocker to control reflex tachycardia

Follow-Up Disposition Admission Criteria 

Suspicion of pheochrom ocytom a in an ill patient m andates alpha-blockade and aggressive volum e expansion in a closely m onitored setting.



Hypertensive urgency or crisis



Cardiac arrhythm ias

Pa ge 3 6 5



End organ com prom ise: congestive heart failure (CHF), m yocardial infarction (MI), renal insufficiency, CVA, abdom inal pain

Discharge Criteria Stable patient with m ild hypertension m ay be referred for prom pt outpatient evaluation.

References 1. Brouwers FM, Lenders JWM, Eisenhofer G, et al. Pheochrom ocytom as as an endocrine em ergency. Rev Endocr Metab Disord. 2003;4:121â€“128. 2. Kercher KW, Novitsky YW, Park A, et al. Laparoscopic curative resection of Pheochrom ocytom as. Ann Surg. 2005;241(6):919â€“928. 3. Lenders JW, et al. Biochem ical diagnosis of pheochrom ocytom a: which test is best? JAMA. 2002;287:1427â€“1434. 4. Manger WM, Eisinhofer G. Pheochrom ocytom a: diagnosis and m anagem ent update. Curr Hypertens Rep. 2004;6:477â€“484. 5. Schifferdecker B, Kodali D, Hausner E, et al. Adrenergic shockâ€”an overlooked clinical entity? Cardiol Rev. 2005;13(2):69â€“72. 6. Westphal SA. Diagnosis of a pheochrom ocytom a. Am J Med Sci. 2005;329(1):18â€“21.

Codes ICD9-CM 227.0

Pa ge 3 6 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phim o sis

Phimosis

Daniel Firestone

Basics Description 

True phim osis is the inability to retract the foreskin over the glans of the penis as a result of scarring.



The inability to retract a norm al, supple foreskin is not true phim osis.



The foreskin is rarely retractable at birth due to norm al adhesions between the glans and the inner prepuce.



Approxim ately 90% are retractable by three years of age, and 99% are retractable by age 17, as the epithelial cells that com prise sm egm a are shed.



Parents should be instructed not to forcibly retract the foreskin.

Etiology Possible causes of true phim osis include: 

Traum a from forcible retraction of the foreskin



Repetitive bouts of diaper derm atitis



Recurrent balanoposthitis



Poor hygiene



Poorly perform ed circum cision



Congenital anom alies

Pa ge 3 6 5

Diagnosis Signs and Symptoms 

Whitish, narrowed preputial opening of the foreskin



Dysuria, hem aturia



Poor urinary stream



Edem a, erythem a, and tenderness of prepuce



Balanoposthitis (inflam m ation of the glans and foreskin)



Ballooning of foreskin on urination in severe cases

Essential Workup 

In the m ajority of cases, no workup is necessary.



In patients with severe stenosis, the com plication of an obstructive uropathy m ay occur.



This should be investigated by: o

Evaluation of kidney function: 

o 

Blood urea nitrogen and creatinine

Renal sonogram

Phim osis secondary to recurrent balanoposthitis should prom pt a workup for diabetes m ellitus: o

Urinalysis, serum glucose, or glycosylated hem oglobin (Hgb A1C)

Differential Diagnosis 

Preputial adhesions are norm al in young children.



Balanoposthitis without phim osis

Treatment

Pa ge 3 6 5

Pre Hospital 

Pre hospital personnel and fam ily m em bers should be instructed not to attem pt retraction of the foreskin prior to m edical evaluation.



Unwarranted attem pts m ay traum atize a norm al, nonretractable prepuce, or convert the situation to a m ore em ergent paraphim osis.

Initial Stabilization 

None required in m ost cases



Exam ination should include an evaluation for potential com plications: o



Obstruction and vascular com prom ise of glans

These occur only in the m ost extrem e cases.

P.855

ED Treatment 

Relieve obstructive uropathy, if present, with urethral catheterization or suprapubic aspiration.



If vascular flow to the glans is com prom ised, a dorsal slit m ust be m ade in the foreskin: o

Perform ed after achieving adequate penile block (see paraphim osis section for m ore detailed description of procedure)

o 

This is rarely necessary in phim osis.

Potent topical steroids for a m ultiweek course have been reported to successfully reduce phim osis: o

Decision to prescribe should only be m ade in conjunction with a urologist

Pediatric Considerations

Pa ge 3 6 5

For foreskin incision, procedural sedation will likely be needed in place of penile-block.

Medication (Drugs) Pain control as required

Follow-Up Disposition Admission Criteria 

Obstructive uropathy



Severe balanoposthitis with ischem ia or necrosis

Discharge Criteria 

Ability to urinate



Adequate urologic follow-up

Issues for Referral 

In uncom plicated cases, provide patients with urologic follow-up for conservative trial of topical steroids, elective dilation of the preputial opening, operative repair, or elective circum cision as necessary.

References 1. Webster TM, Leonard MP: Topical steroid therapy for phim osis. Can J Urol. 9:1492,2002. 2. Dewan PA, Tieu HC. Phim osis: Is circum cision necessary? J Pediatr Child Health. 1996;32(4):285â€“289. 3. Pontari MA. Phim osis and paraphim osis. In: Seidm an EJ, Hanno PM, eds. Current urologic therapy. 3rd ed. Philadelphia, PA: WB Saunders, 1994:392â€“397.

Pa ge 3 6 5

4. Super DM. Phim osis. In: Hoekelm an R, et al., eds. Prim ary pediatric care. St. Louis: CV Mosby, 1987: 1232â€“1234.

Miscellaneous SEE ALSO: Paraphim osis

Codes ICD9-CM 605

Pa ge 3 6 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pityriasis Ro sea

Pityriasis Rosea

Nate Rudman

Basics Description 

A com m on papulosquam ous rash of unknown etiology



Classically m anifests by a herald patch involving the trunk and proxim al extrem ities

Etiology 

Unknown; weak evidence exists for an infectious (viral) cause



Herpes virus 6 and 7 have been suggested



Medications have been associated with a pityriasislike eruption: o

Barbiturates

o

Captopril

o

Clonidine

o

Gold

o

Isotretinoin

o

Metronidazole

o

Penicillam ine

Pa ge 3 6 5

Diagnosis Signs and Symptoms 

Herald patch: o

Solitary, erythem atous, slightly raised papule 2â€“10 cm in diam eter

o 

Seen in 50â€“90% of cases

Secondary eruption: o

Widespread salm on colored, elliptic, finely scaling 1-cm m acular or papular lesions

o

Longest axis along lines of skin tension (a â€œfir treeâ€• distribution)

o

Generally follows herald patch by seven to 14 days

o

Lesions are concentrated on the trunk and proxim al extrem ities.



Pruritus accom panies rash in up to 75% of cases



Prodrom al sym ptom s m ay be seen in 5%:



o

Fever

o

Headache

o

Malaise

o

Arthralgias

o

GI sym ptom s

Atypical presentations including oral involvem ent and inverse pityriasis rosea are m ore com m on in children.





Oral lesions: o

Punctate hem orrhages

o

Ulcerations

o

Erythem atous m acules, and vesicles

Lesions concentrated on the face and distal extremities with m inim al trunk involvem ent characterize inverse pityriasis: o

Atypical form s of individual lesions occasionally occur

Pa ge 3 6 5

including papular, urticarial, pustular, and purpuric

Essential Workup 

Syphilis testing: o

Secondary syphilis can m im ic pityriasis rosea

o

RPR or VDRL is required if the diagnosis is in question.

o

Especially with history of chancre or absence of herald patch



KOH preparation m ay be needed to differentiate the herald patch from tinea corporis: o

Atypical form s of individual lesions occasionally occur including papular, urticarial, pustular, and purpuric.

P.857

Differential Diagnosis 



Herald patch: o

Num m ular eczem a

o

Tinea corporis

Generalized eruption: o

Secondary syphilis

o

Drug eruption

o

Guttate psoriasis

o

Kaposi sarcom a

o

Lichen planus

o

Occult m alignancy

o

Scabies

o

Seborrheic derm atitis

o

Tinea versicolor

Pa ge 3 6 5

Treatment Initial Stabilization None required

ED Treatment Pityriasis is treated sym ptom atically.

Medication (Drugs) 

Diphenhydram ine: adult: 50 m g PO q.i.d.; peds: 5 m g/kg/d div. q.i.d.



Hydrocortisone: adult: 1% cream t.i.d.; peds: 1% cream t.i.d.



Prednisone: adult: 15â€“40 m g per day; peds: 0.25â€“0.5 m g/kg per day



Ultraviolet B (UVB): five daily erythem ogenic doses

Follow-Up Disposition Discharge Criteria Pityriasis rosea is a self-lim ited disease; adm ission is not required.

References 1. Allen R, Janniger CK, Schwartz RA. Pityriasis rosea. Cutis. 1995;56(4):198â€“202. 2. Bjornborg A. Epiderm al-derm al inflam m atory conditions of unknown etiology. In: Fitzpatrick TB, et al., eds. Derm atology in general m edicine. 4th ed. New York: McGraw-Hill,1993:1117â€“1123. 3. Gonzalez LM, Allen R, Janniger CK, Schwartz RA. Pityriasis rosea:

Pa ge 3 6 6

an im portant papulosquam ous disorder. Int J Derm atol. 2005 Sep;44(9):757â€“64. 4. Hartley AH. Pityriasis rosea. Pediatr Rev. 1999;20(8):266â€“269.

Codes ICD9-CM 696.3

ICD10 L42

Pa ge 3 6 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Placenta Previa

Placenta Previa

Roneet Lev

Basics Description 

Im plantation of placenta over the internal cervical os



Uterine enlargem ent and cervical dilation cause placental vessels near the cervix to tear, resulting in vaginal bleeding



Placenta previa seen on ultrasound before 28 weeks frequently â€œm igratesâ€• and does not end up as placenta previa at term .



Twenty percent of all antepartum hem orrhage



Classifications: o

Total placenta previa: cervical os is com pletely covered by placenta.

o

Partial placenta previa: cervical os is partially covered by placenta.

o

Marginal placenta previa: edge of placenta is at m argin of cervical os.

o

Low-lying placenta: placenta edge is close to cervical osâ€”60% chance of vaginal birth.

Etiology 

Unknown

Pa ge 3 6 6



Incidence: 1/300 births = 0.33% of pregnancies



Maternal m ortality: 0.03%



Perinatal m orbidity and m ortality: Triple increase: o



Associated with preterm delivery and fetal anom alies

Factors affecting location of im plantation: o

Abnorm al endom etrial vascularization

o

Delayed ovulation

o

Prior traum a to endom etrium

Risk Factors 

Multiparity (1/20 grand m ultiparous patients versus 1/1,500 nulliparous)



Multifetal gestations (40% increase)



Prior C-section (up to 6 tim es increase; increases with num ber of prior C-sections; 1.9â€“4.1%)



Increased m aternal age (triple increase if age >30 years com pared with age <20 years)



Previous placenta previa (4â€“8% recurrence)



Sm oking (2â€“4 tim es increase)

Associated Conditions 

Intrauterine growth retardation (20%)



Congenital abnorm alities (double increase in incidence)



Abnorm al fetal presentation (30%)



Prem ature rupture of m em branes



Vasa previa: Fetal vessels course through m em branes and cover os.



Placenta accreta, increta, percreta (growth of placenta into uterine wall)

Diagnosis

Pa ge 3 6 6

Signs and Symptoms Painless vaginal bleeding in second half of pregnancy is placenta previa until proven otherwise.

History 

Painless bright red vaginal bleeding in 70% of patients



Uterine contraction in 20% of patients



Occurs at >20 weeksâ€™ gestation



First episode of bleeding typically occurs at 27â€“32 weeks.



Inciting factorsâ€”usually no cause; recent intercourse or heavy exercise m ay contribute.



Initial bleeding is often self-lim ited and not lethal.



Many cases are discovered on routine ultrasound, and patients are asym ptom atic.

Physical Exam 

Never do a digital exam ination or instrum ent probing of the cervix in second-trim ester vaginal bleeding until placenta previa is ruled out.



If obstetric (OB) consult is not readily available, do a partial speculum insertion to identify if blood is from the os or vaginal lesion.



Blood seen at patient's feet is a sign of heavy bleeding.



Hypotension and tachycardia m ay indicate hem orrhagic shock.



Fetal heart tones should be m onitored along with other vital signs.

Essential Workup 

Ultrasonogragraphy is diagnostic procedure of choice.



Placental edge at <2 cm of cervical os is placenta previa and will require C-section delivery.

Pa ge 3 6 6

Tests Lab 

CBC, platelets



Type and cross-m atch.



Kleihauer-Betke (KB)â€”detects >5 m L of fetal cells in m aternal circulation (it takes only 0.1 m L to sensitize m other if Rh negative)



If coagulopathy suspected (rare): PT/PTT, fibrin-split products (FSP), fibrinogen (<300 m g/dL is abnorm al)



Rh status



Wall clot testâ€”fill red top tube and tape to wall; if no clot in 6 m inutes, assum e coagulopathy.

Imaging 

Transabdom inal ultrasound: 93â€“97% accurate: o

False-negative: obesity, posterior or lateral placenta, fetal head over cervical os

o 

False-positive: overdistended bladder

Transperineal (translabial) ultrasoundâ€”reported 100% accuracy



Transvaginal ultrasound: 100% accurate, generally safe: o

Place probe no m ore than 3 cm into vagina and do not contact the cervix.

o

Best to determ ine distance of placental edge to internal os



MRI: m ay be useful in evaluating placental abnorm alities such as accreta and percreta

P.859

Differential Diagnosis

Pa ge 3 6 6



Placenta abruption



Uterine rupture



Fetal vessel rupture



Cervical/vaginal laceration



Cervical/vaginal lesions



Congenital bleeding disorder



Spontaneous abortion



â€œBloody showâ€• of labor

Treatment Pre Hospital 

Patient with vaginal bleeding at >24 weeks should be transported to a facility that can handle high risk and prem ature delivery.



Place patient in left lateral recum bent position if hypotensive in second half of pregnancy.



O 2 and IV as with other patients

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Two large-bore IVs with norm al saline (NS) or lactated Ringers (LR)



Left lateral recum bent position if hypotensive in second half of pregnancy



Fluid resuscitation



Blood transfusion for hem atocrit (Hct) <30 or hypotension not responding to fluids



FFP if coagulopathy



Fetal m onitoring (heart rate [HR] <120 or >160 is abnorm al)

Pa ge 3 6 6



Im m ediate OB consultation

ED Treatment 

Volum e resuscitation with two large-bore IVs with NS or LR



Blood transfusion to keep Hct 30â€“35%



RhoGAM if m other is Rh negative



Fetal m onitoring



Keep NPO and at bed rest until considered stable by OB.



Tocolytics (m agnesium sulfate) if preterm labor



Antenatal steroids between 24 and 34 weeks for preterm labor



Em ergency C-section or delivery for continued bleeding or fetal com prom ise

Medication (Drugs) 

Magnesium sulfate: 6 g IV over 20 m in, then 2â€“4 g/h; adjust to contractions



RhoGAM: 1 vial (300 Âµg) IM; m ay need m ore than one vial if KB indicates >15 m L of fetal RBS

Follow-Up Disposition Admission Criteria Adm it all patients >20 weeks gestation with vaginal bleeding caused by placenta previa.

Discharge Criteria 

Incidental finding of placenta previa by ultrasound at <28

Pa ge 3 6 6

weeks with no vaginal bleeding or uterine contractions 

Patients at â‰¥28 weeks with no active bleeding and no uterine contractions m ay be discharged after OB consultation to ensure follow-up.



Advise: pelvic rest (no intercourse or tam pons in vagina) and return precautions if bleeding occurs; bed rest if patient is bleeding, m ay resum e norm al activity if incidental finding and no vaginal bleeding



Seventy percent of patients will have a second episode of bleeding.

References 1. Cunningham FG, Leveno KJ, Bloom SL, et al. William sâ€™ Obstetrics. 22nd ed. New York: McGraw-Hill; 2005. 2. Hacker NF, Moore JG. Essentials of Obstetrics and Gynecology. 4th ed. Philadelphia: WB Saunders; 2004. 3. Marx JA, Hockberger RS, Walls RM, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 4. Neilson JP. Interventions for Suspected Placenta Praevia. Cochrane Library, issue 4. Oxford: Update Software; 2002. 5. Scott JR, Gibbs RS, Karlan BY, et al. Danforth's Obstetrics and Gynecology. 9th ed. Philadelphia: Lippincott William s & Wilkins; 2003.

Codes ICD9-CM 641.10

ICD10 044.1

Pa ge 3 6 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Plant, Po iso ning

Plant, Poisoning

Kirk Cumpston

Diagnosis Signs and Symptoms Herbs 



Shave grass and horsetail: o

CNS stim ulant

o

Confusion

o

Ataxia

Pokeweed, juniper berries, senna: o

Fulm inant gastroenteritis

o

Abdom inal pain/colic

o

Pokeweed (bradycardia, heart block, tachycardia, ventricular fibrillation [VFib])





Pennyroyal oil: o

Hepatorenal syndrom e

o

Pulm onary toxicity

o

Seizures

o

Com a

o

Abortifacient

Sassafras root: o

Nausea/vom iting

o

Vertigo

Pa ge 3 6 6



o

Hallucinations

o

Shock

o

Respiratory depression

Cham om ile, chrysanthem um s: histam ine-releasing/anaphylactic reactions:



o

Angioedem a

o

Bronchospasm

o

Hypotension

o

Shock

o

Death

Tonka beans, sweet woodruff (natural coum arin): o







Hem orrhage

Nutm eg: o

Nausea, vom iting

o

Chest pain

o

Abdom inal pain

o

Agitation, feelings of doom

o

CNS stim ulation, then suppression

o

Metabolic acidosis

o

Shock

Ginseng: o

Tachycardia

o

Hypertension

o

Hypoglycem ia

o

Increased GI m otility

Jim son weed (locoweed, datura): o

Anticholinergic toxidrom e: 

Dry m outh, skin, eyes



Dilated pupil



Tachycardia



Altered m ental status

Indoor/Outdoor Plants

Pa ge 3 6 7















Buckthorn, coyotillo, tullidora (Karwinskia hum boldtiana): o

Ascending m otor neuropathy, like Guillain-BarrÃ©

o

Respiratory failure

Poison hem lock (Conium m aculatum ): o

Nicotinic toxicity, rhabdom yolysis, renal failure

o

Nausea/vom iting

o

Bradycardia/tachycardia

o

Ascending paralysis

Water hem lock (Cicuta m aculata): o

Cholinergic toxicity, rhabdom yolysis, renal failure

o

Nausea/vom iting

o

Seizures

Yew (Taxus spp): o

Inhibits sodium and calcium channels

o

Nausea/vom iting

o

Bradycardia/dysrhythm ias

May apple: o

Antim itotic, m ultisystem organ failure

o

Nausea/vom iting

o

Encephalopathy

Ackee (Blighia sapida): o

Eating unripe fruit

o

Hypoglycem ia

o

Metabolic acidosis

o

Hepatotoxicity

o

Seizures

Pyrrolizidine alkaloids (Sym phytum , Senecio, Crotalaria, Heliotropium ): o

Liver converts into highly reactive pyrroles.

o

Hepatic veno-occlusive disease

o

Spectrum of hepatic disease from hepatitis to fulm inant hepatic failure

Pa ge 3 6 7



Lectins group (castor bean and rosary pea): o

CNS depression

o

Seizures

o

Severe gastroenteritis

o

Multisystem organ failure can occur within 24 hours (rare).



Colchicine group (autum n crocus and glory lily): o

Three phases: 

Gastrointestinal (24 hours): severe abdom inal pain, nausea, vom iting, diarrhea



Multisystem failure (2â€“7 days): ascending paralysis, adult respiratory distress syndrom e (ARDS), dissem inated intravascular coagulation (DIC), pancytopenia, cardiac arrhythm ias, hepatic failure, renal failure, delirium



Recovery (>7 days): resolution of organ system s failure, rebound of leukocytosis, alopecia

o

Requires large am ount of plant (>0.8 m g/kg of the pharm aceutical colchicineis lethal)



Solanine group (com m on nightshade, woody nightshade, potato tubers, Jerusalem cherry): o

Sym ptom s begin 2â€“4 hours after ingestion.

o

Nausea, vom iting, diarrhea

o

Headaches

o

Muscle weakness

o

Lethargy

o

Hallucinations

o

Central nervous system depression

Nicotine-Containing Plants (Tobacco Plants) 

Rapid onset



Abdom inal pain/nausea/vom iting

Pa ge 3 6 7



Initially tachycardia/hypertension followed by bradycardia/hypotension





CNS stim ulation initially: o

Trem or

o

Seizures

o

Confusion

o

Restlessness

CNS depression later: o

Decreased m ental state

o

Com a

o

Hypotonia/decreased reflexes/m otor paralysis occur sequentially.



Grayanotoxin-containing plants (rhododendrons and azaleas):



o

Dose-dependent bradycardia

o

Hypotension

o

CNS depression

o

Most ingestions asym ptom atic

Cyanogenic plants (seeds of apples, pear, and crab apple; cassava; and bam boo): o

Headache

o

Dyspnea

o

Cyanosis

o

Convulsions

o

Metabolic acidosis

o

Com a, cardiovascular collapse

o

Identical to cyanide poisoning owing to inhibition of oxidative phosphorylation



Cardiac glycosides-containing plants (foxglove, oleander, yellow oleander, lily of the valley): o

Resem bles digoxin toxicity

o

Nausea/vom iting

Pa ge 3 6 7





o

Alteration in vision

o

Cardiac effect: 

Bradydysrhythm ias



Tachydysrhythm ias

Aconite (m onkshood, wolfsbane): o

Sodium channel opener

o

Ventricular dysrhythm ias

o

Cardiovascular collapse

o

Paresthesias, seizures

Hallucinogenics (m arijuana, m orning glory, catnip, peyote, juniper):



o

Mood alterationâ€”euphoria or depression

o

Dry m outh/thirst

o

Tachycardia

o

Toxic psychosis/panic reactions

Oxalate-containing plants (dieffenbachia, philodendron): o

Local tissue destruction of cornea or m ucous m em branes

o

Edem a/pain

o

If oral exposure, potential airway com prom ise

o

Nausea/vom iting

P.861



Gastrointestinal sym ptom s: o

Irritation of oral m ucosa from calcium oxalate crystallization (philodendron)

o

Irritation of gastric m ucosa (daffodil, narcissus)

o

Irritation of intestinal m ucosa (pokeweed, horse chestnut)

Pediatric Considerations 

Often present with lip, tongue, and oropharyngeal

Pa ge 3 6 7

irritation and swelling from oxalate crystal-containing plants: o

Potential for airway com prom ise



Usually consum e leaves and seeds



Nicotine group: 1 or 2 cigarettes potentially lethal



Jim son weed:



o

Seeds highly concentrated

o

100 seeds equals 6 m g of atropine

o

Lethal at 4â€“5 g of leaf

Yellow oleander: o

Two leaves lethal in 12.5-kg child

Essential Workup 

Identification of ingested m aterial



Workup depends on plant ingested.

Tests Lab 

Electrolytes, BUN, creatinine, glucose, liver function tests (LFTs)



Arterial blood gas (ABG): o

Check pH

o

Methem oglobinem ia

o

Oxygen saturation



Digoxin level for cardioglycoside plants



Cyanide level for cyanogenic plants

Imaging 

ECG: dysrhythm ias/bradycardia



Chest radiograph

Differential Diagnosis 

Altered m ental status: o

Drug use/alcohol

Pa ge 3 6 7

o

Seizures

o

Traum a

o

Cerebrovascular accident (CVA)

o

Hypoglycem ia



Digoxin toxicity



Gastroenteritis



Agents causing m etabolic acidosis (use m nem onic MUD PILES, as defined in Acidosis)



Cardiotoxic drugs

Treatment Pre Hospital 

Nontoxic houseplants: o

African violet

o

Alum inum plant

o

Baby's tears

o

Bird's nest fern

o

Corn plant

o

Creeping Charlie

o

Creeping Jenny

o

Gardenia

o

Grape ivy

o

Jade plant

o

Parlor palm

o

Peacock plant

o

Piggyback begonia

o

Prayer plant

o

Rubber tree

o

Snake plant

o

Spider plant

Pa ge 3 6 7

o

Swedish ivy

o

Velvet plant

o

Wandering Jew

o

Wax plant

o

Zebra plant



Collect seeds, leaves, spores in paper bag.



Contact local botanist.



Syrup of ipecac not recom m ended in setting of severe GI distress, altered m ental status.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) IV: o

Aggressive volum e replacem ent for dehydration/hypotension

o

Initiate pressors for hypotension unresponsive to fluids



Cardiac m onitoring



Supportive care for m ost ingestants

ED Treatment 

Gastric decontam ination: o

Gastric lavage for recent (<1 hour) ingestion of plant with serious potential toxicity

o 

Adm inister activated charcoal.

Oxalate crystal irritation from dieffenbachia and philodendron:



o

Local wound care

o

Close follow-up

o

Protection of airway

Gastric decontam ination, fluid therapy, and supportive care for: o

Solanine group

Pa ge 3 6 7

o 



Lectins group

Jim son weed poisoning: o

Physostigm ine in severe cases or benzodiazepines

o

Consult toxicologist.

Cyanogenic group poisoning: o

Cyanide antidote kit

o

In Europe, hydroxocobalam in and DMAP followed by sodium thiosulfate.



Grayanotoxin group poisoning: o



Colchicine group: o



Atropine for significant bradycardia

Multidose activated charcoal

Cardiac glycosides group: o

Digoxin fab fragm ents m ay be useful; initial em piric dose 5â€“10 vials.



o

Correct hyperkalem ia. (Avoid calcium )

o

Magnesium

Nicotine group: o

Airway control (owing to neurom uscular paralysis)

o

Atropine for sym ptom atic bradycardia

Medication (Drugs) 

Atropine: 0.5 m g (peds: 0.02 m g/kg) IV, repeat 0.5â€“1.0 m g IV



DMAP: 3.25 m g/kg IV



Hydroxocobalam in: 50 tim es cyanide dose or 50 m g/kg IV



Magnesium : 2â€“4 g IV



Physostigm ine: 0.5â€“2 m g IV



Cyanide antidote kit: o

Inhale am yl nitrite am pule for 30 seconds every m inute until sodium nitrite given.

Pa ge 3 6 7

o

Sodium nitrite: 10 m L of 3% solution or 300 m g IV over 3â€“5 m inutes (peds: 0.15â€“0.33 m L/kg)

o

Monitor m ethem oglobin levels to keep <30%.

o

Sodium thiosulfate: 50 m L IV of 25% solution or 12.5 g (peds: 1.65 m L/kg)



Digoxin Fab fragm ents: em piric dose 5â€“10 vials



Sodium bicarbonate 8.4%: one am pule IV push until narrowing of QRS com plex

Follow-Up Disposition Admission Criteria 

Dysrhythm ias for cardiac m onitoring



Intractable vom iting



Refractory hypotension



Evidence of end organ dam age



Altered m ental status

Discharge Criteria 

Baseline m ental status



Tolerating fluids



Norm al cardiac activity



No delayed sequelae

Pediatric Considerations 

Lower threshold to adm it children: o

Tend to eat m ore concentrated parts

o

Lower doses are lethal.

o

Sym ptom s m ore nonspecific

References

Pa ge 3 6 7

1. Bryant SM, Aks SE. â€œAre you taking any m edications?â€• Herbal toxicities and their m anifestations in the ED. Em erg Med Pract . 2005;7(1):1â€“24. 2. Graem e K, Braitberg G, Kunkel D, et al. Toxic plants. In: Auerbach PS, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001:1108. 3. Palm er M, Betz JM. Plants. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicological Em ergencies. 7th ed. New York: McGraw-Hill; 2002:1151â€“1182.

Codes ICD9-CM NEC 988.1

ICD10 T62.2

Pa ge 3 6 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pleural Effusio n

Pleural Effusion

Scott B. Murray Edward Ullman

Basics Description 

Norm al conditions: o

Pleural space contains about 30 m L of clear, protein-free fluid that helps facilitate m ovem ent of the pulm onary parenchym a within the thoracic space.

o

Fluid form ation and reabsorption is governed by the hydrostatic and colloid forces acting at the parietal and visceral surfaces.

o

Norm ally, the sum of these forces results in m ovem ent of fluid into the pleural space from the parietal surface and reabsorption at the visceral surface.

o

Lym phatics help rem ove any excess fluid.

o

Alteration of any of the above factors results in excess fluid accum ulation and pleural effusion.



Transudative effusion: o

Results from alteration of system ic hydrostatic and colloid factors

o

An ultrafiltrate of serum , containing little protein or

Pa ge 3 6 8

cells o

Pleural surface is not involved in the prim ary pathologic process.



Exudative effusion: o

Results from pathologic disease of the pleural surface or disruption of lym phatic reabsorption

Etiology 

Transudative effusions: o

Congestive heart failure ([CHF] right or left ventricular)

o

Peritoneal dialysis

o

Cirrhosis with ascites

o

Atelectasis (pulm onary em bolism [PE] or m alignancy causing obstruction)



o

Nephrotic syndrom e

o

Myxedem a

o

Hypoproteinem ia

o

Meigs syndrom e

Exudative effusions: o

Pulm onary (pneum onia, abscess) or pleural infection 

Uncom plicated parapneum onic effusion



Loculated paraneum onic effusion



Com plicated parapneum onic effusion (infected pleural fluid)



Em pyem a (frank pus in pleural space)



Viral, bacterial, tuberculosis (TB), parasitic, fungal

o

Pericarditis

o

Neoplasm , m etastasis, m esotheliom a

o

Pulm onary em bolization or infarction

o

Intraabdom inal disorders: 

Pancreatitis, hepatitis, cholecystitis

Pa ge 3 6 8

o

o

o



Subdiaphragm atic abscess



Esophageal rupture



Peritonitis



Meigs syndrom e

Rheum atologic disease: 

Lupus



Rheum atoid arthritis



Sarcoidosis

Traum a: 

Hem othorax



Chylothorax

Drugs: 

Medications causing drug induced lupus



Nitrofurantoin, m ethysergide, dantrolene, PTU



Warfarin, m esalam ine, fluoxetine, m ethotrexate



Crack cocaine

Diagnosis Signs and Symptoms History 

Dyspnea on exertion or at rest



Cough with large effusion



Pleuritic chest pain with inflam m ation of pleura



Prim ary pathologic process (CHF, pneum onia, pulm onary em bolus, pancreatitis), not the pleural effusion, is often the source of sym ptom s.

Physical Exam 

Decreased breath sounds



Increased egophony

Pa ge 3 6 8



Dullness to chest percussion



Pleural rub



Search for the prim ary cause of pleural effusion.

Tests Lab 

CBC



Electrolytes, blood urea nitrogen/creatinine, glucose, LDH, serum protein



Pulse oxim etry or arterial blood gas



Coagulation profile



Pleural fluid analysis to determ ine if transudate or exudate: o



Check pleural and serum protein and LDH

Criteria for exudates: o

Pleural fluid protein/serum protein >0.5

o

Pleural fluid LDH/serum LDH >0.6

o

Pleural fluid LDH >2/3 upper lim it of norm al serum LDH



Pleural fluid studies to determ ine etiology of exudate: o

Gram stain, AFB stain, routine and m ycobacteria culture

o

Wright stain identifies presence of m esothelial cells, m acrophages, plasm a cells, lym phocytes, PMNs, eosinophils, and m alignant cells

o

Eosinophilia seen with PE, hem othorax, fungal infection, asbestosis, or drug-induced causes

o

RBC and Hct: 

5,000â€“100,000/m m 3 nonspecific



>100,000/m m 3 suggestive of m alignancy, catam enial, pulm onary em bolus, or infarction



Pleural fluid Hct >0.5 serum Hct defines

Pa ge 3 6 8

hem othorax 

Malignancy, TB, aortic rupture



Heparinize and chill hem orrhagic sam ples to be sent for cytology

o

WBC: 

1,000â€“10,000/m m 3 nonspecific



>10,000/m m 3 suggestive of parapneum onic effusion, em pyem a, pancreatitis, rheum atologic, m alignancy, or TB

o

Glucose: 

Levels <50% of serum glucose suggestive of rheum atologic effusion, bacterial em pyem a, m alignancy, or esophageal rupture.

o

Triglyceride: 

Triglycerides >100 m g/dL suggest chylous effusion from disruption of thoracic duct

o

Am ylase: 

Am ylase >200 IU/L suggests pancreatitis, esophageal rupture, m alignancy, TB, or em pyem a.

o

pH: 

Send in a chilled heparinized arterial blood gas syringe

 o

pH <7.0 suggests bacterial em pyem a

Cytology identifies m alignant cells.

P.863

Imaging 

Chest radiograph: o

Upright chest radiographâ€”blunting of the costophrenic angle:

Pa ge 3 6 8

o



Most sensitive radiographic sign



Requires at lease 250 m L of fluid

Presence of subpulm onic effusions m ay be indicated by loss of supradiaphragm atic vascular m arkings or an increased space between the gastric bubble and pulm onary parenchym a.

o

Provides hints to the prim ary source (m alignancy, pneum onia).

o

Obtain lateral decubitus film s to reveal layering of fluid seen with sim ple effusions. 

Suspect a loculated effusion or alternative diagnosis if effusion fails to layer.



Ultrasound: o

Detects sm aller fluid volum es than an upright chest x-ray

o

Indicated as a guide for thoracentesis, particularly if a difficult tap is anticipated

Alert 

Consider PE as a cause of unexplained pleural effusion and obtain the correct diagnostic test.



Obtain lateral decubitus film s prior to perform ing thoracentesis to avoid m isdiagnosis and procedural com plications.

Diagnostic Procedures/Surgery 

Diagnostic/therapeutic ED thoracentesis: o

Indication: 

Diagnose new effusion in toxic-appearing patient.



Suspected parapneum onic effusions (including patients with previously diagnosed effusions)



Sym ptom atic dyspnea caused by large effusions

Pa ge 3 6 8



Diagnostic thoracentesis of a nonparapneum onic effusion in a stable patient can be deferred until after the patient has been adm itted.

o

Correct coagulopathy if present. 

Platelets >50,000/m m 3



Prothrom bin and partial throm boplastin tim e less than twice norm al level.

o

Position patient upright with arm s crossed in front to elevate scapula.

o

Identify superior border of effusion via percussion, ultrasound, or egophony.

o

Mark area one interspace below this in the posterior axillary line or the m id-scapular line.

o

Prepare area with Betadine, dry, and drape for sterile field.

o

Anesthetize with 2% lidocaine.

o

Attach 3-way stop-cock between needle and syringe. Enter superior border of rib with needle bevel down, gently aspirating while advancing. 

Use a 20-gauge needle for sim ple diagnostic aspiration.



Use a 16- to 18-gauge needle/catheter (com m ercial kit) for therapeutic aspiration.



Caution: entering inferior aspect of rib risks lacerating neurovascular bundle

o

Advance catheter over or through needle once pleural space entered: 

Minim um of 100 cc required for basic studies (protein, LDH, cell count, and culture)â€”m ore required for cytology and additional studies



Avoid withdrawing >1500 cc to prevent post-expansion pulm onary edem a.

Pa ge 3 6 8



Intraprocedural chest pain m ay indicate trapped lung or pneum othorax; stop procedure and obtain chest radiograph.

o

After obtaining fluid, withdraw needle, apply pressure, dress, and obtain postprocedural chest radiograph for pneum othorax



Indication for tube thoracostom y: o

Clinical em pyem a: 

o

Aspiration of pus

Com plicated parapneum onic effusion = pneum onia with:

o



pH <7.0, or



Pleural glucose <0.5 serum glucose, or



Pleural gram stain dem onstrates bacteria

Hem othorax

Differential Diagnosis 





Intraparenchym al densities: o

Lobar collapse

o

Mass, tum or, infiltrative disease

o

Pneum onia

Pleural densities: o

Pleural scaring

o

Mesotheliom a, m etastatic disease

Other: o

Herniated abdom inal contents

o

Paralyzed diaphragm

Treatment Pre Hospital

Pa ge 3 6 8



Place high-flow oxygen



Apply cardiac m onitor and pulse oxim eter



Initiate IV line access

Initial Stabilization 

ABCs



High-flow oxygen for shortness of breath



Em ergency thoracentesis for significant respiratory com prom ise

ED Treatment 

Identify and treat underlying prim ary pathologic process: o

CHF, pneum onia, intra-abdom inal infection



Surgical consult if em pyem a found



Interventional radiology or pulm onology for loculated effusions

Follow-Up Disposition Admission Criteria 

Respiratory com prom ise



Unknown cause of the effusion



Prim ary process requires hospitalization



Presence or suspected parapneum onic effusion or em pyem a



Observation for 6 hours or adm ission for potential com plications of thoracentesis:



o

Pneum othorax

o

Postexpansion pulm onary edem a

Intensive care unit adm ission for severe hem odynam ic and

Pa ge 3 6 8

respiratory com prom ise

Discharge Criteria 

Source of the pleural effusion is known



No evidence of respiratory com prom ise exists



Majority of effusions will resolve if the prim ary process is treated appropriately



Patient m ust be reliable and have access to a telephone, a supportive social environm ent, and adequate follow-up.

Issues for Referral Palliative care patients with recurrent effusions due to malignancy m ay present to the ED requesting therapeutic thoracentesis and discharge: 

Arrange appropriate follow-up with their oncologist or pulm onologist prior to discharge.

References 1. Blok B, Ibrado A. Thoracentesis. In: Roberts JR, Hedges JR: Clinical Procedures in Em ergency Medicine. 4th ed. Tarrytown, NY: Elselvier, 2004.171â€“185. 2. Kosowsky JM. Pleural disease. In: Marx JA, et al. Rosen's em ergency m edicine: Concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002. 3. Vukich DJ. Diseases of the pleural space. Em erg Med Clin North Am . 1989;7(2).

Miscellaneous SEE ALSO: Pulm onary Em bolism ; Pneum onia; Hem othorax; CHF; Pancreatitis; System ic Lupus Erythem atous; Procedural: Tube Thoracostom y

Codes

Pa ge 3 6 9

ICD9-CM 511.9

ICD10 J90w

Pa ge 3 6 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o cystis C arinii Pneum o nia

Pneumocystis Carinii Pneumonia Alan M. Kumar

Basics Description 

Most com m on opportunistic infection in patients with HIV



Believed to be transm itted by respiratory-aerosol route: o

Cysts colonize respiratory tract

o

Cysts rupture and m ultiple trophozoites release and form foam y exudate in alveoli.



Most cases of Pneum ocystis carinii pneum onia (PCP) believed to represent reactivation of latent disease, although person-to-person transm ission suggested.

Etiology 

Controversy surrounds the classification of Pneum ocystis as a parasite or fungus



Pneum ocystis occurs in hosts with altered cellular im m unity: o

HIV infection (m ost com m on, especially when CD4 counts <200 cells/m m 3 )

o

Cancer

o

Corticosteroid treatm ent

o

Organ transplantation

Pa ge 3 6 9

o

Malnutrition

Pediatric Considerations PCP in children is typically m ore severe.

Diagnosis Signs and Symptoms 

Subacute presentation



Fever



Cough with none or m inim al am ount of white sputum



Dyspnea on exertion or at rest: o

Progressive over days (m ost com m on in nonâ€“HIV-im m unocom prom ised hosts)

o

Indolent, developing over weeks to m onths (m ore com m on in HIV-positive hosts)

o

Oxygen desaturation with exercise



Chest pain



Chills



Fatigue



Weight loss



Tachypnea



Tachycardia



Crackles and rhonchi on lung exam ination



Up to 7% of patients can be asym ptom atic



Patients on inhaled pentam idine prophylaxis m ay have m ilder sym ptom s: o

Increased incidence of pneum othorax

o

Increased incidence of extrapulm onary disease

Essential Workup N/A

Pa ge 3 6 9

Tests Lab 

Arterial blood gas: o

Obtain in all cases of PCP.

o

Calculate the A-a gradient (usually increased).

o

Adjunctive corticosteroid therapy for A-a gradient >35 or PaO 2 <70



CBC



Electrolytes, blood urea nitrogen/creatinine, glucose



LDH: o

Elevated in HIV-positive patients with PCP com pared to non-PCP pneum onia

o 

Higher levels correlated with poorer prognosis

Blood cultures

Imaging 

Chest radiograph: o

Classically reveals bilateral interstitial or central alveolar infiltrates

o

Radiograph norm al in up to 25% of patients with PCP

o

Early or m ild infection associated with decreased sensitivity

o

o

Atypical presentations include: 

Lobar infiltrates



Cysts



Pneum othoraces



Pleural effusions



Nodular infiltrates

Prophylaxis with aerosolized pentam idine is a risk factor for developing predom inantly upper lobe.

o

Chest radiograph abnorm alities can persist for m onths after treatm ent.

Pa ge 3 6 9



High-resolution chest CT: o

High sensitivity for PCP in HIV-positive patients.

o

Reveals patchy ground-glass attenuation

Diagnostic Procedures/Surgery 

Induced sputum : o

Definitive diagnosis requires presence of Pneum ocystis organism s in an appropriately stained respiratory specim en

o

Specificity approaches 100%, but sensitivity depends on quality of induced sputum and lab expertise.

o

Less sensitive in patients on inhaled pentam idine prophylaxis and nonâ€“HIV-positive patients



Bronchoalveolar lavage: o

Perform if the induced sputum is nondiagnostic and the suspicion for PCP is still high

o

Sensitivity of 80â€“100%

Differential Diagnosis Constellation of dyspnea, fever, diffuse radiographic infiltrates, m inim al or nonproductive cough, and slow progressive course suggests atypical cause of the pneum onia: 

Tuberculosis



Mycoplasm a



Legionella



Chlam ydia pneum oniae



Viral pneum onia (especially cytom egalovirus)

P.865

Pa ge 3 6 9

Treatment Pre Hospital Provide supplem ental oxygen for sym ptom atic patients.

Initial Stabilization 

ABCs



Provide adequate oxygenation with nasal cannula up to 100% nonrebreather.



Perform endotracheal intubation in those with refractory hypoxem ia despite m axim al oxygenation or hypercarbic respiratory failure.



500â€“1,000 cc 0.9% NS IV bolus for hypotension, sepsis, dehydration

ED Treatment 

Initiate antibiotics: o

IV Bactrim is the first-line agent.

o

IV pentam idine for those who cannot tolerate Bactrim

o

Oral therapy is an option for well-appearing patients.

o

Alternative regim ens include trim ethoprim dapsone, clindam ycin-prim aquine, and atovaquone.

o 

Continue antibiotics for 21 days.

Adjunctive corticosteroids in patients with A-a gradient >35 or PaO 2 <70: o



Must start within first 72 hours of treatm ent

Isolate suspected PCP patients from others who are im m unocom prom ised.

Medication (Drugs) 

Atovaquone: 750 m g (peds: dosing not established) PO q12h

Pa ge 3 6 9



Clindam ycin/prim aquine: clindam ycin 900 m g (peds: dosing not established) IV q8h or 300â€“450 m g PO q6h and prim aquine 15â€“30 m g (peds: dosing not established) PO per day



Pentam idine: 4 m g/kg/24h IV over 1 hour (peds: 150 m g/m 2 IV per day for 5 days, then 100 m g/m 2 IV per day for 16 days)



Prednisone: 40 m g (peds: dosing not established) PO q12h for 5 days, 40 m g PO per day for 5 days, then 20 m g PO per day for 11 days (IV m ethylprednisolone at 75% of the prednisone dose m ay be substituted)



Trim ethoprim /Dapsone: trim ethoprim 15â€“20 m g/kg/d IV div. q8h plus dapsone 100 m g PO per day (peds: dosing not established)



Trim ethoprim /sulfam ethoxazole (Bactrim ): trim ethoprim 15â€“20 m g/kg/d IV div. q6h and sulfam ethoxazole 100 m g/kg/d IV div. q6h (peds: dosing sam e)

Pediatric Considerations 

Treatm ent of choice is IV Bactrim , followed by IV pentam idine.



Dosing for alternative m edications not yet established (consult pediatric infectious disease specialist).

Follow-Up Disposition Admission Criteria 

Moderate to severe disease (PaO 2 <70 or A-a gradient >35)



Inability to digest m edications

Pa ge 3 6 9



Inability to return for careful follow-up

Discharge Criteria 

Nontoxic clinical appearance



Mild disease state (no hypoxem ia or A-a gradient)



Ability to tolerate m edications



Close follow-up arranged



If results of induced sputum not available, add m acrolide to em pirical regim en.

References 1. Moe AA, Hardy WD. Pneum ocystis carinii infection in the HIV-seropositive patient. Infect Dis Clin North Am . 1994;8(2):331â€“364. 2. Santam auro JT, Stover DE. Pneum ocystis carinii pneum onia. Med Clin North Am . 1997;81(2):299â€“318. 3. Stansell JD, Huang L. Pneum ocystis carinii pneum onia. In: Sande MA, Volberding PA, eds. The m edical m anagem ent of AIDS. 5th ed. Philadelphia, PA: WB Saunders,1997.

Codes ICD9-CM 486 Pneum onia, organism unspecified 136.3 Pneum ocystosis

ICD10 J18 Pneum onia, organism unspecified B59+ Pneum ocystosis

Pa ge 3 6 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o m ediastinum

Pneumomediastinum Jennifer De La Pena Leon D. Sanchez

Basics Description 

Presence of air or gas within the m ediastinum



May occur spontaneously or as result of traum a or other pathologic processes



Spontaneous pneum om ediastinum : o

Caused by extrapleural tracheobronchial tears: 

Increased alveolar pressure or overdistension



Term inal alveolar rupture into the lung interstitium



Dissection of air into the hilum and subsequently the m ediastinum along a pressure gradient



Mediastinal air then dissects into the fascial planes m ost com m only into the tissues of the neck

o

Often in setting of a Valsalva m aneuver, in association with bronchospasm or inhalational drug use

Pa ge 3 6 9

o 

Most com m only in young m en

Relatively rare, occurs in one in 30,000â€“40,000 hospital adm issions

Etiology 

Prim ary or spontaneous pneum om ediastinum : o

o

Associated with forced Valsava m aneuvers: 

Illicit inhalation drug use (cannabis, cocaine)



Childbirth



Forceful straining during exercise



Straining at stool



Coughing



Sneezing



Vom iting



Inflation of party balloons



Pulm onary function testing

Has been rarely described after dental extraction/procedures.



Secondary pneum om ediastinum : o

Secondary to thoracic barotraum a

o

Positive-pressure ventilation

o

Esophageal rupture (Boerhaave syndrom e)

o

In association with m ediastinal infection caused by gas-form ing organism s



Rarely develops into a tension pneum om ediastinum : o

Life-threatening event

o

Usually in patients on positive pressure ventilation

Diagnosis Signs and Symptoms

Pa ge 3 7 0



Chest pain: o

Sharp

o

Pleuritic

o

Often positional



Dyspnea



Neck pain: o

Occurs in association with dissection of air into soft tissues of neck

o

Often described as â€œneck swelling,â€• â€œneck pain,â€• â€œthroat pain,â€• or â€œdifficulty swallowingâ€•



Subcutaneous em physem a o

Most com m only located to the supraclavicular area and anterior neck



Ham m an crunch: Presence of a crinkling or crepitant sound that varies with heartbeat

Essential Workup 

Exclude secondary causes, notably esophageal rupture



Chest radiography

Tests Lab CBC if there is suspicion of m ediastinitis

Imaging 

Chest radiograph: o

Most valuable initial test

o

Im portant to include lateral view because m ediastinal air is often m issed on posterior-anterior view

o

Excludes pneum othorax

o

Identification of a pleural effusion or parenchym al infiltrate suggests an esophageal rupture.

Pa ge 3 7 0

o 

Negative in up to 30% of cases

Chest CT: o

Im aging test of choice if suspicion is high but chest radiograph is negative



Esophagram with Gastrografin: o

Study of choice to exclude diagnosis of esophageal rupture

Differential Diagnosis 

Pericarditis



Pneum othorax



Pulm onary em bolus



Pneum onia



Coronary ischem ia



Aortic dissection

Treatment Initial Stabilization 

IV line



Oxygen



Cardiac m onitoring



Pulse oxim etry

P.867

ED Treatment 

Spontaneous pneum om ediastinum : o

Does not require specific treatm ent

o

Efforts should focus on pain relief and reassurance once diagnosis is confirm ed.

Pa ge 3 7 0

o

High-flow oxygen will facilitate the reabsorption of nitrogen and provide com fort.

o

Condition is self-lim iting and m ay be expected to resolve over two to five days



Secondary pneum om ediastinum : direct therapy toward underlying cause

Follow-Up Disposition Admission Criteria 

Secondary pneum om ediastinum



Associated pneum othorax



Possibility of esophageal rupture has not been excluded



Abnorm al vital signs

Discharge Criteria 

Spontaneous pneum om ediastinum



Norm al vital signs



No pneum othorax



Period of observation in the ED with im provem ent in sym ptom s



Close outpatient follow-up

References 1. Brody S, Anderson G, Gutm an J. Pneum om ediastinum as a com plication of â€œcrackâ€• sm oking. Am J Em erg Med. 1988;6:241â€“243. 2. Chen SC, Lin FY, Chang KJ. Subcutaneous em physem a and pneum om ediastinum after dental extraction. Am J Em erg Med. 1999;17(7):678â€“680.

Pa ge 3 7 0

3. Dekel B, Paret G, Szeinberg A, et al. Spontaneous pneum om ediastinum in children: clinical and natural history. Eur J Pediatr. 1996;155:695â€“697. 4. Gerazounis M, Athanassiadi K, Kalantzi N, et al. Spontaneous Pneum om ediastinum : a rare benign entity. 5. Jougin JB, Ballester M, Delcam bre F, et al. Assessm ent of spontaneous pneum om ediastinum : experience with 12 patients. Ann Thorac Surg. 2003;75(6):1711â€“1714. 6. Newcom b AE. Spontaneous pneum om ediastinum : a benign curiosity or a significant problem ? Chest. 2005;128(5):3298â€“3302. 7. Panacek E, Singer A, Sherm an B, et al. Spontaneous pneum om ediastinum : clinical and natural history. Ann Em erg Med. 1992;21:1222â€“1227.

Codes ICD9-CM 518.1 Interstitial em physem a

ICD10 J98.2 Interstitial em physem a

Patient Teaching Prevention Caution against use of inhalational drugs or any activity associated with Valsalva-type or breath-holding m aneuvers.

Pa ge 3 7 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o nia, Adult

Pneumonia, Adult

Jason Imperato

Basics Description 

6th leading cause of death in the United States o

Num ber-one infectious cause

o

5 m illion cases per year

o

500,000 hospital adm issions per pear

o

Most deaths occur in the elderly or im m unosuppressed.





Com orbid conditions: o

Advanced age

o

Cigarette sm oking

o

Chronic obstructive pulm onary disease (COPD)

o

Diabetes m ellitus

o

Alcoholism

o

Malnutrition

o

Im m unosuppression

o

Sickle cell disease

o

Congestive heart failure

o

HIV/AIDS

Com plications: o

Sepsis

Pa ge 3 7 0

o

Lung abscess

o

Em pyem a

o

Extrapulm onary com plications (e.g. m eningitis)

o

Respiratory failure

Etiology 

Classification based on the setting of initial infection



Com m unity acquired: o

Streptococcus pneum oniae

o

Haem ophilus influenzae

o

Klebsiella pneum oniae

o

Moraxella catarrhalis

o

Staphylococcus aureus

o

â€œAtypicalsâ€•:

o





Mycoplasm a pneum oniae



Chlam ydia pneum oniae



Legionella pneum ophila

Viruses: 

Influenza virus



Parainfluenza virus

Nosocom ial acquired (Includes above plus the following): o

Pseudom onas aeruginosa

o

Staphylococcus aureus

o

Aneorobes

o

Aspiration pneum onias are typically polym icrobial

Diagnosis Signs and Symptoms History 

Cough

Pa ge 3 7 0



Sputum production



Fever



Chills



Rigors



Shortness of breath



Pleuritic chest pain



â€œAtypicalâ€• pneum onia is often present differently: o

Viral prodrom e

o

Gradual onset

o

Nonproductive cough

o

Low-grade fever

o

Absence of pleurisy and rigors

Physical Exam 



Abnorm al vital signs: o

Tachypnea

o

Tachycardia

o

Hypoxia

o

Fever

Pulm onary exam ination: o

Dullness to percussion

o

Increased tactile frem itus

o

Egophony

o

Coarse rales

o

Rhonchi

o

However, pneum onia m ay be present in the absence of consolidation

Geriatric Considerations 

Elderly patients have a higher m orbidity and m ortality from pneum onia.



Often present with atypical features.

Essential Workup

Pa ge 3 7 0

Pneum onia is both a clinical as well as a radiographic diagnosis.

Tests Lab 

Nonspecific for identifying the etiology of the pneum onia



CBC with differential: o

WBC count >15,000/m m 3 suggests a bacterial cause.

o

A very high or very low WBC count predicts increased m orbidity.



Serum chem istries



Pulse oxim etry



Arterial blood gas



Sputum gram stain and culture



Blood cultures

Imaging Chest radiograph: 

Chest radiograph findings are nonspecific for predicting a particular infectious etiology



May be deferred in young, healthy patients



The absence of chest radiograph findings should not preclude antim icrobial therapy in those with clinical pneum onia.



Findings suggestive of pneum onia include: o

Segm ental or subsegm ental infiltrate

o

Air bronchogram s

o

Abscess

o

Cavitation

o

Em pyem a

o

Pleural effusion

Diagnostic Procedures/Surgery Diagnostic thoracentesis:

Pa ge 3 7 0



Perform ed for large effusions, enigm atic pneum onia, and patients who fail to respond to standard therapy

Differential Diagnosis 

Bronchitis



Pneum othorax



COPD



Asthm a



Congestive heart failure



Pulm onary em bolism



Foreign body aspiration



Occupational or environm ental exposure



Tum or

Treatment Pre Hospital 

Supplem ental oxygen



IV access



Consider inhaled bronchodilators.



Consider endotracheal intubation in patients with severe respiratory distress.

Initial Stabilization 

Supplem ental oxygen



IV access



Consider inhaled bronchodilators.



Consider endotracheal intubation in patients with severe respiratory distress.



IV fluid resuscitation

P.869

Pa ge 3 7 0

ED Treatment 

Em piric antim icrobial therapy is necessary before definitive etiology is established.



The Am erican Thoracic Society has set guidelines for em piric therapy





Outpatient m anagem entâ€”no cardiopulm onary disease: o

Advanced generation m acrolide (azithrom ycin)

o

OR doxycycline

Outpatient m anagem entâ€”cardiopulm onary disease: o

Second or third generation cephalosporin (cefuroxim e)

o

OR Î²-lactam ase inhibitor com bination (am oxicillin/clavulanate)

o

PLUS m acrolide (azithrom ycin)

o

Alternatively, extended spectrum fluoroquinolone (levofloxacin) as a single agent



Inpatient m anagem entâ€”noncritical care setting o

Second generation cephalosporin (cefuroxim e) OR third generation cephalosporin (ceftriaxone) OR Î²-lactam and Î²-lactam ase inhibitor com bination (am picillin-sulbactam )

o

PLUS m acrolide (azithrom ycin or clarithrom ycin)

o

Alternatively, extended spectrum fluoroquinolone (levofloxacin) as a single agent

o

May add clindam ycin or m etronidazole if aspiration is suspected



Inpatient m anagem entâ€”critical care setting: o

Third generation cephalosporin with antipseudom onal activity (ceftazidim e)

o

May add vancom ycin for drug-resistant S. pneum oniae

Pa ge 3 7 1

Medication (Drugs) 

Am oxicillin-clavulanate (Augm entin): 500 m g PO q12h



Am picillin-sulbactam (Unasyn) 1.5â€“3.0 g IV q6h



Azithrom ycin: 500 m g PO on day one and 250 m g PO on days 2 through 5



Ceftazidim e: 1 g IV q8h



Ceftriaxone: 1â€“2 g IV every day



Cefuroxim e: 0.75 and 1.5 g IV q8h



Clindam ycin: 150 and 450 m g PO q.i.d. or 300â€“600 m g IV q.i.d.



Levofloxacin: 500 m g PO/IV every day



Vancom ycin: 1 g q12h

Follow-Up Disposition Admission Criteria 

Decision to adm it is based on a scoring system based on age, com orbid illnesses, physical exam , and laboratory findings.



Good clinical judgm ent should supersede a strict interpretation of the scoring system .



Age >50 years old



Significant com orbid illnesses o

COPD

o

Diabetes m ellitus

o

Chronic renal failure

o

Chronic liver failure

Pa ge 3 7 1







o

Congestive heart failure

o

Neoplastic disease

o

Cerebrovascular disease

o

Post-splenectom y

o

Im m unosuppression

o

Chronic alcohol abuse

o

Malnutrition

o

Pregnancy

Physical exam ination findings: o

Altered m ental status

o

Respiratory rate >30

o

Systolic blood pressure <90

o

Tem perature <35Â°C or >40Â°C

o

Pulse >125

Laboratory findings: o

Arterial pH < 7

o

.35

o

BUN >30 m g/dL

o

Sodium <130 m Eq/L

o

Glucose >250 m g/dL

o

Hem atocrit <30%

Additional considerations: o

Previous hospitalization within the last year for pneum onia

o

Failure to respond to outpatient therapy

o

Social conditions that prevent safe outpatient care

Discharge Criteria 

Age <50 years old



No com orbid illnesses



Nontoxic appearance



Norm al vital signs



Norm al laboratory studies

Pa ge 3 7 1



Prim ary care follow up arranged within 72 hours

Issues for Referral Follow up with prim ary care within 72 hours.

References 1. Am erican Thoracic Society. Guidelines for the initial m anagem ent of adults with com m unity-acquired pneum onia: diagnosis, assessm ent of severity, and initial antim icrobial therapy. Am Rev Respir Dis. 1993;148:1418â€“1426. 2. Bartlett JG, Mundy LM. Com m unity-acquired pneum onia. N Engl J Med. 1995;333(24):1618â€“1624. 3. Moran GJ, Talan DA. Pneum onia. In Marx J, et al, eds: Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis: Mosby, 2002: 986â€“1000. 4. Pim entel L, McPherson SJ. Com m unity-acquired pneum onia in the em ergency departm ent. A practical approach to diagnosis and m anagem ent. Em erg Med Clin N Am . 2003;21:395â€“420.

Miscellaneous SEE ALSO: Pneum onia, Pediatric

Pa ge 3 7 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o nia, Pediatric

Pneumonia,

Pediatric Gary D. Zimmer Karen P. Zimmer

Basics Description 

Mechanism is often unknown.



Sources are oropharyngeal aspiration (m ost com m on) or hem atogenous.



Distribution depends on the organism : interstitial ( Mycoplasm a pneum onia, virus), lobar (Streptococcus pneum oniae), abscesses (Staphylococcus aureus), or diffuse (Pneum ocystis carinii)

Etiology 

Haem ophilus influenza type b is becom ing rare secondary to m ass im m unization.



Less than 2 weeks: o

Group B Streptococcus species

o

Enteric gram -negative organism s

o

Respiratory syncytial virus (RSV)

o

Herpes sim plex virus

o

S. aureus

Pa ge 3 7 1





2 weeks to 3 m onths: o

Chlam ydia trachom atis

o

Parainfluenza virus

o

RSV

o

S. pneum oniae

o

S. aureus

o

H. influenza

o

Bordetella pertussis

3 m onths to 8 years: o







Viral (predom inate): 

RSV



Parainfluenza virus



Influenza virus



Adenovirus

o

S. pneum oniae

o

H. influenza in unim m unized children

o

Group A streptococci

o

S. aureus

o

B. pertussis

Older than 8 years: o

M. pneum oniae m ost com m on

o

Viral

o

S. pneum oniae

Recent im m igrants from developing countries: o

Mycoplasm a tuberculosis

o

H. influenza

o

B. pertussis

Im m unocom prom ised (e.g., HIV, cancer): o

P. carinii

o

Mycoplasm a avium com plex

o

M. tuberculosis

o

Klebsiella pneum oniae

Pa ge 3 7 1

o 

Pseudom onas aeruginosa

Less com m on: o

Fungal (coccidioidom ycosis, histoplasm osis)

o

Rickettsia (Q fever)

Diagnosis Signs and Symptoms 



General (in all ages): o

Fever

o

Hypoxia

o

Tachycardia

o

Tachypnea, retractions

o

Rash (up to 10% of cases); usually m aculopapular

o

Nonspecific sym ptom s of toxicity

o

Pulm onary

o

Cough

o

Decreased breath sounds, ventilation

o

Dullness to percussion

o

Rales

Infants younger than 6 m onths: o

Altered behavior: listless, irritable

o

Apnea

o

Conjunctivitis (Chlam ydia <1 m onth old)

o

Cyanosis

o

Grunting

o

Poor feeding

o

Tem perature instability (hypotherm ia/hypertherm ia)

o

Vom iting

o

Pulm onary

o

Nasal congestion

Pa ge 3 7 1



o

Nasal flaring

o

Wheezing

o

Staccato cough (Chlam ydia)

Children older than 5 years: o

Pleuritic chest pain

o

Rigors, chills

o

Productive cough

Essential Workup 

Pulse oxim etry



Chest radiograph: o

Gold standard for diagnosis

o

Should be ordered for patients with signs of lower respiratory tract infection and patients <36 m onths old with m arked leukocytosis or neutrophilia (WBC >20,000 or absolute neutrophil count [ANC] >9,000)

o

Much overlap between viral and bacterial findings

o

Viral and M. pneum oniae tend to show interstitial infiltrates, often perihilar and peribronchial

o

Bacterial pneum onias m ay show focal lobar consolidation, focal alveolar infiltrates, and possibly effusion or pneum atocele.

o

Round pneum onia pathognom onic of S. pneum onia

o

Lateral decubitus film s m ay aid in dem onstrating effusion.

Tests Lab 

CBC with differential: o

Patients with bacterem ia tend to have leukocytosis with left shift.

o

Sensitivity and specificity are poor.

o

Patients with WBC â‰¥20,000 or ANC >9,000 are at

Pa ge 3 7 1

increased risk of pneum ococcal bacterem ia. o

B. pertussis usually has elevated WBC with lym phocytosis.



Blood culture: o

Low yield (<10â€“20%)

o

Probably worthwhile in toxic patients requiring hospitalization



Arterial blood gas (ABG) m ay be useful in determ ining degree of respiratory insufficiency in critically ill patients.



Electrolytes to exclude syndrom e of inappropriate ADH secretion (SIADH) and in hypotensive children



Sputum for Gram stain and culture m ay be obtained in older children with suspected bacterial infection.





Mycoplasm a IgM or cold agglutinin titers: o

Useful if suspecting this organism

o

More likely positive with severe illness

Nasopharyngeal washes for direct fluorescent antibody and culture: o

Identify RSV, Chlam ydia trachom atis, and B. pertussis infections

Imaging 

Chest radiographs are still the im aging m odality of choice:



Posteroanterior (PA) and lateral film s should be obtained whenever possible.



CT provides additional detail and better identification of underlying lung pathology, but adds little as an initial testing m odality.

Diagnostic Procedures/Surgery Pleural fluid (if present) for culture, Gram stain, protein, glucose, and cell counts

Differential Diagnosis

Pa ge 3 7 1



Reactive airway disease (asthm a, bronchiolitis [age <2 years])



Aspiration: o

Gastroesophageal reflux

o

Vascular ring

o

H-type tracheoesophageal fistula

o

Foreign body

o

Hydrocarbon



Congestive heart failure



Congenital:



o

Cystic fibrosis

o

Sequestered lobe

o

Congenital lobe absence

o

Hem angiom a

Neoplasm

P.871

Treatment Pre Hospital 

Pulse oxim etry



Adm inister high-flow oxygen for respiratory distress.



IV fluids (0.9% norm al saline [NS] 20 m L/kg initial bolus) for volum e depletion, hypotension



Support and intubation for respiratory failure

Initial Stabilization 

If m oderately or severely ill: o

Secure airway, as appropriate; intubate for clinical

Pa ge 3 7 1

respiratory failure. o

High-flow oxygen

o

IV hydration (0.9% NS 20 m L/kg initial bolus) and resuscitation if in shock or hypovolem ia



Monitor



Apply pulse oxim etry; ABG if inadequate ventilation



Check bedside glucose in severely illâ€“appearing infants and toddlers: o

If hypoglycem ic, adm inister glucose D 2 5 at 2 m L/kg IV for toddlers or D 1 0 at 5 m L/kg IV for neonates.

ED Treatment 

Continue prehospital therapy



Early antibiotic therapy should be broad enough to address local resistance patterns in your area.



Often have concurrent reactive airway disease that needs specific treatm ent with bronchodilator (albuterol or levalbuterol)



Perform thoracentesis if pleural effusion com prom ising respiratory function or for diagnostic tests.

Medication (Drugs) 

Initiate IV antibiotic therapy for m oderate to severely ill children who require adm ission.



IV antibiotics: o

Neonate: 

Am picillin, and cefotaxim e or gentam icin



Erythrom ycin for suspected C. trachom atis or B. pertussis pneum onia

o

Infant 1â€“2 m onths of age: 

Am picillin and cefotaxim e

Pa ge 3 7 2



Erythrom ycin for suspected C. trachom atis or B. pertussis

o

Children 3 m onths and older: 

Cefotaxim e, cefuroxim e, or ceftriaxone



Vancom ycin for suspected or confirm ed penicillin-resistant S. pneum oniae



Macrolide (i.e., azithrom ycin) for suspected M. pneum oniae



Outpatient em piric antibiotic therapy: o

Infants <2 m onths old: 

Outpatient treatm ent generally not recom m ended

o

o



Children 3 m onths to 5 years: 

Am oxicillin



Am oxicillin-clavulanate



Trim ethoprim -sulfam ethoxazole



Erythrom ycin-sulfisoxazole



Clarithrom ycin

Children 5â€“18 years: 

Azithrom ycin



Clarithrom ycin

Unusual organism s require specific therapy in coordination with infectious disease consultation.



Medication dosing: o

Albuterol (0.5% solution or 5 m g/m L): nebulizer 0.015 m g (0.03 m L)/kg per dose up to 5 m g per dose q10â€“20 m in as needed; m etered dose inhaler (with spacer; 90 Âµg per puff) 2 puffs q10â€“20 m in up to total of 10 puffs

o

Am oxicillin: 80 m g/kg/24h q12h PO

o

Am oxicillin-clavulanate: 30 m g/kg/24h q12h PO

o

Am picillin: 100â€“150 m g/kg/24h q6h IV

Pa ge 3 7 2

o

Azithrom ycin: 10 m g/kg/24h daily for 1 day, then 5 m g/kg/24h daily for 4 days

o

Cefotaxim e: 75 m g/kg/24h q8h IV, m ax. 2 g q8h

o

Ceftriaxone: 100 m g/kg/24h q12hâ€“q24h IV, m ax. 2 g q12h

o

Cefuroxim e: 100 m g/kg/24h q8h IV, m ax. 2 g q8h

o

Clarithrom ycin: 15 m g/kg/24h q12h PO, m ax. 500 g q12h

o

Erythrom ycin: 40 m g/kg/24h q6h PO or IV, m ax. 2 g/d

o

Erythrom ycin-sulfisoxazole: 40 m g/kg/24h as erythrom ycin q8h PO, m ax. 2 g/d

o

Gentam icin: 5â€“7.5 m g/kg/24h q8hâ€“q12h IV

o

Trim ethoprim -sulfam ethoxazole: 6â€“10 m g/kg/24h as TMP q12h PO

o

Vancom ycin: 10 m g/kg/24h q6h IV, m ax. 1,000 m g q6h

Follow-Up Disposition Admission Criteria 

Toxic appearance



Respiratory distress or failure



Dehydration/vom iting



Apnea



Infants <2 m onths old



Infants <6 m onths old with lobar pneum onia



Hypoxia (O 2 saturation <92% on room air [sea level])



Pleural effusion

Pa ge 3 7 2



Poor response to outpatient oral therapy



Im m unocom prom ised children



Concern about noncom pliant parents

Discharge Criteria 

Most cases are m ild and can be discharged hom e if no evidence of hypoxia, significant work-of-breathing, dehydration, vom iting, or noncom pliance.



Ensured follow-up within 1â€“2 days

References 1. Bachur R, Perry H, Harper MB. Occult pneum onias: em piric chest radiographs in febrile children with leukocytosis. Ann Em erg Med. 1999;33:166â€“173. 2. Baraff LJ. Managem ent of fever without source in infants and children. Ann Em erg Med. 2000;36:602â€“614. 3. Juvn T, Mertsola J, Waris M, et al. Etiology of com m unity-acquired pneum onia in 254 hospitalized children. Pediatr Infect Dis J. 2000;19:293â€“298. 4. McCracken GH. Etiology and treatm ent of pneum onia. Pediatr Infect Dis J. 2000;19:373â€“377.

Miscellaneous SEE ALSO: Asthm a

Codes ICD9-CM 486 482.9 480.9

ICD10

Pa ge 3 7 2

P23.9

Pa ge 3 7 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o tho rax

Pneumothorax

William Porcaro David Feldman

Basics Description 

Presence of free air in the intrapleural space



Spontaneous pneum othorax is due to atraum atic rupture of alveolus, bronchiole, or bleb.



Prim ary spontaneous pneum othorax (two thirds of incidences): o

No underlying pulm onary pathology present

o

Rupture of sm all subpleural cyst or bleb

o

Prim arily young and healthy patients (20â€“40 years old), with tall and thin body habitus



Secondary spontaneous pneum othorax from underlying pulm onary pathology (see Etiology, below)



Tension pneum othorax: o

Air continues to enter pleural space through bronchoalveolar disruption and becom es trapped via â€œball-valveâ€• m echanism

o

Intrapleural pressure increases

o

Venous return to right heart decreases, resulting in decrease in cardiac output

Pa ge 3 7 2

o

Mediastinum shifts toward uninvolved side m echanically interfering with right atrial filling

o

Ventilation com prom ised and ventilation/perfusion m ism atch resulting in hypoxem ia

Etiology 

Idiopathic



Airway disease:



o

Chronic obstructive pulm onary disease (COPD)

o

Asthm a

o

Cystic fibrosis

Infections: o

Necrotizing bacterial pneum onia

o

Tuberculosis

o

Fungal pneum onia

o

Pneum ocystis carinii



Neoplasm



Interstitial lung disease: o

Sarcoidosis

o

Idiopathic pulm onary fibrosis

o

Lym phangiom yom atosis

o

Tuberous sclerosis

o

Pneum oconioses



Connective tissue diseases



Pulm onary infarction



Endom etriosis



Blunt chest traum a



Penetrating traum a to neck or trunk



Iatrogenic: o

Central line placem ent

o

Other vascular access procedure

Pa ge 3 7 2

Diagnosis Signs and Symptoms 

Severity of sym ptom s is generally proportional to size of the pneum othorax.



Chest pain on the ipsilateral side: o

Sharp, pleuritic pain

o

Sudden onset

o

Dull ache in delayed presentations



Shortness of breath



Tachypnea



Heart rate <120 generally seen in sim ple spontaneous pneum othoraces



Rarely cough, asym ptom atic, or generalized m alaise



Tension pneum othorax: o

Hypotension

o

Tachycardia, heart rate >120

o

Diaphoresis

o

Cyanosis

o

Cardiovascular collapse

o

Tracheal deviation

Tests Lab Aterial blood gas offers little over oxygen saturation: 

Drop in oxygen saturation m ay be the earliest finding in a tension pneum othorax

Imaging 

Chest radiograph: o

Upright chest radiograph: 

Patients unable to tolerate upright chest

Pa ge 3 7 2

radiograph can be taken in decubitus position with the suspected side up o

Absence of lung m arkings distal or peripheral to the visceral pleural white line

o

Displacem ent of m ediastinum or anterior junction line

o

Deep sulcus sign: 

On frontal view, larger lateral costodiaphragm atic recess than on opposite side



Diaphragm m ay be inverted on side with deep sulcus

o

A rough estim ate of pneum othorax size is sufficient to m ake clinical decisions.



ECG: o

Often necessary to rule out cardiac etiologies of chest pain

o

Nonspecific changes include T-wave inversion, left axis deviation, and decreased R-wave am plitude.



Chest CT: o

Very sensitive for sm all pneum othorax but has little practical advantage over chest radiograph



Ultrasound: o

User experience required

o

Rapid at bedside

o

Lack of lung sliding and com et-tail artifact m ay signify pneum othorax

Differential Diagnosis 

Exacerbation of COPD



Asthm a



Pulm onary em bolus



Myocardial infarction



Pericarditis



Pneum om ediastinum

Pa ge 3 7 2



Dissection of aortic aneurysm



Chest wall pain



Pleuritis



Acute abdom inal processes

Treatment Pre Hospital Cautions: 

Suspected tension pneum othorax requires im m ediate needle thoracostom y

Initial Stabilization 

Cardiac m onitor



Pulse oxim etry



Oxygen 100% via nonrebreather face m ask



IV access



Suspected tension pneum othorax requires either im m ediate needle thoracostom y or tube thoracostom y.



Needle thoracostom y: o

Im m ediate placem ent indicated in unstable patients with a tension pneum othorax

o

14- to 18-gauge angiocatheter in the second intercostal space at m idclavicular line or fourth or fifth intercostal space at anterior axillary line

ED Treatment 

Nontraum atic pneum othorax estim ated at <15% collapse and no cardiovascular or respiratory com prom ise: o

Observe with 100% oxygen support for four to six hours.

o

Repeat chest radiograph and discharge if unchanged

Pa ge 3 7 2



Sim ple aspiration: o

Indications: 

Sim ple pneum othorax with only 15â€“30% collapse



Increase in size of a sm all pneum othorax during observation

o

Placem ent of aspiration catheter (typically 8 Fr) with three-way stopcock 

Aspirate air until resistance or 3 L air aspirated P.873



If the pneum othorax is no longer visible on two subsequent chest radiographs at four-hour intervals, rem ove catheter.



If a final chest radiograph is norm al two hours after the catheter is rem oved, the patient m ay be discharged.



A second aspiration m ay be attem pted if the pneum othorax does not resolve.



Heim lich valve: o

Indicated when <30% collapse after failure of aspiration

o

Attach Heim lich valve to aspiration catheter or chest tube.





Suction: o

Indicated when the Heim lich valve fails

o

Attach aspiration catheter to suction at 20 cm H 2 O

o

Observe in ED for one hour

Tube thoracostom y: o

Indications: 

Suspicion of a tension pneum othorax

Pa ge 3 7 3



Gunshot wound to the chest



Clinical evidence of a pneum othorax following blunt chest traum a or penetrating chest traum a



Presence of a pneum othorax of any size in patient receiving positive pressure ventilation

o



Pneum othorax with >30% collapse



Most cases of secondary pneum othorax



Definitive therapy after needle thoracostom y

Tube size: 

Sm all-caliber (7â€“14 Fr) tube for prim ary spontaneous pneum othoraces



20â€“28 Fr for secondary spontaneous pneum othorax



28 Fr when there is detectable pleural fluid or an anticipated need for m echanical ventilation

o

Following insertion, the tube should be connected to a water-seal device.

o

A Heim lich valve m ay be used instead of a water-seal device in stable patients without a pleural effusion.

o

Re-expansion edem a is a rare com plication requiring supportive care.



Possible com plications: o

Intercostal vessel bleeding

o

Inadequate drainage: 

Kinked tube



Clogged tube



Com m unication outside of pleural cavity with leak

o

Re-expansion pulm onary edem a: 

Treatm ent with fluid resuscitation

Pa ge 3 7 3

Medication (Drugs) 



Local anesthetic: o

1% Lidocaine with Epinephrine 1:100,000

o

Max dose: 7 m g/kgâ€“500 m g

Consider conscious Sedation in stable awake patients

Follow-Up Disposition Admission Criteria 

Tension pneum othorax



Chest tube required

Discharge Criteria 

<15% collapse, no expansion while in the ED or successful aspiration with catheter rem oved o

Discharge with follow-up in 24 hours and one week for chest radiograph to assure re-expansion.



Reliable patients with the thoracic vent and successful aspiration or secured catheter and Heim lich valve: o

Discharge with 24- and 48-hour follow-up

o

At 48-hour follow-up

o

Clam p catheter, observe for two hours, and repeat chest radiograph

o

Rem ove thoracic vent or catheter if no re-expansion

o

Observe for two hours and repeat chest radiograph

o

If no re-expansion, discharge with 24-hour and one-week follow-up



Discharge instruction should include prom pt return for new onset of chest pain or dyspnea.

Pa ge 3 7 3



Patients without re-expansion at one week require a cardiothoracic surgery consult

References 1. Baum ann MH, Noppen M. Pneum othorax. Respirology 2004;9:157â€“164. 2. Baum ann MH, Strange C, Heffner JE, et al. Managem ent of spontaneous pneum othorax: an Am erican College of Chest Physicians Delphi consensus statem ent. Chest. 2001;119:590. S193. 3. Beng ST, Mahadevan M. An Uncom m on Life-Threatening Com plication After Chest Tube Drainage of Pneum othorax in the ED. Am J Em erg Med. 2004;Vol 22:N7. 4. Chan SSW. Em ergency Bedside Ultrasound to Detect Pneum othorax. Academ ic Em erg Med. 2003;10:N1. 5. Light RW. Pleural diseases. 4th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2001. 6. Miller AC, Harvey JE. Guidelines for the m anagem ent of spontaneous pneum othorax. Standards of Care Com m ittee, British Thoracic Society. BMJ 1993;307:114. S193. 7. Sahn SA, Heffner JE. Spontaneous pneum othorax. N Engl J Med. 2000;342:868. S193.

Codes ICD9-CM 512.8

ICD10 J93.9

Pa ge 3 7 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning, Antido tes

Poisoning,

Antidotes Suzan Mazor

Treatment N-Acetylcysteine (NAC) 

Indications: o





Acetam inophen overdose

Warnings: o

Unpleasant odor, nausea, vom iting

o

Most effective if given in first 8 hours postingestion

Dose: o

PO: 140 m g/kg, then 70 m g/kg q4h for 17 doses

o

IV: (consult poison center) 150 m g/kg in 200 m L D 5 W over 15 m inutes, then 50 m g/kg in 500 m L D 5 W over 4 hours, then 100 m g/kg in 1,000 m L D 5 W over 16 hours

Pediatric Considerations This volum e of D 5 W m ay need to be reduced in dosing pediatric patients to avoid fluid overload/hyponatrem ia.

Atropine 

Indications:

Pa ge 3 7 3



o

Bradycardia owing to drugs

o

Organophosphate insecticides

Warnings: o

Myasthenia gravis, narrow-angle glaucom a, hypertension, coronary ischem ia, and urinary obstruction



Dose: o

Adult: 0.5â€“1.0 m g IV

o

Pediatric: 0.02 m g/kg (m in. 0.1 m g) IV

o

Large repeated doses needed in organophosphate poisoning

Benztropine (Cogentin) 

Indications: o



Acute dystonic reactions

Warnings: o

Carbam ates, m yasthenia gravis, narrow-angle glaucom a, hypertension, coronary ischem ia, and urinary obstruction



Dose o

Adult: 1â€“2 m g IV (for acute reaction) or PO (to prevent reaction)

o

Pediatric: 0.02 m g/kg IV (for acute reaction) or PO (to prevent reaction)

Benzodiazepine 

Indications: o



Warnings: o



Agitation, stim ulant drugs, seizures

Respiratory/CNS depression

Dose: o

Midazolam : 

Adult: 1 m g IV/IM every 2â€“3 m inutes PRN

Pa ge 3 7 3

 o

Pediatric: 0.1 m g/kg IV/IM

Diazepam : 

Adult: 2â€“5 m g IV/IM, repeat in 10â€“15 m inutes



Pediatrics: 0.1 m g/kg IV/IM

Bicarbonate, Sodium 

Indications: o

Cyclic antidepressant poisoning, m etabolic acidosis, urinary alkalinization



Warnings: o

May cause congestive heart failure (CHF), excessive alkalosis, hypokalem ia



Dose: o

Serum alkalinization: 

o

1 m Eq/kg IVP

Urine alkalinization: 

100â€“150 m Eq in 1 L DW at 2â€“3 m L/kg/h IV, goal urine pH 7â€“8

Black Widow Spider Antivenin (Lactrodectus Mactans) 

Indications: o

Severe hypertension, m uscle spasm s not alleviated by analgesics and m uscle relaxants; consider in extrem es of age (<5 or >65 years), pregnant wom en with threatened abortion



Warnings: o

Equine serum derivedâ€”im m ediate hypersensitivity, serum sickness 10â€“14 days

o

Prem edicate for anaphylaxis if know equine serum hypersensitivity.



Dose:

Pa ge 3 7 3

o

1â€“2 vials IV slowly over 15â€“30 m inutes

Botulin Antitoxin Trivalent A,B,E 

Indications: o



Clinical botulism , prior to onset of paralysis

Warnings: o

Binds only free toxins

o

Not for infant botulism

o

Equine serum derivedâ€”im m ediate hypersensitivity, serum sickness 10â€“14 days

o

Prem edicate for anaphylaxis if know equine serum hypersensitivity.

o 

Adm inister slow IV push.

Dose: o

1â€“2 vials IV q4h for 4 or 5 doses

Calcium 





Indications: o

Hyperkalem ia with cardiac toxicity

o

Hydrofluoric acid burn

o

Calcium channel blocker overdose

o

Citrate, oxalate, phosphate poisoning

Warnings: o

Avoid in digoxin toxicity, hypercalcem ia.

o

Calcium chloride (CaCl) corrosive to skin, SC tissue

o

Incom patible with certain IV solutions

o

Adm inister slow IV push

Dose: o

Adult: 5â€“10 m L of 10% Ca chloride, or 10â€“20 m L of 10% Ca gluconate

o

Pediatric: 0.1â€“0.2 m L/kg of 10% Ca chloride, or 0.2â€“0.3 m L/kg of 10% Ca gluconate

Calcium Edta (Edetate Disodium)

Pa ge 3 7 3



Indications: o



Lead, chrom ium , nickel, m anganese, zinc toxicity

Warnings: o

Nausea, vom iting, chill, nephrotoxicity, hypercalcem ia



Dose: o

20â€“30 m g/kg over 24 hours as six divided doses or continuous IV infusion, follow lead (Pb) level

P.877

Coral Snake Antivenin (Micrurus Fulvius) 

Indications: o



Eastern or Texas coral snake

Warnings: o

Equine serum derivedâ€”im m ediate hypersensitivity, serum sickness 10â€“14 days

o

Prem edicate for anaphylaxis if know equine serum hypersensitivity.



Dose: o

4â€“10 vials IV over 15â€“30 m inutes

Cyanide Antidote Kit 

Indications: o



Warnings: o



Cyanide poisoning

Hypotension, m ethem oglobinem ia

Dose: o

Am yl nitrite: 1â€“2 am p crushed, inhaled

o

Sodium nitrite: 

Adult: 300 m g in 10 m L IV over 5 m inutes



Pediatric: 0.3 m L/kg of 3% solution IV

Pa ge 3 7 3

o

Sodium thiosulfate: 

Adult: 12.5 g IV, m ay repeat in 1 hour



Pediatric: 50 m g/kg IV

Dantrolene 



Indications: o

Malignant hypertherm ia

o

Neuroleptic m alignant syndrom e

o

Serotonin syndrom e

o

Muscle rigidity

Warnings: o



Muscle weakness, respiratory depression, hepatitis

Dose: o

1â€“2 m g/kg IV bolus, repeat q10â€“15 m in PRN, m ax. 10 m g/kg

Deferoxamine (Desferal) 

Indications: o



Iron toxicity

Warnings: o

Do not treat for >24 hours, risk for delayed adult respiratory distress syndrom e (ARDS).

o 

Hypotension if >15 m g/kg/h, flushing, urticaria

Dose: o

10â€“15 m g/kg/h IV, m ay increase in severe iron (Fe) poisoning

Digoxin Antibody (Digibind) 

Indications: o



Digoxin, digitoxin toxicity

Warnings: o

Falsely elevated digoxin levels after use

o

Developm ent of CHF/atrial fibrillation in patients requiring digoxin

Pa ge 3 7 3



Dose: o

One vial (40 m g) binds 0.6 m g digoxin.

o

Num ber of vials = digoxin level (ng/m L) Ã— weight (kg)/100

o

Dose estim ate: acute overdose 10â€“20 vials, chronic overdose 4â€“6 vials

Dimercaprol (Bal) 

Indications: o



Arsenic, gold, m ercury, lead-induced encephalopathy

Warnings: o

Renal toxicity, fever, nausea, vom iting, urticaria, cholinergic sym ptom s



Dose: o

3 m g/kg deep IM q4h for 2 days, then q12h for 7 days; follow m etal levels

o

For Pb level >100 Âµg/dL: 4â€“5 m g/kg IM q4h until Pb <50 Âµg/dL, in conjunction with EDTA

Diphenhydramine (Benadryl) 

Indications: o



Antihistam ine, acute dystonic reaction

Warnings: o

Sedation, excitation in children, anticholinergic sym ptom s



Dose: o

Adult: 25â€“50 m g IV/IM/PO q4hâ€“q6h

o

Pediatric: 0.5â€“1 m g/kg IV/IM/PO q4hâ€“q6h

Dmsa (Succimer, Chemet) 

Indications: o



Pediatric lead poisoning

Warnings: o

Caution in renal im pairm entâ€”urinary elim ination

Pa ge 3 7 4

o 

Nausea, vom iting diarrhea

Dose: o

10 m g/kg PO q8h for 5 days, then q12h for 14 days, then reassess blood lead levels

Epinephrine 

Indications: o

Angioedem a, anaphylaxis, acute asthm a, spinal shock, beta-blocker overdose



Warnings: o



Dysrhythm ias, hypertension, trem or, anxiety

Dose: o

o

Hypotension/shock: 

Adult: 1â€“4 Âµg/m in IV infusion



Pediatric: Start IV infusion at 0.1 Âµg/kg/m in.

Mild-m oderate reactions: 

Adult: 0.3â€“0.5 m g SC



Pediatric: 0.01 m g/kg SC

Ethanol 

Indications: o





Methanol or ethylene glycol toxicity

Warnings: o

Disulfiram reaction, CNS sedation

o

Hypoglycem ia in pediatric population

o

Increase dose during dialysis, for chronic alcoholics.

Dose: o

IV: 10 m L/kg load as 10% solution over 1 hour, then 1 m L/kg/h m aintenance

o

PO: 1.5 m L/kg as 100-proof solution, then 0.3 m L/kg/h m aintenance

o

Goal: ethanol level of 100â€“150 m g/dL

Flumazenil (Romazicon)

Pa ge 3 7 4



Indications: o



Benzodiazepine overdose

Warnings: o

Contraindicated in tricyclic antidepressant (TCA) overdose



o

Lowers seizure threshold

o

Induces benzodiazepine withdrawal

Dose: o

Adult: 0.2 m g IV slow, repeat q2â€“3m in to 1 m g m ax.

o

Pediatric: 0.01â€“0.05 m g/kg IV over 30 m inutes to 1 hour

P.878

Fomepizole (4-MP, Antizol) 

Indications: o



Warnings: o



Methanol or ethylene glycol toxicity

Nausea, dizziness, headache

Dose: o

15 m g/kg load, then 10 m g/kg q12h for 4 doses, then 15 m g/kg q12h

Glucagon 

Indications: o

Beta-blocker or calcium channel blocker overdose with bradycardia/hypotension

o 

Hypoglycem ia

Warnings: o

Nausea, vom iting, hyperglycem ia

o

Hypotension from diluent (phenol-containing)

Pa ge 3 7 4



Dose: o

o

Beta-blocker or calcium channel blocker overdose: 

Adult: 5â€“10 m g IV over 1 m inute



Pediatric: 0.15 m g/kg IV over 1 m inute

Hypoglycem ia: 

Adult: 0.5â€“1 m g IM/IV/SC



Pediatric: 0.025â€“0.1 m g/kg IM/IV/SC (m ax. 1 m g per dose)

Insulin/Glucose 

Indications: o

Calcium channel blocker overdose with severe hypotension/sym ptom atic bradycardia refractory to other therapies

o 

Hyperkalem ia

Warnings: o

Experim ental therapy: consult a poison control center/m edical toxicologist.

o

Follow serum glucose q15m in for 1 hour after the first bolus or after any increase in dose, then q1h



Dose: o

o

Bolus: 

0.5â€“1.0 IU/kg regular insulin, followed by



25 g glucose (1 am p D 5 0 )

Maintenance: 

Insulin 0.5 IU regular insulin per kg/h, titrate to 1.0 IU regular insulin per kg/h



Glucose D 1 0 start at 100 m L/h (10g/h) and titrate to keep glucose â‰¥100 m g/dL

Methylene Blue 

Indications: o

Methem oglobinem ia with dyspnea or >25%

Pa ge 3 7 4



Warnings: o



G6-PD deficiency

Dose: o

1â€“2 m g/kg slow IV as 1% solution, repeat in 1 hour

Narcan 

Indications: o



Warnings: o



Opiate poisoning, em piric treatm ent of com a

Acute opiate withdrawal, severe agitation

Dose: o

Adult: 0.4â€“2.0 m g IV or IM, repeat to 10 m g

o

Pediatric: 0.1 m g/kg IV or IM

Octreotide 

Indications: o



Warnings: o



Sulfonylurea overdose with hypoglycem ia

Use with caution in diabetic patients.

Dose: o

Adult: 50 Âµg SC q6h

o

Pediatric: 4â€“5 Âµg/kg/d SC div. q6h

Oxygen, Hyperbaric 

Indications: o



Carbon m onoxide (CO) poisoning

Warnings: o

Tym panic m em brane (TM) perforation, seizures owing to oxygen toxicity

o 

Difficulty m onitoring patient

Dose: o

100% oxygen at 2â€“3 atm

Penicillamine

Pa ge 3 7 4



Indications: o

Arsenic, copper, lead, m ercury with/following BAL or EDTA



Warnings: o

Contraindicated in penicillin allergy, renal insufficiency



Dose: o

o

Lead: 

Adult: 250â€“500 m g per dose PO q8hâ€“q12h



Pediatric: 25â€“40 m g/kg/d PO in 3 div. doses

Arsenic: 

100 m g/kg/d PO divided in four doses for 5 days (m ax. 1 g/d)

o

Mercury: 

Adult: 250 m g PO q.i.d.



Pediatric: 20â€“30 m g/kg/d PO in 4 div. doses

Phentolamine 

Indications: o

Hypertensive crisis: stim ulants, sym pathom im etics, MAO-tyram ine reaction, and extravasated pressors

o 

Warnings: o



Reversal of cocaine-m ediated vasospasm

Hypertension, tachycardia, dysrhythm ias

Dose: o

o

Hypertension (HTN): 

Adult: 1â€“5 m g IV bolus



Pediatric: 0.02â€“0.1 m g/kg bolus

Extravasation: 

Adult: 5 m g diluted in 10â€“15 m L saline SC



Pediatric: 0.1 m g/kg diluted in 10â€“15 m L saline SC

Pa ge 3 7 4

Physostigmine 

Indications: o



Warnings: o



Severe anticholinergic syndrom e

Contraindicated in TCA overdose

Dose: o

Adult: 0.5â€“1.0 m g IV, repeat in 10 m in PRN

o

Pediatric: 0.02 m g/kg IV, repeat in 10 m in PRN

P.879

Pralidoxime (2-PAM, Protopam) 



Indications: o

Organophosphate toxicity

o

Reversal of nicotinic effects

o

Reactivates enzym e

o

Use in conjunction with atropine

Warnings: o

Myasthenic crisis if m yasthenia gravis

o

Nausea, headache, dizziness, laryngospasm , m uscle rigidity



Dose: o

Adult: 1â€“2 g in 100 m L NaCl over 15 m inutes, repeat in 1 hour PRN, repeat in 6 hours if nicotinic sym ptom s return

o

Pediatrics: 25â€“50 m g/kg over 15 m inutes, repeat in 1 hour PRN, repeat in 6 hours if nicotinic sym ptom s return

Protamine 

Indications: o

Reversal of heparin anticoagulation

Pa ge 3 7 4





Warnings: o

Hypersensitivity in patients with fish allergy

o

Avoid benzyl alcohol diluent in neonates.

Dose: o

1 m g for each 100 IU heparin, half dose if 30â€“60 m inutes, and quarter dose if 2 hours after heparin bolus

Pyridoxine (Vitamin B 6) 



Indications: o

Isoniazid-induced seizures

o

Gyrom itra m ushroom

Warnings: o



None, nontoxic

Dose: o

Isonicotinic acid hydrazide (INH)â€“induced seizures: 

Unknown ingested am ount: 5 g for adult or 1 g for pediatrics



Dose (m g) = am ount INH ingested (m g)



Gyrom itra: 25 m g/kg IV over 30 m inutes to 1 hour

Digoxin Antibody (Digibind) 

Indications: o

Significant envenom ation by Crotaline species: rattlesnake, cottonm outh, water m occasin, pit viper



Warnings: o

Equine or ovine derived productsâ€”im m ediate hypersensitivity, serum sickness 10â€“14 days

o

Prem edicate for anaphylaxis if know equine/ovine serum hypersensitivity.



Dose: o

Equine-derived (Wyeth-Ayerst polyvalent):

Pa ge 3 7 4

o



Mild: 5 vialsâ€”infuse slowly



Moderate: 10 vialsâ€”infuse slowly



Severe: 15 vialsâ€”infuse slowly

Ovine-derived (Crofab): 

4â€“6 vials slowly; m ay repeat dose of 4â€“6 vials if control of envenom ation not achieved, then 2 vials q6h for 3 doses

Vitamin K (Phytonadione, Aqua Mephyton) 

Indications: o



Warnings: o



Reversal of Coum adin anticoagulation

Hypersensitivity from IV adm inistration

Dose: o

2â€“10 m g IM/SC/slow IV, m ay repeat in 8 hours

o

2â€“10 m g PO, m ay repeat in 12â€“48 hours

Pa ge 3 7 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning, G astric Deco ntam inatio n

Poisoning,

Gastric Decontamination Frank LoVecchio

Basics Description Modalities to decontam inate the GI tract of poisons

Treatment Pre Hospital Alert 

Ipecac contraindicated in am bulance setting



Controversies: o

Hom e use of ipecac in general is not recom m ended. 

In extrem ely rare cases (e.g., very prolonged transit tim es, protecting airway), consider ipecac adm inistration only after consultation with regional poison control center.

o

Decreased tim e to activated-charcoal adm inistration when given in pre hospital setting

Pa ge 3 7 4

o

Decreased drug absorption in a sim ulated ingestion while volunteers were lying in left lateral versus right lateral decubitus position

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs): o

Secure airway for decreased m ental status/inability to protect airway.



o

Intravenous access

o

Cardiac m onitor

With altered m ental status from overdose: o

Naloxone

o

Thiam ine

o

Dextrose (or Accu-Chek)

ED Treatment 

Ipecac: o

General: 

Derived from the roots of the plant Cephaelis acum inata



Exerts em etic action by direct gastric irritation and centrally m ediated chem oreceptive trigger-zone stim ulation



Delays adm inistration of activated charcoal



Offers no advantage over activated charcoal alone when both treatm ents potentially effective

o

Dosage: 

Older than 12 years: 30 m L



Ages 1 through 12 years: 15 m L



Ages 6 m onths to 1 year: 5â€“10 m L plus 15 m L clear fluid

o

Indications:

Pa ge 3 7 5

 o

No utility in ED

Adverse effects: 

Vom iting m ay com plicate and worsen clinical presentation.



Delay to adm inistration of activated charcoal or oral antidotes

o

Contraindications: 

Caustics (acids and alkali) ingestion



Hydrocarbon ingestion



Ingestion of agents that rapidly depress m ental status

 

Patients actively vom iting

Orogastric lavage: o

General: 

Placem ent of large-bore tube (32â€“36 Fr) in stom ach for rem oval of ingested toxins



Effectiveness of orogastric lavage depends on tim e interval since ingestion, tim ing of last m eal, and toxin ingested.



Protected airway essential prior to any attem pts at orogastric lavage

o

Indications: 

Presentation within 1 hour of taking a potentially lethal ingestion with no known antidote

 o

o

Poisoned intubated patient

Adverse effects: 

Intubation of respiratory tree



Esophageal or gastric perforation



Charcoal aspiration



Patient discom fort

Contraindications:

Pa ge 3 7 5



Large pills (lim ited by lavage-tube port size) ingestion



Caustics (acids and alkali) ingestion



Hydrocarbon ingestion



Ingestion of agents that rapidly depress m ental status



Unprotected airway

P.881

o

Pediatric considerations: 

Avoid in children



Unlikely to result in any clinically significant pill extraction secondary to sm aller-bore orogastric tube (i.e., 18 Fr)

 o

Risk of aspiration increased in children

Controversies: 

Several random ized, controlled trials have docum ented no benefit when lavage plus activated charcoal is com pared with activated charcoal alone.



Activated charcoal: o

General: 

Prepared by treating heated wood pulp, which creates a large surface area to bind toxins



Mainstay of gastric decontam ination



Effective when contents have reached sm all intestine

o

Dose: 

1â€“2 g/kg of body weight or an activated charcoal-to-drug ratio of 10:1; often m ixed with sorbitol (see below)

Pa ge 3 7 5

 o

Oral or nasogastric-tube adm inistration

Indications: 

Adm inister in every toxic ingestion (see below for exceptions).



Optim al for toxic ingestions presenting within 1 hour of ingestion

o

Adverse effects: 

Vom iting and constipation



Charcoal aspiration and subsequent charcoal pneum onitis

o

o

o

Contraindications: 

Caustic ingestions



Unprotected airway



Bowel obstruction or ileus

Drugs not effectively bound to charcoal: 

Metals (borates, brom ide, iron, lithium )



Alcohols



Potassium



Potassium cyanide (poorly absorbed)



Hydrocarbons



Caustics

Pediatric considerations: 

Mix with palatable substance (cola or juice) to facilitate intake or adm inister via gastric tube.

o

Controversies: 

Random ized, controlled trials have shown a slightly worse outcom e and higher com plication rate when asym ptom atic patients received charcoal versus nothing.



An extrem ely sm all m inority of patients are likely to benefit from gastric lavage.



Multiple-dose activated charcoal:

Pa ge 3 7 5

o

General: 

Used in toxic ingestions that are well absorbed by charcoal and undergo enterohepatic circulation

o

Dose: 

1 g/kg followed by 0.5 g/kg q2hâ€“q6h



Never use cathartics in conjunction with m ultiple-dose activated charcoal.

o

Indications: 

Theophylline



salicylates



Multiple-dose activated charcoal m ay decrease area under the curve for such drugs as phenobarbital, phenytoin, and carbam azepine, but has not been proven to im prove outcom e.



Cathartics: o

General: 

Used in com bination with activated charcoal to prevent constipation and to enhance gastrointestinal transit tim e



Lim ited data available to dem onstrate any decreased absorption when a cathartic (sorbitol) is added to activated charcoal



Cathartics alone are of no proven benefit and should be avoided.



Never use cathartics in conjunction with m ultiple-dose activated charcoal.

o

Dose: 

Magnesium citrate: 10% solution: 250 m L (peds: 4 m L/kg)



Magnesium sulfate: 15â€“20 g (peds: 250 m g/kg)

Pa ge 3 7 5



Sorbitol: 0.5â€“1 g/kg to a m ax. 100 g of 70% solution (peds: >1 year old: 0.5â€“1 g/kg as a 35% solution to a m ax. 50 g) PO m ixed in the activated charcoal slurryâ€”use only in first dose.

o

o

Adverse effects: 

Dehydration



Hyperm agnesem ia



Diarrhea



Abdom inal discom fort

Contraindications: 

Pre-existing dehydration



Renal disease (cathartics containing m agnesium )

 o

Avoid in children

Controversies: 

No proven benefit with som e cases of harm reported



Whole-bowel irrigation: o

General: cleansing of bowel

o

Indications: 

Toxins not well absorbed by charcoal such as toxic iron and lithium ingestions



Toxins in sealed containers (body packers) without signs of gastrointestinal perforation

 o

Toxic, sustained-release product ingestions

Dose: 

Polyethylene glycol (Colyte, Go-Lytely)



Solution at 2 L/h in adults (0.5 L/h in children) until rectal excretions clear



Adm inister via nasogastric tube with activated charcoal via continuous or bolus m ethod as

Pa ge 3 7 5

indicated. o

o

Adverse effects: 

Bloating



Rectal irritation



Frequent bowel m ovem ents

Contraindications: 

Mechanical or pharm acologic ileus



Bowel obstruction



Intestinal perforation



Unprotected airway

Follow-Up N/A

References 1. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients with acute toxic ingestions or derm al or inhalation exposure. Ann Em erg Med. 1995;25:570â€“585. 2. Ellenhorn MJ, Schoonwald S, Ordog G, et al. Gut decontam ination. In: Ellenhorn MJ, ed. Ellenhorn's Medical Toxicology. 2nd ed. Baltim ore: William s & Wilkins; 1997:66â€“78. 3. Perrone J, Hoffm an RS, Goldfrank LR. Special considerations in gastric decontam ination. Em erg Med Clin. 1994;12:285â€“299. 4. Pond SM, Lewis Driver DJ, William s GM, et al. Gastric em ptying in acute overdose: a prospective random ized controlled trial. Med J Aust . 1995;163:345â€“349.

Miscellaneous SEE ALSO: Poisoning; Poisoning, Toxidrom es; Poisoning, Antidotes

Pa ge 3 7 5

Codes ICD9-CM 977.9 Unspecified drug or m edicinal substance

ICD10 T47.6 Antidiarrheal drugs

Pa ge 3 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning, To xidro m es

Poisoning,

Toxidromes Kirk Cumpston

Basics Etiology N/A

Mechanism 

Anticholinergic: o

Adrenergic im balance results from inhibition of acetylcholine at receptors.



Cholinergic: o

Excess parasym pathetic stim ulation and cholinergic crisis result from inhibition of acetylcholinesterase or increased activity at acetylcholine receptor.



Opiates: o

Differ in their agonist and antagonist properties at various opioid receptor sites

o

Âµ-Receptor stim ulationâ€”full agonist

o

K and Î´ receptors share partial agonist and antagonist properties.



Sym pathom im etic: o

Stim ulation of sym pathetic effector organs

Pa ge 3 7 5

(particularly CNS) 

Withdrawal: o

Hyperactivity of sym pathetic nervous system predom inates.

Diagnosis Signs and Symptoms 

Toxicologic m nem onics: o

Use the following m nem onics to rem em ber the substances and drugs that can present each sign or sym ptom :



Anion gap acidosis: A CAT MUD PILES: o

AKA

o

CO/cyanide

o

Acetam inophen in fulm inant hepatic failure

o

Toluene

o

Methanol

o

Urem ia

o

DKA

o

Paraldehyde, phenform in/m etform in, prophylene glycol



o

Iron/INH

o

Lactic acidosis

o

Ethylene glycol

o

Salicylates, Starvation ketosis

Increased osm olar gap: ME DIE: o

Methanol

o

Ethylene glycol

o

Diuretics (m annitol, glycerol, sorbital) Diluents (propylene glycol)

Pa ge 3 7 5



o

Isopropyl alcohol

o

Ethanol

Seizures: OTIS CAMPBELL: o

Organophosphates

o

Tricyclic antidepressants

o

INH/insulin

o

Sym pathom im etics, salicylates

o

Cam phor/cocaine/citalopram

o

Am phetam ines, anticholinergic agents

o

Methylxanthines (theophylline, caffeine), m ushroom s (m onom ethyl hydrazine group)

o

PCP, pethidine (Dem erol), propoxyphene, plants (nicotine, water hem lock)







o

Benzodiazepine withdrawal, bupropion

o

Ethanol withdrawal

o

Lithium , lidocaine

o

Lead, lindane

Mydriasis: AAAS: o

Antihistam ines

o

Antidepressants

o

Anticholinergics/atropine

o

Sym pathom im etics

Miosis: COPS: o

Cholinergic/clonidine

o

Opiates/organophosphates/olanzapine

o

Phenothiazines/pilocarpine/pontine bleed

o

Sedative hypnotics

Hypertension: CT SCAN: o

Cocaine

o

Theophylline

o

Sym pathom im etics

o

Caffeine

Pa ge 3 7 6













o

Anticholinergics/am phetam ines

o

Nicotine

Hypotension: CRASH: o

Cocaine/calcium channel blockers

o

Reserpine/antihypertensives/beta-blockers

o

Antidepressants/am inophylline

o

Sedative-hypnotics

o

Heroin/other opioids

Bradycardia: PACED: o

Propranolol (beta-blockers)

o

Anticholinesterase inhibitors drugs

o

Clonidine/calcium channel blockers

o

Ethanol/alcohols

o

Digoxin

Tachycardia: FAST: o

Free base (cocaine)

o

Anticholinergic/antihistam ines/am phetam ines

o

Sym pathom im etics/solvent abuse

o

Theophylline

Hypotherm ia: COOLS: o

Carbon m onoxide

o

Opiates

o

Oral hypoglycem ics

o

Liquor

o

Sedative hypnotics

Hypertherm ia: NASA o

Neuroleptic m alignant syndrom e, nicotine

o

Antihistam ines/Alcohol withdrawal

o

Salicylates, sym pathom im etics, serotonin toxicity

o

Anticholinergics, antidepressants

Rapid respiration: PANT: o

PCP, paraquat, pneum onitis

Pa ge 3 7 6







o

ASA (acetylsalicylic acid)

o

Noncardiogenic pulm onary edem a

o

Toxin-induced m etabolic acidosis

Slow respiration: SLOW: o

Sedative-hypnotics (Î³-hydroxybutyrate [GHB])

o

Liquor

o

Opiates

o

Weed

Diaphoresis: SOAP: o

Sym pathom im etics

o

Organophosphates

o

Acetylsalicylic acid

o

PCP

Drugs that cause pulm onary edem a: MOPS: o

Meprobam ate, m ethadone

o

Opiates, organophosphates

o

Phenobarbital, propoxyphene, phenothiazines

o

Salicylates, sm oke inhalation, solvents

Toxidromes 



Cholinergic: SLUDGE BAM: o

Salivation

o

Lacrim ation

o

Urination

o

Diarrhea

o

Em esis

o

Bronchorrhea, bronchospasm , bradycardia

o

Abdom inal discom fort

o

Miosis

Anticholinergic: o

Hypertherm ia (â€œHot as a hare, red as a beetâ€•)

o

Dry skin (â€œDry as a boneâ€•)

o

Dilated pupils (â€œBlind as a batâ€•)

Pa ge 3 7 6

o

Delirium (â€œMad as a hatterâ€•)

o

Tachycardia

o

Hypertension

o

Hypertherm ia

o

Urgency retention

o

Decreased bowel sounds

P.883









Sym pathom im etic: o

Diaphoresis

o

Mydriasis

o

Tachycardia

o

Hypertension

o

Hypertherm ia

o

Seizures

Opiate: o

Miosis

o

Hypovolem ia

o

Com a

o

Bradycardia

o

Hypotension

Withdrawal (alcohol, benzodiazepine, barbiturates): o

Mydriasis

o

Tachycardia

o

Hypertension

o

Hypertherm ia

o

Trem or

o

Agitation

o

Hallucinations

o

Seizures

Withdrawal (opioid):

Pa ge 3 7 6

o

Nausea

o

Vom iting

o

Diarrhea

o

Abdom inal cram ps

o

Mydriasis

o

Piloerection

o

Tachycardia

o

Lacrim ation

o

Salivation

o

Hypertension

o

Yawning

o

Cram ps

Dermatologic 



Dry skin: o

Antihistam ines

o

Anticholinergics

Bullae: o





Barbiturates/carbon m onoxide

Acneiform rash: o

Dioxins

o

Brom ides

o

Chlorinated

o

Hydrocarbons

Flushed or red appearance: o

Anticholinergics

o

Disulfiram reactions

o

Niacin

o

Boric acid

o

Scom broid poisoning

o

Monosodium glutam ate

o

Carbon m onoxide (frequently postm ortem )

o

Cyanide (rare)

Pa ge 3 7 6

o 



Vancom ycin

Cyanosis: o

Ergotam ines

o

Methem oglobinem ia form ing: 

Nitrite



Nitrate



Dapsone



Aniline dye



Phenazopyridine



Benzocaine (caines)



Chloroquine

Odors: o

Bitter alm onds: cyanide

o

Carrots: cicutoxins

o

Fruity: diabetic ketoacidosis (DKA), isopropanol

o

Garlic: organophosphates, arsenic

o

Gasoline: petroleum distillates

o

Mothballs: naphthalene, cam phor

o

Pears: chloral hydrate

o

Pungent odor: ethchlorvynol

o

Oil of wintergreen: m ethyl salicylate

o

Rotten eggs: hydrogen sulfide

o

Peanut butter: Vacor

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)

ED Treatment Depends on ingested substance (see related chapter)

Pa ge 3 7 6

References 1. Erickson TB. Toxicology update: a rational approach to managing the poisoned patient. Em erg Med Pract. 2001;3(8). 2. Keyes DC, Dart RC. Initial diagnosis and treatm ent of the poisoned patient. In Dart RC, ed. Medical Toxicology. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 2004:21â€“31.

Miscellaneous SEE ALSO: Poisoning; Poisoning Antidotes; Poisoning, Gastric Decontam ination

Pa ge 3 7 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning

Poisoning

Mark B. Mycyk

Basics Description 

Poisoning m ay be intentional or unintentional.



Patients with change in m ental status without clear cause should have poisoning (intoxication, overdose) considered in differential diagnosis.

Etiology 



Intentional: o

Depression

o

Suicide

o

Hom icide

o

Recreational drug abuse

Unintentional (accidental): o

Com m on cause in children

o

Therapeutic error (e.g., double dose)

o

Recreational drug experim entation

Pediatric Considerations 

Accidental ingestionsâ€”typically young children (ages 1â€“5 years)



Consider child abuse if inconsistent or suspicious history.

Pa ge 3 7 6

Diagnosis Signs and Symptoms 







Neurologic: o

Lethargy

o

Agitation

o

Com a

o

Hallucinations

o

Seizures

Respiratory: o

Tachypnea/bradypnea/apnea

o

Inability to protect airway

Cardiovascular: o

Dysrhythm ias

o

Conduction blocks

Vital signs: o

Varies depending on toxic substance

o

Hypertherm ia/hypotherm ia

o

Tachycardia/bradycardia

o

Hypertension/hypotension

Selected Toxidromes (see Poisoning, Toxidromes) 

Anticholinergic: o

Altered m ental status (confusion, delirium , lethargy)

o

Dry skin and m ucous m em branes

o

Fixed dilated pupils

o

Tachycardia

o

Hypertherm ia

o

Flushing

Pa ge 3 7 6

o 

Urinary retention

Cholinergic: o

Secretory overdrive (salivation, lacrim ation, urination, diaphoresis)





o

Miosis

o

Bronchospasm /wheezing

Opiate: o

CNS and respiratory depression

o

Pinpoint pupils

Sym pathom im etic: o

CNS excitation

o

Seizures

o

Tachycardia

o

Hypertension

o

Diaphoresis

Essential Workup 

Accurately identify ingestant(s).



Send som eone to patient's hom e to obtain product(s) if necessary.



Accurately identify tim e of ingestion.



Call poison control center or toxicologist for help.

Tests Lab 

Electrolytes, BUN/creatinine, glucose



Calculate anion gap: Na - (Cl+HCO 3 ) o

Norm al anion gap: 8â€“12

o

Use m nem onic A CAT MUD PILES for elevated anion gap acidosis: 

Alcoholic ketoacidosis



Cyanide, carbon m onoxide



ASA, other salicylates

Pa ge 3 7 6





Toluene



Methanol, m etform in



Urem ia



Diabetic ketoacidosis



Paraldehyde, phenform in



Iron, INH



Lactic acidosis from other causes



Ethylene glycol



Starvation ketosis

Serum osm ol gap: o

Calculate osm ol gap if elevated anion gap acidosis from potential toxic alcohol.

o

Most sensitive early in poisoning

o

Norm al osm ol gap does not com pletely rule out toxic alcohol ingestion.

o

Calculated osm olality = 2(Na + ) + glucose/18 + BUN/2.8 + ethanol (in m g/dL)/4.6.

o

Osm ol gap = m easured osm olality â€“ calculated osm olality.

o

Use m nem onic ME DIE A when osm ol gap >10 

Methanol



Ethanol



Diuretics (m annitol, glycerin, sorbitol)



Isopropyl alcohol



Ethylene glycol



Acetone



Pregnancy test



Acetam inophen level for suicidal ingestions



Toxicology screen

Imaging 

ECG for dysrhythm ias or QRS/QT changes



CT of head for altered m ental status not clearly owing to

Pa ge 3 7 7

toxin 

Chest radiograph if suspected aspiration or pneum onia

Differential Diagnosis Causes of Altered Mental Status 

Intracranial m ass, bleeding



Infection, sepsis



Endocrine abnorm alities



Hypotherm ia



Hypoxia



Metabolic abnorm alities



Psychogenic

Treatment Pre Hospital 



Search for clues at scene: o

Pills/pill bottles

o

Drug paraphernalia

o

Witnesses

o

Transport all drugs and pill bottles for identification.

Restrain uncooperative patients for patient and health care giver protection.





Consider co-m orbid conditions: o

Traum a

o

Medical illness

o

Environm ental exposure

Pre hospital adm inistration of activated charcoal m ay optim ize decontam ination if prolonged transport tim e.

Initial Stabilization

Pa ge 3 7 7



Airway, breathing, and circulation m anagem ent (ABCs): o

Endotracheal intubation as needed for airway protection, oxygenation, ventilation, and orogastric lavage







o

Supplem ental oxygen for hypoxia

o

Pulse oxim etry

o

Cardiac m onitor

o

IV access

Hypotension: o

Adm inister 0.9% norm al saline (NS) IV fluid bolus.

o

Trendelenburg

o

Vasopressors for persistent hypotension

Bradycardia: o

Atropine

o

Cardiac pacing

If altered m ental status, adm inister com a cocktail: thiam ine, D 5 0 W (or Accu-Chek), naloxone

P.875

ED Treatment Decontamination 

See Poisoning, Gastric Decontam ination.



Prevents system ic absorption of ingested toxin



Orogastric lavage: o

Consider in potentially lethal ingestions without known antidote within 1 hour of ingestion.

o 

Protected airway essential prior to lavage

Activated charcoal: o

Most effective within a few hours of m ost toxic ingestions

Pa ge 3 7 7

o

Contraindicated if caustic ingestion, unprotected airway, or bowel obstruction

o

Drugs not effectively bound to charcoal: m etals (borates, brom ide, iron, lithium ), alcohols, potassium



Whole-bowel irrigation: o

Polyethylene glycol (Colyte, Go-Lytely) evacuates bowel without causing electrolyte disturbances.

o

Consider in toxins not well adsorbed by charcoal (e.g., iron and lithium ), body packers/stuffers, sustained release ingestions.

o

Contraindicated if bowel obstruction, perforation, or hypotension

Enhanced Elimination Enhances rem oval of system ically absorbed toxin: 





Multiple-dose activated charcoal: o

Theophylline

o

Carbam azepine

o

Phenobarbital

Urinary alkalinization: o

Salicylates

o

Phenobarbital

Hem odialysis/hem operfusion: o

Lithium

o

Salicylates

o

Theophylline

o

Toxic alcohols

Seizures 

Treat initially with diazepam or lorazepam .



For persistent seizures, consider phenobarbital.



Phenytoin not indicated in toxicologic seizures: o

Indicated only if seizures secondary to idiopathic

Pa ge 3 7 7

epilepsy, posttraum atic, or status epilepticus

Antidotes 

See Poisoning, Antidotes.



Acetam inophen: N-acetylcysteine



Anticholinergic: physostigm ine



Benzodiazepines: flum azenil



Beta-blockers: glucagon



Calcium channel blockers: calcium chloride/gluconate, insulin



Carbon m onoxide: oxygen, hyperbaric oxygen



Coum adin: vitam in K 1



Cyanide: cyanide antidote kit



Digoxin: Digibind



Ethylene glycol: ethanol, 4-m ethylpyrazole



Iron: deferoxam ine



Isoniazid (INH): pyridoxine (vitam in B 6 )



Methanol: ethanol, 4-m ethylpyrazole



Methem oglobinem ia: m ethylene blue



Opiates: naloxone



Organophosphates: atropine, pralidoxim e



Tricyclic antidepressants: NaHCO 3

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg PO



Dextrose: D 5 0 W one am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam : 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV every 10â€“15 m inutes



Lorazepam : 2â€“6 m g (peds: 0.05â€“0.1 m g/kg) IV every 10â€“15 m inutes

Pa ge 3 7 7



Naloxone (Narcan): 0.4â€“2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Altered m ental status



Cardiopulm onary instability



Suicidal



Laboratory abnorm alities



Potential for decom pensation from delayed acting substance

Discharge Criteria 

Psychiatrically clear



Detoxified



Hem odynam ically stable

Issues for Referral 

Patients with unintentional (accidental) poisoning require poison prevention counseling.



Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.



Consider substance abuse referral for patients.

References 1. Dem orest RA, Posner JC, Osterhoudt KC, et al. Poisoning prevention education during em ergency departm ent visits for childhood poisoning. Pediatr Em erg Care. 2004;20(5):281â€“284. 2. Ford MD, Delaney KA. Initial approach to the poisoned patient. In:

Pa ge 3 7 7

Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:14. 3. Goldfrank LR, Flom enbaum NE, Lewin NA, et al. Vital signs and toxic syndrom es. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. Norwalk, CT: Appleton & Lange, 2002:37â€“40. 4. Hoffm an RS, Goldfrank LR. The poisoned patient with altered consciousness. JAMA. 1995;274:562â€“569. 5. Kulig K. Initial m anagem ent of toxic substances. N Engl J Med. 1992;326:1678â€“1682.

Miscellaneous SEE ALSO: Poisoning, Antidotes; Poisoning, Gastric Decontam ination; Poisoning, Toxidrom es

Codes ICD9-CM 977.9

ICD10 T65.9

Pa ge 3 7 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po lio

Polio

Philip Shayne

Basics Description 

Caused by poliovirus infection



Incubation period 9â€“12 days



Duration <1 week



Clinical m anifestations are defined as follows: o

Subclinical (i.e., not apparent) 90â€“95%

o

Abortive poliom yelitis 4â€“8%: 

Clinically indistinct from m any other viral infections (fever, m yalgias, m alaise)

 o

Only suspected to be polio during an epidem ic

Nonparalytic poliom yelitis 1â€“2%: 

Differs from abortive poliom yelitis by the presence of m eningeal irritation

 o

Course sim ilar to any aseptic m eningitis

Paralytic poliom yelitis 0.1%, which is further subdivided: 

Spinal paralytic poliom yelitis (frank polio)



Bulbar paralytic poliom yelitis (10% of paralytic polio): paralysis of m uscle groups innervated by cranial nerves; involves the circulatory and

Pa ge 3 7 7

respiratory centers of the m edulla with high m ortality  o

Mixed bulbospinal poliom yelitis

Postpoliom yelitis syndrom e: 

New onset of m uscle weakness, pain, and atrophy



Occurs m any years after the active illness, usually in the previously affected lim b



Gradual progression

Etiology 

Polioviruses: o

Picornaviruses

o

Sm all, nonenveloped, RNA viruses of the enterovirus genera



Fecal-oral route transm ission



Hum ans are the only natural host and reservoir.



Poliovirus selectively destroys m otor and autonom ic neurons.



Natural (wild) virus is com pletely elim inated in North and Latin Am erica.



Oral poliovirus vaccine (OPV): o

Accounts for only poliom yelitis seen in the United States (8â€“10 cases per year of vaccine associated paralysis [VAP])

o

Incidence of VAP: 1 in 700,000

o

Use no longer recom m ended in United States

Diagnosis Signs and Symptoms

Pa ge 3 7 7

History 

Malaise



Anorexia/nausea/vom iting



Upper respiratory tract sym ptom s

Physical Exam 

Fever (37â€“39Â°C)



Headache, photophobia



Nuchal rigidity



Neurologic changes: o

Muscle soreness that becom es severe m uscle spasm , progressing rapidly to spotty flaccid weakness and paralysis

o

Asym m etric paralysis m ore prom inent in the lower than the upper extrem ities

o

Urinary retention (50% of paralytic cases)

o

Reflexes: 

Initially hyperactive, then absent

o

Apprehensive and irritable, occasionally drowsy

o

No sensory loss associated with the m otor deficit

Pediatric Considerations 

More likely to have a biphasic acute course: o

Viral-type syndrom e for 1â€“2 days

o

Sym ptom -free period of 2â€“5 days

o

Then an abrupt onset of the m ajor illness

Essential Workup 

Clinical diagnosis



Differentiate from other causes of acute paralysis.



Notify public health officials when diagnosis suspected.

Tests Lab

Pa ge 3 7 7



CBC: o



WBC norm al or m ildly elevated

Diagnosis confirm ed by: o

Com paring acute with convalescent sera for antigen titers

o

Isolation of virus from blood or cerebrospinal fluid (CSF)

Diagnostic Procedures/Surgery CSF analysis: 

Abnorm alities typical of aseptic m eningitis (increased lym phocytes and elevated protein)



Poliovirus rarely isolated from the CSF

Differential Diagnosis 

Abortive poliom yelitis is sim ilar to m any viral illnesses.



Nonparalytic poliom yelitis is indistinguishable from any viral, aseptic m eningitis.



Paralytic poliom yelitis: o

Guillain-BarrÃ© (not febrile, sym m etrical, not ill appearing)

o

Acute transverse m yelitis

o

Diphtheria

o

Botulism

o

Tick paralysis

o

Encephalitis

P.885

Treatment

Pa ge 3 7 8

Alert Rare fatal case com es from respiratory insufficiency, which requires prom pt ventilatory support.

Initial Stabilization Aggressive pulm onary toilet and early intubation m andated for respiratory insufficiency

ED Treatment 

Supportive and sym ptom atic m anagem ent



Analgesics for severe m uscle pain and spasm



Bed rest to prevent augm entation or extension of paralysis



Paralytic poliom yelitis tends to localize to a lim b that has been the site of intram uscular injection or injury within 2â€“4 weeks prior to the onset of infection: o

Avoid any unnecessary tissue dam age in suspected cases.



No antiviral agents available

Prevention 



Inactivated poliovirus vaccine (IPV): o

Costly

o

Painful

o

No conferred im m unity

o

However, no vaccine-associated paralysis (VAP)

Oral poliovirus vaccine (OPV) o

Accounted for only poliom yelitis seen in the United States (8â€“10 cases per year of vaccine-associated paralysis [VAP])

o

Incidence of VAP: 1 in 700,000

o

Confers im m unity to unvaccinated contacts by fecal-oral spread

o

Inexpensive

Pa ge 3 7 8

o

No longer recom m ended

Follow-Up Disposition Admission Criteria All acute phase paralytic poliom yelitis for strict bed rest and observation for respiratory sym ptom s: 

Isolate from nonvaccinated personnel.

Discharge Criteria No evidence of nervous system involvem ent and no danger of contact with nonvaccinated population: 

Deterioration of m uscle strength usually ends after 3â€“5 days.

References 1. Alexander L, Birkhead G, et al. Ensuring preparedness for potential poliom yelitis outbreaks: recom m endations for the US poliovirus vaccine stockpile from the National Vaccine Advisory Com m ittee (NVAC) and the Advisory Com m ittee on Im m unization Practices (ACIP). Arch Pediatr Adolesc Med. 2004:158:1106â€“1112. 2. Am erican Academ y of Pediatrics. Poliom yelitis prevention: revised recom m endations for use of inactivated and live oral poliovirus vaccines. Pediatrics. 1999;103:171â€“172. 3. Centers for Disease Control. Poliom yelitis in the United States: updated recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Morb Mortal Wkly Rep. 2000;49:RR-5. 4. Kirkpatrick BD, Alston WK. Current im m unizations for travel. Curr Opinion Infect Dis. 2003;16(5):369â€“374.

Pa ge 3 7 8

5. Minor PD. Eradication of polio by vaccination. Virology. 2000;268:231â€“232. 6. Mulder DW. Clinical observations on acute poliom yelitis. Ann NY Acad Sci. 1995;753:110. 7. Trojan DA, Cashm an NR. Post-poliom yelitis syndrom e. Muscle Nerve. 2005;31(1):6â€“19.

Codes ICD9-CM 045.1

Pa ge 3 7 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po lycythem ia

Polycythemia

David N. Zull

Basics Description 

Increase in circulating red blood cells above the norm al range: o

Men: hem oglobin (Hgb) >17 g/dL, hem atocrit (Hct) >50%

o 

Wom en: Hgb >15g/dL, Hct >45%

Sym ptom s are related to blood viscosity, which increases exponentially at Hct >55%.

Genetics 

Most cases are acquired disorders.



Rare genetic disorders with polycythem ia include: o

Prim ary fam ilial congenital polycythem ia (PFCP)

o

High affinity hem oglobin variants

o

Bisphosphoglycerate deficiency

o

von Hippel-Lindau syndrom e

o

Chuvash polycythem ia

o

Congenital m ethem oglobinem ia.

Etiology 

Relative polycythem ia:

Pa ge 3 7 8

o

Resulting from decrease in plasm a volum e/dehydration

o

Gaisbock syndrom e: obese, hypertensive, m iddle-aged sm okers with chronic elevations in Hct



Prim ary polycythem ia vera: o

Stem cell disorder characterized by panhyperplasia of all bone m arrow elem ents leading to increased production of RBCs, WBCs, and platelets. Erythrocytosis is the m ost prom inent feature. 

Proliferative stage: increase in RBCs, m egakaryocytes, platelets



Stable phase: return of blood counts to norm al values owing to replacem ent of m arrow by fibrosis



Spent phase: extensive m arrow fibrosisâ€” peripheral cytopenia



Secondary polycythem ia: o

Appropriately increased erythropoietin caused by tissue hypoxia:

o



Chronic pulm onary disease



Sleep apnea



Congenital heart disease (cyanotic)



High altitude



Sm oking



Carbon m onoxide (CO) poisoning (chronic)

Inappropriate autonom ous erythropoietin production: 

Tum ors: renal cell carcinom a (CA), hepatic CA, Wilm s tum or, vascular cerebellar tum ors, ovarian tum ors



Benign renal disease: renal cysts, polycystic kidney disease, renal artery stenosis or infarction, focal glom erulonephritis (GN),

Pa ge 3 7 8

hydronephrosis, postâ€“renal transplant o

o

o

Blood doping: 

Recom binant erythropoietin abuse



Autologous transfusions

Drug abuse: 

Chronic cocaine abuse



Androgenic steroids

Miscellaneous: 

Viral hepatitis



Cushing syndrom e



Prim ary aldosteronism



Uterine leiom yom ata

Diagnosis Signs and Symptoms History 

General: o

Dyspnea

o

Weakness

o

Sweating

o

Weight loss

o

Epistaxis

o

Pruritusâ€”generalized, attacks associated with water contact or cooling

o 

Gout

Neurologic: o

Headache

o

Vertigo/dizziness/tinnitus

o

Fluctuating dem entia

Pa ge 3 7 8

o

Paresthesias

o

Scotom a, blurred vision

o

Chorea

o

Cerebrovascular accident/transient ischem ic attack (CVA/TIA)





Cardiovascular: o

Congestive heart failure

o

Angina/m yocardial infarction

o

Deep vein throm bosis (DVT)

o

Hypertension

Extrem ities: o

Erythrom elalgia: 

Secondary to capillary sludging



Burning pain in the feet or hands associated with warm th and erythem a of the affected areas





Worse at night



Relief with cooling



Pulses intact

o

Digital artery occlusion

o

Painful ulcers of fingers and toes (digital ischem ia)

GI: o

Hepatom egaly/splenom egaly

o

Epigastric discom fort/early satiety

o

Peptic ulcer disease/GI bleed

o

Budd-Chiari syndrom e (hepatic vein throm bosis)â€”ascites and peripheral edem a

Physical Exam 

Hypertension



Ruddy com plexion/plethora



Splenom egaly (75% in polycythem ia vera [PV])



Hepatom egaly (30% in PV)



Erythem a/rubor of hands and feet

Pa ge 3 7 8

Essential Workup CBC with platelets

Tests Lab 

First priority is distinguishing relative from true erythrocytosis: o

Volum e repletion IV or PO, then repeat CBC

o

If persistent Hct >52% (m ales) or >47% (fem ales), obtain red blood cell m ass and plasm a volum e by nuclear m edicine.

o

Red blood cell m ass <35 m g/kg (m ales) or <31 m g/kg (fem ales) is norm al.

o

Decreased plasm a volum e with norm al RBC m ass verifies relative erythrocytosis.



Second priority is distinguishing polycythem ia vera from secondary erythrocytosis: o

Arterial oxygen saturations <92% suggest hypoxia related.

Diagnostic Criteria for Polycythemia Vera 

Category A: o



A1: increased RBC m ass: 

Male: >35 m L/kg



Fem ale: >32 m L/kg

o

A2: oxygen saturation >92%

o

A3: splenom egaly

Category B: o

B1: platelets >400,000/m m 3

o

B2: WBC >12,000/m m 3

o

B3: B 1 2 >900 pg/m L; unbound vitam in B 1 2 binding capacity >2,200 pg/m L

Pa ge 3 7 8



Diagnosis established by either of these com binations: o

Presence of all three category A criteria

o

A1 + A2 + any two category B criteria

Imaging Abdom inal CT scanning can detect a nonpalpable spleen.

Diagnostic Procedures/Surgery Bone m arrow aspirate and biopsy can be a helpful adjunct to diagnose polycythem ia vera.

Differential Diagnosis See Etiology P.887

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs) with em phasis on fluid resuscitation if no evidence of congestive heart failure (CHF)

ED Treatment 

Em ergency m anagem ent of hyperviscosity syndrom e or Hct >60%



Fluid resuscitation to achieve hem odilution: o



Withhold if evidence of CHF

Em ergency phlebotom y of 250â€“500 m L of blood over 1â€“2 hours replacing with an equal am ount of 0.9% norm al saline (NS)



Rem oval of 1,000â€“1,500 m L of blood over 24 hours with a goal of Hct <60 or relief of sym ptom s:

Pa ge 3 7 8



o

Keep Hct >45

o

Replace with an equal am ount of 0.9% NS.

Phlebotom ize the elderly and those with cardiovascular disease m ore slowly: o



Every other day phlebotom y

Em ergent surgery with polycythem ia: o

Phlebotom ize to Hct of 45 to avoid throm botic com plications postoperatively.



Throm bocytosis therapy: o

Adm inister aspirin if platelet count is 500,000â€“1,500,000/m m 3 and there are no hem orrhagic com plications.



Treat pruritus with diphenhydram ine.

Chronic Therapy 

Phlebotom y: m aintain Hct at 45% for m en and 42% for wom en.



Iron supplem entation is contraindicated.



Interferon-alpha: o

Especially helpful for refractory pruritus and painful splenom egaly

o 

Suggested in sym ptom atic patients <60 years

Anagrelide: o

Specific for throm bocytosis

o

No risk of leukem ia, ideal for younger patients with postphlebotom y throm bocytosis

o

Effective alone and can decrease need for or frequency of chem otherapy



Hydroxyurea: o

Mainstay of therapy, especially for patients older than 60 years, with frequent phlebotom y requirem ents, throm botic episodes, or refractory throm bocytosis

Pa ge 3 7 9



Im atinib (Gleevec)â€”possible alternative to hydroxyurea



Busulfan, P 3 2 : o

Severe refractory disease

o

High risk of leukem ic transform ation

Pregnancy Considerations Tem porary rem ission during pregnancy, no treatm ent usually needed

Pediatric Considerations 

Defined by Hct >65% (sam ple m ust be obtained >6 hours postdelivery)



One percent to 5% of neonates; up to 50% of neonates with intrauterine growth retardation



Etiology: o

Maternal-fetal hypoxem ia secondary to m aternal diabetes, hypertension, or sm oking



Placental transfusion: o

If signs of hyperviscosity syndrom e, partial exchange transfusion with saline

Geriatric Considerations Caution with speed of phlebotom y and fluid resuscitation as noted

Medication (Drugs) 

Aspirin: 325 m g initially, then 80 m g/d



Diphenhydram ine: 25â€“50 m g PO q.i.d.

Follow-Up Disposition Admission Criteria

Pa ge 3 7 9



New diagnosis of polycythem ia



Hct >60% without sym ptom s



Sym ptom s of hyperviscosity: o

Unstable vital signs/significant com orbidities

o

Inability to com ply with outpatient treatm ent or follow-up

Discharge Criteria 

Previous diagnosis of polycythem ia, Hct <60, and asym ptom atic



Stable vital signs

Issues for Referral All patients should be referred to a hem atologist.

References 1. Berlin N. Polycythem ia vera. Hem atol Oncol Clin North Am . 2003;17:1191â€“1210. 2. Elliott MA, Tefferi A. Throm bosis and haem orrhage in polycythaem ia vera and essential throm bocythaem ia. Br J Haem atol. 2005;128:275â€“290. 3. Finazzi G, Barbui T. Risk-adapted therapy in essential throm bocythem ia and polycythem ia vera. Blood Rev. 2005;19(5):243â€“252. 4. Hoffm an R, Benz EJ, Shattil SJ, et al., eds. Hem atology: Basic Principles and Practice. 4th ed. Orlando, FL: Elsevier; 2005. 5. Passam onti F. Life expectancy and prognostic factors for survival in patients with polycythem ia vera and essential throm bocythem ia. Am J Med. 2004;117:755â€“761. 6. Stuart BJ. Polycythem ia vera. Am Fam Physician. 2004;69:2139â€“2144.

Codes ICD9-CM

Pa ge 3 7 9

238.4

ICD10 D45

Pa ge 3 7 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po stpartum Hem o rrhage

Postpartum

Hemorrhage Marco Coppola Clyde Turner

Basics Description 

Im m ediate: hem orrhage occurring within 24 hours after delivery



Delayed: hem orrhage occurring m ore than 24 hours after delivery: o

Often 1â€“2 postpartum

Etiology 



Im m ediate: o

Uterine atony

o

Lower genital lacerations

o

Retained placental tissue

o

Placenta accreta

o

Uterine rupture

o

Uterine inversion

o

Puerperal hem atom a

o

Coagulopathies

Delayed:

Pa ge 3 7 9



o

Retained products of conception

o

Postpartum endom etritis

o

Withdrawal of exogenous estrogen

o

Puerperal hem atom a

Coagulopathies: o

Pre-existing idiopathic throm bocytopenic purpura

o

Throm botic throm bocytopenic purpura

o

Von Willebrand disease

o

Dissem inated intravascular coagulation (DIC)

Associated Conditions If bleeding is present at other sites, consider coagulopathy

Diagnosis Signs and Symptoms 

Ongoing blood loss, usually painless



Significant hypovolem ia, resulting in:



o

Tachycardia

o

Tachypnea

o

Narrow pulse pressure

o

Decreased urine output

o

Cool, clam m y skin

o

Poor capillary refill

o

Altered m ental status

Maternal tachycardia and hypotension m ay not occur until blood loss >1,500 m L.

Essential Workup 

Abdom en and pelvic exam ination to assess for uterine atony, retained products, or other anatom ic abnorm ality



Type and cross-m atch for packed RBC

Pa ge 3 7 9



Rapid hem oglobin determ ination

Tests Lab 

CBC, platelets



Prothrom bin tim e, partial throm boplastin tim e



Fibrinogen level



Type and cross-m atch

Imaging Ultrasound m ay be helpful to evaluate for retained products in delayed postpartum hem orrhage.

Differential Diagnosis Consider puerperal hem atom as if perineal, rectal, or lower abdom inal pain in conjunction with tachycardia and hypotension.

Treatment Alert 

Patients with postpartum hem orrhage m ay be hem odynam ically unstable.



IV access and fluid resuscitation is im portant.

Initial Stabilization 

Attem pt to sim ultaneously control bleeding and stabilize hem odynam ic status.





Manage airway and resuscitate as indicated: o

Supplem ental oxygen

o

Cardiac m onitor

IV fluid resuscitation with norm al saline or lactated Ringer solution

Pa ge 3 7 9



Foley catheter

P.889

ED Treatment 

Managem ent of uterine atony: o

Bim anual m assage

o

Oxytocin (Pitocin) adm inistered IV/IM

o

Methylergonovine (Methergine) or ergonovine (Ergotrate) IM if oxytocin fails

o



Avoid if known hypertensive



Onset in m inutes

15-Methyl prostaglandin F 2 Î ± (PGF 2 Î ± ; Hem abate) intram uscularly if above fails: 

o 

Relatively contraindicated in asthm a

Surgery if m edical intervention fails

Inspect closely for genital tract laceration: o

Repair required if â‰¥2 cm

o

Use 00 or 000 absorbable suture; continuous, locked recom m ended.



Managem ent of uterine inversion (acute): o

Reposition uterus using Johnson m aneuver or Harris m ethod.

o

Use left hand on abdom inal wall to stabilize fundus of uterus.

o

Place right hand with fingers spread into vagina and push steadily on inverted part to reduce.

o

If unsuccessful, give terbutaline IV or m agnesium sulfate to produce cervical relaxation, and reposition.

o

Surgery if unsuccessful or if subacute or chronic inversion



Managem ent of coagulopathies:

Pa ge 3 7 9

o

Fresh frozen plasm a, platelets, cryoprecipitate as indicated

o

Careful attention to volum e status

o

Continuous reassessm ent

Medication (Drugs) 

Uterotonicsâ€”stim ulate uterine contraction to control bleeding: o

Ergonovine (Ergotrate): 0.2 m g IM; avoid if known hypertensive

o

Methylergonovine (Methergine): 0.2 m g IM; 0.2 m g PO q6h; avoid if known hypertensive

o

15-Methyl PGF 2 Î ± (Hem abate): 0.25 m g IM; m ay repeat in 15â€“60 m inutes

o

Oxytocin (Pitocin): 20â€“40 IU in 1 L norm al saline at 200 m L per hour; do not use for resuscitation



Cervical relaxation agents facilitate uterine inversion reduction: o

Magnesium sulfate 20%: 2 g IM bolus over 10 m inutes

o

Terbutaline: 0.25 m g IV; avoid if hypotensive

Follow-Up Disposition Admission Criteria 

All patients with im m ediate postpartum hem orrhage require adm ission to a closely m onitored setting.



Early obstetrics consultation recom m ended

Pa ge 3 7 9



Early surgical intervention dependent on cause



Intensive care unit setting if DIC or evidence of hem odynam ic com prom ise



Patients with endom etritis should be adm itted for parenteral antibiotics.

Discharge Criteria 

Delayed postpartum hem orrhage that is easily controlled without excessive bleeding



Outpatient m anagem ent with m ethylergonovine 0.2 m g PO every 6 hours m ay be considered in consultation and close follow-up with obstetrician

References 1. Druelinger L. Postpartum em ergencies. Em erg Med Clin North Am . 1994;12:219â€“237. 2. Gilstrap LC, Ram in SM. Postpartum hem orrhage. Clin Obstet Gynecol. 1994;37:824â€“830. 3. Mallon W, Henderson S. Labor and delivery. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 2479â€“2481. 4. Roberts WE. Em ergent obstetric m anagem ent of postpartum hem orrhage. Obstet Gynecol Clin North Am . 1995;22:283â€“302.

Codes ICD9-CM 666.10 Other im m ediate postpartum hem orrhage, unspecified as to episode of care or not applicable

ICD10 O46.8 Other antepartum hem orrhage

Pa ge 3 7 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po stpartum Infectio n

Postpartum

Infection Timothy Stallard Marco Coppola

Basics Description 





Early postpartum endom etritis (PPE): o

Develops within 48 hours

o

Most often com plicating cesarean section

Late PPE: o

Develops after three days to six weeks

o

Usually following vaginal delivery

Septic pelvic throm bophlebitis is a diagnosis of exclusion with two distinct clinical presentations, either of which m ay present with postpartum pulm onary em bolus: o

Acute throm bosis: m ost com m on right ovarian vein, usually occurring in first 48 hours as acute, progressive lower abdom inal pain

o

Enigm atic fever: â€œpicket fenceâ€• spiking fevers and tachycardia

Etiology 

Polym icrobial infection result of ascending spread from

Pa ge 3 8 0

lower genital tract 

Anaerobic (up to 80%) and aerobic (~70%): o

o

o

o

Gram -positive aerobes: 

Group A, B streptococcus



Enterococci



Gardnerella vaginalis

Gram -negative aerobes: 

Escherichia coli



Enterobacter

Anaerobes: 

Bacteroides



Peptostreptococcus

Other genital m ycoplasm as com m on in late PPE: 

Ureaplasm a urealyticum



Mycoplasm a hom inis



Chlam ydia trachom atis

Diagnosis Signs and Symptoms 

Persistent fever and chills



Localized pain and swelling



Lower abdom inal pain



Foul-sm elling lochia



Cervical m otion tenderness, uterine tenderness



Absence of other sources of infection: o

Genital tract infection should be assum ed until ruled out

Essential Workup 

Abdom inal and pelvic exam ination

Pa ge 3 8 0



Cervical cultures for chlam ydia



Transcervical endom etrial cultures

Tests Lab 

CBC



Urinalysis and culture



Blood cultures

Imaging 

CT or MRI for ovarian vein throm bosis



Ultrasound is sensitive for abscess

Differential Diagnosis Fever from other sources: 



<6 hours: o

Early streptococcal infection

o

Transfusion reaction

o

Thyroid crisis

<48 hours: o









Atelectasis

<72 hours: o

Urinary tract infection

o

Pneum onia

3â€“5 days: o

Mastitis

o

Breast engorgem ent

o

Necrotizing fasciitis

3â€“7 days: o

Mastitis

o

Septic throm bophlebitis

7â€“14 days: o

Abscess

Pa ge 3 8 0



>2 weeks: o

Mastitis

o

Pulm onary em bolism

Treatment Initial Stabilization 

Manage airway and resuscitate as indicated: o

Prom pt evaluation of respiratory and hem odynam ic status

o

Supplem ental oxygen, cardiac m onitor, and pulse oxim etry, as needed

o

Venous access; support circulatory status with crystalloid and pressors, if needed

P.891

ED Treatment 

IV antibiotics and close observation: o

Several choices are appropriate for initial therapy: 

Cefoxitin



Ticarcillin/clavulanate (Tim entin)



Im ipenem cilastatin (Prim axin)



Meropenem



Am picillin/sulbactam (Unasyn)



Piperacillin/tazobactam plus doxycycline



Clindam ycin plus gentam icin or antipseudom onal third-generation cephalosporin



Heparin if suspicion or evidence of throm bophlebitis



Infected wound or abscess should be opened to establish

Pa ge 3 8 0

drainage. 

Necrotizing fasciitis requires wide surgical dÃ©bridem ent, parenteral antibiotics, and adjunctive hyperbaric oxygen therapy.



Peritonitis requires im aging to evaluate cause: AAS, CT

Medication (Drugs) 

Am picillin/sulbactam : 3 g IV q6h



Cefoxitin: 2 g IV q6h



Clindam ycin: 900-m g load, then 600 m g IV q6hâ€“q8h



Gentam icin: 2-m g/kg load, then 1â€“1.5 m g/kg IV q8h



Heparin: 80-IU/kg loading dose, then 18 IU/kg/h IV



Im ipenem cilastatin: 500 m g IV q6h



Meropenem : 1.0 g IV q8h



Mezlocillin: 4 g IV q6h



Piperacillin/tazobactam : 4.5 g IV q8h



Ticarcillin/clavulanate: 3.1 g IV q4h

Follow-Up Disposition Admission Criteria Patients with endom etritis or suspicion for septic pelvic throm bophlebitis should be adm itted.

Discharge Criteria Nontoxic, m ildly sym ptom atic patient with late PPE m ay be considered for outpatient m anagem ent in consultation and close follow-up with obstetrics.

Pa ge 3 8 0

References 1. Calhoun BC, Brost B. Em ergency m anagem ent of sudden puerperal fever. Obstet Gynecol Clin North Am . 1995;22(2):357â€“367. 2. Druelinger L. Postpartum em ergencies. Em erg Med Clin North Am . 1994;12(1):219â€“237. 3. Faro S. Postpartum endom etritis. Clin Perinatol. 2005;32(3):803â€“814. 4. French LM. Antibiotic regim ens for endom etritis after delivery. Cochrane Database Syst Rev. 2004(4);CD001067.

Codes ICD9-CM 615.9

ICD10 O23.5

Pa ge 3 8 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pre-Eclam psia/Eclam psia

Pre-Eclampsia/Eclampsia Elaine Sapiro

Basics Description 

Spectrum of disease



Severity ranges from pregnancy-induced hypertension (PIH) to hypertension with proteinuria (pre-eclam psia) to pre-eclam psia with seizures (eclam psia).



Usually occurs late third trim ester: o

May also present up to 30 days post-partum

Etiology 





Diffuse arteriolar vasospasm : o

Secondary endothelial activation

o

Microthrom bi form ation

o

Tissue ischem ia

Heightened vascular perm eability: o

Edem a

o

Vascular congestion

Risk factors: o

Extrem es of reproductive age (<20 or >35 years)

o

Prim agravida

o

Multiple gestations

Pa ge 3 8 0

o

Molar pregnancy, hydrops fetalis

o

Sm oking, hypercholesterem ia

o

Diabetes, collagen vascular diseases

o

Pre-existing hypertension or renal disease

Diagnosis Signs and Symptoms 

PIH: o

Blood pressure (BP) >140/90; SBP >130 or DBP >80 on two occasions

o

Rapid weight gain often precedes hypertension (>2 lb/wk)



Pre-eclam psiaâ€”PIH plus: o

Proteinuria: 

May see wide fluctuation



Single urine sam ple m ay be negative even in severe cases

o 

Dependent edem a progressing to constant edem a

Severe pre-eclam psia: o

Epigastric or right upper quadrant pain m im icking cholelithiasis due to hepatocellular necrosis with edem a and stretch of capsule

o

Abdom inal pain with nausea and vom iting

o

Throm bocytopenia

o

Hyper-reflexia

o

Severe and worsening headache with possible visual disturbances including blindness

o 

Oliguria, proteinuria > 3+ dipstick, BP>160/110

Eclam psiaâ€”PIH or pre-eclam psia plus: o

Seizures, tonic-clonic

Pa ge 3 8 0

o

Pre-, peri- or postpartum up to 30 days after delivery

o

Unrelenting, severe headache with or without visual changes often precede seizures.

o

Up to 2% of wom en with pre-eclam psia progress to eclam psia.

Essential Workup 

History: o

o



Early pre-eclam psia: 

Weight gain



Leg swelling

Advanced pre-eclam psia: 

Abdom inal pain



Shortness of breath



Headache



Visual changes

Physical exam ination: o

Pay attention to blood pressure with m ultiple m easurem ents, as needed.

o

Carefully palpate abdom en, especially the right upper quadrant.

o

Perform a careful neurological exam , noting deep tendon reflexes, m ental status, and visual acuity.

Tests Lab 

Urinalysis: o

Protein >1 requires 24-hour protein.

o

Urine sedim ent for RBC, WBC, casts



CBC, liver function tests (HELLP syndrom e)



Blood urea nitrogen/creatinine, uric acid



Urine toxicology: o

Sym pathom im etics m ay cause hypertension,

Pa ge 3 8 0

seizures. 

Cerebrospinal fluid: o

Infection, hem orrhage causing seizures

Imaging 

Head CT after airway stabilization: Evaluate for intracranial m asses, hem orrhage.



Em ergency ultrasound for estim ated gestational age, fetal viability



Fetal m onitoring, stress test

Differential Diagnosis 

Pre-eclam psia: o

PIH, chronic hypertension

o

Pregnancy-aggravated hypertension: 

Chronic hypertension with superim posed PIH or pre-eclam psia



o

Flare in underlying renal or collagen vascular disease

o

Hydatiform m ole

o

Hydrops fetalis

o

Drug abuse

Eclam psia: o

Epilepsy

o

Encephalitis

o

Meningitis

o

Encephalopathy

o

Brain tum or

o

Intracranial hem orrhage

P.893

Pa ge 3 8 0

Treatment Initial Stabilization 

Airway, breathing, and circulation



100% oxygen, m aternal cardiopulm onary m onitoring



Place patient in left lateral decubitus position (reduces pressure on inferior vena cava, enhancing cardiac return/output).



Treat seizures, m agnesium sulfate (MgSO 4 ) )â€” first line.

ED Treatment 

Tocographic and fetal m onitoring



Seizure prophylaxis for severe pre-eclam psia: MgSO 4



Treat hypertension with hydralazine, labetalol.



Avoid diuretics in pre- and peripartum patients: o

Can induce placental hypoperfusion and fetal hypoxia as patient is typically intravascularly volum e depleted



Obstetrical consultation: o

All cases along PIH-pre-eclam psia-eclam psia spectrum

o

Expectant m anagem ent: <30 weeks gestation, delivery >30 weeks

o

Em ergent delivery for severe sym ptom s: induction (consider in pre-eclam psia) vs. caesarean section (eclam psia)

Medication (Drugs) 

Anti-seizure: o

Magnesium sulfate: 2â€“4 g IV; followed by 2 g/hr IV drip or 10 g IM:

Pa ge 3 8 1



MgSO 4 drip should not exceed 1 g/m in.



Serum Mg goal: 4â€“7 m Eq/L



Mg toxicity: hypotension, loss of patellar reflex, respiratory depression



Calcium gluconate: 1 g IV to reverse hyperm agnesem ia

o

Valium : 5â€“10 m g IV if no response to MgSO 4

o

Phenytoin: 15â€“18 m g/kg IV, not to exceed 25â€“50 m g/m in, for persistent seizure activity



Anti-hypertension: o

Hydralazine: 5â€“20 m g IV

o

Labetalol: 10 m g IV initially, then 5â€“10 m g increm ents for desired effect

Surgery Em ergency caesarean section for severely pre-eclam ptic and all eclam ptic patients

Follow-Up Disposition Admission Criteria 

Pre-eclam psia



Eclam psia



HELLP syndrom e



Intensive care unit, Labor and Delivery, operating room

Discharge Criteria 

Asym ptom atic patients with negative work-up for pre-eclam psia (i.e., isolated hypertension)



Close obstetric follow-up assured

Pa ge 3 8 1

References 1. Cunningham FG, MacDonald PC, Grant NF, eds. William sâ€™ obstetrics. 20th ed. Norwalk, CT: Appleton & Lange,1997. 2. Evans SD. Pre-eclam psia/Eclam psia. In: Rosen P, Barkin RM, Hayden SR, et al. eds. Rosen's 5-m inute em ergency m edicine consult. 1st ed. Philadelphia, PA: Lippincott, William s & Wilkins,1999. 3. Houry D, Abbott JT. Acute com plications of pregnancy. In: Marx JA, ed. Rosen's em ergency m edicine. 5th ed. St. Louis, MO: CV Mosby, 2002: 2413â€“2433 4. Wagner LK. Diagnosis and m anagem ent of pre-eclam psia. Am Fam Physician. 2004;1570(12):2317â€“2324. 5. Walker JJ. Severe pre-eclam psia and eclam psia. Baillieres Clin Obstet Gynaecol. 2000;14(1):57â€“71.

Codes ICD9-CM 642.40 Mild or unspecified pre-eclam psia 642.50 Severe pre-eclam psia 642.60 Eclam psia 780.30 Convulsions

ICD10 O14.9 O15.0

Pa ge 3 8 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pre-excitatio n Syndro m es

Pre-excitation

Syndromes Richard Wolfe Eric Glasser

Basics Description 

A group of conditions characterized by antegrade ventricular activation or retrograde atrial activation via an accessory pathway distinct from the norm al cardiac conduction system : o

Connects the atria and the ventricles by bypassing the atrioventricular (AV) node

o

Conduction is faster and the refractory period is shorter.

o 

Sum of vectors allows for shorter pulse rate intervals

Accessory pathways are sm all bands of tissue that failed to separate during developm ent: o

Kent bundle connects atrium to ventricle bypassing the AV node 

Results in delta waves and the Wolff-Parkinson-White (WPW) syndrom e

o

Jam es fiber connects atrium to his bundle or lower AV

Pa ge 3 8 1

node o

Mahain fibers: 

Allows a range of connections



Atrium to distal right bundle



Atrium to the right ventricle near the AV annulus





AV node to the ventricle



His bundle to ventricle

Allows for early depolarization of the ventricles generating rapid supraventricular tachycardias



WPW syndrom e: o

Syndrom e caused by ventricular pre-excitation via an accessory AV pathway, the bundle of Kent

o

Conduction m ay be anterograde, retrograde, or both

o

Type A, or orthodrom ic, is the m ost com m on (70%). 

Im pulse travels down the AV node and then up the retrograde pathway.



A circuit is created that potentiates reentrant tachycardia.

o



Type B or antidrom ic: 

Less com m on than Type A



The circuit operates in the opposite direction

Lown-Ganong-Levine syndrom e: o

Rare pre-excitation syndrom e with an accessory pathway in the AV node, usually Jam es fiber





Com plications: o

Atrial flutter (5%)

o

Atrial fibrillation (10â€“20%)

o

Paroxysm al SVT (40â€“80%)

The m ajority of patients with accessory pathways never becom e sym ptom atic.



Risk of death is very low (0.1â€“4%).

Pa ge 3 8 1



Pre-excitation with wide com plex tachycardia is m ost at risk for ventricular dysrhythm ias.



Prevalence is estim ated at 0.1â€“0.3% of the population.



Males are affected twice as often as fem ales.



Most are young and healthy.

Pediatric Considerations 

Most supraventricular tachycardias in children are the result of AV nodal reentry.



10% are the result of an identified pre-excitation syndrom e.

Genetics 

Recent m olecular genetic investigations indicate that pre-excitation disorders m ay have a substantial genetic com ponent.



Pre-excitation disorders are som etim es inherited as single gene disorders.

Etiology 

Idiopathic



In association with structural heart disease: o

Cardiom yopathy

o

Transposition of the great vessels

o

Mitral valve prolapse

o

Ebstein anom aly

Diagnosis Signs and Symptoms History 

Asym ptom atic

Pa ge 3 8 1



Palpitations: o

Fast or irregular



Chest Pain



Dyspnea



Dizziness



Nausea



Diaphoresis

Physical Exam 



Tachycardia up to 250 bpm : o

Rapid and regular

o

Supraventricular tachycardia

o

Irregular (atrial fibrillation)

Signs of instability: o

Chest pain

o

Hypotension

o

Change in m ental status

o

Rales

o

Cyanosis

Essential Workup 

The diagnosis is m ade on the 12-lead ECG



Pre-existing history



Stable patients m ust be carefully m onitored and reassessed for signs of instability.

Tests Lab 

Cardiac enzym es only if signs of ischem ia



Consider electrolytes

Imaging ECG: 

Com plications of the pre-excitation syndrom e:

Pa ge 3 8 1



o

Atrial fibrillation

o

Atrial flutter

o

SVT

WPW syndrom e o

Short pulse rate (PR) <0.12 seconds

o

Prolonged quasi-random signal (QRS) >0.10 seconds

o

Delta wave: Sm all slurred upstroke at the beginning of the QRS





Lown-Ganong-Levine syndrom e: o

PR interval less than 0.12 seconds

o

Norm al QRS upstroke and duration

o

Absence of a delta wave

Mahaim tachydysrhythm ia: o

QRS axis between 0 and â€“75Â°

o

QRS duration of 0.15 seconds or less

o

R-wave in lead 1

o

rS com plex in lead V1

o

Precordial transition in lead V4 or later

o

Cycle length between 220 and 450 m secs

Diagnostic Procedures/Surgery Radiofrequency catheter ablation: 

Definitive diagnosis and therapeutic procedure for accessory pathways that is not perform ed on an em ergent basis

P.895

Differential Diagnosis 

AV nodal re-entry SVT



Ventricular tachycardia

Pa ge 3 8 1

Treatment Pre Hospital 

Supplem ental oxygen



Monitor



Synchronized cardioversion: o

Signs of instability

o

Atrial fibrillation with WPW- wide com plex tachycardia



Pre hospital use of adenosine: o

Stable patients do not require em ergent conversion.

o

Unstable patients should undergo cardioversion not adenosine.

Initial Stabilization 



Unstable patients: o

Synchronized cardioversion starting with 50 J-m in

o

Increase increm entally until sinus rhythm is restored

Stable patients with wide com plex tachycardia: o

Procainam ide

ED Treatment 

Vagal m aneuvers such as a Valsalva: o

Right carotid artery m assage for no m ore than 10 seconds

o

Auscultate the artery first for a bruit that would contraindicate this procedure



Fluid replacem ent and Trendelenburg if the patient has m ild hypotension



Pharm acologic conversion if carotid m assage fails: o

Adenosine

o

Verapam il

Pa ge 3 8 1



Irregular wide com plex tachycardia: o

Procainam ide or m agnesium is effective

o

Never use calcium -channel blockers, beta-blockers, or digoxin 

These m edications block the AV node.



Conduction occurs exclusively down the faster accessory pathway.



Precipitation of ventricular dysrhythm ias

Pediatric Considerations 

Children m ay develop ventricular rates up to 320 bpm that are poorly tolerated.



Cardiovert unstable children with 0.5â€“2 J/kg.



Vagal m aneuvers and adenosine are safe in stable children.

Medication (Drugs) 

Adenosine: 6 m g rapid IV bolus over 1â€“2 seconds; if ineffective, repeat with 12 m g (peds: 0.1 m g/kg rapid IV push, repeat with 0.2 m g/kg)



Magnesium : 2 g IV bolus



Procainam ide: 6â€“13 m g/kg IV at 0.2â€“0.5 m g/kg/m in until either arrhythm ia controlled, QRS widens 50%, or hypotension, then 2â€“6 m g/m in, m ax. dose of 1,000 m g



Only to be used in stable narrow com plex tachycardia o

Diltiazem : 0.25 m g/kg IV over 2 m in followed in 15 m in by 0.35 m g/kg IV over 2 m in

o

Esm olol: 0.5 m g/kg over 1 m in; m aintenance infusion at 0.05 m g/kg/m in over 4 m in, then 0.1â€“0.2 m g/kg/m in continuously

o

Verapam il: 2.5â€“5 m g IV bolus over 2 m in; m ay

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repeat with 5â€“10 m g q5â€“30m in to m ax. 20 m g

Follow-Up Disposition Admission Criteria 

Patients with signs of instability require adm ission to a m onitored bed.



Failure of outpatient therapy for continuous pharm acologic control or ablation

Discharge Criteria 

The m ajority of patients will be stable and can be discharged once converted to sinus rhythm



Consider low-dose verapam il prophylaxis

Issues for Referral 

Follow-up should be arranged with a cardiologist.



Electrophysiologic studies with possible ablative therapy during the outpatient workup

References 1. Rosner MH, Brady WJ Jr, Kefer MP, Martin ML, Electrocardiography in the patient with the Wolff-Parkinson-White syndrom e: diagnostic and initial theraputic issues. Am J Em erg Med. Nov 1999;17:705â€“714. 2. Stahm er SA, Cowan R, Tachydysrhythm ias. Em erg Med Clin North Am 2006;24(1):11â€“40 3. Wellens HJ, Brugada P, Penn OC, The Managem ent of Preexcitation Syndrom es. JAMA, 1987 May;257(17):2325â€“2333. 4. Xie B, Thakur RK, Shah CP, Hoon VK, Clinical differentiation of narrow QRS com plex tachycardia, Em erg Med Clin North Am . 1998

Pa ge 3 8 2

May;16(2):295â€“330. 5. Redfearn DP, Krahn AD, Skanes AC, Yee R, Klein GJ Use of m edications in Wolff-Parkinson-White syndrom e. Expert Opin Pharm acother. 2005;6(6):955â€“963.

Codes ICD9-CM 426.7

ICD10 I45.6

Pa ge 3 8 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pregnancy, Traum a in

Pregnancy,

Trauma in A. Antoine Kazzi Ziad N. Kazzi

Basics Description 

Fetal and m aternal injury specific to pregnancy is evident after the first trim ester: o

Increased rate of fetal loss, but not m aternal m ortality



Likelihood of fetal injury increases with the severity of m aternal insult.



Physiologic hypervolem ia of pregnancy m ay lead to an underestim ation of blood loss: o

Clinical shock m ay be apparent only after a 30% m aternal blood loss.



Abdom inal findings are less evident in the gravid patient.



Minor traum a can also lead to fetal injuries (at least 50% of fetal losses).



Less frequent bowel injury



More frequent retroperitoneal hem orrhage due to the engorgem ent of pelvic organs and veins

Pa ge 3 8 2



Increased m orbidity and m ortality with pelvic fractures due to pelvic and uterine engorgem ent





Fetal or uterine traum a includes o

Placental abruption

o

Fetal m aternal hem orrhage

o

Prem ature labor

o

Uterine contusion or rupture (prior C section)

o

Fetal dem ise

o

Prem ature m em brane rupture

o

Hypoxem ic or anatom ic fetal injury (skull fracture)

Abruption occurs in up to 50% of severe traum a and 1â€“5% of m inor injuries: o

Accounts for up to 50% of fetal loss

o

May occur with no external bleeding (20%)

o

Occurs after 16 weeks of gestation

o

Early sym ptom s of vaginal bleeding, uterine contractions, or abdom inal/uterine tenderness had a sensitivity of 52% and specificity 48% for a preterm delivery or adverse outcom e.

o 

Hallm ark is uterine contractions

Fetal/m aternal hem orrhage (FMH) occurs in m ore than 30% of severe traum a: o

Isoim m unization of Rh-negative m others (with as little as 0.03 cc of FMH)



Penetrating traum a results in direct injury to fetus, m aternal shock, and prem ature delivery

Etiology 

Traum a occurs in about 7% of all pregnancies



Most com m on cause of nonobstetric m orbidity and m ortality in pregnancy



Rate of fetal loss varies between 3.4 and 38%



Motor vehicle accidents (48â€“84%)

Pa ge 3 8 2



Falls



Dom estic violence



Direct abdom inal traum a



Penetrating (stab or gunshot)



Electrical or burn

Diagnosis Signs and Symptoms 

Abdom inal pain



Uterine contraction



Vaginal bleeding, leakage of fluid



Contusion, lap belt m arks

Essential Workup 

Identify m aternal condition first o



Airway m anagem ent and resuscitate as indicated

Determ ine the gestational age (EGA) to assess viability o

Estim ate LMP

o

Fundal height (FH); EGA = FH (cm ) Ã— 8/7 after week 16



o

Doppler fetal heart tones

o

Sonography (m ay m iss sm all abruptions)

Fetal/m aternal m onitoring for >4â€“6 hours o

Only m onitor viable fetuses (typically with an EGA > 24 weeks)

o

Abruption does not occur if no contractions during first 4 hours of m onitoring

o

More than 8 contractions per hour over 4 hours is associated with an adverse outcom e

o

If m ore than 1 contraction every 10 m in, there is a

Pa ge 3 8 2

20% incidence of abruption o

The occurrence of bradycardia, poor beat-to-beat variability, or type II â€œlateâ€• deceleration indicates fetal distress.

o

An abnorm al tracing has a sensitivity and specificity of 62, and 49% of predicting adverse fetal outcom es.

o

A norm al tracing com bined with a norm al physical exam has a negative predictive value of nearly 100%.

Tests Lab 

CBC, urinalysis



Blood gas and electrolyte panel



Type, Rh, and screening of blood



The Kleihauer-Betke (KB) stain: o

Identifies FMH in vaginal fluid or blood

o

Indicated when quantification of FMH is im portant

Imaging 

Shield the uterus if possible, but obtain necessary m aternal radiographs.



Less than 1% of traum a victim s are exposed to m ore than 3 radiation-absorbed doses (rad).



No adverse effects are expected with exposure to radiation up to 10 rads



In a large retrospective study, there was no increase in the relative risk of adverse effects in neonates exposed to radiation in utero.



The rad exposure is estim ated at the following: o

C-spine and chest x-rays: <0.005 rad

o

Fem ur: <0.012 rad

o

AP pelvis, spine, KUB: 0.14â€“0.5 rad each

Pa ge 3 8 2

o

IV push: 0.2â€“0.8 rad

o

CT head: <0.05 rad; thorax: <1 rad; upper abdom en: <3 rad; lower abdom en/pelvis: 3â€“9 rad





Ultrasonography: o

Evaluate for solid organ injury or hem operitoneum

o

Fetal heart activity

o

Gestational age

o

Am ount of am niotic fluid (am niotic fluid index)

o

It m isses 50â€“80% of placental abruptions.

Test vaginal fluid with Nitrazine paper (turns blue) and for ferning.



With stable penetrating traum a, triple-contrast CT is advocated, particularly with stab wounds

P.897

Treatment Pre Hospital Cautions: 

Patients in late second and third trim ester should be transported to a traum a center.



Advise traum a center early of pregnancy and estim ated gestational age (EGA) to facilitate m obilization of appropriate resources.



Place patient (while on backboard) in the left lateral recum bent position to avoid supine hypotension (after 24 weeks EGA).



Mast suit inflation over the abdom en is contraindicated

Pa ge 3 8 2

Initial Stabilization 

Direct therapy at the m other with no delays due to pregnancy: o

Manage airway and resuscitate as indicated.



Cardiac, pulse-oxim etry, and cardiotocographic m onitoring



Tilt patient or board 15â€“30Â° to the left (or m anually displace uterus to left).

ED Treatment 

Lactated ringers preferred for IV fluids: o

Large volum es of NS m ay induce a hyperchlorem ic acidosis.



Replace estim ated blood loss in a 3:1 ratio.



Resort to transfusions after 1 L of estim ated blood loss or if hypovolem ia persists after 2 L of crystalloid.



Nasogastric tube decom pression (higher risk of aspiration in pregnancy)



Foley catheterization to assess urinary output



If diagnostic peritoneal lavage is necessary, use supraum bilical open technique.



Use tocolytic therapy only for hem odynam ically stable patients: o

Contraindicated if cervix dilated >4 cm or if FMH and abruption have not been reasonably ruled out.

o

Use tocolytics only when over 8 contractions/hour have lasted >4 hours.



A perim ortem cesarean delivery m ay be attem pted within 4â€“5 m inutes of cardiopulm onary arrest, See Cesarean Section, Em ergency.



In m inor traum a after the 20th week, fetal and m aternal m onitoring is best done in the labor and delivery area.

Pa ge 3 8 2

Medication (Drugs) 



RhoGAM in all Rh-negative wom en (within 72 hours): o

50 Âµg IM in wom en <12 weeks pregnant

o

300 Âµg IM in wom en >12 weeks pregnant

24-hour recheck for ongoing FMH: o

Repeat Rh im m une globulin if needed (if FMH > 30 m L)



Tocolytics: m agnesium sulfate 4 g IV



Avoid aspirin, hypnotics, nonsteroidals, vasopressors



Contraindicated: chloram phenicol, Dilantin, gentam icin, sulfonam ides, tetracyclines

Follow-Up Disposition Admission Criteria 

Vaginal bleeding or am niotic fluid leakage



Fetom aternal hem orrhage



Abdom inal pain



Uterine contractions



Evidence of fetal distress



Abruption placenta



Hem operitoneum or visceral or solid organ injury



Fetal survival begins at the 24th week (9.9%): o

Survival becom es significant after the 26th week (54.7%)

Discharge Criteria 

All the following criteria m ust be m et



No uterine contractions for m ore than four hours of

Pa ge 3 8 2

tocodynam om etry 

No evidence of fetal distress



No vaginal bleeding or am niotic fluid leakage



No abdom inal pain or tenderness



Tim ely obstetric follow-up



Specific instructions to return if any of the above sym ptom s occur



Discharge only in consultation with obstetrics

References 1. ACOG Educational Bulletin. Obstetric aspects of traum a m anagem ent. Int J Gynecol Obstet. 1999;64:87â€“94. 2. Connolly AM, Katz VL, Bash KL, McMahon MJ, Hansen WF. Traum a and pregnancy. Am J Perinatol. 1997;14:331â€“336. 3. Curet MJ, et al. Predictors of outcom e in traum a during pregnancy: Identification of patients who can be m onitored for less than 6 hours. J Traum a. 2000;49(1):18â€“24. 4. Grossm an N. Blunt traum a in pregnancy. Am Fam Physician. 2004;70:1303â€“1310,1313. 5. Kuhlm an RS, Cruikshank DP. Maternal traum a during pregnancy. Clin Obstet Gynecol. 1994;37(2):274â€“293. 6. Lavery JP, Staten-McCorm ick M. Managem ent of m oderate to severe traum a in pregnancy. Obstet Gynecol Clin North Am . 1995;22(1):69â€“90. 7. Pearlm an MD, Tintinalli JE. Evaluation and treatm ent of the gravida and fetus following traum a in pregnancy. Obstet Gynecol Clin North Am . 1991;18:371. 8. Van Hook JW. Traum a in pregnancy. Clin Obstet Gynecol. 2002;45(2):414â€“424.

Miscellaneous

Pa ge 3 8 2

SEE ALSO: Cesarean Section, Em ergency

Codes ICD9-CM 760.5

ICD10 P00.5

Pa ge 3 8 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pregnancy, Unco m plicated

Pregnancy,

Uncomplicated James Walker

Basics 

Pregnancy is not a disease process but rather a physiologic state.



All wom en of reproductive age with abdom inal pain are considered pregnant until proven otherwise.

Description 

The changes in pregnancy occur from the production of large am ounts of placental horm ones: o



Placental progesterone and estrogen

Feedback m echanism s between m aternal and fetal endocrine system s

Pediatric Considerations 

Range for m enarche in the United States is 11â€“15 years old



Pregnant adolescents who present to the ED m ay be either unaware of the pregnancy or reluctant to adm it it: o

Assum e pregnancy in adolescents, regardless of the chief com plaint.

Pa ge 3 8 3

Etiology 

Preceding signs and sym ptom s can be explained by elevations in various horm one levels or changes in anatom y that are a function of the progression of the pregnancy.



Placental hum an chorionic gonadotropin (HCG): o

Prevents the norm al involution of the corpus luteum at the end of the m enstrual cycle.

o

Causes the corpus luteum to secrete even larger quantities of estrogen and progesterone.

o

Elevated HCG levels are responsible for nausea and vom iting.



Placental progesterone: o

Causes decidual cells in the endom etrium to develop and provide nutrition for the early em bryo

o

Decreases contractility of the gravid uterus and risk of spontaneous abortion

o 

Helps estrogen prepare the breasts for lactation

Placental estrogen: o

Responsible for enlargem ent of uterus, breasts, and m am m ary ducts

o

Enlargem ent of fem ale external genitalia, relaxation of pelvic ligam ents, sym physis pubis, and sacroiliac joints

Diagnosis The diagnosis of pregnancy and som e of its potential com plications focus on the utilization of three diagnostic tools: 

History and physical



Horm onal assays

Pa ge 3 8 3



Ultrasonogaphy

Signs and Symptoms 

Am enorrhea accom panied by nausea and vom iting in a sexually active wom an



Am enorrhea: o

The m ost com m on cause of secondary am enorrhea in a wom an of reproductive age is pregnancy.



Nausea and vom iting (m orning sickness)



Breast tenderness (m astodynia)



Urinary frequency



Headache



Low back pain



Pica



Edem a of feet and ankles



Weight gain



Easy fatigability, generalized m alaise



Increase in abdom inal girth



Constipation



Heartburn



Excessive eructation

History Determ ine first day of last m enstrual period (FDLMP) 

40% of wom en cannot accurately rem em ber their FDLMP

Physical Exam Pelvic exam ination: 

Estim ate expected date of delivery by determ ining uterine fundal height.



Detect abnorm al pelvic pain or m asses

Tests Lab

Pa ge 3 8 3





Pregnancy tests o

Î² subunit of HCG

o

Progesterone (P)

Measurem ent of Î²-hCG: o

Most urinary pregnancy tests have a sensitivity of 25 m IU/m L.

o

Hom e pregnancy tests are not that accurate.

o

Positive hom e pregnancy tests should be confirm ed by serum HHCG levels

o



Serum level of HCG: 

Radioim m unoassay



Im m unoradiom etric assay



Fluoroim m unoassay



Enzym e-linked im m unosorbent assay

Serum progesterone (P) level is an indicator of the viability of the pregnancy and m ay be utilized to predict the outcom e of the pregnancy: o

A serum P level of <5 ng/m L is indicative of a nonviable pregnancy (spontaneous abortion or ectopic pregnancy).

o

P level 25 ng/m L denotes a viable pregnancy.

Imaging 

Ultrasonography is used to confirm pregnancy in the setting of abdom inal pain, vaginal bleeding, or som e other potential obstetric com plication: o

Can estim ate gestational age

o

Confirm intrauterine or ectopic pregnancy.

o

Evaluate fetal viability.

o

Identify fetal abnorm alities: 

Transabdom inal ultrasound vs. transvaginal ultrasound.

o

Transvaginal ultrasound is m ore sensitive but m ore

Pa ge 3 8 3

difficult to perform . o

Transvaginal ultrasound is contraindicated in the setting of prem ature rupture of m em branes and third-trim ester bleeding.



When used in com bination with HCG levels, ultrasound is a very helpful tool in detecting abnorm al/problem pregnancy.

Differential Diagnosis Any wom an who is of the age to be sexually active who presents to the ED should be assum ed to be pregnant until proven otherwise.

Pediatric Considerations Assum e pregnancy in the adolescent regardless of the chief com plaint. P.899

Treatment Pre Hospital 

Assum e that the patient is pregnant.



Adm inister m edications only when necessary to avoid teratogenetic side effects or placental-fetal com prom ise (i.e., epinephrine)



If greater than 24 weeksâ€™ gestation, transport in left lateral recum bent position.

Initial Stabilization 

Advanced cardiac life support, advanced traum a life support m easures as needed: oxygen, cardiac m onitor, IV

Pa ge 3 8 3

access, and fluids 

If greater than 24 weeksâ€™ gestation, place in the left lateral recum bent position

ED Treatment The goal is to optim ize m aternal condition to im prove fetal condition.

Medication (Drugs) 

First trim ester is when organogenesis is occurring.



Fetal m alform ation continues beyond the first trim ester.



Before using any drug, refer to its Food and Drug Adm inistration safety classification in pregnancy: o

This classification system categorizes drugs as A, B, C, D, and X, with category A being the safest and category X being the m ost toxic.



Analgesics: acetam inophen is the preferred OTC analgesic.



Aspirin and NSAIDs are not teratogenic but are best utilized in consultation with an obstetrician.



Propoxyphene, codeine, hydrocodone, m eperidine, and m orphine have no known teratogenic affect and can be used for the control of severe pain in pregnancy for short periods of tim e (three to four days)



Antibiotics: selecting the right antibiotic in a gravid fem ale is dependent on three factors: o

Maternal drug allergies

o

Gestational age

o

Type of infections and associated pathogens

Follow-Up

Pa ge 3 8 3

Disposition Admission Criteria 

Pregnant wom en with the following obstetric com plications should be adm itted to the hospital: o

Hyperem esis gravidarum with inability to tolerate oral fluids



o

Com plicated urinary tract infection

o

Ectopic or m olar pregnancy

o

Septic abortion

o

Preterm labor

o

Prem ature rupture of m em branes

o

Pre-eclam psia/eclam psia

o

Severe pregnancy-induced hypertension

Pregnant wom en with m edical conditions that would warrant adm ission in a nongravid fem ale

Discharge Criteria Wom en without the above conditions m ay be discharged from the ED.

References 1. Barnhart K, Esposito M, Coutifars C. An update on the m edical treatm ent of ectopic pregnancy. Obstet Gynecol Clin North Am . 2000;27:653â€“667. 2. Barnhart K, Sim han H, Kam elle SA. Diagnostic accuracy of ultrasound above and below the beta-hCG discrim inatory zone. Obstet Gynecol. 1999;94:583â€“587. 3. Bree RL, Edwards M, Bohm -Valez M, et al. Transvaginal sonography in the evaluation of norm al early pregnancy: correlation with hCG level. Am J Roentgenol. 1989;153:75â€“79. 4. Cole LA, Khanilan SA, Sutton JM, et al. Accuracy of hom e pregnancy tests at the tim e of m issed m enses. Am J Obstet Gynecol. 2004;190:100â€“105.

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5. Davies S, Byrn F, Cole LA. Hum an chorionic gonadotropin testing for early pregnancy viability and com plications. Clin Lab Med. 2003;23:257â€“264. 6. Dogra V, Paspulati RM, Bhatt S. First trim ester vaginal bleeding evaluation. Ultrasound Q. 2005;21:69â€“85. 7. Filkins K, Koos BJ. Ultrasound and fetal diagnosis. Curr Opin Obstet Gynecol. 2005;17:185â€“195. 8. Paul M, Schaff E, Nichols M. The roles of clinical assessm ent, hum an chorionic gonadotropin assays, and ultrasonography in m edical abortion practice. Am J Obstet Gynecol. 2000;183(2 suppl):S34â€“S43.

Codes ICD9-CM V22.2

ICD10 O36.7

Pa ge 3 8 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Priapism

Priapism

David Barlas

Basics Description 

Penile erection (engorgem ent of corpora cavernosa) in the absence of sexual arousal that is prolonged and frequently painful



Low-flow priapism : o

Most com m on m echanism

o

Poor venous outflow

o

Usually painful

o

Ischem ia and throm bosis from stagnant, hypoxic blood can occur after a few hours.

o 

Fibrosis and im potence are late sequelae.

High-flow priapism : o

Rare

o

Penile arterial laceration with uncontrolled inflow of arterial blood

o

Usually painless

o

Presentation m ay be later than in low-flow priapism .

o

Ischem ia and im potence are uncom m on.

Etiology 

Idiopathic

Pa ge 3 8 3



Pharm acologic agents: o

Intracavernosal injectables for the treatm ent of im potence:

o

o

o







PGE-1



Papaverine



Phentolam ine

Psychotropics: 

Phenothiazines



Butyrophenones



Trazodone



Sedative-hypnotics



Selective serotonin uptake inhibitors (SSRIs)

Antihypertensives: 

Prazosin



Hydralazine



Phenoxybenzam ine



Guanethidine

Rarely im plicated agents: 

Sildenafil (Viagra)



Anticoagulants



Cocaine



Marijuana



Ethanol



Androstenedione

Hem atologic disorders predisposing to sludging of blood: o

Sickle cell anem ia

o

Leukem ia

o

Multiple m yelom a

o

Polycythem ia

Penile and perineal traum a can result in arterial laceration and high-flow priapism .



Spinal traum a m ay cause priapism from loss of inhibitory

Pa ge 3 8 4

adrenergic tone. 

Rare causes: o

Pelvic neoplasm s and infections

o

Dialysis

o

Parenteral nutrition solutions containing a fat em ulsion

Pediatric Considerations Sickle cell anem ia is the cause of m ost priapism in children.

Diagnosis Signs and Symptoms History Type of priapism m ay be determ ined by history: 



Low-flow priapism : o

Painful

o

Predisposing condition or m edication

High-flow priapism : o

Painless

o

Penile traum a

Physical Exam 

Diagnosis is clinically apparent.



Penile im plants



Traum a



Urinary retention

Tests Lab 

Com plete blood count



Coagulation studies

Pa ge 3 8 4



Sickle cell evaluation m ay be indicated.

Imaging 

Duplex Doppler ultrasound can verify and localize the arterial laceration in high-flow priapism .



Angiography enables localization and em bolization of the arterial laceration in high-flow priapism .

Diagnostic Procedures/Surgery Intracavernosal blood gas analysis: 

Can help differentiate type of priapism



Because of the possibility of penile arterial injury, a urologist should perform this procedure.



High-flow priapism : near-norm al values



Low-flow priapism : acidosis and hypoxia (O 2 <30 torr)

Differential Diagnosis 

Penile erection from sexual arousal is usually painless and transient.



Penile im plants are a benign cause of â€œpriapism .â€•

Treatment Pre Hospital 

IV



O2



Analgesia

Initial Stabilization 

O2



Analgesia and sedation



Intravenous hydration



Urgent urologic consultation

Pa ge 3 8 4

P.901

ED Treatment 

Managem ent of specific causes: o

o

Sickle cell anem ia: 

RBC transfusion



Exchange transfusion



Hyperbaric oxygen if other m easures fail

Leukem ia: 

o



Chem otherapy

Arterial injury: 

Expectant m anagem ent is an option.



Angiographic localization



Em bolization

Terbutaline (Î²-agonist): o

May be adm inistered in consultation with urologist to initiate treatm ent of low-flow priapism , but m ay not be effective alone



Intracavernosal injection/aspiration: o

Invasive technique that should be perform ed by urologist if m edical therapy for low-flow priapism fails.

o

If specialty care is unavailable for several hours, ED physician m ay perform procedure as follows: 

Sterile prep of area



Adm inister local anesthesia to the glans, or perform a pudendal nerve block or penile nerve block (inject plain lidocaine around the base of the penis).



Position yourself to the right of the patient and grasp the penile shaft with your left hand.

Pa ge 3 8 4



Enter the corpus cavernosum with a 19-gauge butterfly needle inserted through the glans laterally at 2- or 10-O'clock position to avoid the ventral urethra and the dorsal neurovascular bundle.



Aspirate blood while â€œm ilkingâ€• the penile shaft; aspirating both corpora cavernosa is unnecessary as they are connected by shunts; aspirate until arterial blood is obtained, often after 20â€“30 m L; irrigation with saline m ay be necessary.



Phenylephrine (preferred), epinephrine, or pseudoephedrine m ay be injected through the butterfly needle if tum escence recurs; m onitor heart rate and blood pressure if these agents are used, and do not adm inister them to patients with cardiovascular or cerebrovascular disease or patients taking m onoam ine-oxidase inhibitors (MAOIs) because of the risk of hypertensive crisis.



Surgical shunt (i.e., corpus cavernosum to spongiosum ) m ay be necessary if the above m easures fail.

Medication (Drugs) 

Phenylephrine: Dilute 1 m g in 100 m L saline; inject 10-m L boluses in the corpus cavernosum .



Epinephrine: Dilute 1 m g in 100 m L saline; inject 1- to 3-m L boluses in the corpus cavernosum , up to 10 m L.



Pseudoephedrine: 60â€“100 m g in the corpus cavernosum



Terbutaline: 0.25â€“0.5 m g SC or 5 m g PO q4hâ€“q6h

Pa ge 3 8 4

Follow-Up Disposition Admission Criteria 

Persistent priapism despite noninvasive treatm ents



Serious underlying disease (sickle cell anem ia, leukem ia)

Discharge Criteria 

Detum escence is com plete and has not recurred after several hours of observation.



Urologic consultation has been obtained.



Short-term follow-up has been arranged.



The patient has been advised to return to the ED if tum escence recurs.



The patient has been warned of the possibility of im potence.

References 1. Hakim LS, Kulaksizoglu H, Mulligan R, et al. Evolving concepts in the diagnosis and treatm ent of arterial high flow priapism . J Urol. 1996;155:541â€“548. 2. Mulhall JP, Honig SC. Priapism : diagnosis and m anagem ent. Acad Em erg Med. 1996;3:810â€“816. 3. Montagne DK, Jarow J, Broderick GA, et al. Am erican Urological Association guideline on the m anagem ent of priapism . J Urol. 2003;170(4 pt 1):1318â€“1324. (Also available at http://www.auanet.org/tim ssnet/products/guidelines/m ain_reports/p riapism /online.pdf). Last accessed June 2006. 4. Paulter SE, Brock GB. Priapism . From Priapus to the present tim e. Urol Clin North Am . 2001;28:391â€“403.

Codes

Pa ge 3 8 4

ICD9-CM 607.3

ICD10 N48.3

Pa ge 3 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pro statitis

Prostatitis

Robert S. Hamilton

Basics Description Five categories: 

Prostatic abscess: o

Once com m on after acute prostatitis, now rare except in im m unocom prom ised patients

o

Fever, rectal pain, and leukocytosis despite treatm ent

o 

Fluctuant m ass on rectal exam

Acute (bacterial) prostatitis: o

Acute febrile illness

o

System ic sym ptom s m ay appear days before localizing urinary sym ptom s appear.

o

Patients m ay appear toxic and usually have a concurrent cystitis.



Chronic bacterial prostatitis: o

About 10% of cases of prostatitis

o

Most com m on cause of recurrent urinary tract infection in m en

o

WBC and bacteria m ay be present in expressed prostatic secretions (EPS)

Pa ge 3 8 4



Chronic nonbacterial prostatitis (also called prostatosis): o

Sam e sym ptom s as chronic bacterial prostatitis but unable to culture organism s from urine or EPS



Prostatodynia: o

Sym ptom s referable to the prostate

o

No inflam m atory cells are found

o

No bacteria cultured from the urine or EPS

Etiology 

Usually a single organism bacterial infection of the prostate



Acute prostatitis: o

Age <35 years: 

Neisseria gonorrhoeae and Chlam ydia trachom atis are usual etiologies

o

Age â‰¥35 years: 

Enterobacteriaceae or Escherichia coli (usual), Klebsiella, Pseudom onas, Enterococcus, and Proteus also seen

o

Rarely m ay be caused by Salm onella, Clostridia, tuberculosis, or fungi

o 

Cryptococcus neoform ans in AIDS patients

Chronic bacterial prostatitis: o

Enterobacteriaceae (80%), Enterococcus (15%), and Pseudom onas aeruginosa



Chronic nonbacterial prostatitis: o

Possible role for Chlam ydia, Ureaplasm a urealyticum , Trichom onas vaginalis, and Mycoplasm a hom inis

Diagnosis

Pa ge 3 8 4

Signs and Symptoms History 

Irritative voiding sym ptom s: o

Frequency, urgency, dysuria



Low back pain



Perineal, suprapubic, or testicular pain



Bladder outlet obstruction and urinary retention



Ejaculatory sym ptom s such as hem atosperm ia



Acute prostatitis:



o

Fever, chills

o

Malaise

o

Arthralgias, or m yalgias

Prim ary sym ptom in chronic prostatitis is relapsing dysuria

Physical Exam 

Acute prostatitis: o

Exquisitely prostate tenderness

o

Warm , swollen

o

Firm or boggy prostate

o

Acutely inflam ed prostate should not be m assaged because m ay precipitate hem atogenous spread of organism s.



In chronic prostatitis, the exam ination is usually norm al.

Tests Lab 

Urinalysis (with m icroscopy) and culture



Acute prostatitis: o

CBC, electrolytes, and blood cultures m ay be helpful in the acutely ill patient.

o

If <35 years old or suspected sexual transm ission, test for syphilis.

Pa ge 3 8 4



Venereal disease research laboratory or rapid plasm a reagin



Chronic prostatitis/prostatodynia: o

Prostatic m assage between voiding m ay be used to capture EPS for gram stain and culture if organism or white cells not present in the urine.

Imaging 

Not indicated in acute prostatitis



If prostatic abscess suspected, prostatic ultrasound or pelvic CT scan with IV and rectal contrast will confirm diagnosis.



Pelvic radiographs m ay reveal prostatic calculi (com m on in m en), which m ay serve as a nidus for infection in chronic prostatitis.

Diagnostic Procedures/Surgery Not applicable in ED

Differential Diagnosis 

Cystitis



Pyelonephritis



Urolithiasis



Vesicular calculi



Sem inal vesiculitis



Proctitis



Perirectal/perianal abscess



Urethritis



Epididym itis



Orchitis



Prostatic infarction



Benign prostatic hyperplasia



Prostatic carcinom a



Other causes of lower back pain (strain, disc disease,

Pa ge 3 8 5

sacroiliac joint disease, etc.)

Treatment Initial Stabilization Initial resuscitative m easures as indicated

ED Treatment 

Prostatic abscess requires urgent urologic consultation and operative m anagem ent



Antibiotic therapy should be initiated in ED (see Medications, below).



Urinary tract instrum entation should be avoided: o

If patient has painful urinary retention in acute prostatitis, suprapubic needle aspiration or suprapubic catheter placem ent should be perform ed.



Many patients will benefit from IV fluid.



Pain control with NSAIDs and narcotic analgesics as needed



Stool softeners



Bed rest



Irritative voiding sym ptom s m ay persist for m onths after antibiotic therapy and m ay be treated with NSAIDs

Medication (Drugs) 

Analgesia: o

Narcotic, analgesic com binations such as hydroxycodone/acetam inophen: 1â€“2 tabs PO q4h

o 

NSAIDs such as ibuprofen: 800 m g PO t.i.d.

Parenteral antibiotic therapy for acute prostatitis

Pa ge 3 8 5

o

Am picillin/sulbactam : 3 g IV q6h

o

Cefotaxim e: 2 g IV q8h

o

Ceftriaxone: 2 g IV qd

o

Ciprofloxacin: 400 m g IV b.i.d.

o

Ofloxacin: 200 m g IV b.i.d. P.903

o

Piperacillin/tazobactam : 3.375 g IV q6h or 4.5 g IV q8h

o 

Ticarcillin/clavulanate: 3.1 g IV q6h

Antibiotics for outpatient treatm ent of acute (â‰¤35 years old) prostatitis, suspected etiology N. gonorrhoeae or C. trachom atis: o

Ceftriaxone: 250 m g IM, then doxycycline 100 m g PO b.i.d. Ã— 10â€“14 days

o

Levofloxacin: 500 m g PO every day for 10â€“14 days

o

Ofloxacin: 400 m g PO Ã— 1, then 300 m g PO b.i.d. Ã — 10â€“14 days



Antibiotics for outpatient treatm ent of acute (>35 years old) prostatitis, suspected etiology Enterobacteriaceae (coliform s); som e authorities recom m end treatm ent for 3â€“4 weeks o

Ciprofloxacin: 500 m g PO b.i.d. Ã— 14 days

o

Levofloxacin: 500 m g PO every day for 14 days

o

Ofloxacin: 200 m g PO b.i.d. Ã— 14 days

o

Trim ethoprim /sulfam ethoxazole: 1 DS tab or 2 regular-strength tablets PO b.i.d. Ã— 14 days



Outpatient therapy for chronic bacterial prostatitis (Enterobacteriaceae, Enterococcus, or P. aeruginosa): o

Ciprofloxacin: 500 m g PO b.i.d. for 4 weeks

o

Levofloxacin: 500 m g PO every day for 4 weeks

Pa ge 3 8 5

o

Ofloxacin: 300 m g PO b.i.d. for 6 weeks

o

Trim ethoprim /sulfam ethoxazole DS: 1 tab PO b.i.d. for 1â€“3 m onths



Prostatodynia/chronic pain syndrom e: o

Doxazosin: 1 m g PO every day

o

Peripheral Î±-adrenergic blocking agents have been used with som e success; consult a urologist

o

Prazosin: 1 m g PO b.i.d./t.i.d.

o

Terazosin: 1 m g PO qhs

Follow-Up Disposition Admission Criteria 



Acute prostatitis: o

Patients who appear ill or toxic

o

Hypotension

o

Urinary retention

Chronic prostatitis: o

Adm ission generally not warranted unless patient has signs or sym ptom s of acute prostatitis.

Discharge Criteria 

Acute prostatitis: o

Patient m ust be nontoxic

o

Able to take fluids and oral m edications (analgesia and antibiotics)

o

Urinate without difficulty

o

Im m unocom petent

o

Relatively free of concurrent underlying disease

o

Have appropriate follow-up care

Pa ge 3 8 5



Chronic prostatitis: appropriate follow-up care should be available

Issues for Referral Patient with either acute or chronic prostatitis should be referred to an urologist.

References 1. Bjerklund Johansen TE. Diagnosis and im aging in urinary tract infection. Curr Opin Urol. 2002;12(1):39â€“43. 2. Hua VN, Schaeffer AJ. Acute and Chronic Prostatitis. Med Clin North Am . 2004;88(2):483â€“494. 3. Lipsky, Benjam in A. Prostatitis and urinary tract infection in m en: what's new; what's true? Am J Med. 1999;106(3):327â€“334. 4. Lum m us WE, Thom pson I. Prostatitis. Em erg Med Clin North Am . 2001;19(3):691â€“707. 5. Robert RO, Lieber MM, Bostwick DG, et al. A review of clinical and pathological prostatitis syndrom es. Urology. 1997;49:809â€“821. 6. Schaeffer A, Stern J. Chronic Prostatitis. Clin Evid. 2003;12(10):994â€“1002. 7. Wagenlehner FM, Naber KG. Antim icrobial Treatm ent of Prostatitis. Expert Rev Anti Infect Ther. 2003;1(2):275â€“82. 8. Wagenlehner FM, Naber KG. Fluoroquinolone antim icrobial agents in the treatm ent of prostatitis and recurrent urinary tract infections in m en. Curr Urol Rep.2004;5(4):309â€“316.

Codes ICD9-CM 601.9

ICD10 N41.9

Pa ge 3 8 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pruritis

Pruritis

Christine Tsien Silvers

Basics Description 

Unpleasant sensation that provokes a desire to scratch



Mediated by unm yelinated C fibers in upper portion of derm is:



o

Transm itted to dorsal horn of spinal cord

o

Via spinothalam ic tract to cerebral cortex

Peripheral m ediators stim ulate C fibers and induce itching: o

Histam ine

o

Serotonin

o

Trypsin

o

Proteases

o

Peptides that release histam ine:

o



Bradykinin



Vasoactive intestinal peptide



Substance P

Bile salts



Prostaglandins (PGE 2 , PGH 2 ) lower threshold to pruritus



Opiates cause pruritus by acting on central receptors.



No single pharm acologic agent effectively treats all kinds of pruritus.

Pa ge 3 8 5



â€œItchâ€“scratchâ€“itchâ€• cycle: o

Itching triggers scratching, which dam ages the skin and stim ulates nerve endings, thereby producing even greater itching.

o

Pathogenic basis for lichen sim plex chronicus and prurigo nodularis

Etiology 

Allergy



Atopy



Endocrine diseases:





o

Thyroid and parathyroid diseases

o

Diabetes m ellitus

Metabolic diseases: o

Kidney disease

o

Liver disease

o

Carcinoid

Neoplasm s: o

Lym phom a

o

Leukem ia

o

Polycythem ia vera



Autoim m une disorders



Infections



Neuropsychiatric causes

Diagnosis Signs and Symptoms History 

Onset: o

Shortly after fresh water bathing in swim m er's itch

Pa ge 3 8 5

o

More intense at night with scabies

o

Paroxysm al with m ultiple sclerosis

o

With sudden changes in tem perature in polycythem ia vera



Location on body (e.g., exposed skin only)

Physical Exam 

Derm atologic: o

Absence of rash

o

Hives/urticaria

o

Grouped papules

o

Interdigital, pubic, axillary, or nipple lesions

o

Generalized m orbilliform eruptions

o

Discrete weeping patches with vesicles

o

Dry skin

o

Jaundice

o

Excoriations

o

Prurigo papules: 

Thickened papular areas of skin from constant rubbing



Psychogenic: o

Constant rubbing in areas patient can readily reach

Essential Workup 

Detailed history is key in the ED workup: o

Onset

o

Character: paroxysm al, burning, pricking

o

Tim e of occurrence, circadian nature

o

Duration

o

Severity

o

Anatom ic area

o

Exacerbating or alleviating factors: 

Water, heat, dryness, dam pness, coolness

Pa ge 3 8 5

o

Medications

o

Use of new topical products: 

Soap



Hair spray



Lotions



Cosm etics



Perfum e

o

Laundry detergents

o

Fabric softeners

o

Fam ily history of atopic derm atitis or skin disease

o

Personal history of allergies or asthm a

o

Pruritus in other fam ily m em bers

o

System ic or associated sym ptom s: 

Night sweats, fever, trem ors, weight loss, fatigue



o

Sexual history, history of HIV or AIDS

o

Social: occupation, hobbies, pets, travel

Characterization of skin lesions: o

Diffuse or localized

o

Location: genitals, interdigital webs, axilla, wrists, etc.

o

Follicular (around the hair)

o

Nonfollicular: 

o

Prim ary lesions: 

o

Papular, pustular, urticarial, or polym orphic

Secondary lesions: 



Insect bites, scabies

Excoriations, lichenification, hyperpigm entation

Signs of system ic disease on physical exam ination

Tests Lab

Pa ge 3 8 5



Lab testing is m ost often unnecessary.



Indications for specific studies vary based on the clinical presentation and should be guided by clinical judgm ent.

Diagnostic Procedures/Surgery 

Skin scrapings for scabies and derm atophytoses



Skin biopsy: o



Perform ed by derm atologist at follow-up visit

Skin culture for bacterial, viral, or fungal infection

Differential Diagnosis Dermatologic 

Xerosis (dry skin)



Insect infestations: o

Scabies: 

o

Pediculosis (lice)

o

Insect bites; 



Localized clusters of papules

Derm atitis: o

Atopic derm atitis

o

Contact derm atitis: 

o

Includes poison ivy contact

Num m ular derm atitis: 



Vesicles and burrows on intertriginous areas

Round eczem atous or vesicular eruption

Drug-induced (suspect when absence of rash): o

Opiates and derivatives

o

Aspirin

o

Quinidine

o

Antim alarials

o

Antifungals

o

Phenothiazines

o

Isoniazid

Pa ge 3 8 5



o

Vitam in B com plex

o

Estrogens, progestins, testosterone

o

Tolbutam ide

Lichen planus: o

Lichenification, hyperpigm entation, skin thickening



Urticaria



Bullous pem phigoid



Eosinophilic folliculitis



Psoriasis



Derm atitis herpetiform is: o

Burning itch



Sunburn



Aquagenic pruritus



Fiberglass derm atitis



Seborrheic derm atitis: o

Scaly plaques on scalp, hairline, eyebrows, central face, and other sebaceous gland-bearing areas like axillae and chest





Swim m er's itch o

Schistosom e cercarial derm atitis

o

Repeated fresh water exposure

o

Itching starts as water evaporates

o

Highly pruritic papules develop hours later

Miliaria rubra (prickly heat)

Infectious 

HIV



Parasites: o

Hookworm

o

Onchocerciasis

o

Ascariasis

o

Trichinosis

P.905

Pa ge 3 8 6

Cholestatic 

Obstructive biliary disease



Prim ary biliary cirrhosis: o



Early sign usually starting on hands and soles

Hepatic cholestasis secondary to drugs: o

Chlorpropam ide

o

Estrogens

o

Phenothiazine

o

Allopurinol



Intrahepatic cholestasis of pregnancy



Extrahepatic biliary obstruction



Chronic hepatitis, especially hepatitis C

Hematologic 

Polycythem ia vera



Iron-deficiency anem ia



Paraproteinem ia



WaldenstrÃ¶m m acroglobulinem ia



Mastocytosis

Neoplastic 

Lym phom a, including Hodgkin disease



Mycosis fungoides



Leukem ia



CNS tum ors



Multiple m yelom a



Carcinoid



Visceral m alignancies: o

Breast, stom ach, lung

Metabolic-Endocrine

Pa ge 3 8 6



Urem ia



Hyperthyroidism



Hypothyroidism



Hyperparathyroidism



Diabetes



Carcinoid

Neurologic 

Multiple sclerosis: o



Paroxysm al itching

Notalgia paraesthetic: o

Local itch of back, m edial shaft scapula



Brain abscess



CNS infarct



Cerebral tum or



Creutzfeldt-Jakob disease

Renal 

Chronic renal failure



Chronic hem odialysis

Rheumatologic 

SjÃ¶gren syndrom e



Derm atom yositis

Psychiatric 

Stress, anxiety, neurotic excoriation



Delusions of parasitosis



Psychogenic pruritus

Treatment ED Treatment

Pa ge 3 8 6



Start with antihistam ines for pruritus of undeterm ined etiology



Em ollients indicated for pruritus secondary to dry skin



Coolants to alleviate itching: m enthol, cam phor, eucalyptus oil, calam ine lotion



Substance P evacuators (capsaicin) block C fibers: o

Burning sensation during first weeks of use

o

Anesthetic can be applied prior



Topical glucocorticoids for contact derm atitis



Perm ethrin cream for scabies and lice when rash is suggestive.



Topical antihistam ines (doxepin) for eczem a, urticaria, bites



Swim m er's itch: o

Control with antihistam ines, cool com presses, calam ine lotion

o

Topical steroids to suppress intense inflam m ation

o

Towel dry im m ediately after leaving water as preventive m easure.



Discontinue m edications that m ay cause allergic reaction.



Ultraviolet light for urem ic pruritus



Treat the underlying cause for pruritis associated with a system ic disease.

Medication (Drugs) 

Oral antihistam ines for histam ine-induced itch: o

Chlorpheniram ine 4 m g (peds: 0.35 m g/kg/24h) PO q.i.d.

o

Diphenhydram ine 25â€“50 m g (peds: 5 m g/kg/24h) PO q.i.d.

o

Hydroxyzine 10â€“25 m g (peds: 2 m g/kg/24h) PO

Pa ge 3 8 6

q.i.d. 

Topical treatm ents o

Capsaicin 0.025%, 0.075% ointm ent: apply up to q.i.d.

o

Doxepin 5% cream : apply q.i.d. for up to 8 days

o

EMLA (2.5% lidocaine + 2.5% prilocaine): apply prior to capsaicin

o

Hydrocortisone, 0.5%, 1%, 2.5%: apply up to q.i.d.

o

Perm ethrin 5% cream : apply from neck down after bath (for infestations): 

Shower thoroughly to rem ove the m edication in 8â€“12 hours

o

White petroleum em ollients: apply after short bath/shower in warm (not hot) water



Corticosteroids for inflam m ation-induced itch



Other system ic treatm ents for specific diseases

Follow-Up Disposition Admission Criteria 

Anaphylaxis



Generalized exfoliating lesions

Discharge Criteria Practical recom m endations for dry skin: 

Take baths with baking soda, bath oils, or colloidal oatm eal



Use m oisturizers frequently during day and im m ediately after bathing



Avoid:

Pa ge 3 8 6

o

Dry air (hum idity less than 40%)

o

Contact irritants (wool, cleansers, etc.)

o

Alkaline soaps and overwashing

o

Alcohol, caffeine, peppery foods (cause vasodilation)

o

Overexposure to heat, hot water

Issues for Referral 

Refer patients with skin lesions to prim ary care physician or derm atologist.



Patients with pruritus without skin lesions should be discharged on antipruritic m edication and referred to a physician for an underlying system ic illness.

References 1. Charlesworth EN, Beltrani VS. Pruritic derm atoses: overview of etiology and therapy. Am J Med. 2002;113 Suppl 9A:25Sâ€“33S. 2. Hiram anek N. Itch: a sym ptom of occult disease. Aust Fam Physician. 2004;33(7):495â€“499. 3. Krajnik M, Zylicz Z. Understanding pruritus in system ic disease. J Pain Sym ptom Manage. 2001;21(2):151â€“68. 4. Lidstone V, Thorns A. Pruritus in cancer patients. Cancer Treat Rev . 2001;27(5):305â€“312. 5. Lonsdale-Eccles A, Carm ichael AJ. Treatm ent of pruritus associated with system ic disorders in the elderly: a review of the role of new therapies. Drugs Aging. 2003;20(3):197â€“208. 6. Moses S. Pruritis. Am Fam Physician. 2003;68(6):1135â€“1142. 7. Singh F, Rudikoff D. HIV-associated pruritus: etiology and m anagem ent. Am J Clin Derm atol. 2003;4(3):177â€“188. 8. Yosipovitch G, Greaves MW, Schm elz M. Itch. Lancet. 2003;361(9358):690â€“694.

Codes ICD9-CM

Pa ge 3 8 6

698

ICD10 L29.9

Pa ge 3 8 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pseudo tum o r C erebri

Pseudotumor

Cerebri Ian Reilly

Basics Description 

Buildup of cerebrospinal fluid (CSF) pressure without m ass lesion and no clear cause



Two proposed m echanism s: o

Increased abdom inal pressure m ay elevate right heart pressures and decrease venous drainage from the head.

o

Vitam in A levels above the saturation of the liver can dam age cell m em branes in the arachnoid granulations.



Associated with obesity



Average age of onset 30 years

Genetics Fem ale predom inance (7:1)

Etiology 

Proposed causative agents: o

Obesity

Pa ge 3 8 6

o

Hypervitam inosis A

o

Steroids/steroid withdrawal

o

Tetracycline antibiotics

o

Oral contraceptive pills

o

Hypertension

o

Recent weight gain

o

Chronic carbon dioxide retention with elevated intracranial pressure

Diagnosis Signs and Symptoms History 

Headache: o

Typically described as constant, bilateral

o

Pressurelike

o

Worse in the m orning

o

Worse with Valsalva m aneuver



Nausea and vom iting



Pulsatile intracranial noise



Diplopia



Dizziness



Scotom a



Transient visual obscurations lasting seconds



Blind spots



Constriction of vision

Physical Exam 

Visual field defects (in up to 90%): o



Typically inferior nasal visual field loss

Papilledem a

Pa ge 3 8 6



Lum bar puncture im proves sym ptom s



Sixth cranial nerve palsy



Loss of visual acuity



Otherwise norm al neurologic exam except: o

Visual changes

o

Abducens palsy

o

Rarely seventh cranial nerve palsy

Pediatric Considerations 

Usually presents with strabism us as opposed to headache and visual field loss



Also associated with obesity and m edications (tetracycline antibiotics, steroids)

Essential Workup 

Thorough history and physical exam



Detailed neurologic assessm ent and funduscopic exam

Tests Lab 

Lum bar puncture: CSF norm al or low protein with a norm al cell count



Opening pressure >25 cm H 2 O or >20 cm H 2 O in nonobese, relaxed patient: o

Be sure patient is lying down with m easurem ent of opening pressure.

o

Observing respiratory variation ensures good transm ission of pressure.



Consider CBC, coagulation studies prior to lum bar puncture.



Im provem ent of sym ptom s with lum bar puncture

Imaging 

Head CT/MRI to rule out m ass lesions (prior to lum bar

Pa ge 3 8 6

puncture) 

Classically the head CT will dem onstrate slitlike frontal horns of the lateral ventricles.



MRI recom m ended in the full workup: o

Can be done as an outpatient

o

Cerebral venous throm bosis can m im ic pseudotum or cerebri in all regards including norm al head CT.

P.907

Differential Diagnosis 

Migraine headache



Hypertensive headache



Anoxic headache



Tension headache



Cluster headache



Subarachnoid hem orrhage



Aneurysm /arteriovenous m alform ation



Meningitis/encephalitis



Subdural hem atom a



Epidural hem atom a



Tum or



Abscess



Trigem inal neuralgia



Tem poral arteritis



Sinusitis



Glaucom a



Central retinal vein/artery occlusion



Congenital optic nerve head elevation



Optic nerve drusen



Labyrinthitis



Optic neuritis

Pa ge 3 8 7



Cerebral venous throm bosis



Chronic carbon dioxide retention

Treatment Pre Hospital Pain control as appropriate

Initial Stabilization 

Airway and circulation m anagem ent as indicated



IV fluid hydration

ED Treatment 

Large-volum e Lum bar puncture of 20â€“30 m L of CSF o

Only if confident of correct diagnosis and head CT dem onstrates open basilar cisterns and fourth ventricle.



Acetazolam ide



Pain control



Neurology consult



Ophthalm ology consult



Neurosurgery consult for acute or im pending visual loss unresponsive to diuretics (for lum boperitoneal shunt)



Optic nerve fenestration another surgical option



Weight loss



Discontinue any drugs that could be causative.



Typically resolves spontaneously

Medication (Drugs) 

Acetam inophen: 650 m gâ€“1 g (peds: 15 m g/kg)

Pa ge 3 8 7



Acetazolam ide: 500 m g slow-release PO b.i.d. (peds: 25 m g/kg/d div. q.i.d./t.i.d. PO/IV)



Ibuprofen: 600â€“800 m g PO (peds: 10 m g/kg PO)



Lasix: 0.5â€“1 m g/kg IV/PO



Morphine: 0.1 m g/kg IV/IM



Prednisone: helpful when severe visual sym ptom s present, 5-day course recom m ended

Follow-Up Disposition Admission Criteria Acute or im pending visual loss

Discharge Criteria 

Consultation obtained from neurology and ophthalm ology



Appropriate follow-up arranged



Tolerating oral diuretics



Pain under control

References 1. Goetz CG, Pappert EJ, eds. Textbook of Clinical Neurology. Philadelphia: WB Saunders,1999. 2. Jones JS, Nevai J, Freem an MP, et al. Em ergency departm ent presentation of idiopathic Intracranial hypertension. Am J Em erg Med . 1999;17(6):517â€“521. 3. Mouvsas TZ, et al. Current neuro-ophthalm ic therapies. Neurol Clin. 2001;19(1):145â€“172. 4. Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Codes

Pa ge 3 8 7

ICD9-CM 348.2

ICD10 G93.2

Pa ge 3 8 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pso riasis

Psoriasis

Stephen R. Hayden

Basics Description 

Chronic skin condition presents with erythem atous plaques with silver scaling



Caucasians and atopics m ost affected



Majority of cases are diagnosed between 10 and 30 years of age.



Equal num ber of adult m ale and fem ale cases



Occurs as the result of defective inhibition of epiderm al proliferation



Several clinical presentations: o

Chronic plaque psoriasis: 

Most com m on form with classic lesions on the extensor surfaces (elbows, kness, occipital scalp, back)

o

Guttate psoriasis: 

Red drop like lesions usually on the trunk



Occurs m ore com m only in children and often after streptococcal infections

o

Pustular psoriasis: 

Collections of pustules on one area of the body,

Pa ge 3 8 7

usually palm s or soles o

Erythroderm ic psoriasis: 

Sim ple confluent erythroderm a or the patient m ay exhibit pustules

o

Light-sensitive psoriasis: 

o

Response to sunburning (Koebner phenom enon)

Inverse flexural psoriasis: 

A variant that causes lesions in flexural areas that don't exhibit scaling due to m oisture in these areas

o

HIV-induced psoriasis: 

May be the first m anifestation of AIDS with an explosive presentation

o

Keratoderm a blennorrhagicum : 

Psoriasis of the penis seen with Reiter syndrom e with a distinctive winding pattern to the lesion (balanitis circinata)

Genetics Autosom al-dom inant inheritance pattern

Etiology 

Affects approxim ately 1â€“2% of people in the United States



Triggers include: o

Drugs: 

Lithium



Beta-blockers



Antim alarials



Steroids



NSAIDs



Alcohol



Tetracycline

Pa ge 3 8 7

o

o



Penicillin



Am iodarone



Morphine



Procaine



Potassium iodide



Sulfapyridine, and sulfonam ides

Infections: 

Streptococcal pharyngitis



HIV



Viral URI

Local traum a: 

Frostbite



Sunburn



Routine skin breaks (Koebner phenom enon)

o

Stress: em otional and physical

o

Winter: 

Low light exposure



Dry weather

o

Cigarette sm oking

o

Horm onal changes such as puberty or m enopause

Diagnosis Signs and Symptoms History 

Patients usually com plain of skin lesions that are not intensely pruritic but m ay itch or burn.



May give a history of previously diagnosed psoriasis



May relate one of the above triggers



Age at first appearance of lesions

Pa ge 3 8 7



Specific location of lesions



Fam ily history of the disease



History of im provem ent with sun exposure, or if recurrent, success of prior regim ens



System ic sym ptom s like fevers or joint pains

Physical Exam 

The classic skin lesion is a round red patch with central plaque of silvery white scale that appears on extensor surfaces: o



The lesions not intensely pruritic, but do itch.

Positive Auspitz sign: o

Erythem a and punctuate bleeding when scales are rem oved.



Scalp lesions m ay be confused with seborrhea: o

Lesions that extend beyond the hair borders indicate psoriasis.



Stippling and pitting of nail and oncolysis: o

Yellow or brown band across the nail will help differentiate psoriasis (+ band) from onychom ycosis (â€“ band)



Approxim ately 10% of patients with plaque psoriasis have concom itant psoriatic arthritis: o



Often affects the DIP joints of the hands and feet.

Asym m etric oligoarticular arthritis: o

Present in 70% of these patients

o

Swelling of the juxtaarticular tissue

o

â€œSausage-shapeâ€• to the affected digits

Essential Workup 

The diagnosis is clinical.



Rarely a biopsy is necessary.



Skin biopsies can confirm the diagnosis or rule out other

Pa ge 3 8 7

conditions in unusual cases.

Tests Lab 

Elevated sedim entation rate and uric acid



Decreased serum album in



Anem ia with vitam in B 1 2 , folate, and iron deficiency



Positive streptococcal cultures and titers



Hypocalcem ia and leukocytosis in pustular disease



Negative rheum atoid factor



Key biopsy traits: o

Dilated tortuous capillaries (Auspitz sign)

o

Hyperkeratosis

o

Epiderm al hyperplasia

o

Munro m icroabscesses

Imaging Plain radiographs of the hands or feet m ay show osteoporosis and bone loss at the distal phalanx: 

Pencil-in-cup deform ation at the MTP or MCP joints



Sacroiliitis and ankylosing spondylitis m ay also be seen on radiographs.

Differential Diagnosis 

Best thought of by region: o

Scalp: seborrhea

o

Flexure creases: 

Candidiasis



Intertrigo



Eczem a

o

Nails: onychom ycosis

o

Trunk and extrem ities: 

Num m ular eczem a

Pa ge 3 8 7



Pityriasis rosea or rubra pilaris



Tinea



System atic lupus erythem atosus



Syphilis



Drug eruption



Atopy



Mycosis fungoides



Squam ous cell carcinom a

Treatment Initial Stabilization 

General resuscitation efforts aim ed at correcting fluid and electrolyte abnorm alities



Treating sepsis if present: o

Cultures of lesions, blood, and urine



Soothing m oist com presses are appropriate



System ic steroids should not be used as they m ay predispose to severe com plications

P.909

ED Treatment 



There are three basic types of treatm ent for psoriasis: o

Topical therapy

o

System ic therapy

o

Phototherapy

Topical therapy is the m ost com m only prescribed treatm ent m odality from the ED.



System ic therapy is usually em ployed only after patients

Pa ge 3 8 7

have failed topical and phototherapy. 

Exceptions where system ic therapy m ay be used: o

Generalized pustular psoriasis

o

Very active psoriatic arthritis

o

Psoriasis which is considered severely disabling



Phototherapy is not an ED treatm ent m odality.



Derm atology consult should be obtained in all severe cases.

Medication (Drugs) 

Mild to m oderate disease: o

Usually topical treatm ent only

o

No single topical agent works best for all people.

o

Em ollients: 

Hydrates and softens plaques



Greasier choices work best, but are poorly tolerated by patients

o

Keratolytics: 

Help to rem ove plaques



Salicylic acid (2â€“10%) is the m ainstay of treatm ent (caution m ust be used in applying near the eyes)

o

Coal-tar preparations: 

Usually used with topical steroids



Ointm ents and sham poos are available

o

Anthralin

o

May be used in com plex treatm ent regim ens with other topical agents and ultraviolet light

o

Topical corticosteroids: 

Mainstay of treatm ent in the United States



Best results are obtained by rotating drugs and

Pa ge 3 8 8

using occlusive dressings. 

Sm all lesions m ay be treated with intralesional Kenalog as m ay psoriatic nails.



Steroids have been im plicated in serious relapses and pustular psoriasis.

o

Vitam in D derivatives: 

o

Topical retinoids (Tazarotene): 



Calcipotriene is applied to lesions twice daily

Particularly useful for scalp lesions

Moderate to severe disease: o

The above-nam ed agents m ay be em ployed along with phototherapy and system ic m edications.

o

Phototherapy: 

Indicated in patients with very large areas of skin involvem ent or refractory to topical treatm ents.



Proper facilities are required for this form of treatm ent.



Ultraviolet B light is usually com bined with one or m ore topical agents and has reports of 80% rem ission.



Ultraviolet B m ay be used alone in guttate psoriasis.



Ultraviolet A light (PUVA) is com bined with a system ic agent (psoralen) which sensitizes the skin to UVA light.



Therapy is usually given two to three tim es per week.

o

System ic agents: m ay be used in various com binations with the above m odalities: 

Methotrexate (im m unosuppressant); assess renal, liver, and hem atologic function prior to

Pa ge 3 8 8

therapy and not to be used during pregnancy 

Etretinate: a retinoid, it causes dryness, scaling, redness, and tenderness of the skin



System ic corticosteroids: not in favor due to iatrogenic Cushing syndrom e; it m ay have a role in acute erythroderm ic psoriasis if patient is extrem ely ill



Cyclosporine: use in conjunction with derm atology consult

o

Psoralens (see above): have no effect unless com bined with UVA light therapy

o

Etanercept (Enbrel): injectable agent that works with the im m une system to reduce inflam m ation

o

Alefacept (Am evive): im m unosuppressant given as injection once per week

Follow-Up Disposition Admission Criteria Acute erythroderm a and acute pustular psoriasis warrant adm ission for supportive therapy and system ic treatm ent as noted above.

Discharge Criteria 

Patients without the above-m entioned form s m ay be discharged.



Advise patients the disease is not contagious.



Warn against excessive scrubbing to loosen scale, as it m ay worsen the disease.



Educate the patient on avoiding m edications that trigger relapses.

Pa ge 3 8 8



Refer patients to the National Psoriasis Foundation (telephone 503-244-7404) for further inform ation

Pediatric Considerations 

37% of all psoriasis cases occur before age 20.



The younger the patient at onset of disease, the worse the course.



The em otional side of this chronic disease m ay be param ount in children whose body im age is being form ed.



In general, topical agents are well tolerated, but PUVA and system ic agents are generally avoided in children.

Pregnancy Considerations Many of the drugs used to treat psoriasis are contraindicated in pregnancy.

References 1. Cam isa C. Psoriasis: a clinical update on diagnosis and new therapies. Cleve Clin J Med. 2000;67(2):105â€“106,109â€“113,117â€“119, S193. 2. Habif T. Psoriasis. In: Habif T, ed. Clinical derm atology. 3rd ed. St. Louis: CV Mosby,1996: 190â€“212. 3. Rogers M. Childhood psoriasis. Curr Opin Pediatr. 2002;14(4):404â€“409. 4. Wood J. Treatm ent of psoriasis. N Engl J Med. 1995;332:581â€“588.

Codes ICD9-CM 696.1

ICD10 L40.9

Pa ge 3 8 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psychiatric C o m m itm ent

Psychiatric

Commitment Jennifer M. Park Lawrence Park

Basics Description Com m itm ent criteria (check specific laws in your state): 

Individual is m entally ill.



Failure to hospitalize or discharge from hospital creates likelihood of serious harm .



Likelihood of serious harm defined as: o

Substantial risk of physical harm to self: threats or attem pts at suicide

o

Substantial risk of physical harm to other persons: hom icidal or violent behaviors, or others are placed in reasonable fear of violent behaviors

o

Very substantial risk of physical im pairm ent owing to inability to protect self resulting from im paired judgm ent; reasonable protection not available in com m unity



No less-restrictive alternative to hospitalization would attenuate risk.

Pa ge 3 8 8



Physician usually m ust sign form attesting that patient m eets one of above criteria.



(1) Often leads to 72-hour m andatory hospitalization, which m ay be followed by petition for psychiatric com m itm ent (2) once the patient is adm itted involuntarily, psychiatrist petitions the court for psychiatric com m itm ent.



If court does not grant petition for com m itm ent, patient m ust be released from psychiatric facility.

Diagnosis Signs and Symptoms 

Civil com m itm ent: confinem ent of an individual



Involuntary com m itm ent: confinem ent against patient's will



Basis of civil com m itm ent: danger to self or others



Psychiatric (civil) com m itm ent: o

Refers to order by judge for continued hospitalization of inpatient in a m ental health facility for treatm ent of psychiatric disease against patient's wishes

o

Based on danger to self or others by reason of m ental illness



Psychiatric com m itm ent not indicated for other causes of dangerous behavior:



o

Anger

o

Antisocial behavior

o

Substance abuse

o

Medical illness

Psychiatric com m itm ent usually involves two steps: o

Initial involuntary hospitalization in psychiatric

Pa ge 3 8 8

facility, m ost com m only initiated by a psychiatrist o

Petition to court for psychiatric com m itm ent

Essential Workup 

Psychiatric evaluation through history/m ental status exam : o

History of psychiatric illness

o

Recent change in behavior or thinking

o

Medication dosages

o

Drugs of abuse: am ount and tim e of last use

o

Disabling thought patterns: hallucinations, delusions, disorganization



Assessm ent of com m itm ent criteria: o

Threat of violence toward self

o

Threat of violence toward others

o

Inability to care for self or severe deficits in judgm ent



Rule out crim inal behavior.



Com plete physical and neurologic exam



Rule out m edical causes for m ental status change, com m only delirium or substance intoxication/withdrawal.

Tests 



Labs as indicated by history and physical: o

Electrolytes, blood urea nitrogen, creatinine, glucose

o

Liver function tests

o

CBC and differential

o

Toxicology screens and m edication levels

o

Urinalysis if infection suspected

Im aging: o

CT of head if injury or structural CNS pathology suspected

Differential Diagnosis

Pa ge 3 8 8



Intoxication or withdrawal



Delirium



Dem entia



Traum atic brain injury



Antisocial behavior

P.911

Treatment Pre Hospital Controversies/ethical considerations: 

Involuntary adm ission leads to loss of basic rights.



Parens patriae power: State's authority to care for citizen who cannot care for self



Police power: State's authority to detain citizen who is danger to self or som eone else

Initial Stabilization 

Initial containm ent by police



Transport patient to facility for psychiatric evaluation.



Ensure patient and staff safety

ED Treatment 

Restrain dangerous patients as needed: o

Nurse or security guard standing outside room

o

Physical restraints

o

Medications given PO, intram uscularly, or intravenously

o

Closely observe patients when using physical restraints or involuntary m edications.

Pa ge 3 8 8



Determ ine if patient requires psychiatric hospitalization.

Medication (Drugs) May be necessary for extrem ely agitated patient

Disposition Discharge Criteria Patients m ay be discharged after initial psychiatric evaluation if they: 

Can care for them selves adequately and



Have no intention of harm to self or others

References 1. Behnke SH, Hilliard JT. The Essentials of Massachusetts Mental Health Law. New York: WW Norton; 1998. 2. Folstein MF, Folstein FE, McHugh PR. The â€œm ini-m ental stateâ€ •: a practical m ethod for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189. 3. Gutheil TG, Appelbaum PS. Clinical Handbook of Psychiatry and the Law. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 2000. 4. LaFond JQ. Law and the delivery of involuntary m ental health services. Am J Orthopsychiatry. 1994;64:209â€“222. 5. Nickens HW. Assessm ent and m anagem ent of the violent patient. In: Dubin WR, Hom ke N, Nichory H, eds. Clinics in Em ergency Medicine: Psychiatric Em ergencies. Vol 4. Edinburgh, Scotland: Churchill Livingstone; 1984:101â€“111. 6. Schouten R. Psychiatry and the law I: inform ed consent, com petency, treatm ent refusal, and civil com m itm ent. In: Stern TA, Herm an JB, eds. Psychiatry Update and Board Preparation. New York: McGraw-Hill; 2000:415â€“419.

Codes

Pa ge 3 8 8

ICD9-CM V70.2 General psychiatric exam ination, other and unspecified

ICD10 Z00.4 General psychiatric exam ination

Pa ge 3 8 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psycho sis, Acute

Psychosis, Acute

Richard Wolfe Robert Vissers

Basics Description 

A severe m ental disorder characterized by derangem ent of personality and loss of contact with reality causing gross disorganization of a person's m ental capacity



The psychosis m ay be secondary to functional (psychiatric) or organic (m edical) causes.



Medical psychoses are generally secondary to system ic or neurologic diseases or neuroactive m edications.



Neurodevelopm ental abnorm alities in the dopam inergic and serotonergic system s are im plicated in functional psychosis.

Etiology Organic 

Autoim m une disease



CNS: o

Alzheim er disease

o

Cerebritis: 

Autoim m une disorders

Pa ge 3 8 9









o

Cerebrovascular accident

o

Encephalitis

o

Encephalopathy

o

Head injury

o

Huntington chorea

o

Migraine

o

Multiple sclerosis

o

Neoplasm s

o

Norm al pressure hydrocephalus

o

Parkinson disease

o

Seizure

Endocrine: o

Addison disease

o

Cushing disease

o

Thyroid dysfunction

o

Parathyroid dysfunction

o

Postpartum psychosis

o

Recurrent m enstrual psychosis

o

Sydenham chorea

Metabolic: o

Intoxication or withdrawal

o

Hypercarbia

o

Hypoglycem ia

o

Hypoxia

o

Porphyria

o

Electrolyte im balance

Nutritional deficiencies: o

Niacin

o

Thiam ine

o

Vitam in B 1 2 and folate

Organ failure: o

Hepatic encephalopathy

Pa ge 3 8 9

o

Renal failure

Pharmacologic 

Psychoactive agents



Benzodiazepines



Chlordiazepoxide



Antidepressants



Antiepileptics



Antibiotics:







o

Isoniazid

o

Rifam pin

Cardiovascular agents: o

Captopril

o

Digoxin

o

Methyldopa

o

Procainam ide

o

Propranolol

o

Reserpine

Drugs of abuse: o

Alcohol

o

Am phetam ines

o

Cocaine

o

Opioids

o

Hallucinogens

Other: o

Steroids

o

Heavy m etals

o

Antihistam ines

o

Cim etidine

o

Disulfiram

Functional 

Brief psychotic disorder:

Pa ge 3 8 9

o 

Usually secondary to acute em otional stress

Schizophreniform disorder: o

Sym ptom s present 1â€“6 m onths



Schizophrenia



Mood disorder with psychotic features or schizo-affective disorder

Diagnosis Signs and Symptoms 



Delusions are erroneous beliefs that: o

Involve a m isinterpretation of perceptions

o

Are clearly im plausible

o

Are often persecutory, religious, or som atic in nature

Hallucinations: o

Sensory experiences that exist only in the m ind of the patient

o

Can involve any sense; auditory and visual are m ost com m on.







Disorganized speech: o

Loose associations

o

Neologism s

o

Perseverations

o

Poverty of content

o

Word salad

Disorganized or catatonic behavior: o

Unable to perform goal-directed behavior

o

Unaware of the environm ent

Negative sym ptom s: o

Flattened affect

o

Poverty of speech

Pa ge 3 8 9

o

Avolition: 



Unable to m aintain goal-directed activities

Features suggesting an organic etiology: o

Sudden onset

o

>40 years old

o

Fluctuating course

o

Confusion

o

Headaches

o

Loss of consciousness

o

Focal neurologic sym ptom s

o

Speech difficulties

o

Abnorm al vital signs

o

Disorientation

o

Psychom otor retardation

o

Visual hallucinations

o

Global im pairm ent of attention and cognitive function

o

Delusions are disorganized.

o

Labile affect

o

Incoherent speech

o

Social im m odesty

Essential Workup 

The workup is case specific and prim arily based on the suspected etiology.



Functional and organic etiologies are generally distinguished by features of the history and physical exam ination described below.



Collateral history is im portant, as the patient history is often unreliable.



Com plete physical exam ination with particular attention to the neurologic exam ination, vital signs, and m ental status exam ination



Mental status exam ination:

Pa ge 3 8 9

o

Orientation

o

Mem ory (short- and long-term )

o

Attention (or calculation)

o

Recall

o

Language

o

Thoughts

o

Perception

o

Mood/Affect

o

Judgm ent

P.913

Tests Lab Laboratory evaluation is needed in patients at risk for an organic etiology: 

Routine â€œscreening labsâ€• not helpful



Specific studies should be guided by the suspected underlying etiologies.



Serum glucose



Toxicologic screen



Serum electrolytes



Urinalysis

Imaging Head CT scan indicated in patients at risk for a neurologic etiology

Diagnostic Procedures/Surgery Lum bar puncture indicated if signs and sym ptom s suggest delirium

Differential Diagnosis See Etiology

Pa ge 3 8 9

Treatment Pre Hospital 

Prevention of violent behavior m ust be established before transport.



Consider police backup to reduce risk of violence and to place restraints.

Controversies Chem ical restraints are rare in field protocols; m ay be an adjunct to physical restraints.

Initial Stabilization Prevention of violence: 

See Violence, Managem ent of

ED Treatment 

Antipsychotic agents are sym ptom specific and therefore useful in both organic or functional psychoses.



High potency, IV antipsychotics, such as haloperidol, are m ost com m only utilized in the ED setting.



Rapid tranquilization m ay be achieved with the addition of a benzodiazepine.



If a specific organic etiology is identified, therapy should be directed toward the treatm ent of the m edical condition.



Treatm ent of adverse effects from antipsychotic m edications: o

Extrapyram idal sym ptom s, dystonia, akathisia, pseudoparkinsonism , and tardive dyskinesia: 

o

Treat with diphenhydram ine or benztropine.

Neuroleptic m alignant syndrom e is a life-threatening com plication:

Pa ge 3 8 9



Characterized by hypertherm ia, m uscle rigidity, autonom ic instability, and altered consciousness



Treat with supportive m easures and dantrolene.



Droperidol has been reported to cause QT prolongation and dysrhythm ias.

Medication (Drugs) 

Antipsychotics: o

Droperidol: 2.5â€“5.0 m g IV or IM

o

Haloperidol: 2â€“5 m g IV or IM or PO; 0.5â€“2.0 m g for elderly

o 

Benzodiazepines o



Risperidone: 1â€“2 m g PO

Lorazepam 1.0â€“2.0 m g IV or IM or PO

Treatm ent of m edication side effects o

Benztropine: 2 m g IM or IV

o

Dantrolene: 1 m g/kg IV repeated to sym ptom resolution or total of 10 m g/kg

o

Diphenhydram ine: 50 m g IV, IM, or PO

Follow-Up Disposition Admission Criteria 

If the cause is determ ined to be m edical in origin, adm ission to the appropriate m edical service is indicated.



Acute psychosis of psychiatric etiology requires adm ission to a psychiatric service.



Safety of staff and patient m ust be m aintained in the

Pa ge 3 8 9

hospital after disposition from the ED, including possible chem ical and physical restraint or a one-on-one sitter. 

If the patient is felt to be a danger to either self or others, the patient cannot be discharged.



Involuntary com m itm ent is required if patient is uncooperative and a threat to self or others.

Discharge Criteria 

If the psychotic behavior was caused by a tem porary, reversible organic cause (e.g., drug intoxication) and the patient is now deem ed to be in control, com petent, and not a danger to self or others, the patient m ay be discharged.



Psychiatric consultation prior to discharge is recom m ended.

References 1. Battaglia J, Moss S, Rush J, et al. Haloperidol, lorazepam , or both for psychotic agitation? A m ulticenter, prospective, double-blind em ergency departm ent study. Am J Em erg. 1997;15:335â€“340. 2. Hutzler JC, Rund DA. Behavioral disorders: Em ergency assessm ent and stabilization. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency m edicine: a com prehensive study guide. 5th ed. New York, NY: McGraw-Hill, 2000. 3. Richards CF, Gurr DE. Psychosis. Em erg Med Clin North Am . 2000;18:253â€“262. 4. Lukens TW, Wolf SJ, Edlow JA, et al. Clinical policy: critical issues in the diagnosis and m anagem ent of the adult psychiatric patient in the em ergency departm ent. Ann Em erg Med. 2006;47(1):79â€“99.

Codes ICD9-CM 297

Pa ge 3 8 9

298 299

ICD10 F23.9

Pa ge 3 8 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psycho sis, M edical vs. Psychiatric

Psychosis,

Medical vs. Psychiatric Kathy Sanders

Basics Description 

Wide variety of m edical and neurological illnesses have psychosis as one of their presenting m anifestations or psychosis em erges during the course of the illness.



Difficult to determ ine whether m edical or psychiatric illness is the cause of psychotic behavior



Nature of im pairm ent determ ines whether a prim arily psychiatric disorder or a secondary psychosis based on a m edical, neurologic, or toxic etiology



Evaluation for underlying m edical or neurologic condition essential for patients with psychotic presentation without previous history of psychosis

Etiology 

Age factor: o

Late adolescence/early adulthood presentation m ore likely to be schizophrenia

o

Middle- to late-life presentation m ore likely to be m edical cause.

Pa ge 3 9 0



Etiology of the CNS im pairm ent that results in a psychotic presentation include: o

Neurological disorders

o

Metabolic conditions

o

Toxic or drug effects

o

Nonorganic or psychiatric

Diagnosis Signs and Symptoms 





Psychosis characterized by: o

Im paired reality testing

o

Inappropriate affect

o

Poor im pulse control

o

Regressive or inappropriate behavior

Hallucinations: o

Auditory

o

Visual

o

Olfactory

o

Tactile

Delusions: o

False beliefs held strongly by the patient even in the face of reasonable evidence to the contrary



Affective sym ptom s include m ania and catatonic states.



Focal and diffuse CNS im pairm ent result in derangem ents of:



o

Thinking

o

Com m unicating

o

Perceiving

Responding inappropriately

Pa ge 3 9 0

Essential Workup 

Careful history and physical exam ination



Laboratory investigation for new or previously undiagnosed psychosis



Use history and physical to guide workup.

Tests Lab 

CBC



Electrolytes, blood urea nitrogen/creatinine, glucose



Toxicology screen



Am m onium level



Urinalysis



Thyroid function tests

Imaging CT head

Diagnostic Procedures/Surgery Lum bar puncture/cerebrospinal fluid analysis

Differential Diagnosis 



Neurological: o

Head traum a

o

Space-occupying lesions

o

Cerebrovascular disease

o

Postanoxic encephalopathy

o

Seizure disorders

Degenerative diseases: o

Alzheim er

o

Pick

o

Huntington's

o

Parkinsonism

o

Hydrocephalus

Pa ge 3 9 0



CNS infections:



Viral



Herpetic



Nonherpetic (e.g., rabies, m um ps, influenza)



Cerebral m alaria



Syphilis



Toxoplasm osis



Trypanosom iasis



Schistosom iasis



Myelin diseases



Multiple sclerosis



Leukodystrophies



Marchiafava-Bignam i disease



Narcolepsy



Endocrine



Thyroid disorders



Parathyroid disorders



Diabetes m ellitus



Pituitary abnorm alities



Adrenal abnorm alities



Postpartum psychosis



Metabolic: o



Electrolyte im balance

End-organ failure: o

Respiratory cardiac

o

Renal

o

Hepatic

o

Pancreatic



Ketoacidosis



Porphyria



Wilson disease



Deficiency diseases:

Pa ge 3 9 0





o

Pernicious anem ia

o

Beriberi, Wernicke-Korsakoff syndrom e

o

Pellagra

o

Pyridoxine deficiency

System ic illnesses: o

Carcinom atosis

o

Infections, sepsis

Viral syndrom es: o

Hepatitis

o

Mononucleosis



Collagen and autoim m une disorders



Postoperative states:



o

Delirium

o

Psychosis

o

Depression

Intoxicants: o

Alcohol

o

Barbiturates



Stim ulants



Hallucinogens



Opiates



Heavy m etals



Brom ide



Organic phosphates



Anticholinergic com pounds



Carbon m onoxide



Industrial agents



Withdrawal states:



o

Alcohol withdrawal (delirium trem ens)

o

Barbiturate withdrawal

Medication side effects: o

Antipsychotics

Pa ge 3 9 0

o

Steroids

o

Sedative-hypnotics

o

Antidepressants

o

Lithium carbonate

o

Cim etidine

o

Disulfiram

o

Belladonna alkaloids

o

Levodopa

o

Anticonvulsants

o

Antituberculous drugs

o

Antiinflam m atory drugs

o

Antihypertensive agents

o

Cardiac drugs digitalis lidocaine propranolol procainam ide

o 

Idiosyncratic drug reaction of any m edication

Psychiatric: o

Schizophrenia

o

Manic-depressive illness

o

Stress reactions including posttraum atic stress disorder (PTSD)

o

Interm ittent explosive disorder

o

Im pulse control disorder

P.915

Treatment Initial Stabilization 

ABCs of psychiatric assessm ent: o

Safety

Pa ge 3 9 0



o

Evaluation

o

Managem ent

If uncooperative and dangerous, control behavior with neuroleptics or benzodiazepines.

ED Treatment 

Determ ine if a m edical cause for psychosis



Treat underlying m edical illness or substance abuse disorder



Psychiatric evaluation for true psychosis



Control psychotic behavior with psychotropic m edications: o

Treatm ent approach based on the severity of the psychotic features of the m edical or psychiatric illness

o

Severe behavioral disturbance of m edical psychosis requires sedating the patient to adequately attend to the m edical workup and treatm ent.

o

The m ore behaviorally unstable the patient, the m ore difficult it is to stabilize m edical derangem ents.



Haloperidol in com bination with lorazepam : o

Safest, fastest, and least disruptive of the ongoing m ental exam ination of the patient

o

Effectively calm s and sedates the behaviorally agitated, psychotic, m edical patient

o

Atypical neuroleptics (olanzapine, risperidone, ziprasidone): 

Targets the lim bic dopam ine neuroreceptors



Im proves both positive and negative sym ptom s of schizophrenia



Few extrapyram idal side effects



Better tolerated than typical neuroleptics



Sedation, weight gain



Olanzapine and ziprasidone can be given

Pa ge 3 9 0

parenterally 

Olanzapine zydus and risperidone m -tab are a dissolving wafer preparation

Medication (Drugs) 



Neuroleptics. o

Haloperidol: 2.5â€“10 m g IM or IV

o

Atypical neuroleptics used in em ergency: 

olanzapine 5â€“10 m g PO or Zydis or IM



risperidone 1â€“2 m g PO or Zydis



ziprasidone 10â€“20 m g IM

Benzodiazepines: o

Diazepam : 5â€“10 m g IV

o

Lorazepam : 0.5â€“2 m g IV or IM

o

Midazolam : 1â€“5 m g IV

Follow-Up Disposition Admission Criteria 

Psychosis prim arily psychiatric (i.e., schizophrenia/m anic depressive)



Adm ission sam e as for involuntary com m itm ent: o

Suicidal/hom icidal behavior

o

Inability to care for self

o

Deranged thought pattern that can be threat to self or others



Psychosis prim arily m edical etiology



Adm ission dictated by specific m edical condition and

Pa ge 3 9 0

behavior

Discharge Criteria 

Stable m edical condition



Not suicidal/hom icidal



Able to care for self



Capable of m aking m edical decisions

Issues for Referral 

Patient's insurance coverage determ ines inpatient psychiatric disposition options.



Case m anagem ent or social services are necessary for psychiatric disposition.

References 1. Cum m ings JL. Secondary psychoses, delusions, and schizophrenia. In: Cum m ings JL, ed. Clinical neuropsychiatry. Orlando, FL: Grune & Stratton, 1985:163â€“182. 2. Goff D, Freudenreich O, Henderson DC. Psychotic patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. St. Louis: Mosby, 2004:155â€“174. 3. Sanders KM. Aggressive and im pulsive patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. St. Louis: Mosby, 2004: 501â€“512.

Codes ICD9-CM 289.9

ICD10 F29

Pa ge 3 9 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pulm o nary C o ntusio n

Pulmonary

Contusion Gregory W. Lampe

Basics Description Transfer of kinetic energy to the lung parenchym a adjacent to traum atic injury: 

Causes disruption of the alveolocapillary m em brane



Developm ent of pulm onary contusion



Microhem orrhage, localized pulm onary edem a, and extravasation of blood into the interstitial and alveolar spaces: o

Arteriovenous shunting

o

Ventilation-perfusion m ism atch

o

Decreased lung com pliance

o

Hypoxem ia

o

Respiratory failure

Etiology 

Blunt or penetrating thoracic traum a



Sudden deceleration



Fall from height



Motor vehicle accident

Pa ge 3 9 0



Assault



Missile

Pediatric Considerations Relatively m ore elastic chest wall m ay transm it greater force to the thoracic contents in children.

Diagnosis Signs and Symptoms History 

Blunt or penetrating thoracic traum a by any m echanism



Mechanism as described by patient, parent or prehospital personnel: o

Seat belt usage

o

Steering wheel dam age

o

Air bag deploym ent



Pleuritic chest pain



Dyspnea



Hem optysis

Physical Exam 



Auscultation: o

Initially norm al or dim inished breath sounds

o

Progresses to wet rales, absent breath sounds

Localized ecchym osis, edem a, erythem a and tenderness of chest wall



Bony stepoffs, crepitus, point tenderness associated with rib fractures



Ecchym osis from seat belt, aka â€œseat belt signâ€•



Ecchym osis from steering wheel im pact



Splinting respirations

Pa ge 3 9 1



Cyanosis, tachycardia, hypotension



Dyspnea, tachypnea

Alert Insidious onset increasing 6â€“12 hours post injury

Essential Workup Chest radiograph: 

Radiographic findings m ay not appear until 6â€“12 hours post injury.



Patchy alveolar infiltrates to frank consolidation.



Associated intrathoracic injury: o

Rib fractures

o

Pneum othorax, hem othorax

o

Widened m ediastinal silhouette

Tests Lab Arterial blood gas m ay reveal hypoxem ia and elevated alveolar-arterial gradient.

Imaging Thoracic CT is useful in detecting pulm onary injury and associated intrathoracic injuries not identified on chest radiograph.

Differential Diagnosis 

Adult respiratory distress syndrom e



Pulm onary laceration, infarction or em bolism



Congestive heart failure



Pneum onia, abscess or other infectious process



Noncardiogenic causes of pulm onary edem a

P.917

Pa ge 3 9 1

Treatment Pre Hospital Thoracic traum a with significant m echanism or pre-existing pulm onary disease should be routed to the nearest available traum a center.

Initial Stabilization 

Manage airway and resuscitate as indicated.



IV line, O 2 , continuous cardiac m onitoring and pulse oxim etry



Control airway: o

Endotracheal intubation indications: 

Severe hypoxem ia (PaO 2 <60 m m Hg on room air, <80 m m Hg on O 2 )

o



Significant underlying lung disease



Im pending respiratory failure

Early intubation and institution of positive end expiratory pressure: 

Correct hypoxem ia and acidosis



Decrease the work of breathing

ED Treatment 

Maintain adequate oxygenation and ventilation.



Monitor O 2 saturation and respiratory rate.



In conscious and alert patient, O 2 adm inistration via face m ask is first-line therapy.



If patient cannot m aintain a PaO 2 >80 m m Hg on high-flow oxygen: o

Continuous positive airway pressure via m ask

o

Nasal bilevel positive airway pressure (BiPAP)

Pa ge 3 9 1



If adequate oxygenation cannot be m aintained with face m ask: o

Continuous positive airway pressure

o

BiPAP

o

Early endotracheal intubation and m echanical ventilation

Alert 

Avoid overhydration: o

IV crystalloid adm inistration needed for resuscitation m ust be balanced with the risk of increasing interstitial pulm onary edem a

o

Frequent re-exam ination and serial chest radiographs are required to m onitor alveolar fluid accum ulation.

Medication (Drugs) 

Steroids have no proven benefit.



Prophylactic antibiotics are not indicated.

Follow-Up Disposition Admission Criteria Patients with pulm onary contusion m ust be adm itted to the hospital for observation in anticipation of delayed-onset respiratory com prom ise.

Discharge Criteria 

Patients with m inim al chest traum a



No evidence of respiratory distress or hypoxem ia:

Pa ge 3 9 1



o

Norm al respiratory rate

o

Pulse oxim etry

o

Chest radiograph

Strict return criteria should be discussed with the patient prior to discharge: o

Shortness of breath

o

Increased pain

o

Inadequate pain control

o

Fever

o

Cough

References 1. Perl M, Gebhard F, Bruckner UB, Ayala A, Braum uller S, Buttner C, Kinzl L, Knoferl MW. Pulm onary contusion causes im pairm ent of m acrophage and lym phocytic im m une functions and increases m ortality associated with a subsequent septic challenge. Crit Care Med. 2005 Jun;33(6):1351â€“1358. 2. Schm ittenbecher P. Lung contusion-lacerations after blunt thoracic traum a in children. J Pediatr Surg. 2005 May;40(5):892. 3. Wanek S, Mayberry JC. Blunt thoracic traum a: flail chest, pulm onary contusion, and blast injury. Crit Care Clin. 2004 Jan;20(1):71â€“81. 4. Eckstein M, Henderson S. Thoracic traum a. In: Marx J, Hockberger R, Walls R, eds. Rosen's Em ergency m edicine: concepts and clinical practice. 6th ed. St. Louis: CV Mosby, 2005, in press.

Pa ge 3 9 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pulm o nary Edem a

Pulmonary Edema

Shamai Grossman Seric Cusick

Basics Description 

Im balance in Starling forces causes an increase in lung fluid secondary to leakage from pulm onary capillaries into the interstitium and alveoli of the lung.



If capacity of lym phatic drainage is exceeded, liquid accum ulates in interstitial spaces surrounding bronchioles and lung vasculature, creating congestive heart failure (CHF).



If increased fluid and pressure tracks into the interstitial space around the alveoli and disrupts the alveolar m em brane, the alveoli are flooded causing pulm onary edem a.



Systolic dysfunction is characterized by a dilated left ventricle with im paired contractility.



Diastolic dysfunction occurs in a norm al or intact left ventricle with im paired ability to relax and receive as well as eject blood.



New York Heart Association classification of CHF: o

Class I: not lim ited in norm al physical activity by

Pa ge 3 9 1

sym ptom s o

Class II: ordinary physical activity results in fatigue, dyspnea, or other sym ptom s



o

Class III: m arked lim itation in norm al activity

o

Class IV: sym ptom s at rest or with any activity

Epidem iology: o

400,000 new cases present yearly.

o

Prevalence is 1â€“2% of the general population.

o

Incidence is greater in m ales than in fem ales for patients aged 40â€“75 years.

o

No sex predilection exists for patients older than 75 years.

o

Incidence of CHF increases with increasing age and affects 10% of population older than 75.

o

30â€“40% of patients with CHF are hospitalized every year.

o

Five-year m ortality after diagnosis was reported as 60% in m en and 45% in wom en.

o

Median survival of 3.2 years for m ales and 5.4 years for fem ales

o

Sudden death accounts for up to 45% of all deaths.

o

In-hospital m ortality rate: 19%

o

African Am ericans are 1.5 tim es m ore likely to die of CHF than whites.

o

Mortality approxim ately 50â€“60% for noncardiogenic pulm onary edem a and up to 80% for cardiogenic shock

Etiology 

Six categories: o

Pulm onary edem a secondary to altered capillary perm eability

o

Pulm onary edem a secondary to increased pulm onary

Pa ge 3 9 1

capillary pressure: pulm onary venous throm bosis, stenosis or veno-occlusive disease, and volum e overload o

Pulm onary edem a secondary to decreased oncotic pressure found with hypoalbum inem ia

o

Pulm onary edem a secondary to large negative pleural pressure with increased end expiratory volum e

o

Pulm onary edem a secondary to lym phatic insufficiency

o

Pulm onary edem a secondary to m ixed or unknown m echanism s



Specific etiologies: o

Cardiogenic/altered capillary perm eability: 

Left heart failure



Ischem ic heart disease



Acute m yocardial infarction



Aortic and m itral valvular disease



Hypertensive heart disease



Cardiom yopathy



Volum e overload



Arrhythm ias



Endocarditis



Myocarditis



Congenital heart disease



Acute rheum atic fever and rheum atic heart disease

 o

o

Septal defects

High cardiac output states: 

Thyrotoxicosis



Beriberi

Urem ia

Pa ge 3 9 1



Respiratory/adult respiratory distress syndrom e/altered capillary perm eability:









o

Pneum onia

o

Inhaled toxins

o

Circulating foreign substances

o

Snake venom

o

Endotoxins

o

Aspiration

o

Acute radiation pneum onitis

o

Dissem inated intravascular coagulation

o

Hypersensitivity pneum onitis

o

Shock lung in association with nonthoracic traum a

o

Acute hem orrhagic pancreatitis

o

Near drowning

Hypoalbum inem ia/decreased oncotic pressure: o

Renal failure

o

Hepatic failure

o

Protein-losing enteropathic

o

Severe derm atologic disease with high protein losses

o

Starvation

Increased negativity of interstitial pressure: o

Rapid decom pression of a pneum othorax

o

Asthm a

Lym phatic obstruction: o

Postâ€“lung transplant

o

Lym phangitic carcinom atosis

o

Fibrosing lym phangitis

Mixed or unknown m echanism : o

High-altitude pulm onary edem a

o

Neurogenic pulm onary edem a

o

Narcotic overdose

o

Pulm onary em bolism

Pa ge 3 9 1

o

Eclam psia

o

Postcardioversion

o

Postanesthesia

o

Postâ€“cardiopulm onary bypass

o

Postextubation

Diagnosis Signs and Symptoms History 



General: o

Weakness

o

Fatigue

o

Anxiety

Respiratory: o

Dyspnea with exertion is the single m ost sensitive test.



o

Dyspnea at rest is also com m on.

o

Orthopnea, paroxysm al nocturnal dyspnea

o

Cough

o

Pink, frothy sputum

o

Noisy respirations

Cardiovascular: o

Nocturnal angina

o

Presence of valvular heart disease

Physical Exam 



General: o

Diaphoresis

o

Cold, ashen, or cyanotic skin

Respiratory:

Pa ge 3 9 1

o

Tachypnea

o

Wheezing, rhonchi, gurgles

o

Moist, crepitant rales noted initially at bases and progressing to apices

o

Dilated alae nasi

o

Inspiratory retraction of the intercostal spaces or supraventricular fossae

o 

Cheyne-Stokes respirations

Cardiovascular: o

Tachycardia

o

Jugular venous distention

o

Abnorm al heart sounds

o

Increased P 2 , S 3 , S 4

o

Pulsus alternansâ€”alternating weak and strong pulses

Essential Workup A careful history and physical should determ ine if the underlying etiology is cardiogenic.

Tests Lab 

B-type natriuretic peptide (BNP): o

A proteohorm one secreted by the left ventricle in response to wall tension

o

Laboratory param eter for the detection and follow-up of heart failure: 

<100 pg/m Lâ€”CHF unlikely to be cause of acute dyspnea

o



100â€“500 pg/m Lâ€”m ay be CHF



>500 pg/m Lâ€”m ost consistent with CHF

BNP is available for point of care testing with 10- to 15-m inute turnaround tim e.

Pa ge 3 9 2

o

May be helpful in determ ining whether dyspnea is secondary to chronic obstructive pulm onary disease or CHF



N-term inal pro-BNP: o

B-natriuretic peptide precursor

o

Can be used concom itantly with Nesiritide

P.919



Serum electrolytes, blood urea nitrogen, creatinine, urinalysis o

Hyperkalem ia with severe low output states

o

Increased creatinine and dilutional hyponatrem ia are observed in severe cases.

o

Mild azotem ia and proteinuria are observed in early and m ild-to-m oderate disease.



Elevated alanine am inotransferase, aspartate am inotransferase, or bilirubin suggests congestive hepatopathy



Cardiac enzym es m ay be useful if ischem ia or infarction is presum ed to be the underlying cause.



Serum lipase if pancreatitis is suspected as the underlying cause



Arterial blood gas m ay help evaluate hypoxem ia, ventilation/perfusion m ism atch, hypercapnia, and acidosis.

Imaging 

Chest radiograph: o

Three phases of pulm onary findings

o

Pulm onary redistribution: 

o

Cephalization of vessels

Interstitial edem a: 

Effusions

Pa ge 3 9 2

o



Kerley B lines



Classic butterfly infiltrate

Frank alveolar infiltrates: 

May be asym m etric and m istaken for pneum onia



ECG: o



Assess for underlying cardiac disorders.

Echocardiography: o

Excludes acute valvular pathology

o

Assessm ent for focal or global left ventricle dysfunction

o

Measurem ent of cardiac output

Differential Diagnosis 

Pneum onia



Asthm a



COPD exacerbation



Pulm onary em bolism



Hyperventilation syndrom e



Pericardial tam ponade



Pneum othorax



Pleural effusion

Treatment Pre Hospital 

IV access



Supplem ental oxygen



100% nonrebreather m ask



Cardiac m onitor



Pulse oxim etry

Pa ge 3 9 2



Sublingual nitrates



Furosem ide



Endotracheal intubation m ay be required in severe cases

Initial Stabilization 

IV access



Supplem ental oxygen



Place patient in an upright position.



Cardiac m onitor



Pulse oxim etry



Control airway as needed



Noninvasive ventilation or endotracheal intubation for im pending respiratory failure

ED Treatment 

Norm otensive or hypertensive patients with cardiogenic pulm onary edem a: o

Rapid-acting nitrates preferably sublingual or Nitrospray

o

IV nitroglycerin

o

Morphine sulfate

o

IV diuretics: 

o

Lasix or Bum ex

IV BNP (Nesiritide) is a balanced vasodilator with no inotropic or chronotropic properties. 

Com pared to dobutam ine, BNP is not proarrhythm ic and has no effect on heart rate and is particularly useful in patients already taking nitrates, as tolerance to Nesritide has not been described.

o

Sodium nitroprusside for afterload reduction can be helpful for severe persistent hypertension but is not recom m ended if cardiac ischem ia m ay be concurrent.

Pa ge 3 9 2

o

Noninvasive ventilatory support: continuous or bilevel positive airway pressure (CPAP or Bi-PAP) m ay decrease the need for intubation, although Bi-PAP m ay be associated with a higher incidence of acute m yocardial infarction.

o

Endotracheal intubation for im pending respiratory failure





Hypotensive patients: o

Avoid nitrates, m orphine, and diuretics

o

Use agents that increase m yocardial contractility: 

Dopam ine



Dobutam ine



Am rinone



Milrinone

Renal dialysis patients: o

Em ergent renal dialysis is the treatm ent of choice.

o

If rapid dialysis cannot be rapidly achieved: 

IV nitroglycerin



IV enalapril or oral captopril m ay be useful

Medication (Drugs) 

Bum ex: 0.5â€“1 m g IV



Captopril: 25â€“50 m g PO t.i.d.



Dobutam ine: begin at 2 m cg/kg/m in IV; titrate to BP, cardiac output, and pulm onary capillary wedge pressure



Enalapril: 1.25 m g IV q6h over 5 m inutes



Furosem ide: 20â€“80 m g IV



Morphine sulfate: 2â€“5 m g IV



Nesiritide: IV bolus of 2 m cg/kg followed by a continuous infusion of 0.01 m cg/kg/m in



Nitroglycerin:

Pa ge 3 9 2

o

Sublingual or Nitrospray: 0.4 m g m ay give repeatedly as SBP tolerates q5m in

o

Paste: 1â€“2 inches

o

IV infusion: begins at 5 m cg/m in and increases by 5â€“10 m cg/m in every few m inutes; titrate to BP



Nitroprusside: begin drip at 10 m cg/m in and increasing by 5â€“10 m cg/m in every few m inutes

Follow-Up Disposition Admission Criteria 





Intensive care unit: o

Intubated patients

o

Patients on Bi-PAP

o

Adult respiratory distress syndrom e

Monitored unit: o

New-onset pulm onary edem a

o

Electrocardiographic changes

Observation: o

Known CHF with m ild to m oderate disease

Discharge Criteria 

Patients with known CHF presenting with m ild pulm onary edem a no concom itant com plaints suggestive of ischem ia: o

Com plete resolution of sym ptom s after ED m anagem ent

o

Norm al oxygenation on room air at the tim e of discharge

o 

No new electrocardiographic changes

Follow-up arranged within the next 48 hours

Pa ge 3 9 2



Low-salt diet



Serial weights to assess fluid accum ulation

References 1. Braunwald E. Pulm onary edem a. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders, 2001:503â€“614. 2. Evaluation and m anagem ent of chronic heart failure in the adult: ACC/AHA practice guidelines. J Am Coll Cardiol. 2001;38:2101â€“2113. 3. Ketai LH, Godwin JD. A new view of pulm onary edem a and acute respiratory distress syndrom e. J Thorac Im aging. 1998;13:147â€“171. 4. McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgm ent in em ergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002 Jul 23;106(4):416â€“422. 5. Pang D, Keenan SP, Cook DJ, et al. The effect of positive pressure airway support on m ortality and the need for intubation in cardiogenic pulm onary edem a. A system atic review. Chest. 1998;114:1186â€“1192. 6. Wright SP, Doughty RN, Pearl A, et al: Plasm a am ino-term inal pro-brain natriuretic peptide and accuracy of heart-failure diagnosis in prim ary care: a random ized, controlled trial. J Am Coll Cardiol. Nov 19,2003;42(10):1793â€“1800.

Miscellaneous SEE ALSO: Congestive Heart Failure

Codes ICD9-CM

Pa ge 3 9 2

518.4

ICD10 J81

Pa ge 3 9 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pulm o nary Em bo lism

Pulmonary

Embolism Alan M. Kumar

Basics Description 

The m ajority of cases arise from throm bi in the deep veins of the lower extrem ities and pelvis.



Throm bi also originate in renal and upper extrem ity veins.



After traveling to lungs, size of throm bus determ ines signs and sym ptom s.

Etiology 

Most with pulm onary em bolism (PE) have identifiable risk factor: o

Recent surgery

o

Pregnancy

o

Previous deep vein throm bosis (DVT)/PE

o

Stroke or recent paraplegia

o

Malignancy

o

Age >50 years

o

Obesity

o

Sm oking

o

Oral contraceptives

Pa ge 3 9 2

o

Major traum a

o

Hem atologic risk factors: 

Factor 5 Leiden



Protein C or S deficiency



Antithrom bin III deficiency



Antiphospholipid antibody syndrom e



Lupus Anticoagulant

Pediatric Considerations 

Throm boem bolic disease is quite rare.



Risk factors in children: o

Presence of central venous catheter

o

Im m obility

o

Heart disease

o

Traum a

o

Malignancy

o

Surgery

o

Infection

Diagnosis Signs and Symptoms 





Most com m on: o

Dyspnea

o

Pleuritic chest pain

o

Tachypnea

General: o

Fevers (rarely >102.0Â°F)

o

Diaphoresis

Pulm onary: o

Cough

Pa ge 3 9 2





o

Hem optysis (rarely m assive)

o

Rales

Cardiovascular: o

Tachycardia

o

Syncope

o

Murm ur

Extrem ities: o

Cyanosis

o

Evidence of throm bophlebitis

o

Lower extrem ity edem a



Abdom inal pain



Sym ptom s sim ilar in elderly but typically m ore subtle if age <40 years

Essential Workup 

Chest radiograph: o

Used to rule out other causes

o

Most com m on findings with PE:

o





Norm al



Nonspecific parenchym al abnorm ality



Atelectasis

Other findings with PE: 

Pleural effusions



Pleural-based opacities (Ham pton hum p)



Elevated hem idiaphragm



Local oligem ia (Westerm ark sign)

ECG: o

To rule out cardiac etiology

o

Usually norm al in PE

o

Other findings include: 

Nonspecific ST-T wave changes (m ost com m on abnorm ality)



Sinus tachycardia

Pa ge 3 9 3



Left axis deviation



Right bundle branch block pattern



S1Q3T3 pattern is uncom m on and not specific enough to rule in/out diagnosis.

Tests Lab 

Arterial blood gas: o

Can show hypoxem ia, hypocapnia, respiratory alkalosis, or elevated A-a gradient



o

PE still possible with norm al A-a gradient

o

Does not aid in diagnosis of PE

CBC: o



Anem ia m ay be contributing factor to dyspnea.

D-dim er enzym e-linked im m unosorbent assay: o

D-dim ers are detectable at levels greater than 500 ng/m L in nearly all patients with PE

o

High sensitivity (close to 100%) with low specificity for PE

o

Of little help as alm ost always elevated in patients with: 

Malignancy



Surgery within three m onths

Imaging 

Ventilation-perfusion scan (V/Q): o

Results reported in probabilities and correlated to clinical suspicion

o

Probability of PE with V/Q results: 

Norm al or near norm al V/Q scan: 4% probability for PE



Low probability V/Q scan with low clinical suspicion: 4% probability for PE

Pa ge 3 9 3



Low probability V/Q scan with high clinical suspicion: 16â€“40% probability for PE



Interm ediate V/Q scan: 16â€“66% probability for PE



High probability V/Q scan with low clinical suspicion: 56% probability for PE



High probability V/Q scan with high clinical suspicion: 96% probability for PE



Spiral chest CT with IV contrast: o

Accurate for identifying PE in proxim al pulm onary tree

o

Will not pick up subsegm ental PE

o

In patients with concordant clinical assessm ent, offers high positive and negative predictive value



Lower-extrem ity duplex ultrasound: o

Used in patients who would otherwise require pulm onary angiogram

o 



Presence of DVT requires sam e anticoagulation as PE.

Pulm onary angiogram : o

Gold standard for diagnosis

o

Used when diagnosis not confirm ed or excluded

o

Higher com plication rate than other m odalities

Echocardiogram : o

Used to assess for right heart strain when throm bolysis is a possibility

P.921

Differential Diagnosis 

Pneum onia



Cardiac dysrhythm ias



Asthm a

Pa ge 3 9 3



Pneum othorax



Aortic dissection



Pericarditis



Myocardial infarction



Rib fracture



Costochondritis



Anxiety disorder

Treatment Pre Hospital 

Initial supplem ental oxygen



Establish IV access



Cardiac m onitor

Initial Stabilization 

ABCs



Provide supplem ental oxygen to m aintain adequate oxygen saturation.



Intubate if unable to provide adequate oxygenation.



Adm inister IV fluids carefully for hypotensive patients: o

Excessive fluid expansion m ay worsen right heart failure.

ED Treatment 



Anticoagulation: o

Prevents additional throm bus from form ing

o

Stabilizes existent clot to prevent m igration

Unfractionated heparin: o

Dose-titration fraught with difficulty leading to inadequate therapy

o

Goal to m aintain partial throm boplastin tim e test

Pa ge 3 9 3

between 1.5 and 2.5 tim es the control value (60â€“80 seconds) 

Low m olecular weight heparin: o

As least as effective as unfractionated heparin in m ultiple prospective random ized trials

o

Therapeutic goal autom atic with weight-based dosing

o

Easier adm inistration and m onitoring than heparin with som e cost benefit





Warfarin: o

Oral therapy for long-term anticoagulation

o

Goal is international norm alized ratio of 2â€“3

Throm bolysis: o

Initiate in hem odynam ically unstable patients with confirm ed PE.

o

Consider in stable patients with PE and right heart strain/failure on echo.



Inferior vena cava filter: o

Indicated in patients who have contraindications to anticoagulation or have been therapeutic on anticoagulation but failed prevention of PE.



Surgical or catheter em bolectom y: o

Consider in those with throm bolysis contraindications or failure, or deem ed unstable for m edical m anagem ent.

o

Case-by-case basis

Medication (Drugs) 

Alteplase: 100 m g (peds: N/A) IV over 2 hours



Enoxaparin: 1 m g/kg (peds: 0.75 m g/kg) SC q12h



Reteplase: 10 U (peds: N/A) IV bolus q30m in Ã— 2



Streptokinase: 250,000 U (peds: 3,500â€“4,000 U/kg) IV

Pa ge 3 9 3

bolus over 30 m inutes, then 100,000 U (peds: 1,000â€“1,500 U/kg) IV m aintenance over 24 hours 



Unfractionated heparin: o

Bolus: 80 U/kg (peds: 75 U/kg) IV over 10 m inutes

o

Maintenance: 18 U/kg (peds: 20 U/kg) IV drip

Warfarin: 5 m g (peds: 0.05â€“0.34 m g/kg/d) PO per day adjust for INR goal 2â€“3

Follow-Up Disposition Admission Criteria 

Adm it all patients with PE for continued treatm ent.



Clinically stable patients with a high suspicion for PE, no contraindication to anticoagulation, and a lack of V/Q scanning or angiographic availability m ay be anticoagulated and studied when resources are available in the m orning.

References 1. Edlow JA.Brown J, eds.Em ergency departm ent m anagem ent of pulm onary em bolism . Em erg Med Clin North Am . 2001;19:995â€“1011. 2. Goldhaber SZ. Pulm onary em bolism . N Engl J Med. 1999;339:93â€“104. 3. Hull, RD, Raskob, GE, Rosenbloo, D et al. Treatment of proxim al vein throm bosis with subcutaneous low-m olecular-weight heparin vs intravenous heparin. An econom ic perspective. Arch Intern Med. 1997;157:289. 4. PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulm onary em bolism . JAMA. 1990;263:2753â€“2759.

Pa ge 3 9 3

5. Quinlan DJ, McQuillan, A, Eikelboom , JW. Low-m olecular-weight heparin com apred with intravenous unfractionated heparin for treatm ent of pulm onary em bolism : a m eta-analysis of random ized, controlled trials. Ann Intern Med. 2004;140:175. 6. Stein P, Fowler S, et al. Multidetector com puted tom ography for acute pulm onary em bolism . N Eng J Med 2006;354:2317â€“2327.

Codes ICD9-CM 415.1

ICD10 I26

Pa ge 3 9 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Purpura

Purpura

Richard Wolfe

Basics Description 

Skin lesions caused by extravasation of blood into the skin or subcutaneous tissue



Increased fragility of capillaries or derm al support



The resultant lesions do not blanch com pletely with pressure (as seen when pressing down through a glass slide).





Nom enclature varies by the size of the lesions: o

Petechiae (<2 m m )

o

Purpuric lesions (2â€“10 m m )

o

Ecchym oses (>10 m m )

Color determ ined by depth and tim e of onset: o

Red if superficial and of recent onset

o

Purple if deep

o

Deep purple, brown, orange, or blue-green with later presentations



Nonpalpable purpura: o

Sim ple hem orrhage or m icrovascular occlusion with ischem ic hem orrhage

o

Generally due to platelet disorder

Pa ge 3 9 3



Palpable purpura: o

Generally due to vasculitis

o

Vasculitic lesions m ay not be palpable in im m unocom prom ised patients

Etiology 



Platelet disorder: o

Dim inished production

o

Altered distribution

o

Increased destruction

o

Abnorm al function

Vasculitis: o

Autoim m une, sm all-vessel leukocytoclastic vasculitis

o

Hypersensitivity to various antigens

o

Form ation of circulating im m une com plexes deposited in walls of postcapillary venules, activate com plem ent that is chem otactic for polym orphonuclear leukocytes

o

Released enzym es dam age vessel walls and cause leakage of blood.

Essential Workup Obtain a com plete m edical history: 

Previous bleeding problem s



Deep venous throm bosis/pulm onary em bolism suggesting factor V Leiden m utation



Splenectom y



Alcohol abuse



Fam ily history of bleeding disorders



High-risk m edications

Tests Lab

Pa ge 3 9 3



Platelet count: Abnorm al counts m ust be verified by m anual exam ination of a peripheral sm ear.



Dissem inated intravascular coagulation (DIC) screen: indicated when patient appears toxic



Prothrom bin tim e/partial throm boplastin tim e



Rapid strep test



Urinalysis



Studies for outpatient m anagem ent o

Bleeding tim e

o

Hepatitis B and C serologies

o

Strep throat culture or antistreptolysin O titer

o

Antinuclear antibodies

o

Cryoglobulins

o

Platelet function studies

o

Serum com plem ents

o

Serum protein electrophoresis

o

von Willebrand disease screen

Differential Diagnosis 

Nonpalpable purpura: o

o

Viral: 

Echovirus



Coxsackie



Measles



Parvovirus B19

Drugs: 

Acetam inophen



Allopurinol



Anticoagulants



Aspirin



Digoxin



Furosem ide



Gold salts

Pa ge 3 9 3

o



Lidocaine



Methyldopa



Penicillin



Phenylbutazone



Quinidine



Quinine



Rifam pin



Steroids



Sulfonam ides



Thiazides

Nutritional deficiencies: 

Vitam in K deficiency



Scurvy

o

Bone m arrow disease

o

Hypersplenism

o

Idiopathic throm bocytopenic purpura (ITP)

o

DIC

o

Throm botic throm bocytopenic purpura

o

Liver or renal insufficiency

o

Throm bocytosis (>1,000,000 plt/cc Spiking elevations of intravascular pressure (childbirth, vom iting, paroxysm al coughing)



o

Hem ophilia

o

Solar purpura (lim ited to sun-exposed areas)

Palpable purpura: o

Viral: 

Echovirus type 9



Coxsackie



Hepatitis B

o

Streptococcal pharyngitis

o

Drugs: 

Allopurinol

Pa ge 3 9 4



Aspirin



Anti-influenza vaccines



Cephalosporins



Gold



Hydralazine



Iodides



Metoclopram ide



Nonsteroidal anti-inflam m atory drugs



Penicillin



Phenylbutazone



Phenytoin



Quinidine



Quinine



Streptom ycin



Sulfonam ides



Thiazides



Ticlopidine

o

Malignancies

o

Autoim m une and connective tissue diseases

o

Gonococcus

o

Meningococcus

o

Pseudom onas (ecthym a gangrenosum )

o

Rocky Mountain spotted fever

o

In im m unocom prom ised hosts: Candida, Aspergillus

o

Occlusion due to organism s living in vessels, generally in im m unocom prom ised patients (m ucorm ycosis, aspergillus, dissem inated strongyloidiasis)

o

Occlusion due to m icrovascular platelet plugs (heparin necrosis)

o

Cold-related gelling or agglutinations (cryoglobulinem ia)

Pa ge 3 9 4

o

Local or system ic coagulation abnorm alities: scarlet fever (rarely â€œstrep throatâ€•), Vibrio vulnificus bacterem ia, â€œm alignant chickenpox,â€• and â€œblack m easlesâ€• (both rare in United States); Coum adin necrosis

o

Em bolization: cholesterol, crystal, throm bus (atrial m yxom a, septic endocarditis, m ultiple m yelom a)

Pediatric Considerations 

Henoch-SchÃ¶nlein purpura



Kawasaki disease



Neonatal: o

Extram edullary erythropoiesis (blueberry m uffin baby)

o

Purpura fulm inans (protein C and S deficiency)

o

Maternal ITP

o

Wiskott-Aldrich syndrom e

P.923

Diagnosis Signs and Symptoms 

Palpable or nonpalpable nonblanching lesions from 0.2â€“1 cm in diam eter: o

Irregular when caused by infectious em boli

o

Regular lesions with leukocytoclastic em boli

o

Massive bleeding from a platelet disorder m ay cause palpable hem atom as



Shape and size:

Pa ge 3 9 4



o

Petechiae (<2 m m )

o

Macular (2â€“10 m m )

o

Ecchym oses (>10 m m )

o

Annular or erythem a m ultiform e (target lesions)

o

Irregular (retiform )

Distribution: o

Generally m ore frequent in lower extrem ities (increased hydrostatic force)

o

Widespread petechiae and ecchym oses seen with dissem inated intravascular coagulation and m eningococcem ia

o

When oral m ucous m em branes involved, consider idiopathic throm bocytopenic purpura.



Hypotension



Altered m ental status



Gingival hem orrhage



Epistaxis



Hem aturia



Fever



Malaise



Arthralgias



Myalgias



Purpura fulm inans:





o

Large, irregular ecchym oses

o

Fever

o

Shock

o

DIC

Pseudom onas (ecthym a gangrenosum ) o

Begins as edem atous, erythem atous papules

o

Bullae form ation in girdle region

Dissem inated gonococcal infection: o

Usually <10 lesions, purpuric papules or

Pa ge 3 9 4

vesicopustules on the extensor surface of hands, dorsal aspect of ankles and toes



o

Fever

o

Arthralgias

Meningococcem ia: o

Sm all areas of skin infarction cause purpura in irregular pattern

o

May involve head, palm s, soles, m ucous m em branes including conjunctivae



o

Fever

o

Headache

Rocky Mountain spotted fever: o

After 4â€“7 days of generalized sym ptom s, erythem atous m acules on distal extrem ities including palm s and soles, then petechial



o

Fever

o

Chills

o

Headache

Henoch-SchÃ¶nlein purpura: o

Appears on extensor aspects of lower extrem ities and buttocks



o

Fades in about 5 days

o

Fever

o

Arthralgias

o

Abdom inal pain

o

Hem aturia

Kawasaki disease: o

Purpura is rare.

Fever, plus four of the following: polym orphous exanthem a, peripheral extrem ity changes, bilateral conjunctivitis, changes of lips and m outh, cervical lym phadenopathy

Pa ge 3 9 4

Treatment Pre Hospital 

IV access



Monitor for: o

Fever

o

Hypotension

o

Altered m ental status

Alert Take respiratory precautions

Initial Stabilization For fever, hypotension, altered m ental status, or generalized ecchym oses: 

Airway support



IV access



Fluid resuscitation



IV antibiotics as soon as possible (ceftriaxone)

ED Treatment 



Presum ptive treatm ent of bacterial infection: o

Meningococcus: Ceftriaxone

o

Pneum ococcus: Ceftriaxone, consider penicillin

Prophylaxis for m eningococcal infection: o

Rifam pin

o

Ciprofloxacin

Medication (Drugs) 

Adults: o

Ceftriaxone: 2 g IV q12h

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

o

Ciprofloxacin (prophylaxis): 500 m g PO single dose

o

Penicillin: 4 m illion units IV q4h

o

Rifam pin (prophylaxis): 600 m g PO q12h for 2 days

Children: o

Ceftriaxone: 100 m g/kg/24h IV q12h

o

Penicillin: 240,000U/kg/24h IV q4h

o

Neonatal sepsis: am picillin 100 m g/kg/24h IV q6h and gentam icin 7.5 m g/kg/24h IV q8h (or cefotaxim e 200 m g/kg/24h IV q6h)

Follow-Up Disposition Admission Criteria 

Unstable vital signs



Altered m ental status



Fever

Discharge Criteria 

Exclusion of life-threatening etiologies: o

Serious bacterial infections

o

Critical throm bocytopenia



Appropriate close follow-up scheduled



Consider follow-up with derm atology (skin biopsy) and hem atology.

References 1. Baselga E. Purpura in infants and children. J Am Acad Derm atol. 1997;37:673â€“705. 2. Cohen YC, Djulbegovic B, Sham ai-Lubovitz O, et al. The bleeding risk and natural history of idiopathic throm bocytopenic purpura in

Pa ge 3 9 4

patients with persistent low platelet counts. Arch Intern Med. 2000;160:1630â€“1638. 3. Coller BS, Schneiderm an PI. Clinical evaluation of hem orrhagic disorders: The bleeding history and differential diagnosis of purpura. In: Hoffm an R, Benz E, Sanford S, Furie B, Cohen H, eds. Hem atology: Basic Principles and Practice. 4th ed. Churchill Livingston; 2004:1975â€“2000 4. Leung AK, Chan KW. Evaluating the child with purpura. Am Fam Physician. 2001;64:419â€“428. 5. Piette WW. Hem atologic disorders. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsm ith LA, Katz SL, eds. Fitzpatrick's Derm atology in General Medicine. 5th ed. New York, NY: McGraw-Hill; 1999:1867â€“1881.

Miscellaneous SEE ALSO: Rash

Codes ICD9-CM 287 Purpura and other hem orrhagic conditions

ICD10 D69.2 Other nonthrom bocytopenic purpura

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pyelo nephritis

Pyelonephritis

Ingrid D. Carter

Basics Description 

Ascension of bacteria from lower urinary tract infection (UTI) into renal parenchym a



Male/fem ale ratio: o

1:5 in first year of life

o

1:10 in children

o

1:50 in reproductive years

o

1:1 in fifth decade and later

Etiology 



Bacteriology: o

E. coli 80â€“95%

o

S. saprophyticus 5â€“15%

o

Proteus m irabilis

o

Klebsiella species

o

Citrobacter freundii

o

Serratia

o

Enterobacter

o

Pseudom onas

Predisposing factors: o

Recent instrum entation:

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o

o

o



Catheterization



Cystoscopy



Indwelling urinary catheter

Urinary obstruction: 

Stricture



Stone



Prostatic enlargem ent

Anatom ic abnorm alities: 

Hypospadias



Ureteral ectopia



Bifid ureter



Renal scarring

Neurologic conditions: 

Neurogenic bladder



Spinal cord injury

o

Abnorm al urodynam ics

o

Previous UTIs (in childhood, m ore than three in past year)

o

Recent pyelonephritis within 1 year

o

Diabetes m ellitus

o

Im m unosuppression

o

Pregnancy

Diagnosis Signs and Symptoms 

Dysuria/urgency/frequency



Back, flank, or abdom inal pain



Body aches, fever, chills, m alaise



Nausea, vom iting



Costovertebral angle tenderness or suprapubic tenderness

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

Ill/toxic appearing



Dehydration



Occult pyelonephritis: o

Invasion of upper urinary tract without clinical sym ptom s

o

Suspect in lower UTI that does not resolve with standard treatm ent.

Pediatric Considerations 

Fever, irritability, lethargy, poor feeding, or jaundice m ay be only sym ptom in infants.



Enuresis in previously toilet-trained child



Hem atogenous spread in neonates and im m unocom prom ised children



Renal scarring: o

More com m on sequelae in young children than in adults



Group B streptococci



Etiologic agents in neonates

Essential Workup 

Urinalysis: o

Clean catch or catheterized urine specim en: catheterized specim en if: 

Vaginal discharge or bleeding



Contam inated specim en (large num ber of squam ous cells)

o

Pyuria: 5â€“10 WBCs, plus leukocyte esterase, plus nitrates: 

o

Hem aturia: 



If not present, consider alternate diagnosis.

White cell castâ€”renal origin of pyuria

Urine culture and sensitivity:

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o

Obtain in: 

Suspected pyelonephritis P.925

o



Unclear diagnosis



Treatm ent failures



Recurrent infections

Greater than 100,000 colony-form ing units (CFU)/m L positive

o

o

10 2 â€“10 4 CFU considered positive in: 

Early infection



Clinical scenario consistent with UTI



Catheter or suprapubic specim en



Males

Identifies bacteria in patient does not respond to therapy

Tests Lab 



CBC: o

Leukocytosis

o

Does not rule in or out upper tract infection

Blood cultures: o

Not needed; positive cultures do not correlate with m ore severe disease.

o

Bacteria identified m ore readily on urine culture, usually E. coli

Imaging 

Usually not required



Helical CT: o

Stranding or inflam m ation and edem a of parenchym a

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o

Obtain helical CT or renal ultrasound if: 

Concom itant stone or obstruction suspected



Diagnosis unclear



Patient very ill or getting worse



At risk for renal em physem a or abscess (diabetes m ellitus, elderly)



Elective evaluation of genitourinary tract in m ales with pyelonephritis

Pediatric Considerations 

Obtain catheter urine specim en: o

Vast m ajority of bag urine specim ens will result in positive cultures owing to contam inants.

o

Helpful only for ruling out disease if culture is negative

o

Catheterized or suprapubic specim en with >1,000 CFU is positive.



Blood cultures usually perform ed for children <1 year of age



All children with first episode of pyelonephritis should have urinary tract im aging perform ed later.





Renal ultrasound: o

Within 48 hours if no clinical im provem ent

o

Within 3â€“6 weeks if clinical im provem ent

Girls 4â€“10 years old: o



Radionuclide isocystogram for vesicoureteral reflux

Boys 4â€“10 years old: o

Voiding cystourethrogram after urine is sterile and bladder spasm has subsided

Differential Diagnosis 

Lower UTI



Pelvic inflam m atory disease

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

Prostatitis



Epididym itis



Urethritis



Nephrolithiasis



Renal abscess



Appendicitis



Diverticulitis



Cholecystitis



Lower lobe pneum onia

Treatment Initial Stabilization Treat shock secondary to urosepsis with 0.9% norm al saline (NS) 500 m L to 1 L (peds: 20 m L/kg) IV fluid bolus

ED Treatment 



Parental antibiotics for: o

Inability to com ply with oral therapy

o

Extrem es of age

o

Failure of oral therapy

o

Urinary obstruction

o

Toxicity

o

Im m unosuppression

o

Pregnancy

o

Suspected antibiotic resistant organism s

Em piric intravenous antibiotics: o

Am inoglycoside (gentam icin) plus am picillin

o

Third-generation cephalosporin (ceftriaxone)

o

Fluoroquinolonesâ€”not approved for children

o

Trim ethoprim -sulfam ethoxazole (TMP-SMX)â€”not for

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use in com plicated pyelonephritis o



In pregnancy: 

Third-generation cephalosporin



Gentam icin/am picillin



Cefazolin



Aztreonam

Outpatient oral antibiotics: o

For nontoxic and otherwise healthy patient: 

Fluoroquinoloneâ€”7-day course



TMP-SMXâ€”10- to 14-day course (if known susceptibility)

o

May adm inister one dose of parenteral antibiotics prior to oral antibiotics: 

Ensures prom pt cessation of bacterial proliferation



Avoids delays in oral antibiotic adm inistration



No literature addressing efficacy



Antiem etics for vom iting



Analgesia for pain

Medication (Drugs) 

Oral antibiotics: o

Ciprofloxacin: 500 m g PO b.i.d.

o

Levofloxacin: 500 m g PO daily

o

Gatifloxacin: 400 m g PO daily

o

Ofloxacin: 200 m g PO b.i.d.

o

TMP-SMX: 160 m g/800 m g PO b.i.d. (only if known susceptibility)



IV antibiotics: o

Am picillin: 1 g IV q6h

o

Cefazolin: 1â€“1.5 g IV q8h

Pa ge 3 9 5

o

Ceftriaxone: 1 g IV q24h

o

Ciprofloxacin: 400 m g IV q12h

o

Gatifloxacin: 400 m g IV daily

o

Gentam icin: 2â€“5 m g/kg IV load

o

Levofloxacin: 500 m g IV daily

o

Piperacillin-tazobactam : 3.375 g IV q8h

o

Ticarcillin-clavulanate: 3.1 g IV q6h

Pediatric Considerations 

Oral antibiotic liquid preparations for children: o

Am oxicillin: 30â€“50 m g/kg/24h PO t.i.d.

o

Am oxicillin/clavulanic acid: 45 m g/kg/24h PO t.i.d.

o

Cefixim e: 8 m g/kg PO daily

o

Cefpodoxim e: 10 m g/kg/24h PO b.i.d.

o

Cephalexin: 50â€“75 m g/kg/24h PO q.i.d.

o

Erythrom ycin/sulfisoxazole: 50 m g EM/kg/24h PO q.i.d.

o

Loracarbef: 15â€“30 m g/kg/24h PO b.i.d.

o

TMP-SMZ: 6â€“12 m g TMP, 30â€“60 m g SMZ per kg/24h PO b.i.d.



Parenteral antibiotics for adm itted children: o

Age 0â€“3 m onths: 

Cefotaxim e (50â€“180 m g/kg/d t.i.d.) plus am picillin (50â€“100 m g/kg/d q.i.d.)



Gentam icin (1â€“2.5 m g/kg/d t.i.d.) plus am picillin

o

Age >3 m onths: 

May substitute ceftriaxone (50â€“100 m g/kg/d b.i.d. to daily) for cefotaxim e

Follow-Up

Pa ge 3 9 5

Disposition Admission Criteria 

Unstable vital signs/toxic appearance



Inability to com ply with oral therapy



Nausea/vom iting



Social situation prevents com pliance.



Pregnancy



Indwelling urinary catheter



Urinary obstruction/anatom ic abnorm alities



Proxim al obstruction (such as kidney stone) places patient at high risk for developm ent of renal abscess or sepsis and so requires em ergent urologic consultation.



Im m unosuppression/diabetes m ellitus



Extrem es of age (children <2â€“6 m onths)



Failure of outpatient therapy/recent antibiotics



If uncertain of diagnosis

Discharge Criteria 

Ability to m aintain oral hydration



Pain controlled with oral analgesic



Follow-up in 48â€“72 hours

References 1. Gibly R. Infections of the urinary tract and m ale genitalia. In: Brillm an JC, Quenzer RW, eds. Infectious Disease in Em ergency Medicine. 2nd ed. Philadelphia: Lippincott William s & Wilkins; 1998: 602â€“629. 2. Lipsky BA. Prostatitis and urinary tract infection in m en: what's new; what's true? Am J Med. 1999;106:327â€“334. 3. Stam m WE, Norrby SR. Urinary tract infection: disease panoram a and challenges. J Infect Dis. 2001;183(suppl 1):S1â€“4. 4. Warren JW, Abrutyn E, Hebel JR, et al. Guidelines for antim icrobial

Pa ge 3 9 5

treatm ent of uncom plicated acute bacterial cystitis and acute pyelonephritis in wom en. Clin Infect Dis. 1999;29:745â€“758.

Codes ICD9-CM 590.80

ICD10 N12

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pylo ric Steno sis

Pyloric Stenosis

Roger Barkin

Basics Description 

Postnatal hypertrophy and hyperplasia of the circular sm ooth m uscle cell layer causing a thickened pylorus and antrum leads to worsening gastric outlet obstruction.



Neuronal nitric oxide synthase (NOS-1) m ay be a genetic susceptibility locus.



Adm inistration of erythrom ycin in infants m ay increase risk of hypertrophic pyloric stenosis.



Jaundice due to transient glucuronyl transferase deficiency



Adult: caused by peptic ulcer disease

Etiology 

Most com m on cause of gastrointestinal obstruction in infants with an incidence of 1 in 150 m ales and 1 in 750 fem ales (average: 3 in 100 live births)



Males affected 5 tim es m ore com m only than fem ales; firstborn m ost com m on



Fam ilial, 15%: o

Child of affected parent has 7% incidence.

o

Recurrence risk in subsequent m ale children is 10%; 2% in fem ales.

Pa ge 3 9 5

Diagnosis Signs and Symptoms History 

Vom iting: o

Gradual onset, usually beginning at around 3 weeks of age

o

Progressive, usually becom ing projectile

o

Nonbilious

o

May be blood tinged (secondary to esophagitis, gastritis, gastric ulceration)



o

Progressively worsening

o

Postprandial

Represents the hypertrophied pylorus: o

Confirm s diagnosis



Constipation or sm all am ount of stools



â€œLean and hungryâ€• infant early in course; dehydrated and uninterested in feeding late in course; failure to thrive



Variable dehydration and wasting depending on duration of sym ptom s



Jaundice in 8% of children



Adult presents with vom iting, anorexia, early satiety, and epigastric pain.

Physical Exam 

Often norm al unless a relaxed abdom en



May feel olive-shaped m ass at lateral m argin of the right rectus abdom inis m uscle in the right upper quadrant (80% of patients), often after vom iting:

Pa ge 3 9 5

o

Best felt im m ediately after vom iting or after the stom ach is em ptied via gastric suction as the dilated body of the stom ach overlies the pylorus

o

Represents the hypertrophied pylorus: 



Helps confirm diagnosis

Peristaltic waves m oving from the left to right in the left upper quadrant, seen best after feeding or just prior to vom iting

Essential Workup If â€œoliveâ€• palpable, further diagnostic evaluation is unnecessary and surgical consultation should be sought; otherwise, im aging studies are indicated.

Tests Lab 

Electrolytes, BUN/creatinine, glucose: o

Hypokalem ic, hypochlorem ic m etabolic alkalosis

o

Norm al electrolytes do not exclude the diagnosis.



Bilirubin elevated



CBC if blood in em esis



Urinalysis for hydration

Imaging 

Abdom inal ultrasound: o

Study of choice

o

Ultrasonic diagnosis hinges on identification and m easurem ent of pyloric m uscle m ass (3-m m ring thickness with 1.5-cm pylorus channel) and observation of fluid m ovem ent through the pylorus

o

Positive predictive value approaches 100%; 19% false-negatives

o

Serial ultrasounds for equivocal or negative study

Pa ge 3 9 6



Upper GI series: o

String sign representing contrast passing through a narrowed gastric outlet

o

95% accurate

o

Rem ove contrast from the stom ach after the study to prevent aspiration.



Supine abdom inal film : o

Not diagnostic; rarely helpful

o

Dilated stom ach and no air distal to the pylorus

o

Most useful with other views to begin evaluation for other abdom inal pathology

Differential Diagnosis 







GI anatom ic/functional disorder: o

Gastroesophageal reflux (GER)

o

Hiatal hernia

o

Obstruction/atresia

o

Gastric or duodenal web

Infection: o

Gastroenteritis

o

Urinary tract infection

o

Sepsis

Metabolic: o

Adrenal insufficiency

o

Inborn error of m etabolism

Feeding problem s: o

Psychosocial: poor m aternal interaction or stress

o

Chalasia

o

Form ula intolerance

o

Overfeeding



Drug withdrawal



Increased intracranial pressure

P.927

Pa ge 3 9 6

Treatment Pre Hospital Fluid resuscitation if significant volum e deficit

Initial Stabilization 

IV access



Rapid bedside glucose test to exclude hypoglycem ia



Correct volum e deficit with 20 m L/kg bolus of 0.9% norm al saline (NS) IV; m ay repeat.

ED Treatment 

Correct electrolyte abnorm alities.



Hydrate with dextrose-containing solution after fluid resuscitation at 1â€“1.5 tim es m aintenance rate: o

Add potassium after ensuring adequate urine output.



Insert nasogastric tube to decom press the stom ach.



Restrict oral intake.



Consult pediatric surgeon for pylorom yotom y.



Adult: proton pum p antagonist (lansoprazole or om eprazole)

Medication (Drugs) 

Lansoprazole: 30 m g daily PO



Om eprazole: 20 m g daily PO

Pa ge 3 9 6

Follow-Up Disposition Admission Criteria 

All pediatric patients should be adm itted to the hospital for rehydration and surgical correction with either an um bilical pylorom yotom y or laparoscopic pylorom yotom y.



Adult patients: Adm it as necessary for rehydration; m ay be scheduled for elective pylorotom y if proton pum p inhibitors fail to im prove this condition.

Discharge Criteria None

References 1. Bishop HC. Diagnosis of pyloric stenosis by palpation. Clin Pediatr. 1973;12(4):226â€“227. 2. Heller RM, Hernanz-Schulm an M. Application of new im aging m odalities to the evaluation of com m on pediatric conditions. J Pediatr . 1999;135:632â€“639. 3. Majon BE, Rosenm an MG, Kleinm an MB. Maternal and infant use of erythrom ycin and other m acrolide antibiotics as rick factors for infantile hypertrophic pyloric stenosis. J Pediatr. 2001;13:380. 4. Najm aldin A, Tan HL. Early experience with laparoscopic pylorom yotom y for infantile hypertrophic pyloric stenosis. J Pediatr. 1995;30â€“37. 5. Feldm an H, Friedm an LS, Sleisenger MH, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders; 1998. 6. Touloukian RJ, Higgins E. The spectrum of serum electrolytes in hypertrophic pyloric stenosis. J Pediatr Surg. 1983;18(4):394â€“397.

Codes

Pa ge 3 9 6

ICD9-CM 537.0

ICD10 K31.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > QT Syndro m e, Pro lo nged

QT Syndrome,

Prolonged Jason A. Tracy

Basics Description 

Alteration in cardiac sodium , potassium or calcium -channel m echanics



Prolonged ventricular repolarization results in lengthening of QT interval on surface ECG: o

â€œPause-dependentâ€• lengthening due to short-long-short sequence in which a sinus beat is followed by an extrasystole (short), then a post-extrasystolic pause (long), concluding with a ventricular extrasystole (short)

o

â€œAdrenergic-dependentâ€• pauses found in congenital cases



Sym ptom s preceded by vigorous exercise, em otional stress, or loud noise.



Nocturnal bradycardia can lengthen QT interval causing sleep-related sym ptom s.



Re-entrant rhythm can lead to torsades de pointes, ventricular tachycardia, and ventricular fibrillation.

Pa ge 3 9 6



Hem odynam ic com prom ise following dysrhythm ia leads to syncope or death.

Genetics 

Six genetic loci identified with sporadic cases due to spontaneous m utations: o

Autosom al-recessive form associated with deafness (Jervell and Lange-Nielsen syndrom es)

o

Autosom al-dom inant form not associated with deafness (Rom ano-Ward syndrom e)

o

Adrenergic stim ulation (fright, exertion, delirium trem ens, and loud auditory stim ulus) becom es prodysrhythm ic in certain genotypes while sleep-related sym ptom s found in others. 

10â€“15% of carriers have baseline norm al QTc.



Death occurs in 1â€“2% of untreated patients per year.

o

Drug-induced QT prolongation m ay also have a genetic background.

o

Congenital form occurs in one in 3,000â€“5,000 with m ortality of 6% by age 40 years.

Pediatric Considerations 

Diagnosis suspected in the young with syncope, cardiac arrest, or sudden death



Syncope following em otional stress or exercise suggestive



Death occurs without preceding sym ptom s in 10% of pediatric patients.

Etiology Drugs: 

Com plete list at http://www.QTDrugs.org



Class Ia antidysrhythm icsâ€”quinidine, procainam ide, disopyram ide

Pa ge 3 9 6



Class III antidysrhythm icsâ€”sotalol, ibutilide, am iodarone



Antibioticsâ€”erythrom ycin, pentam idine, chloroquine, trim ethoprim -sulfam ethoxazole



Antifungal agentsâ€”ketoconazole, itraconazole



Psychotropic drugsâ€”phenothiazines, haloperidol, risperidone, STCAs



Cisapride



Antihistam ines



Organophosphates



Electrolyte abnorm alities



Hypokalem ia



Hypom agnesem ia



Hypocalcem ia



Cardiac



Bradyarrhythm ias



Arteriovenous block



Mitral valve prolapse



Myocarditis



Myocardial ischem ia



CNS



Subarachnoid hem orrhage



Stroke



Congenital (idiopathic)



Other



Protein-sparing fasting



Anorexia nervosa



Hypothyroidism



Hypotherm ia

Diagnosis

Pa ge 3 9 6

Signs and Symptoms History 

Syncope



Near syncope



Light-headedness



Dizziness



Seizure



Sudden death

Essential Workup 

A detailed history: o

Medications

o

Congenital deafness

o

Syncope or sudden death: 



Fam ily history of syncope or sudden death

Cardiac m onitor: o

ECG

o

QTc (QT corrected for heart rate) >0.44 seconds in m en and >0.46 seconds in wom en

o

QT m easured from beginning of quasi-random signal to end of T wave: 

Measured best in the lim b leads and should be averaged over three to five beats



There is no expert consensus on best heart rate correction (QTc) form ula.



Bazett form ula (QT divided by square root of RR interval) is m ost com m only used



Increase in QT variability

o

T-wave abnorm alities (T-wave alternans, biphasic)

o

Appearance of U waves

o

Ventricular tachycardia

o

Ventricular fibrillation

Pa ge 3 9 6

o

Torsades de pointes

Tests Lab 

Full electrolytes including calcium and m agnesium



Toxicology screen

Imaging Echocardiography to exclude other cardiac causes

Diagnostic Procedures/Surgery 

ECG stress testing to induce a prolonged QT interval in suspected cases



Holter m onitoring of QTc



Genetic counseling/testing in suspected congenital form s



Fam ilial ECG testing

Differential Diagnosis 

Myocardial infarction



Hypertrophic cardiom yopathy



Valvular defect

P.929

Treatment Pre Hospital 

Supplem ental oxygen



IV access



Monitor

Alert

Pa ge 3 9 6



Stable patients with prolonged QT interval transported without intervention



Cardioversion for unstable patients with confirm ed torsades de pointes



Magnesium sulfate for stable patients with evidence of torsades de pointes

Initial Stabilization 

IV access



Monitor



Determ ine hem odynam ic stability



Unstable patients require im m ediate cardioversion

ED Treatment 

IV m agnesium sulfate for torsades de pointes



IV potassium to serum levels of 4.5â€“5 m Eq/L



Tem porary transvenous cardiac pacing (rates between 90 and 110 beats/m in) for recurrences of torsades de pointes refractory to m agnesium sulfate therapy (shortens QTc)



IV isoproterenol for refractory cases of hem odynam ically unstable patients with acquired long QT (ineffective in congenital cases) and inability to transvenous pace



Rem ove any offending m edications and correct m etabolic derangem ents



Consultation with cardiology in those with sym ptom atic long QT as Î²-blockers at m axim um doses are to be started



No ED treatm ent needed (in consultation with cardiology) for those with suspected idiopathic long QT and no history of syncope, fam ily history of sudden cardiac death or ventricular arrhythm ias



Pacem aker or defibrillator placem ent with or without cervicothoracic stellectom y (to reduce adrenergic

Pa ge 3 9 7

stim ulation) m ay be required in high-risk patients. 

Beta-blockers prevent 70% of cardiac events in congenital cases.

Medication (Drugs) 

Isoproterenol: 1Âµg/m in (peds: 0.1â€“1.0 Âµg/kg/m in) IV continuous infusion, titrate for effect, up to 10 Âµg/m in



Magnesium sulfate: 2 g (peds: 25â€“50 m g/kg) IV bolus over 2â€“3 m inutes followed by IV infusion at 2â€“4 m g/m in



Propanolol: 2â€“3 m g/kg/d (peds: 2â€“3 m g/kg/d) PO (in consultation with cardiology)

Follow-Up Disposition Admission Criteria 

Sym ptom atic prolonged QT



Syncope



Cardiac dysrhythm ia



Possible cardiac or ischem ic event



Metabolic abnorm ality

Discharge Criteria Asym ptom atic prolonged QT in consultation with cardiology

References 1. Al-Khatib SM, LaPointe NM, Kram er JM, et al. What clinicians should know about the QT interval. JAMA. 2003;289:2120â€“127. 2. Khan IA. Clinical and therapeutic aspects of congenital and

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acquired long QT syndrom e. Am J Med. 2002;112:58â€“66. 3. Meyer JS, Mehdirad A, Salem BI, et al. Sudden arrhythm ia death syndrom e: Im portance of the long QT syndrom e. Am Fam Phys. 2003;68:483â€“488. 4. Olgin JE, Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Braunwald E, Zipes DP, Libby P, eds. Braunwald: Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders 2001:867â€“870. 5. Vincent GM. Ventricular arrhythm ias: long QT syndrom e. Cardiol Clin. 2000;18:309â€“325.

Miscellaneous SEE ALSO: http://www.QTDrugs.org

Codes ICD9-CM 427

ICD10 I49.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rabies

Rabies

Matthew Kippenhan

Basics Description CNS infectious disease of m am m als caused by the rabies virus: 

Negative-stranded RNA genom e, fam ily Rhabdoviridae, genus Lyssavirus

Etiology 

Epidem iology: o

30,000â€“70,000 hum an cases worldwide per year: 

Especially com m on in southeast Asia, Philippines, Africa, South Am erica, and the Indian subcontinent

 o

Dogs and foxes are m ain reservoirs.

United States has two to three hum an cases per year: 

Most clinical cases in the United States com e from foreign travel and bat exposures.



Wild anim als account for 93% of cases, dom estic anim als for 6.8%.



Raccoons, skunks, bats, foxes, woodchucks, groundhogs are reservoirs.



Lasionycteris (Silver haired) and Pipistrellus

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(Eastern pipistrelle) bats are associated with m ost cases. 

Thought not enough to constitute exposure, squirrel, rat, m ouse, ham ster, guinea pig, gerbil, chipm unk, rabbit are also reservoirs.



Mode of transm ission: o

Infected saliva of host passed to uninfected anim al

o

Bite: m ost com m on

o

Nonbite: scratch, abrasion, m ucous m em brane contact with saliva, bat aerosol exposure

o

Corneal and solid organ transplant procedures

o

Not considered transm ission risk: petting rabid anim al; contact with blood, urine, or feces of rabid anim al



Progression after infection: o

Virus m ultiplies in local tissue (i.e., m uscle)

o

Virus taken up into peripheral nerves through acetylcholine receptors

o

Virus transported to CNS via retrograde axoplasm ic flow

o

Once in CNS, rapid replication and dissem ination causes encephalitis.

o

Centrifugal spread of virus to peripheral nerves, including salivary glands

Diagnosis Signs and Symptoms 

Five stagesâ€”latent period, prodrom e, encephalitis, com a, death (or recovery) o

Latent period: 1â€“3 m onths (range 10 days to >6

Pa ge 3 9 7

years):

o



Virus incubation in peripheral tissues



Shorter period for head or neck bite

Prodrom eâ€”duration 1â€“7 days: 

Fever, headache, m alaise, m yalgias, anorexia, sore throat, nausea, and vom iting



Paresthesias or fasciculations around bite site give clue to diagnosis.

o

Encephalitisâ€”duration 2â€“7 days: 

Anxiety, agitation, hallucinations, confusion or delirium , m uscle spasm s, seizure, persistent high fever



Aerophobiaâ€”pharyngeal spasm from draft of air



Hydrophobiaâ€”violent involuntary m uscle contraction of diaphragm , pharyngeal, laryngeal and accessory respiratory m uscles when attem pting to swallow (seen in two thirds of cases)



Autonom ic instability, dysrhythm ias, m yocarditis



Brainstem involvem entâ€”diplopia, facial paralysis

o

Com a: 

Apnea from respiratory center involvem ent, vascular collapse, flaccid paralysis, adult respiratory distress syndrom e, syndrom e of inappropriate diuretic horm one

 o

Most die within 2 weeks

Death (or recovery): 

Fatal if no pre- or postexposure prophylaxis given

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

Single case report in 2004 of survival without prophylaxis

 

Residual neurologic deficits likely persist.

Three m anifestations of disease: o

Classic (encephalitic) accounts for about 80% of cases.

o

Dum b rabies (Paralytic) accounts for about 20%: ascending paralysis m im icking Guillain-BarrÃ©.

o

Nonclassic (atypical) rabies (<1%): neuropathic pain, sensory or m otor deficits, choreiform m ovem ents, m yoclonus, and seizures

History 

Bite wound or other known exposure



Bat found in room with person unable to give history (i.e., child, intoxicated): assum e exposure



Travel to endem ic areas



Unprovoked attack carries higher risk of infection.

Physical Exam 

Fever



Bat bite often not visible on exam



Altered m ental status, seizures, encephalopathy



Percussion m yoedem aâ€”m uscle m ounds at percussion site



Autonom ic m anifestationsâ€”dilated pupils, perspiration, hypersalivation, orthostatic hypotension

Essential Workup 

Saliva: o

Rabies RNA by reverse transcription, polym erase chain reaction (PCR)

o 

Virus isolation in cell culture

Serum â€”rabies antibodies: o

Positive titers are diagnostic if not vaccinated

Pa ge 3 9 7

o 

Earliest positive day 6

Cerebrospinal fluidâ€”m ildly elevated WBC and protein, norm al glucose: o

Virus isolation

o

Rabies antibodies are diagnostic, even if im m unized.

Tests Lab 

CBC



Electrolytes, blood urea nitrogen, creatinine, glucose



Blood cultures/urinalysis: o



Search for other infection/illness

Neck biopsyâ€”reverse transcriptase/polym erase chain reaction (RT/PCR), im m unofluorescent staining for viral antigen

Imaging 

CT headâ€”other causes of altered m ental status, seizure, encephalopathy



Chest radiographâ€”other infectious etiologies

Diagnostic Procedures/Surgery Lum bar puncture P.931

Differential Diagnosis 

Other causes of encephalitis: o

Herpesvirusesâ€”HSV1, VZV

o

Enterovirus (coxsackie, echovirus, poliovirus)

o

Arboviruses (West Nile virus, Eastern/Western Equine Encephalitis, LaCrosse, St. Louis)



Tetanus

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

Delirium trem ens



Psychosis



Paralytic form â€”Guillain-BarrÃ©, polio, tick-bite paralysis, im m une-m ediated polyneuritis

Treatment Pre Hospital 

Thoroughly wash wound with soap and water.



If safely able, capture wild anim al for sacrifice and testing.

Initial Stabilization 

ABCs



Intubation as needed



Treatm ent of seizures

ED Treatment 

Wound cleansing with soap and virucidal agent



Tetanus im m unization



Determ ine if exposure requires treatm ent: o

Dom estic anim al bite: 

Hom e m onitoring of anim al for 10 days



If anim al displays no signs of illness, patient does not need post-exposure prophylaxis.

o

Wild anim al bite: 

Rabies testing of sacrificed anim al head



May delay postexposure prophylaxis (PEP) pending results

 o

Treat if anim al not captured.

All unprovoked attacks should be assum ed at high risk for exposure.



PEP:

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o

Passive im m unization with hum an rabies im m une globulin (HRIG)

o



HRIGâ€”20 IU/kg: 

One half infiltrated in and around wound



Rem ainder given IM (gluteus okay)

Active im m unization with rabies vaccine: o

Rabies vaccineâ€”1 m l (2.5 IU) IM days 0, 3, 7, 14, 28

o

Three vaccines availableâ€”equally safe and efficacious: 

Hum an diploid cell vaccineâ€”Im ovax, Im ovax ID (IM and intraderm al form s)

o



Rabies vaccine adsorbed



Purified chick em bryo cell vaccineâ€”RabAvert

Adm inistration location: 

Deltoid in adults or anterior thigh in children



Not given in gluteusâ€”reported failures with inadvertent adm inistration into subcutaneous fat



For those with pre-exposure prophylaxis and rabies exposure:





o

Do not require HRIG

o

Need vaccine booster on days 0 and 3

If care delayed after rabies exposure: o

HRIG not indicated m ore than 7 days after exposure

o

Vaccine should be adm inistered as usual.

Pre-exposure prophylaxis: o

Rabies vaccine on days 0, 7, 21, 28

o

Target groupsâ€”veterinarians, anim al handlers, virus laboratory workers, foreign travelers in endem ic regions

Pediatric Considerations Treat as in adults.

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Pregnancy Considerations Treatm ent considered safe during pregnancy

Follow-Up Disposition Ensure adequate access for subsequent vaccine adm inistration post rabies exposure.

Admission Criteria Patient with encephalitis or high suspicion of rabies

Discharge Criteria 

Stable patient



No evidence of reaction to vaccine

Issues for Referral Public health and CDC for suspicious cases

References 1. Centers for Disease Control and Prevention. Hum an Rabies Preventionâ€”United States, 1999. Recom m endations of the Advisory Com m ittee on Im m unization Practices. Morb Mortal Wkly Rep. 1999;48(RRâ€“1):1â€“21. 2. Centers for Disease Control and Prevention. Investigation of rabies infections in organ donor and transplant recipientsâ€”Alabam a, Arkansas, Oklahom a and Texas. MMWR Morb Mortal Wkly Rep. 2004;53:586â€“589. 3. Centers for Disease Control and Prevention. Recovery of a Patient from Clinical Rabiesâ€”Wisconsin. Morb Mortal Wkly Rep. 2004;53(50):1171â€“1173. 4. Krebs J, Mandel E, et al. Rabies Surveillance in the United States during 2003. J Am Vet Med Assoc. 2004;225:1837â€“1849.

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Miscellaneous SEE ALSO: Encephalitis; Meningitis

Codes ICD9-CM 71.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Radiatio n Injury

Radiation Injury

Robert Feldman

Basics Description 

Radiation in this chapter refers to ionizing radiation.



Alphaâ€”helium nucleus; does not penetrate skin



Betaâ€”electron; penetrates tissue a few cm



Gam m aâ€”photon; penetrates body



Neutronâ€”very penetrating; not detected by Geiger counter, but neutron em itter will also give off gam m a radiation



Radioisotope/radionuclideâ€”chem ical elem ent that em its radiation from its nucleus: o

Radioactivity cannot be destroyed, only relocated or shielded.

o

Being radioactive does not change elem ent's other chem ical and physical properties, such as heavy m etal toxicity.



Exposure/irradiationâ€”patient has been in presence of ionizing radiation: o



Whole body or only certain areas m ay be exposed.

Contam inationâ€”radioactive m aterial where it is not desired

Pa ge 3 9 8



Internalâ€”within body (e.g., lung)



Externalâ€”outside body (skin, hair, clothing)



Doseâ€”am ount of radiation energy absorbed by tissue: o

Units and conversions: 

1 gray (Gy) = 100 rad



1 sievert (Sv) = 100 rem



For beta and gam m a radiation:



1 Gy = 1 Sv = 100 rad = 100 rem

Alert Contact regional or federal authorities for guidance if radiation incident is suspected.

Pediatric Considerations 

Children are m ore sensitive to radiation injury.



Potassium iodide is m ost protective for children and should be given prom ptly if contam ination with radioactive iodine is suspected.

Pregnancy Considerations 

Developing fetus is very sensitive to radiation.



Pregnant staff should not care for radioactively contam inated patients.

Etiology 

Ionizing radiation leads to cellular injury.



Dam age to blood vessels leads to endarteritis and loss of tissue blood supply.



Higher rates of cell division within an organ m ake it m ore sensitive to radiation:



o

Bone m arrow and GI tract are very sensitive.

o

Skin and nerve are less sensitive.

Acute radiation syndrom e (ARS) occurs in stages following whole-body exposure:

Pa ge 3 9 8

o

Prodrom al: Acute radiation injury leads to acute inflam m ation (0â€“48 hours).

o

Latent: If the acute phase of injury is survived, inflam m ation and sym ptom s subside (0â€“2 weeks).

o

Manifest illness: At higher radiation doses, organ failure then develops.

o 

Recovery, or death (usually from infection), follows.

Sources of radiation include m edical devices and therapeutics, and industry.



Absolute lym phocyte count (ALC, all values listed per m m 3 ) can help differentiate ARS from psychosom atic illness.

Diagnosis 

Diagnosing contam ination is fairly easy.



Diagnosing and quantifying exposure is m ore difficult and will probably require expert consultation.

Signs and Symptoms 

Vary based on dose, see â€œTerrorism with Ionizing Radiation General Guidance Pocket Guideâ€• (from VA or DOD, see References)



Overall: o

Whole-body exposure: syndrom e sim ilar to high-dose chem otherapy toxicity

o

ARS progresses m ore rapidly the higher the absorbed dose.



Local exposure: o

Early resem bles therm al or ultraviolet (UV) burn

o

Later resem bles ischem ic ulcer

History

Pa ge 3 9 8



Recognized exposure: o



Occupational, m edical, transportation accident

Unrecognized or clandestine exposure: o

Radiological dispersal device RDD, concealed, or unrecognized source

o

Industrial and m edical radiography sources m ay be pellets only a few m illim eters in diam eter, and are highly radioactive.

o

Suspect if m ultiple patients present with sym ptom s of ARS at any stage, burns without history of therm al exposure, or ischem ic ulcers in unusual locations (e.g., hand from handling unrecognized source, hip from placing source in pocket).

Physical Exam 

Whole-body exposure: o

Nausea, vom iting: 

Within 3â€“6 hours for >100 rad exposure; sooner with higher exposures



Vom iting within 1 hour of exposure indicates potentially lethal injury (>600 rad).

o

Confusion and weakness (>200 rad)

o

Fever:

o



Acutely, from inflam m ation



During m anifest illness, from infection

Hair loss, hem orrhage, diarrhea m ay develop with doses >300 rad.



Derm al exposure: o

Initial erythem a

o

Blistering and ischem ic necrosis m ay follow.

Essential Workup 

Survey for radiation using a Geiger counter, which can be

Pa ge 3 9 8

found in any nuclear m edicine or radiation therapy departm ent: o

Any probe style is okay for survey.

o

Cover probe with exam glove: 

Prevents contam ination of probe



Blocks alpha radiation, but will detect beta/gam m a

o

Measure background radiation away from patient.

o

Move probe slowly over patient's skin: 

1â€“2 cm from skin



Move probe only 2â€“3 cm /s.



Contam ination is greater than two tim es background.



Note any contam inated areas.



Follow system atic pattern to avoid m issing areas.

 

Rem em ber to survey palm s, soles, hair.

Absolute lym phocyte count is best indicator of severity of ARS: o

<1,000/m m 3 â€”m oderate exposure, 200â€“600 rad

o

<500/m m 3 â€”severe exposure, >600 rad

Tests Lab 

CBC with differential every 4â€“6 hours (for 24 hours or until stable)



Swab both nares and survey for inhaled contam inants.



Type and cross



24-hour stool for radioassay if GI contam ination suspected



24-hour urine for radioassay if any internal contam ination is suspected

Diagnostic Procedures/Surgery

Pa ge 3 9 8



Whole-body gam m a cam era (without collim ator) is best for ruling out internal contam ination with am ericium , or low levels of other radioisotopes, if suspicion is high and survey with Geiger counter is negative.



Cytogenetics allows m ore accurate dose assessm ent: o

10 m L blood in lithium -heparin tube (EDTA also acceptable)

o

Draw 24 hours postexposure.

o

Refrigerate (4Â°C) and ship cold to Arm ed Forces Radiobiology Research Institute (AFRRI).

o

Only lim ited num ber of sam ples can be processed owing to resources required.

Differential Diagnosis 

System ic illness: lym phopenia, weakness, nausea: o

Psychologic effects are com m on in both exposed and unexposed patients, and m ay m im ic ARS: 

Radiation casualty with vom iting from ARS should have falling ALC; if ALC norm al and stable, consider psychologic stress reaction or other type of illness.



o

Hem atologic m alignancy

o

Chem ical warfare agents (blister/m ustard)

o

HIV disease, im m unosuppression

Skin injuries: o

Ischem ic ulcer

o

Brown recluse spider bite

o

Bacterial infection

o

Pyoderm a gangrenosum

P.933

Pa ge 3 9 8

Treatment 

Em ergent m edical care takes precedence over decontam ination: o

No known case where live, contam inated patient was so radioactive as to be an im m ediate hazard to em ergency personnel



Do not underestim ate psychologic im pact of any incident involving â€œradiationâ€• on staff (and public): o

Get early support from hospital or outside experts to counsel staff.



Personal protective equipm ent (PPE): o

Must provide protection from dust (particulate respirator, e.g., N-95, gown, gloves, hair, and shoe covers)

o

Radiography aprons are of no valueâ€”they do not protect against m ost gam m a radiation.

Pre Hospital 

Treat life threats (airway, breathing, and circulation m anagem ent [ABCs]).



Assess any bom bing scene for radioactive contam ination (RDD).



Rem oving clothing will elim inate about 80% of external contam ination.



Survey for residual contam ination: o

No contam ination: patient m ay be cared for as usual.

o

If contam ination is present, assess m edical condition: 

Stableâ€”proceed with decontam ination.



Unstableâ€”provide necessary care and transport; use sheets to control contam ination.

Pa ge 3 9 8

Initial Stabilization 

ABCs



Assess for contam ination



If patient condition perm its, perform decontam ination before patient enters (and contam inates) facility



Minim ize staff exposure: o

Tim eâ€”lim it tim e in contam inated area, rem ove contam inated m aterial often.

o

Distanceâ€”use long-handled instrum ents to handle contam inated m aterial.

o

Shieldingâ€”place contam inated m aterial in a lead container (available in nuclear m edicine departm ent); radiography lead aprons are not effective.

ED Treatment 

Hospital issues o

Activate hospital disaster plan, if indicated, to m obilize resources.

o

Designate contam inated and â€œcleanâ€• treatm ent areas.

o

Appoint a tem porary radiation safety officer (RSO) for incident to survey all patients and staff and all m aterials leaving treatm ent area: 

Hospital RSO if available



Any staff m em ber who is trained to use Geiger counter and dosim eters m ay fill RSO role initially if necessary.

o

Patients and m aterials that are not contam inated do not need decontam ination or containm ent.

o

Call for expert assistanceâ€”hospital radiation safety officer, local Departm ent of Nuclear Safety, health

Pa ge 3 9 8

departm ent, Radiation Em ergency Assistance Center/Training Site (REAC/TS) or AFRRI (see References). 

Staff issues: o

Provide PPE and psychologic support as described above.

o

Assign pregnant personnel to â€œcleanâ€• areas only.



Decontam ination: o

Priorities: wounds > m ucous m em branes > intact skin

o

Use fenestrated drapes to shield adjacent skin.

o

Use soap and water; no harsh chem icals.

o

Diaper wipes work well for intact skin; wipe from edges of area to center, then lift away.

o

Irrigate woundsâ€”collect and survey runoff, avoid splashing.

o

Resurvey frequently to assess effectiveness of decontam ination.

o

Do not abrade skin.

o

If contam ination cannot be rem oved, cover area to prevent spread and m ove onâ€”residual contam ination can be controlled.



Treat vom iting and dehydration: o

Antiem etics (5-HT3 antagonist, e.g., ondansetron 4 m g IV)

o 

IV fluids

Decorporation agents for internal decontam ination are specific to each radionuclide: o



Contact REAC/TS for guidance.

Potassium iodide is useful only to prevent thyroid uptake of radioactive iodine (found in nuclear reactors), and only

Pa ge 3 9 9

if given within a few hours after contam ination; see VA/DOD Pocket Guide for dosage (see References). 

Cytokines and transfusions m ay be needed with doses >200 rad.



RDD: o

Necessary surgery m ust be done im m ediately (36â€“48 hours), or else delayed 1â€“2 m onths, with exposure >200 rad.

o

Any bom bing victim m ust be assessed for radioactive contam ination until RDD ruled out by assessm ent of scene.

o

Preserve evidence for crim inal investigation.

Medication (Drugs) Potassium iodide: 

Adults: 130 m g PO



Peds: o

3â€“18 years: 65 m g PO

o

1 m onth to 3 years: 32 m g PO

o

<1 m onth: 16 m g PO

Follow-Up Disposition When in doubt, adm it for serial CBC and obtain consultation.

Admission Criteria 

Lym phocyte count <1,000 at 24â€“48 hours postexposure



Lym phocyte count decreased 50% at 24â€“48 hours



Suspect acute exposure >200 rad.

Pa ge 3 9 9



Significant traum a or other illness



Uncontrolled vom iting

Discharge Criteria 

No residual contam ination



No evidence of acute exposure >100 rad



Tolerating oral fluids

Issues for Referral 

Internal contam ination: Contact REAC/TS for guidance.



External contam ination that cannot be rem oved



Any patient with radiation exposure will require dose assessm ent and risk counseling.



Skin injuries m ay require m onths of treatm ent and require expert consultation to guide dÃ©bridem ent.

References 1. Arm ed Forces Radiobiology Research Institute. Medical Managem ent of Radiological Casualties. 2nd ed. 2003. Available at http://www.afrri.usuhs.m il/. 2. Managem ent of Terrorist Events Involving Radioactive Material. NCRP Reportno. 138. Bethesda, MD: National Council on Radiation Protection; 2001. 3. Medical Radiobiology Advisory Team (MRAT): Call (301)295-0530. 4. Potassium iodide dosing: inform ation available at http://www.fda.gov/cder/guidance/4825fnl.htm . 5. Radiation Em ergency Assistance Center/Training Site (REAC/TS). Inform ation available at http://www.orisa.orav.gov/reacts/guides/m anage.htm 6. Step-by-step guidance for radiation incident m anagem ent: available at http://www.orau.gov/reacts/guidance.htm . 7. 24-hour em ergency line: (865) 576-1005 (ask for REACTS). 8. VA/DOD. Terrorism with Ionizing Radiation General Guidance Pocket Guide. Available at http://www.oqp.m ed.va.gov/cpg/cpg.htm

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Miscellaneous SEE ALSO: Chem ical Weapons Poisoning

Codes ICD9-CM NEC 990

Pa ge 3 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rapid Sequence Intubatio n

Rapid

Sequence Intubation Christopher Ross

Treatment Initial Stabilization 

Preparation: o

Have patient in appropriately m onitored area where resuscitation m ay be instituted.

o

Assem ble appropriate m edicines.

o

Apply cardiorespiratory m onitor, pulse oxim eter, and blood pressure (BP) m onitor.

o



Test laryngoscope blade: 

Adult: nos. 3 or 4 Macintosh (curved) blade



Child <8 years: no. 2 Macintosh blade



Term infant: no. 1 Miller (straight) blade



Prem ature infant: no. 0 Miller blade

Obtain endotracheal tube: o

Adult m an: 7.5â€“8.5 French

o

Adult wom an: 7.0â€“8.0 French

o

Child â‰¥4 years: age in years/4, or length based (Broselow tape)

o

Use cuffed endotracheal tube for children >8 years

Pa ge 3 9 9

and adults. o

Use uncuffed endotracheal tube for children <8 years.

o

Test endotracheal tube balloon with 15 m L syringe via inflation.

o

Use stylet for endotracheal tube; do not extend beyond distal endotracheal tube.

o 



End-tidal CO 2 m onitor

At bedside: o

Bag-valve m ask with functioning high-flow oxygen

o

Functioning suction with Yankhauer tip

Establish two IV lines: o

10 m l syringe

o

Water-soluble lubricant

o

Tape

o

Crash cart

o

Surgical airway backup tray

o

Evaluate the airway for potential difficulty.

o

Assess thyrom ental distance (distance between the thyroid cartilage and the inside of the anterior aspect of the m andible).

o 

Assess patient's ability to open m outh: o



Distances less than 5 cm m ay predict difficulty.

Distances less than 3 cm m ay predict difficulty.

Assess m obility of C spine: o

Flexion less than 35 degrees and extension less than 80 degrees m ay predict difficulty.



Assess faucial pillars, soft palate and uvula (Mallam pati classification) by having patient open m outh: o

Loss of visualization of posterior anatom ical structures m ore predictive of difficulty.



Assess m outh for dentition, palate, and tongue.

Pa ge 3 9 9



Medication drawn up and labeled

ED Treatment 

Preoxygenation: o

Oxygen (100%) for five m inutes if clinically practical; will allow nitrogen washout and give three to five m inutes before desaturation <90% occurs. Four m axim al inspirations with 100% oxygen are equally effective in a cooperative patient

o

Do not bag, as inflation of stom ach increases aspiration risk.



Pretreatm ent (three m inutes before paralytic): o

Vecuronium (defasciculating dose) or rocuronium

o

Atropine:

o

o 



For children <5 years



Before ketam ine adm inistration

Lidocaine: 

Increased intracranial pressure (ICP)



Ocular traum a



History of reactive airway disease

Fentanyl: for increased ICP

Induction and paralysis: o

Induction agent im m ediately before paralytic agent: 

Etom idate: m inim al hem odynam ic effects; therefore, best for hypotensive patients



Thiopental: for increased ICP; m ay cause hypotension, so use in hem odynam ically stable patients.

 o

Ketam ine: for status asthm aticus

Paralytic agent: 

Succinylcholine: Avoid in ocular traum a, hyperkalem ia, two days after severe crush injury/burn, or in congenital neurom uscular

Pa ge 3 9 9

disorders; if contraindication present, use alternative agent.  o

Alternative agents: rocuronium , vecuronium

Im m ediately apply cricoid pressure and release only after intubation successful.

o

Position the patient.

o

If no suspicion of a cervical spine injury, position the patient in the optim um â€œsniffingâ€• position.

o

If suspicion of cervical spine injury, an assistant should provide m anual in-line axial stabilization while rem oving the anterior portion of the cervical spine collar.



Placem ent of endotracheal tube: o

Intubate the trachea one m inute after the succinylcholine adm inistered



For Macintosh blade: o

Holding the laryngoscope in the left hand, sweep the patient's tongue up and to the left and into the space between the base of the tongue and the epiglottis, which should allow visualization of the glottis.



For Miller blade: o

Insert the blade com pletely and slowly withdraw which will allow the airway to fall into view as the epiglottis is held out of the way.

o

Lift handle anteriorly and inferiorly to elevate the m andible, tongue and epiglottis.



Do not rotate or â€œcrankâ€• or â€œcockâ€• on the laryngoscope or the blade m ay break the teeth.



Place tube through vocal cords with direct visualization of glottis.



Lim it attem pts to <30 seconds and ventilate briefly with bag-valve m ask between attem pts.

Pa ge 3 9 9



After placem ent, cuff should be inflated and placem ent confirm ed with sym m etric chest expansion, equal breath sounds bilaterally, end tidal CO 2 m onitor, and chest radiograph.



Secure the endotracheal tube with tape or a com m ercially available device.



Adm inister adequate sedation and neurom uscular relaxation as necessary.



Place nasogastric tube to decom press the stom ach.



Special clinical situations: o

Head injury or penetrating globe injury: 

Prevent ICP rise: lidocaine, vecuronium (defasciculating dose) fentanyl to prevent sym pathetic discharge.



Prevent vagally stim ulated bradycardia with atropine.



Sedation with etom idate or thiopental (if hem odynam ically stable)



Muscle relaxants/paralytic agents: succinylcholine or vecuronium

o

Status asthm aticus: Use ketam ine to sedate.

o

Status epilepticus: Use thiopental to sedate (raises seizure threshold) if hem odynam ically stable.

o

Multiple traum a/hem orrhagic shock: Use etom idate to sedate.

P.935

Medication (Drugs) 

Atropine: 0.02 m g/kg (m in. dose 0.1 m g to m ax. dose 4

Pa ge 3 9 9

m g IV)



o

Onset: <1 m inute

o

Indications: 

For pediatric intubations to prevent bradycardia



When ketam ine is used as induction agent

Etom idate: 0.3 m g/kg o

Onset: <1 m inute

o

Duration of action: 5 m inutes

o

Indications: 

For hem odynam ically unstable patients of cardiac and hypovolem ic causes

 o

Asthm atics, as it does not release histam ine

Cautions: 

Partial seizures (not generalized)



Nausea and vom iting



Myoclonus



Patients who have pre-existing adrenal suppression



Fentanyl: 2â€“4 Âµg/kg o

Onset: <90 seconds

o

Duration: 20â€“30 m inutes

o

Cautions: 

Respiratory depression (which can be reversed with naloxone 2 m g [adults] or 0.1 m g/kg [ped])

o 



Hypotension in hypovolem ia



Truncal rigidity

Indication: increased ICP

Ketam ine: 1.5â€“2 m g/kg IV o

Indication: status asthm aticus

o

Cautions: 

Head traum a (increases ICP)

Pa ge 3 9 9



Ischem ic heart disease (increases BP, heart rate, and m yocardial oxygen dem and)

 



Em ergence reactions

Lidocaine: 1.0 m g/kg IV: o

Onset: 1â€“3 m inutes

o

Indication: increased ICP

Rocuronium : 0.6 m g/kg IV: o

Onset: 1â€“3 m inutes

o

Duration: 30â€“35 m inutes

o

Cautions: tachycardia

o

Indications: when succinylcholine is contraindicated as paralytic agent in ocular traum a, in hyperkalem ia, two days after crush or burn injury, or in m alignant hypertherm ia



Succinylcholine: 1.0â€“1.5 m g/kg IV: o

Onset: <1 m inute

o

Duration: three to eight m inutes

o

Cautions: 

Bradyarrhythm ias



Increased intraocular or ICP



Hyperkalem ia (renal failure, neurom uscular disorders, or rhabdom yolysis)



2 days after burn or crush injury



Malignant hypertherm ia



Indication: paralytic of choice owing to rapid onset and short duration of onset



Thiopental: 3.0â€“5.0 m g/kg IV: o

Onset: 30â€“60 seconds

o

Duration: 5â€“10 m inutes

o

Cautions: 

Hypotension



Laryngospasm

Pa ge 4 0 0

 o

Bronchospasm via histam ine release

Indications: increased ICP in hem odynam ically stable patients



Vecuronium : o

Dosage: 

Defasciculating dose: 1 m g (adults), 0.01 m g/kg to m ax. 1 m g (pediatric)



Intubating dose: 0.8â€“0.15 m g/kg

o

Onset: 2â€“4 m inutes

o

Duration: 25â€“40 m inutes

o

Cautions: prolonged recovery tim e especially in obese or elderly or if hepatorenal dysfunction

o

Indications: when succinylcholine is contraindicated as paralytic agent in ocular traum a, in hyperkalem ia, 2 days after crush or burn injury, or in m alignant hypertherm ia

Follow-Up Disposition Admission Criteria Intensive care unit adm ission for all intubated patients

References 1. Chung D, Lam A. Essentials of Anesthesiology. 3rd ed. Philadelphia: WB Saunders; 1997. 2. Reichm an E, Sim on R. Em ergency Medicine Procedures. McGraw-Hill; 2004 3. Walls RM. Rapid sequence intubation in head traum a. Ann Em erg Med. 1993;22:1008â€“1013. 4. Walls RM. Airway. In: Marx J, ed. Rosen's Em ergency Medicine:

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Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.

Miscellaneous SEE ALSO: Airway Managem ent.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rash, Pediatric

Rash, Pediatric

Bruce Webster

Basics 

Lesion m orphology: o

Macule: 

Localized nonpalpable changes in skin color



Purpura or petechiae (nonblanching with pressure)



Maculopapule



Slightly elevated lesions with localized changes in skin

o

o

o

Papule: 

Solid, elevated lesions <5 m m in diam eter



Keratotic (rough-surfaced lesion)



Nonkeratotic (sm ooth lesion)



Palpable purpura (nonblanching with pressure)

Plaque: 

Solid, elevated lesions >5 m m in diam eter



Often results from a confluence of papules

Nodule: 

Solid, elevated lesions extending deep into the derm is or subcutaneous tissue >5 m m in diam eter

Pa ge 4 0 0

o

Wheal: 

Circular, irregular lesions varying from red to pale

o

Vesicle: 

o

Bullae: 

o

Clear, fluid-filled lesions >5 m m in diam eter

Pustules: 



Clear, fluid-filled lesions <5 m m in diam eter

Pus-filled lesions

Secondary lesions: o

Scales: 

Thin plates of dried cornified epithelium partially separated from the epiderm is

o

Lichenification: 

o

Dried plaques resulting in skin furrowing

Erosion: 

Moist surface uncovered by rupture of vesicles or bullae

o

Excoriation: 

o

Linear loss of the skin secondary to traum a

Ulcer: 

Deep loss of the skin involving the epiderm is and a variable am ount of the derm is and subcutaneous tissue



Configuration: o

Circles or arcs

o

Serpiginous (creeping or worm like)

o

Iris grouping (bull's eye appearance)

o

Irregular grouping

o

Zosteriform grouping

o

Linear grouping

o

Retiform grouping

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Description 

The color of a lesion or the entire skin m ay be due to a num ber of substances: o

Red or red-brown lesions result from oxyhem oglobin found in RBCs.

o

The m acular erythem atous lesions seen in viral exanthem a usually represent dilated superficial cutaneous vessels.

o

Purpura and petechiae result from leakage of RBCs out of the vascular space.

o

Hypopigm entation or hyperpigm entation represent postinflam m atory change from either increases or decreases in m elanin production.

o

Depigm entation refers to the total loss of pigm ent secondary to autoim m une effect (vitiligo) or in congenital disorders from a genetic inability to produce m elanin (albinism ).



Scales represent a proliferative disorder of epiderm al cell turnover.

Etiology 

Papulosquam ous: o



Infections: 

Viral or bacterial



Rickettsial or fungal

o

Allergic reactions

o

Autoim m une disorders

Purpura and petechiae: o

Clotting or platelet disorder

o

Vascular fragility disease

o

Vasculitis

o

Overwhelm ing infection

Pa ge 4 0 0





Vesicobullous: o

Infection

o

Drug reaction

o

Autoim m une disorder

Ulcer: o

Infection

o

Vascular insufficiency

Diagnosis Signs and Symptoms 

Fever (consider infectious exanthem as)



Pruritus



Joint pain



Abdom inal pain

Essential Workup 

Obtain a detailed history: o

Age-group: conditions, distribution and appearance m ay vary with age

o

Developm ent, progression, pattern and duration of the rash

o

Lesions synchronous or asynchronous

o

Associated sym ptom s

o

Prodrom esâ€”cough, rhinorrhea, pharyngitis, fever, m eningis m al sym ptom s, fever, pruritus



o

Fam ily history, exposures, im m unizations

o

Generic derm atoses

o

Atopic derm atitis

o

Psoriasis

Classify the rash based on the prim ary lesions:

Pa ge 4 0 0

o

Papulosquam ous

o

Vesicobullous

o

Purpuric

Tests Lab 

Indicated if the rash is purpuric: o

Com plete blood count (CBC) with platelet count

o

Bleeding screen (prothrom bin test, partial throm boplastin tim e, bleeding tim e, dissem inated intravascular coagulation [DIC] screen)



Indicated if fever present: o

CBC

o

Electrolytes, blood urea nitrogen, creatinine to evaluate dehydration and scarlatiniform rash (exclude glom erulonephritis)

o

Viral culture and titers for suspected exanthem s

o

Bacterial blood cultures for suspected system ic bacterial infection



Lum bar puncture if m eningococcus or other m eningitides or encephalitis suspected

Imaging 

Chest radiograph for suspected pulm onary involvem ent



Potassium hydroxide preparations: o

Indicated with scaling lesions to differentiate derm atophytosis from num m ular eczem a and pityriasis rosea

o

Superficial scale sam ple from active border of lesion rem oved from the skin with a scalpel or the edge of a glass slide

o

Place on a slide and add 1 drop of 10% KOH.

o

Place a coverslip and heat slowly without boiling.

Pa ge 4 0 0

Allow to set for a few m inutes and scan for hyphae. 

Wood lam p: o



Useful in derm atophytosis and erythrasm a

Scabies preparations: o

Most of the m ite population resides on the hands and feet.

o

Place a drop of m ineral oil on the lesion. Scrape with a no. 15 blade to produce speck of blood

o

Exam ine under low power for the m ite, ova, larva, or fecal m atter.

Differential Diagnosis Maculopapular Rash 



Solid, skin colored or yellow: o

Keratotic

o

Wart

o

Corn or callus

o

Nonkeratotic

o

Molluscum contagiosum

o

Sebaceous cyst

o

Basal and squam ous cell carcinom a

o

Nevi

Solid, brown: o

CafÃ© au lait patch

o

Nevi

o

Freckle

o

Melanom a

o

Photoallergic/Phototoxic drug eruption

o

Tinea nigra palm aris hypopigm entation

P.939

Pa ge 4 0 0



Solid, red, nonscaling: o

Nonpurpuric

o

Exanthem s: 

Rubeola, rubella or roseola



Scarlet fever



Toxin-producing staphylococcal or streptococcal disease



Erythem a infectiosum (fifth disease)



Rubellalike rash (echoviruses, coxsackie A viruses)





Varicella (early m anifestations)



Variola (sm allpox: early m anifestations)



Epstein-Barr virus



Enterovirus or adenovirus



Mycoplasm a



Kawasaki disease



Erythem a m ultiform e



Localized, pruriginous



Insect bites. Scabies



Allergic or irritant contact derm atitis

Purpuric: o

Bacterem ia sepsis 

Meningococcem ia, pneum ococcem ia, gonococcem ia, H influenzae



Endocarditis



Plague



DIC



Rocky Mountain spotted fever (RMSF)



Henoch-SchÃ¶nlein purpura



Idiopathic throm bocytopenic purpura



Leukem ia



Underlying bleeding disorder

Pa ge 4 0 0





Ecthym a gangrenosum



Rarely, pityriasis rosea

Solid, red, scaling: o

o

Without epithelial disruption: 

Tinea corporis, capitis, pedis, or cruris



Pityriasis rosea



Secondary syphilis



Lupus erythem atosus

With epithelial disruption: 

Papular urticaria



Eczem a



Seborrheic, diaper, contact, or stasis derm atitis



Im petigo



Candidiasis



Tinea corporis, capitis, pedis, or cruris

Vesiculobullous Rash 

Herpes virus: varicella, variola (sm allpox),



Herpes sim plex/zoster



Hand-foot-and-m outh syndrom e



Scabies



Drug hypersensitivity, toxic epiderm al necrolysis



Staphylococcal scalded skin syndrom e (SSS)



Im petigo, bullous im petigo



Cat-scratch disease



Derm atitis herpetiform is



Eczem a



Erythem a m ultiform e



Lichen planus

Pustular 

Acne



Folliculitis

Pa ge 4 0 1



Candidiasis



Gonococcem ia



Meningococcem ia

With Fever, Consider 

Infection



Drug reaction



System ic inflam m atory disease (juvenile rheum atoid arthritis, system atic lupus erythem atosus, etc.)

Treatment Pre Hospital Field m anagem ent is indicated when there are signs of system ic instability: 

Airway m anagem ent using precautions to avoid exposure to respiratory secretions; IV access



Identify rashes with a potentially life-threatening illness or need for special isolation.

Initial Stabilization Aggressive, em piric m anagem ent of children with a purpuric rash associated with fever or unstable vital signs: 

Airway support, IV access, pressors if cardiovascular collapse





IV antibiotics should be adm inistered as soon as possible: o

Cefotaxim e or ceftriaxone

o

Plus doxycycline if RMSF is considered

Fluid resuscitation as if burn with SSS or toxic epiderm al necrolysis

ED Treatment

Pa ge 4 0 1



Specific ED treatm ent should be directed to the underlying etiology.



Diphenhydram ine should be used when an allergic reaction is suspected.

Medication (Drugs) 

Acetam inophen: 10â€“15 m g/kg PO/PR q4hâ€“q6h



Cefotaxim e: 50 m g/kg IV q6h; m ax. dose, 12 g/24h



Ceftriaxone: 50 m g/kg IV q12h; m ax. dose, 4 g/24h



Diphenhydram ine: 1.25 m g/kg PO/IM/IV q6h



RSMF: o

Doxycycline: 100 m g PO/IV q12h (older than 8 years) or chloram phenicol 12.5 m g/kg/dose q6h (m ax. 500 m g/dose)



Kawasaki disease: o

Im m une globulin: 2 g/kg IV over 10â€“12 hours and aspirin 25 m g/kg/dose PO q6h



Varicella: o

Acyclovir: 800 m g PO q.i.d. (peds: 20 m g/kg/dose) with pulm onary or CNS involvem ent; give 10â€“12 m g/kg/dose IV q8h in the im m unocom prom ised patient; no aspirin should be used



Toxic shock syndrom e or SSS: o

Nafcillin or oxacillin: 2 g IV q4h (peds: 200 m g/kg/d IV q4h); alternative: cefazolin 2 g IV q8h (peds: 100 m g/kg/d IV q8h)



Scarlet fever: o

Penicillin V: 500 m g PO q.i.d. (peds: 250 m g PO q.i.d.) for 10 days; alternative: erythrom ycin 250â€“500 m g PO q.i.d. (peds: 12.5 m g/kg/dose PO q.i.d.) Ã— 10 days, or azithrom ycin 500 m g PO per

Pa ge 4 0 1

day (peds: 12 m g/kg/d PO per day) for 5 days

Follow-Up Disposition Admission Criteria 

Hospital adm ission is determ ined by the underlying disorder.



Adm it life-threatening conditions: m eningococcem ia, RMSF, toxic shock syndrom e, Kawasaki disease.



Other illnesses associated with system ic illness or potential deterioration; SSS, rubeola, and varicella, as well as others, m ay require inpatient care.

Discharge Criteria 

Discharge instructions should be based on the underlying disorder.



Exanthem s associated with self-lim ited entities in stable children: o

Follow-up with prim ary care physician or derm atologist should be arranged.

References 1. Mancini AJ. Childhood exanthem s: a prim er and update for the derm atologist. Adv Derm atol. 2000;16:337. 2. Pom eranz AJ. The system atic evaluation of the skin in children. Pediatr Clin North Am . 1998;45:49â€“63.

Miscellaneous SEE ALSO: Henoch-SchÃ¶nlein Purpura; Staphylococcal Scalded Skin

Pa ge 4 0 1

Syndrom e

Codes ICD9-CM 782.1

ICD10 R21

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rash

Rash

Owen Lander J. Scott Goudie

Basics Description Abnorm al skin lesions that can be classified into broad categories: 

Erythem a/Red m acular lesions from dilatation of superficial vasculature



Vesicobullous lesions form ed by disruption of epiderm al/derm al integrity and filling with exudative fluid, com m only allergic/infectious/system ic inflam m atory response



Purpura and petechiae from failure of norm al vascular integrity/hem ostatic m echanism s



Nodules from prolonged inflam m atory response



Urticaria from contact/system ic allergic response, histam ine release

Etiology 

Maculopapular: o

Infections: 

Viral



Bacterial



Rickettsial

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





Fungal



Parasitic

o

Allergic reaction

o

Autoim m une disease

Purpura/petechiae: o

Clotting pathway dysfunction

o

Platelet dysfunction, qualitative or quantitative

o

Vasculitis

o

System ic infection, sepsis

Vesicobullous: o

Localized: 

Allergic reaction



Mechanical/physical traum a: heat, radiation, sunburn

 o

Infections

Generalized (system ic): 

Infections



Allergic reaction/anaphylaxis



Autoim m une

Diagnosis Signs and Symptoms History 

Age



Im m une status (HIV, chem otherapy, diabetes, steroids)



Previous episodes/prior history of lesions/reactions



Sick contacts



Chronologic and physical evolution



Associated sym ptom s, pruritus, fever, abdom inal pain,

Pa ge 4 0 1

m yalgias/arthralgias 

Prodrom e: fever, headache, cough, odynophagia, rhinorrhea



Environm ental exposure: tick bite, unusual flora, diet, travel



Recent change in m edication



Fam ily history

Physical Exam 

Prim ary lesion appearance: o

Macule: 

Nonraised areas of distinct coloration



Blanching lesions are inflam m atory; nonblanching lesions are either altered pigm entation or petechiae/purpura.

o

Papule: 

Raised, palpable lesions <5 m m in diam eter, nonfluid filled



Hem orrhagic, nonblanching lesions palpable purpura

o

Vesicles: 

o

Bullae: 

o

Sm all, raised, clear fluid-filled lesions (<5 m m )

Large, raised, clear fluid-filled lesions (>5 m m )

Pustules: 

As vesicles and bullae, but containing purulent fluid

o

Nodule: 

Solid, raised lesion >5 m m seated in deeper layer of skin and tissue



Secondary changes: o

Scaling, lichenification, excoriation, fissuring all result from m anipulation/scratching or

Pa ge 4 0 1

proliferation/shedding of epiderm al cells o

Erosions/ulcers from varying degrees of tissue loss (superficial to deep) from loss of vascular supply/tissue integrity



Distribution: o

Characterized as central/peripheral, confluent/scattered, m ucosal/nonm ucosal, presence of palm /sole involvem ent



Associated signs/sym ptom s: o

Pruritus associated with allergic reactions, system ic and contact

o

Fever with infection/drug reaction/system ic inflam m atory response, viral exanthem a com m on in children



Vital signs: o

Abnorm al vital signs, airway com prom ise, respiratory distress, hem odynam ic instability present in severe disease.

Essential Workup 

Identify system ic illness: o

Fever

o

Abnorm al vital signs

o

Nausea, vom iting, abdom inal pain, generalized distribution, altered m ental status

o

Signs/Sym ptom s of local infectious source: 

Pharyngitis, abscess, foreign body, m eningism us signs



Categorize the lesions: o

Maculopapular

o

Vesicobullous

o

Petechial

Pa ge 4 0 1

Tests Lab 

Presence of fever, system ic sym ptom s, or possible infection warrants blood work: o

CBC with differential, electrolytes, blood urea nitrogen/creatinine

o

Blood cultures, viral cultures

o

Gram stain and culture of purulent lesions

o

Tzanck sm ear for suspected herpetic lesions

o

Venereal disease research laboratory/rapid plasm a reagin for suspected syphilis



Suspected autoim m une disorders (Lupus, rheum atoid arthritis, juvenile rheum atoid arthritis, Sjogren syndrom e) o

CBC, ESR, particular assays in consultation with rheum atologist (ANA, antineutrophil cytoplasm ic antibody, etc.)



Petechiae/Purpura warrant com plete coagulation evaluation: o

CBC with platelets

o

Partial throm boplastin tim e, prothrom bin tim e, international norm alized ratio

o

Dissem inated intravascular coagulation (DIC) screen: fibrinogen, fibrin split products, haptoglobin, LDH

Imaging Chest radiograph indicated for respiratory sym ptom s, possible infectious/autoim m une etiology.

Diagnostic Procedures/Surgery 

Lum bar puncture for altered m ental status, m eningeal signs, suspected m eningococcus



Biopsy under derm atologic consultation to differentiate

Pa ge 4 0 1

allergic/autoim m une/infectious processes. 

Nikolsky test: expansion of bullous lesion with lateral stress at m argin indicates epiderm al/derm al disruptive process



Scrapings: Indicated to rule out topical fungal infections and parasites o

Potassium hydroxide preparation from edge of lesion reveal hyphae

o

Plain m ineral oil to rule out scabies in pruritic linear lesions of hands

Differential Diagnosis 

Diffusely erythem atous rashes: o

Toxic shock syndrom e (TSS): exotoxin, 90% Staphylococcus aureus, desquam ation 2 weeks after early rash, end organ involvem ent

o

Toxic epiderm al necrolysis (TEN): constitutional sym ptom s, adults, drug related, positive Nikolsy test result, full-thickness desquam ation, oral lesions prom inent

o

Staphylococcal scalded skin syndrom e (SSSS): exotoxin, fever, m alaise, flaccid bullae later, superficial desquam ation, oral lesions rare, children



o

Kawasaki syndrom e

o

Generalized exfoliative erythroderm a

o

Lupus

o

Cutaneous T-cell lym phom a

Vesicobullous lesions: o

Anaphylaxis

o

Stevens-Johnson syndrom e: continuum with TEN, drug related, constitutional sym ptom s, m ucous m em branes involved, sym m etric blistering P.937

Pa ge 4 0 2

o

Toxic epiderm al necrolysis

o

Pem phigus vulgaris: fulm inant, usually 40â€“65 years, painful, flaccid bullae, positive Nikolsky test result, oral lesions, antiepithelial antibody by biopsy

o

Bullous pem phigoid: m ore elderly population, oral lesions less com m on, positive Nikolsky test result, basem ent m em brane antibody by biopsy

o

Sm allpox

o

Dissem inated herpes sim plex, zoster/varicella, vaccinia



Maculopapular and local lesions: o

Gonococcem ia: sexually active, polyarthritis, tenosynovitis, hem orrhagic pustules with erythem atous base

o

Secondary syphilis

o

Erysipelas

o

Pustular psoriasis

o

Ecthym a gangrenosum : with gram -negative sepsis, discrete lesions, few in num ber, peripheral, evolve from m acule to pustule to an erythem atous base



o

Envenom ations

o

Malignancy

Petechial/purpuric lesions: o

Meningococcem ia

o

Gonococcem ia

o

Pneum ococcem ia

o

DIC

o

Rocky Mountain spotted fever (RMSF): pronounced prodrom e of fever, headache, m yalgia, rash, peripheral m oves to palm s/soles, system ic

Pa ge 4 0 2

o

Babesiosis: sim ilar to RMSF, rash less often, frequent co-infection with Lym e



o

Henoch-SchÃ¶nlein purpura

o

Multiple system ic illnesses (see Purpura)

Nonlethal diagnoses: o

Maculopapular lesions: 

Psoriasis



Tinea



Pityriasis rosea



Seborrheic derm atitis



Intertrigo



Lichen planus



Lym e disease



Phototoxic and photoallergic reactions



Viral exanthem s (m ostly in children, see Rash, Pediatric)

o



Contact derm atitis



Scabies



Eczem a



Im petigo



Candidiasis



Urticaria



Nevi



Hypopigm entation



Warts

Vesicobullous lesions: 

Herpes sim plex



Zoster



Vaccinia



Contact allergic derm atitis



Coxsackie (hand, foot, m outh)



Echovirus

Pa ge 4 0 2

o



Scabies



Insect bites

Petechial/purpuric lesions: 

Usually reflect system ic infection/inflam m ation/vasculitis

o



Few trivial causes



Actinic purpura in elderly



Traum atic

Pustular lesions: 

Trivial causes m ust be localized, have no associated sym ptom s, and no petechial com ponent.



Folliculitis



Candidiasis



Acne

Treatment Pre Hospital 

Managem ent is dictated by presence of hem odynam ic instability, airway com prom ise, and concern for infectious exposure.

Alert Universal precautions, m asks if infectious etiology suspected

Initial Stabilization 

Aggressive, presum ptive m anagem ent of potentially lethal presentations: o

Petechial lesions

o

Fever

o

Dissem inated erythem atous or vesicobullous lesions

Pa ge 4 0 2



Treat for anaphylaxis if acute, urticarial, known exposure, or respiratory distress.



Treat resuscitation of dissem inated bullous or exfoliative disease as a severe therm al burn.

ED Treatment 

Treatm ent directed for underlying cause



Antibiotics if life threatening infectious em ergency suspected: o

SSSS: nafcillin/oxacillin

o

TSS: penicillin G and clindam ycin: 

Rem oval of the offending agent, supportive care, if any clinical suspicion treat as infectious



o

RMSF: doxycycline or chloram phenical

o

Meningococcem ia: ceftriaxone or penicillin G

If varicella or dissem inated herpes is suspected, initiate acyclovir.



Sym ptom atic treatm ent of pruritus (diphenhydram ine or hydroxyzine)



Steroid therapy reserved for clear allergic reactions, relapse of known steroid responsive disease, or in consultation with derm atologist



Allergic reactions treated aggressively: o

Diphenhydram ine

o

H2-blocker

o

Steroids

o

Epinephrine if respiratory com prom ise

Medication (Drugs) 

Acetam inophen: 625 m g PO/PR q4hâ€“q6h (peds: 60 m g/kg/24h)

Pa ge 4 0 2



Acyclovir: 10 m g/kg/dose IV q8h



Cefotaxim e: 1â€“2 g IV q6h (peds: 100â€“200 m g/kg/24h)



Ceftriaxone: 1â€“2 g IV q12h (peds: 100â€“200 m g/kg/24h)



Chloram phenicol: 50 m g/kg/24h IV divided q6h (peds: sam e)



Clindam ycin: 900 m g IV q8h (peds: 40 m g/kg/24h)



Diphenhydram ine: 50 m g PO/IM/IV q6h (peds: 5 m g/kg/24h)



Doxycycline: 100 m g PO q12h (peds: 4.4 m g/kg/24h divided, m ax. 100 m g; not recom m ended <8 years old)



Epinephrine: 0.1â€“0.5 m g SC/IM (1:1000 solution), m ay repeat SC q15m in (peds: 0.01 m g/kg/dose)



Hydroxyzine: 25â€“100 m g PO q6h (peds: 50 m g/24h)



Methylprednisolone: 125 m g IV q24h (peds: 0.5â€“2 m g/kg/24h)



Nafcillin/oxacillin: 2 g IV q4h (peds: 150 m g/kg/24h)



Penicillin G: 6 m illion units IV q6h or 2 m illion units IV q2h (peds: 400,000 U/kg/24h)

Follow-Up Disposition Admission Criteria 

Potentially lethal diagnoses



All patients receiving IV antibiotic/fluid support



Patients with significant bullous/exfoliative disorders



Associated system ic sym ptom s



Metabolic/Electrolyte disorders

Discharge Criteria

Pa ge 4 0 2



Lim ited lesions



Viral exanthem s



Absence of system ic signs or sym ptom s m ay discharge to follow-up with prim ary care physician/derm atologist

References 1. Brady WJ, DeBehnke D, Crosby DL. Derm atological em ergencies. Am J Em erg Med. 1994;12(2):217â€“237. 2. Cydulka RK. Derm atologic disorders. In: Marx JA, ed. Marx: Rosen's em ergency m edicine: concepts and clinical practice. St. Louis, MO: Mosby, 2002. 3. Fitzpatrick TB, et al. Color atlas and synopsis of clinical derm atology. New York: McGraw-Hill, 2001. 4. Forstater AT, Neuberger KJ. Life threatening derm atoses. In: Harwood-Nuss A, ed. The clinical practice of em ergency m edicine. Philadelphia, PA: JB Lippincott Co, 2001. 5. Habif TP. Clinical derm atology: a color guide to diagnosis and treatm ent. St. Louis, MO: Mosby, 2003.

Codes ICD9-CM 709.9

ICD10 R21

Pa ge 4 0 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Reactive Arthritis

Reactive Arthritis

Christine Yang-Kauh

Basics Description 

Culture-negative arthritis after extra-articular infection, usually enteritis or venereal disease



System ic disease with widely varying extra-articular sym ptom s



â€œReiter syndrom eâ€• is the classic triad of: o

Arthritis

o

Nongonoccocal urethritis/cervicitis

o

Conjunctivitis



Num ber-one cause of inflam m atory arthritis in young m en



Men >wom en by 5â€“10:1 in venereal infection



Men = wom en in enteric infection



Peak onset 15â€“35 years of age



First episode of arthritis usually resolves in 3â€“6 m onths



10â€“20% Recurrence or chronic disease



1% severe or fatal disease o

Keratoderm a blenorrhagica is a predictor of poor outcom e



Rate of chronic disease varies with etiologic organism and presence of HLA-B27.

Pa ge 4 0 2

Genetics 

Genetic predisposition plays a strong role.



HLA-B27 seen in 70â€“80% of patients

Etiology 

Different m echanism s m ay be used depending on the infectious agent.



Infection-triggered aseptic arthritis: o

Ongoing im m une response to persistent bacterial antigen

o

Autoim m une response or antigenic cross-reactivity with HLA-B27 (i.e., enteric organism s)



Chronic infection with a sm all am ount of a slow-growing, difficult to culture organism : o



Chlam ydia, m ycoplasm a, borrelia

First episode of arthritis typically occurs 1â€“6 weeks after infection with: Salm onella, Shigella, Yersinia, Cam pylobacter, and Chlam ydia



Case reports of m any other agents, including HIV, C. Difficile and intravesicular BCG

Diagnosis Signs and Symptoms 

History of dysentery, urethritis, or cervicitis 1â€“6 weeks prior



Musculoskeletal: o

o

Asym m etric oligoarthritis 

Usually lower extrem ities



May be m igratory

Dactylitis: â€œsausageâ€• digits

Pa ge 4 0 2

o

Enthesitis: inflam m ation of the tendinous insertions into bone

o













Low back pain



Alternating buttock pain

o

Achilles tendonitis

o

Plantar fasciitis

General: o

Fever

o

Weight loss

o

Malaise

Eyes: o

Conjunctivitis with m ild nonpurulent discharge

o

Uveitis, iritis,

Mouth: o

Oral ulcers: erythem atous, painless, transient

o

Often unnoticed

Cardiovascular: o

Rare dysrhythm ia

o

Pericarditis or aortic regurgitation in chronic disease

Gastrointestinal o



Sacroiliitis:

Diarrhea 1â€“6 weeks prior

Genitourinary: o

Nonpurulent urethritis: 

Dysuria, urinary frequency



Occasional hem aturia

o

Cervicitis

o

Balanitis circinata: 



Shallow, painless, red penile lesions

Skin, nails: o

Keratoderm a blennorrhagica: 

Clear vesicles on an erythem atous base that

Pa ge 4 0 2

evolve to hyperkeratotic lesions





Com m only on soles, palm s



Associated with severe disease

o

Onycholysis

o

Nail yellowing and hyperkeratosis

Neurologic: o

Rare transient neurologic dysfunction: 

Nerve palsies, hem iplegia

Essential Workup 

Includes a search for the etiologic infection by history and exam ination, especially in wom en where cervicitis is often asym ptom atic



Joint aspiration should be perform ed to rule out septic arthritis or crystal arthropathy.

Tests Lab 

Urethral or cervical swab for Chlam ydia infection: o

Preferably direct fluorescent antibody or DNA probes for chlam ydial ribosom al RNA



CBC with differential m ay show a m oderate neutrophilic leukocytosis and anem ia.



ESR m ildly elevated



C-reactive protein and C3/C4 levels m ildly elevated



Rheum atoid factor, ANA and HLA-B27 m ay be considered for further rheum atologic work-up.



Stool cultures if ongoing dysentery



HIV testing should be considered, especially if use of im m unosuppressive therapy is contem plated

Imaging 

Radiograph of affected joints:

Pa ge 4 0 3

o

Usually norm al

o

Soft tissue swelling and effusion m ay be seen.

o

Enthesitis (periosteal spurs with indistinct m argins and fluffy periostitis at the sites of tendinous insertions) m ay be noted, especially of the lower extrem ities.



Radiograph of lum bar spine, sacroiliac joints: o

Unilateral sacroiliitis in early disease (10%)

o

Bilateral in chronic disease (70%)

o

Asym m etric spondylitis

o

Syndesm ophytes

P.941

Diagnostic Procedures/Surgery Arthrocentesis with fluid analysis should be perform ed: 

Synovial fluid shows inflam m ation (usually between 2â€“50,000 cells/m L) with neutrophilia.



Fluid glucose is norm al.



Fluid is gram stain and culture negative

Differential Diagnosis 

Gonococcal arthritis



Ankylosing spondylitis



Psoriatic arthritis



Arthritis related to inflam m atory bowel disease



Occult celiac disease



Undifferentiated spondyloarthropathy



Lym e disease



BehÃ§et syndrom e



Rheum atoid arthritis



Still's disease

Pa ge 4 0 3



Sarcoid arthritis



Gout/pseudogout



Rheum atic fever



Viral arthropathy

Treatment Initial Stabilization 

Supportive care



IV fluids if hypovolem ia due to dysentery



Ice to inflam ed joints

ED Treatment 

High-dose NSAIDs are the m ainstay of therapy: o

A m inim um of 1 m onth of NSAID treatm ent at m axim um dosage is m andatory before evaluating effectiveness



Sulfasalazine for NSAID failure or contraindication



Treat urethritis/cervicitis if present or suspected: o

Doxycycline or azithrom ycin

o

Prolonged (up to 3 m onths) of antibiotic treatm ent for chlam ydia-associated arthritis m ay im prove recovery.

o

Partners should also be treated.



Antibiotics are not indicated for enteric disease.



Local corticosteroids injections m ay be helpful for severe arthritis or enthesitis.



In persistent or aggressive disease, im m unom odulating therapies m ay be initiated in consult with a rheum atologist: o

System ic corticosteroids

Pa ge 4 0 3

o

Azathioprine

o

Methotrexate

Medication (Drugs) 

Azathioprine: 1â€“2.5 m g/kg/d PO q12hâ€“q24h



Azithrom ycin: 1 g (peds: 10 m g/kg) PO for 1 day



Doxycycline: 100 m g (peds: 5 m g/kg/d, div.) PO q12h for 10 days (consider prolonged therapy)



Ibuprofen: 2,400 m g/d, div. (peds: 20â€“40 m g/kg/d) PO q6hâ€“q8h



Indom ethacin: 75â€“200 m g/d (peds: 1â€“2 m g/kg/d) PO q6hâ€“q12h



Methotrexate: 7.5â€“25 m g (peds: 0.5â€“1 m g/kg; m axim um , 15â€“25 m g) PO per week for aggressive unrem itting disease



Sulfasalazine: 1â€“3 g (peds: 30â€“60 m g/kg/d; m ax., 2 g) PO q6h, for NSAID failure or contraindication

Pregnancy Considerations 

Doxycycline is contraindicated in pregnancy.



Azithrom ycin m ay be safe.



Am oxicillin: 500 m g PO t.i.d. for 7 days



Erythrom ycin: base 500 m g PO q6h Ã— 7 days

Follow-Up Disposition Admission Criteria 

Concom itant disease(s) that require adm ission

Pa ge 4 0 3



Unrem itting pain or inability to am bulate

Discharge Criteria Most patients can be discharged.

Issues for Referral 

Close follow-up with a rheum atologist or a prim ary care physician is required.



Physical therapy and vocational counseling m ay help.

References 1. Am or B. Reiter's syndrom e: diagnosis and clinical features. Rheum Dis Clin North Am . 1998;24(4):677â€“695. 2. Flores DF, Marquez J, Garza M, Espinoza LR. Reactive arthritis: newer developm ents. Rheum Dis Clin N Am . 2003;29:37â€“59. 3. Kataria RK, Brent LH. Spondyloarthropathies. Am Fam Physician. 2004;69:2853â€“2860. 4. Sibilia J, Lim bach FX. Reactive arthritis or chronic infectious arthritis? Ann Rheum Dis. 2002;61:580â€“587.

Codes ICD9-CM 716.80

ICD10 M02.9

Pa ge 4 0 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rectal Pro lapse

Rectal Prolapse

Scot Hill

Basics Description Three types of rectal prolapse: 

Full-thickness rectum protrudes through anus; by far m ost com m on.



Partial thickness or m ucosal prolapse: o



Only m ucosal layer protrudes through anus.

Internal or occult prolapse: o

May be partial or full thickness

o

Never protrudes through anus

o

May be difficult to diagnose

Etiology 



Cause unclear and m ultifactorial: o

Chronic constipation/straining at stool

o

Laxity of sphincter: 

Pelvic floor traum a/weakness



Neurologic disease

More com m on in wom en, peak in seventh decade.

Pediatric Considerations 

Very rare after age 4 years

Pa ge 4 0 3



True rectal prolapse unusual in children; m ore likely partial or intussusception



Consider chronic diarrhea, parasites, cystic fibrosis (CF) as contributing causes.

Diagnosis Signs and Symptoms 

Protruding rectum



Mucous or bloody discharge



Sensation of rectal m ass



Tenesm us



Constipation or incontinence

History History with em phasis on bowel obstruction and duration of prolapse: 

Often progressive sym ptom s over tim e with self-reducing prolapse initially

Physical Exam Rectal exam inationâ€”m ust differentiate prolapse, hem orrhoids, or intussusception: 

True prolapse shows circum ferential circular folds in beefy m ucosa of protruding rectum .



Mucosal prolapse rarely m ore than a few centim eters of protrusion; will not contain m uscular layer



Internal hem orrhoids identified by folds of m ucosa radiating out like spokes in wheel



Intussusception identified by placing exam ining finger between protruding rectum and anus

Essential Workup Careful physical exam ination

Pa ge 4 0 3

Tests Lab 

No lab test necessary for uncom plicated prolapse



Preoperative testing for incarcerated, going to OR

Imaging No im aging is necessary for uncom plicated prolapse.

Differential Diagnosis 

Prolapsed internal hem orrhoids



Prolapsed polyp



Other rectal m ass

Treatment Pre Hospital 

Position of com fort



Prevent m ucosal desiccation with m oist gauze.



Avoid traum a to m ucosa.

Initial Stabilization Stabilization generally not needed in sim ple prolapse P.943



Incarcerated or ischem ic prolapse: o

NPO

o

IV fluids

o

Prepare for surgery.

ED Treatment 

Reduce prolapse:

Pa ge 4 0 3



o

Gentle steady pressure

o

Invert m ucosa through lum en from distal.

o

Sedation as needed to relax sphincter

If prolapse incarcerated or ischem ic: o

Adm ission for reduction and surgical correction before swelling creates full-thickness necrosis

Alert 

Constriction of blood flow to rectum by anal sphincter can lead to ischem ia, possible loss of gut.



Tim ely reduction decreases risk.



Surgical intervention required for ischem ic m ucosa.

Medication (Drugs) Sedation and pain m edication only as needed

Follow-Up Disposition Admission Criteria 

Necrotic or ischem ic m ucosa



Inability to reduce acute prolapse

Discharge Criteria 

Reduced rectal prolapse



Stable and tolerating PO



Instructions to reduce pressure on rectum : o

Correct constipation: 

Stool softeners



Increase fluid intake.

Pa ge 4 0 3

o

Avoid prolonged sitting or straining.

Issues for Referral Refer for workup including: 

Search for leading lesion.



Refer for definitive surgical repair of recurrent prolapse.



Testing for CF in children

References 1. Heine JA, Wong WD. Rectal prolapse. In: Mazier PW, et al., eds. Surgery of the colon, rectum , and anus. Philadelphia: WB Saunders; 1995:515â€“537.

Miscellaneous SEE ALSO: Hem orrhoid

Codes ICD9-CM 569.1

ICD10 K62.3

Pa ge 4 0 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rectal Traum a

Rectal Trauma

Elaine Sapiro

Basics Description 

Injury to rectal m ucosa



Sim ple contusion to full-thickness laceration with extension into peritoneum or perineum



Two thirds of rectum is extraperitoneal.

Etiology 



Penetrating traum a: o

Gunshot wounds account for 80%.

o

Knife wounds

o

Im palem ent injuries

Blunt traum a; less frequent cause of rectal injury: o

Motor-vehicle collision

o

Motorcycle accident

o

Waterskiing and watercraft accidents: 

o

Falls and crush injuries

o

Pelvic fractures: 



Hydrostatic pressure injury

Bony fragm ents penetrate rectum

Foreign body: o

Autoeroticism

Pa ge 4 0 4



o

Anal intercourse

o

Assault

o

Ingestion of sharp objects

Iatrogenic traum a is m ost com m on cause of rectal injury: o

Barium enem a: 

Perforation occurs in 0.04% patients; 50% m ortality.

o

Colonoscopy: 

0.2% perforation rate; increased risk with polypectom y

o

Urologic and obstetric-gynecologic procedures

o

Episiotom y

Pediatric Considerations 

Rectal injury m ay result from therm om eter insertion.



Any rectal traum a in young children should raise the suspicion of nonaccidental traum a.

Diagnosis Signs and Symptoms 

Perineal, anal, or lower abdom inal pain



Signs of perforation or peritonitis: o

Guarding

o

Rebound tenderness

o

Fever



Pelvic fracture



Rectal bleeding



Obstipation



History of anal m anipulation, foreign body insertion, sexual abuse

Pa ge 4 0 4

Essential Workup 

History: o

Tim e and m echanism of injury

o

Suspect rectal injury in all patients with gunshot wound, stab wound, or im palem ent injury to trunk, buttocks, perineum , or upper thigh.

o

Consider in any patient with history of anal m anipulation com plaining of lower abdom inal or pelvic pain



Physical exam ination: o

Inspect and palpate thoroughly the buttocks, anus, and perineum .

o

Identify entrance and exit wounds if penetrating traum a.

o

Perform digital rectal exam ination to assess for gross blood or guaiac-positive stool; note position of prostate.

o

Assess perineal integrity: speculum and bim anual exam in all fem ale patients, thorough genitourinary exam in all m ale patients.



Anoscopy and sigm oidoscopy: o

Must be perform ed if rectal injury is suspected by history or exam

o

Irrigate and suction feces and blood.

o

Avoid insufflating large am ount of air during sigm oidoscopy: 

Can force stool into peritoneum if proxim al bowel perforation exists



Evidentiary exam required in cases of sexual assault.

Tests Lab

Pa ge 4 0 4



CBC



Type and screen



Urinalysis

Imaging 

Supine/Upright abdom inal film s, pelvic radiographs: o

Evaluate for pneum operitoneum or extraperitoneal and extrarectal densities suggesting perforation.

o

Identify location, size, and shape of foreign body.

o

Identify pelvic fracture or diastasis of sym physis pubis, which m ay accom pany rectal injury.



Retrograde urethrogram if high-riding prostate noted on rectal exam .



Contrast enem a helpful only in situations where perforation is unclear: o

Use water-soluble contrast (e.g., gastrografin)

Differential Diagnosis 

Colon injuries



Genitourinary injuries

Treatment Alert 

Airway m anagem ent and resuscitation as indicated



Spinal precautions if blunt traum a



Fluid resuscitation if blood loss, hypotension



Prehospital personnel should not attem pt to rem ove foreign body from rectum .

Initial Stabilization In penetrating or blunt abdom inal traum a, follow traum a protocols:

Pa ge 4 0 4



Prim ary survey



Resuscitation



Secondary survey



Treatm ent

P.945

ED Treatment 

Adm inister tetanus prophylaxis if needed.



Adm inister broad-spectrum antibiotics if significant m ucosal disruption or signs of peritonitis are present (see Medications).



Place Foley catheter after excluding urethral injury.



Obtain surgical consultation for: o

Peritonitis

o

All traum atic rectal m ucosal lacerations

o

Objects >10 cm from anal verge

o

Sharp objects whose rem oval m ay provoke m ucosal injury

o 

Inability to extract foreign body in ED

Rectal foreign body rem oval in ED: o

Determ ine location and type of foreign object.

o

Provide adequate IV sedation and use gentle digital sphincter dilation to increase likelihood of successful ED extraction.

o

Adm inister local anesthesia to m axim ize anal sphincter dilation.

o

Place patient in lithotom y position: 

Use obstetric, ring, or biopsy forceps, tenaculum , or suctioning device to aid extraction.



Apply suprapubic pressure.

Pa ge 4 0 4

 o

Have patient bear down during procedure.

Other m ethods: 

Pass Foley catheter above foreign body, inflate balloon and apply gentle traction to release suction and perm it extraction.



Plaster of Paris: Fill hollow object and insert gauze or instrum ent to serve as â€œhandleâ€• ; place above or adjacent to foreign body; when hard, pull on inset handle to perm it extraction.

o

Sigm oidoscopy to evaluate m ucosal injury following extraction

Medication (Drugs) 

Antibiotics with coverage against gram -negative and anaerobic organism s: o

Am picillin/sulbactam : 

o

Cefotetan: 

o

Adults: 3.1 g IV (peds: 75 m g/kg IV)

Additional anaerobic coverage: o

Clindam ycin: 

o

Adults: 600â€“900 m g IV (peds: 10 m g/kg IV)

Metronidazole: 



Adults: 3.375 g IV (peds: 75 m g/kg IV)

Ticarcillin/clavulanate: 



Adults: 2 g q6h IV (peds: 80 m g/kg q6h IV)

Piperacillin/tazobactam : 

o

Adults: 2 g q12h IV (peds: 40 m g/kg IV)

Cefoxitin: 

o

Adults: 3 g q6h IV (peds: 50 m g/kg IV)

Adults: 1 g IV (peds: 15 m g/kg IV)

Com bination therapy:

Pa ge 4 0 4

o

Adults: Am picillin 500 m g IV q6h, gentam icin 1â€“1.7 m g/kg IV, and m etronidazole 1 g IV

o

Peds: Am picillin 50 m g/kg IV q6h, gentam icin 1â€“1.7 m g/kg IV, and m etronidazole 15 m g/kg IV



Sedation and analgesia: o

Fentanyl: 2â€“3 Âµg/kg IV (peds and adults)

o

Midazolam : 0.01â€“0.2 m g/kg IV (peds and adults)

Surgery 

Rectal foreign body rem oval in operating room .



General anesthesia is required to rem ove high-riding or sharp object.



Laparotom y is last resort.

Follow-Up Disposition Admission Criteria 

Perforation



Significant bleeding



Unstable vital signs



Abdom inal pain



Torn anal sphincter



Foreign body that requires extraction in operating room



Broken glass or other sharp object in rectum requiring surgical rem oval

Discharge Criteria 

Stable vital signs



No abdom inal pain



Norm al sigm oidoscopy/anoscopy exam

Pa ge 4 0 4

References 1. Carrillo EH, Som berg LB, Ceballos CE, et al. Blunt traum atic injuries to the colon and rectum . J Am Coll Surg. 1996;183:548â€“552. 2. Coates WC. Anorectum . In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1343â€“1359. 3. Cohen JS, Sackier JM. Managem ent of colorectal foreign bodies. J R Coll Surg Edinb. 1996;41:312â€“315. 4. Fry RD. Anorectal traum a and foreign bodies. Surg Clin North Am . 1994;74:1491â€“1505. 5. Janicke DM, Pundt MR. Anorectal disorders. Em erg Med Clin North Am . 1996;14:757â€“788.

Codes ICD9-CM 863.45 Injury to gastrointestinal tract without m ention of open wound into cavity, rectum

ICD10 S36.6 Injury of rectum

Pa ge 4 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Red Eye

Red Eye

Camie J. Sorensen

Basics Description 

May be caused by alm ost any eye disorder



Often benign, though m ay represent system ic disease



Red eye is due to vascular engorgem ent of conjunctiva.



Main causes include inflam m atory, allergic, infection, or traum a.



Inflam m atory etiology includes uveitis (anterior and posterior), episcleritis (70% are idiopathic), scleritis (50% associated with system ic disease).



Allergic etiology is due to histam ine release and increased vascular perm eability, resulting in swelling of conjunctiva (chem osis), watery discharge, and pruritis; usually bilateral involvem ent.



Infectious etiology is either bacterial (purulent m ucous discharge), viral (watery or no discharge), or fungal.



Traum atic causes of red eye include corneal abrasions, conjunctival hem orrhage, and foreign bodies.

Etiology 

Anterior uveitis, iritis (perilim bic injection)



Posterior uveitis

Pa ge 4 0 4



Pinguecula



Pterygium



Hem orrhage



Episcleritis



Scleritis



Bacterial conjunctivitis (diffuse injection)



Viral conjunctivitis (diffuse injection)



Blepharitis



Dry eye syndrom e



Acute angle closure glaucom a



Endophthalm itis



Allergic reaction



Ophthalm ia neonatorum



Dacryocystitis



Canaliculitis



Conjunctival tum or



Foreign body



Corneal ulcer/abrasion/erosion



Occult perforation



Acute angle closure glaucom a



Endophthalm itis



Orbital cellulites



System ic inflam m atory reactions (see list in Differential Diagnosis Section)

Diagnosis Signs and Symptoms 

Discharge



Pruritis



Pain

Pa ge 4 0 4



Foreign body sensation



Ectropion, entropion



Eyelash against globe (trichiasis)



Conjunctival injection



Corneal abrasion, ulcer, or opacity



Anterior cham ber cells or flare



Photophobia (from m ovem ent of an inflam ed iris)



Proptosis



Preauricular (viral conjunctivitis) lym phadenopathy



Subm andibular lym phadenopathy



Rosacea (m ay cause blepharitis)



Facial or skin lesions (herpes)



Sinusitis



Otitis



Pharyngitis

History 

Obtain tim e of onset



Patient's occupation (i.e., m etal worker)



Associated signs and sym ptom s (headache, blurring vision)



Other com orbidities

Physical Exam 

Thorough physical exam ination



Ophthalm ologic: o

Visual acuity

o

Pupil exam ination

o

Confrontational visual field exam

o

Extraocular m uscle function

o

Slit-lam p exam ination with fluorescein

o

Lid eversion

o

Funduscopy and tonom etry when applicable

Essential Workup

Pa ge 4 0 5



Address and rule-out system ic causes of red eye.



Com plete full physical exam as described above.

Tests 

Tests should be directed toward the suspected etiology of red eye: o

Dacryocystitis: culture discharge

o

Corneal ulcers: ophthalm ologist m ay scrape the cornea for cultures.

o

Bacterial conjunctivitis: 

Moderate discharge: obtain conjunctival swab for routine culture and sensitivity (usually Staphylococcus aureus, Streptococcus, and Haem ophilus influenzae in children); however, not always needed as conjunctivitis is often treated presum ptively



Severe discharge: Neisseria gonorrhoeae and Chlam ydia

Lab 

Often not indicated



Useful if etiology is thought to be system ic disease



If bilateral, recurrent, granulom atous uveitis is suspected, send CBC, ESR, ANA, venereal disease research laboratory, FTA Ab, purified protein derivative, ACE level, CXR (sarcoidosis and tuberculosis [TB]), Lym e titer, and HLA-B27, toxoplasm a, and cytom egalovirus (CMV) titers

Imaging Obtain plain film s and/or CT scan of the orbits if suspect foreign body, orbital disease, or traum a.

Differential Diagnosis 

Local: infection, allergy, traum a (also see list in Etiology

Pa ge 4 0 5

section) 

System ic (generally an inflam m atory reaction): o

Arthritic disease

o

Ankylosing spondylosis

o

Ulcerative colitis

o

Reiter syndrom e

o

TB

o

Herpes

o

Syphilis

o

Sarcoidosis

o

Toxoplasm a

o

CMV

Treatment Initial Stabilization N/A

ED Treatment 

Treatm ent is based on cause of red eye.



Direct therapy toward specific etiology.



Medication as indicated (See Medication Section)



Special rem inders: o

Differentiate between a corneal abrasion and a corneal ulcer.

o

Eye patching is no longer routinely recom m ended for abrasions and is contraindicated for corneal ulcers or abrasions with high infection risk (contact lens wearers, abrasions from tree branches or fingernails).

o

Update tetanus im m unization for corneal injury.

Pa ge 4 0 5

o

Do not wear contact lenses.

o

Do not spread infection from the affected eye to the unaffected eye.

o

Diagnosis of conjunctivitis caused by neisseria gonorrhea or chlam ydia requires treatm ent of system ic infection for the individual as well as treatm ent of all sexual partners.

o

Always include work-up and treatm ent of system ic disease if this is suspected.

Special Topics Corneal Abrasion 

Nonâ€“contact lens wearer: o



Ointm ent or drops: 

Erythrom ycin ointm ent every 4 hours



Polytrim drops four tim es a day

Contact lens wearers need pseudom onal coverage: o

Tobram ycin ointm ent every 4 hours

o

Tobram ycin, ofloxacin, or ciprofloxacin drops four tim es a day



Dilate eyes with cyclopentolate 1â€“2%, 2â€“4 drops daily to prevent pain from iritis.



Abrasions will heal without patching.

P.947

Corneal Ulcer 



Nonâ€“contact lens wearer: o

Polytrim ointm ent four tim es a day

o

Ofloxacin, ciprofloxacin drops q2hâ€“q4h

Contact lens wearers need pseudom onal coverage: o

Tobram ycin, ofloxacin, or ciprofloxacin drops

Pa ge 4 0 5

q2hâ€“q4h o

Tobram ycin or ciprofloxacin ointm ent every hour as needed (optional)



Severe or vision-threatening corneal ulcers: o

Central, larger than 1.5 m m or with significant anterior cham ber reaction

o

Treat as aforem entioned and add increased frequency of antibiotic drops such as one drop every 15 m inutes for 3 doses then every 15 m inutes for 2â€“6 hours then every 30 m inutes around the clock

o

Ophthalm ology consult for further recom m endations, which m ay include ciprofloxacin 500 m g PO b.i.d. or fortified antibiotic drops m ade by pharm acist



Ulcers from herpes sim plex or zoster: o

Add trifluridine (Viroptic) 1%, 2 gtt 9 tim es/day or vidarabine 3% ointm ent 5 tim es/day (ointm ent preferred for children).



Traum a or uveitis: Rule out foreign body.

Medication (Drugs) 



Antibiotic drops: o

Ciprofloxacin 0.3%: 1â€“2 gtt q1hâ€“q6h

o

Gentam ycin 0.3%: 1â€“2 gtt q4h

o

Ofloxacin 0.3%: 1â€“2 gtt q1hâ€“q6h

o

Levofloxacin 0.5%: 1â€“2 gtt q2h

o

Polytrim : 1 gtt q3â€“6h

o

Sulfacetam ide 10%: 0.3% 1â€“2 gtt q2hâ€“q6h

o

Tobram ycin 0.3%: 1â€“2 gtt q1hâ€“q4h

o

Trifluridine 1%: 1 gtt q2hâ€“q4h

Antibiotic ointm ents: o

Bacitracin: 500 U/g one half-inch ribbon of ointm ent

Pa ge 4 0 5

q3hâ€“q6h o

Ciprofloxacin 0.3%: one half-inch ribbon of ointm ent q6hâ€“q8h

o

Erythrom ycin 0.5%: one half-inch ribbon of ointm ent q3hâ€“q6h

o

Gentam ycin 0.3%: one half-inch ribbon of ointm ent q3hâ€“q4h

o

Neosporin: Â½-inch ribbon of ointm ent q3hâ€“q4h

o

Polysporin: one half-inch ribbon of ointm ent q3hâ€“q4h

o

Sulfacetam ide 10%: one half-inch ribbon of ointm ent q3hâ€“q8h

o

Tobram ycin 0.3%: one half-inch ribbon of ointm ent q3hâ€“q4h

o

Vidarabine: one half-inch ribbon of ointm ent 5 tim es/day



Mydriatics and cycloplegics: o

Atropine 1%, 2%: 1â€“2 gtt per day to q.i.d.

o

Cyclopentolate 0.5%, 1%, 2%: 1â€“2 gtt p.r.n. dilation

o

Hom atropine 2%: 1â€“2 gtt b.i.d.â€“t.i.d.

o

Phenylephrine 0.12%, 2.5%, 10%: 1â€“2 gtt t.i.d.â€“q.i.d.

o 

Tropicam ide 0.5%, 1%: 1â€“2 gtt PRN dilation

Corticosteroid antibiotic com bination drops (use only with ophthalm ology consultation):



o

Blepham ide: 1â€“2 gtt q1hâ€“q8h

o

Cortisporin: 1â€“2 gtt q3hâ€“q4h

o

Maxitrol: 1â€“2 gtt q1hâ€“q8h

o

Pred G: 1â€“2 gtt q1hâ€“q8h

o

TobraDex: 1â€“2 gtt q2hâ€“q6h

Glaucom a agents (always use with ophthalm ology

Pa ge 4 0 5

consultation): o

Acetazolam ide: 250â€“500 m g PO per day to q.i.d.

o

Betaxolol 0.25%, 0.5%: 1â€“2 gtt b.i.d.

o

Carteolol 1%: 1 gtt b.i.d.

o

Levobunolol 0.25%, 0.5%: 1 gtt per day to b.i.d.

o

Dipivefrin 1%: 1 gtt b.i.d.

o

Mannitol: 1â€“2 g/kg IV over 45 m inutes

o

Pilocarpine 0.25%, 0.5%, 1%, 2%, 3%, 4%, 6%, 8%, 10%: 1â€“2 gtt t.i.d.â€“q.i.d. (use only if m echanical closure is ruled out)

o

Tim olol 0.25%, 0.5%: 1 gtt b.i.d.

Follow-Up Disposition Admission Criteria 

Endophthalm itis



Perforated corneal ulcers



Orbital cellulites



Concurrent injuries (i.e., traum a)



New or suspected diagnosis of system ic disease

Issues for Referral 

Dacryocystitis



Corneal ulcer



Scleritis



Angle closure glaucom a



Uveitis



Proptosis



Orbital cellulitis



Vision loss

Pa ge 4 0 5



Uncertain diagnosis



Gonorrheal or Chlam ydia conjunctivitis

References 1. Kunim oto DY, Kanitkar KD, Makar MS. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 4th ed. Lippincott William s & Wilkins, 2004. 2. Leibowitz HM. â€œPrim ary Care: The Red Eye.â€• New Eng J Med . 2000;343(5).

Miscellaneous SEE ALSO: Chalazion; Conjunctivitis; Corneal Abrasion; Corneal Burn; Corneal Foreign Body; Dacryocystitis; Globe Rupture; Hordeolum; Hyphem a; Iritis; Optic Artery Occlusion; Optic Neuritis; Orbital Cellulitis; Ultraviolet Keratitis; Visual Loss; Vitreous Hemorrhage

Codes ICD9-CM 077.9 Viral conjunctivitis NOS 372.01 Serous conjunctivitis

ICD10 H10 Conjunctivitis

Pa ge 4 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Renal C alculus

Renal Calculus

Jennifer Kolodchak

Basics Description 

Urinary tract obstruction



Interm ittent distention of the renal pelvis of proxim al ureter produces pain.



Kidney stones: o

Most com m on cause of renal colic

o

Theories of stone form ation: 

Urinary supersaturation of solute followed by crystal precipitation



Decrease in the norm al urinary proteins inhibiting crystal growth



Urinary stasis from a physical anom aly, catheter placem ent, neurogenic bladder, or the presence of a foreign body

o

Stone com position: 

75%: calcium in conjunction with phosphate and/or oxalate



15%: m agnesium phosphate (struvite)



Associated with infections caused by urea-splitting organism s (e.g., Pseudom onas,

Pa ge 4 0 5

Proteus, Klebsiella) along with an alkalotic urine  

5% uric acid

90% of urinary calculi radiopaque

Etiology 

1% of the population



Three tim es m ore com m on in m en than wom en

Pediatric Considerations 

Rare in children



When present, indication of an overt m etabolic or genetic disorder



Painless hem aturia com m on presentation (up to 30%)



Pediatric patients younger than 16 years com prise approxim ately 7% of all cases of renal stones.



1:1 sex distribution



Causes of stone form ation: o

Metabolic abnorm alities (50%) 

Most com m on etiologies of stone form ation in the pediatric population

o

Urologic abnorm alities (20%)

o

Infection (15%)

o

Im m obilization syndrom e (5%)

Diagnosis Signs and Symptoms History 

Sudden onset of severe pain in the costovertebral angle, flank, and lateral abdom en



Colicky or constant pain: o

Patient cannot find a com fortable position.

Pa ge 4 0 5



Hem aturia



Nausea/Vom iting



Restlessness



Diaphoresis



History of prior stone form ation



Abdom inal tenderness is not generally present.

Physical Exam 

Obtain vital signs: o

Fever suggests an occult infection.

o

Hypotension with an altered m ental status is suggestive of urosepsis.



Abdom inal exam : o

Pain on palpation, rebound tenderness, and or guarding suggests a m ore serious intraabdom inal process.

o

Palpate the abdom inal aorta for tenderness or pulsatile enlargem ent suggestive of an aneurysm .



Genitourinary exam : o

Exam ine the genitalia for evidence of epididym itis, torsion, or testicular m asses.

Essential Workup Urinalysis: 

Microscopic hem aturia present in >80%



Gross hem aturia



Absent urinary blood in 10%



No correlation between the am ount of hem aturia and the degree of urinary obstruction



WBC/Bacteria suggestive of infection

Tests Lab

Pa ge 4 0 6



CBC: o

WBC >15,000 suggestive of concom itant infection



Urine culture



Electrolytes, glucose, blood urea nitrogen, and creatinine



Pregnancy test when suggestive

Imaging 

CT: o

Helical CT has replaced IV pyelogram (IVP) as test of choice.

o

Detect calculi as sm all as 1 m m in diam eter

o

Directly visualizes com plications, such as hydroureter, hydronephrosis, and ureteral edem a

o

Advantages over IVP: 

Perform ed rapidly



Does not require IV contrast m edia



Detects other nonurologic causes of sym ptom s, such as abdom inal aortic aneurysm s (AAA)

o

Nonenhanced helical CT in the evaluation of renal colic:

o





Sensitivity of 97%



Specificity of 96%



Accuracy of 97%

Indications: 

First-tim e diagnosis



Persistent pain



Clinical confusion with pyelonephritis

IVP: o

Establishes diagnosis in 95%

o

Dem onstrates the severity of obstruction

o

Scout film prior m ay localize stones that would otherwise be obscured by the dye.

o

Postvoiding film

Pa ge 4 0 6



Useful to identify stones at the ureteral vesicular junction or distal ureter that are obscured by a full bladder.



Kidney, ureter, and bladder (KUB) radiograph: o

Indicated when allergy to IVP dye and when renal scanning and ultrasound (US) not available

o

Assists in locating radiopaque stones and the exclusion of other pathologies in nonpregnant patients

o

Difficult to distinguish radiopaque body: 

Phlebolith



Bowel contents



Obstruction within the urinary tract on the KUB



Oblique film s assist in localizing suspicious calcifications

P.949



US: o

For patients who are not candidates for IV contrast

o

Useful in the detection of larger stones and hydronephrosis

o

Provides anatom ic inform ation only

o

Helpful in diagnosing obstruction and localizing stones in the proxim al and distal portions of the ureter

o

o

Ability to detect hydronephrosis: 

Sensitivity of 85â€“94%



Specificity of 100%

Lim itations: 

May m iss stones <5 m m in size



May m iss an obstruction in the early phase of renal colic

Pa ge 4 0 6



Tim e delay until the onset of pyelocaliectasis even after total obstruction

Pregnancy Considerations 

Every effort should be m ade to m inim ize ionizing radiation exposure to the fetus.



US becom es the im aging m odality of choice.

Diagnostic Procedures/Surgery 

Ureteroscopy

Differential Diagnosis 

Do not m iss a catastrophe m im icking renal colic.



Dissecting or rupturing AAA



Pyelonephritis



Papillary necrosis (sickle cell disease, NSAID analgesic abuse, diabetes, or infection)



Renal infarction (vascular dissection or arterial em bolus)



Ectopic pregnancy



Ovarian cyst/torsion



Appendicitis (subacute prodrom e differentiates)



Biliary tract disease (right upper quadrant tenderness m akes renal calculi unlikely)



Musculoskeletal strain (worsening of discom fort during physical exam m aneuvers)



Lower lobe pneum onia (auscultate the lungs)

Treatment Pre Hospital Parenteral opiates m ay be required for pain control with long transport tim es.

Pa ge 4 0 6

Initial Stabilization 

Rapid dipstick urine test for blood: o

Positive test in conjunction with clinical findings sufficient to begin analgesic therapy.



Provide adequate analgesia when diagnosis suspected on clinical and laboratory findings.

ED Treatment 

Hydration: o

Initiate IV crystalloid infusion with 1 L of NS infused over 30â€“60 m inutes followed by 200â€“500 m L/h

o

Bolus volum e com prom ised patients with 500-m L increm ents until urine output adequate



Analgesics (dem erol, m orphine, ketorolac)



Antiem etics (prochlorperazine, ondansetron, droperidol, Vistaril)

Pregnancy Considerations Avoid NSAIDs in pregnancy, particularly in third trim ester

Medication (Drugs) 

Hydrom orphone (dilaudid): 1â€“4 m g (peds: 0.015 m g/kg/dose) IM/IV/SC q4hâ€“q6h PRN. Reduce dose in opiate naÃ¯ve patients.



Hydroxyzine hydrochloride (Vistaril): 25â€“50 m g (peds: 0.5â€“1 m g/kg/dose) IM (not IV) q4hâ€“q6h



Ketorolac (Toradol): 30â€“60 m g IM or 30 m g (peds: 0.5m g/kg/dose up to 1 m g/kg/24â€“48 hours) IV (alone or with opiates). Reduce dose to 30 m g IM or 15 m g IV if >65 years or <50 kg



Meperidine (Dem erol): 50â€“100 m g (peds: 1â€“1.75

Pa ge 4 0 6

m g/kg/dose) q3hâ€“q4h IV/IM 

Morphine sulfate: 2â€“10 m g (peds: 0.1â€“0.2 m g/kg/dose q2hâ€“q4h) IM/IV/SC q2hâ€“q6h PRN. May redose m ore frequently if needed.



Ondansetron (Zofran): 4 m g (peds: 0.1 m g/kg Ã— 1) IM/IV



Prochlorperazine (Com pazine): 5â€“10 m g IM/IV q4hâ€“q6h; 25 m g suppository PR



Prom ethazine (Phenergan): 12.5â€“25 m g (peds: 0.25â€“1 m g/kg) IM/IV q4hâ€“q6h

Follow-Up Disposition Admission Criteria 

Obstruction in the presence of infection m andates im m ediate urologic intervention.



Intractable pain with refractory nausea and vom iting



Severe volum e depletion



Urinary extravasation



Hypercalcem ic crisis



Solitary kidney and com plete obstruction



Relative adm ission indications (discuss with urologist): o

High-grade obstruction

o

Renal insufficiency

o

Intrinsic renal disease

o

Stone size <5 m m usually pass spontaneously; those >8 m m rarely do.

Discharge Criteria 

Norm al vital signs

Pa ge 4 0 6



No evidence of concom itant urinary tract infection



Adequate analgesia



Able to tolerate PO fluids to m aintain hydration status



Reliable patient with an adequate hom e situation



Appropriate outpatient follow-up arranged



Norm al renal function



Provide a urine strainer to collect the stone for possible future stone analysis.



Arrange urologic follow-up.

References 1. Bartosh SM. Medical m anagem ent of pediatric stone disease. Urol Clin N Am . 2004;31:575â€“587. 2. Javier I, Escobar JL II, Eastm an ER, et al. Selected urologic problem s. In: Marx ed. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002. 3. Loughlin KR, Kerr LA. The current m anagem ent of urolithiasis during pregnancy. Urol Clin N Am . 2002;29:701â€“704. 4. Sheley RC, et al. Helical CT in the evaluation of renal colic. Am J Em erg Med. 1999;17:279.

Codes ICD9-CM 592.0

ICD10 N20.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Renal F ailure

Renal Failure

Matthew N. Graber

Basics 

Acute renal failure (ARF): o

Deterioration of renal function over hours to days resulting in the inability to excrete nitrogenous waste products and to m aintain fluid and electrolyte hom eostasis

o 

May be reversible or lead to chronic renal failure

Chronic renal failure: o

Deterioration of renal function over an extended period of tim e that results in: 

The accum ulation of nitrogenous waste products



The inability to m aintain fluid and electrolyte hom eostasis

o



Acidosis



Anem ia

Less likely to be reversible than acute renal failure

Description 

Decline in glom erular filtration



Disrupts the extracellular fluid volum e, electrolyte, and acid-base status



Results in accum ulation of nitrogenous waste

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Etiology 

Prerenal failure: o

Caused by renal hypoperfusion

o

Renal tissue rem ains norm al unless severe/prolonged hypoperfusion.



Intrarenal failure: o



Postrenal failure: o



Caused by diseases of the renal parenchym a

Due to acute obstruction of the urinary tract

Iatrogenic causes include: o

Am inoglycoside antibiotics

o

Radiocontrast m aterial adm inistration

o

NSAIDs

o

Angiotensin converting enzym e inhibitors

Diagnosis Signs and Symptoms Acute Renal Failure (ARF) 

Often asym ptom atic and com m only diagnosed with incidental laboratory findings



Oliguria (<400 m L/d urine production)



Fluid overload: o

Dyspnea

o

Hypertension

o

Jugular venous distention

o

Pulm onary edem a

o

Peripheral edem a

o

Ascites

o

Pericardial effusion

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o 

Pulm onary effusion

Nausea/vom iting

Prerenal Failure 

Absolute or relative volum e deficit



Dry m ucous m em branes



Hypotension



Tachycardia



Low cardiac output



Congestive heart failure (CHF)



System ic vasodilation: o

Sepsis

o

Anaphylaxis

Geriatric Considerations Elderly patients are particularly susceptible to prerenal failure.

Intrarenal (Intrinsic) Failure 





Renal artery throm bosis: o

Flank or abdom inal pain

o

Atrial fibrillation

o

Recent m yocardial infarction

Renal vein throm bosis: o

Nephrotic syndrom e (see Nephrotic Syndrom e)

o

Pulm onary em bolus (see Pulm onary Em bolism )

o

Flank pain

Glom erulonephritis/vasculitis: o



Recent infection: 

Sinusitis



Rash (palpable purpura)



Pulm onary hem orrhage

Hem olytic-urem ic syndrom e (HUS): o

Preceded by a viral or bacterial infection

o

Upper respiratory infection or diarrhea

Pa ge 4 0 6



Throm botic throm bocytopenic purpura (TTP): o

Mild elevation of blood urea nitrogen (BUN)/creatinine (Cr)



o

Fever

o

Altered m ental status

o

Headache

o

Seizures

o

Anem ia

o

Com a

Allergic interstitial nephritis after drug ingestion: o

Fever

o

Rash

o

Arthralgias

Postrenal Failure 

Benign prostatic hyperplasia



Prostatitis



Abdom inal or flank pain



Distended bladder



Oliguria or anuria

Complications of ARF Uremic Syndrome 

Pericarditis



Pericardial effusion



Cardiac tam ponade



Ileus



Altered m ental status



Asterixis



Reflex abnorm alities



Restless leg syndrom e



Focal neurologic abnorm ality



Seizures

Hematologic Disorders

Pa ge 4 0 7



Anem ia



Increased bleeding tim e



Leukocytosis

Essential Workup 



Electrolytes: o

Hyperkalem ia

o

Hyponatrem ia

o

Hyperphosphatem ia

o

Hypocalcem ia

o

Hyperm agnesem ia

o

Metabolic acidosis

o

Elevated anion gap

BUN/Cr: o



Elevated in ratio determ ined by cause of renal failure

Urinalysis (UA): o

Centrifuged specim en helps to distinguish between different etiologies of ARF.

o 

Exam ined for casts, blood, WBCs, and crystals

CBC: o

Anem ia with chronic renal failure

Tests Lab N/A

Prerenal 



UA: o

Specific gravity >1.018

o

Osm olality >500 m m ol/kg

o

Sodium <10 m m ol/L

o

Hyaline casts

BUN/Cr ratio >20

Pa ge 4 0 7



Rapid recovery of renal function when renal perfusion norm alized

Intrarenal 

BUN/Cr ratio <10â€“15



Glom erulonephritis/Vasculitis:





o

UA with red cell or granular casts

o

Com plem ent and autoim m une antibodies

HUS or TTP: o

UA norm al

o

Anem ia

o

Throm bocytopenia

o

Schistocytes on blood sm ear

o

Elevated lactate dehydrogenase (LDH)

Nephrotoxic acute tubular necrosis (ATN): o



UA: 

Brown granular or epithelial cell casts



Specific gravity (SG) 1.010



Urine osm olality <350 m m ol/kg



Urine Na >20 m m ol/L

Ethylene glycol ingestion: o

UA: calcium oxalate crystals

o

Anion gap m etabolic acidosis

o

Osm olal gap

P.951



Rhabdom yolysis: o

UA: hem e positive without red cells

o

Elevated serum K + , PO 4 , m yoglobin, creatine phosphokinase-MM, uric acid

o 

Decreased serum Ca 2 +

Tubulointerstitial disease

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

Allergic interstitial nephritis: o

UA with WBC casts, WBCs, RBCs, and proteinuria

o

System ic eosinophilia

Postrenal UA: 

Usually norm al



May have som e hem aturia but no casts or protein

Imaging 

Ultrasound: o





Helical CT scan: o

Without contrast sensitive for obstruction

o

May detect intrarenal changes

Duplex scan for: o



Renal artery or vein throm bosis

Renal arteriogram : o



98% sensitive for excluding obstruction

Definitive diagnosis or renal artery throm bosis

Inferior vena cava and renal vessel venogram for renal vein throm bosis



IV pyelogram : o

Avoid contrast with renal insufficiency as it m ay worsen renal function.

Diagnostic Procedures/Surgery ECG: 

Hypertension secondary to volum e overload m ay cause ischem ia.



CHF



Sensitive for significant, acute electrolyte changes o

Hyper- and hypokalem ia

o

Hypo- and hypercalcem ia

o

Hypo- and hyperm agnesia

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Treatment Initial Stabilization 

ABCs: o

Supplem ental oxygen for hypoxia



IV fluids (NS or Ringer) for volum e depletion



Correct electrolyte disturbances.



Indications for em ergent dialysis: o

Life-threatening hyperkalem ia

o

Intractable hypertension or pulm onary edem a

o

Fluid overload unresponsive to other treatm ents

o

BUN >100 m g/dL

o

Cr >10 m g/dL: 

Chronic renal failure patients on regular dialysis m ay have a baseline elevated creatinine that by itself is not an indication for em ergent dialysis.

o

Metabolic acidosis (pH <7.2)

o

Severe urem ia causing pericarditis



Avoid nephrotoxins.



Monitor urine output.

ED Treatment Prerenal 

Treat hypoperfusion: o

Consider packed RBC for blood loss, anem ia, or lack of response after two boluses.



Invasive cardiac m onitoring if unable to assess cardiac failure versus hypovolem ia



Adm inister 0.9% NS fluid challenge cautiously to avoid fluid overload in liver failure with ascites:

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o

Response: good indicator of the degree to which hypovolem ia is a factor

Intrarenal 

Glom erulonephritis: o

Im m unosuppressive agents (glucocorticoids) or plasm a exchange





ATN: o

Mannitol

o

Furosem ide

o

Calcium channel blockers

o

Furosem ide

o

Dialysis

Hyponatrem ia: o



Fluid restriction with norm al saline

Hyperkalem ia: o

Sodium polystyrene sulfonate for asym ptom atic with K + >5.5 m Eq/L

o

For K + >6.5 m Eq/L or ECG abnorm alities consistent with hyperkalem ia 

Albuterol via nebulizer



Glucose and insulin: onset 30â€“60 m inutes, duration several hours



Furosem ide if patient not anuric



Sodium bicarbonate: onset <15 m inutes, duration 1â€“2 hours



Dialysis for intractable hyperkalem ia



Metabolic acidosis: o

Consider sodium bicarbonate for pH <7.2 or HCO 3 <15 m Eq/L.

o 

Dialysis

Hyperphosphatem ia: o

Calcium carbonate

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o 

Alum inum hydroxide

Myoglobinuria: o

Aggressive fluid resuscitation with 0.9% NS

o

Mannitol if patient not m aintaining appropriate urine output

o

Sodium bicarbonate to alkalinize the urine: 

This is a considerable sodium load; use caution in anuric/oliguric patients.



Calcium gluconate: for cardiac and neurom uscular protection

Alert Ca gluconate is only indicated by EKG by widened PR, QT, or QRS intervals. Peaked T waves alone are not an indication.

Medication (Drugs) 

Albuterol 5 m g via nebulizer



Alum inum hydroxide (Am phojel): 500â€“1,500 m g PO



Calcium carbonate (Os-Cal): 250â€“3,000 m g PO



Calcium gluconate: 10 m L of 10% solution over 5 m in IV



Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m L/kg) IV



Furosem ide: 20â€“400 m g IV push



Insulin: 10 IU regular IV with dextrose



Mannitol: 12.5â€“25 g IV push



Sodium bicarbonate: 1â€“2 m Eq/kg IV



Sodium polystyrene sulfonate (Kayexalate): 1 g/kg up to 15â€“60 g PO or 30â€“50 g retention enem a in sorbitol q6h

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Follow-Up Disposition Admission Criteria 

New-onset ARF



Hyperkalem ia/Significant electrolyte abnorm alities



Fluid overload with hypoxia/CHF

Discharge Criteria 

Stable



Norm al electrolytes

Issues for Referral Refer to prim ary physician for progressive worsening renal function in an otherwise stable patient.

References 1. Albright RC. Acute renal failure: a practical update. Mayo Clin Proc . 2001;76(1):67â€“74. 2. Brady HR, Brenner BM. Acute renal failure. In: Isselbacher KJ, Braunwald E, Wilson JD, et al, eds. Harrison's principles of internal m edicine. 15th ed. New York: McGraw-Hill, 2001:1541â€“1550. 3. Brady HR, Brenner BM, Clarkson MR, et al. Acute renal failure. In: Brenner BM, ed. Brenner and Rector's the kidney. 6th ed. Philadelphia, PA: WB Saunders, 2000:1201â€“1262. 4. Prough DS. Physiologic acid-base and electrolyte changes in acute and chronic renal failure patients. Anesthesiol Clin North Am . 2000;18(4):809â€“833. 5. Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med. 1996;334(22):1448â€“1460.

Codes ICD9-CM 584.9 Acute renal failure, unspecified

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585 Chronic renal failure

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Renal Injury

Renal Injury

Albert Jin

Basics Description 

Kidneys are located in the retroperitoneal space and are surrounded by adipose tissue and loose areolar connective tissue.



Lie along the lower two thoracic vertebrae and first four lum bar vertebrae



Left kidney is positioned slightly higher than the right.



Kidneys are not fixed: o

Shift with the diaphragm and are supported by the renal arteries, veins, and adipose tissue to the renal (Gerota) fascia

Etiology 

Most com m on of all urologic injuries



Occurs in approxim ately 8â€“10% of all abdom inal traum a



Blunt renal traum a accounts for 80â€“85% of all renal injuries and is five tim es m ore com m on than penetrating injury: o

Mechanism s include m otor-vehicle accidents, falls, dom estic violence, and contact sports.

o

Pathophysiology includes rapid deceleration and

Pa ge 4 0 7

displacem ent m echanism s. o

About 20% of cases are associated with intraperitoneal injury.



Mechanism s responsible for significant renal injury alm ost never affect the kidney alone: o

Most often disrupt and injure other vital organs that can be responsible for patient m ortality



Renal injuries are classified according to type and severity of the injury: o

Grade I: renal contusion; subcapsular hem atom a, nonexpanding without parenchym al laceration

o

Grade II: hem atom a nonexpanding, perirenal hem atom a confined to retroperitoneum ; laceration <1 cm parenchym al depth of renal cortex

o

Grade III: laceration >1 cm parenchym al depth of renal cortex without collecting system rupture or urinary extravasation

o

Grade IV: parenchym al laceration extending through renal cortex, m edulla, and collecting system ; m ain renal artery or vein with contained hem orrhage

o

Grade V: com pletely shattered kidney; avulsion of renal hilum that devascularized kidney

Pediatric Considerations 

The kidney is the organ m ost com m only dam aged by blunt abdom inal traum a.



Contributing factors: o

Relatively larger size of kidneys com pared with adults

o

Tenth and eleventh ribs are not com pletely ossified until the third decade of life.



Significant abdom inal injury occurs in about 5% of nonaccidental traum a cases but is the second m ost

Pa ge 4 0 8

com m on cause of death after head injury.

Diagnosis Signs and Symptoms History 

Mechanism of injury and kinem atics are im portant factors.



In blunt traum a, note the type and direction (horizontal or vertical) of any deceleration or com pressive forces.



In penetrating traum a, note the characteristic of the weapon (type and caliber), distance from the weapon, or the type and length of knife or im paling object: o

Injuries result from a com bination of kinetic energy and shear forces of penetrating object.

Physical Exam 

Gross hem aturia is a com m on presentation even with m inor renal traum a: o

Severity of renal traum a does not correlate with the am ount of blood in the urine.



Flank m ass or ecchym osis



Tenderness in the flank, abdom en, or back



Fracture of the inferior ribs or spinal transverse processes



Nausea and vom iting

Essential Workup 

In 1989, Mee et al. published the hallm ark article (10-year prospective study) that established guidelines for the evaluation and treatm ent of blunt renal traum a: o

Major renal lacerations represent significant reparable renal injuries.

o

Adult patients at risk for having sustained m ajor

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lacerations: 

Gross hem aturia, or



Microhem aturia (â‰¥ 3â€“5 RBCs/hpf) with shock (systolic blood pressure â‰¤ 90) in the field or on arrival in the ED, or



History of sudden deceleration without hem aturia or shock

o

IV contrast-enhanced CT scan is the procedure of choice in identifying urologic injury.

o

Guidelines are not applicable in cases of penetrating renal traum a or in children.



Adults with blunt renal traum a and gross hem aturia, or m icrohem aturia in the presence of shock, require renal im aging for further evaluation of renal injury.



In adults with penetrating renal traum a, significant injuries to the kidney and ureter can occur without hem aturia: o

Location of penetrating wound in relation to urinary tract is m ost im portant factor in deciding need for radiographic im aging.



Im portant to rule out co-existing injuries

Tests Lab 

Urinalysis: Gross hem aturia or >50 RBCs/HPF in adults and >20 RBC/HPF in children is suggestive of renal injury.



Baseline laboratory values including hem atocrit and blood urea nitrogen/creatinine should be obtained.

Imaging 

Plain abdom inal film s: o

May show fractured inferior ribs or transverse processes, a unilateral enlarged kidney shadow, or

Pa ge 4 0 8

obscuring of the psoas m argin 

IV pyelogram (IVP): o

Bolus infusion IVP with nephrotom ography study of choice in institutions without 24-hour availability of CT 

Rapid injection of 1.5â€“2 m L of contrast m aterial per kilogram of body weight to a m axim um or 150 m l after obtaining a prelim inary kidney, ureter, and bladder



Postinfusion supine film is obtained followed by 1-, 2-, and 3-m inute supine film s.

o

Allows evaluation for renal viability and function

o

Extravasation reflects injury to the collecting system .

o

Nonvisualization of a kidney m ay indicate renal pedicle injury or parenchym al shattering.

o

Abnorm al findings are often nonspecific and require m ore definitive studies.



Ultrasound: o

Role in evaluation of renal injury is controversial.

o

May show size of perirenal hem atom a and whether it is expanding or resolving

o

Otherwise, exam is nonspecific and does not provide enough inform ation.

P.953



CT scan: o

An IV contrast-enhanced helical CT scan is the diagnostic procedure of choice.

o

Superior anatom ic detail and diagnostic accuracy of 98% for renal injury

o

Sensitive indicator of m inor extravasation,

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parenchym al laceration, vascular injury, and nonrenal injuries

Pediatric Considerations 

Major blunt renal traum a can occur in the absence of gross hem aturia or shock.



Meta-analysis has defined 50 RBC/hpf as the m icroscopic quantity below which im aging can be om itted and no significant injuries m issed.



CT scan is the im aging m odality of choice.

Differential Diagnosis 

Renal parenchym al injury



Renal vascular injury



Ureteral injury



Bladder or urethral injury

Treatment Pre Hospital 

Obtain details of injury from prehospital providers.



IV access



Penetrating wounds or evisceration should be covered with sterile dressings.

Initial Stabilization 

Airway m anagem ent and resuscitation: o

Adequate IV access

o

Fluid resuscitation, initially with 2 L of crystalloid (NS or lactated Ringer solution), followed by blood products as needed



Rule out potential life-threatening injuries first.

Pa ge 4 0 8

ED Treatment 

Im m ediate laparotom y in the acutely injured patient who is hem odynam ically unstable with presum ed hem operitoneum and renal injury



All penetrating renal traum a requires renal exploration unless com plete radiographic staging reveals an injury which can be m anaged nonoperatively.



Managem ent of renal injuries: o

Classes I and II: Contusions and m inor lacerations with stable vital signs and urographically norm al renal function can be m anaged nonoperatively.

o

Class III: renal lacerations with urinary extravasation: 

Controversy between operative versus nonoperative m anagem ent



Managem ent should be based on degree of injury using CT scanning.

o

Classes IV and V: Shattered kidney or renal pedicle injuries and hem odynam ically unstable patients require em ergent laparotom y.

o

All ureteral injuries require operative repair.

Follow-Up Disposition Admission Criteria Patients with significant renal injury require hospitalization for definitive laparotom y or observation.

Discharge Criteria

Pa ge 4 0 8



Adult traum a patients without hem aturia, shock, or no renal injury confirm ed radiographically



Adult blunt traum a patient with m icrohem aturia (â‰¥ 3â€“5 RBCs/hpf) but no shock (systolic blood pressure â‰¤ 90)



Pediatric blunt traum a patient with â‰¤ 50 RBC/hpf and no other co-existing m ajor organ injuries

Issues for Referral Outpatient referral to urologist should be m ade for m icrohem aturia to ensure that it does not represent a m ore serious underlying condition.

References 1. Mee SL et al. Radiographic assessm ent of renal traum a: a ten-year prospective study of patient selection. J Urol. 1989;(141):1095. 2. Peterson N. Genitourinary traum a. In: Felicano D, et al, eds. Traum a. 3rd ed. Stam ford, CT: Appleton & Lange, 1996:661â€“694. 3. Santucci RA, et al. Evaluation and m anagem ent of renal injuries: consensus statem ent of the renal traum a subcom m ittee. BJU Int. May 2004;93(7):937â€“954. 4. Schneider R. Genitourinary system . In: Rosen P, et al, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002:437â€“456. 5. Stein J, Kaji D, Eastham J, et al. Blunt renal traum a in the pediatric population: Indications for radiographic evaluation. Urology. 1994;(44):406â€“410. 6. Wessells H, McAninich J. Update on upper urinary tract traum a. AUA Update Series. 1996;(15):110â€“115.

Codes ICD9-CM 866.00

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ICD10 S37.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Reperfusio n Therapy, C ardiac

Reperfusion

Therapy, Cardiac Shamal Grossman

Basics Description 

Throm bolytic therapy: o

Reduces m orbidity and m ortality in ST-segm ent elevation m yocardial infarction (MI)

o

Maxim um benefit is achieved when started within 6 hours after infarct.

o

The earlier throm bolytics are started, the m ore m yocardium salvaged.



Percutaneous coronary intervention (PCI): o

Balloon inflation results in overstretching of vessel wall and partial disruption of intim a, m edia, and adventitia, resulting in enlargem ent of lum en and outer diam eter of diseased vessel.

o

Stent placem ent decreases early and late loss in lum inal diam eter seen with percutaneous translum inal coronary angioplasty (PTCA).

o

PCI provides greater coronary patency and throm bolysis in MI III flow than do throm bolytics.

Pa ge 4 0 8

o

Lower risk of bleeding than with throm bolytics

o

Im m ediate knowledge of extent of disease

o

Meta-analysis suggests im proved survival with PCI for ST-segm ent elevation MI when com pared with throm bolytic therapy (6.5% vs. 4.4%); however, im proved outcom es m ay be contingent on operator and institutional expertise.

o

Particularly useful when throm bolytic therapy is contraindicated

o

PTCA has a 30% restenosis rate in first 6 m onths.

o

Stents reduce restenosis rate to 20%.

o

Medication coated stents m ay reduce to 5% or less.

o

PCI should be strongly considered within first 48 hours after a nonâ€“ST-segm ent elevation MI with concom itant use of glycoprotein IIb/IIIa inhibitors.



Glycoprotein IIb/IIIa inhibitors: o

Antiplatelet agents that bind to platelet receptor glycoprotein IIb/IIIa and inhibit platelet aggregation

o

Reduce m ortality and reinfarction rate in patients in whom PCI is planned

o

Recent data suggest reduced m ortality in all patients with unstable angina and nonâ€“Q-wave infarction.

o

Not indicated for patients with ST-elevation MI, unless also undergoing PCI



Unfractionated heparin and low m olecular weight heparin: o

Adjuncts in treatm ent with throm bolytics, glycoprotein IIb/IIIa inhibitors, and PCI

o

Low m olecular weight heparin has been associated with less re-occlusion, enhanced late patency, and reduced reinfarction rates when com pared with unfractionated heparin.



Clopidogrel m ay be of benefit acutely when added to

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standard therapy by reducing the odds of acute MI patients having another occluded artery, or a second heart attack or death by 36% after one week of hospitalization 

Statin therapy reduces clinical events in patients with stable coronary artery disease. This m ay also extend to patients experiencing an acute ischem ic coronary event.

Etiology Ischem ic MI is caused by occlusion of a coronary artery, usually as a result of a throm botic event.

Diagnosis Signs and Symptoms 

Chest pain, heaviness, or pressure feeling



Shortness of breath



Arm , neck, or back pain



Weakness or fatigue



Nausea, vom iting



Diaphoresis



Palpitations



Dizziness or syncope

Essential Workup 

History is critical in assessing window for use of both throm bolytics and PTCA.



ECG: o

Will be norm al approxim ately 50% of tim e

o

Must be com pared with prior tracings if available

o

New ST-segm ent changes or T-wave inversions are suspicious for unstable angina or nonâ€“Q-wave infarct.

Pa ge 4 0 9

o

1 m m depression of the ST segm ent below the baseline, 80 m s from the J point, is characteristic of unstable angina or nonâ€“Q-wave infarct.

o

New left bundle branch block, or new ST-segm ent elevation 1 m m in two contiguous lim b leads or 2 m m in two contiguous precordial leads suggests Q-wave infarct.



Chest radiograph: m ay be helpful if aortic dissection is being considered



Hem e stool test: helpful in establishing baseline

Tests Lab 

Cardiac enzym es



Baseline creatinine, hem atocrit, and coagulation profile are all appropriate in initial work-up.

Differential Diagnosis 

Aortic dissection



Anxiety



Biliary colic



Costochondritis



Esophageal spasm



Esophageal reflux



Herpes zoster



Hiatal hernia



Mitral valve prolapse



Peptic ulcer disease



Psychogenic sym ptom s



Panic disorder



Pericarditis



Pneum onia



Pulm onary em bolus

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Treatment Pre Hospital 

IV access



Oxygen



Cardiac m onitoring



Sublingual nitroglycerin for sym ptom relief



Aspirin



Controversies: o

Whether to bypass closer EDs in favor of hospitals capable of prim ary PTCA; follow local em ergency m edical service protocols.

Alert 

All chest pain should be treated and transported as a possible life-threatening em ergency.



Therapy with throm bolytics and glycoprotein IIb/IIIa inhibitors in the field is not currently standard of care.

Initial Stabilization 

Place patient on m onitor.



Obtain IV access.



Oxygen



Nitrates

P.955

ED Treatment 

Aspirin



Clopidogrel m ay be of benefit acutely

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



Throm bolytics: o

Unless contraindicated

o

If PCI is not readily available within 90 m inutes

PCI is preferred for both diagnostic and therapeutic options.



PCI and throm bolytic therapy m ust be used with either unfractionated heparin or a low m olecular weight heparin, such as enoxaparin.



Low m olecular weight heparin: o

Kinetics m ore predictable

o

Requires no m onitoring

o

Less potential for platelet activation

o

Lower bleeding rate

o

Is at least as effective as unfractionated heparin in treatm ent of acute coronary syndrom es



Glycoprotein IIb/IIIa inhibitors

Medication (Drugs) 

Aspirin: 80â€“325 m g PO



Enoxaparin (Lovenox): 1 m g/kg SQ q12h



Clopidogrel (Plavix): 300 m g PO load, 75 m g PO per day



Glycoprotein IIb/IIIa inhibitor: o

Abcixim ab (ReoPro): for use before PCI only; 0.25 m g/kg IV bolus

o

Eptifibatide (Integrilin): 180 Âµg/kg IV over 1â€“2 m inutes, followed by continuous IV infusion of 2 Âµg/kg per m inute up to 72 hours

o

Tirofiban (Aggrastat): 0.4 Âµg/kg per m inute for 30 m inutes, then 0.1 Âµg/kg per m inute for 48â€“108 hours



Heparin: 80 U/kg IV bolus, then 18 U/kg per hour

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

Metoprolol: 5 m g IV bolus and/or 25â€“50 m g PO



Throm bolytics: o

Anisoylated plasm inogen streptokinase activator com plex: 30 m g IV over 2â€“5 m inutes; patients should also receive m ethylprednisolone 250 m g IV.

o

Recom binant tissue plasm inogen activator (Reteplase): 10 m illion-unit IV bolus, repeat dose after 30 m inutes; patients should also receive heparin 5,000 IU IV bolus, then infuse 1,000 IU per hour for 48 hours, keeping activated partial throm boplastin tim e (aPTT) 1.5â€“2.5.

o

Streptokinase: 1.5 m illion units over 60 m inutes; patients should also receive m ethylprednisolone 250 m g IV.

o

Tissue plasm inogen activator: 15 m g IV bolus, then 0.75 m g/kg (m ax. 50 m g) over 30 m inutes, then 0.5 m g/kg (m ax. 35 m g) over 60 m inutes; patients should also receive heparin 5,000 IU IV bolus, then infuse 1,000 IU per hour for 48 hours keeping aPTT 1.5â€“2.5

o

Urokinase: 1.5 IU IV over 2 m inutes, then 1.5 IU IV over next 90 m inutes

o

Contraindications: 

Active internal bleeding



History of cerebrovascular accident in past 6 m onths



History of a hem orrhagic cerebrovascular accident



Recent (within 2 m onths) intracranial or intraspinal surgery or traum a



Intracranial neoplasm , arteriovenous m alform ation, or aneurysm

Pa ge 4 0 9



Known bleeding diathesis



Severe, uncontrolled hypertension



Pregnancy



Head traum a within past m onth



Traum a or surgery within past 2 weeks that m ay result in closed-space bleed

Follow-Up Disposition Admission Criteria All patients being considered for reperfusion therapy should be adm itted to a telem etry or intensive care unit setting.

Discharge Criteria No patient being considered for reperfusion therapy should be discharged hom e from ED.

References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and nonâ€“ST-segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970â€“1062. 2. Gibson CM. Prim ary angioplasty com pared with throm bolysis: New issues in the era of glycoprotein IIb/IIIa inhibition and intracoronary stenting. Ann Intern Med. 1999;130:841â€“847. 3. Lieu TA, Gurley RJ, Lundstrom RJ, et al. Prim ary angioplasty and throm bolysis for acute m yocardial infarction: An evidence based sum m ary. J Am Coll Cardiol. 1996;27:737â€“750. 4. Ryan TJ, Antm an EM, Brooks NH, et al. ACC/AHA practice guidelines for the m anagem ent of patients with acute m yocardial

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infarction. J Am Coll Cardiol. 1996;28:1328â€“1428. (See also 1999 Web update at http://www.acc.org.) 5. SchÃ¶m ig H, Kastrati A, Dirschinger J, et al. Coronary stenting plus platelet glycoprotein IIb/IIIa blockade com pared with tissue plasm inogen activator in acute m yocardial infarction. N Engl J Med. 2000;343:385â€“391.

Miscellaneous SEE ALSO: Acute Coronary Syndrom e: Myocardial Infarction

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Reperfusio n Therapy, C erebral

Reperfusion

Therapy, Cerebral Kama Guluma

Basics Description 

Cerebrovascular accident (CVA) or stroke is a focal interruption of blood supply to the brain:



o

Onset m ay be sudden and com plete or gradual.

o

Course m ay be progressive or stuttering.

o

Transient ischem ic attack (TIA): 

Sym ptom s that resolve within 24 hours



May predict m ore com plete throm botic CVA

The National Institutes of Health Stroke Scale (NIH-SS) can be used to delineate severity of a CVA (by com puting the total of subcategory scores, to a m axim um of 42) as follows: o

1a. Level of consciousness (LOC): alert = 0; drowsy = 1; stuporous = 2; com a = 3

o

1b. LOC questions: answers both correctly = 0; one correctly = 1; none correct = 2

o

1c. LOC com m ands: obeys both correctly = 0; one correctly = 1; none correctly = 2

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o

2. Best gaze: norm al = 0; partial gaze palsy = 1; forced deviation = 2

o

3. Visual: no visual loss = 0; partial hem ianopia = 1; com plete hem ianopia = 2; bilateral hem ianopia = 3

o

4. Facial palsy: norm al, sym m etric = 0; m inor paralysis = 1; partial paralysis = 2; com plete paralysis = 3

o

5 to 8. Best m otor (com puted for each arm and leg): no drift = 0; drift = 1; som e effort against gravity = 2; no effort against gravity = 3; no m ovem ent = 4; untestable (e.g., am putation or joint fusion) = 9

o

9. Lim b ataxia: absent = 0; present in 1 lim b = 1; present in two lim bs = 2

o

10. Sensory (pinprick): norm al = 0; partial loss = 1; dense loss = 2

o

11. Best language: no aphasia = 0; m ild to m oderate aphasia = 1; severe aphasia = 2; m ute = 3

o

12. Dysarthria: norm al articulation = 0; m ild to m oderate dysarthria = 1; unintelligible = 2

o

13. Neglect/inattention: no neglect = 0; partial neglect = 1; com plete neglect = 2



Cerebral reperfusion therapy involves the IV adm inistration of a throm bolytic agent: o

To effect rapid dissolution of an acute cerebrovascular throm boem bolic occlusion

o

Interventional endovascular techniques enable site-specific intra-arterial throm bolysis or m echanical rem oval of the occlusion.

Etiology 

Ischem ic CVA is caused by occlusion of a cerebral artery: o



Prim arily from a throm botic or em bolic event

Throm botic CVA is caused by in situ occlusion:

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o

Clot form ation at an ulcerated atherosclerotic plaque or other prothrom botic endothelial abnorm ality

o

Hypercoagulable states: 

Antithrom bin III, protein C or protein S deficiencies

o



Sludging: 

Sickle cell disease



Polycythem ia vera

Em bolic CVA is caused by acute obstruction by an intravascular em bolus from : o

Cardiac m ural throm bus form ed in: 

Fibrillating atrium



Hypokinetic ventricle (m yocardial infarction, cardiom yopathy, failure)

 o

Ventricular aneurysm

A prosthetic cardiac valve or an abnorm al native valve

o

Aortic, carotid, or cerebrovascular atherosclerotic plaques



Other occlusive events include: o

Vascular dissection of the aorta, cerebral, vertebral, carotid, or innom inate arteries

o

Cerebral vasospasm induced by: 

Subarachnoid hem orrhage (SAH)



Vasoconstrictive agents (e.g., cocaine)

Diagnosis Signs and Symptoms History

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

Occlusive event that m ight benefit from em ergent reperfusion therapy with IV throm bolysis: o

Acute focal neurological deficits presenting within 3 hours of onset



Tim e of sym ptom onset is critical: o

If tim e of onset cannot be firm ly established, the tim e the patient last felt norm al or was last seen norm al should be a surrogate.



Historical elem ents that m ay suggest an etiology other than routine throm boem bolic stroke: o

Severe, sudden headache in SAH

o

Acute neck strain in vertebral dissection

o

Injury to the anterior neck in carotid dissection

o

Tearing back pain in aortic dissection

o

Recent or concom itant drug abuse in vasospastic occlusions

Physical Exam Abnorm al neurological exam findings warrant consideration for cerebral reperfusion therapy: 

Especially sym ptom s within a distinct vascular supply territory of the brain (see below)

Middle Cerebral Artery 

Contralateral hem iplegia (upper > lower)



Contralateral hem isensory deficits



Contralateral hom onym ous hem ianopia



Expressive or receptive aphasia (dom inant hem isphere)



Contralateral neglect

Posterior Cerebral Artery 

Cortical blindness in half the visual field



Visual agnosia



Third nerve palsy

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

Thalam ic syndrom es: o

Abnorm al m ovem ents (chorea or hem iballism us)

o

Hem isensory deficit

Vertebrobasilar System 

Im paired vision, visual field defects



Nystagm us, vertigo, dizziness



Facial paresthesia, dysarthria



Cranial nerve palsies



Contralateral sensory deficits (pain and tem perature)



Lim b ataxia, abnorm al gait

Anterior Cerebral Artery 

Contralateral hem iplegia (lower >upper)



Hem isensory loss



Apraxia



Confusion, im paired judgm ent

Lacunar (deep subcortical) 

Pure m otor hem iplegia (m ost com m on), or pure sensory hem iplegia



Dysarthria and contralateral hand ataxia (clum sy hand), or dysarthria with facial weakness



Ataxic hem iparesis

Essential Workup 

STAT bedside blood glucose testing



Im m ediate noncontrast head CT scan: o

Can differentiate between ischem ic and hem orrhagic CVA

o

Can reveal other etiologies

o

May be norm al in the first 24 hours of an ischem ic CVA: 

Very likely norm al in the first 3 hours

Pa ge 4 1 0



Early signs of ischem ia (e.g., edem a) should prom pt a re-evaluation of tim e of onset.



ECG to assess for dysrhythm ia, pericarditis or m yocardial infarction

Tests Lab 

CBC, serum electrolytes and glucose, blood urea nitrogen, creatinine, prothrom bin tim e (PT)/partial throm boplastin tim e (PTT)



Urine pregnancy test



Urine toxicology screen



Liver function tests in selected patients, such as those prone to liver dysfunction

Imaging 

Multim odal MRI (with perfusion- and diffusion-weighted protocols): o

Can detect ischem ic CVA alm ost im m ediately after onset



Perfusion brain CT can reveal a perfusion deficit im m ediately after onset.



Carotid ultrasound



Chest radiograph

Diagnostic Procedures/Surgery Cerebral angiography m ay be a useful diagnostic and therapeutic adjunct: 

Considered in consultation with a neurologist and interventional radiologist

Differential Diagnosis 

Intracranial hem orrhage (ICH)



Seizure

Pa ge 4 1 0



Com plex m igraine



Bell palsy or other focal neuropathies



Hypoglycem ia and other m etabolic abnorm alities



Dural sinus throm bosis



Intracranial neoplasm



Intracranial traum a



Meningitis, encephalitis, or brain abscess



Vasculitis



Air em bolism or decom pression illness



Spinal cord lesion



Psychogenic

P.957

Treatment Pre Hospital 

Screening for CVA: o

o

Assessing for deficits: 

Dysarthria, facial weakness



Arm or leg weakness

Notification and pre-arrival m obilization of ED and hospital resources



Blood-glucose testing should be perform ed: o

Hypoglycem ia can cause focal neurological sym ptom s that m im ic a CVA.

o

Treat with adm inistration of dextrose.

Initial Stabilization 

Supplem ental oxygen to correct hypoxia

Pa ge 4 1 0



IV access and norm al saline bolus to correct hypotension



Cardiac m onitoring and pulse oxim etry



Naloxone, thiam ine, and dextrose (if hypoglycem ic) for altered m ental status



Rapid sequence intubation if airway protection is warranted or ventilatory insufficiency is evident

ED Treatment 

Exclude other diagnoses in the differential, especially vascular dissection and ICH.



Throm bolytic therapy should be reserved for patients with ischem ic strokes caused by throm bosis or em bolism .





Inclusion criteria for IV throm bolytic therapy: o

Age â‰¥18 years of age

o

Clearly defined onset of sym ptom s within 3 hours

o

Noncontrast head CT without evidence of hem orrhage

Absolute contraindications to IV throm bolytic therapy: o

ICH on pretreatm ent head CT scan

o

Prior ICH

o

Clinical presentation consistent with SAH

o

Known arteriovenous m alform ation or aneurysm

o

CVA, serious brain injury or intracranial surgery within previous 3 m onths

o

Active internal bleeding

o

Major surgery within previous 14 days

o

Pregnancy

o

Pericarditis

o

Known bleeding diathesis: 

Platelet count <100,000/m m 3



International norm alized ratio >1.7, PT >15 seconds



Prolonged PTT



Current anticoagulant use

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



Use of heparin within 48 hours

o

Systolic blood pressure (SBP) >185 m m Hg

o

Diastolic blood pressure (DBP) >115 m m Hg

Relative contraindications to IV throm bolytics: o

Rapid im provem ent of neurological sym ptom s

o

Mild CVA

o

Gastrointestinal or genitourinary bleeding with 21 days



o

Recent lum bar puncture

o

Recent arterial puncture at a noncom pressible site

o

Seizure at the tim e stroke was observed

o

Blood-glucose level <50 or >400 m g/dL

Treat BP >185/110 m m Hg with nitropaste or 1â€“2 doses of labetalol, or nicardipine: o

Do not aggressively norm alize BP.

o

Stroke patient m ay be dependant on an elevated m ean arterial pressure for cerebral perfusion.

o

Avoid throm bolytic therapy if BP cannot be reduced with m inim al intervention



Adm inister IV tissue plasm inogen activator (TPA).



Avoid antiplatelet agents and anticoagulants for 24 hours.



Monitor arterial BP during the first 24 hours after treatm ent with TPA and aggressively treat a S BP >180 or a DBP >105: o

Check BP every 15 m inutes for 2 hours, then every 30 m inutes for 6 hours, then every hour for 24 hours.

o

Keep BP <180/105 m m Hg using m edication such as labetalol or nicardipine.

o

Consider nitroprusside for hypertension unresponsive to labetalol or nicardipine, or for a DBP >140 m m Hg.



Monitor for signs of ICH:

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o

Up to a 6% increased risk with TPA: 



Prim arily in patients with a NIH-SS >20

o

Decreased LOC

o

Increased weakness

o

Headache

o

Acute hypertension or tachycardia

o

Nausea or vom iting

If ICH suspected, obtain em ergent head CT to confirm diagnosis:



If present, treat as follows: o

Discontinue TPA.

o

Obtain blood sam ples for PT, PTT, platelet count, fibrinogen level.

o

Prepare cryoprecipitate, fibrinogen and platelets, and infuse as needed.

o 

Obtain neurosurgical consultation

Patients who have presented after 3 hours but within 6 hours of sym ptom onset: o

Consider intra-arterial throm bolysis or m echanical recanalization if available.

Medication (Drugs) 

Nitropaste: 1â€“2 inches to anterior chest wall



Labetalol: 10 m g IV over 1â€“2 m inutes; then, if needed: o

repeat or double dose q10m inâ€“q20m in up to a m ax. of 300 m g, or

o 

start a drip at 2â€“8 m g/m in

Nicardipine: 5 m g/hr as a drip; titrate upwards in 2.5 m g/hr increm ents q5m in, up to a m ax. of 15 m g/hr



Nitroprusside: 0.5â€“1.0 m g/kg/m inute, continuous IV drip, titrated to BP param eters

Pa ge 4 1 0



TPA: 0.9 m g/kg IV, m ax. 90 m g: o

Give 10% of dose as a bolus.

o

Followed im m ediately by the rem ainder infused over the subsequent 60 m inutes



Cryoprecipitate and fibrinogen: 6â€“8 U IV



Platelets: 6â€“8 U IV

Follow-Up Disposition Admission Criteria All patients given throm bolytic or other reperfusion therapy for a CVA should be adm itted to an intensive care setting for frequent neurological checks and vital sign assessm ents.

Discharge Criteria N/A, see Adm ission Criteria

References 1. Adam s HP, Adam s RJ, Brott T, et al. Guidelines for the early m anagem ent of patients with ischem ic stroke; a scientific statem ent from the Stroke Council of the Am erican Stroke Association. Stroke. 2003;34:1056â€“1083. 2. Albers GW. Advances in intravenous throm bolytic therapy for treatm ent of acute stroke. Neurology. 2001;57(S2):S77â€“S81. 3. Furlan A, Higashida R, Wechsler L, et al. Intraarterial pro-urokinase for acute ischem ic stroke (PROACT II). JAMA. 1999;282:2003â€“2011. 4. Leary M, Saver JL, Gobin PY, et al. Beyond tissue plasm inogen activator: Mechanical intervention in acute stroke. Ann Em erg Med. 2003;41:838â€“846.

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5. The NINDS rt-PA Stroke Study Group. Tissue plasm inogen activator for acute ischem ic stroke. New Eng J Med. 1995;333:1581â€“1587.

Codes ICD9-CM ICD-9 for total body throm bolysis: 39.96 ICD-9 for infusion therapy: 99.29 CPT: 907.84

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Respirato ry Distress

Respiratory

Distress Erik D. Barton

Basics Description Respiratory distress, shortness of breath, or dyspnea is a com m on com plaint for patients presenting to the ED.

Etiology 



Upper airway obstruction: o

Epiglottitis

o

Croup syndrom es

o

Laryngotracheobronchitis

o

Foreign body

o

Angioedem a

o

Retropharyngeal abscess

Cardiovascular: o

Pulm onary edem a/congestive heart failure (CHF)

o

Dysrhythm ias

o

Cardiac ischem ia

o

Pulm onary em bolus

o

Pericarditis

o

Tam ponade

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o 

Air em bolism

Pulm onary: o

Asthm a

o

Chronic obstructive pulm onary disease (COPD)/em physem a





o

Pneum onia

o

Bronchiolitis

o

Aspiration

o

Adult respiratory distress syndrom e (ARDS)

o

Pulm onary edem a

o

Pleural effusion

o

Toxic inhalation injury

Traum a: o

Pneum othorax

o

Tension pneum othorax

o

Rib fractures

o

Pulm onary contusion

o

Fat em bolism with long bone fractures

Neurom uscular: o

Guillain-BarrÃ© syndrom e

o

Myasthenia gravis



Metabolic/System ic/Toxic



Anaphylaxis



Anem ia



Acidosis



Hyperthyroidism



Sepsis



Septic em boli from IV drug use or infected indwelling lines



Salicylate intoxication



Drug overdose



Am phetam ines



Cocaine

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

Sym pathom im etic



Obesity



Psychogenic: o

Anxiety disorder

o

Hyperventilation syndrom e

Pediatric Considerations 

Respiratory failure is m ost com m on cause of cardiac arrest in infants.



Croup syndrom es include: o

Viral

o

Spasm odic

o

Bacterial

o

Congenital defects

o

Noninflam m atory causes (foreign body, gastroesophageal reflux, traum a, tum ors)





Most com m on cause of upper airway obstruction: o

Younger than 6 m onths: congenital laryngom alacia

o

Older than 6 m onths: viral croup

Epiglottitis: o

Highest incidence at ages 2â€“4 years

o

Abrupt onset

o

Fever

o

Respiratory distress and stridor

o

Difficulty swallowing oral secretions

o

Restlessness and anxiety

Pregnancy Considerations 

Am niotic fluid em bolism during or after delivery



Septic em bolism from septic abortion or postpartum uterine infection

Pa ge 4 1 1

Diagnosis Signs and Symptoms 

Tachypnea



Dyspnea



Tachycardia



Anxiety



Diaphoresis



Cough (â€œbarking,â€• productive)



Stridor



Hoarse voice



Difficulty swallowing or handling oral secretions



Upper airway rhonchi (wheezes)



Lower airway crackles (rales)



Increased work of breathing



Accessory and intercostal m uscle use



Hypoxem ia



Hypocapnia or hypercapnia if severe



Respiratory acidosis



Cyanosis



Lethargy, then obtundation

History 

Previous history of asthm a, COPD, cardiac disease, or dysrhythm ia, CHF, foreign body aspiration



Recent fever or upper respiratory tract infection, cough, sputum production, sore throat, system ic disease, anxiety disorder



Recent chest or long bone traum a



IV drug use or indwelling catheters

Physical Exam 

Observe: m ental status, level of distress, work of

Pa ge 4 1 1

breathing, jugular venous pressure, skin color 

Feel/Palpate: distal pulses, heart perioperative m yocardial infarction, chest wall, peripheral edem a



Percuss: lungs for dullness or resonance, abdom inal distention or hepatom egaly



Auscultate: heart sounds, m urm urs, lung wheezes or crackles, neck for upper airway stridor, abdom en bowel sounds

Pediatric Considerations 

Evaluate retractions, behavior, respiratory rate, breath sounds, and skin color.



Weak cry, expiratory grunting, nasal flaring, tachypnea and tachycardia, retractions, and cyanosis in neonates

Essential Workup 

Pulse oxim etry



Cardiac and blood pressure (BP) m onitoring



ECG if suspected cardiac etiology

Tests Lab 

ABG for severity and acid-base determ ination



CBC



Electrolytes, blood urea nitrogen/creatinine, glucose



Blood, sputum , urine cultures for fever or sepsis



Brain natriuretic peptide for undifferentiated shortness of breath or CHF severity



Urinary output m onitoring for CHF



Toxicology screen or salicylate level if suspected

Imaging 

Chest radiograph for: o

Pneum onia

Pa ge 4 1 1

o

Pneum othorax

o

Hyperinflation

o

Atelectasis

o

CHF/Pulm onary edem a



Spirom etry (peak expiratory flow rates) for asthm a, COPD



Neck radiographs to assess epiglottis and soft tissue spaces, foreign body



Fiberoptic laryngoscopy to assess epiglottis, vocal cords, and pharyngeal space



CT angiography or ventilation/perfusion scan for pulm onary em bolus

Pediatric Considerations 

Chest/neck radiograph m ay show foreign body or â€œsteeple signâ€• in croup syndrom es.



Chest fluoroscopy m ay be used to assess inspiratory and expiratory excursions if foreign body is suspected.

Diagnostic Procedures/Surgery 

Bronchoscopy for foreign body in trachea or bronchus



Pulm onary artery (Swan-Ganz) catheter for severe CHF, ARDS, pulm onary edem a

Differential Diagnosis See Etiology P.959

Treatment Pre Hospital

Pa ge 4 1 1



Assum e a position of com fort for patient



100% oxygen: o

Assisted bag-valve m ask (BMV) ventilation if obtunded



Airway adjunct devices (oral or nasal) to m aintain patency if tolerated



Intubation for severe respiratory distress



Needle aspiration of suspected tension pneum othorax

Initial Stabilization 

ABCs



Ensure patent airway; BVM assist or intubate for severe distress or arrest



IV fluids if hypotensive



100% oxygen by face m ask: o

Use cautiously in patients with severe COPD or chronic CO 2 retention.



Monitor BP, heart rate, respirations, pulse oxim etry



Advanced cardiac life support for dysrhythm ias or arrest

ED Treatment 

Treat underlying etiology as appropriate.



CHF or pulm onary edem a: o

Diuretics

o

Nitroglycerin

o

Nitroprusside if hypertensive

o

Pulm onary artery catheter if severe

o

Noninvasive positive-pressure ventilation (NPPV) or intubation if severe



Asthm a, bronchiolitis, COPD: o

Bronchodilators

o

Steroids

o

Antibiotics for infection

Pa ge 4 1 1

o 



ARDS, aspiration, toxic lung injury: o

Mechanical ventilation as needed

o

Steroids controversial

Pneum onia: o



NPPV or intubation if severe

Antibiotics

Pneum othorax: o

Im m ediate decom pression if suspected tension pneum othorax

o 





Aspiration or tube thoracostom y (see Pneum othorax)

Pleural effusion: o

Determ ine etiology

o

Diagnostic and sym ptom atic thoracentesis

Croup: o

Cool, m isted air or oxygen

o

Steroids

o

Racem ic epinephrine

o

Antibiotics for bacterial infection

Epiglottitis: o

Im m ediate airway stabilization with intubation or tracheostom y in operating room if possible

o 





Antibiotics for Haem ophilus influenzae

Anaphylaxis, angioedem a: o

IV steroids

o

H 1 /H 2 -blockers

o

SQ or IV epinephrine

o

Early intubation

Retropharyngeal abscess o

Drainage

o

IV antibiotics

o

Ear/Nose/Throat consult

Cardiac:

Pa ge 4 1 1



o

Treat dysrhythm ias or ischem ia

o

Anticoagulation or throm bolysis for PE

o

Pericardiocentesis for tam ponade

o

NSAIDs or aspirin for pericarditis

Neurom uscular: o

Support ventilation

o

Pyridostigm ine brom ide or neostigm ine for m yasthenia gravis



Metabolic/toxic: o



Treat underlying cause

Psychogenic: o

Anxiolytics

Pediatric Considerations 

Transtracheal jet ventilation if unable to intubate (cricothyrotom y not recom m ended in children younger than 10 years)





Bronchiolitis: o

Bronchodilators

o

Antivirals for respiratory syncytial virus

o

Antibiotics for infection

Spasm odic croup: o



Very sensitive to m isted air

Bacterial croup (m em branous laryngotracheobronchitis): o

Treat Staphylococcus aureus

Pregnancy Considerations 

Supportive oxygen therapy and heparin for PE or am niotic fluid em bolism



IV antibiotics for septic em bolism

Medication (Drugs)

Pa ge 4 1 1

Refer to specific etiologies

Follow-Up Disposition Admission Criteria 

Continued supplem ental oxygen requirem ent



Cardiac or hem odynam ic instability: o

Requiring IV therapy or hydration

o

Requiring close airway observation or repeated treatm ents



As required by underlying cause or significant com orbid disease

Discharge Criteria 

Correction of underlying disease



Stable airway



Acute supplem ental oxygen not required

Issues for Referral Refer to specific etiologies

References 1. Ausiello D, Goldm an L. Eds. Cecil Textbook of Medicine. 22nd ed., Philadelphia, PA: WB Saunders, 2004:492â€“583,1523â€“1524. 2. Sigillito RJ, DeBlieux PM. Evaluation and initial m anagem ent of the patient in respiratory distress. Em erg Med Clin North Am . 2003;21(2):239â€“258. 3. William s SA, Hutson HR, Speals HL. Dyspnea. In: Em ergency m edicine: Concepts and clinical practice. 4th ed. St. Louis, MO: Mosby, 1998: 1460â€“1469.

Codes

Pa ge 4 1 1

ICD9-CM 786.09 Respiratory Distress 770.89 peds <28 days

ICD10 R06.00 Dyspnea NOS R06.02 Shortness of breath R06.09 Other form s of dyspnea P22.9 peds <28 days

Pa ge 4 1 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Resuscitatio n, Neo nate

Resuscitation,

Neonate David A. Listman

Basics Description 

Annually, alm ost 1 m illion deaths worldwide are related to birth asphyxia



10% of newborns require som e assistance at birth.



1% of newborns require extensive resuscitation.



Consider not initiating resuscitation if: o

Newborns confirm ed to be less than 23 weeks gestation or 400 g



o

Anencephaly

o

Babies with confirm ed Trisom y 13 or 18

APGAR (activity, pulse, grim ace, appearance, respiration) scores do not guide resuscitation: o

Do not wait to assign APGAR scores prior to starting resuscitation.

o

APGAR scoreâ€”5 categories with score of 0, 1 or 2 in each at 1 and 5 m inutes 

Heart rate: 0 = absent, 1 = <100, 2 = >100



Respirations: 0 = absent; 1 = slow, irregular; 2

Pa ge 4 1 2

= good, crying 

Muscle tone: 0 = lim p; 1 = som e flexion; 2 = active m otion



Reflex irritability: 0 = no response; 1 = grim ace; 2 = cough, sneeze, cry



Color: 0 = blue or pale; 1 = pink body and blue extrem ities; 2 = all pink

Genetics Consider not initiating resuscitation in Trisom y 13 and 18

Etiology 

Newborns transition from dependence on the placenta to dependence on the lungs for oxygen.



Hypoxia initially causes tachypnea followed by prim ary apnea.



Stim ulation m ay cause resum ption of breathing during prim ary apnea.



Continued hypoxia leads to secondary apnea.



Secondary apnea requires assisted ventilation.



Antepartum risk factors associated with need for resuscitation include: o

Maternal diabetes

o

Pregnancy-induced hypertension

o

Chronic hypertension

o

Anem ia

o

Previous fetal or neonatal death

o

Bleeding in second or third trim ester

o

Maternal infection

o

Maternal cardiac, renal pulm onary, thyroid or neurologic disease

o

Polyhydram nios

o

Oligohydram nios

Pa ge 4 1 2



o

Prem ature rupture of m em branes

o

Postterm gestation

o

Multiple gestation

o

Size-dates discrepancy

o

Drug therapy

o

Maternal substance abuse

o

Fetal m alform ation

o

Dim inished fetal activity

o

No prenatal care

o

Age <16 or >35 years

Intrapartum risk factors associated with need for resuscitation include:



o

Em ergency C-section

o

Forceps or vacuum assist

o

Breech or other abnorm al presentation

o

Prem ature labor

o

Precipitous labor

o

Chorioam nionitis

o

Prolonged rupture of m em branes

o

Prolonged second stage of labor

o

Fetal bradycardia

o

Non reassuring fetal heart tracing

o

General anesthesia

o

Uterine tetany

Narcotics adm inistered to m other within 4 hours: o

Meconium -stained am niotic fluid

o

Prolapsed cord

o

Abruptio placenta

o

Placenta previa

Pa ge 4 1 2

Diagnosis Signs and Symptoms History Risk factors as above predict the need for resuscitation

Physical Exam 

Respirationsâ€”rate and effectiveness



Heart rateâ€”by auscultation or palpation of um bilical cord



Color

Tests Lab 

Bedside blood glucose m easurem ent



Blood gas

Imaging Chest radiograph

Diagnostic Procedures/Surgery 

Endotracheal intubation: o

Straight blades Miller 1 for full term , Miller 0 for preterm

o

o

Endotracheal tubes: 

2.5 below 1,000 g or 28 weeks



3.0 1,000â€“2,000 g or 28â€“34 weeks



3.5 2,000â€“3,000 g or 34â€“38 weeks



4.0 above 3,000 g or 38 weeks

Have stylet, end tidal CO 2 detector, suction, tape, m econium aspirator available



Um bilical vein catheterization: o

Tie um bilical tape around base of cord.

o

Prefill syringe attached to um bilical catheter (3.5 or 5 Fr.).

Pa ge 4 1 2

o

Cord below cord clam p

o

Identify um bilical vein (large, thin-walled and single).

o

Insert catheter into um bilical vein directed cephalad.

o

Advance 2â€“4 cm until blood flows freely into syringe.

o

Inject drugs/fluids as appropriate.

o

Secure catheter with suture.

P.961

Treatment Pre Hospital 

Resuscitation should be started by prehospital personnel.



Neonatal resuscitation equipm ent should be available.



Pay particular attention to heat retention and warm ing.

Initial Stabilization 

If m econium , poor respiratory effort, poor m uscle tone, cyanosis, or prem aturity are present proceed with resuscitation.



Initial steps include: o

Warm the baby.

o

Position (neck slightly extended, sniffing position) and clear the airway (m econium m ay necessitate intubationâ€”see below).



o

Dry; stim ulate (flick feet, rub trunk or extrem ities).

o

Provide oxygen.

Meconium :

Pa ge 4 1 2

o

Meconium present and baby is not vigorous: 

Insert endotracheal tube.



Suction with endotracheal tube (ETT) m econium aspiration device.



Slowly withdraw tube.



Repeat as necessary until little m econium is recovered or heart rate (HR) is not m aintained.

o

Meconium present and baby is vigorous.

o

Suction m outh then nose with bulb or suction catheter.



If re-evaluation within 30 seconds reveals apnea or HR <100 proceed with: o

Positive pressure ventilation with 100% oxygen

o

Self-inflating or flow-inflating (anesthesia type) bag

o

Proper-fitting m ask

o

First breath m ay require high pressure necessitating occlusion of â€œpop-offâ€• valve.



o

Rate of 40â€“60 breaths per m inute

o

Pressure of 30â€“40 cm H 2 O

o

If prolonged, place nasogastric (NG) tube.

If re-evaluation after 30 seconds of positive pressure ventilation with 100% oxygen reveals HR <60 proceed with: o

Continued positive pressure ventilation and chest com pressions

o

Two-thum b technique while hand encircle torso

o

Two-finger technique: 

Com press approxim ately one third the anterior posterior (AP) diam eter of chest and release.

o

3 com pressions followed by one ventilation

o

120 events per m inute (90 com pressions and 30 breaths)

Pa ge 4 1 2



If after 30 seconds HR is >60, stop com pressions.



If after 30 seconds HR is >100, stop positive pressure ventilator (PPV).



If after 30 seconds HR still <60, adm inister epinephrine (IV or via ET tube)

ED Treatment 

If evidence of blood loss or poor response to resuscitation, adm inister volum e expander.



Norm al saline, Ringer Lactate, O-negative blood (cross-m atched if tim e perm itting)





If severe m etabolic acidosis is suspected or proven: o

Ensure adequate ventilation.

o

Adm inister sodium bicarbonate.

If hypoglycem ia is proven or suspected, treat with IV dextrose.



If heart rate and color im prove, but respiratory effort and tone are poor and m other received narcotics within 4 hours, treat with naloxone hydrochloride. o

Contraindicated in m others addicted to narcotics or receiving m ethadoneâ€”can precipitate seizures.



Persistent distress m ay indicate pneum othorax.



Know or suspected diaphragm atic hernias should be treated with im m ediate endotracheal intubation and placem ent of NG tube.



Consider discontinuation of resuscitation if 15 m inutes of absent HR.

Medication (Drugs) 

Dextrose: 2â€“4 m L/kg of D 1 0 W given IV (um bilical vein)



Epinephrine: 0.1â€“0.3 m L/kg of 1:10,000 solution, m ay

Pa ge 4 1 2

be given IV or via ET-tube 

Naloxone hydrochloride: 0.1 m g/kg. Adm inister IV or via ETT, can adm inister IM or SC, but onset of action is delayed.



Sodium bicarbonate: 2 m Eq/kg 4 m L/kg of 4.2% solution (0.5 m Eq/cc). Adm inister slowly via IV route (um bilical vein).



Volum e expanders: norm al saline, Ringer's lactate, blood. Initial dose 10 cc/kg, m ay be repeated, all given IV (um bilical vein).

Follow-Up Disposition Admission Criteria 

All newborns require adm ission.



If significant resuscitation is necessary, adm it to newborn intensive care unit

References 1. Fowlie PW, McGuire W. Im m ediate care of the preterm infant. BMJ . 329(9):845â€“848. 2. Kattwinkel J, editor. Textbook of neonatal resuscitation. 4th ed. Elk Grove Village, IL: Am erican Academ y of Pediatrics; 2000.

Codes ICD9-CM 769 Respiratory distress syndrom e Cardiorespiratory distress syndrom e of newborn

Pa ge 4 1 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Resuscitatio n, Pediatric

Resuscitation,

Pediatric Brian Clyne Michelle McMahon-Downer

Basics Description 

Respiratory and/or circulatory failure leads to tissue hypoxia, acidosis, and cell death.



Multisystem organ failure subsequently develops.



Respiratory failure: o

Tachypnea

o

Slow, irregular breathing pattern prearrest

o

Decreased or absent breath sounds; inadequate ventilation

o

Retractions, accessory m uscle use, expiratory grunting, nasal flaring

o

Mottled skin, cyanosis

o

Altered level of consciousness (LOC): irritability, agitation, lethargy, weak or absent cry, decreased response to pain

o

Poor m uscle tone

o

Weak or absent cough or gag reflex

Pa ge 4 1 2





Early shock (com pensated): o

Vital signs initially com pensated

o

Orthostatic changes or isolated tachycardia

o

Slightly delayed cap refill (>2 seconds)

o

Warm , dry skin in early septic shock

Late shock (uncom pensated): o

Tachycardia, tachypnea, prearrest bradycardia

o

Hypotension, weak peripheral pulses

o

Mottled, pale, cool extrem ities with m arkedly decreased capillary refill



o

Decreased urine output progressing to anuria

o

Decreased LOC, seizures, com a

o

Fever or hypotherm ia in septic shock

Cardiopulm onary arrest: o

Final com m on pathway of progressive deterioration of respiratory and circulatory function

Signs and Symptoms 

History from caregivers/parents of onset, progression, inciting, contributing or predisposing traum a/exposure/conditions, associated findings, past m edical history, fam ily history, m edications, ingestions



History of preceding events from prehospital personnel

Physical Exam 

Airway assessm ent: o

Look, listen, feel for air exchange and ventilation; observe for stridor, signs of obstruction.



Breathing assessm ent: o

Respiratory rate: tachypnea or slow/irregular pattern (m ore om inous)

o

Observe for grunting, nasal flaring, head bobbing, retractions, abdom inal distention, chest expansion.

Pa ge 4 1 2

o

Pulse oxim etry: reflects hem oglobin oxygen saturation, not necessarily oxygen delivery

o

Auscultation: assess for wheezing, rales, dim inished breath sounds



Circulatory assessm ent: o

Pulse: tachycardia or bradycardia (m ore om inous); orthostatic changes noted easily.

o

Blood pressure (BP): Typical SBP in children is 90 m m Hg plus (age in years tim es two) m m Hg. Hypotension is a late finding; widened pulse pressure in early septic shock.

o

Peripheral pulse presence and strength (brachial/fem oral [<1 year] or carotid [>1 year])

o

Capillary refill: delayed >2 seconds with poor perfusion

o 

Skin: m ottled, pale, or cyanotic with poor perfusion

Mental status assessm ent: o

Observe for signs of decreased CNS perfusion: decreased responsiveness, irritability, confusion, agitation, poor m uscle tone, sluggish pupillary response, posturing



Com plete set of vital signs including rectal tem perature, oxim etry, and orthostatics when appropriate.

Tests Lab 

Workup directed by history, assessm ent of ABCs, and likely etiologies



Arterial blood gas with oxim etry to assess oxygenation, ventilation, acid-base status



Glucose, electrolytes; do bedside glucose.



Other m etabolic and toxicology studies as indicated

Pa ge 4 1 3



Sepsis evaluation including lum bar puncture, urine and blood cultures as indicated

Imaging 

Chest radiograph to evaluate pulm onary or cardiac etiologies



Lateral decubitus or inspiratory/expiratory film or laryngoscopy/bronchoscopy for suspicion of foreign body



ECG



Echocardiogram



Cervical spine film s and other traum a studies as indicated



CT scan of head for neurologic findings

Differential Diagnosis 

Cardiopulm onary failure in children is usually the result of prim ary respiratory failure but is the potential end point of all untreated or unresponsive critical illness.



Respiratory: o

Upper airway obstruction: croup, epiglottitis, peritonsillar or retropharyngeal abscess, foreign body, tracheitis, congenital abnorm alities

o

Lower airway obstruction: asthm a, pneum onia, bronchiolitis, foreign body, cystic fibrosis

o

Thoracic traum a, near drowning



Hypovolem ia: traum a, diarrhea/vom iting, burns



Cardiovascular: congenital/acquired heart disease, m yocarditis, pericarditis, congestive heart failure, dysrhythm ias



Infectious: sepsis, m eningitis, gastroenteritis, peritonitis



CNS: status epilepticus, epidural/subdural hem atom a



Metabolic: diabetic ketoacidosis, hypoglycem ia, hypernatrem ia, hypo/hyperkalem ia, acidosis



Toxicologic: CO poisoning, cardiotoxic agents

Pa ge 4 1 3



Near sudden infant death syndrom e (SIDS)/apparent life-threatening event (ALTE)



Consider child abuse when history is inconsistent with the illness or pattern of injury.

Treatment Pre Hospital 

Priority is to stabilize ABCs; m onitor.



Avoid prolonged on-scene tim es; rapid transport of critically ill child is crucial.



Recognize respiratory or circulatory failure; intervene early.



Recognize im pending arrest and provide life-sustaining procedures during transport.



Autom ated external defibrillator for ventricular fibrillation and pulseless ventricular tachycardia in children 1 year and older



Tim ely notification of ED to allow proper preparation



Gather history from fam ily/bystanders about preceding events, past m edical history, m edications, allergies.

Initial Stabilization 

Early recognition and stabilization of respiratory failure or shock



Diagnose and treat im m ediately life-threatening conditions sim ultaneously.



Em pirical intervention is required



ABCDE evaluation: o

Airway: Assess patient ability to speak/cry; listen for stridor; observe for traum a.

Pa ge 4 1 3

o

Breathing: Observe for tracheal deviation, signs of chest injury or pneum othorax; observe chest excursion, auscultate; apply oxygen.

o

Circulation: Evaluate pulses, heart rate, BP, capillary refill.

o

Disability: Determ ine m ental status and assess for neurologic deficits; check stat glucose.

o

Exposure/Environm ent: Fully expose for rapid skeletal survey while preventing hypotherm ia.



Obtain pertinent history from em ergency m edical services or fam ily.

P.963

ED Treatment 

Broselow Pediatric Em ergency Tape relates patient's length to weight and thus to appropriate drug dosages and equipm ent sizes.



Airway: o

Secure for every resuscitation.

o

Open airway with head tilt, chin lift, or m odified jaw thrust (if traum a suspected).

o

Clear secretions, blood, foreign body with suction.

o

Tem porary stabilization with oropharyngeal or nasopharyngeal airway, bag-valve m ask assistance

o

Intubation as necessary using appropriate tube size ([16 + age in years]/4 or size sim ilar to patient's little finger or nares)

o

Position of endotracheal tube (ETT) at lips (cm ) = 3 tim es diam eter of tube (m m )

o

Use adjunctive device, as applicable.

o

Postintubation: Confirm tube placem ent with

Pa ge 4 1 3

colorim etric CO 2 device, continuous ETCO 2 m onitoring, auscultation. 

Rapid-sequence intubation: preoxygenation, pretreatm ent, paralysis with induction cricoid pressure, intubation, confirm ation of placem ent, postintubation m onitoring o

Prem edications: atropine to prevent bradycardia, lidocaine following head injury

o

Induction agents: m idazolam , thiopental, etom idate, ketam ine

o

Paralytics: succinylcholine, pancuronium , vecuronium , rocuronium



Breathing: o

Oxygenate with supplem ental O 2 , nonrebreather m ask; assist ventilation with bag-valve m ask or control ventilation if intubation perform ed.

o

Treat conditions that lim it ability to oxygenate/ventilate: pneum othorax, hem othorax, cardiac tam ponade, circum ferential burns.



Circulation: o

Obtain intravascular access: IV, intraosseous, central access.

o

Fluid resuscitate with crystalloid (NS or lactated Ringer solution) bolus at 10â€“20 m L/kg and repeat if necessary; correct hypovolem ia.

o

Control obvious sources of bleeding: Apply direct pressure; elevate.

o

Consider transfusion of packed RBCs after crystalloid replacem ent in traum a.

o

Consider vasopressor in decom pensated shock: epinephrine, dopam ine, norepinephrine.

o

Consider inotrope in com pensated shock: dobutam ine, m ilrinone.

Pa ge 4 1 3



Cardiopulm onary resuscitation: o

Provide blood flow to vital organs while restoring spontaneous circulation.

o

Infant younger than 1 year: Check for pulse at brachial or fem oral artery.

o 

Child 1â€“8 years: Check for pulse at carotid artery.

Cardiac dysrhythm ias: o

Usually secondary to respiratory insufficiency or m etabolic disturbance

o

Treat rhythm disturbance as per published algorithm s.

o

Unstable tachydysrhythm ia m ay require adenosine, lidocaine, am iodarone, cardioversion, or defibrillation.

o

Unstable bradydysrhythm ia m ay require atropine, epinephrine, or pacing.

o

Pulseless rhythm s: ventricular fibrillation, pulseless ventricular tachycardia, pulseless electrical activity, asystole; m ay require epinephrine, defibrillation, lidocaine, am iodarone



Continuously m onitor patient

Medication (Drugs) 

First or loading dose unless otherwise noted



Adenosine: 0.1 m g/kg



Am iodarone: 5 m g/kg IV rapid



Atropine: 0.02 m g/kg IV, m inim um 0.1 m g



Calidum chloride: 20 m g/kg IV



Cardioversion: 0.5 J/kg



Defibrillation: 2 J/kg initial, then 4 J/kg



Epinephrine: 0.01 m g/kg IV first dose (0.1 m L/kg 1:10,000

Pa ge 4 1 3

IV); 0.1 m g/kg IV subsequent or ETT doses (0.1 m L/kg 1:1,000 IV); higher doses (0.1â€“0.2 m g/kg IV) m ay be considered for refractory arrest 

Etom idate: 0.3 m g/kg IV



Ketam ine: 1â€“2 m g/kg IV



Lidocaine: 1â€“1.5 m g/kg IV



Midazolam : 0.1 m g/kg IV



Naloxone: 0.1 m g/kg IV



Pancuronium : 0.1 m g/kg IV



Rocuronium : 0.6â€“1.2 m g/kg IV



Sodium bicarbonate: 1 m Eq/kg IV



Succinylcholine: 1â€“1.5 m g/kg IV



Vecuronium : 0.1â€“0.3 m g/kg IV

Follow-Up Disposition Admission Criteria 

All patients requiring resuscitation



All patients with im pending or existent respiratory or cardiovascular com prom ise



Survivors of cardiopulm onary arrest require an intensive care unit equipped to m anage critically ill children: o

Continually m onitor patients for any signs of decom pensation after resuscitation.

o

Consider transferring patient if the child's acuity exceeds hospital capabilities.



Consultation as appropriate depending on specific pathophysiology

References

Pa ge 4 1 3

1. Am erican Heart Association in Collaboration with the International Liaison Com m ittee on Resuscitation. Guidelines 2000 for Cardiopulm onary Resuscitation and Em ergency Cardiovascular Care: International Consensus on Science, part 10. Pediatric Advanced Life Support. Circulation. 2000;102(8)Supplem ent: 291â€“342. 2. Bardella IJ. Pediatric advanced life support: a review of the AHA recom m endations. Am erican Heart Association. Am Fam Physician. 1999;60(6):1743â€“1750. 3. Brown K, Bocock J. Update in Pediatric Resuscitation. Em erg Med Clinic North Am . 2002;20(1):1â€“26. 4. Patterson MD. Resuscitation update for the pediatrician. Pediatr Clin North Am . 1999;46(6):1285â€“1303. 5. Pediatric Advanced Life Support Task Force, International Liaison Com m ittee on Resuscitation. Use of Autom ated External Defibrillators for Children: An Update. Circulation. 2003;107(25):3250â€“3255. 6. Wright JL, Patterson MD. Resuscitating the pediatric patient. Em erg Med Clinic North Am . 1996;14(1):219â€“231. 7. Zaritsky AL, Nadkarn VH, Berg RA, et al. Pediatric advanced life support. Dallas, TX: Am erican Heart Association, 2002.

Pa ge 4 1 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Retinal Detachm ent

Retinal

Detachment David A. Harter

Basics Description 



Three types of retinal detachm ents: o

Rhegm atogenous retinal detachm ents (RRD)

o

Tractional retinal detachm ents (TRD)

o

Exudative retinal detachm ents (ERD)

RRD: o

Most com m on

o

Violation of sensory retina allows vitreous to separate the sensory and pigm ented parts of retina from each other.

o

Acute event, flashes secondary to tearing of nerve fibers, floaters secondary to bleeding; from ruptured retinal vessels



TRD: o

Contraction of fibrous vitreous bands pulls the sensory retina off the pigm ented retina.

o

Chronic and progressive

o

Asym ptom atic unless hem orrhage or retinal tear

Pa ge 4 1 3

occurs 

ERD: o

Subretinal collections of serous fluid separate retinal layers without violating either layer.

o

Affected part of retina changes with head position.

Etiology 

RRD: o

Myopia

o

Marfan syndrom e

o

Structural degeneration of underlying anatom y of vitreous body, sensory or pigm ented retina

o 

Traum a

TRD: o

Proliferative diabetic retinopathy

o

Vasculopathy

o

Perforating injury

o

Chorioretinitis: 

Retinopathy of prem aturity, sickle cell disease, or toxocariasis

o 

Traum a

ERD: o

Tum ors of the choroid or retina (m elanom a, retinoblastom a)

o

Inflam m atory disorders (Coates or Harada disease, posterior scleritis)

Diagnosis Signs and Symptoms 

Flashes of light

Pa ge 4 1 3



Floaters



â€œNight shadeâ€• obscuring visual field



Peripheral/Central vision loss or other visual field defects



Asym ptom atic

Essential Workup 



History: o

Age

o

Speed of onset

o

Associated sym ptom s

o

Previous episodes

Physical: o

Com plete ophthalm ologic exam ination

o

Thorough neurologic exam ination to exclude cerebrovascular accident/transient ischem ic attack

P.965

Tests Lab As needed to workup underlying diseases

Imaging Visual field testing

Differential Diagnosis 

Senile retinoschisis



Juvenile retinoschisis



Choroidal detachm ent

Treatment

Pa ge 4 1 4

ED Treatment 

Bed rest



Ophthalm ologic consultation

Follow-Up Disposition Admission Criteria Need for surgical repair

Discharge Criteria 

Any patient retinal detachm ent seen by an ophthalm ologist and deem ed safe to go hom e



Chronic retinal detachm ents are repaired over the sam e tim e course as it took to create them .



ERD resolves with treatm ent of the underlying problem .

References 1. Albert D, Jakobiec F, Azar D, et al, eds. Principles and practice of ophthalm ology. 2nd ed. Philadelphia, PA: WB Saunders, 2000. 2. Morgan A, Hem phill R. Acute visual change. Em erg Med Clin North Am . 1998;16(4):825â€“843. 3. Regillo C, Benson W. Retinal Detachm ent. Opthalm ic Surgery. 3rd ed. Philadelphia, PA: Elsevier Science, 2003 4. Rhee D, Pyfer M, eds. The Wills eye m anual office and em ergency room diagnosis and treatm ent of eye disease. 3rd ed. Philadelphia, PA: Lippincott William s & Wilkins, 1999. 5. Shingleton B, O'Donoghue M. Blurred vision. N Engl J Med. 2000;343(8):556â€“562. 6. Whitm ore P. Sudden painless visual loss retinal causes. Clin Geriatr Med. 1999;15(1):15â€“23

Pa ge 4 1 4

Codes ICD9-CM 361.9

Pa ge 4 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Retro pharyngeal Abscess

Retropharyngeal Abscess Lee Shockley Kurt Whitaker

Basics Description 

Infection in the retropharyngeal space, which lies anterior to the prevertebral space, posterior to the pharyngeal m ucosa; skull base to carina



Prim arily a disease of young children: o

Peak incidence at 3â€“5 years of age (90% under age 6; one third less than 6 m onths)

o

Suppurative infection which begins in the posterior pharyngeal nodes

o

Nodes regress during later childhood, explaining the decreasing incidence after age 5.

o 

Disease still reported in all age groups.

Anatom y: o

Space lies between the m iddle cervical and alar fascia.

o

Contiguous with the superior and posterior m ediastinum



Prognosis is very good with prom pt diagnosis, IV

Pa ge 4 1 4

antibiotics, and surgical drainage. 

Com plications: o

Airway com prom ise

o

Sepsis

o

Aspiration pneum onia

o

Spontaneous perforation

o

Necrotizing fasciitis

o

Mediastinitis

o

Throm bosis of the internal jugular vein

o

Erosion into the carotid artery

o

Recurrent abscess

o

Cranial nerve palsies (IX, X, XII)

Etiology 

Causes: o

Often preceded by viral or bacterial upper respiratory infection (45%)



o

May also follow oropharyngeal traum a (27%)

o

Substantial portion idiopathic (28%)

Bacteriology: o

Strep viridans

o

Staph aureus

o

Staph epiderm idis

o

Other gram positives

o

Anaerobes

o

Acid-fast bacilli

o

Polym icrobial abscesses predom inate

Diagnosis Signs and Symptoms

Pa ge 4 1 4

History 

Fever



Dysphagia



Decreased oral intake



Stridor, dyspnea



Irritability



Pain with neck m ovem ent



Neck swelling



Ill appearing

Physical Exam 

Fever (100%)



Torticollis (75%)



Pharyngitis (60%)



Stridor/drooling (20â€“40%)



Bulging of posterior pharynx (25%)



Pain on neck extension (m ore than flexion)



Trism us



Dysphonia



Respiratory distress

Tests Lab 

CBC: o

May have leukocytosis, often profound



Blood cultures



Throat cultures



No lab test will m ake diagnosis.

Imaging 

Lateral soft tissue neck radiographs: o

Specificity: 100%

o

Sensitivity: 80â€“88%

Pa ge 4 1 4

o

Film taken in inspiration with neck slightly extended

o

Increased suspicion if widening of the: 

Retropharyngeal space anterior to C2 to >7m m , or greater than half of the width of the vertebral body



Space anterior to C6 to >14 m m in preschool children or >22 m m in adults







Chest radiograph: o

Mediastinal widening

o

Aspiration

Ultrasound of neck: o

Low sensitivity

o

Not recom m ended

CT of neck with IV contrast: o

Sensitivity: 85â€“100%

o

Specificity: 45â€“88%

o

Can aid in operative planning

o

May not distinguish abscess from cellulitis

P.967

Differential Diagnosis 

Tonsillopharyngitis



Epiglottitis



Croup



Foreign body



Tracheitis



Meningitis



Retropharyngeal hem orrhage



Dystonic reactions



Cervical osteom yelitis



Epidural abscess

Pa ge 4 1 4



Other deep space infection of the neck

Treatment Pre Hospital 

Keep child calm and com fortable; parent m ay hold the child.



Pulse oxim etry, cardiac m onitor



Supplem ental oxygen



Suction and intubation equipm ent ready



Airway control will be required: o

Airway com prom ise

o

Prior to lengthy transport

Initial Stabilization 

Assess and control airway.



Provide supplem ental oxygen.



IV access, but this should be delayed if airway com prom ise suspected: o

Child to be kept calm until airway controlled.

ED Treatment 

Patient non per os



Surgical consultation (ear/nose/throat if available)

Medication (Drugs) 

Gram positives and anaerobes should both be covered: o

Am picillin and sulbactam (40 m g/kg/d, div. q8h)

o

Clindam ycin (40 m g/kg/d, div. q8h) and cefuroxim e (50â€“100 m g/kg/d, div. q6hâ€“q8h)

Pa ge 4 1 4

o

Metronidazole (50 m g/kg/d, div. q8h) and ceftriaxone (50â€“75 m g/kg/d)

o

Antibiotic choice m ay be tailored to local preferences and susceptibilities.

o

Should be changed when culture results and sensitivities return



Rapid sequence intubation drugs m ay be required.

Follow-Up Disposition Admission Criteria 

All patients with retropharyngeal abscess should be adm itted to the hospital for IV antibiotics and surgical drainage.



Intensive care unit adm ission: o

Airway com prom ise

o

Sepsis

o

Altered m ental status

o

Hem odynam ic instability

o

Infants and toxic-appearing children

Discharge Criteria None

References 1. Brook I. Microbiology and m anagem ent of peritonsillar, retropharyngeal, and parapharyngeal abscesses. J Oral Maxillofac Surg. Decem ber 2004;62(12):1545â€“1550. 2. Craig FW, Schunk JE. Retropharyngeal abscess in children: clinical presentation, utility of im aging, and current m anagem ent. Pediatrics.

Pa ge 4 1 4

June 2003;111(6 Pt 1):1394â€“1398. 3. Philpott CM, Selvadurai D, Banerjee AR. Paediatric retropharyngeal abscess. J Laryngol Otol. 2004 Dec;118(12):919â€“26.

Codes ICD9-CM 478.24

ICD10 J39.0

Pa ge 4 1 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Reye Syndro m e

Reye Syndrome

Brian D. Euerle

Basics Description 

Reversible clinicopathologic syndrom e of unknown etiology



Prim ary m itochondrial injury



Decreased enzym e activity:



o

Krebs cycle

o

Gluconeogenesis

o

Urea biosynthesis

Fatty infiltration: o

Liver: 

Hyperam m onem ia due to decreased conversion from am m onia to urea

o



Hepatorenal syndrom e m ay be the end result.



Rapid recovery of liver function in survivors

Brain: 

Encephalopathy of unclear etiology



Cytotoxic edem a



Deteriorating level of consciousness reflects increasing intracranial pressure.



Herniation is the m ost com m on cause of death.



Norm al recovery of neurologic function in

Pa ge 4 1 5

survivors





o

Skeletal and m yocardial m uscle

o

Fatty infiltration and distorted m itochondria

Fewer than 10% of cases occur before the age of 1 year: o

Average age is 7 years.

o

Peak age is 4â€“11 years.

Regional differences: o

Highest incidence in the m idwestern states

o

Lower incidence in the states of the southeast and far west



More com m on in whites than in blacks



Peak incidence is in winter and early spring.



Reyelike syndrom e: o

Describes conditions resulting in defects in urea and fatty acid m etabolism , toxicologic injury, and im paired gluconeogenesis

Etiology 

Not known with certainty



Multifactorial causes have been epidem iologically im plicated: o

Antecedent viral syndrom e

o

Influenza A or B

o

Varicella

o

Diarrhea illness

o

Genetic predisposition

o

Exposure to salicylates

o

Other undefined factors

Diagnosis

Pa ge 4 1 5

Signs and Symptoms 

Usually the patient is afebrile.



Tachycardia



Hyperventilation

History 

Biphasic history m arked by an infectious phase (viral illness or prodrom e) followed by an encephalopathic stage



Profuse and repeated vom iting: o



Typically 4â€“5 days after the start of the viral illness

Marked behavioral changes, including delirium and com bativeness, disorientation, and hallucination

Physical Exam 

No focal neurologic signs



Hepatom egaly in 40% of cases



Pancreatitis



Clinical staging of Reye syndrom e with Lovejoy classification: o

Stage 0: 

o

o

o

Wakeful

Stage I: 

Vom iting



Lethargy



Sleepiness

Stage II: 

Disorientation



Delirium



Com bative/stuporous



Hyperventilation



Hyperreflexia



Appropriate response to noxious stim uli

Stage III:

Pa ge 4 1 5

o



Obtunded



Com a



Hyperventilation



Inappropriate response to noxious stim uli



Decorticate posturing



Preservation of pupillary light reflexes



Preservation of oculovestibular light reflexes

Stage IV: 

Deeper com a



Decerebrate rigidity



Loss of oculovestibular reflexes



Dilated, fixed pupils



Dysconjugate eye m ovem ents in response to caloric stim ulation

o



Stage V: 

Seizures



Absent deep tendon reflexes



Respiratory arrest



Flaccid paralysis



No papillary response

Infantsâ€”atypical presentation: o

Tachypnea

o

Apnea

o

Irritability

o

Seizures

o

Hypoglycem ia

Essential Workup 

Establish the presence of encephalopathy and liver abnorm alities



Laboratory testing to assess for characteristic biochem ical abnorm alities



Liver biopsy confirm s the diagnosis.

Pa ge 4 1 5

Tests Lab 

Liver function tests: o

A threefold or greater rise in AST, ALT

o

Serum am m onia level greater than 1.5â€“3 tim es norm al: 

Transient 24â€“48 hours after m ental status changes



Level >300 Âµg/dL associated with poor prognosis

o

Serum bilirubin should be norm al or slightly elevated.



Hypoglycem ia m ay be present, especially in infants.



Elevated blood urea nitrogen



Ketonuria



The prothrom bin tim e m ay be prolonged due to decreased liver-dependent clotting factors (II, VII, IX, X).



Norm al platelet count and blood sm ear



Negative toxicology screen

Imaging 

Head CT scan: o



May show diffuse cerebral edem a

Lum bar puncture: o

Perform after head CT

o

Edem a is diffuse and lum bar puncture is not contraindicated.



o

Measure opening pressure.

o

Less than 8 leukocytes/m m 3

Percutaneous liver biopsy: o

Useful in patients with atypical presentation (1 year old, recurrent, fam ilial)

Pa ge 4 1 5

o

Gastroenterology consult

P.969

Differential Diagnosis 

Inborn errors of m etabolism : o

Disorders of the urea cycle

o

Disorders of fatty acid oxidation

o

System ic carnitine deficiency

o

Organic acidem ias

o

Disorders of the electron transport chain



Hypoglycem ia



Toxin exposure: o

Toxic encephalopathy without liver dysfunction (Gall syndrom e)







o

Lead

o

Hydrocarbons

Drug intoxication: o

Acetam inophen

o

Salicylates

o

Ethanol

Infection: o

Sepsis

o

Meningitis

o

Encephalitis

o

Varicella hepatitis

Traum a, head

Treatment

Pa ge 4 1 5

Pre Hospital 



Decreased m ental status: o

Glucose

o

Narcan

Com a: o

Assist respirations with bag-valve m ask.

Initial Stabilization 

Place on a cardiorespiratory m onitor.



Supplem ental oxygen



Rapid-sequence intubation if airway m anagem ent required



Glucose if m ental status is altered: o

10% glucose solution IV

o

Rate of two thirds m aintenance requirem ent after dehydration is corrected.

o

Follow serum glucose hourly; m aintain glucose between 125â€“175 m g/dL.



Avoid early overhydration.

ED Treatment 

Institute treatm ent before the liver biopsy.



Vitam in K: o





Indicated if prothrom bin tim e is elevated.

Fresh-frozen plasm a: o

To control bleeding

o

To correct a severe coagulopathy

Interventions aim ed at lowering intracranial pressure (ICP): o

Stage III or greater

o

Stage II with serum am m onia >300 Âµg/L: 

Intubation using rapid-sequence protocol



Hyperventilation



Fluid restriction

Pa ge 4 1 5



Barbiturate com a



Osm otically active agents:





Mannitol



Furosem ide

Monitor ICP: 

Subarachnoid bolt



Intraventricular cannula

Medication (Drugs) 

D 5 0 W: 1â€“2 m L/kg/dose (0.5â€“1.0 g/kg) IV over the age of 3 years



D 2 5 W: 2â€“4 m L/kg/dose (0.5â€“1.0 m g/kg) IV under the age of 3 years; m aintenance infusion 10% dextrose solution at a rate of two-thirds m aintenance



Fresh-frozen plasm a: 10 m L/kg/dose q12hâ€“q24h IV or PRN



Lasix: 1 m g/kg IV



Mannitol: 0.25â€“1.0 g/kg IV q4hâ€“q6h



Pentobarbital: 3â€“20 m g/kg IV slowly while m onitoring blood pressure; m aintenance infusion 1â€“2 m g/kg/h; m aintain level at 25â€“40 Âµg/dL



Vitam in K: 1â€“2 m g/dose (infants and children); 2â€“10 m g/dose (adolescents)

Follow-Up Disposition Admission Criteria 

All children with suspected Reye syndrom e should be

Pa ge 4 1 5

adm itted to the intensive care unit. 

Hospital capable of ICP m onitoring

References 1. Arrowsm ith JB, Kennedy DL, Kuritsky JN, Faich GA. National patterns of aspirin use and Reye syndrom e reporting, United States, 1980 to 1985. Pediatrics. 1987;79:858â€“863. 2. Belay ED, Bresee JS, Holm an RC, et al. Reye's syndrom e in the United States from 1981 through 1997. N Engl J Med. 1999;340:1377â€“1382. 3. Bhutta AT, Savell VH, Schexnayder SM. Reye's syndrom e: down but not out. South Med J. 2003;96:43â€“45. 4. Boenning DA. Reye syndrom e. In: Barkin RM, ed. Pediatric em ergency m edicine. 2nd ed. St. Louis, MO: Mosby YearBook,1997:845â€“847. 5. Chow EL, Cherry JD, Harrison R, et al. Reassessing Reye syndrom e. Arch Pediatr Adolesc Med. 2003;157:1241â€“1242. 6. Kaufm an RE. Reye's syndrom e and salicylate use, by Karen M. Starko, MD, et al. Pediatrics. 1980;66:859â€“864. 7. Arrowsm ith, J, et al. National patterns of aspirin use and Reye Syndrom e reporting, United States, 1980 to 1985. Pediatrics. 1987;79:858â€“863. Pediatrics 1998; 102. 259â€“62. 8. National Institutes of Health Consensus Conference. Diagnosis and treatm ent of Reye's syndrom e. JAMA. 1981;246:2441â€“2444. 9. Orlowski JP, Hanhan UA, Fiallos MR. Is aspirin a cause of Reye's syndrom e? A case against. Drug Saf. 2002;25:225â€“231.

Codes ICD9-CM 331.81

ICD10 G93.7

Pa ge 4 1 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rhabdo m yo lysis

Rhabdomyolysis

Marcelo Sandoval

Basics Description Syndrom e associated with m uscle injury and system ic release of creatine phosphokinase (CPK), m yoglobin, potassium , phosphate, urate com plicated by: 

Myoglobin-induced renal failure in 30%



Hyperkalem ia m ay lead to sudden death.



Hypocalcem ia and acidosis also dangerous



Volum e loss due to fluid sequestration in injured or necrotic m uscle



Dehydration due to underlying illness



Com partm ent syndrom e in individual m uscle groups due to traum a and IV hydration fluid sequestration in dam aged tissue



Hepatic dysfunction in 25%



Dissem inated intravascular clot (DIC)

Etiology 

Often m ultiple causes in sam e patient



Muscle injury, such as traum a/crush, burn, electrical shock



Muscle exertion: o

Strenuous exercise

Pa ge 4 1 5

o

Marathon running

o

Exercise in hot hum id conditions

o

Exercise by individuals with an inherited m yopathy or with poor physical training





o

Status epilepticus, delirium trem ens

o

Tetanus

o

Psychotic agitation

Muscle ischem ia: o

Extensive throm bosis

o

Multiple em bolism

o

Generalized shock

o

Sickle cell crisis

Surgery: o

Im m obilization

o

Hypotension

o

Ischem ia due to vessel clam ping



Massive blood transfusion



Hypotherm ia, hypertherm ia



Prolonged im m obile state without traum a



Drugs/toxins: o

Alcohols

o

Cocaine, am phetam ines and analogues (m etham phetam ine and ecstasy)

o

Toluene

o

Opiates

o

LSD, PCP

o

Caffeine

o

Carbon m onoxide

o

Snake or bee/hornet venom

o

Hem lock

o

Buffalo fish

o

Tetanus toxin

Pa ge 4 1 6

o 

Mushroom poisoning (Tricholom a equestre)

Medications: o

HMG-CoA reductase inhibitors (statin) and other cholesterol-lowering agents

o

Propofol, succinylcholine, halogenated anesthetic gases

o

INH, zidovudine, antim alarials

o

Methylxanthines

o

Colchicine

o

Corticosteroids

o

Itraconazole

o

Erythrom ycin

o

Diuretics

o

Haloperidol, phenothiazines

o

Cyclosporine

o

Antihistam ines

o

Barbiturates



Neuroleptic m alignant syndrom e



Metabolic disorders:



o

Hypokalem ia

o

Hypophosphatem ia

o

Hyper and hyponatrem ia

o

Diabetic ketoacidosis, hyperosm olar state

o

Hypoxia

o

Hyperthyroid state (rare)

o

Pheochrom ocytom a (rare)

Infections: o

Viral: 

Coxsackievirus



Herpesviruses



HIV



Influenza B

Pa ge 4 1 6



Cytom egalovirus, Epstein-Barr virus, adeno/echovirus

o

o

Bacterial: 

Legionnairesâ€™ disease



Pyom yositis



Salm onellosis



Shigellosis



Staph, Strep species



Listeria



Tetanus



Toxic shock syndrom e



Tularem ia



Gas gangrene



Bacillus cereus

Parasitic (m alaria falciparum ), protozoan (leptospirosis), rickettsial



Genetic disorders: o

McArdle disease

o

Tarui disease

o

CPT deficiency

o

These inherited m yopathies can exacerbate any other cause.



Im m unologic disorders: derm atom yositis, polym yositis



Idiopathic

Diagnosis Signs and Symptoms History 

Can vary dram atically, reflect underlying disease process

Pa ge 4 1 6



Crush, traum a, exercise, drug/alcohol use, recent surgery, im m obilization, m edications, infections, fever are all com m on and im portant to ask about.



Ask about reddish brown urine and decreased urine output.

Physical Exam 

Hypotherm ia/hypertherm ia



Alert/obtunded



Muscle pain (only 50%), tenderness, swelling; diffuse or localized



Neurovascular status of involved m uscle groups if suspect com partm ent syndrom e



Hypovolem ic state, dry m ucous m em brane, poor skin turgor, tachycardia, hypotension



Decreased urine output



Change in urine color

Essential Workup 

History and physical are insensitive in m aking the diagnosis.



Serum and urine m yoglobin levels often norm al due to rapid m etabolism and excretion



Serum CPK level is criterion standard and m ust be sent if any clinical suspicion exists.



CPK level not always predictive of renal failure but m ost often associated with level >15,000.



Early ECG to look for signs of severe hyperkalem ia or hypocalcem ia before serum levels available.



Urine dipstick test positive for hem e but absent for RBCs suggests rhabdom yolysis.



Microscopic urinalysis to look for pigm ented tubular casts



Because of rapid urinary excretion of m yoglobin, up to 26% of patients with rhabdom yolysis have negative urine

Pa ge 4 1 6

dipstick test. 

Serum electrolytes (potassium , calcium , m agnesium , phosphorus, bun, creatinine, uric acid, bicarbonate)



Measure com partm ent pressure if com partm ent syndrom e suspected.

Tests Lab In addition to above consider: 

ABG



Urine/Serum m yoglobin, but m ay be too transient to be useful



Serum glucose



Liver function tests, including GGTP, LDH, album in



Toxicology screen in absence of physical injury



Prothrom bin tim e/partial throm boplastin tim e, platelet count, fibrinogen, fibrin-split products if DIC is suspected

P.971

Imaging 

Renal ultrasound to evaluate for renal failure (sm all shrunken kidneys) or renal obstruction (hydronephrosis)



MRI is 90â€“95% sensitive in visualizing m uscle injury but does not change initial ED treatm ent.

Differential Diagnosis The following conditions m ay present with elevated serum CPK but m ay not lead to com plications of rhabdom yolysis: 

Nontraum atic m yopathies including m uscular dystrophies



Chronic renal failure



Intram uscular injections

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

Myocardial injury



Stroke

Treatment Pre Hospital 

Need for rapid extrication in case of crush injury



Early IV norm al saline before extrication: o

Prevents com plications of restored blood flow to injured lim b (hypovolem ia, acute renal failure [ARF], hyperkalem ia, etc.)



â€œCrush injury cocktailâ€• during extrication is 1.5 L 0.9% NS/hr; consider adding 1 am p (40 m eq) bicarbonate and 10 g of m annitol to each liter (controversial).

Initial Stabilization 

Airway m anagem ent and resuscitate as indicated



Im m obilization of traum a/crush injuries



IV saline for hypovolem ia at rate of 1 Lâ€“1.5 L per hour until volum e restored: o

Restoration of volum e within 6 hours helps prevent renal failure.



Even if the patient is not dehydrated, aggressively hydrate with saline to keep urine flow and protect tubules from dam age due to m yoglobin precipitation.



Avoid furosem ide and other loop diuretics, as they m ay worsen renal failure.



Mannitol supported by anim al studies and retrospective clinical studies, but not prospective



Bicarbonate infusion to alkalinize urine (pH 6.5) also controversial:

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o

A retrospective study suggests use when CPK level >30,000, but not prospectively studied.

ED Treatment 

Directed toward treating or reversing the cause of rhabdom yolysis and com plications



Prevent ARF: IV fluid, keep urine output >300 cc/hr with or without m annitol.



Hyperkalem ia: IV fluid, dextrose, insulin, sodium polystyrene sulfonate (Kayexalate), calcium gluconate, hem odialysis, m onitor/ECG



Acidosis: bicarbonate IV (keep urine pH >6.5)



Overdose: activated charcoal, lavage, antidote



Infection: broad-spectrum antibiotics



Com partm ent syndrom e: fasciotom y (com partm ent pressure >35 m m Hg)



Neuroleptic m alignant syndrom e: dantrolene, brom ocriptine



Need for hem odialysis: refractory to treatm ent, hyperkalem ia, hyperphosphatem ia, hyperuricem ia, volum e overload, overdose

Medication (Drugs) 

Bicarbonate: 50â€“100 m L of 8.4% solution IV (peds: 1 m Eq/kg up to 50â€“100 m Eq); do not continue if urine pH fails to go above 6.5.



Mannitol: 10 g in first liter of one-half isotonic saline; continue only if able to achieve diuresis of >300 cc/hr.

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Follow-Up Disposition Admission Criteria 

Because it is im possible to predict which patients will develop com plications, all patients with significant elevated CPK or with sym ptom s suggestive of rhabdom yolysis m ust be adm itted.



Adm it to m onitored bed patients with electrolyte abnorm alities.



Adm it to intensive care unit bed patients who m ight require hem odialysis or closer fluid and electrolyte m onitoring.

Discharge Criteria No patients suspected of having rhabdom yolysis should be discharged from the ED.

References 1. Bhanushali MJ. The evaluation and m anagem ent of patients with neuroleptic m alignant syndrom e. Neurol Clin. 2004;22(2):389â€“411. 2. Brown CV, Rhee P, Chan L. Preventing renal failure in patients with rhabdom yolysis: do bicarbonate and m annitol m ake a difference? Jrnl of Tr-Inj Inf & Crit Care. 2004;56(6):1191â€“1196. 3. Cheney P. Early m anagem ent and physiologic changes in crush syndrom e. Crit Care Nurs Q. 1994;17(2):62â€“73. 4. Gonzalez D. Crush syndrom e. Crit Care Med. January 2005;33(1 Suppl):S34â€“S41. 5. Pina EM, Mehlm an CT. Rhabdom yolysisa prim er for the orthopaedist. Orthop Rev. 1994;23(1):28â€“32. 6. Prendergast BD, George CF. Drug-induced rhabdom yolysis m echanism s and m anagem ent Postgrad Med J. 1993;69(811):333â€“336.

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7. Rosenbaum HK. Malignant hypertherm ia and m yotonic disorders. Anesthesiol Clin North Am erica. 2002;20(3):623â€“664. 8. Sauret JM, Marinides G, Wang GK. Rhabdom yolysis. Am Fam Physician. 2002;65: 907â€“912. 9. Sinert R, Kohl L, Rainone T, et al. Exercise-induced rhabdom yolysis. Ann Em erg Med. 1994;23(6):1301â€“1306. 10. Vanholder Sever, Erek, et al. Rhabdom yolysis. J Am Soc Nephrol. 2000;11(8):1553â€“1561. 11. Viswswaran, Jayaram a. Rhabdom yolysis. Crit Care Clin. 1999;15(2):415â€“428. 12. Walsh RJ. Toxic m yopathies. Neurol Clin. 2005;23(2):397â€“428. 13. Zager RA. Rhabdom yolysis and m yohem oglobinuric acute renal failure [Editorial Review]. Kidney Int. 1996;49(2):314â€“326.

Codes ICD9-CM 728.89

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rheum atic F ever

Rheumatic Fever

Jon D. Mason

Basics Description 

Constellation of sym ptom s and signs (Jones Criteria)



Follows group A Streptococcal infection (GAS).



Recent resurgence in the western United States



Rem ains a m ajor cause of cardiac m orbidity and m ortality worldwide.



Rheum atic fever (RF) is m ost com m on in the 5- to 15-year age range.

Etiology 

GAS infection



Inflam m atory, autoim m une response following GAS infection

Diagnosis Two m ajor or one m ajor and two m inor elem ents of the Jones criteria plus evidence of a recent GAS infection

Signs and Symptoms

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Major Manifestations (Jones Criteria) 



Migratory polyarthritis in 60â€“75% of initial attacks: o

Can involve knees, ankles, elbows, and wrists

o

Lower extrem ities joints m ore com m only involved

o

Rheum atic arthritis generally responds to salicylates.

Carditis occurs in one third of new cases; prednisone used in severe cases: o

Pericardium , m yocardium , and endocardium m ay be affected (pancarditis).

o

Myocarditis m ay lead to heart failure but is frequently asym ptom atic.

o

Valvular disease and endocarditis are m ost serious sequelae of acute renal failure (ARF).

o

Carditis heralded by a new m urm ur, tachycardia, gallop rhythm , pericardial friction rub, or congestive heart failure (CHF)



Chorea occurs in 10% of cases: o

Sydenham chorea predom inantly affects teenage girls.

o

Purposeless, uncoordinated m ovem ents of the extrem ities

o

Movem ents m ore apparent during periods of anxiety and disappear with sleep.

o 

Chorea m ay be the sole m anifestation of ARF.

Erythem a m arginatum occurs in <5% of cases: o

Nonpruritic pink eruptions with central clearing and well-dem arcated irregular borders

o 

Usually seen on the trunk and the extrem ities

Subcutaneous nodules in 10% of patients: o

Crops of sm all subcutaneous, painless nodules located m ost com m only on extensor surfaces

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Minor Manifestations 



Clinical: o

Fever (>38Â°C)

o

Arthralgia

Laboratory: o

Elevated acute-phase reactants

o

Prolonged pulse rate interval

Supporting Evidence of Recent GAS Throat Infection 

Positive throat culture or rapid antigen test



Elevated or increasing antibody testâ€”antistreptolysin-O (ASO) titer

History Fever, sore throat, joint pains, or unusual m ovem ents of extrem ities

Physical Exam Heart m urm ur consistent with m itral or aortic disease

Tests Lab 

Rapid antigen strep test



Throat culture



ASO titer



ECG



CBC



Erythrocyte sedim entation rate or C-reactive protein



Other rheum atic serology tests to rule out other diseases

Imaging 

Chest radiograph



Echocardiogram

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Differential Diagnosis 

Juvenile rheum atoid arthritis



Infective endocarditis



Reiter syndrom e



System ic lupus erythem atosus



Postgonococcal arthritis



Other infectious causes of arthritis and carditis o

Coxsackie B virus and Parvovirus

P.973

Treatment Initial Stabilization Som e patients in CHF will need airway m anaged.

ED Treatment 

Pericardial effusions m ay need drainage.



In severe carditis, start steroids.



In case of severe chorea, start haloperidol.



Penicillin IM, IV, or PO



Nonsteroidal anti-inflam m atory agents

Medication (Drugs) 

Aspirin: 4â€“8 g/d (peds: 100 m g/kg/d) PO q4hâ€“q6h



Digoxin: 0.25â€“0.5 m g (peds: 0.04 m g/kg) IV



Erythrom ycin: 250 m g (peds: 30â€“50 m g/kg/d) q6h PO for 10 days

Pa ge 4 1 7



Furosem ide: 20â€“80 m g (peds: 1 m g/kg/dose) IV



Haloperidol: 2â€“10 m g (peds: 0.01â€“0.03 m g/kg/d) q6h IM or PO



Penicillin (benzathine benzylpenicillin): 1.2 m illion U (peds: 600,000 U for under 27 kg) IM acutely and m onthly thereafter (prophylaxis)



Penicillin VK: 500 m g (peds: 250 m g) PO q8h for 10 days (acute treatm ent)



Prednisone: 1â€“2 m g/kg/d for 14 days with taper for the next 2 weeks

Follow-Up Disposition Most patients with a new diagnosis should be adm itted for stabilization and further evaluation of the severity of the heart disease.

Admission Criteria 

CHF



New diagnosis



Uncontrolled chorea



Uncontrolled pain



Pericardial effusion

Discharge Criteria 

Control of pain



Stable cardiovascular status

Issues for Referral All patients need close follow up with their prim ary physician and a cardiologist.

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References 1. Bisno AL et al. Practice guidelines for the diagnosis and m anagem ent of group A streptococcal pharyngitis. (Infectious Disease Society of Am erica.) Clin Infec Dis. 2002;35:113. 2. Kaplan EL. Rheum atic Fever. In: Kasper DL, et al, eds. Harrison's principles of internal m edicine. 16th ed. New York, NY: McGraw Hill, 2005: 1977â€“1979. 3. Lennon D. Acute rheum atic fever in children: recognition and treatm ent. Pediatr Drugs. 2004;6(6):363â€“373. 4. Pinals RS. Polyarthritis and fever. N Engl J Med. 1994;330(11):769â€“774. 5. Stollerm an GH. Rheum atic fever in the 21st century. Clin Infect Dis. 2001;806â€“814. 6. Tani LY et al. Rheum atic fever in children younger than 5 years: is the presentation different? Pediatrics. 2003;112:1065â€“1068.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rib F racture

Rib Fracture

Gregory W. Lampe

Basics Description 

Result of m ajor or m inor thoracic traum a



Can be classified as traum atic or pathologic

Etiology 

Blunt thoracic traum a: o

Sim ple fall, fall from height

o

Motor vehicle accident

o

Assault

o

Missile



Penetrating traum a is a less likely cause.



Ribs usually break at the point of im pact or the posterior angle: o



Structurally weakest region

Pathologic fractures associated with m inor traum a or significant underlying disease: o

Coughing or sneezing

o

Advanced age

o

Osteoporosis

o

Neoplasm

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Pediatric Considerations 

Relatively elastic chest wall m akes rib fractures less com m on in children.



Consider nonaccidental traum a for infants and toddlers without appropriate m echanism .

Diagnosis Signs and Symptoms History 

Blunt thoracic traum a by any m echanism



Mechanism as described by patient, parent or prehospital personnel:



o

Seat belt usage

o

Steering wheel dam age

o

Air bag deploym ent

Localized chest wall pain that increases with deep inspiration, coughing, m oving



Pleuritic chest pain



Dyspnea

Physical Exam 

Point tenderness



Pain referred to fracture site with palpation of the involved rib elsewhere



Bony stepoff



Crepitus



Localized edem a



Erythem a



Ecchym osis: o

Ecchym osis from seat belt, a.k.a. â€œseat belt

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signâ€• o

Ecchym osis from steering wheel im pact



Intercostal m uscle spasm



Splinting respirations



Hypoxia, tachypnea, respiratory distress



Auscultation shows norm al or dim inished breath sounds.

Essential Workup 

Diagnosis is initially m ade on clinical grounds.

Alert 

The first three ribs are relatively protected and require significant im pact to fracture, indicating possible intrathoracic injury.



Ribs 9 through 12 are relatively m obile and their fracture suggests possible intraabdom inal injury.



Multiple rib fractures m ay be associated with flail chest and pulm onary contusion.

Tests Lab Arterial blood gas m ay reveal hypoxem ia and elevated alveolar-arterial gradient: 

Not indicated for sim ple, uncom plicated rib fractures



May consider in patients with m ultiple rib fractures or preexisting pulm onary disease

Imaging 

Chest radiography is indicated to rule out associated intrathoracic injury but m isses up to 50% of rib fractures: o

May reveal associated intrathoracic pathology: 

Pneum othorax



Hem othorax



Pneum om ediastinum

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o



Pulm onary contusion



Widened m ediastinal silhouette

Pulm onary contusion appears within 6 to 12 hours after injury: 

Ranges from patchy alveolar infiltrates to frank consolidation



Indications for rib radiograph series: o

Suspected fractures of ribs 1 through 3 or 9 through 12

o

Multiple rib fractures

o

Elderly patients with preexisting pulm onary disease or suspected pathologic fractures



CT of the chest m ay be required to rule out intrathoracic injuries.



CT or ultrasound of the abdom en m ay be required to rule out associated intraabdom inal injuries.

Differential Diagnosis 

Rib contusion or intercostal m uscle strain



Costochondral separation



Sternal fracture and dislocation



Nontraum atic causes of chest pain: o

o

o

Cardiovascular: 

Myocardial ischem ia or infarction



Pericarditis



Aortic dissection



Pulm onary em bolism

Pulm onary: 

Infections



Inflam m ation



Barotraum a

Musculoskeletal: 

Costochondritis

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 o

o

Cervical or thoracic spine disease

Gastrointestinal: 

Esophageal reflux or spasm



Mallory-Weiss tear



Biliary or renal colic



Peptic ulcer disease



Gastritis, pancreatitis, hepatitis

Derm atologic: 

Herpes zoster



Chest wall tum or

P.975

Treatment Initial Stabilization 

For sim ple fractures, generally no significant stabilization is required.



Multiple fractures, elderly patients or significant underlying lung disease: o

Manage airway and resuscitate as indicated.

o

Control airway: 

Endotracheal intubation indicated for patients with severe hypoxem ia (PaO 2 <60 m m Hg on room air, <80 m m Hg on 100% O 2 ) or im pending respiratory failure

ED Treatment 

Sim ple fractures: o

Pain control:

Pa ge 4 1 7



Key to m aintaining adequate pulm onary function, avoiding atelectasis and subsequent pneum onia

o

Intercostal nerve blocks with 0.5% bupivacaine are safe and effective: 

Provides 6â€“12 hours of pain relief



Intercostal nerve block should be perform ed posteriorly, two to three fingerbreadths from the vertebral m idline.



Inject 0.5â€“1 m L just under the inferior surface of the rib where the neurovascular bundle is located.



Aspirate first to be certain the intercostal vessels have not been punctured.

o

Deep breathing or incentive spirom etry should be encouraged with adequate pain control.

o

Avoid binders or banding of the chest wall because these restrict ventilation and prom ote atelectasis.



Multiple fractures, elderly patients, or significant underlying lung disease: o

Pain control and pulm onary toilet

o

Search for associated injuries; treat exacerbation of underlying lung disease.

o

Intercostal nerve blocks for m ultiple fractures are safe and effective providing 6â€“12 hours of pain relief.

o

For the adm itted patient, thoracic epidural analgesia or patient-controlled analgesia (PCA) are effective.

Medication (Drugs) 

Multiple acetam inophen/narcotic analgesic com binations

Pa ge 4 1 8

are available; see Alert below. 

Acetam inophen: 300 m g/codeine 30 m g (peds: 0.5â€“1 m g/kg codeine) PO q4hâ€“q6h



Acetam inophen: 500 m g/hydrocodone 5 m g PO q4hâ€“q6h



Acetam inophen: 750 m g/hydrocodone 7.5 m g PO q4hâ€“q6h



Acetam inophen: 325 m g/hydrocodone 10 m g PO q4hâ€“q6h



Acetam inophen: 325 m g/oxycodone 5 m g PO q6h



Bupivacaine 0.5%: 0.5â€“1 m L per injection for intercostal nerve blocks



Hydrom orphone: 2â€“8 m g (peds: 0.03â€“0.08 m g/kg) PO q4hâ€“q6h



Hydrom orphone: 1â€“4 m g (peds: 0.015 m g/kg) IV/IM/SC q4hâ€“q6h



Morphine sulfate: 0.05â€“0.1 m g/kg IV/IM/SC q2hâ€“q6h



PCA using hydrom orphone or m orphine sulfate are effective.

Alert 

Consider thoracic epidural analgesia: o

Patients with intractable pain

o

Oversedation

o

Hypoventilation from narcotic analgesics



Avoid NSAIDs due to the risk of gastrointestinal bleeding.



The dose of acetam inophen/narcotic analgesic com binations is lim ited by the hepatic toxicity of acetam inophen.



The m axim um acetam inophen dose is 1 g per dose and 4 g per day (peds: 15 m g/kg/dose).

Pa ge 4 1 8

Follow-Up Disposition Admission Criteria 

Intractable pain



Com prom ised pulm onary function



Multiple fractures, fractures of the first three ribs



Associated pneum othorax, pneum om ediastinum , pulm onary contusion, or intrathoracic pathology



Elderly patients and patients with significant underlying lung disease: o

Chronic obstructive pulm onary disease, congestive heart failure, pulm onary fibrosis, asthm a



Inadequate pain control on oral analgesics

Discharge Criteria 

Patients with norm al pulm onary function, no underlying pulm onary injury, and adequate pain control on oral analgesics



Strict return criteria should be discussed with the patient prior to discharge: o

Shortness of breath

o

Increased pain

o

Inadequate pain control

o

Fever

o

Cough

References 1. Flagel BT, Luchette FA, Reed RL, Esposito TJ, Davis KA, Santaniello JM, Gam elli RL. Half-a-dozen ribs: The breakpoint for m ortality. Surgery. October 2005;138(4):717â€“725. 2. Matthes G, Stengel D, Bauwens K, Seifert J, Radem acher G, Mutze S, Ekkernkam p A. Predictive factors of liver injury in blunt m ultiple

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traum a. Langenbecks Arch Surg. 2005 Nov 1;1â€“5. 3. Hanak V, Hartm an TE, Ryu JH. Cough-induced rib fractures. Mayo Clin Proc. July 2005;80(7):879â€“882. 4. Bulger EM, Edwards T, Klotz P, Jurkovich GJ. Epidural analgesia im proves outcom e after m ultiple rib fractures. Surgery. August 2004;136(2):426â€“430. 5. Eckstein M, Henderson S. Thoracic traum a. In: Marx J, Hockberger R, Walls R, eds. Rosen's Em ergency m edicine: concepts and clinical practice. 6th ed. St. Louis, MO: CV Mosby,2005 in press.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ring/C o nstricting Band Rem o val

Ring/Constricting Band Removal Carl K. Hsu Bradley Peckler

Basics Description 

Prim ary constricting band: A band tightened around an appendage causes swelling and pain (e.g., a hair knotted around a toddler's toe).



Secondary constricting band: Injury or disease process that causes swelling and edem a as a result of tightness against the band (e.g., im pacted ring with an underlying fracture of the finger)



Untreated, the constricting band m ay becom e em bedded and interrupt skin integrity.

Pediatric Considerations In the preverbal child, a constricting band m ay be a m anifestation of child abuse or neglect.

Geriatric Considerations The cognitively im paired nursing hom e resident or Alzheim er patient m ay be unable to give an indication of injury or pain.

Etiology

Pa ge 4 1 8

Tourniquet syndrom e m ay result from allergic, derm atologic, iatrogenic, endocrinologic, infectious, m alignant, m etabolic, physiologic, or traum atic conditions, or related to pregnancy.

Diagnosis Signs and Symptoms 

A constricting band with swollen tissue and skin, m ost com m only a finger



Other locations include wrist, ankle, toe, um bilicus, ear lobe, nipple, septum or nares of nose, penis, scrotum , vagina, labia, uvula or tongue.



Pain on m anipulation of the appendage or constricting band

Essential Workup 

Prim ary constricting band: Diagnosis m ade by history and physical exam with special attention to neurovascular status.



Secondary constricting band: Diagnosis of underlying pathology m ay depend on results of im aging and laboratory test results.

Tests Lab 

Usually not indicated for acute treatm ent



Measurem ent of electrolytes, blood urea nitrogen, and creatinine; thyroid function tests; and Tzanck sm ear of vesicular lesions m ay be useful in identifying the underlying diagnosis.

Imaging

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Plain film s for evaluation of underlying fracture or foreign body after band rem oval

Differential Diagnosis Any condition causing m arked swelling and edem a predisposing to the tourniquet syndrom e

Treatment Pre Hospital Rem ove rings and other potential constricting bands before developm ent of tourniquet syndrom e: 

Particularly in regions of extrem ity traum a

Initial Stabilization Pain m anagem ent or procedural sedation as needed

ED Treatment 

Rem oval of the constricting band either by advancing the band distally or by division



The m ost benign m ethods should be attem pted first.



These adjuvant m ethods m ay be used alone or in com bination: o

Elevation of the affected extrem ity m ay decrease vascular congestion.

o

Cooling the extrem ity with ice or cold water m ay reduce edem a and erythem a.

o

Lubrication with soap or m ineral oil m ay allow slippage over an inflam ed or edem atous area.

o

Digital block with 1â€“2% lidocaine without epinephrine decreases the discom fort of rem oval and m anipulation of an underlying injury.

Pa ge 4 1 8

o

A digital block m ay, however, increase local swelling.

o

Gauze or a needle holder m ay be used to m anipulate the band.



The distal swollen finger, especially the proxim al interphalangeal, is an im portant obstacle in constricting band rem oval.



Distal to proxim al edem a reduction by sequential com pression: o

Self-adherent tape is wrapped from distal to proxim al to form a sm ooth and decom pressed area over which the band is advanced.

o

A Penrose surgical drain or a finger cut from a sm all glove is stretched to fit over the distal swelling before attem pted rem oval.

o

With lubrication, the proxim al end of the drain is pulled under the ring to form a cuff around the ring; the cuff with distal traction applied advances the band over the decom pressed area.

o

Suture m aterial (no. 0 silk, dental floss, or um bilical tape) is wrapped under tension in a tight layer advancing over the edem a in a distal to proxim al direction; the proxim al tail of the suture m aterial or floss is tucked under the ring; with lubrication, the tail under tension is pulled distally and unwound, forcing the ring over the layered suture m aterial and decom pressed area.

P.977



Constricting band rem oval by division: o

Scissors m ay be used to first lift and then cut the offending fibrous band constricting a toddler's toe or

Pa ge 4 1 8

penis. o

A no. 11 scalpel blade with cutting edge up m ay be sufficient to cut constricting bands form ed by hair, fibers, or plastic ties.

o

A topical com m ercially available depilatory agent m ay be used to divide a tourniquet form ed by a suspected hair obscured by local edem a.

o

A handheld wire cutter/stripper m ay divide sm all-girth m etallic rings with m inim um discom fort to the underlying injury; this type of rem oval m ay, however, im part a crush defect to the ring, m aking repair difficult.

o

A long-handled bolt cutter, available in m ost operating room s or hospital engineering departm ents, m ay be used to divide large-girth or broad-sized rings: 

Long handles provide significant m echanical advantage needed to cut large rings.



The reinforced cutting blades m ay not easily fit through a constricting band with adjacent swollen tissue and skin.

o

A standard hand-powered, m edically approved ring cutter (Steinm ann pin cutter with a MacDonald elevator) m ay be used to divide sm all-girth m etallic constricting bands m ade of soft m etals (gold/silver): 

This m ethod has the advantage of a cleaner cut for subsequent repair of the ring.



The disadvantage is that the handheld ring cutter is labor intensive and m ay aggravate the pain of an underlying injury.

o

A m otorized high-revolution-per-m inute cutting device m ay be used to rapidly divide constricting

Pa ge 4 1 8

bands irrespective of girth and size of the ring; it m ay be AC powered or pneum atically driven in the operating suite. 

Cutting procedure: o

The initial cut is m ade on the band on the volar aspect of the extrem ity.

o

A tenaculum m ay be used to spread the band in softer m etals.

o

For a second cut, the band should be rotated 180Â°on the extrem ity, allowing the second cut on the band over the volar aspect of the extrem ity.



Motorized cutting: o

Rem ove flam m able solvents from the work area.

o

Protective eyewear should be worn by everyone present, including the patient.

o

Place a thin alum inum splint (shaped to the curvature of the ring) between the patient's skin and the ring as a shield to protect underlying tissue.

o

Cool splint and cutting surface with ice water irrigations before and during the cutting procedure.

o

Lim it cutting with m otorized device to 5 seconds during 60â€“90 second intervals between ice water irrigations to avoid producing local excessive heat.



Postdivision care: o

Underlying injuries should be irrigated thoroughly to rem ove m etallic dust to avoid foreign body reaction and granulom a form ation.

o

Tetanus prophylaxis should be provided if indicated.

Follow-Up

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Disposition Admission Criteria 

Neurovascular com prom ise or injury requiring surgical repair



Concom itant infection or necrosis

Discharge Criteria Successful band rem oval with restoration of circulation

References 1. Cresap CR. Rem oval of a hardened steel ring from an extrem ity swollen finger. Am J Em erg Med. 1995;13:318â€“320. 2. Fasano FJ Jr, Hansen RH. Foreign body granulom a and synovitis of the finger: a hazard of ring rem oval by the sawing technique. J Hand Surg. 1987;12:621â€“623. 3. Hsu CK, Neblett M, Mansur M and Mok S. Hair tourniquet syndrom e: division by a topical depilatory agent. Unpublished data. 4. Krishna S, Paul RI. Hair tourniquet of the uvula. J Em erg Med. 2003;24(3):325â€“326. 5. Peckler B, Hsu CK. Tourniquet syndrom e: a review of constricting band rem oval. J Em erg Med. 2001;20(3):253â€“262. 6. Roberts JR, Hedges JR. Clinical Procedures in Em ergency Medicine. 3rd ed. Philadelphia, PA: WB Saunders; 1997. 7. Rosen P, Chan TC, Vilke GM, et al. Atlas of Em ergency Procedures. St. Louis, MO: Mosby; 2001.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ro cky M o untain Spo tted F ever

Rocky

Mountain Spotted Fever Moses S. Lee

Basics Description Rickettsial invasion of sm all blood vessels: 

Causes direct vascular dam age



Superim posed vascular dam age owing to im m unologic phenom ena

Etiology Acute infection by Rickettsia rickettsii via tick vector: 

Derm acentor andersoni (wood tick) in the western states



Derm acentor variabilis (dog tick) in the eastern states

Diagnosis Signs and Symptoms 

Fever in nearly all cases



Tick bite reported within 14 days of rash in 60â€“70%



Rash: o

Initial rash (3â€“5 days)

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o



Macular, red, and flat



Blanches under pressure



1â€“4 m m diam eter

In hours to days: 

o

o

Becom es darker, papular, dusky, and palpable

In 2â€“3 days: 

Petechial or purpuric



Positive Rum pel-Leede test



May coalesce or ulcerate

In severe disease, necrosis of dependent peripheral parts m ay occur.

o

Location: 

Begins in flexor surfaces of wrist and ankles



Spreads centripetally



Fifteen percent with centrifugal spread to palm s and soles



Triad of fever, headache, and rash in 50%: o

Often not identified when patient initially presents for care







Pulm onary: o

Nonproductive cough

o

Chest pain

o

Dyspnea

o

Rales

Gastrointestinal: o

Associated with fatal Rocky Mountain spotted fever

o

Secondary to vasculitis

o

Nausea/vom iting

o

Abdom inal pain/distention

o

Ileus

o

Hepatosplenom egaly

Neurologic:

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o

Focal or generalized neurologic m anifestation in two thirds





o

Meningism us

o

Severe, unrem itting headache

o

Encephalitis

Other: o

Generalized edem a

o

Dehydration

o

Malaise

o

Myalgia

o

Retinal hem orrhage and conjunctivitis

Com plications: o

Dissem inated intravascular coagulation (DIC)

o

Noncardiogenic pulm onary edem a

o

Acute renal failure

o

Severe or fatal in advanced age, m ale sex, African Am erican, chronic alcohol abuse, G6PD deficiency

Essential Workup Clinical diagnosis

Tests Lab 

Serology: o

Diagnose by single titer >1:64 or fourfold increase

o

Methods: 

Im m unofluorescent antibody



Com plem ent fixation



Indirect hem agglutination test



Indirect im m unofluorescence assay (IFA) is reference standard.



CBC: o

Norm al WBC count

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

o

Throm bocytopenia

o

Anem ia

Electrolytes, BUN/creatinine, glucose: o





Hyponatrem ia <130 m Eq/L

Liver profile: o

Elevated AST

o

Lactate dehydrogenase (LDH)

Arterial blood gas (ABG) for: o

Hypoxia

o

Respiratory alkalosis



Coagulation profile if DIC suspected



Microbiology:



o

Im m unohistologic antibody stain of skin biopsy

o

Isolation of R. rickettsii (tim e consum ing/expensive)

o

Polym erase chain reaction (PCR) assay

Cerebrospinal fluid (CSF): o

Pleocytosis and increased protein

Imaging 

Chest radiograph for pulm onary edem a



Echocardiography: o

Decreased left ventricular contractility

Differential Diagnosis 



Other tickborne diseases: o

Ehrlichiosis: older adults

o

Relapsing fever

o

Lym e disease: erythem a chronicum m igrans (ECM)

o

Tularem ia

o

Babesiosis

o

Colorado tick fever

Infectious diseases: o

Meningococcem iaâ€”late winter, early spring;

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m aculopapular or petechial rash o

Measlesâ€”late winter, early spring; severe prodrom e

o

Rubellaâ€”palm s and soles spared

o

Varicellaâ€”does not have rash in extrem ities P.979





o

Infectious m ononucleosisâ€”palm s and soles spared

o

Dissem inated gonococcal infectionâ€”pustular lesions

o

Typhusâ€”rash starts at trunk with centrifugal spread

o

Secondary syphilis

o

Scarlet fever

o

Kawasaki diseaseâ€”red cracked lips

o

Toxic shock syndrom e

o

Gastroenteritis

o

Staphylococcal sepsis

Inflam m atory causes: o

Allergic vasculitis

o

Throm botic throm bocytic purpura

o

Collagen vascular disease

o

Juvenile rheum atoid arthritis

Heat illness

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) IV fluid bolus for dehydration



Oxygen for hypoxia

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ED Treatment 

Correct fluid and electrolyte deficits.



Initiate antibiotic therapy im m ediately on clinical and epidem iologic findings: o

Doxycyclineâ€”drug of choice

o

Chloram phenicol in pregnant and allergic patients

o

Sulfonam ides m ake infection worse.



Adm inister acetam inophen for fever.



Adm inister high-dose steroids for severe cases com plicated by extensive vasculitis, encephalitis, or cerebral edem a.



Treat com plications: o

DIC

o

Adult respiratory distress syndrom e (ARDS)

o

Congestive heart failure (CHF)

Medication (Drugs) 

Acetam inophen: 1 g (peds: 15 m g/kg) PO q4h



Chloram phenicol: 75 m g/kg/24h PO or IV q6h for 5â€“7 days and 48 hours after defervescence



Doxycycline: 100 m g (peds: 2 m g/kg for those <45 kg) PO or IV b.i.d. for 5â€“7 days and 48 hours after defervescence



Solu-Medrol: 125 m g (peds: 1â€“2 m g/kg) IV push

Pediatric Considerations 

Highest incidence in the 5â€“9-year-old age group



Two thirds of cases occur in children younger than 15 years.



Doxycycline is used in children owing to potential for fatal cases.

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Pregnancy Considerations Use chloram phenicol in pregnant patients.

Follow-Up Disposition Admission Criteria Moderate to severe sym ptom s

Discharge Criteria 

Mild, early disease



Notify fam ily because of clustering.

References 1. Bolgiano EB, Sexton J. Tick-borne illness. In: Rosen P, Barkin R, et al., eds. Em ergency m edicine. 4th ed. St. Louis, MO: Mosby; 1998:2598â€“2629. 2. Centers for Disease Control and Prevention. Inform ation available at http://www.cdc.gov/ncidod/dvrd/rm sf. 3. Fischer JJ. Rocky m ountain spotted fever: when and why to consider the diagnosis. Postgrad Med. 1990;87:109â€“118. 4. Masters EJ, Olson GS, Weiner SJ, et al. Rocky Mountain spotted fever: a clinician's dilem m a. Arch Intern Med. 2003;163:769â€“774.

Codes ICD9-CM 82.0

ICD10 A77.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ro seo la

Roseola

Moses S. Lee

Basics Description 

Incubation period of 5â€“15 days



Mode of acquisition unknown: o

Horizontal spread by oral shedding suggested

o

It is spread person to person, but not very contagious.



Pathophysiology: o

Com plex im m une response (cytokines, antibody responses, T-cell reactivity)

Etiology 

Exanthem subitum



Hum an herpesvirus 6 (HHV-6):



o

Large, double-stranded DNA

o

Closely related to hum an cytom egalovirus

Peak incidence at 6â€“12 m onths; 90% occurrence within first year



Highest incidence in late spring and early sum m er

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Diagnosis Signs and Symptoms 

Sudden, high fever 39.4â€“41.2Â°C (103â€“106Â°F)



Febrile seizures in 5â€“35%



Absence of physical findings: o

Child looks well



Tem perature norm alizes in 3â€“4 days



Maculopapular eruption from trunk to arm s and neck after tem perature norm alization: o

Rash fades within 3 days.



Enlarged lym ph nodes



Diarrhea



Irritability



Erythem atous papules in pharynx (Nakayam a spots)



Rarely causes severe or fatal dissem inating diseases: o



Infectious m ononucleosis syndrom e of hepatitis

Reactivation in im m unocom prom ised individuals

Pediatric Considerations 

Most newborns are seropositive for HHV-6 owing to transplacental antibodies.



By age 1â€“2 years, >90% of infants seropositive

Essential Workup Clinical diagnosis: 

High fever in well-appearing child

Tests Lab 

CBC: o

Initial increase in WBC, then norm alization with lym phocytosis

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



HHV-6 DNA: o

Detected by polym erase chain reaction (PCR)

o

Available at research level

IgM appears early and declines as IgG is produced.

P.981

Differential Diagnosis Fever of unknown origin 

Scarlet fever: o

â€œSandpaperâ€• rash, Pastia lines, and strawberry tongue



Measles (rubeola): o



Rocky Mountain spotted fever: o



Koplik spots, cough, coryza, conjunctivitis, and fever

Rash begins at ankles and wrists.

Rubella: o

Fever after rash



Fifth disease (erythem a infectiosum )



Dengue fever



Pneum ococcal bacterem ia



Meningitis

Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)

ED Treatment 

Supportive



Antipyretics:

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o

Acetam inophen

o

Ibuprofen

Medication (Drugs) 

Acetam inophen: 650 m g (peds: 15 m g/kg) PO q4h



Ibuprofen: 200â€“600 m g (peds: 5â€“10 m g/kg; suspension 100 m g/5 m L; oral drops 40 m g/m L) PO q6h

Follow-Up Disposition Admission Criteria Fever in child who is toxic and does not respond to initial supportive care

Discharge Criteria Usually, all patients m ay be discharged.

References 1. Asano Y, Yoshikawa T, Suga S, et al. Clinical features of infants with prim ary hum an herpesvirus 6 infection (exanthem subitum , roseola infantum ). Pediatrics. 1994;93:104â€“108. 2. Hall CB, Long CE, Schnabel KC, et al. Hum an herpesvirus-6 infection in children: a prospective study of com plications and reactivation. N Engl J Med. 1994;331:482â€“438. 3. Nelson WE, ed. Textbook of Pediatrics. Philadelphia: WB Saunders; 1996:890â€“892. 4. Stoeckle MY. The spectrum of hum an herpesvirus 6 infection: from roseola infantum to adult disease. Annu Rev Med. 2000;51:423â€“430.

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Codes ICD9-CM 57.8

ICD10 B09

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rubella

Rubella

Moses S. Lee

Basics Description 

Transm ission via droplets from respiratory secretions



Moderately contagious: o

Especially during rash eruption and infants with congenital rubella syndrom e (CRS)



Up to 50% m ay be subclinical.



Infants with congenital rubella shed large quantities of virus for several m onths.



Infectious period 7 days before to 5 days after appearance of rash



Incubation period: 14â€“21 days

Etiology 

Also known as Germ an m easles or 3-day m easles



Rubella virus (fam ily: Togaviridae, genus: Rubivirus)



Live, attenuated virus vaccine indications: o

All children older than 12 m onths and entering school

o

All wom en of childbearing age

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Diagnosis Signs and Symptoms 

Acute viral disease



Low-grade fever



Malaise



Headache



Upper respiratory tract sym ptom s



Rash: o

Rash is fainter than m easles rash and does not coalesce.

o

Red m acular rash evolving to pink-red m aculopapules with occasional pruritus





o

Begins in face with rapid caudal spread

o

Com pleted in first day and disappears in 3 days

o

May have hem orrhagic m anifestations

Lym phadenopathy: o

Postauricular

o

Occipital

o

Posterior cervical

Com plications: o

Uncom m on, tend to occur m ore in adults

o

Congenital rubella syndrom e (CRS)â€”infected wom en in first trim ester

o

o

Arthritis: 

More com m on in wom en (up to 79%)



Chronic arthritis is rare.



Begins after 2â€“3 days of illness



Knees, wrists, fingers affected

Hem orrhagic m anifestations: 

Secondary to throm bocytopenia



More com m on in children

Pa ge 4 2 0

o

Neurologic sequelae: 

Encephalitis m ost com m on in adults

Essential Workup Clinical diagnosis

Tests Lab 

CBC: o



Decreased WBC, platelets (m ore com m on in children)

Urinalysis (UA): o

Hem aturia



Reverse transcriptase polym erase chain reaction (PCR)



Enzym e-linked im m unosorbent assay (ELISA) to detect rubella IgM



Rubella antibody titer: o

Acute and convalescent serum specim ens

o

Hem agglutination-inhibition test m ost com m on

o

Definitive diagnosis in acute infection

o

Com pare infant with m aternal sera for CRS.

o

False positives in parvovirus, infectious m ononucleosis, rheum atoid factor



Pharynx: o

Virus m ay be isolated from pharynx 1 week before and until 2 weeks after rash onset (valuable epidem iologic tool).



Cerebrospinal fluid (CSF): o

Few WBCs (m onocytes) in encephalitis

Differential Diagnosis 

Scarlet fever: o

â€œSandpaperâ€• rash, Pastia lines, and strawberry tongue

Pa ge 4 2 0



Measles (rubeola): o



Roseola infantum : o



Spring and fall

Rocky Mountain spotted fever: o



Koplik spots, cough, coryza, conjunctivitis, and fever

Rash begins at ankles and wrists.

Rheum atoid arthritis

P.983

Treatment Pre Hospital Use N95 filter m ask for potential respiratory transm ission.

Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)

ED Treatment 

Sym ptom atic therapy



Antipyretics and antiinflam m atory agents:



o

Acetam inophen

o

Ibuprofen

Isolate rubella patients from susceptible persons (e.g., pregnancy).



Vaccine: o

Measles-m um ps-rubella (MMR) vaccine

o

Rubella vaccine is live attenuated virus.

o

Indications: 

Older than 12 m onths and entry to school



Susceptible postpubertal fem ales

Pa ge 4 2 0



High-risk groups (colleges, m ilitary, places of em ploym ent)



Unim m unized contacts



Health care workers and wom en of childbearing age born before 1957

o

Contraindicated in pregnant wom en

o

Avoid pregnancy for 3 m onths after vaccination.

o

One dose confers probable lifelong protection.

o

Com m on com plaints are fever, lym phadenopathy, and arthralgia.



Im m une globulin: o

Will not prevent virem ia, but m ay m odify sym ptom s

Medication (Drugs) 

Acetam inophen: 650 m g (peds: 15 m g/kg) PO q4h



Ibuprofen: 200â€“600 m g (peds: 5â€“10 m g/kg; suspension 100 m g/5 m L; oral drops 40 m g/m L) PO q6h



Im m une globulin: 0.5 m L reconstituted vial SC (0.25â€“0.50 m L/kg)

Follow-Up Disposition Admission Criteria 

Congenital rubella syndrom e



Encephalitis

Discharge Criteria 

Most patients m ay go hom e.



Inquire regarding vaccination status of fam ily m em bers.

Pa ge 4 2 0

References 1. Banatvala JE, Brown DW. Rubella. Lancet. 2004;363:1127â€“1137. 2. Centers for Disease Control. Rubella and congenital rubella United States, 1984â€“1986. MMWR Morb Mortal Wkly Rep 1987(b);36:664â€“675. Available at http://www.cdc.gov/nip/publications/pink/rubella.pdf. 3. Maldonado Y. Rubella virus (Germ an or three-day m easles). In: Behrm an RE, Kliegm an R, Jensen HB, eds. Nelson Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000:951â€“953. 4. Reef SE, Frey TK, Theall K, et al. The changing epidem iology of rubella in the 1990s. JAMA. 2002;287:464â€“472.

Codes ICD9-CM 56.9

ICD10 B06.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sacral F racture

Sacral Fracture

Jaime B. Rivas

Basics Description 

Sacral fractures are rarely isolated injuries (<5%).



They are frequently associated with pelvic fractures.



They are defined by the orientation of the fracture line.



Mechanism : o

Axial com pression

o

Direct posterior traum a

o

Massive crush injury

Fracture Classification Transverse 



High sacral: o

Fall from height

o

Rare m otor weakness

o

Can see cauda equina syndrom e (CES)

Low sacral: o

Direct blow

o

Associated rectal tears

o

Possible cerebrospinal fluid leaks

o

Rare m otor weakness, can see CES

Vertical

Pa ge 4 2 0







Alar (zone 1): o

Sciatica

o

L5 root injury

o

Neurologic deficit infrequent

Foram inal (zone 2): o

Bowel/bladder dysfunction

o

L5, S1, S2 root injury

o

Sciatica

o

Foot drop

o

Neurologic deficit frequent

Canal (zone 3): o

Bowel/Bladder dysfunction

o

Sciatica

o

L5, S1 root injury

o

Sexual dysfunction

o

Neurologic deficit very frequent

Diagnosis Signs and Symptoms 

Pain in buttocks, perirectal area, and posterior thigh



Swelling and ecchym osis over the sacral prom inence



Possible sacral nerve dysfunction: o

Absence or dim inished anal sphincter tone is an im portant finding.

o

Bowel or bladder incontinence

Essential Workup 

History and exam ination with attention to loss of anal sphincter tone, sensation in the perineum , and bowel and bladder sphincter control

Pa ge 4 2 1



Sacral fractures rarely occur in isolation; look for associated injuries.



Rectal exam will elicit pain in the sacrum .



Displacem ent can be assessed with bim anual rectal exam .

Tests Imaging 

Only 30% of sacral fractures detected on radiograph



Rostrally and caudally angulated anteroposterior views and cone-down views of the lum bosacral junction m ay help.



CT scan m ay better delineate the fracture and associated injuries.

Differential Diagnosis Contusion P.985

Treatment Pre Hospital 

Sacral fractures are frequently associated with other spine and intraabdom inal injuries.



Im m obilize with backboard and C-spine collar.

Initial Stabilization 

Manage airway, breathing, and circulation as needed.



Early im m obilization in unstable pelvis or spine fractures



Pain control with NSAIDs or narcotic analgesics

Pa ge 4 2 1

ED Treatment 

Vertical unstable fractures require a rapid and thorough assessm ent for life-threatening injuries, and orthopaedic consultation (see Pelvic Fracture).



Nondisplaced isolated sacral fractures are treated sym ptom atically with bed rest.



Surgery m ay be required for fractures associated with neurologic injury.



Early orthopedic referral



Early application of cold com presses

Follow-Up Disposition Admission Criteria 

Critically injured traum a patient with unstable pelvic fracture



Neurologic im pairm ent

Discharge Criteria 

All other types of isolated sacral fractures



Consider interm ediate or assisted care setting for elderly patients.

References 1. Cwinn AA. Pelvis and hip. In: Rosen P, et al., eds. Em ergency m edicine: concepts and clinical practice. 4th ed. St. Louis, MO: CV Mosby, 1998: 739â€“762. 2. Pollack C. Pelvic traum a. In: Harwood-Nuss A, et al., eds. The clinical practice of em ergency m edicine. 2nd ed. Philadelphia, PA: Lippincott-Raven, 1996.

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3. Sim on R, Koenigsknecht S. Traum atic conditions of the hip and fractures of the pelvis. In: Sim on R, et al., eds. Em ergency orthopedics: the extrem ities. 4th ed. New York: McGraw-Hill, 2001: 356â€“362, 411â€“413.

Miscellaneous SEE ALSO: Pelvic Fracture

Codes ICD9-CM 805.6

ICD10 S32.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Salicylate Po iso ning

Salicylate

Poisoning Michele Zell-Kanter

Basics Description 

Respiratory alkalosis and m etabolic acidosis: o

Secondary to inhibition of Krebs cycle and uncoupling of oxidative phosphorylation



Dehydration, hyponatrem ia or hypernatrem ia, hypokalem ia, hypocalcem ia: o



Owing to increased sweating, vom iting, tachypnea

Noncardiogenic pulm onary edem a: o

Because of toxic effect of salicylate on pulm onary endothelium resulting in extravasation of fluids



Pharm acokinetics of salicylate change from first order to zero order in overdose setting.

Geriatric Considerations 

Greater m orbidity



Respiratory distress/altered m ental status indicative of severe toxicity



Diagnosis of salicylate intoxication delayed because underlying disease states m ask signs and sym ptom s

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Pediatric Considerations 

Children exhibit faster onset and m ore severe signs and sym ptom s than adults: o

Results from salicylate being distributed m ore quickly into target organs such as brain, kidney, and liver



Respiratory alkalosis (hallm ark of salicylate poisoning in adults) m ay not occur in children.



Metabolic acidosis occurs quicker in children than in adults.



Hypoglycem ia m ore com m on than hyperglycem ia

Diagnosis Signs and Symptoms Gastrointestinal 

Nausea



Vom iting



Epigastric pain



Hem atem esis

Pulmonary 

Tachypnea



Noncardiogenic pulm onary edem a

CNS 

Tinnitus



Deafness



Delirium



Seizures



Com a

Essential Workup 

Guidelines for assessing poisoning severity:

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o



Acute ingestion of: 

<150 m g/kgâ€”considered nontoxic



150â€“300 m g/kgâ€”m ild to m oderately toxic



>300 m g/kgâ€”potentially lethal

Salicylate level: o

At presentation and then every 2 hours until the level begins to decline

o

Make certain units are correct, generally m g/dL.

o

In the chronic overdose setting: Manage patient on clinical findings and not level alone: 

Clinical findings better indication of severity than plasm a salicylate levels

 o

Done nom ogram not valid

Salicylate levels needed to achieve anti-inflam m atory effect (20â€“25 m g/dL) approach toxic levels.

Tests Lab 

Arterial blood gas (ABG): o

Respiratory alkalosis

o

Metabolic acidosis



CBC



Electrolytes, BUN/creatinine, glucose:



o

Anion gap m etabolic acidosis

o

Hypokalem ia

o

Baseline renal function

Urinalysis: o

Urine pH



PT/PTT with significant ingestions



Ferric chloride test: o

Purple if salicylate present

o

Positive 30 m inutes postingestion

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

In the presence of salicylate, Phenistix will turn brown-purple and m ay detect concentrations as low as 20 m g/dL,

Imaging 

Abdom inal flatplate radiograph for concretions



Chest radiograph for pulm onary edem a

Differential Diagnosis Acute Salicylate Poisoning Considered with change in m ental status, unexplained noncardiogenic pulm onary edem a, m ixed acid-base disorder: 

Methanol



Ethylene glycol



Conditions causing noncardiogenic pulm onary edem a

Chronic Salicylate Poisoning 

Im pending m yocardial infarction



Alcohol withdrawal



Organic psychoses



Sepsis



Dem entia

P.987

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



Naloxone, thiam ine, glucose (or Accu-Chek) for altered m ental status

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

IV rehydration with 0.9% norm al saline (NS) for hypotension

ED Treatment Morbidity and m ortality from chronic salicylate poisoning are m uch greater than from acute poisoning: 

Manage chronic intoxication m ore aggressively.

Gastric Decontamination 

Perform gastric lavage for ingestion >150 m g/kg and: o

Patient com atose (after airway control) or at risk of having seizures

o

If patient presents within 1-hour postingestion and has an intact gag reflex 

If no gag reflex is present, intubate with cuffed endotracheal tube prior to perform ing gastric lavage.



Adm inister activated charcoal plus sorbitol im m ediately or postlavage.



Whole-bowel irrigationL o

For concretions visible on plain abdom inal radiograph

o

For ingestion of sustained-release preparation

o

If salicylate levels continue to increase despite appropriate m anagem ent

Enhanced Elimination 

Alkalinization: o

Enhances elim ination of ionized salicylate

o

Indications:

o



Acidosis



Presence of sym ptom s



Elevated salicylate levels

One or two am pules of sodium bicarbonate followed by IV D 5 W with three am pules sodium bicarbonate

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

Goal: urine pH of 7.5â€“8 at 3â€“6 m L/kg/h rate



Add 20â€“40 m Eq KCl per liter to avoid hypokalem ia.



Avoid fluid overload with congestive heart failure (CHF), coronary artery disease.

 

Closely m onitor serum potassium .

Indications for hem odialysis include: o

CHF

o

Noncardiogenic pulm onary edem a

o

CNS depression

o

Seizures

o

Unstable vital signs

o

Severe acid-base disorder

o

Hepatic com prom ise

o

Coagulopathy

o

Underlying disease state com prom ising elim ination of salicylate

o

Absolute salicylate level should not be used as sole criterion for m aking decision to dialyze without considering patient's clinical status unless level is >80â€“100 m g/dL in acute ingestion.



Lower threshold to dialyze patients with chronic overdose

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Sorbitol: 1â€“2 g/kg to m ax. 100 g (peds: >1 year old: 1â€“1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in

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activated charcoal slurryâ€”use only with first dose 

Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Monitor patients with salicylate levels >25 m g/dL until level drops below 25 m g/dL and sym ptom s abate.



ICU adm ission for altered m ental status, m etabolic acidosis, pulm onary edem a

Discharge Criteria Salicylate level <25 m g/dL and sym ptom s have resolved

References 1. Donovan JW, Akhtar J. Salicylates. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia, PA:WB Saunders; 2001:275â€“280. 2. Juurlink DN, McGuigan MA. Gastrointestinal decontam ination for enteric-coated aspirin overdose: what to do depends on who you ask. J Toxicol Clin Toxicol. 2000;38:465â€“470. 3. Rivera W, Kleinschm idt KC, Velez LI, et al. Delayed salicylate toxicity at 35 hours without early m anifestations following a single salicylate ingestion. Ann Pharm acother. 2004;38:1186â€“1188.

ICD9-CM 965.1

ICD10 T39.0

Pa ge 4 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sarco ido sis

Sarcoidosis

Alex Manini Tracy Wimbush

Basics Description 

Chronic, m ultisystem disorder characterized in affected organs by an accum ulation of T lym phocytes and m ononuclear phagocytes, noncaseating epithelioid granulom as, and derangem ents of the norm al tissue architecture



Prevalence 10â€“40/100,000 in the United States and Europe



Affects individuals of both sexes and alm ost all ages, races, and geographic locations



Ratio of blacks to whites ranges from 10:1â€“17:1.

Etiology Unknown

Diagnosis Signs and Symptoms

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History 





Constitutional: o

Fatigue

o

Fever

o

Anorexia

o

Weight loss

Respiratory: o

Dyspnea

o

Chest pain

o

Cough

o

Hem optysis (rare)

Neurologic: o

May affect any aspect but m ost com m only: cranial nerve palsy (usually CN VII)





Cardiac: o

Shortness of breath

o

Palpitations

o

Chest pain

Renal: o



Flank pain

Polyarthralgia

Physical Exam 

Constitutional: o



Respiratory: o



Fever

Dyspnea

Skin: o

Erythem a nodosum

o

Subcutaneous nodules

o

Maculopapules

o

Plaques

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

o

Infiltrative scars

o

Lupus pernio

Ocular: o



Acute anterior uveitis

Neurologic: o

May affect any aspect but m ost com m only: cranial nerve palsy (usually CN VII)



Cardiac: o

Conduction abnorm alities: 

Congestive heart failure due to infiltrative cardiom yopathy









Papillary m uscle dysfunction



Dysrhythm ias



Repolarization abnorm alities

Renal: o

Nephrolithiasis

o

Nephrocalcinosis

Lofgren syndrom e: o

Bilateral hilar adenopathy

o

Erythem a nodosum

o

Often accom panied by joint sym ptom s

Polyarthralgias

Pediatric Considerations 

Children <4 years old classically present with triad of rash, uveitis, and arthritis.



Children â‰¥4 years old present sim ilar to adults.

Essential Workup 

Physical exam ination with em phasis on lung, skin, eye, liver, and heart



Pulse oxim etry



ECG

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

Pulm onary function testing



Slit-lam p eye exam ination

Tests Lab 

Serum angiotensin-converting enzym e inhibitor (ACE) level



Basic chem istry panel



Liver function test: m ild, usually asym ptom atic, elevation of transam inases



Serum calcium : hypercalcem ia due to over synthesis of vitam in D



Urine analysis: hypercalciuria

Imaging Chest radiograph: 

Stage 0: norm al chest radiograph



Stage 1: bilateral hilar lym phadenopathy



Stage 2: lym phadenopathy and pulm onary infiltrates



Stage 3: pulm onary infiltrates only



Stage 4: pulm onary fibrosis

Diagnostic Procedures/Surgery Biopsy: 

Dem onstrates noncaseating granulom as and exclusion of other diseases producing sim ilar histologic picture

Differential Diagnosis 

Lym phom a



Mycobacterial infection



Parathyroid disease

P.989

Pa ge 4 2 2

Treatment Pre Hospital Oxygen by nasal cannula or nonrebreather

Initial Stabilization Provide adequate oxygenation with nasal cannula or face m ask.

ED Treatment 

Patients should be observed without therapy, if possible, due to the potential of spontaneous im provem ent.



Initiating steroids in patients dem onstrating one of the following: o

Sym ptom atic or progressive stage II pulm onary disease



o

Malignant hypercalcem ia

o

Severe ocular disease

o

Neurologic or cardiac sarcoid

o

Stage III pulm onary disease

Consider topical corticosteroids and cycloplegic agents alone for anterior uveitis.



Oxygen if needed for respiratory support

Medication (Drugs) 

Prednisone: o

10â€“20 m g/d for hypercalcem ic nephropathy

o

20â€“40 m g/d for patients with generally m ild to m oderate disease

o

40â€“80 m g/d for neuro sarcoid

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Follow-Up Disposition Admission Criteria 

Any patient who is hypoxem ic



Patients with m oderate to severe sym ptom s

Discharge Criteria 

Life-threatening illness has been ruled out



Follow-up is established

References 1. Am erican Thoracic Society. Statem ent on sarcoidosis. Am J Crit Care Med. 1999;160:736â€“755. 2. English J, Patel P, Greer G. Sarcoidosis. J Am Acad Derm atol. 2001;44:725â€“743. 3. Newm an L, Rose C, Maier L. Sarcoidosis. N Engl J Med. 1997;336:1224â€“1234. 4. Shetty A, Gedalia A. Sarcoidosis: a pediatric perspective. Clin Pediatr. 1998;37:707â€“717.

Codes ICD9-CM 135

ICD10 D86.9

Pa ge 4 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Scabies

Scabies

James Hwang

Basics Description 

Mites m ate on skin surface and gravid fem ale burrows into strateum corneum to lay eggs: o



Anim al scabies burrow but cannot reproduce.

Sym ptom s result from delayed type IV hypersensitivity reaction to m ite, eggs, saliva, and feces: o

Inflam m atory reaction is responsible for intense pruritus, which is the hallm ark of the disease.

o

Norwegian scabies (crusted scabies) is an atypical, highly contagious form of severe scabies: 

Seen in disabled, im m unocom prom ised, and institutionalized patients

General Prevention Despite m ore than 2,500 years existence, an effective way to prevent scabies is still not known.

Epidemiology Over the past two decades, the num ber of patients with scabies is increasing.

Etiology

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

Produced by the hum an scabies m ite, Sarcoptes scabiei var. hom inis, or from anim al m ites



It is transm itted by direct skin-to-skin contact or, less frequently, by infected bedding or clothing.



Mites subsist on a diet of dissolved hum an tissue (do not feed on blood) and can live up to 4 days off a host's body.



On average, the num ber of m ites on a host at any tim e is approxim ately 10â€“15: o

Main difference between Norwegian scabies and regular scabies is the num ber of m ites present on the hostâ€”patients with Norwegian scabies are infected with thousands of m ites.

Diagnosis Signs and Symptoms History 

Generalized, intensely pruritic eruption: o



Pruritus is intensified at night.

Onset 10â€“30 days after exposure and infestation; re-infestation provokes im m ediate (within 1â€“4 days) pruritus: o

Patients with Norwegian scabies are usually im m unocom prom ised, have a decreased inflam m atory response, and have less pruritus.

Physical Exam Often m inim al cutaneous findings: 

Prim ary lesion: linear, elevated, white-gray burrow (up to 1-cm long, width of a hum an hair) with sm all vesicle containing black dot at the end (m ites barely visible to

Pa ge 4 2 2

naked eye) 

Found sym m etrically in web spaces of fingers, flexor surfaces of wrists and elbows, waistline, axillary folds, penis, scrotum , vulva, and areola



Head and neck rarely affected in adults but m ore com m only in infants and children



Secondary lesions: crusted papules, nodules, excoriations, and secondary im petigo or folliculitis seen on back, shoulders, axilla, waist, buttocks, and flexor aspects of elbows



Secondary lesions usually m ore num erous and prom inent than burrows but also m ay be few if topical steroids used o

Norwegian scabies produce gross scaling with hyperkeratotic plaques on hands, feet, scalp, and pressure-bearing areas.

Pediatric Considerations 

Eruption m ay be seen from head to toe.



Distribution typically involves the proxim al half of the foot and heel.



Neonatal scabies is associated with poor feeding, poor weight gain, and frequent super infection.

Essential Workup 

Careful history and skin exam for characteristic lesions



The diagnosis is easily m issed and should be considered in any patient with persistent generalized pruritus.

Tests Lab May be indicated in im m unocom prom ised patients or in patients with system ic infection

Diagnostic Procedures/Surgery

Pa ge 4 2 2



Scrape skin with no. 15 blade and m ineral oil (adheres scraped m aterial to blade) and observe under low-power m icroscope for m ites, eggs, or fecal m aterial.



A negative scraping does not exclude infestation.

Differential Diagnosis 

Atopic derm atitis, derm atitis herpetiform is, papular urticaria folliculitis, lichen planus



Pruritic urticarial papules and plaques of pregnancy



Adult linear IgA bullous derm atosis



Syphilis, pediculosis, pityriasis rosea, im petigo, seborrheic derm atitis, and lym phom a

Treatment Pre Hospital Maintain universal precautions.

Initial Stabilization No specific stabilization necessary in routine cases

ED Treatment 

Treat patient and all persons in im m ediate contact with topical scabicide.



Perm ethrin is 89â€“92% effective and is best tolerated.



Less than 2% of perm ethrin is absorbed into the skin, m aking its potential toxicity low. P.991



Crotam iton is 50â€“60% effective and used when other scabicides are not tolerated.

Pa ge 4 2 3



Iverm ectin has shown excellent results, particularly with resistant or crusted scabies, though is not yet FDA approved for oral use.



Lindane is slightly less effective and is potentially toxic to the CNS: o

Lindanes absorption is about 10%, with side effects of seizure, nausea, headache, vertigo, am blyopia, and irritability.



o

Don't use in pediatric patients.

o

Its use is prohibited in states such as California.

Sulfur is the oldest known treatm ent of scabies and is the drug of choice for infants younger than 2 m onths and for pregnant or lactating wom en.



Crusted scabies first require rem oval of hyperkeratotic scale with 6% salicyclic acid in petroleum jelly to facilitate entry of scabicide.



Treatm ent failures: o

Treatm ent failures are frequent in Norwegian scabies, and use of several agents including oral m edications is often necessary.

o

Machine wash and dry in hot cycles (60Â°C) or dry clean all clothes and bedding worn within 2 days of treatm ent; vacuum household floors, carpets, m attresses, and furniture.

o

Em phasize that itching m ay continue for 1 to 4 weeks after m ites are killed due to skin inflam m atory reaction.

o

Topical steroids and oral antihistam ines reduce pruritic sym ptom s.

o

Relapses can occur from untreated areas such as the scalp and subungal regions.

o

Re-evaluate after 2 weeks for recurrence; retreat if

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live m ites found. o

Treatm ent failures tend to arise from poor patient understanding.

Medication (Drugs) Scabicides 

Crotam iton 10% lotion or cream : Apply topically from neck down in adults and entire skin surface in children qhs for 2 nights, then rinse off 48 hours after last application.



Iverm ectin 3 m g tablets: Single oral dose of 200 m cg/kg provides antiscabietic activity for 6 weeks (pregnancy category C).



Lindane 1% lotion or cream : Apply topically from neck down and rinse off after 8â€“12 hours; contra-indicated in infants, pregnancy, lactation, excessive excoriations, or seizure disorder.



Perm ethrin 5% cream (Elim ite): Apply topically from neck down in adults and entire skin in children qhs, rinse off after 8â€“14 hours (pregnancy class B, unknown safety in breastfeeding): o

Sulfur 5% or 10% precipitated in petrolatum : Apply topically nightly for 3 consecutive nights and wash off 24 hours later.

Antipruritics Low Sedating/Selective Antihistamines: 

Certirizine (Zyrtec): adults and peds >6 years old: 5â€“10 m g PO per day; 6â€“12 m onths: 2.5 m g PO per day; 12â€“24 m onths: 2.5 m g PO per day to b.i.d.; 2â€“6 years old: 2.5â€“5 m g PO per day

Pa ge 4 2 3



Fexofenadine (Allegra): adult and peds >12 years old: 180 m g PO per day or 60 m g PO b.i.d.; 6 m onths to 5 years old: 15â€“30 m g PO b.i.d.; 6â€“11 years old: 30 m g PO b.i.d. o

Loratadine (Claritin): adults and peds >6 years old: 10 m g PO per day; 2â€“5 years old: 5 m g PO per day

Sedating/Nonselective Antihistamines: 

Diphenhydram ine (Benadryl): adults and peds >12 years old: 25â€“50 m g PO q4hâ€“q6h; 2â€“6 years old: 6.25 m g PO q4hâ€“q6h; 6â€“12 years old: 12.5â€“25 m g PO q4hâ€“q6h



Doxepin: 25â€“50 m g PO b.i.d., peds: dosing currently unavailable



Hydroxyzine HCl (Atarax): adults and peds >12 years old: 25â€“100 m g PO q6hâ€“q8h; <6 years old: 2 m g/kg/d PO divided q6hâ€“q8h; 6â€“12 years old: 12.5â€“25 m g PO q6hâ€“q8h

Follow-Up Disposition Admission Criteria Patients with severe topical or system ic super infection

Discharge Criteria Non-toxic appearing patients with routine sym ptom s

Issues for Referral Refractory or relapsing cases

References 1. Burkhart CG, Burkhart CN, Burkhart K. An epidem iologic and

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therapeutic reassessm ent of scabies. Cutis. 2000;65:233â€“240. 2. Chosidow O. Scabies and pediculosis. Lancet. 2000;355:819â€“826. 3. Huynh TH, Norm an RA. Scabies and Pediculosis. Derm atology Clinics. 2004;22(1)7â€“11. 4. Potts J. Eradication of ectoparasites in children. How to infestations of lice, scabies and chiggers. Postgrad Med. 2001;110:5759, 63â€“64. 5. Steen CJ, Carbonaro PA, Schwartz RA. Arthropods in derm atology. J Am Academ y of Derm atology. 2004;50(6):819â€“842.

Codes ICD9-CM 133.0

ICD10 B86

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Scapho id F racture

Scaphoid Fracture

Robyn Heister Girard

Basics Description 

The scaphoid is the m ost com m only fractured carpal bone.



This bone is the stabilizer between the distal and proxim al carpal rows: o

Injury m ay result in arthritis, avascular necrosis, or m alunion.



Fractures are m issed on initial radiographs 10â€“15% of the tim e, and delayed diagnosis greatly increases risk of com plications.



The blood supply to the scaphoid enters distally; the m ore proxim al the fracture, the higher the risk for avascular necrosis.

Etiology Generally results from a fall on an outstretched (dorsiflexed) hand (FOOSH injury)

Diagnosis

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Signs and Symptoms History FOOSH injury

Physical Exam 

Pain and tenderness in the anatom ic snuffbox (m ay be elicited with direct palpation or axial loading of the thum b)



Dorsal wrist pain distal to the radial styloid and decreased range of m otion of the wrist and thum b



Rarely, incidental dam age to the superficial branches of the radial nerve results in sensory changes.

Pediatric Considerations 

Carpal fractures are rare in children (and the elderly), as the distal radius usually fails first.



If present, carefully evaluate m echanism .

Tests Imaging 

Radiographic im aging should include three views of the wrist: PA, lateral, and scaphoid view (wrist prone and in ulnar deviation).



Pay special attention to the m iddle third, or waist, of the bone: 70% of injuries occur here.



Fracture m ay be identified by subtle findings such as a displaced fat pad.



10â€“15% of all fractures are not visible on radiographs at the tim e of injury.



Bone scintigraphy or MRI as early as 3 days postinjury can rule-out fracture and allow for earlier rehabilitation: o

CT is not reliable.

Diagnostic Procedures/Surgery

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If fracture is open or associated injuries are identified, urgent surgical intervention m ay be indicated.

Differential Diagnosis 

Bennett fracture



Rolando fracture



Extra-articular fracture at the base of the thum b m etacarpal



Gam ekeeper thum b



DE Quervain tenosynovitis



Perilunate dislocation



Scapholunate dissociation



Lunate fracture or dislocation

P.993

Treatment Initial Stabilization 

Evaluate patient for other injuries.



Dress open wounds.



Im m obilize with thum b in neutral position, ice, and elevate.

ED Treatment 

Appropriate evaluation m ust include assessm ent of m echanism of injury and point of m axim al tenderness.



Exam ine with special attention to skin integrity and neurovascular status.



Place in thum b spica splint any tim e snuffbox tenderness is present.

Pa ge 4 2 3



Counsel patient regarding risk of m alunion and avascular necrosis.

Medication (Drugs) Pain control with NSAIDs or narcotics as needed

Follow-Up Disposition Admission Criteria Open fracture or presence of other m ore serious injuries

Discharge Criteria Closed injuries, with 72-hour orthopaedic follow-up

Issues for Referral 

If fracture is angulated or displaced >1 m m , im m ediate orthopaedic referral is indicated.



All scaphoid or suspected scaphoid injuries m ust be referred to orthopaedics.



If no radiographic abnorm alities found on initial radiograph, refer to orthopaedics or prim ary MD after placing in thum b spica splint in 7 to 10 days with repeat radiographs at that tim e.

References 1. Eisenhauer MA. Wrist & Forearm . In: Rosen P, et al., eds. Em ergency m edicine: Concepts and clinical practice. 5th ed. St. Louis, MO: Mosby-Year Book, 2002:535â€“539. 2. Kum ar S, O; Connor A, Dsespois M, Galloway H. Use of early m agnetic resonance im aging in the diagnosis of occult scaphoid

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fractures: the CAST Study. N Z Med J. 2005;11;118(1209):U1296. 3. Perron AD, Brady WJ, Keats TE, et al. Orthopedic Pitfalls in the ED: Scaphoid Fracture. Am J Em erg Med. 2001;19(4)310â€“316. 4. Pillai A, Jain M. Managem ent of clinical fractures of the scaphoid:results of an audit and literature review. Euro J Em erg Med. 2005;12(2):47â€“51. 5. Plancher KD. Methods of Im aging the Scaphoid. Hand Clinics. 2001;17(4):703â€“721. 6. Rockwood CA Jr, Green DP, Bucholz RW, et al. eds. Fractures in Adults. 4th ed. Lippincott Raven Press, 1996. 7. Uehara DT. The hand in em ergency m edicine. Em erg Clin North Am . 1993;11(3):781â€“96.

Miscellaneous SEE ALSO: Lunate Fracture and Dislocations

ICD9-CM 814.01

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Schiz o phrenia

Schizophrenia

Joshua L. Roffman Donald C. Goff

Basics Description 

A chronic psychotic disorder characterized by delusions, hallucinations, disorganization, and negative sym ptom s



Onset typically early in adulthood



Com orbid substance abuse (alcohol and stim ulants) is com m on.



Approxim ately 10â€“15% of patients com m it suicide.



Violence m ay result from im paired judgm ent, paranoia, and com m and hallucinations.



Patients with schizophrenia can have abnorm ally high pain thresholds that can com plicate the detection of m edical illness.



Prem orbid phase: o

Developm ent of negative sym ptom s with deterioration of personal, social, and intellectual functioning



Active phase: o

Precipitated by a stressful event

o

Developm ent of active delusions, hallucinations, and

Pa ge 4 2 4

bizarre behavior 

Residual phase: o

Patients are left with im paired social and cognitive ability.

Etiology 

Genetic com ponent (concordance rate of 50% in m onozygotic twins)



Specific genes rem ain uncertain.



Stressors during pregnancy m ay increase risk.



Influenza during second trim ester



Birth com plications

Diagnosis Signs and Symptoms The Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria require the presence of at least two of the following sym ptom s for m ore than 6 m onths: 

Delusions (fixed, false beliefs) o

Bizarre, paranoid, or grandiose:

o

Often involve the conviction that others are tam pering with one's m ind or body





Hallucinations: o

Typically hearing voices

o

May involve any sensory m odality

Thought disorder: o

Disorganized speech ranging from odd, idiosyncratic logic to incoherence



Grossly disorganized or catatonic behavior



Negative sym ptom s

Pa ge 4 2 4

o

Apathy

o

Flat affect

o

Social isolation

o

Anhedonia

Essential Workup 



Obtain history from additional sources: o

Friends or fam ily

o

Assists in establishing the diagnosis

Evaluate potential dangerousness to self or others: o

The content of delusions and the nature of auditory hallucinations should be explored to assess safety.



Medical and neurologic screening o

Assessm ent for drug-induced psychosis (see Psychosis, Medical vs. Psychiatric)

o

Evaluate for acute delirium : 

Schizophrenia does not affect orientation or m em ory.

Tests Lab 

Toxicology screen



Electrolytes, blood urea nitrogen, creatinine, glucose, calcium



Thyroid panel (see Psychosis, Medical vs. Psychiatric)

Imaging Head im aging only with suspicion of neurologic etiology

Differential Diagnosis 

Delirium



Drug-induced psychosis



Huntington disease



Tem poral lobe epilepsy

Pa ge 4 2 4



Bipolar (m anic depressive) disorder



Psychotic depression



Delusional disorder



Schizotypal personality:



Brief psychotic episode o

Sim ilar sym ptom s that occur with duration of less than 1 m onth



Schizophreniform disorder: o

Sim ilar sym ptom s that occur with duration between 1 and 6 m onths

P.995

Treatment Pre Hospital 

Pre hospital personnel m ust protect them selves from harm .



Patients can display unpredictable and violent behavior toward them selves and others.



Patients m ay require restraints to protect them selves or em ergency m edical services crew.



Know local laws as they apply to involuntary restraint.

Initial Stabilization 

Safety of health care workers and patient is param ount.



Patient m ay require a quiet room .



Presence of security staff



Physical or chem ical restraints as appropriate



Agitation m ay be treated with a high-potency antipsychotic

Pa ge 4 2 4

and benzodiazepine: o

Haloperidol com bined with lorazepam is synergistic.

o

Ziprasidone and olanzapine m ay be adm inistered IM for agitation.



Negative sym ptom s tend to be less responsive to pharm acotherapy than psychotic sym ptom s.

ED Treatment 

Psychiatric consultation after m edical evaluation is com pleted



High-potency conventional antipsychotic agents (haloperidol, fluphenazine): o

Minim al cardiovascular effects (droperidol and thioridazine affect QT interval)

o

Oral and IM adm inistration can produce extrapyram idal sym ptom s:

o



Dystonia



Parkinsonism



Akathisia (restlessness of lower extrem ities)

IV haloperidol associated with fewer extrapyram idal sym ptom s



Low-potency conventional agents (chlorprom azine, thioridazine):



o

Fewer extrapyram idal sym ptom s

o

More sedating

o

Orthostatic hypotension

o

Anticholinergic side effects

Atypical antipsychotic agents (risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole): o

Better tolerated with fewer extrapyram idal sym ptom s

o

Risperidone and quetiapine can cause orthostatic hypotension

Pa ge 4 2 4

o

Ziprasidone delays cardiac repolarization (QT interval)

o

Clozapine is the only agent that is clearly m ore effective for psychotic sym ptom s: 

Requires weekly m onitoring of WBC due to agranulocytosis

 

Highly sedating, anticholinergic, hypotensive

Risperidone Consta, haloperidol decanoate, and fluphenazine decanoate are long-acting depot preparations.



If a conventional antipsychotic agent is adm inistered, patients younger than age 40 should be started on benztropine (Cogentin) 2 m g b.i.d. for 10 days to reduce the risk of dystonic reactions.

Medication (Drugs) 

Aripiprazole (Abilify): 5â€“30 m g/d



Olanzapine (Zyprexa): 10â€“30 m g/d



Risperidoxe (Risperdal): 4â€“8 m g/d



Thioridazine (Mellaril): 50â€“800 m g/d



Chlorprom azine (Thorazine): 300â€“800 m g/d



Clozapine (Clozaril): 200â€“900 m g/d



Fluphenazine (Prolixin): 5â€“20 m g/d



Haloperidol (Haldol): 5â€“20 m g/d, acute agitation; 5â€“20 m g IV/IM repeat q30m inâ€“q60m in



Lorazepam (Ativan): acute agitation; 2â€“4 m g IV/IM repeat q30m inâ€“q60m in



Olanzapine (Zyprexa): 10â€“20 m g/d



Quetiapine (Seroquel): 250â€“750 m g/d



Risperidone (Risperdal): 4â€“12 m g/d



Thioridazine (Mellaril): 5â€“30 m g/d

Pa ge 4 2 4



Ziprasidone (Geodon): 80â€“160 m g/d

Follow-Up Disposition Admission Criteria 

Adm it if patient is a danger to self or others or is gravely disabled.



Criteria for involuntary hospitalization vary by state.



Patients with new-onset psychosis should also be adm itted for evaluation and stabilization.

Discharge Criteria 

Patients not a danger to self or others and able to perform activities of daily living



Psychiatric follow-up is arranged.



Psychotic sym ptom s m ay persist at tim e of discharge.

References 1. Goff D. A 23 year old m an with schizophrenia. JAMA. 2002;287:3249â€“3257. 2. Goff D, Heckers S, Freudenreich O. Schizophrenia. In: Nemeroff C, ed. Med Clin North Am . 2001;85:663â€“689.

Miscellaneous SEE ALSO: Psychosis, Acute

Codes ICD9-CM 295.90

Pa ge 4 2 4

ICD10 F20

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sciatica/Herniated Disc

Sciatica/Herniated Disc Ruth Granlund

Basics Description Pain that radiates from the back into buttocks and lower extrem ity distal to knee, with or without sensory or m otor deficits: 

95% sensitive, 88% specific for herniated disc (HD)



Peaks fourth to fifth decade



2â€“10% of low back pain



95% L5 or S1 nerve root



50â€“80% im prove with conservative m anagem ent



5â€“10% require surgery

Etiology 

Protrusion of colloidal gel (nucleus pulposus) through weakened surrounding fibrous capsule (annulus fibrosis)



Risk factors: o

Sm oking

o

Repetitive lifting/twisting

o

Vehicular/m achinery vibration

o

Obesity

o

Sedentary lifestyle

Pa ge 4 2 4

Diagnosis Signs and Symptoms History 

Low back pain precedes onset of leg pain



Leg pain predom inates with tim e



Sharp, well localized, radiates distal to knee



Exacerbated by activities that increase intradiscal pressure:



o

Valsalva m aneuver

o

Cough

o

Nerve-root tension (sitting, straight leg raise)

Relieved by decreasing pressure/tension: o

Lying supine

o

Walking

Physical Exam 

Neurologic exam (m otor; sensory; DTRs) o

o

o



L4 root/L3-4 disc: 

Knee extension/hip adduction



Anterom edial leg/knee/m edial m alleolus



Patella reflex

L5 root/L4-5 disc: 

Great toe and foot dorsiflexion



Dorsom edial foot/first web space



No reflex

S1 root/L5-S1 disc: 

Foot plantarflexion



Posterior leg/lateral m alleolus/dorsolateral foot



Achilles reflex

Rectal exam (tone, sensation)

Pa ge 4 2 4



Straight leg raise: o

Elevate ipsilateral leg by heel 30â€“60 degrees with or without dorsiflex foot.



o

Reproduces radicular pain past knee

o

80% sensitive for HD

Crossed straight leg raise test (pathognom onic): o

Elevate contralateral leg

o

Pain in involved leg

o

Less sensitive but very specific for HD

Essential Workup 

Com plete history and physical exam



See below for test indications.

Tests Lab Indicated if clinical suspicion for differential diagnoses (DDX), not lim ited to: 

CBC



ESR/CRP



Urine analysis

Imaging N/A

PA/Lateral of LS spine 

Helps to rule out som e DDX



Indications: o

Extrem es of age (<20, >55 years)

o

Unresolved back pain (>4â€“6 weeks) despite conservative treatm ent

o

Red flags on history and physical exam : 

Traum a



Constitutional sym ptom s (fever, unexplained

Pa ge 4 2 5

weight loss, m alaise) 

History of cancer



Im m unocom prom ised



IV drug abuse



Recent bacterial infection



Worse at night/awakens patient from sleep



Fever



Midline point tenderness



Neurologic deficits

MRI (Criterion Standard) 

Indications: o

Acute severe neurologic deficits (order from ED)

o

Suspicion of infectious etiology of back pain:

o



Epidural abscess



Osteom yelitis



Discitis

Six weeks failed conservative therapy (order on outpatient basis)



Disc disease (>25%): o

Incidental finding on MRI in asym ptom atic patients

o

No relationship between extent of protrusion and degree of sym ptom s

CT Myelogram 

Rarely used alternative for MRI



CT better at bone details

Diagnostic Procedures/Surgery Postvoid residual (PVR): 

Overflow incontinence



PVR >100 m L

Differential Diagnosis

Pa ge 4 2 5

Low Back Pain/Referred Pain 

Pneum onia, pulm onary em bolus



Pancreatitis



Pyelonephritis, renal calculi



Ectopic pregnancy, pelvic inflam m atory disease



Abdom inal aortic aneurysm (AAA)



Peripheral vascular disease (claudication)



Lum bosacral strain



Hip/SI joint (infection, fracture, bursitis)



Degenerative joint disease



Herpes zoster



Psychologic: o

Functional

o

Secondary gain (drug seeking, disability)

Sciatica Irritating lesion affecting a lum bosacral nerve anywhere along its route: 

Thalam us/Spinothalam ic tum or/Hem orrhage



Spinal cord (m yelopathy): o

Intraspinal tum or/hem atom a/infection (epidural abscess, discitis, osteom yelitis)



Root (radiculopathy): o

Intradural: tum or, infection

o

Extradural: HD, lum bar spine/foram inal stenosis (pseudoclaudication), spondylolisthesis, cyst, tum or, infection



Plexus (plexopathy): tum or, AAA, infection (iliopsoas abscess), hem atom a (retroperitoneal)



Peripheral nerve(neuropathy): toxic/m etabolic/nutritional, infection, traum a, ischem ia, infiltration, com pression, entrapm ent

Pa ge 4 2 5

Pediatric Considerations 

Usually secondary to traum a or serious underlying m edical disease (i.e., leukem ia); consider com plete workup





<10 years o

Infection

o

Tum or

o

Arteriovenous m alform ation

â‰¥10 years: o

Traum atic HD

o

Spondylolisthesis

o

Scheuerm ann disease

o

Tum or

Pregnancy Considerations 

Ectopic pregnancy



Labor



Pyelonephritis



Musculoskeletal

P.997

Treatment Pre Hospital Full spine precautions for traum a victim s

Initial Stabilization Evaluate for neurosurgical em ergency.

ED Treatment 

Pain relief:

Pa ge 4 2 5



o

NSAIDs first line

o

Muscles relaxants, narcotics as needed in acute phase

Conservative treatm ent (4â€“6 weeks): o

Avoid com plete bed rest

o

Lim ited exercise in acute phase as tolerated

o

Gradually increase activity as tolerated

o

Low back and pelvic stretching followed by ice

o

Avoid m ovem ents that load lower back or exacerbate pain:





Heavy lifting



Trunk twisting



Bending, leaning, stooping



Bodily vibration

Studies have shown chiropractic care is effective and favored by som e patients.



Therapies of unproven benefit: o

Transcutaneous electrical nerve stim ulation (TENS)

o

Traction

o

Back brace/corset

o

Ultrasound

o

Diatherm y

o

Acupuncture, acupressure

o

Massage

Medication (Drugs) 

NSAIDs: o

Ibuprofen (Motrin, Advil): 600â€“800 m g (peds: 5â€“10 m g/kg/dose) PO t.i.d.â€“q.i.d.



o

Ketorolac (Toradol): 15 m g IM/30 m g IM Ã—1

o

Naproxen (Naprosyn, Aleve): 500 m g PO b.i.d.

Muscle relaxants (short term ):

Pa ge 4 2 5

o

Cyclobenzaprine (Flexeril): 10â€“20 m g PO t.i.d.

o

Diazepam (Valium ): 2â€“10 m g (peds: 0.1 m g/kg/dose) PO t.i.d.â€“q.i.d.

o

Methocarbam ol (Robaxin): 1,000â€“1,500 m g PO q.i.d.



Opioids (short term ): o

Hydrom orphone (Dilaudid): 2â€“4 m g PO/0.5â€“2 m g IM/IV q4hâ€“q6h PRN

o

Morphine sulfate: 2â€“10 m g (peds: 0.1 m g/kg/dose) IM/IV q2hâ€“q4h PRN

o

Tylenol #3: 1â€“2 PO q4hâ€“q6h PRN

o

Vicodin: 1â€“2 PO q4hâ€“q6h PRN

Follow-Up Disposition Admission Criteria 

Severe or progressive neurologic deficit



Infection/neoplasm



Unstable fracture



Inability to m anage as outpatient (social situation/pain)

Discharge Criteria Patient able to am bulate, follow instructions, has reliable hom e situation, and planned follow-up

References 1. Brisby H. Nerve root injuries in patients with chronic low back pain. Orthop Clin North Am . 2003;34(2):221â€“230. 2. Della-Giustina DA. Em ergency departm ent evaluation and treatm ent of back pain. Em erg Med Clin North Am .

Pa ge 4 2 5

1999;17(4):877â€“893. 3. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363â€“370. 4. Haas M, Sharm a R, Stano M. Cost-effectiveness of m edical and chiropractic care for acute and chronic low back pain. J Manipulative Physiol Ther. October 2005;28(8):555â€“563. 5. Herkowitz HN, Garfin SR, Balderston RA, et al. Rothm an-Sim one: the spine, 4th ed. Philadelphia, PA: WB Saunders, 1999. 6. Roh JS. Degenerative disorders of the lum bar and cervical spine. Orthop Clin North Am . 2005;36(3):255â€“262. 7. Wheeler AH. Diagnosis and m anagem ent of low back pain and sciatica. Am Fam Physician 1995;52(5):13331341.

Codes ICD9-CM 722.10

ICD10 M51.1 G55.1

Pa ge 4 2 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sebo rrheic Derm atitis

Seborrheic

Dermatitis Ian Glen Ferguson

Basics Description 

Com m on, chronic inflam m atory skin disorder



Erythem atous, greasy, yellow, scaly, and crusting papulosquam ous lesions



Affects areas of high sebaceous gland concentration



Periods of rem ission and exacerbation are frequent in adults.

Etiology 

Etiology is m ultifactorial with genetic, environm ental, and horm onal influences.



Malassezia furfur: o

Lipophilic yeast

o

Im portant cofactor which m ay cause T-cell depression

o

Increased sebum and activation of the alternate com plem ent pathway



Disease flares are com m on with physical and em otional stress or illness.

Pa ge 4 2 5



Factors that m ay predispose patients to develop seborrheic derm atitis or m ore extensive or refractory disease:



o

Parkinson disease

o

Paralysis

o

AIDS

o

Congestive heart failure

o

Im m unosuppression of prem ature infants

Medications reported to induce or aggravate the condition include: o

Buspirone

o

Carbam azepine

o

Cim etidine

o

Gold

o

Griseofulvin

o

Haloperidol

o

Interferon-Î±

o

Lithium

o

Phenothiazines

o

Phenytoin

o

Prim idone

o

Stanozolol

o

Thiothixene

Diagnosis Signs and Symptoms Infants 

Onset typically at 1 m onth of age and usually resolves by 12 m onths

Pa ge 4 2 5



Flexural fold involvem ent m ay appear as diaper derm atitis: o

Frequently develops a bacterial or fungal superinfection



Cradle cap: o

Thick greasy, adherent scale on the vertex of the scalp

o

May be accom panied by inflam m ation or secondary infection

Young Children Blepharitis is a white scale adherent to eyelashes, lid m argins with erythem a: 

Resistant to treatm ent and persistent

Adolescents and Adults 

Classic seborrheic derm atitis: o

Minor itching with greasy, fine, dry, white scaling overlying red, inflam ed skin



Exacerbated by avoidance of washing



Usually bilateral and sym m etrical:



o

Scalp, forehead, eyebrows, eyelids

o

Areas of facial hair

o

External ear canals, posterior auricular folds

o

Nasolabial folds

o

Posterior neck

o

Presternal, naval, and body folds: 

Axillary, infram am m ary



Groin, and anogenital

May cause areas of hypopigm entation in dark skinned individuals

Essential Workup Diagnosis is m ade clinically through history and physical

Pa ge 4 2 5

exam ination.

Tests Lab 

Potassium hydroxide preparations of skin scrapings m ay suggest yeast involvem ent.



Fungal culture m ay help exclude tinea capitis as an alternate diagnosis.

Imaging None required

Diagnostic Procedures/Surgery Skin biopsy: 

Not usually required



May help to exclude other diagnoses



Consider if the diagnosis is unclear or the condition fails to respond to treatm ent

Differential Diagnosis 

Atopic derm atitisâ€”characteristically affects antecubital and popliteal fossa in adults: o

Axillary involvem ent favors the diagnosis of seborrheic derm atitis.

o

Pruritus, oozing, and weeping support the diagnosis of atopic derm atitis.

o 

Strong fam ily history of atopy

Candidiasis: o

Presence of pseudohyphae on cytologic exam ination with potassium hydroxide does not exclude seborrheic derm atitis.



Derm atophytosis: o

May occur in the groin area

o

Can be difficult to distinguish from seborrheic

Pa ge 4 2 6

derm atitis o 



Generally distributed asym m etrically

Histiocytosis X: o

Infants affected m ay display scaling.

o

Associated splenom egaly

o

Reddish-brown papules or vesicles

o

Purpuric lesions

o

System ic signs such as fever and adenopathy

Leiner disease: o

Prevalent in infant fem ales

o

Rapid onset in second to fourth m onth of life

o

Com plem ent dysfunction

o

Severe generalized erythem atous, and exfoliative seborrheic derm atitis

o 

Severe diarrhea and failure to thrive

Lupusâ€”erythem atous m alar rash of the nose and m alar em inences: o

Chronic, or discoid, lupus: 

Discrete erythem atous papules or plaques



Thick adherent scale



When rem oved reveals a â€œcarpet tackâ€• appearance



Psoriasis vulgaris: less likely confined to scalp



Rosacea: usually with central facial erythem a or forehead involvem ent



Tinea capitis: Presence of hyphae on cytologic exam ination with potassium hydroxide is suggestive of tinea.



Tinea versicolor: o

Presence of short hyphae with spores (spaghetti and m eatball pattern) with potassium hydroxide

Pediatric Considerations Infants with seborrheic derm atitis and cradle cap m ay present with

Pa ge 4 2 6

concurrent atopic derm atitis.

Alert 

Seborrheic derm atitis is one of m any conditions that m ay cause erythroderm a (generalized exfoliative derm atitis): o

Severe scaling erythem atous derm atitis involving 90% or m ore of the body

P.999

Treatment Initial Stabilization None required

ED Treatment 

Seborrheic derm atitis is a chronic condition: o

Em ergent treatm ent is not required unless secondary infection is present



Patient education: o

Early treatm ent when condition flares

o

Em phasize hygiene and dem onstrate proper cleansing of scaly lesions.

o

Increase frequency of showering.

o

Wash all affected areas.

o

Moderate exposure to sunlight m ay be beneficial as UV-A and UV-B light inhibit the growth of Malassezia furfur.

Pa ge 4 2 6

Medication (Drugs) 

Pharm acologic options are often utilized in a m ultifaceted approach.



Therapy is directed at im proving hygiene, reducing inflam m ation, and decreasing the reservoir of lipophilic yeast and the sebum that supports its growth.



Severe cases require rem oving scales and cornified nonviable epithelium to facilitate further treatm ent.



Soften scales with m ineral oil prior to washing.



Keratolytics rem ove cornified epithelium : o

Salicylic acid (Kerasol)

o

Salicylic acid and sulfur (Sebulex) 



Coal tar: o

Antibacterial

o

Antipruritic properties

o

Slows epiderm al cell production

o

May soften thick scalp scales

o

DHS tar, T/Gel, Tegrin Dandruff, Pentrax 



5â€“10 m inute application to hair or skin daily

5â€“10 m inute application to hair or skin daily

Antidandruff sham poo: o

Use daily to decrease scaling and itching

o

Zinc pyrithione: 

Head and Shoulders, Dandrex, DHS Zinc, Zincon, or X Seb

o

Selenium sulfide: 





Exsel or Selsun

Topical antifungal preparations: o

Use daily

o

Ketoconazole cream or sham poo 1%, 2%

Topical corticosteroids: o

Effective anti-inflam m atory action

Pa ge 4 2 6

o

May be used with antifungal and antidandruff sham poo

o

Can cause cutaneous atrophy and telangiectasias

o

Frequent use m ay hasten recurrence of lesions, and foster dependence from rebound effect.

o

o

Low potency: 

Hydrocortisone 1%, 2%, 2.5%



One or two tim es/day



May be applied to scalp as well

Moderate and high-potency agents: 

Indicated only for conditions refractory to less potent agents



Use only briefly.



Use only on torso and extrem ities.



Do not use on delicate skin, such as the face, genitals, or flexures.

o

o



Moderate potency: 

Triam cinolone acetonide



Fluocinolone acetonide

High potency: 

Clobetasol propionate



Betam ethasone dipropionate

Blepharitis: o

Sodium sulfacetam ide ophthalm ic ointm ent or solution

o

Gentle cleansing with baby sham poo

Follow-Up Disposition

Pa ge 4 2 6

Admission Criteria 

Adm ission unlikely unless severe secondary infection or erythroderm a is present.



Severe and sudden attacks of seborrheic derm atitis m ay be the initial presentation of an im m unocom prom ised patient: o

May warrant adm ission for further evaluation of the underlying disease process

Discharge Criteria 

Patients can be discharged with the recom m ended m edications and follow-up.



Im provem ent should be seen within 7â€“10 days but m ay take m onths to resolve com pletely.



Adolescent and adult form s m ay persist as a chronic derm atitis.



Provide return precautions for signs of secondary bacterial or fungal infections: o

Fever, erythem a, tenderness, or ulceration

Issues for Referral Consider referral to a qualified derm atologist when the diagnosis rem ains elusive or the condition fails to respond to therapy.

References 1. Gee BC. Seborrheic derm atitis. Clin Evid. Decem ber 2004;(12):2344â€“2352. 2. Habif TP. Clinical derm atology. 3rd ed. St. Louis, MO: CV Mosby, 1996. 3. Hurwitz S. Clinical pediatric derm atology. 2nd ed. Philadelphia, PA: WB Saunders, 1993. 4. Johnson BA, Nunley, JR. Treatm ent of Seborrheic Derm atitis. Am Fam Physician. 2000;61:9.

Pa ge 4 2 6

Codes ICD9-CM 690.10

ICD10 L21.9

Pa ge 4 2 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Seiz ure, Adult

Seizure, Adult

Atul Gupta Rebecca Smith-Coggins

Basics Description 

Generalized seizures: o

Classically tonic-clonic (grand m al)

o

Begins as m yoclonic jerks followed by loss of consciousness

o

Sustained generalized skeletal m uscle contractions

o

Nonconvulsive generalized seizures: 

Absence seizures (petit m al); brief episodes of sudden im m obility and blank stare



Partial seizures: o

Sim ple: 

Brief sensory or m otor sym ptom s without loss of consciousness (i.e., jacksonian)

o

Com plex: 

Mental and psychological sym ptom s



Affect changes



Confusion



Autom atism s



Hallucinations

Pa ge 4 2 6

 

Associated with im paired consciousness

Status epilepticus: o

Seizure lasting longer than 1 hour

o

Serial seizures that produce an enduring epileptic condition for longer than 1 hour

o

Life-threatening em ergency with m ortality rate of 10â€“12%

Pediatric Considerations 

Febrile seizure is a generalized seizure occurring between 3 m onths and 5 years of age: o

Typically lasts less than 15 m inutes

o

Associated with a rapid rise in tem perature

o

Without evidence of CNS infection or other definitive cause

Etiology 

Meningitis, abscess, encephalitis



Ischem ic or hem orrhagic stroke



Prim ary or m etastatic neoplasm



Metabolic abnorm alities



Electrolytes (hypernatrem ia, hyponatrem ia, hypocalcem ia)



Hypo/hyperglycem ia



Hypoxia



Urem ia



Toxins/Drugs: o

Lidocaine

o

TCAs

o

Cocaine

o

Alcohol withdrawal



Eclam psia



Hypertensive encephalopathy



Traum a

Pa ge 4 2 6



Congenital abnorm alities



Idiopathic

Diagnosis Signs and Symptoms 

Altered level of consciousness



Involuntary, repetitive m uscle m ovem ents: o



Seizures have abrupt onset: o



Tonic posturing or clonic jerking

Aura m ay precede a focal seizure

Duration is usually 90â€“120 seconds: o

Im paired m em ory of the event

o

Postictal state is a brief period of confusion and som nolence following a seizure.





Evidence of recent seizure activity: o

Confusion or som nolence

o

Acute intraoral injury

o

Urinary incontinence

o

Posterior shoulder dislocation

o

Tem porary paralysis (Todd paralysis)

Other findings m ay suggest etiology of seizure: o

Fever and nuchal rigidity (CNS infection)

o

Needle tracks; stigm ata of liver disease (drugs and alcohol)

o

Head traum a: 

Papilledem a (increased intracranial pressure)



Lateralized weakness, sensory loss, or asym m etric reflexes

Essential Workup

Pa ge 4 2 6



A thorough history is the m ost valuable part of the workup:



o

Witness accounts

o

History of prior seizures

o

Presence of acute illnesses

o

Past m edical problem s

o

History of substance use

Patients with chronic seizure disorder and typical seizure pattern m ay need to have only serum glucose and anticonvulsant levels checked.



New-onset seizure m andates workup: o

Electrolytes including calcium , phosphorus

o

Head CT

o

Search for specific underlying cause.

o

Patient's condition and resources for follow-up determ ine whether all these tests need to be done in the ED.

Pediatric Considerations 

Children with first febrile seizure should receive fever workup as dictated by clinical condition.



Frequently, there is a fam ily history of febrile seizure.



CBC, blood culture, urinalysis, chest radiograph if any signs of respiratory distress



Lum bar puncture for first febrile seizure: o

Consider strongly if age <1 year.

o

Lethargy or poor feeding

o

Exam difficult

o

Unreliable follow-up

Tests Lab 

Serum anticonvulsant levels

Pa ge 4 2 7



Other labs as indicated by concom itant disease

Imaging 



Noncontrast head CT: o

Persistent or progressive alteration of m ental status

o

Focal neurologic deficits

o

Seizure associated with traum a

CT scan with contrast should be obtained in HIV-positive patients to rule out toxoplasm osis.



MRI is sensitive for low-grade tum ors, sm all vascular lesions, early inflam m ation, and early cerebral infarcts: o

Consider electively in new-onset seizures.

Diagnostic Procedures/Surgery 

EEG m ay be arranged as an outpatient with neurology.



Bedside EEG m ay be perform ed in ED if suspicious for nonconvulsive status epilepticus or psychogenic seizures.

Differential Diagnosis 

Syncope (m ay also have incontinence, twitching, and jerking)



Hyperventilation syndrom e



Psychogenic seizures



Transient ischem ic attacks



Sleep disorders

P.1001

Treatment Pre Hospital

Pa ge 4 2 7

Anticonvulsant as per local protocol

Initial Stabilization 

Airway m anagem ent as indicated



Pulse oxim etry, oxygen with suction available: o

C-spine precautions

o

Rapid sequence intubation if patient cannot control airway, hypoxic, or head traum a

o

IV access, rapid glucose, and if hypoglycem ic give IV dextrose 1 am p

o

Lorazepam or diazepam for active seizures

ED Treatment 

Phenytoin or phenobarbital as second-line drugs



Rectal paraldehyde or pentobarbital com a for refractory patients



Treat the underlying cause if identifiable (hypoglycem ia, infection, etc.).



Load with anticonvulsants if levels are low.



Fosphenytoin is an option in patients for whom IV Dilantin is considered unsafe.



If no cause is identifiable in new-onset seizure patient, begin single-agent anticonvulsant therapy (e.g., phenytoin).



Notify appropriate departm ent of m otor vehicles.

Pediatric Considerations 

Fever control with acetam inophen and ibuprofen



Anticonvulsants are not necessary for febrile seizures.



Anticonvulsants should be prescribed in conjunction with neurologist.

Pa ge 4 2 7

Medication (Drugs) 

Acetam inophen: 10â€“15 m g/kg PO or PR



Diazepam : 0.2 m g/kg IV per dose (m ax. 20 m g), 0.5 m g/kg PR



Fosphenytoin: 15â€“20 m g/kg at rate of 100â€“150 m g/m in IV



Ibuprofen: 5â€“10 m g/kg PO



Lorazepam : 0.1 m g/kg IV per dose (m ax. 10 m g)



Paraldehyde: 0.3â€“0.5 m L/kg PR 1:1 in m ineral oil (peds: 0.3 m L/kg PR 1:2 in m ineral oil)



Phenobarbital: 15â€“20 m g/kg IV at rate of 1 m g/kg/m in



Phenytoin: 15â€“20 m g/kg IV at rate of 40â€“50 m g/m in (peds: use rate of 0.5â€“1.0 m g/kg/m in)

Follow-Up Disposition Admission Criteria 

Patients with status epilepticus should be adm itted to the intensive care unit.



Patients with seizures secondary to underlying disease (e.g., m eningitis, intracranial lesion) m ust be adm itted for appropriate treatm ent and m onitoring.



Patients with poorly controlled repetitive seizures should be adm itted for m onitoring.



Delirium trem ens

Discharge Criteria 

Patient with norm al workup and appropriate neurology follow-up

Pa ge 4 2 7



Uncom plicated seizure in patient with chronic seizure disorder



Seizure secondary to reversible cause (e.g., hypoglycem ia, alcohol withdrawal)



Sim ple febrile seizure

References 1. ACEP Clinical Policies Com m ittee Clinical Policies Subcom m ittee on Seizures. Clinical policy: Critical issues in the evaluation and m anagem ent of adult patients presenting to the em ergency departm ent with seizures. Ann Em erg Med. 2004;43(5):605â€“625, 1511â€“1920. 2. Bradford JC, Kyriakedes CG. Evaluation of the patient with seizures: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):203â€“220. 3. Gilad R, Lam pl Y, Gabby U, et al. Early treatm ent of a single generalized tonic-clonic seizure to prevent recurrence. Arch Neurol. 1996;53(11):1149â€“1152. 4. Roth HL, Drislane FW. Seizures. Neurol Clin. 1998;16(2):257â€“284. 5. Shepherd SM. Managem ent of status epilepticus. Em erg Med Clin North Am . 1994;12(4):941â€“961. 6. Stenklyft PH, Carm ona M. Febrile seizure. Em erg Med Clin North Am . 1994;12(4):989â€“999.

Codes ICD9-CM 780.39

Pa ge 4 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Seiz ure, F ebrile

Seizure, Febrile

John Santamaria

Basics Description 

Occurs between 6 m onths and 5 years of age associated with fever: o

No evidence of intracranial infection or other defined CNS prim ary cause

o

Average age of onset is 18â€“22 m onths

o

Children with previous nonfebrile seizures are excluded.



Most com m on pediatric convulsive disorder: o

Affects 2â€“4% of young children in United States



Occurs in norm al children with a system ic viral illness



High-risk children: o

History of febrile seizure in im m ediate fam ily m em bers



o

Delayed neurologic developm ent

o

Males

Subgroups: o

Sim ple febrile seizures: 

Brief, self-lim ited lasting <10â€“15 m inutes, resolve spontaneously

Pa ge 4 2 7

 o



Generalized without any focal features

Com plex febrile seizures: 

Duration >15 m inutes



Focal features



More than one seizure within a 24-hour period

Risk of recurrence: o

One third of cases

o

Early age of onset, history of febrile or afebrile seizures in first-degree relatives, and tem perature <40Â°C during initial seizure increase the likelihood of recurrence.



Risk of subsequent epilepsy: o

Greatest for those with prior abnorm al neurologic developm ent, a com plex first febrile seizure, or a fam ily history of afebrile seizures

o

Only slightly greater than the general population if first febrile seizure is sim ple and neurologic developm ent is norm al

o

Not affected by the use of prophylactic m edications

Alert Because this is usually self-lim ited, intervention m ust be individualized in relation to airway, breathing and seizure m anagem ent.

Etiology Com m on childhood infections: 

Upper respiratory illnesses



Otitis m edia



Roseola



Gastrointestinal infections



Shigella gastroenteritis

Pa ge 4 2 7

Diagnosis Signs and Symptoms Fever Seizure m ay occur concurrent with recognition of the febrile illness.

Seizure Generalized tonic-clonic seizure m ost com m on: 



Tonic phase: o

Muscular rigidity

o

Apnea and incontinence

o

Self-lim ited and last only a few m inutes

Other seizure types: o

Staring with stiffness

o

Lim pness

o

Jerking m ovem ents without prior stiffening

History Careful history and physical exam ination help confirm the diagnosis and rule out other etiologies: 

Sym ptom s/Evidence of infectious illness



Duration of fever



Medication exposure/toxin



Traum a/Occult traum a



Developm ental level



Fam ily history of seizures



Com plete description of the seizure



Presence of m eningism us, tense/bulging fontanelle, preexisting altered m ental status



Evidence of focal deficits or increased intracranial pressure

Physical Exam

Pa ge 4 2 7

See History

Tests Lab 

Routine laboratory studies are not indicated.



Evaluate for a source of fever if a serious bacterial infection is suspected:



o

WBC

o

Urinalysis

o

Blood and urine cultures

Electrolytes and bedside glucose in infants and children with vom iting or diarrhea

Imaging 

Chest radiograph only in patients with significant respiratory sym ptom s



Head CT: o

Indicated with traum atic injuries, focal neurologic findings, or inability to exclude elevated intracranial pressure



Lum bar puncture not routinely indicated: o

Indications: 

<12â€“18 m onths of age



History or irritability, decreased feeding, lethargy

o



Physical signs of m eningitis



Com plex seizure



Prolonged postictal state



Antibiotics altering presentation



Abnorm al m entation after postictal state

Indications: >18 m onths old: 



Signs/Sym ptom s of CNS infection present

Electroencephalogram :

Pa ge 4 2 7

o

Not helpful in the initial evaluation of febrile seizure

o

May be indicated if developm ental delay, underlying neurologic abnorm ality, or focal seizure

o

Does not help predict recurrences or risk for later epilepsy



Anticonvulsant levels



Toxicologic studies of blood and urine if history and physical exam suggestive

P.1003

Differential Diagnosis 

Febrile delirium



Febrile shivering with pallor and perioral cyanosis



Breath-holding spell during febrile event



Acute life-threatening event



Other causes of seizure: o

Afebrile seizure occurring during febrile event

o

Sudden discontinuance of anticonvulsants

o

Infection: 

Meningitis/Encephalitis



Acute gastroenteritis, often with dehydration

o

Head traum a

o

Toxicologic: 

Anticholinergics



Sym pathom im etics



Other

o

Hypoxia

o

Metabolic disease

o

Intracranial m asses

o

CNS vascular lesions

Pa ge 4 2 7

Treatment Pre Hospital 

Protect the airway



Oxygen



Support breathing as needed



Cautions: o

Keep the child from incurring injury while actively convulsing.

o

Respiratory insufficiency and apnea occur secondary to overaggressive treatm ent with benzodiazepines.

o

Sim ple febrile seizures are self-lim ited and generally require no anticonvulsant therapy or ventilatory support.

Initial Stabilization 

Support the airway and breathing.



Benzodiazepines rarely needed: o

Prolonged seizures or com prom ised patients

o

Lorazepam , diazepam , or m idazolam

o

Rectal diazepam or IM m idazolam m ay be easily adm inistered with good efficacy.

ED Treatment 

Rarely is pharm acologic intervention required; usually self-lim ited.





Seizures refractory to benzodiazepines: o

Phenytoin or fosphenytoin

o

Phenobarbital

o

Work-up to exclude other etiologies

Adm inister antipyretics acutely and routinely for at least the next 24 hours:

Pa ge 4 2 8

o 

Acetam inophen or ibuprofen (m ay use both)

Appropriate antibiotic treatm ent for specific bacterial disease, if identified

Medication (Drugs) 

Acetam inophen: 15 m g/kg PO, PR



Diazepam : 0.2â€“0.3 m g/kg IV; 0.5 m g/kg PR



Fosphenytoin: 20 m g/kg IV over 20 m inutes



Ibuprofen: 10 m g/kg PO



Lorazepam : 0.1 m g/kg IV



Midazolam : 0.1 m g/kg IV; 0.2 m g/kg IM



Phenobarbital: 20 m g/kg IV over 20 m inutes or IM



Phenytoin: 20 m g/kg IV over 30â€“45 m inutes

Follow-Up Disposition Admission Criteria Recurrent or prolonged seizures

Discharge Criteria 

Sim ple febrile seizures: o

Norm al neurologic exam ination

o

Source of fever is appropriately treated as outpatient



Reassurance to parents



Aggressive treatm ent of fever with antipyretics is generally recom m ended despite absence of evidence that this reduces recurrences.



Oral diazepam during febrile illness m ay reduce risk of recurrence; prophylactic anticonvulsants with other

Pa ge 4 2 8

anticonvulsants rarely indicatedâ€”controversial and only after extensive discussion.

References 1. Am erican Academ y of Pediatrics, Provisional Com m ittee on Quality Im provem ent, Subcom m ittee on Febrile Seizures. Practice param eter: the neurodiagnostic evaluation of the child with a first sim ple febrile seizure. Pediatrics. 1996;97:769â€“771. 2. Barata I. Pediatric Seizures. Critical Decisions in Em ergency Medicine. 2005;19(6):1â€“21. 3. Depieso AD, Teach SJ. Febrile seizures. Pediatr Em erg Care. 2001;17(5):384â€“387. 4. Warden CR, Zibulewsky J, Mace S, et al. Evaluation and m anagem ent of febrile seizures in the out-of-hospital and em ergency departm ent settings. Ann Em erg Med. 2003;41(2):215â€“222.

Miscellaneous SEE ALSO: Anticholinergic Poisoning; Seizures, Pediatric

Codes ICD9-CM 780.39

Pa ge 4 2 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Seiz ure, Pediatric

Seizure, Pediatric

John Santamaria

Basics Description Sudden, abnorm al discharges of neurons resulting in a change in behavior or function

Etiology 

Febrile seizures



Infection



Idiopathic



Traum a



Toxicologic:



o

Ingestion

o

Drug action

o

Drug withdrawal

Metabolic: o

Hypoglycem ia

o

Hypocalcem ia

o

Hypo/Hypernatrem ia

o

Inborn errors of m etabolism



Perinatal hypoxia



Intracranial hem orrhage



CNS structural anom aly or m alform ation

Pa ge 4 2 8



Degenerative disease

Diagnosis Signs and Symptoms Neonates 

Subtle abnorm al repetitive m otor activity: o

Facial m ovem ents

o

Eye deviations

o

Eyelid fluttering

o

Lip sm acking/sucking



Respiratory alterations



Apnea



Seizure activity:



o

Focal or generalized tonic seizures

o

Focal or m ultifocal clonic seizure

o

Myoclonic m ovem ents

Generalized problem s (m etabiolic, infection, etc) m ay present with focal seizures.

Older Infants and Children 



Generalized seizures: o

Tonic-clonic

o

Tonic

o

Clonic

o

Myoclonic

o

Atonic (â€œdropâ€•)

o

Absence

Partial or focal seizures: o

Sim ple: 

Consciousness m aintained

Pa ge 4 2 8

o

Sim ple partial seizures: 

Motor, sensory, and/or cognitive sym ptom s



Motor activity is focal: one part or side.



Paresthesias, m etallic tastes, and visual or auditory hallucinations

o

o

Com plex: 

Consciousness im paired



Com plex partial seizure

Siim ple partial seizure progresses with im paired consciousness: 

Aura precedes altered consciousness; auditory, olfactory, or visual hallucination

 

May generalize

Status epilepticus: o

Generalized is m ost com m on.

o

Sustained partial seizures

o

Absence seizures

o

Persistent confusion; postictal period

History 

Determ ine whether seizures are febrile or afebrile.



Determ ine type of seizure: o

Partial versus generalized

o

Presence of eye findings, aura, m ovem ents, cyanosis

o

Duration

o

State of consciousness, postictal state

o

Predisposing conditions/history/fam ily history (syndrom es with a genetic com ponent)



A careful neurologic exam should be perform ed: o

Ophthalm oscopic evaluation

o

Skin evaluation to identify neurocutaneous diseases such as tuberous sclerosis



Rapid glucose testing for those in status epilepticus

Pa ge 4 2 8

Tests Lab 

Bedside glucose test



Perform ed in young infants and those in status epilepticus



Select studies in other children reflecting history and physical exam ination:



o

Electrolytes

o

Blood urea nitrogen

o

Creatinine

o

Glucose

o

Calcium

o

Magnesium

o

CBC

o

Toxicologic screen

Patients on anticonvulsant therapy: o



Drug levels

Febrile seizure: o

Laboratory studies to evaluate for a serious underlying bacterial infection, if suspected

Imaging 

Head CT: o

Focal seizure

o

New focal neurologic abnorm ality

o

Suspected intracranial hem orrhage or m ass lesion

o

New-onset status epilepticus without identifiable cause

o 



Not routinely indicated for first afebrile seizure

Lum bar puncture: o

Suspicion of m eningitis or encephalitis

o

CT first if suspect increased intracranial pressure

MRI:

Pa ge 4 2 8

o 

Rarely urgently indicated for seizures

EEG: o

Generally indicated in children with an afebrile seizure as a predictor of risk of recurrence and classify the seizure type/epilepsy syndrom e

o

Postictal slowing seen within 24â€“48 hours of a seizure and m ay be transient; delay EEG if possible.

o

Rarely helpful in the acute setting

P.1005

Differential Diagnosis 





Neonates: o

Apnea due to other causes

o

Jitters or trem ors

o

Gastroesophageal reflux

Infants and toddlers: o

Breath-holding spells

o

Night terrors

Children and adolescents: o

Migraine headache

o

Syncope

o

Tics

o

Pseudoseizures

o

Hysteria

Treatment Pre Hospital Cautions:

Pa ge 4 2 8



Many conditions m ay be m istaken for seizures (see Differential Diagnosis, below).



Im m obilize cervical spine if traum a suspected.



Check fingerstick glucose or adm inister dextrose as appropriate.

Initial Stabilization 

Airway, breathing, and circulation support if actively seizing



Airway: o

Oxygen/Monitor pulse oxim etry.

o

Nasopharyngeal airway preferred over oral airway

o

Bag valveâ€“m ask support, if hypoventilating or persistently hypoxic

o

Intubation if seizures are refractory and bag valveâ€“m ask support is unsuccessful



IV access



If hypoglycem ic, dextrose



Maintain spine precautions if traum a suspected.

Alert Airway and breathing m ust be stabilized concurrent with m anagem ent of ongoing seizures, if present.

ED Treatment Status Epilepticus 

Benzodiazepine: o

Lorazepam is preferred due to its longer duration of action.

o

Valium is acceptable.

o

If IV access is not available: 

Diazepam m ay be given per rectum ; use a TB syringe or 14-gauge Angiocath catheter or

Pa ge 4 2 8

feeding tube. 

Midazolam IM is also effective if IV access is not available.





Phenytoin: o

If benzodiazepines fail

o

For longer-term control

o

Fosphenytoin easier to adm inister

Phenobarbital: o

Use if benzodiazepines and phenytoin fail to break the seizure.

o

Risk of respiratory depression greatly increases if a benzodiazepine has also been given.



Alternative therapies in the event of refractory status epilepticus



Consultation appropriate: o

Paraldehyde (per rectum )

o

Barbiturate com a: 

Barbiturate (pentobarbital) com a requires intubation and EEG m onitoring to be sure the seizure is suppressed

 o

Associated hypotension

General anesthesia: 

A final resort



Continuous EEG is needed to be sure the seizure is abolished.



Neonates: o

Phenobarbital is acceptable first-line therapy.

o

Preferred m aintenance drug

Alert Note: Aggregate response to second- and third-line agents is less than 10%.

Pa ge 4 2 8

Medication (Drugs) 

D 1 0 : 5 m L/kg IV for neonates



D 2 5 : 2 m L/kg IV for children



Diazepam : 0.2â€“0.3 m g/kg IV; 0.5 m g/kg PR



Fosphenytoin: 20 m g/kg IV over 20 m inutes



Lorazepam : 0.1 m g/kg IV



Midazolam : 0.1 m g/kg IV, 0.2 m g/kg IM



Paraldehyde: 0.3 m L/kg PR m ixed 1:1 with cottonseed or olive oil, m ax. dose is 5 m L



Pentobarbital: 10â€“15 m g/kg IV over 1â€“2 hours; m aintenance: 1â€“3 m g/kg/h IV



Phenobarbital: 20 m g/kg IV over 20 m inutes



Phenytoin: 20 m g/kg IV over 30â€“45 m inutes

Follow-Up Disposition Admission Criteria 

Intensive care unit: o

Active status epilepticus, intubated, or persistent m ental status changes



Inpatient unit: o

Status epilepticus resolved in the ED

o

Underlying cause of seizure not resolved or controlled

o

Intracranial hem orrhage

o

Mass lesion

o

Meningitis/Encephalitis

o

Drug

o

Toxin ingestions

Pa ge 4 2 9

Discharge Criteria 

The child is alert with norm al m ental status and neurologic exam .



No evidence of an underlying cause requiring hospitalization



Reliable parent or caregiver



Hom e telephone



Provide seizure precautions and aftercare instructions



Follow-up with a prim ary care physician or pediatric neurologist

References 1. Appleton R, Choonara I, Martland T, et al. The treatm ent of convulsive status epilepticus in children. The Status Epilepticus Working party. Arch Dis Child. 2000;83:415â€“419. 2. Barata I, Pediatric Seizures. Critical Decisions in Em ergency Medicine. 2005;19:1â€“10. 3. Bleck TP, Managem ent Approaches to Prolonged Seizures and Status Epilepticus. Epilepsia. 1999;40:S59â€“S63. 4. Cantor RM, Santam aria JP, eds. Pediatric em ergency guide. Dallas, TX: Am erican College of Em ergency Physicians, 1997. 5. Hirtz D, et al. Practice param eter: evaluating a first nonfebrile seizure in childrenreport of the Quality Standards Subcom m ittee or the Am erican Academ y of Neurology, the Child Neurology Society, and the Am erican Epilepsy Society. Neurology. 2000;55:616â€“623. 6. Vining EPG. Pediatric seizures. Em erg Med Clin North Am . 1994;12:973â€“988.

Miscellaneous SEE ALSO: Seizures, Febrile

Pa ge 4 2 9

Codes ICD9-CM 780.31

Pa ge 4 2 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sepsis

Sepsis

Richard Wolfe Nathan Shapiro

Basics Description 

System ic inflam m atory response triggered by an infection in the host and m ediated by chem ical m essengers: o

Decreased peripheral vascular resistance

o

Elevated cardiac output in response to vasodilatation

o

Later in septic shock, m yocardial depression, and reduced cardiac output (due to injury at the cellular level or m ediators acting on the heart)

o

Multiple organ dysfunction syndrom e (MODS) if sepsis is ineffectively treated





Adult respiratory distress syndrom e (ARDS)



Acute tubular necrosis and kidney failure



Hepatic injury and failure



Dissem inated intravascular coagulation

Sepsis is classified by the system ic inflam m atory response syndrom e (SIRS): o

Tem perature >38Â°C or <36Â°C

o

Heart rate >90 beats/m inute

o

Respiratory rate >20/m inute or PaCO 2 <32 m m Hg

Pa ge 4 2 9

o

WBC >12,000/m m 3 , <4,000/m m 3 , or >10% band form s



Sepsis: two or m ore of the SIRS criteria with an underlying infection



Severe sepsis: o

Sepsis with organ dysfunction as m anifested by one of the following:





Acidosis



Renal dysfunction



Acute change in m ental status



Pulm onary dysfunction



Hypotension



Throm bocytopenia or coagulopathy



Liver dysfunction

Septic shock: o

Sepsis-induced hypotension despite fluid resuscitation

o

Systolic blood pressure (BP) <90 m m Hg or reduction of >40 m m Hg from baseline

Etiology 



Gram -negative bacteria m ost com m on: o

Escherichia coli

o

Pseudom onas aeruginosa

o

Rickettsiae

o

Legionella species

Gram -positive bacteria: o

Enterococcus species

o

Staphylococcus aureus

o

Streptococcus pneum oniae



Fungi (Candida species)



Viruses

Pediatric Considerations

Pa ge 4 2 9



Children with a m inor infection m ay have m any of the findings of SIRS.



Major causes of pediatric bacterial sepsis o

Neisseria m eningitis

o

Streptococcal pneum oniae

o

Haem ophilus influenzae

Diagnosis Signs and Symptoms Physical Exam 





General: o

Fever

o

Tachycardia

o

Tachypnea

o

Hypotherm ia (poor prognosis)

o

Hypoxem ia

o

Diaphoresis

Cardiovascular: o

BP

o

Norm al early in sepsis

o

Hypotension when septic shock occurs

o

Poor perfusion with septic shock: 

Prolonged capillary refill



Cool and clam m y extrem ities

Gastrointestinal/Genitourinary: o

Abdom inal pain

o

Nausea, vom iting

o

Diarrhea

o

Dysuria/Frequency

Pa ge 4 2 9

o

Reduced urine output

o

Abdom inal tenderness: 

Diffuse



Localized to right upper quadrant (liver or gallbladder source)



Right lower quadrant (appendicitis with or without abscess)



Suprapubic area or lower quadrants (urinary tract or pelvic source or diverticulitis)

o

Flank pain: 



With pyelonephritis or retroperitoneal abscess

Pulm onary: o

Shortness of breath

o

Tachypnea: 

Present even when the lungs are not the source of sepsis

o 

Productive cough

Derm atologic: o

Any rash is im portant.

o

Localized erythem a with lym phangitis (streptococcal or staphylococcal cellulitis)

o

Rash involving palm s of hands and soles of feet (rickettsial infection)

o

Petechiae scattered on the torso and extrem ities (m eningococcem ia)

o

Ecthym a gangrenosum (pseudom onas septicem ia)

o

Round, indurated, painless lesion with surrounding erythem a and central necrotic black eschar

o

Decubitus ulcers

o

Indwelling catheter: 

Surrounding skin erythem atous with or without purulent drainage

Pa ge 4 2 9



CNS: o

Change in m ental status

o

Confusion

o

Delirium

o

Com a

o

Neck stiffness (m eningitis)

Essential Workup 

Careful history and physical exam ination



Guides further evaluation and initiation of appropriate antibiotic therapy

Tests Lab 

Serum lactate: o



>4 m m ol/L defines severe sepsis

CBC with differential: o

Leukocytosis is insensitive and nonspecific.

o

Neutrophil count <500 cells/m m 3 should prom pt isolation and em piric IV antibiotics in chem otherapy patients.

o

>5% bands on a peripheral sm ear is an im perfect indicator of infection.

o

Hem atocrit: 

Needed to determ ine whether adequate oxygen delivery can be achieved



Patients should be m aintained with a hem atocrit >30% and hem oglobin >10 g/dl.

o

Platelets: 

May be elevated in the presence of infection or sepsis-induced volum e depletion



Low platelet count is a significant predictor of bacterem ia and death.

Pa ge 4 2 9



Electrolytes, blood urea nitrogen, creatinine, glucose: o

Low bicarbonate suggests inadequate perfusion.

o

Renal dysfunction or failure indicates a worse prognosis.



Ca, Mg, Ph



C-reactive protein



Cortisol level



International norm alized ratio/prothrom bin tim e/partial throm boplastin tim e



Type and screen



Liver function tests



Arterial blood gas: o

Mixed acidâ€“base abnorm alities: respiratory alkalosis with m etabolic acidosis



Blood cultures: o

From two different sites

o

One m ay be drawn through an indwelling central line (i.e., Broviac).



Urine analysis and culture

Imaging 

Chest radiograph: o

Determ ine whether pneum onia is the infectious source.

o

Fluffy, bilateral infiltrates m ay indicate that ARDS is already present.

o

Free air under the diaphragm indicates the source of the infection in intraperitoneal and a surgical intervention.



Soft tissue plain film s: o

Indicated if extrem ity erythem a or severe pain

o

Air in the soft tissues associated with necrotizing or gas-form ing infection

Pa ge 4 2 9

P.1007



CT scan of the abdom en and pelvis o

Suspicion of abdom inal source of infection: 

Diverticulitis, appendicitis, necrotizing pancreatitis, m icroperforation of the stom ach or bowel, or form ation of an intra-abdom inal abscess



Abdom inal ultrasound: o



Pelvic ultrasound: o



Indicated for suspected cholecystitis

Tubo-ovarian abscess or endom etritis

Transesophageal echo: o

When endocarditis is suspected to detect the presence of any valvular vegetations



MRI: o

May be useful to identify soft tissue infections or epidural abscess

Diagnostic Procedures/Surgery 

Lum bar puncture: o

Indicated when m eningeal signs are present or altered m ental status without a source of infection

o

Cerebrospinal fluid analysis: 

Cell count and differential, tube 1



Total protein and glucose, tube 2



Culture and gram stain, tube 3



Cell count and differential, tube 4



Depending on the clinical situation: cytology, venereal disease research laboratory, AFB stain/culture, fungal stain



Central venous access:

Pa ge 4 2 9

o

Central venous pressure (CVP) and ongoing m easurem ent of central venous oxim etry catheter m ay be helpful in guiding resuscitation.

Differential Diagnosis 

Pancreatitis



Traum a



Toxic shock syndrom e



Anaphylaxis



Adrenal insufficiency



Drug or toxin reactions



Heavy m etal poisoning



Hepatic insufficiency



Neurogenic shock

Treatment Pre Hospital Aggressive fluid resuscitation for hypotension

Initial Stabilization 

ABCs



Supplem ental oxygen to m aintain PaO 2 >60 m m Hg



Intubation and m echanical ventilation if shock or hypoxia are present



Adm inister 0.9% NS IV

ED Treatment 

Early goal-directed therapy: o

500 cc boluses of 0.9% saline up to 1â€“2 liters em pirically

o

Place central line

Pa ge 4 3 0

o

Continue 500 cc saline boluses until CVP >8 cm H 2 O

o

If the m ean arterial pressure <65 m m Hg and CVP >8, then initiate pressors: 

Dopam ine or norepinephrine to raise blood pressure



Norepinephrine is preferred if tachycardia or dysrhythm ias are present.



Phenyl epinephrine for cases where shock is refractory to other pressors



If the ScvO 2 <70 and HCT <30, transfuse 2 units PRBCs.



If ScvO 2 >70 and HCT >30, then add dobutam ine.



Adm inister antibiotics early based on the m ost likely organism s or site of infection.



If no source identified after initial assessm ent: o

Norm al im m une function: 

Second- or third-generation cephalosporin and gentam icin



Nafcillin and gentam icin



Add vancom ycin if there is a history of m ethicillin resistant staphylococcus aureous or the patient resides in a nursing facility or there is a history of recent hospitalizations.

o

Im m unocom prom ised host: 

Piperacillin and gentam icin



Ceftazidim e and either nafcillin or vancom ycin and gentam icin



If source identified, or highly suspected, treat the m ost likely organism s: o

Pulm onary source: 

Second- or third-generation cephalosporin and gentam icin, and possibly erythrom ycin

o

Intra-abdom inal source:

Pa ge 4 3 0

o



Am picillin and m etronidazole and gentam icin



Cefoxitin and gentam icin

Urinary tract source: 

Am picillin or piperacillin and gentam icin

Pediatric Considerations 

Antibiotic therapy based on age: o

<3 m onths (2 drugs): am picillin and gentam icin or cefotaxim e (50â€“180 m g/kg/d div. q4hâ€“q6h)

o

â‰¥3 m onths: cefotaxim e or ceftriaxone (50â€“100 m g/kg/d div. q12hâ€“q24h)



Initiate vasopressors after no response to 60 m L/kg IV fluid.



Avoid hyponatrem ia and hypoglycem ia.



Dexam ethasone for children with bacterial m eningitis: o

0.15 m g/kg q6h for 4 days

Medication (Drugs) 

Am picillin: 1â€“2 g (peds: 50â€“200 m g/kg/24h) IV q4hâ€“q6h



Cefoxitin: 1â€“2 g (peds: 100â€“160 m g/kg/24h) IV q6hâ€“q8h



Ceftazidim e: 1â€“2 g (peds: 100â€“150 m g/kg/24h) IV q8hâ€“q12h



Dopam ine: 1â€“5 Âµg/kg/m in (renal dose); 5â€“10 Âµg/kg/m in (pressor dose)



Gentam icin: 1â€“1.5 m g/kg (peds: 2â€“2.5 m g/kg q8h) IV q8h



Metronidazole: load with 1 g (peds: 15 m g/kg) IV, then 500 m g (peds: 7.5 m g/kg q6h)



Nafcillin: 1â€“2 g IV q4h (peds: 50 m g/kg/24h div.

Pa ge 4 3 0

q4hâ€“q6h) 

Norepinephrine: 2â€“8 Âµg/m in



Piperacillin: 3â€“4 g IV q4hâ€“q6h



Vancom ycin: 500 m g (peds: 10 m g/kg) IV q6h

Follow-Up Disposition Admission Criteria Sepsis with toxicity, septicem ia, or septic shock requires adm ission generally to an intensive care unit.

Discharge Criteria None

References 1. Carcillo JA, Cunnion RE. Septic shock. Crit Care Clin. 1997;13:553â€“574. 2. Cunha BA. Antibiotic treatm ent of sepsis. Med Clin North Am . 1995;79:351â€“558. 3. Hollenberg SM, Ahrens TS, Annane D, et al. Practice param eters for hem odynam ic support of sepsis in adult patients: 2004 update. Crit Care Med. 2004;32(9):1928â€“1948 4. Jacobs RF, Sowell MK, Moss MM, et al. Septic shock in children: bacterial etiologies and tem poral relationships. Pediatr Infect Dis J. 1990;9:196â€“200. 5. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatm ent of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368â€“1377. 6. Shapiro NI, Wolfe RE, Moore RB, et al. Mortality in Em ergency Departm ent Sepsis (MEDS) score: a prospectively derived and

Pa ge 4 3 0

validated clinical prediction rule. Crit Care Med. 2003;31(3):670â€“676.

Codes ICD9-CM 38.9

ICD10 A41.9

Pa ge 4 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Serum Sickness

Serum Sickness

Kelly Corrigan

Basics Description 

Type III hypersensitivity reaction



When a foreign protein or drug (the antigen) is injected, the body's im m une system responds by form ing antibodies to the foreign m aterial and subsequently form s com plexes com posed of the antigen, antibody, and com plem ent.



These com plexes then deposit in tissue, inciting an inflam m atory response: o

C3a and C5a act as anaphylatoxins.

o

C5a is strongly chem otactic for neutrophils.

o

The neutrophils then infiltrate the vessel wall at the site of the im m une com plex deposition and release enzym es like collagenase and elastase that dam age vessel walls.



Occurs 7â€“10 days after the prim ary exposure to the antigen



Usually starts 12â€“36 hours after ingestion if there is an initial im m unizing exposure



The tim e course for this process is 4â€“14 days.

Etiology

Pa ge 4 3 0

Serum Sickness 

Vaccines containing foreign serum such as pneum ococcal vaccine or rabies.



Antivenom and tetanus inoculations m ade with horse protein

Serum Sicknesslike Reaction 

Drugs that act as haptens



Penicillins, am oxicillin



Cephalosporins (i.e., Cefaclor)



Sulfonam ides (i.e., Bactrim )



Thiazides



Gold



Thiouracils



Hydantoins



Phenylbutazone



Aspirin



Streptom ycin



Rarely observed when anim al-derived proteins are used as vaccines and im m une globulins

Diagnosis Signs and Symptoms History 

Fever



Rash (urticarial or m orbilliform )



Arthralgias



Myalgias



Lym phadenopathy



Facial and neck edem a

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

Splenom egaly



Proteinuria



Peripheral neuritis



Myocarditis/Pericarditis



Anaphylaxis

Essential Workup 

History of a possible offending agent and tim e course of 4â€“14 days before onset of sym ptom s



Physical exam ination revealing rash as well as joint, m uscular, cardiac, neurologic, or renal insult

P.1009

Tests Lab 

Decreased com plem ent levels



CBC, possible eosinophilia



Elevated ESR



Hypergam m aglobulinem ia



Proteinuria or hem aturia

Diagnostic Procedures/Surgery Biopsy is the only m eans of definitive diagnosis.

Differential Diagnosis 

Vasculitides (e.g., polyarteritis nodosa, Goodpasture, Wegener)



Rashes (e.g., erythem a m ultiform e, toxic epiderm al necrolysis)



Im m unologic (e.g., system atic lupus erythem atosus, polym yositis, anaphylaxis)



Infectious (e.g., tickborne disease, Rocky Mountain

Pa ge 4 3 0

spotted fever, m ononucleosis)

Treatment Initial Stabilization ABCs if a severe system ic reaction is present

ED Treatment 

Sym ptom atic relief until the disease spontaneously resolves in 1â€“13 weeks



Antihistam ines



Antipyretics



NSAIDs



Prednisone is controversial.

Medication (Drugs) 

Acetam inophen: 325â€“650 m g PO/PR (peds: 10â€“15 m g/kg) q4hâ€“q6h



Diphenhydram ine: 50â€“100 m g (peds: 5 m g/kg/d, div.) q6hâ€“q8h



Ibuprofen: 200â€“800 m g PO (peds >6 m onths: 5â€“10 m g/kg) q6hâ€“q8h



Prednisone: 0.052 m g/kg PO (peds: 12 m g/kg) per day, 2-week taper

Follow-Up Disposition

Pa ge 4 3 0

Admission Criteria 

Involvem ent of the airway



Relapse of sym ptom s and signs after initial steroids



Im m unosuppression



Concom itant serious disease



Sociologic considerations

Discharge Criteria Stable; m ost cases are self-lim iting in 23 weeks.

References 1. LoVecchio F, Curry SC, Welch S, et al. Incidence of im m ediate and delayed hypersensitivity to Centruroides antivenom . Ann Em erg Med. 1999;34:615â€“619. 2. Piessens WF. System ic im m une com plex disease. In: Ruddy S, ed. Kelley's textbook of rheum atology. 6th ed. Philadelphia, PA: WB Saunders, 2001. 3. Poley GE, Slater JE. Drug and vaccine allergy. Im m unol Allergy Clin North Am . 1999;19:409â€“419. 4. Rosenwasser LJ. The vasculitic syndrom es. In: Goldm an L, ed. Cecil textbook of m edicine. 21st ed. Philadelphia, PA: WB Saunders, 2000:1525â€“1527. 5. Winkelstein JA, Fries LF. The com plem ent system and im m unopathology. In: Middleton E, ed. Allergy: principles and practice. 5th ed. St. Louis, MO: Mosby Year Book, 1998:63â€“64.

Codes ICD9-CM 999.5

ICD10 T80.6

Pa ge 4 3 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sexual Assault

Sexual Assault

Ingrid D. Carter

Basics Description Specific legal definition varies from state to state: 

Defined as forced sexual contact without consent



Any unwanted touching or fondling via force, threat of force, or if person is unable to give consent



Continuum from unwanted touching and fondling to forced penetration of vagina, anus, oral cavity

Etiology 

78â€“82% of fem ale rape victim s are raped by som eone they know.



50% of rape victim s older than 30 years old are assaulted by intim ate partner.



Am ong wom en suffering physical abuse by partner, 33â€“46% report being sexually assaulted.



Age distribution of fem ale rape victim s: o

11â€“17 years old: 32%

o

18â€“24 years old: 22%

o

50 years old: 22%

Pa ge 4 3 1

Diagnosis Signs and Symptoms 

Victim s m ight not disclose assault: o

Approxim ately 70% of rape victim s do not tell their doctors.

o

Most will reveal history only in response to direct questions.



Tachycardia or pounding heart beat



Headaches



Nausea



Back pain



Skin problem s



Menstrual sym ptom s



Sudden weight change



Sleeping disorders



Abdom inal pain



Trouble breathing



Associated injuries: o

Of those with injuries, 70% report no injury at presentation.

o

Lacerations of perineum

o

Vulvar traum a

o

Laceration of vaginal wall (m ore com m on in younger patients near introitus)

o

Multiple contusions

o

Abrasions

o

Hum an bite

o

Lacerations or puncture wound to extrem ity

o

Burns

o

Depressed skull fracture

Pa ge 4 3 1

Pediatric Considerations 

Must follow local laws regarding child abuse



Patient m ost likely never had pelvic exam previously; if possible, involve specialist.



Use sm allest speculum possible.



Use toys and dolls to have child explain what happened.



Early psychiatric intervention necessary

Essential Workup 

Obtain written consent prior to any exam , test, or treatm ent.



Allow patient to pause and proceed at com fortable pace.



Allow advocate to stay with patient during exam with patient's consent.

History 

Obtain com plete history even if patient does not wish to file charges, including: o

Tim e and place of assault

o

Physical description of assailants

o

Num ber of assailants

o

Types of penetration: vaginal, oral, rectal

o

Assailant ejaculation, if assailant used condom

o

Any bodily fluid exchange

o

Use of force, weapons, restraints, drugs or alcohol

o

If victim has m em ory loss or loss of consciousness

o

Victim 's activity since assault: 

Changed clothes



Douched



Bathed



Urinated



Defecated



Ate

Pa ge 4 3 1



Tam pon use

o

Full gynecologic history

o

Last voluntary intercourse

o

Sperm m ay be m obile up to 5 days in cervix and 12 hours in vagina.



Address all physical com plaints.

Physical Exam 

Use local evidence kit even if victim unsure if reporting to police.



Fem ale chaperone required if m ale physician



If clothes soiled, photograph prior to undressing with patient's consent.



Note em otional state of victim .



Note general appearance of clothes: o

Staining

o

Tears

o

Mud

o

Leaves

o

Wood lam p for sem inal stains

o

Have patient disrobe while standing on sheet and place all clothes in paper bag. 

Plastic causes m old and increases bacteria counts.



o

Have only patient handle clothing.

o

Arrange for change of clothes.

Com plete physical should be done with em phasis on: o

Abrasions

o

Lacerations

o

Bites

o

Scratches

o

Foreign bodies

o

Ecchym oses

Pa ge 4 3 1

o

Dried sem en on skin

P.1011



Forensic collection: o

Fingernail scrapings

o

Scalp or pubic hair sam ples

o

If oral penetration, swab between teeth for acid phosphatase (assay for sem en) and sperm .

o 

Throat culture for gonorrhea/chlam ydia if oral sex

Gynecologic exam : o

Explain all steps and allow patient to pace exam .

o

Com b and collect pubic hair per local protocol.

o

Lubricate speculum with water.

o

Look for genital traum a even in asym ptom atic patients.

o

May use toluidine blue to identify sm all pelvic lacerations from traum atic intercourse: 

o

Best applied to vaginal m ucosa at introitus

Special attention to hym en as one of m ost com m on places for traum a

o

Lacerations to vaginal wall near introitus m ore com m on in younger patients

o

Aspirate secretions pooled in posterior fornix and place in sterile container to be exam ined for sperm and acid phosphates: 

If no secretions in posterior fornix, wipe with cotton tip.



Swab and m icroscopically exam ine for sperm and acid phosphates.

o

Swabs for gonorrhea and chlam ydia: 

Controversial; evidence can be used by defense

Pa ge 4 3 1

to show prom iscuity. o

Colposcope allows visualization of sm all lesions and ability to photograph findings.

o

Rectal exam and cultures for gonorrhea and chlam ydia if penetration or attem pted penetration

Tests Lab 

Syphilis serology



Hepatitis band C panel



HIV testing and counseling



Drug testing (if suspect victim was drugged, can be used against victim if other agents detected)



Blood type



Pregnancy test



Gonorrhea culture



Chlam ydia culture



Other labs as needed based on injuries

Imaging As indicated by injuries

Diagnostic Procedures/Surgery As indicated by injuries

Treatment Initial Stabilization Treat life-threatening injuries.

ED Treatment 

Place patient in quiet, private room .

Pa ge 4 3 1



Assure patient of confidentiality regarding nam e and reason for visit.



Regularly assure patient of safety.



Enforce nonjudgm ental behavior by staff.



Designate nursing and m edical provider for entire stay who is fam iliar with evidence collection kit.



Have sexual assault nurse exam iner (SANE) perform exam if available.



Contact com m unity or in-hospital advocate to stay with patient while in ED.



Alert hospital security to possibility of assailant presenting to ED.



Contact police if patient consents or local law requires.



Collect evidence as outlined above and according to local law.



Adm inister pregnancy prophylaxis if not currently pregnant: o

Estim ated risk of pregnancy is 2â€“4% if wom an not using contraceptives.

o

Horm onal therapy if within 72 hours: 

Levonorgestrel 0.75 m g stat and repeat in 12 hours (preferred) or



Ethinyl estradiol 100 Âµg stat and repeat in 12 hours

o

72 hours to 7 days post-assault 

Consult obstetrics and gynecology (ob/gyn) for possible intrauterine device (IUD) placem ent.



Adm inister prophylactic therapy for gonorrhea, chlam ydia, trichom onas: o

Ceftriaxone 125 m g IM

o

Doxycycline 100 m g PO b.i.d. for 7â€“10 days or

o

Azithrom ycin 1 g PO (single dose)

Pa ge 4 3 1

o

Flagyl 2 g PO (single dose)



Consider prophylactic therapy for HIV.



Consider prophylactic therapy or vaccine for Hepatitis B.

Follow-Up Disposition Admission Criteria Serious traum atic injury

Discharge Criteria 

Medical follow-up for culture and HIV test results



Offer m ental health services and counseling.



Safe place for patient to go to

References 1. Burgess AW, Fawcett J. The com prehensive sexual assault assessm ent tool. Nurse Pract. 1996;21:66. 2. Dunn SFM, Gilchrist VJ. Sexual assault. Prim Care. 1993;20:359â€“373. 3. Dupre AR, Ham pton HL, Morrison H, et al. Sexual assault. Obstet Gynecol Surv. 1993;45:640â€“648. 4. Levine DL, Kaufm an LE. Rape and sexual violence: the adult and adolescent fem ale victim . In: Bernstein E, Bernstein J, eds. Case Studies in Em ergency Medicine and the Health of the Public. Boston: Jones & Bartlett; 1996:100â€“112.

Codes ICD9-CM V71.5

ICD10

Pa ge 4 3 1

T74.2

Pa ge 4 3 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sho ck

Shock

Nathan Shapiro Christopher Fischer

Basics Description 

Inadequate supply of blood flow to tissues to m eet the dem ands of the tissues



Nutrient requirem ents are not fulfilled.



Toxic m etabolites are not rem oved.



If untreated, inevitable progression from inadequate perfusion to organ dysfunction and ultim ately to death.



Main com ponents of blood flow: o

Cardiac output

o

Blood volum e

o

Peripheral resistance of arteriolar and venous system (system ic vascular resistance [SVR])



Major categories of shock: o

Hypovolem ic shock: 

Decreased blood volum e



Suspect hem orrhage if acute onset



Severe dehydration if progressive onset and elevated hem atocrit, blood urea nitrogen, and creatinine

Pa ge 4 3 1



Decrease in cardiac output leads to com pensatory increase of the SVR in an attem pt to norm alize perfusion pressure.

o

Obstructive (cardiogenic) shock: 

Decreased cardiac output and tissue hypoxia with adequate intravascular volum e and m yocardial dysfunction



Venous congestion with increase in central venous pressure

o



Com pensatory increase in SVR



Causes of decreased cardiac output



Cardiac dysfunction with reduced contractility



Obstruction to inflow of blood to the heart



Obstruction to outflow of blood from the heart

Septic shock: 

An initial infectious insult overwhelm s the im m une system .



Biochem ical m essengers (leukotrienes, histam ines, prostaglandins) cause vessel dilatation.



Capillary endothelium becom es disrupted and the vessels leak.



Drop in SVR leads to inadequate tissue perfusion.



Secondarily, decreased cardiac output from â€œcardiac stunâ€• resulting in cold septic shock

o

Neurogenic shock: 

Spinal chord insults disrupt sym pathetic stim ulation to vessels.



Loss of sym pathetic tone causes arteriodilating and vasodilatation.

Pa ge 4 3 2



Lesions proxim al to T4 disrupt sym pathetic, spares vagal innervation causing bradycardia.

o

Anaphylactic shock: 

An antigen stim ulates the allergic reaction.



Mast cells degranulate.



Histam ine releases along with autocoids stim ulate an anaphylaxis cascade.

o



Vascular sm ooth m uscle relaxes.



Capillary endothelium leaks.



Drop SVR leads to inadequate tissue perfusion.

Pharm acologic agents m ay cause shock through sm ooth m uscle dilation or m yocardial depression.

Etiology See differential diagnosis.

Diagnosis Signs and Symptoms 



Generalized shock: o

Hypotension

o

Decreased peripheral pulses

o

Tachycardia

o

Tachypnea

o

Decreased urine output

o

Diaphoresis

o

Obtundation

o

Lethargy

Hypovolem ic shock: o

Cold and clam m y extrem ities

o

Pallor

Pa ge 4 3 2









o

Flattened neck veins

o

Decreased capillary refill

o

Narrowed pulse pressure

Cardiogenic shock: o

Chest pain/pressure

o

Dyspnea

o

Orthopnea

o

Jugular venous distention

o

Cool, clam m y, sweaty extrem ities

o

Rales

o

Wheezes

o

Dullness at lung bases

o

S3 gallop

Septic shock: o

Warm flushed extrem ities

o

Strong pulses

o

Hypertherm ia

o

Hypotherm ia

o

Purpura or petechial rash

Anaphylactic shock: o

Warm flushed extrem ities

o

Urticaria

o

Stridor

o

Throat tightness

o

Hoarseness

o

Wheezing

Neurogenic shock: o

Flaccid paralysis

o

Loss of rectal tone

o

Hypotension with bradycardia

Essential Workup 

Identify type or types of shock present.

Pa ge 4 3 2



Identify underlying cause of shock.

Tests Lab 





Hem oglobin/Hem atocrit: o

Low hem oglobin and hem atocritâ€”hem orrhage

o

Very high hem atocritâ€”dehydration

o

Poor m arker with acute hem orrhage

WBC: o

Highâ€”nonspecific m arker of infection

o

Lowâ€”neutropenic infections

Electrolytes: o

Low CO 2 â€”acidosis

o

Increased blood urea nitrogen (gastrointestinal hem orrhage)

o

Increased Na, K, Cl, blood urea nitrogen/creatinine (dehydration)





Blood glucose: o

High (diabetic ketoacidosis or septic shock)

o

Low (pediatric sepsis)

Prothrom bin tim e/partial throm boplastin tim e o

Increased in dissem inated intravascular co-agulation, septic shock, and liver disease



Cardiac enzym es



Urinalysis:



o

High glucose/ketones (DKA or septic shock)

o

WBCs and bacteria in urosepsis

Beta-hum an chorionic gonadotropin: o

Wom en of childbearing age at risk for a ruptured ectopic pregnancy



Lactic acid level: o

Anaerobic m etabolism , cell dysfunction, and organ

Pa ge 4 3 2

dam age leads to release of lactic acids when organ dem ands exceed nutrient supply. o

Good surrogate m arker of shock state

Imaging 

ECG: o

Assess for ischem ia and other disorders of cardiac m uscle: 

Electrical alternans or low voltage with cardiac tam ponade

 







Right heart strain with pulm onary em bolism

Chest radiograph: o

Pneum onia

o

Pulm onary edem a

o

Pneum othorax

o

Hem othorax

o

Pulm onary infarction

o

Traum atic injuries

Echocardiography: o

Tam ponade

o

Wall m otion abnorm alities (m yocardial ischem ia)

o

Right ventricle strain (pulm onary em bolus)

o

Aortic dissection

Abdom inal ultrasound: o

Intraperitoneal hem orrhage

o

Ectopic pregnancy

CT abdom en: o

Requires that the patient first be stabilized

o

In the setting of abdom inal traum a and in search for suspicion of abdom inal infection

Differential Diagnosis 

Hypovolem ic shock:

Pa ge 4 3 2

o

Abdom inal traum a, blunt or penetrating

o

Abortionâ€”com plete, partial, or inevitable

o

Anem iaâ€”chronic or acute

o

Aneurysm sâ€”abdom inal, thoracic, dissecting

o

Aortogastric fistula

o

Arteriovenous m alform ations

o

Blunt traum a

o

Burns

o

Diabetes

o

Diarrhea P.1013





o

Diuretics

o

Ruptured ectopic pregnancy

o

Epistaxis

o

Fractures (especially long bones)

o

Hem optysis

o

Gastrointestinal bleed

o

Mallory-Weiss tear

o

Penetrating traum a

o

Placenta previa

o

Postpartum hem orrhage

o

Retroperitoneal bleed

o

Severe ascites

o

Splenic rupture

Toxic epiderm al necrolysis: o

Vascular injuries

o

Vom iting

Cardiogenic shock: o

Cardiom yopathy

o

Conduction abnorm alities and arrhythm ias

Pa ge 4 3 2



o

Myocardial infarction

o

Myocardial contusion

o

Myocarditis

o

Pericardial tam ponade

o

Pulm onary em bolus

o

Tension pneum othorax

o

Valvular insufficiency

o

Ventricular septal defect

Vasogenic shock: o

Acute respiratory distress syndrom e

o

Bacterial infection

o

Bowel perforation

o

Cellulitis

o

Cholangitis

o

Cholecystitis

o

Endocarditis

o

Endom etritis

o

Fungem ia

o

Infected indwelling prosthetic device

o

Intraabdom inal infection or abscess

o

Mediastinitis

o

Meningitis

o

Myom etritis

o

Pelvic inflam m atory disease

o

Peritonitis

o

Pyelonephritis

o

Pharyngitis

o

Pneum onia

o

Septic arthritis

o

Throm bophlebitis

o

Tubo-ovarian abscess

o

Urosepsis

Pa ge 4 3 2



Anaphylactic: o

Drug reaction (m ost com m only to aspirin, beta-lactam antibiotics)

o

Exercise (rare)

o

Food allergy (peanuts, tree nuts, shellfish, fish, milk, eggs, soy, and wheat account for 90% of food related anaphylaxis)





o

Insect sting

o

Latex

o

Radiographic contrast m aterials

o

Synthetic products

Pharm acologic: o

Antihypertensives

o

Antidepressants

o

Benzodiazepines

o

Cholinergics

o

Digoxin

o

Narcotics

o

Nitrates

Neurogenic: o

Spinal chord injury

Treatment Initial Stabilization 

Large-bore IV access: o

When possible, central venous access and m onitoring



Fluid resuscitation in noncardiogenic shock patients



Control bleeding with direct pressure m easures.



Long bone traction



Stabilization of pelvis with sheet or com m ercial device or

Pa ge 4 3 2

external fixation

ED Treatment 

Hypovolem ic shock: o

Identify source of volum e depletion

o

Aggressive fluid resuscitation keeping systolic blood pressure (SBP) >100 m m Hg until definitive treatm ent

o

2â€“3 L crystalloid initially

o

Packed red blood cells if 2â€“3 L crystalloids do not im prove SBP

o

Identify source of bleeding and rapidly m ove toward definitive treatm ent.

o

Dopam ine and epinephrine in refractory shock after m axim al fluid and blood product resuscitation with delayed hem orrhage control

o

Thoracotom y and aortic cross-clam ping in refractory shock with penetrating torso traum a



Cardiogenic shock: o

Ease work of breathing with intubation

o

Insult-specific therapy (e.g., throm bolytics for MI, pericardiocentesis for pericardial tam ponade)

o 



Treat dysrhythm ias.

Septic shock: o

Aggressive crystalloid fluid resuscitation

o

Titrate fluid to urine output >30 cc/h

o

Blood product transfusion to m aintain HCT 30â€“35%

o

Early antim icrobial therapy

o

Inotropic support as needed

o

Dopam ine or norepinephrine infusion

Anaphylactic shock: o

Intubation for airway com prom ise

o

Epinephrine

Pa ge 4 3 2

o

Subcutaneous in noncritical settings

o

Intravenous drip for im m ediate life threats or refractory hypotension

o

H-1 blockers (diphenhydram ine)

o

H-2 blockers (cim etidine)

o

Corticosteroids (hydrocortisone or m ethylprednisolone)

o

Nebulized Î² 2 -antagonists for bronchospasm

o

Patients taking beta-blockers m ay be m ore likely to experience severe sym ptom s of anaphylaxis that m ay m anifest as paradoxical bradycardia, profound hypotension, and severe bronchospasm .





Pharm acologic shock: o

Supportive therapy

o

Decontam ination of overdoses with charcoal

o

Inotropic agents as needed

o

Drug specific antidotes

Neurogenic shock: o

Supportive therapy

o

Traction and fracture stabilization

o

Corticosteroids

Medication (Drugs) 

Albuterol: 2.5 m g/2.5 cc nebulizer PRN



Calcium gluconate: 100â€“1,000 m g IV



Cim etidine: 300 m g IV



Diphenhydram ine: 50â€“100 m g IV over 3 m inutes



Dobutam ineâ€”5â€“40 Âµg/kg/m in IV: o

Dopam inergic: 1â€“3 Âµg/kg/m in IV

o

Beta effects: 3â€“10 Âµg/kg/m in IV

o

Alpha/Beta effects: 10â€“20 Âµg/kg/m in IV

Pa ge 4 3 2

o 

Alpha effects: 20 Âµg/kg/m in IV

Epinephrine: o

1â€“4 Âµg/m in IV infusion

o

SQ/IM 1:1000 0.1â€“0.3 m g repeat q5m inâ€“q20m in Ã— 3 PRN

o 

IV 1:10,000 10 m L (1 m g) over 10 m in IV

Glucagon: 1â€“5 m g IV bolus initial, then 1â€“20 m g/h infusion



Hydrocortisone: 5â€“10 m g/kg IV



Methylprednisolone: 1â€“2 m g/kg IV



Naloxone: 0.01 m g/kg IV initial, titrate to effect



Norepinephrine start: 2â€“4 Âµg/m in IV, titrate up to 1â€“2 Âµg/kg/m in IV



Phenylephrine: 40â€“180 Âµg/kg/m in IV

Follow-Up Disposition Admission Criteria 

All patients in shock need to be adm itted.



Intensive care unit (ICU) criteria: o

All patients with persisting shock need ICU m onitoring.



Patients with shock definitively reversed m ay be adm itted to non-ICU setting (e.g., tension pneum othorax that has been decom pressed and chest tube placed).

Discharge Criteria Patients who are in shock should not be discharged hom e from the ED.

Pa ge 4 3 3

References 1. Kline JA. Shock. In: Marx J, et al. eds. Rosen's em ergency m edicine: concepts and clinical practice. St. Louis, MO: Mosby Year Book, 2002: 33â€“47. 2. Rivers E, Nguyen B, Havstad S, et al. Early goal directed therapy in the treatm ent of severe sepsis and septic shock. N Engl J Med. 2001;345:1368â€“1377. 3. Shapiro NI, Howell M, Talm or D. â€œA Blueprint for a sepsis protocol. Academ ic Em ergency Medicine. 2005;12:4:352â€“359.

Codes ICD9-CM 785.5 785.51

ICD10 R57.9

Pa ge 4 3 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sho ulder Dislo catio n

Shoulder

Dislocation Doodnauth Hiraman Wallace Carter

Basics Description 

Shoulder very dynam ic joint prone to injury



Anterior dislocation (90â€“96%): o

Injury is from direct or indirect forces on the abducted and externally rotated arm .

o

Injury m ay also result from a direct blow to posterior lateral aspect of shoulder.



Posterior dislocation: o

Often m issed

o

Forces on the adducted and internally rotated arm result in posterior dislocation of hum eral head in relation to glenoid fossa.

o

Most com m on m echanism is seizure and sudden contraction of all the posterior m uscle groups.

o

Other m echanism s include electrocution and direct blow to anterior shoulder.



Inferior dislocation (rare):

Pa ge 4 3 3

o

Luxatio erecta

o

Hyperabduction of arm , tear of rotator cuff, and rotation of arm 180Â° above head

o

Com m only seen after a fall from a height: 

Arm has struck object on descent and is thrust above the head.

o

Often accom panied by neurovascular injury and fracture

Pediatric Considerations 

Dislocation is rare in children: o

Epiphysial fractures m ust be suspected.

Geriatric Considerations Dislocation is often accom panied by fracture.

Etiology 

Falls from height



Im pact injuries



Distraction injuries of upper arm



Seizures



Electrocution

Diagnosis Signs and Symptoms 

Severe pain in the affected shoulder



Anterior dislocation: o

Shoulder is squared off.

o

Prom inent acrom ion process and palpable anterior fullness

o 

Arm is held in slight abduction and external rotation.

Posterior dislocation:

Pa ge 4 3 3

o

Coracoid process is prom inent, with a palpable posterior bulge.

o 

Arm is held in slight adduction and internal rotation.

Inferior dislocation (luxatio erecta): o

Rare but easy to identify

o

Arm is shortened and fixed above head as if raised to ask a question.



Head of hum erus m ay be palpable on the lateral chest wall.

Essential Workup 

Evaluate neurovascular status of distal arm .



Retest neurovascular status after any m anipulation.



Dislocation requires prom pt treatm ent: o

Incidence of posttraum atic arthritis increases with tim e dislocation is untreated.

o

Plain film s of the shoulder should be obtained im m ediately.

o

Even in clinically obvious cases, film s should be obtained before m anipulation unless a significant delay will result.

o

An im pacted hum eral head fracture m ay be converted to a displaced hum eral head fracture if m anipulated.

Tests Imaging 

At least two views should be obtained: o

Anteroposterior: 

o

Trans-scapular Y or axillary view: 



To visualize dislocation or fracture

To visualize if anterior or posterior

Anterior dislocation:

Pa ge 4 3 3

o

Posterolateral com pression fracture of the hum eral head (Hills-Sachs deform ity)

o

Corresponding lesion on anterior glenoid rim is the Bankart lesion: 

o

These do not require treatm ent.

Fractures of the greater tuberosity of the hum eral head are seen in 15â€“35%: 

If there is >1-cm displacem ent after reduction, surgical intervention m ay be necessary.



Posterior dislocation: o

Often m issed on anteroposterior film 

Degree of overlap on radiographic film is sm aller and displaced superiorly, producing the m eniscus sign.



Rotated hum erus yields â€œlight bulb on a stickâ€• finding on anteroposterior view.

o

Reverse Hill-Sachs deform ity from com pression fracture of the anterior m edial hum eral head m ay also be seen.

Differential Diagnosis 

Fracture of the hum eral head



Fracture of the hum eral shaft



Acrom ioclavicular injury



Septic shoulder joint



Hem arthrosis in shoulder joint



Scapular fracture



Cervical spine injury

P.1015

Pa ge 4 3 3

Treatment Pre Hospital Neurovascular injury should be identified and the arm splinted in the position of m ost com fort.

Initial Stabilization 

Airway m anagem ent and resuscitate as indicated.



Exclude m ore serious injuries especially in m ultitraum a patient.



Ensure no injury to axillary nerve or vessels.

ED Treatment 

Adequate analgesia and m uscle relaxation are essential for successful reduction: o

Procedural sedation with a short-acting opioid and a benzodiazepine or

o

Methohexital or etom idate alone

o

In the co-operative patient, intra-articular block only (20 cc of lidocaine 1% or bupivacaine 0.5%) into shoulder joint



Anterior dislocation reduction techniques: o

Scapular m anipulation: 

Patient seated, traction to arm in horizontal plane, countertraction with other hand on clavicle



Second person adducts tip of scapula m edially, m oving glenoid fossa

o

Stim son: 

Patient in prone position with arm dangling over side, hang 10â€“15 lb around wrist; m uscle fatigued over 20â€“30 m inutes

Pa ge 4 3 3

o



Can concurrently use scapular m anipulation



Only one person required

Traction/Countertraction: 

Patient in supine position with continuous longitudinal traction to affected arm



Countertraction from sheet wrapped around chest



Arm internally or externally rotated if unsuccessful after several m inutes

o

External rotation: 

Patient supine; elbow at 90Â°; gentle, slow external rotation of arm



Should be done slowly and with cooperative patient



Posterior dislocation reduction techniques: o

May use Stim son or traction/countertraction techniques with m anipulation of hum eral head anteriorly



Inferior dislocation (luxatio erecta) reduction techniques: o

Patient in supine position; gentle longitudinal traction to distract hum eral head

o

Gentle countertraction with sheet draped over trapezius and chest

o 

Arm slowly rotated from 180â€“0Â°

Postreduction care: o

Post reduction film s

o

Place in sling and swath or shoulder im m obilizer im m ediately after reduction.

o

Shoulder should rem ain im m obilized for 2â€“3 weeks in young patients.

o

Im m obilization tim e should be less in older patients to avoid frozen shoulder.

Pa ge 4 3 3

Medication (Drugs) 

Bupivacaine 0.5%: 20 cc intra-articular to shoulder



Diazepam : 5â€“10 m g IV (peds: 0.2 m g/kg)



Etom idate: 0.2 m g/kg IV (adult and peds)



Fentanyl: 50â€“100 Âµg IV (peds: 2â€“4 Âµg/kg)



Lidocaine 1%: 20 cc intra-articular to shoulder



Methohexital: 1â€“1.5 m g/kg IV (peds: not routinely used)



Midazolam : 2â€“5 m g IV (peds: 0.035â€“0.1 m g/kg)



Morphine: 2â€“8 m g IV (peds: 0.1 m g/kg)



Propofol: 1â€“2 m g/kg IV

Follow-Up Disposition Admission Criteria 

Failure to reduce shoulder m ay require adm ission for reduction under general anesthesia or open reduction.



Patients with neurovascular com prom ise

Discharge Criteria 

Patients with successful reductions, confirm ed by plain film s, m ay be discharged with shoulder in appropriate im m obilizer and with orthopaedic follow-up.



Recurrent dislocation m ay require elective surgery.



Patients with residual neuropraxia from injury or m anipulation m ay be safely discharged with instructions that m ost sym ptom s will resolve, but should have neurology follow-up.

Pa ge 4 3 3

Issues for Referral 

Patients with residual neuropraxia should be advised to see a neurologist.



Routine orthopaedic consultation should be advised with all successful reductions.

References 1. Hendey GW. Necessity of radiographs in the em ergency departm ent m anagem ent of shoulder dislocations. Ann Em erg Med. 2000;36(2):108â€“113. 2. Kahn J. The Role of Post-Reduction X-rays after Dislocation. Acad Em erg Med. 2001;8(5):521. 3. McNam ara RM: Reduction of anterior shoulder dislocations by scapular m anipulation. Ann Em erg Med. July 1993;22(7):1140â€“1144. 4. Perrron AD, et al. Acute com plications associated with shoulder dislocation at an academ ic Em ergency Departm ent. J Em erg Med. 2003;24(2):141â€“145. 5. Quillen DM, et al. Acute Shoulder Injuries. Am Fam ily Physician. 2004;70(10):1947â€“1954. 6. Ufberg JW, et al. Anterior Shoulder Dislocations: Beyond Traction-Countertraction. J Em erg Med. 2004;27(3):301â€“306.

Codes ICD9-CM 831.00 S43.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sick Sinus Syndro m e

Sick Sinus

Syndrome David F. M. Brown Jennifer L. Chan

Basics Description Definition Dysfunction of the sinus node's autom aticity and conductivity to the atria

Mechanism 

Caused by progressive degeneration of the cardiac conduction system



Characterized by periods of unexplained sinus node dysfunction leading to bradyarrhythm ias often without appropriate atrial or junctional escape rhythm s



Dysfunction from failure of im pulse generation or conduction to atrial tissue



Syndrom e includes: o

Chronic sinoatrial (SA) nodal dysfunction

o

Frequently depressed pacem akers

o

Arteriovenous nodal conduction disturbances

o

Sluggish return of SA nodal activity after DC

Pa ge 4 3 4

cardioversion

Etiology Intrinsic Causes 

Sinus node fibrosis



Coronary artery or SA nodal artery disease



Cardiom yopathy



Hypertensive heart disease



Infiltrative cardiac or collagen vascular disease



Surgical traum a



Inflam m atory diseases: o

Rheum atic heart disease

o

Chagas

o

Pericarditis

Extrinsic Causes 

Drugs: o

Beta-blockers, calcium -channel blockers, clonidine

o

Digoxin, am iodarone

o

Lithium , phenytoin



Autonom ically m ediated syndrom es



Hyperkalem ia/Hypokalem ia



Ischem ia



Hypothyroidism



Hypotherm ia



Hypoglycem ia



Sepsis/Infection

Pediatric Considerations Associated with m ajor cardiovascular surgical interventions (e.g., repair of transposition of the great vessels)

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Diagnosis Signs and Symptoms History 

Asym ptom atic



Palpitations/Fatigue



Syncope/Presyncope



Chest pain



Shortness of breath



Sudden death

Physical Exam 

Bradycardia



Alternating bradycardia and atrial tachycardia



Altered m ental status



Cyanosis



Transient ischem ic attack/stroke



Tachypnea

Essential Workup 

Ascertaining etiology



12-lead ECG



Chest radiograph

Tests Lab 

Serum electrolytes (including m agnesium and calcium )



Cardiac m arkers



Digoxin level, if appropriate



Thyroid function testing

Imaging ECG: 

Inappropriate sinus bradycardia

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

Sinus pauses or sinus exit block



Atrial fibrillation with slow ventricular response



Prolonged pauses after cardioversion or carotid m assage



Bradyarrhythm ias m ay alternate with supraventricular tachydysrhythm ia.

Differential Diagnosis 

Other bradyarrhythm ias



Electrolyte derangem ents



Medication toxicity: beta-blockers, calcium -channel blockers, clonidine, digoxin



Excessive vagal tone

P.1017

Treatment Pre Hospital 

Advanced life support transport



Oxygen supplem entation



Cardiac m onitoring



Atropine if bradycardic and hem odynam ically unstable



Transcutaneous pacing for unstable patients

Initial Stabilization 

Atropine if a bradydysrhythm ia is causing unstable signs/sym ptom s: angina, m ental confusion, or hypotension



Transcutaneous pacing if atropine unsuccessful



If this fails, em ergent transvenous pacing

ED Treatment

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

Supraventricular tachydysrhythm ia alternating with bradycardia: o

Unstable: 

Cardiovert



Anticipate subsequent profound bradycardia

o

Stable patients:

o

Cardiac m onitoring 

Digoxin, diltiazem , verapam il, or m agnesium can be used



Any m edication m ay cause profound bradycardia.



Bradycardias: o

Discontinuation of m edications that alter sinus node function

o

Identifying other rem ediable causes of SA nodal depression

o

Warm ing in the setting of hypotherm ia as atropine m ay cause m yocardial instability



Anticoagulation patients with atrial fibrillation and bradycardia/tachycardia syndrom e.

Medication (Drugs) 

Atropine: 0.5â€“1.0 m g IV/ET: o

Repeat q5m in as necessary, m ax. dose of 0.04 m g/kg (peds: 0.02 m g/kg, m inim um , 0.1 m g)



Diltiazem : 0.25 m g/kg IV over 2 m inutes followed in 15 m inutes by 0.35 m g/kg IV over 2 m inutes



Verapam il: 2.5â€“5 m g IV bolus over 2 m inutes o

May repeat with 5â€“10 m g q15â€“30m in m ax. 20 m g

o

Peds: <1 year: 0.1â€“0.2 m g/kg over 2 m inutes; repeat q30m in 1â€“15 years: 0.1â€“0.3 m g/kg over 2

Pa ge 4 3 4

m inutes, m ax. dose 5 m g/dose, can repeat once. 

Digoxin: 0.5 m g IV initially then 0.25 m g IV q4h until desired effect (m ax. 1 m g IV)



Isoproterenol: 2â€“3 m cg/m in IV, titrate to goal heart rate/blood pressure, m ax. 10 m cg/m in (peds: 0.1 m cg/kg/m in)â€”do not co-adm inister with epinephrine



Epinephrine: 1 m g IV (peds: 0.01 m g/kg IV)â€”for cardiac arrest



Glucagon: 0.05â€“0.15 m g/kg IV (peds: 0.05â€“0.10 m g/kg)



Heparin: load 80 IU/kg IV; infusion at 18 IU/kg/h



Magnesium : 1â€“2 g IV

Follow-Up Disposition Admission Criteria 

New onset



Sym ptom atic: congestive heart failure, syncope, chest pain



Persistent bradyarrhythm ia or tachydysrhythm ia



Advanced age older than 60 years



Patients should be adm itted to a telem etry floor with cardiology consultation.



Most will require perm anent pacing.

Discharge Criteria 

Asym ptom atic, otherwise healthy patients can be evaluated as outpatients.



Holter m onitoring



Exercise testing

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Issues for Referral 

Need for form al cardiac electrophysiology evaluation



Need for perm anent pacem aker placem ent

References 1. Brady W, Harrigan R. Evaluation and m anagem ent of bradyarrhythm ias in the em ergency departm ent. Em erg Med Clin North Am . 1998;16(2):361â€“388. 2. Kaushuk V, Leon A, Forrester J, et al. Bradyarrhythm ias, tem porary and perm anent pacing. Crit Care Med. 2000;28:N121â€“N128. 3. Mangrum J, DiMarco M. Prim ary care: the evaluation and m anagem ent of bradycardia. N Engl J Med. 2000;342:703â€“709. 4. Rubenstein JJ, Schulm an CI, Yurchak PM, et al. Clinical spectrum of the sick sinus syndrom e. Circulation. 1972;46:513.

Miscellaneous SEE ALSO: Bradydysrhythm ia

Codes ICD9-CM 427.81

ICD10 I49

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sickle C ell Disease

Sickle Cell Disease

Steven H. Bowman

Basics Description 

Affects m ultiple organ system s



Inherited autosom al-recessive disorder caused by a single am ino acid substitution in hem oglobin gene



Abnorm al hem oglobin (hem oglobin S) polym erizes under stress, deform s RBC, resulting in hem olysis, vaso-occlusion, tissue ischem ia, and infarction.



Occurs in people of African, Mediterranean, Middle Eastern, and Indian descent



Severity is variable, even am ong the sam e phenotype.



Vaso-occlusion, ischem ia, and infarction crises occur in essentially all organ system s: o

Bone/Joint crises: 

Vaso-occlusion of bone m icrovasculature causes infarction.



Dactylitis â€œhand-foot syndrom eâ€• occurs at ages 6â€“24 m onths.

o

Chest crisis or syndrom e: 

Vaso-occlusion of pulm onary vasculature with infarcts

Pa ge 4 3 4



Fat em bolism , viral and bacterial infections m ay contribute.

o



High m ortality (2â€“14%)



More com m on in children



Difficult to distinguish from pneum onia

Splenic sequestration: 

Splenic sinusoids becom e congested with sickled RBCs and obstruct outflow.



High m ortality (12â€“20%)



May be rapidly fatal



More com m on in children younger than 5 years, rare in adults

o

Aplastic crisis: 

Bone m arrow suppression usually occurs secondary to viral infection.



Increased baseline hem olysis in patients with sickle cell disease requires m axim um erythropoiesis.

o



Decrease in hem atocrit m ay be severe.



Generally self-lim ited



More com m on in children

Cerebrovascular accident/transient ischem ic attack (TIA): 

Secondary to infarction in children; hem orrhage in adults



Peak incidence between ages 9 and 15 years; prevalence 5â€“20%

 o

Often preceded by TIAs

Bacterial infection: 

Sepsis is the leading cause of death in patients with sickle cell disease.



Ability to fight encapsulated organism s is

Pa ge 4 3 4

im paired secondary to decreased splenic function. 

Children younger than 5 years have 400-fold increase in pneum ococcal infections.



Streptococcus pneum oniae, Haem ophilus influenzae, Staphylococcus aureus, Escherichia coli, and Salm onella are leading organism s.



Sites: lung, CNS, bone, kidney

Genetics Genotypes/phenotypes/severity/incidence in African Am ericans: 

SS, sickle cell disease, m arked severity, 0.3%



SC, SC disease, m ild to m oderate severity, 0.1%



Stahl, Î²-thalassem ia, m ild to m oderate severity, <0.1%



AS, sickle cell trait, no m anifestation of disease, 8%

Etiology Com m on crisis precipitants: 

Infection (bacterial and viral)



Dehydration



Hypoxem ia



Acidosis



Surgery/Traum a



Weather changes



Pregnancy



Toxins

Diagnosis Signs and Symptoms 

May present with either: o

Painful episode

Pa ge 4 3 4



o

Com plications of the disease

o

Com bination of above

Acute painful episodes: o

o

o 

Bone/Joint crisis: 

Pain in extrem ities, back, sternum , or joints



Variable swelling, warm th



Variable joint effusion



Hand-foot syndrom e in infants

Abdom inal crisis: 

Abdom inal pain without peritonitis



Variable nausea, vom iting, diarrhea

Priapism â€”prolonged painful erection

Com plications/Progression of disease: o

o

o

Chest crisis (or syndrom e): 

Pleuritic chest pain



Cough with variable hem optysis



Dyspnea



Tachypnea



Rales

Splenic sequestration crisis: 

Abdom inal pain



Splenom egaly



Variable nausea, vom iting



Fatigue, lethargy



Pallor



Tachycardia



Hypotension, syncope, shock

Aplastic crisis: 

Variable fever, headache, nausea, vom iting



Fatigue



Pallor



Tachycardia

Pa ge 4 3 5

o

o

Cerebrovascular accident/TIA 

Focal neurologic deficit



Mental status changes

Infections: 

Fever



Localizing signs

P.1019

Pediatric Considerations 

Infections com m only precipitate crisis.



Patients im m unization history (pneum ococcal and H. influenzae) m ust be confirm ed.



Acute sickle cell com plications in children carry high m orbidity and should be screened for aggressively.

Essential Workup Conduct a thorough physical exam .

Tests Lab 

CBC: o

Anem ia m ay be profound.

o

Com pare with prior values if available.

o

Leukocytosis is com m on and does not necessarily indicate infection.





Reticulocyte count: o

Generally elevated >5.0% in SS individuals

o

A low count m ay indicate an aplastic crisis.

Consider the following if indicated: o

Urinalysis: 

Asym ptom atic hem aturia is a com m on finding.

Pa ge 4 3 5



Urinary tract infection m ay precipitate pain crisis and requires aggressive treatm ent.

o

Electrolytes, blood urea nitrogen/creatinine, glucose

o

Blood cultures

o

Type and screen (or cross)

o

Urine pregnancy test in wom en

Imaging 

Radiographs should be directed to confirm diagnoses: o

Chest radiograph if pneum onia or chest syndrom e suspected



o

Extrem ities if osteom yelitis suspected

o

IV contrast m ay exacerbate or precipitate a crisis.

Head CT/MRI to evaluate stroke.

Differential Diagnosis Sickle cell crises m ay m im ic or obscure m ore serious underlying pathology (e.g., acute abdom en, m yocardial infarction, nephrolithiasis): 

Suspect other diagnoses if pain is m ore severe or atypical.

Treatment Initial Stabilization 



Identify and treat high m orbidity com plications: o

Sepsis

o

Splenic sequestration

o

Chest crisis

o

Central venous access

Assess pain and initiate therapy.

ED Treatment

Pa ge 4 3 5



Analgesia: o

Choice of analgesic agent depends on patient, severity of episode, and prior agents.

o

Evaluate patient frequently and titrate m edications accordingly for relief of pain.



Hydration: o

1.5â€“2 tim es m aintenance after correction of deficits

o

Oral hydration if patient can tolerate fluids by m outh

o

Parenteral IV solution 0.45% NS for adults and children, or 0.2% NS for infants

o 

Monitor fluids closely.

Com plication-specific therapy: o

Oxygen: chest syndrom e, pneum onia

o

Antibiotics: sepsis, pneum onia, osteom yelitis

o

Acute sim ple transfusion: sequestration crisis, blood loss, accelerated hem olysis

o

Exchange transfusion m ay be required for m ore severe com plications: cerebrovascular accident.

Medication (Drugs) 

Severe/m oderate pain: o

Hydrocodone: 0.15/m g/kg/dose PO q4h

o

Hydrom orphone: 0.01â€“0.02 m g/kg/dose IV q3hâ€“q4h or 0.04â€“0.06 m g/kg/dose PO q4h

o

Ketorolac: 30 m g IV initial, then 15â€“30 m g q6hâ€“q8h

o

Meperidine: 0.75â€“1.5 m g/kg/dose IV q2hâ€“q4h

o

Morphine: 0.1â€“0.15 m g/kg/dose IV q3hâ€“q4h or 0.3â€“0.6 m g/kg/dose PO q4h



Mild pain: o

Acetam inophen: 1 g (peds: 15 m g/kg/dose) PO q4h

Pa ge 4 3 5

o

Codeine: 0.5â€“1 m g/kg/dose PO

o

Ibuprofen: 800 m g (peds: 5â€“10 m g/kg/dose) PO q8h

Follow-Up Disposition Admission Criteria 

Refractory pain crisis



Signs of bacterial infection or fever of undeterm ined etiology



Chest syndrom e



Sequestration crisis



Aplastic crisis



Cerebrovascular accident or TIA



Refractory priapism



Sym ptom atic anem ia

Discharge Criteria 

Resolution of pain crisis



No indications for adm ission

References 1. Beutler E. Sickle cell anem ia. In: Beutler E, et al, eds. William s hem atology. 6th ed. New York, NY: McGraw-Hill, 2001:581â€“605. 2. Claster S, Vichinsky EP. Managing sickle cell disease. BMJ. 2003;327(7424):1151â€“1155 3. Stephens C. Sickle cell disease: a review of the state-of-the-art em ergency m anagem ent and outcom e-effective therapy. Em erg Med Rep. 1999;20(18):183. 4. Stuart MJ, Nagel RL. Sickle-cell disease. Lancet.

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2004;364(9442):1343â€“1360. 5. Steinberg M. Managem ent of sickle cell disease. N Engl J Med. 1999;340(13):1021. 6. Wang W, et al. Sickle cell anem ia and other sickling syndrom es. In: Lee G, et al, eds. Wintrobe's clinical hem atology. 11th ed. Baltim ore, MD: Lippincott William s & Wilkins, 2004:1263â€“1311.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sinusitis

Sinusitis

Lee Shockley Maria Moreira

Basics Description 

Inflam m ation of the m ucous m em branes lining the paranasal sinuses



Acute bacterial sinusitis is diagnosed when signs and sym ptom s last fewer than 3â€“4 weeks.



Subacute sinusitis occurs when signs and sym ptom s last 3 weeks to 3 m onths.



Chronic sinusitis occurs when signs and sym ptom s last longer than 3 m onths in spite of antibiotic treatm ent.



Nosocom ial sinusitis is associated with nasogastric and nasotracheal tubes.



Viral sinusitis is 20â€“200 tim es m ore com m on than bacterial sinusitis.



Com plication of sim ple viral upper respiratory tract infection or allergic rhinitis



As m ucous m em branes becom e inflam ed, sinus ostia narrow and block drainage.



Air is absorbed and negative pressure develops, resulting in transudate form ation.

Pa ge 4 3 5



Bacteria are trapped and m ultiply resulting in suppuration and converting the viral infection to a bacterial infection.



Foreign bodies, nasal polyps, tum ors, or traum atic fractures can lead to obstruction of ostia.



Im m unocom prom ised patients and patients with im paired m ucociliary m ovem ent are also predisposed to sinusitis.

Etiology 







Acute sinusitis: o

Haem ophilus influenzae

o

Streptococcus pneum oniae

o

Moraxella catarrhalis

o

Staphylococcus aureus

Chronic sinusitis: o

Staphylococcus aureus

o

Peptostreptococcus

o

Fusobacterium

o

Bacteroides

o

Aspergillus

Nosocom ial sinusitis: o

S. aureus

o

Streptococcal species

o

Pseudom onas

o

Klebsiella

Im m unocom prom ised patients with sinusitis: o

The usual bacterial pathogens

o

Fungal pathogens (Aspergillus)

Pediatric Considerations 

Ethm oid and m axillary sinuses are present at birth.



Frontal and sphenoid sinuses do not em erge until age 6â€“7 years



Sinusitis is m ore com m on in children than adults.

Pa ge 4 3 5



Periorbital/orbital cellulitis is a com m on com plication of ethm oid sinusitis in children. o

Periorbital swelling, fever, ptosis, proptosis, and painful or decreased extraocular m ovem ents

Diagnosis Signs and Symptoms History 

Facial pain



Headache



Halitosis



Cough



Purulent nasal discharge



Fever



Frontal sinusitis: o

Pain of the lower forehead

o

Pain worsened when lying on the back and im proves when upright



Maxillary sinusitis: o

Malar facial pain

o

Maxillary dental pain

o

Referred ear pain

o

Pain worsens with head upright or bending forward and im proves with reclining





Ethm oid sinusitis: o

Retro-orbital pain

o

Periorbital edem a

Sphenoid sinusitis (very uncom m on): o

Pain over the occiput or m astoid

Pa ge 4 3 5

o 

Pain worse when lying on back or bending forward

Recent history of nasotracheal intubation suggests nosocom ial sinusitis: o

Involves atypical pathogens such as Pseudom onas and gram -negative organism s



Rhinocerebral m ucorm ycosis: o

Rare but rapidly progressive fungal infection

o

Occurs in diabetic and other im m unocom prom ised patients

o

Orbital and facial pain out of proportion to physical signs

o

Lethargy, headache in a system ically ill-appearing patient

o

Black eschar or pale area on the palate or nasal m ucosa

Physical Exam 

Edem a of the nasal m ucous m em branes



Pus in the nares or posterior pharynx



Warm th, tenderness, and possibly cellulitis over the affected sinus

Essential Workup 

Clinical diagnosis based on history and physical exam



Transillum ination is not a reliable indicator of sinus disease.



Im aging is unnecessary in uncom plicated cases (see below).

Tests Lab Laboratory studies are not helpful for diagnosis or m anagem ent.

Imaging

Pa ge 4 3 5



Plain film radiography: o

Norm al plain film s do not rule out bacterial involvem ent.

o

A Water view m ay help in the diagnosis of m axillary sinusitis.

o 

Opacification or air fluid level in involved sinus

CT: o

Preferred to plain film s if im aging is necessary

o

May assist in diagnosing com plications of sinusitis

Diagnostic Procedures/Surgery 



Sinus aspirate culture: o

Gold standard for m aking a m icrobial diagnosis

o

Not used in routine m edical practice

Functional endoscopic sinus surgery (FESS): o

Restores physiologic sinus ventilation and drainage

Pediatric Considerations 

FESS is a safe and effective treatm ent in children.



FESS is indicated when the following failed: o

Maxim al m edical therapy

o

Adenoidectom y

o

Culture-directed system ic antibiotics

Differential Diagnosis 

Migraine and cluster headache



Dental pain



Trigem inal neuralgia



Tem porom andibular joint disorders



Tem poral arteritis



Uncom plicated viral or allergic rhinitis



Nasal polyp, tum or, or foreign body



CNS infection

Pa ge 4 3 6

Pregnancy Considerations 

Pregnancy rhinitis: o

Nasal congestion during last 6 or m ore weeks of pregnancy

o

Disappears within 2 weeks after delivery

P.1021

Treatment Initial Stabilization Toxic-appearing patients m ay require airway intervention and fluid resuscitation: 

First dose of antibiotics in ED

ED Treatment 

Cost-effective approach favors appropriate antibiotic therapy and no testing.



Establishing good drainage with topical or oral decongestants and m ucor-evacuants



Reducing edem a with topical corticosteroids in chronic sinusitis



Hum idification and saline spray are beneficial adjuncts to pharm acologic therapy.



Reserve antibiotics for patients with: o

Pain and discharge for m ore than 7 days in spite of decongestant and analgesic treatm ent

o 

Severe sym ptom s

Acute sinusitisâ€”antibiotic choices if no antibiotic treatm ent in the previous m onth:

Pa ge 4 3 6

o

Am oxicillin, am oxicillin-clavulanate, cefpodoxim e, or cefuroxim e



Acute sinusitisâ€”antibiotic choices if antibiotic treatm ent in the previous m onth (>30% risk of drug resistant S. pneum oniae): o

Am oxicillin-clavulanate, gatifloxacin (adult), levofloxacin (adult), m oxifloxacin (adult)



Acute sinusitisâ€”clinical failure after 3 days of antibiotic treatm ent: o

Am oxicillin-clavulanate or cefpodoxim e (m ild to m oderate disease)

o

Gatifloxacin, levofloxacin, m oxifloxacin (severe disease in adults)



Acute sinusitisâ€”patient with penicillin or cephalosporin allergy: o

Clarithrom ycin, azithrom ycin, trim ethoprim -sulfam ethoxazole, doxycycline, erythrom ycin ethyl succinate/sulfam ethoxazole, gatifloxacin, levofloxacin, m oxifloxacin, or trim ethoprim -sulfam ethoxazole



Acute sinusitisâ€”aspergillosis: o



Ear-nose-throat (ENT) consultation

Chronic sinusitis: o

3-m onth course of antibiotics, douche, and topical steroids

o

ENT consultation

Medication (Drugs) Antibiotics 

Am oxicillin: 250â€“500 m g PO t.i.d. (peds: 40 m g/kg/d PO

Pa ge 4 3 6

t.i.d.) 

Am oxicillin-clavulanate: 250â€“500 m g PO t.i.d. (peds: 40 m g/kg/d, based on the am oxicillin com ponent, PO t.i.d.) or 875/125 m g PO b.i.d.



Azithrom ycin: 500 m g PO once then 250 m g PO per day for 4 days per day (peds: 5â€“10 m g/kg/d, based on the am oxicillin com ponent PO)



Cefpodoxim e: 100â€“400 m g PO b.i.d. (peds: 10 m g/kg/d PO b.i.d.)



Cefuroxim e: 250â€“500 m g PO b.i.d. (peds: 15 m g/kg/d PO b.i.d.)



Clarithrom ycin: 500 m g PO b.i.d. (peds: 7.5 m g/kg/d PO b.i.d.) or clarithrom ycin XL 1000 m g per day



Doxycycline: 100 m g PO b.i.d.



Erythrom ycin ethyl succinate-sulfam ethoxazole: 50 m g/kg/d (based on the erythrom ycin com ponent) PO t.i.d.â€“q.i.d. (peds)



Gatifloxacin: 400 m g PO per day (adult)



Levofloxacin: 250â€“500 m g PO per day (adult)



Moxifloxacin: 400 m g PO per day (adult)



Trim ethoprim -sulfam ethoxazole: 1 double-strength tablet PO b.i.d. (peds: 8â€“12 m g/kg/d, based on the trim ethoprim com ponent, PO b.i.d.)

Decongestants 

Topical: not to be used for m ore than 3 days



Oxym etazoline hydrochloride 0.05%: 2â€“3 gtt or sprays per nostril b.i.d.



Phenylephrine hydrochloride 0.5%: 2â€“3 sprays per nostril q3hâ€“q4h; oral: if longer than 3 days of treatm ent



Pseudoephedrine: 60 m g PO q4hâ€“q6h

Mucor-Evacuants

Pa ge 4 3 6



Guaifenesin: 5â€“20 m L PO q4h (peds: 5â€“10 m L/dose if 6â€“12 years old, 2.5â€“5 m L if 2â€“6 years old)

Corticosteroids for Chronic Sinusitis 

Beclom ethasone dipropionate: 1 spray/nostril per day/b.i.d./t.i.d.



Dexam ethasone sodium phosphate: 2 sprays/nostril b.i.d./t.i.d.

Follow-Up Disposition Admission Criteria 

Evidence of spread of infection beyond the sinus cavity



Toxic-appearing patients



Im m unocom prom ised/Diabetic patients with extensive infection



Multiple sinus involvem ent



Frontal sinus involvem ent



Extrem es of age



Severe com orbidity



ENT evaluation and aspiration if patient is severely ill, im m unocom prom ised, or pansinusitis- and ill-appearing

Discharge Criteria 

Most cases of uncom plicated sinusitis m ay be m anaged as outpatients.



Follow up with prim ary care physician or ENT specialist if sym ptom s persist >7 days despite antibiotic therapy.

Issues for Referral 

Com plications of acute infection

Pa ge 4 3 6



Im m unocom prom ised patients



Nasal polyps



Chronic rhinosinusitis

References 1. Ah-See K. Acute sinusitis. Clin Evid. Decem ber 2003;(10):567â€“573. (Update in: Clin Evid. 2004 Jun;(11):710â€“717). 2. Am erican Academ y of Pediatrics. Subcom m ittee on Managem ent of Sinusitis and Com m ittee on Quality Im provem ent. Clinical practice guideline: m anagem ent of sinusitis. Pediatrics. Septem ber 2001;108(3):798â€“808. (Erratum in: Pediatrics. Novem ber 2001;108(5):A24. Pediatrics. May 2002;109(5):40.) 3. Anon JB. Acute bacterial rhinosinusitis in pediatric m edicine: current issues in diagnosis and m anagem ent. Paediatr Drugs. 2003;5Suppl1:25â€“33. 4. Com bs JT: Antibiotics and sinusitis. Pediatrics. April 2001;107(4):619â€“625. 5. Ellegard EK. Clinical and pathogenetic characteristics of pregnancy rhinitis. Clin Rev Allergy Im m unol. June 2004;26(3):149â€“159. 6. Hickner JM, Bartlett JG, Besser RE, Gonzales R, Hoffm an JR, Sande MA; Centers for Disease Control and Prevention. Principles of appropriate antibiotic use for acute rhinosinusitis in adults: background. Ann Em erg Med. June 2001;37(6):703â€“710. 7. Josephson GD, Gross CW. Diagnosis & m anagem ent of acute & chronic sinusitis. Com pr Ther. Novem ber 1997;23(11):708â€“714. 8. Lieser JD, Derkay CS. Pediatric sinusitis: when do we operate? Curr Opin Otolaryngol Head Neck Surg. February 2005;13(1):60â€“66. 9. Poole MD. A focus on acute sinusitis in adults: changes in disease m anagem ent. Am J Med. May 3, 1999;106(5A):38Sâ€“47S; discussion 48Sâ€“52S. 10. Ragab SM, Lund VJ, Scadding G. Evaluation of the m edical and

Pa ge 4 3 6

surgical treatm ent of chronic rhinosinusitis: a prospective, random ised, controlled trial. Laryngoscope. May 2004;114(5):923â€“930. 11. Scheid DC, Ham m RM. Acute bacterial rhinosinusitis in adults: part I. Evaluation. Am Fam Physician. Novem ber 2004;70(9):1685â€“1692. 12. Scheid DC, Ham m RM. Acute bacterial rhinosinusitis in adults: part II. Treatm ent. Am Fam Physician. 2004 Nov 1;70(9):1697â€“1704. 13. Slavin RG. Sinusitis: Current Diagnostic and Treatm ent Strategies. Am J Ther. July 1996;3(7):525528.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Skin C ancer

Skin Cancer

Michael K. Doney

Basics Description 



Basal cell carcinom a: o

Cells arise from epiderm is.

o

Most com m on skin cancer m ore than 75% of total

o

Most im portant risk factor is sun exposure.

o

Locally invasive without risk of distant m etastasis

Squam ous cell carcinom a: o

Second m ost com m on skin cancer

o

Most arise from precancerous actinic keratoses lesions.

o

Most im portant risk factor is sun exposure, especially sunburn.

o 

Risk of regional lym ph node and distant m etastasis

Melanom a: o

Arises from m elanin-producing cells

o

Most im portant risk factor is sun exposure, especially sunburn.

o

Additional risk factors: 

Multiple com m on m elanocytic nevi



Atypical nevi

Pa ge 4 3 6



Im m unosuppression



Positive fam ily history



History of nonm elanom a skin cancer (basal cell or squam ous cell carcinom a)

o

Risk of regional lym ph node and distant m etastasis

Etiology Sun exposure

Diagnosis Signs and Symptoms 



Basal cell carcinom a: o

Papule or nodule with waxy or pearly appearance

o

Central depression or erosion often present

o

May be single or m ultiple

o

Pigm ented form m ay be brownish or stippled

o

Usually painless

o

Rarely m etastasizes

o

May be locally invasive

o

Usually appears in sun-exposed areas of skin

Squam ous cell carcinom a: o

Characteristic lesion is raised, firm , keratotic papule or plaque.

o

Usually asym ptom atic but m ay be ulcerated and painful.



Melanom a: o

Pigm ented skin lesion

o

Features suggestive of m elanom a (the ABCDs of m elanom a): 

Asym m etry (not regularly round or oval)

Pa ge 4 3 6



Border irregularity (notched or poorly defined); Bleeding (spontaneous)



Color variegation (shades or com binations of brown, tan, red, white, or blue-black)



Diam eter exceeding 6 m m

o

Lesions rarely sym ptom atic unless ulcerated

o

Malignant m elanom a 

Presentation related to affected organ system



Lym phangitic spread with local to regional lym phadenopathy



Typical visceral sites of hem atogenous spread include liver, lung, bone, and brain.

Essential Workup Suspicious lesions require biopsy, a procedure rarely done in ED.

Tests Lab 

No specific testing is required.



Tests of liver enzym es and function are ordered if suspicion of m etastatic m elanom a exists.

Imaging 

Chest radiograph m ay show pulm onary involvem ent by m etastatic m elanom a.



Head or body CT scan m ay show visceral involvem ent by m etastatic m elanom a.

Differential Diagnosis 

For basal cell carcinom a: o

Squam ous cell carcinom a

o

Bowen disease

o

Actinic keratosis

o

Paget disease

Pa ge 4 3 6

o

Benign nevus

o

Melanom a

P.1023





For squam ous cell carcinom a: o

Actinic keratosis

o

Basal cell carcinom a

o

Keratoacanthom a

o

Wart

For m elanom a: o

Atypical nevus

o

Com m on nevus

o

Actinic keratosis

o

Pigm ented basal cell carcinom a

o

Squam ous cell carcinom a

Treatment ED Treatment 

No specific ED treatm ent



Treat com plications of visceral involvem ent by m etastatic m elanom a or locally invasive basal cell carcinom a.

Follow-Up Disposition Admission Criteria 

Usually adm ission occurs only because of visceral

Pa ge 4 3 7

involvem ent or invasive spread. 

Adm ission is rarely required because of the lesions them selves.

Discharge Criteria Patients are generally discharged with advice on seeking additional consultation.

Issues for Referral Discharged patients should be advised to consult a derm atologist or experienced prim ary care physician.

References 1. Bernstein SC, Lim KK, Brodland DG, Heidelberg KA. The m any faces of squam ous cell carcinom a. Derm atol Surg. 1996;22(3):243â€“254. 2. Lear JT, Sm ith AG. Basal cell carcinom a. Postgrad Med J. 1997;41:538â€“542. 3. Marks R. An overview of skin cancers: incidence and causation. Cancer. 1995;75:607â€“612. 4. Rivers JK. Melanom a. Lancet. 1996;347:803â€“807. 5. Rubin AI, Chen EH, Ratner D. Basal-cell carcinom a. N Engl J Med. Novem ber 24, 2005;353(21):2262â€“2269.

Codes ICD9-CM 172.9 Malignant m elanom a of skin, site unspecified 173.9 Other m alignant neoplasm of skin, site unspecified

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sleep Apnea

Sleep Apnea

Mark Sagarin

Basics Description 

Airway closing at the level of nasopharynx or oropharynx during sleep: o

Decreased tone during REM sleep

o

Affects about 3% of m iddle-aged m en and about 1.5% of m iddle-aged wom en

o 



Most patients are undiagnosed.

Groups at risk: o

Obese

o

Men

o

Age older than 40 years

o

Upper airway anom alies

o

Hypertrophy

o

Myxedem a (hypothyroidism )

o

Alcohol/Sedative abuse

o

Long-distance truck drivers

Associated illness: o

Various dysrhythm ias, particularly atrial fibrillation

o

Right and left heart failure

o

Myocardial infarction

Pa ge 4 3 7

o

Stroke

o

Motor vehicle accidents

o

Hypertension poorly controlled by m edical therapies

Genetics Unknown

Etiology 

Excessive soft tissue obstructs airway during sleep.



Sleep is disrupted, resulting in daytim e drowsiness.

Diagnosis Signs and Symptoms 

Snoring in com bination with observed apnea



Daytim e drowsiness



Sleep disturbance



Irritability

Physical Exam 

Hypertension, hypoxem ia



Obesity



Craniofacial anom alies



Enlarged tonsils



Elevated jugular veins (secondary to pulm onary hypertension)

Essential Workup 

Pulse oxim etry



ECG



Chest radiograph



Sleep study (polysom nogram ): o

Required for diagnosis

Pa ge 4 3 7



Never indicated as part of the em ergency evaluation

Tests Lab Consider arterial blood gas.

Imaging 

Consider lateral neck soft-tissue radiograph to rule out other etiologies of upper airway obstruction.



Chest radiograph to assess other etiologies of hypoxem ia



Chest CT rarely indicated; consider prim arily to rule out pulm onary em bolism .

Diagnostic Procedures/Surgery 

Polysom nogram establishes diagnosis: o



Not a consideration for ED m anagem ent

Various operative interventions have been tried: o

Most intend to reduce or bypass the excessive pharyngeal/airway resistance that occurs during sleep.

o

Varying levels of success; no good random ized trials

o

Not a consideration for ED m anagem ent.

Differential Diagnosis 

Central sleep apnea: o

Neurologic, rather than obstructive, cause of apnea during sleep



Chronic obstructive pulm onary disease



Asthm a



Left heart failure



Prim ary pulm onary hypertension



Narcolepsy



Idiopathic hypersom nia

Pa ge 4 3 7

Treatment Initial Stabilization Chin lift/jaw thrust m aneuver, oxygen as needed, oral or nasal airway devices

ED Treatment 

Supplem ental oxygen as needed



Bag-valve m ask ventilation m ay be difficult.



Consider using two nasals and one oral airway, and a two-person technique to ensure a good seal. P.1025



Noninvasive ventilation with continuous positive airway pressure



May obviate need for intubation in setting of hypoxem ia or hypercarbia

Alert 

Endotracheal intubation: o

Most patients have redundant soft tissue in the oropharynx and upper airway and thus m ay be difficult to intubate.

o

Consider and plan several possible m ethods of definitive airway control.

o

Have alternative laryngoscope blades and devices (laryngeal m ask airway, bougie) available.

o

Be prepared to perform cricothyroidotom y if necessary.

o

Use neurom uscular blockade only if successful oral intubation is reasonably likely and bag ventilation is

Pa ge 4 3 7

easy. o

Sweep the tongue out of the way when perform ing laryngoscopy.



Positive end-expiratory pressure for ventilated patients

Medication (Drugs) 

No specific m edications useful in ED to treat this chronic disorder



See Airway Managem ent for details on induction agents and neurom uscular blockade.

Follow-Up Disposition Admission Criteria 

Ventilatory failure, especially if intubation was necessary



Hem odynam ic instability

Discharge Criteria 

Maintenance of O 2 saturation >85% for several hours using oxygenation or ventilation equipm ent available to the patient at hom e



Very low likelihood of decom pensation overnight



Patients with sleep apnea who present after m otor-vehicle crashes: o

Manage initially like other blunt traum a patients.

o

Later, consider the increased risk with sleep apnea and intervene to prevent future accidents.

Issues for Referral

Pa ge 4 3 7



Consider referral of patients with suspected sleep apnea to a pulm onologist.



Encourage weight loss and refer to a prim ary care physician for assistance with this.



Cardiology referral is appropriate when sleep apnea is com plicated by heart failure or dysrhythm ias.

References 1. Am erican Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med. 1994;150[Suppl 5, Pt 1]:1463â€“1473. 2. Caples SM, Gam i AS, Som ers VK. Obstructive sleep apnea. Ann Intern Med. Febraury 1, 2005;142(3):187â€“197. 3. den Herder C, Schm eck J, Appelboom DJ, de Vries N. Risks of general anaesthesia in people with obstructive sleep apnea. BMJ. 2004;329(7472):955â€“959. 4. Fuchs BD, McMaster J, Sm ull G, et al. Underappreciation of sleep disorders as a cause of m otor vehicle crashes. Am J Em erg Med. 2001;19(7):575â€“578. 5. Gibson GJ. Obstructive sleep apnea syndrom e: underestim ated and undertreated. Br Med Bull. 2005;72:49â€“65. 6. Hillm an DR, Loadsm an JA, Platt PR, Eastwood PR. Obstructive sleep apnea and anaesthesia. Sleep Med Rev. Decem ber 2004;8(6):459â€“471. 7. Hudgel DW. Treatm ent of obstructive sleep apnea. Chest. 1996;109:1346â€“1358. 8. Hung J, Whitford EG, Parsons RW, et al. Association of sleep apnoea with m yocardial infarction in m en. Lancet. 1990;336(8710):261â€“264. 9. Man GCW. Obstructive sleep apnea: diagnosis and treatm ent. Med Clin North Am . 1996;80(4):804â€“820. 10. McDonald JP. A review of surgical treatm ent for obstructive sleep apnoea/hypopnoea syndrom e. Surgeon. October

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2003;1(5):259â€“264. 11. Obenza Nishim e E, Liu LC, Coulter TD, et al. Heart failure and sleep-related breathing disorders. Cardiol Rev. 2000;8(4):191â€“201. 12. Parish JM, Som ers VK. Obstructive sleep apnea and cardiovascular disease. Mayo Clin Proc 2004;79(8):1036â€“1346. 13. Strollo PJ, Rogers RM. Obstructive sleep apnea. N Engl J Med. 1996;334(2):99â€“101. 14. Victor LD. Obstructive sleep apnea. Am Fam Physician. 1999;60(8):2279â€“2286. 15. Wright J, White J. Continuous positive airways pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2000;(2):CD001106. 16. Young T, Peppard PE, Gottlieb DJ. Epidem iology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165(9):1217â€“1239. 17. Young T, Skatrud J, Peppard PE. Risk factors for obstructive sleep apnea in adults. JAMA. 2004;291(16):2013â€“2016.

Codes ICD9-CM 780.57

ICD10 G47.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Slipped C apital F em o ral Epiphysis

Slipped

Capital Femoral Epiphysis Judd L. Glasser

Basics Description 

Fem oral epiphysis translates, or â€œslips,â€• relative to the fem oral head/neck.



Classified: o

Degree of displacem ent: 

(Mild, grade 1)


(Moderate, grade 2) one-third to one-half translation

 o



(Severe, grade 3) >one-half translation

Tem poral: 

Acute (<3 weeks of sym ptom s)



Chronic (>3 weeks of sym ptom s)

Peak age at onset 13â€“15 years for boys and 11â€“13 years for girls



Most patients are obese.



Male patients predom inate (8:3).



Approxim ately one third of cases involve bilateral joint.

Etiology

Pa ge 4 3 7



True etiology rem ains elusive.



Association with endocrine abnorm alities: o

Especially hypothyroidism and treatm ent with growth horm one

Diagnosis Signs and Symptoms 

Presents with lim p or exertional lim p



Pain in the knee, thigh, groin, or hip (referral of pain along the obturator nerve): o

Vague and dull for weeks in chronic slipped capital fem oral epiphysis (SCFE)

o

Severe and sudden onset in an acute SCFE



Com m only presents with the leg externally rotated



Flexion is restricted (cannot touch thigh to abdom en).

History 

May present with chronic hip pain with exertion



May have acute pain following m inor traum a



May have acute on chronic pain

Physical Exam 

Observe resting position of the leg.



If suspicion of SCFE, do not am bulate the patient.

Tests Lab Without diagnostic radiographic abnorm ality, the practitioner should consider the following tests to help risk stratify possible alternative diagnoses: 

CBC with differential

Pa ge 4 3 8



Sedim entation rate



C-reactive protein

Imaging 

Anteroposterior and frog-leg lateral radiograph film s of both hips should be obtained: o

Widened or irregular physis

o

Bird's beak appearance of the actual slipping of the epiphysis off of the fem oral head



Klein line (line drawn parallel lateral fem oral neck does not transect epiphysis)

Differential Diagnosis 

Legg-Calve-Perthes: o

Typically seen in 4â€“9-year-old age range



Septic arthritis of hip



Osteom yelitis



Toxic Synovitis



Fem ur or pelvic fractures

P.1027

Treatment Pre Hospital Patient should be im m obilized for transport, as with suspected hip fracture or dislocation.

Initial Stabilization 

Im m obilize hip.



Keep nonâ€“weight-bearing.

Pa ge 4 3 8



Do not attem pt reduction.

ED Treatment 

SCFE is an urgent orthopaedic condition; delay in diagnosis m ay lead to chronic irreversible hip joint disability.



Consult orthopaedics im m ediately for definitive im m obilization or operative intervention.

Medication (Drugs) Pain m anagem ent is appropriate; avoid PO m edications, as often acute SCFE m ay be m anaged with em ergent surgical fixation.

Follow-Up Disposition Admission Criteria 

Patients with acute or acute on chronic (unstable) SCFE require orthopaedic adm ission for urgent operative fixation (usually single central pinning).



Chronic SCFE m ay be m anaged with delayed operative fixation.

Discharge Criteria 

None



It is too difficult to achieve com plete nonâ€“weight-bearing status, which is required to prevent further slippage, avascular necrosis, and chondrolysis

References 1. Aronsson DD, Loder RT. Treatm ent of the unstable (acute) slipped capital fem oral epiphysis. Clin Orthop Related Res. 1996;322:99110.

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2. Causey AL, Sm ith ER, Donaldson JJ, et al. Missed slipped capital fem oral epiphysis: illustrative cases and a review. J Em erg Med. 1995;13(2):175â€“189. 3. Loder RT. Slipped capital fem oral epiphysis. Am Fam Physician. 1998;57(9):2135â€“2142 4. Uglow MG, Clarke NMP. The m anagem ent of slipped capital fem oral epiphysis. J Bone and Joint Sur. 2004;86-B:631â€“635.

Codes ICD9-CM 732.2

ICD10 M93.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sm all-Bo w el Injury

Small-Bowel

Injury Barry J. Knapp II

Basics Description 

Penetrating: visceral injury (96% gunshot wound, 50% stabbing)â€”serosal tear, bowel wall hem atom a, perforation, bowel transection, m esenteric hem atom a/vascular injury



Blunt: o

Mortality rate from sm all bowel injury is 33%.

o

Deceleration injury at fixed points (e.g., ligam ent of Treitz)

o

Shearing m echanism s near fixed points (e.g., ileocecal junction, adhesions)

o

Com pressive force against anterior spine

o

Bursting or â€œblowoutâ€• at antim esenteric m argin from sudden closed-loop intralum inal pressure rise

o 

Mesenteric tears m ay initially be asym ptom atic.

Associated injuries: o

Liver and splenic lacerations; thoracic and pelvic

Pa ge 4 3 8

fractures o

Seatbelt syndrom e: abdom inal wall ecchym osis, sm all bowel injury; chance fracture of L1, L2

Etiology 

Penetrating: o

Sm all bowel is the second m ost com m only injured organ (32%) in anterior abdom inal stabbing.

o

Sm all-bowel injury is m ost com m on in gunshot wounds (49%).

o

About 80% of sm all-bowel injuries are caused by gunshot wounds, 60% by stab wounds.



Blunt: o

Third m ost com m only injured organ (5â€“10% of all blunt traum a victim s)

o

Lap belts

o

Motor vehicle accidents

o

Nonvehicular traum a: abuse/assault, bicycle handlebars, large-anim al kick

Pediatric Considerations 

Penetrating: air-gun accidents at close range (<10 feet)



Blunt: o

Less com m on in children (1â€“8% of all blunt pediatric traum a)

o

Lower chance of intestinal injury in vehicular accidents when both shoulder and lap belts are worn.

o

Consider the possibility of nonaccidental traum a.

Diagnosis Signs and Symptoms

Pa ge 4 3 8



Delays in diagnosis are com m on.



Presence of a â€œseatbelt signâ€• doubles the risk for sm all bowel injury.



Initial presentation m ay be m ild: o

Uniform ly, patients will progress to serious signs/sym ptom s.







Awake, alert patients: o

Abdom inal tenderness (87â€“98%)

o

Abdom inal pain (85%)

o

Peritoneal signs (67%)

Many patients will have: o

Abdom inal wall bruising (54%)

o

Hypotension (38%)

o

Guaiac-positive rectal exam (5%)

Sm all-bowel injury m ay initially be obscured by abnorm al m ental status, severe associated injuries.



Sm all-bowel injury not initially apparent m ay be indicated by:



o

Progressive abdom inal pain

o

Intestinal obstruction

o

Decreased urine output

o

Tachycardia

Delays in diagnosis add to m orbidity and m ortality: o

Mortality is 2% when diagnosis is m ade within 8 hours, 31% when m ade after 24 hours.

Essential Workup 

Initial physical exam should note all wounds and areas of tenderness.



Serial abdom inal exam and vital signs



For m edically unstable patients, diagnostic peritoneal lavage is superior to ultrasound in determ ining presence of a hollow viscus injury.

Pa ge 4 3 8



Com puted tom ography (CT) scan for all m edically stable patients

Tests Lab 

No diagnostic test has proven highly sensitive in the prediction of sm all-bowel injury.



Serum am ylase, lipase, and liver function tests have poor sensitivity for acute injury.

Imaging 

Plain radiography of chest/abdom en: o

Not useful for sm all-bowel injury

o

Incidence of pneum operitoneum visible on plain radiograph is 8%.



CT: o

Diagnostic standard for solid-organ injury and head traum a but is less sensitive for hollow viscous injuries

o

Newest generation helical CT scanners have a sensitivity of 88% and a specificity of 99%.

o

The use of oral contrast is controversial.

o

Blunt traum a: 

Used in stable patients



Indications in blunt traum a include abdom inal distention, absent bowel sounds, blood in the nasogastric tube, abdom inal abrasions or contusions, gross hem aturia, lap belt injury, assault/abuse as m echanism , abdom inal tenderness, traum a score <12.



Specific signs for sm all-bowel injury on CT are pneum operitoneum (sensitivity 50â€“75%) and extravasation of contrast (sensitivity 12%).

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

Signs on CT suggestive of sm all-bowel injury include unexplained free intraperitoneal fluid (m ost sensitive 73%), thickened bowel wall >3 m m (61% sensitive), intram ural hem atom as (75â€“88% sensitive), interloop fluid, m esenteric streaking.

o

Penetrating: CT is not recom m ended because sensitivity is only 14%; false-negative result rate is 18%.



Ultrasonography: not sensitive in hollow viscous injury because air in bowel m akes visualization difficult

Diagnostic Procedures/Surgery 

Diagnostic peritoneal lavage: o

Invasive but helpful in unstable patients or in patients with clinically suspicious but nondiagnostic abdom inal CT

o

Sensitive for hem operitoneum but not source of bleeding

o

Positive if RBC count of >100,000/m m 3

o

Lavage am ylase >20 IU/L and leukocyte count >500/m m 3 (late m arkers of sm all-bowel injury)

o

Lavage m icroscopy for succus/vegetable m atter/feces is specific for sm all-bowel injury but not sensitive.

o

Lavage alkaline phosphatase (>3 IU/L) is reported to be a useful im m ediate m arker of sm all-bowel injury.



Laparoscopy: plays a key role in diagnosing sm all-bowel injury in stable patients with progressive signs or sym ptom s

P.1029

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Differential Diagnosis 

Hem operitoneum owing to vascular insult



Solid visceral organ injury or gastric/colon/rectum perforation



Vertebral injury and associated ileus

Pediatric Considerations Delay in diagnosis of 1â€“2 days is com m on and m ay increase m orbidity.

Treatment Pre Hospital Alert 

Patients should be transported to the nearest traum a center.



Do not attem pt to replace eviscerated abdom inal contents; cover with m oist gauze, blanket, and transport.



Do not rem ove im paled objects in the abdom en; stabilize the object with gauze and tape and transport.

Initial Stabilization 

Standard advanced traum a life support protocols, including airway, breathing, and circulation m anagem ent



Aggressive fluid resuscitation, central line suggested with pressure infusion of warm ed intravenous fluid (lactated Ringer solution or norm al saline)



Decom pression using a nasogastric tube, then CT contrast adm inistration, as indicated



Cover eviscerated sm all bowel with m oist gauze; do not rem ove im paled foreign body in ED.

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ED Treatment 

Im m ediate transfer to operating room is required for patients with an indication for laparotom y: o

Evisceration

o

Abdom inal pain with hypotension

o

Positive diagnostic peritoneal lavage or abdom inal CT

o

Thoracic abdom inal herniation visualized on chest radiograph

o

Im paled foreign body

o

Penetrating gunshot wound to the abdom en

o

Tetanus and antibiotic prophylaxis for penetrating abdom inal wounds and blunt injury requiring surgical exploration



Local wound exploration is safe for abdom inal stab wounds.



Serial abdom inal exam inations and observation for otherwise stable patients



Judicious analgesia as blood pressure perm its after diagnosis is established

Medication (Drugs) 

Cefotetan (Cefotan): 1â€“2 g (peds: 20 m g/kg) IV or



Cefoxitin (Mefoxin): 1â€“2 g (peds: 40 m g/kg) IV or



Ceftizoxim e (Cefizox): 1â€“2 g (peds: 50 m g/kg) IV plus



Flagyl: 500 m g (peds: 7.5 m g/kg) IV

Follow-Up Disposition

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Admission Criteria 

Indication for laparotom y



Abnorm al m ental status/intoxication with abdom inal injury



Presence of abdom inal pain, tenderness (even with a negative work-up) m andates adm ission for observation and serial exam s.



Stab and gunshot wounds that violate the abdom inal fascia, positive diagnostic peritoneal lavage, or worsening findings on clinical exam

Discharge Criteria 

Minim al m echanism blunt traum a in a sober patient with norm al exam result who has no abdom inal pain and will receive adequate follow-up



Explicit discharge instructions to return for worsening signs/sym ptom s are im portant to identify those with unsuspected injury.



Penetrating wounds that do not violate abdom inal fascia

References 1. ACEP Policies Com m ittee. Critical Issues in the evaluation of adult patients presenting to the em ergency departm ent with acute blunt abdom inal traum a. Ann Em erg Med. 2004;43(2):278â€“290. 2. Fakhry SM, Brownstein M, Watts DD, et al. Relatively short diagnostic delays (<8 hours) produce m orbidity and m ortality in blunt sm all bowel injury: an analysis of tim e to operative intervention in 198 patients from a m ulticenter experience. J Traum a. 2000;48:408â€“415. 3. Hanks PW, Brody JM. Blunt injury to m esentery and sm all bowel: CT evaluation. Rad Clin North Am . 2003;41(6):1171â€“1182. 4. Marx JA. Abdom inal Traum a. In: Rosen P. et al. Marx: Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: CV Mosby, 2002:415â€“436.

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5. Sikka R. Unsuspected internal organ traum atic injuries. Em erg Med Clin North Am . 2004;22(4):1067â€“1180.

Codes ICD9-CM 863.20 Injury to gastrointestinal tract; sm all intestine, without m ention of open wound into cavity; unspecified site

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sm o ke Inhalatio n

Smoke Inhalation

Trevonne M. Thompson

Basics Description 

Suspect sm oke inhalation in anyone involved in a fire within a closed space or with a history of loss of consciousness.



May cause direct injury to the upper (supraglottic) airway structures



May cause chem ical/irritant effect to lower airway structures



May cause system ic toxicity from inhaled substances

Etiology 

Direct heat injury from heated gases/sm oke: o

Lim ited to supraglottic structures because of the heat dissipating properties of the upper airway





Irritant effect from sm oke com ponents: o

Acid and aldehyde gases

o

Oxidants

System ic toxicity from inhaled cellular toxins: o

Carbon m onoxide

o

Hydrogen cyanide

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Alert 

Inhalation of steam can be rapidly fatal: o

Steam has approxim ately 4,000 tim es the heat-carrying capacity of hot air.

o

Can rapidly cause obstructive glottic edem a, therm ally induced tracheitis, and hem orrhagic edem a of the bronchial m ucosa

Diagnosis Signs and Symptoms History Exposure to a fire or heavy sm oke 

Typically in a confined space



Maintain high index of suspicion with history of loss of consciousness

Physical Exam 

May have a norm al physical exam ination with sym ptom s developing during the 24-hour interval following exposure







Upper airway (supraglottic): o

Nasopharyngeal irritation

o

Hoarseness

o

Stridor

o

Cough

Lower airway: o

Chest discom fort

o

Hem optysis

o

Bronchospasm

o

Bronchorrhea

May have sym ptom s and signs of carbon m onoxide and/or

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cyanide toxicity

Alert 

The following signs are suggestive of significant inhalation injury: o

Facial and upper cervical burns

o

Carbonaceous sputum

o

Singed eyebrows and nasal vibrissae

Essential Workup 

Pulse oxim etry: o

May be falsely elevated in cases of carbon m onoxide exposure



Arterial blood gas m easurem ent: o

Hypoxia

o

Metabolic acidosis in cases of carbon m onoxide or hydrogen cyanide



Chest radiography: o

Initial radiograph typically norm al

o

May show signs of pulm onary injury over the next 24 hours

Tests Lab 

Electrolytes, blood urea nitrogen, creatinine, glucose



CBC



Coagulation profile



Creatine phosphokinase: o



Carboxyhem oglobin: o



When clinically indicated in burn patients

To evaluate for potential carbon m onoxide exposure

Cyanide level: o

In suspected cases of cyanide exposure, do not wait

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for the level before initiating therapy. o

May send lactate level as a m arker of cyanide toxicity



Pregnancy test

Imaging Bronchoscopy and radionuclide scanning m ay be done to evaluate extent of injury: 

Typically not done in the ED

P.1031

Diagnostic Procedures/Surgery 

Peak expiratory flow rate: o



Low peak flow associated with m ore severe injury

PaO 2 /FiO 2 ratio: o

A ratio of <300 after initial resuscitation is associated with developm ent of respiratory failure.

Differential Diagnosis 

Irritant gas exposure



Asphyxiant gas exposure



Cardiogenic pulm onary edem a



Chronic obstructive pulm onary (COPD) exacerbation



Asthm a exacerbation



Pneum onia

Treatment Pre Hospital 

100% oxygen by face m ask

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

Intubation for patients with agonal breathing



Rapid transport to ED for those with stridor: o

May need advanced airway m anagem ent



Albuterol nebulizer therapy for bronchospasm



Rapid glucose m easurem ent for those with altered m ental status

Initial Stabilization 

100% oxygen via face m ask



Intubation: o

Respiratory distress: 

Drooling



Stridor

o

Refractory hypoxia

o

CNS depression

o

Significant facial/upper airway burns



Establish IV access.



Consider IV dextrose, naloxone, and thiam ine for altered m ental status.

ED Treatment 

Inhaled or nebulized albuterol as needed for bronchospasm



Corticosteroids as needed for patients with history of asthm a or COPD





Intubated patients: o

Low endotracheal tube cuff pressure

o

Frequent suctioning

o

Positive end expiratory pressure

If indicated, treat for carbon m onoxide toxicity: o

100% oxygen

o

Hyperbaric oxygen in appropriate cases when available



If indicated, treat for cyanide toxicity:

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o

100% oxygen

o

Am yl nitrite/sodium nitrite: 

Contra-indicated in cases of significant carbon m onoxide exposure

o 

Sodium thiosulfate

No role for prophylactic antibiotics

Medication (Drugs) 

Albuterol nebulization: 2.5â€“5 m g in 2.5 m l of norm al saline every 20 m inutes o

Alternatively, 10 m g nebulizer treatm ent continuous over 1 hour



Dextrose: D 5 0 W 1 am pule (50 m L or 25 g) (peds: D 2 5 W 2â€“4 m g/kg) IV



Methylprednisolone 125 m g IV (peds: 1â€“2 m g/kg)



Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM



Prednisone: 60â€“80 m g PO (peds: 1â€“2 m g/kg)



Sodium thiosulfate 12.5 g (50 m L of 25% solution) slow IV infusion (peds: 412.5 m g/kg or 1.65 m L/kg of 25% solution)



Thiam ine (vitam in B1): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Intensive/Burn care unit: o

Intubated

o

Significant associated burns

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o

Persistent dyspnea, hoarseness, odynophagia, carbonaceous sputum



General m edical adm ission: o

Persistent cough

o

Asthm a/COPD patients with bronchospasm

o

Significant carbon m onoxide or cyanide exposure

o

Com orbid m edical illnesses

Discharge Criteria 

Minim al exposure history



Asym ptom atic



Significant exposure history, asym ptom atic after 4â€“6 hours of observation

Issues for Referral 

In cases of significant associated burn injuries, transfer to burn facility as appropriate.



In cases of significant carbon m onoxide toxicity, transfer to hyperbaric oxygen facility as appropriate.

References 1. Am erican Burn Association. Inhalation injury: diagnosis. J Am Coll Surg. 2003;196(2):307â€“312. 2. Lee-chiong TL. Sm oke inhalation injury. Postgrad Med. 1999;105(2):55â€“62. 3. Miller K, Chang A. Acute inhalation injury. Em erg Med Clin North Am . 2003;21(2):533â€“557.

Miscellaneous SEE ALSO: Cyanide; Carbon Monoxide; Hyperbaric Oxygen

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Snake Enveno m atio n

Snake

Envenomation Adam Black Timothy Erickson

Basics Description 

Pit viper venom : o

Mixture of proteolytic enzym es and throm bin-like esterases: 

Enzym es cause local m uscle and subcutaneous tissue necrosis.



Esterases have anticoagulant effect, leading to dissem inated intravascular coagulation (DIC) in severe envenom ations.



Bite location: o

Head or trunk biteâ€”m ore severe than on extrem ities

o

Lower extrem ity bites m ay have delayed presentation.



Severe envenom ation: o

Direct bite into artery or vein

o

All coral snake venom (prim arily neurotoxic)

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

Bite m ark significance: o

Venom ous snake: classically includes one or two puncture m arks

o

Nonvenom ous snake: horseshoe-shaped row of m ultiple teeth m arks



Twenty-five percent of all pit viper bites are dry and do not result in envenom ation.

Etiology Venom ous snakes indigenous to United States: 

Pit vipers: o

Account for 95% of all envenom ations



Rattlesnakes, cottonm ouths, and copperheads



Coral snakes (Elapidae): o

More severe envenom ations

o

Western coral snakes are found in Arizona and New Mexico.

o

More venom ous eastern coral snakes found in Carolinas and Gulf states



International exotic venom ous snakes: o

Zoos, illegal im portation, sm uggling

Pediatric Considerations 

Sm all children are m ost likely target for snake envenom ations.



Those who freeze with fear in response to snake are also m ore susceptible to m ultiple envenom ations.



Because of their low body weight, sm aller children and infants are m ore vulnerable to severe envenom ation.

Diagnosis

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Signs and Symptoms Local 





Classic skin changes: o

One or two puncture wounds

o

Pain and swelling at site

Swelling and edem a of involved extrem ity: o

Within 1 hour in severe envenom ations

o

Tender proxim al lym ph nodes

Ecchym osis, petechiae, and hem orrhagic vesicles develop within several hours.

Systemic 

Weakness



Diaphoresis



Dizziness



Nausea



Scalp paresthesias



Periorbital fasciculations



Metallic taste



Severe bites can lead to: o

Coagulopathies and DIC

o

Hypotension

o

Shock

o

Pulm onary edem a

o

Hem aturia

o

Rhabdom yolysis

o

Renal failure

o

Cardiac dysfunction

o

Throm bocytopenia



Potential com partm ent syndrom e in involved extrem ity



Coral snake venom : o

Prim arily neurotoxic:

Pa ge 4 4 0

o



Weakness



Diplopia



Confusion



Delayed respiratory depression

Local effects m ay be deceivingly m inim al.

Essential Workup History 

Description of snake



Geographic location of bite

Physical Exam 

Careful exam of wound site and involved extrem ity: o



Essential in judging severity of envenom ation

Careful assessm ent for anaphylactic reactions

Tests Lab 

CBC



PT/PTT



DIC panel



Electrolytes, BUN/creatinine, glucose



Creatine phosphokinase (CPK)



Urinalysis



Type and cross-m atch with m oderate to severe envenom ation.

Differential Diagnosis 



Nonpoisonous snakes: o

Sm ooth, tapered body

o

Narrow head

o

Round pupils

o

No rattles

Pit vipers:

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

o

Triangular or arrow-shaped head

o

Vertical or elliptical pupils

o

Rattles

Coral snakes in United States: o

â€œRed on yellowâ€”kill a fellowâ€•

o

â€œRed on blackâ€”venom lackâ€•

Treatment Pre Hospital 

Retreat well beyond striking range of snake.



Im m obilize extrem ity in functional position at level of heart.



Keep physical activity m inim al.



Rem ove rings, watches, and all constrictive clothing.



If snake is killed, transport in closed container: o

If snake is indigenous to region, positive identification not essential.

o 

Even severed head can envenom ate.

Controversies: o

Incision and suction of bite wound is not recom m ended: 

Can lead to further wound contam ination with hum an m outh flora.



Incision attem pts by inexperienced can lead to severe tendon, nerve, and vascular dam age.

o

Tourniquets, cryotherapy, and electrocautery: 

o

Contraindicated owing to tissue dam age

Although m echanical suction devices do exist, no clinical trials support their use.

P.1033

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Pediatric Considerations 

Increased urgency in transport to hospital setting is indicated: o

Envenom ation m ore likely to be severe

o

Because of relatively low body weight of sm all child

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)â€” two IVs



Vigorous hydration with 0.9% norm al saline (NS) to m aintain intravascular volum e and renal blood flow



Monitor.



Im m obilize bitten extrem ity.

ED Treatment 

Supportive care



Observe for com partm ent syndrom e.



Repeated m easurem ents of extrem ity circum ference: o

Measure every 15â€“20 m inutes until local progression/swelling subsides.



Analgesia



Tetanus prophylaxis if needed



Broad-spectrum antibiotics for m oderate to severe envenom ations



Steroids not indicated except for reactions to antivenin (see below)



Wound severity: o

Minim al: 

o

Local swelling and tenderness

Moderate: 

Extrem ity swelling

Pa ge 4 4 0

 o

Evidence of system ic toxicity

Severe: 

Obvious toxicity



Unstable vitals



Coagulopathy



Coral snake, Mojave rattlesnake



Lab abnorm alities

Antivenin 

Crotalidae antivenin: o

Fundam ental treatm ent for pit viper envenom ation

o

Effective for rattlesnakes, cottonm ouths, and copperheads

o

Most effective if given within 4â€“6 hours of bite

o

Skin test with diluted horse serum (in antivenin kit) before antivenin adm inistration

o

Treatm ent com plications include anaphylaxis and serum sickness.

o

Dosage (each vial contains 10 m L of antivenin) by wound severity:

o



Minim al/m oderate: 10 vials



Severe: 15â€“20 vials

Victim s of severe envenom ations who develop positive skin test with horse serum : 

May still receive antivenin



Pretreat with diphenhydram ine and corticosteroids.



Monitor closely for anaphylaxis with epinephrine at bedside.



CroFab: o

New affinity-purified ovine Fab antibody fragm ent antivenin

o

Minim izes hypersensitivity reactions

Pa ge 4 4 0

o

Dosing: four to six vials regardless of patient size; m ay require two to four additional vials if sym ptom s persist

o

CroFab vials dissolved in 250â€“500 m L 0.9% NS, infused over 30â€“60 m inutes



Coral snake antivenin: o

Effective against m ore toxic eastern coral snake but not against western coral snakes

o

After proper skin testing, three to five vials of antivenin is recom m ended.

o

Treatm ent com plications are sam e as those with Crotalidae antivenin.

o

International exotic venom ous snakes: Specific antivenins m ay be available at local zoos.

Treatment Assistance 

Contact local poison control center, local zoo, or herpetologist.



Call Antivenom Index at (602) 626-6016 in Tucson, Arizona, for assistance in treatm ent of exotic snakes not indigenous to United States.

Pediatric Considerations 

Proportionally m ore antivenin per body weight



Children often require standard adult doses.

Follow-Up Disposition Admission Criteria 

Twenty-four-hour observation for patients requiring antivenin adm inistration

Pa ge 4 4 0



ICU adm ission for: o

Evidence of m oderate to severe envenom ation, especially in children

o

All victim s of coral snake bites, sym ptom atic exotic snake envenom ations

Discharge Criteria Suspicious bite that shows no signs or sym ptom s of envenom ation for 6â€“8 hours and has norm al lab panel: 

Discharge with follow-up in 24 hours.



Observe lower extrem ity bites for up to 12 hours because of possible delayed toxicity.



Coral snake and Mojave rattlesnake bites m ay require 24-hour observation period.



Dry bites occur in up to 25% of pit viper bites.

References 1. Bebarta V, Dart RC. Effectiveness of delayed use of Crotalidae polyvalent im m une Fab (ovine) antivenom . J Toxicol Clin Toxicol. 2004;42(3):321â€“324. 2. Dart RC, McNally J. Efficacy, safety, and use of snake antivenom s in the United States. Ann Em erg Med. 2001;37:181â€“188. 3. Erickson T, Herm an BE, Bowm an MA. Snake envenom ations. In: Strange G, Ahrens WR, et al., eds. Pediatric Em ergency Medicine. New York: McGraw-Hill; 2002:676â€“679. 4. Gold BS, Barish RA, Dart RC. North Am erican snake envenom ation: diagnosis, treatm ent and m anagem ent. Em erg Med Clin North Am . 2004;22(2):423â€“443. 5. Gold BS, Dart RC, Barish RA. Current concepts: bites of venom ous snakes. N Engl J Med. 2002;347:347â€“357. 6. Holstege CP, Miller A, Werm uth M, et al. Crotalid envenom ation. Crit Care Clin. 1997;13:889â€“921. 7. Lawrence WT, Giannopoulos A, Hansen A. Pit viper bites: rational

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m anagem ent in locales in which copperheads and cottonm ouths predom inate. Ann Plast Surg. 1996;36(3):276â€“285. 8. Offerm an SR, Bush SP, Moynihan JA, et al. Crotaline Fab antivenom for the treatm ent of children with rattlesnake envenom ation. Pediatrics. 2002;110:968â€“971. 9. Richardson WH, Offerm an SR, Clark RF. Snake envenom ations. In: Erickson T, Ahrens W, Aks SE, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2005:548â€“555. 10. Trinh HH, Hack JB: Use of CroFab antivenin in the m anagem ent of a very young pediatric patient copperhead envenom ation. J Em erg Med. 2005:29(2):159â€“162.

Codes ICD9-CM 989.5

ICD10 T63.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spider Bite, Black Wido w

Spider Bite,

Black Widow Paul Arnold

Basics Description Syndrom es caused by envenom ation by black widow spider bite

Mechanism 

Venom s contain potent neurotoxins: o

Disrupt presynaptic nerve term inal m em branes causing neurotransm itter release at the neurom uscular junction (acetylcholine) and in autonom ic and cortical tissues (norepinephrine)

o

Initially, postsynaptic term inals are overstim ulated, then blockaded, and neurotransm itters rapidly becom e depleted.



Morbidity and m ortality are dose dependent.



Severity of envenom ation depends on: o

Prem orbid health of victim : 

Hypertension or cardiovascular disease increase risk

o

Size and age of victim : 

Children (i.e., sm aller size for a given dose of

Pa ge 4 4 1

venom ) are at greater risk of m orbidity and m ortality. o

Num ber of bites

o

Location of bite wounds

o

Size and condition of spider

Etiology Black widow spider features: 

Appearance: o

Black with red m arkings shaped like an hourglass or a pair of spots on the ventral aspect of the globular abdom en

o

Fem ales have 25- to 50-m m leg spans and 15-m m -long bodies.



Found throughout North Am erica, except the far north and Alaska



Prefer dark, cozy hideaways outdoors and close to the ground



Most bites occur during the warm er m onths when spiders are defending their webs and egg clutches.



Fem ales are responsible for hum an envenom ations.

Diagnosis Signs and Symptoms History 

History of spider bite very unreliable and species usually not identified



Local com plaints: o

Pain: 

Sharp or burning at the site

Pa ge 4 4 1



Onset within m inutes of the bite



Usually resolves spontaneously after a few m inutes or hours



May becom e worse and spread proxim ally from the bite



System ic com plaints: o

Onset within 20â€“30 m inutes of bite

o

Neurologic: 

Painful m uscle cram ps and spasm s



Entire body m ay becom e progressively involved or sym ptom s m ay rem ain regional.



Arm bites m ay lead to arm and chest m uscle tightness and dyspnea.



Leg bites m ay lead to abdom inal pain and leg spasm s.

o

Cutaneous dysesthesia and hyperesthesia

o

Perspiration, nausea, vom iting, tachycardia

o

Abdom inal pain

o

Restlessness, headache, agitation, and a sense of im pending death

Physical Exam 

Skin findings: o

Often there is nothing to see or palpate at the wound site but any or all of the following m ay be observed: 

Two pinpricks from the spider's fangs



Tender and blanched skin with surrounding erythem a (â€œtarget lesionâ€•)





Urticaria



Piloerection



Swelling



Local sweating

Neurologic findings:

Pa ge 4 4 1

o

Tetanic contractions of extrem ities with trem ors

o

Spasm and rigidity in the thighs and abdom en

o

Autonom ic instability with diaphoresis, nausea, vom iting, tachycardia or bradycardia



Less com m on system ic findings: o

Fever

o

Hypertension

o

Arrhythm ias

o

Dyspnea

o

Pulm onary edem a

o

Seizures

o

Shock

o

Acute toxic psychosis

Course 

Rarely fatal



In m ost untreated patients, sym ptom s peak after 2â€“3 hours and then begin to resolve, occasionally recurring episodically over the following few days.



In otherwise healthy adults, com plete resolution of sym ptom s occurs within 2â€“3 days.



Persistent neurologic sym ptom s can last weeks to m onths: o

Fatigue

o

Generalized weakness or m yalgias

o

Paresthesias

o

Headache

o

Insom nia

o

Im potence

o

Polyneuritis

Essential Workup Diagnosis is based on: 

Clinical presentation

Pa ge 4 4 1



Careful inquiry to elicit the spider bite history



Identification of the spider (if it has been caught)

Tests Lab 

No specific blood tests for black widow spider venom



WBC can be m ildly elevated but is usually norm al.



Electrolytes, glucose, calcium , blood urea nitrogen, creatinine, am ylase, liver function tests, creatinine kinase, troponin, pregnancy test, and prothrom bin tim e/partial throm boplastin tim e tests o

Appropriate to assess abdom inal or chest pain and rule out alternative diagnoses

o

Usually norm al

P.1035



ABGs in rare cases with pulm onary edem a



ECG and cardiac m onitoring for: o

Elderly

o

Presence of chest pain, unstable vital signs or dysrhythm ias

Imaging 

Chest radiograph for respiratory com plaints



Abdom inal im aging to rule out other causes of pain

Diagnostic Procedures/Surgery Calcium gluconate infusion considered by som e to be a good diagnostic test due to dram atic but tem porary relief it provides

Differential Diagnosis 

A high fever and WBC count should prom pt consideration of alternatives to spider bites (e.g., infection).

Pa ge 4 4 1



Acute surgical abdom en (e.g., appendicitis, cholecystitis, pancreatitis): o

Black widow spider victim s are restless instead of quiet (the posture favored by m ost patients with peritoneal irritation).

o

The abdom inal wall rigidity is also unexpectedly nontender.



Sym pathom im etics (e.g., cocaine, am phetam ines): o

Tetanic m uscle contractions uncom m on in conscious, nonseizing sym pathom im etic toxicity patients



Muscular injury or strain



Hypertensive em ergency



Myocardial infarction

Treatment Pre Hospital 

Im m obilize the wound site and apply cool com presses or ice for com fort during transport to hospital.



Supportive m easures (analgesics, anxiolytics) m ay be required for patients with system ic sym ptom s.



Venom extraction devices (e.g., Sawyer extractor) have been recom m ended anecdotally but are probably ineffective if >10 m inutes has elapsed since the bite.

Alert Every effort should be m ade by caregivers at the scene to find and bring in the responsible spider for identification.

Initial Stabilization 

ABCs: o

Support airway and respiration if pulm onary edem a

Pa ge 4 4 1

is present o 

Stabilize dysrhythm ias

Control seizures

ED Treatment 

Cleanse the bite site thoroughly.



Tetanus prophylaxis



Benzodiazepines for agitation and restlessness



Antiem etics for nausea and vom iting



Analgesics



Muscle cram ps/spasm therapyâ€”com binations of the following work synergistically: o

Benzodiazepines

o

Narcotics

o

Calcium gluconate: 

Com m only advocated but consensus is lacking on its utility



May provide dram atic but tem porary relief



Effects m ay be transient and m ultiple doses m ay be required



Antihypertensive agents for sym ptom atic hypertension



Specific antivenin: o

Indications: 

Younger than 16 years or older than 65 years or prem orbid com prom ised health status



Sym ptom s do not respond to sym ptom atic m easures.



Significant hypertension



Respiratory distress



Sym ptom atic and pregnant



Consider using for persistent sym ptom s even several days after envenom ation.

o

Always perform a skin test for sensitivity to horse

Pa ge 4 4 1

serum first (test kit included in the antivenin package). o

Watch for hypersensitivity reaction in first 20 m inutes: 

o

Consider pretreatm ent with antihistam ines.

Due to the sm all quantity of antivenin used, if serum sickness reactions occur, they are usually m ild.

o

Effectiveness is usually apparent within 2 hours of the first treatm ent and repeated doses are rarely necessary.

o

Antivenin probably helps to prevent persistent neuropathic sym ptom s and m ay be worth considering for that indication even if the acute stage illness is m ild.

Medication (Drugs) 

Antivenin: 1 am pule (2.5 m L) diluted into 50 m L NS (peds: sam e dose) IV over 1 hour



Calcium gluconate: 10â€“20 m L of 10% solution IV q2hâ€“q4h PRN



Morphine sulfate: 2â€“10 m g (peds: 0.1 m g/kg) IV or IM PRN (titrate to patient response)

Follow-Up Disposition Admission Criteria 

Elderly, pregnant or sym ptom atic young patients



Significant cardiovascular sym ptom s and signs, or severe

Pa ge 4 4 1

hypertension, particularly in presence of prem orbid cardiac disease or chronic hypertension 

Respiratory distress or pulm onary edem a



Persistent sym ptom s not responding to aggressive m anagem ent and specific antivenin

Discharge Criteria 

Asym ptom atic patients with no positive identification of a black widow spider can be released after observation for 1 to 2 hours.



Asym ptom atic patients with no com orbid illness with a positive identification of the black widow spider should be observed for a m inim um of 4 to 6 hours and discharged if their condition does not change.



All discharged patients m ust be instructed about what to watch for in term s of relapsing sym ptom s and to seek appropriate follow-up if needed.



Discharged patients who received antivenin should be instructed to watch for signs of serum sickness.

References 1. Allen C. Arachnid envenom ations. Em erg Med Clin North Am . 1992;10(2):288â€“291. 2. Boyer Hassen LV, McNally JT. Spider bites. In: Auerbach PS, ed. Wilderness m edicine: m anagem ent of wilderness and environm ental em ergencies. 3rd ed. St. Louis, MO: Mosby Year Book, 1995:769â€“786. 3. Clark MD, et al. Clinical presentation and treatm ent of black widow spider envenom ation: a review of 163 cases. Ann Em erg Med. 1992;21(7):782â€“787. 4. Isbister GK, White J. Clinical consequences of spider bites: recent advances in our understanding. Toxicon. 2004;43:477â€“492.

Codes

Pa ge 4 4 1

ICD9-CM 989.5

ICD10 T63.3

Pa ge 4 4 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spider Bite, Bro w n Recluse

Spider Bite,

Brown Recluse Paul Arnold

Basics Description Local or system ic illness caused by brown recluse spider bite envenom ation

Etiology Brown recluse spider features: 

Appearance: o

Delicate body and legs spanning 10 to 25 m m

o

Light- to m edium -brown with darker violin-shaped m arking visible on the upper aspect of the head

o 

Three pairs of eyes

Found widely throughout the southern half of North Am erica



Habitat: typically any warm and dry location indoors or outdoors such as wood piles, bundles of rags, cellars, or attics



Spider not aggressive



Hum ans are bitten when they disturb a spider in its habitat.

Pa ge 4 4 2

Mechanism 

Venom is a com plex cocktail of enzym es and peptides: o

Causes hem olysis and tissue necrosis

o

Triggers com plem ent cascades, platelet aggregation, throm bosis, and release of inflam m atory m ediators.

o

Result is direct cytotoxic effects, coupled with indirect toxicity due to inflam m ation and vascular com prom ise.



System ic toxicity is due to an inflam m atory or allergic response to venom antigenic properties.



Toxicity proportional to: o

The am ount of venom and

o

The am ount of venom relative to the size of patient

Pediatric Considerations Children are m ore vulnerable to a given am ount of venom than healthy adults.

Diagnosis 

Rem em ber the lim ited range of brown recluse spiders and the rarity of arachnidism as a cause of necrotic skin wounds.



Diagnosis m ust be based not only on the clinical presentation but also on a reliable history of spider bite.



In the absence of a reliable spider bite by history, other possible diagnoses m ust be carefully sought and excluded.

Signs and Symptoms History 

Local wound sym ptom onset: o

Typically delayed 1â€“24 hours after bite

Pa ge 4 4 2

o

Usually asym ptom atic but m ay experience m inor stinging and burning sensation



System ic features: o

Rare com plication

o

Develop during the first 1â€“3 days after the bite

o

Severity is proportional to the am ount of venom injected.

o

Patient m ay report: 

Fever, chills, m alaise



Nausea, vom iting, diarrhea



Myalgias, m uscle cram ps, arthralgias



Petechial or urticarial rash

Physical Exam 

Bite wound: o

Usually no visible injury if exam ined within first 1â€“3 days

o

Less com m only, there m ay be pinprick, local blanching and induration, or erythem a.

o

Tissue injury m ay develop at bite site: 

Blister m ay form in the center of the blanched area with circum ferential erythem a.



Blister m ay gradually enlarge and darken with the developm ent of skin and subcutaneous fat necrosis over 3â€“4 days.



Necrosis develops m ost extensively where subcutaneous fat is greatest.



Lower extrem ity blisters spread distally under the influence of gravity.



Local response is not dependent on the extent of envenom ation and cannot be used to predict the severity of subsequent system ic illness.



Other:

Pa ge 4 4 2

o

Exam ination is otherwise usually unrem arkable.

o

Patient m ay have petechial or urticarial rash.

Course 

Skin lesions: o

Vast m ajority of patients recover fully with no sequelae.

o

Lesions rarely evolve into ulcerative necrosis over the following days or weeks.

o

Healing by secondary intention m ay take weeks to m onths.

o 

Ulcers can recur even years later.

Rare com plications include: o

Hem olysis, which m ay lead to hem oglobinuria and acute renal failure

o

Dissem inated intravascular coagulation

o

Shock

Essential Workup Careful inquiry required to elicit the spider bite history

Tests Lab 

Spider venom can be detected in skin lesions, but widespread clinical testing is not available yet.



CBC, electrolytes, blood urea nitrogen, creatinine, prothrom bin tim e/partial throm boplastin test for baseline m onitoring



Urinalysis for evidence of system ic hem olysis

Imaging Soft-tissue radiograph of bite site is indicated if the differential includes suspected gas-form ing organism , infection of ulcers.

Differential Diagnosis

Pa ge 4 4 2



Necrotic ulcers: o

Soft-tissue infection

o

Neoplastic lesion

o

Lym e disease

o

Cutaneous anthrax

o

Other arachnid envenom ation

o

Stevens-Johnson syndrom e

o

Erythem a nodosum

o

Diabetic ulcer

o

Bed sore

o

Lower-lim b vascular insufficiency with secondary ulcer

o 

Chem ical burn

Other etiologies of hem olytic anem ia, DIC, anaphylactoid reactions

P.1037

Treatment Pre Hospital 

Im m obilize wound site.



Cover bite with cool com presses.



Transport to hospital when patient experiences im m ediate onset of sym ptom s.



Supportive m easures for patients with system ic sym ptom s



Venom extraction devices (e.g., Sawyer extractor) have been recom m ended anecdotally but are probably ineffective if >10 m inutes has elapsed since bite.

Pa ge 4 4 2

Alert Every effort should be m ade by caregivers at the scene to find and bring in the responsible spider for identification.

Initial Stabilization IV fluids, oxygen, cardiac m onitoring if the patient is experiencing system ic collapse

ED Treatment 

Cleanse the bite site thoroughly



Tetanus prophylaxis



Antibiotics: o

Appropriate if wound appears infected

o

Not indicated prophylactically

o

Antistaphylococcal (first-generation cephalosporin or penicillinase-resistant penicillins)



Controversial and unproven m easures include: o

Topical or system ic steroids

o

Hyperbaric therapy

o

Topical nitroglycerin

o

Local electric shock

o

Dapsone: 

Screen for G6PD deficiency before initiating



Monitor for m ethem oglobinem ia, hem olysis, and leukopenia during therapy.

o

Excision of necrotic wound: 

Not indicated in the first 8 weeks because m ay cause m ore severe ulcer form ation

 o

Can be considered at a later date

Specific antivenin is of proven benefit if system ic toxicity develops but is of debatable value if only a skin lesion is present.



System ic problem m anagem ent:

Pa ge 4 4 2

o

Standard supportive care and interventions should be em ployed for shock, seizures, DIC, and com a

o

Analgesics for pain control

o

Hem oglobinuria: 

Treated with IV fluids and alkalinization



Monitor renal, fluid, and electrolyte status



Transfusion for significant anem ia

o

Dialysis in the event of acute renal failure

o

Specific antivenin: 

Therapeutic value reduced if given >4 to 6 hours after envenom ation (m ost cases present m ore than 6 hours after presum ed bite)



Before use, weigh low m ortality of brown recluse bites against risk of side effects of antivenin.



Always perform a skin test for sensitivity to horse serum beforehand.



Watch for hypersensitivity reaction in first 20 m inutes.



Pretreat with antihistam ines.



Due to sm all dose of antivenin, risk of serum sickness is low.

Medication (Drugs) 

Antivenin: 1 am pule (2.5 m L) diluted into 50 m L NS (peds: sam e dose) IV over 1 hour



Dapsone: progressive dosage of 50â€“500 m g b.i.d. for 2 weeks (peds: 2 m g/kg/24 h PO for 2 weeks)



Methylprednisolone: 125 m g IV bolus followed by prednisone 30â€“50 m g/d for 5 days (peds: m ethylprednisolone 1â€“2 m g/kg IV, prednisone 1â€“2

Pa ge 4 4 2

m g/kg PO) 

Morphine sulfate: 2â€“10 m g (peds: 0.1 m g/kg) IV or IM PRN

Pediatric Considerations 

Use dapsone only in severe cases because of potential for side effects such as: o

Hepatitis

o

Methem oglobinem ia

o

Hem olytic anem ia

o

Leukopenia

Follow-Up Disposition Admission Criteria 

Significant local reaction, signs of system ic toxicity, reaction to antivenin



Lower threshold for children, patients with com orbidities

Discharge Criteria 

No evidence of system ic toxicity or severe progression of local wound necrosis after envenom ation



Daily reassessm ent, including blood work, until 3 to 4 days after envenom ation to guard against the risk of system ic toxicity.



Patients should be advised about prolonged course for skin healing with consideration for surgical excision after 8 weeks.

Pediatric Considerations Longer observation period before disposition of asym ptom atic cases

Pa ge 4 4 2

because of the higher m ortality in this population

References 1. Henrique da Silva P, et al. Brown spiders and loxoscelism . Toxicon . 2004;44:693â€“709. 2. Isbister GK, White J. Clinical consequences of spider bites: recent advances in our understanding. Toxicon. 2004;43:477â€“492. 3. Krywko DM, Gom ez HF. Detection of Loxosceles Species Venom in Derm al Lesions: A Com parison of 4 Venom Recovery Methods. Ann Em erg Med. 2002;39:475â€“480. 4. Mold JW, Thom pson DM. Managem ent of Brown Recluse Spider Bites in Prim ary Care. J Am Board Fam Pract. 2004;17:347â€“352. 5. Swanson DL, Vetter RS. Bites of Brown Recluse Spiders and Suspected Necrotic Arachnidism . New Eng J Med. 2005;352:700â€“707. 6. Vetter RS, Bush SP. The Diagnosis of Brown Recluse Spider Bite Is Overused for Derm onecrotic Wounds of Uncertain Etiology. Ann Em erg Med. 2002;39:544â€“546.

Codes ICD9-CM 989.5

ICD10 T14.0

Pa ge 4 4 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spinal C o rd Syndro m es

Spinal Cord

Syndromes Judd L. Glasser

Basics Description 

Anterior cord syndrom e: o

Results from flexion or axial loading m echanism or direct cord com pression from vertebral fractures, dislocations, disc herniation, tum or, or abscess

o

Rarely caused by laceration or throm bosis to the anterior spinal artery



Brown-SÃ©quard syndrom e: o

Hem isection of the spinal cord classically as a result of a penetrating wound

o 

Rarely unilateral cord com pression

Central cord syndrom e: o

Most com m only occurs in elderly patients who have pre-existing cervical spondylosis and stenosis

o

Forced hyperextension causes buckling of the ligam entum flavum , creating a shearing injury to the central portion of the spinal cord.



Dorsal cord syndrom e:

Pa ge 4 4 2

o 

Associated with hyperextension injuries

Com plete cord syndrom e: o

Blunt or penetrating traum a that results in com plete disruption of spinal cord

o

Sym ptom s that rem ain >24 hours generally are perm anent.

Etiology Spinal cord syndrom es result from localized disruption of neurotransm ission and exhibit m ixed m otor and sensory deficits. The m ost com m on m echanism is traum a: 

Patients with arthritis, osteoporosis, m etastatic disease, or other chronic spinal disorders are at risk of developing spinal injuries as the result of even m inor traum a.

Diagnosis Signs and Symptoms History Acute loss of m otor and or sensory function usually following a traum atic event

Physical Exam 

Anterior cord syndrom e: o

Bilateral spastic paralysis and loss of pain and tem perature sensation below the level of the lesion

o

Preservation of dorsal colum n function (proprioception and position sense)



Brown-SÃ©quard syndrom e (lateral cord syndrom e): o

Ipsilateral spastic paresis and loss of dorsal colum n function (proprioception and position sense)

o

Contralateral loss of pain and tem perature sensation

Pa ge 4 4 3

o 

Deficits usually begin two levels below the injury

Central cord syndrom e: o

Loss of m otor function affects upper extrem ities m ore severely than lower extrem ities.

o

Most profound deficits occur in the distal upper extrem ities.

o 

Sensory loss is m ore variable.

Dorsal cord syndrom e: o

Loss of proprioception, position sensation, and coordination below the level of the lesion



Com plete cord syndrom e: o

Flaccid paresis below the level of the injury

o

Low blood pressure and heart rate, flushed skin, priapism m ay be present (loss of sym pathetic tone).





Sensory deficit levels: o

C-2â€”occiput

o

C-4â€”clavicular region

o

C-6â€”thum b

o

C-8â€”little finger

o

T-4â€”nipple line

o

T-10â€”um bilicus

o

L-1â€”inguinal region

o

L-5â€”dorsum of the foot

o

S-5â€”perianal area

Motor deficit levels: o

C-5â€”elbow flexion

o

C-7â€”elbow extension

o

C-8â€”finger flexion

o

T-1â€”finger abduction

o

L-2â€”hip flexion

o

L-3â€”knee extension

o

L-4â€”ankle dorsiflexion

Pa ge 4 4 3

o

S-1â€”ankle plantar flexion

Tests Lab 

Basic pre-operative laboratory studies are indicated.



Consider sed rate and C-reactive protein to risk-stratify other potential diagnoses.

Imaging 

All areas of clinical suspicion should be im aged with plain radiographs.



CT of the spine when plain film s are norm al or am biguous: o

CT allows assessm ent of the spinal canal and any im pingem ent by bone fragm ents.



MRI is the im aging m odality of choice for detection of spinal cord dam age; in the acute setting, the indications for MRI are: o

Neurologic deficits not explained by plain film s or CT

o

Clinical progression of a spinal cord lesion

o

Determ ination of acute surgical candidacy

o

Disadvantages of MRI include the inability to adequately m onitor the patient while undergoing the study and the incom patibility with certain m etal devices.

Diagnostic Procedures/Surgery 

Myelography is used with CT when MRI is not available or cannot be perform ed.



A lum bar puncture m ay be required if considering Guillain-BarrÃ©.

Differential Diagnosis 

Dorsal root injury



Peripheral nerve injury

Pa ge 4 4 3



Guillain-BarrÃ© syndrom e



Multiple sclerosis



Transverse m yelitis



Epidural abscess

P.1039

Treatment Pre Hospital 

Full spinal im m obilization



IV access should be established for fluid resuscitation in the setting of neurogenic shock.



Patients should be transported to the nearest traum a center.

Pediatric Considerations Cervical collars m ust be the appropriate size for the child; splinting the head and body with towels and tape is a reasonable alternative.

Initial Stabilization 

Spinal im m obilization m ust be m aintained at all tim es.



Intubation m ust proceed with in-line spinal im m obilization.



IV fluids should be adm inistered at m aintenance levels unless shock is present: o

Spinal traum a m ay cause hypotension due to loss of sym pathetic tone; fluid adm inistration is first-line treatm ent.

o

Other causes of hypotension (e.g., hem orrhage) should be sought before being attributed to SCI.

o

Generally hypovolem ic shock causes tachycardia,

Pa ge 4 4 3

whereas neurogenic shock results in bradycardia. o

If BP does not im prove after a fluid challenge and no other cause for hypotension can be found, vasopressor use m ay be necessary; Î±-agonist is preferred.

ED Treatment 

Other injuries m ust be treated as indicated.



Level of spinal cord injury (SCI) should be determ ined as a baseline to follow for im provem ent or deterioration.



A neurosurgeon m ust be consulted once an SCI is suspected even when plain film s are norm al; early surgical decom pression or im m obilization m ay reduce m orbidity.



The patient with an SCI should be m anaged at an appropriate regional traum a or spinal center: o

If necessary, transfer should occur as soon as m anagem ent of other injuries allow.



High-dose m ethylprednisolone (MP) is started as soon as possible in the patient with SCI: o

The greatest benefit is reported when infusion is begun within 8 hours of injury.

o

MP has not been established as having a definitive clinically significant benefit, and high-dose steroids do increase the likelihood of im m une system com prom ise and gastrointestinal (GI) tract bleeding; however, MP is still considered standard of care in m ost practice settings

o

To prevent GI tract bleeding with steroid use, concurrently start the patient on IV H2 blockade.



IV antibiotics and tetanus prophylaxis are given to patients with a penetrating injury.



IV vasopressor support m ay be required to treat neurogenic shock.

Pa ge 4 4 3

Medication (Drugs) 

MP: 30 m g/kg IV loading dose given over 15 m inutes in the first hour followed by a 5.4 m g/kg/h continuous infusion for the next 23 hours (adults and peds)



Fam otidine: 20 m g IV (peds: 0.6â€“0.8 m g/kg/24h q8hâ€“q12h)



Phenylephrine: 0.5â€“2 Âµg/kg bolus then 50â€“100 Âµg/m in drip

Follow-Up Disposition Admission Criteria All patients with spinal cord syndrom e m ust be adm itted to an intensive care unit setting.

Discharge Criteria No patient with sym ptom s suggestive of SCI should be discharged.

References 1. Am erican College of Surgeons, Com m ittee on Traum a. Advanced traum a life support course for physicians. Chicago: College of Surgeons, 1993: 193â€“203. 2. Bracken MB, et al. A random ized controlled trial of m ethylprednisolone or naloxone in the treatm ent of acute spinal cord injury. N Engl J Med. 1990;322(20):1405â€“1411. 3. Dum ont RJ, Verm a S, Okonkwo DO, et al. Acute spinal cord injury, part II: contem porary pharm acotherapy. Clin Neuropharm acol. 2000;24(5):265â€“279.

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4. Gerling MC, Davis DP, Ham ilton RS, Hayden SR. Effects of cervical spine im m obilization technique and laryngoscope blade selection on an unstable cervical spine in a cadaver m odel of intubation. Ann Em erg Med. 2000;36(4):293â€“300. 5. Hockberger RS, Kirshenbaum KJ. Spinal traum a. In: Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002:329â€“370.

Codes ICD9-CM 952.00-952.19

ICD10 T09.3

Pa ge 4 4 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spinal Injury: Lum bar

Spinal Injury:

Lumbar Bret Ginther

Basics Description 

Flexion com pression fracture: o

Wedge com pression: 

If <50% anterior com pression of the vertebral body, injury considered stable

o



No ligam entous injury



No neurologic deficit

Burst fracture: 

Vertebral body fracture with retropulsion of bone into the neural canal



Kyphosis evident on lateral radiograph



Posterior ligam entous injury



Anterior com pression, lower extrem ities, calcaneal fractures

 

Possible neurologic deficit

Flexion distractionâ€”lap belt injury: o

Abdom inal injuries likely

o

Chance fracture:

Pa ge 4 4 3



Purely bony injury; fracture line through spinous process, pedicles, and vertebral body

o



No kyphosis evident on lateral radiograph



Often no neurologic deficit

Facet dislocation: 

Mostly soft-tissue injury; no fracture



Com plete disruption of posterior ligam ents and intervertebral disc

 



Neurologic deficit m ay be present.

Flexion rotation: o

Unstable injury

o

Neurologic deficit often present

Extension: o

Unstable, uncom m on

o

Disruption of anterior longitudinal ligam ent and intervertebral disc

o 

Neurologic sequelae rare but possible

Shear injuriesâ€”translational injuries: o

Anterior, posterior, or lateral translation of superior vertebral segm ent over the inferior segm ent



o

Com plete ligam entous disruption

o

Neurologic deficit present

Sim ple fractures: o

o

Isolated spinous process fracture: 

Ligam entous disruption



No neurologic deficit

Isolated transverse process fracture: 

Ligam entous disruption



Neurologic deficit possible; rare isolated root injury

Etiology 

Blunt traum a with axial distraction, axial com pression, or

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translational forces applied to lum bar region 

Fall from height landing on the feet (associated calcaneal fractures) or on the buttocks



Motor vehicle accidents (MVA)

Pediatric Considerations 

Rare reports of child abuse presenting as lower extrem ity flaccid paralysis owing to lum bar spine fracture



Spinal cord term inates at L3 in newborn and recedes to T12 by adulthood; direct cord dam age possible in children with high lum bar fractures.



End plate avulsion fractures: Adolescent injury usually at L4â€“5 or L5â€“S1 level; ligam ent pulls off vertebral body end plate; associated neurologic findings usually resolve with excision of end plate fracture.

Diagnosis Signs and Symptoms 

Pain or localized tenderness to palpation in lum bar m idline



Ecchym osis or deform ity overlying lum bar region; palpable deform ity; paraspinal m uscle spasm



Increased interspinous distance by palpation



Step-off (anterior or posterior displacem ent of spinous process) by palpation



Neurologic deficits referable to lum bar spinal nerves: o

Loss of bladder control

o

Motor: hip flexion (L1â€“4), leg extension (L3, L4), ankle dorsiflexion (L4, L5), toe extension (L5)

o

Sensory: inguinal crease (L1), m edial thigh (L2â€“3), knee (L4), lateral calf (L5)

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o 

Reflexes: knee jerk (L2â€“4)

Pain m ay be m asked by associated distracting injuries (e.g., pelvis, calcaneal fractures).



Patients with m ultiple injuries and altered m ental status have an unreliable clinical exam ination and require im aging evaluation.

Essential Workup 

Following criteria associated with higher risk of thoracolum bar (TL) spine injuries and should be im aged:



TL pain or tenderness to palpation



Decreased level of consciousness (Glasgow Com a Scale <14)



Drug intoxication



Neurologic deficits (described above)



Painful, distracting injuries



Severe injury m echanism (e.g., rollover MVA, auto versus pedestrian, fall >10 feet)



Lum bar radiographs (described under Im aging)



Careful neurologic exam ination including: o

Assessm ent of rectal tone

o

Postvoid residual urinary catheterization

o

Bulbocavernosus and crem asteric reflexes

Tests Lab Standard traum a labs, as indicated: 

CBC



Chem istry panel



Co-agulation studies



Urinalysis

Imaging

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

Lum bar radiography with m inim um of anteroposterior and lateral views. Characteristics of unstable fractures include: o

Widening of interspinous, interlam inar, or interpedicular distance



o

Kyphosis >20Â°

o

Translation >2 m m

o

Vertebral body height loss >50%

o

Articular process fracture

Radiographs m ay not help diagnose burst fractures in 25% of cases.



If a fracture is identified, entire spine should be im aged to evaluate potential associated spinal injuries.



Spinous process fracture, transverse process fracture, or sim ple transverse sacral fracture require lum bar flexion-extension film s if patient is neurologically intact and there is no evidence of unstable injury.



CT or MRI should be perform ed for further evaluation of suspected fractures or fractures identified on plain films to assess spinal cord integrity.

Differential Diagnosis 

Contusion



Pathologic fracture (m etastatic cancer)



Osteoporosis



Pelvic fracture



Traum atic herniated disc



Low posterior rib fracture



Tuberculous spondylitis (Pott disease)



Ankylosing spondylitis



Osteogenesis im perfecta (pediatric)



Congenital scoliosis with hem ivertebra (m istaken for lateral wedge fracture)



Child abuse

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P.1047

Treatment Pre Hospital It is difficult to determ ine whether an injury is stable in the field; any patients with suspected spinal injuries should be im m obilized to prevent further injury.

Initial Stabilization 

Im m obilization while tending to im m ediate life-threatening conditions



Airway, breathing, and circulation m anagem ent

ED Treatment 

Maintain spinal im m obilization.



High-dose m ethylprednisolone protocol for any neurologic deficit



Consultation with orthopaedic spine or neurosurgery service



Appropriate analgesia



The following stable injuries m ay be treated conservatively if CT confirm s stability of injury and patient is neurologically intact:



o

Isolated spinous process, transverse process fracture

o

Chance fracture

o

Anterior wedge com pression (<50%) fracture

o

Stable burst fracture

Total contact orthotic devices m ay be useful; lim ited activities; sleep prone; avoid pillows and soft m attresses,

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which m ay worsen deform ity.

Medication (Drugs) 

Narcotic pain m edication in absence of contraindications



High-dose steroid protocol: Methylprednisolone: 30 m g/kg IV load over 1 hour, then 5.4 m g/kg per hour for the next 23 hours; initiate in ED within 8 hours of injury if possible.

Follow-Up Disposition Admission Criteria Patients with traum atic lum bar fractures should be adm itted for stabilization procedures, parenteral pain control, m anagem ent of possible ileus, and evaluation for associated injuries.

Discharge Criteria 

Neurologically intact patients with stable injuries evaluated in conjunction with a spine surgeon



Patients with sim ple com pression (wedge) fractures with no neurologic deficit m ay be considered for outpatient m anagem ent if adequate pain control and appropriate follow-up can be arranged.



Sim ple transverse sacral fracture, isolated spinous process fracture, and isolated transverse process fracture m ay also be considered for outpatient m anagem ent.



The patient m ust be neurologically intact with a stable living situation; CT scan and flexion-extension film s m ust confirm fracture stability.

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References 1. Denis F. Spinal instability as defined by the three-colum n spine concept in acute spinal traum a. Clin Orthop. 1984;189:65â€“76. 2. Gabos P, Tuten H, Leet A, et al. Fracture-dislocation of the lum bar spine in an abused child. Pediatrics. 1998;101:473â€“477. 3. Holm es J, Panacek E, Miller P, et al. Prospective evaluation criteria for obtaining thoracolum bar radiographs in traum a patients. J Em erg Med. 2003;24:1â€“7. 4. Krueger MA, Green DA, Hoyt D, et al. Overlooked spine injuries associated with lum bar process fractures. Clin Orthop. 1996;327:191â€“195. 5. Petersilge C, Em ery S. Thoracolum bar burst fracture: evaluating stability. Sem in Ultrasound CT MR. 1996;17:105â€“113. 6. Savitsky E, Votey S. Em ergency departm ent approach to acute thoracolum bar spine injury. J Em erg Med. 1997;15:49â€“60.

Codes ICD9-CM 805.4 Fracture of vertebral colum n without m ention of spinal cord lesion; fourth cervical vertebra

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spine Injury: C ervical, Adult

Spine Injury:

Cervical, Adult Gary M. Vilke

Basics Description 

Injury to the neck that results in injury to the spinal cord, cervical spine, or the ligam ents supporting the cervical spine.



May have m ore than one m echanism concurrently

Flexion Injuries 

Sim ple wedge fracture: usually a stable fracture



Anterior subluxation: disruption of the posterior ligam ent com plex without bony injury; potentially unstable injury



Clay shoveler fracture: avulsion fracture of the spinous process of C-7, C-6, or T-1; stable fracture



Flexion teardrop fracture: extrem ely unstable fracture and m ay be associated with acute anterior cervical cord syndrom e



Atlanto-occipital dislocation: unstable injury



Bilateral facet dislocation: can occur from C-2â€“C-7; unstable injury

Flexion/Rotation Injuries

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

Unilateral facet dislocation â€œlockedâ€• vertebra: stable injury



Rotary atlanto-axial dislocation: unstable injury

Extension Injuries 

Extension teardrop fracture: an avulsion fracture of the anterior inferior corner of the involved vertebral body; unstable in extension and stable in flexion



Posterior arch of C-1 fracture: arch is com pressed between the occiput and the spinous process of the axis during hyperextension; unstable fracture.



Avulsion fracture of the anterior arch of the atlas: horizontal fracture of C-1 and prevertebral soft-tissue swelling on the lateral C-spine



Hangm an fracture: traum atic spondylolisthesis of the axis involving the pedicles of C-2; unstable fracture



Hyperextension dislocation: described as the syndrom e of the paralyzed patient with a radiographically norm al appearing C-spine

Extension-Rotation Injury Pillar fracture: generally stable fracture

Vertical Compression (Axial Loading) Injuries 

Jefferson fracture: burst fracture of both the anterior and the posterior arch of C-1; extrem ely unstable fracture



Burst fracture: a com m inuted fracture of the vertebral body with variable retropulsion of the posterior body fragm ents into the spinal canal

Etiology 

Blunt traum a is the m ajor cause of neck injuries: o

Autom obile accidents account for >50%.

o

Falls account for approxim ately 20%.

Pa ge 4 4 4

o

Sporting accidents account for 15%.

o

Minor traum a in patients with severe arthritis m ay result in cervical injuries.



Penetrating traum a

Diagnosis Signs and Symptoms 

Neck pain, tenderness on palpation



Num bness, weakness, paresthesias of upper or lower extrem ities



Always assum e a C-spine injury in any patient with: o

Altered m ental status (unconscious, intoxicated, drugs, or hypoxia) following traum a or if events unknown but traum a likely

o

Inability to com m unicate (m entally retarded, language barrier, or intubated) following traum a or if events unknown but traum a likely



o

Distracting injury

o

Blunt traum a involving head or neck

Incom plete Cervical Cord Syndrom es (see separate chapter): o

Brown-SÃ©quard syndrom e: hem isection of cord from penetrating injury (ipsilateral m otor paralysis/contralateral sensory hypesthesia)

o

Anterior cord syndrom e: cervical flexion injury causing cord contusion (paralysis/hypesthesia with sparing of position/touch/vibratory sensations)

o

Central cord syndrom e: patients with cervical degenerative arthritis with forced hyperflexion (deficits greater in upper extrem ities relative to

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lower extrem ities)

Tests Imaging 

Standard radiographs include three separate views: lateral, anterior-posterior, and open-m outh view of the odontoid while still im m obilized.



Lateral radiograph m ust include C1-T1; a swim m er's view m ay be necessary to view lower levels.



Supine oblique views m ay help in identifying subtle rotational injuries.



CT should be obtained when C-spine fractures, dislocations, or soft-tissue swelling is seen on plain film s or for unexplained neck pain/neuro deficit with norm al radiograph.



CT (helical) is considered a good alternative to plain film s, and is favored in certain patients, including intubated blunt traum a patients.



Flexion-extension views m ay be needed to evaluate for dynam ic ligam entous injuries if static radiographs are negative and the alert, cooperative patient still com plains of pain.



MRI has becom e a valuable tool in evaluation of patients with neurologic deficits, including spinal cord injury without radiographic abnorm ality

Differential Diagnosis 

Cervical m uscle strain injury (whiplash)



C-spine dislocation



Cervical fracture dislocation



Com plex or sim ple cervical fractures

P.1041

Pa ge 4 4 4

Treatment Pre Hospital 

If C-spine injury suspected, im m obilize with a hard collar, neck pads, and backboard.



Im m obilized patients require constant observation in case of vom iting.



Im m obilize C-spine in patients with penetrating neck wounds only if a neurologic deficit is present.



If the weapon is still em bedded, im m obilize the neck to avoid further injury and do not rem ove the im paling object unless it is directly im peding breathing.

Initial Stabilization 

Im m obilize the spine using a rigid collar and backboard, plus tape/towels or lightweight foam pads along the side of the neck.



Stabilize the airway, establish IV access, and support circulation: o

Preferred m ethod is careful orotracheal rapid-sequence intubation with in-line spinal im m obilization.

o

Fiberoptic intubation set should be at the bedside and considered if available.

ED Treatment 

Assess patient for other injuries; rem em ber that the abdom inal exam in a C-spineâ€“injured patient is unreliable and further objective testing is indicated.



Patients m ay be clinically cleared and do not require

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C-spine radiograph if they have no: o

Altered level of alertness

o

Intoxication

o

Posterior m idline cervical spine tenderness

o

Distracting painful injury

o

Focal neurologic deficit



If a neurologic deficit is present, consult neurosurgery.



If the radiographs or CT is abnorm al, consult neurosurgery or the orthopaedic spine service.



If the radiographs are norm al but the alert and cooperative patient is having severe neck pain, consider flexion-extension film s, CT, or MRI; if abnorm al, consult neurosurgery.



High-dose steroid protocol should be initiated for patients with neurologic deficits due to fractures or dislocations.

Medication (Drugs) High-dose steroid protocol: 

Methylprednisolone: 30 m g/kg IV bolus then 5.4 m g/kg/h over the next 23 hours; begin within 8 hours of injury

Follow-Up Disposition Admission Criteria 

C-spine fractures or dislocations associated with a neurologic deficit or any unstable fracture or dislocation should be adm itted to the intensive care unit or m onitored setting.

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

Stable C-spine fractures or dislocations should be adm itted.



Isolated spinous process fractures that are not associated with any neurologic deficit or instability on plain film s



Sim ple cervical wedge fractures with no neurologic deficit

Discharge Criteria 

Patients with acute cervical strain â€œwhiplashâ€•



Musculoskeletal injuries that are associated with m ild to m oderate pain, no neurologic deficit, and norm al radiographs



Patients with radiographically norm al C-spine but continuous pain should be discharged with a hard collar and appropriate orthopaedic follow-up.

References 1. Hockberger R, Kirshenbaum K. Spine. In: Rosen P, et al, eds: Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002:329â€“370. 2. Hoffm an JR, Mower WR, Wolfson AB, et al. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt traum a. N Engl J Med. 2000;343:94â€“99. 3. Holm es JF, Mirvis SE, Panacek EA, et al. Variability in com puted tom ography and m agnetic resonance im aging in patients with cervical spine injuries. J Traum a. 2002;53:524â€“530. 4. Richards PJ. Cervical spine clearance: a review. Injury, Int J Care inured. 2005;36:248â€“269. 5. Van Goethem JW, Maes M, Ozsarlak O, et al. Im aging in spinal traum a. Eur Radiol. 2005;15:582â€“590.

Codes ICD9-CM 952.0

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ICD10 S14.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spine Injury: C ervical, Pediatric

Spine

Injury: Cervical, Pediatric Steven Riley

Basics Description 

Accounts for 2% of pediatric traum a-caused hospital adm issions in the United States



Children younger than 8 years: o

Anatom ic differences lead to predom inance of C1-3 injuries.



o

Relatively larger head

o

Weaker cervical m usculature

o

Ligam entous laxity

o

Horizontally oriented facets

Children aged 8â€“12 years: o





Increased incidence of pancervical injuries

Children older than 12 years: o

Injury patterns consistent with those of adults

o

Lower cervical spine injuries m ore com m on

o

Evident radiographically

Spinal cord injury without radiographic abnorm ality (SCIWORA)

Pa ge 4 4 5

o

Occurs in approxim ately 20% of pediatric cervical spine injuries

o

More com m on in children younger than 8 years

o

Sym ptom s m ay be transient and have resolved by tim e of evaluation:

o



Paresthesias



Burning sensation down spine



Weakness

Sym ptom s often occur im m ediately after injury but m ay have delayed onset (i.e., m inutes to days).

Etiology 

Motor vehicle and pedestrian accidents



Falls



Sports injuries

Diagnosis Signs and Symptoms 

Cervical spine pain



Lim ited range of m otion



Neurologic deficit that m ay be transient



May be m asked by altered m ental status or distracting injury





General signs: o

Hypotension

o

Bradycardia

o

Hypoventilation or apnea

Neck signs: o

Tender to palpation over cervical spine

o

Lim ited range of m otion

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o 

Respiratory signs: o







Torticollis

Diaphragm atic breathing

Abdom inal signs: o

Ileus

o

Fecal incontinence

o

Absent rectal tone

Genitourinary signs: o

Priapism

o

Urinary retention

Neurologic signs: o

Paresthesias or sensory deficit

o

Focal weakness

o

Paralysis:

o



Partial cord syndrom es



Quadriplegia

Absent reflexes

Pediatric Considerations Preverbal child m ay be unable to express sym ptom s and m ay not cooperate during exam .

Essential Workup 

Obtain cervical spine radiographs for: o

Cervical spine tenderness

o

Altered m ental status

o

Neurologic deficit (even if transient)

o

Distracting injury or m echanism of injury (i.e., in preverbal child)



Rem em ber, the National Em ergency X-Radiography Utilization Study C-spine decision rule does not apply to children.



Additional im aging studies (CT, MRI) m ay be indicated if

Pa ge 4 4 5

plain radiographs are inconclusive and clinical exam ination suggests injury.

Tests Imaging Cervical spine radiographs: 

Standard initial views: anteroposterior, lateral, and odontoid



Identifies approxim ately 80% of fractures, dislocations, and subluxations



Need to visualize all seven cervical vertebrae.



Space between anterior arch of C-1 and anterior aspect of odontoid process: o



5 m m or sm aller in children and 3 m m in adults

Thickening of prevertebral soft tissue: o

Suggests underlying fracture or ligam entous injury

o

Also occurs with neck flexion, expiration, swallowing

o

Too m uch variability exists for m easurem ents to be highly sensitive.

o

Soft tissue below the glottis should be approxim ately twice as thick as above the glottis.



Pseudosubluxation of C-2: o

Norm al variant

o

A result of ligam entous laxity and often resolves by age of 8 years

o

C-2 anteriorly displaced on C-3

o

Posterior cervical line retains norm al relationships.

o

Line drawn between anterior aspect of spinous processes of C-1 and C-3 should pass within 2 m m of anterior aspect of spinous process of C-2.

o

Larger than 2-m m space suggests underlying hangm an fracture.

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o 

Anterior vertebral wedging of C-3 and C-4: o



Can be applied only at C1-3

May be m istaken for com pression fracture

Epiphysial growth plates m ay resem ble fractures: o

Posterior arch of C-1 fuses by 4 years of age.

o

Anterior arch of C-1 fuses by 10 years of age.

o

Base of odontoid fuses with body of C-2 by 7 years of age.

Flexion and extension views: 

Lim ited use



May be useful if suspected occult ligam entous injury: o

Negative cervical spine film s

o

No neurologic abnorm alities

CT scan: 

If fracture suspected despite negative plain radiographs



For further definition of fracture identified on plain radiographs



If need for differentiating between synchondrosis and fracture

MRI: 

Suspected spinal cord injury with or without abnorm alities found on plain radiographs or CT

Differential Diagnosis 

Cervical m uscle strain



Torticollis



Cervical adenitis



Retropharyngeal abscess



Meningitis

P.1043

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Treatment Pre Hospital Im m obilize all infants and children with potential cervical spine injuries: 

Appropriate size cervical collar



Tape, towels, padding in com bination with car seat or spine board



Larger head creates cervical flexion.



Place padding under neck, shoulders, and back.



Align external auditory m eatus with shoulder.

Initial Stabilization Maintain cervical spine im m obilization: 

Log roll patient.



One person needs to be devoted to in-line cervical spine im m obilization if intubation is required.

ED Treatment 

Any traum a patient with neurologic deficit consistent with spinal cord injury requires m ethylprednisolone (see Medications).



Neurosurgical consultation: o

True subluxation

o

Fracture

o

Transient or persistent neurologic deficit

Medication (Drugs) First Line Methylprednisolone: loading dose 30 m g/kg IV over 1 hour;

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m aintenance infusion 5.4 m g/kg/h over next 23 hours; initiate within 8 hours of injury

Follow-Up Disposition Admission Criteria 

Altered m ental status



Signs/sym ptom s of spinal cord injury



Fracture



Obtain appropriate consultation: o

Neurosurgery

o

Orthopaedic Spine

Discharge Criteria 

Com pletely norm al m ental status



No radiographic abnorm alities



No transient or persistent neurologic deficit



Educate parents: o

SCIWORA can present with delayed onset of sym ptom s.

o

Patient should return to hospital if paresthesias, weakness, or paralysis is present.

References 1. Cirak B, Ziegfeld S, Knight V, et al. Spinal injuries in children. J Pediatr Surg. 2004;39:607â€“612. 2. Brown R, Brunn MA, Garcia VF. Cervical spine injuries in children: a review of 103 patients treated consecutively at a level 1 pediatric traum a center. J Pediatr Surg. 2001;36:1104â€“1114. 3. Patel JC, Tepas JJ III, Moh H. Pediatric cervical spine injuries:

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defining the disease. J Pediatr Surg. 2001;36:373â€“376. 4. Viccellio P, Sim on H, Pressm an B, et al. A prospective m ulticenter study of cervical spine injury in children. Pediatrics. 2001;108(2):e20. 5. Swischuk LE. Em ergency Im aging of the Acutely Ill or Injured Child . 4th ed. Baltim ore, MD: William s & Wilkins; 2000.

Codes ICD9-CM 952.0 Spinal cord injury without evidence of spinal bone injury, cervical

ICD10 514.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spine Injury: C o ccyx

Spine Injury:

Coccyx Gary Schwartz

Basics Description 

Often from a fall with the victim in sitting position



Fall usually occurs from standing height.



Can occur during childbirth



More com m on in wom en

Etiology See Description

Diagnosis Signs and Symptoms 

Tenderness localized over the coccyx



Ecchym osis over the gluteal fold



Pain with sitting, leaning forward, and with defecation

History Obtain history of accident:

Pa ge 4 4 6



Including earlier events that m ight influence m echanism of fall or insult

Physical Exam Diagnosis can often be m ade on physical exam ination: 

Rectal exam to assess tenderness or m obility of coccyx



Isolated coccyx fractures should have no neurologic deficits.

Essential Workup 

Most often isolated injury



If other spinal injury is suspected, spinal im m obilization should be instituted.

Tests Imaging Routine radiographic im aging unnecessary: 

Concern about unnecessary radiation to gonads when diagnosis can be m ade clinically



Im aging is indicated if concern for other spine injuries.



Radiographs can be hard to interpret because coccyx has norm al variant positions that can be confused with fracture.



Lateral radiograph is best view for fracture or dislocation.

Differential Diagnosis 

Coccygodynia



Levator ani syndrom e



Pilonidal cyst



Perirectal abscess

P.1045

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Treatment Initial Stabilization 

Usually none required



Spinal im m obilization as indicated



If patient unstable, consider other diagnoses.



Medicate for pain

ED Treatment 

Pain m edication



Reduce displaced coccyx fracture, but rarely necessary

General Measures Recom m end donut-shaped seat cushion for com fort.

Medication (Drugs) First Line 

Medication for pain if needed



Stool softener

Surgery Reduction m ay be attem pted if displaced coccygeal fracture evident: 

Rarely needed or successful

Follow-Up Disposition Admission Criteria Adm ission is generally not required.

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Discharge Criteria Coccygeal fracture can be m anaged as an outpatient unless other injury m akes adm ission necessary.

References 1. Cwinn, AA. Pelvis. In: Marx J. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:632â€“633. 2. Gutierrez PR, Mas Martinez JJ, Arenas J. Salter-Harris type I fracture of the sacro-coccygeal joint. Pediatr Radiol. 1998;28:734.

Codes ICD9-CM 805.6 Fracture of vertebral colum n without m ention of spinal cord injury, sacrum and coccyx, closed

ICD10 S39.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spine Injury: Tho racic

Spine Injury:

Thoracic Richard D. Zane

Basics Description 

The following forces account for m ost thoracic fractures and dislocations:



o

Axial com pression

o

Flexion-rotation

o

Shear

o

Flexion-distraction

o

Extension

Three anatom ically distinct colum ns; if two of the three colum ns are disrupted, the spinal colum n is unstable: o

Posterior colum n: posterior bony arch and interconnecting ligam entous structures

o

Middle colum n: posterior aspects of the vertebral bodies, posterior annulus fibrosis, and the posterior longitudinal ligam ent

o

Anterior colum n: anterior longitudinal ligam ent, anterior annulus fibrosis, and anterior vertebral body

Major vs. Minor Fractures

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





Minor: o

Isolated articular fracture

o

Transverse process fracture

o

Spinous process fracture

o

Pars interarticularis fracture

Major: o

Com pression fracture

o

Burst fracture

o

Seat-belt injury

o

Fracture-dislocation

Com pression fracture (anterior or lateral flexion): o

Fracture of anterior portion of vertebral body with intact m iddle colum n



o

May be posterior colum n disruption

o

Type A: fracture through both end plates

o

Type B: fracture through superior end plate

o

Type C: fracture through inferior end plate

o

Type D: both end plates intact

Burst fracture (axial loading): o

Fracture through m iddle colum n of spine

o

May have spreading of posterior elem ents and lam ina fractures with possible retropulsion into the spinal canal and potential neurologic com prom ise

o

Type A: fracture through both end plates

o

Type B: fracture through superior end plate

o

Type C: fracture through inferior end plate

o

Type D: burst in m iddle colum n with rotational injury leading to subluxation

o

Type E: burst in m iddle colum n with asym m etric com pression of anterior colum n



Seat-belt injury (flexion-distraction): o

Distraction of posterior and m iddle colum ns with

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anterior colum n intact o

Typically caused by lap belts used without shoulder harness

o

Type A: through bone

o

Type B: prim arily ligam entous

o

Type C: disruption of bone through m iddle colum n

o

Type D: through ligam ents and disc with no m iddle colum n fracture



Fracture-dislocations: o

Failure of all three colum ns following com pression, tension, rotation, or shear forces

o

Type A: flexion-rotation; fall from height

o

Type B: shearâ€”violent force across long axis of trunk

o

Type C: flexion-distraction; bilateral facet dislocation

Etiology 

Thoracic spine is rigid due to the rib cage and the costovertebral articulations: o



The spinal canal is narrowest in the thoracic spine.

Because traum atic thoracic spine fractures require enorm ous forces, m otor-vehicle accidents or falls from height account for m ost fractures: o

A sm all percentage is caused by penetrating injuries (see Spinal Cord Syndrom es).

o

50% of all spinal fractures and 40% of all spinal cord injuries occur at the thoracolum bar junction (T11-L2).

Diagnosis Signs and Symptoms

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

Significant force is required to produce thoracic vertebral fractures.



Pain at the fracture site or im pingem ent of nearby structures by bone fragm ents



Because of the stabilizing influence of the rib cage, a trem endous am ount of force is needed to cause thoracic spine dislocations: o

Concom itant internal injury should be suspected.

o

Thoracic spine fracture-dislocation is less com m on than thoracolum bar fracture-dislocation but has higher incidence of neurologic im pairm ent.



Com m on signs and sym ptom s: o

Localized soft-tissue defect

o

Pain or tenderness

o

Localizedâ€”pain and tenderness over spinous process

o

Referredâ€”paraspinal, anterior chest, or abdom en

o

Paraspinal m uscle spasm

o

Paresthesia or dysesthesia

o

Weakness (focal or global)

o

Distal areflexia, flaccid plegia

o

Bowel or bladder incontinence

o

Priapism

o

Loss of tem perature control

o

Spinal shockâ€”hypotension with bradycardia

Essential Workup 

Rapid evaluation of airway, breathing, and circulation



Prim ary and secondary traum a survey



Detailed neurologic exam , including rectal tone and perianal sensation



Thorough spine exam for deform ity or tenderness



Any m idline tenderness elicited on exam ination,

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distracting injury, or intoxication m andates plain film spine radiography. 

If fracture present, determ ine whether it is stable or unstable.



Assess for bulbocavernous reflex in spinal shock.

P.1049

Tests Imaging 

Midline pain or tenderness, severe m otor-vehicle accident, or falls from height are indications for anteroposterior and lateral plain film views of the spine.



Thin-cut CT scanning is indicated in any patient with evidence of spinal fracture on plain film s to assess spinal canal integrity or in patients with norm al plain film s and significant pain or tenderness and m echanism for severe injury.



Any finding of a fracture anywhere in the thoracic spine m andate im aging of the entire spine with plain radiograph.

Differential Diagnosis 

Arthritis (degenerative and rheum atoid)



Ankylosing spondylitis



Spina bifida



Congenital m alform ation



Neoplasm



Pathologic fracture

Treatment

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Pre Hospital 

If the patient's positioning initially prevents placem ent of a long spinal board, then a short board should be placed until the patient is fully extricated.



Patients with neurologic deficit should be transported directly to a traum a center.

Initial Stabilization 

Manage airway and resuscitate as indicated.



Airway intervention should be done with in-line cervical im m obilization.



Preserve residual spinal cord function and prevent further injury by stabilizing the spine.

ED Treatment 

Perform all needed resuscitation and diagnostic tests with the patient in full spinal im m obilization



If spinal cord injury is suspected, consider the adm inistration of high-dose steroids and consult a spine surgeon.



If spinal fracture or ligam entous injury is suspected without neurologic im pairm ent, arrange CT or MRI scanning while consulting neurosurgery or orthopaedic surgery.



Pain control should be adm inistered as soon as possible; NSAIDs, opiates, and benzodiazepines are the m ainstays of treatm ent.



Neurogenic hypotension presents with bradycardia or norm al heart rate, rather than the tachycardia seen with hypovolem ic shock: o

Neurogenic hypotension should be treated with crystalloid bolus but m ay require vasopressors.

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Medication (Drugs) 

High-dose steroid protocol



Solu-Medrol: 30 m g/kg IV bolus followed im m ediately by an infusion of 5.4 m g/kg/h for the next 23 hours if started within 3 hours of injury; continue for 48 hours if started 3â€“8 hours after injury; not recom m ended >8 hours after injury

Follow-Up Disposition Admission Criteria 

Patients with significant spinal cord or colum n injury should be treated in a regional traum a center.



Unstable spinal colum n injury



Cord or root injury



Ileus



Pain control



Concom itant traum atic injury

Discharge Criteria Stable m inor fractures after orthopaedic or neurosurgical evaluation

References 1. Bagley LJ, et al, Im aging of spinal traum a. Radiol Clin North Am . January 1, 2006;44(1):1â€“12, vii. 2. Block BE, et al. Thoracic and lum bar spine injuries in children. Contem p Orthop. 1994;29(4):243â€“555. 3. Brandser EA, El-Khoury GY. Thoracic and lum bar spine traum a. Radiol Clin North Am . 1997;35(3):533â€“557.

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4. Chiles BW III, Cooper PR. Acute spinal injury. N Engl J Med. 1996;334(8):514â€“520. 5. El-Khoury GY, Whitten CG. Traum a to the upper thoracic spine: anatom y, biom echanics, and unique im aging features. Am J Roentgenol. 1993;160:95â€“102. 6. Hockberger RS, et al. Spine. In: Rosen P, et al, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002: 329â€“369. 7. Rivas LA, et al, Multislice CT in thoracic traum a. Radiol Clin North Am . May 1, 2003;41(3):599â€“616.

Codes ICD9-CM 952.10

ICD10 S24.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Splenic Injury

Splenic Injury

Albert Jin

Basics Description 

The spleen is form ed by reticular and lym phatic tissue and is the largest lym ph organ.



The spleen lies in the left upper quadrant between the fundus of the stom ach and the diaphragm .

Etiology 

The spleen is the m ost com m only injured intraabdom inal organ: o

In nearly two thirds of cases, it is the only dam aged intraperitoneal structure



Motor-vehicle accidents (auto-auto, pedestrian-auto) are the m ajor cause (50â€“75%), followed by blows to the abdom en (15%) and falls (6â€“9%)



Mechanism of injury and kinem atics are im portant factors in evaluating patients for possible splenic injury.



Splenic injuries are graded by type and severity of injury: o

Grade I: superficial laceration

o

Grade II: m ore extensive laceration or subcapsular hem atom a

o

Grade III: laceration >3 cm involving trabecular

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vessels o

Grade IV: laceration involving segm ental or hilar vessels

o

Grade V: shattered spleen

Pediatric Considerations 

Poorly developed m usculature and relatively sm aller anteroposterior diam eter increase the vulnerability of abdom inal contents to com pressive forces.



Rib cage is extrem ely com pliant and less prone to fracture in children but provides only partial protection against splenic injury.



Splenic capsule in children is relatively thicker than that of an adult; parenchym a of spleen seem s to contain m ore sm ooth m uscle than in adults.



Significant abdom inal injury occurs in only about 5% of child abuse cases but is the second m ost com m on cause of death after head injury.

Diagnosis Signs and Symptoms History 

In blunt traum a, note the type and direction (horizontal or vertical) of any deceleration or com pressive forces: o

Injuries are caused by com pression of the spleen between the anterior abdom inal wall and the posterior thoracic cage or vertebra (e.g., lap-belt restraints).



In penetrating traum a, note the characteristic of the weapon (type and caliber), distance from the weapon, or

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the type and length of knife or im paling object: o

Injuries result from a com bination of the kinetic energy and shear forces of penetration.

Physical Exam 



System ic signs from acute blood loss: o

Syncope, dizziness, weakness, confusion

o

Hypotension or shock

Local signs: o

Left upper quadrant (LUQ) abdom inal tenderness

o

Palpable tender m ass in LUQ (Balance sign)

o

Referred pain to the left shoulder (Kehr sign)

o

Abdom inal distention, rigidity, rebound tenderness, involuntary guarding



Contusions, abrasions, or penetrating wounds to the chest, flank, or abdom en m ay indicate underlying spleen injury.



Fractures of lower left ribs are com m only seen in association with splenic injuries.

Pediatric Considerations Age-related difficulties in com m unication, fear-induced uncooperative behavior, or a concom itant head injury m ake clinical exam ination less reliable.

Essential Workup 

Physical exam is neither specific nor sensitive for splenic injury.



Adjunctive im aging studies are required.

Tests Lab 

No hem atologic laboratory studies are specific for diagnosis of injury to the spleen.



Obtain baseline hem oglobin, type and cross-m atch, and

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chem istries.

Imaging 

Plain abdom inal radiographs: o

Too nonspecific to be of value

o

Chest radiograph findings suggestive for splenic injury include left lower rib fracture(s), elevation of left hem idiaphragm , or left pleural effusion



Ultrasound (US; FAST exam ): o

Can be done at bedside, especially if the patient is too unstable to go to CT

o

Prim ary role is detecting free intraperitoneal blood, which m ay suggest splenic injury.

o

Does not im age solid parenchym al dam age well

o

Technically com prom ised by uncooperative patient, obesity, substantial bowel gas, and subcutaneous air



CT scan: o

Procedure of choice in stable patient

o

Depicts the presence and extent of splenic injury and adjacent organs, including the retroperitoneum

o

Provides the m ost specific inform ation in patients stable enough to go to the CT scanner

Diagnostic Procedures/Surgery Diagnostic peritoneal lavage (DPL): 

Extrem ely sensitive for the presence of hem operitoneum although nonspecific for source of bleeding and does not evaluate retroperitoneum

Differential Diagnosis 

Intraperitoneal organ injury, especially liver



Injury to retroperitoneal structures



Thoracic injury

P.1051

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Treatment Pre Hospital 

Obtain details of injury from prehospital providers.



Insert two large-bore IVs.



Penetrating wounds or evisceration should be covered with m oist, sterile dressings.

Initial Stabilization 

Airway m anagem ent (including C-spine im m obilization)



Standard traum a resuscitation m easures: o

Adequate IV access, including central lines and cutdowns, as dictated by the patient's hem odynam ic status

o

Fluid resuscitation, initially with 2 L of crystalloid (NS or lactated Ringer solution), followed by blood products as needed

ED Treatment 

Im m ediate laparotom y m ay be appropriate in the acutely injured patient who is hem odynam ically unstable with presum ed hem operitoneum and splenic injury.



Most patients with acute splenic injury either are hem odynam ically stable or stabilize rapidly with relatively sm all am ounts of fluid resuscitation.



Adjunctive diagnostic procedures supplem enting the physical exam should be perform ed early in the evaluation, followed by laparotom y when indicated by positive diagnostic findings.

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

Gunshot wounds to the anterior abdom en are routinely explored in operating room .



Stab wounds can be m anaged by local wound exploration, followed by US or DPL when intraperitoneal penetration is suspected.



Operative versus nonoperative m anagem ent: o

Patients with signs and sym ptom s of intraperitoneal hem orrhage, those with operative indications based on im aging/diagnostic procedures, and those who fail nonoperative m anagem ent should undergo laparotom y.

o

Splenectom y versus splenic salvage depends on the grade of splenic injury.

o

Patient selection for nonoperative m anagem ent includes hem odynam ic stability, no evidence of other intraabdom inal injury, isolated splenic injury confirm ed by im aging study (m ost com m only CT scan).

Geriatric Considerations Patients older than 55 years should be considered for operative m anagem ent due to decreased physical tolerance to traum atic insult and reduced physiologic reserve.

Pediatric Considerations 

Nonoperative m anagem ent of splenic injuries is considered safe: o

Concerns for overwhelm ing postsplenectom y infection/sepsis

Follow-Up

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Disposition Admission Criteria All patients with splenic injury require hospitalization for definitive laparotom y or observation with serial abdom inal exam inations, serial hem atocrit determ inations, and bed rest.

Discharge Criteria Only asym ptom atic patients objectively dem onstrated not to have splenic or other traum atic injury m ay be discharged.

References 1. Dupuy DE, Raptopoulos V, Fink MP. Current concepts in splenic traum a. J Intens Care Med. 1995;10:76â€“90. 2. Esposito T, Gam elli R. Injury to the spleen. In: Felicano D, et al, eds. Traum a. 3rd ed. Norwalk, CT: Appleton & Lange, 1996:525â€“550. 3. Jurkovich Gregory J. and C. Jam es Carrico. Managem ent of the Acutely Injured Patient. In:Sabiston Textbook of Surgery. 15th ed. Philadelphia, PA: W.B. Saunders Com pany, 1997: 320V323. 4. Marx J. Abdom inal traum a. In: Rosen P, et al, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002: 415â€“436. 5. Peitzm an A, et al. Injury to the spleen. Curr Probl Surg. 2001;38(12):932â€“1008.

Codes ICD9-CM 865.00

ICD10 S36.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spo ndylo lysis/Spo ndylo listhesis

Spondylolysis/Spondylolisthesis Joel Kravitz

Basics Description Spondylolysis 

Bony defect at the pars interarticularis (the isthm us of bone between the superior and inferior facets): o



Can be unilateral or bilateral

Type 1â€”dysplastic: congenital defect of the neural arch or intra-articular facets



Type 2â€”isthm ic: stress fracture from repetitive m icrotraum a through the neural arch



Type 3â€”degenerative: long-standing segm ental instability



Type 4â€”traum atic



Type 5â€”pathologic: generalized or focal bone disease

Spondylolisthesis 

The slipping forward of one vertebra upon another



Spondylolysis can contribute to spondylolisthesis, which is noted in approxim ately 5% of the population.



Of those with spondylolysis, 50% will have som e degree of

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spondylolisthesis develop during their lifetim e, and 50% of those will be sym ptom atic: o

Literature does not associate athletic activity with increased slippage.



Spondylolisthesis predisposes to sciatica.



Spondylolisthesis is divided into four grades based on degree of slippage (Meyerding grading system ):



o

Grade I: up to 25% of the vertebral body width

o

Grade II: 26â€“50% of vertebral body width

o

Grade III: 51â€“75% of vertebral body width

o

Grade IV: 76â€“100% ofvertebral body width

The m ost com m on location for spondylolisthesis is L-5 displaced on the sacrum (85â€“95%), followed by L-4 on L-5.

Pediatric Considerations 

Spondylolysis is one of the m ost com m on causes of serious low back pain in children, although it is m ost often asym ptom atic.



Sym ptom s m ost often present during adolescent growth spurt between ages 10 and 15 years.



Seen com m only in athletic teens; particularly in sports involving back hyperextension (e.g., gym nastics, diving, football).



Acute sym ptom s are related to traum a.

Etiology Unknown; theories include congenital pars anom alies, bone-density alterations, and recurrent subclinical stress injury.

Diagnosis

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Signs and Symptoms History 

Onset often gradual, unless traum atic



Often associated with feeling of stiffness or spasm in paravertebral m uscles



Pain in the back and proxim al legs that is aggravated by standing and walking



Sitting or forward bending relieves pain



Pain occurs after varying am ounts of exercise, with standing, or with coughing: o

Aggravating/Alleviating factors: for exam ple, repetitive hyperextending m ovem ents



Relief of pain with rest is variable and slow and usually requires sitting or stooping.



System ic/Neurologic sym ptom s: m inim al, unless significant traum a or â€œslipâ€•

Physical Exam 



Hyperlordotic posture: o

Trunk m ay appear shortened.

o

Rib cage approaches iliac crests.

Ham string tightness: o



Knees flexed to allow patient to stand upright

Only â€œtypicalâ€• finding is one-legged hyperextension: o

Standing on one leg and leaning backward reproduces pain on ipsilateral side.



Palpation m ay reveal step-off with a prom inent spinous process of L-5 in significant spondylolisthesis.



Neurologic exam is usually norm al: o

If abnorm al, pain and sensorim otor loss is in a derm atom al distribution.

o

Consider herniation or spondylolisthesis.

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Pediatric Considerations 

Spondylolysis in a child younger than 10 years is rare; these patients should be watched for: o

Constant pain lasting several weeks

o

Pain occurring spontaneously at night

o

Pain that interferes repeatedly with school, play, or sports

o

Pain associated with m arked stiffness, lim itation of m otion, fever, or neurologic signs

o

Pain at the lum bosacral junction

Tests Imaging 

Lum bosacral spine radiographs: o



Lateral and oblique radiographs of spine m ost helpful

Spondylolysis will m anifest as a radiolucent defect in the pars interarticularis, visible as a â€œcollarâ€• or â€œbroken neckâ€• on the oblique view â€œScottie dogâ€•: o



Majority (85â€“95%) found at L5-S1 level

Spondylolisthesis will m anifest as forward slipping of one vertebral body on another (on lateral).



SPECT scanningâ€”better specificity for linking back pain to spondylolysis



CT scan: o

Pathology m ore clearly dem onstrated than plain film s

o

Can identify other spinal pathology

o

Plays an im portant role for orthopaedics in m anagem ent decisions through identification of new stress fractures and healing of old stress fractures



Outpatient evaluation unless history of recent traum a



MRIâ€”exact role not yet clarified in literature:

Pa ge 4 4 8

o

Useful for defining root im pingem ent and foram inal narrowing

Pediatric Considerations 

Lower threshold for ordering im aging studies



Progressive slipping m ore likely to occur than in adults.

Differential Diagnosis 

Tuberculosis



Discitis



Bone or spinal cord tum or



Pyelonephritis



Retroperitoneal infection



Injury to m uscles or joints of back



Congenital hip dislocation



Rickets



Ruptured intervertebral disc



Vascular claudication

P.1053

Treatment Pre Hospital Spinal precautions are not needed unless there is a history of recent traum a.

Initial Stabilization Vigorous attem pts at traction should not be pursued.

ED Treatment 

Pain control and m uscle relaxants as clinically needed

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

Supportive therapy if sym ptom s are m ild



Restrict activities if repetitive traum a is likely aggravating cause (e.g., sports) for 3â€“6 weeks, followed by re-introduction of activity when asym ptom atic.



Consider antilordotic braces (controversial) or physical therapy



Orthopaedic consult or referral if sym ptom s are m oderate to severe or unresponsive to supportive care



Surgical intervention typically consists of spinal fusion in the flexed position: o

50% of sym ptom atic patients with spondylolisthesis m ay require surgery.



All sym ptom atic patients with grade III or IV spondylolisthesis should probably undergo surgery.



Exercises are not of proven benefit.

Pediatric Considerations 

Activity restriction is not necessary if m inim al or no sym ptom s.



Literature suggests good outcom e for young athletes with conservative treatm ent.

Medication (Drugs) 

Muscle relaxants: o

Exam pleâ€”m ethocarbam ol: 1,000â€“1,500 m g PO q.i.d. (peds: safety and effectiveness for children younger than 12 years not established)



NSAIDs: o

Exam pleâ€”ibuprofen: 200â€“800 m g PO t.i.d.â€“q.i.d. (peds: 5â€“10 m g/kg PO q6h)



Opioids:

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o

Exam pleâ€”m orphine sulfates: 0.1 m g/kg up to 2â€“4 m g increm ents IV.

Follow-Up Disposition Admission Criteria 

Inability to walk



Inability to cope at hom e due to pain or social situation



Progressive neurologic deficit

Discharge Criteria 

Orthopaedic follow-up arranged



Social support system in place



Pain control



Patient education

Pediatric Considerations Close follow-up is m andatory.

References 1. Congeni J, McCulloch J, Swanson K. Lum bar spondylolysis. A study of natural progression in athletes. Am J Sports Med. 1997;25(2):248â€“253. 2. Debnath UK, Freem an BJ et al. Clinical outcom e and return to sport after the surgical treatm ent of spondylolysis in young athletes. J Bone Joint Surgery. March 2003;85(2);244. 3. Iwam oto J, Takeda T, Wakano K. Returning athletes with severe low back pain and spondylolysis to original sporting activities with conservative treatm ent. Scand J Med Sci Sports. Decem ber 2004;14(6);337. 4. Miller SF, Congeni J, Swanson K. Long-term functional and

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anatom ical follow-up of early detected spondylolysis in young athletes. Am Jour Sports Med. June 2004;32(4);928. 5. Nachem son A. Newest knowledge of low back pain. Clin Orthop. 1992;279:8. 6. Satndaert CJ. Spondylolysis. Phys Med Rehab Clin North Am . 2000;11(4):785â€“801. 7. Skinner H. Disorders, diseases and injuries of the spine. In: Current diagnosis and treatm ent in orthopedics. Norwalk, CT: Appleton & Lange,1995:206â€“211. 8. Vitek G. Spine conference spondylolysis and spondylolisthesis. Ortho News Magazine. May 1995. Available at: http://www.nm is.com /onm /htm l/sponconf-spon.htm .

Codes ICD9-CM 721.90 756.12

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spo ntaneo us Bacterial Perito nitis

Spontaneous Bacterial Peritonitis Michael Schmidt Amer Aldeen

Basics Description 

Infection of ascites fluid without an evident intra-abdom inal surgically treatable source: o

Ascites polym orphonuclear leukocyte count >250 cells/m m 3 with a positive bacterial ascites culture



Must be distinguished from secondary bacterial peritonitis: o

Nonsurgical m anagem ent of secondary bacterial peritonitis carries 100% m ortality.

o

Surgical m anagem ent of spontaneous bacterial peritonitis (SBP) carries 80% m ortality.

Etiology Mechanism 

Portal hypertension causes translocation of bacteria through edem atous gut m ucosa to lym ph nodes to the peritoneal cavity.



Transient bacterem ia with low serum com plem ent



Im paired activity of reticuloendothelial system

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phagocytosis and opsonization 

Patients with a total protein concentration <1 g/dL have a 20% risk of developing SBP during the first year after diagnosis of ascites.



Usually seen in the setting of cirrhosis



Rare in other conditions causing ascites (nephrotic syndrom e or congestive heart failure)



Predom inant organism s o

Escherichia coli 43%

o

Streptococci 28%

o

Klebsiella 11%

o

Polym icrobial 5%

o

Enterobacter 4%

o

Staphylococci 3%

o

Pseudom onas 1%

o

Proteus, Citrobacter, Enterococcus

o

Gram positives account for 50% of cases in patients who are on prophylactic therapy with fluoroquinolones.

Diagnosis Signs and Symptoms 13% of patients with SBP have absolutely no signs or sym ptom s of infection.

History 

Abdom inal pain, often very m ild



Fever, chills



Diarrhea



Worsening ascites

Pa ge 4 4 8



Altered m ental status

Physical Exam 

Fever is the m ost com m on sign: o

A lower threshold for fever (>37.8Â°C or >100.4Â°F) is m aintained for cirrhotic patients due to baseline hypotherm ia



Altered m ental status



Ascites: o

Only clinically obvious ascites (shifting dullness and fluid wave) is associated with developm ent of SBP.



Abdom inal tenderness: o

Developm ent of a rigid abdom en does not occur because of the separation of visceral and parietal pleura due to ascites.

Essential Workup Paracentesis is the m ainstay of diagnosis: 

Procedure: o

Location (with patient supine): 

4 cm cephalad and m edial to anterior superior iliac spine



2 cm caudad to the um bilicus (ensure bladder em ptying beforehand)

o

Total 40 m L should be aspirated: 

10 m L for each culture bottle



10 m L for cell count and chem istries (red top, purple top EDTA, and sterile container)

o

Inoculate culture bottles with ascitic fluid im m ediately at the bedside.

o

Coagulopathy does not need to be corrected before the procedure (except for platelets <20K)

Tests

Pa ge 4 4 9

Lab 

Im portant ascites fluid assays: o

Cell count and diff (PMN >250 cells/m m 3 )

o

Total protein <1 g/dL

o

Album in (serum -ascites album in gradient >1.1 g/dL is consistent with portal hypertension)

o

Am ylase

o

Culture and gram stain

o

Glucose >50 m g/dL

o

Ascites leukocyte esterase on dipstick has excellent negative predictive value for SBP.



CBC with differential



Basic m etabolic panel



Prothrom bin tim e/partial throm boplastin tim e



Liver function tests (including album in)



Blood cultures



Urinalysis and culture

Imaging 

Abdom inal ultrasound: o

Confirm s presence of ascites

o

Helps guide paracentesis



Chest radiograph



Abdom inal radiographs: flat plate and upright to evaluate for perforation or obstruction

Differential Diagnosis 



Alcohol hepatitis: o

Fever, leukocytosis, abdom inal pain +/- ascites

o

Ascites PMN <250 cells/m m 3

Secondary bacterial peritonitis: o

Due to perforation or abscess

o

Usually polym icrobial

Pa ge 4 4 9





o

Ascites total protein >1 g/dL

o

Ascites glucose <50 m g/dL

Culture-negative neutrocytic ascites: o

Ascites PMN >250 cells/m m 3

o

Ascites culture negative

o

Can be due to tuberculosis or m alignancy

Monom icrobial nonneutrocytic bacterascites: o

PMN <250 cells/m m 3

o

Ascites culture positive, due to colonization phase of SBP



Polym icrobial bacterascites: o

PMN <250 cells/m m 3

o

Ascites culture positive with m ultiple organism s, due to accidental gut perforation (1 in 1,000 paracenteses)

P.1055

Treatment Initial Stabilization 

ABCs



Aggressive IV fluid resuscitation



Prom pt antibiotic treatm ent for septic shock

ED Treatment 

Adm inister platelets before paracentesis only if <20 K



Give antibiotics if ascites PMNs >250 cells/m m 3 o

First choice: third-generation cephalosporin

o

Second choice: am picillin-sulbactam or aztreonam

Pa ge 4 4 9

o

Avoid am inoglycosides.

o

Give antibiotics for 5 days and extend to 10 if no im provem ent in 48 hours.



IV album in is helpful in preventing renal im pairm ent and reducing m ortality.

Medication (Drugs) 

Album in: 1.5 g/kg IV on day 1, 1 g/kg on day 3



Aztreonam : 0.5â€“2 g IM/IV q6hâ€“q12h



Cefotaxim e: 2 g IV (peds: 50â€“180 m g/kg/24h) q8h



Ceftriaxone: 2 g IV (peds: 50â€“75 m g/kg/24h) q8h



Ciprofloxacin: 500 m g PO b.i.d.



Ofloxacin: 400 m g PO b.i.d.

Follow-Up Disposition Prognosis: 

Mortality due to SBP itself is low.



In-hospital noninfectionâ€“related m ortality is 20%



One-year and two-year m ortality rates after an episode of SBP are 70â€“80%, respectively.

Admission Criteria 

Adm it all patients for IV antibiotics and gastroenterology consultation



Intensive care unit adm ission for septic shock or severe hepatic encephalopathy

Discharge Criteria If patients refuse adm ission, a dose of IV ceftriaxone and a course of

Pa ge 4 4 9

oral fluoroquinolones followed by close follow-up are appropriate.

Issues for Referral Hepatology or gastroenterology referral m ay be indicated for patients.

Alert 

Issues with continuous abdom inal peritoneal dialysis (CAPD) o

Sym ptom s: cloudy peritoneal fluid (90%), abdom inal pain (80%), and fever (50%)

o

Signs: abdom inal tenderness 70%

o

Diagnosis: peritoneal WBC >100 cells/m m 3 with positive gram stain or culture

o

Microbiology: 

50+% of cases are due to gram positives, m ost com m only staphylococci.



E. coli is an uncom m on cause of peritonitis in patients with CAPD.

o

Treatm ent: 

Antibiotics are given through the intraperitoneal route.



1st choice: cefazolin (1 g IP per day) + ceftazidim e (1 g IP per day)



Vancom ycin (2 g IP every week) is alternative to cefazolin. 

Am ikacin 2 m g/kg/d IP

References 1. Castellote J, Lopez C, Gornals J et al. Rapid diagnosis of spontaneous bacterial peritonitis by use of reagent strips. Hepatology . 2003;37:893. 2. Grabeau CM, Crago SF, Hoff LK, et al. Perform ance standards for therapeutic abdom inal paracentesis. Hepatology. 2004;40:484.

Pa ge 4 4 9

3. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous album in on renal im pairm ent and m ortality in patients with cirrhosis and spontaneous bacterial peritonitis. New Engl J Med. 1999;341:403. 4. Such J, Runyon BA. Spontaneous bacterial peritonitis. Clin Infect Dis. 1998;27:669.

Miscellaneous SEE ALSO: Hepatic Encephalopathy; Hepatitis; Hepatorenal Syndrom e

Codes ICD9-CM 567.2

ICD10 K65.9

Pa ge 4 4 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spo ro tricho sis

Sporotrichosis

Maggie Ferng

Basics Description 

Lym phocutaneous: o

Disease with or without hem atogenous spread after traum atic inoculation with soil or plant m aterial



o

Inoculation of fungus into skin/soft tissue

o

Secondary to anim al bites/scratches, traum a

o

Increased risk: farm ers, gardeners, forestry workers

Pulm onary: o

Inhalation of conidia aerosolized from soil/plant decay

o

Increased risk: alcoholics, diabetics, chronic obstructive pulm onary disease, steroid use



Multifocal extracutaneous: o

Cutaneous inoculation or hem atologic spread

o

Increased risk: HIV/im m unosuppressed patients

Etiology 

Fungal infection caused by Sporothrix schenckii: o

Dim orphic fungus

o

Occurs as m old on decaying vegetation, m oss, and soil in tem perate and tropical environm ents

Pa ge 4 4 9



Anim al vectors, notably cats and arm adillos

Diagnosis Signs and Symptoms 

Several clinical m anifestations/syndrom es



Determ ined by m ode of inoculation and host factors

Lymphocutaneous 

Most com m on m anifestation



Initial lesions appear days to weeks after inoculation.



Begin as papule, becom e nodular, often ulcerate: o

Distal extrem ities m ore com m only involved

o

Size: m illim eters to 4 cm

o

Pain is absent or m ild.

o

Drainage is nonpurulent.



System ic sym ptom s usually absent



Secondary nodular lesions develop along lym phatics draining original site.



May wax and wane over years if untreated

Fixed Cutaneous 

Plaquelike or verrucous lesion at site of inoculation



Ulceration uncom m on



Do not m anifest lym phangitic progression.

Extracutaneous 

Osteoarticular: o

Most com m on extracutaneous m anifestation

o

Joint inflam m ation, effusion, and pain

o

Single or m ultiple joint involvem ent of extrem ities

o

Indolent onset, few system ic sym ptom s

o

Tenosynovitis, osteom yelitis, and bursitis

Pa ge 4 4 9





Pulm onary: o

Syndrom e resem bles m ycobacterial infection.

o

Fever, weight loss, fatigue

o

Productive cough, hem optysis

Less com m only associated sites: o

Chronic lym phocytic m eningitis

o

Ocular adnexa, endophthalm itis

o

Genitourinary, sinuses

Multifocal Extracutaneous (Disseminated) 

Low-grade fever, weight loss



Diffuse cutaneous lesions



Arthritis/Osteolytic lesions/Parenchym al involvem ent



Can be fatal if untreated



Often occurs in im m unocom prom ised host

Essential Workup Diagnosis dependent on isolation S. schenckii from site of infection

Tests Lab 

Blood tests not indicated with cutaneous disease



Cultures of sputum , synovial fluid, cerebrospinal fluid (CSF), blood as indicated by extracutaneous m anifestations



No reliable serologic assays available

Imaging 

Lym phocutaneous/Fixed cutaneous: o

Biopsy reveals pyogranulom atous inflam m ation, cigar-shaped yeast



Pulm onary: o



Chest radiograph reveals cavitary lesions

Extracutaneous/Dissem inated:

Pa ge 4 4 9

o

CSF reveals lym phocytic m eningitis, increased protein/decreased glucose.

o

Consider bone scan in im m unocom prom ised host.

Diagnostic Procedures/Surgery Pulm onary: 

Gram stain of sputum m ay yield yeast.



Sputum cultures often positive

Differential Diagnosis 







Lym phocutaneous: o

Leishm aniasis

o

Nocardiosis

o

Mycobacterium m arinum

o

Tularem ia

Fixed cutaneous: o

Bacterial pyoderm a

o

Foreign-body granulom a

o

Inflam m atory derm atophyte infections

o

Blastom ycosis

o

Mycobacteria

o

Chrom oblastom ycosis

Osteoarticular: o

Rheum atoid arthritis

o

Gout

o

Tuberculosis

o

Bacterial arthritis

o

Pigm ented villonodular synovitis

Pulm onary and m eningitis: o

Histoplasm osis

o

Coccidioidom ycosis

o

Cryptococcal disease

o

Mycobacterial infections

Pa ge 4 4 9

P.1057

Treatment Initial Stabilization Airway/Hem odynam ic stabilization for severely ill patients with extracutaneous m anifestations

ED Treatment 

Lym phocutaneous/Fixed cutaneous: o

o

Itraconazole (drug of choice): 

Better tolerated



More expensive



Potential for hepatotoxicity

Saturated solution of potassium iodide (SSKI): 

Less expensive



Bitter taste and side effects (anorexia, nausea, diarrhea) lead to lim ited acceptability.



o

Local heat therapy (>35Â°C) inhibits fungal growth.

o

Therapy m ay take 3â€“6 m onths.

Pulm onary: o

Itraconazole or am photericin B in early disease: 

o

Effective in about 30% of cases

More advanced disease often requires resection plus am photericin B.





Osteoarticular: o

Itraconazole: first line

o

Am photericin B if refractory

Dissem inated:

Pa ge 4 5 0

o

Itraconazole in stable, im m unocom petent patients

o

Am photericin B indicated in: 

Acutely ill



Meningitis (m ay need 5-fluorocystine as adjunct)

 

Im m unosuppressed host

HIV and sporotrichosis: o

Suppressive therapy with itraconazole is recom m ended after initial infection.

Medication (Drugs) 

Am photericin B: start 0.25 m g/kg IV per day, advance to 0.5â€“1.5 m g/kg IV per day, for 1- to 2.5-g course



Itraconazole: o

For lym phocutaneous: 100â€“200 m g PO per day for up to 6 m onths

o 

For pulm onary/osteoarticular 200 m g PO per day.

SSKI: 5 gtt in water or juice t.i.d.; increase by 5 gtt/dose each week up to a m ax. 40â€“50 gtt t.i.d. as tolerated, for 6â€“12 weeks or until lesions resolve

Follow-Up Disposition Admission Criteria 

System ic signs/sym ptom s



Pulm onary, CNS, m ultifocal disease



Im m unosuppressed host with dissem inated disease

Discharge Criteria

Pa ge 4 5 0



Lym phocutaneous/Fixed cutaneous form , nontoxic



Im m unosuppressed host, only if occult dissem inated disease ruled out

References 1. Bustam ante B, Cam pos PE. Endem ic sporotrichosis. Curr Opin Infect Dis. 2001;14(2):145â€“149. 2. Kauffm an CA. Sporotrichosis. Clin Infect Dis. 1999;29:231â€“237. 3. Rex JH, Okhuysen PC. Sporothrix schenckii. In: Mandel GL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases. 5th ed. New York, NY: Churchill Livingstone, 2000: 2695â€“2699.

Codes ICD9-CM 117.1

ICD10 B42.9

Pa ge 4 5 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Staphylo co ccal Scalded Skin Syndro m e

Staphylococcal Scalded Skin Syndrome Timothy J. Mader Laura A. Matzkin

Basics Description 

Results from the actions of a soluble epiderm olytic exotoxin produced by Staphylococcus aureus: o

Produced at a distant site of infection or colonization

o

Dissem inates hem atogenously

o

Lyses desm osom es of granular cells in the superficial epiderm is

o 

Results in generalized intraderm al exfoliation

Disease of infants and children younger than 6 years: o

Adults have specific staph antibodies allowing them to localize, m etabolize, and excrete the staph toxins.

o

Infants, children, and som e im m unocom prom ised are unable to m etabolize and excrete toxin efficiently.



Presentation determ ined by age and extent of the rash: o

Classic staphylococcal scalded skin syndrom e

o

Pem phigus neonatorum

Pa ge 4 5 0

o 

Bullous im petigo

Typically, coagulase positive phage group II Staphylococcus: o

Group I and group III also im plicated

Etiology 

Colonization often without overt infection



Concurrent infection or break of skin barrier:



o

Minor skin abrasions

o

Circum cision site

o

Conjunctivitis

o

Um bilicus/Om phalitis

o

Im petigo

o

Endocarditis and septicem ia

Often no focus identified

Diagnosis Signs and Symptoms 



Constitutional sym ptom s: o

Malaise

o

Fever

o

Irritability

Diffuse tender scarlatiniform erythem atous rash (sandpaperlike) resem bling a â€œsunburnâ€•â€” erythroderm a





Areas of prom inence: o

Around the flexor areas of the neck

o

In intertriginous areas, especially axilla and groin

o

Near the eyes and m outh

Increased erythem a in skin creases

Pa ge 4 5 0



Facial edem a with radial crusting fissures around the eyes, nose, and m outh



Child m ay appear well, ill, or overtly toxic.



Flaccid bullae: o

Within 1â€“3 days after onset of cariniform rash

o

Initially over flexures (axillae, groin, body orifices)

o

Bullae m igrate through epiderm is with light lateral pressure; epiderm is separates with m inor pressure (Nikolsky sign).

o

Rupture within hours

o

Epiderm is separates with m inor traum a.

o

Epiderm is is shed in sheets.

o

Denuded areas are m oist, sensitive, and painful.

o

Com plete healing within 2 weeks, no scarring



Purulent conjunctivitis



Mucous m em branes are not affected



Com plications are rare: o

Hypotherm ia

o

Fluid and electrolyte im balance

o

Secondary infection

o

Pneum onia

o

Septicem ia

o

Cellulitis

o

Osteom yelitis

Essential Workup 

Clinical presentation is diagnostic.



Determ ine location/source of toxin producing Staphylococcus.



Tests

Lab 

CBC and urinalysis:

Pa ge 4 5 0

o 

Electrolytes: o



Assess for sepsis if source is not obvious.

Indicated if signs of dehydration or extensive rash

Blood cultures: o

Rarely positive

Diagnostic Procedures/Surgery 

Fluid aspirated from bullae: o

Sterile in staphylococcal scalded skin syndrom e

o

Consistent with hem atogenous dissem ination of the toxin



Isolation of staphylococci from a site other than the blisters: o



Com m only conjunctivae, nasopharynx, or blood

Skin biopsy or frozen histologic section: o

Determ ine level of epiderm al/derm al separation (cleavage is in granular layer of derm is).

o

Indicated for children on m edications, those older than 6 years and in cases of m ixed presentation

P.1059

Differential Diagnosis 

Infection: o

o

Scarlet fever: 

Involves the m ucous m em branes



Strawberry tongue:



Painful desquam ation does not occur.

Bullous im petigo: 

o

Turbid or cloudy bullae fluid

Bullous varicella: 

Tzanck prep or viral base reveals giant cells.

Pa ge 4 5 0

 o

5 days after the onset of varicella

Toxic shock syndrom e: 

Rapid developm ent of clinical signs and sym ptom s

 



Mucous m em brane and m ultiorgan involvem ent

Toxic epiderm al necrolysis or drug eruption: o

Much m ore com m on in adults

o

Severely afflicted m ucous m em branes

o

Full thickness epiderm al necrosis

Derm atologic: o

Erythem a m ultiform e

o

Epiderm olysis hyperkeratosis

o

Epiderm olysis bullosa

o

Pem phigus vulgaris



Scald injury



Secondary rash of an underlying disorder: o

Lym phom a

o

Aspergillosis

o

Irradiation

o

Graft-versus-host reaction

o

Kawasaki disease

Treatment Initial Stabilization 

Managem ent is sim ilar to an extensive second-degree burn: o

Large total body-surface area involvem ent will require IV fluids.



Provide adequate analgesia.



Undress and place child on sterile linen.

Pa ge 4 5 0



Lim it handling of child.



Apply m oist sterile dressings.



Avoid excess heat loss.

ED Treatment 

Topical burn cream s are of no proven benefit.



Steroids are contra-indicated.



IV antibiotics effective against penicillinase-resistant S. aureus:



o

Cefazolin

o

Nafcillin

Oral antibiotics for m ild involvem ent: o

Dicloxacillin

o

Erythrom ycin

o

Cephalexin

Medication (Drugs) 

Cefazolin: 50â€“100 m g/kg/24h IV div. q.i.d.



Cephalexin: 25â€“100 m g/kg/24h PO div. q.i.d.



Dicloxacillin: 12â€“25 m g/kg/24h PO div. q.i.d.



Erythrom ycin: 30â€“50 m g/kg/24h PO div. q.i.d.



Nafcillin: 1â€“2 g IV q6h (peds: newborns, 50â€“100 m g/kg/24h IV div. q6h; children, 100â€“200 m g/kg/24h IV div. q6h)

Follow-Up Disposition Admission Criteria

Pa ge 4 5 0



Children younger than 1 year



All toxic-appearing children



Widespread skin involvem ent



Dehydration and/or electrolyte derangem ent

Discharge Criteria 

Older well-appearing children with m ild involvem ent



Oral antibiotics for 7 days



Follow-up within 48 hours

References 1. Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. Philadelphia, PA: WB Saunders, 1998:1055â€“1057. 2. Freedberg Irwin M, et al. Fitzpatrick's Derm atology in General Medicine. McGraw-Hill. 6th ed., 2003: Ch 195. 3. Gem ell CG. Staphylococcal scalded skin syndrom e. J Med Microbiol . 1995;43(5):318â€“327. 4. Ladhani L. Recent developm ents in staphylococcal scalded skin syndrom e. Clin Microbiol Infect. 2001;7(6):301â€“307.

Codes ICD9-CM 695.1

ICD10 L00

Pa ge 4 5 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sterno clavicular Jo int Injury

Sternoclavicular Joint Injury Robert S. Chang Wallace Carter

Basics Description 

Sternoclavicular joint (SCJ) is the only joint that connects the upper lim b to the trunk.



Am ong least frequently injured joints in the body



Traum a from vehicular or athletic injuries through direct or indirect m echanism



Congenital or atraum atic dislocation rarely seen

Etiology 

Injury to the SCJ can be from sprains, subluxations, and dislocations.



The SCJ can dislocate anteriorly or posteriorly.



Anterior dislocation is m ore com m on: o

Caused by a posteriorly directed force to the anterolateral aspect of the shoulder

o

Reciprocal anterior displacem ent of the m edial clavicle

o

May be associated with pneum othorax, hem othorax, pulm onary contusion, and rib fractures

Pa ge 4 5 1



Posterior dislocation results from : o

Anterior-to-posterior blow to the m edial clavicle

o

Anteriorly directed force to the posterolateral aspect of the shoulder

o

Reciprocal posterior displacem ent of the m edial clavicle



Posterior dislocation is a surgical em ergency: o

Indications for im m ediate reduction: 

Com pression/Tear of trachea, esophagus, or great vessels



Recurrent laryngeal nerve



Brachial plexus in the m ediastinum

Pediatric Considerations 

The m edial epiphyseal growth plates of the clavicles are last to ossify and fuse between ages 22 and 25 years: o



Up until fusion, growth plate weakest part of the joint

Fractures through the m edial epiphysis m im ic SCJ dislocations: o

Classified as Salter-Harris type I or II fractures

o

True dislocations of the SCJ are extrem ely rare in children because of the strong ligam entous attachm ents.

Diagnosis Signs and Symptoms 

Pain localized to the m edial clavicle and SCJ



Affected arm supported across the chest by the contralateral arm



Inability to abduct or externally rotate arm

Pa ge 4 5 1



If the SCJ is dislocated, shoulder appears shortened: o

Head tilts toward injured side due to sternocleidom astoid m uscle spasm



In anterior dislocation, m edial end of the clavicle is visibly prom inent and palpable.



In posterior dislocation, there m ay be a sulcus of the SCJ area through which the lateral border of the m anubrium m ay be palpated. o

Dislocation m ay be m asked by significant swelling over the sternoclavicular region.

o

Venous congestion in the neck or upper extrem ities

o

Asym m etric upper extrem ity pulses

o

Neuropraxia

o

Shortness of breath, hoarseness, dysphagia

o

Signs of shock: 

Suggest life-threatening im pingem ent of the posteriorly displaced clavicle upon structures in the m ediastinum



If subluxed or sprained, the SCJ is tender on direct palpation and with shoulder m ovem ent: o

No deform ity or significant AP m obility

Essential Workup 

Com plete traum a evaluation for other life-threatening injuries



Special attention to respiratory, neurologic, and vascular status



Appropriate analgesia for patient com fort

Tests Imaging 

Routine plain chest radiographs difficult to evaluate SCJ injury:

Pa ge 4 5 1

o

May dem onstrate asym m etry of the SCJ com pared with contralateral side

o

More useful to assess co-existing bony, pulm onary, and m ediastinal injury



Rockwood or serendipity view: o

Radiograph beam aim ed at m anubrium at 40Â° cephalic tilt allows view of both SCJs.



Ultrasound can reliably dem onstrate posterior SCJ dislocations: o

Currently used in operating room setting to evaluate reduction and vascular structures

o

Advantage of being noninvasive, portable, and sim ple to use

o

May be useful in the initial ED evaluation of unstable patients with chest traum a



MRI provides superior soft tissue (ligam ent and cartilage) detail of the SCJ and sternum : o



Lim ited utility in the ED setting

CT scan is best to evaluate the SCJ: o

Useful when plain film s are inconclusive

o

Accurately differentiates fractures from dislocations

o

Dem onstrates the position of the m edial end of the clavicle

o

Shows detailed anatom y of the thoracic outlet and m ediastinum

Differential Diagnosis 

Sternoclavicular sprain/subluxation



Medial clavicle fracture



Septic joint



Osteoarthritis

Pa ge 4 5 1

Treatment Pre Hospital 

Attention to airway and vital signs, and neurovascular status of the affected extrem ity



The affected arm should be splinted in the position of com fort before transport to the ED.

Initial Stabilization 

Endotracheal intubation if indicated: o



Then im m ediate m edial clavicular reduction

Em ergent SCJ reduction for: o

Hoarseness

o

Dysphagia

o

Sensation of throat tightness

o

Neurovascular com prom ise: 

Upper extrem ity weakness



Paresthesia



Dim inished pulses



Signs of shock



Orthopaedic and thoracic surgical consults



Analgesia and sedation as needed

P.1061

ED Treatment 

Anterior dislocations m ay be reduced in the ED: o

Procedural sedation for adequate pain control and m uscle relaxation

o

Rolled towel placed between the shoulder blades in the supine position:

Pa ge 4 5 1



Longitudinal traction applied to the extended arm with shoulder abducted 90Â°



Assistant applies gentle inward pressure over the displaced end of the clavicle.



After reduction, im m obilize using a well-padded figure-of-eight dressing.

o

Many anterior dislocations rem ain unstable after reduction.

o

Surgery rarely indicated as deform ity is m ainly cosm etic



Posterior dislocations require urgent reduction best achieved in the operating room under general anesthesia: o

If surgeon not im m ediately available, em ergent reduction in the ED m ay be necessary: 

Relieve serious airway, neurologic, or vascular com prom ise.



After airway secured, sm all incision is m ade directly over the m edial clavicle.



A sterile towel clam p used to grasp m edial clavicular head and gentle anterior traction applied to reduce the dislocation.

Medication (Drugs) 

Procedural sedation



Atropine: used in pediatric patients in conjunction with ketam ine to decrease hypersalivation (peds: 0.02 m g/kg IM/IV., m inim um dose of 0.1 m g)



Etom idate: 0.1 m g/kg IV



Fentanyl: 1â€“2 Âµg/IV q2m inâ€“q3m in



Ketam ine: 1â€“2 m g/kg IV



Midazolam : 0.01 m g/kg (peds: 0.05â€“0.1 m g/kg) IV

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q2m inâ€“q3m in

Follow-Up Disposition Admission Criteria 

All posterior dislocations of the SCJ require adm ission for prom pt reduction in the OR and evaluation for potential intrathoracic com plications.



Co-existing injury significant enough to warrant hospitalization

Discharge Criteria 

SCJ sprains



Anterior dislocations of the SCJ without neurovascular com prom ise or other significant injury



Appropriate outpatient orthopaedic follow-up arranged

References 1. Doss A, Lang IM, Roberts I, et al. Posterior Sternoclavicular joint dislocation in childrenâ€”Role of spiral com puted tom ography. Pediatr Em erg Care. 2005;21(5):325â€“326. 2. Ferrera PC, Wheeling HM. Sternoclavicular joint injuries. Am J Em erg Med. 2000;18(1):58â€“61. 3. Gobet R, Meuli M, Alterm att S, et al. Medial clavicular epiphysiolysis in children: the so-called sterno-clavicular dislocation. Em erg Radiol. 2004;10(5):252â€“255. 4. Medvecky MJ, Zuckerm an JD. Sternoclavicular joint injuries and disorders. AAOS Instructional Course Lectures. 2000;49:397â€“406. 5. Salgado RA, Ghysen D. Posttraum atic posterior sternoclavicular dislocation: case report and review of the literature. Em erg Radiol.

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2002;9:323â€“325. 6. Yeh GL, William s GR. Conservative m anagem ent of sternoclavicular injuries. Orthop Clin North Am . 2000;31(2):189â€“203.

Codes ICD9-CM 810.01

ICD10 S49.9

Pa ge 4 5 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Stevens-jo hnso n Syndro m e

Stevens-johnson Syndrome James Comes Herbert G. Bivins

Basics Description 

Stevens-Johnson syndrom e (SJS) is a severe m ucocutaneous disease: o

Blistering of less than 10% of the body surface area

o

95% of patients have m ucous m em brane lesions.

o

85% have conjunctival lesions.

o

Lesions often involving face, neck, and central trunk regions becom e confluent over hours to days.



Erythem a m ultiform e (EM), SJS, and toxic epiderm al necrolysis (TEN) m ay be considered variants of the sam e disease.

Etiology 

The m ost com m on causes include m edications and infections: o

Dam age to the skin is thought to be m ediated by cytotoxic T lym phocytes and m ononuclear cells aim ed at keratinocytes expressing (drug-related) antigens.

o

Cytokines from activated m ononuclear cells probably

Pa ge 4 5 1

contribute to cell destruction and system ic sym ptom atology. 

Causative m edications: Antibiotics (e.g., Penicillin, Sulfonam ides), anticonvulsants, oxicam s, NSAIDs, and allopurinol have been associated with these severe cutaneous drug reactions.



Infections: Mycoplasm a pneum onia and herpes sim plex are well-recognized causes of erythem a m ultiform e and SJS.

Diagnosis Signs and Symptoms History 

Prodrom e: fever, headache, m alaise, upper respiratory infection (URI) sym ptom s, arthritis, arthralgias, and m yalgias prior to m ucocutaneous lesions



Skin: m ild to m oderate skin tenderness followed by skin pain, burning sensation, and paresthesias



Eye: conjunctival burning or itching



Mucous m em branes: painful m icturition, painful swallowing

Physical Exam 

Rash: target lesions, erythem atous or purpuric m acules with or without confluence, and raised flaccid blisters or bullae with skin detachm ent that spread with lateral pressure (Nikolsky sign) on erythem atous areas



Mucous m em brane: erythem atous tender erosions of the m outh, pharynx, trachea, genitalia, or anus; possibly pseudom em brane form ation



Eye: m ild to severe conjunctivitis with possible form ation of pseudom em branes and corneal ulcers

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Essential Workup A com plete history and physical exam ination with careful attention to m ucous m em branes, percentage of blistering, and identification of likely etiology

Tests Lab 

Electrolytes



Liver enzym es



CBC



Urinalysis

Imaging Chest radiography if pneum onia is a consideration

Diagnostic Procedures/Surgery Skin biopsy of lesions and m ucous m em branes dem onstrates necrosis of the entire epiderm al layer with form ation of subepiderm al split above basem ent m em brane.

Differential Diagnosis 

EM m ajor:



Overlapping SJS and TEN (skin detachm ent between 10% and 30% of the body surface area plus widespread m acules or flat atypical target lesions)



Toxic epiderm al necrolysis (skin detachm ent greater than 30% of the body surface area plus widespread m acules or flat atypical targets)



Therm al burns



Phototoxic reactions



Exfoliative derm atitis



Bullous fixed drug eruptions



Graft-versus-host disease in bone m arrow transplant patients

Pa ge 4 5 2

Pediatric Considerations Staphylococcal scalded skin syndrom e is in the pediatric differential diagnosis of severe blistering m ucocutaneous diseases. P.1063

Treatment Initial Stabilization 

Endotracheal intubation and ventilatory support m ay be required for im pending respiratory failure (m ore com m only associated with TEN).



IV fluids

ED Treatment Recognize and treat underlying infections: 

Sepsis is the prim ary cause of death, frequently from gram -negative pneum onia.



Secondarily infected cutaneous lesions can be treated with dÃ©bridem ent of blisters, com presses, and system ic antibiotics.



Corticosteroids are controversial.



Prophylactic antibiotics m ay be indicated if system ic steroids are given.



Mild system ic sym ptom s m ay be treated with acetam inophen or NSAIDs, provided they are not the cause of the m ucocutaneous reaction.



Mucous m em brane lesions are extrem ely painful and m ay require parenteral analgesics.



Large extensive bullae should be dÃ©brided, ideally in a

Pa ge 4 5 2

burn unit.

Medication (Drugs) 

Acetam inophen: 650â€“975 m g PO/PR (peds: 15 m g/kg/dose)



Acyclovir: 5â€“10 m g/kg IV q8h (for herpes sim plex virus infections)



Ibuprofen: 300â€“800 m g PO (peds: 5â€“10 m g/kg/dose)



Morphine sulfate: 0.1 m g/kg/dose IV

Follow-Up Disposition Admission Criteria 

Patients with SJS should be adm itted to the hospital.



Patients with extensive epiderm al detachm ent should be adm itted to a burn center or a specialized intensive care unit.

Discharge Criteria Patients with erythem a m ultiform e m inor m ay be discharged with appropriate and tim ely follow-up.

Issues for Referral Patients m ust be m ade aware of the likely offending drug (and its class) and that it m ust never be adm inistered to them again.

References 1. Fritsch PO, Sidoroff A. Drug-induced Stevens-Johnson syndrom e/toxic epiderm al necrolysis. Am J Clin Derm at. 2000;1(6):349â€“360.

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2. Roujeau JC, Kelly JP, Naldi L, et al. Medication use and the risk of Stevens-Johnson syndrom e or toxic epiderm al necrolysis. N Engl J Med. 1995;333:1600â€“1607. 3. Wolff K, Johnson RA, Suurm ond D. Stevens- Johnson Syndrom e and Toxic Epiderm al Necrolysis. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Derm atology. 5th ed. Mc Graw-Hill; 2005: 144â€“147.

Codes ICD9-CM 695.1

Pa ge 4 5 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sting, Bee

Sting, Bee

Daniel T. Wu

Basics Description 



Injection of hym enoptera venom causes: o

Release of biologic am ines

o

Local or system ic allergic reactions

Reactions are: o

Usually IgE-m ediated type I hypersensitivity reactions

o

Rarely type III (Arthrus) hypersensitivity reactions

Etiology 

Hym enopteraâ€”order of the phylum Arthropoda



Includes bees, wasps, hornets, and fire ants

Diagnosis Signs and Symptoms History History and physical exam â€”keys to diagnosis

Physical Exam

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N/A

Five Types of Reactions to Stings 

Local reaction: o

Most com m on type of reaction

o

Local pain, erythem a, and edem a at sting site

o

Sym ptom s occur im m ediately and resolve within 1â€“2 hours



Large local reaction: o

Sim ilar to local reaction, but affects larger area or entire lim bs



o

Peaks at 48 hours and can last several days

o

Mild to m oderate fever

System ic reaction: o

Includes anaphylaxis

o

Can be fatal (usually owing to respiratory failure)

o

Respiratory:

o

o



Wheezing



Coughing



Stridor



Shortness of breath



Hoarseness



Angioedem a

Gastrointestinal: 

Nausea



Vom iting



Diarrhea



Abdom inal pain

Cardiovascular: 

Hypotension



Chest pain



Tachycardia



Shock

Pa ge 4 5 2

o

o

Other: 

Urticaria



Pruritus



Flushing

Sym ptom s occur within 15â€“20 m inutes and last up to 72 hours





Toxic reaction: o

Result of m ultiple stings and large doses of venom

o

Sym ptom s sim ilar to anaphylaxis

Unusual reactions: o

Owing to unusual im m une response

o

Vasculitis

o

Nephrosis

o

Serum sickness

o

Neuritis

o

Encephalitis

o

Reaction delayed (days to weeks after sting)

Essential Workup 

History and physical key to diagnosis



No radiologic or laboratory test will confirm hym enoptera envenom ation or anaphylaxis.

Tests Lab CBC, electrolytes, BUN, creatinine, glucose, arterial blood gases (ABGs): 

Not routine



Consider when significant system ic effects present

Diagnostic Procedures/Surgery ECG 

When significant system ic effects in patients at risk for

Pa ge 4 5 2

cardiovascular disease

Differential Diagnosis 

Insect bites som etim es cause pain; stings always cause pain.



Cellulitis: o

Difficult to distinguish between large local reactions and cellulitis

o

Infections of hym enoptera envenom ations are rare and usually caused by wasp envenom ations.

o

Local reaction can resem ble periorbital cellulitis.



Gout



Soft tissue traum a



System ic/toxic reactions: o

Pulm onary em bolus

o

Anaphylaxis from different agent

o

Hyperventilatory syndrom e/anxiety

o

Acute coronary syndrom e

Treatment Pre Hospital Most deaths occur within first hour owing to either respiratory obstruction or anaphylaxis causing cardiovascular and respiratory collapse.

Initial Stabilization Acute Severe Systemic Reaction/Anaphylaxis 

Airway, breathing, and circulation m anagem ent (ABCs): o

Intubation/ventilation with rapidly increasing signs of laryngeal com prom ise

Pa ge 4 5 2

o

Oxygen

o

0.9% norm al saline (NS) IV access



Epinephrine SC/IV



Antihistam ines IV



When signs of system ic reactions: o

Assess for patent airway.

o

Establish IV access.

ED Treatment 

System ic reactions: o

Epinephrine for respiratory sym ptom s/hypotension

o

Antihistam inesâ€”H 1 (diphenhydram ine) and H 2 (cim etidine) blockers

o

Steroids (prednisone, m ethylprednisolone)

o

Inhaled Î²-agonist for wheezing/shortness of breath

o

For persistent hypotension: 

0.9% NS IV fluid resuscitation



Vasopressor (epinephrine/Î±-adrenergic) for hypotension resistant to IV fluids



Rem oval of rem nants of stinger at site of envenom ation (bees m ay leave stingers with venom sacs) by scraping, not squeezing



Local reactions: o

Cool com press

o

Elevation

o

Rem ove constrictive clothing or jewelry

o

Topical antihistam ine/topical steroidal cream as needed

o

Oral antihistam ine or steroids as needed

P.1065

Pa ge 4 5 2

Medication (Drugs) 

Albuterol, Î²-agonist (inhaled): 3 m g in 5 m L solvent (peds: 0.1 m g/kg of 5 m g/m L concentration) via nebulization



Cim etidine: 300 m g (peds: 5 m g/kg) IV, IM, or PO



Diphenhydram ine: o

50â€“100 m g (peds: 1 m g/kg) IV for severe reactions

o

25â€“50 m g (peds: 1 m g/kg) PO q.i.d. for severe local reactions



Epinephrine: o

0.1 m g: 1 m L of 1:10,000 dilution (peds: 0.01 m g/kg = 0.1 m L/kg of 1:10,000 dilution up to 1 m L) IV over 5 m inutes for shock

o

0.3â€“0.5 m g (0.3 m Lâ€“0.5 m L of 1:1,000 dilution; peds: 0.01 m g/kg up to 0.5 m g) SC for severe reactions but not in shock



Methylprednisolone: 125 m g (peds: 1â€“2 m g/kg) IV



Norepinephrine: 4â€“12 Âµg/m in (peds: 0.1 Âµg/kg/m in) titrated continuous infusion



Prednisone: 60 m g (peds: 1â€“2 m g/kg) PO

Follow-Up Disposition Admission Criteria 

Worsening sym ptom s, airway com prom ise



Persistent unstable vital signs require ICU adm ission.



Life-threatening reaction requires 24-hour observation.



System ic reaction requires m inim um of 6 hours of

Pa ge 4 5 2

observation.

Discharge Criteria 

Minim al isolated local reaction



System ic reactions that resolve and do not recur during 6-hour observation period

Issues for Referral Follow-up: 

Provide patients with life-threatening reactions em ergency anaphylaxis kits (EpiPen; peds: EpiPen Jr. if <15 kg) and m edical identification bracelets (Medi-Alert).



System ic reaction requires follow-up for possible im m unotherapy.

References 1. Bahna SL. Insect sting allergy: a m atter of life and death. Pediatr Ann. 2000;29:753â€“758. 2. McDougle L, Klein G, Hoehler FK. Managem ent of hym enoptera sting anaphylaxis: a preventive m edicine survey. J Em erg Med. 1995;13:9â€“13. 3. Moffitt JE. Stinging insect hypersensitivity: a practice param eter update. J Allergy Clin Im m unol. 2004;114:869â€“886. 4. Reism an R. Insect stings. N Engl J Med. 1994;331:523â€“527. 5. Reism an RE. Stinging insect allergy. Clin Allergy. 1992;76:863â€“893.

Codes ICD9-CM 989.5

ICD10 T63.4

Pa ge 4 5 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sting, Sco rpio n

Sting, Scorpion

Frank LoVecchio

Basics Description 

Scorpion venom is neurotoxic.



Sodium channels opening



Prolonged firing of neurons



Autonom ic, som atic, and cranial nerve excitation occurs.



Sym ptom s begin within m inutes of bite.



Sym ptom s persist 1â€“48 hours

Etiology 

Centruroides species found in southern United States, Mexico, Central Am erica, and Caribbean



Many other species in Asia, Africa, Israel, South Am erica, and Middle East

Pediatric Considerations 

Can be m isdiagnosed with seizures, am phetam ine poisoning or m eningitis



Higher m ortality and severity of illness

Pa ge 4 5 3

Diagnosis Signs and Symptoms 

Onset within m inutes and progresses to m axim um severity in about 1â€“2 hours but m ay persist for up to 48 hours.



Scorpion species determ ines sym ptom atology (Centruroides sculpturatus, also known as Centruroides exilicauda or bark scorpion is the only species to cause sym ptom s in the United States).

Local Tissue Effects 

No erythem a



Pain



Hyperesthesia

Autonomic Effects 



Sym pathetic sym ptom s: o

Tachycardia

o

Hypertension

o

Hypertherm ia

o

Pulm onary edem a

o

Agitation

o

Perspiration

Parasym pathetic effects: o

Hypotension

o

Bradycardia

o

Hypersalivation

Somatic Effects 

Involuntary m uscle contractions



Restlessness

Cranial Nerve Effects 

Roving eye m ovem ents



Blurred vision

Pa ge 4 5 3



Nystagm us



Tongue fasciculations



Loss of pharyngeal m uscle control

Essential Workup 

Identification of scorpion species is not needed if scorpion is native to United States (see above).



High clinical suspicion in endem ic areas



Grade severity of envenom ation: o

Grade I: local pain and/or paresthesias at site

o

Grade II: local pain and pain and/or paresthesias at a rem ote site

o

Grade III: either cranial/autonom ic or som atic skeletal neurom uscular dysfunction

o

Grade IV: both cranial/autonom ic and som atic skeletal m uscle dysfunction

Tests Lab 

Grade I and II envenom ations: o







None

Grade III and IV envenom ations: o

Blood urea nitrogen, creatinine

o

Electrolytes

o

Urinalysis

o

CBC

Severely agitated patients: o

Creatine kinase

o

Urine m yoglobin

Severe respiratory distress: o

Arterial blood gases (ABG)

Imaging

Pa ge 4 5 3



Chest radiograph for respiratory sym ptom s



ECG for tachycardia

Differential Diagnosis 

Snake, spider, insect envenom ation



Tetanus



Diphtheria



Botulism



Overdose/dystonic reaction



Seizures



Infections

P.1067

Treatment Pre Hospital 

Evaluate ABCs



IV access

Initial Stabilization 

ABCs



Endotracheal intubation, if necessary



IV



O2



Monitor

ED Treatment 

Mild envenom ationsâ€”grade I and II: o

Oral analgesics

o

Tetanus prophylaxis

Pa ge 4 5 3



Severe envenom ationsâ€”grade III and IV: o

Antivenom (no longer available in United States)

o

Tetanus prophylaxis

o

Hypertensive urgencies/em ergencies: 

o

Standard therapy such as labetalol

Hypotension: 

IV fluid resuscitation and pressor therapy with dopam ine

o

Severe agitation: 

o

Midazolam

Treatm ent for rhabdom yolysis, if present

Medication (Drugs) 

Antivenom : current trial for new FAB product



Dopam ine: 2â€“5 Âµg/kg/m in IV; increase in 5â€“10 Âµg/kg/m in as needed



Midazolam : 1â€“2 m g (peds: 0.01â€“0.05 m g/kg) IV



Labetalol: 20 m g (peds:0.3â€“1.0 m g/kg/dose) q10m in



Fentanyl: 50â€“150 m cg (peds: 1â€“5 m cg/kg) IV



Tetanus: 0.5 m L IM (peds: sam e dose)

Pediatric Considerations Antivenom doses are the sam e in children because dosage is based on venom burden.

Follow-Up Disposition Admission Criteria

Pa ge 4 5 3



Grade III and IV envenom ations require adm ission to intensive care unit.



If antivenom is given with resolution of sym ptom s, observe for 1â€“2 hours if asym ptom atic.

Discharge Criteria 

Grade I and II envenom ations



Grade III and IV envenom ations given antivenom with resolution of sym ptom s can be discharged.



If patient received antivenom , discuss signs and sym ptom s of delayed serum sickness.



Discuss possibility of persistence of pain and paresthesias at site.



Encourage patient to return for progression of sym ptom s.

Pediatric Considerations Toddlers are m ore likely to have early airway involvem ent.

References 1. LoVecchio F, McBride C Scorpion envenom ations in young children in central Arizona. J Toxicol Clin Toxicol. 2003;41(7):937â€“940. 2. Sofer S. Scorpion envenom ation. Intens Care Med. 1995;21(8):626â€“628. 3. Walter GE, Bilden EF, Gibly RL. Envenom ations. Crit Care Clin. 1999;15(2):353â€“386.

Codes ICD9-CM 989.5

ICD10 T63.2

Pa ge 4 5 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Strepto co ccal Disease

Streptococcal

Disease Scott Sherman

Basics Description 

In the late 1980s, an increase was seen in the frequency of an aggressive streptococcal infection that afflicted otherwise healthy patients aged 20â€“50 years who did not have underlying predisposing diseases.



Dubbed â€œflesh-eating bacteriaâ€• in British press



Rapid progression of shock and m ultiorgan dysfunction, with death occurring in m any afflicted patients within 1â€“2 days



Streptococcal toxic shock syndrom e (Strep TSS): o

o

Portal of entry for streptococci: 

Vagina



Pharynx



Mucosa



Skin



In 50% of cases, the site of entry is unknown.

Nonsteroidal anti-inflam m atory drugs appear to m ask or predispose patients to streptococcal toxic shock

Pa ge 4 5 3

syndrom e. o

Most cases occur sporadically.

o

Occasional outbreaks in long-term care facilities and hospitals



Necrotizing fasciitis: o

Mortality rate 30â€“70%

o

Infection of the subcutaneous tissue with progressive destruction of the fascia and fat

o

Often fatal over a course of 24â€“96 hours

o

Described by Meleney in 1924, but progression in his patients was slower (over 7â€“10 days) with lower m ortality rate (20%).



Streptococcal m yositis: o

A rare group A beta-hem olytic streptococcal infection was reported only 21 tim es from 1900â€“1985.

o

Swelling and erythem a develop late.

o

Difficult to differentiate from gas gangrene secondary to Clostridium species infection

o

Mortality rate 80â€“100%

o

Aggressive surgical dÃ©bridem ent is essential.

Streptococcal Toxic Shock Syndrome Case Definition Isolation of group A beta-hem olytic streptococcus from sterile or nonsterile body site, and: 

Hypotension



Two or m ore of the following: o

Renal im pairm ent

o

Coagulopathy

o

Liver abnorm alities

o

Acute respiratory distress

o

Extensive tissue necrosis (necrotizing fasciitis)

Pa ge 4 5 3

o

Erythem atous rash

Etiology 

Streptococci: o

Catalase-negative spheric cocci

o

Divided into two groups: alpha and beta: 

On ability to lyse erythrocytes on an agar plate



Beta-hem olytic streptococci fully lyse erythrocytes

o

Further divided into Lancefield groups by variations in an antigen in the cell wall (C carbohydrate)

o

Group A beta-hem olytic streptococcus: 

Possesses another antigen, the M protein, which is associated with the virulence of the bacteria



Strep TSS: o

Occurs when a susceptible host is infected with a virulent strain

o

M protein types 1, 3, and 28 are m ost com m on.

o

Possesses pyrogenic exotoxins (e.g., A, B, and C)

o

Produces fever and shock via activation of tum or necrosis factor and interleukins

o

Risk factors for developm ent of strep TSS: 

Patients generally younger than 10 years or older than 60 years of age





Cancer



Renal failure



Leukem ia



Severe burns



Corticosteroids

Necrotizing fasciitis: o

Group A beta-hem olytic streptococcus is causative in 10% of cases.

o

Mixed anaerobic and aerobic organism s are found in

Pa ge 4 5 3

70% of cases. o

Staphylococcus aureus, Clostridium species, and other enteric organism s

Diagnosis Signs and Symptoms 



Presents as: o

Strep TSS

o

Necrotizing fasciitis/m yositis

Pain is the m ost com m on initial sym ptom : o

Often abrupt in onset and severe

o

Occurs in 85% of cases

o

Often requiring palliative IV narcotics

o

Usually involves an extrem ity

o

May m im ic peritonitis, pelvic inflam m atory disease, pneum onia, acute m yocardial infarction, or pericarditis



Fever is the m ost com m on sign: o

Can present with hypotherm ia, especially if patient is in shock



Altered m ental status is present in 55% of patients.



Soft-tissue infection (erythem a and swelling) present in 80% of patients: o

70% progress to necrotizing fasciitis or m yositis: 

Indistinct borders, blisters, bullae



No lym phangitis or lym phadenopathy



Most patients will require surgical procedure (e.g., fasciotom y, surgical dÃ©bridem ent, exploratory laparotom y, intra-ocular aspiration, am putation, or hysterectom y).

Pa ge 4 5 4





Influenzalike syndrom e in 20%: o

Fever

o

Chills

o

Myalgias

o

Nausea, vom iting

o

Diarrhea

Shock: o

Present at adm ission or within 4â€“8 hours in all patients

o

Persists despite fluids, antibiotics, and pressors in all but 10%



Renal failure: o

Precedes onset of shock in m any cases

o

Dialysis often necessary

o

Kidney function returns to norm al within 4â€“6 weeks in survivors.



Adult respiratory distress syndrom e: o

Occurs in 55% of patients and develops after hypotension

o

Mechanical ventilation required in 90% of patients with adult respiratory distress syndrom e

P.1069

Essential Workup 

Suspect necrotizing fasciitis when pain is out of proportion to exam ination.



Rapid adm inistration of broad-spectrum antibiotics



Early surgical consultation

Tests Lab

Pa ge 4 5 4



CBC with differential: o

Mild leukocytosis with left shift initially



Electrolytes, blood urea nitrogen, and creatinine



Calcium level: o

Hypocalcem ia in association with fat necrosis from necrotizing fasciitis



Urinalysis: o



Hem oglobinuria if renal involvem ent

Serum creatine phosphokinase level that is elevated or rising correlates with necrotizing fasciitis or m yositis



Aerobic and anaerobic blood cultures



Wound cultures



Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio and dissem inated intravascular coagulation (DIC) panel

Imaging 

Plain film s: o

Gas in soft tissues in 25â€“75% of cases of necrotizing fasciitis

o

Not com m only associated with group A beta-hem olytic streptococcal infection

o 



More com m on in m ixed anaerobic infections

CT scan: o

Asym m etric thickening of deep fascia

o

Gas

MRI: o

High signal intensity of the fascia in T2-weighted im ages

Differential Diagnosis 

Sepsis



Cellulitis

Pa ge 4 5 4



Erysipelas



Necrotizing fasciitis/m yositis secondary to infection by another pathogen

Treatment Initial Stabilization 

Maintain airway, breathing, and circulation.



Treat shock with fluids and pressors as needed: o

Hypotension is often intractable, and up to 10â€“20 L per day m ay be required.



Intubation and m echanical ventilation for: o

Adult respiratory distress syndrom e

o

Severe shock

o

Ventilatory failure

ED Treatment 

Broad-spectrum antibiotics im m ediately after cultures: o

Penicillin (or a cephalosporin)

o

Anaerobic coverage (clindam ycin or m etronidazole)

o

Gram -negative coverage (am inoglycoside, third-generation cephalosporin, or ciprofloxacin)



Early surgical consultation for dÃ©bridem ent: o



Im m ediate surgery indicated if: 

Extensive necrosis or gas



Com partm ent syndrom e



Profound system ic toxicity

Aggressive group A beta-hem olytic streptococcal infections do not respond well to penicillin.



Clindam ycin has been found to be a potent suppressor of bacterial toxin synthesis and inhibits M-protein synthesis.

Pa ge 4 5 4



Reports of successful use of IV im m unoglobulin



Hyperbaric oxygen therapy rem ains controversial.

Medication (Drugs) Invasive Streptococcal Disease 

Clindam ycin: 900 m g (peds: 40 m g/kg per day) q6hâ€“q8h IV, and Penicillin G: 4 m illion units (peds: 250,000 IU per day) IV q4hâ€“6h, or



Vancom ycin: 15 m g/kg q12h (peds: 10 m g/kg q6h) IV if patient has penicillin allergy

Polymicrobial Necrotizing Fasciitis and Fournier Gangrene 

Metronidazole: 15 m g/kg IV loading dose, then 7.5 m g/kg IV q6h, and Ticarcillin/clavulanic acid: 3.1 g (peds: 200 m g/kg per day) IV q6h, or



Am picillin/sulbactam : 3 g (peds: 200 m g/kg per day) IV q6h, or



Piperacillin/tazobactam : 3.375 g IV q6h

Follow-Up Disposition Admission Criteria Intensive care unit adm ission for all patients with suspected invasive streptococcal infection

Discharge Criteria None

Pa ge 4 5 4

References 1. Ahm ed S, Ayoub E. Severe, invasive group A streptococcal disease and toxic shock. Pediatr Ann. 1998;27:287â€“292. 2. Am erican Academ y of Pediatrics, Com m ittee on Infectious Disease. Severe invasive group A streptococcal infections: a subject review. Pediatrics. 1998;101:136â€“140. 3. Stevens DL. The flesh-eating bacterium : What's next? J Infect Dis. 1999;179:(suppl 2)S366â€“374. 4. Stevens DL. Invasive group A streptococcus infections. Clin Infect Dis. 1992;14:2â€“13.

Codes ICD9-CM 038.0 Streptococcal septicem ia

ICD10 B95.5

Pa ge 4 5 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Strido r

Stridor

Gregory Ciottone

Basics Description Im pedance of air m ovem ent through the upper airway, which causes high-pitched audible wheezing and vibratory harsh sounds evident on auscultation over larynx during inspiration.

Etiology 

Congenital: o





Laryngom alacia

Ectopic thyroid: o

Laryngeal webs/rings

o

Vocal cord dysfunction

Infection: o

Bacterial tracheitis

o

Epiglottitis

o

Viral croup

o

Peritonsillar abscess

o

Retropharyngeal abscess

o

Supraglottitis

o

Uvulitis (e.g., Quincke disease)

o

Ludwig angina

o

Diphtheria

Pa ge 4 5 4

o 





Tetanus

Extrinsic com pression: o

Traum a

o

Hem atom a

o

Vascular anom alies (e.g., rings)

Intralum inal obstruction of the trachea: o

Foreign body

o

Cyst

o

Invasive tum ors

o

Squam ous cell

o

Lym phom as

o

Thyroid carcinom as

o

Laryngeal or tracheal papillom a

Subglottic stenosis: o

Postoperative scarring

o

After radiation therapy



Angioedem a



Vocal cord dysfunction: o

Congenital

o

Surgical injury

o

Postintubation traum a

o

Thyroid m alignancy

o

Mediastinal m ass

Diagnosis Signs and Symptoms 

Anxiety



Audible wheezing or grunting with inspiration



Increased respiratory rate



Effort required for inspiration:

Pa ge 4 5 4

o

Nasal flaring

o

Use of accessory m uscles



Intercostal retractions



Paradoxic diaphragm atic m ovem ent (late finding)



Dyspnea



Cough



Fever



Drooling



Sore throat



â€œHot potatoâ€• voice in adults



Trism us: o

Peritonsillar abscess, retropharyngeal abscess, Ludwig angina



Respiratory distress: o

Agitation

o

Diaphoresis

o

Cyanosis

o

Decreased respiratory rate

o

Som nolence

Essential Workup Visualization of the upper airway: 

Radiographic if sym ptom s very m ild; be careful!



Direct visualization in operating room with a surgeon prepared to perform a cricothyrotom y or tracheostom y is the safest approach.

Tests Lab These tests are not helpful and thus avoidable; m ay upset child even m ore.

Imaging

Pa ge 4 5 4

Radiograph of lateral neck: 

Not essential



Only done in extrem ely m ild cases

Diagnostic Procedures/Surgery 

Fiberoptic laryngoscopy: o

Should be perform ed with an intubating fiberoptic laryngoscope in a setting where a rapid surgical airway can be obtained



Direct laryngoscopy: o

Diagnostic study of choice

o

Should be perform ed in a setting where a rapid surgical airway can be obtained

Differential Diagnosis 

Bronchospasm



Malingering (patient breathing against a closed glottis)

P.1071

Treatment Pre Hospital 

Keep child calm , with m other if possible.



Supply blow-by oxygen.



Maintain adequate airway.



Use bag-valve m ask (BVM) if respiratory status deteriorates.



Intubate if BVM ineffective.



Provide rapid transport with ED notification.

Pa ge 4 5 4

Initial Stabilization 

In children: Avoid agitation. Supply blow-by oxygen.



Use 100% nonrebreathing-type face m ask

Pediatric Considerations 

Avoid agitating child.



Watch for rapid deterioration of respiratory status.

ED Treatment 

Airway m anagem ent: o

Stridor com prises a difficult airway passage: 

Be prepared to create an airway surgically before intubation.



If tim e perm its, perform intubation in OR with surgeon and pediatric anesthesiologist present.



Intubate with tube one or two sizes sm aller than would be norm ally used.



Oral awake intubation: o

Ketam ine induction

o

Patient is sedated but continues to ventilate during procedure.



Avoid blind nasotracheal intubation.



Provide surgical airway if intubation fails or sudden deterioration in respiratory status occurs.



Postintubation ceftriaxone in cases of infectious cause



Sedation/Paralysis for duration of intubated status after airway is secured.

Medication (Drugs) 

Atropine: 0.02 m g/kg IV



Ceftriaxone: 1â€“2 g IV

Pa ge 4 5 5



Diazepam : 2â€“10 m g IV (peds: 0.2â€“0.3 m g/kg)



Etom idate: 0.3 m g/kg IV



Fentanyl: 3 Âµg/kg IV



Ketam ine: 1â€“2 m g/kg IV or 4â€“7 m g/kg IM



Lidocaine: 1.5 m g/kg IV



Midazolam : 1â€“5 m g IV (0.07â€“0.30 m g/kg for induction)



Vecuronium : 0.1 m g/kg IV

Controversies 

Heliox therapy



Racem ic epinephrine therapy



Early intubation

Follow-Up Disposition Admission Criteria All cases of stridor m andate adm ission of patient to hospital.

Discharge Criteria N/A

References 1. Beckm an DB. Diagnostic dilem m a: vocal cord dysfunction. Am J Med. 2001;110:731â€“741. 2. Chang AB. A review of cough in children. J Asthm a. 2001;38:299â€“309. 3. Gupta VK. Heliox adm inistration in the pediatric intensive care unit: an evidence based review. Pediatri Crit Care Med. 2005;6(2):204â€“211. 4. Konarzewski W. Adult epiglottitis: an under-recognized, life

Pa ge 4 5 5

threatening condition. Br J Anaesth. 2001;86:456â€“457. 5. Levy RJ. Pediatric airway issues. Crit Care Clin. 2000;16:489â€“504. 6. McGahey-Oakland PR. A wheezing toddler. J Pediatr Healthcare. 2005;19(3):176â€“177. 7. Nakam ura H. Acute epiglottitis: a review of 80 patients. J Laryngol Otol. 2001;115:31â€“34. 8. Verghese ST. Pediatric otolaryngologic em ergencies. Anesthesiol Clin North Am . 2001;19:237â€“256.

Codes ICD9-CM 786.1 Stridor

ICD10 R06.1

Pa ge 4 5 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Subarachno id Hem o rrhage

Subarachnoid

Hemorrhage John W. Morehouse Rebecca Smith-Coggins

Basics Description Bleeding into the subarachnoid space and cerebrospinal fluid (CSF): 

Spontaneous or traum atic



Spontaneous m ost often results from cerebral aneurysm rupture



If traum atic, represents severe head injury

Epidemiology 

Incidence is 6â€“10 per 100,000 individuals.



Affects 30,000 in North Am erica annually



Results in death or severe disability in 40â€“60%.



Uncom m on prior to third decade; incidence peaks in sixth decade

Risk Factors 

Fam ily history



Hypertension



Sm oking

Pa ge 4 5 5



Alcohol abuse



Cocaine, m etham phetam ine, and ecstasy (MDMA) use



Gender (fem ale:m ale = 1.6:1)



African Am erican and Japanese ethnicity

Genetics 

Three- to seven-fold increased risk with first degree relatives with subarachnoid hem orrhage (SAH)



Autosom al dom inant polycystic kidney disease: o

Strongest genetic association, but represents only 2% of SAH patients

Pediatric Considerations 

Most often due to arteriovenous m alform ation in children



Although rare in children, SAH is a leading cause of pediatric stroke.



Aneurysm s that occur are m ore likely to rupture and to be giant (>25 m m ).

Etiology 

â€œCongenital,â€• saccular, or Berry aneurysm rupture (80â€“90%) o

Occur at bifurcations of m ajor arteries

o

Incidence increases with age.

o

Aneurysm s m ay be m ultiple in 20â€“30%.



Nonaneurysm al perim esencephalic hem orrhage (10%)



Rem aining 5% of causes include: o

Mycotic (septic) aneurysm due to syphilis or endocarditis



o

Arteriovenous m alform ations

o

Vertebral or carotid artery dissection

o

Intracranial neoplasm

o

Pituitary apoplexy

Severe closed head injury

Pa ge 4 5 5

Diagnosis Signs and Symptoms History 

Classically a severe, sudden headache: o

Often described as â€œthunderclapâ€• or â€œworst headache of lifeâ€•

o

Headache is often occipital or nuchal, but m ay be unilateral.

o

Usually develops within seconds and peaks within m inutes



o

Distinct from prior headaches

o

Headache often m axim al at onset

Sentinel headaches and m inor bleeding occur in 20â€“50%: o

May occur days to weeks prior to presentation and diagnosis



Seizures, transient loss of consciousness, or altered level of consciousness occur in m ore than 50% of patients.



Vom iting occurs in 70%.



Syncope, diplopia, and seizure are particularly high-risk features for SAH.

Physical Exam 

Focal neurological deficits occur at the sam e tim e as the headache in one third: o

Third cranial nerve (CN) palsy (the â€œdown and outâ€• eye) occurs in 10â€“15%.

o

Isolated CN VI palsy or papillary dilation m ay also occur.

Pa ge 4 5 5



Nuchal rigidity develops in 25â€“70%.



Retinal hem orrhage m ay be only clue in com atose patient.

Essential Workup 

Com plete neurologic exam ination and funduscopic exam



Em ergent noncontrast head CT scan: o

Diagnoses 93â€“98% of SAH if perform ed within 12 hours

o

Thin cuts (3 m m ) through base of brain im prove diagnostic yield.

o

CT is less sensitive after 24 hours or if hem oglobin is less than 10 g/l.



Lum bar puncture (LP) and CSF analysis m ust be perform ed if CT negative and history suggests possibility of SAH,

Pregnancy Considerations 

Incidence slightly increased in pregnancy



Workup should include CT scan and LP.

Tests Lab 

Baseline CBC, platelets, and differential



Electrolytes, renal and liver function tests



Co-agulation studies



Cardiac m arkers: o



Troponin-I elevated in 10â€“40%

CSF analysis (see below)

Imaging 

Chest radiograph for pulm onary edem a: o



Occurs in up to 40% with severe neurological deficit

Four-vessel digital subtraction cerebral angiography is traditional im aging standard.



Spiral CT angiography m ore sensitive and m ore useful for

Pa ge 4 5 5

operative planning. 

Magnetic resonance angiography: o



MRI is less sensitive for hem orrhage.

Transcranial Doppler ultrasound m ay be useful in detecting vasospasm .

Diagnostic Procedures/Surgery 

LP: o

Presence of erythrocytes in CSF indicates SAH or traum atic tap.

o

If traum atic tap suspected, LP should be perform ed one interspace higher.

o

Dim inishing erythrocyte count in successive tubes suggests but does not firm ly establish a traum atic tap.

o

Xanthochrom ia is diagnostic of SAH if perform ed 12 hours after onset.

o

An elevated opening pressure m ay indicate SAH, cerebral venous sinus throm bosis, or pseudotum or cerebri.



ECG: o

ST-segm ent elevation or depression

o

QT prolongation

o

T-wave abnorm alities

o

Often m im ics ischem ia or infarction

o

Sym ptom atic bradycardia, ventricular tachycardia, and ventricular fibrillation

Differential Diagnosis 

Neoplasm



Arterial dissection



Aneurysm (unruptured)



Arteriovenous m alform ation

Pa ge 4 5 5



Migraine



Pseudotum or cerebri



Meningitis



Encephalitis



Hypertensive encephalopathy



Hyperglycem ia or hypoglycem ia



Tem poral arteritis



Acute glaucom a



Subdural hem atom a



Epidural hem atom a



Intracerebral hem orrhage



Throm boem bolic stroke



Sinusitis



Seizure disorder



Cerebral venous sinus throm bosis

P.1073

Treatment Pre Hospital 



Initial assessm ent and history is helpful: o

Level of consciousness

o

Glasgow Com a scale score

o

Gross m otor deficits

o

Other focal deficits

Patients with SAH m ay need em ergent intubation for rapidly deteriorating level of consciousness.



IV access should be established.



Provide supplem ental oxygen.

Pa ge 4 5 5



Monitor cardiac rhythm .



Patients should be transported to a hospital with em ergent CT scan and intensive care unit capability.

Initial Stabilization 

Manage airway, resuscitate as indicated: o

Rapid sequence intubation

o

Pretreat with lidocaine, fentanyl and de-fasciculating dose of nondepolarizing paralytic to blunt increase in intracranial pressure (ICP) during intubation.



o

Cardiac m onitoring and pulse oxim etry

o

Establish adequate IV access.

Obtain urgent neurosurgical consultation.

ED Treatment 



Major goals: o

Prevent rebleeding.

o

Manage ICP, cerebral vasospasm .

Blood pressure (BP) control: o

Goal m ean arterial pressure 100â€“120 m m Hg, systolic BP <180

o

Adequately treat pain.

o

Correct hypovolem ia: 

Central venous pressure >8 m m Hg and urine output >50 m L/h

o

Labetalol, hydralazine, nitroprusside or nicardipine for hypertension

o

Treat hypotension with volum e expansion.

o

Elevate head of bed to 30Â°

o

Prevent increases in ICP from vom iting and defecation with antiem etics and stool softeners.

o

Treat increased ICP with controlled ventilation and m annitol.

Pa ge 4 5 5



Cerebral vasospasm m ay cause secondary ischem ia and infarction after SAH: o

Nim odipine im proves outcom e: 

o 

Should start within 96 hours of SAH

Monitor with transcranial Doppler.

Seizures should be m anaged with IV benzodiazepine or diazepam and phenytoin: o



Prophylactic anticonvulsants not indicated

Correct tem perature, electrolyte, glucose, or pH abnorm alities.



Treat coagulopathy, throm bocytopenia, and severe anem ia.



Maintain norm al pO 2 and pCO 2 with controlled ventilation if necessary.



Monitor for and correct pulm onary edem a and cardiac arrhythm ias.



No current indication for use of glucocorticoid or antifibrinolytic therapies



When stable, expedited transfer to hospital with neurosurgical capabilities is m andatory.

Medication (Drugs) 

Diazepam : 5â€“10 m g (peds: 0.2â€“0.3 m g/kg) IV/IM q10â€“15 m inutes PRN; m ax. 30 m g (peds: 10 m g)



Fentanyl:1â€“3 m cg/kg (adults and peds) IV q1hâ€“q4h PRN



Fosphenytoin:15â€“20 phenytoin equivalents (PE) per kg (adults and peds) IV Ã— 1; m aintenance 4â€“6 m g/kg/d IV



Hydralazine: 10â€“20 m g (peds: 0.1â€“0.5 m g/kg IV) q30m inâ€“q4h PRN



Labetalol: 20 m g IV bolus, then 40â€“80 m g q10m in; m ax.

Pa ge 4 5 6

300 m g; follow with IV continuous infusion 0.5â€“2 m g/m in (peds: 0.4â€“1 m g/kg/h IV continuous infusion; m ax. 3 m g/kg/h) 

Lidocaine: 1â€“1.5 m g/kg IV Ã— 1 (adults and peds)



Lorazepam : 2â€“4 m g (peds: 0.03â€“0.05 m g/kg per dose; m ax. 4 m g per dose) IV q15m in PRN



Midazolam : 1â€“2 m g (peds: 0.15 m g/kg IV Ã— 1) IV q10m in PRN



Morphine: 2â€“10 m g (peds: 0.05â€“0.2 m g/kg IV) q2hâ€“q4h PRN



Nicardipine: 5â€“15 m g/h IV continuous infusion (peds: safety not established)



Nim odipine: 60 m g PO/NGT q4h; (peds: safety not established)



Nitroprusside: 0.25â€“10 m cg/kg/m in IV continuous infusion (adults and peds)



Ondansetron: 4â€“8 m g (peds: 0.1â€“0.15 m g/kg m ax. 4 m g) PO/IM/IV t.i.d. PRN



Phenytoin: 15â€“20 m g/kg IV load at m ax. 50 m g/m in; m ax. 1.5 g; m aintenance 4â€“6 m g/kg/d IV; (adult and pediatric)



Prom ethazine:12.5â€“25 m g (peds >2 years old: 0.25â€“1 m g/kg; m ax. 25 m g/dose) PO/IM/IV q4hâ€“q6h hours PRN

Surgery 

Per neurosurgical consultant



Early operative intervention m ay prevent vasospasm and im prove outcom e.

Follow-Up

Pa ge 4 5 6

Disposition Admission Criteria 

All patients with SAH should be adm itted to an intensive care unit.



Patients with negative CT findings and equivocal LP findings should be adm itted.

Discharge Criteria 

Patients with negative CT and LP findings and onset of sym ptom s less than 2 weeks



Outpatient follow-up for headache treatm ent and further evaluation

Prognosis 

Mortality is 12% before arrival to hospital.



Ultim ately fatal in m ore than 50%.



In cases of â€œsentinel bleedâ€• or early detection of aneurysm al rupture, outcom es are im proved with early surgical or interventional approaches.

References 1. Claassen J, Vu A, Kreiter KT, et al. Effect of acute physiologic derangem ents on outcom e after subarachnoid hem orrhage. Crit Care Med. March 2004;32(3):832â€“838. 2. Edlow JA. Diagnosis of subarachnoid hem orrhage in the em ergency departm ent. Em erg Med Clin North Am . February 2003;21(1):73â€“87. 3. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hem orrhage. N Engl J Med. January 6, 2000;342(1):29â€“36. 4. Shah KH, Richard KM, Nicholas S, Edlow JA. Incidence of traum atic lum bar puncture. Acad Em erg Med. February 2003;10(2):151â€“154. 5. Uysal E, Yanbuloglu B, Erturk M, Kilinc BM, Basak M. Spiral CT

Pa ge 4 5 6

angiography in diagnosis of cerebral aneurysm s of cases with acute subarachnoid hem orrhage. Diagn Interv Radiol. June 2005;11(2):77â€“82.

Codes ICD9-CM 430 Subarachnoid hem orrhage, Meningeal hem orrhage Ruptured: Berry aneurysm (Congenital) Cerebral aneurysm NOS

ICD10 I60 Subarachnoid haem orrhage I60.9 Subarachnoid haem orrhage, unspecified I69.0 Sequelae of subarachnoid haem orrhage S06.6 Traum atic subarachnoid haem orrhage

CPT 62270 Lum bar puncture, diagnostic

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Subdural Hem ato m a

Subdural

Hematoma Colleen Campbell

Basics Description 



Classification of subdural hem atom a (SDH): o

Acute: diagnosis within the first 3 days

o

Subacute: diagnosis 3 days to 3 weeks

o

Chronic: diagnosis after 3 weeks

CT description: o

Rarely crosses m idline

o

Does cross suture lines

o

Inner m argins are often seen to be irregular.

Acute 

Most com m only due to acceleration-deceleration forces and less com m only from direct traum a



Sagittal m ovem ent of the head causes stretch of parasagittal bridging veins.



Other bleeding sites include: o

Laceration of dura

o

Venous sinus injury

o

Cortical arteries

Pa ge 4 5 6

o

Nontraum atic injuries: 

Intracerebral aneurysm rupture



Arteriovenous m alform ation



Co-agulation disorder



Arterial hypertension



Drug or alcohol abuse

Chronic Encapsulated hem atom a m ost likely caused by repeated sm all hem orrhages of bridging veins.

Etiology Acute 

Most com m on type of intracranial hem atom a (66â€“70%)



Represents 26â€“63% of blunt head injury



Motor vehicle crash (MVC) is m ost com m on cause overall.



Falls and assault m ore com m only result in isolated SDH (72%) than do MVCs (24%).



Elderly patients and those with seizure disorders are at increased risk.



Mortality is related to presenting signs and sym ptom s as well as com orbidities: o

Less than one half present as sim ple extra-axial collectionâ€”22% m ortality rate

o

About 40% of patients will have com plicated SDH: 

Parenchym al laceration or intracerebral hem atom a): m ortality rate >50%

o

Third group associated with contusionâ€”30% m ortality rate with functional recovery of 20%

Chronic 

Most com m on in babies or old people with atrophy: o

Associated with infarction in underlying brain

Pa ge 4 5 6



75% of patients are >50 years old.



Less than one half have history of traum a.



50% are alcoholic.



Epilepsy, shunting procedures, and coagulopathy are also associated.

Pediatric Considerations 

May occur secondary to traum a at birth



Nonaccidental traum a m ore com m on

Diagnosis Signs and Symptoms Acute 

One fifth has diagnosis discovered at autopsy.



Most com m only m isdiagnosed as intoxication or cerebrovascular accident (CVA)



Headache and altered m ental status: o

50% unconscious at discovery

Subacute/Chronic 

Headaches, nausea, vom iting, and seizures are frequent sym ptom s.



Presentation varied: o

Fluctuating m ental status

o

Unsteady gait

o

Slow progression of deficits

Pediatric Considerations Im aging is necessary in infants with persistent vom iting, new seizures, lethargy, irritability, bulging or tense fontanels.

Physical Exam

Pa ge 4 5 6

N/A

Acute 

Headache and altered m ental status



Most com m on clinical signs are hem iparesis or hem iplegia:



o

Seen in 40â€“65%

o

SDH opposite m otor deficit in 60â€“85%

Pupillary abnorm ality seen in 28â€“79%: o

SDH will be on sam e side of pupillary abnorm ality in 70â€“90%.



Seizures m ay be seen in about 10% initially.



Papilledem a in less than one third

Chronic Presentation is varied and m im ics other diseases.

Essential Workup 



Obtain directed history: o

Mechanism of injury kinetics

o

Neurologic status: baseline and at-scene

o

Com plicating factors: 

Past m edical history, m edications



Allergies, drug use

Rapid neurologic assessm ent: o

Glasgow Com a scale ([GCS] after fluid resuscitation m ost im portant)

o



Brainstem reflexes: 

Anisocoria



Pupillary light reflex



Corneal, gag, oculocephalic/oculovestibular

Head im aging

Tests Lab

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

Arterial blood gas, CBC, electrolytes with glucose, prothrom bin tim e (PT), partial throm boplastin tim e (PTT)



Blood ethyl alcohol, drug screen

Imaging Head CT in co-ordination with other necessary traum a workup

Acute 

Characteristic CT finding is crescent-shaped clot overlying hem ispheric convexity.



Most (60%) associated with other intracranial lesions

Chronic 

MRI is the test of choice as lesion m ay be isodense on CT from 2â€“3 weeks.



CT m ay show hypodense lesion after 3 weeks.



Spinal radiographs

Pediatric Considerations Ultrasound can be used to visualize cerebral structures if fontanelles are patent.

Differential Diagnosis Acute 

Diffuse axonal injury



Cerebral contusion



Intracerebral bleed



Subdural hygrom a



Epidural hem atom a



Shaken baby/battered child syndrom e

Chronic 

Pseudotum or cerebri



Brain tum or



Dem entia

Pa ge 4 5 6



Meningitis



CVA/Transient ischem ic attack



Cerebral atherosclerosis



Toxic, m etabolic, respiratory, or circulatory causes

P.1075

Treatment Initial Stabilization 

Manage airway and resuscitate as indicated: o

Hypoxia is a strong predictor of outcom e.

o

Maintain SAO 2 >95%

o

Rapid sequence intubation (RSI) is indicated for GCS <9 or for evidence of increased intracranial pressure (ICP). 

Routine hyperventilation is no longer recom m ended due to resultant dim inished cerebral perfusion pressure.



Controlled ventilation to m aintain PCO 2 35â€“40 m m Hg

o

NS to m aintain m ean arterial pressure (MAP) 100â€“110 is necessary: 

A single episode of systolic blood pressure <90 is associated with poor outcom e.

o

Spine precautions

o

Elevate head of bed 20â€“30Â° (only after adequate fluid resuscitation to avoid resultant decrease in cerebral blood flow [CBF]).



Not considered helpful:

Pa ge 4 5 6

o

Steroids

o

Antibiotic prophylaxis

o

Hyperventilation (unless herniation is im m inent)

o

Fluid restriction

o

Calcium -channel blockers

ED Treatment Acute 

Early neurosurgical intervention (<4 hours) in com atose patients shows reduced m ortality: o

Burr holes m ay be used as tem porizing m easure in deteriorating patients.

o

ICP m onitoring is indicated for patients with abnorm al CT who are intubated.



Nonoperative treatm ent m ay be indicated for sm all SDH: o

<20 m L of blood, <1 cm , m idline shift <5 m m , no m ass effect, no neurologic deficit



o

This requires frequent neurologic reassessm ent.

o

10% go on to require operative intervention.

Maintain euvolem ic state with isotonic fluids: o

Arterial line placem ent to m onitor MAP, PO 2 , and PCO 2

o 

Foley Catheter to m onitor I/O status

Control ICP: o

Prevent pain, posturing, and increased respiratory effort: 

Sedation with benzodiazepines



Neurom uscular blockade with vecuronium or pancuronium in intubated patients

 o

Etom idate is a good induction agent.

Mannitol m ay be used once euvolem ic: 

Shown to increase MAP >cerebral perfusion pressure and CBF as well as decrease ICP

Pa ge 4 5 7



Keep osm olality between 295 and 310.



Use furosem ide (Lasix) as an adjunct only if norm ovolem ic.

o

Treat hypertension: 



Labetalol, nicardipine, or hydralazine

Treat hyperglycem ia if present: o

Associated with increased m ortality in traum atic brain injury



Treat and prevent seizures: o

Diazepam and phenytoin (Dilantin): 

Prophylactic anticonvulsants not indicated

Medication (Drugs) 

Diazepam : 5â€“10 m g (peds: 0.2â€“0.3 m g/kg) IV/IM q10m inâ€“q15m in PRN; m axim um , 30 m g (peds: 10 m g)



Dilantin: adults and peds: load 18 m g/kg at 25â€“50 m g/m in



Etom idate: 0.3 m g/kg IV for induction of RSI



Hydralazine: 10â€“20 m g (peds: 0.1â€“0.5 m g/kg IV) q30m inâ€“q4h PRN



Labetalol: 20 m g IV bolus, then 40â€“80 m g q10m in; m ax. 300 m g; follow with IV continuous infusion 0.5â€“2 m g/m in; (peds: 0.4â€“1 m g/kg/h IV continuous infusion; m ax. 3 m g/kg/h)



Lasix: adults and peds: 0.5 m g/kg IV



Lidocaine: as preinduction agent, 1.5 m g/kg IV



Mannitol: adults and peds: 0.25â€“0.5 g/kg IV q4h



Midazolam : 1â€“2 m g (peds: 0.15 m g/kg IV Ã— 1) IV q10m in PRN



Nicardipine: 5â€“15 m g/hr IV continuous infusion (peds: safety not established)

Pa ge 4 5 7



Pentobarbital: 1â€“5 m g IV q6h



Thiopental: as induction agent, 20 m g/kg IV

Follow-Up Disposition Admission Criteria 

Acute SDH patients should be adm itted to the operating room or intensive care unit by the neurosurgical service.



Subacute subdurals should be adm itted to a m onitored setting.

Discharge Criteria Patients with chronic SDH often can be m anaged as outpatients in conjunction with neurosurgery, adequate hom e resources, and appropriate follow-up.

Issues for Referral All patients need neurosurgical evaluation im m ediately.

References 1. Bedell E, Prough DS: Anesthetic m anagem ent of traum atic brain injury. Anesth Clinics N. A. June 2002;20,2:417â€“439. 2. Goetz. Text of Clinical Neurology. 2nd ed. Elsevier 2003 3. Ono JI, Yam aura A, et al. Outcom e prediction in severe head injury: analyses of clinical prognostic factors. J Clin Neurosci. 2001;8(2):120â€“123. 4. Stieg PE, Kase CS. Neurologic em ergencies: intracranial hem orrhage diagnosis and em ergency m anagem ent. Neurol Clin. 1998;16(2):373â€“390. 5. Zink BJ. Traum atic brain injury outcom e: concepts for em ergency care. Ann Em erg Med. 2001;37(3):318â€“332.

Pa ge 4 5 7

Codes ICD9-CM 852.20 S06.5

Pa ge 4 5 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sudden Infant Death Syndro m e (SIDS)

Sudden

Infant Death Syndrome (SIDS) Roger Barkin Thea James

Basics Description 

Sudden, unexpected death of an infant less than 1 year old, who was typically well before being placed down to sleep



Death rem ains unexplained after being thoroughly investigated by autopsy, exam ination of the death scene, investigation of the circum stances, and review of the fam ily and infant m edical histories.



The m ajor cause of death in infants from 1 m onth to 1 year of age; the incidence has declined m arkedly since the initiation of the â€œBack to Sleepâ€• program in 1994: o

1983â€“1991: 5,000â€“6,000 deaths/year in the United States

o 

1999: 2,648 deaths in the United States

Peak occurrence of sudden infant death syndrom e (SIDS) between 2 and 4 m onths of age: o

88% occur before 5.5 m onths of age

Pa ge 4 5 7

o

2% occur after 12 m onths of age



60:40 m ale-to-fem ale ratio



Higher incidence reported in fall and winter



Recent respiratory infection com m on



Sleeping on back (supine) reduces incidence significantly (Back to Sleep). Practice of infants sleeping on their backs began earlier in Europe than in the United States, resulting in lower rates occurrence.

Etiology 

Most likely m ultifactorial



Many researchers suggest that SIDS infants have predisposing conditions that m ake them m ore vulnerable to norm al internal and external stresses that occur in infant life.



Proposed and unproven hypotheses: dysrhythm ias, hyperthyroidism , m ast cell activation, infection, anem ia, m ineral and electrolyte abnorm alities/im balances, airway obstruction, suffocation, congenital diseases, neurologic events, occult traum a



Associations/Risk factors for SIDS appear to be environm ental and behavioral, including m aternal, prenatal, and postnatal.

Maternal Influences Prevalent in SIDS Infants 

Prenatal cigarette sm oking



Maternal age <20 years during first pregnancy



Maternal low weight gain



Illicit drug use



Short intervals between pregnancies



Prenatal illness, sexually transm itted diseases, urinary tract infections

Pa ge 4 5 7

Other Possible Risk Factors and Associations 

Intrauterine growth retardation



Low birth weight



Exposure to environm ental sm oking



Hypertherm ia, including heavy bed linens, blankets



Bed sharing



Infant gastrointestinal illnesses and listlessness have been reported in proxim ity to SIDS deaths.

Diagnosis Signs and Symptoms History 

No significant pre-existing signs or sym ptom s to alert caretakers



Unpredictable, unpreventable



Most infants appear norm al when put to bed and are subsequently found dead.



Death occurs quickly while the infant is sleeping.



Typically the event is silent; no signs of suffering.



No clinical or pathologic explanation for death

History Apparent Life-Threatening Episode (ALTE) 

Prolonged period of apnea (>20 seconds), lasting long enough to cause changes in skin colorâ€”cyanosis, pallor, and occasionally erythem a



Lim pness, choking, gagging



Appears well when evaluated by clinicians after recovery from ALTE; infant should be transported to hospital for evaluation, adm ission, and m onitoring.

Pa ge 4 5 7



Link with SIDS has been suggested

Physical Exam 

The infant is seem ingly healthy and well appearing, well developed, and well nourished prior to the event; often appears well when evaluated after the episode if brief and self-lim ited.



Survivors m ay experience com plications of pulm onary edem a, aspiration pneum onia, and neurologic sequelae secondary to hypoxia, including seizures.

Essential Workup 

SIDS is a diagnosis of exclusion. An evaluation for other prim ary or contributing conditions is m andatory.



A diagnosis of SIDS is preceded by the m ultifactorial work-up.

Thorough Investigation of the Death Scene 

Where the infant slept and conditions in sleeping space (tem perature, bedding, bed sharing)



Position in which infant was sleeping; what (if anything) it was doing



Interview the parents, fam ily m em bers, caregivers



Collect and exam ine potentially relevant item s from the death scene



Maintain sensitivity toward fam ily; investigation could be difficult for them .

Investigate Infant and Family Case Histories 

History connected to infant: prenatal, perinatal, and postbirth m edical history



Fam ily m edical and social history, particularly m other



Fam ily is very vulnerable at the tim e of the investigation; ultim ately, it m ay help them through grieving process.

Pa ge 4 5 7



Could reveal a preventable cause: o

Could reveal no preventable cause; helping the fam ily to realize that there was nothing that they could have done to prevent the child's death



Investigate other possible risk factors

Tests Lab 

Selective studies reflecting episode and whether patient survives



Arterial blood gas



CBC



Electrolytes, including calcium , m agnesium , and phosphorous



Liver function tests



Toxicology screen



Blood culture and other sepsis workup as indicated



Urinalysis and culture



ECG



EEG

Imaging 

Chest radiograph, if ongoing resuscitation or to exclude pulm onary disease



Radiologic skeletal survey to exclude abuse (often done by pathologist)



If child survives, CT. Consider upper GI to exclude reflux

Diagnostic Procedures/Surgery 

Autopsy: o

Som e states require an autopsy in all SIDS cases

o

Is im portant that postm ortem exam ination be done, especially because SIDS is a diagnosis of exclusion

Pa ge 4 5 7

o

Involves m icroscopic exam ination of vital organs through tissue sam ples, as well as gross exam ination

o

Previous postm ortem findings in SIDS cases: 

Congenital cardiom yopathies



Cardiac rhabdom yom as



Tuberous sclerosis P.1077





Rare genetic diseases



Viral m yocarditis



Intracranial arteriovenous m alform ations

ECG of surviving fam ily m em bers m ay suggest fam ily disorder such as prolonged QT syndrom e.

Differential Diagnosis 



Cardiovascular: o

Dysrhythm ia

o

Myocarditis

o

Tuberous sclerosis

o

Cardiom yopathy

o

Congenital heart disease

Respiratory: o

Asphyxiation

o

Drowning

o

Gastroesophageal reflux



Infection



Overwhelm ing infection:



o

Bronchiolitis/Respiratory syncytial virus

o

Bronchopneum onia

o

Pertussis

o

Tracheobronchitis

CNS:

Pa ge 4 5 7



o

Cerebral edem a

o

Subdural hem atom a

o

Meningitis

o

Encephalitis

o

Arteriovenous m alform ation

Gastrointestinal: o





Pancreas: o

Cystic fibrosis

o

Islet cell hyperplasia

o

Hypertrophy or neoplasm

Endocrine: o



Enterocolitis with diarrhea

Congenital adrenal hyperplasia/hypoplasia

System ic: o

Dehydration

o

Sepsis

o

Intoxication, overdose

o

Hypertherm ia

o

Intoxication

o

Infantile apnea

Treatment 

Initiate optim al resuscitation at the scene; transport the infant to ED and continue the protocols en route.



On rare occasion and under m edical direction, resuscitations have been aborted and pronounced at the scene; consideration m ust be given to the em otional, social, and clinical circum stances.

Initial Stabilization 

Assess and support airway, breathing, circulation, and

Pa ge 4 5 8

blood glucose (bedside). 

Adm inister appropriate m edications per protocols by endotracheal tube if other IV access unobtainable (lidocaine, epinephrine, atropine, and naloxone).



Monitor vital signs: blood pressure, heart rate, respirations, and oxygen saturation continuously.



Conduct a thorough physical exam ination; look for accidental as well as intentional traum a.



Assess the scene and fam ily m em bers.

ED Treatment 

Resuscitate patient per established protocols, seam lessly continuing efforts initiated by prehospital personnel.



If the resuscitation is unsuccessful and no obvious diagnosis is found, the parents should not be told that SIDS is the cause of death. o

When speaking with the parents, it is appropriate to include SIDS am ong the possible causes of death.

o

A diagnosis cannot be m ade until com pletion of an autopsy, investigation of circum stances and death scene, and exploration of case m edical histories of the infant and fam ily.

Family Support 

If resuscitation is unsuccessful, attention should then be focused on the fam ily; if resuscitation is ongoing, com m unication and support of fam ily is essential.



All fam ily m em bers and caregivers are affected; they experience grief, guilt, failure, and inadequacy.



Som e parents want to spend quiet tim e holding their infants after an unsuccessful resuscitation.



Fam ily is defined variably am ong different cultures and could be m ore extensive than nuclear or traditional

Pa ge 4 5 8

extended fam ily; ED personnel should attem pt to be sensitive to cultural needs and expectations of the fam ily. 

Fam ily should be offered support in the ED and supplied with resources of support for beyond the day of their infant's death; the local, state, and national SIDS Foundation resources should be m ade available.



Support m ay be obtained from Sudden Infant Death Syndrom e Alliance, 1314 Bedford Avenue, Suite 210, Baltim ore, MD 21208 (800-221-7437)

Emergency Personnel Support 

ED debriefing should be conducted for all staff who were involved in the infant's care, including em ergency m edical service personnel; this can be im portant to allow people to express their feelings and freely process the event in a supportive setting.



The child's prim ary care physician should be involved in follow-up and supporting fam ily.

Follow-Up Disposition Admission Criteria Adm it all infants who have ALTE for evaluation and m onitoring after initial resuscitation and stabilization.

Discharge Criteria None

Issues for Referral 

All survivors should have a pediatric consultation.



Patients dying require an autopsy.

Pa ge 4 5 8



Fam ilies m ay need support.

References 1. Alteim er WA. A pediatrician's view: crib death and m anaged care. Pediatr Ann. 1995;24:345â€“346. 2. Am erican Academ y of Pediatrics, Task Force on Infant Sleep Position and Sudden Infant Death Syndrom e. Changing concepts of sudden infant death syndrom e: im plications for infant sleeping environm ent and sleep position. Pediatrics. 2000;24:650â€“656. 3. Carroll-Pankhurst C, Mortim er EA Jr. Sudden infant death syndrom e, bed baring, parental weight, and age at death. Pediatrics. 2001;108:1239â€“1240. 4. Dwyer T, Ponsby A. SIDS epidem iology and incidence. Pediatr Ann. 1995;24:350â€“352. 5. Krous HF, Beckwith B, Byard RW, et al: Sudden infant death syndrom e and unclassified sudden infant deaths: a definitional and diagnostic approach. Pediatrics. 2004;114:234. 6. Paris CA, Rem ler R, Daling IR: Risk factors for sudden infant death syndrom e: changes associated with sleep position recom m endations. J Pediatr. 2001;139:771.

Miscellaneous SEE ALSO: Resuscitation, Neonatal; Resuscitation, Pediatric

Codes ICD9-CM 798.0

ICD10 R95

Pa ge 4 5 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Suicide, Risk Evaluatio n

Suicide, Risk

Evaluation Lawrence Park Jennifer M. Park

Basics Description 

The intentional taking of one's own life



Suicidal ideation:



o

Passive: no real plan or intent

o

Active: with plan and intent to die

Suicidal gesture: self-injurious behavior not intended to cause death (e.g., superficial cutting, cigarette burns, head banging)



Reckless behavior: not taking prescribed m edications, taking too m uch of prescribed m edications, running into traffic



Risk-to-rescue ratioâ€”lethality of plan com pared with likelihood of rescue: o

High risk-to-rescue ratio indicates increased severity of attem pt.

Etiology 

29,199 suicides in United States (1999)

Pa ge 4 5 8



11.4 deaths per 100,000 population



Two peaks in age group m ost at risk for suicide: o

Age 15â€“24 years (third leading cause of death in this age group)

o

Age >60 years (highest rates of any age group, increasing incidence with age)

Risk Factors for Suicidal Behavior 

Alcohol or drug abuse



History of physical or sexual abuse



History of head injury or neurologic disorder



Cigarette sm oking



Positive fam ily history of suicide attem pt



Prior psychiatric diagnosis: o

90% of patients who com m it suicide

o

Depression (bipolar or unipolar)

o

Substance abuse

o

Anxiety/Panic disorders

o

Schizophrenia

o

Personality disorders

o

Chronic severe m edical illness

o

Epilepsy

o

AIDS

o

Huntington disease

o

Stroke

o

Traum atic brain injury

o

Cancer

o

Multiple sclerosis

o

Spinal cord injuries

o

Hypertension

o

Cardiopulm onary disease

o

Peptic ulcer disease

o

Chronic renal failure

Pa ge 4 5 8



o

Cushing disease

o

Rheum atoid arthritis

o

Porphyria

Gender: o

Wom en are three tim es m ore likely to attem pt suicide.

o 



Men are three tim es m ore likely to com plete suicide.

Psychological: o

Im pulsivity/Aggression

o

Depression

o

Anxiety

o

Hopelessness

o

Self-consciousness/social disengagem ent

o

Poor problem -solving abilities

o

Social

o

Widowed

o

Divorced

o

Separated

o

Lack of social supports

o

Recent loss of relationship

o

Anniversary of loss

Environm ental: o

Rural areas

o

Access to firearm s

o

Poverty

o

Unem ploym ent

Risk Factors for Completed Suicide 

Male



Age >60 years



White or Native Am erican



Widowed/Divorced



Living alone

Pa ge 4 5 8



Unem ploym ent/Poverty



Past suicide attem pt

Methods of Suicide 

Firearm s (m ost com m on am ong m en and wom en, three of five com pleted suicides)



Overdose (second m ost com m on am ong wom en); m ost com m on m eans of suicide attem pt (70% of failed attem pts are by overdose)



Hanging (second m ost com m on am ong m en)

Populations at Highest Risk for Completing Suicide 

Depressionâ€”especially psychotic depression



Anxiety and panic disorder



Alcohol or drug intoxication



Schizophrenia



Adolescents

Others at Risk for Completing Suicide 

Recent discharge from psychiatric facility



Past history of suicidal ideation or suicide attem pt



Serious physical illness is present up to 70% of all suicides, particularly in elderly patients.



Prisoners



Doctors



Victim s of violence/abuse



Persons expecting secondary gain through attem pt

Decreased Risk for Suicide 

Patients with m ood disorders (m ajor depression and bipolar disorder) treated with lithium



Patient with m ajor depression treated with electroconvulsive therapy

Pa ge 4 5 8



Patients with schizophrenia treated with clozapine



Patients with m ajor depression treated with selective serotonin reuptake inhibitors (SSRI) not shown to decrease suicide rates

Diagnosis Signs and Symptoms 

Depressed m ood



Verbalization of suicidal ideation



Hopelessness



Helplessness



Anger/Aggression



Im pulsivity



Psychotic sym ptom s (com m and auditory hallucinations)

Essential Workup 

Obtain history to assess risk: o

Asking about suicide does not increase risk for attem pt



Degree of suicidal ideation



Plan: im m ediate risk of self-injury? o

Means available to com plete plan

o

Activity toward initiating plan

o

Patient's expectations of lethality of plan



Intent: reasons, goal



Risk-to-rescue ratio



Plan or intent to harm others?



Presence of acute precipitants: o



Recent losses, lack of social supports

Risk factors:

Pa ge 4 5 8

o

History of past suicide attem pts

o

Psychiatric review of sym ptom s: depression, psychosis, panic/anxiety



o

Chronic m edical illness

o

Alcohol or drug abuse

Serial assessm ent of m ental status, consistency of responses



â€œWhy didn't you attem pt suicide?â€•



Collateral inform ation from outpatient treaters, fam ily, friends

Safety Plan 

Would the patient im m ediately seek help if suicidal ideation recurred?



Elim ination of m eans of suicide



Access to other m eans of suicide



Support and supervision in the outpatient setting



Prom pt outpatient follow-up with psychiatric therapy



Patient investing in not attem pting suicide



Reasons for living?



Safety contracts are not useful

Tests 

Blood alcohol level



Serum toxicology screen: aspirin, acetam inophen, and other m edications



Urine drug screen: o

Many psychiatric facilities require toxicology screen before placem ent.



ECG, carbon m onoxide (as indicated)



Im aging not routinely indicated

P.1079

Pa ge 4 5 8

Differential Diagnosis 

Norm al despondency



Bereavem ent



Adjustm ent disorder with depressed m ood



Major depressive disorder



Bipolar disorder



Organic m ental disorder (head injury, dem entia, delirium )



Schizophrenia



Panic and anxiety disorders



Alcohol or drug abuse



Borderline personality disorder



Antisocial personality disorder



Accidental death



Attem pted hom icide

Pediatric Considerations 

Suicide is third leading cause of death am ong young people 15â€“24 years of age.



More than 5,000 adolescents com m it suicide every year.



Rapidly increasing in young black m ales, ages 10â€“14 years



Less evidence available to link suicide in youth to overt psychiatric illness



Stresses: o

Prior attem pts

o

Fam ily disruption

o

History of psychiatric disorder

o

Depression

o

Disciplinary crisis

o

Broken rom ance

o

School difficulties

Pa ge 4 5 9



o

Bereavem ent

o

Rejection

o

History of physical or sexual abuse

Early warning signs: o

Progressive declining schoolwork

o

Multiple physical com plaints

o

Substance abuse

o

Disrupted fam ily relations

Geriatric Considerations 

Suicide rates highest in age >65 years



Com pleted suicide: 83% m en



Risk factors: divorced, widowed, m ale, social isolation



Tend to use m ore lethal m ethods



Lower ratio of attem pts to com pletions

Treatment Pre Hospital 

Restraint of potentially dangerous patient who refuses transport to treatm ent facility; involve police.



Risk to m edics on the scene in cases of firearm s or other weapons



Know state and local laws, availability of m obile crisis units, and when to involve the police departm ent.

Initial Stabilization 

Prevent any ability to elope.



Search the patient. o

Rem ove sharp objects, belts, shoelaces, and other articles that could be use for self-injury.



Appropriate supervision

Pa ge 4 5 9

ED Treatment 

Voluntary adm ission to psychiatric facility



Involuntary adm ission if patient refuses voluntary



For involuntary psychiatric adm ission, patient m ust have psychiatric disorder and one of the following: o

Risk for danger to self

o

Risk for danger to others

o

Unable to care for self owing to extrem ely poor judgm ent

Medication (Drugs) Treat underlying psychiatric disorder.

Follow-Up Disposition Admission Criteria 

If patient endorses suicidal ideation with plan and intent, then adm ission m ay be needed for safety.



If im pulsivity, anger, or aggression hinder ability to control behavior

Discharge Criteria 

Patient has no suicidal ideation.



Patient agrees to return to ED im m ediately or seek psychiatric help if suicidal ideation recurs.



Patient has passive suicidal ideation without plan or intent.



Good support network or placem ent in appropriate crisis housing

Pa ge 4 5 9



Appropriate outpatient psychiatric follow-up ensured



In som e cases, patients who express suicidal ideation while intoxicated m ay be discharged if no longer suicidal once they are sober.



Som e patients with borderline personality disorder and chronic suicidal ideation are discharged after careful psychiatric evaluation, in consultation with long-term outpatient caregivers.

References 1. Connor KR, Duberstein PR, Conwell Y, et al. Psychological vulnerability to com pleted suicide: a review of em pirical studies. Suicide and Life-Threatening Behavior. 2001;31(4):367â€“385. 2. Harwitz D, Ravizza L. Suicide and depression. Em erg Med Clin North Am . 2000;18(2):263â€“71, ix 3. Lagom asino IT, Stern TA. Approach to the suicidal patient. In Stern TA, Herm an JB, Slavin PL, eds. The MGH guide to psychiatry in prim ary care. New York, NY: McGraw-Hill, 1998:1522. 4. Mann JJ. A current perspective of suicide and attem pted suicide. Ann Intern Med. 2002;136(4):302â€“311.

Codes ICD9-CM 300.9

ICD10 Z91.5

Pa ge 4 5 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Supraventricular Tachycardia

Supraventricular Tachycardia James Adams Jason Liebzeit

Basics Description 

Rhythm that originates ectopically above the His bundle



Heart rate of 100 beats/m in or greater



Irregular narrow com plex supraventricular tachycardia (SVT): o





Most com m on form of SVT seen in the ED



10% of people over 75 years of age have AF.

o

Atrial flutter

o

Multifocal atrial tachycardia

Regular narrow com plex SVT: o

o 

Atrial fibrillation (AF):

Arteriovenous nodal re-entry: 

60% of SVT



Typically present age 30â€“40 years



70% are wom en.

AV re-entry involving an accessory pathway

Wide com plex SVT: o

Aberrant conduction or a bundle branch block is

Pa ge 4 5 9

present. o

Conduction is outside of the norm al His-Purkinje system .

o

More com m on in younger patients without structural disease

o

Always suspect a ventricular rhythm with a wide com plex rhythm

Etiology 

Atrial tachycardia: o

Precipitated by a prem ature atrial or ventricular contraction



o

Electrolyte disturbances

o

Drug toxicity

o

Hypoxia

Junctional tachycardia: o

AV nodal re-entry

o

Myocardial ischem ia

o

Structural heart disease

o

Pre-excitation syndrom es: 

o 

Wolff-Parkinson-White (WPW) syndrom e

Drug and alcohol toxicity

AF: o

Hypertension

o

Coronary artery disease

o

Hypothyroidism

o

Heavy alcohol intake

o

Mitral valve disease

o

Chronic pulm onary disease

o

Pulm onary em bolus

o

WPW syndrom e

o

Hypoxia

o

Digoxin toxicity

Pa ge 4 5 9



o

Chronic pericarditis

o

Idiopathic AF

Atrial flutter: o

Ischem ic heart disease

o

Valvular heart diseases

o

Congestive heart failure

o

Myocarditis

o

Cardiom yopathies

o

Pulm onary em bolus

o

Other pulm onary disease

Diagnosis Signs and Symptoms 

Palpitations (m ost com m on)



Lightheadedness, pressure in the head



Dyspnea



Diaphoresis



Dizziness



Weakness



Chest discom fort



Syncope



Prom inent neck veins



Signs of instability: o

Mental status changes

o

Chest pain/ischem ia

o

Acute pulm onary edem a

o

Hypotension

History 

Abrupt onset of palpitations, lightheadedness, weakness,

Pa ge 4 5 9

chest pain 

Insidious onset of generalized weakness and m alaise

Physical Exam 





Vital signs: o

Tachycardia

o

Blood pressure norm al or hypotensive

o

Respiratory rate norm al or tachypneic

Cardiac: o

Regular or irregularly irregular rhythm

o

JVD m ay be present in setting of heart failure

Pulm onary: o

Rales m ay be present in setting of heart failure.

Essential Workup 

ABCs, assess stable vs. unstable



History: o

Current sym ptom s

o

Previous episodes

o

Prior cardiac history

o

Medications: 

o 

Over-the-counter, decongestants

Illicit drug use

ECG: o

Regular or irregular?

o

Quasi random signal com plex narrow or wide?

o

P waves present or absent: 

Regular or irregular?

Tests ECG 

Atrial flutter: o

Regular atrial rate usually greater than 300

Pa ge 4 5 9

o

Beat-to-beat uniform ity of cycle length, polarity, and am plitude

o

Sawtooth flutter waves directed superiorly and m ost visible in leads II, III, aVF

o

AV block, usually 2:1, but occasionally greater or irregular



Multifocal atrial tachycardia: o

Three distinctly different P waves with varying pulse rate intervals



Atrial tachycardia: o

Rate of 100â€“200 beats/m in

o

P wave precedes QRS and is m orphologically different from the sinus P wave.



Junctional tachycardia: o

There is usually 1:1 conduction, with ventricular rates equaling the atrial rate.

o

May be either paroxysm al or sustained

o

Ventricular rates faster than 200 beats/m in in an adult suggest an accessory pathway syndrom e such as WPW syndrom e.

o

Absence of preceding P waves

o

Often retrograde P waves buried in the QRS

o

Paroxysm al junctional tachycardia rates range from 120â€“200 beats/m in.

o

Nonparoxysm al junctional tachycardia rates rarely exceed 130 beats/m in.

Lab Studies are indicated when underlying m etabolic abnorm alities or ischem ia is considered: 

CBC



Electrolytes



Cardiac enzym es

Pa ge 4 5 9



Thyroid function

Imaging Chest radiograph: 

Assess cardiac size



Evaluate for pulm onary process



More useful in AF/flutter

Differential Diagnosis 



Sinus tachycardia: o

Sepsis

o

Hypovolem ia

o

Pericardial tam ponade

o

Acute m yocardial infarction

o

Drug intoxication

o

Infection

Wide com plex tachycardias: o

Distinguish between supraventricular with aberrancy or ventricular origins.

P.1081

Treatment Pre Hospital 

Supplem ental oxygen



IV access



Monitor

Initial Stabilization 

IV access

Pa ge 4 5 9



Oxygen



Monitor



Determ ination of unstable versus stable patient m ade by determ ining whether the patient has organ perfusion (if patient is awake and talking, there is usually tim e to try other m ethods before cardioversion even with low BP).

ED Treatment 

AF: o

Most likely diagnosis when the rhythm is irregular

o

When unstable, then im m ediate cardioversion

o

When stable, rate control is a priority: 

Beta-blockers or calcium -channel blockers, am iodarone, and digoxin



Cardioversion in stable patients should not be attem pted unless the dysrhythm ia is known to be acute (<24 hours in duration), otherwise anticoagulation is the first step.



WPW syndrom e: o

Consider direct current cardioversion or am iodarone, flecainide, or procainam ide.

o

Avoid adenosine, beta-blockers, calcium -channel blockers, and digoxin.



In regular narrow com plex SVTs: o

Vagal m aneuvers will occasionally term inate the dysrhythm ia: 

Carotid m assage (though beware of carotid disease, especially in elderly)



Ice to face in children (m am m alian diving reflex)

 o

Valsalva m aneuver

If this is unsuccessful, adenosine is the drug of choice.

Pa ge 4 6 0



Wide com plex SVT: o

Try to determ ine whether ventricular tachycardia or SVT with aberrancy: 

Brugada criteria

o

Verapam il is absolutely contraindicated.

o

Adenosine should be reserved for SVT with aberrancy and is rarely indicated.

o

Electrical cardioversion: 

Fewer potential com plications than anti-arrhythm ic drugs when m echanism unknown

o

Antidysrhythm ic drugs: 

IV procainam ide and IV am iodarone



Lidocaine is less effective, although som etim es m ore readily available.



Bretylium lacks any evidence of efficacy.

Pediatric Considerations 

SVT is the m ost com m on dysrhythm ia seen in young adults and children without underlying heart disease.



Aberrant conduction: o

WPW syndrom e and atrioventricular nodal re-entry tachycardia are the two m ost com m on form s of SVT seen in children.



Use verapam il only over 1 year of age.

Medication (Drugs) 

Adenosine: 6 m g (peds: 0.1 m g/kg up to 6 m g) rapid IVP; if no response after 1â€“2 m inutes, then 12 m g (peds: 0.2m g/kg up to 12 m g), m ay repeat 12 m g (0.2 m g/kg)



Am iodarone: load with 15 m g/m in IV over 10 m inutes

Pa ge 4 6 0

(peds: 5 m g/kg over 20â€“60 m inutes), then 1 m g/m in IV for 6 hours 

Digoxin: 0.5 m g IV initially, then 0.25 m g IV q4h



Diltiazem : 0.25 m g/kg IV (usually 10â€“20 m g) over 2 m inutes, followed in 15 m inutes by 0.35 m g/kg IV over 2 m inutes



Esm olol: 0.5 m g/kg IV over 1 m inute; m aintenance infusion, 0.05 m g/kg/m in IV over 4 m inutes, then 0.1â€“0.2 m g/kg/m in IV continuously



Lidocaine: 100 m g IV



Metoprolol: 5â€“15 m g slow IV push at 5-m inute intervals to total of 15 m g



Procainam ide: 20â€“30 m g/m in IV up to 17 m g/kg, m ay increase to 50 m g/m in for m ore urgent situations



Propranolol: 0.1 m g/kg div. into equal doses at 2- to 3-m inute intervals



Sotalol: load 10 m g/m in IV up to 1.0â€“1.5 m g/kg body weight



Verapam il: 2.5â€“5.0 m g IV bolus over 2 m inutes; m ay repeat with 5â€“10 m g q15â€“30m in to m ax. of 20 m g

Follow-Up Disposition Admission Criteria 

Possible cardiac ischem ic event



Persistent supraventricular tachycardia



Other underlying m etabolic abnorm alities

Discharge Criteria Term inated rhythm without organ hypoperfusion

Pa ge 4 6 0

References 1. Atkins DL, Dorian P, Gonzalez ER, et al. Treatm ent of tachyarrhythm ias. Ann Em erg Med. 2001;37:S91â€“S109. 2. Chauhan VS, Krahn AD, Klein GJ, et al. Supraventricular tachycardia. Med Clin North Am . 2001;85(2):193â€“223. 3. Connors S, Dorian P. Managem ent of supraventricular tachycardia in the em ergency departm ent. Can J Cardiol. 1997;13(Suppl A):19Aâ€“24A. 4. Gupta AK, Thakur RK. Wide QRS com plex tachycardias. Med Clin North Am . 2001;85(2):245â€“266, ixx. 5. Obel OA, Cam m AJ. Supraventricular tachycardia: ECG diagnosis and anatom y. Eur Heart J. 1997;18(Suppl C):C2â€“C11.

Codes ICD9-CM 427.0 Supraventricular tachycardia, unspecified 427.3 Atrial fibrillation and flutter 427.6 Prem ature beats 785.0 Tachycardia, unspecified

ICD10 I47.1 Supraventricular tachycardia I48 Atrial fibrillation and flutter

Pa ge 4 6 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sym patho m im etic Po iso ning

Sympathomimetic Poisoning Sean Patrick Nordt James W. Rhee

Basics Description 

Direct or indirect stim ulation of adrenergic receptors in sym pathetic and central nervous system s



Often no correlation between dosage and degree of toxicity



Cocaine m ay also block sodium channels of cardiac m yocytes, leading to â€œtricyclicâ€• or class 1aâ€“type dysrhythm ias.

Pediatric Considerations 

Sym pathom im etic poisoning in children m ay present sim ilarly to m eningitis or other system ic illness.



Urinary toxicology screening m ay be only way to discover sym pathom im etic poisoning in children presenting with altered m ental status.



Methylphenidate (Ritalin, Concerta) and other sym pathom im etics used for attention deficit/hyperactivity disorder (ADHD) m ay cross-react with altered m ental status.

Pa ge 4 6 0

Etiology 

Sym pathom im etic toxicity can result from use of any sym pathetically active drug, including: o

All am phetam ines, m etham phetam ines, and derivatives (ecstasy, MDMA)



o

Cocaine

o

Phencyclidine (PCP)

o

Lysergic acid diethylam ide (LSD)

o

Decongestants (rare)

Drug delivery routes: inhalation, injection, snorting, or ingestion

Diagnosis Signs and Symptoms Vital Signs 

Tachycardia: o

Bradycardia possible for cocaine and som e other decongestants



Increased blood pressure: o

Severely intoxicated patients m ay be hypotensive.



Tachypnea



Hypertherm ia: o

Often present, m ay be severe, and is often overlooked

CNS 

Anxiety



Headache



Agitation



Altered m entation

Pa ge 4 6 0



Diaphoresis



Seizures



Stroke



Dystonia (rare)

Cardiovascular 

Palpitations



Chest pain



Myocardial ischem ia or infarction



Tachydysrhythm ias



Cardiovascular collapse



Murm ur (e.g., endocarditis)

Other 

Dilated pupils



Dry m ucous m em branes



Urinary retention m ay cause enlarged bladder.



Needle track m arks or abscesses on extrem ities should be sought.



Increased or decreased bowel sounds



The presence of diaphoresis and bowel sounds m ay help to differentiate sym pathom im etic toxicity from anticholinergic poisoning.

Essential Workup 

Monitor vital signs: o

o

Increased tem perature (>40Â°C possible): 

Core tem perature recording essential



Peripheral tem perature m ay be cool.



Indication for urgent cooling



Om inous prognostic sign

Blood pressure: 

Severe hypertension can lead to cardiac and neurologic abnorm alities.

Pa ge 4 6 0

 

Late in course, hypotension m ay supervene.

ECG: o

Signs of cardiac ischem ia

o

Ventricular tachydysrhythm ias

o

Reflex bradycardia

Tests Lab 



Urinalysis: o

Blood

o

Myoglobin

Electrolytes, BUN/creatinine, glucose: o

Hypoglycem ia m ay contribute to altered m ental status.

o

Acidosis m ay accom pany severe toxicity.

o

Rhabdom yolysis m ay cause renal failure.

o

Hyperkalem iaâ€”life-threatening consequence of acute renal failure



Coagulation profile to m onitor for potential dissem inated intravascular coagulation (DIC): o



Creatine phosphokinase (CPK): o



INR, PT, PTT, platelets

Markedly elevated in rhabdom yolysis

Urine toxicology screen: o

For other toxins with sim ilar effects (e.g., cocaine)

o

Som e am phetam inelike substances (e.g., m ethcathinone) m ay not be detected.



Aspirin and acetam inophen levels if suicide attem pt a possibility



Arterial blood gas (ABG)

Imaging 

Chest radiograph:

Pa ge 4 6 0



o

Adult respiratory distress syndrom e

o

Noncardiogenic pulm onary edem a

Head CT for: o

Significant headache

o

Altered m ental status

o

Focal neurologic signs

o

Subarachnoid hem orrhage, intracerebral bleed

Diagnostic Procedures/Surgery 

Lum bar puncture for: o

Suspected m eningitis (headache, altered m ental status, hyperpyrexia)

o

Suspected subarachnoid hem orrhage and CT norm al

Differential Diagnosis 

Sepsis



Thyroid storm



Serotonin syndrom e



Neuroleptic m alignant syndrom e



Pheochrom ocytom a



Subarachnoid hem orrhage



Drugs that cause delirium : o



Anticholinergics: 

Belladonna alkaloids



Antihistam ines

o

Tricyclic antidepressants

o

Cocaine

o

Ethanol withdrawal

o

Sedative/hypnotic withdrawal

o

Hallucinogens

o

Phencyclidine

Drugs that cause hypertension and tachycardia: o

Sym pathom im etics

Pa ge 4 6 0



o

Anticholinergics

o

Ethanol withdrawal

o

Phencyclidine

o

Caffeine

o

Phenylpropanolam ine

o

Ephedrine

o

Monoam ine oxidase inhibitors

o

Theophylline

o

Nicotine

Drugs that cause seizures: o

Anticholinergics

o

Cam phor

o

Carbam azepine

o

Carbon m onoxide

o

Chlorinated hydrocarbons

o

Cholinergics (organophosphate insecticides)

o

Cocaine

o

Cyanide

o

Ethanol withdrawal

o

Hypoglycem ics

o

Isoniazid

o

Lead

o

Lithium

o

Local anesthetics

o

Phencyclidine

o

Phenothiazines

o

Phenytoin

o

Propoxyphene

o

Salicylates

o

Sedative/hypnotic withdrawal

o

Strychnine

o

Theophylline

Pa ge 4 6 0

P.1083

Treatment Pre Hospital 

Patient m ay be uncooperative or violent.



Secure IV access.



Protect from self-induced traum a.

Initial Stabilization 

ABCs



Establish IV 0.9% NS access.



Cardiac m onitor



Naloxone, dextrose (or Accu-Chek), and thiam ine if altered m ental status

ED Treatment 

Decontam ination: o

Gastric lavage: 

Consider if recent (1â€“2 hours) or life-threatening ingestion



Instill activated charcoal through large-bore orogastric tube both before and after lavage.

o

Adm inister activated charcoal with sorbitol.

o

Whole-bowel irrigation with polyethylene glycol solution for body packers



Hypertensive crisis: o

Initially adm inister benzodiazepines if agitated.

o

Alpha-blocker (phentolam ine) as second-line agent

o

Nitroprusside for severe, unresponsive hypertension

Pa ge 4 6 1

o

Avoid beta-blockers, which m ay exacerbate hypertension.



Agitation, acute psychosis: o

Adm inister benzodiazepines.

o

Use butyrophenones (e.g., haloperidol) with caution to m anage agitation: 

May lower seizure thresholds and m ay prolong QT duration



Dysrhythm ias: o

Sodium bicarbonate is treatm ent of choice for ventricular dysrhythm ias and heart blocks indicative of sodium channel blocking effects with cocaine poisoning (e.g., widened QRS com plex on electrocardiography).

o

Lidocaine for ventricular dysrhythm ias refractory to alkalinization, benzodiazepines, and supportive care



Hypertherm ia: o

Benzodiazepines if agitated

o

Active cooling if tem perature >40Â°C:

o



Tepid water m ist



Evaporate with fan.

Paralysis: 

Indicated if m uscle rigidity and hyperactivity contributing to persistent hypertherm ia



Rhabdom yolysis: o

Adm inister benzodiazepines.

o

Hydrate with 0.9% NS.

o

Maintain urine output at 1â€“2 m L/m in

o

Hem odialysis (if acute renal failure and hyperkalem ia occur)



Seizures: o

Maintain airway

Pa ge 4 6 1

o

Adm inister benzodiazepines

o

Phenobarbital if unresponsive to benzodiazepines

o

Phenytoin contraindicated

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 100 g PO



Dextrose: D 5 0 W one am p: 50 m L or 25 g (peds: D 2 5 W 2â€“4 m L/kg) IV



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Lorazepam (benzodiazepine): 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV



Nitroprusside: 1â€“8 Âµg/kg/m in IV (titrated to blood pressure)



Phenobarbital: 15â€“20 m g/kg at 25â€“50 m g/m in until cessation of seizure activity



Phentolam ine: 1â€“5 m g IV over 5 m inutes (titrated to blood pressure)



Sodium bicarbonate: 1 or 2 am ps (peds: 1â€“2 m Eq/kg) IV push



Sorbitol: 1â€“2 g/kg to m ax. of 100 g PO m ixed in activated charcoal slurry (peds: >1-year-old: 1â€“1.5 g/kg as 35% solution to m ax. of 50 g); avoid repeat doses of sorbitol

Follow-Up Disposition Admission Criteria

Pa ge 4 6 1



Adm it all body packers or stuffers to hospital.



Severe m anifestations of toxicity to m onitored bed:



o

Seizures

o

Dysrhythm ias

o

Hypertherm ia

o

Rhabdom yolysis

o

Severe hypertension

o

Altered m ental status

Ischem ic chest pain

Discharge Criteria Mildly intoxicated patients can be observed and treated in ED until resolution of clinical m anifestations.

References 1. Albertson TE, Derlet RW, Van Hoozen BE. Metham phetam ine and the expanding com plications of am phetam ines. West J Med. 1999;170:214â€“219. 2. Callaway CW, Clark RF. Hypertherm ia in psychostim ulant overdose. Ann Em erg Med. 1994;24:68â€“76. 3. Derlet RW, Albertson TE. Em ergency departm ent presentation of cocaine intoxication. Ann Em erg Med. 1989;18:182â€“186. 4. McCarron M, et al. Acute phencyclidine intoxication: incidence of clinical findings in 1000 cases. Ann Em erg Med. 1981;10:237â€“242. 5. Richards CF, Clark RF, Holbrook T, et al. The effects of cocaine and am phetam ines on vital signs in traum a patients. J Em erg Med. 1995;13:59â€“63.

Codes ICD9-CM 971.2 Poisoning by drugs prim arily affecting the autonom ic nervous system , sym pathom im etics (adrenergics)

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Synco pe

Syncope

Sam Keim Amy Baldwin

Basics Description 

Transient loss of consciousness associated with loss of postural tone



Ultim ately, it is the lack of oxygen to the brainstem reticular-activating system , which results in a loss of consciousness and postural tone.



Most com m only, an inciting event causes a drop in cardiac output.



Cerebral perfusion is re-established by autonom ic regulation as well as the reclined posture, which results from the event.



Accounts for 3% of ED visits

Geriatric Considerations 

Elderly with highest incidence as well as increased m orbidity



>One third will have num erous potential causes.

Etiology 

Neurally m ediated syncope:

Pa ge 4 6 1

o

Reflex response causing vasodilatation and bradycardia with resulting hypoperfusion

o

Vasovagal (com m on faint): 

Often incited by pain or fear



Prodrom al findings are usually present.



Typically lasts less than 20 seconds



Tilt-table testing is the gold standard to diagnose.

o



Carotid sinus syncope: 

Cough, sneeze



Gastrointestinal stim ulation (e.g., defecation)



Micturition

Orthostatic: o

Positional changes cause abrupt drop in venous return to heart.

o

Volum e depletion: 

Severe dehydration (e.g., vom iting, diarrhea, diuretics)

 o



Hem orrhage (see Hem orrhagic Shock)

Autonom ic failure: 

Diabetic or am yloid neuropathy



Parkinson disease



Drugs (e.g., beta blockers) and alcohol

Cardiac arrhythm ias: o

Typically sudden and without prodrom al sym ptom s

o

Tachydysrhythm ia or bradydysrhythm ia

o

Inherited syndrom es (e.g., long QT syndrom e, Brugada syndrom e)

o

Pacem aker/im plantable cardioverter defibrillator m alfunction



Structural cardiac or cardiopulm onary disease: o

Valvular disease (especially aortic stenosis)

Pa ge 4 6 1



o

Hypertrophic cardiom yopathy

o

Acute m yocardial infarction

o

Aortic dissection

o

Pericardial tam ponade

o

Pulm onary em bolus

Neurologic: o

Transient spike in intracranial pressure that exceeds cerebral perfusion pressure



o

Postsyncopal headache is alm ost universal.

o

May be presentation of a subarachnoid hem orrhage

Cerebrovascular steal syndrom es

Diagnosis Signs and Symptoms History 





Prodrom al sym ptom s: o

Lightheadedness

o

Diaphoresis

o

Dim m ing vision

o

Nausea

o

Weakness

The following findings suggest an underlying life threat: o

Sudden event without warning

o

Chest pain or palpitations

Six Ps of a syncope history: o

Pre-Prodrom e activities

o

Prodrom e sym ptom sâ€”visual sym ptom , nausea

o

Predisposing factorsâ€”age, chronic disease, fam ily history of sudden death

Pa ge 4 6 1

o

Precipitating factorsâ€”stress, postural sym ptom s

o

Passerby witnessâ€”what did they see?

o

Postictal phase, if anyâ€”suggests seizure

Physical Exam 

Evaluate for traum a.



Orthostatic vital signs



Check for difference in blood pressure in both arm s suggesting aortic dissection or subclavian steal syndrom e.



Careful cardiovascular exam ination, including m urm urs, bruits, and dysrhythm ias



Rectal exam ination to check for gastrointestinal (GI) bleeding



Urine pregnancy test in reproductive age fem ale



Careful neurologic exam ination

Pediatric Considerations 

Warning signs of a potential serious underlying disease: o

Syncope during exertion

o

Syncope to loud noise, fright, extrem e stress

o

Syncope while supine

o

Fam ily history of sudden death at young age (<30 years)

Essential Workup 



ECG im m ediately upon arrival to check for: o

Ischem ia

o

Dysrhythm ias

o

Block

o

Long QT interval

o

Wolff-Parkinson-White syndrom e

Detailed history and physical exam ination will determ ine diagnosis in 85% of those who eventually obtain a diagnosis.

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Tests Lab 

Driven by history and physical exam ination



CBC in suspected occult hem orrhage



Serum bicarbonate: o

Norm al with m ost syncopal events

o

Marked decreased bicarbonate obtained less than 1 hour after the event: 

Suggestive of a grand m al seizure rather than syncope



If due to seizure, should norm alize 1 hour after the event



Cardiac enzym es in suspected ischem ia



Pregnancy test in reproductive age fem ale



Electrolytes in patients with profound dehydration or diuretic use

Imaging 

ECG and m onitoring until cardiac etiology ruled out



Chest radiograph if congestive heart failure (CHF), dissection, or m assive pulm onary em bolism suspected



Head CT if abnorm al neurologic exam ination or transient ischem ic attack suspected



Echocardiogram if concern for structural defects

P.1085

Differential Diagnosis 

Seizure is m ost com m only m istaken for syncope: o

Key differentiating factor is postictal confusion.

o

Brief tonic m ovem ents and urinary incontinence m ay

Pa ge 4 6 1

be seen with syncope. 

Metabolic disorders (e.g., hypoxem ia, hyperventilation, hypoglycem ia)



Toxicologic



Stroke



Psychogenic syncope

Treatment Pre Hospital 

Oxygen



Cardiac m onitoring



IV access

Initial Stabilization 

Advanced cardiac life support (ACLS) interventions for unstable patients



Oxygen



Cardiac m onitoring



IV access with norm al saline fluid bolus in suspected hypovolem ia



Consider com a cocktailâ€”dextrose, thiam ine, and naloxone for persistent altered m ental status

ED Treatment 

ACLS interventions for dysrhythm ias



Standard regim ens for acute m yocardial infarction



Control blood pressure for subarachnoid hem orrhage and aortic dissection

Pa ge 4 6 1

Medication (Drugs) 

Dextrose: D 5 0 W 1 am p (50 m L or 25 g) IV (peds: D 2 5 W 2â€“4 m L/kg IV)



Naloxone: 2 m g IV or IM (peds: 0.1 m g/kg)



Thiam ine: 100 m g IV or IM (peds: 50 m g)

Follow-Up Disposition Admission Criteria 

San Francisco Syncope Rule identifies patients at high risk for serious short-term outcom es (â€œCHESSâ€•)



o

History of CHF

o

Hem atocrit <30%

o

Abnorm al ECG

o

Patient com plaint of shortness of breath

o

Systolic BP <90

Other recom m endations: o

Suspected cardiac syncope m ust be adm itted to m onitored bed

o

GI bleeds consider intensive care unit bed

o

Adm it elderly patients with syncope.

Discharge Criteria 

Neurally m ediated syncope or orthostatic syncope from volum e depletion m ay be evaluated on outpatient basis with close follow-up, if patient is reliable and has a good social structure.



Driving restrictions until cleared

References

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1. Brignole M, et al. Task force report: Guidelines on m anagem ent (diagnosis and treatm ent) of syncope. Eur Heart J. 2001,22(15):1256â€“1306. 2. Brignole M, et al. ESC Guidelines on m anagem ent (diagnosis and treatm ent) of syncopeâ€”Update 2004. Eur Heart J. 2004;25(22):2054â€“2072. 3. Hayes OW. Evaluation of syncope in the em ergency departm ent. Em erg Med Clin North Am . 1998;16(3):601â€“615. 4. Massin M, et al. Syncope in pediatric patients presenting to an em ergency departm ent. The J of Ped. 2004;145(2):223â€“228. 5. Meyer MD. Evaluation of the patient with syncope: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):189â€“201. 6. Quinn J, et al. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcom es. Ann Em erg Med. 2004;43(2):224â€“232. 7. Quinn J, et al. Death rates of Em ergency Departm ent patients with syncope: can the San Francisco Syncope Rule predict long-term m ortality? Acad Em erg Med. 2005;12(5), abstract 004.

Codes ICD9-CM 780.2

ICD10 R55

Pa ge 4 6 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Syndro m e o f Inappro priate Antidiuretic Ho rm o ne Secretio n (SIADH)

Syndrome of Inappropriate

Antidiuretic Hormone Secretion (SIADH) Arunachalam Einstein

Basics Description 

Norm al regulation of water balance: o

Antidiuretic horm one (ADH): 

Integral part of the hom eostatic m echanism that controls water balance



Increases water perm eability of the kidney collecting tubules resulting in water reabsorption



Released when hypothalam ic osm oreceptors, left atrial stretch receptors, and carotid baroreceptors detect water deprivation



Hyponatrem ia: o

Serum sodium <135 m Eq/L

o

Excess extracellular water relative to sodium

o

Depletional hyponatrem ia: 

Sodium depletion can be caused by diet,

Pa ge 4 6 2

gastrointestinal losses, diuretic use, renal or adrenal disease. 

Often accom panied by extracellular fluid volum e depletion



Hyponatrem ia associated with clinical signs of dehydration



Increased hem atocrit, blood urea nitrogen (BUN), creatinine

 o

Urinary sodium excretion <20 m Eq/L

Dilutional hyponatrem ia: 

Increased extracellular water in presence of norm al or increased total body sodium



Can be caused by increased fluid intake (oral, IV), drugs that cause water retention, and m edical conditions causing water retention



Euvolem ia or edem a



Norm al or decreased hem atocrit, BUN, creatinine



Urinary sodium excretion >20 m Eq/L



Inappropriate ADH secretion is a form of dilutional hyponatrem ia.



Definition of SIADH: o

ADH secretion in absence of hyperosm olality or hypovolem ia

o

Criteria for definition: 

Hyponatrem ia



Hyposm olality of the plasm a



Continued renal excretion of sodium in absence of diuretics



No clinical evidence of volum e depletion



Urine osm olality greater than appropriate with respect to plasm a osm olality

Pa ge 4 6 2

 o

Norm al renal, adrenal, and thyroid function

Inappropriate ADH secretion can originate from the hypothalam us or extrahypothalam ic tissue.

Etiology 









ADH-producing tum ors: o

Sm all-cell lung cancer

o

Pancreatic cancer

o

Prostate cancer

o

Pituitary tum or

o

Thym om a

o

Lym phom a

Pulm onary disease: o

Pneum onia

o

Tuberculosis

o

Lung abscess

o

Chronic obstructive pulm onary disease

CNS disorders: o

Meningitis

o

Encephalitis

o

Cerebrovascular accident

o

Head traum a

Com m on drugs: o

Chlorpropam ide

o

Vincristine

o

Carbam azepine

o

Tricyclic antidepressants

o

Fluoxetine

o

Narcotics

o

Anticonvulsants

Other: o

Positive pressure ventilation

o

AIDS

Pa ge 4 6 2

o

Idiopathic

Diagnosis Signs and Symptoms 



Serum sodium <130 m Eq/L: o

Weakness

o

Lethargy

o

Weight gain

o

Headache

o

Anorexia

Sodium serum <120 m Eq/L: o

Mental status change

o

Seizure

o

Com a



Chronic hyponatrem ia: 50% asym ptom atic



High m ortality when hyponatrem ia develops acutely

Essential Workup 

Exclude depletional hyponatrem ia.



Exclude other causes of dilutional hyponatrem ia.



Electrolytes, BUN, creatinine, glucose: o

Hyponatrem ia (serum sodium <135 m m ol/L)

o

Serum hyposm olality (serum osm olality <280 m Osm /kg)





Urine osm olality: o

Inability to excrete a dilute urine

o

Urine osm olality >100 m Osm /kg

Urine sodium : o

Continued urinary excretion of sodium

o

Urinary sodium >20 m Eq/L

Pa ge 4 6 2



Exclude other causes of hyponatrem ia.

Tests Lab 

Serum protein



Lipid levels



Serum osm olality



Liver and thyroid function test



Morning cortisol level

Imaging Chest radiograph and CT head to screen for pathology causing SIADH

Differential Diagnosis Causes of Hyponatremia 





Increased extracellular fluid (dilutional hyponatrem ia): o

Renal failure

o

Cardiac failure

o

Liver cirrhosis

Norm al extracellular fluid (dilutional hyponatrem ia): o

SIADH

o

Physical and em otional stress

o

Myxedem a

o

Sheehan syndrom e

o

Reset osm ostat syndrom es

Decreased extracellular fluid (depletional hyponatrem ia): o

Excessive sweating

o

Vom iting

o

Diarrhea

o

Third-space sequestration

o

Diuretics

o

Aldosterone deficiency: 

Addison disease

Pa ge 4 6 2

o

Salt-losing nephropathies: 



Renal tubular acidosis

Pseudohyponatrem ia: o

Hyperproteinem ia

o

Hyperlipidem ia

o

Hyperglycem ia

P.1087

Treatment Initial Stabilization 

Severe sym ptom atic hyponatrem ia with CNS m anifestations



Endotracheal intubation for patients in need of airway protection:



o

IV access

o

Naloxone, thiam ine, dextrose (or Accu-Chek)

o

Treat seizures with benzodiazepines.

Proceed to hyponatrem ia treatm ent.

ED Treatment 

Initial treatm ent of hyponatrem ia caused by SIADH is the sam e for all causes of euvolem ic/hypervolem ic hyponatrem ia.



Mildly sym ptom atic hyponatrem ia, chronic hyponatrem ia with m inim al sym ptom s, asym ptom atic hyponatrem ia: o

Serum sodium usually >125 m Eq/L

o

Fluid restriction 800 to 1000 m L/d alone or in conjunction with:

Pa ge 4 6 2

o



0.9% NS infusion



IV furosem ide

Correct serum sodium by no m ore than 0.5 m Eq/L/h: 

Too rapid correction of serum sodium levels can induce central pontine m yelinolysis, associated with developm ent of bulbar palsy, quadriplegia com a, and death.



Severe hyponatrem ia: o

Sym ptom atic patient, serum sodium <125 m Eq/L

o

Increase serum sodium by no m ore than 12 m Eq/L in first 24 hours at rate of 0.5â€“1 m Eq/L/h.

o

Target level 125 m Eq/L

o

Treat patients with significant neurologic sym ptom s with 3% saline solution.

o 

Serum sodium laboratory testing every 1â€“2 hours

Acute life-threatening hyponatrem ia: o

Serum sodium usually <120 m Eq/L

o

Associated with seizures or com a

o

Clinical goal: Stop seizure and im prove neurologic status.

o

Therapeutic goal: sam e as for severe hyponatrem ia

o

Adm inister 3% saline solution for significant neurologic sym ptom s.

o

IV furosem ide to prom ote a prom pt diuresis and induce a negative fluid balance

o

Once serum sodium 125 m Eq/L, further IV fluid should be in form of 0.9% saline solution.

o

Restoration of serum sodium to norm al levels should take place over >48 hours.



Most effective treatm ent of SIADH is successful eradication of the underlying cause.



Drugs that inhibit the secretion or the renal effect of ADH

Pa ge 4 6 2



Indicated when SIADH not self-lim ited and cause cannot be rem oved



Dem eclocycline (blocks renal effect of ADH)

Medication (Drugs) 

Dem eclocycline: 300 m g PO b.i.d.



Hypertonic saline solution (3% NaCl): 250â€“500 m L: o

25â€“100 m L/h

o

Lim it rate in rise of serum sodium to 0.5â€“1.0 m Eq/L/h.

o

Discontinue when a resolution in hyponatrem ic seizure is obtained, or serum sodium 125 m Eq/L reached.

o

Rise in serum sodium by 4â€“6 m Eq/L usually sufficient to stop seizures



Isotonic saline solution (0.9% NS): standard m aintenance rates



Lasix: 1 m g/kg up to 20â€“40 m g IV push

Follow-Up Disposition Admission Criteria 

Severe life-threatening hyponatrem ia



Sym ptom atic hyponatrem ia



Serum sodium <125 m Eq/L regardless of sym ptom s



New-onset SIADH in which underlying cause m ust be diagnosed and treated



Com plications secondary to the underlying cause of SIADH

Pa ge 4 6 2



Patient's com pliance an issue

Discharge Criteria Asym ptom atic chronic hyponatrem ia: 

Serum sodium >125 m Eq/L



No unstable com orbid factors



Known diagnosis of SIADH

References 1. Adrogue HJ, Madias NE. Prim ary care: Hyponatrem ia. New Eng J Med. May 25, 2000;342:1581â€“1589. 2. Fried LF, Palevsky PM. Hyponatrem ia and hypernatrem ia. Med Clin North Am . 1997;81(3):585â€“609. 3. Miller M. Syndrom e of excess antidiuretic horm one release. Crit Care Clin. 2001;17(1):1123. 4. Sorensen JB, Anderson MK, Hansen HH. Syndrom e of inappropriate secretion of antidiuretic horm one (SIADH) in m alignant disease. J Intern Med. 1995;238(2):97â€“110. 5. Spigset O, Hedenm alm K. Hyponatrem ia and the syndrom e of inappropriate antidiuretic horm one secretion (SIADH) induced by psychotropic drugs. Drug Saf. 1995;12(3):209â€“225.

Miscellaneous SEE ALSO: Hyponatrem ia

Codes ICD9-CM 253.6

ICD10 E22.2

Pa ge 4 6 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Syno vitis, To xic

Synovitis, Toxic

James E. Colletti Dick Kuo

Basics Description 

Acute inflam m ation of the hip joint in children associated with joint effusion



Disease process is self-lim iting.



Num ber-one cause of hip pain in children younger than 10 years of age



Also referred to as transient synovitis and irritable hip syndrom e.



Age group m ost affected is 3â€“6 years.



2:1 m ale predom inance



Right hip is affected m ore than the left.

Etiology 

Cause of toxic synovitis (TTS) is unknown.



Infectious etiology is suspected because there is a preceding upper respiratory illness in a large num ber of cases.

Pa ge 4 6 3

Diagnosis Signs and Symptoms History 

Unilateral hip pain, acute onset



Painful lim p



Pain in anterom edial thigh and knee



Refusal or inability to bear weight



Recent or current upper respiratory infection

Physical Exam 

Low-grade fever



Nontoxic appearing



Lim itation of hip m edial rotation and abduction



Preferred external rotation, abduction, and flexion



Pain over anterior portion of hip with palpation

Tests Lab 

CBC, erythrocyte sedim entation rate (ESR), C-reactive protein (CRP): o



Norm al or elevated

One investigation concluded that if two out of following four criteria are present, there is a 95% sensitivity and 91% specificity for septic arthritis (SA):



o

Severe pain and spasm

o

Tem perature >38Â°C

o

ESR >20 or CRP >1

o

Tenderness on palpation

An investigation by Kocher et al. utilized the following clinical data to differentiate TTS from SA: o

History of fever

o

Non-weight bearing

Pa ge 4 6 3



o

ESR â‰¥40 m m /hr

o

WBC >12,000 cell/m m 3

An elevated CBC or ESR alone does not differentiate TTS from SA or osteom yelitis: o

If both CBC and ESR/CRP are norm al, m ore serious causes of hip pain are less likely.

Imaging 



Plain hip film s (anteroposterior and frog-leg view): o

Usually norm al

o

May detect an effusion or other causes of hip pain

MRI (rarely indicated): o

Very useful in diagnosing Legg-CalvÃ©-Perthes (LCP) disease

o

Can detect abnorm alities in TTS

o

An investigation by Lee suggested that signal intensity alteration in the bone m arrow of the affected hip m ight differentiate TTS from SA.



Bone scan: o

Used to differentiate LCP disease from TTS

o

Can detect osteom yelitis

o

The increased radiation is usually reserved for recurrent cases or cases in which the diagnosis is still in question.

o

Negative bone scan decreases the likelihood of infection, fracture, or tum or.



Ultrasound to rule out joint effusion if high suspicion for septic arthritis



If a joint effusion is present, an ultrasound-guided joint aspiration should be perform ed to rule out septic arthritis.

Diagnostic Procedures/Surgery Joint aspiration:

Pa ge 4 6 3



Not necessary if the patient is afebrile with a norm al CBC and ESR/CRP



Abnorm al joint fluid analysis indicates SA (see Arthritis, Septic)

Differential Diagnosis 

SA



Osteom yelitis



Soft-tissue infection



LCP disease



Slipped capitol fem oral epiphysis



Juvenile rheum atoid arthritis



Rheum atic fever



Chondrolysis



Gaucher disease



Osteosarcom a



Ewing sarcom a



Osteoid osteom a



Leukem ia



Tuberculosis of the hip



Fracture



Lym e disease



Psoas abscess



Sickle cell crisis

P.1089

Pediatric Considerations 

Second event m ay occur in 4â€“17% within 6 m onths of initial event



Association of TTS with LCP disease



2â€“10% of patients with TTS later develop LCP disease:

Pa ge 4 6 3

o

Suggested that TTS m ay represent an early stage of LCP disease.

Treatment ED Treatment 

Conservative treatm ent



Bed rest in position of com fortâ€”flexion and external rotation



Initiate NSAIDs.



Antibiotics and steroids are not indicated.



Som e authors recom m end no weight-bearing for 7â€“10 days following im provem ent and return of norm al hip function, citing increased risk for recurrence.



Close follow-up essential with repeat radiographs due to association with LCP

Medication (Drugs) 

Ibuprofen: 200â€“600 m g (peds >6 m onths old: 5â€“10 m g/kg/dose) PO q6h



An investigation by Fink dem onstrated that ibuprofen decreased sym ptom s duration.

Disposition Admission Criteria Patients with severe joint pain or a large effusion m ay require hospitalization for bed rest and analgesics.

Discharge Criteria All patients who have been excluded for m ore serious diagnosis of hip

Pa ge 4 6 3

pain and diagnosed with toxic synovitis can be discharged from the hospital with good follow-up.

References 1. Della-Giustina K, Della-Giustina D. Em ergency departm ent evaluation and treatm ent of pediatric orthopedic injuries. Em erg Med Clin North Am . 1999;17(4):895â€“922. 2. Do T. Transient synovitis as a cause of painful lim ps in children. Curr Opin Pediatr. 2000;12:48â€“51. 3. Eich G, et al. The painful hip: evaluation of criteria for clinical decision-m aking. Eur J Pediatr. 1999;158:923â€“928. 4. Hoffer FA, Zawin JK, Rand FF, et al. Joint effusion in children with an irritable hip: US diagnosis and aspiration. Radiology. 1993;187:459â€“463. 5. Kerm ond S, Fink M, Graham K, Carlin JB, Barnett P. A random ized clinical trial: should the child with transient synovitis of the hip be treated with nonsteroidal anti-inflam m atory drugs? Ann Em erg Med. Septem ber 2002;40(3):294â€“299. 6. Kocher MS, Mandiga R, Zurakowski D, Barnewolt C, Dasser JR. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg. 2004;86:1629â€“1635. 7. Koop S, Quanbeck D. Three com m on causes of childhood hip pain. Pediatr Clin North Am . 1996;43:1053â€“1066. 8. Lee S, et al. Septic arthritis versus transient synovitis at MR im aging: prelim inary assessm ent with signal intensity alterations in bone m arrow. Radiology. 1999;211:459â€“465. 9. Spock A. Transient synovitis of the hip joint in children. Pediatrics. 1959;24:1042. 10. Tachidjian MS. Acute transient synovitis of the hip. In: Tachidjian MS, ed. Pediatric orthopedics. Philadelphia, PA: WB Saunders, 1990:1461â€“1465.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Syphilis

Syphilis

JiWon E. Lee

Basics Description 

Sexually transm itted disease



One hundred thousand new cases per year in United States



Acquired via m ucous m em branes/disrupted skin



Spirochetes m ultiply at site of inoculation and spread via lym phatics and bloodstream : o

Prim ary syphilis: 

o

Secondary syphilis: 

o

Focal enarteritis, prim ary pathologic lesion

Replication and hem atogenous spread

Secondary/tertiary syphilis: 

Granulom atous reaction



Infectious during prim ary and secondary stages



Cofactor transm ission of HIV

Etiology Treponem a pallidum : 

Spirochete bacteria

Pa ge 4 6 3

Diagnosis Signs and Symptoms Primary (Early) Syphilis 

Two- to three-week incubation period



Chancre: o

Painless papule at site of inoculation

o

Clean-based, circular, sharply defined borders:

o 



Solitary lesions



Com m only on penis, vulva, and rectum



Bilateral regional lym phadenopathy

Heal spontaneously in 3â€“6 weeks

Rectal chancre: o

Painful or painless

o

Rectal irritation/discharge

o

Painless enlargem ent of lym ph nodes

Secondary (Early) Syphilis 

Twenty-five percent with untreated infection



Weeks to m onths after initial infection



Rash (m ost com m on):



o

Sym m etric, diffuse, m aculopapular rash

o

Starts on trunk and flexor extrem ities

o

Classic involvem ent of palm s and soles: 

Discrete, red/reddish-brown



0.5â€“2 cm in diam eter

Condylom a lata: o

Large, raised, gray/white lesions

o

Warm , m oist areas: 

Mucus m em branes in m outh and perineum



Intertriginous areas



Flat rectal warts

Pa ge 4 6 3





System ic sym ptom s: o

Fever, headache, m alaise, anorexia, sore

o

throat, m yalgias, and weight loss

Diffuse lym phadenopathy: o

Palpable nodes at inguinal, axillary, posterior cervical, fem oral, and/or epitrochlear regions

o 

Painless, firm , and rubbery

Less com m on: o

â€œMoth-eatenâ€• alopecia

o

Syphilitic m eningitis



Loss of lateral third of eyebrows



Painless m ucosal lesions (m ucous patches)



Heal spontaneously in 1â€“2 m onths

Latent Syphilis 

Period of no sym ptom s but positive serology: o



Cerebrospinal fluid (CSF) is norm al.

Late latent not infectious except for fetal transm ission in pregnant wom en



Persists for lifetim e or develops into tertiary syphilis

Tertiary (Late) Syphilis 

Years after initial infection (up to 20 years): o



Destructive stages of disease

Neurosyphilis (m ost com m on): o

o

Asym ptom atic: 

Positive CSF-VDRL



CSF pleocytosis (10â€“100 lym phocytes)



Elevated CSF protein at 50â€“100 m g/dL

Meningitis: 

Aseptic; CSF with positive VDRL, higher protein, and lower glucose (com pared with above)



Cranial nerve palsy, including isolated eighth

Pa ge 4 6 3

nerve palsy o

General paresis: 

Progressive dem entia



Loss of cortical function



Argyll Robertson pupils (sm all fixed pupils that do not react to strong light, but do react to accom m odative convergence)

o

Tabes dorsalis (neuropathy): 

Degeneration of posterior colum ns/posterior or dorsal roots of spinal cord



Paresthesias, abnorm al gait, and lightning (sudden, severe) pain of extrem ities/trunk



Progressive loss of reflexes, vibratory/position sensation





Positive Rom berg sign



Vision: optic atrophy



Pupils: Argyll Robertson pupils



Urinary incontinence

Gum m as: o

Late benign syphilis of cutaneous skin/viscera: 

o



Bone, brain, abdom inal viscera, and so on

Granulom atous, cellular hypersensitivity Reaction: 

Round, irregular, or serpiginous shape



â€œGreat poxâ€•

Cardiovascular: o

Thoracic aneurysm (ascending m ost com m on): 

Dilated aorta and aortic valve regurgitation

o

Aortic insufficiency

o

Coronary throm bosis



Destructive lesions of skeletal structures or skin



HIV infected: o

Strong association with syphilis

Pa ge 4 6 4

o

Increased incidence of neurosyphilis

Congenital Syphilis In utero infection: 

Age <2 years: o

Hepatosplenom egaly, rash, condylom a lata, snuffles, jaundice (nonviral hepatitis), and so on



Older children (syphilis stigm ata): o

Interstitial keratitis, nerve deafness, anterior bowing of shins, frontal bossing, m ulberry m olars, Hutchinson teeth, saddle nose, and so on

Essential Workup Rapid plasm a reagin (RPR)

Tests Lab 

Serology: o

Nontreponem al test: 

Rapid plasm a reagin (RPR)



Venereal Disease Research Laboratories (VDRL)



Positive 2 to 4 weeks after chancre appears



Early false-negatives, especially â‰¤7 days after prim ary chancre



Repeat negative test in 2 weeks and correlate with disease activity. P.1091



Two percent false-positive rate



Fourfold change in titer clinically significant



One hundred percent sensitivity in secondary syphilis

Pa ge 4 6 4

 o

Nonreactive after successful treatm ent

Treponem al antibody test: 

Fluorescent treponem al antibody absorption (FTA-ABS)



Hem agglutination assay for antibody to T. pallidum (MHA-TP)





More sensitive and specific



One percent false-positive rate



Confirm atory test



Reacive for lifetim e



More costly and harder to perform

Dark-field m icroscopy: o

Identifies treponem es from prim ary and secondary lesions: 

Suspicious early lesions with negative serology (early prim ary syphilis)





False-negatives with ointm ents, cream s



Oral specifm en unsuitable

CSF analysis: o

Tertiary syphilis: 

Positive VDRL



Greater than five lym phocytes per m illiliter



Protein >45 m g/dL

Differential Diagnosis 

Genital ulcer: o

Chancroid (painful)

o

Genital herpes: 

Vesicular, m ultiple lesions

o

Lym phogranulom a venereum

o

Granulom a inguinale

o

Superficial fungal infection

o

Carcinom a

Pa ge 4 6 4



Secondary syphilis: o

Pityriasis rosea

o

Drug-induced rash

o

Acute febrile exanthem s

o

Psoriasis

o

Lichen planus

o

Scbies

o

Infectious m ononucleosis

Treatment Initial Stabilization Lower blood pressure and establish IV access for aortic dissection.

ED Treatment 

Treatm ent other than penicillin with increased relapse rate: o



Desensitize those allergic to penicillin.

Pregnancy: o

Teat with penicillin even in latent syphilis.

o

If patient allergic to penicillin, adm it for desensitization.



Jarisch-Herxheim er reaction: o

Transient febrile reaction to therapy

o

May be owing to antigen liberation from spirochetes or com plem ent cascade activation

o

Peaks at 8 hours, resolves in 24 hours

o

Sym ptom s: 

Fever, headache, m alaise, worsening rash

o

Treat with antipyretics.

o

No serious sequelae

Pa ge 4 6 4



Recom m ended testing: o

Sexual partners

o

Concom itant sexually transm itted diseases Including HIV

o

Repeat serology test in 6 and 12 m onths.

Medication (Drugs) 



Early prim ary, secondary, latent (<1 year): o

Benzathine penicillin G: 2.4 m illion U IM

o

Doxycycline: 100 m g PO b.i.d. for 14 days

o

Tetracycline: 500 m g PO q.i.d. for 14 days

Latent (>1 year) except neurosyphilis: o

Benzathine penicillin G: 2.4 m illion U IM weekly for 3 weeks



o

Doxycycline: 100 m g PO b.i.d. for 4 weeks

o

Tetracycline: 500 m g PO q.i.d. for 4 weeks

Neurosyphilis: o

Penicillin G: 3â€“4 m illion U IV q4h for 10â€“14 days

o

Procaine penicillin: 2.4 m illion U IM daily plus Probenecid: 500 m g PO q.i.d. for 10â€“14 days



Congenital syphilis: o

Penicillin G: 50,000 Âµg/kg IM q8hâ€“q12h for 10â€“14 days or

o

Procaine penicillin: 50,000 Âµg/kg IM daily for 10â€“14 days

Follow-Up Disposition

Pa ge 4 6 4

Admission Criteria 

Neurosyphilis requiring IV antibiotics



Pregnant wom en allergic to penicillin requiring desensitization

Discharge Criteria Follow-up care: 

Measure for falling titers in 6 m onths and 1 year after treatm ent.



Tertiary/latent (>1 year): o

Measure for falling titers in 3, 6, 12, and 24 m onths after treatm ent.

References 1. Hook EW. Syphilis control: a continuing challenge. N Eng J Med. 2004;351:122. 2. McKinzie J. Sexually transm itted disease. Em erg Med Clin North Am . 2001;19:723â€“743. 3. Centers for Disease Control and Prevention (CDC). Prim ary and secondary syphilis in United States, 2002. MMWR Morb Mortal Wkly Rep. 2003;52:1117. 4. Schacter J. Classification of latent syphilis. Sex Transm Dis. 2005;32:143. 5. Tim m erm ans M. Neurosyphilis in the m odern era. J Neurol Neurosurg Psychiatry. 2004;75:1727.

Codes ICD9-CM 97.0 (090â€“099)

ICD10 A53.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > System ic Lupus Erythem ato sus

Systemic

Lupus Erythematosus Steven Furer

Basics Description 

Lupus is a chronic autoim m une disease with a peak onset between the ages of 15 and 40 years characterized by flares and rem issions.



It is a m ultisystem disease with diverse clinical m anifestations: o

Arthritis

o

Cardiac:

o

o



Endocarditis



Myocarditis



Congestive heart failure



Conduction abnorm alities



Atherosclerosis



Myocardial infarction

Renal: 

Glom erulonephritis



Renal failure

Pulm onary:

Pa ge 4 6 4

o



Pleural effusion (usually exudative)



Pneum onitis



Pulm onary hem orrhage



Pulm onary em bolism



Pneum onia



Pleuritis



Pulm onary edem a



Pulm onary hypertension

Neurologic: 

o

o

Lupus cerebritis

Vascular: 

Vasculitis



Throm bosis



Atherosclerosis

Gastrointestinal (GI): 

Peritonitis



Mesenteric vasculitis and ischem ia



Pancreatitis

Pediatric Considerations 

Neonatal lupus m ay occur when m aternal autoantibodies cross the placenta.



Congenital heart block is the m ost serious com plication.

Geriatric Considerations 

Ten tim es greater risk of m yocardial infarction due to atherosclerosis



High incidence of osteoporosis related to chronic steroid use

Genetics 

More com m on in fem ales than m ales (ratio, 9:1)



More com m on in African Am ericans



Higher frequency of system atic lupus erythem atosus and

Pa ge 4 6 4

other autoim m une diseases am ong first-degree relatives

Etiology 

Autoantibody production against cell nucleus and cytoplasm ic structures leading to inflam m atory changes, vasculitis, and im m une com plex deposition in m ultiple organ system s



A significant percentage of patients have an associated antiphospholipid syndrom e: o

Characterized by antibodies against cellular phospholipid com ponents

o 



Tendency toward recurrent vascular throm bosis

Lupus is a chronic disease with exacerbating factors: o

Infection

o

Sun exposure

o

Traum a

o

Medications

o

Stress

o

Diet

Drug-induced lupus is a m ilder disease that eventually resolves once the m edication is discontinued: o

Chlorprom azine

o

Methyldopa

o

Procainam ide

o

Hydralazine

o

Isoniazid

o

Quinidine

Diagnosis 

Four of the 11 criteria from the following list are needed to m ake the diagnosis:

Pa ge 4 6 4

o

Malar rash

o

Discoid rash

o

Photosensitivity rash

o

Oral ulcers

o

Arthritis

o

Serositis

o

Neurologic disorders

o

Hem atologic disorders

o

Im m unologic disorders

o

Renal disorders

o

Antinuclear antibodies

Signs and Symptoms 





System ic: o

Fatigue

o

Fever

o

Weight loss

o

Dyspnea

Skin: o

Malar rash (butterfly facial)

o

Discoid rash (raised red patches)

o

Photosensitivity rash (subacute cutaneous lupus)

Musculoskeletal: o

Myalgias

o

Joint pain

o

Arthritis: 

Defined as two or m ore peripheral joints with warm th, tenderness, or effusion

 

Polyarthritis, sym m etric, or m igratory

Heart: o

Chest pain

o

Pericardial rub

o

Murm ur

Pa ge 4 6 4









Vascular: o

Vasculitis

o

Throm bosis

o

Atherosclerosis

o

Peripheral vascular disease

Lungs: o

Dyspnea

o

Tachypnea

o

Pleural rub

o

Rales

Nervous system : o

Psychosis

o

Depression

o

Headache

o

Seizures

o

Peripheral neuropathies

o

Stroke

o

Cranial nerve deficits

GI: o

Painless oral ulcers

o

Abdom inal pain

o

Guarding or rebound tenderness

o

Positive stool guaiac suggests m esenteric ischem ia

Essential Workup 

Thorough history and physical exam needed to distinguish between m ajor and m inor flare-ups



Major flare-ups: o

CBC

o

Electrolytes, blood urea nitrogen, creatinine, glucose

o

Urinalysis

o

Erythrocyte sedim entation rate (ESR)

o

Chest radiograph, ECG, and pulse oxim etry for

Pa ge 4 6 5

cardiorespiratory sym ptom s P.1093

Tests Lab 

CBC: o

Leukopenia, throm bocytopenia

o

Degree of hem atologic disorders suggests degree of disease activity.



ESR: o

May be elevated during acute exacerbations, but this test tends to rem ain high m onths after a flare-up has ceased.



Partial throm boplastin tim e: o





May be elevated in patients with lupus anticoagulant

Urinalysis: o

Protein

o

Casts

o

Hem aturia

o

WBCs

Am ylase is elevated in m esenteric ischem ia and pancreatitis.



Send antinuclear antibody, rheum atoid factor (RF), anti-streptolysin O (ASO) titer if diagnosis unclear.



Anti-Sm and anti-dsDNA are diagnostic.



A false-positive venereal disease research laboratory (VDRL) is supportive of the diagnosis.



Joint aspirate typically shows fluid with fewer than 3,000 WBCs.

Imaging

Pa ge 4 6 5



Chest radiograph: o

Pneum onitis

o

Pneum onias

o

Pleural effusion

o

Cardiom egaly



ECG



Echocardiogram

Differential Diagnosis 

Hypotension m ay be due to shock secondary to a m ajor flare-up or secondary to acute steroid withdrawal in the known lupus patient.





Other autoim m une diseases: o

Rheum atic fever

o

Rheum atoid arthritis

o

Derm atom yositis

o

Overlap syndrom es

Skin changes: o

Urticaria

o

Erythem a m ultiform e



Idiopathic throm bocytopenic purpura



Multiple sclerosis



Epilepsy

Treatment Initial Stabilization ABCs

ED Treatment 

Mainstays include nonsteroidal anti-inflam m atory drugs (NSAIDs), antim alarials, corticosteroids, and

Pa ge 4 6 5

im m unosuppressive drugs. 

Special attention m ust be given to CNS and renal involvem ent as well as infections; these are the m ain determ inants of m orbidity: o

Atherosclerosis is a leading cause of death in the older lupus patients.



Mild flare-upsâ€”arthralgias, m yalgias, and fatigue, rash: o

NSAIDs, acetyle salicylic acid (ASA), topical steroids for rash, sunscreen

o 

If not sufficient, begin low-dose prednisone.

Major flare-upsâ€”life- or organ-threatening: o

Methylprednisolone

o

Anticoagulation for throm bosis; give blood products early if needed.

o

Psychotropics for neuropsychiatric sym ptom s

o

Anticonvulsants for seizures

o

If poor response, consult rheum atology before starting cytotoxic m edications such as azathioprine or cyclophospham ide.



Chronically: o

Prednisone taper

o

NSAIDs

o

Rheum atologist initiated:

o



Antim alarials; quinacrine, chloroquine



Cyclophospham ide



Azathioprine



Methotrexate

Horm onal therapy, thalidom ide, and m onoclonal antibodies are under investigation.

Medication (Drugs)

Pa ge 4 6 5



Methylprednisolone: 15 m g/kg/d IV up to 1 g; consult rheum atologist for peds dosing



Prednisone 5â€“30 m g (peds: <0.5 m g/kg) PO daily for m inor flare



Prednisone 1â€“2 m g/kg/d PO m ajor flare in adults



Ibuprofen 800 m g (peds: 5â€“10 m g/kg) PO t.i.d.

Follow-Up Disposition Admission Criteria 

Patients who have end-organ disease such as renal or CNS involvem ent, pericarditis, pancreatitis, or GI sym ptom s



Those with severe end-organ or life-threatening m anifestations should be adm itted to the intensive care unit.



Patients with lupus should be treated as im m unocom prom ised and suspected or diagnosed infections should be treated aggressively.

Discharge Criteria 

Patients m ay be discharged hom e with m ild flare-ups if afebrile, well hydrated, and not ill-appearing



Erythrocyte sedim entation rate (ESR) should not be used as disposition criteria, as it m ay be elevated long after a flare-up has subsided.

Issues for Referral 

Lupus is a chronic disease and patients m ust be followed adequately by a rheum atologist or a capable prim ary care physician.

Pa ge 4 6 5

References 1. Boum pas DT, Austin HA 3rd. System ic lupus erythem atosus: em erging concepts. Part 1: Renal, neuropsychiatric, cardiovascular, pulm onary, and hem atologic disease. Ann Intern Med. 1995;122(12):940â€“950. 2. Boum pas DT, Fessler BJ. System ic lupus erythem atosus: em erging concepts. Part 2. Derm atologic and joint disease, the antiphospholipid antibody syndrom e, pregnancy and horm onal therapy, m orbidity and m ortality, and pathogenesis. Ann Intern Med. 1995;123(1):42â€“53. 3. Buyon JP. System ic lupus erythem atosus. B. Clinical and laboratory features. In: Klippel JH, ed. Prim er on the rheum atic diseases. 12th ed. Atlanta, GA: Arthritis Foundation, 2001:335â€“346 4. Hahn BH. Managem ent of system ic lupus erythem atosus. In: Kelley WN, et al., eds. Textbook of rheum atology. 5th ed. Philadelphia, PA: WB Saunders, 1997:1040â€“1056. 5. Lahita RG. Clinical presentation of system ic lupus erythem atosus. In: Kelley WN, et al., eds. Textbook of rheum atology, 5th ed. Philadelphia, PA: WB Saunders, 1997:1028â€“1039. 6. Ruiz-Irastorza G, Kham ashta MA. System ic lupus erythem atosus. Lancet. 2001;357:1027â€“1032.

Codes ICD9-CM 710.0

ICD10 M32.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tachydysrhythm ias

Tachydysrhythmias James Adams Jason Liebzeit

Basics Description 

Any disturbance of the heart's rhythm resulting in a rate greater than 100 beats/m in; caused by disorders of im pulse form ation or conduction



Re-entry is the m ost com m on underlying m echanism for tachydysrhythm ia: o

Ventricular dysrhythm ias result from a re-entrant circuit established as a result of drugs, ischem ia, m etabolic abnorm alities, or scarred or infiltrated m yocardial tissue.

o

Supraventricular dysrhythm ias usually result from reentrant pathways or AV nodal re-entry.



Sinus tachycardia: o

Narrow com plex regular rhythm at a rate of 100â€“150 beats/m in 

Infants and young children can obtain rates of 170â€“225 beats/m in.

o

Functional response to physiologic stress

Pa ge 4 6 5

o

Caused by increased catecholam ine tone or decreased vagal stim ulation



Supraventricular tachycardia (SVT): o

A narrow com plex tachycardia that originates above the His bundle 

One of the m ost frequent cardiac disturbances evaluated in the ED



Most com m on dysrhythm ia seen in young adults and children without underlying heart disease





Irregular SVT: o

Atrial fibrillation (AF)

o

Atrial flutter

o

Multifocal atrial tachycardia

Regular SVT: o

Atrial tachycardia 

Any rapid dysrhythm ia from a nonsinus focus above the AV node

o

Junctional tachycardia: 

Regular tachycardia without preceding depolarization waves



Ventricular tachycardia (VT): o

Three or m ore consecutive ventricular ectopic beats at a rate of 100 beats/m in.

o

Most com m on initiating rhythm in sudden death in patients with previous m yocardial infarction

o

Always suspect a ventricular rhythm with a wide com plex rhythm , especially in the older patient.

o

Sustained VT that persists for 30 seconds or m ore and polym orphic VT require term ination because they are usually unstable and degenerate into ventricular fibrillation (VF).

o

Need to distinguish between m onom orphic VT and

Pa ge 4 6 5

SVT with aberrant conduction 

Torsades de pointes: o

Paroxysm al form of VT with undulating axis and prolonged baseline QT interval

o

Secondary to either congenital or acquired abnorm alities of ventricular repolarization

o

Often the result of drug therapy or electrolyte disturbances



VF: o

Oscillations without evidence of discrete QRST m orphology

o

Accounts for 80â€“85% of sudden cardiac deaths 

Frequently results from degeneration of sustained VT

Alert Wide com plex tachycardias can be supraventricular in origin.

Genetics Rare cases of autosom al dom inant atrial tachycardias without structural heart disorders

Etiology 

Sinus tachycardia: o

Acute m yocardial infarction

o

Anem ia

o

Anxiety

o

Congestive heart failure (CHF)

o

Drug intoxication

o

Hyperthyroidism

o

Hypovolem ia

o

Hypoxia

o

Infection

o

Pain

Pa ge 4 6 5



o

Pericardial tam ponade

o

Pulm onary em bolus

Atrial tachycardia: o

Precipitated by a prem ature atrial or ventricular contraction







o

Electrolyte disturbances

o

Drug toxicity

o

Hypoxia

Junctional tachycardia: o

AV nodal re-entry

o

Myocardial ischem ia

o

Structural heart disease

o

Pre-excitation syndrom es

o

Drug and alcohol toxicity

AF: o

Hypertension

o

Coronary artery disease

o

Hypothyroidism

o

Alcohol intake

o

Mitral valve disease

o

Chronic obstructive pulm onary disease

o

Pulm onary em bolus

o

Wolf-Parkinson-White (WPW) syndrom e

o

Hypoxia

o

Digoxin toxicity

o

Chronic pericarditis

o

Idiopathic atrial fibrillation

Atrial flutter: o

Ischem ic heart disease

o

Valvular heart disease

o

CHF

o

Myocarditis

Pa ge 4 6 5

o

Cardiom yopathies

o

Pulm onary em bolus

o

Electrolyte abnorm alities

o

Recent cardiac surgery

P.1095









Multifocal atrial tachycardia: o

Hypoxic effects of chronic lung disease

o

Theophylline toxicity

VT: o

Dilated cardiom yopathy

o

Cardiac ischem ia

o

Hypoxia

o

Cardiac scarring/fibrosis

o

After cardiac surgery or congenital anom aly repair

o

Digoxin toxicity

o

Long QT syndrom e

o

Electrolyte abnorm alities

Torsades de pointes (polym orphic VT): o

Drug toxicity (antiarrhythm ic class IA and IC agents)

o

Hypokalem ia

o

Hypom agnesem ia

o

Congenital QT prolongation

VF: o

Acute m yocardial infarction (m ost com m on)

o

Chronic ischem ic heart disease

o

Hypoxia

o

Acidosis

o

Anaphylaxis

o

Electrocution

o

Shock

Pa ge 4 6 6

o

Hypokalem ia

o

Initiation of quinidine therapy

o

Massive hem orrhage

Diagnosis Signs and Symptoms 

Asym ptom atic: o

Frequent with SVT

o

Rare with sustained VT



Palpitations



Lightheadedness



Dyspnea



Diaphoresis



Dizziness



Weakness



Chest discom fort



Angina



Syncope: o

Sudden loss of consciousness suggests VF.



Prom inent neck veins



Signs of instability: o

Hypotension

o

Pulm onary edem a

o

Chest pain

o

Mental status changes

History 

Acute onset of palpitations, lightheadedness, generalized weakness, or shortness of breath: o

May be asym ptom atic

Pa ge 4 6 6



Sudden collapse, often preceded for m inutes-hours by chest pain



Prior history of cardiac disease com m on (ischem ia, CHF)

Physical Exam 

Sinus tachycardia: o

Vital signs: 



SVT: o

o

Vital signs: 

Tachycardia



Blood pressure (BP) norm al or hypotensive

Skin: 



Cool, diaphoretic if hypoperfusing

VT: o

Awake or unconscious

o

Vital signs:

o

o



Tachycardia



BP norm al or hypotensive

Cardiac: 

Splitting of heart sounds



Gallop rhythm

Skin: 



Tachycardia

Cool, diaphoretic if hypoperfusing

VF: o

Unconscious

o

Vital signs: 

o

Absent

Skin: 

Cool, m ottled

Essential Workup 

ABCs

Pa ge 4 6 6



Determ ination of unstable versus stable patient



Detailed history: P.1096

o

Current sym ptom s

o

Previous episodes

o

Cardiac history

o

Drug use: 

Illicit, prescribed, over-the-counter such as decongestants



12-lead ECG and rhythm strip to categorize the tachycardia: o

Determ ine whether the rhythm is regular or irregular.

o

Determ ine whether the com plexes are narrow or wide.

o

P waves present or absent

o

AV dissociation, sinus capture beats, fusion beats

Tests Lab Studies are indicated to evaluate underlying m etabolic abnorm alities or ischem ia: 

CBC



Electrolytes



Cardiac enzym es



Thyroid function tests

Imaging ECG: 

SVT:

Pa ge 4 6 6



o

Narrow-com plex, rate usually 130â€“160

o

Uniform ity of polarity and am plitude

o

No P waves visible

AF: o

Irregular, narrow quasi-random signal (QRS) com plexes, rate 110â€“130

o 

Irregular P waves with uniform m orphology

Atrial flutter: o

Regular atrial rate, usually greater than 300

o

Beat-to-beat uniform ity of cycle length, polarity, and am plitude

o

Sawtooth flutter waves directed superiorly and m ost visible in leads II, III, aVF

o

AV block usually 2:1, but occasionally greater or irregular



Multifocal atrial tachycardia: o

Three distinctly different conducted P waves with varying pulse rate intervals



VT: o



QRS is usually 0.12 seconds and often 0.14 seconds.

Torsades de pointes: o

Ventricular rate greater than 200 beats/m in

o

QRS structure displays an undulating axis, with the polarity of the com plexes appearing to shift around the baseline.

o

Occurrence is often in short episodes of less than 90 seconds.



VF: o

ECG shows oscillations without evidence of discrete QRST m orphology.

o

Oscillations are usually irregular and occur at a rate of 150â€“300 beats/m in.

Pa ge 4 6 6

o

When the am plitude of m ost oscillations is 1 m m , the term â€œcoarseâ€• is used.

o

â€œFineâ€• VF is used for oscillations <1 m m

Differential Diagnosis See â€œEtiologyâ€•

Treatment Pre Hospital Cardiopulm onary resuscitation if pulseless

Initial Stabilization 

IV access



Oxygen



Cardiac m onitor



Determ ine rhythm .

ED Treatment 



Irregular narrow com plex (A fib): o

Rate control

o

Beta-blockers or calcium -channel blockers

o

Anticoagulation if onset is greater than 24 hours

o

Cardioversion for severe hem odynam ic com prom ise

Regular narrow com plex tachydysrhythm ia: o

Vagal m aneuvers occasionally term inate the dysrhythm ia: 

o

Beware of carotid disease in elderly.

Adenosine: 

Rapid onset and short half-life



90% effective in term inating SVTs



May be diagnostic (can reveal underlying

Pa ge 4 6 6

AF/atrial flutter) 

Stable wide com plex tachycardia: o

Determ ine whether VT or SVT with aberrancy.

o

Adm inistration of AV nodal-blocking agents (verapam il, adenosine) m ay result in VF: 

With WPW, use am iodarone, flecainide, procainam ide, or DC cardioversion.

o

Electrical cardioversion should be utilized owing to fewer potential com plications than antidysrhythm ic drugs when m echanism unknown.

o

Antidysrhythm ic drugs include procainam ide and am iodarone. 

Lidocaine is less effective although som etim es m ore readily available.





Polym orphic VT with prolonged QT (torsades de pointes): o

Magnesium , overdrive pacing, am iodarone

o

Correct underlying abnorm al electrolytes

Polym orphic VT with norm al QT: o

Ejection fraction (EF) norm al 

Beta-blockers, lidocaine, am iodarone, or procainam ide

o

EF abnorm al: 

Am iodarone or lidocaine; then synchronized cardioversion

o 

Treat ischem ia and correct electrolytes.

Monom orphic VT: o

EF norm al 

Procainam ide, am iodarone, sotalol, lidocaine; then synchronized cardioversion

o

EF abnorm al 

Am iodarone or lidocaine, then synchronized cardioversion

Pa ge 4 6 6



VF or pulseless VT: o

Defibrillation up to 3 tim es (200 J, 200â€“300 J, 360 J)

o

If persistent or recurrent VF/VT then intubate, establish IV, and look for underlying causes.

o

Chest com pressions: 100/m in

o

Epinephrine: 1 m g IV, repeat q3â€“5m in, or vasopressin once, then epi

o

Repeat defibrillation at 360 J

o

Add antidysrhythm ics: am iodarone, lidocaine, m agnesium , or procainam ide; then bicarb. 

Shock at 360 J after drug given.

P.1097

Medication (Drugs) 

Adenosine: 6 m g (peds: 0.1 m g/kg up to 6 m g) rapid IV push; if no response after 1â€“2 m inutes, then 12 m g (peds: 0.2 m g/kg up to 12 m g), m ay repeat 12 m g (0.2 m g/kg)



Am iodarone: o

VT/SVT: 15 m g/m in (peds: 5 m g/kg IV over 20â€“60 m inutes, m ax. 15 m g/kg/day IV) IV over 10 m inutes, followed by 1 m g/m in IV over the next 6 hours and then 0.5 m g/m in over 18 hours

o

VF/pulseless VT: 300 m g (peds: 0.5 m g/kg) IV push; m ay give 150 m g IV push 3â€“5 m inutes after if no response, m ax. 2.2 g in 24 hours



Epinephrine:1 m g (peds: 0.01 m g/kg) IV push q3â€“5m in; 2.5 m g (peds: 0.1 m g/kg) endotracheally q3â€“5m in

Pa ge 4 6 6



Lidocaine: 1â€“1.5 m g/kg [100 m g] (peds: 1 m g/kg) IV push, m ay repeat q5â€“10m in, m ax. dose 3 m g/kg



Magnesium sulfate: 2 m g IV push over 2 m inutes (peds: 25â€“50 m g/kg, m ax. 2 g, IV over 10â€“20 m inutes)



Procainam ide: o

VF/pulseless VT: 30 m g/m in (peds: not recom m ended) IV load until rhythm resolves, hypotension, QRS widens >50% or m ax. 17 m g/kg, then 1â€“4 m g/m in IV

o

Perfusing VT: 20 m g/m in (peds: 15 m g/kg IV over 30â€“60 m inutes) IV load until rhythm resolves, hypotension, QRS widens > 50% or m ax. 17 m g/kg, then 1â€“4 m g/m in IV

o

SVT: 15â€“17 m g/kg IV at 20â€“30 m g/m in OR 100 m g IV q5m in slow IV push until rhythm resolves or m ax. dose 1000 m g (peds: 3â€“6 m g/kg IV over 5 m inutes, m ax. 100 m g/dose, m ay repeat q5â€“10m in as needed to total dose 15 m g/kg)



Vasopressin: 40 units (peds: not recom m ended) IV push once

Follow-Up Disposition Admission Criteria 

VT or VF



Possible cardiac ischem ic event



Persistent SVT



Underlying m etabolic abnorm alities

Discharge Criteria

Pa ge 4 6 6

Term inated supraventricular rhythm without organ hypoperfusion

Issues for Referral Electrophysiologic testing: 

Diagnostic but not required em ergently



Determ ines therapy for accessory pathways

References 1. Am erican Heart Association. ACLS guidelines. 2000. 2. Atkins DL, Dorian P, Gonzalez ER. Treatm ent of tachyarrhythm ias. Ann Em erg Med. 2001;37:S91â€“S109. 3. Connors S, Dorian P. Managem ent of supraventricular tachycardia in the em ergency departm ent. Can J Cardiol. 1997;13(Suppl A):19Aâ€“24A. 4. Dagres N, Gutersohn A, Wieneke H, Sack S, Erbel R. A new hereditary form of ectopic atrial tachycardia with autosom al dom inant inheritance. Int J Cardiol. February 2004;93(2-3):311â€“313. 5. Obel OA, Cam m AJ. Supraventricular tachycardia: ECG diagnosis and anatom y. Eur Heart J. 1997;18(Suppl C):C2â€“C11.

Codes ICD9-CM 427.0â€“427.9 785.0

Pa ge 4 6 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tem po ral Arteritis

Temporal Arteritis

Andrew A. Aronson

Basics Description 

Chronic vasculitis of large- and m edium -size vessels that occurs am ong individuals over 50 years of age



Tem poral arteritis m ost com m only causes inflam m ation of arteries originating from the arch of the aorta.



Other vessels, including veins, are som etim es involved.



Although usually clinically silent, involvem ent of the thoracic aorta occurs in a significant m inority of patients, and aortic aneurysm m ay result.



Thoracic aortic aneurysm is a late m anifestation with an incidence 17 tim es those without tem poral arteritis.



Abdom inal aortic aneurysm is about twice as com m on in those with tem poral arteritis.



Pathologic specim ens feature patchy m ononuclear granulom atous inflam m ation resulting in a m arkedly thickened intim a and occlusion of the vessel lum en.



Occlusive arteritis m ay involve throm bosis of the ophthalm ic artery resulting in ischem ic optic neuritis and visual loss.



Inflam m ation of arteries supplying the m uscles of

Pa ge 4 6 7

m astication results in jaw claudication. 

Hepatic involvem ent is seen in about 25% of cases.



Age is the greatest risk factor: o

Rare in patients <50 years old

o

>90% are >60 years old



Increased prevalence in Northern latitude



Two to four tim es m ore com m on in wom en



Rare in African Am erican patients, com m on in whites

Genetics 

Genetic predisposition is linked to HLA-DR4â€”60% prevalence.



There is a strong association with polym yalgia rheum atica.

Etiology Unknown

Diagnosis Presence of any three or m ore of the following in patients with vasculitis: 

Erythrocyte sedim entation rate greater than 50



Age greater than 50 years



New onset of headache, or change in quality of headache



Tenderness or decreased pulsation of tem poral artery



Abnorm al artery biopsy

Signs and Symptoms 



May present with acute, subacute, or chronic sym ptom s: o

Headache is the single m ost frequent sym ptom .

o

Often boring or lancinating in quality

o

Often described as unilateral over a tem ple

Tongue or jaw claudication upon m astication is com m on

Pa ge 4 6 7

sym ptom s. 



Constitutional sym ptom s: o

Fatigue

o

Malaise

o

Anorexia

o

Weight loss

o

Weakness

o

Arthralgias

o

Low-grade fever

Visual findings: o

Findings are usually in one eye.

o

Develop weeks to m onths after the onset of other sym ptom s

o

May fluctuate, but visual im pairm ent does not usually im prove over tim e, even with treatm ent

o

Diplopia

o

Ptosis

o

Extraocular m uscle weakness

o

Scotom ata

o

Blurred vision

o

Am aurosis fugax

o

Blindness



Sore throat, dysphagia, and cough



Scalp tenderness, especially over the tem poral artery



Pulsations over tem poral artery:



o

Increased pulsations early in disease

o

Decreased pulsations late in the disease

Erythem a, warm th, swelling, or nodules over scalp arteries



Bruits or decreased pulses over large arteries



Rare findings: o

Respiratory sym ptom s

Pa ge 4 6 7







o

Ischem ic chest pain

o

Congestive heart failure

Neurologic problem s: o

Occurs in up to one third of patients

o

Neuropathies

o

Transient ischem ic attacks

o

Cerebral vascular accidents

Occult m anifestations include: o

Glossitis

o

Lingual infarction

o

Tongue infarction

o

Raynaud phenom enon

o

Tum orlike lesions: 

Breast



Ovarian



Uterine m ass

40% do not present with the classic features of headache, scalp tenderness, visual changes, or jaw claudication.



Frequently associated with polym yalgia rheum atica (up to 50%):



o

Stiffness

o

Aching pain in the proxim al m uscles

o

Worse in the m orning and decreasing with exercise

Associated synovitis, especially in the knees, is com m on.

Essential Workup 

Focused physical exam ination with em phasis on: o

Tem poral artery and scalp abnorm alities

o

Com plete neurologic exam ination

o

Ophthalm ic exam ination including visual acuity and visual field testing

P.1099

Pa ge 4 6 7



Funduscopy: o

Often norm al initially

o

Iritis and fine vitreous opacities m ay be early findings.



o

Optic nerve edem a

o

Hyperem ia of the disk

o

Pallor

o

Hem orrhage

o

Scattered cotton-wool spots

o

Vessel engorgem ent and exudates are seen later.

Any pulse differences in the extrem ities or bruits over large arteries should be noted.

Tests Lab 

Elevated erythrocyte sedim entation rate, usually greater than 100 m m /h



C-reactive protein above 2.45 m g/dL



A m ild norm ochrom ic anem ia is typical; platelets tend to be elevated, white cell count can be norm al or slightly elevated and differential is usually norm al.



Liver function tests and prothrom bin tim e m ay be elevated; creatine phosphokinase, tests of renal function and urinalysis are generally norm al.



Elevation in interleukin-6 (IL-6) is seen during flares.

Imaging 

Doppler ultrasound: o

Decreased blood flow in tem poral, facial, and ophthalm ic arteries

o

Presence of a halo is highly suggestive of active tem poral arteritis.

Pa ge 4 6 7



Angiogram : o



Sm ooth, tapered occlusions or stenosis

MRI: o

Indicated for exam ination of large arteries

Diagnostic Procedures/Surgery Tem poral artery biopsy: 

Multiple sections should be done in 24â€“48 hours and no longer than 96 hours after initiation of steroids.



Gold standard for diagnosis

Differential Diagnosis 

Vasculitides: o

Polyarteritis nodosa

o

Hypersensitivity vasculitis

o

System ic lupus erythem atosus

o

Takayasu arteritis

o

Wegener granulom atosis



Throm bosis of retinal, ophthalm ic, or tem poral arteries



Lym e disease

Treatment Pre Hospital 

Sym ptom s m ay be confused with stroke.



Initiate appropriate m onitoring and oxygen.



Patients m ay be hypotensive from one of the rare sequelae (aortic dissection, abdom inal aortic aneurysm , or m yocardial infarction).

Initial Stabilization Although rare, patients m ay present with vascular catastrophe such

Pa ge 4 6 7

as aortic dissection or m yocardial infarction and need appropriate aggressive early m anagem ent.

ED Treatment 

Steroids: o

Strong clinical indications are required if started before tem poral artery biopsy.

o

Early treatm ent significantly reduces the incidence of blindness.

o

Steroids effectively control system ic and local sym ptom s within days to weeks.

o

Treatm ent with prednisone m ay continue for yearsâ€”usual disease length is 3â€“4 years.

o

Sustained steroid therapy m ay accelerate osteopenia, cause cataracts, and potentiate hyperglycem ia and hypertension.



Sym ptom atic pain m anagem ent with NSAIDs or salicylates

Medication (Drugs) 

Ibuprofen: 400 m g PO every 4 hours



Methylprednisolone (Solu-Medrol): 125 m g IV



Prednisone: 60â€“100 m g PO per day that is not tapered for several weeks

Follow-Up Disposition Admission Criteria 

Patients with im pending vascular com plications

Pa ge 4 6 7



Patients with associated acute visual loss

Discharge Criteria 

Less sym ptom atic patients without evidence of end-organ involvem ent



Able to be seen in follow-up within 1â€“2 days

Issues for Referral 

Rheum atology



Ophthalm ology if associated with visual sym ptom s

References 1. Calvo-Rom ero JM. Giant cell arteritis. Postgrad Med J. 2003;79:5115115. 2. Levine SM, Hellm ann DB. Giant cell arteritis. Curr Opin Rheum atol . 2002;14:310. 3. Nordberg E, Noirberg C. Giant cell arteritis: strategies in diagnosis and treatm ent. Curr Opin Rheum atol. 2004;16:25â€“30.

Codes ICD9-CM 446.5

ICD10 M31.6

Pa ge 4 6 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tem po ral M andibular Jo int Injury/Syndro m e

Temporal Mandibular Joint Injury/Syndrome Timothy J. Mader Gregory R. Murphy

Basics Description 

Myofacial pain causing tem porom andibular dysfunction



Tem porom andibular joint (TMJ) pain: o

Originates from the joint (capsulitis, traum atic arthritis, acute disk displacem ent) or m uscles of m astication (spasm )



TMJ clicking: o

Highly correlated with disk displacem ent

o

May be norm al finding; present as a transient finding in 30â€“40% of the population



TMJ m otion: o

Typical range is 42â€“55 m m (m axillary to m andible incisors).

o

Lim ited by adhesions within the joint or disk displacem ent or trism us from m uscle spasm



TMJ locking:

Pa ge 4 6 7

o

Open locking (dislocation): typically from yawning consequent to joint laxity and easily reduce

o

Closed locking: results from disk displacem ent and is difficult to correct

Etiology TMJ dysfunction is poorly understood: 

Multifactorial: bruxism , traum a, m alocclusion

Diagnosis Signs and Symptoms History 

Preauricular pain: o

Constant

o

Dull and aching

o

May be referred to the ipsilateral ear, head, or neck

o

Exacerbated by m andible m ovem ent (pathognom onic)



o

More conspicuous at night and m ay cause insom nia

o

Often worsens through the day

Tongue, lip, or cheek biting

Physical Exam 





Joint sounds: o

Popping or clicking sensation with TMJ articulation

o

A palpable or audible click with opening and closing

Malalignm ent and lim ited range of m otion: o

Dentoskeletal m alocclusion or lateral deviation

o

Open or closed locking of the jaw

Tenderness over the m uscles of m astication and TMJ: o

Masseter m uscle m ost com m only painful

Pa ge 4 6 7

Essential Workup 

Diagnosis based on clinical presentation



Exclude other causes of headache and facial pain.

Tests Lab No specific laboratory tests are indicated. P.1101

Imaging Panorex is the screening radiograph of choice: 

May dem onstrate fracture or intra-articular pathology (i.e., tum or, or degenerative joint disease) but usually unrem arkable

Differential Diagnosis 

Acute coronary syndrom e



Carotid artery dissection



Intracranial hem orrhage (subarachnoid hem orrhage)



Tem poral arteritis



Trigem inal or glossopharyngeal neuralgia



Vascular headache



Intraoral and dental pathology



Herpes zoster



Salivary gland disorder, otitis, and sinusitis



Elongated styloid process pain

Treatment

Pa ge 4 6 8

Pre Hospital Provide com fort and reassurance

ED Treatment 

Acute therapeutic options: o

Patient reassurance and educationâ€”â€œusually m ild and self-lim itedâ€•

o

Analgesics and anxiolytics

o

Urgent reduction of open or closed locking (Montgom ery 2000)â€”m ay require procedural sedation

o 

Physical therapyâ€”m oist heat or ice packs

Outpatient m anagem ent: o

Com bination pharm acotherapy

o

Hom e physical therapyâ€”m oist heat or ice packs and m echanically soft diet

o

Occlusal appliance worn during sleep

o

Referral to dentist or oral-m axillofacial surgeon

Medication (Drugs) 

Narcotic analgesics



NSAIDs



Anxiolytics



Muscle relaxants



Sedative-hypnotics

Follow-Up Disposition

Pa ge 4 6 8

Discharge Criteria 

Treat as outpatients with pain m edication, m uscle relaxants, and warm com presses.



Referral to Otolaryngologist

References 1. Gray RJM, Davies SJ. Em ergency treatm ent of acute tem porom andibular disorders: part I. Dent Update. 1997;24:170â€“173. 2. Gray RJM, Davies SJ. Em ergency treatm ent of acute tem porom andibular disorders: part II. Dent Update. 1997;24:186â€“189. 3. Montgom ery MT. Extraoral facial pain. Em erg Med Clin North Am . 2000;18(3):577â€“600.

Codes ICD9-CM 524.60

ICD10 K07.6

Pa ge 4 6 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tendo n Laceratio n

Tendon Laceration

Robert Marsan Jr. Elisa Aumont Verena Valley

Basics Alert Tendons near lacerations m ust be explored through com plete range of m otion to rule out injury.

Description Based on m echanism 

External traum a: o

o

Penetrating traum a: 

Gunshot wounds



Glass



Knives



Foreign bodies

Blunt traum a: 

Crushing force or avulsion from hyperextension of a joint



Internal traum a: o

Entrapm ent/Laceration from bony fracture (rare)

Etiology

Pa ge 4 6 8

Tendon injuries grossly categorized into those affecting upper versus lower extrem ities: 

Upper-extrem ity injuries frequently related to the workplace, hom e, an assault, or attem pted suicide



Lower-extrem ity injuries m ost often associated with work or m otor vehicle accident

Diagnosis Signs and Symptoms 

Pain is the cardinal sym ptom



Functional deficit



Soft-tissue dam age:



o

Swelling

o

Ecchym osis

o

Lacerations

o

Hem orrhage

Abnorm al resting position of the extrem ity or large joint instability increases suspicion for tendon injury.

Essential Workup 



A careful history: o

Mechanism , tim e of injury

o

Hand position during injury

o

Hand dom inance

o

Drug allergies

o

Medications

o

Past m edical history

o

Tetanus-vaccination status

Physical exam should follow the orthopaedic schem e of look, feel, m ove:

Pa ge 4 6 8

o

Perform neurovascular exam before local anesthesia is instilled.

o 

Exam ine each digit separately.

Flexor digitorum profundus injuries: o

Present with inability to flex the distal interphalangeal joint

o

Exam involves stabilizing the proxim al interphalangeal joint in full extension while the patient attem pts to flex distal interphalangeal joint.



Flexor digitorum superficialis injuries: o

Present with inability to flex the proxim al interphalangeal joint of a digit

o

Usually established by m eans of standard superficialis tendon test: 

While holding the uninjured digits in full extension, the patient attem pts to flex the affected finger at the proxim al interphalangeal joint.

 o

Falsely negative if profundus is functional

The distal interphalangeal joint extension test: 

May m ake this diagnosis m ore apparent



Patient is asked to m ake a precision pinch between the thum b and the injured finger.



Then asked to flex the proxim al interphalangeal joint so that the distal interphalangeal joint is hyperextended



Confirm s the integrity of the flexor digitorum superficialis



Forearm and wrist flexor injuries: o

Present with inability to flex ulnar or radial side of wrist or to flex the wrist while opposing the thum b to the little finger

Pa ge 4 6 8



Extensor tendon injuries: o

Found by weakness or lack of extension of the distal phalanx against resistant

o

Indicates partial or com plete disruption

o

Best determ ined with patient placing palm on flat surface and asking the patient to attem pt to extend the fingers individually



o

Palpate each tendon.

o

Loss of norm al tension indicates injury

Further explore tendons and wounds after local anesthesia (1% lidocaine or 0.5% bupivacaine) in a bloodless, well-lit surgical field: o

Tendons near lacerations m ust be explored through com plete range of m otion.

o

Best elucidates tendon injuries distal or proxim al to a skin wound

Pediatric Considerations 

More difficult to get an adequate exam ination



The healing process is usually quicker and m ore often associated with com plete return to pre-injury function.

Tests Lab Wounds first exam ined >12 hours after injury or wounds with evident infection should be cultured.

Imaging 

Radiographs are frequently needed to identify radiopaque foreign bodies or fractures.



High-frequency ultrasound can be used to identify com plete tendon lacerations: o

Partial tendon lacerations difficult to im age

Pa ge 4 6 8

o

A water bath m ay help when attem pting to im age a painful extrem ity.



Ultrasound guidance m ay help to guide rem oval of foreign bodies.

Differential Diagnosis 

Always rule out an associated foreign body or fracture.



Partial lacerations are com m on but m ore difficult to diagnosis than com plete disruptions because they m ay dem onstrate intact function: o

Alterations of the norm al resting hand position m ay indicate partial laceration.



Lacerations over the m etacarpophalangeal joint should be considered the result of a hum an bite until proven otherwise: o

Look for associated extensor tendon injury while m etacarpophalangeal joint flexed.



Lacerations over the proxim al interphalangeal joint m ay involve the lateral bands or the central slip of the extensor m echanism : o



BoutonniÃ¨re deform ity from im proper repair

Disruption of the extensor tendon distal to the central slip results in a m allet finger deform ity.



Avulsion of the flexor digitorum superficialis distally m ay be present with or without an associated avulsion fracture: o

Suspect when a grasping finger is hit by a fast-m oving object (jam m ed finger).

P.1103

Pa ge 4 6 8

Treatment Pre Hospital 

Do not rem ove foreign m atter from the patient in the field.



Im m obilize and transport patient.



Apply direct pressure to control hem orrhage.



Assess distal neurovascular status for signs of com prom ise.



Contact m edical control before any attem pted reduction.

Initial Stabilization 

Evaluate extrem ity and control hem orrhage with direct pressure.



Rem ove all jewelry or constricting bands.

ED Treatment 

Pain control as required



Adm inister tetanus toxoid as needed.



Copious irrigation with 1 L norm al saline



Broad-spectrum antibiotic, such as a first-generation cephalosporin (Cefazolin)



Tendon lacerations associated with hum an bites: o

Must be copiously irrigated

o

Place on IV antibiotics with coverage of oral anaerobes (am picillin/sulbactam )

o 

Im m obilized and elevate the hand

Rem ove all foreign bodies and provide debridem ent of avascular tissue.



Partial tendon lacerations that involve m ore than 20% of the cross-sectional area of the tendon m ust be repaired.



Sim ple extensor tendon lacerations m ay be repaired in the ED:

Pa ge 4 6 8

o

Use a 4-0 or 5-0 nonabsorbable suture in a figure-of-eight or a m odified Kessler stitch.



All suspected flexor tendon, wrist, and distal forearm tendon lacerations require consultation by a hand surgeon, ideally within 12 hours.



Tendon lacerations over the proxim al interphalangeal joint m ay result in a boutonniÃ¨re deform ity: o



Refer to a hand surgeon.

The superficial nature of m ultiple tendons, nerves, and vessels on the volar aspect of the wrist renders them easily vulnerable to penetrating traum a: o

â€œSpaghetti wristâ€• or â€œfull houseâ€• 

Volar wrist laceration with at least 10 structures involved



Requires prom pt consultation with a hand surgeon



Tendon lacerations associated with fractures require referral for operative repair.



If a surgeon is not prom ptly available: o

Irrigate copiously.

o

Close skin without repair of tendon.

o

Im m obilize injured hand with a bulky volar dressing and splint

o

Wrist in 20â€“30Â°of flexion

o

Metacarpal joint in 60â€“70Â°of flexion

o

Interphalangeal joints in 10â€“15Â°of flexion

Medication (Drugs) 

Am picillin/sulbactam : 3 g IV q6 (peds: 200 m g/kg per day IM or IV div. q6h)



Cefazolin: 1 g IV piggyback (peds: 100 m g/kg per day IM

Pa ge 4 6 8

or IV div. q6h, followed by 40 m g/kg per day PO q.i.d. for 5â€“7 days) 

Tetanus toxoid: 0.5 m L IM (peds: younger than 7 yearsâ€”diphtheria-pertussis-tetanus vaccine preferred; in those older than 7 years, adult dose tetanus toxoid if im m unization series not com pleted), tetanus im m une globulin, as required, 250 IU adm inistered IM

Follow-Up Disposition Admission Criteria 

Patients with infected tendon lacerations m ust be adm itted for operative debridem ent.



Any patients with tendon injury secondary to hum an bite m ust be adm itted for operative debridem ent and IV antibiotics.



Any patients with significant flexor tendon laceration m ay be adm itted for tim ely operative repair or transferred to the nearest hand surgeon.

Discharge Criteria 

Patients with an extensor tendon laceration that is not infected, nor associated with other significant injury or underlying fracture, which was repaired by the ED physician and is now properly splinted, m ay be discharged with tim ely surgical follow-up.



Patients with an extensor tendon laceration requiring surgeon referral for repair (wrist, forearm , proxim al interphalangeal joint), which has been properly treated and splinted, with the patient placed on antibiotics, m ay

Pa ge 4 6 9

be discharged for tim ely surgical follow-up.

References 1. Blaivas M, Lyon M, Brannam L, et al. Water bath evaluation technique for em ergency ultrasound of painful superficial structures. Am J Em erg Med. 2004;22:589â€“593. 2. Dogan T, Celebiler O, Gorungluoglu R, et al. A new test for superficialis flexor tendon function. Ann Plast Surg. 2000;45:93â€“96. 3. Hudson DA, de Jager LT. The spaghetti wrist: sim ultaneous laceration of the m edian and ulnar nerves with flexor tendons at the wrist. J Hand Surg (Br). 1993;18:171â€“173. 4. Jozsa LG, Kannus P. Hum an Tendons: Anatom y, Physiology and Pathology. Cham paign, IL: Hum an Kinetic, 1997. 5. Lee DH, Robbin ML, Galliott R, et al. Ultrasound evaluation of flexor tendon lacerations. J Hand Surg (Am ). 2000;25:236â€“241. 6. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the em ergency departm ent: Closed tendon injuries of the hand. Am J Em erg Med. 2001;19:76â€“80. 7. Stahl S, Kaufm an T, Bialik V. Partial lacerations of flexor tendons in children: prim ary repair versus conservative treatm ent. J Hand Surg (Br). 1997;22B:377â€“380.

Codes ICD9-CM 848.9 Other and ill-defined sprains and strains, unspecified site of sprain and strain 880.2 Open wound of shoulder and upper arm â€“ With tendon involvem ent 881.2 Open wound of elbow, forearm , wrist â€“ With tendon involvem ent 882 Open wound of hand except finger(s) alone 883 Open wound of finger(s) 894 Multiple and unspecified open wound of lower lim b

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ICD10 T14.6

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tendo nitis

Tendonitis

James Killeen

Basics Description 



Overuse syndrom e: o

Synovial cells increase in thickness

o

Excess synovial fluid collection

o

Constant irritation

If no further injury occurs, the process m ay last from 48 hours to 2 weeks.



Continuous irritation causes fibrosis with tendon thickening and stenosing tenosynovitis.

Etiology 

Mechanical overload or repetitive m icrotraum a to the m usculotendinous unit: o

o

Intrinsic factors: 

Inflexibility



Muscle weakness or im balance

Extrinsic factors: 



Excessive deviation, frequency, or activity

Chem otactive and vasoactive chem ical m ediators are released: o

Vasodilatation and cellular edem a increasing the

Pa ge 4 6 9

num ber and activity of PMNs

Diagnosis Signs and Symptoms History 

Repetitive stress and m echanical overload



The classic inflam m atory signs include pain, warm th, erythem a, and swelling.



Pain will resolve quickly after initial m ovem ent only to becom e a throbbing pain after exercise.

Physical Exam 

Defined as inflam m ation of the tendon only



There is a poor distinction between tendonitis and tenosynovitis (degree of inflam m ation).



Clinical findings: o

Warm th

o

Presence of an effusion

o

Decreased range of m otion

o

Instability

o

Pain on m otion

o

Tenderness over tendon site

Specific Conditions Supraspinatus Tendonitis 

Supraspinatus and other rotator cuff tendons: o



Com pressed between hum erus and acrom ion

Overuse of the extrem ity m ay lead to m icrotraum a of the tendons fibers.



Neer classification: o

Stage 1: 

Age<25

Pa ge 4 6 9



Involved in sports requiring repetitive overhead m otion (e.g., swim m ers or pitchers)

o

o



Edem a and hem orrhage of the tendon



Flexion-abduction m otion will elicit pain.



â€œDull achesâ€•

Stage 2: 

Age 25â€“40



Pain is constant and worsens at night.



Active m otion is lim ited by pain.



Passive range of m otion is preserved.



Diffuse intense pain



Fibrosis and thickening of the tendon

Stage 3: 

Partial or com plete tendon tears.



Raising the hum erus in a forced forward flexion while preserving scapular rotation causes im pingem ent.

Calcific Tendonitis 

Age older than 40 years with unknown etiology



Any tendon of the rotator cuff can be affected, but there is a predisposition for the supraspinatus.



Most cases are asym ptom atic and are found on routine radiographs.



Calcium is deposited within the tendon over tim e, undergoes spontaneous resorption causing pain.



Acute attacks m ay develop from crystal release.

Bicipital Tendonitis 

Pain to the anterior shoulder, which radiates down the radius



Discom fort when rolling on the shoulder or trying to reach a hip pocket or back zipper

Pa ge 4 6 9



Focal tenderness is between the greater and lesser tuberosities of the hum erus.





Yergason test: o

Elbow at 90Â° and arm against the body

o

Pain increases with resisted supination of wrist.

Speeds test: o

Pain along the bicipital groove with resisted forward flexion and forearm supination

Lateral Epicondylitis (Tennis Elbow) 

Rotational repetitive m otion causes pain.



Dull ache on the outside of the elbow that increases with grasping and twisting



Inflam m ation at the insertion of the com m on extensor tendon at lateral epicondyle of hum erus



Resisted active dorsiflexion of the wrist on extension of the m iddle finger against resistance can reproduce pain with the elbow extended.



Inflam m ation at site of insertion of the flexor carpi-radialis on the m edial epicondyle: o

Bowlers, golfers, pitchers

o

Active flexing of the wrist against resistance causes pain.

Wrist/Hand 

Inflam m atory changes of the synovial lining between tendons and the retinaculum



De Quervain tenosynovitis: o

Inflam m ation of the abductor pollicis longus and extensor pollicis brevis

o

Finkelstein's test: 

Patient m akes fist with thum b curled in palm .



Wrist is deviated in the direction of the ulna.

Pa ge 4 6 9

 o

Pain occurs in first extensor com partm ent.

Osteoarthritis of the carpal m etacarpal joints or GC tenosynovitis causes the sam e pain.

Trigger finger 

Proxim al portion of the palm ar flexor tendon sheath becom es stenosed and catches as the finger is m oved.



Sym ptom s vary from pain to locking in flexion.

Ankle 

Achilles tendonitis: o

Overuse injury com m only seen in m ales

o

Traum a or system ic disease causing inflam m ation

o

With repeated stress, scar tissue form ation and degeneration of the tendon will occur.

o

Patient will have pain, reduced range of m otion, or m orning stiffness



Achilles tendon rupture o

Seen m ore com m only in 30- to 40-year-old recreational athletes

o

â€œPopping sensationâ€•

o

Acute weakness, inability to continue activity

o

Feels like being kicked or hit in back of leg

o

May initially have a gap by palpation, followed by ecchym osis and a boggy sensation

o

Inability to plantar flex the foot with com plete rupture

o

Thom pson's test: 

Patient lies prone with the feet hanging over the edge of the bed.



Physician squeezes the calf m uscles and looks for plantar flexion

Pediatric Considerations

Pa ge 4 6 9



Apophysitis occurs in children at an ossification center subject to traction:





o

Little League elbow at the m edial epicondyle

o

Osgood-Schlatter syndrom e at tibial tubercle

Avascular necrosis (AVN): o

Presents with pain and swelling around a joint

o

Can occur at various locations

o

Well-recognized sites: 

Capitellum of the hum erus



Head of the fem ur



Tarsal navicular



Metatarsal head



Diagnosis is m ade by plain radiographs.

Radiographs are often required to rule out fracture, AVN, osteochondritis dissecans, or bony tum or.

P.1105

Essential Workup Physical exam ination

Tests Lab CBC, erythrocyte sedim entation rate only if m ore serious infection suspected

Imaging 

Radiographs: o

Extra-articular from articular etiologies

o

â€œSECONDSâ€•: 

Soft tissue swelling



Erosions

Pa ge 4 6 9







Calcifications



Osteoporosis



Narrowing



Deform ity



Separation

Ultrasound: o

Evaluate joint effusions

o

More sensitive than MRI

o

Lim ited use in the em ergency setting

o

Focal tendon thickening

o

Focal hypoechoic areas

o

Irregular and ill-defined borders

o

Peritendinous edem a

MRI: o

Internal m orphology of the tendon and the surrounding structures

o

Helps diagnose retrocalcaneal bursitis and insertional tendonitis

o

Reveals tendon thickening and increased signal with chronic tendon abnorm alities



Scintigraphy: o

99 Technetium pertechnetate phosphate (binds with plasm a protein) and concentrates in joint space (Bursitis)

Differential Diagnosis 

Septic arthritis



Fracture



Osteoarthritis

Treatment

Pa ge 4 6 9

Pre Hospital Im m obilize injured extrem ity as indicated.

Initial Stabilization Ice, im m obilization pending work up

ED Treatment General 

Rest



NSAIDs



Ice (10â€“20 m inute intervals)



Range of m otion exercises



Local injection for pain control



Outpatient m anagem ent



Adm it only for surgery or severe disability



Allow 6â€“12 weeks to heal

Calcific Tendonitis 

Low-energy radio shock wave therapy has recently shown significant pain relief: o



Thought to increase the resorption of calcium

Cim etidine has been used to decrease pain and calcium deposits.

Trigger Finger 

Conservative treatm ents such as rest, splinting (thum b-spica) and NSAIDs for m ost



Som e physicians suggest cortisone injections, (84â€“91% cure rate).



Surgical release of A-1 Pulley m ay be required.

De Quervain Tenosynovitis 

Rest, ice, NSAIDs



Thum b spica splint for 3â€“5 days often helps.

Pa ge 4 7 0

Achilles Tendonitis 

Rest, ice, NSAIDs



Orthotics or heel wedges



Cryotherapy has shown to be useful in controlling inflam m ation.



Recent studies have described successful ultrasound-guided injection of polidocanol: o

Sclerosing agent

o

Decrease neovascularization and sym ptom s of chronic tendinosis



Achilles rupture should be splinted posteriorly in slight plantar flexion: o

Refer to orthopaedics, as patients often need surgery

Medication (Drugs) 

Ibuprofen: 400â€“800 m g PO q6hâ€“q8h (m ax. 2400 m g per day); peds: 5â€“10 m g/kg/dose PO q4hâ€“q6h (m ax. 50 m g/kg/d)

Follow-Up Disposition Admission Criteria Adm it patients if require surgery or other m ore serious illness/injury

Discharge Criteria Most patients m ay be m anaged as outpatients with appropriate referral.

References

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1. Magosch P, Lichtenberg S, Haberm eyer. Radial shock wave therapy in calcifying tendinitis of the rotator cuffâ€”a prospective study. Z Orthop Ihre Grenzgeb. Novem ber 1, 2003;141(6):629â€“636. 2. Rom pe JD. Shock wave therapy for calcific tendinitis of the shoulder: a prospective clinical study with two-year follow-up. Am J Sports Med. Novem ber 1, 2003;31(6):1049â€“1050. 3. Wilder RP, Sethi S. Overuse injuries: tendinopathies, stress fractures, com partm ent syndrom e, and shin splints. Clin Sports Med. 23 (2004)55â€“81 61. 4. Yokoyam a M, Aono H, Takeda A, Morita K. Cim etidine for chronic calcifying tendinitis of the shoulder. Reg Anesth Pain Med. May 1, 2003;28(3):248â€“252.

Codes ICD9-CM 726.90

Pa ge 4 7 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Teno syno vitis

Tenosynovitis

James Killeen

Basics Definition Inflam m ation of the tendon and tendon sheath

Description 

Caused by inflam m ation, overuse or infection



Synovial sheaths cover tendons as they pass through osseofibrous tunnels: o

Visceral and parietal layers of the synovium lubricate and nourish the tendons.

o



Infection can be introduced into tendon sheath. 

Skin wound



Hem atogenous spread

Flexor tenosynovitis (FTS) of hand: o

Typically infectious etiology

o

Penetrating injury especially at flexion creases of the finger is m ost com m on m echanism .

o

High-pressure â€œinjectionâ€• injury to fingers 

Air tools



Paint sprayers



Hydraulic equipm ent



May appear m inor on the surface but are

Pa ge 4 7 0

associated with high incidence of FTS

Etiology 



De Quervain tenosynovitis: o

Caused by overuse

o

Inflam m atory in nature

GC tenosynovitis: o



Neisseria Gonorrhea

Nongonococcal infectious tenosynovitis: o

Staphylococcus aureus and Streptococci are m ost com m on in penetrating injuries.

o

Pasteurella m ultocida is com m on with cat bites.

o

Eikenella corrodens is com m on in hum an bites.

o

Pseudom onas is seen in patients with diabetes or m arine-associated injuries.

o

Mycobacterium species m ay occur in im m unocom prom ised patients.

Diagnosis Signs and Symptoms Cardinal signs of Kanavel for FTS include: 

Tenderness and sym m etric swelling along flexor tendon sheath (sausage digit)



Flexed position of the digit



Pain with passive extension of the finger

Hand 

De Quervain tenosynovitis: o

Repetitive pinching m otion of thum b and fingers 

Assem bly-line workers



Carpenters

Pa ge 4 7 0

 o

Landscaping or weeding

Pain in the radial aspect of the wrist becom es worse with activity and better with rest.

o

Pain occurs on palpation along the radial aspect of the wrist.

o

Pain occurs with passive range of m otion of the thum b.

o

Finkelstein test: 

Pain occurs with ulnar deviation of the wrist with the thum b cupped in a closed fist.



GC tenosynovitis: o

Most com m only affects teenagers, young adults

o

Seen in the ankle, hand or wrist

o

More com m only seen in wom en

o

Vaginal or penile discharge usually absent

o

Fever, chills, polyarthralgia are com m on.

o

Erythem a, tenderness to palpation, and painful range of m otion of the involved tendon

o

Derm atitis m ay be present. 

Hem orrhagic m acules or papules on the distal extrem ities or trunk

Forearm Traum atic tenosynovitis is seen after a direct blow to the lower portion of the forearm .

Ankle 

Stenosing tenosynovitis: o

Com m only seen at the inferior retinaculum of the peroneus tendon

o

Patients are usually m ore than 40 years old and have som e predisposing traum a.

o

Motion increases the pain.

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

Rheum atoid tenosynovitis: o

Medially, the posterior tibial and flexor hallucis longus tendons are com m only involved.

o

Laterally, the peronei are involved.

o

Anteriorly, the anterior tibial tendon is involved.

o

Motion increases the pain.

o

Spontaneous rupture m ay occur.

History 

Assess for infectious etiology: o

History of sexually transm itted disease exposure, penile or vaginal discharge





Obtain history of m echanism : o

High-pressure injections

o

Puncture wounds, bites

o

Environm ental exposures

Assess tetanus status and com orbid factors (e.g., diabetes and im m unocom prom ised).

Physical Exam 

Assess Kanavel signs.



Docum ent neurovascular status.



Identify signs and sym ptom s of system ic illness as well as other potential sites of infection.

Essential Workup Thorough history and physical exam ination will often lead to appropriate diagnosis.

Tests Lab 

CBC, erythrocyte sedim entation rate (ESR): o



May be of assistance in infectious etiology

GC cultures (urethra, cervix, rectum or pharynx) m ay be

Pa ge 4 7 0

useful. 

Liver function tests m ay be elevated with dissem inated Neisseria gonorrhea infection.

Imaging 

Radiographs are low yield, unless a retained radiopaque soft tissue foreign body is suspected.



MRI has proven accurate in assisting the diagnosis of tenosynovitis: o

Generally unnecessary in ED

Differential Diagnosis 

Ankle, soft tissue injuries



Bursitis



Carpal tunnel syndrom e



Cellulitis



Com partm ent syndrom e



Endocarditis



Felon



Gonorrhea



Gout and pseudogout



Hand infections



High-pressure hand injuries



Soft-tissue hand injuries



Soft-tissue knee injuries



Reiter syndrom e



Rheum atic fever



Rheum atoid arthritis

P.1107

Pa ge 4 7 0

Treatment Pre Hospital 

Delay to definitive treatm ent leads to significant increased m orbidity and loss of function.



Elevation and im m obilization of the affected extrem ity should be perform ed.

Initial Stabilization 

Managem ent airway and resuscitate as indicated: o

Septic shock



Elevation, im m obilization of affected extrem ity



IV Access



Tetanus status

Procedure 

Diagnostic arthrocentesis is indicated if joint effusion is present with tenosynovitis: o

Most patients with dissem inated GC infection have co-existing septic arthritis.

o

Cultures are negative in 50% of patients.

o

25% GC arthritis is polyarticular.

o

Joint fluid glucose is norm al.

o

WBC usually are less than 50,000 and a Gram stain is positive in 25% of the patients.

ED Treatment Hand 



High-pressure injection injuries to hand: o

Surgical em ergency

o

Im m ediate hand surgery consultation

o

Pain m anagem ent

Infectious FTS of hand:

Pa ge 4 7 0



o

Im m ediate hand surgery consultation

o

Broad spectrum antibiotic coverage

De Quervain tenosynovitis: o

Rest, NSAID agents, and thum b spica splint

o

Consider lidocaine/corticosteroid injection if condition is unresponsive.



GC tenosynovitis: o

Adm it for IV antibiotic therapy.

o

Penicillin or first-generation cephalosporins for initial therapy

o

Second-generation cephalosporins for an alternative

o

Surgical drainage m ay be indicated if antibiotics do not im prove the condition.

o 

Pain m anagem ent

Nongonococcal infectious tenosynovitis: o

If diagnosis is equivocal, the patient should receive IV antibiotic therapy and consultation with a hand surgeon.

o

Cover for Staphylococcus, Streptococcus as well as anaerobic bacterial infection.

o

Consider coverage for Pseudom onas for the diabetic or im m unocom prom ised patient.

o

Am inoglycosides m ay be added for double coverage.

o

Pain m anagem ent

Forearm Traum atic tenosynovitis: 

Rest, ice, elevation, im m obilization



NSAIDs

Ankle 

Stenosing tenosynovitis: o

Rest, ice, elevation, im m obilization

Pa ge 4 7 0

o 

NSAIDs

Rheum atoid tenosynovitis: o

Rest, ice, elevation, im m obilization

o

NSAIDs

Medication (Drugs) 

Cefazolin: 1â€“2 g IV q8h (peds: 50â€“100 m g/kg/d IV div. q8h)



Cefotetan: 1â€“2 g IV q12h (peds: 50â€“100 m g/kg/d IV div. q12h)



Cefoxitin: 1â€“2 g IV q8h (peds: 80â€“160 m g/kg/d IV div. q6hâ€“q8h)



Ceftriaxone: 1â€“2 g IV q12h (peds: 50â€“100 m g/kg/d IV div. q12h)



Clindam ycin: 600â€“900 m g IV q8h (peds: 20â€“40 m g/kg/d div. q8h)



Penicillin G: 12â€“24 m IU IV div. q4hâ€“q6h (peds: 100,000â€“400,000 IU/kg/d IV div. q4hâ€“q6h)



Tim entin: 3.1 g IV q6h (peds: 200â€“300 m g/kg/d IV div. q4hâ€“q6h)



Tobram ycin: 1 m g/kg IV q8h or 5 m g/kg IV q24h (peds: 2â€“2.5 m g/kg IV q8h)



Zosyn: 3.375 g IV q6h (peds: 200â€“400 m g/kg/d IV div. q6hâ€“q8h)

Follow-Up Disposition 

Patients with FTS require im m ediate consultation with a

Pa ge 4 7 1

hand specialist and adm ission. 

Patients presenting 24â€“48 hours m ay have m ore conservative therapy to include im m obilization, elevation IV antibiotics, and close observation.



Surgical debridem ent indicated if patient is not im proved within the first 24 hours, or physical findings are not resolved within 48 hours.



Patients presenting longer than 48 hours require surgical debridem ent in the operating room .



The hand surgeon m ay attem pt continuous catheter irrigation of the tendon sheath.

Admission Criteria Infectious or high-pressure etiologies for tenosynovitis should be adm itted.

Discharge Criteria Inflam m atory etiologies can be m anaged as outpatients with appropriate referral.

References 1. Em ergency Orthopedics, The Extrem ities. 3rd ed. New Jersey: Appelton & Lange, 1995. 2. Hausm an MR, Lisser SP. Hand infections. Orthopedic Clinic North Am erica. 1992;23(1):171â€“185. 3. Richie CA, Briner WW. Corticosteroid injection for treatm ent of de Quervain's tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Pract. March 1, 2003;16(2):102â€“106. 4. White PH. Regional problem s of the arm and leg in children. In: Maddison PJ, et al., eds. Oxford textbook of rheum atology. Vol. 1. New York, NY: Oxford University Press, 1993:80â€“84. 5. Wilder RP, Sethi S. Overuse injuries: tendinopathies, stress fractures, com partm ent syndrom e, and shin splints. Clin Sports Med. 2004;(23):55â€“81,61.

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6. Zarin M, Ahm ad I. Surgical treatm ent of de Quervain's disease. J Coll Physicians Surg Pak. March 1, 2003;13(3):157â€“158.

Codes ICD9-CM 727.00

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Testicular To rsio n

Testicular Torsion

Edward Newton

Basics Description 

Rotation of the testicle around the sperm atic cord and vascular pedicle



Congenital abnorm ality of the genitalia: o

High insertion of the tunica vaginalis on the sperm atic cord

o

Redundant m esorchium

o

Perm its increased m obility and twisting of the testicle on its vascular pedicle



The anatom ic abnorm ality is generally bilateral, so both testicles are susceptible to torsion.



Rotation often occurs m edially (two thirds of cases): o

Ranges from incom plete (90â€“180Â°) to com plete (360â€“1080Â° degrees) torsion

o

Depending on the degree of torsion: 

Vascular occlusion occurs



Infarction of the testicle after m ore than 6 hours ofwarm ischem ia



Testicular salvage: o

73â€“100% with less than 6 hours ischem ia

Pa ge 4 7 1

o

Up to 70% at 6â€“12 hours

o

Less than 20% after 12 hours

o

It is still worthwhile to attem pt to salvage the testicle up to 24 hours after the onset.



Testicular infarction leads to atrophy and m ay ultim ately decrease fertility.



Bim odal distribution of torsion: o

Peak incidences in infancy and adolescence

o

85% of cases of occur between ages 12 and 18 years, with a m ean of 13 years.

o

Torsion is rare after age 30 but still possible.

Diagnosis Signs and Symptoms History 

Sudden onset of unilateral testicular pain



Scrotal swelling and erythem a



Less com m only, torsion m ay present with pain in the inguinal or lower abdom inal area.



Up to 40% of patients m ay describe previous sim ilar episodes that rem itted spontaneously: o

Represents spontaneous torsion and detorsion



Nausea and vom iting occur in 50% of cases.



Low-grade fever occurs in 25%.



Often a history of m inor traum a to the testicle preceding the onset of pain.



Sym ptom s of urinary infection (dysuria, frequency, and urgency) are absent.

Physical Exam

Pa ge 4 7 1



In distinguishing torsion from epididym itis, localized tenderness is helpful early; however, once significant scrotal swelling occurs, the anatom y becom es indistinct.



The affected testicle m ay lie transversely as opposed to the norm al vertical lie.



Crem asteric reflex is frequently absent on the affected side with testicular torsion.



Prehn sign: o

Relief of pain on elevation of the testicle in epididym itis

o

Worsening or no change in the pain with torsion

o

Considered unreliable

Essential Workup 

The presentation of an â€œacute scrotum â€• in a child or adolescent requires rapid assessm ent and im m ediate consultation with an urologist.



These patients require noninvasive flow studies or surgical exploration to confirm torsion.



25â€“30% of these patients ultim ately prove to have testicular torsion.

Tests Lab 

Elevated WBC count with a left shift is present in 50% of cases.



Urinalysis is usually norm al, but up to 20% of cases of torsion have pyuria.



There are no laboratory tests specific for testicular torsion.

Imaging Alert

Pa ge 4 7 1



There are lim itations of all flow studies: o

Reflect only the current state of perfusion

o

Spontaneously detorsed testicle m ay show norm al or even increased flow.

o 

Still at high risk for recurrent torsion

Traditional criterion standard has been technetium -99m radionuclide scans: o

Decreased flow in the torsed testicle com pared with the unaffected side

o 

Frequent tim e delays in obtaining scans

Doppler ultrasound: o

Assess testicular blood flow.

o

Has replaced nuclear scanning:

o



Less invasive



More readily available test



Com parable results

Overall sensitivity and specificity of 98% and 100%, respectively

o

Epididym itis will reveal increased flow due to inflam m ation.

o

Torsion will reveal decreased or no blood flow.

o

Color-flow Doppler is the m ost com m only available.

o

Use of Doppler contrast m aterial m ay enhance the accuracy.

Pediatric Considerations 

All im aging techniques have technical lim itations when in infants: o

Testicular vessels are very sm all.

o

Am ount of blood flow to the testicle under norm al conditions is m inim al.



Scrotal exploration m ay be required.

Pa ge 4 7 1

Diagnostic Procedures/Surgery 

Scrotal exploration can be done rapidly under local anesthesia to diagnose and treat torsion.



The â€œbell-clapperâ€• deform ity of both testicles should be corrected by orchiopexy.

Differential Diagnosis 

Testicular neoplasm



Epididym itis/Orchitis



Torsion of the appendix testis



Testicular traum a or rupture of the testicle



Incarcerated inguinal hernia



Testicular tum or



Acute hydrocele



Henoch-SchÃ¶nlein purpura



Other intraabdom inal conditions: o

Appendicitis

o

Pancreatitis

o

Renal colic

P.1109

Treatment Pre Hospital 

There is no definitive treatm ent that can be rendered in the field.



Prehospital personnel need to recognize the urgency of acute testicular pain in young patients.



These patients should be transported to the ED

Pa ge 4 7 1

im m ediately.

Initial Stabilization IV fluid, analgesics as appropriate

ED Treatment 

Exam ination of testicle to exclude prim ary neoplasm



Establish the diagnosis and m obilize appropriate urologic care.



Applying an ice pack to the scrotum relieves pain: o



Can prolong the viability of the ischem ic testicle

If definitive care is likely to be delayed beyond 4â€“5 hours from the onset of torsion, m anual detorsion m ay be attem pted: o

Externally rotate the affected testicle opposite the usual m edial direction of torsion.

o

Continue until pain is relieved or norm al anatom y is restored.

o

All patients who undergo m anual detorsion m ust be surgically explored.

Medication (Drugs) Analgesia

Follow-Up Disposition Admission Criteria 

Patients with confirm ed torsion m ust be adm itted for scrotal exploration and bilateral orchiopexy.

Pa ge 4 7 1



Flow studies that are inconclusive and technical failures m andate further investigation by surgical exploration of the scrotum .



Adm ission for urgent surgical exploration of an acute scrotum is m andatory if there is any potential delay in obtaining a flow study: o

Patients in whom apparent spontaneous detorsion has occurred should undergo exploration for bilateral orchiopexy.

Discharge Criteria 

Patients with negative scrotal exploration and those with norm al flow studies can be discharged with appropriate urologic follow-up.



Param eters for return to ED m ust be discussed because of the possibility of recurrent torsion.



Patients with an obvious diagnosis other than testicular torsion can be referred for care.

References 1. Al Mufti RA, Ogedegbe AK, Laferty K. The use of Doppler ultrasound in the clinical m anagem ent of acute testicular pain. Br J Urol. 1995;76:625â€“627. 2. Arce JD, Cortes M, Vargas JC: Sonographic diagnosis of acute sperm atic cord torsion. Rotation of the cord: a key to the diagnosis Pediatr Radiol. 2002;32:485â€“491. 3. Burgher SW. Acute scrotal pain. Em erg Med Clin North Am . 1998;16:781â€“809. 4. Kafla N, Veyrac C, Baud C et al: Ultrasonography of the sperm atic cord in children with testicular torsion: im pact on the surgical strategy. J Urol. 2004;1721692-5. 5. Sessions AE, Rabinowitz R, Hulbert WC et al: Testicular torsion: direction, degree, duration and disinform ation. J Urol.

Pa ge 4 7 1

2003;169:663â€“665. 6. Sidhu PS. Clinical and im aging features of testicular torsion: role of ultrasound. Clin Radiol. 1999;54:343â€“352.

Codes ICD9-CM 608.2

ICD10 N44

Pa ge 4 7 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tetanus

Tetanus

Daniel T. Wu

Basics Description 

Rare disease in the United States but still prevalent in third world countries



About 40 cases per year in the United States



500,000â€“1,000,000 cases worldwide



Incubation period: o

o

Inoculation to the appearance of the first sym ptom s: 

48 hours to 3 weeks or m ore



<7 daysâ€”poor prognosis

Period of onset: 

Poor prognosis if <48 hours from first sym ptom to first reflex spasm



Neonatal tetanus: o

Due to infected um bilical stum p

o

Sym ptom onset in second week of life when m aternal antibodies decrease

o

Rare in United States but com m on in third world countries

o

Worldwide, accounts for over half of all tetanus infections

Pa ge 4 7 2



Mortality rates as high as 20%.

Etiology 

Clostridium tetani: o

Slender, m otile, heat-sensitive, anaerobic gram -positive rod with a term inal spherical spore

o

Spore characteristics

o

Resistant to oxygen, m oisture, tem perature extrem es



o

Can survive indefinitely until they germ inate

o

Ubiquitous in soil and feces

When inoculated into a wound or devitalized tissue or injected IV as a contam inant of street drugs, the spores germ inate under anaerobic conditions and produce two toxins.



Toxins: o

Tetanolysin: 

Dam ages tissue



Does not cause clinical m anifestations of tetanus infection

o

Tetanospasm in: 

Powerful neurotoxin



Disrupts the release of neurotransm itters such as gam m a-am inobutyric acid (GABA)



Responsible for the clinical m anifestations



Muscle spasm s



Autonom ic instability



Uncontrolled m otor activity

Diagnosis

Pa ge 4 7 2

Signs and Symptoms Generalized 

Most com m on type accounting for about 80% of all cases



Initial presentation:





o

Muscle stiffness and pain

o

Trism us (initial)

o

Risus sardonicus (characteristic facial appearance)

System ic sym ptom s: o

Irritability

o

Restlessness

o

Diaphoresis

Later m anifestations: o

Muscle group rigidity

o

Sudden burst of tonic contractions of m uscle groups causing:

o



Opisthotonos



Flexion and adduction of the arm s



Clenching of fists



Extension of the lower extrem ities

Diaphragm atic spasm or paralysis: 



May com prom ise respiration

Hypersym pathetic state (m ost com m on cause of death): o

Begins in the second week

o

Dysrhythm ias

o

Blood pressure (BP) changes

o

Diaphoresis

o

Hypertherm ia

Local 

Less com m on form of disease accounting for about 17% of all cases



Manifested by localized spasm s around area of initial

Pa ge 4 7 2

infection m ay: o

Be m ild

o

Persist for m onths before resolving

o

Evolve to generalized form (13%)

Cephalic 

Rare variant of disease



Follows head injury or otitis m edia



Spasm of lower cranial and facial m uscles: o



Cranial nerve palsies, CN VII m ost com m on

May progress to generalized tetanus

Neonatal 

Generalized form of tetanus that occurs during the first few weeks of life



Often caused by infection of um bilical stum p



Clinical m anifestations: o

Irritability

o

Poor suck

o

Facial grim acing

o

Muscle spasm s with touch



Very high m ortality rate (50â€“100%)



Incubation period 1â€“2 weeks

History 

Investigate source of infection.



Acute skin wound is not necessary to contract infection.



>25% of infections occurred in the absence of known acute traum a.



Infections can occur from abscesses, ulcers and gangrene.



Elicit tetanus im m unization status.

Essential Workup 

Perform com plete physical exam ination focusing on

Pa ge 4 7 2

cardiovascular and respiratory status, neurological and cranial nerve exam . 

Diagnosis of tetanus is clinical: o

Suspect in all cases of trism us.

o

No wound recalled in one fifth of cases

o

Full tetanus im m unization alm ost elim inates diagnosis.

Tests Often of lim ited or no benefit for diagnosis but useful for ruling out other etiologies or assessing com plications of disease

Lab 

CBC



Electrolytes, blood urea nitrogen, creatinine, glucose: o

For hypocalcem ia



Strychnine level



Arterial blood gas, pulse oxim etry: o



Wound culture for C. tetani: o



Positive only about 30% of tim e

C. tetani titers: o



For oxygenation status

Will only be useful after the fact

Cerebrospinal fluid analysis: o

Norm al with tetanus

o

For m eningitis

Imaging CT brain for altered m ental status: 

Norm al

P.1111

Pa ge 4 7 2

Differential Diagnosis 

Strychnine poisoning



Jaw m uscles usually spared or not involved early in strychnine poisonings



Dystonic reaction to dopam ine blockade



Meningitis



Rabies



Encephalitis



Peritonitis



Alveolar abscess



Tetany/Hyperventilation syndrom e



Hysteria



Dislocated m andible/tem porom andibular joint syndrom e



Bell palsy (cephalic form , before trism us)

Treatment Pre Hospital 

Evaluate airway carefully: o

Endotracheal intubation com plicated by trism us, vocal cord paralysis, and facial/neck rigidity



Avoid excessive stim ulation because it m ay provoke tetany of m usculature.

Initial Stabilization 

ABCs: o

Prophylactic intubation

o

Require neurom uscular blockade due to trism us

o

Establish IV 0.9% NS

o

Monitor BP and cardiac rhythm (autonom ic instability).

Pa ge 4 7 2



Adm inister benztropine or diphenhydram ine to exclude dystonic reaction.

ED Treatment 



Focuses on three goals: o

Stabilizing the patient and supportive care

o

Neutralizing the toxin

o

Rem oving any rem aining organism

Stabilization and supportive care: o

Secure airway: 

o

Prophylactic intubation m ay be necessary.

Paralytic agent m ay be needed in the setting of trism us: 

Succinylcholine should be used with caution due to the risk of hyperkalem ia from up-regulation of acetylcholine receptors.

o

Treat m uscle spasm s with benzodiazepines; if large doses fail, can adm inister dantrolene.



Autonom ic instability therapy: o

Occurs days to weeks after the onset of sym ptom s

o

Tachydysrhythm ia and hypertension: 

No treatm ent universally effective



Alpha- and beta-blockers can be tried, but m ay cause worsening of sym ptom s (labetalol has been used for its alpha and beta blocking affects).



Clonidine, m agnesium , m orphine, fentanyl, and epidural anesthesia m ay be tried.

o

Hypotension: 

Rule out septicem ia and hypovolem ia.



Initiate dopam ine or dobutam ine when low cardiac output.



Neutralization of the toxin

Pa ge 4 7 2







Hum an tetanus im m une globulin (TIG): o

3000â€“6000 U IM for both adults and children

o

Adm inister before dÃ©bridem ent of wound.

o

Neutralizes unbound toxins

o

No effect on toxin already bound in CNS

Rem oval of rem aining organism : o

Lim its the severity of the infection

o

DÃ©bridem ent rem oves any necrotic tissue.

Antibiotics are effective in elim inating Clostridium tetani: o

Metronidazole is the antibiotic of choice.

o

Penicillin is a viable alternative.

Prevention 

Prim ary vaccination series should be com pleted by age 18 m onths, and children receive the booster at ages 4, 11, and then every 10 years after.



Diphtheria, pertussis, and tetanus vaccine for children under 7



Tetanus diphtheria (Td) can be used for children >7 years and adults.



Clinical tetanus does not confer im m unity.



For clean wounds o

Td should be given if unknown prior vaccination history or greater than 10 years since last booster.



For tetanus prone wounds o

Td should be given if unknown vaccination history or >5 years since last booster.

o

TIG should be given if unknown vaccination or has never received the prim ary series.

Medication (Drugs)

Pa ge 4 7 2



Benztropine: 1â€“2 m g IV



Chlorprom azine 10â€“50 m g IM



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.4 m g/kg) IV



Diphenhydram ine: 50 m g IV



Dobutam ine: 2.5â€“15 Âµg/kg/m in IV



Dopam ine: 2â€“20 Âµg/kg/m in IV



Doxycycline: 100 m g IV q12h



Erythrom ycin: 500 m g IV q6h



Labetalol: 20 m g (peds: 0.3â€“1 m g/kg/dose) IV q10m in up to 300 m g PRNâ€”start infusion 2 m g/m in (peds: 0.4â€“1 m g/kg/hr m ax. 3 m g/kg/hr as needed)



Metronidazole: 1.0 g (peds: 15 m g/kg) load, followed by 500 m g (7.5 m g/kg) IV q6h



Penicillin G potassium : 1.2 m IU (peds: 100,000 IU/kg/24h) IV q6h for 10 days



Propranolol 0.5â€“1 m g (peds: 0.01â€“0.1 m g/kg) IV



TIG (tetanus im m une globulin): o

250 IU IM

o

Adm inister in separate site from Td toxoid

o

For unim m unized or incom pletely im m unized in presence of tetanus prone wound



Td 0.5 m L IM

Follow-Up Disposition Admission Criteria All patients should be adm itted to an intensive care setting.

Discharge Criteria

Pa ge 4 7 2

None for suspected generalized tetanus

References 1. CDC Tetanus Surveillanceâ€”United States 1998â€“2000. MMWR. 2003;52(ss-3):1â€“7. 2. CDC. Tetanus. Epidem iology and prevention of Vaccineâ€”Preventable Diseases. 8th ed. (The Pink Book) 3. Hsu SS, Tetanus in the Em ergency Departm ent: a current review. J Em erg Med. 2001;20:357â€“365. 4. McQuillan GM, Serologic im m unity to diphtheria and tetanus in the United States. Ann Intern Med. 2002;136:660â€“666. 5. Pickering L, Ed 2003: Report of the com m ittee on infectious diseases. 26th ed. Am erican Academ y of Pediatrics, 2003. 6. Thawaites CL. Preventing and treating tetanus. Brit Med J. 2003;326:188â€“119.

Codes ICD9-CM 37.0

ICD10 A35

Pa ge 4 7 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Theo phylline Po iso ning

Theophylline

Poisoning Gerald Maloney

Basics Description 

Acute overdose: o

Ingestion within 8-hour interval in patient with no prior theophylline use



Acute-on-chronic overdose: o

Single excessive dose in patient previously receiving usual therapeutic doses for â‰¥24 hours



Chronic intoxication: o

Accum ulation of theophylline >20 m g/L associated with prior therapeutic use for â‰¥24 hours secondary to: 

Drugâ€“drug, drugâ€“diet, or drugâ€“disease interactions

 

Use of serial excessive doses

Electrolyte shifts and hypotensive effects occur only in acute overdoses: o

Tachyphylaxis to these effects occurs with m aintenance therapy.

Pa ge 4 7 3

o

As result of cellular shifts between extracellular and intracellular fluids

Etiology 

Acute ingestions require larger concentrations to achieve specific toxic effects than acute-on-chronic or chronic overdoses.



Drugâ€“drug interactions: o

o

Inhibiting theophylline m etabolism : 

H 2 -receptor antagonists



Macrolide antibiotics



Fluoroquinolones



Allopurinol



Influenza vaccine



Interferons

Enhances theophylline m etabolism (leads to toxicity when discontinued):





Carbam azepine



Barbiturates



Sm oking



Rifam pin

Chronic theophylline accum ulation: o

Uncontrolled congestive heart failure

o

Liver disease (cirrhosis or severe hepatitis)

o

Acute viral infections

Diagnosis Signs and Symptoms 

Cardiovascular: o

Sinus or supraventricular tachycardias:

Pa ge 4 7 3

o



Multifocal atrial tachycardia



Caused by Î² 1 -receptor stim ulation

Hypotension: 

In acute or acute-on-chronic ingestions only



Associated with theophylline >35 m g/L



Owing to vasodilatation induced by Î² 2 -receptor stim ulation



May be refractory to fluids, positioning, and conventional vasopressors



Central nervous system : o

Trem or

o

Mental status changes

o

Seizures with theophylline level: 

Greater than 100 m g/L in acute overdose



Greater than 30 m g/L in acute-on-chronic intoxication



As low as 20 m g/L in chronic intoxication



Seizures are seen in 14% of chronic intoxications and 5% of acute intoxications.



Gastrointestinal: o

Nausea, vom iting: 

Protracted and m ay be refractory to antiem etics at usual doses

o

Abdom inal pain

o

Pharm acobezoar: 

From sustained-release dosage form s in acute ingestions

 

Delays peak concentrations

Miscellaneous: o

Hypokalem ia: 

As low as 1.5 m Eq/L



Owing to Î²-receptor stim ulation

Pa ge 4 7 3

o

Hyperglycem ia

o

Leukocytosis

o

Hypercalcem ia, hypophosphatem ia, hypom agnesem ia

Essential Workup 

Serum theophylline concentration: o



Finding of â‰¥20 m g/L confirm s diagnosis.

Detailed history to differentiate acute from acute-on-chronic from chronic intoxication

Tests Lab 

Theophylline level: o

Repeat every 2 hours until decreasing to confirm im m ediate absorption is com plete and peak value has occurred.

o

Serious m orbidity in acute overdose if â‰¥100 m g/L

o

Massive caffeine ingestions can yield detectable or toxic theophylline determ inations with conventional lab testing.



CBC



Electrolytes: o



Transient hypokalem ia

Serum acetam inophen level (for intentional ingestions)

Imaging 

KUB (kidneys, ureters, bladder): o

Undissolved sustained-release tablets or pharm acobezoars m ay appear as radiopacities.

o 

Bead-filled capsules m ay appear as radiolucencies.

Ultrasound of stom ach m ay detect intact sustained-release dosage form s.

Differential Diagnosis

Pa ge 4 7 3



Caffeine/Î²-agonist bronchodilator overdose



Am phetam ines



Sym pathom im etics



Anticholinergic agents



Drug withdrawal syndrom es



Pheochrom ocytom a



Thyrotoxicosis

P.1113

Treatment Pre Hospital Alert Bring pill bottles/pill sam ples in suspected overdose.

Initial Stabilization 



Airway, breathing, and circulation m anagem ent (ABCs): o

Cardiac m onitor

o

Isotonic crystalloids as needed for hypotension

Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status



Cardiovascular: o

Initiate beta-blockers or calcium channel blockers for rate control with supraventricular tachyarrhythm ia: 

Adenosine is antagonized by theophylline and will not be effective.

o

Adm inister isotonic crystalloid intravenous fluid resuscitation for hypotension: 

With treatm ent failure, consider beta-blocker to

Pa ge 4 7 3

reverse theophylline-induced Î² 2 -receptorâ€“stim ulated vasodilation. 

If vasopressors are needed, choose pressor that is not a Î²-agonist, such as phenylephrine.

o 

Treat ventricular dysrhythm ias conventionally.

Seizures: o

Adm inister benzodiazepines.

o

Phenytoin is contraindicated; it is usually ineffective and m ay paradoxically worsen seizures in theophylline intoxications.

ED Treatment Decontamination 

Perform gastric lavage for severe (â‰¥50 m g/kg) acute overdoses presenting within 1 hour of ingestion: o

Ensure airway is adequately m aintained prior to initiating lavage.



Adm inister activated charcoal.



Adm inister cathartics with first dose only of activated charcoal.



Multidose charcoal: o

Especially with sustained-release products

o

Binds theophylline, which back-diffuses to sm all intestine



o

For m ild to m oderate toxicity

o

25 g q2h until theophylline level â‰¤20 m g/L

Initiate whole-bowel irrigation with sustained-release products: o

Adm inister until a clear, colorless rectal effluent or serum theophylline <20 m g/L

o 

1â€“2 L/h of polyethylene glycol

Treat protracted vom iting with m etoclopram ide or 5-HT 3

Pa ge 4 7 3

-receptor antagonists. 

Avoid ipecac.

Electrolyte Disturbances 

Treat hypokalem ia in acute ingestions cautiously: o

Relative hypokalem ia owing to Î²-receptorâ€“m ediated intracellular shift of extracellular potassium

o

Aggressive correction leads to potentially serious hyperkalem ia as theophylline concentrations decrease.



Most electrolyte im balances respond to beta-blocker therapy: o

Generally not indicated because of absence of associated m orbidity and potential for beta-blockerâ€“induced bronchospasm in pulm onary patients

Extracorporeal Elimination 

Hem operfusion: m ore efficacious



Hem odialysis: faster availability



Initiate hem odialysis or hem operfusion if theophylline level: o

Greater than or equal to 100 m g/L in acute ingestions

o

Greater than or equal to 60 m g/L in acute-on-chronic or chronic intoxications

Medication (Drugs) 

Activated charcoal: 1g/kg PO, if dose ingested is known, 10 g/1 g theophylline ingested, no one dose >100 g



Diazepam : 0.1 m g/kg IV q5â€“10m in until seizures controlled, up to 30 m g

Pa ge 4 7 3



Diltiazem : 0.25 m g/kg IV bolus; m ay repeat after 15 m inutes, then 5â€“15 m g/h infusion for control of heart rate in patients with contraindication to beta-blockade



Esm olol: 500 Âµg/kg IV bolus, followed by 50 Âµg/kg/m in infusion; increase by 50 Âµg/kg/m in increm ents to m ax. of 200 Âµg/kg/m in



Metoclopram ide: 10 m g IV bolus; m ay repeat to m ax. of 1 m g/kg



Ondansetron: 0.15 m g/kg IV bolus up to m ax. of 32 m g total



Polyethylene glycol (high m olecular weight): 1â€“2 L/h via nasogastric tube

Follow-Up Disposition Admission Criteria 

Acute overdoses with serum theophylline concentrations >100 m g/L



Acute-on-chronic or chronic theophylline with either serum concentration >60 m g/L or patient >60 years old



Seizures, or fluid and vasopressor refractory hypotension in a patient with serum theophylline concentration >30 m g/L



Unchanged or rising serial serum theophylline concentrations (two or m ore) >30 m g/L in acute or acute-on-chronic ingestion of sustained-release theophylline

Discharge Criteria 

Two consecutive (â‰¥2 hours apart) decreasing serum

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theophylline concentrations with m ost recent concentration <30 m g/L 

Mildly sym ptom atic or asym ptom atic patient m eeting above criterion and no evidence of suicidal intention

References 1. Henderson A, Wright DM, Pond SM. Managem ent of theophylline overdose patients in the intensive care unit. Anaesth Intensive Care. 1992;20:56â€“62. 2. Olson KR, Benowitz NL, Woo OF, et al. Theophylline overdose: acute single ingestion vs. chronic repeated overm edication. Am J Em erg Med. 1985;3:386â€“394. 3. Shannon MW. Com parative efficacy of hem odialysis and hem operfusion in severe theophylline intoxication. Acad Em erg Med. 1997;4:674â€“678. 4. Shannon MW. Life-threatening events after theophylline overdose. Arch Intern Med. 1999;159:989â€“994. 5. Stork CM, Howland MA, Goldfrank LR. Concepts and controversies of bronchodilator overdose. Em erg Med Clin North Am . 1994;12:415â€“436.

Codes ICD9-CM 974.1 Poisoning by water, m ineral and uric acid m etabolism drugs; purine derivative diuretics

ICD10 T48.6 Poisoning by agents prim arily acting on sm ooth and skeletal m uscles and the respiratory system ; antiasthm atics, not elsewhere classified

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tho racic Outlet Syndro m e

Thoracic

Outlet Syndrome Anna Cheh

Basics Description 

Sym ptom s produced by com pression at the thoracic outlet of the brachial plexus, subclavian vein, or subclavian artery



Subdivided into three categories depending on the predom inant sym ptom s: o

Neurologic 

About 95% of patients



Prevalence is higher in fem ales.



True (1â€“3%)â€”those with objective findings



Disputed (90%)â€”those with no or lim ited objective findings

o

Venous: 

Com pression or throm bosis of the subclavian vein

o



4% of patients



Prevalence is higher in m en age 20â€“35 years

Arterial:

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

Rareâ€” <1%



Men and wom en are equally affected.



Bim odal age distribution of young adults and patients >50 years of age



Bony abnorm alities (cervical rib, first thoracic rib, or clavicle) are the m ost com m on causes.



Right extrem ity is m ore com m only affected.

Etiology 



Sagging m usculature with descent of the shoulder girdle: o

Aging

o

Obesity

o

Heavy breasts

Droopy shoulder syndrom e (weakness of the trapezius m uscle)



Inadequate intrascalene triangle: o



Anterior or m iddle scalene hypertrophy or spasm

Anatom ic anom alies: o

Congenital bands

o

Supernum erary ribs

o

Cervical rib

o

High, rudim entary, or anom alous first thoracic rib

o

Congenital or traum atic laxity of the costoclavicular joint



o

Separation of the sternoclavicular joint

o

Anom alous m uscles: 

Axillopectoral m uscle



Chondroepitrochlear m uscle



Subscapularis-teres-latissim us m uscle

Traum a: o

Fracture of the clavicle

o

Injuries to the cervical vertebrae

o

Dislocation of the head of the hum erus

Pa ge 4 7 4

Diagnosis Signs and Symptoms History 

May be positional or exacerbated by repetitive use (i.e., working overhead)



Supraclavicular tenderness



Usually insidious in onset and progressive



Can occur or worsen suddenly after traum a



True neurogenic: o

Caused by congenital anatom ical anom alies

o

Pain

o

Paresthesias

o

Num bness

o

Weakness of the arm and hand: 

o 

Usually in C8â€“T1 nerve distribution

Vasom otor sym ptom s

Disputed neurogenic: o

Often associated with traum a

o

Includes above sym ptom s but not in a neuroanatom ic distribution

o

Protean of other com plaints of the shoulder, neck, head, and chest

Physical Exam 

General: o

o

Shoulder asym m etry: 

Drooping



Hypertrophy

Deform ity of the clavicle

Pa ge 4 7 4

o 





Cervical rib on palpation of the supraclavicular area

Arterial com pression: o

Supraclavicular bruit

o

Dim inished pulse

o

Ischem ic sym ptom s: 

Cool



Claudication



Color changes

Venous com pression: o

Venous engorgem ent

o

Arm swelling

o

Edem a

Neurological com pression: o

Elevated arm stress test (EAST): 

Evaluates arterial, venous, and neurologic thoracic outlet syndrom e (TOS)



Arm s abducted 90Â° from the thorax and elbows flexed at 90Â°



Shoulders braced slightly back of the frontal plane



Fists are open and closed for 3 m inutes.



Early heaviness and fatigue of the arm



Gradual onset of hand num bness



Progressive aching through the arm and top of shoulder

o

Adson test: 

Arm down, patient rotates head toward extrem ity, looks up, and inhales.

 o

Not as reliable as EAST

During testing: 

Check for pulse dim inution.



Reproduction/Exacerbation of sym ptom s

Pa ge 4 7 4



If radial pulse is norm al during the test, a neurologic cause should be suspected.



Neither test is very sensitive nor specific.

P.1115

Essential Workup 

Careful history and physical exam



ECG to rule out cardiac ischem ia

Tests Imaging 

Perform as outpatient except in case of lim b-threatening ischem ia and/or suspicion of venous throm bus



Chest radiograph: o

o 



Assess for anatom ic abnorm alities: 

First rib



Cervical rib



Clavicle deform ity

Pulm onary disease

Cervical spine series: o

Fracture

o

Scoliosis

Arteriogram : o

Indications: 

Obliteration of the radial pulse on EAST



Blood pressure is 20 m m Hg less than the opposite lim b.





Suspected subclavian stenosis



Bruit or abnorm al supraclavicular pulsations



Peripheral em boli in the upper extrem ity

Venography:

Pa ge 4 7 4

o

Indicated if edem a, peripheral unilateral cyanosis, or distended thoracic and extrem ity veins



Neurogenic TOS: o

No gold standard testâ€”diagnosis rem ains m ostly clinical.

o

Nerve conduction studies helpful in confirm ing the clinical diagnosis and in identifying other disorders in the differential diagnosis

o

MRI required to assess for spinal cord disease or a herniated cervical disk

Differential Diagnosis 

Cardiac ischem ia



Cervical spondylosis or disk disease



Carpal tunnel syndrom e or nerve entrapm ents



Pancoast tum or; other neck/m ediastinum m alignancies



Neuritis



Myositis



Raynaud disease



Multiple sclerosis or degenerative spinal cord disease



Shoulder inflam m atory diseasesâ€”arthritis, rotator cuff injury, bicipital tendonitis



Atherosclerotic or throm boem bolic disease

Treatment ED Treatment 

Heparinization if signs of arterial or venous throm bosis



Vascular surgery consult for signs of ischem ia



Initial m anagem ent: o

The m ajority im prove with conservative treatm ent

Pa ge 4 7 4

consisting of physical therapy and m edications for sym ptom atic relief. 

Surgery reserved for failure of m edical therapy: o

70â€“90% of patients experience som e to com plete relief postoperatively

Medication (Drugs) 

Cyclobenzaprine (Flexeril): 10 m g PO t.i.d.



Diazepam : 5 m g PO t.i.d.



Ibuprofen: 800 m g PO t.i.d.



Methocarbam ol (Robaxin): 1,000â€“1,500 m g PO t.i.d.



Soothing linim ents or ointm ents

Follow-Up Disposition Admission Criteria 

Ischem ia



Venous throm bosis



Arterial throm bosis



Intractable pain

Discharge Criteria 

Nonâ€“lim b-threatening neurologic findings



Absence of arterial or venous throm bosis

Issues for Referral Neurologic, orthopaedic, or vascular surgery consultation is indicated according to the pathologic condition.

References

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1. Atasoy E. Thoracic outlet com pression syndrom e. Orthop Clin North Am . 1996;27:265â€“303. 2. Mackinnon SE, Novak CB. Thoracic outlet syndrom e. Curr Probl Surg. 2002;39(11):1070â€“1145. 3. Hand Clin. 2004;20(1)

Miscellaneous SEE ALSO: http://www.ninds.nih.gov

Codes ICD9-CM 353.0

ICD10 G54.0

Pa ge 4 7 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Thro m bo tic Thro m bo cyto penic Purpura

Thrombotic Thrombocytopenic Purpura Timothy Pavek

Basics Description 

Throm botic throm bocytopenic purpura (TTP) is a severe disorder of abnorm al clotting affecting m ultiple organ system s.





Classically characterized by pentad of: o

Throm bocytopenia

o

Hem olytic anem ia

o

Mild renal dysfunction

o

Neurologic signs

o

Fever

Associated with acquired or congenital deficiency of plasm a von Willebrand factorâ€“cleaving protease (VWFcp).

Classic Course 

Acute onset



Fulm inant course lasting days to a few m onths



Nearly always fatal outcom e without treatm ent:

Pa ge 4 7 4



o

Greater than 90% m ortality without treatm ent

o

Reverses to >90% survival with m odern treatm ent

Clinical presentations include: o

Idiopathic

o

Fam ilial, chronic or relapsing

o

Drug-induced: 

Allergic or im m une m ediated (quinine, ticlopidine, clopidogrel)



Dose-related toxicity (m itom ycin C, cyclosporine)

o

Pregnancy, postpartum associated: 

10â€“25% of cases

o

Bone m arrow transplantation associated

o

Infection



More com m on in the 3rdâ€“6th decades of life



Uncom m on in pediatric or geriatric populations



Wom en affected about twice as frequently as m en

Etiology 

Unknown prim ary stim ulant; possibly system ic endothelial cell dam age results inactivation of coagulation pathway



Platelet aggregation and fibrin deposition occurring in arterioles and capillaries leading to m icrothrom bi and obstruction to blood flow



Platelet aggregation leads to: o

Consum ption of platelets in excess of bone m arrow's ability to respond, producing throm bocytopenia

o 

Widespread m icrovascular hyaline throm botic lesions

Microvasculature obstruction with platelet aggregates leads to: o

Red cell hem olysis

o

Accum ulation of hem e breakdown products

o

Anem ia

Pa ge 4 7 4



End organ ischem ia results from diffuse throm bosis in sm all vessels: o

Most com m on in heart, brain, kidney, pancreas, and adrenal glands

o 

Lungs and liver relatively spared

Deficiency of vWF-cleaving protease causes failure of control of coagulation pathway.

Genetics 

Som e cases are genetic/fam ilial.



VWFcp was recently identified as new m em ber of ADAMTS fam ily and designated ADAMTS13.



Mutations in ADAMTS13 gene cause autosom al recessive form of chronic relapsing TTP.

Diagnosis Signs and Symptoms Five Major Clinical Features: Classic Pentad 

Throm bocytopenia: o



Microangiopathic and hem olytic anem ia: o



Platelet count <20,000/m m 3

Hb <10 g/dL (<6 g/dL in 40%)

Neurologic sym ptom s: o

Presenting com plaint in 60%, occur in 90%

o

Typically fluctuating

o

Headache

o

Altered m entation (confusion, stupor, com a)

o

Behavioral or personality changes

o

Focal sensory or m otor deficits or aphasia

o

Seizures

Pa ge 4 7 5

o 



Spontaneous intracranial hem orrhage

Renal insufficiency: o

Usually m ild

o

Creatinine <3.0 m g/dL

Fever: o

Occurs in acute episodes and prodrom al syndrom es

History 









General: o

Weakness

o

Fatigue

o

Fever

o

Malaise

Hem orrhage: o

Easy bruising

o

Epistaxis

o

Menorrhagia

o

GI bleeding

o

Loss or change in vision

GI com plaints: o

Nausea

o

Anorexia

o

Diarrhea

o

Abdom inal pain

Neurologic: o

Headache

o

Confusion

o

Seizure

o

Behavioral or personality changes

o

Focal sensory or m otor deficits or aphasia

Changes in vision or blindness

Physical Exam

Pa ge 4 7 5



Purpura



GI hem orrhage: hem atem esis, hem atochezia, m elena



Epistaxis



Jaundice



Shock



Altered m ental status (confusion, stupor, com a)



Focal sensory or m otor deficits



Pulm onary infiltrates and edem a



Alteration of vision, retinal hem orrhage or detachm ent, occlusive retinopathy (Purtscher retinopathy)



Abnorm alities of cardiac conduction

Essential Workup Clinical Diagnosis 

Because of success of treatm ent, base diagnosis on: o

o 

Identification of two m ajor findings: 

Throm bocytopenia



Microangiopathic hem olytic anem ia

Exclude other m ajor differential diagnoses.

Com prehensive history and physical exam with directed laboratory testing targeted at identification of m ajor sym ptom s and signs, com plications, and exclusion of m ajor differential diagnoses



Identify possible drug-associated disease and avoid reexposure.

Tests Lab 

CBC/platelet count/reticulocyte count: o

Anem ia: hem oglobin <10 g/dL

o

Throm bocytopenia <20,000/m m 3

o

Increased reticulocyte count

Pa ge 4 7 5



Coagulation studies: o





Peripheral blood sm ear: o

Macroangiopathic changes

o

Schistocytes

o

Helm et cells

o

Nucleated RBCs

Coom bs test: o



Norm al

Negative direct Coom bs test

Electrolytes, BUN, creatinine, glucose: o

Mild elevation of BUN, creatinine

o

Hyperkalem ia owing to RBC lysis

P.1117



Lactate dehydrogenase (LDH): o

Elevated five to ten tim es

o

Elevated owing to both hem olysis and diffuse tissue ischem ia



Bilirubin: o



Urinalysis: o



Increased unconjugated bilirubin

Hem aturia (m icroscopic to gross)

ADAMTS13 assay m ay be used to distinguish chronic recurring TTP, TTP secondary to presence of ADAMTS13 inhibitor, and hem olytic-urem ic syndrom e (HUS). o

ADAMTS13 deficiency does not detect all patients who m ay respond to plasm a exchange transfusions.

Diagnostic Procedures/Surgery 

Biopsy: o

Confirm s diagnosis

o

Reveals hyaline lesions in sm all vessels

Pa ge 4 7 5

o

Contraindicated during fulm inant presentation (hem orrhage risk)



EEG: o

To predict need for anticonvulsant therapy

Imaging CT head: 

For altered m ental status to rule out intracranial hem orrhage

Differential Diagnosis 

HUS: o

Triad of throm bocytopenia, schistocytosis, and renal dysfunction



o

Neurologic sym ptom s unusual

o

Often preceded by infectious prodrom e and diarrhea

Dissem inated intravascular coagulation: o

Causes deposition of fibrin in m icrovasculature and not hyaline

o 



Coagulation studies abnorm al

Idiopathic throm bocytopenic purpura (ITP): o

No evidence of hem olysis

o

LDH and bilirubin norm al

Pregnancy-related throm bocytopenia: o

Pre-eclam psia, eclam psia

o

Pregnancy-associated hem olysis

o

HELLP (hem olysis, elevated liver enzym es, and low platelets)



Evans syndrom e: o

Autoim m une hem olytic anem ia

o

Prom inence of m icrospherocytes rather than schistocytes

o

Positive direct Coom bs test

Pa ge 4 7 5



Malignant hypertension



Bacterial sepsis



Subacute bacterial endocarditis



Autoim m une disorders (e.g., system ic lupus erythem atosus [SLE])



Dissem inated m alignancy



Heparin-associated throm bocytopenia



Prosthetic valves or severely calcified aortic stenosis

Treatment Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)



0.9% norm al saline (NS) IV fluid resuscitation for shock or GI hem orrhage



RBC transfusions: o



For significant anem ia or bleeding com plications

Platelet transfusions: o

Reserve for life-threatening hem orrhage (e.g., CNS bleeds) or required invasive procedures

o

May aggravate the throm botic, m icrovascular obstructive process and worsen the end organ ischem ia and shock

ED Treatment 

Fresh frozen plasm a (FFP) or fresh unfrozen plasm a: o

Initiated as bridge to exchange transfusions on diagnosis of TTP

o

Success rate approaching 64%

o

Provides a platelet-antiaggregating factor absent or dim inished in patient's own serum

Pa ge 4 7 5

o

Used prophylactically to prevent recurrence in chronic relapsing variant



Plasm a exchange transfusions: o

Most im portant com ponent of treatm ent

o

Com bination of plasm apheresis and infusion of FFP

o

Plasm apheresis rem oves: 

Im m une com plexes responsible for endothelial dam age and initiation of TTP



Circulating proaggregation factors prom oting platelet aggregation

o

o

Perform daily until: 

Platelet count norm alizes



Neurologic sym ptom s im prove



LDH norm alizes

Im provem ent of renal function m ay lag behind other findings.

o

Taper frequency based on em piric judgm ent of response; m ay need to resum e if relapse occurs.

o



Com plications include: 

Allergy or serum sickness



Secondary infection



Hypotension

Corticosteroids: o

Unproven therapeutic benefit

o

May lim it im m unologically m ediated endothelial dam age and decrease splenic sequestration of platelets and dam aged RBCs

o

Supportive benefit if adrenal glands dam aged through hem orrhage or ischem ia



Antiplatelet or im m unosuppressive drugs: o

Aspirin and dipyridam ole m ost com m only used

o

Sulfapyrazine, dextran, and vincristine use have been

Pa ge 4 7 5

reported.





o

Used with variable effectiveness

o

Can worsen bleeding com plications

o

Heparin is ineffective.

Splenectom y: o

Historically recom m ended

o

Of uncertain efficacy

Dialysis: o

For renal failure

Medication (Drugs) 

Aspirin: 325â€“650 m g PO q4hâ€“q6h



Dipyridam ole: 75â€“100 m g PO q.i.d.



FFP: o

Plasm a infusion: 30 m L/kg/d (75â€“100 m L/h)

o

Plasm a exchange transfusion: 3â€“4 L/d



Methylprednisolone: 0.75 m g/kg q12h



Prednisone: 1â€“2 m g/kg/d (high dose up to 200 m g/d)



Vincristine: 2 m g IV q4dâ€“q7d for 4 doses

Follow-Up Disposition Admission Criteria 

Newly diagnosed serious platelet disorder, especially with bleeding com plications or altered m ental status or renal dysfunction



ICU adm ission for TTP with active bleeding or neurologic findings:

Pa ge 4 7 5

o

Transport to tertiary care center with appropriate specialty care facilities.

References 1. Elliot MA, Nichols WL. Throm botic throm bocytopenic purpura and hem olytic urem ic syndrom e. Mayo Clin Proc. 2001;76:1154â€“1162. 2. Proia A, Paesano R, Torcia F, et al. Throm botic throm bocytopenic purpura and pregnancy: a case report and a review of the literature. Ann Hem atol. 2002;81(4):210â€“214. 3. Reddy PS, Deauna-Lim ayo D, Cook JD, et al. Rituxim ab in the treatm ent of relapsed throm botic throm bocytopenic purpura. Ann Hem atol. 2005;84(4):232â€“235. 4. Vesely SK, George JN, Lam m le B, et al. ADAMTS13 activity in throm botic throm bocytopenic purpura-hem olytic urem ic syndrom e: relation to presenting features and clinical outcom es in a prospective cohort of 142 patients. Blood. 2003;102(1):60â€“68.

Codes ICD9-CM 446.6

ICD10 M31.1

Pa ge 4 7 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Thum b F racture

Thumb Fracture

John MacKay Jr.

Basics Description 

Distal phalangeal fractures: o

Blunt traum a, hyperextension of the thum b, axial loading of the thum b

o

Tuft fracture is a fracture sim ilar to that in other digits in which the distal phalanx is crushed and fragm ented.

o

It m ay be open or closed and associated with nailbed injury.

o 

It is treated as a soft tissue injury.

Proxim al phalangeal fractures and thum b m etacarpal fractures: o

Blunt traum a to the thum b: 

Axial loading of the thum b with the m etacarpal phalangeal (MP) joint flexed, hand closed or the thum b MP joint otherwise stabilized

o

Bennett fracture: 

Oblique intra-articular fracture of the ulnar aspect of the base of the thum b m etacarpal with the larger distal fragm ent displaced

Pa ge 4 7 5

o

Rolando fracture: 

Com m inuted Y-shaped intra-articular fracture of the ulnar base of the thum b m etacarpal with the large distal fragm ent displaced

Etiology 

Falls



Motor vehicle accidents



Sports, especially downhill or alpine skiing



Basketball



Baseball



Football



Rugby

Diagnosis Signs and Symptoms 

Pain, swelling, and deform ity of the thum b



Exam should include the thenar em inence for pain or deform ity.



The thum b m ay be rotated distal to the fracture site.



The base of the thum b m ay appear radially deviated relative to the rest of the hand in the resting position.



Occasionally, there m ay be dam age to the thum b digital nerves.

Pediatric Considerations 

Fractures to the thum b som etim es occur in children. o

Consider nonaccidental traum a.

o

Do not neglect appropriate pain m anagem ent in children.

Physical Exam

Pa ge 4 7 6

Im m obilize thum b pending definitive evaluation.

Essential Workup Radiography as noted below

Tests Imaging 

Plain radiography of affected areas



Avoid testing stress of thum b m etacarpophalangeal joint, as in testing for gam ekeeper thum b, until all plain radiography is com plete.

Differential Diagnosis 

Extra-articular fracture of the base of the thum b m etacarpal



Scaphoid fracture



Gam ekeeper thum b

P.1119

Treatment Pre Hospital 

Dress open wounds.



Im m obilization in neutral position



Elevation and cold to reduce swelling



Age-appropriate social m anagem ent

Initial Stabilization Im m obilize thum b pending definitive evaluation.

ED Treatment

Pa ge 4 7 6



Thum b spica splint with the thum b in neutral position, as if holding a beverage can



Splint instructions should be provided to patient.

Medication (Drugs) Pain control with oral analgesic preparations

Surgery 

72-hour orthopedic referral



Counsel patient that there is a strong likelihood of the need for operative repair.

Follow-Up Disposition Admission Criteria Open fracture, presence of m ultiple traum a, or other m ore serious injuries

Discharge Criteria Closed injuries, referral, and explain frequent need for operative fixation

Issues for Referral 72-hour orthopaedic referral

References 1. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 2nd ed. New York, NY: Churchill Livingstone; 1983. 2. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York, NY: Churchill

Pa ge 4 7 6

Livingstone; 1990. 3. Antosia RE, Lyn E. Hand. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosbyâ€“Year Book; 2002: 493â€“506. 4. Chaffin TH. Phalangeal fractures. In: Hart RG, Uehara DT, Wagner MJ, et al., eds. Em ergency and Prim ary Care of the Hand. Dallas, Tex: ACEP; 2001:111â€“122. 5. Sullivan JH, Tsonis GD. Metacarpal fractures. In: Hart RG, Uehara DT, Wagner MJ, et al., eds. Em ergency and Prim ary Care of the Hand . Dallas, Tex: ACEP; 2001:99â€“110.

Codes ICD9-CM 816.00 Fracture of one or m ore phalanges of hand, closed

ICD10 S62.5

Pa ge 4 7 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tibial Plateau F racture

Tibial Plateau

Fracture Binh T. Ly

Basics Description 

Synonym : tibial condylar fracture



Fracture or depression of the proxim al tibial articulating surface



Valgus or varus force applied in com bination with axial loading: o

Lateral plateau fractures: 

Occurs classically after pedestrian struck by a vehicle bum per



Lateral aspect of the knee with a m edially directed force

o

Medial plateau fractures are m uch less com m on and require significant force.



Younger patients are m ore resistant to depressed plateau fractures.



Elderly patients are m ore prone to depression-type fractures.

Schatzki Classification of Plateau Fractures

Pa ge 4 7 6



Type 1: o

Split fracture of the lateral tibial plateau without depression of the plateau

o

Occurs in younger patients

o

Cancellous bone of the plateau resists depression.

o

Usually occurs from a valgus force in com bination with axial load



Type 2: o

Com bination of split fracture and depression of lateral plateau

o

The m echanism is sim ilar to type 1 injury.

o

Patients tend to be in their fourth decade of life or older.

o 





Have weaker subchondral bone

Type 3: o

Local depression of the lateral plateau

o

Injuries m ay be unstable.

Type 4: o

Fracture/Depression of the m edial plateau

o

Requires m uch m ore force (varus and axial loading)

o

Be suspicious for associated injuries.

o

Dam age to other structures: 

Popliteal artery



Peroneal nerve



Lateral collateral ligam ent



Medial m eniscus



Cruciate ligam ents

Type 5: o

Bicondylar fracture

o

High-energy injury

o

Associated injuries: 

Popliteal vessel injury

Pa ge 4 7 6





Peroneal nerve injury



Com partm ent syndrom e

Type 6: o

Bicondylar, grossly com m inuted fracture of the plateau

o

Diaphyseal-m etaphyseal dissociation

o

Violent force, usually a fall from a height

o

Associated neurovascular injuries and com partm ent syndrom e

Etiology Mechanism of Injury 

Fall from a height causing fem oral condyles to im pact on tibial surface



Vehicle bum per injury (forces directed lateral to m edial)



Violent twisting force (e.g., skiing)



Associated injuries include: o

Ligam entous (collaterals, cruciates)

o

Meniscal

o

Neurovascular (peroneal nerve and popliteal vessels)

Pediatric Considerations 

Tibial plateau fractures are rare in children: o

Dense cancellous bone of the tibial plateau

Diagnosis Signs and Symptoms 

Painful, swollen knee



Inability to bear weight



Knee effusion (hem arthrosis)



Lim ited active and passive range of m otion of the knee

Pa ge 4 7 6



Tenderness along the proxim al tibia and joint line



Possible varus or valgus deform ity of the knee



Possible joint instability due to associated ligam entous injury

Physical Exam Decision aids for the use of radiography: 

Ottawa knee ruleâ€”knee radiographs are indicated if any of the following are present: o

Age >55 years

o

Tenderness of the fibular head

o

Isolated patellar tenderness

o

Inability to flex to 90Â°

o

Inability to transfer weight for four steps both im m ediately after the injury and in the ED

o 

Lim ping is allowed.

Pittsburgh knee ruleâ€”knee radiographs are indicated in fall or blunt traum a and the following are present: o

Age <12 or >55 years 

Pittsburgh knee rule should be applied with caution to patients <18 years old.

o

Inability to bear weight fully for four steps on both toe pads and heel pad of each foot

o 

Lim ping is not allowed.

Neurovascular exam ination: o

High-energy m echanism carries risk for neurovascular injury and com partm ent syndrom e.

o

Check popliteal, posterior tibial, and dorsalis pedis pulses.

o

Check integrity of peroneal nerve: 

Ankle and great toe dorsiflexion



Sensation in dorsal webspace between great and second toes

Pa ge 4 7 6



Plain radiography: o

Anteroposterior (AP) and cross-table lateral views of the knee and proxim al tibia

o

Cross-table lateral view m ay dem onstrate lipohem arthrosis (fat-fluid level).

o

Oblique views m ay identify fractures not apparent on other film s.

o

Pay attention to areas of ligam entous attachm ent where avulsion fractures m ay take place: 

Medial and lateral fem oral condyles



Tibial spine (intercondylar em inence)



Fibular head

P.1121

Tests Imaging 

Tibial plateau view: o

AP view with the knee in 10â€“15Â° of flexion helps visualize depressions.



Sunrise view of the patella: o

Useful in identifying fractures of the patella not visualized on AP or lateral views



CT scan m ay reveal occult fractures not seen on plain radiographs: o

Further delineates extent of fractures



MRI can be used to better elucidate soft tissue injuries.



Arthrocentesis to look for fat globules: o

If m echanism strongly suggests fracture

o

Effusion present without fracture on plain radiographs.

Pa ge 4 7 6





Arteriography is indicated if: o

High-energy m echanism

o

Schatzker type 4, 5, or 6 fracture

o

Alteration in distal pulses

o

Expanding hem atom a

o

Bruit

o

Injury to anatom ically related nerves

Com partm ent pressure m easurem ents are indicated if: o

Pain not over fracture site

o

Pain on passive stretch

o

Paresthesias

o

Abnorm ality of pulses

o

Intracom partm ental pressures >30 m m Hg are an indication for em ergent orthopaedic consultation.

Differential Diagnosis 

Knee dislocation



Proxim al fibula fracture



Fem oral condyle fracture



Patella fracture



Tibial subcondylar fracture



Tibial tuberosity fracture



Tibial spine fracture



Cruciate ligam ent tears



Collateral ligam ent tears



Meniscal tears

Pediatric Considerations Include oblique views as part of routine radiography.

Treatment

Pa ge 4 7 6

Pre Hospital Cautions: 

In high-energy m echanism s, associated m ajor injuries take precedence.



Im m obilize to prevent further neurological or vascular injury.

Initial Stabilization 

Stabilization of the m ultiple-injury traum a patient



Long-leg splint



Ice



Elevation



Frank dislocations with vascular com prom ise m ay need im m ediate reduction in ED.

ED Treatment 

Nonâ€“weight-bearing



Pain control



Nondisplaced fractures or m inim ally displaced (<8 m m ) lateral plateau fractures without ligam entous injury: o

Aspiration of hem arthrosis and injection of local anesthetic

o

Exam ination for ligam entous instability

o

If knee is stable:

o



Com pressive dressing



Ice and elevation for 48 hours



Nonâ€“weight-bearing/crutches

If knee is unstable, then urgent orthopaedic consultation is warranted.



Open fractures: o

Rem ove contam inants.

o

Apply m oist sterile dressing.

o

Assess tetanus im m unity.

Pa ge 4 7 7

o

Antibiotics

o

Em ergent orthopaedic consultation

Medication (Drugs) 

Open fractures



Cefazolin: 2 g IV (peds: 50 m g/kg)



Gentam icin: 2â€“5 m g/kg IV (peds: 2.5 m g/kg)



Tetanus toxoid if indicated



Vancom ycin: 1 g IV loading dose (peds: 10 m g/kg) if penicillin allergy

Follow-Up Disposition Admission Criteria 

Open fractures for debridem ent, irrigation, and IV antibiotics



Com m inuted, bicondylar fractures for traction



High-energy m echanism s for observation of neurovascular status and developm ent of com partm ent syndrom e



Pain control

Discharge Criteria Nondisplaced or m inim ally displaced, stable fractures of the lateral plateau

References 1. Em paranza JI, Aginaga JR. Validation of the Ottawa Knee Rules. Ann Em erg Med. 2001 Oct;38(4):364â€“368. 2. Seaberg DC, Yealy DM, Lukens T, et al. Multicenter com parison of

Pa ge 4 7 7

two clinical decision rules for the use of radiography in acute, high-risk knee injuries. Ann Em erg Med. 1998;32:813. 3. Sim on RR, Koenigsknecht SJ. Em ergency Orthopedics: The Extrem ities. 4th ed. New York, NY: McGraw-Hill; 2001. 4. Stiell IG, Greenberg GH, Wells GA, et al. Prospective validation of a decision rule for the use of radiography in acute knee injuries. JAMA 1996;275(8):611â€“615. 5. Watson JT, Wiss DA. Fractures of the proxim al tibia and fibula. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's Fractures in Adults, 5th ed. Philadelphia, PA: Lippincott William s & Wilkins; 2001:1801â€“1838.

Codes ICD9-CM 823-00

ICD10 S82.1

Pa ge 4 7 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tibial/F ibular Shaft F racture

Tibial/Fibular

Shaft Fracture Tyler F. Vadeboncoeur Seth K. Williams

Basics Description Fracture Description 

Tibia



Open versus closed



Extent of soft tissue dam age



Gustilo-Anderson classification of open fractures: o

o

o

Type I: 

Wound <1 cm



Little soft-tissue dam age



No crush injury

Type II: 

Wound >1 cm



Moderate soft-tissue dam age



Little or no devitalized soft tissue

Type IIIâ€”severe soft-tissue injury: 

Aâ€”adequate soft-tissue coverage of bone



Bâ€”tissue loss/periosteal stripping

Pa ge 4 7 7

 

Câ€”neurovascular injury requiring surgery

Anatom ic location: o

Proxim al, m iddle, or distal third

o

Articular extension



Displacem ent



Degree of shortening



Angulation



Configuration: o

Spiral, transverse, or oblique

o

Com m inuted, with butterfly fragm ent or m ultiple fragm ents



Fibula: o

Proxim al: 

Associated with peroneal nerve injury



Disruption of ankle syndesm osis (Maisonneuve fracture)

o

Middle

o

Distal

Pediatric Considerations 



Nonphyseal fracture patterns: o

Com pression (torus)

o

Incom plete tension-com pression (greenstick)

o

Plastic/Bowing deform ity of fibula m ay occur.

o

Com plete fractures

Physeal fracture patterns: o

Tibial shaft fractures m ay extend to the physis in Salter-Harris II pattern.

Etiology 

High-energy versus low-energy injury



Am ount of soft-tissue injury is prognostic and is determ ined by the degree of energy involved.

Pa ge 4 7 7



Indirect forceâ€”frequently low-energy traum a: o

Rotary and com pressive forces often result in oblique and spiral fractures. 



Skiing, fall, child abuse

Direct forceâ€”high-energy traum a: o

Direct blow to leg often results in transverse and com m inuted fractures. 

Pedestrian versus auto, m otor vehicle crash (MVC)

o

Bending force over a fulcrum often produces com m inution with a wedge-shaped butterfly fragm ent. 

Skier's boot top, football tackle, MVC

Pediatric Considerations 

Bicycle spoke injury: o

Foot and lower leg get caught between fram e and wheel spoke.

o

Crush injury is the prim ary problem .

o

Initial benign appearance of the soft tissues is often deceiving: 

o

Full-thickness skin loss can occur in days.

Orthopaedic surgery consultation should be obtained on all spoke-injury patients with associated fractures.



Toddler fracture: o

Spiral fracture involving the distal third of the tibia with intact fibula secondary to rotational force (turning on planted foot)

o

Age range is 9 m onths to 6 years, m ost often when learning to walk.

o

Fractures in m idshaft or m ore transverse are suspicious of nonaccidental traum a.

Pa ge 4 7 7

Diagnosis Signs and Symptoms History 

History of traum a



Pain usually im m ediate, severe, and well localized to the fracture site

Physical Exam 

Visible or palpable deform ity at the fracture site



Significant soft-tissue dam age with high-energy traum a



Inability to bear weight if tibia involved: o



May be able to walk if isolated fibula fracture

Foot drop on affected leg from peroneal nerve injury as it wraps around fibular head



Com partm ent syndrom e

Pediatric Considerations 

Rely on parents for historical inform ation.



Child m ay present lim ping with no obvious deform ity.

Essential Workup 

Careful assessm ent of soft tissues



Careful neurovascular exam ination (com pare with contralateral side)



Exam ine for associated injuries.



Com pletely expose patient and put into gown.



Assessm ent for com partm ent syndrom e

Alert Compartment Syndrome 

Relatively com m on com plication of tibia fractures and m ay

Pa ge 4 7 7

not appear until 24 hours after injury 

Pain disproportionate from that expected



Swollen, tight com partm ent, with pain on palpation of com partm ent



Pain on passive stretch of foot, toes



Sensory deficit



Motor weakness is late finding.



Pulselessness is not a sign of com partm ent syndrom e: o

Palpable pulses are alm ost always present in com partm ent syndrom e unless there is underlying arterial injury.



Four leg com partm ents: anterior, lateral, deep posterior, and superficial posterior







Anterior com partm ent: o

Deep peroneal nerve

o

Sensation of first web space

o

Ankle and toe dorsiflexion

o

Anterior tibial artery feeds dorsalis pedis artery

Lateral com partm ent: o

Superficial peroneal nerve

o

Sensation of dorsum of foot

o

Foot eversion

Deep posterior com partm ent: o

Tibial nerve

o

Sensation to sole of foot

o

Ankle and toe plantarflexion

o

Posterior tibial and peroneal arteries

P.1123



Superficial posterior com partm ent: o

Branch of sural cutaneous nerve

Pa ge 4 7 7

o

Sensation to lateral foot

Tests Imaging Anteroposterior and lateral views of the leg, knee, and ankle

Diagnostic Procedures/Surgery Com partm ent pressures: 

Pressures >30 m m Hg are an indication for orthopaedic consultation and fasciotom y.

Pediatric Considerations Oblique radiograph to detect nondisplaced fractures

Differential Diagnosis 

Stress fracture



Pathologic fracture



Osteom yelitis

Pediatric Considerations 

Sarcom a



Pathologic fracture



Osteom yelitis



Nonaccidental traum a

Treatment Pre Hospital 

Look for associated injuries in high-energy m echanism s.



Assess for neurologic or vascular com prom ise.



Adequate im m obilization is essential to prevent further injury.

Initial Stabilization

Pa ge 4 7 7



Manage airway and resuscitate as indicated.



Life-threatening injuries take precedence.



Elevate and im m obilize extrem ity.



Apply ice.



Strict NPO



Pain control

ED Treatment 

Closed fractures: o

Gentle attem pt at reduction if fracture displaced (do not attem pt m ultiple reductions)

o



Well-padded long-leg posterior splint



Knee in 10â€“20Â° of flexion

o

Avoid circum ferential cast.

o

If pain persists after im m obilization, suspect:

o 

Im m obilization:



Com partm ent syndrom e



Nerve com pression

Crutches

Open fractures: o

Rem ove contam inants and cover wound with m oist sterile dressing.

o

Antibiotics

o

Tetanus prophylaxis

o

Im m obilization with well-padded long-leg posterior splint

o

Im m ediate orthopaedic surgery consultation for dÃ©bridem ent and fracture fixation



Isolated fibula fracture: o

Usually treated sym ptom atically: 

Padded splint



Elevation



Ice

Pa ge 4 7 7

 o

Nonâ€“weight-bearing until swelling resolves

Crutches if nonâ€“weight-bearing

Medication (Drugs) 

Open fractures gram -positive cocci coverage: Cefazolin 2 g loading dose then 1 g (peds: 50 m g/kg/day) IV/IM q8h



Gustilo-Anderson type III add gram -negative rod coverage: Gentam icin 3â€“5 m g/kg (peds: 2.5 m g/kg) IV q8h



Farm ing accident add Clostridium species coverage: Penicillin G 10 m illion IU (peds: 250,000â€“400,000 IU/kg/d) IV q6h



Tetanus toxoid 0.5 m L IM and tetanus im m une globulin 250 U IM as indicated by the type of wound and the num ber of prim ary im m unizations



If penicillin allergy: Vancom ycin 1 g (peds: 10 m g/kg) IV q12h

Follow-Up Disposition Admission Criteria 

Multiple traum a



High-energy m echanism



Soft-tissue involvem ent



Risk for com partm ent syndrom e



All open fractures



Displaced, angulated, transverse, shortened, com m inuted, and otherwise unstable fractures

Pa ge 4 7 8



Intra-articular involvem ent



Neurovascular com prom ise



Inadequate pain control



Pathologic fracture



Nonaccidental traum a in children

Discharge Criteria 

Minim ally displaced fracture with low-energy injury m echanism



Close orthopaedic follow-up



Return param eters for com partm ent syndrom e in a reliable patient



If fracture is m ore than 24 hours old, com partm ent syndrom e is unlikely if it has not occurred; discharge criteria m ay be m ore liberal.

References 1. Court-Brown CM. Fractures of the tibia and fibula. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's fractures in adults. 5th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2001: 1939â€“2000. 2. Trafton PG. Tibial shaft fractures. In: Browner BD, Jupiter JB, Levine AM, et al., eds. Skeletal traum a: basic science, m anagem ent and reconstruction, 3rd ed. Philadelphia, PA: WB Saunders, 2003: 2131â€“2255. 3. Watson JT. Treatm ent of unstable fractures of the shaft of the tibia. J Bone Joint Surg. 1994;76A(10):1575â€“1584.

Codes ICD9-CM 823.80 823.81

ICD10 S82.2

Pa ge 4 7 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tick Bite

Tick Bite

Jonathan A. Edlow

Basics Description 





Tick bite patient concerns: o

Tick rem oval

o

Local effect of the bite

o

Possibility of acquiring a tickborne illness: 

Often fear contracting Lym e disease



Want to be tested or treated for Lym e

Tickborne diseases in North Am erica: o

Lym e disease

o

Babesiosis

o

Ehrlichiosis

o

Rocky Mountain spotted fever

o

Relapsing fever

o

Tularem ia

o

Colorado Tick fever

o

Q-fever

o

Tickborne encephalitis (Powassan fever)

o

Tick paralysis

Additional tickborne diseases found in Europe: o

Tickborne encephalitis

Pa ge 4 7 8

o

Boutonneuse fever (R. connori)

o

Other spotted fever rickettsiae

Etiology 

Specific tickborne infections are discussed in other chapters.



Tick bite can be from different species of ticks of two m ajor types: o

Soft ticks (Ornithodoros): 

Cause tickborne relapsing fever



Only feed for m inutes and therefore alm ost never provoke a visit to the ED

o

Hard ticksâ€”especially Ixodes and Derm acentor: 

Feed for several days to a week and therefore m ay lead to an ED visit.



Lym e disease transm ission: o

Species of tick, stage of developm ent, duration of attachm ent, and geography m ay all play a role in the possibility of developing Lym e disease.

o

Most cases of Lym e are associated with bites from nym phal I. scapularis ticks.

o

Most cases are transm itted only after the tick has been attached for 24â€“48 hours: 

Degree of engorgem ent is a m arker for duration of attachm ent.

Diagnosis Signs and Symptoms History 

The patient has usually m ade the diagnosis them selves,

Pa ge 4 7 8

although som etim es they m istake the tick for skin tags or other skin lesions. 

Ask regarding duration of tick attachm ent, as this m ay influence the decision to prescribe antibiotic prophylaxis.

Physical Exam Directly exam ine the skin and the tick: 

Try to identify the tick species.



Estim ate degree of engorgem ent.

Alert 

Som e of the tickborne infections are potentially fatal and m ust be diagnosed based on history, physical and epidem iological context.



Because the drug of choice for som e of these infectionsâ€”doxycyclineâ€”is not usually prescribed for em piric therapy for acutely ill febrile patients: o

Ask about the potential for tick bites in the history of febrile patients and consider using this drug in the appropriate settings.

Essential Workup Accurate history and physical exam searching for presence of tick

Tests Lab Testing for Lym e disease is not indicated: 

Such antibody testing would only reflect prior exposure to Borrelia burgdorferi



No treatm ent im plications whatsoever for the current bite

Diagnostic Procedures/Surgery 

Testing of the tick itself is not recom m ended.



See treatm ent for tick rem oval.

P.1125

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Treatment Initial Stabilization Rem ove tick: 

Early rem oval reduces the likelihood of transm ission of tickborne infections.

ED Treatment 

Tick rem oval m ethod: o

Grasp the tick with very fine forceps, as close to the skin as possible, and gently lift up over 30â€“120 seconds. 

Most ticks will com e out.



Do not to squeeze the tick, which could inject infectious m aterials.



If m outhparts are left in the skin, although this could lead to local infection or foreign body reaction, it has no im plications for transm ission of tickborne diseases.

o

Another described m ethod: 

Inject an intraderm al wheal of lidocaine with epinephrine beneath the tick.

 o

Tick m ay crawl out of its own accord.

Methods not to use include: 

Burning the tick with a m atch



Covering it with petroleum jelly or other noxious agents



Lym e disease prophylaxis:

Pa ge 4 7 8

o

Indicated if the tick is an engorged Ixodes scapularis nym ph, or if the physician decides to prophylax

o

Doxycycline 200 m g for one dose

o

For children, there is no studied single-dose regim en: 

Prescribe am oxicillin (25â€“50 m g/kg) for 10 days in divided doses.



No data supporting prophylactic antibiotics for other tickborne diseases.

Pediatric Considerations 

Several studies used 10 days of am oxicillin in children for prevention of Lym e disease: o

No patients in the treated groups developed Lym e or seroconverted.

Pregnancy Considerations Although there are no high quality data on antibiotic prophylaxis for Lym e disease in pregnant wom en, som e authors recom m end having a very low threshold for treating pregnant wom en with tick bites (using am oxicillin).

Follow-Up Disposition Admission Criteria 

Tick bite and sym ptom s or signs of tick paralysis



Tick bite leading to a soft tissue infection sufficiently severe to require adm ission

Discharge Criteria All other patients, the vast m ajority, are safely discharged.

Issues for Referral

Pa ge 4 7 8



Follow-up with prim ary care physicians if there are issues regarding local bacterial infection from the bite (cellulites) or subsequent sym ptom s and signs of one of the tickborne infections listed above.



Seek m edical attention in the event of a febrile illness and to report the history of the tick bite to that physician.

References 1. Edlow JA. Erythem a m igrans. Med Clin North Am . 2002;86:239â€“260. 2. Edlow JA. Introduction to tick-borne diseases; 1997, updated 2005. Em ergency Medicine on-line Textbook. Boston Medical Publishing Corporation. 3. Needham GR. Evaluation of 5 popular m ethods for tick rem oval. Pediatrics. 1985;75:997â€“1002. 4. Fix AD, Strickland T and Grant J. Tick bites and Lym e disease in an endem ic setting. JAMA. 1998;279:206â€“210. 5. Nadelm an, RB et al; Prophylaxis with single dose doxycycline for the prevention of Lym e disease after an Ixodes scapularis tick bite. New Eng J Med. 2001;245:79â€“84. 6. Sood SK, et al. Duration of tick attachm ent as a predictor of the risk of Lym e disease in an area in which Lym e disease is endem ic. J Infect Dis. 1997;175:996â€“999.

Miscellaneous SEE ALSO: Lym e Disease; Rocky Mountain Spotted Fever

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tinea Infectio ns, C utaneo us

Tinea

Infections, Cutaneous Timothy Young Mark Richmond

Basics Description 

Superficial fungal infections of the hair, skin, or nails: o



Usually confined to the stratum corneum layer

Tinea requires keratin for growth, so does not involve m ucosa.

Etiology 

Derm atophytes: o

Microsporum

o

Trichophyton

o

Epiderm ophyton

o

Malassezia furfur, a yeast, is the etiologic agent of tinea versicolor (not a true tinea).



Traum a or m aceration of the skin m ay allow fungal entry into skin.

Pediatric Considerations 

Fungi can be spread from toys and brushes.

Pa ge 4 7 8



Tinea unguium is rare in children and is associated with Down syndrom e, im m unosuppression, and tinea pedis or capitis.

Diagnosis Signs and Symptoms 

Tinea capitis: o

Children are predom inately affected.

o

Most contagious derm atophytosis

o

Alopecia, dandrufflike scaling

o

Kerion: 

Boggy, inflam m atory m ass that exudes pus and causes cervical lym phadenopathy

o

â€œBlack dotsâ€• from infected hairs broken off at the scalp



Tinea corporis (â€œringworm â€•): o

Arm s, legs, and trunk

o

Sharply m arginated, annular lesion with raised m argins and central clearing

o

Hair follicle involvem ent m ay produce indurated papules and pustules



o

Lesions m ay be single, m ultiple, or concentric.

o

Pets are often a vector.

Tinea cruris (â€œjock itchâ€•): o

Erythem atous, scaly, m arginated patches involving the perineum , thighs, and buttocks

o

Associated with heat, hum idity, and tight-fitting undergarm ents

o 

Unlike candidiasis, scrotum and penis are spared.

Tinea pedis (â€œathlete's footâ€•):

Pa ge 4 7 8



o

Scaling, m aceration, fissuring between the toes

o

Risk factors: 

Advanced age



Im m unocom prom ised status



Hot and hum id clim ates



Infrequent changing of socks

o

More com m on in adults than children

o

â€œTrichophytidâ€• reaction: 

Vesicular eruption rem ote from the infection



Involving hands, m im ics dyshidrotic eczem a

Tinea unguium : o

One type of onychom ycosis

o

Yellow or brown discoloration with thickening and debris under the nails



o

Onycholysis: loosening of the nail from its bed

o

May involve the plantar surface of the foot

Tinea versicolor: o

Most com m on in warm m onths

o

Round or oval superficial brown, yellow, or hypopigm ented m acules that m ay coalesce

o

Upper trunk, arm s, and neck

o

Facial involvem ent is com m on in children.

Essential Workup 

Diagnose by clinical exam .



If diagnosis is in doubt, confirm with m icroscopy before starting oral antifungals because of possible side effects.

Tests Lab Fungal cultures are slow-growing and should not be routinely done.

Diagnostic Procedures/Surgery

Pa ge 4 7 9



Wood lam p is insensitive: o

Not all fungi fluoresce

o

Trichophyton, the m ost com m on cause of tinea infections, does not fluoresce.

o

Microsporum fluoresces green

o

Malassezia (tinea versicolor) fluoresces yellow to yellow-green.

o

Erythrasm a (nontinea corynebacterial infection) will fluoresce coral red.



Microscopy: o

Cleanse area with 70% ethanol.

o

Scrape active m argin of lesion with #10 or #15 scalpel blades.

o

Place scrapings on a glass slide, add a drop of 10â€“20% potassium hydroxide solution, and cover with a coverslip.

o

The presence of septate hyphae confirm s derm atophyte infection.

o

Budding yeasts and short hyphae (â€œspaghetti and m eatballsâ€•) confirm s Malassezia.

Pediatric Considerations 

Methods to obtain fungal elem ents for culture or m icroscopy: o

Brushing the hair with a toothbrush

o

Rolling a m oistened cotton swab

o

Collecting skin cells with transparent tape

Differential Diagnosis 

Tinea capitis: im petigo, pediculosis, alopecia areata, seborrheic derm atitis, and psoriasis



Tinea corporis: im petigo, herpes sim plex, Lym e disease, verruca vulgaris, psoriasis, num m ular eczem a, granulom a

Pa ge 4 7 9

annulare, herald patch of pityriasis rosea, erythem a m ultiform e, urticaria, seborrheic derm atitis, and secondary syphilis 

Tinea cruris: im petigo, seborrheic derm atitis, psoriasis, candidal infection, irritant and allergic contact derm atitis, and erythrasm a



Tinea pedis: scabies, erythrasm a, candida, allergic and contact derm atitis, and psoriasis



Tinea unguium : psoriasis, derm atitis, lichen planus, and congenital nail dystrophy



Tinea versicolor: vitiligo, secondary syphilis

Treatment Initial Stabilization None required except in im m unocom prom ised or septic patients

ED Treatment 

Topical antifungals do not penetrate hair or nails: o

Use in conjunction with system ic agent for tinea capitis or unguium .



Tinea capitis: o

Griseofulvin has traditionally been first line.

o

Newer oral antifungals, including terbinafine, itraconazole, and fluconazole, are preferred. 

Retained in tissues longer



Allows for shorter treatm ent courses without a decrease in efficacy

o

Terbinafine is now considered the drug of choice by m ost.

o

Pill form m ay be crushed in food.

Pa ge 4 7 9

o

Selenium sulfide or ketoconazole sham poo reduces transm issibility.

o

Kerion m ay respond m ore rapidly with addition of prednisone.



Tinea corporis, cruris, and pedis: o

Topical terbinafine or im idazoles (ketoconazole, m iconazole, and clotrim azole) are first line.

o

Topical terbinafine has been shown to be as effective as or m ore effective than the im idazoles with a shorter course. P.1127

o

Oral therapy m ay be necessary for cases resistant to topical treatm ent or for im m unocom prom ised patients.

o

Keep the area dry (talc powders) and frequently change socks and underclothes



Tinea unguium : o

Requires oral therapy and longer course than other tinea infections

o

Terbinafine had a slightly higher cure rate than im idazoles or griseofulvin in a m eta-analysis.

o

Ciclopirox 8% nail lacquer approved for treatm ent but low cure rates: 



May enhance oral therapy

Tinea versicolor: o

Topicals are first line therapy: 

Selenium sulfide 2.5% sham poo was as effective as topical ketoconazole

o

Oral ketoconazole, itraconazole, or fluconazole have been used with cure rates up to 97% but are not as

Pa ge 4 7 9

safe as topicals.

Medication (Drugs) 

Ciclopirox 8% nail lacquer: Apply to affected nails daily, m ax. 48 weeks; rem ove with alcohol every 7 days (peds: sam e).



Clotrim azole: Apply 1% cream to affected area b.i.d. for 2â€“4 weeks (peds: sam e).



Fluconazole: tinea unguium â€”150â€“300 m g/wk pulse therapy for 3â€“6 m onths for fingernails, 6â€“12 m onths for toenails; tinea corporis, cruris, and pedis: 150 m g PO weekly for 2â€“4 weeks; tinea versicolor: 400 m g PO single dose (peds: 6 m g/kg/d for 3â€“6 weeks for tinea capitis)



Griseofulvin: tinea capitisâ€”500 m g PO per day for 4â€“6 weeks (peds: 10â€“20 m g/kg up to 500 m g PO per day until hair regrows, usually 6â€“8 weeks)



Itraconazole: tinea capitis: adults and peds: 3â€“5 m g/kg PO per day for 2â€“4 weeks; tinea unguium : 200 m g PO per day for 3 m onths; tinea versicolor: 400 m g PO per day for 3â€“7 days; contraindicated in congestive heart failure



Ketoconazole: 2% topical cream per day for 2 weeks; tinea capitis, corporis, cruris, pedisâ€”200 m g PO per day for 4 weeks (peds: 3.3â€“6.6 m g/kg PO per day for 4 weeks); tinea versicolorâ€”400 m g PO Ã— 1 or 200 m g per day for 7 days (contraindicated with terfenadine and astem izole); soda increases absorption 65%



Miconazole: Apply cream to affected area b.i.d. for 2â€“4 weeks (peds: sam e)



Prednisone: adultsâ€”none (peds: 1 m g/kg PO per day for 2 weeks)

Pa ge 4 7 9



Selenium sulfide: 2.5% sham poo to affected area for 10 m inutes for 1â€“2 weeks (peds: sam e)



Terbinafine: 1% topical cream b.i.d. for 2â€“3 weeks; tinea unguium â€”250 m g PO daily for 6 weeks for fingernails, 12 weeks for toenails (peds: <20 kgâ€“67.5 m g/d, 20â€“40 kg 125 m g/d, >40 kg 250 m g/d at sam e interval as adult; tinea pedis: 250 m g PO daily for 2 weeks; tinea capitis: 250 m g/d for 4 weeks [dose by weight as for tinea unguium for 4 weeks])



Tolnaftate: Apply 1% cream /powder/solution to affected area b.i.d. for 2â€“3 weeks (peds: sam e)

Alert 

The oral antifungals m ay rarely cause hepatotoxicity: o

Consider checking liver transam inases prior to initiating therapy.

Pediatric Considerations Topical preparations are preferred when possible.

Pregnancy Considerations 

There are few studies addressing the use of antifungal m edications during pregnancy in hum ans.



The im idazoles have shown adverse effects in anim als.



Risk-to-benefit ratio m ust be considered; elective antifungal therapy is generally not recom m ended in pregnancy.



Topical clotrim azole m ay be used.

Follow-Up Disposition

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Admission Criteria 

Invasive disease in im m unocom prom ised host



Kerion with secondary bacterial infection

Discharge Criteria 

Most patients m ay be m anaged as outpatients.



Children m ay return to school once appropriate treatm ent has been initiated.

Issues for Referral Patients started on oral antifungals should be referred for follow up to m onitor therapy and advised regarding sym ptom s of hepatitis.

References 1. Gupta AK, Ryder JE, Johnson AM. Cum ulative m eta-analysis of system ic antifungal agents for the treatm ent of onychom ycosis. Br J Derm atol. 2004 Mar;150(3):537â€“544. 2. Gupta AK, Ryder JE, Nicol K, Cooper EA. Superficial fungal infections: an update on pityriasis versicolor, seborrheic derm atitis, tinea capitis, and onychom ycosis. Clin Derm atol. Septem ber to October, 2003;21(5):417â€“425. 3. Huang DB, Ostrosky-Zeichner L, Wu JJ, Pang KR, Tyring SK. Therapy of com m on superficial fungal infections. Derm atol Ther. 2004;17(6):517â€“522. 4. Schwartz RA. Superficial fungal infections. Lancet. Septem ber 25, 2004;364(9440):1173â€“1182. 5. Sladden MJ, Johnston GA. Com m on skin infections in children. Brit Med J. July 10, 2004;329(7457):95â€“99.

Codes ICD9-CM 110.9

ICD10

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B35.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To luene Po iso ning

Toluene Poisoning

Kirk Cumpston

Basics Etiology 

Volatile hydrocarbon



Abused for its euphoric effect



Used as organic solventâ€”found in: o

Glue

o

Coolants

o

Paints and paint thinners

o

Petroleum products

o

Aerosolized household products

o

Correction fluid

Pediatric Considerations 

Prevalent in adolescent age group: o

Inexpensive â€œhighâ€• with readily available sources

o 

Many psychosocial problem s

Develop chronic neurologic dysfunction

Mechanism 

Rapidly absorbed by inhalation



Readily crosses bloodâ€“brain barrier, reaching high

Pa ge 4 7 9

concentrations in brain 

Alveolar excretion and liver m etabolism



Methods of intoxication: o

Sniffingâ€”sim ple inhalation of substance directly from container

o

Huffingâ€”vapors inhaled through cloth saturated with substance

o

Baggingâ€”vapors inhaled from bag containing substance



Toxic range: o

100 ppm â€”im pairm ent of psychom otor and perceptual perform ance

o

500â€“800 ppm â€”headache, drowsiness, nausea, weakness, and confusion

o

>800 ppm â€”convulsions, ataxia, staggering gait for several days

o

10,000â€“30,000 ppm â€”anesthesia within 1 m inute

Diagnosis Signs and Symptoms Acute 



Neurologic: o

Depression

o

Euphoria

o

Ataxia

o

Seizures

Cardiac: o



Fatal dysrhythm ias

Pulm onary

Pa ge 4 7 9

o

Chem ical pneum onitis



Electrolytes



Hypokalem ia



Gastrointestinal:







o

Abdom inal pain

o

Nausea, vom iting

o

Hem atem esis

Renal: o

Renal tubular acidosis

o

Hem aturia

o

Proteinuria

Musculoskeletal: o

Diffuse weakness

o

If high anion gap m etabolic acidosis, hippuric acid

Electrolytes o

Hypocalcem ia

o

Anion gap m etabolic acidosis

Chronic 







Neurologic: o

Peripheral neuropathies

o

Encephalopathy

o

Optic atrophy

o

Clonus

Cardiac: o

Dysrhythm ias

o

Dilated cardiom yopathy

Renal: o

Distal renal tubular acidosis

o

Renal failure

o

Fanconi's syndrom e

Musculoskeletal: o

Rhabdom yolysis

Pa ge 4 8 0

Essential Workup Physical clues to diagnosis: 

Presence of agent on lips, nose, or clothes (gold paint has highest concentration)



Perioral eczem atous derm atitis from chronic huffing or bagging can be covered by beard.



Odor of agents

Tests Lab 





Arterial blood gas (ABG): o

Acidosis

o

Hypoxia if chem ical pneum onitis

Electrolytes, BUN, creatinine, glucose: o

Hypokalem ia

o

Norm al or high anion gap m etabolic acidosis

o

Hyperchlorem ia

o

Im paired renal function

Calcium and phosphorus: o



Severe hypocalcem ia/hypophosphatem ia com m on

Urinalysis: o

Check for m yoglobin (rhabdom yolysis)

o

Hem aturia and protein often present



Creatinine kinase if suspect rhabdom yolysis



Alcohol levelâ€”often coingestant



Liver enzym es, prothrom bin tim e (PT), partial throm boplastin tim e (PTT), INR, if hepatic dysfunction suspected



Urine for hippuric acid (m etabolite of toluene)

Imaging 

ECG:

Pa ge 4 8 0

o 



For atrial and ventricular dysrhythm ias

Chest radiograph: o

Indicated if dyspnea or low oxygen saturation

o

Chem ical pneum onitis

CT: o

For altered m ental status/chronic exposure

o

Cerebral/cerebellar atrophy

P.1129

Differential Diagnosis 

Alcohol intoxication



Methanol



Ethylene glycol



Salicylate



Heavy-m etal exposure



Guillain-BarrÃ© syndrom e



Other hydrocarbon exposure



Metabolic abnorm alities

Treatment Pre Hospital 

Rapid onset of toxicity



Death possible with sudden cardiac dysrhythm ias



Forced em esis is not indicated: o

Aspiration is possibility owing to decreased level of consciousness.

Initial Stabilization 

Airway, breathing, and circulation m anagem ent (ABCs)

Pa ge 4 8 0



Cardiac m onitor



0.9% norm al saline (NS) IV access



Naloxone, thiam ine, and check glucose if altered m ental status

ED Treatment 

Treat cardiac dysrhythm ias in standard fashion.



Correct m etabolic abnorm alities: o

Potassium

o

Calcium

o

Phosphate



Acidosis resolves with IV fluids.



If rhabdom yolysis: o



Maintain high urine output.

Gastric decontam ination for oral ingestion: o

Charcoal does not bind hydrocarbons well.

Medication (Drugs) 

Dextrose: D 5 0 W, one am p: 50 m L or 25 g (peds: D 2 5 W, 2â€“4 m L/kg) IV



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM

Follow-Up Disposition Admission Criteria 

Altered m ental status

Pa ge 4 8 0



Dysrhythm ias



Hepatic dysfunction



Renal failure



Rhabdom yolysis



Severe m etabolic derangem ents



Refractory hypokalem ia

Discharge Criteria After 4â€“6 hours of observation: 

Mental status at baseline



No evidence of cardiac, m etabolic, or neurologic derangem ent

References 1. Filley C, Kleinschm idt-Dem asters B. Toxic leukoencephalopathy. N Engl J Med. 2001;345:425â€“432. 2. Horowitz R. Arom atic hydrocarbons. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:803â€“812. 3. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:1195â€“1196. 4. Tang HL, Chu KH, Cheuk A, et al. Renal tubular acidosis and severe hypophosphataem ia due to toluene inhalation. Hong Kong Med J. 2005;11(1):50â€“53.

Codes ICD9-CM 982.0

ICD10 T52.2

Pa ge 4 8 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To o thache

Toothache

Franklin D. Friedman

Basics Description Pain caused by irritation of the root nerves located in pulpal tissue (the pulp is the tooth's center and its neurovascular supply).

Etiology 

Dental: o

Dental caries (hard structures dem ineralized by bacteria)

o

Pulpitis (inflam ed pulp secondary to infection)

o

Reversible pulpitis is m ild inflam m ation of the tooth pulp caused by caries encroaching on the pulp.

o

Irreversible pulpitis is the result of an untreated carious lesion causing severe inflam m ation of the pulp and to severe, persistent and poorly localized discom fort.

o

Periapical abscess (necrotic pulp and subsequent abscess)

o

Postextraction pain (dry socket, infection)

o

Root canal pain

o

Cracked-tooth syndrom e (pain, cold sensitivity, crack difficult to visualize)

Pa ge 4 8 0



Periodontal disease: o

Gingivitis and periodontitis (gingivitis with loss of periodontal ligam ent attachm ent)

o

Periodontal abscess (gum boil)

o

Pericoronitis (gingival inflam m ation from m alerupted tooth)

o

Acute necrotizing ulcerative gingivitis (gingival pain, ulcers with/without pseudom em branes)

o

Denture stom atitis

o

Herpetic gingivostom atitis

o

Aphthous ulcers (canker sores)

o

Traum atic ulcers

Diagnosis Signs and Symptoms 

Tooth pain: o

May be referred to jaw, ear, face, eye, and neck (sensory distribution of fifth cranial nerve)

o

Pain often associated with chewing, changes in tem perature, and recum bency



Malodorous breath



Fever and chills



Foul taste in m outh



Dental caries



Pain on percussion/palpation of tooth and gum s



Abscess



Facial swelling or erythem a



Cervical adenopathy



Trism us: o

Decreased m axim al interincisal opening (norm al

Pa ge 4 8 0

opening, 35â€“50 m m )

Essential Workup 

Obtain full m edical and dental history.



Ask about drug allergies, especially antibiotics and analgesics.



Assess need for preâ€“dental-procedure antibiotic prophylaxis:



o

Rheum atic fever

o

Cardiac valve replacem ents

o

Orthopaedic joint replacem ents

o

Mitral valve prolapse or valvular heart disease

Physical exam ination: o

Inspect and palpate lips, salivary glands, floor of the m outh, lym ph nodes of the neck.

o

Identify periodontal abscess.

o

Evaluate for deep-space infection.

o

Teeth should be percussed for tenderness and m obility.

o

Dental num eric system used in adults: 

Maxillary: right to left 1â€“16; m andibular: left to right 17â€“32 (peds: A-J and K-T)



Alternatively identifying teeth by their location is also appropriate (i.e., left, rear-m ost, upper m olar, or right, center lower incisor).



If physical exam conflicts with patient's history and intra-oral source of pain is not apparent consider other sources of pain.



Nonodontogenic etiologies of pain



Factitious pain/drug-seeking behavior

Tests Lab

Pa ge 4 8 0

No such tests needed except in patients with signs of system ic toxicity and those patients with perceptible deep fascial space infection.

Imaging 

Panoram ic and periapical radiograph views if suspicion exists about dental infection or fracture



CT or MRI to evaluate deeper infections

Differential Diagnosis 

Sinusitis



Otitis m edia



Pharyngitis



Peritonsillar abscess



Tem porom andibular joint syndrom e, which usually presents with pain around the ear



Trigem inal neuralgia



Vascular headache



Herpes zoster



Cardiac ischem ia

Pediatric Considerations 

Tooth eruption in a child or infant m ay cause oral pain, irritability, low-grade fever, diarrhea, and decreased food intake.



Facial swelling with fever and leukocytosis >15,000 cells/m m 3 suggests a nonodontogenic source



Children have a m axim um of 20 deciduous teeth, ten upper and ten lower.

Treatment

Pa ge 4 8 0

Pre Hospital 

Maintain patent airway in patients with severe facial swelling or trism us.



The patient should be kept in a sitting position if possible.

Initial Stabilization 

Airway m anagem ent for deep-space infection and airway com prom ise



Early pain m anagem ent as indicated

ED Treatment 

Appropriate analgesia



Nonsteroidal anti-inflam m atory pain m edication is the first-line therapy for uncom plicated dental pain.



Opiate analgesics are an alternative therapy.



Dental anesthetic field block: o

Injected along the buccal surface of the affected tooth



o

Specific nerve block for m ultiple teeth

o

Long-acting anesthetic (e.g., bupivacaine)

Antibiotics if dental infection is present: o

Penicillin is the antibiotic of choice, if patient is not allergic.

o

Erythrom ycin or clindam ycin for patients with penicillin allergy or for predom inance of anaerobes



Localized periapical and periodontal abscesses should be incised, drained, and irrigated: o



Drain m ay be placed for 24 hours.

Saline rinses at hom e four tim es a day and dental referral in 24 hours

P.1131

Pa ge 4 8 0

Medication (Drugs) 

Antibiotics: o

Clindam ycin: 150â€“450 m g PO q6h (ped: 25â€“30 m g/kg/24h [m ax. 2 g] q6h) 

o

IV dose 300â€“900 m g (peds: 6â€“10 m g/kg)

Erythrom ycin: 500 m g PO q6h (peds: 30â€“50 m g/kg/24h [m ax. 2 g] q6h)

o

Penicillin VK: 500 m g PO q6h (peds: 25â€“50 m g/kg/24h [m ax. 3 g] q6h

o

Penicillin G potassium aqueous: 4 m U IM/IV q4h (peds: 250,000â€“400,000 U/kg/d IM/IV div. q4hâ€“q6h, m ax: 24 m U/d)



Analgesics: o

Acetam inophen: 650â€“1,000 m g PO q4h (peds: 15 m g/kg/dose q4h)

o

Acetam inophen and codeine #3: 1â€“2 tablets PO q4â€“6h (peds: elixirâ€”codeine 12 m g/5 m L)

o

Acetam inophen and oxycodone: 1 or 2 tablets PO q6h (peds: 0.05â€“0.15 m g/kg/dose [m ax. 10 m g])

o

Ibuprofen: 400â€“800 m g PO q8h (peds: 10 m g/kg PO q6h)

o

Ketorolac: 30 m g IV, 60 m g IM q6h (peds: 1 m g/kg per dose IM)

o

Morphine sulfate: 2â€“8 m g SC or IV q2h (peds: 0.1 m g/kg per dose SC or IV q2h)

Pediatric Considerations Teething infants m ay be helped by over-the-counter topical anesthetics and oral analgesics.

Pa ge 4 8 1

Follow-Up Disposition Admission Criteria 

Suspicion of deep fascial space infections (e.g., Ludwig angina, retropharyngeal abscess)



Facial cellulitis proxim al to the eye



Extensive trism us



Inability to m aintain nutrition and hydration stasis



Evidence of system ic toxicity

Discharge Criteria Patients with toothache and localized dental infections can be discharged from the ED.

Issues for Referral Patients treated in the ED should be referred to a dentist or dental surgeon prom ptly.

References 1. Am sterdam JT. Dental disorders. In Marx JA, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby; 2002:892â€“908. 2. Annino DJ, Goguen LA. Pain from the oral cavity. Otolaryngol Clin of North Am . 2003:6;1127â€“1135. 3. Dodson TB, Kaban LB. Special considerations for the pediatric em ergency patient. Em erg Med Clin North Am . 2000:18;539â€“548. 4. Douglass AB. Com m on dental em ergencies. Am Fam Physician. 2003:67;511â€“516. 5. Klokkevold P. Com m on dental em ergencies: Evaluation and m anagem ent for em ergency physicians. Em erg Med Clin North Am . 1989;7:29â€“63.

Pa ge 4 8 1

Codes ICD9-CM 521.0 Dental caries, unspecified 522.0 Pulpitis 525.9 Unspecified disorder of the teeth and supporting structures 528.3 Cellulitis and abscess (of oral soft tissue) 873.63 Tooth (broken)

Pa ge 4 8 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To rtico llis

Torticollis

Andrew Chang

Basics Description 

â€œTwisted neckâ€•



A fixed or dynam ic posturing of the head and neck



Synonym : cervical dystonia

Etiology Local 





Acute wry neck: o

Develops overnight without provocation

o

Most prevalent

o

Self-lim ited, sym ptom s resolve in 1 to 2 weeks

Cervical spine: o

Fracture

o

Dislocation, subluxation

o

Infections

o

Spondylosis

o

Tum or

o

Scar tissueâ€“producing injuries

o

Ligam entous laxity in atlantoaxial region

Inflam m atory disease causing m uscular dam age:

Pa ge 4 8 1



o

Myositis

o

Lym phadenitis

o

Tuberculosis

Infections of surrounding soft tissues: o

Nasopharyngeal abscess

o

Retropharyngeal abscess

o

Cervical adenitis

o

Tonsillitis

o

Meningitis

o

Mastoiditis

o

Sinusitis

o

Posttraum a

Compensatory 

Tilt with essential head trem or (patient tilts head to suppress trem or)



Ocular m uscle palsy

Central 



Idiopathic spasm odic torticollis: o

Fem ale > Male

o

Onset 31â€“60 years old

Dystonias: o

Torsion dystonia

o

Generalized tardive dystonia

o

Wilson disease

o

L-Dopa therapy

o

Acute (neuroleptic drugs)

Pediatric Considerations Local 

Congenital: o

Odontoid hypoplasia

Pa ge 4 8 1



o

Hem ivertebrae

o

Spina bifida

o

Arnold-Chiari syndrom e

o

Pseudotum or of infancy

o

Hypertrophy or absence of cervical m usculature

Otolaryngologic: o

Vestibular dysfunction

o

Otitis m edia

o

Cervical adenitis

o

Pharyngitis

o

Retropharyngeal abscess

o

Pharyngitis

o

Mastoiditis



Esophageal reflux



Syrinx with spinal cord tum or



Traum a:



o

Cervical fracture/dislocation

o

Clavicular fractures

Juvenile rheum atoid arthritis

Compensatory 

Strabism us (fourth cranial nerve paresis)



Congenital nystagm us



Posterior fossa tum or

Central Dystonias: 

Torsion dystonia



Drug induced



Cerebral palsy

Pa ge 4 8 1

Diagnosis Signs and Symptoms 

Interm ittent painful spasm s of sternocleidom astoid (SCM), trapezius, and other neck m uscles



Head is rotated and twisted to one direction.



Pure flexion (anterocollis) or extension (retrocollis) is rare: o

Represents sym m etric involvem ent of m uscles



Neck m ovem ents vary from jerky to sm ooth.



Sym ptom s usually aggravated by standing, walking, or stressful situations



Usually does not occur with sleep



Congenital form : o

First sign m ay be a firm , nontender enlargem ent of the SCM m uscle visible at birth.



Psychological factors (e.g., depression, anxiety) m ay play a role.

History 

Interm ittent painful spasm s of SCM, trapezius, and other neck m uscles



Although the m ajority of antipsychotic m edicationâ€“induced dystonic reactions occur between 12 and 23 hours, one case report described torticollis 26 hours after IM haloperidol.



Pure flexion (anterocollis) or extension (retrocollis) is rare: o



Represents sym m etric involvem ent of m uscles

Sym ptom s usually aggravated by standing, walking, or stressful situations.



Usually does not occur with sleep



Psychological factors (e.g., depression, anxiety) m ay play

Pa ge 4 8 1

a role.

Physical Exam 

Head is rotated and twisted to one direction.



Neck m ovem ents vary from jerky to sm ooth.



Congenital form : o

First sign m ay be a firm , nontender enlargem ent of the SCM m uscle visible at birth.

Essential Workup 

Geared toward diagnosing life-threatening etiologies above



Distinguish torticollis from other causes of neck stiffness (m eningism us)



Good m edication/ingestion history



Cervical spine film s to evaluate for fracture except patients with chronic paroxysm al episodes

Tests Lab No specific tests helpful

Imaging CT or MRI of cervical spine if retropharyngeal abscess or tumor suspected

Diagnostic Procedures/Surgery Som e patients who do not respond to m edical therapy (such as botulinum toxin injections) m ay benefit from elective surgical treatm ent, such as selective peripheral denervation.

Differential Diagnosis 

CNS infections



Tum ors of soft tissue or bone



Basal ganglia disease

Pa ge 4 8 1



Abscess of cervical glands



Myositis of cervical m uscles



Cervical disk lesions

P.1133

Treatment Pre Hospital 

Ensure patent airway.



Cervical spine precautions for any history of traum a



Support head

Initial Stabilization 

Cervical spine im m obilization if fracture is suspected



If airway m anagem ent is necessary, rapid sequence intubation is the m ethod of choice.

ED Treatment 

Drug (e.g., phenothiazine) induced: o



Diphenhydram ine or benztropine

Acquired: o

If less than 1 week in duration, recom m end soft collar and rest.

o

If less than 1 m onth in duration, consider outpatient orthopaedic referral for possible traction.



Miscellaneous: o

Physical therapy

o

Massage

o

Local heat

o

Analgesics

Pa ge 4 8 1

o

Sensory biofeedback

o

Transepiderm al neurostim ulation

o

Surgery

Medication (Drugs) 

Benztropine (for drug-related dystonia): 1â€“2 m g IM or slow IV, followed by 3â€“5 days PO



Botulinum toxin A (used for failed drug therapy): 50â€“200 IU IM



Clonazepam (second-line drug): 0.5 m g PO t.i.d.



Diphenhydram ine (for drug-related dystonia): 25â€“50 m g IV or IM, followed by 3â€“5 days PO (peds: 5 m g/kg/24h div. q6h IV, IM, or PO)



Trihexyphenidyl (a first-line drug): 2â€“5 m g/d PO, advance to 30 m g/d



Valium : 2â€“5 m g IV, 2â€“10 m g PO t.i.d. (peds: 0.1â€“0.2 m g/kg/dose IV or PO q6h)

Follow-Up Disposition Admission Criteria 

Cervical spine fracture



Diagnosis is in doubt



Infectious causes



Toxic appearance



Unable to m aintain adequate fluid intake



No support system

Discharge Criteria

Pa ge 4 8 1

None of the above and sym ptom s adequately controlled with oral m edications

Issues for Referral 

Many non-drug induced patients with torticollis m ay need to be referred for possible therapy, such as with botulinum toxin.



Som e patients who fail m edical treatm ent m ay benefit from surgical treatm ent.

References 1. Braun V, Richter HP. Selective peripheral denervation for spasm odic torticollis: 13-year experience with 155 patients. J Neurosurg Spine. 2002;97:207â€“212. 2. Dauer WT, Burke RE, Greene P, et al. Current concepts on the clinical features, aetiology and m anagem ent of idiopathic cervical dystonia. Brain. 1998;121:547â€“560. 3. Duane DD. Spasm odic torticollis. Adv Neurol. 1988;49:135â€“150. 4. Jhee SS, Zarotsky V, Mohaupt SM, et al. Delayed onset of oculogyric crisis and torticollis with intram uscular haloperidol. Ann Pharm acother. 2003;37:1434â€“1437. 5. Kahn ML, Davidson R, Drum m ond DS. Acquired torticollis in children. Orthop Rev. 1991;20:667â€“674. 6. Sm ith DL, DeMario MC. Spasm odic torticollis: a case report and review of therapies. J Am Board Fam Pract. 1996;9:435â€“441.

Codes ICD9-CM 723.5

ICD10 M43.6

Pa ge 4 8 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To xic Epiderm al Necro lysis

Toxic

Epidermal Necrolysis Andrew Chang Hong K. Choi

Basics Description 

One of the m ost fulm inant and potentially fatal of all derm atologic disorders



Skin sloughing at the derm al-epiderm al interface results in the equivalent of a second-degree burn; can affect up to 100% of total body surface area.



May extend to involve gastrointestinal (GI) m ucosa (esophagitis, GI bleeding), respiratory m ucosa (dyspnea, bronchial hypersecretion, respiratory failure), and renal epithelium (glom erulonephritis)



Hypothesized to be a type IV hypersensitivity reaction



Current classification system proposes three categories within the spectrum of Stevens-Johnson syndrom e (SJS) and toxic epiderm al necrolysis (TEN) based on percentage of total body surface area (BSA): o

SJS: Less than 10% of BSA

o

Overlap SJS-TEN: 10â€“30% of BSA

Pa ge 4 8 2

o 

TEN: m ore than 30% of BSA

More com m on in older patients (m ore m edications), HIV patients (m ore m edications, im m unocom prom ised), system atic lupus erythm atosus patients, and bone m arrow transplant recipients



Mortality rate is about 30%, usually due to secondary sepsis from S. aureus and P. aeruginosa



Synonym s: o

Lyell syndrom e

o

Fixed drug necrolysis

o

Epiderm olysis necroticans com bustiform is

o

Epiderm olysis bullosa

Etiology 

Dose-independent drug reactions are the usual cause of toxic epiderm al necrolysis: o

Drugs introduced within previous 1â€“3 weeks are m ost likely candidates.

o

Frequently im plicated drugs include sulfonam ide antibiotics, anticonvulsants (phenytoin, phenobarbital, carbam azepine, lam otrigine), nonsteroidal anti-inflam m atory drugs (oxicam s, pyrazolones, sulindac), allopurinol, and the antiretroviral drug nevirapine.



Others: severe m ycoplasm al infections, graft versus host disease, idiopathic cases (com bined less than 4%).

Diagnosis Signs and Symptoms History

Pa ge 4 8 2



Prodrom e: 1 to several days of fever, conjunctivitis, pharyngitis, cough, m alaise, pruritis, cutaneous tenderness, erythem a, anorexia, m yalgias, arthralgias, dysuria, vom iting, or diarrhea



Mucous m em branes are com m only affected 1â€“3 days before skin lesions appear (oropharynx, eyes, genitalia, anus, esophageal and intestinal m ucosa, respiratory epithelium ).

Physical Exam 

Skin: o

Rash usually begins on face (scalp usually spared) and trunk as erythem atous m acules, irregular targetlike bullae, or diffuse ill-defined erythem a.

o

Widespread epiderm olysis, denuding of skin surfaces, flaccid bullae, and sheetlike sloughing of epiderm is generally progress over 3â€“4 days but can progress rapidly over hours.

o

Nikolsky sign: with lateral pressure the skin denudes and sloughs from separation of epiderm is from derm is



Oral m ucosa: initial swelling and erythem a followed by blistering and ulceration of the lips and oral m ucosa



Ocular lesions (pseudom em branes, synechiae or adhesions, keratitis, corneal erosions)

Essential Workup 

Diagnosis is m ade clinically: o

Based on history and characteristic skin and m ucous m em brane lesions



Ophthalm ology consultation is required for eye involvem ent (evaluation and rem oval of pseudom em branes and adhesions).

Pa ge 4 8 2

Tests Lab 

No confirm atory laboratory tests exist.



CBC: norm ocytic anem ia, leukocytosis, lym phopenia/neutropenia, and throm bocytopenia m ay be present.



Erythrocyte sedim entation rate m ay be elevated as a result of system ic inflam m ation.



Serum chem istry: electrolyte derangem ents if extensive fluid losses: o



Prerenal azotem ia.

Urinalysis m ay show hem aturia (urethral m ucosal erosion, glom erulonephritis) or casts (acute tubular necrosis).



Bacterial sam pling of skin, and blood cultures



SCORTEN: prognostic score including m ortality: o

Age above 40 years

o

Malignancy

o

Tachycardia above 120/m in

o

Initial percentage of epiderm al detachm ent above 10%

o

Blood urea nitrogen above 27 m g/dL

o

Serum glucose level above 252 m g/dL, 7 serum bicarbonate level below 20 m Eq/L

Imaging Chest radiograph should be done if pneum onitis or Mycoplasm a pneum oniae is suspected.

Diagnostic Procedures/Surgery Biopsy by consulting derm atologist to rule out autoim m une bullous diseases, staphylococcal scalded skin syndrom e, and other diagnoses. 

Results not im m ediately available to ED physician.

Pa ge 4 8 2

Differential Diagnosis 

SJS



Erythem a m ultiform e m ajor (EMM) o

Differentiation of TEN from EMM:

o

Etiology: TEN is m ainly drug induced; EMM occurs m ainly after herpes sim plex virus (HSV) infection

o

Lesions: 

TEN: widely distributed, m ainly on the trunk and face, nonspecific, targetlike lesions that often are confluent and too num erous to count



EMM: lim ited in num ber, sym m etric and acral distribution, typical target type (at least three concentric rings) with or without blisters

o

Prognosis: EMM is usually benign; recurrence of disease is com m on (30%); therapeutic prevention of EMM due to HSV is prevention of HSV recurrence



Staphylococcal scalded skin syndrom e (SSSS): o

Differentiation of TEN from SSSS:

o

Age: TEN: prim arily adults (but m ay occur in children); SSSS: prim arily affects children.

o

Etiology: 

TEN m ost often represents an idiosyncratic, drug-induced, dose-independent reaction and hence does not require treatm ent with antibiotics.



SSSS results from infection and requires antibiotics.

P.1135

o

Pain: painful in TEN; painless in SSSS

o

Mucous m em branes: involved with TEN; usually

Pa ge 4 8 2

spared with SSSS o

Skin cleavage: derm al-epiderm al junction in TEN; intraepiderm ally in SSSS (both can produce a positive Nikolsky sign).



Autoim m une bullous diseases (pem phigus vulgaris, bullous pem phigoid)



Scarlet fever



Toxic shock syndrom e



Chem ical or therm al scalds



Kawasaki syndrom e

Treatment Pre Hospital 

Transport to facility with burn center.



Care during transport should be gentle to avoid skin traum a.



IV catheter should be avoided for short transport if hem odynam ically stable (m ore sterile conditions in ED).



Avoid using adhesive m aterials.

Initial Stabilization 

If intubation is required, gentle technique m ust be used to m inim ize m ucosal dam age.



Meticulous sterile technique



Peripheral IV line is preferred over central line to decrease risk of sepsis.



Cardiac m onitor, pulse oxim eter, nasogastric tube, Foley catheter

ED Treatment 

Identify and stop any causative m edication.

Pa ge 4 8 2



Aggressive fluid resuscitation with lactated Ringer solution as in burn care (Parkland form ula): o

Urine output should be m aintained at a rate of at least 0.5 m L/kg per hour.



Pain should be controlled with IV opiates.



Warm ing m easures and frequent core tem perature evaluation are im portant.



Antibiotics are usually withheld because toxic epiderm al necrolysis is often drug induced.



If available, cover with biologic dressings (e.g., Biobrane): o

Reduces pain, decreases caloric and evaporative losses, and facilitates healing.



Antibiotic drops for eyes



Petroleum jelly application to lips



Prevention of peptic stress ulcers



Topical antibiotics are unproven, but m ay be applied with the exception of silver sulfadiazine (sulfonam ide derivative).



Tim ely adm ission to burn unit/intensive care unit



Tim ely derm atologic and ophthalm ologic consultation



System ic corticosteroids are no longer recom m ended: o

Retrospective studies show no benefit and suggest greater risk of death from infection.

Medication (Drugs) There are no established treatm ent regim ens; however, the following experim ental therapies are under investigation: 

Cyclosporin A: 3 m g/kg/d



Cyclophospham ide: 300 m g/d



Intravenous im m unoglobulin: 0.4â€“1 g/kg/d



Anti-TNF-Î± Antibodies: inflixim ab 5 m g/kg/dose

Pa ge 4 8 2

Follow-Up Disposition Admission Criteria All patients with suspected toxic epiderm al necrolysis should be adm itted to a burn unit (if burn unit is unavailable and transfer is not possible, then adm it to intensive care unit).

Issues for Referral Transfer to facility with burn unit has been shown to improve patient outcom e.

References 1. Bachot N, Roujeau JC. Differential Diagnosis of Severe Cutaneous Drug Eruptions. Am J Clin Derm atol. 2003;4:561â€“572. 2. Bastuji-Garin S, et al. SCORTEN: A Severity-of-Illness Score for Toxic Epiderm al Necrolysis. J Invest Derm atol. 2000;115(2):149â€“153. 3. Becker DS. Toxic epiderm al necrolysis. Lancet. 1998;351:1417â€“1420. 4. Ghislain PD, Roujeau JC. Treatm ent of severe drug reactions: Stevens-Johnson Syndrom e, Toxic Epiderm al Necrolysis and Hypersensitivity syndrom e. Derm atol Online J. 2002;8(1):5. 5. Nassif A, et al. Toxic epiderm al necrolysis: Effector cells are drug-specific cytotoxic T cells. J Allergy Clin Im m unol. 2004;114(5):1209â€“1215. 6. Paquet P, et al. Novel Treatm ents for Drug-Induced Toxic Epiderm al Necrolysis (Lyell's Syndrom e). Int Arch Allergy Im m unol. 2005;136(3);205â€“216. 7. Prendiville J. Stevens-Johnson Syndrom e and Toxic Epiderm al

Pa ge 4 8 2

Necrolysis. Adv Derm atol. 2002;18:151â€“173. 8. Prins C, et al. Treatm ent of Toxic Epiderm al Necrolysis with High-Dose Intravenous Im m unoglobulins. Arch Derm atol. 2003;139:26â€“32. 9. Wolkenstein P, Revuz J. Toxic epiderm al necrolysis. Derm atol Clin. 2000;18(3):485â€“495.

Codes ICD9-CM 695.1 Necrolysis, toxic epiderm al

ICD10 L51.2

Pa ge 4 8 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To xic Sho ck Syndro m e

Toxic Shock

Syndrome Michelle Canham

Basics Description 

Toxic shock syndrom e (TSS) is a severe, acute life-threatening illness caused by toxin-producing strains of Staphylococcus aureus or, to a lesser extent, by group A streptococci (GAS, Streptococcal TSS).



S. aureus produces an exotoxin, toxic shock syndrom e toxin (TSST-1): o



Produced by 20% of S. aureus isolates

GAS produces pyrogenic exotoxinsâ€”m ost com m only exotoxins A (SPEA) and B (SPEB).



The exotoxins are superantigens, a significant factor in the production of sym ptom s associated with TSS.



Biologic properties of superantigens include the ability to: o

Activate up to 20% of T-cells at one tim e resulting in m assive cytokine production

o

Induce fever directly on the hypothalam us or indirectly via interleukin-1 (IL-1) and tum or necrosis factor (TNF) production

Pa ge 4 8 3



o

Enhance delayed hypersensitivity

o

Suppress neutrophil m igration and im m unoglobulin

o

Enhance host susceptibility to endotoxins

Massive vasodilation occurs: o

Causes rapid m ovem ent of serum proteins and fluids from the intravascular to the extravascular space, causing hypotension.

Etiology 

Initially TSS was a disease of young, healthy m enstruating fem ales due to highly absorbent tam pons: o

Changes were m ade to reduce the absorbency and com position of tam pons.



Approxim ately one half of reported TSS cases are nonm enstrual including:



o

Surgical wounds

o

Postpartum wound infections

o

Mastitis

o

Septorhinoplasty

o

Sinusitis

o

Osteom yelitis

o

Arthritis

o

Burns

o

Nasal packing (nasal tam pons)

o

Cutaneous and subcutaneous lesions

30â€“50% of healthy adults and children carry S. aureus in the nasal vestibule, vagina, and rectum and/or on the skin.



GAS infections often begin within 24â€“72 hours at the site of m inor traum a, often without a visible break in the skin.

Pa ge 4 8 3

Diagnosis Signs and Symptoms Criteria for Diagnosisâ€”CDC Case Definition 

Fever >38.9Â°C (102.0Â°F)



Hypotension (systolic blood pressure [BP] <90 m m Hg) or shock



Diffuse, blanching nonpruritic m acular erythroderm a rash



Subsequent desquam ation 1â€“2 weeks after the onset of illness (particularly involving palm s and soles)



Multisystem involvem entâ€”at least three of the following o

Gastrointestinal: Profuse diarrhea or vom iting at onset of illness

o

Musculoskeletal: Severe m yalgias or greater than a twofold increase in creatine phosphokinase (CPK)

o

Mucosal inflam m ation: conjunctival, vaginal, or pharyngeal hyperem ia

o

Renal: increase in blood urea nitrogen (BUN) or creatinine greater than two tim es norm al upper lim it, or sterile pyuria without evidence of infection

o

Hepatic: total bilirubin or transam inases greater than two tim es norm al upper lim it



o

Hem atologic: throm bocytopenia <100,000/m m 3

o

CNS: disorientation, confusion, or hallucinations

Negative results on the following tests, if obtained: throat, or cerebrospinal fluid (CSF) cultures, rise in titer to Rocky Mountain spotted fever (RMSF), leptospirosis, or rubeola.

Other 

Tachycardia frequently present



Can rapidly progress to m ultisystem dysfunction (acute respiratory distress syndrom e or dissem inated

Pa ge 4 8 3

intravascular co-agulation) 

Most com m on initial sym ptom of strep TSS is diffuse or localized painâ€”abrupt in onset, severe, and usually precedes physical findings



Approxim ately 80% of strep TSS have clinical signs of soft-tissue infection.

Essential Workup 

Clinical diagnosis using diagnostic criteria with the absence of other causes of illness



A thorough history and physical exam ination

Tests Lab 

CBC: o

Leukocytosis or leukopenia, m arked bandem ia com m on



Electrolytes, BUN, creatinine, glucose: o



Calcium , m agnesium : o



Two-fold increase

Hepatic function: o



Norm al or sterile pyuria without evidence of infection

CPK: o



Hypocalcem ia/Hypom agnesem ia often present

Urinalysis: o



Elevated BUN and creatinine com m on

Elevated total bilirubin, AST, ALT

Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), platelets: o

Throm bocytopenia <100,000 platelets/m m 3



Arterial blood gas



Culture the site of injury/infection if possible



Blood, urine, throat, and CSF cultures as indicated:

Pa ge 4 8 3

o

The case definition does not require a positive blood culture for S. aureus, but does for Streptococcus organism s.



Serology for RMSF, rubeola, and leptospirosis



Hepatitis B surface antigen

Imaging Chest radiograph to rule out other sources of system ic illness

Differential Diagnosis 

Staphylococcal scalded skin syndrom e: o

In children <5 years old

o

Initial m acular rash followed by the form ation of ill-defined bullae that can be rubbed off revealing a shiny, m oist epiderm is (positive Nikolsky sign)



Scarlet fever: o

Preceding streptococcal pharyngitis

o

Rash begins on the upper chest, neck, and back spreading to the rem ainder of the trunk, sparing the palm s and soles.

o

Hypotension absent

P.1137



Kawasaki disease: o

Fever, conjunctival hyperem ia, and erythem a of the m ucous m em branes

o

Not associated with renal failure, hypotension, or throm bocytopenia



Stevens-Johnson syndrom e: o

Severe, m ultisystem involvem ent

o

Mucosal involvem ent prom inent with involvem ent of the m outh, conjunctivae, vagina, anus, and urethral

Pa ge 4 8 3

m eatus 



Leptospirosis: o

Transm itted through contact with infected anim als

o

Fever, headache, severe m yalgias, and conjunctivitis

o

Truncal rash that only desquam ates in children

RMSF: o

Rash is pink and m acular, beginning on the wrists, palm s, ankles, and soles spreading to the trunk and face.

o 

Petechiae appear after 4 days.

Meningococcem ia: o

Meningitis present

Treatment Initial Stabilization 

ABCs



Aggressive m anagem ent of circulatory shock with IV fluids and pressors

ED Treatment Hypotension Aggressive fluid replacem ent: 

During the first 24 hours, m ay require 4â€“20 L of crystalloid and/or fresh-frozen plasm a (colloid)



Caution: Large am ounts of IV fluids and pressor agents used to treat refractory hypotension can result in the rapid onset of pulm onary edem a.



Pressors (dopam ine) if fluid correction fails to restore norm al arterial pressure

Pa ge 4 8 3

Infection Management 

Search for and treat the focus of infection.



Rem ove the source of infection (e.g., tam pon, nasal or wound packing).



Som e authorities recom m end wom en with tam pon-related TSS to have vaginal irrigation with saline or povidone-iodine solution.



Early surgical/gynecologic consultation if drainage or debridem ent of infectious sites necessary



Antibiotics: o

Recom m ended but have not been shown to not alter the course

o

Clindam ycin is a potent suppresser of bacterial toxin synthesis.

o

Clindam ycin alone for a drained infected focus

o

Clindam ycin plus a Î²-Lactam aseâ€“resistant penicillin (nafcillin or oxacillin) for deep-seated infections or bacterem ia



IV im m unoglobulin (IVIG) treatm ent: o

May be efficacious in streptococcal toxic shock, but no controlled trials to prove efficacy in staphylococcal TSS

o

May initiate if no response to fluids, pressors, and antibiotics in patients with pulm onary edem a and hypotension

Medication (Drugs) 

Clindam ycin: 600â€“900 m g (peds: 20â€“40 m g/kg/24h) IV q6hâ€“q8h



Dopam ine: 2â€“20 Âµg/kg/m in IV, titrate to BP

Pa ge 4 8 3



IVIG: 400 m g/kg over several hours



Nafcillin: 1.5 g (peds: 100 m g/kg/24h) IV q4h



Oxacillin: 1â€“2 g (peds: 50â€“100 m g/kg/24h) IV q4h

Follow-Up Disposition Admission Criteria 

Most cases require adm ission.



Intensive care unit adm ission for critically ill/shock

Discharge Criteria None

References 1. Centers for Disease Control and Prevention. Toxic-shock syndrom e United States. MMWR. 1999;48(LMRK):60â€“70. 2. Hauser AR. Another toxic shock syndrom e: streptococcal infection is even m ore dangerous than the staphylococcal form . Postgrad Med. 1998;104:31â€“43. 3. Marx JA, et al., eds. Rosen's em ergency m edicine clinical practice. 5th ed. St. Louis, Mo: Mosby, 2002:1806â€“1810. 4. Stevens, DL. The toxic shock syndrom es. Infect Dis Clin North Am . 1996;10:727.

Codes ICD9-CM 785.5 785.59

ICD10 A48.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > To xo plasm o sis

Toxoplasmosis

Ann Buchanan

Basics Description 

Toxoplasm a gondiiâ€”intracellular protozoan parasite: o

Three form s: 

Tachyzoite: asexual invasive form



Tissue cyst: persists in tissues of infected hosts during chronic phase



Oocyst: contains sporozoites and produced during sexual cycle in cat intestine



Transm ission: o

Ingesting tissue cysts or oocysts: 

Ingesting undercooked m eat



Vegetables contam inated with oocysts



Contact with cat feces, through cat or soil

o

Transplacental

o

Blood product

o

Organ transplantation

Etiology 

70% of adults seropositive



Asym ptom atic in m ost im m unocom petent patients



Chorioretinitis:

Pa ge 4 8 3

o

Usually secondary to congenital transm ission

o

Does not becom e sym ptom atic until 20â€“30 years of age

Diagnosis Signs and Symptoms Four types of infection

Immunocompromised Host 



CNS: o

Subacute presentation (90%)

o

Encephalitis

o

Headache

o

Altered m ental status

o

Fever

o

Seizures

o

Cranial nerve palsies

o

Spinal cord lesions

o

Cerebellar signs

o

Meningitislike sym ptom s

o

Movem ent disorders

o

Neuropsychological sym ptom s: 

Psychosis



Paranoia



Dem entia



Anxiety



Agitation

Pulm onary: o

Pneum onitis

o

Prolonged febrile illness

Pa ge 4 8 3

o

Nonproductive cough

o

Dyspnea

Immunocompetent Host 

10% with sym ptom s



Lym phadenopathy



Fever



Malaise



Headache



Sore throat



Night sweats



Maculopapular rash



Urticaria



Self-lim ited process; resolves in 2â€“12 m onths



Rarely presents with pneum onitis or encephalitis

Ocular Toxoplasmosis 

Blurred vision



Scotom a



Pain



Photophobia



Retina: o

Sm all clusters of yellow-white, cottonlike patches

Congenital Toxoplasmosis 

Results from an asym ptom atic acute infection during pregnancy





First trim ester: o

Spontaneous abortion

o

Stillbirth

o

Severe disease up to 25% of the tim e

Second or third trim ester: o

50â€“60% chance of acquiring congenital toxoplasm osis

Pa ge 4 8 4

o

2% fatal



Most asym ptom atic at birth



Delayed onset: o

CNS disease

o

Ocular disease (blindness m onths to years later)

o

Lym phadenopathy

o

Hepatosplenom egaly

Essential Workup 

Diagnose via: o



Isolation of organism : 

Blood



Cerebrospinal fluid (CSF) for encephalitis



Bronchoalveolar lavage for pneum onitis



Am niotic fluid



Aqueous hum or

o

Detection of tachyzoites in tissues or body fluids

o

Dem onstrating characteristic lym ph node pathology

Thorough ocular exam ination: o

Retinal exam ination

o

Visual acuity

Tests Lab 

LDH >600/UL associated with toxoplasm osis



CBC: o

Atypical lym phocytes



Arterial blood gas/pulse oxim etry for pulm onary sym ptom s



IgG antibodies: o

High num ber of false-positive and false-negative results

o

Com m on tests: 

Sabin-Feldm an dye test

Pa ge 4 8 4





Indirect fluorescent antibody



Agglutination



Enzym e-linked im m unosorbent assay test

Im m unoglobulin M (IgM) antibodies: o

Absence excludes diagnosis in im m unocom petent host

o

Diagnoses acute infection

o

Appear in 5 days

o

Disappear in weeks to m onths

o

Neonatal testing differentiates from m aternal infection.

Imaging 

Chest radiograph for pulm onary sym ptom s: o



CT head with contrast: o



Pneum onitis associated with reticulonodular pattern

Multiple bilateral hypodense ring enhancing lesions

MRI brain: o

High signal abnorm alities on T2-weighted im ages

Diagnostic Procedures/Surgery Brain biopsy for encephalitisâ€”definitive diagnosis P.1139

Differential Diagnosis 

Cryptococcal m eningitis



CNS lym phom a



Pneum ocystis carinii pneum onia



Cytom egalovirus retinitis

Treatment

Pa ge 4 8 4

Initial Stabilization 

Treat seizures in standard fashion with diazepam and phenytoin.



Initiate oxygen if hypoxia due to pneum onitis.

ED Treatment Immunocompetent 

Toxoplasm ic lym phadenitis: o

No antibiotics unless sym ptom s severe and persistent

o

Treat sym ptom atic patients with Pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin for 2â€“4 weeks.

o

Reassess to determ ine if longer therapy needed.

Immunocompromised 

Confirm ed acute infection by serology/sym ptom s: o

Treat with pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin for 4â€“6 weeks after resolution of sym ptom s.

o



Alternative m edications: 

Trim ethoprim -sulfam ethoxazole



Pyrim etham ine and folinic acid plus dapsone

CNS sym ptom s plus a lesion on CT or MRI: o

Treat em pirically with pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin.

o

Brain biopsy or CSF to confirm diagnosis

o

Adm inister anticonvulsants only if confirm ed prior seizures: 



Poorer outcom e for patients on anticonvulsants

Chronic asym ptom atic infection: o

No therapy required

o

Prophylaxis options for toxoplasm osis in AIDS

Pa ge 4 8 4

patients: 

Trim ethoprim -sulfam ethoxazole: 1 tablet daily or 2 tablets twice a week



Pyrim etham ine (75 m g/week) and dapsone (200 m g/week)



Fansidar (pyrim etham ine-sulfadoxine) 3 tablets every 2 weeks

Ocular 

Treat with pyrim etham ine and sulfadiazine for 1 m onth: o



May add clindam ycin

Adm inister system ic steroids with m acula or optic nerve involvem ent.

Acute Acquired Infection in Pregnancy 

Initially treat with spiram ycin pending confirm atory tests.



After the infection is docum ented, initiate treatm ent with:



o

Sulfadiazine in the first 16 weeks

o

Pyrim etham ine and sulfadiazine after 16 weeks

Studies suggest m aternal-fetal transm ission is rapid and treatm ent m ay have little effect.



Treat congenital infection with sulfadiazine, pyrim etham ine, and folinic acid for 12 m onths.

Medication (Drugs) 

Clindam ycin: o

600 m g (peds: 20â€“40 m g/kg/24h) IV q6h

o

300 m g (peds: 8â€“20 m g/kg/24h) PO q6h



Dapsone: 100 m g PO daily



Folinic acid: 5â€“10 m g PO daily in conjunction with pyrim etham ine



Pyrim etham ine: 100 m g b.i.d. on first day loading dose,

Pa ge 4 8 4

then 25â€“50 m g PO daily (peds: 1 m g/kg/24h PO b.i.d. for 1â€“2 days, then 0.5 m g/kg/24h) 

Sulfadiazine: 500 m gâ€“2 g (peds: 100â€“200 m g/kg/24h) PO q6h



Trim ethoprim -sulfam ethoxazole: 5 m g/kg of trim ethoprim com ponent IV or PO q6h

Follow-Up Disposition Admission Criteria 

Acute infection with severe system ic sym ptom s



Im m unocom prom ised patients with: o

Toxoplasm osis encephalitis

o

Pneum onitis

o

Sepsis

Discharge Criteria 



Im m unocom petent patients with: o

Mild sym ptom s

o

Ocular

Maternal/Congenital infection with m ild sym ptom s

References 1. Chang HR. The potential role of azithrom ycin in the treatm ent of prophylaxis of toxoplasm osis. Int J STD AIDS. 1996;(Suppl 1):18â€“22. 2. Fung HB, Kirschenbaum HL. Treatm ent regim ens for patients with toxoplasm ic encephalitis. Clin Ther. 1996;18:1037â€“1056. 3. Ram sey RG, Bean AD. Neuroim aging of AIDS. I. Central nervous system toxoplasm osis. Neuroim aging Clin North Am .

Pa ge 4 8 4

1997;7:171â€“186. 4. Rodriguez JC, Martinez MM, et al. Evaluation of different techniques in the diagnosis of toxoplasm a encephalitis. J Med Microbiol. 1997;46:597â€“601. 5. Sciam m arella J. 2002 July 6. Toxoplasm osis. http://www.em edicine.com /em erg/topic601.htm . Accessed 2005 April 15.

Codes ICD9-CM 130.9

ICD10 B58.9

Pa ge 4 8 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transfusio n C o m plicatio ns

Transfusion

Complications Jason Prystowsky

Basics Epidemiology 

Som e type of transfusion reaction occurs in 2% of units given during or within 24 hours of use.



Febrile nonhem olytic: 0.5â€“6% (1â€“38% in platelets)



Allergic: 1â€“3%



Anaphylaxis: 0.002â€“0.005%



Acute hem olytic reaction: 0.0026â€“0.00142%



Delayed hem olytic reaction: 0.02â€“0.009%



Circulatory overload: <1%



Congestive heart failure: 1:100



Alloim m unization: 1% to RBC antigens; 10 HLA



Graft-versus-host disease: 0.005â€“0.002%



TRALI (transfusion-related lung injury): 0.02â€“0.0005%, 13% of reported transfusion-related deaths



Iron overload: after >100 RBC units



Infectious agent: o

Bacteria: RBC 1:1,000, platelets 1:2,000

o

Hepatitis C: 1:1,935,000

Pa ge 4 8 4

o

Hepatitis B: 1:205,000

o

HTLV I and II: 1:2,993,000

o

HIV: 1:2,135,000

o

HAV: 1:1,000,000

o

B19 Parvovirus: 1:40,000

o

Parasites: Babesia and m alaria: <1:1,000,000

o

Parasites: Trypanosom a cruzi: 1:42,000

Acute Intravascular Hemolytic Transfusion Reaction 

Mortality and m orbidity correlate with am ount of incom patible blood transfused (sym ptom s can occur with as little as 5â€“20-m L exposure)



Occurs im m ediately from : o

ABO incom patibility

o

Blood type identification error

o

Incom patible transfused cells im m ediately destroyed by antibodies



Intravascular hem olysis causing activation of coagulation system leading to inflam m ation, shock, and DIC



Mediators (cytokines) released during inflam m atory response



Renal failure: o

Cytokines cause local release of endothelin in kidney, causing vasoconstriction.

o

Leads to parenchym al ischem ia and acute renal failure



Respiratory failure owing to pulm onary edem a/adult respiratory distress syndrom e (ARDS): o

Free hem oglobin (Hb) causes vasoconstriction in pulm onary vasculature.

Other Transfusion-Related Complications

Pa ge 4 8 4





Hem olysis because of Rh incom patibility: o

Mild, self-lim iting

o

1/200 units transfused

Febrile nonhem olytic transfusions reaction: o

Most com m on transfusion reaction

o

Tem perature increases at least 1Â°C with chills

o

Antigen-antibody reaction to transfused blood com ponents (WBCs, platelets, plasm a)

o

Usually m ild

o

Occurs with m ultiparous wom en or m ultiple transfusions (recurs in 15% of patients)

o

Febrile nonhem olytic transfusion reaction is diagnosis of exclusion.



Allergic transfusion reaction: o

Occurs in 1% of transfusions

o

Usually seen with im m unoglobulin A (IgA)â€“deficient patients

o

Urticaria alone is not reason to stop transfusion.

o

Antihistam ine m ay be used as therapy or prophylactically.

Delayed Reactions 

Infection: o

HIV, hepatitis B, hepatitis C 

Blood screened for viruses



Blood treated to inactivate viruses



Blood donors with recent history of travel or poor health are deferred from donating.

o

Delayed extravascular hem olytic reaction: 

Occurs 7â€“10 days after transfusion



Antigen-antibody reaction that develops after transfusion



Coom bs test is positive.

Pa ge 4 8 4

o



Usually asym ptom atic



Blood bank analysis detects antibody.

Electrolyte im balance: 

Hypocalcem ia: calcium binds to citrate



Hypokalem ia: citrate m etabolized to bicarbonate, which drives potassium intracellular

o

Graft-versus-host disease: 

Usually fatal >90%



Im m unologically com petent lym phocytes transfused into im m unocom petent host



Host unable to destroy new WBCs



Donor WBCs recognize host as foreign and attack host's tissues.

o

Anaphylactic reaction: 

Can occur with <10 m L of exposure



Generalized flushing, urticaria, laryngeal edem a, bronchospasm , profound hypotension, shock, or cardiac arrest could occur.



Treat with subcutaneous epinephrine, supportive hem odynam ic and respiratory care.

o

TRALI (transfusion-related lung injury): 

Sym ptom s typically begin with 1â€“2 hours of transfusion



3rd m ost com m on cause of fatal transfusion



Difficult to distinguish from ARDS



Treat with supportive care.



Disease is typically self-lim ited within 96 hours.



Diuretics are contraindicated.

Pa ge 4 8 5

Diagnosis Signs and Symptoms 











General: o

Fevers

o

Chills

o

Burning at infusion site

o

Urticaria/pruritus/skin erythem a

Pulm onary: o

Dyspnea

o

Bronchospasm

o

Respiratory distress/failure

Cardiovascular: o

Tachycardia

o

Hypotension

o

Substernal chest pain/tightness

GI: o

Nausea

o

Vom iting

o

Diarrhea

Hem atologic: o

Bleeding

o

Hem oglobinuria

o

Oozing from surgical wounds

o

Jaundice

o

Dissem inated intravascular coagulation (DIC)

Miscellaneous: o

Low back pain

o

Renal failure (oliguria/anuria)

Essential Workup 

Recognize clinical findings of transfusion reaction.



Recheck identifying inform ation of blood and patient

Pa ge 4 8 5

com patibility.

Tests Lab 

CBC



Electrolytes, BUN, creatinine, glucose: o

For electrolyte abnorm alities



Prothrom bin tim e (PT), partial throm boplastin tim e (PTT)



Serum calcium



Fibrinogen, fibrin degradation products P.1141



Bilirubin (direct/indirect)



Coom bs test



Hem oglobinem ia: o

Pink or red supernatant of plasm a or serum indicates hem olysis.



Urinalysis: o

Hem oglobinuria: dipstick positive blood without RBC on m icro

Lab Findings Indicating Hemolysis 

Throm bocytopenia (<100,000)



Fibrinogenopenia (<150 m g/L)



Fibrin degradation products



Prolonged activated PTT (aPTT)



Spherocytosis

Lab Findings Indicating Hemolysis 

Coom bs test is positive.



Elevated indirect bilirubin



Posttransfusion hem oglobin/hem atocrit does not show

Pa ge 4 8 5

expected rise.

Imaging 

Chest radiograph: diffuse patch infiltrates without cardiom egaly.



ECG for dysrhythm ia, sign of electrolyte abnorm ality

Differential Diagnosis 

Sepsis



Anaphylaxis/allergic reaction to m edication

Treatment Initial Stabilization 

Im m ediately stop infusion: o

Severity of reaction proportional to am ount of blood transfused



Airway, breathing, and circulation m anagem ent (ABCs)



Supplem ental oxygenâ€”intubation and m echanical ventilation if needed



Recheck blood-identifying inform ationâ€”patient's bracelet, blood labels, call blood bank

ED Treatment 

Hypotension: o

0.9% norm al saline (NS) hydration with two large-bore IVs



o

Trendelenburg position

o

Dopam ine

Prevention of renal failure: o

Maintain urine output of 100 m L/h

o

Adequate hydration

Pa ge 4 8 5



o

Furosem ide or m annitol if oliguric

o

Dopam ine infusion at 2 Âµg/kg/m in

Febrile reactions: o

Antipyretics (acetam inophen/nonsteroidal anti-inflam m atory drug [NSAID])





o

Antihistam ine (diphenhydram ine) IV

o

Steroids (Solu-Medrol)

Allergic reactions: o

Antihistam ine (diphenhydram ine) IV

o

Epinephrine for respiratory sym ptom s

o

Steroids (Solu-Medrol)

Redraw blood sam ple for repeat ABO/Rh typing, direct antiglobulin testing.



Foley catheter to m onitor urine output



Replenish calcium if hypocalcem ia develops.



Treat DIC.

Medication (Drugs) 

Calcium gluconate: 10 m L of 10% (peds: 100 m g/kg/dose) solution slow IV push



Dopam ine: 2â€“20 Âµg/kg/m in IV



Diphenhydram ine: 25â€“50 m g (peds: 1.25 m g/kg) IV or PO



Epinephrine (1:1,000): 0.3â€“0.5 m L (peds: 0.01 m L/kg) SC



Solu-Medrol: 125 m g (peds: 2 m g/kg) IV

Follow-Up

Pa ge 4 8 5

Disposition Admission Criteria 

Acute hem olytic transfusion reaction, pulm onary com plications, anaphylaxis, sepsis: o



Require ICU m onitoring

Delayed hem olytic transfusion reactions for evaluation/treatm ent

Discharge Criteria 

Uncom plicated febrile or allergic reaction

References 1. Dodd RY, Notari EP, Stram er SL. Current Prevalence and incidence of infectious disease m arkers and estim ated window-period risk in the Am erican Red Cross blood donor population. Transfusion. 2002;42:975 to 979. 2. Hoffm an R, Benz E, Shattil S, et al., eds. Hem atology: Basic Principles and Practice. 3rd ed. New York: Churchill Livingstone; 2000. 3. Kruskall MS, Mintz PD, Bergin JJ, et al. Transfusion therapy in em ergency m edicine. Ann Em erg Med. 1988;17:327â€“335. 4. Kuriyan M, Carson J. Blood transfusion risks in the intensive care unit. Crit Care Clin. 2004;20:237â€“253.

Codes ICD9-CM 99.8

ICD10 T80.9

Pa ge 4 8 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transient G lo bal Am nesia

Transient

Global Amnesia Kama Guluma

Basics Description 

Transient global am nesia (TGA) has the following features: o

Episode of am nesia with abrupt onset

o

No focal neurological signs or sym ptom s

o

Tem porary, severe, anterograde am nesia:

o



Acute inability to form new m em ories



Perm anent m em ory gap after the episode

Tem porary long-ranging retrograde am nesia: 

More recent m em ories at m ore risk



Previously encoded m em ories are only tem porarily unavailable

o

Gradually shrinks, until only rem aining m em ory deficit is the m em ory gap induced by the anterograde am nesia



Incidence between 3.4â€“10 per 100,000 people: o



23.5 per 100,000 in people over age 50

The average age of patients is 61: o

TGA is rare before age 40.

Pa ge 4 8 5



The m ajority of attacks last between 1 and 8 hours (range 15 m inutes to 7 days).

Etiology 

The exact etiology of TGA is unknown.



Speculated causes: o

Migraine

o

Transient ischem ic attack

o

Seizure

o

Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunction



SPECT and PET have shown som e abnorm alities of regional cerebral blood flow.



Recent studies using MRI and internal jugular vein ultrasonography suggest transient cerebral venous congestion: o

Specifically in the setting of internal jugular vein incom petence

o

Resulting in dysfunction of selectively vulnerable hippocam pal structures

Diagnosis Signs and Symptoms History 

Often precipitated by stressful condition: o

Cough, valsalva

o

Physical exertion

o

Sexual intercourse

o

Extrem e fright or shock

o

Intense heat or cold

Pa ge 4 8 5





Patient will likely feel that som ething is wrong: o

May ask â€œhow did I get here?â€•

o

Will be generally aware of attack

May have other subtle transient sym ptom s at onset, such as headache, dizziness, nausea



Historical features that are helpful in excluding other diagnoses are: o

Onset of attack witnessed, with no seizure activity or epileptiform features noted

o

No history of seizures in prior 2 m onths

o

No history of recent traum atic brain injury

o

Acute anterograde am nesia with relatively preserved rem ote m em ory

Physical Exam 

Marked anterograde am nesia



Most cases (up to 90% in case series) will dem onstrate repetitive questioning.



The neurological and general exam norm al



The TGA patient will not have findings of an acute confusional state or dem entia. The patient will not: o

Be som nolent, inattentive or globally confused

o

Confabulate

o

Be disoriented to nam e, birth date, address, phone num ber, date

o

Have problem s perform ing com plex tasks and following com plex com m ands



Aphasia, apraxia, and agnosia are not findings consistent with TGA.

Essential Workup 

True TGA can be diagnosed with a careful history and physical alone.

Pa ge 4 8 5



If clinical diagnosis is certain, no other workup is essential.

Tests Testing is only indicated when the diagnosis is uncertain.

Lab 

CBC, com prehensive chem istries including glucose, liver function tests, NH3, thyroid studies, and urine analysis for organic m etabolic etiologies where im plicated



Tox screen, alcohol level for toxicological etiologies where suspected

Imaging Head CT for intracranial m ass or bleed

Diagnostic Procedures/Surgery 

Lum bar puncture and cerebrospinal fluid analysis for encephalitis



Electrocardiogram for seizure if indicated

Differential Diagnosis 

Since TGA is a unique and very characteristic entity: o

There is little in the way of a differential diagnosis to consider.



Other entities m ay present som ewhat sim ilarly, but will have historical or exam features that readily distinguish them from TGA: o

Acute confusional state/Korsakoff syndrom e/m etabolic disorder: 

Alcohol, m edication, or toxin ingestion



Decreased attention or other findings of an encephalopathy



Ability to lay down new m em ory if allowed tim e to encode

Pa ge 4 8 5

o

Com plex partial seizures/epileptic am nestic attacks: 

Witnessed epileptiform activity or features



Short duration (typically less than 30 m inutes)



No repetitive questioning



Frequent and rapid recurrences

P.1143

o

Psychogenic am nesia: 

Younger patient with a known psychiatric stressor



Psychiatric history, or history of personality changes



Typically no anterograde am nesia (only a retrograde gap)



Psychogenic m em ory loss for personal identification, nam e, birthdate, etc.

o

Tem poral lobe brain lesion or encephalitis affecting the tem poral lobe: 

Typically with other associated neurological sym ptom s (e.g., visual field cut)

 o

Progressive and perm anent am nesia

Previously unrecognized Alzheim er dem entia: 

Mem ory loss for personal inform ation such as date, phone num ber, address



Signs of additional global cognitive im pairm ent

Treatment ED Treatment 

TGA is a self-lim ited, relatively benign entity.

Pa ge 4 8 6



Observe the patient for im provem ent.



Assum ing a true diagnosis of TGA, no acute treatm ent, beyond reassurance of the patient and fam ily, is indicated.

Follow-Up Disposition Admission Criteria 

Adm ission for further observation for patients without significant im provem ent at the tim e of disposition



Patients with uncertain diagnosis



Patients showing a trend towards resolution, but who have suboptim al social support at hom e

Discharge Criteria 

A clear diagnosis of TGA



Resolving or resolved am nesia



Good social support

Issues for Referral 

Refer patients with recurrent episodes of TGA to a neurologist.



Selected case series have revealed that patients in this subgroup have a different prognosis: o

May have sustained focal cerebral blood flow abnorm alities on specialized im aging

o

More likely to go on to develop clinical epilepsy

References 1. Brown J. ED Evaluation of Transient Global Am nesia. Ann Em erg Med. 1997;30:522â€“526. 2. Fredericks JAM. Transient Global Am nesia. Clin Neurol Neurosurg.

Pa ge 4 8 6

1993;95:265â€“283. 3. Lam pl Y, Sadeh M, Lorberboym M. Transient global am nesiaâ€”not always a benign process. Acta Neurol Scand. 2004;110:75â€“79. 4. Lewis SL. Aetiology of transient global am nesia. Lancet 1998;352:397â€“399. 5. Pantoni L, Lam assa M, Inzitari D. Transient global am nesia: a review em phasizing pathogenic aspects. Acta Neurol Scand. 2000;102:275â€“283. 6. Sander D, Winbeck K, Etgen T, Knapp R, KlingelhÃ¶fer J, Conrad B. Disturbance of venous flow patterns in patients with transient global am nesia. Lancet. 2000;356:1982â€“1984. 7. Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM. Internal jugular vein incom petence and intracranial venous anatom y in transient global am nesia. J Neurol Neurosurg Psych. 2005;76;509â€“513.

Codes ICD9-CM 437.7

Pa ge 4 8 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transient Ischem ic Attack

Transient

Ischemic Attack Renee Hsia Rebecca Smith-Coggins

Basics Description 

Classically a tem porary neurologic deficit that resolves within 24 hours due to transient decrease in blood supply: o



80% resolve in less than 30 m inutes.

Modern definitions m ore tissue-based rather than tim e-based: o

Infarction can occur if sym ptom s last m ore than an hour.



Contrasts with other ischem ic neurologic conditions: o

Stroke in evolutionâ€”neurologic deficits that continue to worsen over m inutes to hours

o

Com pleted strokeâ€”persistent deficit after 3 weeks despite im provem ent

Etiology Mechanism Transient hypoperfusion of portion of brain from :

Pa ge 4 8 6



Low flow state from atherosclerotic lesions of large arteries (e.g., internal carotid origin, m iddle cerebral artery stem , junction of vertebral and basilar artery)



Em bolus from heart or proxim al atherosclerotic plaque



Throm bus form ation in involved vessel



Vasculopathiesâ€”carotid or vertebral dissection, Takayasu, Moyam oya disease

Diagnosis Signs and Symptoms 

The vessel and extent of involvem ent dictate neurologic deficits.



Carotid artery (anterior circulation): o

Manifests signs and sym ptom s of both anterior cerebral artery (ACA) and m iddle cerebral artery (MCA)



ACA: o

Motor and sensoryâ€”contralateral leg >arm , Â± face

o

Speechâ€”anarthria (speechlessness), dysarthria, perseveration

o

Visionâ€”am aurosis fugax, or blurred vision on one side of field of vision of both eyes opposite to side of diseased artery

o 

Contralateral neglect

MCA: o

Motor or sensoryâ€”contralateral arm and face greater than leg

o

If dom inant hem isphere involved, receptive or expressive aphasia, or both

o

Mentationâ€”inattention, neglect, apraxia

Pa ge 4 8 6

o

Visionâ€”hom onym ous hem ianopsia, gaze preference to side of infarct



Vertebrobasilar artery (posterior circulation): o

Hallm ark

o

Visionâ€”diplopia or hom onym ous field defect

o

Other features: dizziness, vertigo, and dysphagia

o

Wallenberg syndrom eâ€”ipsilateral cranial nerve deficits, contralateral m otor weakness, gait and lim b ataxia, and incom plete Horner syndrom e (anhydrosis usually absent)

o

â€œDrop attackâ€•â€”sudden onset of inability to walk, often with vertigo, headache, neck pain, and nausea/vom iting



Lacunes/Subcortical areas: o

Pure m otor or sensory deficits

o

Motor deficit is unilateral and equal in face/arm /leg.

o

Ataxic hem iparesis

o

Dysarthria

Essential Workup 

Neurologic evaluation that assesses level of consciousness, vision, cranial nerves, m otor and sensory, coordination, speech, and signs of neglect



Noncontrast head CT to rule out hem orrhage



Cardiac m onitoring and ECG to diagnose atrial fibrillation, acute m yocardial infarction, or other cardiac abnorm alities



Glucose level

Tests Lab 

CBC: Assess for anem ia or signs of hyperviscosity (elevated hem atocrit or throm bocytosis).



Electrolytes: Rule out hyponatrem ia or other abnorm alities

Pa ge 4 8 6

that can m im ic stroke 

Coagulation studies Â± throm bophilic studies (if throm bophilia suspected): o

Investigate for hypercoagulable state or as baseline for possible anticoagulation therapy.



Tox screen: particularly in younger sym ptom atic patients for cocaine or am phetam ine-induced ischem ia



Arterial blood gases



Blood cultures and erythrocyte sedim entation rate: if bacterial or nonbacterial endocarditis suspected

Imaging 

Noncontrast head CT: o

Prim arily to assess for hem orrhage

o

Sensitivity of greater than 90% for subarachnoid bleed

o

Ischem ic evidence on CT often does not appear unless im aged >6 hours after sym ptom onset.



Carotid duplex scan: o

Indicated when a high-grade carotid obstruction is suspected or with crescendo transient ischem ic attacks

o

Can detect stenosis of >60% but cannot distinguish 95% from 100% occlusion

o

Positive findings would suggest candidacy for urgent carotid endarterectom y or anticoagulation.



Echoâ€”m ay dem onstrate cardioem bolic phenom enon (m ural throm bus, tum or, or valvular vegetation)



MRIâ€”Identifies and distinguishes ischem ia and infarcts earlier than CT but is less sensitive for hem orrhage: o

Better study for posterior circulation (m agnetic resonance angiography)

o

Detects posterior bleeding better

Pa ge 4 8 6



Angiographyâ€”gold standard for detection of both stenosis and aneurysm of cerebral blood vessels: o

Cost, availability, and invasiveness m ay preclude its use.

Differential Diagnosis 

Subarachnoid/Intracerebral hem orrhage



Subdural/Epidural hem atom a



Brain aneurysm or arteriovenous m alform ation



Giant cell arteritis



Air em bolism



Migraine headache



Todd's paralysis



MÃ©niÃ¨re disease



Benign positional vertigo



Vestibular neuronitis



Epilepsy



Brain tum or/m ass



Syncope



Peripheral nerve or nerve root com pression



Dem entia



Encephalopathy



Wernicke encephalopathy



Carotid dissection after neck traum a



Hypoglycem ia



Diabetic ketoacidosis/hyperosm olar com a



Multiple sclerosis



Hyperventilation

Pediatric Considerations 

Severe dehydration with associated hypernatrem ia



Congenital heart disease



Sickle cell anem ia

Pa ge 4 8 6



Meningitis



Acute and congenital hem iplegia of childhood



Moyam oya disease: o

Rare prim ary vascular disease defined by diffuse cerebral arterial narrowing that m anifests as reoccurring TIAs

P.1145

Treatment Pre Hospital Cautions: 

Initial assessm ent of neurologic deficits crucial because they m ay com pletely resolve before arrival at ED



Avoid glucose-containing fluids unless low glucose level confirm ed.

Initial Stabilization 

Airway: support as needed



Breathing: oxygen



Circulation: careful hydration avoiding cerebral edem a and decreased cerebral blood flow (CBF)

ED Treatment 

Hypertension: o

Only patients suspected to have neurologic findings from hypertension (e.g., hypertensive encephalopathy) should be treated acutely with agents such as nitroprusside, nicardipine, or labetalol.

Pa ge 4 8 6

o

Avoid precipitous drops in blood pressure because stroke requires m aintaining perfusion to brain.



Early evaluation to prevent transient ischem ia becom ing infarct



Neurology consult



Antiplatelet therapy with aspirin



Full anticoagulation of heparin m ay be used with atrial fibrillation or with neurology consultation if patient is having recurrent sym ptom s or m inor stroke.



Transition to warfarin with target international norm alized ratio of 2.5 for patients with atrial fibrillation



Patients with aspirin failure can be started on clopidogrel, ticlopidine, or aspirin-dipyridam ole.



Patients with TIA and high-grade carotid stenosis (>70%) benefit from carotid endarterectom y (tim ing controversial but within 1â€“2 weeks at latest).

Medication (Drugs) 

Aspirin: 50â€“325 m g PO daily



Aspirin-dipyridam ole: 25/200 m g PO b.i.d.



Clopidogrel: 75 m g PO daily



Heparin: 5000 IU SC q8hâ€“q12h, or 5,000â€“7,500 IU IV bolus; 1,000 IU/h infusion



Labetalol 20 m g/m in IV bolus, then 20â€“80 m g q10m in; m ax. 300 m g; infusion 0.5â€“2 m g/m in IV



Nicardipine: 5 m g/h IV infusion, increase by 2.5 m g/h q5m inâ€“q15m in; m ax. 15 m g/h, pediatric dosing unavailable



Nitroprusside (adults and peds): 0.25â€“10 Âµg/kg/m in IV



Ticlopidine: 250 m g PO b.i.d.

Pa ge 4 8 6

Follow-Up Disposition Admission Criteria 

Controversial, disposition decisions are best m ade in conjunction with neurology.



Work-up should include evaluation for a surgically reversible cause and m edical treatm ent with anticoagulants.



Consider adm ission for TIAs when appropriate im aging studies are not available or in high-risk populations: o

Patients already taking aspirin, clopidogrel, aspirin-dipyridam ole, ticlopidine, or warfarin

o

Possible cardioem bolic stroke (e.g., atrial fibrillation),

o

â€œCrescendoâ€• TIAs (m ore than three ischem ic events in a 72-hour period that increase in frequency, duration, or severity of sym ptom s)

o

Johnston's â€œhigh-riskâ€• group (>60 years, diabetes, duration >10-m inutes, weakness with TIA, speech im pairm ent with TIA)

Discharge Criteria 

Com pletely asym ptom atic patients with extensively investigated condition or patients presenting with TIAs greater than 1 week before ED visit m ay be discharged as long as appropriate follow-up is ensured.



Patients with contraindications to antiplatelet therapy or surgery m ay be discharged if stable.



Prognosis: o

5â€“20% of those who experience a TIA will have a

Pa ge 4 8 7

stroke in 1 m onth and 50% within 1 year, o

High risk for recurrence: known high-grade lesion, cardioem bolic source, crescendo TIA (three TIAs in 72 hours), and TIAs despite antiplatelet therapy

o

30â€“325 m g of aspirin daily reduces risk of stroke by 20% after prior stroke or TIA.

Pediatric Considerations All children with TIA require adm ission for close m onitoring of blood pressure, fluid status, and neurologic status in pediatric intensive care.

References 1. Albers GW, et al. Supplem ent to the guidelines for the m anagem ent of transient ischem ic attacks: a statem ent from the Ad Hoc Com m ittee on Guidelines for the Managem ent of Transient Ischem ic Attacks, Stroke Council, Am erican Heart Association. Stroke . 1999;30:2502â€“2511. 2. Albers GW. A review of published TIA treatm ent recom m endations. Neurology. 2004;62:S26â€“S28. 3. Scott PA, Barsan WG. Stroke, transient ischem ic attack, and other central focal conditions. In: Tintinalli JE, et al., eds. Em ergency m edicine. 5th ed. New York, NY: McGraw-Hill; 2000: 1430â€“1439. 4. Shah KH, Edlow JA. Transient ischem ic attack: review for the em ergency physician. Ann Em erg Med. 2004;43:592â€“604.

Codes ICD9-CM 435.9

ICD10 G45.9

Pa ge 4 8 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transplant Rejectio n

Transplant

Rejection Richard Wolfe Mark Langdorf

Basics Description 

A transplant recipient's im m une response to a graft's genetically dissim ilar antigens resulting in rejection of the transplanted organ



The diagnostic challenge is differentiating rejection from infection, surgical com plications, and the side effects of m edication.



(HLA) incom patibility: o

MHC antigens are tissue cell surface antigens that m ost often lead to transplant rejection of solid organ transplants.



Antibodies blood group incom patibility: o

Of m uch less im portance than HLA com patibility in graft survival

o

May result in hyperacute rejection of prim arily vascularized grafts, such as kidney and heart



Three phases of rejection:

Pa ge 4 8 7

o

Hyperacute: 

Occurs in the im m ediate postoperative period



Antibody reaction to red cells or HLA antigens



Endothelial dam age occurs, probably as a result of enzym es released from polym orphonuclear leukocytes.



Platelets accum ulate, throm bi develop, and tissue necrosis occurs.

 o

Rare with careful donor-recipient m atching

Acute: 

Usually occurs within the first m onths after transplantation but m ay happen at any tim e if im m unosuppressants are stopped



T cell-dependent process whereby inflam m atory cells infiltrate the allograft releasing cellular and hum oral factors that destroy the graft



Presents with constitutional sym ptom s and signs of transplant organ insufficiency.

o

Chronic: 

Occurs over years



Results in the gradual failure of the transplanted organ

Genetics 

MHC antigens: o

Encoded by the HLA com plex

o

MHC class I genes: 

Encoded by genes of the HLA-A, HLA-B, or HLA-C loci on chrom osom e 6

 o

Present on all nucleated cells

MHC class II genes: 

Encoded by genes of the HLA-D region



Expressed only on B lym phocytes, activated T

Pa ge 4 8 7

lym phocytes, m onocytes, m acrophages, Langerhans cells, dendritic cells, endothelium , and epithelial cells o

MHC class III genes: 

Located between the HLA-B and HLA-D loci



Determ ines the structure of three com ponents of the com plem ent system : C2, C4, and factor B

Etiology 

Reduction or noncom pliance with m edication



Medication interactions with cyclosporine, tacrolim us or sirolim us m ay lead to rejection because of lower blood levels: o

Phenobarbital, phenytoin, carbam azepine, rifam pin, isoniazid



Kidney transplant rejection: o

Early rejection caused by T and B lym phocytes, which attack m icrovasculature and im pair graft perfusion

o

Chronic rejection from progressive nephrosclerosis of renal vessels



Cardiac transplant rejection: o

Acute rejection occurs in 75â€“85% of patients within the first 3 m onths.

o

Accelerated atherosclerosis is the hallm ark of chronic rejection and presents as congestive heart failure (CHF), ventricular dysrhythm ias, hypotension, syncope, or sudden death.





Lung transplant rejection: o

Rejection develops early

o

Only 25â€“40% develop chronic rejection.

Liver transplant rejection: o

Com m only follows reduction in im m unosuppression regim en

Pa ge 4 8 7



Bone m arrow transplant rejection: o

Acute graft-versus-host disease (im m une attack of donor m arrow on lung tissue)

o

Chronic graft-versus-host disease (incidence, 25â€“50% of patients)

o

Marrow rejection: 

Destruction of the graft by im m unologically active cells in the host



Most frequent in patients with aplastic anem ia who do not receive total body radiotherapy or in patients receiving m ism atched or unrelated transplants

Diagnosis Signs and Symptoms 



Renal transplant rejection: o

Progressive system ic hypertension

o

Fever

o

Swelling

o

Tenderness over the allograft

o

Decreased urine output

Heart transplant rejection: o

Fever: tem perature >38Â°C

o

Shortness of breath

o

Rales

o

Nausea, vom iting

o

Chest pain: 

Not related to ischem ia because the heart is denervated

o

Hypotension or poorly controlled hypertension

Pa ge 4 8 7

o 





New arrhythm ias

Lung transplant rejection: o

Cough

o

Dyspnea

o

Fever

o

Rales

o

Rhonchi

Liver transplant rejection: o

Fever

o

Right upper quadrant pain

o

Jaundice

Bone m arrow transplant rejection: o

Fever

o

Generalized wasting

o

Dyspnea

o

Cough

o

Hypoxia

o

Chest pain

o

Rash

o

Mucositis

o

Keratoconjunctivitis

o

Dysphagia

o

Abdom inal pain

o

Diarrhea

o

Jaundice

o

Encephalopathy

o

Seizures

Tests Lab 

General: o

CBC

Pa ge 4 8 7

o

Blood levels of im m unosuppressant m edications (see Medications): 

Levels m ay not represent trough if patient took m edication prior to ED visit.

o 

Blood cultures

Renal transplant rejection: o

Electrolytes, blood urea nitrogen, creatinine

o

Urinalysis: 

Presence of leukocytes m ay be seen during rejection as well as with infection.



Fractional excretion of sodium to help differentiate rejection from iatrogenic causes



Heart transplant rejection: o



Lung transplant rejection: o



Cardiac troponin T

ABG

Liver transplant rejection: o

Liver function tests: 

Late acute rejection presents with elevated bilirubin and transam inases.



Bone m arrow transplant rejection: o

Arterial blood gas

o

Liver function tests

P.1147

Imaging 

General: o

Chest radiograph: 

Diffuse infiltrates are seen in early acute lung rejection, but when rejection occurs >1 m onth after transplantation, radiographs m ay be

Pa ge 4 8 7

norm al or unchanged. 

Bone m arrow transplant rejection: interstitial infiltrates, pleural effusion, pulm onary edem a



Renal transplant rejection: o

Renal ultrasound 

Dem onstration of hydronephrosis im plies obstructive uropathy and warrants urgent percutaneous nephrostom y.



Heart transplant rejection: o

ECG: 

Com m only dem onstrates two P waves because the native sinus node is left in place



Decreased quasi-random signal voltage, new S3, or new CHF or atrial arrhythm ias suggest rejection.

o 

Echocardiogram

Liver transplant rejection: o

Ultrasound

o

CT

Diagnostic Procedures/Surgery 

Renal transplant rejection: o



Heart transplant rejection: o



Allograft biopsy

Endom yocardial biopsy

Lung transplant rejection: o

Pulm onary function tests

o

Bronchoscopy/Biopsy

Differential Diagnosis 

Infections: o

Wide variety of bacterial, m ycobacterial, fungal, viral, and parasitic pathogens can cause opportunistic

Pa ge 4 8 7

infections in transplant patients. 

Im m unosuppressant toxicity



Drug interactions with im m unosuppressant m edication



Renal transplant rejection: o

Any disorder that can affect the native kidneys can also occur in the transplant recipient.

o

o

Iatrogenic nephrotoxicity: 

Cyclospine, Tacrolim us



May be exacerbated by other m edication

Urinary tract infection/pyelonephritis: 

Classic organism s as with native kidney infections



Tubulointerstitial nephritis caused by the BK-polyom a virus (incidence 3â€“5%)

o

Acute occlusion of the transplant renal artery or vein: 

Acute occlusion usually occurs within the first posttransplant week (incidence 0.5â€“8%) and causes oligoanuria and acute renal failure.



o

Peritransplant hem atom a

o

Urinary leak

o

Lym phocele

o

Obstructive uropathy

o

Bleeding after renal graft biopsy

Lung transplant rejection: o

Cytom egalovirus pneum onia is the m ost com m on pathogen in transplanted lungs.

o

Aspergillus is the m ost com m on fungal infection.

o

Upper respiratory infection or bronchitis: 

o 

Mim ic chronic lung rejection

Medication-induced pneum onitis

Liver transplant rejection: o

Ascending cholangitis

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

Occurs because the biliary stent is left in place for m onths after surgery and can be colonized

o

Cholestatic hepatitis from Azathioprine

o

Methotrexate-induced hepatotoxicity

Treatment Pre Hospital Avoid aggressive fluid resuscitation.

Initial Stabilization 

ABCs



Shock state treated with IV fluids and pressor agents



Treat hypertensive crisis like other hypertensive em ergencies.

ED Treatment 

For kidney, heart, lung and liver rejection, adm inister IV m ethylprednisolone: o

Stress-dose corticosteroid coverage is also indicated in any ill-appearing transplant patient.



Avoid blood transfusions because these need special screening to prevent transm ission of disease.



Heart transplant rejection: o

Pressors and inotropics work as usual in the transplanted heart.

o

Atropine will have no effect on bradycardia because there is no vagal innervation.

o

Use dopam ine, epinephrine drips, or external pacing to increase heart rate if bradycardia is sym ptom atic.



Com m on im m unosuppressive regim ens are cyclosporine, prednisone, and azathioprine or tacrolim us (form erly

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known as FK506), and prednisone. 

Mycophenolate m ofetil: o

May reduce incidence of chronic allograft nephropathy, with less hypertension and hyperuricem ia than earlier regim ens

Medication (Drugs) 

Cyclosporine: 5â€“6 m g/kg PO q12h; m aintenance dose determ ined by blood level: 250â€“400 ng/m L (initial) 125â€“200 ng/m L (long term )



Cyclosporine m icroem ulsion: 4â€“5 m g/kg PO q12h; m aintenance dose determ ined by blood level: 250â€“400 ng/m L (initial) 125â€“200 ng/m L (long term )



Tacrolim us: 0.1 m g/kg PO q12h; m aintenance dose determ ined by blood level 10â€“20 ng/m L (initial) 5â€“10 ng/m L (long term )



Azathioprine: 1.5â€“2.5 m g/kg PO per day (adjusted for blood counts); blood-level m onitoring not used in clinical practice



Mycophenolate m ofetil: 1.0â€“1.5 g PO q12h (adjusted according to gastrointestinal adverse effects and blood counts); blood-level m onitoring not used in clinical practice



Prednisone: 0.5 m g/kg/day (initial) 0.1 m g/kg/d (long term )



Sirolim us: 2â€“5 m g PO per day (adjusted according to level); blood level:10â€“20 ng/m L (initial) 5â€“15 ng/m L (long term )

Disposition Admission Criteria

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

Adm it transplant recipients with fever, shortness of breath, signs or sym ptom s of rejection, abdom inal pain, or other signs of organ infection.



Adm it to the intensive care unit patients who are septic or have cardiopulm onary com prom ise.

Discharge Criteria Nontoxic patients in whom rejection or serious infection has been excluded m ay be discharged with close follow-up.

Issues for Referral Treatm ent decisions should be m ade in consultation with the patient's oncologist, transplant surgeon, or organ specialist.

References 1. Andrews PA. Renal transplantation. Br Med J. 2002;324:530â€“534. 2. Buckley RH. Transplantation im m unology: Organ and bone m arrow. Journal of Allergy and Clinical Im m unology. 2003;111(2): 3. Deng MC. Cardiac transplantation. Heart. 2002;87:177â€“184. 4. Jain A, Khanna A, Molm enti EP, et al. Im m unosuppressive therapy. Surg Clin North Am . 1999;79:59â€“76. 5. Yen KT. Pulm onary com plications in bone m arrow transplantation: a practical approach to diagnosis and treatm ent. Clin Chest Med. 2004;25(1):189â€“201. 6. Noble-Jam ieson G, Barnes N. Diagnosis and m anagem ent of late com plications after liver transplantation. Arch Dis Child. 1999;81:446â€“451. 7. Sternbach GL, et al. Em ergency departm ent presentation and care of heart and heart/lung transplant recipients. Ann Em erg Med. 1992;21:1140. 8. Suthanthiran M, Strom TB. Mechanism s and m anagem ent of acute renal allograft rejection. Surg Clin North Am . 1998;78:77â€“94. 9. Venkat KK, Venkat A. Care of the renal transplant recipient in the

Pa ge 4 8 8

em ergency departm ent. Ann Em erg Med. 2004;44(4):330â€“341

Codes ICD9-CM 996.52

ICD10 T86.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Traum a, M ultiple

Trauma, Multiple

Daniel Davis

Basics Description 

Standardized approach for rapid assessm ent of the traum a patient



Although presented as a sequential m ethod for gathering inform ation, m any of these steps can be perform ed sim ultaneously: o

Life-threatening injuries m ust be im m ediately addressed and treated before going on to the next level of care.



With any change in the patient's status, the prim ary survey should be repeated.

Etiology Variety of causes such as: 

Motor vehicle/m otorcycle crashes



Falls from heights



Assault



Airplane crashes



Train derailm ents



Results of m ass-casualty weapons



Terrorism

Pa ge 4 8 8

Diagnosis 

Triage to a m ajor traum a center is determ ined by local protocols.



Injured patients with a need for surgical, neurosurgical, or orthopaedic intervention should be transported to a m ajor traum a center.



Prim ary survey should be perform ed at the scene and en route.

Signs and Symptoms 

Prim ary survey (ABCDE): o

Airway, cervical spine: 

Look, listen, and palpate from nose/m outh to trachea/bronchial tree.



Assess airway patency.



Evaluate gag reflex.



Cervical spine m ust be im m obilized.



Ability to speak or effective m ovem ent of air with respiration indicates patency.



Gurgling, stridor, wheezing, snoring, choking, or absence of air m ovem ent requires im m ediate intervention.



Manage airway com prom ise before next step in prim ary survey.

o

Breathing: 

Awake, alert patient with norm al speech and good air m ovem ent suggests effective breathing.



Sym m etric chest wall rise/fall, equal breath sounds, norm al respiratory rate, and oxygen

Pa ge 4 8 8

saturation at 95% or m ore suggest effective breathing. 

Asym m etric chest m ovem ent, unequal breath sounds, abnorm al respiratory rate, decreased oxygen saturation, inadequate air m ovem ent, or an obtunded patient suggests ineffective breathing.



Decreased unilateral breath sounds, tracheal shift, hyperexpansion, hyperresonance to percussion, subcutaneous air, hypoxia, or hem odynam ic com prom ise raises concerns about tension pneum othorax.



Decreased breath sounds with dullness to percussion suggest hem othorax.



Manage patients im m ediately with needle thoracostom y followed by tube thoracostom y.

o

Circulation: 

Adequate circulating blood volum e m ust be m aintained.



Prim ary assessm ent includes blood pressure, heart rate, pulse quality, and end organ function (e.g., m entation, urine output, capillary refill).



Tachycardia and oliguria indicate early shock; hypotension is a late finding.

o

Disability: 

Assess level of consciousness, gross m otor function, and pupil size/reactivity.



Glasgow com a scale is m ost com m only used; score of 8 or lower indicates severe head injury/com a.



Spinal cord injuries are grossly assessed by

Pa ge 4 8 8

observing m ovem ent of all extrem ities. 

Pupil size and reactivity to light m easure brainstem function.

o

Exposure: 



Patient should be undressed com pletely.

Secondary survey: o

After the prim ary survey has been com pleted

o

Patient stabilized at each level

o

Com plete physical exam from head to toe is perform ed.

o

â€œTubes and fingers in every body cavityâ€•

Physical Exam Initial stabilization should begin sim ultaneously with essential workup.

Essential Workup 

Prim ary and secondary survey



Cervical spine and chest radiographs are m andatory for m ajor traum a patients.



Pelvic radiographs should be perform ed with clinical suspicion of pelvic traum a or with hem odynam ic instability.



Hem oglobin/Hem atocrit, arterial blood gas, blood type



Urine dip for blood



Urinalysis if dip positive result



Urine-based pregnancy test for any fem ale patient of child-bearing age

Tests Lab Baseline co-agulation and chem istry studies with m assive injury or hem orrhage

Pa ge 4 8 8

Imaging 

Loss of consciousness, posttraum atic am nesia (anterograde or retrograde), or persistent altered level of consciousness is indication for head CT.



Significant blunt and penetrating chest traum a requires objective evaluation of the heart and great vessels with echocardiography, CT scan, angiography, or direct visualization.



Blunt abdom inal traum a requires objective evaluation using ultrasound, abdom inal CT or diagnostic peritoneal lavage, depending on patient's condition: o

Hem odynam ically stable patients should have an abdom inal CT with IV contrast.

o

Unstable patients should have an abdom inal ultrasound (FASTexam ) or diagnostic peritoneal lavage.



Extrem ity injury: o

Radiographs

o

Suspected vascular dam age requires angiography or duplex ultrasound.

P.1149

Treatment Initial Stabilization 

The initial treatm ent should parallel the prim ary survey with injuries treated before addressing the next assessm ent level.

Pa ge 4 8 8



Airway with cervical spine control: o

Jaw thrust, suctioning, and oropharyngeal or nasopharyngeal airways provide initial airway support.

o

Rapid sequence intubation is the airway m anagem ent option of choice for m ultiple traum a patients: 

Insertion of a Com bitube or laryngeal m ask airway (LMA) or cricothyroidotom y m ay be necessary.



Breathing: o

100% oxygen and respiratory m onitoring

o

Tension pneum othorax should be diagnosed clinically and decom pressed on an em ergency basis with a needle thoracostom y below the axilla or above the second rib in the m idclavicular line: 

o

Tube thoracostom y should follow.

Open chest wounds should be covered with an adherent dressing and a tube thoracostom y perform ed.

o

Respiratory distress from flail segm ent or pulm onary contusion should prom pt early intubation with m echanical ventilation and positive end expiratory pressure.

o

Hyperventilation should be avoided except with im pending herniation or intracranial hypertension resistant to other therapies; end-tidal carbon dioxide m onitoring should be strongly considered, especially with m anual ventilation.



Circulation: o

Two large-bore IV lines with constant hem odynam ic and cardiac m onitoring should be placed: 

Alternatives include central lines, venous

Pa ge 4 8 8

cutdowns (e.g., saphenous or fem oral), or intraosseous lines. o

Aggressive fluid replacem ent with three parts fluid for every one part circulatory volum e loss rem ains the standard of care; adjust fluids based on ongoing assessm ent. 

2 L initial bolus in adults, 20 m L/kg in children



Whole blood, or autotransfused blood, for hem orrhagic shock or uncontrolled bleeding

o

Pericardial tam ponade requires em ergent pericardiocentesis/pericardial window.

o

External bleeding should be m anaged with direct pressure.



Disability: o

Head injury with Glasgow com a scale of 8 or lower should initiate treatm ent for elevated intracranial pressure with m annitol or hypertonic saline, rapid-sequence intubation, oxygenation, and controlled ventilation to a Pco 2 of 35 m m Hg.

o

Elevate head 20â€“30Â°, m aintaining spine im m obilization.

ED Treatment 

Definitive treatm ent is often surgical.



Prom pt stabilization, early recognition of the need for operative intervention, and appropriate traum a surgical consultation are param ount.

Medication (Drugs) Dictated by need for specific interventions

Pediatric Considerations

Pa ge 4 8 9

Intraosseous lines are an alternative to IV lines for fluids and m edications.

Follow-Up Disposition Admission Criteria 

Most m ajor traum a patients should be adm itted for observation, m onitoring, and further evaluation.



Patients with significant injuries or hem odynam ic instability should be adm itted to an intensive care unit.



Patients requiring frequent assessm ents should be adm itted to a m onitored setting.

Discharge Criteria Minor traum a patients with negative objective work-up/im aging m ay be observed in the ED for several hours and then discharged.

References 1. Com m ittee on Traum a, Am erican College of Surgeons. Advanced Traum a Life Support. St. Louis, MO: Mosby; 1997. 2. Gin Shaw SL, Jordan RC. Multiple traum as. In: Marx J, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby; 2002:242â€“255. 3. Krantz BE. Initial assessm ent. In: Feliciano DV, et al., eds. Traum a. Stam ford, CT: Appleton & Lange; 1996:123.

Codes ICD9-CM 959.80 Injury to other specified sites, including m ultiple

ICD10

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T07

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tricho m o nas

Trichomonas

JiWon E. Lee

Basics Description 

Sexually transm itted disease



Causes urogenital infections:



o

May cause prem ature rupture of m em brane or

o

preterm labor in pregnancy

Prevalence: o

Five m illion cases per year in United States

o

Fifteen percent of wom en seen in sexually transm itted disease (STD) clinics



May facilitate transm ission of HIV

Etiology Trichom onas vaginalis: 

Flagellated protozoan: o

Com m only found in urethra, bladder, and Skene gland

Diagnosis

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Signs and Symptoms Female 

Vaginitis: o

Often asym ptom atic (25%): 



50% develop sym ptom s within 6 m onths.

o

Vaginal discharge (50â€“75%), pruritis (50%),

o

dysuria (25%), and dyspareunia: 

Discharge yellow-green, to gray/white frothy



Inflam m ation of vaginal walls



If chronic, scant discharge and m ild pruritis

Cervix: o

Diffuse erythem a (10â€“33%)

o

Punctate hem orrhage known as colpitis m acularis or strawberry cervix (2%)



Abdom inal pain



Elevated vaginal pH (>5.5)

Male 

Usually asym ptom atic (90%)



Urethritis: o

Twenty percent of nonspecific urethritis

o

Scant discharge

o

Dysuria



Prostatitis



Epididym itis



Reversible sterility

Essential Workup â€œHanging-dropâ€• slide test: 

80â€“90% sensitive in sym ptom atic patients



Saline wet m ount on cervical sm ears (from vaginal vault) or spun urine:

Pa ge 4 8 9

o

Many polym orphonuclear leukocytes (PMNs)

o

Motile, pear-shaped flagellated trichom onas (slightly larger than leukocytes, seen in 60%)

Tests Lab 

Culture: o

95% percent sensitivity: 

Prostate m assage before collection Increases sensitivity in m ales.



Im m unofluorescence and/or Im m unoassay: o

Available but expensive

Differential Diagnosis 

Urinary tract infection (UTI)



Gonorrhea



Chlam ydia



Candidal vaginitis



Nonspecific vaginitis

P.1151

Treatment ED Treatment 

Fem ale: o

Metronidazole 2 g PO once: 

o

90â€“95% cure rate

Resistant infections: 

Metronidazole 500 m g PO b.i.d. for 7 days or

Pa ge 4 8 9

 o

Metronidazole gel (less effective)

o

If refractory to m etronidazole: 

o 

Metronidazole 375 m g PO b.i.d. for 7 days

Treat sexual partner to prevent re-exposure.

If allergic, m ay have to desensitize to m etronidazole

Pregnant: o

First trim ester: 

Clotrim azole 100 m g vaginal suppository for 7 days (70% effective)

o

After first trim ester: 





Metronidazole as above

Males (urethritis): o

Metronidazole 2 g PO once

o

Tinidazole 2 g PO once

o

Metronidazole 500 m g PO b.i.d. for 7 days or

o

Metronidazole 375 m g PO b.i.d. for 7 days

Avoid concom itant alcohol use with m etronidazole: o

Precipitate Antabuse reaction



Test and treat sexual partners.



Test for concom itant sexually transm itted diseases, syphilis, and HIV.

Follow-Up Disposition Discharge Criteria All patients

References 1. Centers for Disease Control and Prevention. Sexually transm itted diseases treatm ent guidelines 2002. MMWR Recom m Rep.

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2002;51(RR-6):1â€“78. 2. Das S. Treatm ent failure of vaginal trichom oniasis in clinical practice. Int J STD AIDS. 2005;16(4):284â€“286. 3. Mam m en-Tobin A. Managem ent of m etronidazole-resistant Trichom onas vaginalis. Int J STD AIDS. 2005;16(7):488â€“490.

Miscellaneous SEE ALSO: Urethritis

Codes ICD9-CM 131.9

ICD10 A59.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tricyclic Antidepressant, Po iso ning

Tricyclic

Antidepressant, Poisoning Steven Aks

Basics Description 

Prim ary m echanism of tricyclic antidepressant (TCA) toxicity:





o

Sodium channel blocking effect (quinidinelike effect)

o

Inhibition of norepinephrine reuptake

o

Alpha blockade

o

Anticholinergic effect

Selective serotonin reuptake inhibitors (SSRIs): o

Wider m argin of safety than TCA

o

Less CNS/cardiovascular toxicity

Nonselective serotonin reuptake inhibitors: o

Serotonin and norepinephrine reuptake inhibitors (SNRIs)

o

Can cause cardiac dysrhythm ias or seizures

o

Venlafaxine (Effexor)

o

See Antidepressants, Poisoning

Etiology 

Tricyclic antidepressants:

Pa ge 4 8 9



o

Am itriptyline

o

Nortriptyline

o

Im ipram ine

o

Doxepin

Newer-generation antidepressants (nontricyclic): o

Have different toxic profile than TCAs

o

See Antidepressants, Poisoning

Diagnosis Signs and Symptoms 

Rapid deterioration m ay occur.



Classic tricyclic antidepressant (TCA) com pounds (im ipram ine, am itriptyline, nortriptyline)â€”greatest cardiovascular toxicity



Newer agents (serotonergic agents)â€”less overall toxicity in overdose

Central Nervous System (CNS) 

Stim ulation or depression



Stim ulation: o

Trem ulousness

o

Agitation

o

Fasciculation

o

Seizures (resulting acidem ia m ay lead to worsening cardiovascular toxicity)



Depression: o

Drowsiness

o

Lethargy

o

Com a

Cardiovascular System

Pa ge 4 8 9



Hypotension



Tachycardia (early; owing to blockade of norepinephrine reuptake and anticholinergic effects)



Bradycardia (late; owing to catecholam ine depletion state)



ECG changes: o

QRS widening (>100â€“120 m illiseconds)

o

Rightward shift in term inal 40 m illiseconds in frontal plane axis (r wave >3 m m in aVR)



Dysrhythm ias: o

Supraventricular tachycardia (SVT)

o

Ventricular arrhythm ias

Anticholinergic Effects (Less Common) 

Dilated pupils



Decreased bowel sounds



Urinary retention

Essential Workup 

ECG: factors associated with TCA poisoning: o

Sinus tachycardia (alm ost always present at som e tim e after poisoning)

o

QRS widening: 

Greater than 100 m illiseconds associated with seizure



Greater than 160 m illiseconds associated with ventricular dysrhythm ia

o

QT prolongation

o

PR prolongation

o

Rightward shifting of term inal 40 m illiseconds QRS axis

o 

R-wave am plitude in aVR >3 m m

Continuous cardiac m onitor

Tests

Pa ge 4 9 0

Lab 

CBC



Electrolytes, BUN, creatinine, glucose



Arterial blood gas (ABG)



Urine toxicology screen: o



Rule out other toxins.

TCA levels: o

Not useful

o

Do not correlate well with degree of toxicity

o

Qualitative screen appropriate to confirm ingestion if necessary

Imaging Chest radiograph for aspiration pneum onia/pulm onary edem a

Differential Diagnosis Drugs That Cause Coma 

Alcohols



Alcohol withdrawal



Anticholinergics



Lithium



Phencyclidine (PCP)



Opioids



Phenothiazines



Sedative hypnotics



Salicylates

Cardiotoxic Drugs 

Antidysrhythm ics (category IA)



Digoxin toxicity



Sym pathom im etics



Anticholinergics

Drugs That Cause Seizures

Pa ge 4 9 0



Alcohol withdrawal



Anticholinergics



Cam phor



Isoniazid



Lindane



Lithium



Phenothiazines



Sym pathom im etics



Toxic alcohols

Treatment Pre Hospital 

Do not be lulled into false sense of security with well-appearing patient: o

Rapid onset of altered m ental status, seizures, and dysrhythm ias occur.



Perform endotracheal intubation if any evidence of com prom ise.



Secure IV access.



Adm inister sodium bicarbonate if any evidence of QRS widening (>100â€“120 m illiseconds):



o

One am pule in adults

o

1â€“2 m Eq/kg in children

Ipecac contraindicated (risk for aspiration with developm ent of depressed m ental status, or seizure)

P.1153

Initial Stabilization

Pa ge 4 9 0



Airway, breathing, and circulation m anagem ent (ABCs): o

Low threshold to intubate patients with altered m ental status



IV 0.9% norm al saline (NS)



Oxygen



Cardiac m onitor: o

For wide com plex rhythm (QRS >100â€“120 m illiseconds) bolus sodium bicarbonate



Naloxone, thiam ine, glucose (Accu-Chek) for altered m ental status



Flum azenil contraindicated in com bined TCA/benzodiazepine overdose

ED Treatment Cardiac Toxicity 

QRS widening (>100â€“120 m illiseconds): o

Bolus with one am p (peds: 1â€“2 m Eq/kg) of sodium bicarbonate; repeat if sudden increase in QRS width

o

Maintain arterial pH of 7.45â€“7.5 with hyperventilation.

o

Initiate sodium bicarbonate infusion if hyperventilation alone does not reach target pH.



Dysrhythm ia: o

Sinus tachycardia requires no treatm ent.

o

Bolus 1â€“2 am ps of sodium bicarbonate (1â€“2 m Eq/kg in children) for sudden change in rhythm

o

Follow advanced cardiac life support (ACLS) protocol with addition of sodium bicarbonate boluses: 

Lidocaine is second-line agent after sodium bicarbonate.

o

Use of class IA (procainam ide) and IC agents and physostigm ine contraindicated

Pa ge 4 9 0

Hypotension 

0.9% NS fluid bolus



Norepinephrine: o

Preferred pressor (over dopam ine)

o

Counters alpha blockade better

o

Dopam ine requires higher doses.

Decontamination 

Gastric lavage: o

For recent ingestion (<1â€“2 hours)

o

Perform ed when airway has been secured in lethargic patient



Adm inister activated charcoal with sorbitol.



Ipecac contraindicated

Seizure 

Diazepam first-line followed by phenobarbital/phenytoin



Neurom uscular paralysis with short-acting agent (rocuronium /vecuronium ) for refractory seizures (m onitor electroencephalogram [EEG])



Sodium bicarbonate bolus to prevent acidosis

Medication (Drugs) 

Activated charcoal slurry: 1â€“2 g/kg up to 90 g PO



Dextrose: D 5 0 W, one am p: 50 m L or 25 g (peds: D 2 5 W, 2â€“4 m L/kg) IV



Diazepam (benzodiazepine): 5â€“10 m g (peds: 0.2â€“0.5 m g/kg) IV



Dopam ine: 2â€“20 Âµg/kg/m in IV infusion titrated to desired effect



Lorazepam (benzodiazepine): 2â€“6 m g (peds: 0.03â€“0.05 m g/kg) IV

Pa ge 4 9 0



Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose



Norepinephrine: 4â€“12 Âµg/m in (peds: 0.05â€“0.1 Âµg/kg/m in) IV infusion titrated to desired effect



Sodium bicarbonate: 1â€“2 am ps IV push (peds: 1â€“2 m Eq/kg); dripâ€”add 3 am ps to 1 L of D 5 W (efficacy of drip is unknown)



Sorbitol: 1â€“2 g/kg to m ax. of 150 g (peds: >1 year old: 1â€“1.5 g/kg as 35% solution to m ax. of 50 g) PO m ixed in activated charcoal slurry this is unnecessary

Follow-Up Disposition Admission Criteria 

Sym ptom atic patients observed >6 hours



Altered m ental status



Dysrhythm ia or conduction delay



Seizure



Heart rate >100 beats/m in 6 hours after ingestion



Coingestion requiring prolonged observation

Discharge Criteria 

Asym ptom atic after 6 hours observation



No alteration in m ental status



Norm al ECG with heart rate <100 beats/m in



Active bowel sounds; tolerated activated charcoal



Psychiatry clearance if there has been suicide attem pt or gesture

References

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1. Brent J. Serotonin reuptake inhibitors, newer antidepressants, and the serotonin syndrom e. In: Ford M, Delaney C, Ling L, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 2. Geis GL, Bond GR. Antidepressant overdose: tricyclics, selective serotonin reuptake inhibitors, and atypical antidepressants. In: Erickson TB, Ahrens W, Aks SE, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2004:297â€“302. 3. Gueye P, Hoffm an JR, Taboulet P. Em piric use of flum azenil in com atose patients: lim ited applicability of criteria to define low risk. Ann Em erg Med. 1996;27:730. 4. Liebelt EL, Francis PD, Woolf AD. ECG lead aVR versus QRS interval in predicting seizures and arrhythm ias in acute tricyclic antidepressant toxicity. Ann Em erg Med.l 1995;26:195â€“201. 5. McCabe JL, Cobaugh DJ, Menegazzi JJ, et al. Experim ental tricyclic antidepressant toxicity: a random ized, controlled com parison of hypertonic saline solution, sodium bicarbonate and hyperventilation. Ann Em erg Med. 1998;32:329â€“333.

Codes ICD9-CM 969.0

ICD10 T43.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Trigem inal Neuralgia

Trigeminal

Neuralgia James M. Leaming

Basics Description 

Also known as tic douloureux



Pain syndrom e recognizable by history alone



Facial pain often accom panied by a brief facial spasm or tic



Pain distribution is unilateral and follows the sensory distribution of cranial nerve V.



Typically radiates to the m axillary (V2) or m andibular (V3) area



At tim es, both distributions are affected.



Mechanism of pain production rem ains controversial: o

Theories suggest that peripheral injury or disease of the trigem inal nerve increases afferent firing in the nerve.

o

Failure of central inhibitory m echanism s m ay be involved as well.



Pain is perceived when nociceptive neurons in a trigem inal nucleus involve thalam ic relay neurons.

Etiology

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

Idiopathic (prim ary idiopathic is m ost com m on)



Redundant or tortuous blood vessel in the posterior fossa resulting in irritation of the nerve root



Space-occupying lesion causing direct com pression of the nerve



Bilateral tic douloureux in younger adult can be seen in m ultiple sclerosis.



Irritation of the nerve during exacerbation of herpes zoster in sam e distribution



Space-occupying lesions (aneurysm , neurofibrom a, m eningiom a)



Dissim ilar m etal containing dental fillings

Diagnosis Signs and Symptoms 

Brief, intense, lancinating pain (tic douloureux)



Unilateral in the distribution of a branch of the trigem inal nerve: o

Bilateral trigem inal neuralgias do occur.



May occur without provocation



May be initiated by tactile stim ulation of face, lips, tongue, or scalp



Pain seldom lasts m ore than a few seconds to several m inutes.



Occurs alm ost exclusively in the m iddle-aged or elderly patient



More com m on in fem ales than m ales



Associated sensory loss in the effected region m ay be found.



Paroxysm al pattern of pain lasting weeks in duration

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Physical Exam 

Physical exam ination findings are norm al.



Carefully exam ine the cranial nerves, including the corneal reflex: o

Any abnorm ality on exam ination suggests pain m ay be from another cause.



Patients report pain following stim ulation of a trigger point.

Essential Workup 

Diagnosis is m ade clinically.



History is of prim ary im portance:



o

Onset, duration of pain

o

Associated constitutional sym ptom s

o

Visual disturbances

o

Associated paraesthesias

o

History of traum a

Cranial nerve exam ination for both sensory and m otor function including visual acuity



Neurologic exam ination for focal deficits



Skin exam ination for presence of rash or other abnorm alities



Dental and oral exam ination

Tests Lab No specific laboratory tests apply for diagnosis of trigem inal neuralgia.

Imaging 

Patients with characteristic history and norm al neurologic exam ination m ay be treated without further workup.



Elective MRI:

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o

To exclude a m ass lesion or aberrant vessel com pressing the nerve roots

Differential Diagnosis 

Multiple sclerosis



Tem porom andibular joint syndrom e



Atypical facial pain



Glossopharyngeal neuralgia



Tem porom andibular joint pain



Com pression of trigem inal roots from tum ors or aberrant vessels



Dental problem s

Treatment ED Treatment 

Appropriate pain relief



Anticonvulsants m ay be effective: o

Carbam azepine m ost often used

P.1155

Medication (Drugs) 

Carbam azepine: begin with 100 m g b.i.d.; can be increased to 600 m g b.i.d. for sym ptom control



Phenytoin is anecdotally successful therapy for neuralgia control: o

Starting doses should be 300 m g daily and increased to control pain.

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Follow-Up Disposition Admission Criteria 

Trigem inal neuralgia with presence of other focal neurologic findings



Positive CT or MRI studies m ay require em ergent neurologic or neurosurgical consultation.



Refractory or recurrent trigem inal neuralgia not responding to outpatient pain m anagem ent or anticonvulsant therapy: o

May require adm ission for surgical intervention and ablation of the trigem inal nerve

Discharge Criteria Patients without any focal neurological findings and im proved pain control in the ED m ay be m anaged as outpatients.

Issues for Referral 

Pain m anagem ent center referral m ay be helpful in refractory pain control: o

Anesthetic blocks of the trigem inal ganglion m ay be helpful.



Referral to a neurologist if the diagnosis is in question



Referral to a neurosurgeon m ay be indicated for refractory patients: o

Percutaneous radiofrequency ablation of a portion of the trigem inal ganglion is com m only perform ed.

o

Less com m only perform ed is trigem inal root decom pression.

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References 1. Cam pbell JK. Trigem inal neuralgia: are all of the treatm ent options being considered?. Headache. January 1997;37(1):H3. 2. Cheshire WP. The shocking tooth about trigem inal neuralgia. N Engl J Med. June 29, 2000;342(26):2003 3. Gouda JJ, Brown JA. Atypical facial pain and other pain syndromes. Differential diagnosis and treatm ent. Neurosurg Clin N Am . January 1997;8(1):87â€“100. 4. Kubitz PK, Wijdicks EF, Bolton CF. Tic douloureux or â€œtic dentaireâ€•. Neurology. January 27, 2004;62(2):333. 5. Liu JK, Apfelbaum RI. Treatm ent of trigem inal neuralgia. Neurosurg Clin N Am . July 2004;15(3):319â€“334. 6. Rasche D, Kress B, Schwark C, et al. Treatm ent of trigem inal neuralgia associated with m ultiple sclerosis: case report. Neurology. 2004;63(9):1714â€“1715. 7. Sweet WH. The treatm ent of trigem inal neuralgia (tic douloureux). N Engl J Med. 1986;315:174.

Codes ICD9-CM 350.1

ICD10 G50.0

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tuberculo sis

Tuberculosis

Vittorio J. Raho

Basics Description Infection with Mycobacterium tuberculosis, an aerobic acid-fast bacillus, resulting in disease

Mechanism 

Most com m on route of infection is by droplet nuclei inhaled through the respiratory tract.



Prim ary tuberculosis: o

Initial infection occurs when organism s enter the alveoli, becom e engulfed by m acrophages, and spread via regional lym ph nodes to the bloodstream .

o

Patients are usually asym ptom atic.

o

May be progressive/fatal in im m unocom prom ised hosts

o

Positive reaction to purified protein derivative (PPD) indicates past exposure or infection.



Reactivation tuberculosis: o

Latent infection becom es active tuberculosis.

o

System ic (15%) and pulm onary (85%) sym ptom s

o

Characterized by a chronic wasting disease

o

Tuberculosis affects about one third of the world's

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population (90 m illion new cases in past decade worldwide, with about 30 m illion deaths). o

Estim ated 10â€“15 m illion people infected in the United States alone

Etiology 



Three tuberculosis epidem ics: o

Global resurgence

o

HIV-infected patients

o

Multidrug-resistant tuberculosis

Conditions that predispose the individual to developing tuberculosis include: o

HIV infection and other im m unocom prom ised states

o

Drug and alcohol abuse

o

Poverty

o

Hom elessness

o

Institutionalization

o

Im m igration from a high-prevalence area

Diagnosis Signs and Symptoms 

Pulm onary tuberculosis: o

Fever

o

Malaise

o

Weight loss

o

Night sweats

o

Chronic cough

o

Hem optysis

o

Pleuritic chest pain

o

Shortness of breath

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

Extrapulm onary tuberculosis: o

CNS infections: 

Meningeal irritation and cranial nerve defects



Malaise



Interm ittent headache



Low-grade fever



Confusion



Meningism us



Diplopia



Hyponatrem ia (due to syndrom e of inappropriate antidiuretic horm one)

 o

Pericarditis: 

o

o

o

o

Acute ischem ic stroke

Pleuritic chest pain increased with recum bency

Renal infection: 

Fever



Flank pain



Sterile pyuria

Spinal tuberculosis (Pott disease): 

Back pain/stiffness



Fever



Point tenderness



Decreased range of m otion

Cervical lym phadenitis: 

Known as Scrofula



Draining sinus tracts m ay form .

Miliary tuberculosis: 

Multi-organ system involvem ent



Diffuse adenopathy



Hepatom egaly



Splenom egaly



Weight loss

Pa ge 4 9 1



Fever

Essential Workup 

Diagnosis difficult due to the variety of clinical presentations



Chest radiography: o

Most valuable test for diagnosing active pulm onary tuberculosis



Skin testing

Tests Lab 

CBC



Electrolytes, blood urea nitrogen, creatinine, glucose



Arterial blood gas for oxygenation/ventilation assessm ent



Sputum staining for acid-fast bacilli (Ziehl-Neelsen stain):



o

Provides a quick presum ptive diagnosis

o

Not im m ediately available

Sputum , cerebrospinal fluid (CSF), blood, urine, or peritoneal fluid culture:



o

Gold standard for diagnosis of tuberculosis

o

Average tim e for positive culture is 3â€“6 weeks.

Lum bar puncture with CSF analysis: o

For suspected tuberculous m eningitis

o

WBC range 0â€“1,500/m m 3 with lym phocyte predom inance

o

Elevated protein

o

Low to norm al glucose

Imaging 

Chest radiograph: o

In prim ary disease, parenchym al infiltrates with unilateral hilar adenopathy are the classic findings.

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o

Reactivation tuberculosis typically appears as cavitary lesions with or without calcification usually in upper lung segm ents.

o

Miliary tuberculosis shows bilateral nodules throughout lungs.

o

Chest radiograph m ay be nondefinitive in AIDS patients.

o

Unilateral pleural effusion in both prim ary and reactivation tuberculosis

o

Tracheal deviation with scarring or atelectasis

o

Ghon focusâ€”calcified scar/healed prim ary focus of infection

o

Ghon com plexâ€”prim ary infiltrate with associated unilateral hilar adenopathy



Spine radiographs for Pott disease: o

May be norm al

o

Anterior wedging of two involved vertebral bodies and destruction of disk



CT chest: o

Better define extent of disease

Diagnostic Procedures/Surgery 

Skin testing: o

Inject 0.1 m L of PPD subcutaneous in the forearm .

o

Positive test indicates prior or current infection with m ycobacterium .

o

Test results read between 48 and 72 hours after adm inistration.

o

Interpretation of positive: 

>5 m m induration



Close contacts with tuberculosis



Positive chest radiographs



HIV

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

Organ transplant or other im m unosuppression



>10 m m induration



IV drug users



Im m igrants from high-prevalence countries



Underlying disease (diabetes, renal failure, m alignancies)



Health care workers



Prison inm ates



Institutionalized (nursing hom e, hom eless shelters)



>15 m m induration



Low-risk individuals

P.1157

Differential Diagnosis 

Bacterial pneum onia



Pneum ocystis Carinii pneum onia



Lung carcinom a



Bronchiectasis



Lung abscess



Lym phom a



Sarcoidosis



Coccidiom ycosis



Histoplasm osis

Treatment Pre Hospital Cautions:

Pa ge 4 9 1



Place patient in respiratory isolation (negative flow).



Place a m ask on the patient to prevent respiratory spread of the disease.



Initiate treatm ent with an IV, oxygen, and pulse oxim etry.



Endotracheal intubation m ay be required in patients with severe hem optysis or respiratory com prom ise.



Providers should wear subm icron-particulate filter m asks (N-95 designation).



Inform close contacts.

Initial Stabilization 

ABCs: o

Control airway as needed.

o

Adm inister oxygen as needed.

o

Place on cardiac m onitor and m easure pulse oxim etry.

o 

Establish IV access with 0.9% norm al saline.

Isolate patients in negative pressure room s with at least six air exchanges per hour.



Protection for health care workers (N-95 m asks)

ED Treatment 

Isolation and strict respiratory precautions



Treatm ent is augm ented due to increasing m ulti-drug resistance.



Any regim en m ust contain at least two drugs to which the tuberculous bacillus is susceptible.



CDC currently recom m ends initial therapy that includes four drugs.



Initial treatm ent is continued for 2 m onths and then tailored depending on culture susceptibilities.



Consult infectious disease specialists when treating HIV patients on antiretroviral therapies.

Pa ge 4 9 1



Directly observed therapy m ay be necessary to ensure com pliance in certain populations.

Medication (Drugs) 

Etham butol: 15â€“20 m g/kg, m ax. 1600 m g (peds: 15â€“20 m g/kg, m ax. 1 g) PO per day



Isoniazid: 5 m g/kg, m ax. 300 m g (peds: 10â€“15 m g/kg, m ax. 300 m g) PO per day



Pyrazinam ide: 15â€“30 m g/kg, m ax. 2 g (peds: 15â€“30 m g/kg, m ax. 2 g) PO per day



Rifam pin: 10 m g/kg, m ax. 600 m g (peds: 10â€“20 m g/kg, m ax. 600 m g) PO per day



Rifabutin: 5 m g/kg, m ax. 300 m g (peds: unknown) PO per day

Follow-Up Disposition Admission Criteria 

Respiratory com prom ise as in other pulm onary infections



Suspicion of diagnosis



Inability to com ply with outpatient therapy



Unavailable outpatient resources (no prim ary care physician)



Involuntary adm ission for noncom pliant outpatients occurs o

Be aware of respective state laws concerning involuntary adm ission (consult infectious disease specialist).

Discharge Criteria

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

Without respiratory com prom ise



Hom e isolation procedure com pliance



Ability and willingness to com ply with long-term therapy



Appropriate outpatient follow-up and treatm ent available



Notification of the public health authorities is m andatory

References 1. Am erican Thoracic Society. Diagnostic standards and classification of tuberculosis. Am Rev Respir Dis. 1990;142:725. 2. Am erican Thoracic Society. Treatm ent of tuberculosis and tuberculosis infection in adults and children. Am J Respir Crit Care Med. 1994;149:1359. 3. Centers for Disease Control and Prevention. Treatm ent of Tuberculosis, Am erican Thoracic Society, CDC, and Infectious Diseases Society of Am erica. MMWR 2003;52(RR11):1â€“77. 4. Isem an MD. Treatm ent of m ultidrug-resistant tuberculosis. N Engl J Med. 1993;329:784. 5. Isem an MD. Tuberculosis. In: Bennett JC, et al., eds. Cecil's textbook of m edicine, 20th ed. Philadelphia, PA: WB Saunders, 1996: 1683â€“1689. 6. Moran GJ, Talan DA. Tuberculosis. In Wolfson AB, et al., eds. Harwood Nussâ€™: Clinical Practice of Em ergency Medicine. 4th ed. Philadelphia, PA. Lippincott William s and Wilkins, 2005:751â€“756. 7. Neville K, Brom berg A, Brom berg R, et al. Escalating threat from tuberculosis: the third epidem ic. Thorax. 1995;50(Suppl 1):537â€“542.

Codes ICD9-CM 011.9

ICD10 A16.9

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Acknowledgement Thanks to the previous edition chapter author, Kathleen A. Raftery.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tularem ia

Tularemia

Ian Greenwald

Basics Description 

Tularem ia is an acute febrile illness caused by the sm all aerobic gram negative coccobacillus Francisella tularensis: o

Organism is highly infectious.

o

Person-to-person transm ission has not been reported.



Hum ans becom e infected through different environm ental exposures: o

Wounds inflicted by infected arthropods

o

Direct contact with infectious anim al tissue or fluid

o

Contact or ingestion of contam inated food, water or soil

o

Inhalation of infected aerosols (e.g., cutting grass with power m owers, which m ay aerolize the organism ).



The four m ajor strains of the bacteria have different virulence and geographic location: o



North Am erican strain is the m ost virulent.

Natural hosts: o

Lagom orphs and other rodents

Pa ge 4 9 2





Natural vectors: o

Ticks

o

Biting flies

o

Mosquitoes

o

Wild rabbits.

Weaponization of tularem ia accom plished during the cold war: o

Because of its infectivity and ability to be aerosolized, it rem ains a potential biological agent for m ass destruction.



Laboratory technicians handling culture specim ens are at high risk: o

F. tularensis cultures should only be m anipulated in a Biosafety Level 3 facility.

Etiology 

Individuals that spend tim e outdoors in endem ic areas at highest risk: o

Farm ers

o

Hunters

o

Forest workers

o

Those that handle anim al carcasses are at highest risk (taxiderm ist and butchers).



Although tularem ia can occur worldwide, it is endem ic in the northern hem isphere: o

Reported nationwide except Hawaii

o

States with the highest incidence include Missouri, Arkansas, South Dakota and Oklahom a.

Pediatric Considerations 

Children in rural areas are at risk because tim e spent outdoors in endem ic areas.



Recent case report in the United States of a child who

Pa ge 4 9 2

developed tularem ia from a com m ercially purchased pet ham ster after sustaining a superficial bite.

Diagnosis Signs and Symptoms 

Tularem ia has different presentations based on route of entry: o

Prim ary route of entry is through skin and m ost often a cutaneous ulcer develops.



Six form s of illness: o

Ulceroglandular: 

Most com m on presentation (70â€“80% of cases).



Inoculated cutaneously through as few as 50 organism s



Initially, a local cutaneous papule



Followed by tender regional adenopathy and constitutional sym ptom s to include fever, chills, m yalgias, and headaches

o

Glandular: 

Rare form



Tender regional lym phadenopathy with no local lesions

o

Ocular: 

Rare form



Organism enters through a splash of infected blood/fluid to the eye or is introduced by eye rubbing after handling infectious m aterials (e.g., rabbit carcass).



Edem a, conjunctivitis, injection, chem osis with

Pa ge 4 9 2

periauricular, subm andibular or cervical lym phadenopathy o

Pharyngeal: 

Rare form



From contam inated food or water.



Severe throat pain with exudative pharyngitis and regional lym phadenitis.

o

Typhoidal (aka septicem ic): 

Unapparent point of entry.



Fever develops along with severe diarrhea, bowel necrosis and pneum onia.



Occurs in 10â€“15% of cases and is m ost lethal if not recognized early and treated with antibiotics

o

Pulm onic: 

Secondary to inhalation



Seen in sheep shearers, farm ers, landscapers, and lab technicians



Fever, dry cough and pleuritic chest pain develop



Pneum onia can occur in 10â€“15% of patients with Ulceroglandular tularem ia and up to 50% of patients with Typhoidal tularem ia.

Physical Exam 

Fever



Tender, well-dem arcated cutaneous ulcer



Tender regional lym phadenopathy; lym ph nodes can develop fluctuance and spontaneously drain.



Exudative pharyngitis (with pharyngeal tularem ia)



Ulcerations of the conjunctiva with pronounced chem osis (with oculoglandular tularem ia)

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Tests Lab 

No rapid diagnostic test available



Routine lab studies nonspecific:



o

CBC can be norm al.

o

ESR m ight be slightly elevated.

Gram stains, cultures and tissue biopsies: o

Often negative



Blood cultures



Enzym e-linked im m unosorbent assay and polym erase chain reaction are available through reference laboratories.



Serum antibody titers: o

Typically do not obtain diagnostic levels until 10 or m ore days after the onset of the illness

o

A single titer of at least 1:160 for tube agglutination is diagnostic for tularensis infection.

Imaging 

Chest radiograph for: o

Consolidative process, pleural effusions and hilar adenopathy



CT scan of chest for: o

Severe pulm onary sym ptom s

o

Other possible etiologies of atypical pneum onia

Differential Diagnosis 

Ulceroglandular tularem ia m im ics include: o

Tuberculosis

o

Cat-scratch disease

o

Syphilis

o

Chancroid

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

o

Lym phogranulom a venereum

o

Toxoplasm osis

o

Sporotrichosis

o

Rat-bite fever

o

Anthrax

Ocular glandular tularem ia m im ics include: o







Adenoviral infection

Pharyngeal tularem ia m im ics include: o

Diphtheria

o

Bacterial pharyngitis

o

Infectious m ononucleosis

o

Adenoviral infection.

Typhoidal tularem ia m im ics include: o

Salm onella

o

Brucellosis

o

Legionella

o

Q fever

o

Malaria

o

Dissem inated fungal or m ycobacterial infections.

Pulm onary tularem ia m im ics include: o

Mycoplasm a

o

Legionella

o

Chlam ydia

o

Tuberculosis.

P.1159

Treatment Pre Hospital

Pa ge 4 9 2



Universal precautions



Airway, breathing, and circulation m anagem ent.



Treat dehydration/hypotension with NS fluid boluses.

Initial Stabilization 

ABCs



Supplem ental oxygen for hypoxia



Fluid resuscitation with norm al saline for intravascular volum e depletion or septic shock



Central line access for unstable patients



Vasopressors for persistent hypotension

ED Treatment 

Fever control with acetam inophen



Early adm inistration of antibiotic therapy after obtaining cultures.



Antibiotic options: o

First-line agents:streptom ycin or gentam icin continued for 10 days.

o

Ciprofloxacin if diagnosis of com m unity-acquired pneum onia in differential diagnosis

o

Tetracyclines or chloram phenicol: 

Continue for 14 days since only bacteriostatic.



Associated with a higher rate of treatm ent failures than the previously m entioned antibiotics.

Pediatric Considerations Streptom ycin or gentam icin are recom m ended as the first-line agents.

Medication (Drugs)

Pa ge 4 9 2



Chloram phenicol: 15 m g/kg IV q6h (adult and peds)



Ciprofloxacin: 400 m g (peds: 15 m g/kg) IV q12h



Doxycycline: 100 m g (peds: if weight â‰¥45 kg, 100 m g; if weight â‰¤45 kg, 2.2 m g/kg) IV q12h



Gentam icin: 5 m g/kg IV or IM q24h (peds: 2.5 m g/kg IV or IM q8h)



Streptom ycin: 1 g IM (peds: 15 m g/kg, not to exceed 2 g/d) q12h

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission for advanced age, neutropenia, severe hypoxem ia, hem odynam ic instability or patients presenting with Typhoidal tularem ia



In-patient floor bed adm ission for m ild to m oderate illness: o

Isolation bed required only for the purpose of ruling out other etiology (e.g., tuberculosis)

Discharge Criteria Outpatient therapy oral or IM therapy for m ild illness with close follow-up

References 1. Brief report: Tularem ia Associated with a Ham ster Biteâ€”Colorado, 2004. MMWR. 2005;53:1202â€“1203. 2. Centers for Disease Control; Sum m ary of notifiable diseases, United States, 1998. MMWR. 1998;46:iiâ€“vii, 3â€“87. 3. Centers for Disease Control; Tularem ia â€” United States,

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1990â€“2000. MMWR. 2002;51:181â€“184. 4. Dennis DT, Inglesby TV, et al. Tularem ia as a Biological Weapon. JAMA. 2001;285:2763â€“2773. 5. Hopla CE: The ecology of tularem ia, Adv Vet Sci Com p Med 1974;18:25. 6. Spach DH, et al. Tick-borne diseases in the United States. N Engl J Med. 1993;329:936â€“947.

Codes ICD9-CM 21.0

ICD10 A21.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tum o r C o m pressio n Syndro m es

Tumor

Compression Syndromes Richard Wolfe Martin J. Carey

Basics Description 

Com plications arising from the com pression or direct infiltration of solid tum ors on neural and vascular structures



Spinal cord com pression: o

Affects over 20,000 patients each year

o

Occurs in 5â€“14% of cancer patients

o

More than 50% of cases are m etastases from lung, breast, or prostate cancer.



Other neurologic tum or com pression: o

Brachial plexus

o

Recurrent laryngeal nerve com pression by m ediastinal lym ph nodes



Superior vena cava syndrom e (SVC): o

Obstruction of returning blood flow in the superior vena cave by com pression, infiltration, or throm bosis

o

Venous hypertension within the area ordinarily

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drained by the SVC o

In severe cases, gradual elevation of the intracranial pressure (ICP) with altered m ental status and com a

o

85% caused by m alignancy

Etiology 





Spinal cord com pression: o

Prostate cancer

o

Breast cancer

o

Lung cancer

o

Renal cancer

o

Multiple m yelom a

o

Melanom a

o

Thyroid cancer

o

Lym phom a

o

Sarcom a

Brachial plexus com pression: o

Lung cancer

o

Breast cancer

SVC syndrom e from tum or com pression: o

Lung cancer (m ost com m on): 

Sm all cell lung cancer prim arily

o

Postirradiation fibrosis

o

Lym phom a

o

Breast cancer

o

Testicular cancer

o

See differential diagnosis for nontum oral causes of the SVC syndrom e

Pediatric Considerations In children with spinal cord com pression, com m on causes are sarcom a, neuroblastom a, germ cell tum ors, and lym phom a.

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Diagnosis Signs and Symptoms History 



Spinal cord com pression: o

History of m alignancy

o

Back or neck pain: 

Prolonged



Worse with rest

o

Paresthesias

o

Difficulty am bulating

o

Constipation

o

Urinary retention

o

Urinary or fecal incontinence

o

Weight loss

Brachial Plexus com pression: o

Neuropathic pain involving the m edial aspect of the upper extrem ity



Intrathoracic vagal nerve com pression: o



Ipsilateral aching facial pain around the ear

SVC syndrom e: o

Orthopnea

o

Dyspnea

o

Tightness of the shirt collar

o

Cough

o

Chest pain

o

Headache

o

Blurred vision

o

Dizziness

o

Syncope

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Physical Exam 







Spinal cord com pression: o

Loss of rectal tone

o

Loss of anal wink

Laryngeal nerve com pression: o

Hoarseness

o

Vocal cord paralysis

Brachial plexus: o

Ulnar paresthesias

o

Weakness and wasting of intrinsic hand m uscles

o

Pan-plexopathy

o

Horner syndrom e

SVC syndrom e: o

Periorbital edem a

o

Conjunctival suffusion

o

Facial swelling

o

Facial plethora

o

Upper extrem ity edem a

o

Findings exacerbated by recum bent or stooped-over position

o

Usually worse in the early m orning hours

o

ICP m ay be elevated in severe cases: 

Altered m ental status



Com a



Papilledem a

Tests Imaging 

Chest radiograph: o

Spinal cord com pression: 

May identify a prim ary lung tum or



Helpful in excluding Tuberculous spondylitis

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o



SVC com pression: 

Mass present in 10%



Pleural effusion in 25%

Plain spinal radiography: o

Will show 85% of m etastases causing com pression

o

A norm al spine (or one showing just degenerative changes) on plain radiology does not exclude the diagnosis of possible cord com pression.



CT: o

More sensitive and specific than plain radiography and radionucleotide im aging in distinguishing benign from m alignant disease in spinal com pression syndrom e

o

To identify m ass and im pingem ent in vena cava obstruction



MRI: o

Study of choice for spinal cord com pression

o

Indicated in patients with back or neck pain and: 

History of cancer



Bowel or bladder dysfunction



Lower extrem ity weakness



Sensory loss

P.1161



Venography: o

Relative contraindication in SVC syndrom e because of possible bleeding

Diagnostic Procedures/Surgery 

CT m yelography: o

Indicated for spinal cord com pression when MRI is unavailable or contraindicated (pacem aker, severe

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claustrophobia). 

An invasive procedure is required to obtain a tum or biopsy in patients with SVC syndrom e: o

Bronchoscopy

o

Mediastinoscopy

o

Scalene node biopsy

o

Lim ited thoracotom y

Differential Diagnosis Spinal Cord Compression 

Intervertebral disk disease



Osteoporotic vertebral fractures



Spondylosis



Spondylitis



Epidural abscess



Prim ary bone tum ors



Arteriovenous m alform ations



Neurologic diseases



Multiple sclerosis



Am yotrophic lateral sclerosis



Transverse m yelitis



Spinal infarction

Superior Vena Cava Syndrome 

Pericardial tam ponade



Nephrotic syndrom e



Cor pulm onale



Cirrhosis: o

Nonm alignant etiologies of SVC syndrom e: 

Goiter



Pericardial constriction



Prim ary throm bosis



Idiopathic sclerosing aortitis

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

Tuberculous m ediastinitis



Fibrosing m ediastinitis



Histoplasm osis



Indwelling central venous catheters

Treatment Initial Stabilization 

Early diagnosis and treatm ent are the keys to an im proved outcom e.



Level of neurologic dysfunction on presentation is a key factor in the prognosis for spinal cord com pression.



Avoid IV line placem ent in upper extrem ities if severe SVC com pression present.

ED Treatment Spinal Cord Compression 

Corticosteroids (dexam ethasone): o

Adm inister in ED.

o

Higher doses alleviate the pain m ore rapidly, but studies indicate no significant difference in outcom e with regard to sphincter function or am bulation between the dose schedules.



Radiotherapy: o

Definitive treatm ent m odality



Pain m edication with narcotics



Oncology, radiotherapy, and neurosurgical consultation for further m anagem ent of tum or/m alignancy



Consider em piric broad spectrum antibiotics prior to the MRI if an epidural abscess is being considered.

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SVC Compression 

Manage the underlying m alignancy with either radiotherapy or chem otherapy.



Elevation of the head of the bed



Judicious use of diuretics will transiently im prove sym ptom s.



Adm inister steroids if respiratory com prom ise.



Urgent oncology referral



Intravascular stents m ay relieve the obstruction m ore rapidly.

Medication (Drugs) 

Dexam ethasone: 1 m g/kg loading dose, followed by 4â€“24 m g q6h



Furosem ide (Lasix): no prior useâ€”40 m g IVP; prior useâ€”double 24h dose (80â€“180 m g IV)



Hydrocodone/Acetam inophen: 5/500 m g PO q4hâ€“q6h



Oxycodone/Acetam inophen: 5/500 m g PO q4hâ€“q6h

Follow-Up Disposition Admission Criteria Adm ission is advisable for all patients presenting with a tum or-com pression syndrom e.

Discharge Criteria None

Issues for Referral

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

Radiation oncology should be consulted in patients presenting with tum or com pression.



Early neurosurgical consultation for patients with spinal cord com pression

References 1. Boogerd W, van der Sande JJ. Diagnosis and treatm ent of spinal cord com pression in m alignant disease. Cancer Treat Rev. 1993;19:129â€“150. 2. Byrne TN. Spinal cord com pression from epidural m etastases. N Engl J Med. 1992;327:614â€“619. 3. Johnston RA. The m anagem ent of acute spinal cord com pression. J Neurol Neurosurg Psychiatry. 1993;56:1046â€“1054. 4. Jordan JE, Donaldson SS, Enzm ann DR. Cost effectiveness and outcom e assessm ent of m agnetic resonance im aging in diagnosing cord com pression. Cancer. 1995;75:2579â€“2586. 5. Stock KW, Jacob AL, Proske M, et al. Treatm ent of m alignant obstruction of the superior vena cava with the self-expanding Wallstent. Thorax. 1995;50:1151â€“1156. 6. Wen PY, Schiff D. Neurologic com plications of solid tum ors. Neurologic Clinics. 2003;21(1).

Codes ICD9-CM 336.9

ICD10 T79.5

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tym panic M em brane Perfo ratio n

Tympanic

Membrane Perforation Andrew Chang

Basics Description 

Perforations can be classified in several ways: o

o

o

Duration: 

Acute (<3 m onths)



Chronic (>3 m onths)

Site: 

Pars tensa



Pars flaccida

Extent: 

Lim ited to one quadrant (<25%)



Two or m ore quadrants



Total perforation

Etiology 

Infection (acute otitis m edia): o

Most com m on cause of an acute perforation



Blunt traum a (slap to the ear)



Penetrating traum a (Q-tip)



Extrusion of tym panostom y tubes

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

Rapid pressure change (diving, flying): o

Rupture usually occurs between 100 and 400 m m Hg (at a depth of 2.6 feet, there is a pressure differential of 60 m m Hg).



Extrem e noise (blast)



Lightning



Acute necrotic m yringitis (Î²-hem olytic streptococcus)



Slag burns (welding or m etalworking)



Com plications of surgical procedures: o

Myringotom y, tym panoplasty, tym panostom y tube insertion

Diagnosis Signs and Symptoms History 

Ear pain (m ild)



Severe pain or com plete hearing loss in the affected ear suggests additional injuries.



Tinnitus



Vertigo (especially if perforation occurs in water)

Physical Exam 

Decreased hearing (partial)



Purulent or bloody discharge from ear canal



Insufflation via pneum atic otoscope: o

Sm all perforations m ay be evident only as an im m obile tym panic m em brane.

o

Holding pressure for 15 seconds (the fistula test) m ay cause nystagm us or vertigo if the pressure is transm itted through the m iddle ear and into a

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labyrinthine fistula. 

Weber test (tuning fork on m idline bone): o

Sound should be equal or louder in the injured ear, consistent with decreased conduction.

o

Sound localizing to the opposite side of injury indicates possible otic nerve injury.



Rinne test: o

Usually norm al (air conduction detected after bone conduction fades) or shows a sm all conductive loss

Essential Workup Clinical exam ination: 

Direct visualization of tym panic m em brane with otoscope



Test hearing in both ears.



Note any nystagm us with changes of position or pressure on the tragus occluding the canal (fistula sign).

Tests Lab If an aural drainage is present, it m ay be desirable to culture the drainage.

Imaging Cranial CT: 

Obtain if clinically indicated to rule out tem poral bone fracture

Differential Diagnosis 

Tem poral bone fracture



Serous otitis m edia



Infectious otitis m edia



Otitis externa



Cerum en im paction



Barotraum a

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

Acoustic traum a



Foreign body



Child abuse

Treatment Initial Stabilization ABCs of traum a care: 

Im m obilize cervical spine and investigate for intracranial injury when indicated.

P.1163

ED Treatment 

Rem ove debris from the ear canal: o

Do not irrigate because this m ay force m ore debris into the m iddle ear.

o

If the tym panic m em brane is not visible because of im pacted cerum en and suspicion for perforation is high, then rem ove cerum en by m anual disim paction or suctioning.



If clinically indicated, obtain CT scan to rule out tem poral bone fracture.



Prescribe antibiotics if there is evidence of infection (use broad-spectrum antibiotic if patient has been scuba diving). Antibiotic choices (7â€“10 days adm inistration): o

Am oxicillin

o

Trim ethoprim -sulfam ethoxazole

o

Cefixim e

o

Augm entin

Pa ge 4 9 4



Prophylactic antibiotics are not indicated.



Analgesics if needed for pain



The use of ototopical m edication is controversial because of the risk of ototoxicity: o

Most advocate an antibiotic-cortisone otic m edication whenever a discharge is present because this m ay treat or prevent an external canal infection and hasten the resolution of the m iddle-ear infection.





Urgent ear-nose-throat (ENT) consultation (indications): o

Vertigo

o

Sensorineural hearing loss

o

Severe tinnitus

o

Active and significant bleeding

o

Facial paralysis

Arrange outpatient ENT follow-up: o

After detailed exam ination and form al audiom etric tests, m ost otolaryngologists practice â€œwatchful waitingâ€• because m ost heal spontaneously.

o

Operative repair (patch or tym panoplasty) is reserved for the 10â€“20% that do not heal spontaneously.



Provide detailed discharge instructions: o

Occlude the ear canal with cotton coated in petroleum jelly or antibiotic ointm ent when showering to prevent entry of water into the m iddle ear, which can be painful.



o

Swim only with fitted earplugs.

o

Avoid forceful blowing of the nose.

Expected outcom e: o

Most perforations heal spontaneously in a few days to several m onths; in one study of children, 70% closed within 1 week, and 94% closed within 1 m onth.

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o

Perforations caused by m olten m etal or electrical burns are less likely to heal spontaneously.

o

Forceful entry of water, as in a water-skiing accident, is m ore likely to lead to infection.

o

Com plications include infection, dislocation of ossicles, perilym ph leak, and cholesteatom a.

Medication (Drugs) 

Am oxicillin: 250â€“500 m g (peds: 20â€“40 m g/kg/24h) PO t.i.d.



Augm entin: 250â€“500 m g (peds: 20â€“40 m g/kg/24h) PO t.i.d.



Cefixim e: 400 m g (peds: 8 m g/kg/24h) per day



Trim ethoprim -sulfam ethoxazole (Bactrim DS): 1 tablet (peds: 6â€“12 m g/kg/24h TMP PO b.i.d.

Follow-Up Disposition Admission Criteria 

Associated injuries requiring adm ission



Severe vertigo im pairing am bulation

Discharge Criteria Alm ost all patients will be discharged.

Issues for Referral N/A

References 1. Berger G. Nature of spontaneous tym panic m em brane perforation

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in acute otitis m edia in children. J Laryngol Otol. 1989;103:1150â€“1153. 2. Gladstone HB, Jackler RK, Varav K. Tym panic m em brane wound healing: an overview. Otolaryngol Clin North Am . 1995;28:913â€“933. 3. Kristensen S. Spontaneous healing of traum atic tym panic m em brane perforations in m an: a century of experience. J Laryngol Otol. 1992;106:1037â€“1050. 4. Kristensen S, Juul A, Gam elgaard NP, et al. Traum atic tym panic m em brane perforations: com plications and m anagem ent. Ear Nose Throat J. 1989;68:503â€“516. 5. Ott MC, Lundy LB. Tym panic m em brane perforation in adults: how to m anage and when to refer. Postgrad Med. 2001;110:81â€“84. 6. Fernandez G, Sharm a VM, Am edee RG. Traum atic perforation of the tym panic m em brane. J La State Med Soc. 2001;153:116â€“118.

Codes ICD9-CM 384.20

ICD10 H72.9

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ultravio let Keratitis

Ultraviolet

Keratitis Yasuharu Okuda

Basics Description Corneal epithelial dam age caused by direct exposure to ultraviolet (UV) light.

Etiology 

Work-related exposures seen in welders, electricians, and m echanics.



Recreational exposures include tanning booths and high-altitude sports.



Occurs with corneal absorption of UV light at wavelengths of 260â€“290 nm .



Related both to intensity and duration of exposure.

Diagnosis Signs and Symptoms History

Pa ge 4 9 4



Elicit history of exposure to UV light.



Sym ptom s typically occur 8â€“12 hours after exposure.



Com plaints m ay include: o

Severe pain

o

Photophobia

o

Tearing

o

Foreign body sensation

Physical Exam 

May have m ildly dim inished visual acuity.



Slit-lam p exam with topical ophthalm ic anesthetics: o

Injected conjunctiva

o

Multiple superficial punctate corneal lesions.

Essential Workup 

Accurate history including: o

Type of exposure

o

Tim ing and duration of exposure



Visual acuity



Com plete ocular exam ination including: o

Extraocular m ovem ents

o

Conjunctiva/sclera/cornea with fluorescein

o

Anterior cham ber checking for cell and flare

o

Eversion of lids to check for foreign bodies

Tests Imaging Orbital radiographs/ultrasound/CT/MRI for suspected intraocular foreign body

Differential Diagnosis 

Infection: o

Bacterial or viral conjunctivitis

o

Corneal ulcers

Pa ge 4 9 4



Allergic conjunctivitis



Foreign bodies



Chem ical burns: o

Acid

o

Alkali



Therm al burns



Traum atic iritis



Corneal abrasion

Treatment Initial Stabilization Apply topical anesthetic agents for pain relief and to obtain m ore thorough physical exam .

ED Treatment 

Initiate short-acting cycloplegic agent.



Apply topical antibiotic ointm ent.



Provide adequate oral analgesia as needed.



Apply eye patching for com fort: o

Soft double patching with m ild pressure for patient com fort

o

If both eyes involved, either patch both eyes or patch the eye that is m ore severely affected.

P.1165

Medication (Drugs) 

Cycloplegic agent:

Pa ge 4 9 5

o

Scopolam ine hydrobrom ide ophthalm ic solution, 0.25%:, one or two drops into affected eye, q6hâ€“q8h.

o

Cyclopentolate hydrochloride ophthalm ic solution, 0.5%:, 1 or 2 drops into affected eye, q6hâ€“q8h.



Topical anesthetic agent: o

Tetracaine hydrochloride ophthalm ic solution, 0.5%:, 1 or 2 drops into affected eye 

Do not prescribe as outpatient as it m ay decrease healing in and increase corneal ulcer form ation.



Topical antibiotic ointm ent: o

Erythrom ycin ophthalm ic ointm ent, 0.5%:, apply to affected eye q.i.d.

Follow-Up Disposition Admission Criteria Patients requiring bilateral patching with severe decreased visual acuity and whose social circum stances m ake it im possible for the patient to take care of his/or her own needs.

Discharge Criteria 

Nearly all patients m ay be discharged from ED following treatm ent with cycloplegics, topical antibiotics, and patching: o



Lesions usually heal com pletely within 24 hours.

Follow up with ophthalm ologist within 24â€“48 hours.

References

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1. Marx JA: Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 2. Xiang H, Stallones L, Chen G, et al. Work-related eye injuries treated in hospital em ergency departm ents in the US. Am J Ind Med. 2005;48(1):57â€“62. 3. Yanoff M, et al. Ophthalm ology. 2nd ed. St. Louis, MO: Mosby; 2004. 4. Yen Y, Lin Hs, Lin Hu, et al. Photokeratoconjunctivitis caused by different light sources. Am J Em erg Med. 2004;22:511â€“515.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urethral Traum a

Urethral Trauma

P. Yiannis Venieris

Basics Description 

Blood at the urethral m eatus, a palpable full bladder, and inability to void are com m on findings with urethral traum a.



Found in 14% of pelvic fractures



High association with bilateral pubic ram i fractures (aka Straddle fractures)



Fem ales: Urethral injuries are rare likely due to short, unexposed, and m obile urethras.



Girls <17 years old: higher injury rate likely from a m ore flexible pelvic ring



Bladder neck m ost com m only injured location.



Males: The urethra is divided into two sections.



Posterior urethra:



o

More com m only injured (~90%)

o

Prostatic portion

o

Mem branous

Anterior urethra: o

Injuries are rare.

o

Bulbar

Pa ge 4 9 5

o 

Penile

Posterior urethra injuries com prise up to 90% of traum a and have the classification schem e detailed below: o

Type 1: Urethra stretched but not ruptured

o

Type 2: Prostatic/m em branous portions disrupted (either partially or com pletely); urogenital diaphragm intact

o

Type 3: Urethral disruption both proxim al and distal to the genitourinary diaphragm

Etiology 



Fem ales: o

Straddle injuries

o

Rare with pelvic fractures

o

Childbirth or vaginal surgery

o

Sexual traum a/abuse

Males: o

Pelvic fractures: especially straddle injuries

o

Penetrating traum a, m utilation

o

Sexual activity/instrum entation

Diagnosis Signs and Symptoms History Traum a

Physical Exam 

Pelvic pain



Triad of blood at the urethral m eatus, inability to urinate, and a palpably full bladder



Blood at the m eatus found in 50% of cases.

Pa ge 4 9 5



â€œHigh-riding prostateâ€• has a sensitivity of <50%. Do not rely on this finding to rule out urethral traum a if suspected.

Essential Workup 

Fem ales: o

Perform a m eticulous vaginal exam to exclude vaginal laceration or other etiologies of bleeding.

o

If traum a is suspected, radiological evaluation of urethra should be perform ed.

o

If this is not possible, suprapubic aspiration or cystostom y should be done.



Male: o

Radiographic evaluation of urethral integrity should be perform ed before urinary catheter placem ent if injury is suspected.

o

If not possible, suprapubic aspiration or cystostom y should be perform ed.

Pediatric Considerations 

If an exam ination of the m ale or fem ale genitals cannot easily be perform ed, exam ination under anesthesia should occur.



An exam ination with procedural sedation or in the operating room , in addition to being better tolerated by the patient, allows the physician to rule out sexual abuse and to confirm that the injury is consistent with the history.

Tests Lab Urinalysis, hem atocrit, blood urea nitrogen, creatinine

Imaging

Pa ge 4 9 5



Retrograde urethrography (RUG): o

Water-soluble contrast is injected via a catheter-tipped syringe at the urethral m eatus.

o

Extravasation of contrast and its relation to the prevesical space and urogenital diaphragm should be noted.

o

Proxim ity of the extravasation to the m eatus and the bladder should be appreciated.

o

If the urethral tear is com plete, there will be no contrast within the bladder and m arked extravasation will occur.

o

A partial tear will dem onstrate contrast m aterial within the bladder with varying am ounts of extravasation.



Excretory urethrography to define proxim al urethral tears.



Cystography



40% of urethral injuries have concom itant bladder injuries.

Diagnostic Procedures/Surgery Urethral traum a warrants urgent urological consultation. P.1167

Differential Diagnosis 

Perineal and vaginal traum a



Bladder injury



Ureter or kidney traum a

Treatment Pre Hospital

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Pre hospital traum a protocols

Initial Stabilization Stabilization of m ultiple traum as takes precedence.

ED Treatment 

Urethral contusions, lacerations, and avulsions are best m anaged by an experienced urologist.



Bladder decom pression is an im portant initial innervation. If urethral Foley catheter placem ent is not possible, suprapubic aspiration/cystostom y m ay need to be perform ed.

Medication (Drugs) Appropriate analgesia

Follow-Up Disposition Admission Criteria 

Concurrent traum atic injuries



Need for em ergent operative m anagem ent of urethral, penile or bladder injuries

Discharge Criteria Isolated urethral injuries frequently m ay be m anaged in the outpatient setting after appropriate urinary catheterization or suprapubic cystostom y with next day urologic follow-up.

Issues for Referral Urologic follow-up is necessary if patient is discharged from ED.

Pa ge 4 9 5

References 1. Goldm an SM, Sandler CM, Corriere JN Jr, et al. Blunt urethral traum a: A unified, anatom ical m echanical classification. J Urology. 1997;157:85â€“89. 2. Rosenstein D, McAninch J. Urological em ergencies. Med Clinics of North Am . 2004;88(2). 3. Sm ith J, Denney P. Im aging of renal traum a. Radiologic Clinics of North Am . 2003;41(4). 4. Walsh P. et al, Cam pbell's Urology. 8th ed. Edition. New York, NY: Saunders Co., 2002

Miscellaneous SEE ALSO: Pelvic Traum a

Codes ICD9-CM 867.0

Pa ge 4 9 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urethritis

Urethritis

Aaron Pessl Kenneth Bramwell

Basics Description 

Urethritis is inflam m ation of the urethra from any cause (usually infection).



Associated with urethral discharge and dysuria



Urethritis m ay develop after exposure to a partner with a sexually transm itted disease (STD), bacterial vaginosis, or a urinary tract infection (UTI).



Urethritis m ay also develop after orogenital contact.

Etiology 

STD



The m ost com m on causes are: o

Neisseria gonorrhoeae (35%)

o

Chlam ydia trachom atis (25â€“50%)

o

Mycoplasm a genitalium and Ureaplasm a urealyticum (30%)



Rarer causes: o

Trichom onas vaginalis

o

Candidal species

o

Herpes sim plex virus

Pa ge 4 9 5

o

Genital warts

o

Alcohol

o

System ic illnesses

o

Urethral foreign bodies

Diagnosis 

Sym ptom s usually develop 1â€“2 weeks after exposure but can take up to 4â€“6 weeks.



Initially m inim al or absent in m any patients

Signs and Symptoms 

Urethral discharge, dysuria



Cloudy first portion of urine



Pyuria



Inguinal adenopathy m ay be present

History 

Assess color, consistency, and quantity of urethral discharge.



Associated sym ptom s of dysuria, urgency, frequency, hem aturia, and hem atosperm ia



Risk factors for STDs: o

Recent new partner or m ultiple sexual partners

o

Sym ptom s of partner

o

Anal/Oral practices

o

Young age

o

Lower socioeconom ic status

Physical Exam 

Staining on undergarm ents



Meatal crusting



Genital lesions

Pa ge 4 9 6



Lym phadenopathy



Palpate testes, epididym is, and sperm atic cord: o



Masses or tenderness

Foreskin, if present, should be retracted to allow exam ination of the glans.

Essential Workup 

Urethral swabs for N. gonorrhea, and Chlam ydia species will confirm the diagnosis.



A rapid plasm a reagin or venereal disease research laboratory should be drawn because STDs frequently occur together.

Tests Lab 

Gram stain and cultures from urethral swabs should be reviewed when the patient is re-evaluated by his or her physician after treatm ent.



DNA am plification (ligase chain reaction [LCR] or polym erase chain reaction [PCR]) can be used on first-void urine or urethral swab: o

Equal efficacy for diagnosing N. gonorrhea and Chlam ydia species



Urinalysis should be perform ed after urethral swabs to identify urinary tract infections.

Differential Diagnosis 

UTI



Prostatitis



Epididym itis



Orchitis



Pelvic inflam m atory disease



Reiter syndrom e

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Pediatric Considerations 

Urethritis in children should arouse suspicion of child abuse.



Because N. gonorrhoeae infects the entire vaginal vault in prepubescents, a speculum exam ination is not required: o

External exam ination and cultures are sufficient.

P.1169

Potential Complications 

Recurrent infections



Ascending UTIs, including pelvic inflam m atory disease and epididym oorchitis



Fallopian tube dam age and infertility



Arthritis



Conjunctivitis, uveitis, and blindness

Treatment Initial Stabilization Most patients will not require significant stabilization.

ED Treatment 

Treatm ent m ay be given em pirically based on probable etiologic causes.



Patients should be treated for both gonorrhea and Chlam ydia.

Medication (Drugs)

Pa ge 4 9 6



Gonorrhea o

Cefixim e: 400 m g PO once

o

Cefpodoxim e: 400 m g PO once

o

Ceftriaxone: 125 m g (peds: 25â€“50 m g/kg) IM/IV once



o

Ciprofloxacin: 500 m g PO once

o

Gatifloxacin: 400 m g PO once

o

Levofloxacin: 250 m g PO once

o

Ofloxacin: 400 m g PO once

o

Spectinom ycin: 2 g IM once

Chlam ydia: o

Azithrom ycin: 1 g (peds: 10 m g/kg/d 1, 5 m g/kg days 2 through 5) PO once

o

Doxycycline: 100 m g PO b.i.d. for 7 days

o

Erythrom ycin base: 500 m g (peds: 40 m g/kg/d div. q.i.d.) PO q.i.d. for 7 days

o

Erythrom ycin ethyl succinate: 800 m g (peds: 30â€“50 m g/kg/d div. q.i.d.) PO q.i.d. for 7 days

o

Levofloxacin: 500 m g PO per day for 7 days

o

Ofloxacin: 300 m g PO b.i.d. for 7 days

Alert Increasing incidence of quinolone-resistant N. gonorrhoeae nationwide

Follow-Up Disposition Admission Criteria Patients should not require adm ission for urethritis unless other com plaints or infections.

Pa ge 4 9 6

Discharge Criteria All patients should be discharged with follow-up arranged at an outside clinic or with their physician.

Issues for Referral 

If child abuse is suspected, child protective services m ust be involved, and the child should be adm itted if a safe hom e situation cannot be ensured.



Sexual partners should be evaluated.



In m any states, STDs require reporting.

References 1. Ingram DL. Neisseria gonorrhoeae in children. Pediatric Ann. 1994;23(7):341â€“345. 2. Lyon CJ. Urethritis. Clinics in Fam ily Practice. March 2005;7(1). 3. MMWR-Recom m endations and Reports. MMWR. Occtober 2002;51(RR-15). 4. Ness RB, Markovic N, Carlson CL, et al. Do m en becom e infertile after having sexually transm itted urethritis? An epidem iologic exam ination. Fertil Steril. 1997;68(2):205â€“213. 5. Nickel P, Naher H. Nongonococcal urethritis. Current Problem s Derm atology. 1996;24:97â€“104.

Codes ICD9-CM 597.80

Pa ge 4 9 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Retentio n

Urinary Retention

Anthony Huynh

Basics Description 

Norm al m icturition sequence: o

As the bladder fills, sensory stretch signals conducted to sacral cord through pelvic nerves and then back through parasym pathetics, supplying the body and neck of the bladder

o

Once m icturition reflex becom es powerful enough, an inhibitory reflex through som atic pudendal nerves from S-2â€“S-3 causes relaxation of external urethral sphincter.

o

Urination occurs if inhibition is m ore powerful than voluntary constriction signals.



Acute urinary retention (AUR): o

Sudden inability to void urine, resulting in bladder distention



More com m on in m en with advancing age than wom en, less com m on in children



Atonic bladder: o

More com m on in wom en

o

Decom pensated bladder that has resulted from years

Pa ge 4 9 6

of infrequent voiding o

Destruction of sensory nerve fibers from the bladder to spinal cord that prevents transm ission of stretch signals and prevents m icturition reflex contractions

o

Loss of bladder control occurs despite intact neurogenic connections to the brain.

o

Bladder fills to capacity and overflows a few drops at a tim e (overflow incontinence).



Autom atic bladder: o

From dam age of the spinal cord above the level of S-2â€“S-3

o

Micturition inhibited due to â€œspinal shockâ€• from the sudden loss of facillatory im pulse from the brainstem and cerebrum

o

Interm ittent straight catheterization facilitates the return of the excitability of m icturition reflex by preventing physical bladder injury.



Neurogenic bladder: o

From partial dam age in spinal cord or brainstem that interrupts inhibition

o

Sacral centers are in a constant state of excitation that even a sm all quantity of urine results in frequent and relatively uncontrollable m icturition.

Etiology 

Benign prostatic hypertrophy: m ost com m on in m en



Multiple sclerosis and diabetes: Most com m on in wom en and m ay be an early m anifestation of neurologic disease in children.



Bladder outlet obstruction: o

Benign prostatic hypertrophy

o

Prostate

o

Cancer

Pa ge 4 9 6









o

Acute prostatitis

o

Stones

o

Blood clots

o

Prostatic congestion

Detrusor m uscle failure: o

Acute spinal cord injury

o

Elderly patients

o

Sym pathom im etics

Neurologic causes: o

Detrusor hyperactivity with im paired contractility

o

Multiple sclerosis

o

Parkinson disease

o

Stroke

o

Herniated disk

o

Diabetes m elitis

o

Dem entia

o

Myasthenia gravis

o

Brain tum or

o

Landry-Guillain-BarrÃ© syndrom e

o

Bladder neck dysfunction

Urethral stricture: o

Meatal stenosis

o

Phim osis

o

Paraphim osis

o

Foreign body constriction

Gynecologic: o

Posturethropexy

o

Postvaginal delivery

o

Infectious

o

Periurethral abscess

o

Urinary tract infection

o

Constipation

Pa ge 4 9 6



Medications that cause AUR: o

Î²-Agonists

o

Î±-Adrenergic stim ulator

o

Narcotics

o

Anticholinergics

o

Musculotropic relaxants

Diagnosis Signs and Symptoms 

History of chronic voiding hesitancy: o

Decreased size and force of urine stream

o

Difficulty holding or initiating urinary stream

o

Feeling of incom plete bladder em ptying or postvoid residual

o

Interruption of urinary stream



Lower abdom inal pain



Distended and tender bladder

History Obtain a thorough history focusing on the size and force of urine stream , feeling of incom plete bladder em ptying, dribbling, and interruption of urinary stream .

Physical Exam Perform a through physical exam focusing on the neurological exam , abdom inal exam checking the bladder size, and prostate exam in m en.

Essential Workup 

Thorough history and physical exam ination



Urinalysis

Pa ge 4 9 6

Tests Lab 

Electrolytes, blood urea nitrogen, creatinine, and glucose



Urinalysis



For renal failure: o

Prostate-specific antigen

o

Urine culture

Imaging 

Ultrasound



CT scan



IV pyelography

P.1171

Treatment Initial Stabilization 

Urinary drainage by catheterization



Caution with history of urethral stricture or traum atic catheter insertion



Defer catheterization in patient with pelvic fracture, prostate displacem ent on rectal exam ination, or blood at the urethral m eatus until retrograde urethrogram .



Suprapubic catheter if urethral catheterization contraindicated or im possible



Palpable bladder essential

ED Treatment 

Drain bladder and m onitor urine output.

Pa ge 4 9 6



Place leg Foley bag before discharge if Foley is to rem ain indwelling.



Initiate therapy for underlying cause of AUR: o

Rapid decom pression following catheter placem ent m ay result in transient gross hem aturia in the chronically distended edem atous bladder.



Postobstructive diuresis: o

Com plication of AUR in the catheterized patient

o

Occurs from a com bination of factors, including osm otic diuresis, involvem ent of natriuretic and diuretic factors, disorder nephron function, altered tubular perm eability, and disturbance of sodium -regulating horm ones

o

Hypovolem ic or hypotensive m ay result in severe cases.



Observe for 4â€“6 hours all patients with chronic or insidious obstructive voiding sym ptom s and urinary retention with particular attention to hourly intake, urinary output, and vital signs.

Medication (Drugs) 

Baclofen (Lioresal) for external sphincter em ptying: 5 m g PO t.i.d., m ax. 80 m g/d (peds: 2â€“7 years old: 10â€“15 m g/24h div. q8h; titrate to m ax dose 40 m g/24h; >8 years old: m ax. dose 60 m g/d div. q8h)



Belladonna and opium (B and O) suppositories to alleviate the constant urge to urinate secondary to bladder spasm , frequently accom panying an indwelling catheter: 1 PO q4hâ€“q6h



Bethanechol (Urecholine) acts on the detrusor to em pty the bladder: 10â€“50 m g PO b.i.d./q.i.d.; SC: 5 m g (peds:

Pa ge 4 9 7

PO 0.6 m g/kg/24h div. q6hâ€“q8h; SC: 0.15â€“0.2 m g/kg/24h div. q6hâ€“q8h) 

Dantrolene (Dantrium ) for external sphincter em ptying: initial 25 m g PO per day, increase frequency to t.i.d.â€“q.i.d., then increase dose by 25 m g/dose at 4- to 7-day intervals (peds [not indicated <5 years old]: >5 years old: initial 0.5 m g/kg/dose PO b.i.d.; increm entâ€”increase frequency to t.i.d.â€“q.i.d. at 4- to 7-day intervals, then increase doses by 0.5 m g/kg)



Diazepam (Valium ) for external sphincter em ptying: IM or IV to 10 m g/dose q3hâ€“q4h PRN, PO: 2â€“10 m g/dose q6hâ€“q8h PRN (peds: IM OR IV 0.04â€“0.2 m g/kg/dose q2â€“4h (m ax. 0.6 m g/kg within an 8-hour period; PO: 0.12â€“0.8 m g/kg/24h div. q6â€“8h)



Doxazosin m esylate (Cardura) for vesical outlet em ptying: initial 1 m g PO per day, after 24 hours, increase to 2 m g PO per day then to 4, 8, 16 m g per day



Meperidine HCl (Dem erol) for external sphincter relaxation: PO, IM, IV: 50â€“150 m g/dose q3â€“4h PRN (peds: PO, IM, IV: 1.0â€“1.5 m g/kg/dose q3hâ€“q4h PRN, m ax. 100 m g)



Oxybutynin (Ditropan) for storage: 5 m g PO b.i.d.â€“t.i.d.



Phenoxybenzam ine HCl (Dibenzyline) for vesical outlet em ptying: 10 m g PO, increase dosage every other day, usually to 20â€“40 m g, b.i.d.â€“t.i.d.



Prazosin HCl (Minipress) for vesical outlet em ptying: initially 1 m g PO b.i.d. to t.i.d., slowly increase to 20 m g/d in divided doses



Tam sulosin (Flom ax) im press irritative and obstructive voiding sym ptom s: 0.4 m g PO every day initially; m ay increase to 0.8 m g PO every day



Alfuzosin (Uroxatral) for vesical outlet em ptying: 2.5 m g

Pa ge 4 9 7

PO t.i.d. 

Pseudoephedrine (Sudafed) for vesical outlet storage: 30â€“60 m g/dose PO q6hâ€“q8h, m ax. 240 m g/24h (peds: <12 years old: 4 m g/kg/24h PO div. q6h)



Terazosin (Hytrin) for vesical outlet em ptying: start 1 m g PO q.h.s., m ax. 20 m g/d



Trim ethoprim without sulfa (Trim pex or Proloprim ) for the duration of catheter insertion, if it is to rem ain indwelling for m ore than 5 days: 100 m g tablets per day or b.i.d.

Follow-Up Disposition Admission Criteria 

Significant postobstructive diuresis requiring IV fluids



Urosepsis

Discharge Criteria 

Good health with support system



No clinical or laboratory evidence of infection



Urology follow-up

References 1. Escobar JI II, Eastm an ER, Hardwood-Nuss AL. Acute urinary retention. In: Marx J, Hockberger R, Walls R, et al. eds. Rosen's em ergency m edicine. 5th ed. St. Louis, MO: Mosby, 2002 2. Gausehe M. Genitourinary surgical em ergencies. Pediatr Ann. 1996;25(8):458â€“464. 3. Nym an MA, et al. Managem ent of acute urinary retention: rapid vs gradual decom pression and risk of com plications. Mayo Clin Proc. 1997;72:951.

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4. Peter JR, Steinhardt GF. Acute urinary retention in children. Pediatr Em erg Care. 1993;9:205â€“207. 5. Sam m BJ, Dm ochowski RR. Urologic em ergencies. Postgrad Med. 1996;100(4):177â€“184.

Codes ICD9-CM 788.20

ICD10 R33

Pa ge 4 9 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Tract F istula

Urinary Tract

Fistula Anthony Huynh

Basics Description 

Fistulae can form between any part of the urinary tract and contiguous structures.



Com m unications between the urinary and gastrointestinal tracts, external perineum , and fem ale reproductive organs are m ost com m on.



Urinary fistulae: o

Typically not owing to prim ary urologic disease

o

Caused by a com plication of gynecologic surgery, childbirth, and gastrointestinal disorders

Etiology 

Vesicointestinal fistulae: o

Com plication of prim ary gastrointestinal disease

o

Diverticulitis: 50â€“60% of cases

o

Colon cancer: 20â€“25% of cases

o

Crohn disease: 10% of cases

o

Radiation enteritis: 7% of cases

o

Pelvic traum a: 5% of cases

Pa ge 4 9 7





o

Bladder cancer: 4% of cases

o

Other causes: 

Appendicitis



Gynecologic cancers



Tuberculosis

Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o

Gynecologic surgery: 80% of cases

o

Occurs 10â€“14 days after surgery

o

Obstetric com plication: 8â€“10% of cases

o

Pelvic irradiation: 6% of cases

o

Pelvic traum a: 4% of cases

Vesicocutaneous fistulae: o

Cervical or uterine cancer

o

Bladder cancer

o

Advanced prostatic cancer

Diagnosis Signs and Symptoms 



Vesicointestinal fistulae: o

Chronic or recurrent urinary tract infections

o

Most infections are caused by Escherichia coli.

o

Mixed organism s account for one third of infections.

o

Pneum aturia: 60% occurrence rate

o

Fecaluria: 40% occurrence rate

o

Abdom inal pain

o

Change in bowel habits

Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o

Constant leakage of urine from the vagina; described as watery vaginal discharge

o

Malodorous urine

Pa ge 4 9 7

o

Perineal derm atitis and m aceration

o

Severe perineal pain if fistula is a com plication of radiation therapy

o



Ureterovaginal fistula: 

Abdom inal pain



Flank tenderness



Fever



Drainage of urine through the operative site

Vesicocutaneous fistulae: o

Constant leakage of urine from bladder through fistula to skin

o

Usually located in perineal region: 

Perineal derm atitis and m aceration at site of leakage

History Thorough history points to diagnosis for urinary tract fistulae.

Physical Exam 

Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o

Clinical diagnosis is usually the key.

o

Speculum exam m ay reveal a sm all, reddened area of granulom atous tissue at site of fistula opening.

o

If uncertain whether vaginal discharge contains urine, give phenazopyridine (Pyridium ), 200 m g orally, and perform speculum exam 1 hour later.

o 

Orange discoloration of discharge confirm s fistula.

Vesicocutaneous fistula: o

Clinical diagnosis with thorough physical exam ination

Tests Lab 

Urinalysis:

Pa ge 4 9 7

o

Undigested food residue with vesicointestinal fistulae

o

Bacteria with vesicovaginal, urethrovaginal, and ureterovaginal fistulae

o

Bacteria and WBC with vesicocutaneous fistula

o

Detect charcoal in urine with the Bourne test after orally ingesting charcoal.



Urine culture: o

E. coli m ajor pathogen with vesicointestinal fistulae

o

One third infected with m ultiple organism s

o

Mixed organism s with vesicovaginal, urethrovaginal, and ureterovaginal fistulae

o

To exclude infection with vesicocutaneous fistula

Imaging 

Cystoscopy with or without fistulography is a reliable m eans of diagnosis.



CT scan has sensitivity close to 100% in diagnosing vesicointestinal fistulae.



Multidetector row CT urography

P.1173

Differential Diagnosis 



Vesicointestinal fistulae: o

Recurrent UTI

o

Other causes of pneum aturia

o

UTI with gas-form ing organism such as clostridia

o

Ferm entation of glucose in urine

o

Recent urinary tract instrum entation

Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o

Urinary incontinence

o

Copious vaginal discharge

Pa ge 4 9 7



Vesicocutaneous fistula: o

Urinary incontinence

Treatment Initial Stabilization Treat urosepsis with IV fluid bolus and IV antibiotics.

ED Treatment 

Vesicointestinal fistulae: o

Rule out com plications from patient's prim ary disease.

o

Obtain cultures if signs of UTI.

o

Initiate broad-spectrum antibiotic if infection found.

o

Antibiotic resistance is com m on.

o

Most patients have received m ultiple antibiotics for recurrent or chronic UTI.

o 

Urologic referral for definitive surgical therapy

Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o

Place Foley catheter for any patient suspected of having a genitourinary fistula.

o

Initiate broad-spectrum antibiotics if a UTI is present

o

Third-generation cephalosporin, fluoroquinolone, or am oxicillin/clavulanate

o 

Prom pt referrals to urologist and gynecologist

Vesicocutaneous fistula: o

Place Foley catheter.

o

Initiate broad-spectrum antibiotics if a UTI is present

o

Treat derm atitis and skin m aceration with: 

Antifungal cream s such as nystatin, clotrim azole, or m iconazole

Pa ge 4 9 7



Protective ointm ent applied to protect skin from m oisture

o

Third-generation cephalosporin, fluoroquinolone, or am oxicillin/clavulanate acid

o

Prom pt urology referral

Medication (Drugs) 

Am oxicillin/clavulanate: 875 m g PO b.i.d. or 500 m g PO t.i.d.



Am picillin/sulbactam : 3 g IV q6h



Cefaclor: 500 m g PO t.i.d.



Cefixim e: 400 m g PO per day



Ceftriaxone: 2 g IV per day



Ciprofloxacin: 400 m g IV or 500 m g PO b.i.d.



Levofloxacin (Levaquin): 500 m g PO per day

Follow-Up Disposition Admission Criteria 

Presence of urosepsis or septic shock



Unable to take oral antibiotics



Dehydration



Com plications from prim ary gastrointestinal disease or pelvic m alignancies



Bowel obstruction



Malnutrition

Discharge Criteria 

No evidence of urosepsis or shock

Pa ge 4 9 7



Able to adm inister oral antibiotics if urinary tract infections present



Able to care for Foley catheter

References 1. Caoili EM, Cohan RH, Korobkin M: Urinary tract abnorm alities: initial experience with m ulti-detector row CT urography. Radiology. February 2002;222(2):353â€“360. 2. Davits RJ, Miranda SI: Conservative treatm ent of vesicovaginal fistulas by bladder drainage alone. Br J Urol. August 1991;68(2):155â€“156. 3. Driver CP, Anderson DN, Findlay K, et al. Vesico-colic fistulae in Gram pian region: presentation, assessm ent, m anagem ent, and outcom e. J R Coll Surg Edinb. 1997;42:182â€“185. 4. Lee RA, Sym m onds RE, William s TJ. Current status of genitourinary fistula. Obstet Gynecol. 1988;72:313â€“319. 5. McVay KT, Marshall FF. Urinary fistulas. In: Gillenwater J, et al., eds. Adult and Pediatric Urology. 3rd ed. St. Louis, MO: Mosby; 1996. 6. Moos RL, Ryan JA. Managem ent of enterovesical fistulas. Am J Surg. 1990;159:514â€“517. 7. Shobeiri SA, Chesson RR, Echols KT. Cystoscopic fistulography: a new technique for the diagnosis of vesicocervical fistula. Obstet Gynecol. 2001;98:1124â€“1126.

Codes ICD9-CM 599.1 Urethral fistula

ICD10 N36.0

Pa ge 4 9 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Tract Infectio ns, Adult

Urinary Tract

Infections, Adult Paul A. Szucs Barnet Eskin

Basics Description 

Colonization of urine with uropathogens and invasion of genitourinary tract (GU)



Defined as urinary sym ptom s with â‰¥102â€“105 Ã— 10 5 CFU/m l of uropathogen and â‰¥10 WBC/m m 3

Uncomplicated Cystitis 

Fem ales aged 13â€“50



Sym ptom s <2â€“3 days



Not pregnant



Afebrile (tem perature <38Â°C)



No flank pain



No costovertebral angle tenderness (CVAT)



Fewer than four urinary tract infections (UTI) in past year



No recent instrum entation or previous GU surgery



No functional/structural GU abnorm ality



No im m unocom prom ising com orbidity



Neurologically intact

Pa ge 4 9 8

Complicated Cystitis 

Do not m eet above criteria



Male gender



Patients with anatom ic, functional, or m etabolic abnorm alities of GU tract



Postvoid residual urine



Catheters



Resistant pathogens



Recent antim icrobial use

Uncomplicated Pyelonephritis 

Renal parenchym al infection



Dysuria, frequency, urgency



Fever, chills, m yalgias



Flank, back or abdom inal pain



CVAT



Nausea, vom iting



Leukocytosis (com m on)

Complicated Pyelonephritis 

Renal parenchym al infection



Tem perature >40Â°C



Urosepsis with septic shock



Intractable nausea, vom iting



Diabetes



Pregnancy



Im m unosuppression



Asym ptom atic (occult)

Etiology Mechanism Organism s colonize periurethral area and subsequently infect the GU tract.

Pa ge 4 9 8

Risk Factors 



Population: o

Newborn, prepubertal girls, young boys

o

Sexually active young wom an

o

Post-m enopausal wom an, elderly m ales

Behavior: o

Sexual intercourse, sperm icides, diaphragm s

o

Elderly fem ales/postm enopausal state: 

Less efficient bladder em ptying, bladder prolapse, alteration of bladder defenses



Increased vaginal pH



Contam ination due to urinary or fecal incontinence (Enterobacteriaceae)

 o

Instrum entation

Elderly m ales due to prostatic hypertrophy and instrum entation



Organism s: o

Escherichia coli (80â€“85%)

o

Staphylococcus saprophyticus (10%)

o

Other (10%): Klebsiella, Proteus m irabilis, Enterobacter spp., Pseudom onas aeruginosa, group D streptococci

Diagnosis Signs and Symptoms Lower Tract Infection (UTI): Cystitis 

Dysuria, frequency, urgency



Hesitancy



Suprapubic pain

Pa ge 4 9 8



Hem aturia

Upper Tract Infection: Pyelonephritis 

Sym ptom s of cystitis: o

Fever, chills

o

Flank pain

o

CVAT

o

Nausea, vom iting, anorexia



Leukocytosis



Up to 50% m ay be without clinical sym ptom s: o

Sym ptom duration >than 5 days or hom eless are risk factors for upper tract infection



Elderly: o

Altered m ental status

o

Anorexia

o

Decreased social interaction

o

Abdom inal pain

o

Nocturia

o

Incontinence

o

Syncope or dizziness

Essential Workup 

Urinalysis (dipstick test, m icroscopy)



Fem ales: pregnancy test



Fem ales: rule out urethritis, vaginitis, pelvic inflam m atory disease (PID)



Males: rule out urethritis, epididym itis, prostatitis.



Males: inquire about anal intercourse and HIV.



Urologic evaluation in young healthy m ales with first UTI is not routinely recom m ended.

Tests Lab

Pa ge 4 9 8



Rapid Urine Screen o

Dipstick (leukocyte esterase + nitrite) m ost effective when urine contains 10 5 CFU/m l

o

Laboratory specim en unnecessary if pyuria and bacteriuria confirm ed by dipstick

o

o

Leukocyte esterase: 

Sensitivity 75â€“96%



Specificity 94â€“98%

Nitrite: 

Sensitivity 35â€“85%



Specificity 92â€“100%



Both tests have excellent negative predictive values.



Urinalysis/Microscopy: o

Obtain if rapid urine screen is unavailable or negative in patients with presum ed UTI.

o

10 WBC/m m 3 in clean catch m idstream urine indicates infection.

o

Bacteria detected in unspun urine indicates >10 5 CFU/m l.



Indications for urine culture: o

Com plicated UTIs

o

Negative rapid urine screen or m icroscopy in patients with presum ed UTI

o

Persistant signs and sym ptom s after 2â€“3 days of treatm ent

o

Recurrence (relapse versus reinfection)

o

Recently hospitalized patients

o

Nosocom ial infections

o

Pyelonephritis

o

Additional labs dictated by clinical setting

Imaging

Pa ge 4 9 8



Indicated for com plicated upper tract disease (see chapter: Pyelonephritis)



Helical CT, IV pyelogram or renal ultrasound if concom itant stone or obstruction suspected

Diagnostic Procedures/Surgery Patients with significant hem aturia, recurrent UTI with sam e uropathogen, or sym ptom s of obstruction need urologic evaluation to identify structural or functional abnorm ality. P.1175

Differential Diagnosis 

Pyelonephritis



Urethritis



Vulvovaginitis



PID/cervicitis



Prostatitis



Epididym itis



Nephrolithiasis



Appendicitis



Diverticulitis

Treatment Initial Stabilization 



Urosepsis/septic shock: o

Manage airway and resuscitate as indicated

o

IV crystalloid

o

Vasopressors as needed

Antibiotics:

Pa ge 4 9 8

o

Fluoroquinolone

o

Antipseudom onal penicillin with am inoglycoside

o

Carbapenem s

o

Third-generation cephalosporin with antipseudom onal activity

ED Treatment Stable Patients 

Prevalence of uropathogens resistant to trim ethoprim -sulfam ethoxazole (TMP/SMX) is increasing (up to 30%).



Antibiotics of choice: o

Fluoroquinolones (95% susceptibility rates)

o

TMP/Sulfam ethoxazole (SMX) (10â€“20% resistance)

o

Nitrofurantoin:

o



15â€“20% resistance



Bacteriostatic

Fluoroquinolones first-line treatm ent in wom en: 

Sulfonam ide intolerance



High frequency of antim icrobial resistance related to recent treatm ent



Live in areas with significant resistance to TMP/SMX (>10â€“20%)



Live in areas with unknown TMP/SMX resistance rates

o

Second or third-generation oral cephalosporins m ay be reasonable alternates (cefuroxim e, cefixim e) in specific circum stances. 

o

require 7-day treatm ent regim ens

Asym ptom atic bacteriuria occurs in 20% of wom en >65 years, 50% of wom en >80 years, and generally should not be treated.

Pa ge 4 9 8

o

Diabetic wom en have increased risk of bacteriuria with Klebsiella spp.

o

Treat dysuria with phenazopyridine.

o

Treat pain with appropriate analgesics.

o

Cranberry juice: 

May prevent the recurrence of UTI



Prevents E. coli from adhering to uroepithelial cells

o

Treatm ent of upper tract diseaseâ€”rule of 2s 

2 L of IV fluid



2 tablets of Tylenol #3



2 g of ceftriaxone or 2 m g/kg of gentam icin



If fever drops by 2Â°C and patient can retain 2 glasses of water



Discharge with fluoroquinolone for 2 weeks.



Follow up in 2 days.

Pregnancy Considerations 

Asym ptom atic bacteriuria in pregnancy



Treat with 3- to 7-day course of antibiotics: o

Cephalexin

o

Nitrofurantoin

o

TMP/SMX: 

SMX should not be used late in pregnancy as kernicterus can result.

o

Am oxicillin



Fosfom ycin also safe and effective in pregnancy



Nitrofurantoin contraindicated in pregnancy if patient G6PD-deficient



Quinolones not recom m ended during pregnancy: o

CNS reactions

o

Blood dyscrasias

o

Effects on collagen form ation

Pa ge 4 9 8

Medication (Drugs) 

Am oxicillin: 500 m g PO q12h or 875 m g PO q12h



Cefixim e: 400 m g PO per day or 200 m g PO q12h



Ceftazidim e: 1â€“2 g IV q8hâ€“q12h



Ceftriaxone: 1â€“2 g IV/IM q24h



Cefuroxim e: 250â€“500 m g PO q12h



Cephalexin: 250â€“500 m g PO q6h



Ciprofloxacin: 100â€“500 m g PO q12h



Fosfom ycin: 3 g single dose



Gentam icin: 2 m g/kg IV or IM q8h



Levofloxacin: 250 m g PO q24h



Nitrofurantoin: 100 m g PO q12 (sustained release)



Norfloxacin: 400 m g PO q12h or 800 m g PO q24h



Ofloxacin: 200 m g PO q12h or 400 m g IV q12h



Phenazopyridine: 200 m g PO t.i.d. for 2 days



o

For sym ptom atic treatm ent of dysuria

o

May turn urine and contact lenses orange

TMP/SMX: 160 m g/800 m g PO q12h or q8hâ€“q10h m g/kg IV q12h

Follow-Up Disposition Admission Criteria 

Inability to com ply with oral therapy



Unstable vital signs



Toxic appearance



Pyelonephritis

Pa ge 4 9 8

o

Intractable sym ptom s

o

Extrem es of age

o

Im m unosuppression

o

Urinary obstruction

o

Consider if coexisting urolithiasis

o

Significant com orbid disease

o

Outpatient treatm ent failure

o

Late in pregnancy

Discharge Criteria 

Well appearing



Stable vital signs



Can m aintain oral hydration



Can com ply with oral therapy



No significant com orbid disease



Adequate follow-up (48â€“72 hours) as needed



Healthy patients with uncom plicated pyelonephritis who respond to treatm ent in ED according to rule of 2s



Pyelonephritis in early pregnancy with good follow-up m ay be treated as outpatients

References 1. Hooton TM. Practice guidelines for urinary tract infection in the era of m anaged care. Int J Antim icrob Agents. 1999;11:241â€“245. 2. Hooton TM, Stam m WE. Diagnosis and treatm ent of uncom plicated urinary tract infection. Infect Dis Clin North Am . 1997;11(3):551â€“581. 3. McLaughlin SP, Carson CC. Urinary tract infections in wom en. Med Clin North Am . March 2004;88(2):417â€“429. 4. Stam m WE, Hooton TM. Managem ent of urinary tract infections in adults. N Engl J Med. 1993;329(18):1328â€“1334. 5. Warren JW, Abrutyn E, Hebel JR, et al. Guidelines for antim icrobial treatm ent of uncom plicated acute bacterial cystitis and acute

Pa ge 4 9 9

pyelonephritis in wom en. Clin Infect Dis. 1999;103(4):843â€“852.

Miscellaneous SEE ALSO: See Urinary Tract Infection, Pediatric

Codes ICD9-CM 599.0

ICD10 N39.0

Pa ge 4 9 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Tract Infectio ns, Pediatric

Urinary

Tract Infections, Pediatric Suzanne Z. Barkin

Basics Description 

Bacteria colonize via retrograde contam ination of rectal or perineal flora:



o

Infantsâ€”often hem atogenous spread

o

Older childrenâ€”vesicoureteral reflux m ajor risk

Urinary tract infection (UTI) is defined by culture with >10,000 organism s/m L on a catheterized or suprapubic specim en.



In infants 0â€“3 m onths old, UTI is associated with a 30% incidence of sepsis.



Predisposing factors: o

Poor perineal hygiene

o

Short urethra of fem ale

o

Fem ale > Male

o

Infrequent voiding

o

Constipation

o

Sexual activity

o

Circum cision probably reduces risk

Pa ge 4 9 9

Etiology 

UTI found in 4â€“7% of febrile infants



Bacterial agents: o

Escherichia coli accounts for 90%.

o

Klebsiella pneum oniae

o

Staphylococcus aureus

o

Enterobacter species

o

Proteus species

o

Pseudom onas aeruginosa

o

Enterococcus species

Diagnosis Alert UTIs in children m ay be difficult to diagnosis without laboratory confirm ation.

Signs and Symptoms 

Often nonspecific



Neonates:





o

Manifestations of sepsis

o

Feeding difficulties

o

Irritability, listlessness

o

Fever, hypotherm ia

1 m onth to 3 years of age: o

Fever

o

Irritability

o

Vom iting, diarrhea

o

Abdom inal pain

o

Poor feeding, failure to thrive

Hem aturia

Pa ge 4 9 9



In girls <2 years, an increased risk is associated with those having â‰¥three factors (<12 m onths old, white, tem p â‰¥39 C, absence of other source of fever, fever â‰¥2 days)



>3 years of age: o

Dysuria

o

Frequency

o

Enuresis

o

Pain: abdom inal, suprapubic, back, costovertebral (CVA)

o

Fever

o

Hem aturia

o

Malodorous cloudy urine

o

System ic toxicity: high fever and chills with CVA tenderness



Com plications: o

Recurrent UTI

o

Pyelonephritis

o

Chronic renal failure: 

Incidence of scarring greatest in children <1 year old



Scarring probably prevented by early detection and intervention

o

Perinephric abscess

o

Bacterem ia/Sepsis

o

Urolithiasis

Essential Workup 

Urinalysis with m icroscopic RBC and WBC counts, and gram stain for bacteria: o

Urinalysis alone has low diagnostic sensitivity in infants.

o

Causes of pyuria besides UTI include chem ical

Pa ge 4 9 9

(bubble bath) or physical (m asturbation) irritation, dehydration, renal tuberculosis, traum a, acute glom erulonephritis, respiratory infections, appendicitis, pelvic infection, and gastroenteritis. o

Leukocyte esterase correlates with presence of pyuria.

o

Positive nitrite test indicates presence of bacteria capable of fixing nitrate.

o

Gram stain of urinary sedim ent is m ore reliable than dipstick m ethods of diagnosis and superior to traditional urinalysis.

o

Up to 80% of urinalyses in neonates with docum ented UTIs m ay be norm al.



Urine culture: o

Specim en should be cultured within 30 m inutes or refrigerated.

o

False-negative results m ay be caused by dilution, im proper culture m edium , recent antim icrobial therapy, fastidious organism s, bacteriostatic agent in urine, and com plete obstruction of ureter.



Urine collection m ethods: o

Clean-catch in cooperative m ale children

o

Plastic bag collection adequate for urinalysis (70% contam ination rate)

o

Clean the perineum (fem ales) and glans (m ales) before application.

o

Can be used to rule out an infection if patient is not placed on antibiotics em pirically and follow-up culture possible



Positive culture usually needs to be confirm ed by suprapubic or catheterized specim en because contam ination is com m on:

Pa ge 4 9 9

o

Bladder catheterization: 

Acceptable in all infants



Higher success rate than suprapubic aspiration



Aseptic technique essential



Discarding the first 1â€“2 m L of urine before collecting specim en reduces contam ination.

o

Suprapubic aspiration: 

Most useful in infants



Full bladder optim al



Less com m only used than catheter



Ultrasound m ay be useful adjunctive m easure to im prove yield.

Tests Lab 

CBC and blood culture for young children with fever or nonspecific sym ptom s and no source on exam



Electrolytes, blood urea nitrogen, creatinine: o

Check if dehydration, pyelonephritis, or recurrent infection.

Imaging 

Children requiring radiologic evaluation: o

Infants <3 m onths of age

o

Males (increased association with anom aly) with first UTI

o

Clinical signs and sym ptom s consistent with pyelonephritis

o

Clinical evidence of renal disease

o

Som e suggest that girls younger than 3 years of age with a first UTI should be studied.

o

Fem ales older than 3 years of age

o

First UTI in patients who have a fam ily history of

Pa ge 4 9 9

UTIs, abnorm al voiding pattern, poor growth, hypertension, urinary tract anom alies or failure to respond prom ptly to therapy o 

Second UTI

Voiding cystoureterogram (VCUG) and ultrasound: o

UTI is associated with vesicoureteral reflux and other genitourinary abnorm alities.

o

Nuclear cystogram is often substituted for VCUG in fem ales.

o

Further evaluation with nuclear m edicine studies depends upon the grade of vesicoureteral reflex and response to treatm ent.

P.1177

Differential Diagnosis 

Infection: o

Volvovaginitis

o

Viral cystitis

o

Urethritis (Neisseria gonorrhea or Chlam ydia trachom atis)



o

Glom erulonephritis

o

Appendicitis

Traum a: o

Chem ical irritation

o

Perineal

o

Sexual abuse

o

Genitourinary

o

Masturbation

o

Foreign body



Nephrolithiasis



Diabetes

Pa ge 4 9 9

Treatment Initial Stabilization 

Treat infants <3 m onths old presum ptively for sepsis if febrile and/or toxic until blood and other appropriate cultures are final.



Airway intervention for septic/acidotic infants with depressed respiratory drive



20 m L/kg bolus 0.9% NS for dehydration, hypovolem ia, or sepsis; m ay repeat

ED Treatment 



Initiate IV antibiotics in all infants <3 m onths old: o

Am picillin and gentam icin in neonates

o

Cephalosporins after 4â€“8 weeks of age

Outpatient oral antibiotic for 7â€“10 days for children discharged: o

Am oxicillin

o

Am oxicillin/clavulanate

o

Am picillin

o

Cephalexin

o

Nitrofurantoin

o

Trim ethoprim -sulfam ethoxazole (TMP-SMX)

Medication (Drugs) 

Am oxicillin: 40 m g/kg/24h PO q8h



Am oxicillin/clavulanate: 40 m g/kg/24h PO q8h



Am picillin: 100 m g/kg/24h IV q6h



Cefotaxim e: 100 m g/kg/24h IV or IM q6â€“8h

Pa ge 4 9 9



Ceftriaxone: 50 m g/kg/24h q12hâ€“q24 h IV or IM



Cephalexin: 50 m g/kg/24h PO q6hâ€“q12h



Gentam icin: 2.5 m g/kg/dose IV q8h if full-term and age >7 days; 2.5 m g/kg/dose IV q12h if full-term and age 0â€“7 days (special dosing regim ens in infants <36 weeks postconceptual age)



Nitrofurantoin: 5â€“7 m g/kg/24h PO q6h



TMP-SMX (Bactrim , Septra suspension): 5 m L liquid (of 40/200 per 5 m L) per 10 kg per dose PO b.i.d.

Follow-Up Disposition Admission Criteria 

Infants <3 m onths of age



Dehydration



Ill appearance/toxicity/sepsis



Suspected pyelonephritis



Urinary obstruction



Vom iting, inability to retain m edications



Im m unocom prom ised patient



Renal insufficiency



Foreign body (indwelling catheter)



Pregnant

Discharge Criteria 

Sufficiently hydrated



Low risk for sepsis or m eningitis



Able to take oral antibiotics; com pliant

Issues for Referral 

Patients requiring adm ission often require a pediatrician,

Pa ge 4 9 9

urologists, or infectious disease consultant. 

Good follow-up is m andatory.

References 1. Am erican Academ y of Pediatrics, Subcom m ittee on Urinary Tract Infection. Practice param eter: the diagnosis, treatm ent and evaluation of the initial urinary tract infection in febrile infants and young children. Pediatrics. 1999;103:843. 2. Dayan PS, Bennett J, Best R, et al. Test characteristics of urine gram stain in infants â‰¤60 days of age with fever. Pediatr Em erg Care. 2002;18:12. 3. Dick PT, Feldm an W. Routine diagnostic im aging for childhood urinary tract infection: a system atic overview. J Pediatr. 1996;15â€“28. 4. Gorelick MH, Hoberm an A, Kearney D, et al, Pediatr Em erg Care. 2003;19:162â€“164 5. Nelson DS, Gurr MB, Schunk JE: Managem ent of febrile children with urinary tract infections. Am J Em erg Med. 1998;16:643â€“647. 6. Peniakov M, Antonelli J, Naor O, et al: Reduction of contam ination of urine sam ples obtained by in-out catheterization by culturing the later urine stream . Pediatr Em erg Care. 2004;6:418. 7. Sm eilie JM, Jodal U, Lax H: Outcom e of 10 years of severe vesicoureteral reflux m anaged m edically. J Pediatr. 2001;139:656.

Miscellaneous SEE ALSO: Urinary Tract Infection, Adult

Codes ICD9-CM 599.0

ICD10

Pa ge 5 0 0

P39.3

Pa ge 5 0 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urticaria

Urticaria

Jeffrey Horton

Basics Description 

Skin m ast cell release of inflam m atory m ediators, prim arily histam ine: o



Increased vascular perm eability and pruritus

Edem a of the epiderm is, upper and m id derm is

Pediatric Considerations 

Urticaria often the result of reactions to foods



Swelling of distal extrem ities and acrocyanosis m ay be prom inent in infants.



Bullae m ay form in the center of the wheal, especially on legs and buttocks.

Etiology Acute 



Drugs: o

Penicillin

o

Sulfa

o

Aspirin, NSAID

o

ACE inhibitors

Foods or additives

Pa ge 5 0 0



Insect bites, stings



Connective tissue, endocrine disorders



Cancers



Pregnancy, m enstrual cycle



Infections: o

Virus (including hepatitis)

o

Bacteria

o

Fungus

o

Parasite



Inhalant or contact allergen



Em otional stress



Physical urticariaâ€”m ore than 20 identified types, including: o

o

o

o

Derm ographism : 

Most com m on form



Reaction to skin pressure



Linear wheals under tight clothing



Areas scratched with a firm object

Cholinergic: 

Monom orphic wheals 2â€“3 m m



Bright red flare and intense pruritus

A response to elevated core tem perature: 

Hot bath



Fever



Exercise

Other rare form s: 

Cold-induced (m ay be fatal in cold im m ersions)



Delayed pressure



Sun exposure



Aquagenic



Vibratory

Chronic

Pa ge 5 0 0



75% idiopathic



Often an unrecognized recurring physical urticaria



May be due to occult or sub-clinical infection or system ic disease

Diagnosis Signs and Symptoms 

Generalized, transient, pruritic, well-circum scribed skin eruptions:



o

May include palm s or soles

o

Erythem atous or white

o

Nonpitting

o

Edem atous plaques (wheals)

o

May be surrounded by white or red ring (flare)

o

May have clear center

o

Intense swelling

o

May see bullae or purpuric lesions

Lesions are various sizes and shapes, haphazard distribution, and m ay becom e confluent.



Wheals usually resolve in 3â€“4 hours



New lesions evolve as old ones resolve.



Acute: <6 weeks



Chronic: >6 weeks



May be associated with system ic features:



o

Hypotension

o

Flushing

o

Headache

o

Dizziness

o

Respiratory distress

May be part of anaphylactic reaction:

Pa ge 5 0 0



o

Respiratory distress and hypotension

o

Angioedem a: 

Edem a of lower derm is



Swelling of face and tongue

Derm ographism : o

Scratch skin with a tongue blade; observe for linear wheal.



Cholinergic: o

Exercise challenge to raise core tem p.



Expose to sunlight.



Cold-induced: o



Aquagenic: o



Suspect angioedem a (see Angioedem a).

Severe reaction with hypotension: o



Apply tap water at differing tem peratures.

Significant m ucosal edem a: o



Place an ice cube on skin for 5 m inutes.

Suspect anaphylaxis

Prolonged, painful, or nonblanching lesions: o

Suspect vasculitis (see Vasculitis)

Essential Workup Com plete history and physical exam : 

Lesion appearance, location, tim ing, duration



Acute versus chronic



Associated sym ptom s, triggers



Co-existing diseases, allergies, m edications



Environm ent, exposures, and new foods



Characteristics and location of hives



Evaluate for sources of infection and signs of system ic diseases.

Tests

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Lab 

Acute cases: not needed



Chronic cases: o

Evaluate for infection or system ic disease: 

CBC with differential, erythrocyte sedim entation rate



Thyroid-stim ulating horm one and thyroid functions

 

Urinalysis, liver function tests

Skin biopsy if urticarial vasculitis suspected (not done in ED)

Imaging 

Acute cases: not needed



Chronic cases: o

Chest, sinus, or dental radiographs m ay help identify subclinical infection.

Treatment Pre Hospital Cautions: 

Patients with severe allergic reactions can progress rapidly to respiratory failure.



Severe reaction: o

Manage airway, oxygen.

o

Parenteral or inhaled Î²-agonist

o

IV crystalloid

o

Vasopressors as needed

ED Treatment

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

Largely sym ptom atic except in severe reactions



Avoid offending agent.



Î²-agonist (parenteral or inhaled): o



H 1-receptor antagonist (first or second generation): o



Severe hives, angioedem a, system ic features

Mainstay of treatm ent

H 2-receptor antagonist: o

May be beneficial as adjunct to H 1 -blocker when no response to H 1 -blocker alone



Corticosteroid (oral): o



Tricyclic antidepressants: o



Potent histam ine blockers

Avoid aspirin, NSAIDs, and opiates: o



Severe or refractory cases

May exacerbate condition

Concurrent use of ketoconazole or m acrolides alters hepatic m etabolism of antihistam ine; use with caution.



Chronic urticaria unresponsive to antihistam ines m ay respond to colchicine or dapsone; topical steroids are not effective.

P.1179

Medication (Drugs) Î²-agonist 

Albuterol (0.5% solution): 0.5 m L nebulized q20m in PRN (peds: 0.01â€“0.05 m L/kg/dose [m ax. 0.5 m L/dose] nebulized q20m in PRN)



Epinephrine (1:1000 solution): 0.1â€“0.5 m g SC or IM

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q10m inâ€“q15m in PRN (peds: 0.01 m g/kg, SC [m ax. single dose not to exceed 0.3 m g] q15m in PRN) 

Terbutaline: 0.25 m g SC q15m inâ€“q30m in PRN (m ax. 0.5 m g q4h); (peds: <12 years old; 0.005â€“0.01 m g/kg [m ax. 0.4 m g/dose] SC q15m inâ€“q20m in Ã— 3 PRN)

H 1-Receptor Antagonist (First Generationâ€”Sedating) 

Diphenhydram ine hydrochloride (Benadryl): 25â€“50 m g PO, IV, or IM, up to q6h (peds: 5 m g/kg/24h divided q.i.d. [m ax. 300 m g/24h])



Hydroxyzine hydrochloride (Atarax): 25â€“50 m g PO or IM up to q.i.d. (peds: 2 m g/kg/24h PO div. q.i.d. or 0.5â€“1 m g/kg IM q4hâ€“q6h PRN)

H 1-Receptor Antagonist (Second Generationâ€”Less Sedating, Not as Effective) 

Cetirizine (Zyrtec): adult and peds â‰¥6 years old: 5â€“10 m g PO q.d. (peds: 2â€“6 years old: 2.5 m g per day to b.i.d.)



Loratadine (Claritin): 10 m g PO b.i.d.



Fexofenadine (Allegra): 60 m g PO b.i.d. or 180 m g PO per day

H 2-Receptor Antagonist (Suggested Dosage) 

Cim etidine (Tagam et): 300 m g PO, IV, or IM b.i.d. (peds: infants <1 year: 10â€“20 m g/kg/24h PO, IV, or IM div. q.i.d.; >1 year old: 20â€“40 m g/kg/24h PO, IV, or IM div. q.i.d.)



Fam otidine (Pepcid): 20 m g IV q12h or 20â€“40 m g PO q.h.s. (peds: 0.6â€“0.8 m g/kg/24h IV [m ax. 40 m g/24h] div. q8hâ€“q12h or 1â€“1.2 m g/kg/24h [m ax. 40 m g/24h]

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PO div. q8hâ€“q12h) 

Ranitidine (Zantac): 150 m g PO b.i.d. (peds: neonate: 2â€“4 m g/kg/24h PO div. q8hâ€“q12h or 2 m g/kg/24h IV div. q6hâ€“q8h; infants and children 4â€“5 m g/kg/24h PO div. q8â€“12h or 2â€“4 m g/kg/24h IV or IM div. q6hâ€“q8h)

Corticosteroid 

Prednisolone: 50 m g PO per day for 3 days (peds: 0.5â€“2 m g/kg/24h [m ax. 80 m g/24h] div. per day to b.i.d. for 3â€“5 days)



Prednisone: 40 m g PO per day or 20 m g PO b.i.d. for 3â€“5 days (peds: 1â€“2 m g/kg/24h [m ax. 80 m g/24h] div. per day to b.i.d. for 3â€“5 days)

Tricyclic Antidepressant 

Doxepin (Sinequan): 10â€“25 m g PO t.i.d. (peds: not approved for under 12 years of age)

Disposition Admission Criteria 

Respiratory distress or failure



Refractory hypotension or shock



Severe refractory cases requiring IV m edications



Other system ic disease or infection

Discharge Criteria 

Norm al ventilation and oxygenation



Norm al blood pressure



Absence of other condition requiring adm ission



Sym ptom s controlled



Adequate ability of caregivers at hom e to m onitor for further exacerbations

References

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1. Habif TP. Skin disease diagnosis and treatm ent. 2nd ed. China: Mosby, 2005 2. Hurwitz S. Clinical pediatric derm atology. Philadelphia, PA: WB Saunders, 1993:516â€“519. 3. Mahm ood T. Urticaria. Am Fam Physician. 1995;51(4):811â€“816. 4. Mahm ood T. Physical urticarias. Am Fam Physician. 1994;49(6):1411â€“1414. 5. Sveum RJ. Urticaria. Post Grad Med. 1996;100(2):77â€“84.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vaginal Bleeding in Pregnancy

Vaginal

Bleeding in Pregnancy Paul Ishimine

Basics Description 

Leading cause of m aternal/fetal m orbidity and m ortality



Early pregnancy hem orrhage (â‰¤20 weeks):



o

Occurs in 30% of all pregnancies

o

50% lead to spontaneous abortion.

Late pregnancy hem orrhage (>20 weeks): o



Occurs in 3â€“5% of all pregnancies

Risk factors: o

Risk factors differ for each underlying cause of vaginal bleeding: 

Advanced m aternal age



Substance abuse (e.g., cocaine, tobacco)



Pelvic inflam m atory disease (PID)



Previous cesarean section



Previous term ination of pregnancy



Dilation and curettage (D&C)



Previous ectopic pregnancy



Increased parity

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

Multiple gestation



Pre-eclam psia



Hypertension



Traum a

Genetics 50â€“60% of m iscarriages due to chrom osom al abnorm alities

Etiology 



Structural lesions: o

Vaginal

o

Cervical

o

Uterine

o

Uterine-placental interface

Hem atologic dysfunction

Diagnosis Signs and Symptoms History 

Intensity and duration of bleeding: o

Am ount

o

Color (dark or bright red)

o

Painful or painless

o

Watery, blood-tinged m ucus, clots or tissue: 

Spontaneous abortion: classically cram py, diffuse pelvic pain



Ectopic pregnancy: classically sharp pelvic pain with lateralization



Placenta previa: classically painless, bright red hem orrhage



Placental abruption: classically painful, dark red

Pa ge 5 0 1

hem orrhage o

Life-threatening conditions m ay present with only m inim al vaginal bleeding



Last m enstrual period



Estim ated duration of gestation



Parity



Fever



Last intercourse



Previous obstetric-gynecologic com plications

Physical Exam 

Vital signs: o

Tachycardia

o

Hypotension

o

Orthostatic changes in pulse or blood pressure

o

Signs of hem odynam ic instability m ay be absent due to pregnancy-related physiologic increase in blood volum e.



Fetal heart tones: o

Fetal cardiac activity seen on transvaginal ultrasound at 6.5 weeks

o

Auscultated with Doppler past 10 weeksâ€™ gestation



Abdom inal exam ination: o

Uterine size

o

Peritoneal signs

o

Firm or tender uterus in late pregnancy suggests abruption



Pelvic exam â€”only in early pregnancy: o

Evaluate source and intensity of bleeding.

o

Determ ine patency of cervical os (perform this with a finger and only in the first trim ester): 

Threatened abortion: os closed

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o



Inevitable abortion: os open



Incom plete abortion: os open or closed



Com plete abortion: os closed



Em broynic dem ise (m issed abortion): os closed

Products of conception m ay be noted in incom plete or com pleted abortion: 

Products of conception in the cervical os can result in profuse bleeding.

o

Evaluate uterine size, tenderness.

o

Evaluate for uterine fibroids or adnexal m asses.

o

Late pregnancy: Do not perform pelvic exam unless in controlled operating room setting: 

Severe hem orrhage m ay ensue.



Placenta previa or vasa previa m ust be ruled out by sonography prior to pelvic exam .

Essential Workup 

CBC



Type and screen



Quantitative HCG in early pregnancy



Urinalysis



Ultrasound: o

Transvaginal ultrasonography provides m ore inform ation than transabdom inal ultrasonography, especially early pregnancy.

Tests Lab 

CBC: o

Dilutional â€œanem iaâ€• is a norm al physiologic change in pregnancy: 



Blood volum e expands by 45%

Quantitative Î²-hum an chorionic gonadotropin (Î²-hCG):

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o

Useful to correlate with ultrasound findings

o

Detectable 9â€“11 days following ovulation

o

Î²-hCG doubles every 48 hours in norm al early pregnancy until 10 weeks of gestation.



Blood typing and Rh: o



Cross-m atch if significant bleeding

Prothrom bin tim e, partial throm boplastin tim e, and dissem inated intravascular coagulation panel in em bryonic dem ise, placental abruption



Blood cultures with septic abortion



Suspected products of conception to lab for identification of chorionic villi

Imaging 

Ultrasound: o

Essential to the evaluation of bleeding in pregnancy 

Transvaginal ultrasound is m ore helpful than transabdom inal ultrasound in early pregnancy bleeding.



Confirm s intrauterine pregnancy (IUP)



Detects gestational sac at 5 weeks or Î²-hCG = 1000â€“2000 IU, yolk sac at 6 weeks, and cardiac activity at 5â€“6 weeks of gestation



Essentially rules out ectopic pregnancy by showing IUP (except in wom en using assisted reproductive technology)



Proves ectopic pregnancy by showing fetal pole outside uterus



Suggests ectopic pregnancy by detecting free fluid in cul de sac or adnexal m ass



Detects retained products of conception

Diagnostic Procedures/Surgery

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



Culdocentesis: o

Lim ited use with ultrasound available

o

Identifies free fluid in cul-de-sac

Suction D&C o

Indicated if suspected incom plete or septic abortion or em bryonic dem ise, gestational trophoblastic disease, blighted ovum to evacuate retained products of conception



Laparoscopy/laparotom y o

Indicated for unstable patients not responsive to resuscitation m aneuvers

o

Definitive diagnosis and treatm ent of ectopic pregnancy

Differential Diagnosis 

Early pregnancy (<20 weeks): o

Im plantation bleeding

o

Threatened abortion

o

Com plete, incom plete, inevitable, em bryonic dem ise (m issed abortion), and septic abortion

o

Ectopic pregnancy

o

Infection (e.g., cervicitis)

o

Traum a

o

Gestational trophoblastic disease

o

Cervical and vaginal lesions (e.g., polyps, ectropion, carcinom a):



Blighted ovum (anem bryonic gestation) o



Bleeding disorders

Late pregnancy (>20 weeks): o

Abruptio placenta (30%)

o

Placenta previa (20%)

o

Bloody show

o

Vasa previa

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o

Cervical/vaginal traum a or pathology

o

Uterine rupture (uncom m on)

o

Bleeding disorders

P.1183

Treatment Pre Hospital 

Unstable vital signs warrant aggressive resuscitation and continuous cardiac m onitoring.



In late pregnancy, position patient on left side to decrease uterine com pression of vena cava.



Consider preferential transport of a wom an greater than 23â€“24 weeks gestation with vaginal bleeding to a facility with obstetric capabilities.

Initial Stabilization 

Airway m anagem ent, resuscitation as indicated



Oxygen



Pulse oxim etry



Cardiac m onitor



Two large-bore IV lines with norm al saline or lactated Ringer solution infusion



Blood transfusion as indicated

ED Treatment 

All wom en with early pregnancy vaginal bleeding m ust be evaluated for ectopic pregnancy, (preferably by transvaginal ultrasound).



Adm inister anti-Rh im m une globulin if patient is

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Rh-negative. 

Suspected ectopic pregnancy: o

Unstable: consider bedside US with em ergent OB consultation for laparoscopy/laparotom y

o

Stable: perform US; if confirm s or suggestive of ectopic pregnancy, obtain OB consultation for surgery or m ethotrexate therapy



Threatened abortion:



Em ergent OB/gyn consultation for heavy/uncontrolled bleeding



Arrange OB/gyn follow-up for m inim al bleeding



Inevitable/incom plete/m issed (em bryonic dem ise) abortion: o

Products of conception in the cervical os can result in profuse bleeding: 

If products of conception cannot be rem oved with gentle traction, obtain em ergent OB/GYN consultation.

o 

Arrange follow-up with OB/GYN if bleeding m inim al.

Com plete abortion: o

Em ergent OB/GYN consultation for heavy/uncontrolled bleeding

o 



Arrange follow-up with OB/GYN if bleeding m inim al.

Septic abortion: o

Initiate broad-spectrum antibiotic therapy.

o

Em ergent OB/GYN consultation for D&C

Late pregnancy vaginal bleeding: o

Hem odynam ic stabilization: 

Fluid resuscitation



Positioning of patient onto left side or displacem ent of uterus laterally to relieve com pression of the inferior vena cava

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

Because of com pensatory hem odynam ic changes during pregnancy, significant hypovolem ia m ay exist with m inim al vital sign abnorm alities.

o

Dissem inated intravascular coagulation: 

Associated with late pregnancy bleeding



Especially with placental abruption



Treated with blood, coagulation factors and platelets

o

Obstetric consultation and rapid transfer to obstetric unit

Medication (Drugs) 

Anti-Rh 0 (D) im m une globulin: <12 weeksâ€”50 m cg IM; >12 weeksâ€”300 m cg IM



Septic abortion: o

Multiple acceptable antibiotic regim ens

o

Must provide polym icrobial coverage

Follow-Up Disposition Admission Criteria 



Early pregnancy vaginal bleeding with: o

Unstable vital signs or significant hem orrhage

o

Ruptured ectopic pregnancy

o

Incom plete abortion (open os)

o

Septic abortion

All patients with late pregnancy vaginal bleeding need to be adm itted to a labor and delivery unit.

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Discharge Criteria 

Threatened abortion (closed os) with stable sym ptom s



Com plete abortion, em bryonic dem ise, blighted ovum with stable sym ptom s



Asym ptom atic, hem odynam ically stable patient with sm all, unruptured ectopic (or suspected ectopic) pregnancy after OB consultation



Controlled bleeding from local vaginal/cervical source

Discharge Instructions 

No strenuous activity, tam pon use, douching, or intercourse



Seek m edical advice for increased pain, bleeding, fever, or passage of tissue

Issues for Referral 

Wom en with known ectopic pregnancy or in whom ectopic pregnancy is suspected need to have beta-HCG levels checked in 48 hours.



Patients with em bryonic dem ise, blighted ovum , or gestational trophoblastic disease need to be referred for uterine evacuation if D&C not perform ed in ED.



Wom en with threatened, inevitable, com plete, or m issed (em bryonic dem ise) abortion should have OB/GYN follow-up with 24â€“48 hours

References 1. Am erican College of Em ergency Physicians Clinical Policies Com m ittee and the Clinical Policies Subcom m ittee on Early Pregnancy: crucial issues in the initial m anagem ent of patients presenting to the em ergency departm ent in early pregnancy. Ann Em erg Med. 2003;41:123â€“133. 2. Coppola PT, Coppola M. Vaginal bleeding in the first 20 weeks of

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pregnancy. Em erg Med Clin N Am . 2003;21:667â€“677. 3. Dyne PL. Vaginal bleeding and other com m on com plaints in early pregnancy. In: Pearlm an MD, et al. eds. Obstetric & gynecologic em ergencies: diagnosis and m anagem ent. New York, NY: McGraw-Hill. 2004:39â€“55. 4. Reardon RF, Jehle DVK. Pelvic ultrasonography. In: Tintinalli JE, et al. eds. Em ergency m edicine: a com prehensive study guide. New York, NY: McGraw-Hill. 2004:715â€“726. 5. Rehm an KS, Johnson TRB. Bleeding after 20 weeksâ€™ gestation: m aternal and fetal assessm ent. In: Pearlm an MD, et al. eds. Obstetric & gynecologic em ergencies: diagnosis and m anagem ent. New York, NY: McGraw-Hill. 2004: 117â€“136.

Miscellaneous SEE ALSO: Abortion, Spontaneous; Abruptio Placenta; Ectopic Pregnancy; Hydatidiform Mole; Placenta Previa; Postpartum Hem orrhage

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vaginal Bleeding

Vaginal Bleeding

Carla Valentine

Basics Description 

Com m on presenting com plaint in EDs



Most cases have benign etiology.



Som e patients m ay have potentially life-threatening conditions.



Most im portant principles in evaluating wom en with vaginal bleeding: o

All wom en capable of childbearing m ight be pregnant.

o

Menstrual and sexual histories do not rule out pregnancy.

Etiology Pregnancy Related 

Early pregnancy: o

Ectopic pregnancy (occurs in 2% of pregnancies)

o

Abortion: 

Threatened



Incom plete



Com plete



Missed

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





Inevitable



Septic

o

Molar pregnancy

o

Traum a

Later pregnancy: o

Placenta previa

o

Placental abruption

o

Molar pregnancy

o

Labor

o

Traum a

Im m ediate postpartum period: o

Postpartum hem orrhage

o

Uterine inversion

o

Retained placenta

o

Endom etritis

Nonpregnant Patients 

Dysfunctional uterine bleeding



Structural abnorm alities



Uterine fibroids



Cervical/Endom etrial polyps



Pelvic tum ors



Atrophic endom etrium : o



Most com m on cause of postm enopausal bleeding

Rare for system ic disorders to present solely with vaginal bleeding:



o

Von Willebrand disease

o

Idiopathic throm bocytopenic purpura

Traum a

Diagnosis

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Signs and Symptoms 

Vaginal bleeding: o

Variable am ounts: 

Average tam pon holds approxim ately 5 cc of blood



Average pad holds approxim ately 5â€“15 cc of blood

o

May be associated with fetal tissue/blood clots



Light-headedness



Fatigue



Weakness



Thirst



Acute hypotension and tachycardia: o

Significant vaginal bleeding due to ectopic pregnancy or ruptured ovarian cyst: 

o

May produce altered m entation

Abdom inal distention or tenderness

Essential Workup 

Qualitative pregnancy test: o



Point-of-care urine-based pregnancy test preferred

Pelvic exam ination: o

Essential for all wom en with vaginal bleeding

o

Speculum /bim anual exam 

o

Assess whether cervical os open or closed.

Delay pelvic exam ination pending ultrasound result in late pregnancy: 

Evaluate for placenta previa as the etiology of vaginal bleeding.

o

Defer exam if patient is near term with possible rupture of fetal m em branes.



Pregnancy test m andatory for all patients with

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childbearing potential 

Early pregnancy: o

Blood type and Rh

o

Ultrasound to confirm intrauterine pregnancy (IUP)

o

Quantitative Î²-hum an chorionic gonadotropin (HCG)

o

Hem atocrit

o

Type and cross-m atch:

o 



Ectopic pregnancy



Low hem atocrit levels



Hem odynam ic instability

Urinalysis

Later pregnancy: o

Type and Rh

o

Fetal heart tones

o

Ultrasound indications: 

No fetal heart tones



No docum ented intrauterine pregnancy



Unknown placental lie

o

Hem atocrit if significant bleeding

o

Type and cross-m atch if placenta previa/abruption or low hem atocrit levels

o

Dissem inated intravascular co-agulation panel if placental abruption: 

Platelets, prothrom bin tim e (PT), partial throm boplastin tim e (PTT)

 

Fibrinogen, fibrin-split products

Early postpartum : o

Ultrasound for retained products

o

Hem atocrit

o

Î²-Hum an chorionic gonadotropin if concerned about retained tissue

Tests

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Lab 

Hem atocrit for wom en with significant bleeding



Platelet count for suspected throm bocytopenia



PT/PTT for suspected coagulopathy

Imaging 

Send any passed tissue or clot for pathology evaluation.



Endom etrial sam pling required if patient older than 35â€“40 years: o

Risk for endom etrial cancer

Treatment Pre Hospital 

Establish IV 0.9% norm al saline with 1-L fluid bolus for significant bleeding or hypotension.



Adm inister high-flow oxygen in pregnant or unstable patients.



In later pregnancy: o

Place patient in left-lateral recum bent position to prevent occlusion of inferior vena cava by uterus.

Initial Stabilization 

Manage airway and resuscitate as indicated.



Place cardiac/pulse oxim eter m onitors.



Oxygen for significant bleeding or unstable patient



Establish two large-bore IV lines and initiate fluid bolus (1â€“2 L) for hypotensive patients: o

Transfuse blood if continued hypotension from blood losses despite IV fluid resuscitation.

ED Treatment

Pa ge 5 0 2



If unstable with surgical condition, arrange for transfer of the patient to the operating room as soon as possible.



RhoGAM for vaginal bleeding, pregnancy, and Rh-negative m other: o

RhoGAM: 300 Âµg IM if >13 weeks pregnant

o

MICRhoGAM 50 Âµg IM if <13 weeks pregnant

Early Pregnancy 

With positive ultrasound result for ectopic pregnancy: o

Definitive treatm ent is surgery.

o

Methotrexate according to standards at treating institution



With positive result for IUP without concerns of heterotopic pregnancy (1/2,600â€“1/30,000): o

Discharge patient with arranged obstetric follow-up with precautions for a threatened m iscarriage.



Ultrasound indeterm inate for IUP or ectopic with Î²-HCG greater than institutional discrim inatory zone: o

Cannot exclude ectopic pregnancy

o

If hem odynam ically stable with little bleeding, outpatient obstetric follow-up within 48 hours: 

Repeat m easurem ent of Î²-hum an chorionic gonadotropin.

o 

Strict return param eters

Ultrasound indeterm inate for IUP or ectopic with Î²-HCG level less than institutional discrim inatory zone: o

Patient stable with low risk for ectopic pregnancy m ay be discharged

o

Repeat m easurem ent of Î²-HCG level and schedule obstetric follow-up within 48 hours.

o

Patient m ay still have an ectopic pregnancy

P.1181

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

Com plete abortion: o

Discharge patient if stable without significant ongoing bleeding







Incom plete abortion: o

Obstetric consultation is required.

o

Dilation and curettage versus expectant m anagem ent

Missed abortion: o

Expectant m anagem ent initially

o

Dilation and curettage: Infection



Persistent/Significant bleeding



Retained products of conception

Septic abortion: o





IV antibiotics and adm ission

Molar pregnancy: o

Chem otherapy

o

Very responsive in early stages of disease

Later pregnancy: 



Placenta previa: o

Obstetric consultation for possible adm ission

o

Expectant m anagem ent

Placental abruption: o

Induction of labor if large

o

Can lead to fetal/m aternal death

o

May require cesarean section

Im m ediate postpartum 

Uterine inversion: o

Prevent by avoiding strong traction on um bilical cord after delivery.

o

Replace uterus im m ediately.

o

Occasionally requires operative m anagem ent

Pa ge 5 0 2



Postpartum hem orrhage: o

Extraction of placenta if retained

o

Hysterectom y if uncontrolled life-threatening bleeding

Early postpartum : 

Retained tissue: o



Dilation and curettage

Endom etritis: o

IV antibiotics



Nonpregnant



Menses:



Nonsteroidal anti-inflam m atory drugs and supportive care



Dysfunctional Uterine Bleeding (DUB)



Younger than 35â€“40 years of age: o

If known anovulatory DUB: 

Provera, 10 m g PO QD for first 10 days of m enstrual cycle

 o

Oral contraceptive pill daily for 7 days 

o 

Warn patient about withdrawal bleeding

Ortho-Novum 1/50 q.i.d. for 7 days

Discharge if stable with gynecologic referral

Patients older than 35â€“40 years of age: o

Ultrasound for any m asses palpated during physical exam

o

Gynecologic referral

o

Uterine sam pling necessary before initiation of horm onal treatm ent: 



Evaluate for endom etrial cancer

Structural abnorm alities: o

Ultrasound for workup of pelvic m asses

o

Fibroids or uterine tum ors 

Conservative m anagem ent or

Pa ge 5 0 2

lum pectom y/hysterectom y o

Papanicolaou sm ear/biopsy for cervical lesions Hem odynam ically unstable



Resuscitate as indicated: o

Monitor, two large bore IVs

o

Bolus of crystalloid solution



Type and crossm atch



Prem arin 25 m g IV slowly over 10â€“15 m inutes q4hâ€“q6h until bleeding stops: o



Not to exceed four doses

Adm it

Medication (Drugs) 

Prem arin 25 m g IV slowly over 10â€“15 m inutes q4hâ€“q6h until bleeding stops (not to exceed 4 doses)



Known anovulatory DUB: Provera 10 m g PO per day for first 10 days of m enstrual cycle (warn patient about withdrawal bleeding)



RhoGAM 300 Âµg IM if >13 weeks pregnant



MICRhoGAM 50 Âµg IM if <13 weeks pregnant

Follow-Up Disposition Admission Criteria 

Ectopic pregnancy not m eeting m ethotrexate discharge criteria: o



Patient unstable

Uterine inversion

Pa ge 5 0 3



Septic abortion



Placental abruption



Postpartum hem orrhage



Endom etritis



Dysfunctional uterine bleeding:



o

Unstable

o

Sym ptom atic or life-threatening anem ia

Newly diagnosed m olar pregnancy

Discharge Criteria 

Stable vital signs



Confirm ed IUP



Ectopic pregnancy m eeting institutional m ethotrexate discharge criteria





Pregnant patient with low-risk for ectopic pregnancy: o

No findings of IUP on ultrasound

o

Levels of Î²-HCG below discrim inatory zone

Nonpregnant patients with vaginal bleeding that are hem odynam ically stable

References 1. Alexander JD, Schneider FD. Vaginal bleeding associated with pregnancy. Prim ary Care: Clin Office Pract. 2000;27:137â€“151. 2. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients presenting with a chief com plaint of vaginal bleed. Ann Em erg Med. 1997;29:435â€“458. 3. Am erican College of Em ergency Physicians. Clinical policy: critical issues in the initial evaluation and m anagem ent of patients presenting to the em ergency departm ent in early pregnancy. Ann Em erg Med. 2003;41:1:123â€“133. 4. Clinical policy: Bravender T, Em ans SJ. Menstrual disorders. Dysfunctional uterine bleeding. Pediatr Clin North Am . 1999;46:545â€“553.

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5. Kaplan BC, Dart RG, Moskos M, et al. Ectopic pregnancy: prospective study with im proved diagnostic accuracy. Ann Em erg Med . 1996;28:10â€“17 6. Shwayder JM. Pathophysiology of abnorm al uterine bleeding. Obstet Gynecol Clin North Am . 2000;27:219â€“234.

Codes ICD9-CM 623.8 Other specified noninflam m atory disorders of vagina

ICD10 N93.9

Patient Teaching Ectopic precautions: Patients should return to the ED im m ediately for increasing abdom inal pain, vaginal bleeding m ore than one pad per hour for 3â€“4 hours, fever >100.4Â°F, syncope, or dizziness. Patients should not be left alone until the diagnosis of ectopic pregnancy can be safely ruled out. Fam ily and friends should also be instructed on the warning signs and sym ptom s of ruptured/bleeding ectopic pregnancies.

Pa ge 5 0 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vaginal Discharge/Vaginitis

Vaginal

Discharge/Vaginitis Donna Felsenstein

Basics Description 

Vaginal discharge



Som e am ount of vaginal discharge is norm al.



Glands in the cervix produce a clear m ucus that m ay turn white or yellow when exposed to air.



Abnorm al discharge is defined by an increased am ount or change in color or o

Vaginitis

o

Irritation or inflam m ation of the vagina

o

Change in the vaginal flora

o

Loss of norm al lactobacillus (e.g., antibiotics)

o

Inability to m aintain norm al vaginal pH (<4.5) resulting in proliferation of norm ally present pathogens

o

Overgrowth of less dom inant organism s such as Gardnerella vaginalis, Mycoplasm a, Mobiluncus, bacteroides species, and Peptostreptococcus



Also caused by introduction of an infective pathogen (e.g.,

Pa ge 5 0 3

trichom onas) 

Im m une dysfunction m ay allow for fungal infections (e.g., diabetes, HIV).

Etiology 

Bacterial vaginosis



Overgrowth of norm ally present bacteria



Infecting bacteria: o

Group A strep; S. aureus



Candidiasis



Trichom oniasis



Chem ical irritant



Foreign body



Atrophic vaginitis



Hypersensitivity



Collagen vascular



Herpes sim plex virus (HSV, vulvovaginitis, cervicitis)



Lichens sclerosis (atrophic)



Fistula

Diagnosis Signs and Symptoms 

Abnorm al discharge



Vulvovaginitis



Localized pain



Erythem a



Edem a



Dysuria



Pruritus



Asym ptom atic

Pa ge 5 0 3



Excoriations



Abnorm al odor

History 

Description and duration of sym ptom s



Description of discharge if any



Tim ing with regard to m enses



Sexual history of patient and â€œpartnersâ€• if possible



Sexual practices



Hygienic practices



Use of oral contraceptives and/or antibiotics



Likelihood of pregnancy



Other sym ptom s (i.e., abdom inal pain; r/o pelvic inflam m atory disease [PID])

Physical Exam 

Abdom inal exam to assess for tenderness



Inspection of vulva, vaginal os, perineal area



Speculum and bim anual exam

Tests Lab 

Î²-Hum an chorionic gonadotropin (Î²-hCG)



pH of discharge with Nitrazine paper (norm al in prem enopausal adults is between 3.5 and 4.1)



Saline wet prep exam of discharge at 400Ã—: clue cells (bacterial vaginosis), m otile trichom onads (Trichom onas species), budding yeast/pseudohyphae, presence of polym orphonuclear leukocytes (PMNs)



Potassium hydroxide (KOH) wet prep exam of discharge for pseudohyphae (Candida species)



KOH prepâ€”â€œWhiffâ€• test



Endocervical swab for gonorrhea (culture- Thayer-Martin

Pa ge 5 0 3

m edia; DNA probe; am plification techniquesâ€”PCR/LCR) and chlam ydia (DNA probe or am plification techniquesâ€”PCR/LCR), 

Viral cultures for HSV, DFA, or Tzanck sm ear for m ultinucleated giant cells if ulcers or vesicles are present.



Consider vaginal C & S(r/o staph/strep)



Urinalysis/Urine culture: (If c/o dysuria)



Rule out sexually transm itted infections: GC/Chlam ydia testing as above; consider RPR to rule out syphilis; w/u of genital ulcers if lesions are present; discuss HIV testing.

Imaging N/A unless fistula is suspected.

Differential Diagnosis 

Urinary tract infection



PID



Derm atitis



Discharge from cervicitis can be m istaken for vaginitis



Chlam ydia trachom atis



Neisseria gonorrhoeae.

Treatment ED Treatment 

Bacterial vaginosis



Vaginal m etronidazole gel for 5 days versus m etronidazole 500 m g PO for 7 days versus m etronidazole PO 2 gm s for 1 dose versus vaginal clindam ycin cream to 7 days versus clindam ycin PO for 7 days.



Special consideration in pregnancy: Rx sym ptom atic wom an with oral m etronidazole; Rx asym ptom atic

Pa ge 5 0 3

pregnant wom en with history of preterm birth with oral m etronidazole 

Rx before certain gynecologic procedures



Advise no alcohol intake if taking m etronidazole up to 24 hours after treatm ent.



Routine treatm ent of m ale sex partner: no



Candidiasis: single oral dose fluconazole versus 3â€“7 days of intravaginal im idazole drug



Routine treatm ent of m ale sex partner: no



Chem ical irritant



Avoid irritant



Use sitz baths, cotton underwear.



Foreign body: rem oval of foreign body; m ay necessitate sedation for rem oval and appropriate antibiotics if infection present



Chlam ydia Cervicitis



One dose azithrom ycin (for cervicitis, not adequate for PID) versus 7 days of doxycycline, ofloxacin. levofloxacin or erythrom ycin



Treat for presum ed concurrent gonococcal infections. P.1185



Routine treatm ent of m ale sex partners: yes



Gonococcal cervicitis



One dose treatm ent with ceftriaxone versus spectinom ycin



In som e locations, quinolone-resistant gonorrhea exists and is on the rise and should not be first-line treatm ent.



Treat for presum ed concurrent chlam ydial infection.



Routine treatm ent of m ale sex partners



HSV



Acyclovir, fam ciclovir or valacyclovir for 7â€“10 days for

Pa ge 5 0 3

initial attack; 5 days for recurrencesâ€”Lidocaine jelly for topical relief 

Rule out other causes of genital ulcers. Offer RPR, HIV testing and counseling



Routine treatm ent of m ale sex partners: only if sym ptom atic; however, patient and partner m ayshed virus asym ptom atically.



Lichen sclerosis



Referral to gynecologist for estrogen cream and further treatm ent



Trichom oniasis



Metronidazole 2 g PO once versus m etronidazole 250 m g PO t.i.d. for 7 days. (avoid ethyl alcohol); versus tinidazole PO.



Routine treatm ent of m ale sex partners: yes



All sexually transm itted causes



Advise patient to avoid sexual contact with partner until partner is evaluated and treated for when appropriate.



Education re: STDs/safer sex/HIV/hepatitis vaccines

Pediatric Considerations 

Ask about new irritants: bubble bath, soap, and laundry detergent.



Consider sexual assault/abuse.

Medication (Drugs) 

Acyclovir: 200 m g PO 5 tim es per day for 10 days or 400 PO t.i.d. tim es per day for 10 days (for initial attack); 200 m g PO 5 tim es per day for 5 days or 400 PO t.i.d. tim es per day for 5 days (for recurrent attack)



Azithrom ycin: 1 g PO Ã— 1

Pa ge 5 0 3



Ceftriaxone: 125 m g IM or 250 m g IM Ã— 1



Ciprofloxacin: 500 m g PO Ã— 1



Clindam ycin 2% cream : 1 applicator PV q.h.s. for 7 days



Clindam ycin 300 m g PO bid Ã— 7 days



Clotrim azole (??): 2â€“100 m g tabs PV q.h.s. Ã— 3 days or 1â€“150 m g tabs PV Ã— 1 or 1 app PV q.h.s. for 7â€“14 days



Doxycycline: 100 m g PO b.i.d. for 7 days (class D)



Erythrom ycin ethyl succinate: 800 m g PO q.i.d. for 7 days



Erythrom ycin base: 500 m g PO q.i.d. for 7 days



Fam ciclovir: 250 m g PO t.i.d. Ã— 7â€“10 days (for initial attack); 125 m g PO b.i.d. Ã— 5 days (for recurrent infection)



Fluconazole: 150 m g PO Ã— 1



Levofloxacin 500 m gPO per day Ã— 7 days



Metronidazole: 2 g PO Ã— 1 or 500 m g PO b.i.d. for 7 days



Metronidazole 0.75% gel PV b.i.d. for 5 days



Miconazole: 200 m g PV q.h.s. for 3 days



Miconazole: 5 g 2% cream PV q.h.s. for 7 days or 100 m g supp PV q.h.s. for 7 days



Spectinom ycin: 2 g IM Ã— 1



Terconazole: 80 m g supp q.h.s. for 3 days or 5 g of 0.8% cream PV q.h.s. for 3 days or 5 g of 0.4% cream PV for 7 days



Tinidazole: 2 g PO once



Tioconazole: 5 g of 6.5% cream PV for 7 days



Valacyclovir 1g PO b.i.d. Ã— 7â€“10 days (for initial attack); 500 m g PO b.i.d. Ã— 3â€“5 days or 1 g PO per day Ã— 5 days (for recurrent attack)

Pa ge 5 0 3

Follow-Up Disposition Admission Criteria 

Dissem inated gonococcal infection



Sepsis secondary to foreign body



PID toxicity



Pain control, consequent inability to urinate or pass stool (HSV)

Discharge Criteria Most can be discharged; follow-up in about 1 week is suggested.

References 1. Botash AS. Vaginitis. Em edicine July 27 2001;2(7). 2. Egan ME, Lipsky MS. Diagnosis of vaginitis. Am Fam Physician. 2000;62(5):1095â€“1104. 3. Quan M. Vaginitis: m eeting the clinical challenge. Clin Cornerstone . 2000;3(2):36â€“37. 4. Sobel JD. Up to Date. Overview of vaginitis

Codes ICD9-CM 616.10

ICD10 N76.0

Pa ge 5 0 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Valvular Heart Disease

Valvular Heart

Disease Liudvikas Jagminas

Basics Description 

Mitral stenosis: o

Obstruction of diastolic blood flow into the left ventricle (LV)



Mitral regurgitation: o

Inadequate closure of the leaflets allows retrograde blood flow into the left atrium (LA).

o

Acute: 

Pressure overload in LA and pulm onary veins causing acute pulm onary edem a

o

Chronic: 

LV volum e overload with dilatation and hypertrophy with LA enlargem ent





Aortic stenosis: o

Resistance to ejection and systolic gradients increase

o

Progressive increase in LV systolic pressure

Aortic regurgitation: o

Acute:

Pa ge 5 0 4



Acute LV pressure and volum e overload leading to left heart failure and pulm onary edem a

o

Chronic: 

Chronic volum e overload with LV dilation and hypertrophy

Etiology Mechanism 



Mitral stenosis: o

Rheum atic fever

o

Cardiac tum ors

o

Rheum atologic disorders (lupus, rheum atoid arthritis)

o

Myxom a

o

Congenital defects

Mitral regurgitation (acute): o

Ruptured papillary m uscle (infarction, traum a)

o

Papillary m uscle dysfunction (ischem ia)

o

Ruptured chordae tendineae (traum a, endocarditis, m yxom atous)

o 



Valve perforation (endocarditis)

Aortic stenosis: o

Congenital aortic stenosis

o

Congenital bicuspid valve

o

Rheum atic aortic stenosis

o

Calcific aortic stenosis

Aortic regurgitation: o

Acute: 

Infective endocarditis



Rupture of sinus of Valsalva



Acute aortic dissection



Chest traum a



Following valve surgery

Pa ge 5 0 4

o

Chronic: 

Bicuspid aortic valve



Rheum atic fever



Weight-loss m edications (Dexfenfluram ine)



Collagen vascular or connective tissue diseases



System atic lupus erythem atosus



Marfan



Turner Syndrom e



Pseudoxanthom a elasticum



Ankylosing spondylitis



Ehlers-Danlos syndrom e



Polym yalgia rheum atica

Diagnosis Signs and Symptoms 

Mitral stenosis: o

Malar flush (â€œm itral faciesâ€•)

o

Prom inent jugular a waves

o

Right ventricular lift

o

Loud S1

o

Opening snap

o

Low-pitched diastolic rum ble

o

Exertional dyspnea

o

Fatigue

o

Palpitations

o

Paroxysm al nocturnal dyspnea

o

Orthopnea

o

Hem optysis

o

System ic em boli

o

Pulm onary edem a

Pa ge 5 0 4



Mitral regurgitation: o

Acute: 

Acute pulm onary edem a



Jugular venous pressure (JVP) exhibits cannon a waves and giant V waves.



Harsh apical crescendo-decrescendo m urm ur radiating to the axilla

o





Palpable thrill at apex



S3 and S4

Chronic: 

Palpitations



Atrial fibrillation



Dyspnea



Orthopnea



Nocturnal paroxysm al dyspnea



Edem a



System ic em boli



Norm al JVP



Left ventricular hypertrophy (LVH)



Apical high-pitched pansystolic m urm ur



Decreased or obscured S1



Widely split S2



S3

Aortic stenosis: o

Exertional angina

o

Syncope (during exercise)

o

Congestive heart failure (initially diastolic failure, then systolic)

o

Arrhythm ias

o

Harsh crescendo-decrescendo systolic m urm ur at aortic focus radiating to carotids

o

Absent aortic com ponent of S2

Pa ge 5 0 4

o

Delayed upstroke in peripheral pulse (pulsus parvus et tardus)



o

S4 gallop

o

Ejection click

Aortic regurgitation: o

Fatigue

o

Dyspnea

o

Paroxysm al nocturnal dyspnea

o

Orthopnea

o

Chest pain

o

Edem a

o

Acute pulm onary edem a

o

High-pitched blowing decrescendo diastolic m urm ur at aortic area

o

Accentuated A2 heart sound

o

Wide pulse pressure

o

Collapsing pulse

o

Duroziez sign (to-and-fro m urm ur)

o

De Musset's sign (head bobbing with systole)

o

Quincke pulse (nail bed pulsations)

o

Austin Flint m urm ur (soft diastolic rum ble)

Essential Workup 

History and sym ptom s



Thorough cardiopulm onary exam ination



ECG: o

o

Mitral stenosis: 

Left atrium enlargem ent



Right ventricular (RV) hypertrophy



Signs of pulm onary hypertension



Atrial fibrillation

Acute m itral regurgitation: 

Q-wave inferior, posterior, or lateral

Pa ge 5 0 4

o

o



LVH



Left axis deviation

Aortic stenosis: 

LVH m ost com m on



Left atrium enlargem ent



Interventricular conduction delay



Com plete AV Block

Aortic regurgitation 

Acute = LV strain



Chronic = LVH and strain

Tests Lab 

Blood cultures: o



Presum ed endocarditis

CBC: o

Anem ia

Imaging 

Chest radiograph: o

o

Mitral stenosis 

Enlarged LA



Prom inent pulm onary veins

Mitral regurgitation: 

LV and LA enlargem ent in chronic cases



Pulm onary edem a and norm al LV and LA dim ensions in acute cases

o

o

Aortic stenosis: 

LVH



Aortic calcification



Pulm onary congestion

Aortic regurgitation: 

Acute = norm al heart, pulm onary edem a

Pa ge 5 0 4



Chronic = enlarged LV and dilated aorta

P.1187



Echocardiogram : o

o

o

o



Mitral stenosis: 

Inadequate separation of valve leaflets



Valve leaflet calcification and thickening



Valve area and gradient

Mitral regurgitation: 

Enlarged LA



Dilated LV

Aortic stenosis: 

Valve m orphology



Valve area and gradient



Thickened or sclerotic

Aortic regurgitation: 

Valve m orphology



Aortic root size



Assess left ventricular size and function.

Cardiac catheterization for acute m itral regurgitation/aortic regurgitation



Spiral CT scan to exclude aortic dissection with acute aortic regurgitation

Treatment Pre Hospital Avoid vasodilators in aortic stenosis

Initial Stabilization

Pa ge 5 0 4



ABCs



Adm inister oxygen



Monitor and m easure pulse oxim etry



IV access

ED Treatment Mitral Stenosis 

Treat sym ptom s of CHF.



Rate control if in atrial fibrillation



Digoxin



Î²-blockers



Heparin (if new onset atrial fibrillation)



Diuretics



Endocarditis prophylaxis/education

Mitral Regurgitation 

Differentiate between acute and chronic MR: o

Acute: 

Afterload reduction (nitroglycerin, m orphine, or sodium nitroprusside)



Diuresis



Intra-aortic balloon pum p (tem porizing for urgent surgery)

o

Chronic 

Diuresis



Nitrates



Hydralazine



Angiotensin-converting enzym e inhibitor



Digoxin



Î²-adrenergic blocker (ventricular rate control)



Calcium antagonist (ventricular rate control)



Heparin (if atrial fibrillation)



Endocarditis prophylaxis/education

Pa ge 5 0 4

Aortic Stenosis 

Gentle diuresis if CHF



Mild hydration if hypotensive and not in CHF



Avoid nitrates and afterload reduction.



Digoxin



Intra-aortic balloon pum p (tem porize for surgery)



Endocarditis prophylaxis/education

Aortic Regurgitation 



Chronic: o

Preload and afterload reduction

o

Digoxin

o

Diuretics

o

Endocarditis prophylaxis/education

Acute: o

Preload and afterload reduction

o

Intra-aortic balloon pum p

o

Urgent surgery

Medication (Drugs) 

Atenolol: 0.3â€“2 m g/kg PO daily, m ax. 2 m g/kg/d (peds: 1â€“2 m g/kg/dose PO daily suggested)



Bum etanide: 0.5â€“1.0 m g IV q2hâ€“q3h PRN; infusion 0.08â€“0.3 m g/h; PO 0.5â€“2 m g t.i.d. (peds: 0.015â€“0.1 m g/kg PO/IM/IV q24hâ€“q48h hours) m ax. dose 10 m g/d



Digoxin: 0.5 m g bolus IV, then 0.25 m g IV q2h up to 1 m g; 0.125â€“0.375 m g PO daily o



Maintenance dose: use 25â€“35% of PO loading dose.

Diltiazem : 0.25 m g/kg IV over 2 m in (repeat in 15 m in PRN with 0.35 m g/kg) then 5â€“15 m g/h



Enalapril: 1.25 m g IV q6h; PO 2.5â€“10 m g b.i.d. (peds:

Pa ge 5 0 4

0.1â€“0.5 m g/kg/d PO div. q12hâ€“q24h; m ax: 0.58 m g/kg/d or 40 m g/d 

Esm olol: IV: 500 m cg bolus, then 50â€“400 m cg/kg/m in



Furosem ide: 20â€“80 m g/d PO/IV/IM; titrate up to 600 m g/d for severe edem atous states (peds: 1 m g/kg IV/IM slowly under close supervision; not to exceed 6 m g/kg)



Heparin: 80 IU/kg IV bolus, then 18 IU/kg/hr drip, adjust to m aintain partial throm boplastin tim e 1.5â€“2X control (international norm alized ratio 2â€“3)



Hydralazine: 10â€“25 m g IV q2hâ€“q4h (peds: 0.1â€“0.5 m g/kg IM/IV q4hâ€“q6h; m ax. 20 m g/dose)



Metoprolol: 5 m g IV q2m in Ã— 3 doses; then 50 m g PO q6h Ã— 48 hours



Nitroglycerin: start at 20 m cg/m in IV and titrate to effect (up to 300 m cg/m in); SL 0.3â€“0.6 m g PRN; Topical 1â€“2 inches of 2% q6h (peds: 0.25â€“0.5 m cg/kg/m in IV, increase by 0.5â€“1 m g/kg/m in; m ax. 20 m cg/kg/m in)



Phentolam ine: 5 m g bolus IV, then 1â€“2 m g/m in IV infusion



Propranolol IV: 1â€“3 m g at 1 m g/m in



Sodium nitroprusside IV: 0.5 m cg/kg/m in; increase in increm ents of 0.5 to 1.0 m cg/kg/m in q5m inâ€“q10m in up to 10 m cg/kg/m in



Am oxicillin: 2 g PO 1h before the procedure; alternatively, 3 g PO 1h before the procedure, followed by 1.5 g PO 6h after the initial dose: o



Pediatric dose: 50 m g/kg PO 1h before procedure

Am picillin: 2 g IV/IM 30 m in before the procedure (peds: 50 m g/kg IV/IM 30 m in before the procedure)



Clindam ycin: 600 m g PO 1h before procedure (peds: 20 m g/kg PO 1h before procedure; not to exceed 600 m g)

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Follow-Up Disposition Admission Criteria 

New onset atrial fibrillation



CHF/pulm onary edem a



Hem odynam ically unstable



Acute m itral or aortic regurgitation



Cardiac ischem ia



Angina



Syncope



Arrhythm ias

Discharge Criteria 

Hem odynam ic stability



Unchanged ECG



Resolution of CHF sym ptom s with diuresis



Chronic m itral regurgitation

References 1. Carabello BA, Crawford FA. Valvular heart disease. N Engl J Med. 1997;337(1):32â€“41.[published erratum appears in N Engl J Med. 1997;337:507]. 2. Carabello BA. Indications for valve surgery in asym ptom atic patients with aortic and m itral stenosis. Chest. 1995;108(6):1678â€“1682. 3. Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recom m endations by the Am erican Heart Association. JAMA. 1997;227:1794â€“1801. 4. Roldan CA, Shively BK, Crawford MH. Value of the cardiovascular exam ination for detecting valvular heart disease in asym ptom atic

Pa ge 5 0 5

subjects. Am J Cardiol. 1996;77:1327â€“1331.

Codes ICD9-CM 424.1 Aortic valve disorders 424.0 Mitral valve disorders

ICD10 I35 Nonrheum atic aortic valve disorders I34 Nonrheum atic m itral valve disorders

Pa ge 5 0 5

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Varicella

Varicella

John C. Wu Mark Richmond

Basics Description 

Com m only known as chicken pox



Classic viral illness of childhood



Most com m on in late winter and early spring



In the prevaccine era, 90% of children were infected by 15 years of age and virtually all persons acquired varicella by adulthood: o



Vaccine has reduced incidence by 74â€“84%.

Adults have a 15 tim es greater risk for death from varicella than children.

Etiology 

DNA virus characterized by latency in dorsal root ganglia and periodic re-activation: o

Presents as herpes zoster or shingles



Virus is transm itted by respiratory route.



Hum ans are only known reservoir.

Pa ge 5 0 5

Diagnosis Signs and Symptoms Varicella causes a spectrum of disease.

Classic Childhood Illness 

Usually affects children ages 2â€“12



Prodrom e of low-grade fever (100â€“103Â°F), headache and m alaise: o



Precedes rash by 1â€“2 days

Classic exanthem : o

Lesions begin on the face, spreading to the trunk and extrem ities.

o

Vesicles, pustules, and sm all scabs on erythem atous base

o

Lesions in varying stages of evolution

o

â€œDew drop on rose petalâ€•

o

Round or oval, 0.5â€“1.0 cm in diam eter

o

Duration of vesicle form ation 3â€“5 days

o

Pruritus, anorexia, and listlessness

o

10- to 21-day incubation period; average is 14 days

o

Infectious from 48 hours before vesicle form ation until all vesicles are crusted (typically 4â€“5 days)

o

Mucous m em brane involvem ent: 



Conjunctiva, oropharynx, vagina

Bacterial superinfection of the skin develops in 1â€“4% of otherwise healthy children.

Neonates Congenital varicella syndrom e: 

Occasionally follows m aternal zoster infection



Cicatricial skin lesions



Lim b hypoplasia or paresis

Pa ge 5 0 5



Microcephaly



Ophthalm ic lesions, congenital cataracts, chorioretinitis

Adolescents and Adults Presents sim ilarly to disease in children but generally of greater severity: 

Extracutaneous m anifestations in 5â€“50%

Immunocompromised Patients 

HIV, transplant patients, leukem ia patients are the highest risk for dissem inated form .



Patients on chem otherapy, im m unosuppression therapy, and long-term corticosteroid therapy



Absolute neutrophil counts and absolute lym phocyte counts <500 are the best predictors of com plicated disease.



More num erous lesions that m ay have hem orrhagic base



Healing m ay take tim es longer



Extracutaneous m anifestations, especially pneum onia, com m on

Pregnant Patients 

Prevalent in young expectant wom en



Produces a m ore severe disease presentation: o

Risk to the fetus of congenital varicella syndrom e greatest in first half of pregnancy

o

Maternal disease severity greatest if infection in second half of pregnancy



Perinatal disease occurs in m other from 5 days predelivery to 48 hours postdelivery.

Extracutaneous Manifestations 

Pneum onitis: o

25 tim es m ore com m on in adults

o

Most com m on in adult sm okers and

Pa ge 5 0 5

im m unocom prom ised children o

Occurs 3â€“5 days after onset of rash

o

Early signs:

o



Continued eruption of new lesions



Fever



New-onset cough

Tachypnea, dyspnea, cyanosis, pleuritic chest pain, and hem optysis





Cerebellar ataxia: o

May develop 5 days after rash

o

Ataxia

o

Vom iting

o

Slurred speech

o

Fever

o

Vertigo

o

Nystagm us

o

Trem or

Cerebritis: o

Develops 3â€“8 days after appearance of rash: 



Duration about 2 weeks

o

Progressive m alaise

o

Headache

o

Meningism us

o

Vom iting

o

Fever

o

Delirium

o

Seizures

Reye syndrom e

Geriatric Considerations Increased risk of extracutaneous m anifestations

Pediatric Considerations

Pa ge 5 0 5



Do not use aspirin for treatm ent of fever associated with Reye syndrom e.



Parents need to be cautioned regarding risk for secondary bacterial infection and possible progression to sepsis.

Pregnancy Considerations Pregnant wom en with no childhood history of varicella and no antibodies to varicella zoster virus (VZV) require varicella zoster im m unoglobulin (VZIG).

Essential Workup 

History and physical are sufficient in uncom plicated cases.



Pneum onitis: o

Chest radiographs classically dem onstrates 2- to 5-m m peripheral densities, m ay coalesce and persist for weeks





Reye syndrom e: o

Am m onia level peaks early.

o

Liver function tests will be elevated

o

Prothrom bin tim e, partial throm boplastin tim e

Cerebritis: o

Lum bar puncture dem onstrates lym phocytic pleocytosis and elevated levels of protein.

Tests Lab 

Rapid identification using direct fluorescent antibody testing



Serologic tests for varicella antibodies

Diagnostic Procedures/Surgery Liver biopsy definitive test for Reye syndrom e

Differential Diagnosis 

Im petigo

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

Dissem inated herpes



Dissem inated coxsackievirus



Measles



Rickettsial disease



Insect bites



Scabies



Erythem a m ultiform e



Drug eruption

P.1189

Treatment Pre Hospital 

Nonim m une transport personnel m ust avoid respiratory or physical contact with patients.



Transport personnel with varicella or herpes zoster should not com e in contact with im m unocom prom ised or pregnant patients.

Initial Stabilization Airway m anagem ent and resuscitate as indicated: 

Protect airway if obtunded.

ED Treatment 

Antipyretics and antipruritics are all that is generally needed for classic childhood illness.



Closely cropped nails and good hygiene help prevent secondary bacterial infection.



Neonatal: o

VZIG for infants if m aternal varicella develops <5

Pa ge 5 0 5

days before delivery or up to 48 hours after delivery o

Of the infants who receive VZIG, 50% will develop varicella and should be kept in strict isolation for the incubation period.

o

IV acyclovir indicated in neonates: 

Chickenpox and not well appearing (poor feeding and tachypnea)





High-risk neonate who did not receive VZIG



Im m unocom prom ised or prem ature neonate

Infants/children to age 12 o

Acyclovir

o

Controversial, not generally needed for uncom plicated patients

o

Must be initiated within 24 hours of disease onset to be efficacious

o

Reduces total lesions by 25%

o

May be considered in children taking corticosteroids, long term salicylate therapy, chronic cutaneous or pulm onary diseases

o

Prophylaxis with VZIG

o

Indicated in susceptible individuals: 

Im m unocom prom ised children at high risk for com plication with a significant exposure



Living in sam e household as a person with active chickenpox or herpes zoster



Playm ate contact >1 hour with person infected with chickenpox or zoster

o

72 hours postexposure for m axim al effect

o

May provide benefit up to 96 hours postexposure for im m unocom prom ised patients

o 

Ineffective once clinical illness is established

Adolescents/adults:

Pa ge 5 0 5

o

Sym ptom atic with antipyretics and antipruritics

o

Acyclovir initiated within 24 hours decreases progression to dissem inated disease



Pregnant wom en: o

Pregnant wom en with no childhood history of varicella and no antibodies to varicella zoster virus (VZV) require VZIG.

o

Acyclovir, when initiated during incubation period or within 24 hours of onset of rash: 

Prophylaxis after exposure is 84% protective



Currently regarded as safe during pregnancy (category B)

o

IV acyclovir for pneum onitis/other com plications: 

Respiratory, neurologic, hem orrhagic rash, or continued fever after 6 days



Im m unocom prom ised patients: o

Acyclovir recom m ended, shortens course

o

Must be initiated within 72 hours of onset

o

Decreases progression to dissem inated disease

o

Foscarnet for acyclovir-resistant disease

o

Interferon

o

Prophylaxis with VZIG for the susceptible im m unocom prom ised patient



Extracutaneous: o

IV acyclovir, or foscarnet if viral resistance

Vaccine 

Children: o

Routine vaccination at 12â€“18 m onths

o

Recom m ended for all susceptible children by 13th birthday



Adolescents and adults: o

Persons >13 years old without history of varicella

Pa ge 5 0 6

o

Two doses separated by 4â€“8 weeks

o

Recom m ended in high-risk groups: 

Healthcare workers



Fam ily m em ber of im m unocom prom ised persons



Susceptible wom en of childbearing age



Teachers, m ilitary, international travelers



Currently no indications for elderly patients, although recent evidence suggests the vaccine decreases m orbidity from herpes zoster and postherpetic neuralgia

o

Postexposure prophylaxis: 

Effectiveness of 70â€“100% if given within 72 hours of exposure



Not effective if >5 days but will produce im m unity if not infected

o

Im m unocom prom ised persons: 

Most im m unocom prom ised persons should not be im m unized.

Medication (Drugs) 

Acyclovir: o

Uncom plicated: 800 m g PO 5 tim es a day for 7 days; adolescents (13â€“18 years old): 20 m g/kg per dose q.i.d. for 7 days (peds: 20 m g/kg suspension PO q.i.d. for 5 days [m ax. 800 m g PO q.i.d.])

o

Im m unocom prom ised: 10 m g/kg IV q8h infused over 1 h or 800 m g PO 5 tim es a day for 7 days (peds: 10â€“12 m g/kg IV q8h infused over 1 hour or 500 m g/m 2 /d IV q8h)



Diphenhydram ine: 25â€“50 m g IV, IM, or PO q4h (peds: 5 m g/kg/d elixir 12.5 m g/5 m L)

Pa ge 5 0 6



Fam ciclovir: 500 m g PO t.i.d.



Foscarnet: 40 m g/kg q8h over 1 hour for 10 or m ore days (peds: sam e)



Hydroxyzine: 25â€“50 m g IM or PO q4hâ€“q6h (peds: 0.5 m g/kg q4hâ€“q6h suspension 10 and 25 m g/5 m L)



Valacyclovir: 1,000 m g PO t.i.d. for 5â€“7 days



VZIG: 625 IU IM (peds: 1 vial per 10 kg IM to a m ax. of 5 vials [each vial contains 125 IU])

Follow-Up Disposition Admission Criteria 

Patients with pneum onia require adm ission: o

Intensive care unit (ICU) for respiratory observation or support



Im m unocom prom ised patients: ICU versus ward, depending on severity of illness



Neonates require adm ission for IV acyclovir.



All adm itted patients m ust be kept in isolation.

Discharge Criteria 

Im m unocom petent children without evidence of Reye syndrom e or secondary bacterial infection



Adults with no evidence of extracutaneous disease

References 1. Am erican Academ y of Pediatrics. Varicella zoster infections. Pickering L, ed. Red Book: 2003 Report of the Com m ittee on Infectious Diseases. 26th ed. Am erican Academ y of Pediatrics, 2003:672â€“686.

Pa ge 5 0 6

2. Arvin AM. Antiviral therapy for varicella and herpes zoster. Sem inars in Pediatric Infectious Diseases 2002;13:1,12â€“21. 3. Chen TM, et al. Clinical m anifestation of varicella-zoster virus infection. Derm atol Clin. 2002;20:267â€“282. 4. Enright AM and Prober C. Antiviral therapy in children with varicella zoster virus and herpes sim plex virus infections. Herpes. 2003;10:2,32â€“37. 5. Gilden D. Varicella zoster virus and central nervous system syndrom es. Herpes. 2004;11:Supp2,89Aâ€“94A. 6. Mohsen AH and McKendrick M. Varicella pneum onia in adults. Eur Respir J. 2003;21:886â€“891.

Miscellaneous SEE ALSO: Herpes Zoster

Codes ICD9-CM 052.9

Pa ge 5 0 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Varices

Varices

John Bailitz

Basics Description 

Increased portal venous pressure results in portal-system ic shunts.



Shunts at gastroesophageal junction result in fragile subm ucosal esophageal varices.

Etiology 

10â€“30% of all cases of upper gastrointestinal (GI) bleeding



90% of upper GI bleeding in patients with cirrhosis



Variceal hem orrhage occurs in 30% of patients with cirrhosis:





o

30% m ortality per episode

o

70% have recurrent bleeding.

In adults: o

Cirrhosis due to alcoholism or chronic hepatitis

o

Storage disease: Wilson or hem ochrom atosis

o

Middle East: Schistosom iasis

In children: o

Intrahepatic obstruction from biliary cirrhosis

o

Î± 1 -antitrypsin deficiency

Pa ge 5 0 6

o

Hepatitis

Diagnosis Signs and Symptoms General 

Weakness and fatigue



Tachycardia



Tachypnea



Hypotension



Cool, clam m y skin; prolonged capillary refill

Abdominal 

Significant active upper GI bleeding: o

Hem atem esis

o

Hem atochezia

o

Melena

o

20â€“40% of total blood volum e loss possible



Abdom inal pain



Stigm ata of severe hepatic dysfunction:



o

Jaundice

o

Spider angiom ata

o

Palm ar erythem a

o

Pedal edem a

o

Hepatosplenom egaly

o

Ascites

History of portal hypertension: o

Most com m only alcoholic cirrhosis

o

Others, including: 

Prim ary biliary cirrhosis



Schistosom iasis

Pa ge 5 0 6



Budd-Chiari syndrom e



Severe congestive heart failure



Sarcoidosis

Cardiovascular Chest pain/shortness of breath

CNS 

Syncope



Confusion and agitation initially



Lethargy and obtundation later

Pediatric Considerations 

Massive hem atem esis: typical initial presentation: o

Hypotension m ay be a late finding.

Essential Workup 

Gastric tube placem ent: o

Determ ines whether patient is actively bleeding

o

Facilitates endoscopic exam

o

Will not increase or cause esophageal variceal bleeding



Em ergent endoscopy

Tests Lab 

Type and cross-m atchâ€”6â€“8 units: o





Significant transfusion requirem ents

ABG for: o

Acidosis

o

Hypoxem ia

CBC: o

Hem atocrit is an unreliable indicator of early rapid blood loss.



Electrolytes, blood urea nitrogen, creatinine, glucose:

Pa ge 5 0 6

o

Evaluate renal function.

o

BUN/Creatinine greater then 30 suggest significant blood in GI tract.



Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio and platelets: o

Coagulopathy

o

Prolonged bleeding tim es

o

Throm bocytopenia

Imaging 

Chest radiograph (portable) for aspiration/perforation



ECG for m yocardial ischem ia

Differential Diagnosis 

Bleeding/perforated peptic ulcer



Erosive gastritis



Mallory-Weiss syndrom e



Boerhaave syndrom e



Aortoenteric fistula



Gastric varices

Treatment Pre Hospital 

Airway stabilization



Treat hypotension 0.9% norm al saline infusion bolus through two large-bore 16-gauge or large IV lines.



Cardiac and pulse oxim etry m onitoring

P.1191

Pa ge 5 0 6

Initial Stabilization 



ABCs with early aggressive airway control/intubation: o

Early intubation = easier intubation

o

For AMS or m assive hem optysis

o

Facilitates em ergency endoscopy

Establish central IV access with invasive intravascular m onitoring for hypotension not responsive to initial fluid bolus.



Replace lost blood as soon as possible: o

Initiate with O-negative blood until type-specific blood available.

o

10 m L/kg bolus in children

o

Fresh-frozen plasm a and platelets m ay be required.



Place gastric tube nasally (awake) or orally (intubated)



Controversy: o

Overly aggressive volum e expansion m ay lead to rebound portal hypertension, rebleeding, and pulm onary edem a.

Pediatric Considerations 

Initiate intra-osseous access if peripheral access unsuccessful in unstable patient.



Most bleeding in children stops spontaneously.



Vital signs changes m ay be a late finding in children: o

Subtle changes in m ental status, capillary refill, m ild tachycardia, or orthostatic changes m ay indicate significant blood loss.

o

Overaggressive correction in infants can quickly lead to significant electrolyte abnorm alities.

ED Treatment Em ergent endoscopy required, used pharm acologic and tam ponade devices as tem porizing m easures

Pa ge 5 0 6

Endoscopy 

Em ergent with active bleeding in nasogastric tube



Procedure of choice in acute esophageal bleeding



Esophageal band ligation equivalent to sclerotherapy with fewer com plications: o

May be difficult to visualize in cases of m assive bleeding



Sclerotherapy with m assive bleeding



Adm inister antibiotics at tim e of procedure to decrease risk for spontaneous bacterial peritonitis: o

Cefotaxim e or ceftriaxone

Pharmacological Therapy 

Octreotide is first-line therapy: o

Com plications include hyperglycem ia and abdom inal cram ping.



Vasopressin replaced by octreotide secondary to high incidence of vascular ischem ia

Balloon Tamponade 

Initiate in m assive uncontrollable bleed.



Sengstaken-Blakem ore and Minnesota tubes



Applies direct pressure but risks esophageal perforation and ulceration



Tem porary benefit only with m assive uncontrolled bleeding in hands of experienced clinician

Refractory Bleeding Therapy 

Interventional radiology: o

Transjugular intrahepatic portosystem ic shunt procedure



Surgical options: o

Portacaval shunt

Pa ge 5 0 6

o

Variceal transection

o

Stom ach devascularization

o

Liver transplantation

Medication (Drugs) 

Cefotaxim e: 2 g (peds: 50â€“180 m g/kg/24h) IV q8h



Ceftriaxone: 2 g (peds: 50â€“75 m g/kg/24h) IV q24h



Octreotide: 50 Âµg bolus, then 50 Âµg/h infusion for 5 days

Follow-Up Disposition Admission Criteria 

Intensive care unit adm ission for actively bleeding varices



Recent history of variceal bleeding



High risk for early rebleeding: o

Age >60 years, renal failure, initial hem oglobin count <8

Discharge Criteria Nonbleeding varices

References 1. Com ar KM, Sanyal AJ. Portal Hypertensive Bleeding. Gastroenterol Clin North Am . 2003: 32;1079â€“1105 2. Ham oui N, Docherty S. Gastrointestinal Hem orrhage: is the surgeon obsolete? Em erg Med Clin North Am . 2003;21:1017â€“1056 3. Harry R, Wendon J. Managem ent of Variceal Bleeding. Curr Opin Crit Care. 2002:8;164â€“170

Pa ge 5 0 7

Miscellaneous SEE ALSO: Cirrhosis; Gastrointestinal Bleeding

ICD9-CM 454.9

ICD10 183.9

Pa ge 5 0 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vasculitis

Vasculitis

Andrew Milstein

Basics Description 

Acute or chronic inflam m ation and necrosis of blood vessels



Im m une com plexes are deposited in vessel walls.



The com plem ent system is activated and stim ulates accum ulation of polym orphonuclear cells at the site and release of lysosom al enzym es.



Vessel wall dam age and necrosis occurs.



Many factors influence the clinical picture.



Size of im m une com plexes:



o

Size of blood vessels affected

o

Site of deposition

o

Degree of perm eability of the affected vessels

o

Usually there is m ultiorgan dysfunction.

Progressive disease course

Etiology Large Arteries 

Takayasu arteritis: o

Seen in m ostly young (<40 years of age) Asian

Pa ge 5 0 7

fem ales o

Affects aorta, proxim al portions of its m ajor branches and pulm onary arteries

o

Inflam m ation of vessels results in gradual stenosis and, less often dilatation and aneurysm form ation.



Streptococcal or tuberculous infections



Tem poral (Giant cell) arteritis



Arteritis associated with Reiter syndrom e and ankylosing spondylitis

Medium Arteries 

Polyarteritis nodosa (PAN): o

May involve any organ system

o

Predilection for the renal and visceral arteries



Wegener granulom atosis



Churg-Strauss syndrom e



BehÃ§et disease



Kawasaki disease

Small Arteries 

Henoch-SchÃ¶nlein purpura



Hypersensitivity vasculitis



Mixed cryoglobulinem ia



Goodpasture syndrom e



Erythem a nodosum

Secondary Causes 

Connective tissue disorders



Malignancy



Infectious Epstein-Barr virus



Lym e disease



Serum sickness



Im m une com plex-m ediated

Pa ge 5 0 7

Diagnosis Signs and Symptoms 

Fever



Fatigue



Weight loss



Diffuse aches and pains



Nondestructive oligoarthritis and neuropathy

Large Arteries 

Dim inished pulses and bruits over several large arteries



Blood pressure discrepancy >10m m Hg between left and right lim bs



Pulse discrepancy >30 m m Hg between the left and right lim bs



Cool extrem ities due to claudication and ulceration



Posturally dependent visual blurring, diplopia



Severe or resistant hypertension



Abdom inal angina



Ischem ic chest pain



Congestive heart failure



Facial or scalp ulcerations



Hair loss



Stroke



Syncope



Visual and sensorineural hearing loss



Postural dizziness

Medium and Small Arteries 

Palpable purpura (nodules, ulcers, livedo papules)



Constitutional upset (persistent low-grade pyrexia, m alaise, weight loss)

Pa ge 5 0 7



Sinusitis



Shortness or breath, cough



Hypertension



Cardiac failure/pericarditis



Nail-fold infarcts, splinter or retinal hem orrhages, Roth spots, scleritis, and episcleritis



Nonspecific abdom en pain, nausea or vom iting, diarrhea



Hem atochezia, m elena, hem atem esis



Bowel infarction, ischem ia, perforation, occlusion, peritonitis (these independently predict increased m ortality)



Acute appendicitis or cholecystitis (due to organ vasculitis)



History of hepatitis (associated with PAN)



Polyarteritis nodosa o

Three of the following 10 criteria are needed to diagnosis polyarteritis nodosa (PAN)



o

Weight loss >4 kg

o

Livedo reticularis

o

Testicular pain or tenderness

o

Myalgias or weakness

o

Mononeuropathy or polyneuropathy.

o

Diastolic blood pressure >90 m m Hg

Wegner granulom atosis: o

Ear, nose, and throat disease

o

Epistasis

o

Nasal and oral ulcerations and necrosis

o

Sinus pain

o

Hearing loss

o

Pulm onary disease

o

Hem orrhage (look for unexplained hypoxia)

o

Pleural effusions

o

Large airway inflam m ation and stenosis

Pa ge 5 0 7

o

Cardiac disease

o

Myocarditis, coronary arteritis, valvulitis, endocarditis, pericarditis

o 

Conduction disturbances

Churg-Strauss syndrom e (CSS): o

Asthm a (which m ay precede CSS by decades)

o

Allergic rhinitis

o

Peripheral blood eosinophile (which fluctuates rapidly especially with steroid treatm ent for associated asthm a)

o

System ic vasculitis affecting two or m ore extrapulm onary organs

o

Cardiac disease accounts for 50% of deaths due to CSS

o

Acute or constrictive pericarditis

o

Heart failure

o

Myocardial infarction

Small Arteries 

Palpable purpura



Abdom inal pain or cram ping



Nausea and vom iting



Diarrhea or constipation (frequently accom panied by the passage of blood or m ucus per rectum )



Rarely intussusception



Hem aturia

Essential Workup 

History and physical exam ination



CBC, erythrocyte sedim entation rate (ESR), urinalysis, blood urea nitrogen, creatinine

Tests

Pa ge 5 0 7

Lab 

Mild leukocytosis



ESR >20 m m /h



Anem ia of chronic disease with hem oglobin <12



ANA and ANCA titers



Both are generally elevated



Elevated ANCA especially sensitive for Wegner granulom atosis



Positive tissue biopsy



Hepatitis B antigen



30% of patients with PAN will be positive.



Usually, the ANCA is negative except with CSS.



Urinalysis: o

Proteinuria and hem aturia

Imaging 

Arteriography: o

Takayasu arteritis

o

Irregular vessel walls

o

Stenosis

o

Poststenotic dilation

o

Aneurysm s

o

Occlusion

o

Increased collateral circulation

o

Majority of patients have lesions above and below the diaphragm .

o

PAN

o

Mesenteric arteriography shows m ultiple berrylike aneurysm s.



Serial CT scans: o

Used in the early phases

o

Sinus CT for cases of Wegner granulom atosis

Pa ge 5 0 7

P.1193



MRI and MRA:



Positron em ission tom ography (PET scan) for Takayasu arteritis







Echocardiography: o

Takayasu arteritis

o

Aortic regurgitation

o

Dilated and thickened aorta

o

Left ventricular hypertrophy

o

Pulm onary hypertension

Ultrasonography: o

Takayasu arteritis

o

Subclavian and com m on carotid artery involvem ent

o

Aorta involvem ent

o

Coronary or pulm onary angiography

o

Takayasu arteritis

o

Coronary stenosis or occlusion

Endoscopy, sigm oidoscopy, and colonoscopy for gastrointestinal (GI) tract involvem ent



Chest radiograph: o

PAN usually has a nonspecific patchy alveolar infiltration.

o

Look for com plications or alternate diagnoses.

Differential Diagnosis 

Throm bosis



Antiphospholipid antibody syndrom e



Extensive according to specific to presenting sym ptom



Renal failure



Arthritis



Purpura

Pa ge 5 0 7



Congestive heart failure (CHF)

Treatment Initial Stabilization Initial stabilization is directed toward CHF, m yocardial infarction, and pulm onary edem a.

ED Treatment 

Takayasu arteritis: o

Corticosteroids: 

Rem ission occurs in 60%.



Relapses occur during steroid taper in 50%.

o

Methotrexate

o

Azathioprine

o

Cyclophospham ide (use for 3â€“6 m onths and then change im m unosuppressants due to drug toxicity)

o

Mycophenolate m ofetil, antitum or necrosis factor, acetylsalicylic acid (new treatm ents with lim ited research)



PAN fulm inate m ultisystem disease: o

Steroids: IV m ethylprednisolone followed by oral prednisolone

o

Cytotoxic agent: IV cyclophospham ide is started at the sam e tim e as the steroids. Repeated intervals (pulsed) at 1 and 4 weeks. If the GI tract is com petent, oral cyclophospham ide can be used.



PAN less severe disease: o

Lower doses of cyclophospham ide (1.5 to 2 m g/kg) and oral steroids



Wegner granulom atosis:

Pa ge 5 0 7

o

Corticosteroids

o

After 3 m onths on cyclophospham ide, Azathioprine m ay be substituted without increased incidence of relapse.

o 

Plasm a exchange m ay be helpful in severe disease.

Hepatitis B associated with PAN: o

Prednisolone for a week, taper off the 2nd week

o

Follow with lam ivudine for at least 6 m onths

o

Plasm a exchange (3 tim es a week for 3 weeks, then taper over 2 weeks until loss of the Hepatitis B e antigen, developm ent of Hepatitis B e antibody, or clinical recovery for 2â€“3 m onths)

o

Another option: com bination of prednisone and alpha-interferon therapy

o 

Antiplatelet agents

Treat CHF or hypertension with diuretics or an angiotensin-converting enzym e (ACE) inhibitor such as captopril in patients with Takayasu arteritis.



Interventional therapy: o

Indicated in certain settings with Takayasu arteritis: 

Renal vascular hypertension



Moderate to severe aortic regurgitation



Severe coarctation of the aorta



Cerebral hypoperfusion



Coronary ischem ia



Progressive aneurysm enlargem ent



Lim b claudication

o

Percutaneous translum inal angioplasty

o

Cardiac bypass

o

Stenting

o

Aneurysm repair

o

Aortic valve replacem ent

Pa ge 5 0 8

Medication (Drugs) 

Azathioprine: 2 m g/kg/d



Captopril (Capoten): 12.5â€“25 m g PO t.i.d. initially (peds: 0.5â€“1 m g/kg/d in 3 doses, m ax. 6 m g/kg/d)



Cyclophospham ide: o

IV: 0.5â€“1 g/m 2 body surface area

o

Oral: 2 m g/kg/d (up to 4 m g/kg) (peds: dose as per consultant)



Furosem ide: 40â€“100 m g IV (peds: 1 m g/kg IV)



Lam ivudine: 100 m g/d



Methylprednisolone: t.i.d. (0.25â€“1 m g) IV



Methotrexate 0.3 m g/kg/week up to 25 m g/kg/week



Prednisolone 1 m g/kg/d PO



Prednisone: 40â€“60 m g/d (peds: 1â€“2 m g/kg/d)

Follow-Up Disposition Admission Criteria 

Patients with evidence of severe disease and end organ dysfunction should be adm itted.



Consult for procedures to revascularize ischem ic organs.

Discharge Criteria Less sym ptom atic patients without evidence of end-organ involvem ent

References 1. Allen NB, Bressler PB. Diagnosis and treatm ent of the system ic and

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cutaneous necrotizing vasculitis syndrom es. Med Clin North Am . 1997;81(1):243â€“259. 2. Hunder GG. Giant cell arteritis and polym yalgia rheum atica. Med Clin North Am . 1997;81(1):195â€“215. 3. Num ano F, Okawara M, Inom ata H, et al. Takayasu's arteritis. Lancet. 2000;356:1023â€“1025. 4. Vanoli M, Diana E, Salvarani C, et al. Takayasu's Arteritis: A Study of 104 Italian Patients. Arthritis & Rheum atism . 2005;53(1):100â€“107. 5. Maruyoshi H, Toyam a K, Kojim a S, et al. Sensorineural Hearing Loss Com bined with Takayasu's Arteritis. Internal Medicine. 2005;44(2):124â€“128. 6. Sem ple D, Keogh J, Forni L, et al. Clinical review: Vasculitis on the intensive care unit-part 1: diagnosis. Critical Care. 2005: 9(1):92â€“97. 7. Sem ple D, Keogh J, Forni L, et al. Clinical review: Vasculitis on the intensive care unit-part 2: treatm ent and prognosis. Critical Care. 2005: 9(2):193â€“197. 8. Sercom be CT. System ic lupus erythem atosus and the vasculitides. In: Marx J, ed. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002 9. Sneller MC, Fauci AS. Pathogenesis of vasculitis syndrom es. Med Clin North Am . 1997;81(1):221â€“237.

Codes ICD9-CM 447.6

ICD10 I77.6

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Veno us Insufficiency

Venous

Insufficiency Calvin A. Brown III

Basics Description A chronic condition of lower extrem ity vascular incom petence

Etiology 

Norm al venous flow is from the superficial to deep veins.



Unidirectional flow is m aintained by m uscular contractions and bicuspid valves.



Valvular incom petence leads to regurgitant blood flow, elevated venous pressures, and distention of superficial veins.



Venous hypertension and endothelial dysfunction results in leakage of protein, red blood cells, and water into extracellular m atrix.



Fibrosis and dim inished oxygen diffusion produces sclerosis, skin breakdown, and ulcer form ation.

Diagnosis

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Signs and Symptoms History 

Asym ptom atic phase: o

Venous dilation ranging from venous flares to sm all varicosities



Sym ptom atic phase: o

Ankle and calf swelling

o

Itching

o

Profuse bleeding

o

Hyperpigm entation

o

Lipoderm atosclerosis

o

Ulcer form ation

Physical Exam 

Varicosities



Dependent ankle/calf edem a



Skin changes:



o

Induration

o

Sclerosis

Venous ulcers: o

Over either m alleoli or m edial portion of the calf with preserved peripheral pulses





Bacterial infection: o

Surrounding cellulitis

o

Rapidly growing ulcer

o

Increased pain

o

Lym phangitis

Leg edem a and ulcers with ascites, periorbital edem a, orthopnea, or an abnorm al cardiac exam suggests other etiologies.

Essential Workup

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Clinical features usually enough to m ake the diagnosis.

Tests Lab 

Lab tests are of little value.



Cardiac m arkers, brain natriuretic, album in, and tests of renal function can be sent if considering other causes of leg edem a.

Imaging Im aging: 

Duplex ultrasonography: o





Assess for DVT or valvular incom petence.

Venography: o

Gold standard

o

Expensive and invasive

Ankle-brachial index: o

If arterial insufficiency is suspected

Diagnostic Procedures/Surgery 

Im m ediate surgical procedures are not required for varicose veins.



Vein stripping, vein ligation, and sclerotherapy are options for cases refractory to m edical m anagem ent: o

Does not im prove healing but reduces ulcer recurrence

Differential Diagnosis 

Leg edem a: o

Congestive heart failure

o

Nephrotic syndrom e

o

Liver failure

o

Lym phatic obstruction

o

Deep venous throm bus

Pa ge 5 0 8

P.1195



Leg ulcers: o

Venous insufficiency

o

Arterial insufficiency

o

Soft-tissue infection

o

Polyarteritis

o

Pyoderm a gangrenosum

Treatment Initial Stabilization 

Leg elevation



Control bleeding with direct pressure.

ED Treatment 

Leg elevation



Com pression stockings



Anticoagulants for confirm ed deep vein throm bosis (DVT)



Steroids for stasis derm atitis



Aspirin



Antibiotics for signs of infection



Astringents: o



Dom eboro solution

Antihistam ines for pruritus

Medication (Drugs) 

Aspirin: 325 m g/d PO



Augm entin: 875 b.i.d. PO

Pa ge 5 0 8



Benadryl: 12.5â€“25 m g q.i.d. PO



Cephalexin: 500 m g q.i.d. PO



Dicloxacillin: 500 m g q.i.d. PO



Coum adin: dose per prothrom bin tim e/international norm alized ratio



Lovenox: 1 m g/kg SC b.i.d.

Follow-Up Disposition Admission Criteria Evidence of cellulitis, lym phangitis, or osteom yelitis m ay require adm ission.

Discharge Criteria 

Bleeding under control



DVT has been ruled out.



No evidence of bacterial infection requiring adm ission



Appropriate follow-up/referral arranged



Hom e services for dressing changes

References 1. Barwell JR, Davies CE, Deacon J, et al. Com parison of surgery and com pression with com pression alone in chronic venous ulceration (ESCHAR study): random ised controlled trial. Lancet. 2004;363(9424):1854â€“1859. 2. Guyton AC, Hall JE. Textbook of Medical Physiology. 10th ed. Philadelphia, PA: WB Saunders; 2000:158â€“159. 3. Marx JA, Hockberger RS, Walls RM Rosen's Em ergency Medicine: Concepts and Clinical Practice. Mosby, 2002:1228. 4. Tintinalli JE, Kelen GD, Stapczynski JS. Em ergency Medicine: A

Pa ge 5 0 8

Com prehensive Study Guide. McGraw-Hill, 2004:1529â€“1530.

Codes ICD9-CM 459.81

ICD10 I87.2

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventilato r M anagem ent

Ventilator

Management Owen Lander

Basics Description 

Ventilation provided by a m achine that generates a controlled flow of gas into a patient's airways



There are several different m odes and strategies of positive pressure ventilation.



Delivery m odes: o

Pressure-cycled: 

Each breath at the set rate is delivered to a set a m axim um pressure.



Markedly reduces the risk of barotraum a



Markedly variable tidal volum es and m inute ventilation as a result of changes in patient chest wall and lung com pliance and spontaneous respiratory efforts

o

Volum e-cycled: 

Each breath at the set rate is delivered to a set volum e.



Provides a consistent and reliable m inute

Pa ge 5 0 8

ventilation, appealing in the initial m anagem ent setting 

Can generate excessive peak pressures, particularly if patient chest wall or lung com pliance decreases



In m ost cases, can be lim ited by protective peak pressure cut-off lim its



Support m odes: o

Control m ode: 

Each breath, triggered or preset, is delivered as a â€œfull breath,â€• whether volum e- or pressure-cycled.

o

Support m ode: 

Relies solely on supplying set support pressure to patient initiated breaths, term inating when expiratory effort is detected

o

Continuous m andatory ventilation (CMV): 

A control m ode that delivers breaths only at the set respiratory rate.



Rarely used because it frequently results in severe air hunger and asynchrony between the patient and the ventilator



In the paralyzed or apneic patient, assist control (AC) is equivalent to CMV.

o

AC: 

Delivers a full breath at the preset respiratory rate



In addition, any inspiratory effort by the patient will also trigger the delivery of full breath at the set volum e or pressure.



Ensures adequate m inute ventilation while avoiding asynchrony in the nonapneic patient.

Pa ge 5 0 9



Can result in over ventilation, hypocarbia and alkalosis in patients with significant spontaneous respiratory effort secondary to pain or agitation



Can result in excessive peak pressures, barotraum as, and breath stacking, particularly in patients with obstructive airway disease requiring prolonged exhalation phases

o

Interm ittent m andatory ventilation (IMV): 

Delivers full breaths at the set respiratory rate



Spontaneous respirations by the patient are allowed but not supported.



Rarely used due to the subjective discom fort of m ixing fully supported breaths with unsupported breaths against the resistance of ventilator tubing and the possibility of delivering a full breath to a patient who has already spontaneously inhaled or is trying to exhale

o

Synchronous interm ittent m andatory ventilation (SIMV): 

Designed to fit a set num ber of full breaths per m inute around any spontaneous respirations of the patient



Will not deliver a preset full breath when the patient is actively breathing



Spontaneous respirations are aided by an adjustable am ount of pressure support.



Has replaced IMV due to m arked increase in patient com fort and synchrony with the ventilator and reduced risk of barotraum as

o

Pressure support ventilation (PSV): 

Provides a set am ount of pressure support whenever inspiratory effort is detected,

Pa ge 5 0 9

term inating when the flow rate of delivered air drops below a certain point indicating that the patient is ready to exhale 

Com fortable for the patient, allowing the patient to breath as m uch and as often as desired with sufficient support



Requires nonapneic patient who have an adequate and appropriate respiratory drive



May be augm ented on som e ventilators with a fail-safe set IMV rate if the patient becom es apneic



Noninvasive positive pressure ventilation (NIPPV): o

Increasingly available

o

Tight-fitting m ask delivers respiratory support without intubation.

o

Essentially a PSV m ode of ventilation with variable positive end expiratory pressure (PEEP)

o

May avoid intubation in m ild to m oderate reversible respiratory failure 

Congestive heart failure



Chronic obstructive pulm onary disease (COPD)



An awake, responsive patient m andatory



Adequate respiratory drive required



Titrated to the sam e goals as full m echanical ventilation.

Diagnosis Signs and Symptoms Indications for m echanical ventilation: 

Apnea

Pa ge 5 0 9



Respiratory distress with altered m entation



Clinically apparent increased work of breathing



Obtundation



Controlled hyperventilation required



o

Head injury

o

Tricyclic overdose

o

Metabolic acidosis

Severe circulatory shock

Tests Lab Aterial blood gas (ABG): 

Within 15 m inutes of initial intubation



Repeat as clinically indicated: o

Changes in clinical status

o

Changes in ventilator settings

o

Significant changes of or inability to obtain noninvasive SaO 2 or ETCO 2 values



PaO 2 >60 m m Hg and saturation > 90%



pH should be 7.20â€“7.5 initially: o

Avoid overly rapid changes in pH via abrupt changes in ventilation.

o

Acutely pH is m ost easily m anaged via changes in the PaCO 2 .

Imaging Chest radiograph: 

Confirm ation of correct placem ent of endotracheal tube

Differential Diagnosis Problem s in providing effective m echanical ventilation: 

Pneum othorax



Hyperinflation

Pa ge 5 0 9



Decreased venous return



Bronchospasm



Pulm onary edem a



Mucous plugging/secretions



Abdom inal distention



Ventilator problem s



Patient asynchrony

P.1197

Treatment Initial Stabilization 

Cardiac m onitor



Blood pressure m onitoring



Pulse oxim etry to ensure SaO 2 >90%



Continuous core tem perature via esophageal or rectal probe if available: o

Critically ill patients because of the risk of hypotherm ia (especially if paralyzed)



End-tidal CO 2 m onitoring when available: o

Can reduce the frequency of serial ABG m easurem ents

ED Treatment 

Ventilator settings should be adjusted to the patient's specific requirem ents:



Mode: o

Volum e-cycled m odes are the first choice, pressure cycled m odes are rarely used except in PSV.

Pa ge 5 0 9

o

SIMV or AC are the initial m odes of choice in the em ergently intubated patient.

o

PSV can be considered in patients with less severe respiratory failure and a robust respiratory drive.



Respiratory rate: o

Initial rate of 8â€“14 breaths per m inute

o

Higher rates for increased ventilation m ust be balanced against increased risk of air trapping and barotraum as.

o

Rates as low as 4â€“6 breaths per m inute m ay be required in severe asthm a to allow for exhalation.



Tidal volum e: o

Traditional volum es of 10â€“12 m L/kg are based on m aintaining norm al pH in patients with norm al lung parenchym a.

o

Increasing evidence of negative effects of higher volum es, especially in patients with prim ary lung pathology support an initial volum e of 8â€“10 m L/kg.

o

Lower volum es of 5â€“8 m L/kg are indicated in patients with severe asthm a/COPD or the presence of acute respiratory distress syndrom e



PEEP: o



3â€“5 cm H 2 O

Positive inspiratory pressure (PIP): o

Should be set if possible, or m onitored, to ensure they rem ain at or below 35 cm H 2 O



All patients should be adequately sedated to tolerate m echanical ventilation: o

Benzodiazepines are the drug of choice due to m uscle relaxing, am nestic, and anxiolytic effects.



Provide analgesia, optim ally m orphine or fentanyl.



Continued paralysis postintubation m ay be required:

Pa ge 5 0 9

o

Reduce the work of breathing in severe shock.

o

Tolerance of hypercapnia and prolonged I:E ratios in severe obstructive lung disease



Bronchodilators should be used in patients with obstructive lung disease.

Meeting the Goals of Ventilation 

Oxygenation: o

Titrate FIO 2 to m aintain SaO 2 >90% and PaO 2 >60 m m Hg

o

Patients with high m etabolic dem and m ay benefit from slightly increased oxygenation.

o

PaO 2 >110 using FIO 2 >0.50 offers no significant benefit and increases the risk of oxygen toxicity.

o

FIO 2 1.0 refractory hypoxia: 

Increm ental increase in PEEP



1â€“2 cm H 2 O at a tim e



Maxim um 10 cm H 2 O



Increased risk of hyperinflation, barotraum a, decreased venous return



Ventilation: o

Titrate m inute ventilation (RR Ã— TV) to achieve pH >7.20 and <7.55

o

PaCO 2 >35 m m Hg and <50 m m Hg (or patient baseline), as feasible within goal pH range

o

Maxim um respiratory rate no higher than allows for com plete exhalation on each breath

o

Maxim um tidal volum e lim ited by PIP and plateau pressures <35 cm H 2 O

Acute Changes 

Often m anifested by abrupt decrease in oxygen saturation and increase in PIP

Pa ge 5 0 9



Patient intolerance/asynchrony is a diagnosis of exclusion.



Delineate ventilator source from patient etiology.



Check tube placem ent.



Deep suction



Stat portable chest radiograph



Stat ABG if noninvasive values in any doubt



Lung exam : o

Wheezes, decreased air m ovem ent â†’ consider bronchospasm .

o

Crackles â†’ consider pulm onary edem a.

o

Absent breath sounds â†’ consider pneum othorax.

o

Prolonged expiratory phase â†’ consider breath stacking, hyperinflation.



Disconnect patient from ventilator, allow for full exhalation, and bag valve with 100% oxygen: o

o

o

Patient bags easily and saturation corrects quickly: 

Ventilator problem



Inappropriate ventilator m ode



Inadequate sedation

Patient is difficult to bag ventilate and oxygenate: 

Tension Pneum othorax



Bronchospasm



Hyperinflation



Mucous plug



Extubation or m ainstem intubation

Patient is relatively easy to bag ventilate, difficult to oxygenate: 

Pulm onary edem a



Pneum othorax



Pulm onary em bolus

Pa ge 5 0 9

Medication (Drugs) 

Midazolam : 0.03â€“0.05 m g/kg IV q5m inâ€“q10m in, titrate to sedation



Lorazepam : 0.03â€“0.05 m g/kg IV q5m inâ€“q10m in, titrate to sedation



Propofol: 0.3â€“0.5 m g/kg IV loading dose, m aintenance initiated at 10 m cg/kg/m in IV infusion. Increase 5â€“10 m cg/kg/m in to adequate sedation.



Morphine: 0.02â€“0.05 m g/kg IV q15m inâ€“q20m in PRN



Fentanyl: 0.5â€“1 m cg/kg IV q10m inâ€“q15m in PRN



Albuterol: 2.5â€“5 m g/5 m L saline q20m inâ€“q30m in via in line endotracheal delivery



Ipratropium Brom ide: 0.5 m g/2.5 saline q4h vial in line endotracheal delivery



Ketam ine: 0.5â€“3 m g/kg/hr (peds: 0.25â€“1 m g/kg/hr) IV infusion

Follow-Up Disposition Admission Criteria Intensive care unit adm ission for all intubated patients

References 1. Hill NS, Levy MM, et al. Ventilator Managem ent Strategies for Critical Care. New York, NY: Marcel Dekker; 2001. 2. MacIntyre N, Branson R. Mechanical Ventilation. Philadelphia, PA: WB Saunders, 2000 3. Pollack CV. Mechanical Ventilation and Noninvasive Ventilatory Support. In: Rosen's Em ergency Medicine Concepts and Clinical

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Practice. Eds. Marx JA, Hockberger RS, Walls RM, et al. 5th ed. St. Louis, MO: Mosby, 2002. 4. Stock MC, Pearl RG. Handbook of Ventilatory Support. Baltim ore, MD: Wlliam s and Wilkins; 1997.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventricular F ibrillatio n

Ventricular

Fibrillation Ra'ed Hijazi

Basics Description 

Ventricular fibrillation (VF) is com pletely disorganized depolarization and contraction of sm all areas of the ventricle without effective cardiac output.



Cardiac m onitor displays absence of quasi-random signal (QRS) com plexes and T waves with the presence of high-frequency, irregular undulations that are variable in both am plitude and periodicity.

Etiology 

Initial rhythm in approxim ately 50â€“70% of patients sustaining sudden cardiac death in the prehospital setting: o

Most often a result of severe m yocardial ischem ia or infarction



Com plication of cardiom yopathy: o

Up to 50% of patients with dilated cardiom yopathy suffer an episode of VF.

o

In hypertrophic cardiom yopathy, unexpected sudden death occurs with reported frequency of up to 3% per

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year. 

Other less com m on causes of VF: o

Blunt chest traum a

o

Hypotherm ia

o

Iatrogenic m yocardial irritation form pacem aker placem ent or pulm onary artery catheter



VF is often preceded by ventricular tachycardia (VT). Conditions predisposing to VT: o

Drug toxicities (cyclic antidepressants, digitalis)

o

Congenital and acquired prolonged QT syndrom es.

o

Short QT syndrom e

o

Brugada syndrom e

o

Idiopathic VF (5â€“10%)

Pediatric Considerations 

Prim ary ventricular dysrhythm ias are extrem ely rare in children.



VF usually results from a respiratory arrest, hypotherm ia, or near drowning.

Diagnosis Signs and Symptoms 

Loss of consciousness, seizure, transient gasping followed by apnea



Absent pulse and heart sounds



Death if the rhythm rem ains untreated

Essential Workup Cardiac m onitor

Tests

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Lab 

Laboratory tests are not useful during resuscitation.



After successful resuscitation, electrolytes including calcium and m agnesium , cardiac enzym es, troponin, and toxicologic screen

Differential Diagnosis Asystole: Fine VF m ay m im ic asystole in a single lead. Check rhythm in another lead for fine fibrillations.

Treatment Alert 

Early defibrillation of VF is the m ost im portant determ inant of survival, and each m inute without defibrillation reduces survival by 7â€“10%.



Supraventricular tachycardia or VT with a pulse m ay degenerate into VF if cardioverted without synchronization.



In a hypotherm ic cardiac arrest (core tem perature less than 30Â°C), if the patient rem ains in VF after the delivery of the first three shocks, rewarm the patient first before further attem pts of defibrillation.



Do not defibrillate any conscious patient.



The subm ission of this chapter precedes the release of the 2005 Am erican Hospital Association guidelines; therefore, som e discrepancies m ay exist following their release.

Controversies 

Biphasic autom atic external defibrillation (AED): o

Multicenter study showed that low-energy (150 J)

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biphasic AED resulted in superior defibrillation rate com pared to the m onophasic AED, resulting in return of spontaneous circulation in a greater percentage of patients. The rates of survival to hospital adm ission and discharge did not differ between the two groups. 

There is no conclusive evidence supporting nonescalating over escalating biphasic defibrillation.



The optim al energy level of biphasic defibrillation has not yet been agreed upon.



CPR before defibrillation for prolonged VF (>5 m in)

Pre Hospital 

ABCs



Follow initial stabilization according to respective prehospital policies and procedures.

Initial Stabilization 



Im m ediate defibrillation with three stacked shocks: o

Monophasic 200 J, 200â€“300 J, 360 J

o

Biphasic escalating 120 J, 150 J, 200 J

o

Biphasic nonescalating 150 J, 150 J, 150 J

Initiate CPR and airway m anagem ent including endotracheal intubation.



Establish IV access.



Adm inister Vasopressin 40 units IV single dose; can be given one tim e only as first drug before Epinephrine or



Adm inister Epinephrine 1 m g IV bolus or 2â€“2.5 m g via endotracheal tube (ETT).



After Vasopressin or Epinephrine, repeat defibrillation with 360 J (or equivalent biphasic joules) within 30â€“60 seconds o

If VF persists, consider antiarrhythm ics: Am iodarone,

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Lidocaine, Magnesium , and/or Procainam ide. P.1199



Epinephrine can be initiated 10â€“20 m inutes after Vasopressin.



Follow each m edication with defibrillation within 30â€“60 seconds at the last energy level used.



Consider sodium bicarbonate for patients with prolonged arrest.



If the patient is successfully resuscitated, start a continuous infusion of the last antiarrhythm ic agent adm inistered to the patient.



If the patient was successfully resuscitated prior to antiarrhythm ic adm inistration, give: o

Am iodarone 150 m g in 100 m L D 5 W over 10 m inutes followed by a m aintenance infusion or

o

Lidocaine 1â€“1.5 m g/kg IV bolus followed by a m aintenance infusion



Begin an evaluation for the cause of the VF arrest recognizing that the m ost likely cause is m yocardial ischem ia.

Pediatric Considerations 

Defibrillation sequence: m onophasic 2 J/kg, 2â€“4 J/kg, 4 J/kg



Currently, there are no recom m endations for biphasic energy levels for pediatrics.

Medication (Drugs)

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

Vasopressin: 40 units IV bolus single dose



Epinephrineâ€”1:10,000 concentration; 1 m g IV bolus, repeat dose q3m inâ€“q5m in: o

Epinephrine via ETT: 1:1,000 concentration; 2â€“2.5 m g diluted in 10 m L NS via ETT



Am iodaroneâ€”300 m g in 20â€“30 m L NS/D 5 W IV bolus, repeat 150 m g in 20â€“30 m L NS/D 5 W IV bolus q3m inâ€“q5m in: o

Am iodarone infusion: 1 m g/m in for first 6 hours then 0.5 m g/m in for 18 hours, additional 150 m g in 100 m l D 5 W over 10 m in; repeat q10m in as needed. Max. cum ulative dose 2.2 g/24h



Lidocaine: 1â€“1.5 m g/kg IV bolus, repeat 0.5â€“.75 m g/kg IV bolus. Max. IV bolus dose is 3 m g/kg: o

Lidocaine via ETT: 2â€“4 m g/kg

o

Lidocaine infusion: 1â€“4 m g/m in (30 to 50 Âµg/kg/m in)



Magnesium sulfate: 1â€“2 g in 10 m L D 5 W IV bolus



Procainam ide: 20â€“50 m g/m in until arrhythm ia suppressed, hypotension, QRS widens by 50%, or a total of 17 m g/kg is reached: o

Procainam ide infusion: 1â€“4 m g/m in



Sodium bicarbonate: 1 m Eq/kg IV bolus



Follow each m edication with a 20 m L NS flush.

Pediatric Considerations 

Epinephrine: 0.01 m g/kg (0.1 m L/kg of 1:10,000) IV/IO repeat with sam e dose q3m inâ€“q5m in or give 0.1â€“0.02 m g/kg (or 0.1â€“0.02 m L/kg of 1:1000): o

Epinephrine via ETT: 0.1 m g/kg (0.1 m L/kg of 1:1000)



Am iodarone: 5 m g/kg IV/IO, m ay repeat 5 m g/kg; m ax. cum ulative dose 15 m g/kg/d

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

Lidocaine: 1 m g/kg IV/IO: o

Lidocaine infusion 20â€“50 Âµg/kg/m in



Magnesium sulfate: 25â€“50 m g/kg IV/IO up to 2 g



Follow each m edication with a 3â€“5 m L NS flush.

Follow-Up Disposition Admission Criteria All patients who survive need adm ission to the intensive/coronary care unit.

Discharge Criteria No patient who suffers a VF arrest m ay be discharged from the ED.

References 1. Am erican Heart Association Guidelines 2000 for Cardiopulm onary Resuscitation and Em ergency Cardiovascular Care. Circulation. 2000;102. 2. ArKern KG, Halperin HR, Field J. New Guidelines for Cardiopulm onary Resuscitation and Em ergency Cardiac Care. JAMA. 2001;285. 3. Blum FC. Adult Medical Resusciation. In: Howell J. et al. eds. Em ergency Medicine. Philadelphia, PA: WB Saunders, 1997 4. Cum m ins RO, ed. ACLS Provider Manual. Dallas, TX: Am erican Heart Association, 2001 5. Hazinski, MF, ed. PALS Provider Manual. Dallas, TX: Am erican Heart Association, 2002 6. Ewy GA. Cardiocerebral Resuscitation: The New Cardiopulm onary Resuscitation. Circulation. 2005;111:2134â€“2142. 7. Vilke GM, et al., The three-phase m odel of cardiac arrest as

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applied to ventricular fibrillation in a large, urban em ergency m edical services system . Resuscitation. March 2005;64(3):341â€“346.

Codes ICD9-CM 427.41

ICD10 149.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventricular Perito neal Shunts

Ventricular

Peritoneal Shunts Richard S. Krause

Basics Description 

Obstruction: Shunt m alfunction im pairs drainage of cerebrospinal fluid (CSF): o

Increases intracranial pressure (ICP)



Rate of increase in ICP determ ines severity.



Overdrainage syndrom e:



o

Assum ing upright posture increases CSF outflow

o

Decreases ICP

o

Produces post-lum bar puncture like headache

Infection: o

A shunt is a foreign body.

o

Conduit between CSF and the peritoneal cavity

o

Staphylococcus epiderm idis and other staphylococcal species in 75% of infections



Slit ventricle syndrom e: o

Prolonged overdrainage causes decreased ventricular size.

o

Interm ittent increases in ICP owing to proxim al

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obstruction

Pediatric Considerations 

If cranial sutures are open, CSF m ay accum ulate without m uch ICP increase: o

Produces relatively nonspecific signs and sym ptom s

Etiology 

Genetic causes



Cerebral lesion or stroke



Post head traum a



Aneurysm



Meningitis.

Diagnosis Signs and Symptoms 



Shunt obstruction: o

Headache, nausea

o

Malaise, general weakness, irritability

o

Decreased level of consciousness or com a

o

Increased head size or bulging fontanelle

o

New-onset seizures, increased seizure frequency

o

Autonom ic instability, decreased upward gaze

o

Apnea/Respiratory arrest

o

Papilledem a: rare

Overdrainage syndrom e: o

Severe headache, focal neurologic signs, m alaise, seizures, com a: 

o

Signs and sym ptom s often postural

Rapid overdrainage m ay cause upward shift of the brainstem :

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



Apnea, bradycardia



Syncope, hypotension



Laryngospasm

o

Subdural hygrom a or hem atom a

o

Chronic overdrainage

o

Pneum ocranium

Shunt infections: o

Fever (m ay be absent)

o

Meningeal signs

o

Local signs of infection (erythem a, swelling, tenderness)

o

Peritonitis

o

Infections usually occur soon after shunt placem ent (about 80% within 6 m onths).



Slit ventricle syndrom e: o

Episodic headache

o

Alternating periods of norm al behavior and lethargy

o

Headache, nausea, and vom iting

Essential Workup 

Suspected shunt m alfunction: o

Manipulation of the pum ping cham ber: 

Cham ber should com press easily and refill within 3 seconds.



Failure to com press easily im plies distal obstruction.



Failure to fill im plies proxim al obstruction.



Up to 40% of m alfunctioning shunts com press/fill norm ally.

o

Head CT

o

Shunt series: 

Radiographs of skull, chest, abdom en



Aids in diagnosis of disconnection, m alposition,

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or kinking of shunt com ponents 

Suspected infection: o

Aspiration of CSF from shunt reservoir (consultation with neurosurgeon): 

May be perform ed using sterile technique and 23-gauge butterfly needle



Slowly aspirate 5â€“10 m L CSF for the studies noted below in the next section.

Tests Lab 

Electrolytes, renal function, and glucose



Anticonvulsant levels



CBC



Suspected infection: o

Analysis of CSF from the shunt reservoir: 

Send culture, cell count, gram stain, glucose, and protein levels.



CSF analysis m ay have norm al early result, especially with prior antibiotic treatm ent.

o

Blood cultures

Imaging 



Cranial CT: o

Evaluate catheter position, ventricular size.

o

Subdural hem atom a or hygrom a

o

Other causes of elevated ICP: 

Enlarged ventricles: shunt m alfunction



Sm aller ventricles: overdrainage

Ultrasound m ay be used to assess ventricular size and position of catheter tip.



Shunt m anom etry: o

High pressure >20 cm H 2 O im plies distal shunt

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obstruction

Differential Diagnosis 

Seizure disorder (idiopathic, toxic, m etabolic)



Infections:



o

CNS infection not related to the shunt

o

System ic infections

Metabolic abnorm alities: o

Hypoglycem ia

o

Hyponatrem ia

o

Hypoxia



Intoxication/Poisoning



Head traum a

P.1201

Treatment Pre Hospital 

Patients with shunt m alfunction are at risk for apnea and respiratory arrest.



Oxygen should be applied with close m onitoring of respiratory status.



If increased ICP is suspected, transport patient with head elevated to 30Â°.

Initial Stabilization Signs of im pending herniation: 

Rapid-sequence intubation and controlled ventilation to Pco 2 about 35 m m Hg o

Pretreat with lidocaine (pediatric: plus atropine).

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o

Thiopental/Etom idate for induction

o

Succinylcholine m ay increase ICP a few m m Hg, although this m ay not be clinically significant.

o

Use only pretreatm ent dose of nondepolarizing agent if depolarizing agent chosen.

o

Nondepolarizing agents (vecuronium , rocuronium ) m ay be preferable.



Forced pum ping of shunt cham ber: o

Flush the device with 1-m L saline solution to rem ove distal obstruction.

o

Allow slow drainage of CSF from the reservoir to achieve pressure <20 cm H2O.



IV m annitol to lower ICP



Ventricular puncture is procedure of last resort if procedures suggested already unsuccessful and neurosurgeon unavailable.



Status epilepticus is treated with benzodiazepines (lorazepam ).

ED Treatment 

Early neurosurgeon consultation



Shunt m alfunction: o

Elevate head of bed to 30Â°.

o

Medical m anagem ent with diuretics (m annitol, furosem ide) m ay be appropriate in certain m ild cases.





Overdrainage syndrom e: o

Maintain patient's supine position.

o

Correct volum e depletion.

Shunt infection: o

System ic antibiotics: 

Vancom ycin plus cefotaxim e or gentam icin if gram -negative suspected

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Medication (Drugs) 

Adult and pediatric doses: o

Atropine: 0.02 m g/kg IV (m inim um 0.1 m g)

o

Cefotaxim e: 30 m g/kg IV (newborn: 50 m g/kg IV)

o

Furosem ide: 1 m g/kg IV

o

Gentam icin: 2â€“5 m g/kg IV

o

Lidocaine: 1 m g/kg IV

o

Mannitol: 1 m g/kg IV

o

Rocuronium : 0.6â€“1 m g/kg IV

o

Succinylcholine: 1.5 m g/kg IV

o

Vancom ycin: 15 m g/kg IV

o

Vecuronium : 0.1â€“0.3 m g/kg IV

Follow-Up Disposition Admission Criteria Patients with shunt com plications require neurosurgical consultation and adm ission to an intensive care unit or other m onitored setting

Discharge Criteria If shunt m alfunction is ruled out, disposition depends on diagnosis and patient condition.

References 1. Goeser CD, McLeary MS, Young LW. Diagnostic im aging of ventriculoperitoneal shunt m alfunctions and com plications. Radiographics. May/June 1998;18(3):635â€“651. 2. Key CB, Rothrock SG, Falk JL. Cerebrospinal fluid shunt

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com plications: an em ergency m edicine perspective. Pediatr Em erg Care. 1995;11:265â€“273. 3. Madsen MA. Em ergency departm ent m anagem ent of ventriculoperitoneal cerebrospinal fluid shunts. Ann Em erg Med. 1986;15:1330â€“1343. 4. Moza K, McMenom ey SO, Delashaw JB Jr. Indications for cerebrospinal fluid drainage and avoidance of com plications. Otolaryngol Clin North Am . August 2005;38(4):577â€“582.

ICD9-CM 996.2 Mechanical com plication of nervous system device, im plant, and graft

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventricular Tachycardia

Ventricular

Tachycardia Daniel C. McGillicuddy

Basics Description 

A wide-com plex tachydysrhythm ia with a quasi-random signal (QRS) >120 and a rate >100



Rapid and regular depolarization of the ventricles independent of the atria and the norm al conduction system



Re-entry: o

Structural heart disease m ost com m on

o

Seen in dilated cardiom yopathy, ischem ia, and infiltrative heart disease, previous m yocardial infarction, scarring





o

May be pharm acologically induced

o

Usually produces a regular and m onom orphic rhythm

Triggered autom aticity: o

Minority of ventricular tachycardia (VT)

o

Caused by repetitive firing of a ventricular focus

Torsades de pointes: o

Polym orphic form of VT

o

Alternating electrical polarity and am plitude

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

o

Prolongation in repolarization necessary

o

Usually pharm acologically induced

Regardless of the m echanism , all VT m ay degenerate to ventricular fibrillation (VF).

Etiology 

Wide com plex tachycardia: o

80% likelihood of being VT

o

20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy



Wide com plex tachycardia and a history of m yocardial infarction:





o

>98% likelihood of being VT

o

Age >35 years 80% risk of VT

o

Age <35 years 75% risk of SVT

Incidence of nonsustained VT: o

0â€“4% in the general population

o

Up to 60% of patients with dilated cardiom yopathy

Associated with increased risk for sudden cardiac death (SCD)

Diagnosis Signs and Symptoms History 

Asym ptom atic



Syncope/Near syncope



Lightheadedness/Dizziness



Shortness of breath



Palpitations



Chest discom fort/pain

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

Diaphoresis



Cannon A waves



Hypotension



Congestive heart failure



Beat-to-beat variability of systolic blood pressure



Variability in heart tones, especially S1

Essential Workup ECG 

Most im portant initial test to differentiate VT from SVT with aberrancy or LBBB



VT: o

Three or m ore consecutive QRS com plexes with a ventricular rate over 100 beats/m in and a QRS duration >120 m illiseconds



Torsades de pointes: o

Polym orphic VT that rotates its axis every 10â€“20 beats



Criterion to determ ine VT: o

Atrial ventricular (AV) dissociation (present in 60â€“75%)

o

Fusion beats (P wave partially activates ventricle in advance of next VT cycle), capture beats (P wave totally activates ventricle)

o

Uniform m orphology (except in the case of torsades)

o

Extrem e axis deviation (â€“90 to +180 degrees)

o

QRS >140 m illiseconds, with right bundle branch block (RBBB) m orphology; or QRS >160 m illiseconds, with LBBB m orphology, but >160 suggests VT regardless of bunch branch m orphology

o

QRS concordance in the precordial leads

o

RBBB pattern with R> Râ€™ is VT 50:1.

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o

LBBB pattern with Q or QS pattern is VT 50:1.

o

Brugada's criteria: (99% sensitivity, 97% specificity) 

R-S interval absent in all precordial leads



R-S interval >100 m illiseconds in any precordial lead

 o

AV dissociation

V-1 R wave >30 m illiseconds; R-S interval >70 m illiseconds, slurred, notched S

o 

Wide QRS with LBBB in precordium

Indicators of SVT with aberrancy include: o

Norm al-axis QRS <140 m illiseconds

o

Absence of Q waves

o

RBBB in V1 with rsRâ€™ triphasic pattern

o

NB: Slowing of im pulse conduction velocity seen with antiarrhythm ic drugs is m ore pronounced at faster rates, so m ay result in wide-com plex SVT (SVT with aberrancy).

Tests Lab 

Cardiac enzym es



Electrolytes, blood urea nitrogen, creatinine, glucose



Magnesium level



Calcium level



Digoxin level if toxicity suspected

Imaging Chest radiograph: 

Cardiom egaly or other cardiac anom alies m ay be apparent.

Diagnostic Procedures/Surgery Esophageal pacing catheters:

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

May be able to detect atrial activity to establish AV dissociation and therefore diagnose VT



Catheters can then be used to overdrive pace if needed.

Differential Diagnosis 

SVT with aberrancy or baseline LBBB



Proarrhythm ia secondary to antidysrhythm ia m edications; suspect if: o

VT m orphology is different than previous episodes of VT.

o

Medications have recently been started or changed.

o

QT interval is greater than 440 m sec.

o

Torsades de pointes

o

If VT continues to recur after cardioversion

Treatment Pre Hospital 

Cautions: o

Transport stable patients suspected of being in VT without attem pting to convert them .

o

Synchronized cardioversion for unstable patients with a pulse

o 

Defibrillation for pulseless VT

Controversies: o

Lidocaine: 

No benefit in the prevention of VT in patients with isolated prem ature ventricular contractions, regardless of the frequency



Infusions are no longer advanced cardiac life support (ACLS) protocol.

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Initial Stabilization Pulseless VT: Defibrillate im m ediately and follow the ventricular fibrillation treatm ent plan. P.1203

ED Treatment 

Unstable patient: o

o

Definition: 

Chest pain



Hypotension



Evidence of worsening heart failure

Initiate im m ediate synchronized cardioversion with 100 J, quickly progressing to 200 J, 300 J, and 360 J if no response. 

If the VT is polym orphic, begin cardioversion at 200 J.

o

Sedate the patient before cardioversion if at all possible.

o

If unable to term inate the VT, adm inister lidocaine and repeat the cardioversion.

o

Antitachycardia overdrive pacing if torsades

o

After successful return of sinus rhythm , begin am iodarone.



Stable patient, m onom orphic VT: o

Norm al cardiac function at baseline: 

Procainam ide or sotalol; m ay also consider am iodarone or lidocaine

o

Im paired cardiac function at baseline: 

Am iodarone bolus, then infusion or lidocaine, then synchronized cardioversion

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

Stable patient, polym orphic VT: o

Norm al QT interval at baseline: 

Correct electrolyte abnorm alities.



Treat ischem ia if present.



Then begin one of the following: beta-blockers, lidocaine, am iodarone, procainam ide, or sotalol.

o

Prolonged QT Torsades de pointes: 

Correct electrolytes.



Magnesium sulfate or overdrive pacing or one of the following: isoproterenol, phenytoin, lidocaine



Isoproterenol is used to overdrive the tachycardia if the patient has no history of coronary artery disease.



Tem porizing m easure until external pacing available

o

Im paired cardiac function at baseline

o

Am iodarone bolus or lidocaine bolus then synchronized cardioversion

Pediatric Considerations 

Prim ary cardiac arrest and VT are rare in children.



Usually secondary to hypoxia and acidosis



VT is tolerated for longer periods in children than adults and is less likely to degenerate to VF.



Infants in VT m ost com m only present with congestive heart failure.



VT in children results from : o

Cardiom yopathy

o

Congenital structural heart disease

o

Congenital prolonged QT syndrom es

o

Coronary artery disease secondary to vasculitis

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o

Toxins, poisons, drugs

o

Severe electrolyte im balances, especially of potassium

Medication (Drugs) 

Adenosine: 6 m g IV push followed by 12 m g IV push if needed in 1â€“2 m inutes (peds: 1 m g/kg, m ax. 6 m g; note: does not convert VT, no longer ACLS protocol)



Am iodarone: 150 m g IV bolus over 10 m inutes, m ay repeat; m ax. cum ulative dose 2.2 g IV/24h; infusion 540 m g IV over 18 hours (0.5 m g/m in) (peds: 5 m g/kg IV or IO over 20â€“60 m inutes, m ax. 15 m g/kg/d)



Isoproterenol: 2â€“10 Âµg/m in, titrate to heart rate (peds: 0.1 Âµg/kg/m in); note: do not give with epinephrine, m ay precipitate VT/VF



Lidocaine: 1â€“1.5 m g/kg bolus IV push first dose, 0.5â€“0.75 m g/kg second dose, and q5m inâ€“q10m in for a m ax. of 3 m g/kg; tracheal adm inistration 2â€“4 m g/kg; m aintenance infusion 1â€“4 m g/m in if converted (peds: 1 m g/kg bolus with infusion 20â€“50 Âµg/kg/m in)



MgSO 4 : 2 g in D 5 W over 5â€“10 m in followed by infusion of 0.5â€“1.0 g/h IV, titrate to control torsades



Procainam ide: 20â€“30 m g/m in until converted or for a total m ax. dose of 17 m g/kg; m aintenance infusion 1â€“4 m g/m in

Follow-Up Disposition

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Admission Criteria 

Adm it sustained VT to a critical care setting.



Adm it nonsustained VT and a history of m yocardial infarction or dilated cardiom yopathy for electrophysiologic studies.

Discharge Criteria 

Rare patients with nonsustained VT and a previous evaluation that revealed no structural heart disease can be discharged: o



At low risk for SCD

Patients with autom atic internal cardiac defibrillators that are well functioning can also be discharged.

Issues for Referral All patients with VT should be followed by a cardiologist.

References 1. Alpert MA, Mukeiji V, Bikkina M, et al. Pathogenesis, recognition, and m anagem ent of com m on cardiac arrhythm ias. South Med J. 1995;88(1):121. 2. Brady WJ, Skiles J. Wide QRS com plex tachycardias; ECG differential diagnosis. Am J Em erg Med. 1999;17(4):376â€“381. 3. Brugada P, Brugada J, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS com plex. Circulation. 1991;83:1649â€“1659. 4. Fogel RI, Prystowsky EN. Managem ent of m alignant ventricular arrhythm ias and cardiac arrest. Crit Care Med. 2000;28(10):165â€“169. 5. Gupta AK, Thakur RK. Wide com plex tachycardias. Med Clin North Am . 2001;85(2)245â€“266. 6. Kudenchuk PJ. Intravenous antiarrhythm ic drug therapy in the resuscitation from refractory ventricular arrhythm ias. Am J Cardiol.

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Novem ber 4, 1999;84(9A):52Râ€“55R. 7. Passm an R, Kadish A. Polym orphic VT, long QT syndrom e and torsades de pointes. Med Clin North Am . 2001;85(2):321â€“341. 8. Saliba WI, Natale A. Ventricular tachycardia syndrom es. Med Clin North Am . 2001;85(2):267â€“304. 9. Wijetunga M. Am iodarone versus Im plantable Defibrillator (AMIOVIRT): background, rationale, design, m ethods, results and im plications. Card Electrophysiol Rev. Decem ber 2003;7(4):452â€“456.

Codes ICD9-CM 427.1

ICD10 I47.2

Acknowledgment Thank you to the prior author on this chapter, Jennifer Audi

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vertebro basilar Insufficiency

Vertebrobasilar Insufficiency Leo Kobayashi

Basics Description 

Inadequate perfusion of vertebrobasilar (VB) arterial circulation from throm botic, em bolic, or low-flow states



Vertebral arteries (VA) derive from subclavian arteries and give rise to the anterior spinal artery and the basilar artery.



Arteries supplying the brainstem and cerebellum originate from the VB system before it branches into the two posterior cerebral arteries (PCA), such that a wide variety of focal neurological deficits arise from VB circulatory dysfunction.

Etiology Mechanism 

Throm bosis: o

VB ischem ia due to underlying VB atherosclerosis and clot form ation



Em bolus: o

VB ischem ia due to em bolization of clot from

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proxim al location 

Low-flow states: o

Hypoperfusion of VB system from system ic (cardiogenic shock) or localized (e.g., subclavian steal) reduction in blood flow





Less com m on etiologies: o

Fibrom uscular dysplasia

o

Hypercoagulable states

Ischem ic m echanism s causing VB insufficiency can herald and lead to VB territory infarcts.



Severe episodes of VB hypoperfusion or loss of circulation can lead to: o

â€œLocked-inâ€• syndrom e: 

o

Quadriplegia with intact consciousness)

â€œTop-of-basilarâ€• syndrom e: 

Pontine and cerebellar dysfunction with dim inished level of consciousness

Diagnosis Signs and Symptoms All history and physical exam item s m ay present interm ittently.

History 

Dizziness/Vertigo (â€œm ild,â€• â€œnonviolentâ€•; m ay be isolated finding)



â€œDrop attackâ€•



Headache



Mental status changes



Paresis/Paresthesia



Seizure

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

Syncope



Visual changes

Physical Exam 

Brainstem : o

â€œCrossedâ€• findings (i.e., ipsilateral facial and contralateral body deficits)

o

Altered m ental status or responsiveness

o

Decreased respiratory drive

o

Horner syndrom e (enophthalm os, ptosis, m iosis, anhidrosis)

o

Internuclear ophthalm oplegia

o

Nausea/vom iting

o

Nystagm us (especially nonfatigable, vertical/rotatory)

o 



Cranial nerves: o

Extra-ocular m uscle paresis (e.g., diplopia)

o

Pupillary abnorm alities

o

Facial paresthesia

o

Facial m uscle paresis

o

Hearing abnorm alities

o

Dysphagia

o

Dysarthria

Cerebral cortex (PCA circulation): o





Paresis/Paresthesias

Visual disturbances (e.g., hom onym ous hem ianopsia)

Cerebellar: o

Ataxia

o

Dysm etria

o

Gait abnorm ality

Cardiovascular: o

Carotid/VA bruit

o

Irregular/Asym m etric/Weak pulses

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Essential Workup 

Em ergent head CT (noncontrast) to evaluate for hem orrhage (parenchym al, subarachnoid, traum atic), large acute infarcts, prior pathology



Thorough neurologic and cardiac exam



12-lead ECG for arrhythm ias and m yocardial ischem ia

Tests Lab 

CBC: o

Anem ia, throm bocytopenia; polycythem ia, throm bocytosis



Coagulation studies (prothrom bin tim e/partial throm boplastin tim e [PTT]/international norm alized ratio): o

Hypo- and hypercoagulable states; baseline values for anticoagulant and fibrinolytic therapies



Electrolytes, blood urea nitrogen, creatinine, glucose



Cardiac m arkers for concurrent m yocardial ischem ia



Urinalysis



Erythrocyte sedim entation rate for system ic vasculitides



Rapid plasm a reagin



Thyroid-stim ulating horm one



lipid profile

Imaging 

Em ergent head CT (noncontrast); consider head and neck CT angiogram (CTA) for possible acute vascular intervention



Chest radiograph; consider chest CTA for cardiopulm onary and great vessel pathology



MRI/Magnetic resonance angiography for im proved characterization of ischem ic lesion and cerebrovascular

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circulation (e.g., congenital VB anom alies, exclusion of VA dissection) 

Echocardiography for intracardiac em bolic source



Cervical Doppler ultrasound



Transcranial Doppler ultrasound

Diagnostic Procedures/Surgery Neuroangiography for diagnosis (directed intra-arterial throm bolytic therapy/angioplasty/stenting/em bolectom y are still under investigation)

Differential Diagnosis 

CNS: o

CVA (hem orrhagic or ischem ic): 

Cerebral



Cerebellar



Brainstem

o

Multiple sclerosis

o

Migraine syndrom es

o

Seizure (focal)

o

Traum atic injury/postconcussive

o

Tum or

o

Vascular m alform ation hem orrhage (arteriovenous m alform ation, subarachnoid)

o 

Peripheral nervous system : o



Brainstem herniation

Vestibular neuronitis

Ear, nose, throat: o

Cerebellopontine angle tum or

o

Ear canal pathology (foreign body, tum or)

o

Labyrinthitis/Otitis m edia

o

MÃ©niÃ¨re disease

o

Paroxysm al positional vertigo

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

Cardiovascular: o

Arrhythm ia

o

Myocardial ischem ia/infarct

o

Aneurysm /Dissection (VA, BA, subclavian artery, aorta)











o

Hypovolem ia

o

Vasculitides

Endocrine: o

Adrenal insufficiency

o

Hypothyroidism

Hem atologic: o

Anem ia

o

Coagulopathy/hypercoagulable state

Infectious: o

Encephalitis/Meningitis

o

Otitis m edia/m astoiditis

o

Septic shock

o

Syphilis

Metabolic: o

Hypoglycem ia; hyperglycem ia

o

Electrolyte im balance

Toxicologic: o

Ataxia: alcohols, lithium , phenytoin

o

Salicylism

o

Serotonin syndrom e

o

Iatrogenic

P.1205

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Treatment Pre Hospital 

ABCs



Fingerstick glucose m easurem ent



Notification: o

Urgent contact with receiving facility if airway com prom ise or hem odynam ic instability

Initial Stabilization 

ABCs



Adm inister oxygen.



Place on cardiac m onitor and pulse oxim eter.



Establish IV access with 0.9% norm al saline.

ED Treatment 

Cerebrovascular perfusion m anagem ent: o

Supportive care

o

Supine position

o

Antiplatelet agent

o

Anticoagulation: 

Consider in consultation with neurology if significant risk factors for em bolic source, unstable or progressive ischem ic sym ptom s.

o

Ideal blood pressure (BP) targets not well-defined; m aintain BPs within patient's expected range (i.e., account for chronic hypertension). 

If hypotensive: fluid resuscitation, vasopressors or blood as indicated



If hypertensive: titratable antihypertensive m edications for severe hypertension (m ean arterial pressure >140 m m Hg, systolic BP >220 m m Hg, diastolic BP >130 m m Hg) or

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hem orrhage/aneurysm /dissection, m yocardial or other end-organ dysfunction 



Gastrointestinal: o

NPO

o

Antiem etics

Consultation: o

Neurology

o

Vascular interventional radiology for neuroangiography

Medication (Drugs) 

Aspirin: 325 m g PO



Clopidogrel: 75 m g PO



Coum adin (dose for atrial fibrillation): 2â€“5 m g PO loading dose



Diphenhydram ine: 25â€“50 m g PO/IV q6hâ€“q8h



Dopam ine (vasopressor dose): 5â€“10 m cg/kg/m in



Heparin (dose for atrial fibrillation): 50â€“60 U/kg IV bolus, then IV infusion at 12â€“18 U/kg/h for target PTT 50â€“70 seconds



Labetalol: 20â€“40 m g IV over 2 m inutes, then 40â€“80 m g IV q10m in (m ax. 300 m g IV)



Meclizine: 25 m g PO q8hâ€“q12h



Nitroprusside: 0.25â€“10 m cg/kg/m in IV infusion (m ax. 10 m cg/kg/m in IV)



Ondansetron: 4 m g IV



Prom ethazine: 12.5â€“25 m g PO/PR/IV q6hâ€“q8h



Ticlopidine: 250 m g PO

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Follow-Up Disposition Admission Criteria 



Intensive care unit adm ission for: o

Altered m ental status with airway issues

o

Concurrent hem odynam ic instability

o

Malignant cardiac arrhythm ias

Adm it to hospital to identify or exclude etiologies of VB ischem ia and to prevent recurrence or progression to VB circulation cerebrovascular accident, especially in the following populations: o

Elderly

o

Inability to am bulate

o

Inability to tolerate oral intake

o

Inability to arrange (expeditious) outpatient follow-up

o

New or changing neurological deficit

o

Persistent dizziness

o

Syncope

o

Vascular risk factors

Discharge Criteria Consider discharge with outpatient follow-up in populations with the following: 

None of above indications to consider adm ission



Alternative explanation for sym ptom atology

References 1. Caplan LR. Vertebrobasilar disease. In: Barnett HJM, Bogousslavsky J, Meldrium H, eds. Advances in Neurology. Philadelphia, PA: Lippincott William s & Wilkins, 2003;92:131â€“140. 2. Lang E, Afilalo M. Vertebrobasilar atherothrom botic disease.

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eMedicine. Updated July 2004. Available at http://www.em edicine.com /em erg/topic834.htm Accessed May 28, 2005 3. Love BB, Biller J. Neurovascular system . In: Goetz CG, ed. Textbook of Clinical Neurology. 2nd ed. Philadelphia, PA: Elsevier, 2003:395â€“423. 4. Savitz SI, Caplan LR. Vertebrobasilar Disease. N Engl J Med. 2005;352:2618â€“2626.

Codes ICD9-CM Transient cerebral ischem ia, 435 Vertebral artery syndrom e, 435.1 Acute, but ill-defined, cerebrovascular disease, 436 Other generalized ischem ic cerebrovascular disease, 437.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vertigo

Vertigo

Jonathan S. Olshaker

Basics Description 

â€œDizzyâ€• describes a variety of experiences, including:



o

Sensations of m otion

o

Weakness, fainting

o

Lightheadedness

o

Unsteadiness

o

Depression

o

True vertigo

Sensation of disorientation in space com bined with a sensation of m otion



Hallucination of m ovem ent either of the self or the external environm ent



Most patients have an organic basis for these sym ptom s.



Maintenance of equilibrium depends on interaction of three system s: visual, proprioceptive, and vestibular. Any disease that interrupts the integrity of above system s m ay give rise to vertigo.



Peripheral vertigo: o

Sudden onset

Pa ge 5 1 3

o

Severe sym ptom s

o

Interm ittent episodes lasting seconds to m inutes, occasionally hours

o

Horizontal or horizontorotary nystagm us (also positional, fatigues, and suppressed by fixation)



o

Norm al neurologic exam

o

Som etim es associated hearing loss or tinnitus

Central vertigo: o

Gradual onset

o

Mild continuous sym ptom s

o

All varieties of nystagm us (horizontal, vertical, rotatory)

o

Absence of hearing loss

o

No positional association

o

Presence of neurologic findings m ost of the tim e

Etiology Peripheral 







Benign paroxysm al positional o

Uncertain etiology

o

Dependent on head position

o

Fatigues

Acute labyrinthitis: o

Associated with hearing deficit

o

Sudden onset

o

May be serous, acute suppurative, toxic, or chronic

Ototoxic drugs: o

Am inoglycosides

o

Antim alarials

o

Erythrom ycin

o

Furosem ide

MÃ¨niÃ©re disease

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o

Episodic vertigo, hearing loss, and tinnitus

o

Vestibular neuronitis

o

Severe vertigo and sym ptom s resolving over days to weeks



o

No hearing deficits

o

Highest incidence in third to fifth decade

Acoustic neurom a: o

Tum or of Schwann cells enveloping the eighth cranial nerve (CN VIII)



o

Develops into central cause

o

Progressive unilateral hearing deficits and tinnitus

o

May also involve CN V, VII, or X

Traum a: o

Rupture of tym panic m em brane, round window, labyrinthine concussion, or developm ent of perilym phatic fistula can all have severe sym ptom s.



Otitis m edia and serous otitis with effusion



Foreign body in ear canal

Central 

Cerebellar hem orrhage: o

Neurosurgical em ergency

o

Sudden onset of headache, vertigo, vom iting, and ataxia



o

Visual paralysis to affected side

o

Ipsilateral CN VI paralysis

Vertebrobasilar artery insufficiency: o

Dysarthria

o

Ataxia

o

Num bness of the face

o

Hem iparesis, headache

o

Diplopia/Visual disturbances

o

Disturbances m ay be transient or exacerbated by

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m ovem ent of the neck. o

Consider in elderly patients with isolated new-onset vertigo without an obvious cause.

o

Can som etim es rapidly progress in the first 24â€“72 hours





Cerebellar infarction: o

Nausea

o

Vom iting

o

Ipsilateral nystagm us

o

Ataxia

Traum a: o

Vertiginous sym ptom s com m on after whiplash injury

o

Postconcussive syndrom e or dam age to labyrinth or CN VIII secondary to basilar skull fracture

o

Vertebral artery injury has been seen after chiropractic m anipulation.



Tem poral lobe epilepsy: o

Associated with hallucinations, aphasia, trancelike states, or convulsions

o 

More com m on in younger patients

Vertebrobasilar m igraines: o

Prodrom e of vertigo, dysarthria, ataxia, visual disturbances, or paresthesias followed by headache

o

Often a fam ily history of m igraines or sim ilar attacks



Tum or



Multiple sclerosis: o

Onset between 20 and 40 years of age

o

All form s of nystagm us

o

May have abrupt onset of severe vertigo and vom iting

o

History of other vague and varying neurologic signs or sym ptom s

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

Subclavian steal syndrom e: o

Exercise of an arm causing shunting of blood from vertebral and basilar arteries into the subclavian artery, resulting in vertigo or syncope

o

Secondary to a stenotic subclavian artery

o

Dim inished unilateral radial pulse or differential systolic blood pressure between arm s



Hypoglycem ia: o

Suspect in diabetic patient or any other patient with unexplained sym ptom s or m ental status change

Diagnosis Signs and Symptoms History 

Does true vertigo exist?



Tim e of onset and the duration of vertigo



Are auditory sym ptom s present?



Are there associated neurologic sym ptom s?



Has there been head or neck traum a?



Past m edical history



Medication history

P.1207

Physical Exam 

Auscultation of the carotid and vertebral arteries for bruits



Pulses and pressures in both arm s



Inspection of the ears: o

Evaluation of hearing (Weber and Rinne tests)

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o

Ocular assessm ent (pupils, fundi, visual acuity, nystagm us)



Cardiac auscultation



Full neurologic exam ination

Essential Workup 

Ask patient to describe the sensation without using the word â€œdizzy.â€•



Determ ine whether the cause is a peripheral or a central process using patient's clinical presentation (see above).

Tests Lab Electrolytes, blood urea nitrogen, creatinine, glucose

Imaging 

ECG for any suspicion of cardiac etiology



Head CT/MRI for evaluation of suspected tum or, central cause, or posttraum atic cause



MRI or angiography for suspected vertebrobasilar insufficiency

Differential Diagnosis 

More likely when â€œdizzinessâ€• actually is lightheadedness or m alaise.



Diabetes m ellitus



Hypothyroidism



Drugs (e.g., alcohol, barbiturates, salicylates)



Hyperventilation



Cardiac (i.e., arrhythm ia, m yocardial infarction, or other etiologies of syncope); peripheral vascular disease (i.e., hypertension, orthostatic hypotension, vasovagal)



Infection/sepsis

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Treatment Initial Stabilization 

ABCs



IV access for dehydration/vom iting



Monitor



Traum a evaluations as indicated



Finger-stick blood glucose

ED Treatment 

Based on accurate diagnosis: o

Central etiologies require m ore aggressive workup than peripheral.

o

Neurosurgical intervention for cerebellar bleed

o

Sym ptom atic treatm ent for peripheral vertigo with appropriate follow-up



Adm inister m edication to control vertiginous sym ptom sâ€”options:



o

Diphenhydram ine

o

Meclizine

o

Prom ethazine

o

Diazepam

Initiate IV antibiotics for acute bacterial labyrinthitis.

Medication (Drugs) 

Diazepam (Valium ): 2.5â€“5 m g IV q8h or 2â€“10 m g PO q8h



Diphenhydram ine (Benadryl): 25â€“50 m g IV, IM, or PO q6h



Meclizine (Antivert): 25 m g PO q6h PRN

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

Prom ethazine (Phenergan): 12.5 m g IV q6h or 25â€“50 m g IM, PO, or PR q6h

Follow-Up Disposition Admission Criteria 

Cerebellar infarct/hem orrhage



Vertebrobasilar insufficiency



Acute suppurative labyrinthitis



Intractable nausea/vom iting



Inability to am bulate

Discharge Criteria 

Patient with peripheral etiology and stable



Issues for referral o

Prim ary care or otolaryngology follow-up for all

o

Otolaryngology follow-up for suspected acoustic neurom a or perilym phatic fistula

References 1. Derebery MD. The diagnosis and treatm ent of dizziness. Med Clin North Am . 1999;83:10. 2. Gizzi M, Riley E, Molinari S. The diagnostic value of im aging the patient with dizziness. Arch Neurol. 1996;53:1299â€“1304. 3. Gom ez CR, et al. Isolated vertigo as a m anifestation of vertebrobasilar ischem ia. Neurology. 1996;47:94â€“97. 4. Herr R, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Em erg Med. 1989;18:6:664â€“672. 5. Olshaker S. Vertigo. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St. Louis, MO: CV Mosby,

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2006: 142â€“149. 6. Rathore S et al. Characterization of Incident Stroke Signs and Sym ptom s: findings from the Atherosclerosis Risk in Com m unities Study. Stroke. Novem ber 2002;33(11):2718â€“2721. 7. Wolf JS, et al. Success of the m odified Epley m aneuver in treating benign paroxysm al/vertigo. Laryngoscope. 1999;109:900.

Miscellaneous SEE ALSO: Dizziness; Labyrinthitis

Codes ICD9-CM 780.4

ICD10 R42

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vio lence, M anagem ent o f

Violence,

Management of Richard Wolfe Robert Vissers

Basics Description 

ED is likely to be scene of violent episodes owing to 24-hour access.



First contact of victim s and perpetrators of violence



High prevalence of intoxicated patients and psychiatric patients





Only reliable predictors: o

Male gender

o

Alcohol or drug abuse

No difference exists in: o

Ethnicity

o

Language

o

Age

o

Education

o

Em ploym ent status

o

Medical diagnosis

Etiology

Pa ge 5 1 4





Functional: o

Psychiatric

o

Schizophrenia

o

Affective

o

Antisocial

o

Borderline

o

Paranoid

o

Adjustm ent disorders

o

Antisocial behavior

Organic: o

CNS related

o

Delirium

o

Dem entia

o

Infection

o

Seizures

o

Cerebrovascular accident

o

Head injury

o

Metabolic

o

Hypoglycem ia

o

Hypoxia

o

Hypotherm ia or hypertherm ia

o

Endocrine disorders

o

Drugs

o

Alcohol and sedatives (withdrawal, intoxication)

o

Cocaine

o

LSD

o

Phencyclidine

o

Anticholinergics

o

Steroids

Pa ge 5 1 4

Diagnosis Alert 

Restrain potentially violent patients.



Seek police aid in control of violent or dangerous patients.

Signs and Symptoms Behaviors suggesting im pending violence: 

Provocative behavior



Anger



Pacing



Loud speech



Tense posture



Pounding, clenching of fists

Essential Workup 





Identify prodrom es of violence: o

Begins with anxiety

o

Then defensiveness

o

Then physical aggression

History: o

Previous threats and violence

o

Psychiatric history

o

Substance abuse

o

Self-m utilation

o

Verbal threats

o

Plans of violence

Physical: o

Focus on identifying and distinguishing associated functional and m edical conditions.

o

Pay careful attention to findings during neurologic and m ental status exam s and note vital signs.

o

Must often be perform ed with the patient under

Pa ge 5 1 4

restraints

Tests Lab 

Com plete blood chem istry if suspected infectious cause for behavior.



Electrolytes, blood urea nitrogen, creatinine, glucose if m etabolic or toxic etiology suspected.



Drug screen if ingestion likely.

Imaging CT head for altered m ental status or head traum a

Treatment Pre Hospital Restrain violent patients and seek police assistance if necessary.

Initial Stabilization 

Prevention of violence: o

o

Deterrence: 

Signs stating weapons not perm itted



Visible security personnel



Metal detectors



Secure single public entrance

Triage to an appropriate assessm ent room : 

Sparse, solid walls



Lockable



Visible



Exits clear of obstruction



Equipm ent free



Panic button

Pa ge 5 1 4

o

Never underestim ate the potential for violence.

o

ED protocols for violent situations

o

Educate staff on preventing, recognizing, and dealing with potentially violent situations.



Approaching the potentially violent patient: o

Im m ediately assess safety.

o

Call security and em ploy physical or chem ical restraint if the patient is violent or threatening, or if there is an im m ediate perceived danger.

o

Rem ove any potential weapons before interview.

o

Maintain open exit for patient and physician.

o

Maintain distance of 6â€“8 feet.

o

Allow patient to ventilate.

o

Develop therapeutic alliance.

o

Be nonjudgm ental; m ake peace offering.

o

Use subm issive posture: 

o

Avoid eye contact.

Leave im m ediately and initiate seclusion or restraint if there is any destabilization of situation or patient behavior.

ED Treatment Verbal de-escalation: 

Situation can be verbally controlled, particularly if situational precipitant can be identified.



Isolation:



Tem porarily isolate patient in an appropriate room before m ore definitive restraint, or to prevent leaving.



Physical restraints: o

Required for patient's safety, the safety of others, and to allow physical exam ination

o

Perform ed by several trained personnel, by protocol, with clear docum entation of indications and rechecks

Pa ge 5 1 4



Chem ical restraint: o

Least restrictive and potentially therapeutic P.1209

o

Before applying physical restraints, patients should be offered voluntary chem ical sedation.

o

Cooperative patients should receive a com bination of an oral benzodiazepine (lorazepam ) and an oral antipsychotic (risperidone).

o

If uncooperative, patients often require physical restraint first.

o

Initial treatm ent should be a m onotherapy using one of the following: 

Benzodiazepines (lorazepam , m idazolam )



Conventional antipsychotic (droperidol, haloperidol)



Consider droperidol instead of haloperidol if rapid sedation desired.

o

May use com bination if single agent ineffective

o

Adm inister every 15â€“30 m inutes until desired effect reached.

o

Side effects of neuroleptics include: 

Dystonic reactions (treat with diphenhydram ine or benztropine)



Neuroleptic m alignant syndrom e (rare)



QT prolongation and torsades de pointes (rare)

Duty to warn: 

Doctor can owe a duty to warn a third party when that third party is in danger because of the m edical or psychologic condition of the patient.

Pa ge 5 1 5

Medication (Drugs) 

Benztropine: 2 m g IM or IV



Diphenhydram ine: 50 m g IV, IM, or PO



Droperidol: 2.5â€“5 m g IV or IM



Haloperidol: 5â€“10 m g IV or IM; 0.5â€“2 m g for elderly people



Lorazepam : 1â€“2 m g IV, IM, or PO



Midazolam : 1â€“2 m g IV, IM, or PO



Risperdal: 1â€“m g PO

Follow-Up Disposition Admission Criteria 

Violence secondary to an associated organic cause that is not tem porary or reversible in the ED



Psychiatric adm ission: o

Violent psychiatric patient requires psychiatric consultation.

o

Patient is considered to be a danger to either self or others.

o

Involuntary com m itm ent if uncooperative

Discharge Criteria Violent behavior was caused by a tem porary, reversible organic cause (drug or alcohol intoxication), and the patient is now deem ed to be in control, com petent, and not a danger to self or others:. 

Psychiatric consultation before discharge recom m ended



If violent act is owing to antisocial behavior, rather than an organic or psychiatric condition, patient m ay be

Pa ge 5 1 5

discharged into police custody, with the warning that the patient m ay be a danger to self or others.

References 1. Blanchard JC, Curtis KM. Violence in the em ergency departm ent. Em erg Med Clin North Am . 1999;17:717â€“731. 2. Hill S, Petit J. The violent patient. Em erg Med Clin North Am . 2000;18:301â€“315. 3. Lukens TW, Wolf SJ, Edlow JA, et al. Clinical policy: critical issues in the diagnosis and m anagem ent of the adult psychiatric patient in the em ergency departm ent. Ann Em erg Med. 2006;47(1):79â€“99. 4. Spivak HR, Prothrow-Stith D. Addressing Violence in the Em ergency Departm ent. Clinical Pediatric Em ergency Medicine. 2003;4(2):135â€“140.

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Visual Lo ss

Visual Loss

Camie J. Sorensen Pascal Juang

Basics Description 

Decrease in visual function (i.e., visual acuity, visual fields, blurry vision)



Visual loss has m any etiologies and can be caused by m ultiple body system s.

Etiology 

Visual system : o

Eyelid or tear film abnorm ality

o

Anterior segm ent (cornea, anterior cham ber, iris, lens)



o

Posterior segm ent (vitreous, retina, optic nerve)

o

Posterior to the eye (optic nerve, chiasm , radiations)

Neurologic: o

Cerebral (cerebrovascular accident [CVA]) or intracranial pathology (m ass lesion)



o

Multiple sclerosis

o

Optic neuritis

o

Migraine

Cardiovascular system :

Pa ge 5 1 5



o

Em bolic

o

Throm botic

o

Ischem ic

o

Hypertensive events

Im m unologic system : o

Infectious including HIV optic neuropathy or cytom egalovirus (CMV) retinitis

o 

Autoim m une causes (uveitis, tem poral arteritis)

Endocrine: o

Diabetic retinopathy

o

Thyroid disease m ay cause diplopia (m uscle hypertrophy) or corneal erosions.



Toxic: o

Methanol (acute severe loss, subacute optic atrophy)

o

Licorice (transient loss, self-lim ited)

o

Digitalis (flashing lights, color changes)

o

Am iodarone (rare cause of optic neuropathy)

Diagnosis 

Categorize visual loss by the properties associated with the decrease in visual function.



Transient (<24 hours): o

Seconds: papilledem a usually (bilateral)

o

Minutes: 

Transient ischem ic attack = am aurosis fugax (unilateral)

 o

Vertebrobasilar artery insufficiency (bilateral)

Minutes to an hour: 

Migraine



Sudden blood pressure changes

Pa ge 5 1 5



Persistent (>24 hours): o

o

o

Sudden and painless: 

Artery or vein occlusion



Vitreous hem orrhage



Retinal detachm ent



Optic neuritis



Tem poral arteritis

Gradual and painless (weeks to years): 

Cataract



Presbyopia



Refraction errors



Open-angle glaucom a



Chronic retinal disease



Macular degeneration



Diabetic retinopathy



CMV retinopathy



CNS tum or

Painful: 

Corneal abrasion or ulcer



Angle closure glaucom a



Optic neuritis



Iritis/uveitis



Keratoconus with hydrops



Monocular: pathology anterior to optic chiasm



Binocular: pathology posterior to optic chiasm



Associated with system ic neurologic sym ptom s of visual field defects: o

CVA (especially posterior or occipital circulation)

o

Mass lesion (pituitary adenom as, aneurysm , m eningiom a, other tum ors)



Malingering

Signs and Symptoms

Pa ge 5 1 5



Flashing lights



New floaters



Decreased vision



Afferent papillary defect



Visual field defects



Eye pain



Lim itation or pain with eye m ovem ents



Conjunctival injection or discharge



Corneal opacity



Cataract



Optic nerve head swelling



Pale retina with a cherry-red spot



Carotid bruits



Neurologic sym ptom s consistent with intracranial or vascular process



Heart m urm ur

History Key elem ents to determ ine: 

Acute or gradual onset?



Length of sym ptom s?



Transient vision loss or perm anent?



Binocular or m onocular?



Degree of vision loss?



Painful or painless? o

Other com orbidities

Physical Exam 

Ophthalm ologic: o

Visual acuity

o

Pupil exam

o

Confrontational visual field exam

o

Extra-ocular m uscle function

Pa ge 5 1 5







o

Slit-lam p exam ination

o

Funduscopy

o

Tonom etry

Cardiovascular: o

Murm urs

o

Carotid bruits

Neurologic exam : o

Optic chiasm and intracerebral lesions

o

Occipital and posterior circulation lesions

General: o

Manifestations of im m une, endocrine, or toxic disorders

Essential Workup Thorough history and physical exam ination as already discussed

Tests Lab May be obtained to determ ine extent of other com orbidity in association with vision loss (i.e., diabetes, cardiovascular disease)

Imaging 

Tests should be directed toward the suspected etiology of visual loss.



Dilated fundus exam m ay be perform ed to assess for posterior segm ent disease.



Erythrocyte sedim entation rate and tem poral artery biopsy m ay be obtained if tem poral arteritis is suspected.



Brain CT, MRI, MR angiography and transcranial Doppler m ay be used to evaluate neurologic sym ptom s and vertebrobasilar artery flow.



Carotid and carotid ultrasound should be obtained urgently if a retinal artery occlusion is diagnosed.

Pa ge 5 1 5

Differential Diagnosis 

Traum a



Neurologic lesion



Infectious



Cardiovascular



Toxic/Metabolic



Autoim m une

P.1211

Treatment 

Direct therapy toward cause of visual loss.



Ophthalm ology consultation for visual loss with an uncertain diagnosis



Two conditions for which treatm ent m ust begin in m inutes: o

Central retinal artery occlusion

o

Chem ical burn

Central Retinal Artery Occlusion 

Clinical criteria: o

Unilateral, painless, acute loss of vision

o

Afferent papillary defect

o

Pale fundus with a cherry-red spot

o

Counting fingers to light perception in 94% of patients



Therapy: o

Im m ediate ophthalm ology consultation

o

Maneuvers and m edications to lower intra-ocular pressure, allowing the em bolus to m ove to the

Pa ge 5 1 5

periphery o

Ocular m assage: direct pressure to eye for 5â€“15 seconds then sudden release, repeat for 15 m inutes

o

Acetazolam ide: 500 m g IV or PO

o

Topical beta-blocker (tim olol or levobunolol 0.5%) b.i.d.

o

Anterior cham ber paracentesis by an ophthalm ologist

o

Referral for cardiac and carotid artery work-up

o

Rule-out tem poral arteritis.

Chemical Burn 

Clinical criteria: o

Alkali worse than acids

o

White eye worse than red eye (white eye indicates that vessels have already sloughed while red eye m eans vessels are intact)

o 

Treat m ace, cem ents, plasters, solvents.

Therapy: o

Copious irrigation of the eyes with LR or NS (nonsterile water is acceptable if others not available); irrigate for m inim um of 30 m inutes

o

Do not try to neutralize acids with alkalis or vice versa.

o

Moist cotton-tipped applicator to sweep furnaces of residual chem ical precipitants

o

Dilate with cycloplegic (atropine, cyclopentolate, tropicam ide).

o

Do not use phenylephrine; it will vasoconstrict already ischem ic conjunctival blood vessels.

o

Erythrom ycin ointm ent every 1â€“2 hours while awake

o

Artificial tears every 1 hour

o

Check intra-ocular pressure.

Pa ge 5 1 5

Medication (Drugs) 



Antibiotic drops: o

Ciprofloxacin 0.3%: 1â€“2 gtt qh1â€“q6h

o

Gentam icin 0.3%: 1â€“2 gtt q4h

o

Ofloxacin 0.3%: 1â€“2 gtt q1hâ€“q6h

o

Levofloxacin 0.5%: 1â€“2 gtt q2h

o

Polym yxin (Polytrim ): 1 gtt q3hâ€“q6h

o

Sulfacetam ide 10%, 0.3%: 1â€“2 gtt q2hâ€“q6h

o

Tobram ycin 0.3%: 1â€“2 gtt q1hâ€“q4h

o

Trifluridine 1%: 1 gtt q2hâ€“q4h

Antibiotic ointm ents: o

Bacitracin: 500 units/g Â½-inch ribbon of ointm ent q3hâ€“q6h

o

Ciprofloxacin 0.3%: Â½-inch ribbon of ointm ent q6hâ€“q8h

o

Erythrom ycin 0.5%: Â½-inch ribbon of ointm ent q3hâ€“q6h

o

Gentam icin 0.3%: Â½-inch ribbon of ointm ent q3hâ€“q4h

o

Neosporin: Â½-inch ribbon of ointm ent q3hâ€“q4h

o

Polym yxin (Polysporin): Â½-inch ribbon of ointm ent q3hâ€“q4h

o

Sulfacetam ide 10%: Â½-inch ribbon of ointm ent q3hâ€“q8h

o

Tobram ycin 0.3%: Â½-inch ribbon of ointm ent q3hâ€“q4h

o 

Vidarabine: Â½-inch ribbon of ointm ent 5 tim es/day

Mydriatics and cycloplegics: o

Atropine 1%, 2%: 1â€“2 gtt per day to q.i.d.

o

Cyclopentolate 0.5%, 1%, 2%: 1â€“2 gtt PRN dilation

Pa ge 5 1 6

o

Hom atropine 2%: 1â€“2 gtt b.i.d.â€“t.i.d.

o

Phenylephrine 0.12%, 2.5%, 10%: 1â€“2 gtt t.i.d.â€“q.i.d.

o 

Tropicam ide 0.5%, 1%: 1â€“2 gtt PRN dilation

Corticosteroidâ€“antibiotic com bination drops (with ophthalm ology consultation): o

Blepham ide (prednisolone): 1â€“2 gtt q1hâ€“q8h

o

Cortisporin (hydrocortisone; neom ycin sulfate; bacitracin zinc; polym ysin B sulfate): 1â€“2 gtt q3hâ€“q4h

o

Maxitrol (dexam ethasone; neom ycin sulfate; polym yxin B sulfate): 1â€“2 gtt q1hâ€“q8h

o

Pred-G (prednisolone acetate; gentam icin sulfate): 1â€“2 gtt q1hâ€“q8h

o

TobraDex (dexam ethasone; tobram ycin; chlorobutanol): 1â€“2 gtt q2hâ€“q26h



Glaucom a agents (always with ophthalm ology consultation): o

Acetazolam ide: 250â€“500 m g PO per day to q.i.d.

o

Betaxolol 0.25%, 0.5%: 1â€“2 gtt b.i.d.

o

Carteolol 1%: 1 gtt b.i.d.

o

Dipivefrin 1%: 1 gtt b.i.d.

o

Levobunolol 0.25%, 0.5%: 1 gtt per day to b.i.d.

o

Mannitol: 1â€“2 g/kg IV over 45 m inutes

o

Pilocarpine 0.25%, 0.5%, 1%, 2%, 3%, 4%, 6%, 8%, 10%: 1â€“2 gtt t.i.d.â€“q.i.d.



Only if m echanical closure is ruled out o

Tim olol 0.25%, 0.5%: 1 gtt b.i.d.

Follow-Up

Pa ge 5 1 6

Disposition Admission Criteria 

Ruptured globe



Hyphem a (depending on severity)



Significant cardiac, carotid, or neurologic disease



Unexplained, progressive vision loss

Discharge Criteria If the diagnosis is certain and visual loss will not progress

References 1. Kunim oto DY, Kanitkar KD, Makar MS. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 4th ed. Lippincott William s and Wilkins, 2004. Website: http://www.eyeatlas.com

Miscellaneous SEE ALSO: Chalazion; Conjunctivitis; Corneal Abrasion; Corneal Burn; Corneal Foreign Body; Dacryocystitis; Globe Rupture; Hordeolum; Hyphem a; Iritis; Red Eye; Optic Artery Occlusion; Optic Neuritis; Orbital Cellulitis; Ultraviolet Keratitis; Vitreous Hem orrhage

Codes ICD9-CM 369.9

ICD10 H54.7

Pa ge 5 1 6

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vitreo us Hem o rrhage

Vitreous

Hemorrhage David Harter

Basics Description Vitreous hem orrhage is a secondary diagnosis; identification of a specific cause is necessary for successful treatm ent: 

Retinal vessel tear secondary to vitreous separation



Sudden tearing of vessels owing to traum a



Spontaneous bleeding owing to neovascularization

Etiology 

Blunt or penetrating traum a



Retinal break/tear/detachm ent



Any proliferative retinopathy



Diabetes m ellitus



Sickle cell disease



Retinal vein occlusion



Eales disease



Senile m acular degeneration



Retinal angiom atosis



Retinal telangiectasia



Peripheral uveitis

Pa ge 5 1 6



Subarachnoid or subdural hem orrhage



Intra-ocular tum or

Diagnosis Signs and Symptoms 

Sudden painless unilateral loss or decrease in vision



Appearance of dark spots (floaters) in visual axis: o

Above findings som etim es accom panied by flashing lights; floaters m ove with head m ovem ents.



Blurred vision, decreased visual acuity



Loss of red reflex



Inability to visualize fundus



Mild afferent papillary defect

Essential Workup 

History with special attention to pre-existing system ic disease and traum a



Com plete ocular exam including: o

Slit lam p

o

Tonom etry

o

Dilated funduscopic exam

Tests Lab 

CBC



Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio if indicated



Electrolytes, blood urea nitrogen, creatinine, glucose

Imaging 

B-scan ultrasound when no direct retinal view is possible

Pa ge 5 1 6

to rule out retinal detachm ent or intraocular tum or 

Fluorescein angiography to define the cause



CT scan/anteroposterior/lateral orbital film s to rule out intra-ocular foreign body

Differential Diagnosis 

Vitreitis (leukocytes in the vitreous)



Retinal detachm ent without hem orrhage

P.1213

Treatment Initial Stabilization 

Bed rest with head of bed elevated



No activity resem bling Valsalva m aneuvers (lifting, stooping, or heavy exertion)

ED Treatment 

Urgent ophthalm ologic consultation is needed with treatm ent based on the cause of the hem orrhage; an exam ination is carried out by the consultant: o

Laser photocoagulation or cryotherapy for proliferative retinal vascular diseases

o 

Repair retinal detachm ents.

Avoid nonsteroidal anti-inflam m atory drugs, aspirin, and other anticlotting agents.



Delayed vitrectom y is needed for blood that does not clear with tim e.

Pa ge 5 1 6

Follow-Up Disposition Admission Criteria Retinal break or detachm ent

Discharge Criteria Retinal break or retinal detachm ent m ust be excluded as cause of hem orrhage.

References 1. Duguid G. Managing ocular flashes and floaters. Practitioner. 1998;242:302â€“304. 2. Ferrone PJ, de Juan E. Vitreous hem orrhage in infants. Arch Ophthalm ogy. 1994;112:1185â€“1189. 3. Hutcheson K, Nguyen A, Preslan M. et. al. Vitreous Hem orrhage in Patients with High-risk Retinopathy of Prem aturity. Am J Optham ol. 2003;136:258â€“263 4. Rhee DJ, Pyfer MF. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 3rd ed. Philadelphia, PA: Lippincott William s & Wilkins; 1999. 5. Shingleton BJ, O'Donoghue MW. Blurred vision.N Engl J Med. 2000;343:556â€“562.

Codes ICD9-CM 379.23 Vitreous hem orrhage

ICD10 H43.1

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo lvulus

Volvulus

Ann Buchanan

Basics Description 

Axial twist of a portion of the gastrointestinal (GI) tract around its m esentery causing partial or com plete obstruction of the bowel



Anatom ic predisposition: redundant/freely m obile segm ent, with close approxim ation of points of fixation of bowel



Precipitated by pathologic distention of the colon



Blood supply com prom ised by venous congestion, leading to gangrene of the bowel and potential infarction due to arterial obstruction

Etiology 

Third m ost com m on cause of colonic obstruction (10â€“15%) following tum or and diverticular disease



Sigm oid (75%): o

Due to redundant sigm oid colon with narrow m esocolon base

o

Most com m on in: 

Elderly



Institutionalized

Pa ge 5 1 6

o



Chronic bowel m otility disorders



Psychiatric diseases

Associated with chronic constipation and concom itant laxative use



Cecal volvulus (22%): o

More com m on in young adults

o

Due to im proper congenital fusion of the m esentery with the posterior parietal peritoneum , causing the cecum to be freely m obile in varying degrees

o

Associated with increased gas production (m alabsorption and pseudoobstruction)

o

Can be seen in pregnancy and after colonoscopy



Transverse colon and splenic flexure (3%)



Gastric volvulus (rare) associated with diaphragm atic defects

Pediatric Considerations 

Midgut volvulus: o

Due to congenital m alrotation in which the m idgut fails to rotate properly in utero as it enters the abdom en

o

Entire m idgut from the descending duodenum to the transverse colon rotates around its m esenteric stalk, including the superior m esenteric artery.

o

Com m on in neonates (75% <1 m onth old; 6â€“20% >1 year old)

o

Sudden onset of bilious em esis (97%) with abdom inal pain

o

May have previous episodes of feeding problem s/bilious em esis

o

In children >1 year old, associated with failure to thrive, alleged intolerance to feedings, chronic interm ittent vom iting, bloody diarrhea

Pa ge 5 1 6

o

Constipation

o

Mild distention since obstruction higher in GI tract

o

May not appear toxic based on degree of ischem ia

Diagnosis Signs and Symptoms History 





Bowel obstruction: o

Colicky, cram ping abdom inal pain (90%)

o

Abdom inal distention (80%)

o

Obstipation (60%)

o

Nausea and vom iting (28%)

Cecal volvulus: o

Sudden onset of pain and distention

o

Asym m etric abdom inal distention

Sigm oid volvulus: o



More insidious onset

Gastric volvulus: o

Triad of Brochard: severe epigastric distension, intractable wretching, inability to pass nasogastric tube (NGT, 30% of patients)

Physical Exam 



Presence of gangrenous bowel: o

Increased pain

o

Peritoneal signs: guarding, rebound, and rigidity

o

Fever

o

Blood on digital rectal exam

o

Tachycardia and hypovolem ia

Cecal volvulus:

Pa ge 5 1 6

o

Often a palpable m ass in the left upper quadrant/m id-abdom en

Essential Workup Plain abdom inal radiograph: 

Suggestive but often inconclusive



Diagnostic finding present in <70% of cases



Sigm oid volvulus: inverted U-shaped loop of dilated colon arising from the pelvis



Cecal volvulusâ€”dilated and displaced: o

Cecum in the left abdom en (kidney shaped), often with dilated loops of sm all bowel

Tests Lab 

May give clues as to the presence of gangrenous bowel but norm al laboratory values do not exclude the diagnosis



CBC: o

Leukocytosis (WBC >20,000) suggests strangulation with infection/peritonitis.





Electrolytes, blood urea nitrogen, creatinine, glucose: o

Anion gap acidosis due to lactic acidosis

o

Prerenal azotem ia due to dehydration

Urinalysis: o

Elevated specific gravity and ketones

Imaging 



Barium enem a o

â€œBird's beakâ€• deform ity at the site of torsion

o

Perform cautiously owing to perforation risk.

o

May be therapeutic

Upper GI series: o

Abrupt ending or corkscrew tapering of contrast seen

Pa ge 5 1 7



CT scan: o

â€œWhirlâ€• sign in cecal volvulus

o

May be useful in sigm oid volvulus to determ ine extent of obstruction



Ultrasound: o

Abnorm al position of the superior m esenteric vein

o

â€œWhirlpoolâ€• sign of volvulus: vessels twirled around the base of the m esentery

Pediatric Considerations 

Diagnosis of m idgut volvulus: o

Duodenum lies entirely to the right of the spine on plain film s.

o

â€œDouble-bubbleâ€• sign on an upright film due to distended stom ach and proxim al duodenal loop

o

Established by upper GI swallow: coiled spring/corkscrew appearance of jejunum in the right upper quadrant

Pediatric Considerations 

Colic



Henoch SchÃ¶nlein purpura



Necrotizing enterocolitis

P.1215

Alert 

Evaluate any child with signs/sym ptom s of obstruction (including bilious vom iting and abdom inal pain) for m alrotation, even if they appear nontoxic.



Delay in diagnosis >1â€“2 hours results in gangrenous bowel necessitating large resection and leading to perm anent parenteral nutrition with its associated

Pa ge 5 1 7

com plications.

Differential Diagnosis 

Obstruction due to colonic tum or or diverticulitis



Sm all bowel obstruction



Ileus



Intussusception



Appendicitis, pelvic inflam m atory disease and salpingitis, especially for cecal volvuli



Ovarian torsion

Treatment Initial Stabilization 

ABCs



Aggressive fluid resuscitation with 0.9% NS bolus of 20 m L/kg (peds) or 2 L bolus (adult)



NGT



Foley catheter

ED Treatment 

Obtain surgical consultation.



Prepare patient for the operating room .



Correct hypovolem ia and electrolyte abnorm alities.



Preoperative broad-spectrum antibiotics, if suspected sepsis or perforation

Definitive Therapy Sigmoid Volvulus 

Nontoxic patient: o

Reduce volvulus nonoperatively with sigm oidoscopy: 

60% successful

Pa ge 5 1 7

 o

40â€“50% recurrence

Follow with elective sigm oid resection and prim ary anastom osis (<3% recurrence)



Toxic patient: o

Em ergent resection of sigm oid and any gangrenous bowel, with placem ent of end-colostom y

Cecal Volvulus 

Em ergent operative reduction followed by cecectom y and prim ary anastom osis (preferred), or cecopexy if the cecum is still viable (higher recurrence).

Pediatric Considerations 

Laparotom y within 1â€“2 hours to reduce risk for ischem ia



Surgical detorsion of bowel with resection of gangrenous bowel and a Ladd procedure is perform ed to prevent recurrent volvulus.

Medication (Drugs) 

Am picillin sulbactam (Unasyn): 3 g (peds: 100â€“200 m g am picillin/kg/24h) IV q6h



Cefoxitin (Mefoxin): 2 g (peds: 80â€“160 m g/kg/24h) IV q6h

Follow-Up Disposition Admission Criteria Adm it all suspected of having a volvulus with a surgical consult.

Issues for Referral

Pa ge 5 1 7

Surgical consultation necessary

References 1. Frizelle EA, Wolff BG. Colonic volvulus. Adv Surg. 1996;29:131â€“139. 2. Madiba TE, Thom son SR. The m anagem ent of sigm oid volvulus. Diseases of the Colon and Rectum . 2000;45(2):74â€“80. 3. Madiba TE, Thom son SR. The m anagem ent of cecal volvulus. Diseases of the Colon and Rectum . 2002;45(2):264â€“267. 4. Mayo A, et al. Volvulus of the stom ach in childhood: The Spectrum of Disease. Pediatric Em ergency Care. 2001;17(5):344â€“348. 5. Rolandelli RH, Roslyn JJ. Colon and rectum . In: Townsend CM Jr. Sabiston textbook of surgery. 16th ed. Philadelphia, PA: WB Saunders, 2001;947â€“950.

Miscellaneous SEE ALSO: Bowel Obstruction

Codes ICD9-CM 560.2

ICD10 K56.2

Pa ge 5 1 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo m iting, Adult

Vomiting, Adult

Scott G. Weiner

Basics Description Three phases: 

Nausea: unpleasant sensation prior to vom iting



Retching: rhythm ic contractions of diaphragm , abdom inal m uscles, intercostals that bring gastric contents up the esophagus



Vom iting: forceful retrograde expulsion of gastric contents through the m outh

Etiology Pathophysiology: 

Vom iting center in m edulla coordinates vom iting through vagus, phrenic, spinal nerves



Irritated by im pulses from the gastrointestinal (GI) tract, pharynx, vestibular system , heart, genitalia, or via stim ulation of chem oreceptor trigger zone (CTZ) in the area postrem a of the brain by m edications or toxins in circulation



CTZ response m ediated by dopam ine D2, serotonin (5-HT3), cholinergic, and histam ine receptors: o

Medications providing sym ptom atic treatm ent of

Pa ge 5 1 7

vom iting antagonize these receptors

Diagnosis Signs and Symptoms History 

Sym ptom duration, frequency, severity



Characteristics of vom iting: tim ing, description, content of vom itus



Associated sym ptom s: pain, fever, diarrhea, neurologic



Past surgical or GI history



Medication and drugs use



Last m enstrual period



Com plete past m edical history

Physical Exam 

Vital signs: o

Fever: appendicitis, gastroenteritis, cholecystitis, hepatitis, bowel perforation

o 

Tachycardia: dehydration

Head, ears, eyes, nose, throat: o

Abnorm al anterior cham ber: glaucom a

o

Dry m ucous m em branes: dehydration

o

Nystagm us: labyrinthitis, stroke, intracranial hem orrhage

o 

Papilledem a: elevated intracranial pressure (ICP)

Abdom en: o

Blood in stool: peptic ulcer

o

Decreased bowel sounds: ileus

o

Distention, high-pitched bowel sounds, scars or hernias: intestinal obstruction

Pa ge 5 1 7

o

Pain: appendicitis, cholecystitis, pancreatitis, perforated viscus, ovarian torsion

o 

Testicular pain: torsion

Neurologic: o

Abnorm al m ental status, cerebellar test abnorm alities, cranial nerve abnorm alities: CNS pathology

Essential Workup The work-up is also aim ed at determ ining the underlying cause of vom iting and excluding dangerous sequelae.

Tests Lab 

CBC: o

Elevated WBC: infectious process (e.g., appendicitis, gastroenteritis)



o

Elevated hem atocrit: dehydration

o

Decreased hem atocrit: GI bleed from ulcer

Electrolytes: o

Prolonged vom iting m ay cause hypochlorem ia, hypokalem ia.

o

Blood urea nitrogen/creatinine >20 m ay indicate dehydration.





Liver function tests: o

Am ylase/Lipase elevation: pancreatitis

o

AST/ALT elevation: hepatitis

o

Alkaline phosphatase elevation: cholecystic etiology

Urine analysis: o

WBC, nitrites, leukocyte esterase, bacteria: urinary tract infection (UTI)

o

Ketones: dehydration, diabetic ketoacidosis (DKA)

o

Pregnancy test in wom en of childbearing age

Pa ge 5 1 7



Toxicology screen/drug levels: o

Indicated in suspected drug toxicity or overdose

Imaging 

Kidney, ureter, bladder/upright: o



CT abdom en/pelvis: o



Suspected appendicitis, obstruction, nephrolithiasis

CT/MRI head: o



Suspected bowel obstruction or perforated viscus

Suspected intracranial etiology

Ultrasound: o

Suspected biliary disease, gonadal torsion, nephrolithiasis

Diagnostic Procedures/Surgery 

ECG: o



Endoscopy: o



Suspected m yocardial infarction

Peptic ulcer disease leading to significant GI bleed

Surgery: o

For certain etiologies of vom iting (e.g., appendicitis, bowel obstruction, gonadal torsion)

Differential Diagnosis 

GI: o

Appendicitis

o

Boerhaave syndrom e

o

Bowel obstruction

o

Cholecystitis, biliary colic

o

Gastric outlet obstruction, gastroparesis

o

Gastritis, gastroenteritis

o

Hepatitis

o

Pancreatitis

o

Peptic ulcer disease, dyspepsia

Pa ge 5 1 7















o

Peritonitis

o

Ruptured viscus

Neurologic: o

Elevated ICP

o

Intracranial blood

o

Labyrinthitis, vertigo

o

Meningitis

o

Migraine

o

Stroke

o

Tum or

Endocrine: o

Adrenal insufficiency

o

DKA

o

Hypoparathyroid, hyperparathyroid

o

Hypothyroid, hyperthyroid

Pregnancy: o

Hyperem esis gravidarum

o

Nausea/vom iting of pregnancy

Drug toxicity: o

Acetam inophen

o

Aspirin

o

Digoxin

o

Theophylline

Therapeutic m edication use: o

Antibiotics

o

Aspirin

o

Chem otherapy

o

Ibuprofen

Drugs of abuse: o

Narcotics/narcotic withdrawal

o

Alcohols

Genitourinary:

Pa ge 5 1 7



o

Gonadal torsion

o

Nephrolithiasis

o

UTI

Miscellaneous: o

Carbon m onoxide poisoning

o

Electrolyte disorders

o

Glaucom a

o

Motion sickness

o

Myocardial infarction

o

Postprocedural (after anesthesia)

o

Self-induced (eating disorders)

o

Sepsis

P.1217

Treatment Pre Hospital Prehospital treatm ent aim ed at stabilizing patient until arrival in the ED where antiem etics can be adm inistered and the work-up of underlying cause of vom iting can proceed: 

Placem ent of IV, oxygen, cardiac m onitor



Begin adm inistration of isotonic fluids in suspected dehydration.



Fingerstick glucose in m ental status change

Initial Stabilization 

Address ABCs.



Urgent fluid resuscitation if vom iting has led to hypovolem ic shock

Pa ge 5 1 8



Urgent antiem etic therapy for patient com fort



Urgent analgesic therapy if indicated

ED Treatment 

Three principles of ED treatm ent: o

Correction of fluid, electrolyte, and nutritional deficiencies as a result of vom iting



o

Identification and treatm ent of underlying cause

o

Suppression or elim ination of sym ptom s

Antibiotics if indicated: UTI, appendicitis, bacterial gastroenteritis



Medications: o

Dopam ine D2 antagonists useful in m ost types of nausea: 

Prochlorperazine, prom ethazine, m etoclopram ide, droperidol

o

Serotonin antagonists useful in chem otherapy-induced nausea: 

o

Dolasetron, odansetron, granisetron

Anticholinergic and antihistam ine agents useful in labyrinthitis, positional vertigo, and m otion sickness: 



Meclizine, diphenhydram ine, scopolam ine

Consultation with surgery, neurology, gastroenterology, urology, and obstetrics depending on underlying etiology

Medication (Drugs) 

Diphenhydram ine: 25â€“50 m g IM/IV/PO



Dolasetron: 12.5 m g IV



Droperidol: 0.625â€“1.25 m g IM/IV



Granisetron: 1 m g IV or 2 m g PO



Hydroxyzine: 25â€“100 m g IM

Pa ge 5 1 8



Meclizine: 25â€“50 m g PO



Metoclopram ide 10 m g IM/IV/PO



Odansetron: 4â€“8 m g IM/IV



Prochlorperazine: 5â€“10 m g IM/IV/PO or 25 m g PR



Prom ethazine: 12.5â€“25 m g POIM/PR



Scopolam ine: one patch 4 hours prior to travel

Geriatric Considerations 

Dopam ine-antagonizing antiem etics have potential cardiac side-effects: o

The doses of these m edications should be reduced in the elderly.



Serotonin antagonists are safer in this population.

Pregnancy Considerations 

Vom iting occurs in 25â€“55% of pregnancies.



Phenothiazine (prom ethazine, chlorprom azine, m etocloprom ide) or serotonin-antagonizing antiem etics (granisetron, ondasetron) m ost com m only used

Follow-Up Disposition Admission Criteria 

Significant underlying disease or sym ptom s necessitating close observation or surgical procedure



Uncontrolled em esis resulting in inability to tolerate food or liquids by m outh



Severe dehydration requiring continued IV fluids



Significant electrolyte disturbances



Unknown etiology of vom iting with inadequate outpatient

Pa ge 5 1 8

follow-up

Discharge Criteria 

Significant underlying pathology is excluded.



Patient is sufficiently hydrated.



Em esis is controlled.



Close follow-up is arranged (preferably within 24â€“36 hours)

References 1. Heilenbach T. Nausea and vom iting. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby, 2002:178â€“185. 2. Lee M. Nausea and vom iting. In: Feldm an M, et al., eds. Sleisenger and Fordtran's Gastrointestinal and Liver Diseases. 7th ed. Philadelphia, PA: Saunders, 2002:119â€“129. 3. Longstreth GF. Approach to the patient with nausea and vom iting. Up to Date on-line text. http://www.uptodate.com . Septem ber 2004. 4. Quigley EM, Hasler WL, Parkm an HP. AGA technical review on nausea and vom iting. Gastroenterology. January 2001;120(1):263â€“286.

Codes ICD9-CM 787.0

ICD10 R11

Pa ge 5 1 8

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo m iting, Pediatric

Vomiting,

Pediatric Mark A. Hostetler

Basics Description 

Forceful retrograde expulsion of gastric contents through the m outh; characterized by nausea, retching, and em esis; no gastric contents are expelled during retching.



Em esis results from sustained contraction of abdom inal m uscles and diaphragm ; at the sam e tim e, the pylorus and antrum contract.

Etiology Mechanism 

Gastrointestinal (GI)/Mechanical: gastroesophageal reflux (GER), m econium ileus, necrotizing enterocolitis, hypertrophic pyloric stenosis, intussusception, m alrotation with m idgut volvulus, Hirschsprung disease, congenital obstructions (atresias, stenoses, and webs), hernia, foreign body/bezoar, paralytic ileus



Metabolic/Endocrine: inborn errors of m etabolism (am ino acidurias, fatty acid oxidation disorders, urea cycle

Pa ge 5 1 8

defects), urem ia, congenital adrenal hyperplasia, kernicterus 

Neurologic: CNS bleeding (often due to traum a), tum or, hydrocephalus



Infectious: otitis m edia, urinary tract infection (UTI), pneum onia, sepsis, m eningitis/encephalitis



Feeding problem s: chalasia, im proper technique (overfeeding, im proper position), m ilk allergy



Other: toxicologic, nonaccidental traum a

Diagnosis Signs and Symptoms 

General: o

Appearance variable depending on the underlying cause

o

Signs of dehydration, including tachycardia, tachypnea, pallor, decreased perfusion, and shock

o

Altered m ental status m ay occur secondary to shock, hypoglycem ia, or extra-abdom inal conditions (sepsis, inborn error of m etabolism , increased intracranial pressure, toxicologic poisoning)



Vom iting characteristics: o

Assess color, com position, onset, progression, and relationship to intake and position.

o

Nonbilious em esis is caused by a lesion proxim al to the pylorus.

o

Bilious (green) em esis indicates obstruction below the am pulla of Vater; in infants, bilious em esis is associated with a m ore serious underlying condition (m alrotation, volvulus, intussusception, bowel

Pa ge 5 1 8

obstruction); m ay also be due to adynam ic ileus or sepsis. o

Bloody em esis involves a lesion proxim al to the ligam ent of Treitz; bright red bloody em esis has little or no contact with gastric juices due to an active bleeding site at or above cardia.

o

â€œCoffee-groundâ€• em esis results from reduction of hem e by gastric juices.

o

Feculent odor suggests lower obstruction or peritonitis.

o

Undigested food in em esis suggests an esophageal lesion or one at or above the cardia.

o

GER: begins shortly after birth, rem ains relatively constant, usually with norm al weight gain

o

Hypertrophic pyloric stenosis: begins insidiously at 3â€“4 weeks and progresses, becom ing increasingly forceful (projectile) after feedings

o

Obstruction and/or ischem ic bowel (m alrotation with m idgut volvulus, intussusception, necrotizing enterocolitis): sudden onset associated with rapid progression to appearing ill out of proportion to the duration of illness; abdom en distended and tender.





Abdom inal: o

Distention suggests obstruction.

o

Peritoneal signs suggest perforation.

Com plications: o

Aspiration

o

Mallory-Weiss tear

o

Boerhaave syndrom e

Essential Workup Exclude life-threatening causes of vom iting.

Pa ge 5 1 8

Tests Lab As indicated by differential considerations: 

Metabolic assessm ent (glucose, electrolytes)



Infection assessm ent (CBC, cultureâ€”urine)



Pregnancy tests for fem ales of childbearing age

Imaging 

Evaluation/Treatm ent of hypovolem ia and hypoglycem ia



As indicated by differential considerations



Abdom inal radiographs (flat plate, upright and decubitus) helpful for evaluation of obstruction or perforation



Pelvic and abdom inal ultrasound for evaluation of hypertrophic pyloric stenosis, intussusception, appendicitis as well as pelvic pathology



Abdom inal CT scan helpful for evaluation of appendicitis, m ass/tum or often requiring contrast

Differential Diagnosis 

Neonate/infant: o

GI/Mechanical: GER, m econium ileus, necrotizing enterocolitis, hypertrophic pyloric stenosis, intussusception, m alrotation with m idgut volvulus, Hirschsprung disease, congenital obstructions (atresias, stenoses, and webs), hernia, foreign body/bezoar, paralytic ileus

o

Metabolic/Endocrine: inborn errors of m etabolism (am ino acidurias, fatty acid oxidation disorders, urea cycle defects), urem ia, congenital adrenal hyperplasia, kernicterus

o

Neurologic: CNS bleeding (often due to traum a), tum or, hydrocephalus

Pa ge 5 1 8

o

Infectious: otitis m edia, UTI, pneum onia, sepsis, m eningitis/encephalitis

o

Feeding problem s: chalasia, im proper technique (overfeeding, im proper position), m ilk allergy

o 

Other: toxicologic, nonaccidental traum a

Child/adolescent: o

GI: gastroenteritis, obstruction (hernia, adhesions, intussusception, foreign body, bezoar), pancreatitis, appendicitis, peritonitis, paralytic ileus, traum a (duodenal hem atom a)

o

Metabolic/Endocrine: diabetic ketoacidosis, urem ia, adrenal insufficiency

o

Infectious: gastroenteritis, UTI, sinusitis, upper respiratory infection, sepsis, m eningitis, encephalitis, pneum onia, hepatitis

o

Neurologic: CNS m ass/tum or, CNS bleeding (often due to traum a), cerebral edem a, concussion, m igraine, kernicterus

o

Other: toxicologic, (nonaccidental) traum a, pregnancy, bulim ia

P.1219

Treatment Pre Hospital Not applicable

Initial Stabilization 

Fluid resuscitation with 0.9% NS IV; caution if concern

Pa ge 5 1 8

about increased intracranial pressure 

Determ ine bedside finger-stick glucose.

ED Treatment 

Continue fluid resuscitation and correction of electrolyte im balance if present.



Decom press stom ach with nasogastric or orogastric tube if abdom en distended or vom iting persistent.



Continue evaluation for underlying cause.



Consider antiem etic m edications.



Surgical consultation if acute abdom en; antibiotics if peritonitis or other system ic infection present

Medication (Drugs) 

Antiem etics helpful once the underlying cause of vom iting has been determ ined; less frequently used in young children.



Antiem etic options in children: o

Metoclopram ide: 10 m g (0.1 m g/kg/dose) PO q6h

o

Ondansetron: 4â€“8 m g (0.1 m g/kg/dose) IV q6h

o

Prochlorperazine: 2.5â€“5 m g (0.1 m g/kg/dose) IV, IM, or PR q6h

o

Prom ethazine: 12.5â€“25 m g (0.25 m g/kg/dose) PO, PR, or IM q6h

Follow-Up Disposition Admission Criteria

Pa ge 5 1 8



Unstable vital signs, including persistent tachycardia or other evidence of hypovolem ia



Serious etiologic condition



Inability to exclude serious etiologic conditions



Intractable vom iting or inability to take oral fluids



Inadequate social situation or follow-up

Discharge Criteria 

Stable; able to tolerate oral fluids



Benign etiology considered m ost likely



Serious or potentially im portant etiologies excluded



Parental understanding of instructions to advance clear liquids slowly and return for continued vom iting, abdom inal distention, decreased urination, fever, lethargy, or unusual behavior

References 1. Hostetler MA, Bracikowski A. Gastrointestinal disorders. In: Marx JA, Hockerberger RS, Walls RM, et al., eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2000:2296â€“2315. 2. Hostetler MA, Schulm an M. Necrotizing enterocolitis presenting in the em ergency departm ent: case report and review of differential considerations for vom iting in the neonate. J Em erg Med. 2001;21(2):165â€“170. 3. Irish MS, Pearl RH, Caty MG, et al. The approach to com m on abdom inal diagnoses in infants and children. Pediatr Clin North Am . 1998;45(4):729â€“772. 4. Kim ura K, Loening-Baucke V. Bilious vom iting in the newborn: rapid diagnosis of intestinal obstruction. Am Fam Physician. 2000;61(9):2791â€“2798. 5. Pearl RH, Irish MS, Caty MG, et al. The approach to com m on abdom inal diagnoses in infants and children. Part II. Pediatr Clin

Pa ge 5 1 9

North Am . 1998;45(6):1287â€“1326.

Codes ICD9-CM 787.03

ICD10 P92.0

Pa ge 5 1 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo n Willebrand Disease

Von Willebrand

Disease Matthew Kippenhan

Basics Description 

Coagulopathy caused by deficiency or dysfunction of von Willebrand Factor (vWF)



vWF functions: o

Mediates platelet-endothelial cell adhesion

o

Carrier protein for factor VIII

Genetics 

Majority of cases are inheritedâ€”m ultiple genetic defects identified.



Type 1â€”quantitative defect of vWF: o

70% of cases

o

Autosom al dom inant

o

vWF deficiency results from decreased synthesis and increased clearance of protein.

o

Manifestation ranges from asym ptom atic to m oderate bleeding.



Type 2â€”qualitative defect of vWF: o

10â€“15% of cases

Pa ge 5 1 9

o

Divided into types 2A, 2B, 2M, 2Nâ€”all are autosom al dom inant except 2N.

o

Decrease in interm ediate and high m olecular weight m ultim er

o

2Nâ€”decreased binding to factor VIII: 

Leads to decreased levels of VIII and thus m ore serious coagulopathy





Type 3â€”absent or severe deficiency in am ount of vWF: o

Rare diseaseâ€”one per m illion cases

o

Autosom al dom inant

o

Severe coagulopathy

vWD genetically associated with sickle cell disease, hem ophilia A, factor XII deficiency, hereditary hem orrhagic telangiectasia, and throm bocytopenia

Etiology 

In addition to genetic causes, acquired form s exist.



Multiple m echanism s:



o

vWF antibody production

o

Decreased synthesis

o

Proteolysis

o

Increased clearance from binding to tum or cells

Seen in association with the following: o

Malignancy: 

Wilm s tum or



Multiple m yelom a



Chronic lym phocytic leukem ia



Non-Hodgkin lym phom a



Chronic m yelogenous leukem ia



Waldenstrom m acroglobulinem ia



Monoclonal gam m opathy of uncertain significance

o

Im m unologic:

Pa ge 5 1 9

o

o



System atic lupus erythem atosus



Rheum atoid arthritis

Medication induced: 

Valproic acid



Ciprofloxacin



Hetastarch



Griseofulvin

Miscellaneous: 

Hypothyroidism



Urem ia



Hem oglobinopathies



Cirrhosis



congenital heart disease



Dissem inated intravascular coagulation

Diagnosis Signs and Symptoms 

Sym ptom s vary dependent on type of disease.



Many type 1 and som e type 2 are asym ptom atic, severe type 2 and type 3 are sym ptom atic: o

Easy bruising

o

Menorrhagia

o

Recurrent epistaxis

o

Gum bleeding

o

Gastrointestinal bleeding

o

Soft-tissue bleeds and hem arthroses

o

Prolonged or excessive procedural bleeding

Pregnancy Considerations 

Pregnancy causes increased vWF levels in patients with

Pa ge 5 1 9

types 1 and 2 disease. 

Pregnancy, labor, and delivery are usually uncom plicated.



vWF levels fall quickly after delivery: o

Patients m ay suffer postpartum bleeding 10â€“28 days after delivery.

History 

Most often diagnosed in pediatric and adolescent populations



Fam ily history



Minor/Moderate recurrent m ucosal bleeding m ost com m on historical clue

Physical Exam 

Most will have norm al exam .



Multiple, large bruises



Deep-tissue hem atom as, hem arthroses

Essential Workup 

Screen and refer for testing if historical concerns or consistent physical findings.



For type 1 diagnosis, patient m ust have significant m ucocutaneous bleeding, laboratory confirm ation, and fam ily history of type 1 disease.

Tests Lab 

CBC: norm al platelet count



Prothrom bin tim e: norm al



Partial throm boplastin tim e: o

Mildly prolonged in 50%

o

Due to low factor VIII levels or co-existent factor deficiency



Measurem ent of vWF level and activity:

Pa ge 5 1 9

o

Ristocetin activityâ€”uses platelet agglutination to determ ine vWF function

o

vWF antigenâ€”tests for vWF level in serum using rabbit antibodies



Bleeding tim e: o

May be norm al in type 1 (50%); prolonged in types 2 and 3

o

Not specific and hard to reproduce; has fallen out of favor for diagnosis

Differential Diagnosis 

Hem ophilia A, B



Platelet defects



Use of antiplatelet drugsâ€”aspirin, NSAIDS



Platelet-type pseudo vWD



Bernard-Soulier syndrom e

P.1221

Treatment Pre Hospital Direct pressure for control of hem orrhage

Initial Stabilization Resuscitation with crystalloid and packed RBCs as needed

ED Treatment 

Desm opressin acetate (DDAVP): o

Prom otes release of vWF from endothelial cells, increases factor VIII levels

Pa ge 5 1 9

o

Maxim al levels obtained at 30â€“60 m inutes, with duration of 6â€“8 hours

o

Effective for type 1; variable effectiveness for type 2; not indicated for type 3

o

Patients m ay use intranasal spray at hom e before m enses or m inor procedures.



vWF replacem ent therapy: o

Hum ateâ€”P Factor VIII concentrate with vWF: 

Treated to reduce virus transm ission risks



Indicated for type 3 vWD and severe bleeding in all types



Doses, length of treatm ent depend on severity of bleeding.

o

Fresh frozen plasm a, cryoprecipitate: 



Less desirable because they carry infection risk

Antifibrinolytic therapy: o

Am inocaproic acid (Am icar) and trasexam ic acid (Cyklokapron)

o 



Block plasm in form ation to prevent clot degradation

Topical agentsâ€”applied directly to bleeding site: o

Gelfoam or Surgicel soaked in throm bin

o

Micronized collagen

o

Fibrin sealant

Avoid antiplatelet agents.

Medication (Drugs) 

Am inocaproic acidâ€”50â€“60 m g/kg PO/IV q4hâ€“q6h



Cryoprecipitateâ€”10â€“12 units initial dose or 2â€“4 bags/10 kg



DDAVPâ€”desm opressin: o

0.3 m cg/kg IV, m ax. 20 m cg

Pa ge 5 1 9

o

0.3 m cg/kg SQ, m ax. 20 m cg

o

300 m cg intranasal

o

Peds: <50kgâ€”150 m cg intranasal



Fresh frozen plasm aâ€”10â€“20 m L/kg IV



Hum ate-P (antihem ophilic factor/vWF com plex, hum an): 40â€“80 IU/kg IV



Transexam ic acid: 20â€“25 m g/kg PO, IV q8h

Follow-Up Disposition Admission Criteria 

Patients with significant bleeding requiring further IV m edical m anagem ent



Observation after m ajor traum a for types 2 and 3 vWD

Discharge Criteria 

Control of hem orrhage



Adequate follow-up and access to m edical therapy

Issues for Referral Hem atology: 

Severe or refractory bleeding



Prior to elective/sem i-elective procedures



Definitive work-up of suspected cases

References 1. Federici A, Mannucci P. Advances in the Genetics and Treatm ent of von Willebrand Disease. Current Opinion in Pediatrics. February 2002;14(1):23â€“33. 2. Federici A. Diagnosis of von Willebrand disease. Haem ophilia. 1998;4:654â€“660.

Pa ge 5 1 9

3. Greer J, Foerster J. Wintrobe's Clinical Hem atology. 11th ed. Philadelphia, PA: Lippincott William s and Wilkins, 2004. 4. Hoffm an. Hem atology: Basic Principles and Practice. 4th ed. Philadelphia, PA: Churchill Livingstone, 2005. 5. Mannucci P. Treatm ent of von Willebrand disease. Haem ophlia. 1998;4:661â€“664. 6. Rick, ME. Treatm ent of von Willebrand Disease. UptoDate. 2004.

Miscellaneous SEE ALSO: Hem ophilia

Codes ICD9-CM 286.4

Pa ge 5 1 9

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Warfarin/C o um adin Overdo se

Warfarin/Coumadin Overdose John Bailitz

Basics Description 

Most com m only prescribed oral anticoagulant: o

Inhibits regeneration of vitam in K cofactor required for hepatic carboxylation of factors II, VII, IX, and X

o

Blocks the coagulation cascade's extrinsic system and com m on pathway

o

Com m only used for venous throm boem bolism and prevention of em bolism with prosthetic heart valves or atrial fibrillation

o

Adjustm ents based on the international norm alization ratio (INR) 

Typical therapeutic range 2.0â€“3.0



2.5â€“3.5 for m echanical valves and antiphospholipid syndrom es:

o

Contraindications include any condition in which the risk of hem orrhage or adverse reaction outweighs clinical benefit. 

Prior hypersensitivity



Skin reactions

Pa ge 5 2 0



Recent surgeries



Active or potential gastrointestinal (GI), intracerebral, or genitourinary (GU) bleeding



Fall risk

Etiology 

Many factors including age, other drugs, diet, and com orbidities affect INR/bleeding versus throm boem bolism : o

o



Increase INR: 

Multiple antibiotics



NSAIDs



Propranolol



Prednisone



Cim etidine



Influenza vaccine



Gingko biloba



Garlic



Cancer



Collagen vascular disease



Congestive heart failure



Age



Liver disease

Decrease INR: 

Carbam azepine



Haloperidol



St. John Wart



Hereditary Coum adin resistance



Hyperlipidem ia

15% of patients have bleeding com plications/year; 4.9% m ajor, up to 0.8% fatal, m ost com m only intracranial hem orrhage (ICH): o

Risk of bleeding directly related to INR

Pa ge 5 2 0



Increases dram atically above 4.0



Inversely related to tim e spent in therapeutic range:

o

Risk factors for bleeding: 

Age >75 years



Past GI bleeding



Hypertension, cerebrovascular disease, severe heart disease



Renal insufficiency



Alcoholism



Occult GI and GU m alignancies

Pregnancy Considerations 

Warfarin: o

Pregnancy class X

o

Crosses the placenta causing spontaneous abortion and birth defects

Diagnosis Signs and Symptoms 

Presentation m ay be occult or dram atic: o

High index of suspicion required to detect potentially life-threatening com plications 

Com plications occur in sub- and supratherapeutic INR range



Subtherapeutic/Low INR: breakthrough throm bosis



Therapeutic and Supratherapeutic: GI, CNS, retroperitoneal bleeding



Skin necrosis: o

Classic lesions of coum adin skin necrosis begin on the

Pa ge 5 2 0

third to eighth day of therapy resulting from capillary throm bosis in subcutaneous fat. o

Associated with protein C deficiency, but m ay occur with protein S deficiency and in patients with norm al levels

o

Eschar in center differentiates lesions from ecchym osis due to excess coum adin therapy

Essential Workup 

Thorough history: o

Many chief com plaints are com plicated by anticoagulation. 

Reason for anticoagulation, recent dose changes, com pliance, recent INR testing, other prescriptions, over the counter, and alternative m edicines



Subtle changes in m ental status, recent â€œm inor falls,â€• or bleeding



Exam ine for vital sign abnorm alities: o

Early hem orrhagic shock

o

Hypertension and bradycardia m ay be secondary to Cushing response in ICH.

o

Cardiac m eds often m ask im portant changes in vital signs.



Exam ine carefully for: o

Pallor, contusions, abrasions, ecchym osis, and skin lesions

o

Check stool for blood.

Tests Lab 

Prothrom bin tim e/partial throm boplastin tim e/INR: o

Significant bleeding m ay occur even in INR

Pa ge 5 2 0

therapeutic range. o 

PTT also elevated with toxicity

CBC: o

HCT inaccurate m easure of acute rapid bleeding

o

Platelets 

Aspirin and ADP inhibitors/Plavix result in norm al platelet levels but qualitative deficits.



Electrolytes, blood urea nitrogen (BUN), creatinine, glucose:



o

Evaluate renal function.

o

Elevated BUN m ay indicate blood in GI tract.

Type and cross-m atch

Imaging Low threshold for CT im aging to detect occult but life threatening bleeding: 

Head CT: o

Minor m echanism s of blunt head traum a without loss of consciousness

o

Detect ICH presenting with only m ild sym ptom s of headache and nausea before the classic gradual progression of sym ptom s to focal deficits and com a



Abdom inal CT: o

Blunt abdom inal traum a without significant tenderness

o

For retroperitoneal hem orrhage

Differential Diagnosis 

All causes of bleeding: o



GI, retroperitoneal, CNS, and traum atic

Skin lesionsâ€”hem orrhagic skin disorders: o

Hem ostatic deficits such as platelet disorders

o

Vascular purpuras including glucocorticoid use,

Pa ge 5 2 0

vitam in C deficiency, purpura fulim nans, dissem inated intravascular coagulation, Henoch-SchÃ¶nlein purpura, protein C deficiency P.1223

Treatment Pre Hospital 

ABCs



Treat hypotension with two large-bore IV lines and 0.9% NS infusion.



Cardiac and pulse oxim etry m onitoring

Initial Stabilization 

Establish central IV access for hypotension not responsive to initial fluid bolus: o



Com pressible sites only

Replace lost blood as soon as possible: o

Initiate with O-negative blood until type-specific blood available.

o

10 m L/kg bolus in children

ED Treatment 

Specific m anagem ent depends on the INR, presence of bleeding, reason for anticoagulation, and reliability of patient: o

o

INR <5 without bleeding: 

Lower or om it next dose.



Recheck INR in 24 hours.

INR 5â€“9 without bleeding:

Pa ge 5 2 0



Om it next 1 or 2 doses.



If at increased risk for bleeding or pre-op, then adm inister vitam in K 2â€“4 m g PO, INR will be lowered in 24 hours.

 o

Recheck INR in 24 hours.

INR >9 without significant bleeding: 

Hold Coum adin and give vitam in K 5â€“10 m g PO; INR will be substantially lowered in 24â€“48 hours

o

INR >20 with m inor or life-threatening bleeding: 

Hold Coum adin



Vitam in K 10 m g by slow IV infusion



Fresh frozen plasm a (FFP) 3â€“4 units, or prothrom bin com plex concentrate or recom binant factor VIIa depending on volum e status and availability



In the setting of controlled bleeding, m aintain the INR at the lower level of therapeutic efficacy: o

1.5â€“2.0 for atrial fibrillation

o

2.0â€“2.5 with a m echanical heart valves

Medication (Drugs) 

Vitam in K1 Phytonadione: o

Side effects: 

Anaphylaxis with IV > IM or PO



Subcutaneous absorption unpredictable



IM adm inistration m ay result in hem atom a form ation.



Breakthrough throm boem bolism with com plete correction



High-dose vitam in K1 risks prolonged warfarin

Pa ge 5 2 0

resistance and m ay precipitate throm boem bolism for up to 1 week o

10 m g IV infusion over 10 m inutes is recom m ended for life threatening active bleeding with effects beginning in 1â€“2 hours



FFP: o

Traditionally 3â€“4 units of FFP (1 L) are given to control continued bleeding in the short term without excessive risk of throm boem bolism .

o

Patient response is variable and m ay not correlate with correction of the INR.

o



Side effects: 

Virus transm ission



Fluid overload

Prothrom bin com plex concentrate (PCC): o

PCC is a fractionation product of FFP containing equal am ounts of factors II, VII, IX, and X.

o

Long shelf life and easy reconstitution into a highly concentrated volum e (500â€“1,000 U/20 cc versus 1 L of FFP per dose)

o

Rapid and quick reversal without volum e overload where available

o

o

Side effects: 

Throm bosis



Less virus transm ission then FFP

For patients with an INR of 2.0â€“3.9, adm inister 25 U/kg, 4.0â€“5.9, 35 U/kg, and >6.0, 50 U/kg



Recom binant factor VIIa: o

Produces a rapid â€œthrom bin burstâ€• reducing INR and bleeding

o

No risk of virus transm ission

o

Sm all volum e

Pa ge 5 2 0

o

Single bolus of 15â€“90 Âµg/kg bodyweight

o

Side effects: 

Throm bosis rare



Expensive

Follow-Up Disposition Admission Criteria 

Active GI, retroperitoneal, or CNS bleeding



Anticoagulated traum a patient with evidence of active bleeding requires: o

Reversal of anticoagulation and blood replacem ent

o

Early surgical consultation for operative intervention

o

Transport to a level one-traum a center after initial stabilization for definitive care.



Skin necrosis requires adm ission for anticoagulation with alternative agents in consultation with a hem atologist.



Subtherapeutic patient m ay require adequate anticoagulation with inpatient heparin or low m olecular weight heparin to prevent a breakthrough throm boem bolism : o

Outpatient Lovenox therapy followed by increased coum adin with close follow-up prevents unnecessary hospitalization

o

Daily average risk or throm boem bolism low for m ost indications

Discharge Criteria 

Asym ptom atic reliable patient with a supratherapeutic INR after consideration of:

Pa ge 5 2 0

o

Indication for anticoagulation, reason for supratherapeutic level, underlying com orbidities, overall risk of bleeding, fall risk, social situation, reliability, and availability of follow up



Asym ptom atic anticoagulated patient with m inor traum a, therapeutic INR, stable hem oglobin, norm al im aging studies, and reliable caretakers, discharge with close follow up.

References 1. Ansell J, Hirsh J. Pharm acology and m anagem ent of the Vitam in K antagonists. Chest. 2004;204Sâ€“233S. 2. Deveras RA, Kessler K. Reversal of warfarin induced excessive anticoagulation with recom binant factor VIIa concentrate. Ann Intern Med. 2002;137:884â€“889 3. Levine MN, Raskob G. Hem orrhagic Com plications of Anticoagulant Treatm ent. Chest 2004;126;287Sâ€“310S.

Pa ge 5 2 0

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Warts

Warts

Gary M. Vilke

Basics Description 

Condylom a acum inata, also known as genital warts or venereal warts



Self-lim iting benign epithelial tum ors lasting m onths to years

Etiology 

Hum an papillom avirus (HPV), usually subtypes 6 and 11



May produce laryngeal papillom atosis in infants from viral exposure at birth



Transm itted by direct sexual contact, contact with contam inated objects, and autoinoculation



Linked to carcinom a of the penis, vulva, anus, and cervix

Diagnosis Signs and Symptoms 

Pedunculated growths, often with cauliflowerlike appearance

Pa ge 5 2 1



Flesh-colored to slightly pigm ented or red



In m en, usually on glans penis, shaft, scrotum , or anus



In wom en, found on labia, vagina, cervix, or anus



May extend into urethra, bladder, or rectum



Can develop in m outh or throat if oral sexual contact

Essential Workup 

Diagnosis m ade by characteristic appearance of lesions: o

If difficult to see, add acetic acid to suspected area, which will cause infected areas to whiten and becom e m ore visible.

o

Biopsy and viral typing not recom m ended for typical lesions.

o

Biopsy indicated if failing therapy, patient im m unocom prom ised, warts are pigm ented, indurated, fixed, or ulcerated



Screen for other sexually transm itted diseases.

Tests Lab Pregnancy test for fem ales

Differential Diagnosis 

Condylom a latum (secondary syphilis)



Herpes sim plex



Prom inent glands around head of penis



Benign or m alignant neoplasm



Molluscum contagiosum

Treatment Initial Stabilization

Pa ge 5 2 1

None required

ED Treatment 

If available m ay use im iquim od, podofilox, podophyllin, trichloroacetic acid, or alternative therapies listed below.





Alternative treatm ents: o

Cryotherapy with liquid nitrogen or dry ice

o

Electrocautery

o

Laser therapy

o

Surgical excision

o

Interferon for use by subspecialists

Provide appropriate referral.

P.1225

Medication (Drugs) 

Im iquim od cream : apply three tim es/week for up to 16 weeks: o



Cream m ay weaken diaphragm s and condom s.

Podofilox 0.5% gel or solution: o

Apply twice daily for 3 days, then rest 4 days; m ay repeat for four cycles

o

Do not use on perianal, rectal, urethral or vaginal lesions.



Podophyllin 15â€“25% in benzoin: weekly topical application: o

Protect surrounding norm al tissue with petroleum jelly.

o

Wash off 1â€“4 hours later

o

Do not use in pregnancyâ€”highly toxic and

Pa ge 5 2 1

teratogenic. o

Do not use on cervix, vagina, or anal canal as m ay cause dysplastic changes.



Trichloroacetic acid, topical 60â€“90%: o

Wash off 6â€“10 hours later.

o

May be repeated weekly

Follow-Up Disposition Admission Criteria 

Dissem inated cases in im m unocom prom ised patients m ay require adm ission.

Discharge Criteria Most patients can be treated as outpatients.

References 1. Centers for Disease Control and Prevention. Sexually transm itted diseases treatm ent guidelines. MMWR. 2002;51:1â€“78. 2. Kodner CM, Nasraty S. Managem ent of genital warts. Am Fam Physician 2004;70:2335â€“2342. 3. Maw R. Critical appraisal of com m only used treatm ent for genital warts. Int J of STD & AIDS. 2004;15:357â€“364.

Codes ICD9-CM 078.19

ICD10 B07

Pa ge 5 2 1

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Weakness

Weakness

Jason Imperato

Basics Description 

Defined as a decrease in physical strength or energy



Often m ultifactorial



Distinguish neurom uscular disorder versus nonneurom uscular disorder



Categories of neurom uscular disorders: o

o

o

Upper m otor neuron (UMN) lesions: 

Deep tendon reflexes (DTR) increased



Plantar reflexes upgoing



Increased m uscle tone



Muscle atrophy absent

Lower m otor neuron (LMN) lesions: 

DTRs decreased to absent



Plantar reflexes absent or norm al



Decreased m uscle tone



Muscle atrophy present



Fasciculations

Neurom uscular junction (NMJ) lesions: 

DTRs norm al



Plantar reflexes norm al or absent

Pa ge 5 2 1

 

Decreased m uscle tone

Categories of nonneurom uscular disorders: o

Infectious

o

Endocrine

o

Metabolic

o

Cardiac

o

Rheum atologic

o

Toxic

o

Psychiatric

Etiology Neuromuscular Disorders 





UMN lesions: o

Multiple sclerosis

o

Am yotrophic lateral sclerosis

o

Transverse m yelitis

o

Poliom yelitis

LMN lesions: o

Guillain-Barre syndrom e

o

Toxic neuropathies

o

Im pingem ent syndrom es

o

Diphtheria

o

Porphyria

o

Seafood toxins

NMJ lesions: o

Myasthenia gravis

o

Lam bert-Eaton syndrom e

o

Botulism

o

Periodic paralysis

o

Tick paralysis

o

Electrolyte im balances

Nonneuromuscular Disorders

Pa ge 5 2 1



Dehydration



Anem ia



Malignancy



Cerebrovascular accident



Head or neck traum a



Myocardial ischem ia



Infection/sepsis:









o

Urinary tract infection

o

Pneum onia

o

Meningitis

o

Mononucleosis

o

HIV

Endocrine abnorm alities: o

Hypothyroidism

o

Adrenal crisis

o

Periodic paralyses

Rheum atologic disorders: o

System ic lupus erythem atosus

o

Polym yalgia rheum atica

Toxins: o

Medications

o

Environm ental

o

Carbon m onoxide poisoning

o

Cocaine

o

Alcohol

Psychiatric: o

Sim ple fatigue

o

Chronic fatigue syndrom e

o

Fibrom yalgia

o

Anxiety

o

Malingering

Pa ge 5 2 1

Diagnosis Signs and Symptoms Altered Physical Strength 



Assessm ent of strength: o

1: No contraction

o

2: Active m ovem ent with gravity elim inated

o

3: Active m ovem ent against gravity

o

4: Active m ovem ent against gravity and resistance

o

5: Norm al power

Change in m uscle tone: o

Flaccidity

o

Spasticity

o

Rigidity



Abnorm al DTRs



Abnorm al plantar reflexes



Muscle atrophy: o

Difference of >1 cm in the leg and thigh and >0.5 cm in the forearm and arm

Systemic Findings 

Weakness



Fatigue



Dizziness



Paresis



Paresthesias



Hoarse voice



Dysphagia



Visual changes



Confusion



Associated sym ptom s:

Pa ge 5 2 1

o

Fever

o

Chest pain

o

Dyspnea

o

Cough

o

Weight loss

o

Rash

o

Dysuria

o

Upper respiratory infection sym ptom s

Essential Workup Clinical suspicion gathered through history and physical exam guides further testing: 

Generalized versus focal



Acute versus chronic



Proxim al versus distal



Ascending versus descending



Sym m etric versus asym m etric



Im proved versus worsened with activity

Tests Diagnostic testing should be broad unless history and physical exam identify the cause of weakness.

Lab 

Serum glucose



CBC



Electrolytes



Blood urea nitrogen and creatinine



Toxin screen



Urinalysis



Thyroid function tests (r/o hypothyroidism )



Erythrocyte sedim entation rate (r/o rheum atologic cause)



Carboxyhem oglobin (r/o CO poisoning)

P.1227

Pa ge 5 2 1

Imaging 

EKG (r/o acute coronary syndrom e)



Chest radiograph (r/o pneum onia)



CT head or MRI head (r/o intracranial pathology)

Diagnostic Procedures/Surgery 

Bedside spirom etry: o

Forced vital capacity, negative inspiratory force, peak expiratory flow rate

o 

May identify those with im pending ventilatory failure

Lum bar puncture: o

In suspected Guillain-BarrÃ© syndrom e: 

Album in-cytologic dissociation in cerebrospinal fluid (protein >400, WBC <10) is virtually diagnostic.



Tensilon test: o

Distinguishes m yasthenic crisis from cholinergic crisis in m yasthenia gravis

Differential Diagnosis 

Multiple sclerosis



Am yotrophic lateral sclerosis



Transverse m yelitis



Poliom yelitis



Guillain-BarrÃ© syndrom e



Diphtheria



Porphyria



Myasthenia gravis



Lam bert-Eaton syndrom e



Botulism



Periodic paralysis

Pa ge 5 2 1



Electrolyte im balances



Dehydration



Malignancy



Infection/Sepsis



Endocrine abnorm alities



Toxins

Treatment Treatm ent is geared to the underlying cause of weakness.

Pre Hospital 

Supplem ental oxygen



IV access



Fingerstick glucose determ ination



Consider endotracheal intubation in patients with severe respiratory distress.

Initial Stabilization 

Supplem ental oxygen



IV access



Endotracheal intubation for im pending ventilatory failure

ED Treatment 

Neurology consult if needed



When the diagnosis is determ ined, specific therapies can be applied: o

Plasm a exchange and/or IV im m unoglobulin (IVIG) for Guillain-BarrÃ© syndrom e

o

Hydrocortisone for adrenal insufficiency

o

Potassium supplem entation for hypokalem ia

o

Dextrose for hypoglycem ia

o

Specific antidotes for botulism and diphtheria

Pa ge 5 2 2

Follow-Up Disposition Admission Criteria 

All patients with new-onset neurom uscular disorders should be adm itted for definitive diagnosis.



Any evidence of im pending ventilatory or circulatory com prom ise warrants intensive care unit adm ission.

Discharge Criteria 

Resolution of sym ptom s



Stable vital signs



Definitive diagnosis and correction of abnorm ality

References 1. Chew WM, Birnbaum er DM. Evaluation of the elderly patient with weakness: an evidence based approach. Em erg Med Clin N Am . 1999;17(1):265â€“278. 2. LoVecchio F, Jacobson S. Approach to generalized weakness and peripheral neurom uscular disease. Em erg Med Clin N Am . 1997;15(3):605â€“623. 3. Reiser RC. Weakness. In Marx J, et al, eds: Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002: 119â€“123.

Pa ge 5 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > West Nile Virus

West Nile Virus

Malik Mamta

Basics Description Infectious agent is arbovirus that is m em ber of the Flaviviridae fam ily.

Etiology 

Vector-borne virus



Transm itted by infected m osquitoes late sum m er/early fall



Wild birds are prim ary reservoir hosts.



Introduced to Western Hem isphere 1999



Infection after blood transfusion and solid organ transplant can occur.



Case reports of occupational exposure and infection of lab workers via percutaneous inoculation exist.

Pregnancy Considerations Infection via transplacental transm ission and breast-feeding has been reported.

Diagnosis

Pa ge 5 2 2



Variable severity of illness: o

80% asym ptom atic

o

20% m ild sym ptom s, flulike illness

o

Approxim ately 1/150 with CNS involvem ent (encephalitis, m eningitis)



Incubation period is usually 2â€“6 days, but can be up to 14 days in average patient, up to 21 days in im m unocom prom ised patients.



Sym ptom s are sudden onset and last <1 week with m ild infection.



Mortality rate in severe cases is estim ated at 7%.



Severity of illness is related to degree of central nervous system invasion by virus.



Im m unocom prom ised patients have prolonged virem ia, delayed developm ent of antibody, and increased likelihood of severe disease.

Alert Geriatric Considerations 

Patients older than age 50 years are at higher risk for developing m ore severe disease and neurologic consequences if infected.



Advanced age is m ost im portant risk factor for death.

Signs and Symptoms History 



General: o

Fever

o

Malaise

o

Anorexia

o

Headache

Neurologic:

Pa ge 5 2 2

o

Altered m ental status (change in level of consciousness, confusion, agitation, irritability)









o

Severe, diffuse m uscle weakness

o

Flaccid paralysis

o

May resem ble Guillain-BarrÃ© syndrom e

o

Seizures

Gastrointestinal: o

Nausea, vom iting, diarrhea

o

Abdom inal pain

Musculoskeletal: o

Myalgia

o

Arthralgia

Respiratory: o

Cough

o

Sore throat

Ophthalm ologic: o

Photophobia

o

Eye pain

Physical Exam 

General: o





Neurologic: o

Altered m ental status

o

Hyporeflexia, areflexia

o

Ataxia

o

Extrapyram idal signs

o

Cranial nerve palsies, paresis

o

Myoclonus

o

Profound m otor weakness

Gastrointestinal: o



Tem perature >38Â°C, 100Â°F

Hepatosplenom egaly

Musculoskeletal:

Pa ge 5 2 2

o 

Hem atologic: o



Nuchal rigidity

Lym phadenopathy

Derm atologic: o

Rash (m aculopapular or m orbilliform on neck, trunk, extrem ities)



Cardiovascular: o



Myocarditis (rare)

Ophthalm ologic: o

Optic neuritis

o

Vitritis

o

Chorioretinitis

Essential Workup Most sensitive screening test is serologic testing of cerebrospinal fluid (CSF) and serum for IgM antibody-capture enzym e-linked im m unosorbent assay [ELISA] and culture: 

Can be detected during first 4 days of illness, and nearly all tests are positive by day 7â€“8; m ay rem ain positive up to 1 year after infection



Procedures for subm itting sam ples vary by state.



Refer to local public health departm ent for guidelines.

Tests Lab 



CSF: o

Pleocytosis with lym phocyte predom inance

o

Elevated protein

o

Norm al glucose

CBC: o

WBC m ay be m ildly elevated (50%) or norm al.

o

Leukopenia m ay be present (15%).

o

Anem ia can occur.

Pa ge 5 2 2



Chem istry: o

Hyponatrem ia som etim es seen: 

Cause uncertain, possibly syndrom e of inappropriate antidiuretic horm one (SIADH) when CNS involvem ent exists

o

Pancreatitis (rare)

o

Fulm inant hepatitis (rare)

Imaging 

CT head usually norm al



MRI can be useful to identify CNS inflam m ation: o

One third of patients show abnorm ality.

o

Im aging findings generally nonspecific, but m ay include enhancem ent of leptom eninges and/or periventricular white m atter or can m im ic dem yelinating process

Diagnostic Procedures/Surgery Lum bar puncture P.1229

Differential Diagnosis 



Other causes of m eningitis: o

Bacterial

o

Viral

o

Tuberculous

o

Fungal

Other causes of viral encephalitis: o

Other arboviruses, especially St. Louis encephalitis virus

o

Enterovirus, particularly in patients 16 years and younger

Pa ge 5 2 2

o

Herpes sim ple virus (HSV)

o

Cytom egalovirus (CMV)

o

Epstein-Barr virus (EBV)

o

Mum ps virus

o

Varicella-zoster virus

o

Rabies virus



Intracranial abscess



CNS vasculitis



Nonspecific viral syndrom e



Gastroenteritis

Treatment Initial Stabilization 

ABCs



Seizure precautions

ED Treatment 

Supportive care



IV fluids for signs of dehydration



For signs of m eningitis, adm inister antibiotics pending results of CSF.



Consider acyclovir if index of suspicion for only treatable cause of viral encephalitis, HSV, is high.



Adm inister antipyretics and pain m edications.



No known effective antiviral therapy or vaccine



No controlled studies proving effectiveness of Interferon-Î±2b, ribavirin, corticosteroids, anticonvulsants, or osm otic agents

Pa ge 5 2 2

Follow-Up Disposition Admission Criteria 

Neurologic sym ptom s



Dehydration



Concerning risk factors (advanced age, im m unocom prom ise)

Discharge Criteria 

No signs of CNS involvem ent (encephalitis, m eningitis)



Able to tolerate oral solutions

References 1. Hayes EB, O'Leary DR. West Nile virus infection: a pediatric perspective. Pediatrics. 2004;113:1375â€“1381. 2. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001;344:1807â€“1814. 3. Petersen LR, Marfin AA, Gubler DJ. West Nile virus. JAMA. 2003;290:524â€“528. 4. Ravindra KV, Freifeld AG, et al. West Nile virus-associated encephalitis in recipients of renal and pancreas transplants: case series and literature review. Clin Infect Dis. 2004;38:1257â€“1260. Epub 2004 Apr 14. 5. Solom on T, Ooi MH, et al. West Nile encephalitis. Br Med J. 2003;326:865â€“869. 6. West Nile Virus: Inform ation and Guidance for Clinicians. Available at http://www.cdc.gov/ncidod/dvbid/westnile/clinicians. 7. Zak I, Altinok D, et al. West Nile virus infection. AJR Am J Roentgenol. 2005 Mar;184(3):957â€“61. Review

Pa ge 5 2 2

Miscellaneous SEE ALSO: Meningitis; Encephalitis

Codes ICD9-CM 066.4

Pa ge 5 2 2

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wheez ing

Wheezing

Stephen K. Epstein

Basics Description 

Result of turbulent airflow: o

High-pitched sound with dom inant frequency at 400 Hz: 

Gas flowing through constricted airways analogous to a vibrating reed

o

Resonant vibration of the bronchial walls when airflow velocity reaches critical values



Caused by airway narrowing between 2 and 5 m m : o

Wheezing is very low pitched with airway diam eters of 5 m m .

o

Airways of <2 m m are unable to transm it sound because the energy is lost as friction heat.



Airway narrowing is caused by a com bination of one or m ore of the following: o

Constriction (as with reactive airway disease)

o

Peribronchial interstitial edem a

o

Inflam m ation

o

Obstruction

Etiology

Pa ge 5 2 3

Pulmonaryâ€”Small Airway 

Asthm a



Acute respiratory distress syndrom e



Anaphylaxis



Aspiration pneum onia: o

Wheezing occurs early in the disease due to intense bronchospasm following the event.



Byssinosis: o

Occupational lung disease of textile workers exposed to cotton dust



Drugs: o

Can precipitate angioedem a or allergic reaction

o

Angiotensin-converting enzym e inhibitors

o

Beta-blockers

o

Aspirin and NSAIDs



Forced exhalation in norm al patients



Hyperventilation



Chronic obstructive pulm onary disease



Chronic cor pulm onale



Chem ical pneum onitis



Carcinoid tum ors



Paroxysm al nocturnal dyspnea



Pulm onary edem a



Pulm onary em bolism : o

Rarely associated with wheezing

o

Focal



Pneum onia



Sleep apnea

Pulmonaryâ€”Large Airway 

Vocal cord dysfunction (paralysis, paradoxical m ovem ent)



Foreign body

Pa ge 5 2 3



Epiglottitis: o

Wheezing associated with stridor in 10% of cases



Diphtheria



Sm oke inhalation



Bronchial tum or



Tracheal tum or

Pediatric Considerations 

Viral bronchiolitis in patients younger than 3 years of age



Asthm a



Croup



Foreign body aspiration



Congenital abnorm alities: o

Tracheom alacia

o

Tracheal stenosis



Cystic fibrosis



Congestive heart failure

Diagnosis Signs and Symptoms 

A whistling sound m ade while breathing: o

Diffuse: 

As with reactive airway disease or pulm onary edem a

o

Focal: 

As with pneum onia or pulm onary em bolism



Dyspnea



Respiratory distress



Chest pain



Cough

Pa ge 5 2 3



Sputum production: o

Frothy (pulm onary edem a)



Stridor



Fever



Cyanosis



Tachypnea



Tachycardia

Essential Workup 

Pulse oxim etry



Peak flow



Chest radiograph

Tests Lab 

Arterial blood gas: o

Som etim es used to determ ine whether patient is fatiguing by noting falling oxygenation, rising CO 2 , and acidosis

o

Clinical assessm ent is a m ore reliable indicator of the need for airway m anagem ent.



WBC: o

Elevated WBC does not distinguish infection from other disorders, as stress causes dem argination.

o

WBC is also elevated in noninfected patients taking steroids.

o

A norm al WBC does not rule out an underlying pneum onia.

Imaging 

Peak expiratory flow: o

To assess function of sm all airways

o

Use to determ ine severity and track the progress of

Pa ge 5 2 3

therapy in patients with reactive airway disease. 

Chest radiograph: o

o 

Assess for diagnosis of pulm onary conditions: 

Pneum onia



Foreign body aspiration

Assess for pulm onary edem a.

ECG: o

Useful when patient at risk for cardiac ischem ia

o

Indicated in all cases in which wheezing is caused by pulm onary edem a



Soft-tissue neck: o

Used to assess for foreign body or obstructing m ass

Diagnostic Procedures/Surgery Bronchoscopy: 

Indicated when obstruction is thought to be causal



Used to retrieve an inhaled foreign body or diagnose an underlying tum or

P.1231

Treatment Pre Hospital 

Supplem ental oxygen



Initiate pulse oxim etry and cardiac m onitoring.



Initiate therapy for underlying condition when indicated:



o

Asthm a

o

Pulm onary edem a

Intubate for respiratory failure or anticipated respiratory

Pa ge 5 2 3

failure.

Initial Stabilization 

ABCs



Intubation for im pending airway failure: o

Prepare for possible foreign body in airway.

o

Anticipate difficult airway.

ED Treatment 

Supplem ental oxygen



Treat the underlying condition.



Bronchodilators: o

Reversibility following the use of Î²-agonists such as albuterol or terbutaline suggests reactive airway disease.



Trial of steroids indicated if wheezing is caused by bronchospasm or noninfectious inflam m ation.





Heliox: o

Less dense than air or oxygen alone

o

Decreases work of breathing

o

More efficacious in large airway disease

o

Not as effective for sm all airway disease

Magnesium sulfate: o

Evidence for benefit only in m oderate to severe asthm atics



Ketam ine: o

For intubation of the asthm atic patient

Medication (Drugs) 

Albuterol: 2.5 m g in 2.5 m L NS q20m in inhaled (peds: 0.1â€“0.15 m g/kg/dose q20m in; m in. dose 1.25 m g)



Methylprednisolone: 60â€“125 m g IV (peds: 1â€“2

Pa ge 5 2 3

m g/kg/dose IV or PO q6h for 24 hours) 

Prednisone: 40â€“60 m g PO (peds: 1 m g/kg/d in single or div. doses)



Racem ic epinephrine: (peds: 0.25â€“0.5 m L nebulized for croup)



Terbutaline: 0.25 m g SC q0.5h for 2 doses (peds: 0.01 m g/kg up to 0.3 m g SC)

Follow-Up Disposition Admission Criteria 

Hypoxia



Persistent or worsening wheezing



Underlying condition requires hospital adm ission

Discharge Criteria 

Im provem ent or resolution of wheezing



Adequate oxygenation

References 1. Boushey HA, Corry DB, Fahy JV. Asthm a. In: Murray JF, Nadel JA, eds. Textbook of respiratory m edicine. 3rd ed. Philadelphia, PA: WB Saunders, 2000:1247â€“1288. 2. Dorland's illustrated m edical dictionary. 28th ed. Philadelphia, PA: WB Saunders, 1994. 3. Fiz JA, et al. Detection of wheezing during m axim al forced exhalation in patients with obstructed airways. Chest. 2000;122(1):186â€“191. 4. Krieger BP When wheezing m ay not m ean asthm a. Postgrad Med. 2002;112(2):101â€“111.

Pa ge 5 2 3

5. White MV. Differential diagnosis in the difficult asthm atic. Im m unol Allergy Clin North Am . 2001;21(3).

Miscellaneous SEE ALSO: Asthm a, Adult; Asthm a, Pediatric

Codes ICD9-CM 786.09

ICD10 R06.2

Pa ge 5 2 3

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wilm sâ€ ™ Tum o r

Wilmsâ€™ Tumor

Joseph H. Kahn

Basics Description 

Solid tum or (nephroblastom a) of the kidney, accounting for 6â€“8% of childhood solid tum ors in the United States



Incidence: 7 cases per m illion children per year



Mean age at diagnosis: 3.2 years (m edian: 2.6 years; range: 3 m onths to 16 years)



Equal m ale-to-fem ale ratio



Overall 5-year survival: 89.5%



Relapse rate: 22%



Stages (10-year survival):



o

I: Lim ited to kidney (94%)

o

II: Spread by direct extension (86%)

o

III: Spread via lym phatic drainage (71%)

o

IV: Spread via hem atogenous m etastasis (36%)

o

V: Involves both kidneys

Favorable versus unfavorable histology: o

10-year survival with unfavorable histology is 36%

Genetics 

Denys-Drash syndrom e (pseudoherm aphroditism , severe glom erulopathy, Wilm s tum or)

Pa ge 5 2 3



WAGR syndrom e (Wilm s tum or, aniridia, genitourinary m alform ation, m ental retardation)



5â€“10% of Beckwith-Wiedem ann syndrom e (hem ihypertrophy, m acroglossia, om phalocele, viscerom egaly) has Wilm s tum or.

Etiology Abnorm al proliferation of m etanephric blastem a without norm al differentiation into tubules and glom eruli

Diagnosis Signs and Symptoms History 

Abdom inal pain



Gross hem aturia

Physical Exam 

Abdom en: o

Abdom inal m ass that is usually sm ooth and 5â€“10 cm in size 



Usually does not cross m idline

Vital signs: o

Hypertension (60%) due to renal ischem ia from tum or pressure on the renal artery

o

Uncom m only, hypertension m ay be due to renin-secreting Wilm s tum or.



Cardiac/Pulm onary: o

Congestive heart failure (CHF) m ay be present.

Alert 

Com plications:

Pa ge 5 2 3

o

Before surgery: m assive bleeding from ruptured tum or, â€œacute abdom en,â€• bowel obstruction

o

After nephrectom y: bowel obstruction (5.1%), urinary tract infection (UTI), pneum onia, hem orrhage (1.9%), vascular injury (1.5%)

o

During and after chem otherapy: neutropenia with fever, renal insufficiency, anem ia, throm bocytopenia, hepatotoxicity, venoocclusive disease of liver (VOD)

o

VOD seen in 4.9% of patients receiving vincristine and actinom ycin-D

o

Associated with throm bocytopenia

o

Can cause liver failure with ascites and elevated international norm alized ratio (INR)

o

Acquired von Willebrand syndrom e is rarely associated with Wilm s tum or.

Essential Workup 

Urinalysis: hem aturia in 25% of patients



Ultrasound can identify m ass and distinguish cystic from solid tum or.

Tests Lab 

Renal function tests



CBC



INR/partial throm boplastin tim e

Imaging 

CT or MRI scan of abdom en to diagnose and stage the disease



Chest radiograph and chest CT scan evaluating for m etastases

Diagnostic Procedures/Surgery

Pa ge 5 2 4

See Treatm ent

Differential Diagnosis 

Infection: UTI



Anatom ic: urinary tract anom aly, hydronephrosis, renal cyst



Neoplasm : neuroblastom a, renal cell carcinom a, sarcom a, lym phom a

Treatment Initial Stabilization Resuscitation as appropriate, including m anagem ent of hypertension, CHF, anem ia, renal failure

ED Treatment Pediatric oncologic/genitourinary referrals after initiating diagnostic evaluation P.1233

Definitive Treatment Surgical rem oval of affected kidney m ay consider partial nephrectom y for sm all tum ors with favorable histology: 

Chem otherapy reflecting type and stage: o

Stage I with favorable histology: vincristine or vincristine plus actinom ycin D

o

Stage II with favorable histology: sam e agents with longer course than stage I

o

Stages III and IV with favorable histology and any stage with unfavorable histology: radiation and

Pa ge 5 2 4

vincristine and actinom ycin D plus doxorubicin

Follow-Up Disposition Admission Criteria 

Hypertension, CHF



Renal insufficiency



Significant anem ia



Pulm onary findings



Poor com pliance



Lack of tim ely follow-up

Discharge Criteria 

Norm al blood pressure



Norm al renal function



Near-norm al hem atocrit



Norm al cardiac and pulm onary exam ination



Reliable parents



Rapid follow-up available

Issues for Referral 

Pediatric oncology referral



Pediatric genitourinary referral

References 1. Czauderna P, Katski K, Kowalczyk J, et al. Venoocclusive liver disease (VOD) as a com plication of Wilm sâ€™ tum our m anagem ent in the series of consecutive 206 patients. Eur J Pediatr Surg. 2000;10:300â€“303. 2. Grundy RG, Hutton C, Middleton H, et al. â€œOutcom e of patients with stage III or inoperable Wilm sâ€™ Tum or treated on the second

Pa ge 5 2 4

United Kingdom Wilm sâ€™ Tum or protocol (UKWT2).â€• Pediatric Blood and Cancer. 2004;42:311â€“319. 3. Haecker FM, von Schweinitz D, Harm s D, et al. â€œPartial nephrectom y for unilateral Wilm s tum or: results of study SIOP 93-01/GPOH.â€• J Urol. 2003;170:943â€“944. 4. Hartm an DJ, MacLennan GT. â€œWilm s Tum or.â€• The Journal of Urology. 2005;172:21â€“47. 5. Ritchey ML, Sham berger RC, Haase G, et al. Surgical com plications after prim ary nephrectom y for Wilm sâ€™ tum or: report from the National Wilm sâ€™ Tum or Study Group. J Am Coll Surg. 2001;192:63â€“68. 6. Wong W, Mauger D. â€œTreatm ent of Wilm s tum or-related hypertension with losartan and captopril.â€• Pediatric Nephrology. 2004;19:805â€“807.

Codes ICD9-CM 189.0

ICD10 C64

Pa ge 5 2 4

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins

Withdrawal,

> Table o f C o ntents > Withdraw al, Alco ho l

Alcohol Lee Shockley

Basics Description 

Chronic alcohol use â€œdown-regulatesâ€• gam m a-am inobutyric acid (GABA) receptors, leading to tolerance (increasing doses or frequency of alcohol use is necessary to achieve the sam e effects).



Tolerance is necessary for withdrawal to occur.



Alcohol dependence is the altered physiologic state induced by chronic alcohol use; associated with inhibition of excitatory glutam atergic pathways and up-regulation of N-m ethyl-D-aspartate (NMDA) receptors.



Dependence is necessary for withdrawal to occur.



Characterized by a hyperadrenergic state that develops 6â€“8 hours after the cessation of drinking and m ay last up to 5 days.



Enhanced excitatory neurotransm ission: o

Increased levels of plasm a and urine catecholam ines (glutam ate effects)

o

Decreased inhibitory activity of presynaptic Î±2

Pa ge 5 2 4

receptors (GABA effects) o

Increased dopam inergic activity (hallucinogenic effects)

Genetics Alcoholism is related to inherited functional variants of genes that alter the m etabolism of alcohol and alter the neurobiologies of reward, executive cognitive function, anxiety/dysphoria, and neuronal plasticity: 

Functional alleles: o

Com m on alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants (flushing reaction)

o

Catechol-O-m ethyltransferase (COMT) Val158Met (executive cognitive function, stress/anxiety response, and opioid function)

o

Opioid receptor m icro1 (OPRM1) Asn40Asp (gatekeeper m olecule in the action of naltrexone)

o

5-HT transporter gene-linked polym orphic region (5-HTTLPR) alters serotonin transporter function (stress response and anxiety/dysphoria)

Geriatric Considerations 

Alcoholism is not uncom m on am ong older adults.



Age-related increase in alcohol sensitivity



Alcohol-related problem s m ay be m isdiagnosed as norm al consequences of aging.

Pediatric Considerations Newborns whose m others are intoxicated during delivery can experience withdrawal sym ptom s, such as trem ors and even seizures.

Pregnancy Considerations Alcohol withdrawal m ay exacerbate the adverse effects of chronic

Pa ge 5 2 4

alcohol abuse on the fetus, particularly neuronal developm ent.

Etiology 

The m ost com m on withdrawal syndrom e seen in the ED



Predisposing factors: acute, prolonged, and chronic ethanol ingestion; m alnutrition



Dose dependence



Am ount and chronicity of alcohol intake related to the severity of the syndrom e: o

â€œKindlingâ€• hypothesis: withdrawal episodes becom e progressively m ore severe

Diagnosis There are four alcohol withdrawal syndrom es: 

Trem ulousness: o

Hypersym pathetic state (norepinephrine storm ): sim ilar to hypothyroidism

o

Withdrawal of anticonvulsant properties of ethyl alcohol

o 

Hypom agnesem ia

Hallucinosis: o

Otherwise clear sensorium



Seizures



Delirium trem ens (DT)

These withdrawal syndrom es m ay occur in isolation or com bination.

Signs and Symptoms History 

Withdrawal is typically seen in patients who are daily drinkers for 3 m onths or m ore or binge drinkers (large quantities for at least 1 week).

Pa ge 5 2 4



Trem ulousness: o

Onset 6â€“8 hours after last drink, duration 2â€“3 days



o

Intention trem or

o

Nausea and vom iting

o

Anxiety

o

Agitation

o

Sleep disturbance

Hallucinosis: o

Onset 7â€“48 hours, duration 1â€“3 days

o

Seen in up to 25% chronic alcoholics

o

Visual hallucinations: five tim es m ore com m on than auditory



o

Auditory hallucinations m ore benign

o

May becom e perm anent

Seizures: o

Onset 7â€“48 hours after last drink (95% first 12 hour

o

Generalized, tonic-clonic

o

3â€“20% have som e focality

o

No aura

o

40% single seizure

o

90% have less than five in a 6-hour period

o

Only 3% develop status epilepticus; should prom pt a search for other etiologies



DTs: o

Onset 3â€“5 days after last drink (up to 14 days), duration 4â€“5 days

o

Global confusion, trem or, agitation, anxiety, delusions, delirium , sleep disturbances, and gastrointestinal distress (nausea, vom iting)

o

Hallucinosis does not necessarily precede DTs.

Pa ge 5 2 4

Physical Exam 





Autonom ic lability: o

Tachycardia

o

Tachypnea

o

Hypertension

o

Low-grade hypertherm ia

o

Diaphoresis

o

Flushing

o

Hyperreflexia

Stigm ata of chronic alcohol abuse: o

Spider angiom ata

o

Rhinophym a

o

Parotid swelling

o

Flushed facies

o

Hepatom egaly, caput m edusae, ascites

o

Cirrhosis

o

Muscle wasting

o

Peripheral neuropathy

Extraocular m uscles paralysis or nystagm us m ay be seen in Wernicke encephalopathy.

Essential Workup 

Com plete vital signs, including rectal tem perature



Rapid blood glucose



Pulse oxim etry

Tests Lab 

Electrolytes, blood urea nitrogen, creatinine, glucose, m agnesium



CBC



Alcohol level (Breathalyzer or serum sam ple)

Pa ge 5 2 4



Urinalysis



Creatine kinase (if the patient has been agitated or struggling)



Drug screen if co-ingestion suspected



Consider coagulation studies.

Imaging 

Electrocardiography: o

o

Adrenergic storm : 

Increased m yocardial dem and



May precipitate ischem ia or infarction

Prolonged QTc interval; possibly related to hypom agnesem ia



CT scan of the brain: o

Abnorm al m ental status

o

Head traum a

o

First-tim e seizure (3â€“6% incidence of unsuspected intracranial pathology)

o 

Focal or status seizures

Chest radiograph for suspected traum a or aspiration

Diagnostic Procedures/Surgery Lum bar puncture and cerebrospinal fluid analysis if m eningitis suspected

Differential Diagnosis 

Withdrawal from sedative-hypnotic drugs



Head traum a



Epilepsy



Encephalopathy



Hypoglycem ia



Hyperthyroidism



Sepsis



Meningitis

Pa ge 5 2 4



Encephalitis



Sym pathom im etic overdose



Pheochrom ocytom a



Anticholinergic poisoning



Psychosis



Electrolyte disorders



Mercury poisoning



Lithium overdose



Cyclic antidepressant overdose



Phenytoin overdose

P.1235

Treatment Pre Hospital 

Cardiac m onitoring



Blood glucose determ ination



IV glucose if necessary: o

Concerns over precipitating Wernicke syndrom e should not delay glucose adm inistration. Thiam ine should be adm inistered where there is a concern; however, thiam ine takes several hours to enter into cells.



Physical or chem ical restraints for agitation



Seizure precautions

Initial Stabilization 

ABCs



Oxygen

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

Correct hypoglycem ia



IV fluids



Initiate tranquilization to prevent the progression of the syndrom e to m ore severe levels and to relieve the sym ptom s



Adm inister thiam ine

ED Treatment Restore inhibitory tone to the CNS: 

Benzodiazepines: o

Standard therapy

o

High doses required owing to cross-tolerance with chronic ethanol ingestion

o

Sym ptom s-triggered therapy is preferred (over fixed-schedule therapy).

o 

Large doses m ay be necessary.

Barbiturates: o

Alternatives to benzodiazepines

o

May also have a synergistic effect in patients with apparent â€œbenzodiazepine resistanceâ€•



Propofol: o

Last-resort drug in refractory DT and status epilepticus

o

Directly activates GABA receptors and inhibits NMDA receptors.



Butyrophenone antipsychotics: o

Haloperidol (low doses)

o

Indicated as adjuncts in the hallucinating patient but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates

o 

Best avoided in the nonhallucinating patient

Beta-blockers: o

Propranolol and atenolol

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o

Used to relieve som e of the signs and sym ptom s

o

Considered adjunctive therapy (especially in patients with existing coronary artery disease [CAD]), but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates.

o

Avoid in patients with contraindications (asthm a, bradycardia, or CHF).



Clonidine: o

Adjunct to treat the hyperadrenergic signs and sym ptom s of alcohol withdrawal, but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates.



Anticonvulsive prophylaxis: o

Phenytoin is not useful in alcohol-withdrawal patients who do not also have an underlying seizure disorder that is not alcohol related. Identify and correct fluid, electrolyte, and nutritional deficiencies:



Adm inister glucose for hypoglycem ia or alcoholic ketoacidosis.



Treat hypovitam inosis syndrom es due to m alnutrition with thiam ine and folate.



Correct electrolyte abnorm alities.



Replete m agnesium : o

25% of chronic alcoholic patients are total-body m agnesium depleted owing to m alnutrition and increased renal losses.

o

Hypom agnesem ic state m akes replenishm ent of potassium difficult and m ay lower patient's seizure threshold.



Bed rest, m inim al physical stim ulation



Minim al use of physical restraints after adequate sedation

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to decrease the risk for rhabdom yolysis associated with agitation and struggling

Medication (Drugs) 

Chlordiazepoxide: 25â€“100 m g PO for m ild reactions; 25 m g IV in repeated doses as necessary for m ore severe reactions



Clonidine: 0.1â€“0.2 m g PO q4hâ€“q6h



Clorazepate: 15â€“30 m g PO q8hâ€“q12h



Diazepam : 5â€“20 m g PO for m ild reactions; 5â€“10 m g IV



Folate: 1â€“4 m g IV or PO



Glucose: 5% solution in IV fluids; 25 g IV bolus in hypoglycem ic patients



Haloperidol: 2â€“10 m g PO, IV, or IM, q60m inâ€“q120m in



Lorazepam : 2 m g PO, repeat q2hâ€“q4h as necessary for m ild reactions; 2 m g IV in repeated doses as necessary for m ore severe reactions



Magnesium sulfate: 2â€“6 g in IV solutions, except in renal failure



Pentobarbital: 260 m g IV loading dose followed by 130 m g in repeated doses q30m in. titrated to light sedation



Propranolol: 0.5â€“1 m g IV; 10â€“40 m g PO for cardiac risk pts: add propranolol 10â€“40 m g PO q6h



Propofol: Loading dose: 0.2 m g/kg IV; m aintenance: 0.1â€“0.2 m g/kg/m in (6â€“12 m g/kg/h) IV: o

Titrated up to 90 m cg/kg/m in IV



Thiam ine: 100 m g IV



Trazodone 50â€“150 m g PO PRN qHS for sleep (m ay repeat once)

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Follow-Up Disposition Admission Criteria 

Moderate to severe sym ptom s or persistent sym ptom s



Im pending DTs, DTs, or patients who fail to resolve their sym ptom s with m oderate am ounts of m edication should be adm itted to an intensive care unit.



Consider adm ission or observation for: o

Age >60 years old

o

First episode of ethanol withdrawal

o

Dehydration

o

Patients with com orbidities

Discharge Criteria Mild to m oderate sym ptom s that can be controlled with oral m edications: 

Having patients self-adm inister their m edications is strongly discouraged.



Consider a detoxification facility

Issues for Referral Patients identified as having alcohol withdrawal should be referred to detoxification centers, addiction specialists, or counselors.

References 1. Bayard M, McIntyre J, Hill KR, et al. Alcohol withdrawal syndrom e. Am Fam Physician. March 15, 2004;69(6):1443â€“1450. 2. Bouchard NC, Meltzer A, Hoffm an RS. Treatm ent of delirium trem ens. Arch Intern Med. March 14 2005;165(5):587; author reply 587. 3. Chang PH, Steinberg MB. Alcohol withdrawal. Med Clin North Am .

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Septem ber 2001;85(5):1191â€“1212. 4. DeBellis R, Sm ith BS, Choi S, et al. Managem ent of delirium trem ens. J Intensive Care Med. May/June 2005;20(3):164â€“173. 5. Holbrook AM, Crowther R, Lotter A, et al. Diagnosis and m anagem ent of acute alcohol withdrawal. Cm aj. March 9 1999;160(5):675â€“680. 6. Lappin R. Propofol in delirium trem ens. Ann Em erg Med. Aug 1998;32(2):271â€“272. 7. Polycarpou A, Papanikolaou P, Ioannidis J, et al. Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev. 2005(3):CD005064. 8. William s D, McBride AJ. The drug treatm ent of alcohol withdrawal sym ptom s: a system atic review. Alcohol. March/April 1998;33(2):103â€“115.

Codes ICD9-CM 291.81

ICD10 F10.3

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Withdraw al, Drug

Withdrawal, Drug

Lee Shockley Maria Moreira

Basics Description 

Gam m a-am inobutyric acid (GABA)â€”m inergic withdrawal: o

Requires physical dependence

o

Characterized by a hyperadrenergic state that develops in 3â€“7 days after the cessation of the drug

o

Enhanced excitatory neurotransm ission

o

Increased levels of plasm a and urine catecholam ines

o

Decreased inhibitory activity of presynaptic Î±2 receptors

o

Sym ptom severity determ ined by the am ount of endogenous norepinephrine released during withdrawal

o 

Severe withdrawal can be life-threatening.

Opiate withdrawal: o

Requires physical dependence

o

Decrease in the exogenous opioid binding causes a catecholam ine release in the locus ceruleus.

o

Syndrom e m ay be tem porarily disabling and very

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uncom fortable. o

Not life-threatening

o

Onset within 4â€“8 hours for heroin, 36â€“72 hours for m ethadone

o

Opiate antagonists adm inistration (e.g., naloxone) can precipitate withdrawal (usually only lasting 20â€“60 m inutes).



Sym pathom im etic postexcitation syndrom e: o

Causes tiredness, depression, and dysphoria

o

Neurotransm itter depletion

o

No serious m etabolic or neurologic com plications

o

May be associated with an increased suicide risk and cravings for the drug, which often result in cycles of binges and transient abstinence

Diagnosis Signs and Symptoms 

GABA-am inergic (benzodiazepines, barbiturates, alcohol): o

Anxiety

o

Depression

o

Agitation

o

Trem ulous

o

Anorexia

o

Nausea, vom iting

o

Confusion

o

Hallucinations

o

Seizures

o

Sleep disturbances (insom nia and nightm ares)

o

Physical signs: 

Diaphoresis

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



Flushing



Tachycardia



Hypertension



Orthostatic hypotension



Tachypnea



Fever



Hyperreflexia, m yoclonus



Seizures, delirium , and autonom ic instability



Markers of severe withdrawal

Opiates: o

o

Mild withdrawal: 

Drug craving



Lacrim ation



Rhinorrhea



Yawning



Diaphoresis



Anxiety



Restlessness



Myalgias, arthralgias



Dysphoria



Mydriasis



Piloerection

More severe withdrawal: 

Nausea, vom iting



Diarrhea



Abdom inal pain



Mild increase in blood pressure, pulse, and respiratory rate

o

Concurrent benzodiazepine withdrawal exacerbates opiate withdrawal sym ptom s.



Sym pathom im etics: o

Postexcitation syndrom e, not true withdrawal

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because continuous use of the drug does not prevent the syndrom e o

Crash (extrem e exhaustion that follows binge usage): 

Lethargy



Psychom otor retardation



Increased appetite or anorexia



Sleep disturbances



Muscle twitching



Depression



Fatigue and dysphoria m ay last 6â€“18 weeks in the abstinent patient



Extinction (episodically evoked cravings that can last for m onths to years after abstinence)

Essential Workup 

Thorough physical exam ination to determ ine nature of withdrawal



Blood glucose

Tests Lab 

Electrolytes, blood urea nitrogen, creatinine, glucose



Drug screens m ay be useful if polysubstance abuse is suspected.

Imaging 

Lum bar puncture and cerebrospinal fluid analysis for withdrawal patients in whom m eningitis suspected



CT scan of the brain for: o

Abnorm al m ental status

o

Head traum a

o

Focal seizures

o

Status seizures

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Differential Diagnosis 





GABA-am inergic: o

Ethanol withdrawal

o

Head traum a

o

Epilepsy

o

Encephalopathy

o

Hypoglycem ia

o

Hyperthyroidism

o

Sepsis, m eningitis

o

Encephalitis

o

Sym pathom im etic overdose

o

Pheochrom ocytom a

o

Anticholinergic poisoning

o

Psychosis

o

Electrolyte disorders

Opiates: o

Sedative-hypnotic and ethanol withdrawal

o

Gastrointestinal diseases

Sym pathom im etics: o

Alcohol or sedative-hypnotic intoxication

o

Acute psychiatric disease (depression or psychosis)

o

Head traum a

o

CNS infection

Treatment Pre Hospital 

Initiate cardiac m onitoring.



Determ ine blood glucose if abnorm al m ental status.



Physical or chem ical restraints for agitated patients

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Initial Stabilization 

ABCs



Correct hypoglycem ia with glucose



Initiate IV fluid for dehydration

P.1237

ED Treatment 

Sedative-hypnotic withdrawal: o

Reinstitution of therapy or the substitution of a sedative-hypnotic drug with a long half-life to facilitate detoxification

o

Beta-blocking agents

o

Adjuncts to lessen the adrenergically m ediated sym ptom s



Opiate withdrawal: o

Phenothiazines and butyrophenones for nausea and vom iting

o

Clonidine reduces the signs and sym ptom s of opiate withdrawal.

o

Com bination therapy with clonidine and the long half-life antagonist naltrexone m ay shorten the withdrawal duration by as m uch as 50% without increasing the severity of sym ptom s.

o

Benzodiazepines: 

o

May help ease som e of the sym ptom s

Rapid opiate detoxification or ultra-rapid opiate detoxification protocols (high-dose naloxone treatm ent while under general anesthesia) followed by antiem etics, sedatives, clonidine, and naltrexone; the safety and efficacy of these protocols have not

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been proved. 

Sym pathom im etics withdrawal: o

Supportive therapy

Medication (Drugs) 

Buprenorphine 8 m g SL on day 1, 15 m g SL on day 2. Maintenance 15 m g SL per day



Chlordiazepoxide: 25â€“100 m g PO for m ild reactions; 25 m g IV in repeated doses as necessary for m ore severe reactions



Clonidine: 0.1â€“0.2 m g PO q4hâ€“q6h



Clorazepate: 15â€“30 m g PO q8hâ€“q12h



Diazepam : 5â€“20 m g PO for m ild reactions; 5â€“10 m g IV in repeated doses as necessary for m ore severe reactions



Glucose: 5% solution in IV fluids; 25 g IV bolus in hypoglycem ic patients



Haloperidol: 2â€“10 m g PO or IV



Lorazepam : 2 m g PO, repeat q2hâ€“q4h as necessary for m ild reactions; 2 m g IV in repeated doses as necessary for m ore severe reactions



Methadone: 5â€“20 m g/d POâ€”only designated m ethadone clinics m ay dispense to outpatients



Naltrexone: 50 m g/d PO



Pentobarbital: 100 m g IV in repeated doses as necessary for m ore severe reactions



Prom azine: 25 m g IM q30m in as needed, up to 125 m g



Propranolol: 0.5â€“1.0 m g IV; 10â€“40 m g PO

Pediatric Considerations 

Treatm ent with opioids is the preferred initial therapy for neonates with neonatal abstinence syndrom e:

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

Medications: o

Chlorprom azine 0.55 m g/kg q6h IM or PO: 

Lim ited usefulness in neonate secondary to side effects of cerebellar dysfunction, decreased seizure threshold, and hem atological problem s

o

Clonidine 0.5â€“1.0 m g/kg single dose followed by m aintenance dose of 3â€“5 m g/kg/d div. q4hâ€“q6h

o

Methadone 0.05â€“0.1 m g/kg q6h

o

Paregoric 0.1 m L/kg or 2 drops/kg with feedings q4h: 

Lim ited usefulness secondary to side effects

o

Phenobarbital 16 m g/kg per 24 hours

o

Tincture of opium (diluted solution) 0.1 m L/kg or 2 drops/kg with feedings q4h

Follow-Up Disposition Admission Criteria 

Sedative-hypnotic: o

Moderate severe or persistent sym ptom s

o

Seizures

o

Psychosis during withdrawal

o

Severe autonom ic instability or delirium should be adm itted to an intensive care unit





Opiates: o

Medical conditions that m ay com plicate withdrawal

o

Intractable vom iting

Sym pathom im etics: o

Extrem ely lethargic or m inim ally responsive m ust be adm itted.

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o

Suicidal patients require psychiatric evaluation and possible adm ission.

Discharge Criteria 

Able to tolerate oral solutions



Not suicidal

References 1. Am erican Academ y of Pediatrics Com m ittee on Drugs. Neonatal Drug Withdrawal. Pediatrics. June 1998;101(6):1079â€“1088. Erratum in: Pediatrics. Septem ber 1998;102(3 Pt 1):660. 2. de Wet C, Reed L, Glasper A, Moran P, Bearn J, Gossop M. Benzodiazepine co-dependence exacerbates the opiate withdrawal syndrom e. Drug Alcohol Depend. October 2004;5;76(1):31â€“35. 3. Ham ilton RJ, Olm edo RE, Shah S, Hung OL, Howland MA, Perrone J, Nelson LS, Lewin NL, Hoffm an RS. Com plications of ultrarapid opioid detoxification with subcutaneous naltrexone pellets. Acad Em erg Med. January 2002;9(1):63â€“68. 4. Lintzeris N, Bell J, Bam m er G, Jolley DJ, Rushworth L. A random ized controlled trial of buprenorphine in the m anagem ent of short-term am bulatory heroin withdrawal. Addiction. 2002 Nov;97(11):1395â€“1404. 5. O'Connor PG, Kosten TR. Rapid and ultrarapid opioid detoxification techniques. JAMA. January 21, 1998;279(3):229â€“334. 6. Olm edo R, Hoffm an RS. Withdrawal syndrom es. Em erg Med Clin North Am . May 2000;18(2):273â€“288. 7. Upthegrove RA, Naik PC. Pharm acological m anagem ent of opiate withdrawal. Hosp Med. May 2001;62(5):277,280â€“281. 8. William s H, Salter M, Ghodse AH. Managem ent of substance m isusers on the general hospital ward. Br J Clin Pract. March 1996;50(2):94â€“98. 9. William s H, Salter M, Ghodse AH. Managem ent of substance m isusers on the general hospital ward. Br J Clin Pract.

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1996;50(2):948. 10. Woods JH, Winger G. Current benzodiazepine issues. Psychopharm acology (Berl). 1995;118(2):107â€“115; discussion, 118, 1201.

Codes ICD9-CM 292.0

ICD10 F11.3 Narcotic withdrawal F13.3 Sedative and hypnotic withdrawal

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wo lff-Parkinso n-White Syndro m e

Wolff-Parkinson-White Syndrome Mitchell Adelstein

Basics Description 

Syndrom e caused by ventricular pre-excitation via an accessory atrioventricular (AV) pathway, the bundle of Kent



Conduction m ay be anterograde, retrograde, or both.



Type A or orthodrom ic is the m ost com m on (70%).



Im pulse travels down the AV node and then up the retrograde pathway: o

A circuit is created that potentiates reentrant tachycardia.



Type B or antidrom ic: o

Less com m on than type A

o

The circuit operates in the opposite direction.

Diagnosis Signs and Symptoms 

Asym ptom atic

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

Palpitations



Dyspnea



Dizziness



Nausea



Abnorm al heart rate: o

Rapid and regular (supraventricular tachycardia [SVT])

o 

Irregular (atrial fibrillation)

Signs of instability: o

Hypotension

o

Change in m ental status

o

Rales

Essential Workup 

Wolff-Parkinson-White (WPW) syndrom e should be considered the underlying etiology in all cases of tachydysrhythm ia.



The diagnosis should be based on the characteristic ECG findings once the patient has converted to a sinus rhythm .

Tests Diagnostic Procedures/Surgery 

ECG in sinus rhythm : o

Short pulse rate, <0.12 seconds

o

Prolonged quasi-random signal (QRS), >0.10 seconds

o

Delta wave: 

Sm all slurred upstroke at the beginning of the QRS

o

ECG m orphology will depend on the degree of preexcitation

Differential Diagnosis 

AV nodal reentry SVT

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

Ventricular tachycardia

Treatment Initial Stabilization Unstable patients: 

Synchronized cardioversion starting with 50 J/m in



Increase increm entally until sinus rhythm is restored.

ED Treatment 

Stable patients with narrow com plex, regular tachycardia: o

Vagal m aneuvers such as Valsalva

o

Right carotid artery m assage for no m ore than 10 seconds: 

Auscultate the artery first for a bruit, which would contraindicate this procedure.

o

Fluid replacem ent and Trendelenburg position if the patient has m ild hypotension



o

Pharm acologic conversion if carotid m assage fails

o

Adenosine

Stable patients with irregular wide com plex tachycardia: o

Procainam ide is the drug of choice.

Alert 

Never use calcium -channel blockers, beta-blockers, or digoxin: o

These m edications prolong the refractory period of the AV node, increasing the rate of transm ission through the accessory pathway, and m ay result in fatal ventricular dysrhythm ias.

P.1239

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Medication (Drugs) 

Adenosine: 6 m g rapid IV bolus over 1â€“2 seconds; if ineffective, repeat with 12 m g (peds: 0.1 m g/kg rapid IV push, repeat with 0.2 m g/kg)



Procainam ide: 6â€“13 m g/kg IV at 0.2â€“0.5 m g/kg/m in until either arrhythm ia controlled, QRS widens 50%, or hypotension, then 2 to 6 m g/m in, m ax. of 1,000 m g

Follow-Up Disposition Admission Criteria 

Patients with signs of instability require adm ission to a m onitored bed.



Failure of outpatient therapy for continuous pharm acologic control or ablation

Discharge Criteria 

Most patients will be stable and can be discharged once converted to sinus rhythm .



Follow-up should be arranged with a cardiologist.

Issues for Referral Electrophysiology studies to assess for radioablation or surgery m ay be perform ed on outpatient basis.

References 1. Al-Khatib SM, Pritchett EL. Clinical features of Wolff-Parkinson-White syndrom e. Am Heart J. 1999;(3 Pt

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1):403â€“413. 2. Donald M. Dysrhythm ias. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St Louis, MO: CV Mosby, 2002:1053â€“1099. 3. Keating L. Electrocardiographic features of Wolff-Parkinson-White syndrom e. Em ergency Medicine Journal. 2003;20(5):491â€“493. 4. Rosner MH. Electrocardiography in the patient with Wolff Parkinson White syndrom e: diagnostic and initial therapeutic issues. Am er J Em er Med. 1999;17(7):705â€“714. 5. Shah CP. Clinical approach to wide QRS com plex tachycardias. Em erg Med Clin North Am . 1998;16:331â€“360. 6. Xie B, Thakur RK, Shah C, et al. Em ergency m anagem ent of cardiac arrhythm ias: clinical differentiation of narrow QRS com plex tachycardias. Em erg Clin North Am . 1998;16:295â€“330. 7. Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 5th ed. Philadelphia, PA: WB Saunders, 1997: 667â€“675.

Miscellaneous SEE ALSO: Pre-excitation Syndrom e

Codes ICD9-CM 426.7

ICD10 I45.6

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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wo und Ballistics

Wound Ballistics

Brian K. Snyder

Basics Description The physical forces that determ ine the wounding potential of gunshot and other penetrating wounds

Etiology 

Wounding potential of bullet is determ ined by m ass and velocity.





The type and severity of a wound is determ ined by: o

Wounding potential

o

Construction and shape of the bullet

o

Orientation upon striking body

o

Deform ity or fragm entation

o

What tissues the bullet traverses

Traditional distinction between low and high m uzzle velocity does not differentiate kind and severity of wounding: o

A civilian hunting rifle or a large caliber handgun with a hollow point bullet m ay produce a m ore severe wound than a round with a full m etal jacket from a â€œhigh-velocityâ€• m ilitary rifle.



Bullets wound by two m ain m echanism sâ€”crush and

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stretch: o

Sonic pressure wave that precedes bullet has no role in wounding.

o

Bullet crushes tissue it directly passes through, form ing perm anent cavity.

o

Stretch is produced by radial energy transferred from bullet as it slows down in tissue, form ing tem porary cavity.

o

A bullet is stabilized in flight by spin transm itted from rifling in the barrel.

o

Spin m inim izes yaw, which is angle between long axis of the bullet and its flight vector.

o

Without spin, a bullet would yaw to its m ost stable flight configuration, which is base and center of m ass forward: 

o

Not aerodynam ically efficient

As bullet enters tissue, spin of bullet is reduced and bullet will yaw.

o

When yaw is 90Â°, a bullet crushes m axim al am ount of tissue, slows down the m ost, and m axim al stretch injury occurs.



Bullets designed to deform in tissue (soft point, hollow point) will expand on im pact:



o

Increases am ount of crush injury

o

Moves bullet center of m ass forward

Jacketed bullets prevent lead stripping in the barrel that occurs at high m uzzle velocities: o

Jacketed bullets do not deform but m ay fragm ent.

o

Fragm entation increases surface area and crush injury.



Bullets striking bone often fragm ent and m ay cause bone fragm ents to becom e secondary projectiles.

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

Wound severity also dependent upon tissue composition and thickness: o

Minim ally elastic tissues, near water-density tissue (brain, liver), fluid-filled (heart, bowel) and dense organs (bone) m ay be injured by the tem porary cavity.

o

More elastic tissue such as lung and skeletal m uscle m ay absorb the energy from tem porary cavity form ation and sustain m inim al dam age.

o

Extrem ities are often not thick enough for the bullet to fully yaw: 

Tem porary cavity form ation is m inim al.



Most dam age is caused by direct crush injury of the bullet, its fragm ents, or secondary projectiles.



Short-range shotgun blasts produce severe wounds with com prom ise of the blood supply: o

In short-range shotgun injuries, pellets m ay be greatly scattered in tissue secondary to the pellets striking each other.



Stab wounds with knives and other sharp instrum ents are low-energy wounds with tissue injury from direct weapon contact.

Diagnosis Signs and Symptoms 

Severe underlying tissue dam age and life-threatening injury m ay occur with even sm all entrance wounds.



A knowledge of how different kinds of weapons and bullets wound, the trajectory of the bullet through the body, and

Pa ge 5 2 7

the effect on different body tissues will allow the physician to carefully evaluate gunshot and stab wounds and their potential m orbidity and m ortality.

History Field personnel can provide inform ation about weapon type and size, distance and angle between the weapon and victim : 

This inform ation m ay not be available or m ay be inaccurate.

Physical Exam Evaluate for entrance and exit wounds: 

May estim ate trajectory and potential for tissue dam age



Exit wounds are often stellate and larger than entranced wounds unless energy is dissipated at skin surface by special bullet type (hollow point, etc.).



With high-velocity projectiles, exit wound m ay be m uch m ore extensive than entrance wound.



Because of elasticity of the skin, bullet can often be palpated subcutaneously.



It is not always possible to differentiate entrance from exit wounds; clinicians do this poorly, so wounds should be only described fully in the m edical record; classification as entrance or exit wounds should be avoided.

Tests Imaging 

Anteroposterior and lateral radiographs help localize bullet: o

With placem ent of m arker at the entrance, wound trajectory can be estim ated

o

Fragm ents, fractures, pneum othoraces, or hem othoraces can be identified.

Pa ge 5 2 7



CT scanning: o

Identify location of projectile.

o

Location and am ount of tissue dam age (especially to the head and brain)



Angiography m ay be necessary if patient has potential vascular injury and surgical exploration not otherwise warranted.

Diagnostic Procedures/Surgery Extent of tissue injury often only apparent on surgical exploration

Treatment Pre Hospital 

Gunshot and stab wounds to chest with unstable vital signs warrant a needle thoracostom y in the side of the chest with entrance wound: o

Relieves tension pneum othorax

o

If no im provem ent, a needle thoracostom y should be placed in the contralateral hem ithorax.

P.1241



Im paled objects or projectiles should not be rem oved: o



Im m obilize with tape and gauze and transport.

Clothing should be preserved if possible: o

Clothing should be cut around holes m ade by the projectiles to preserve evidence.



Patient should be transported to the closest traum a center.



Hypotensive patient m ay be taken directly to the

Pa ge 5 2 7

operating room .

Initial Stabilization Stabilize airway, breathing, and circulation.

ED Treatment 

Im paled objects should be rem oved only in operating room .



In the ED, estim ate tissue injury based on above principles.



Wound care includes appropriate exploration, irrigation, and dÃ©bridem ent of devitalized tissue.



All bullets are contam inated with bacteria and are not sterilized by being fired: o

All nongrazing bullet wounds warrant em piric antibiotics.



Early traum a, orthopaedic, and vascular surgery consultation is necessary.

Medication (Drugs) Prophylactic antistaphylococcal antibiotics should be prescribed for several days: 

Cefazolin: 1 g IV q6h



Cephalexin: 500 m g PO q6hâ€“q8h



For penicillin allergic patients or patients at risk for m ethicillin-resistant S. aureus then vancom ycin 1 g IV q12h or clindam ycin 300 m g PO q6h can be prescribed



Intra-abdom inal wounds require broader coverage (m any regim ens available) such as cefotetan 1 g IV q6h or the com bination of ciprofloxacin 500 m g IV q12h with m etronidazole 500 m g IV q8h

Pa ge 5 2 7

Follow-Up Disposition Admission Criteria 

Patients with neurovascular com prom ise and extensive tissue dam age m ust be adm itted for appropriate surgical intervention.



Patients with injury to the head, neck, torso, or abdom en should be adm itted.



Patients with injury from high-velocity projectiles or gunshot wounds should be adm itted to a m onitored setting for observation of neurovascular status.

Discharge Criteria Patients with m inor penetrating extrem ity traum a or stabbing victim s found not to have significant injury m ay be discharged with appropriate follow-up.

Issues for Referral Em ergent consultation of appropriate surgical specialists should be obtained in patients with potential injuries to vascular or nervous structures.

References 1. Fackler, ML. Gunshot wound review. Ann Em erg Med. 1996;28:194â€“203. 2. Santucci, RA and Chang Y. Ballistics for physicians: Myths about wound ballistics and gunshot injuries. J Urology. 2004;171:1408â€“1414. 3. Swan KG, Swan RC. Principles of ballistics applicable to the treatm ent of gunshot wounds. Surg Clin Am er. 1991;71:221â€“239.

Codes

Pa ge 5 2 7

ICD9-CM E922.9 Unspecified firearm m issile (Gunshot wound NOS, Shot NOS)

ICD10 W43

Pa ge 5 2 7

Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright Â©2007 Lippincott William s & Wilkins > Back o f Bo o k > Appendix > Appendix

Appendix

Emergency Medications Pediatric (Pediatric dose should not generally exceed Drug

Adult

adult dose)

Abcixim ab

0.25 m g/kg IV, then 0.125 N/A

(ReoPro)

m g/kg/m in infusion

Adenosine

6m g IV (rapid) Give 12 m g 0.1 m g/kg IV (rapid);

(Adenocard) (3

IV if no response after 2

give 0.2 m g/kg if no

m g/m L)

m in

response after 2 m in

Albuterol

2.5 m g (0.5 m L) by

0.03 m L (0.15

(Ventolin,

inhalation; m ay repeat;

m g/kg/dose) by

Proventil) (0.5%

MDI available.

inhalation; m ay

soln: 5m g/m L)

repeat

Alteplase (t-PA,

15 m g IV bolus, then 0.75 N/A

Activase)

m g/kg (m ax 50 m g) over 30 m in, then 0.5 m g/kg (m ax 35 m g) over next 60 m in

Am iodarone

Cardiac arrest: 300 m g IV Cardiac arrest: 5 push

m g/kg IV push

Wide com plex tachycardia: Wide com plex 150 m g IV over 10 m in

tachycardia: 5/m g/kg

Pa ge 5 2 7

IV over 20â€“60 m in Am rinone,

0.75 m g/kg over 10â€“15

0.75 m g/kg over

inam rinone

m in; Infusion: 5â€“10

10â€“15 m in;

Âµg/kg/m in

Infusion: infants & children: 5â€“10 Âµg/kg/m in; neonates 3â€“5 Âµg/kg/m in

Anistreplase

30 IU IV over 2â€“5 m in

N/A

5 m g IV q5 m in to 10 m g

N/A

(APSAC) Atenolol

total Atropine (0.1,

0.5â€“1.0 m g IV/ET

0.4, 1 m g/m L)

0.02 m g/kg IV/ET (m in 0.1 m g/dose)

Bicarbonate,

1 m Eq/kg/dose IV q10m in 1 m Eq/kg/dose IV q10

sodium 44, 50

PRN (per ABG)

m Eq/50 m L

m in PRN (per ABG); dilute

Calcium chloride

500 m g/dose IV slowly

20 m g/kg/dose IV

(10% soln: 100

q10m in PRN

slowly q10 m in PRN

m g/m L, 1.36 m Eq Ca Âµ/m L Crystalloid (0.9% Flush: 1â€“2 liters IV over Flush: 20 m L/kg IV NS, LR)

20â€“30 m in

over 20â€“30 m in

Defibrillation

200 joules/dose; double for 2 joules/kg/dose; subsequent dose;

double for subsequent

synchronized: 50â€“100

dose; synchronized:

joules

0.5â€“1.0 joules/kg/dose

Dexam ethasone

5â€“10 m g IM/IV

(Decadron) (4, 24

0.15â€“0.60 m g/kg/dose IM/IV

m g/m L) Dextrose

25â€“50 g IV

0.5â€“1.0 g (2â€“4 m L

Pa ge 5 2 8

(D-50-W: 25 g/50

D-25-W)/kg/dose IV

m L) Diazepam

5â€“10 m g IV

0.2â€“0.3 m g/kg/dose

(Valium ) (5

IV q2â€“5m in slowly;

m g/m L)

0.2â€“0.5 m g/kg/dose PR q5m in

Digibind (40-m g

3â€“5 vials for

Dose (in no. of vials)

vial binds 0.6 m g chronicoverdose;10â€“20

= [(serum digitoxin

dig)

concentration in

vials for acute over dose

ng/m L) (weight in kg)] Ã· 100 Digoxin

Load: 0.5 m g IV initially

Initial loading dose:

followed by 0.25 m g q6h Ã <2 ys: 10 Âµg/kg — 2

2â€“5 ys: 6â€“9 Âµg/kg 5â€“10 ys: 4â€“8 Âµg/kg

Diltiazem

15â€“20 m g (0.25 m g/kg) N/A IV over 2 m in; infusion: 5â€“15 m g/h

Dobutam ine

2â€“20 Âµg/kg/m in IVdrip 2â€“15 Âµg/kg/m in IV

(Dobutrex) (250

m ax 40 Âµg/kg/m in

drip

m g/vial) Dopam ine (40,

5â€“20 Âµg/kg/m in IV drip 5â€“20 Âµg/kg/m in IV

80, 160 m g/m L)

drip

Enalapril

1.25 m g IV over 5 m in

N/A

(enalaprilat)

then 1.25â€“5 m g IV q6h

Enoxaparin

1 m g/kg

N/A

Asystole: 1 m g IV

Asystole: 0.1 m L

q3â€“5m in

(1:10,000) (0.01

(Lovenox) Epinephrine

Pa ge 5 2 8

Anaphylaxis/allergy: 0.3

m g)/kg/dose IV

m L (1:1000) SC q15â€“20

q3â€“5m in PRN. ET,

m in PRN

IO and subsequent IV doses, 0.1 m L (1:1000) (0.1 m g)/kg/dose q3â€“5m in PRN Anaphylaxis/allergy: 0.01 m g/kg (0.1 m L of 1:1000) SC, q15â€“20m in PRN

Epinephrine,

0.5â€“0.75 m L/dose by

0.25â€“0.75 m L/dose

racem ic

inhalation; m ay repeat

by inhalation; m ay

(Vaponefrin)

repeat

(2.25% soln) Eptifibatide

180 Âµg/kg IV, then 2

N/A

(Integrilin)

Âµg/kg/m in infusion

Esm olol

Load: 500 Âµg/kg over 1

Load: 100â€“500

m in

Âµg/kg IV over 1 m in

Infusion: 50â€“200

Infusion: 25â€“100

Âµg/kg/m in to m ax 0.3

Âµg/kg/m in

m g/kg/m in (m ax 300 m g total dose) Fentanyl

0.5â€“1 Âµg/kg/dose slow 1â€“2 Âµg/kg/doses

(Sublim aze) (50

IV up to 50â€“100

low IV upto 4

Âµg/m L)

Âµg/dose

m g/kg/dose

Flum azenil

0.2 m g IV, then 0.3 m g

0.01 m g/kg IV to m ax

followed by 0.5 m g q m in

of 0.2 m g

up to 3 m g Fosphenytoin

15â€“20 m g phenytoin

15â€“20 m g phenytoin

equivalents/kg IV/IM

equivalents/kg IV/IM

Pa ge 5 2 8

Furosem ide

20â€“40 m g IV

1 m g/kg IV

1 m g q5m in, m ax 5 m g

0.03â€“0.1 m g/kg

(Lasix) (10 m g/m L) Glucagon

IV/IM/SC q5â€“20m in, m ax 1 m g Heparin

Hydralazine

80 IU/kg IV, then 15â€“18 50â€“75 IU/kg then IU/kg/h

15â€“25 IU/kg/h

10â€“20 m g IM/IV

0.1â€“0.2 m g/kg/dose

(Apresoline) (20

IV/IM; m ax 20 m g

m g/m L) Insulin, regular

DKA: 2â€“10 units/h IV

DKA: 0.05â€“0.2 units/kg/h IV drip

Isoproterenol

2â€“10 Âµg/m in

(200 Âµg/m L)

0.05â€“2 Âµg/kg/m in IV drip

Labetalol

Load: 20 m g/dose IV

Load: 0.25â€“1.0

(Norm odyne) (5

q10m in upto 300 m g

m g/kg/dose IV slow

m g/m L)

Maintenance: 0.5â€“2

push; m ay repeat i

m g/m in

0.4â€“1 m g/kg/h, m ax 3 m g/kg/h

Lidocain

Load: 1â€“1.5 m g/kg/dose Load: 1 m g/kg/dose

(Xylocaine) (10,

IV (or ET) q5â€“10m in PRN IV (or ET) q5â€“10m in

20 m g/m L)

up to 3â€“5 m g/kg m ax 3

PRN upto 3â€“5 m g/kg

m g/kg

Maintenance: 20

Maintenance: 1â€“4m g/m in Âµg/kg/m in IV drip IV drip Lorazepam

0.5â€“2 m g IV/IM/PO up to 0.05â€“0.15

(Ativan) (2, 4

5 mg

m g/kg/dose IV/IM

m g/m L) Magnesium

1â€“2 g IV Pree clam psia: 25â€“50 m g/kg over

sulfate

4 mg

10 m in

Pa ge 5 2 8

Mannitol (200,

Load: 0.5â€“1g/kg

Load: 0.5â€“1 g/kg

250 m g/m L)

Maintenance: 0.25â€“0.5

Maintenance:

g/kg

0.25â€“0.5 g/kg

5 m g IV q5m in to 15 m g

N/A

Metoprolol

total Midazolam

1â€“2.5 m g, m ax 2.5â€“5

0.05â€“0.1

(Versed) (1

mg

m g/kg/dose IV

Morphine (8, 10,

0.1â€“0.2 m g/kg/dose

0.1â€“0.2 m g/kg/dose

15 m g/m L)

IV/IM up to 15 m g

IV/IM

Naloxone

1â€“2 m g IV, IM, ET

0.1 m g/kg/dose IV

Nitroglycerin

5 Âµg/m in IV drip, titrate

0.25â€“0.5

(Tridil) (0.5 m g,

up as needed

Âµg/kg/m in IV drip,

m g/m L)

(Narcan) (0.4, 1 m g/m L)

0.8 m g, 5 m g, 10

titrate up as needed

m g/m L) Nitroprusside

Norepinephrine

0.10 Âµg/kg/m in up to 5.0 0.10 Âµg/kg/m in up to Âµg/kg/m in

5.0 Âµg/kg/m in IV

0.5 Âµg/m in IV up to 30

0.05â€“0.1

Âµg/m in

Âµg/kg/m in IV and titrate m ax 1â€“2 Âµg/kg/m in

Pancuronium

0.1â€“0.15 m g/kg/dose IV 0.04â€“0.1

(Pavulon) (1,2

q30â€“60 m in

m g/m L) Phenobarbital

m g/kg/dose IV q30â€“60m in

Load: 15â€“20 m g/kg/dose Load: 15â€“20

(65, 130 m g/m L) IV (<25â€“50 m g/m in)

m g/kg/dose IV(<1 m g/kg/m in)

Phenytoin

Seizure load: 10â€“20

Seizureload: 10â€“20

(Dilantin) (50

m g/kg/dose IV (<40

m g/kg/dose IV (<0.5

Pa ge 5 2 8

m g/m L)

m g/m in) up to 1000 m g;

m g/kg/m in);

fosphenytoin (Cerebyx)

fosphenytoin

perm its m ore rapid

alternative

adm inistration, also Procainam ide

Load: 20 m g/m in IV to

Load: 2â€“6

m ax dose 17 m g/kg

m g/kg/dose over 5

Infusion: 1â€“4 m g/m in

m in (m ax dose: 100 m g/dose); repeat dose q5â€“10m in PRN up to a total m ax of 15 m g/kg; do not exceed 500 m g in 30 m in Maintenance: 20â€“80 Âµg/kg/m in by continuous infusion

Propranolol

1 m g IV over 10 m in q5m in 0.01â€“0.1

(Inderal) (1

to total dose 5 m g

m g/m L)

m g/kg/doses low IV over 10 m in; m ax 1 mg

Reteplase

10 IU IV over 2 m in,

(Retavase)

repeat in 30 m in

Streptokinase

1.5 m illion IU over 1 h

N/A

N/A

infusion Succinylcholine

1â€“1.5 m g/kg/dose IV

1â€“1.5 m g/kg/dose

(Anectine) (20

upto 150 m g

IV

30â€“50 m g IV bolus

N/A

0.25 m g SC

0.01 m L/kg/dose SC

m g/m L) Tenecteplase (TNKase) Terbutaline

Nebulized:

Pa ge 5 2 8

0.01â€“0.03 m g/kg/dose in 2m L saline Thiopental

3â€“5 m g/kg IV

2â€“5 m g/kg IV

Tirofiban

0.4 Âµg/kg/m in for 30 m in N/A

(Aggrastat)

then 0.1 Âµg/kg/m in

Vasopressin

40 U I.V

N/A

Vecuronium

0.1 m g/kg/dose IV

0.1 m g/kg/dose IV

2.5â€“5.0 m g IV; then

N/A

(Norcuron) (10 m g/m L) Verapam il

5â€“10 m g IV

Figure 0.1. Sensory derm atom al segm ents. (Reproduced with perm ission from Harwood-Nuss A, Wolfson AB, Linden CH, et al. eds. The clinical practice of em ergency m edicine, 3rd ed. Philadelphia; Lippincott William s & Wilkins, 2001:1789. )

Page 5286

Pediatric Vital Signs and Resuscitation Equipment Sizes 6

1

m

2 5 0

o 1 y y y T n y e e e e t e a a a r h a r r r ms r s s s A 2 8 1 1 2 3 p â k 0 3 0 5 p € g k k k k r “

g g g g

o 4 xi k mg at e W ei g ht Vital Signs 6 8 9 9 9 1 B0 9 6 9 9 1 P Â Â Â Â Â 2 (s ± ± ± ± ± Â y 1 2 3 2 2 ± st 0 9 0 5 0 1

Page 5287

ol

9

ic ) m m H g 1 1 1 1 1 7 2 3 2 1 0 5 H 5 0 5 5 0 R 4 3 3 2 2 2 0 8 9 8 7 1 R Â Â Â Â Â Â R ±±±±±± 1 1 1 4 6 4 0 0 1 Resuscitation 8 1 2 2 4 7 J 6 0 6 0 0 D

J J J J J

ef ib ri ll at io n 2 4 5 7 2 2 â â â â 0 5 C € € € € â â

Pa ge 5 2 8

a “ “ “ “ € € r 4 8 1 1 “ “ di J J 0 3 4 7 o

J J 0 0

v

J J

e rs io n 8 8 8 1 1 1 SF â â 0 0 2 u

€ € F F F

ct

“ “

io

1 1

n

0 0

c

F F

at h et e r Airway 1 1 1 2 2 2 L (s â â (s (s â a t) € € t/ t/ € r

“ “ c) c) “

y

2 2

3

n

(s (s

(s

g

t) t)

t/

o

c)

sc

Pa ge 5 2 8

o p e bl a d e 3. 3. 4. 4. 5. 6. E0 5 0 5 0 5 n â â â

â

d € € €

€

ot “ “ “

“

r 3. 4. 4.

5.

a 5 0 5

5

c h e al tu b e ( m m ) 1 1 1 1 1 1 L 0. 2 2 3. 6. 9. ip 5

5 5 5

â € “t

Pa ge 5 2 9

ip le n gt h ( m m ) Tubes 5 8 1 1 1 1 /

0 0 0 2

N 6

â

a

€

s

“

o

1

g

2

a st ri c tu b e 5 5 8 1 1 1 fe â fe 0 0 0 U e € e F F F ri di “ di ol ol ol n n 8 n e e e a g fe g y y y r tu e tu

Pa ge 5 2 9

y b di b c e n e at

g

h

tu

et

b

e

e

r 1 1 1 1 2 2 0 4 6 4 0 8 C â â â â â â h € € € € € € e “ “ “ “ “ “ st 1 2 2 2 2 3 tu 2 0 0 4 8 2 b e (F r e n c h )

Temperature Conversion: Celsiusâ†” Fahrenheit

Page 5292

F

F

a

a

h

h

r

r

C e C e el n el n si h si h u ei u ei s t s t 3 9 3 1 4. 3. 8. 0 2 6 6 1. 4 3 9 3 1 4. 4. 9. 0 6 3 0 2. 2 3 9 3 1 5. 5. 9. 0 0 0 4 2. 9 3 9 3 1 5. 5. 9. 0 4 7 8 3. 6 3 9 4 1 5. 6. 0. 0 8 4 2 4. 3 3 9 4 1 6. 7. 0. 0

Page 5293

2 1 6 5. 1 3 9 4 1 6. 7. 1. 0 6 8 0 5. 8 3 9 4 1 7. 8. 1. 0 0 6 4 6. 5 3 9 4 1 7. 9. 1. 0 4 3 8 7. 2 3 1 4 1 7. 0 2. 0 8 0. 2 8. 0

0

3 1 4 1 8. 0 2. 0 2 0. 6 8. 7

7

Â°F = 9/5 Ã— Â°C + 32

Weight Conversion: Poundsâ†” Kilogram

Page 5294

1 4. 1 4 0 5 1 9. lb 3 0 8 k lb 9 g

k g

2 9. 1 5 0 0 2 4. lb 7 0 4 k lb 3 g

k g

3 1 1 5 0 3. 3 8. lb 6 0 9 0 lb 6 k

k

g

g

4 1 1 6 0 8. 4 3. lb 1 0 5 4 lb 0 k

k

g

g

5 2 1 6 0 2. 5 8. lb 6 0 0 8 lb 4 k

k

g

g

6 2 1 7

Page 5295

0 7. 6 2. lb 2 0 5 1 lb 7 k

k

g

g

7 3 1 7 0 1. 7 7. lb 7 0 1 5 lb 1 k

k

g

g

8 3 1 8 0 6. 8 1. lb 2 0 6 8 lb 4 k

k

g

g

9 4 1 8 0 0. 9 6. lb 8 0 1 2 lb 8 k

k

g

g

1 4 2 9 0 5. 0 0. 0 3 0 7 lb 6 lb 2 k

k

g

g

kg = lb Ã— 2.2

Pa ge 5 2 9

Rapid-Sequence Intubation 1. Preo xyg enat e with 100 % oxy gen 2. Lido cain e: 1 m g/ kg IV push (opt iona l for seve re HTN /â†‘ ICP/ bron chos pas m)

Page 5297

3. Defa scic ulati ng dose (opt iona lâ€” see tabl e belo w) 4. Atro pine : 0.02 m g/ kg IV push (for child ren < 5 year s old) 5. WAI T 3

Pa ge 5 2 9

MIN UTE S 6. Succ inylc holi ne: 1.5 m g/ kg IV push 7. Sed ativ e age nt (opt iona l): eto m id ate 0.2â €“0. 4 m g/ kg or thio

Pa ge 5 2 9

pent al* 3â€“ 5 m g/ kg (for â†‘ ICP) IV push 8. Appl y cric oid pres sure 9. WAI T 30 SEC OND S 10. Intu bate whe n opti m al cond ition

Pa ge 5 3 0

s achi eve d * Avoid in traum a and hypovole m ia.

Neuromuscular Blocking Agents D o D s o a s g a e g ( e p (f a a

D

r s

u

A al p O r g y r n a e ti o s ti n c * e o t ) ) t n S R

3 4

u S

0 â

c I:

â €

Page 5301

ci 1

€ “

n â

“ 6

yl €

6 m

c “

0 in

h 2

s

ol m i g n / e k g R R 0. 2 3 o S 0 m0 c I: 6 in m u 0. m

in

r 6 g o â / n € k i “ g u 1. m2 m g / k g M : 0. 6 m g

Pa ge 5 3 0

/ k g V R 0. 2. 2 e S 0 5 5 c I: 1 â â u 0. m € € r 0 g “ “ o 1 / 5 4 n 5 k m0 i â g in m u €

in

m“ 0. 2 5 m g / k g M : 0. 1 m g / k g A M 0. 3 2

Pa ge 5 3 0

tr : 0 â 0 a 0. 4 € â c 4 m“ € u mg 5 “ ri g / m 3 u / k in 5 mk g

m

g

in

P M 0. 3 4 a : 0 â 5 n 0. 1 € â c 1 m“ € u mg 5 “ r g / m6 o / k in 0 n k g

m

i g

in

u m * fas pro, fasciculati on prophylax is/defascic ulating dose; RSI, rapid-seq uence intubation ;

Pa ge 5 3 0

M, m aintena nce dose.

Sedative and Induction Agents Do Se sa da ge

Du

tiv IV On rat e

P set ion

Eto 0.2 60 3â mi â€“ s

€“5

da 0.6

mi

te m g

n

/kg Fe ind 60 30 nt uct s

â€“

an ion

60

yl :

mi

2â

n

€“1 0 Âµ g/k g sed

Page 5305

ati on (tit rat e): 2â €“4 Âµ g/k g Ke 2.0 30 15 ta m g â€“ m i mi /kg 60 n ne

s

Mi ind 2

1â

da uct m i €“2 zol ion n

h

am : 0.0 7â €“0 .3 mg /kg sed ati on (tit rat e): 0.0

Pa ge 5 3 0

2â €“0 .04 mg /kg Thi 3â 20 5â op €“5 â€“ €“1 en m g 40 0 tal /kg s

mi n

Page 5307