1600 John F. Kennedy Blvd. Suite 1800 Philadelphia, PA 19103–2899
ESSENTIAL EMERGENCY MEDICINE: FOR THE HEALTHCARE PRACTITIONER Copyright # 2007 by Saunders, an imprint of Elsevier Inc.
ISBN: 978–1–4160–2971–7
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editor assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book.
Library of Congress Cataloging-in-Publication Data Essential emergency medicine : for the healthcare practitioner / [edited by] Steven W. Salyer. – 1st. p. ; cm. Includes bibliographical references. ISBN 1–4160–2971–0 1. Emergency medicine–Handbooks, manuals, etc. I. Salyer, Steven W. [DNLM: 1. Emergencies–Handbooks. 2. Emergency Medicine–Handbooks. WB 39 E768 2007] RC86.7.E785 2007 616.02'5–dc22
2007000839
Acquisitions Editor: Rolla Couchman Developmental Editor: Mary Beth Murphy Project Manager: Bryan Hayward Design Direction: Steven Stave
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Dedication To my wife Sally, my daughter Laura Emilie, and my son Zachary who gave up so much “daddy” time while I wrote and edited this second book. And to all those Physician Assistants and physicians who have chosen the profession of Emergency Medicine and who still go to work everyday still caring about the lives, hearts, and souls of their patients. And a special prayer for all those men and women on the frontiers of freedom who everyday defend our way of life and keep us all free. God bless all of you!
Contributors GREG A. ABRAHAMIAN, MD Assistant Professor of Surgery, Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Renal Transplantation
JONATHON ALLEN, MD Department of Emergency Medicine, Medical College of Georgia, Augusta, Georgia Chapters 08. Diabetic Ketoacidosis; Hyperglycemic Hypersmolar Nonketotic Coma; 19. Acute Renal Failure
CULLEN ARCHER, MD Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Ectopic Pregnancy; Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia)
MICHAEL A. AROCHO, MD,CPT, USAF United States Air Force Chapter 17. Lead; Mercury
SIMEON W. ASHWORTH, DO,CPT, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapter 03.Toxicodendron Dermatitis
DAVE BARRY, MD, MAJ, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 17. Barbituates; Hallucinogens
CHARLES R. BAUER, MD,CPE, FACS, FACPE, FACEP Director, Center for Public Health Preparedness & Biomedical Research, Professor of Surgery & Emergency Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18. Abdominal Trauma; Pelvic Trauma; Thoracic Trauma; Trauma in the Pregnant Patient
ROGER MATTHEW BAUTISTA, MD,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 07.Tetanus; 10. Ovarian Cysts
MARY ANN BROWNING, FNP Family Nurse Practitioner, Oregon Health & Sciences University, Instructor, Department of Emergency Medicine, Portland, Oregon Chapters 04. Jaundice and Hepatitis; 13. Dehydration in Children; 19. Urinary Tract Infections in Adults
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CONTRIBUTORS
JOHN H.CALHOON, MD Professor, Department of Surgery, Chief, Division of Cardiothoracic Surgery, University of Texas Health Science Center, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
JASON CAPRA, MD United States Air Force, Medical Corps Chapter 17.Cyanide
BARBARA A.CARR, MD,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Spider Bites and Scorpion Stings; 12. Acute Ankle Injuries
ROBERT L.CLOUTIER, MD Oregon Health and Sciences University, Department of Emergency Medicine, Portland, Oregon Chapter 13. Electrolyte and Fluid Management in Pediatric Patients
JIMMY COOPER, MD CAPT, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapter 02. Permanent Pacemakers
STEPHEN A.CRANDALL, MD Division of Emergency Medicine, University of Washington, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Asthma
CHRISTOPHER B.CROWELL, MD University of Washington, Emergency Medicine Residency, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Abdominal Pain
RICHARD L. DAGROSA, MD U.S. Air Force, Medical Corps Chapter 07. Herpes Virus
CHARLES P. DAVIS, MD, PHD Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 19.Common Disorders of the Penis
MOHAMUD DAYA, MD Associate Professor of Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapter 17.Clonidine; Phenytoin
MARC L. DAYMUDE, MD, FACEP United States Army, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 01. Abdominal Aortic Aneurysm (AAA); Appendicitis; Hernias; Intestinal Obstruction; Thoracic Aortic Dissection
Contributors
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JOHN T. DEEL, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
CARRY DEPOLD, PA-C Physician Assistant, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 12. Elbow Injuries; 17. IronToxicity
GERALD D. DEPOLD, PA-C, MPAS Captain, Army Medical Specialist Corps Chapters 06.Thermal Burns; 12. Elbow Injuries
DIANE DEVITA, MD, FACEP Staff Physician, DEM MAMC, Assistant Clinical Professor, University of Washington Chapter 13. Asthma
AMY K. DITZEL, PA-C Family Practice Physician Assistant Chapters 07, Influenza; 10. Emergent Pelvic and Abdominal Pain; Genital Herpes
MARTIN A. DOCHERTY, MD, MAJOR, USAR Clinical Instructor, Division of Emergency Medicine, Washington University School of Medicine, Attending Physician, Barnes-Jewish Hospital, St. Louis, Missouri Chapters 02.Congestive Heart Failure; Hypertensive Emergencies; 07. HIV Infections; 08. Geriatric Emergencies
GARY W. DUFRESNE, DO,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 09. Seizures and Status Epilepticus
JENNY E. DUNLAVY, MD,CPT, USAF Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas Chapters 06. Snakebite Injuries; 12. Foot Injuries
STEVE DURNING, MD, FACP Director, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland Chapter 02. Mitral Valve Prolapse
TERRY EMANUEL, PA-C, MPAS Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Lactic Acidosis; 19. End-Stage Renal Disease
x CONTRIBUTORS
ALFREDO ESPINOZA, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Liver Transplantation
ROBERT M. ESTERL, MD Professor of Surgery, Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Renal Transplantation
BARBARA M. FISHMAN, MD Associate Professor, Department of Medicine, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Acid^Base Problems; Fluid and Electrolyte Emergencies; 17.Cocaine
JEFF FOXWORTH, PA-C Division of Plastic Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18.Trauma Overview
MARK S. FUNK, MD Department of Obstetric and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Sexual Assault
RYAN GARNER, MD United States Air Force, Medical Corps Chapter 13. Neonatal Emergencies; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot
DAVID GLENDENING, MD Associate Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 15. Adult Bacterial Pneumonias
VINITA GOYAL, MD Department of Obstetrics and Gynecology, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 10. Miscarriage (Abortion)
ROBERT D. GRAYDON, PA-C, MPAS Faculty Associate, Department of Surgery, Division of Emergency Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Acute Ethanol Withdrawal; 17.General Principles of the Poisoned Patient; Anticholinergics; Ethanol Intoxication; Ethylene Glycol; Opioids
Contributors
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LEN GRUPPO, PA-C,CPT, SP, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 02. Acute Pericarditis; Cardiac Examination; Evaluation of Cardiac Chest Pain
GLENN HALFF, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. LiverTransplantation
BENJAMIN P. HARRISON, MD, FACEP, LTC, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapters 03.Toxicodendron Dermatitis; 08. Adrenal Insufficiency; 12. Hand Injuries
KATHERINE ANNE HARRISON, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 10. Pelvic Inflammatory Disease; Toxic Shock Syndrome; Vulvovaginitis; 12. Shoulder Injuries
GUYON J. HILL, MD,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 03.Toxic Epidermal Necrolysis; 06. Lightning Injuries; 17. Hydrocarbons; Isoproponal; Methanol
DAVID A. HNATOW, MD Associate Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 04.Gastrointestinal Bleeding; Acute and Chronic Pancreatitis; 06.Chemical Burns
REX L. HOBBS, JR., MPAS, PA-C Assistant Professor, UT Southwestern Medical Center-Dallas, Dallas, Texas Chapters 07. Diphtheria; 09. Bell’s Palsy; Botulism; Multiple Sclerosis; Myasthenia Gravis; Neurological Examination
JULIE HUSLEY, PA-C Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 13. Bronchiolitis; Constipation; Sudden Infant Death Syndrome and Apparent Life-Threatening Event Syndrome
JENNIFER JAMUL, PA-C Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 07. Foodborne and Waterborne Infections
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CONTRIBUTORS
ROY JOHNSON III, MD Uniformed Services University of the Health Sciences, Andrews Air Force Base Chapters 13. Pediatric Airway Management; Pediatric Analgesia and Sedation; 17. Cyanide; Theophylline
SCOTT B. JOHNSON, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
MELISSA KAGARISE, MMS, PA-C Department of Physician Assistant Studies, Saint Francis University, Lorretto, Pennsylvania Chapter 13. Pediatric Pneumonia; Pharyngotonsillitis; 15. Aspiration Pneumonia
SANDEEP J. KHANDHAR, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
C.GORDON KING, MD Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 08. Fluid and Electrolyte Emergencies
JOHN T. KODOSKY, PA-C, MMS Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center, San Antonio, Texas Chapters 04. Peptic Ulcer Disease; 18. Head and Brain Trauma
ADAM CLAY KOERTNER, MD,CAPT United States Air Force, Medical Corps Chapter 08. Hyperthyroidism and Thyroid Storm (Thyrotoxicosis); Hypothyroidism and Myxedema Coma
CHRISTOPHER M. KREBS, MD,CPT, MC, USA Uniformed Services University of the Health Sciences, Andrews Air Force Base, Maryland Chapter 17.Theophylline
DAVID W. KUHNS, MD, FACEP Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapters 03. Urticaria; 13. Kawasaki Disease
KHIM K. LAM, MD Department of Obstetrics and Gynecology, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 10. Abruptio Placentae; Amniotic Fluid Embolism
Contributors
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LINDA L. LAWRENCE, MD, FACEP COL, USAF, MC Chief of Medical Staff, Emergency Medicine Consultant to Air Force Surgeon General Chapter 13. Neonatal Emergencies; Pediatric Airway Management; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot; Pediatric Analgesia and Sedation
DEREK R. LINKLATER, MD, FACEP, FAAEM Assistant Program Director, Darnall Army Community Hospital EM Residency Program, Assistant Clinical Professor of Emergency Medicine, Texas A&M School of Medicine, Assistant Clinical Professor of Military and Emergency Medicine, USUHS School of Medicine Chapter 15. Pulmonary Embolism
REENIE LOPEZ, PA-C Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 13. Febrile Seizures
CLIFFORD C. LUTZ, MD MAJOR, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 06. Hymenoptera Stings
JUSTIN MADILL, DO CPT, MC, USA Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 06. Submersion Incidents
ANANTHA K. MALLIA, DO Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 17. AcetaminophenToxicity; Cyclic Antidepressant Toxicity; Digitalis Glycoside Toxicity
MARGARET MANN-ZEBALLOS, MD Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 19. Prostatitis
DANIEL F. MCBRIDE, MD United States Army, Medical Corps Chapter 13. Otitis Media
SAMUEL TIMOTHY MCILRATH, MD Medical College of Georgia, Augusta, Georgia Chapter 13. Pediatric Bacteremia, Sepsis, and Meningitis; Pediatric Diarrhea
xiv CONTRIBUTORS
JOHN MCMANUS, MD, MCR, FACEP, LTC, MC, USA Clinical Investigator at Army Institute of Surgical Research, Brooke Army Medical Center, San Antonio, Texas; Adjunct Assistant Professor Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapters 06. Altitude-Related Conditions; Frostbite; Hypothermia; 13.Cardiopulmonary Arrest in Children
CHRISTOPHER R. MCNEIL, MD,CPT, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 02. Automatic Implantable Cardioverter-Defibrillators; Cardiac Arrhythmias; Cardiac Tamponade; Prosthetic Heart Valve Dysfunction; Heart Transplant; 08. Rhabdomyolysis; 13. Pediatric Cardiopulmonary Resuscitation; Pediatric Diabetes and Pediatric Diabetic Ketoacidosis
SUMERU GHANSHYAM MEHTA, MD,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Heat Injuries; 10. OvarianTorsion; 19.Torsion of the Testicle
CARL MENCKHOFF, MD, FACEP, FAAEM Associate Professor, Residency Director, Department of Emergency Medicine, Medical College of Georgia, Augusta, Georgia Chapters 01.Wound Management; 12. Injuries to the Forearm and Wrist; Injuries to the Lower Leg
KAZUO MIHATA, MD United States Air Force, Medical Corps Chapter 13. Neonatal Emergencies; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot
MICHAEL A. MILLER, MD, LTC, MC, USA Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapter 17. Amphetamines; Lithium; Organophosphorus and Carbamate Insecticides Poisoning
JAMES ALAN MORGAN, DO,COL, MC, USA (RET) Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 06. Marine Fauna Evenomations; 15. Acute Respiratory Distress Syndrome; Hemoptysis; 17.Carbon Monoxide
JULIE ANN MORGAN, MD,COL, MC, USA (RET) Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Electrical Injuries; Marine Fauna Evenomations; 15. Acute Respiratory Distress Syndrome; Hemoptysis; 17.Carbon Monoxide
KARI MURPHEY, PA-C Emergency Medicine Physician Assistant, Medical College of Georgia, Augusta, Georgia Chapter 19. Renal Stones
Contributors
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YOKO NAKAMURA, MD Visiting Physician, Department of Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapter 17.Clonidine; Phenytoin
ALICIA NASIR, RN, BSN Andrews Air Force Base, Maryland Chapter 02. Mitral Valve Prolapse
JAVED M. NASIR Medical Student, Uniformed Services University of the Health Sciences Chapter 13. Acute Rheumatic Fever
ROBERT NOLAN, DO,CPT, MC, USA Chief Resident, Emergency Medicine, Madigan-University of Washington, Tacoma, Washington Chapter 15. Pneumothorax
BRENDA OSWALD, PA-C, MHE Physician Assistant in Emergency Department at Medical College of Georgia, Assistant Emergency Medicine Physician Assistant Residency Director, Clinical Faculty with Physician Assistant Department, Augusta, Georgia Chapter 12, Injuries to the Forearm and Wrist; Injuries to the Lower Leg
STACEY BLACK PEARLMAN, PA-C, MPAS Saint Vincent Hospital at Worcester Medical Center, Worcester, Massachusetts Chapter 15.The Basics of Ventilator Management in the Emergency Department; Ventilator Settings and Ongoing Monitoring of Critical Patients in the Emergency Department; Sedation and Analgesia in the Intubated Patient
JAMES A. PFAFF, MD,COL, MC, USA (RET) Brooke Army Medical Center, Department of Emergency Medicine, Fort Sam Houston, Texas Chapter 05. Dental Emergencies; Maxillofacial Injuries; Ophthalmological Emergencies; Otolaryngolical Emergencies; Pharyngitis; Sialolithiasis; Sinusitis; Dental Trauma
KRISTEN A. PLASTINO, MD Assistant Professor, Program Coordinator, Sex Education Program, Associate Residency Program Director, Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Placenta Previa
ERIC R. PRESSER Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
xvi CONTRIBUTORS
LON RAMEY, PA-C Faculty Associate, Division of Neurosurgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18. Spinal Cord Injuries
JAKE ROBERTS, DO,CPT Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Urinary Tract Infections in Children
DAWN F. RONDEAU, RN, MS, ACNP-CS Acute Care Nurse Practitioner, Washington State University, Pullman, Washington Chapter 13. Upper Respiratory Emergencies in Children
STEVEN W. SALYER, PA-C,CPT, USA (RET) Emergency Medicine Physician Assistant, San Antonio, Texas Chapters 09. Ataxia, Dizziness, and Vertigo; Headaches; 12. Basic Principles of Orthopedic Injuries; Acute Back Pain; 13.The Pediatric Patient: An Overview; Seizures and Status Epilepticus; 15.Chronic Obstructive Pulmonary Disease; 18. Genitourinary Tract Trauma; Pediatric Trauma
KATHLEEN M. SAMSEY, MD,CPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 12. Hip Trauma
JOHN ROBERT SCOTT, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 11. Blood Transfusions; 13. Reye’s Syndrome
MICHAEL K. SHAFE´, MD, FACEP, FAAEM Assistant Professor Department of Emergency, Medical College of Georgia, Augusta, Georgia Chapters 08. Disseminated Intravascular Coagulation; 11. Acute Bleeding Diathesis; Hemophilia; Sickle Cell Anemia
MARK S. SHORT, PA-C,CAPT U.S. Army Chapter 12. Hand Injuries
SEAN MICHAEL SILER, DO,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 06. Diving Injuries
JACQUELYN L. SIMONDS, PA-C, MPAS Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapters 10. Breast Abscesses and Mastitis; 13. Kawasaki Disease
Contributors
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HOWELL J. SMITH III, PA-C,CPT, USA (RET) Orthopedic Physician Assistant, Veterans Administration, Tampa, Florida Chapter 12. Acute Knee Pain
K.VINCENT SPEEG, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. LiverTransplantation
RICHARD J. SPITZ, MD Clinical Assistant Professor, Department of Surgery, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 03. Erythema Multiforme; 08. Alcoholic Ketoacidosis
LAURA ANN SPIVAK, MD Medical Toxicology, Oregon Health and Science University, Department of Emergency Medicine, Oregon Poison Center, Portland, Oregon Chapter 17. Arsenic; Beta-Blocker Overdose; Calcium-Channel Blockers; Caustic Ingestions
MARK STEVENS, PA-C,CPT, USA (RET) Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 17. Salicylates
BENJAMIN H.TAYLOR, PHD, PA-C Medical College of Georgia, Augusta, Georgia Chapters 03. Exfoliative Dermatitis; 12. Infections of the Bones and Joints
RALPH TERPOLILLI, MD Associate Professor, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 09. Acute Stroke Syndromes
SHAWN M.VARNEY, MD, LTCOL, USAF, MC Flight Commander, 959 MSFS, Wilford Hall Medical Center, Lackland Air Force Base, Texas Chapters 04. Diverticulosis and Diverticulitis; 08. Hypoglycemia
BROOKE ASHLEY VEALE, PA-C Assistant Professor, Department of Physician Assistant Studies, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas Chapters 07. Malaria; 14. Panic Disorder; Generalized Anxiety Disorder; Conversion Disorder; Personality Disorders; Paranoid Personality Disorder; Schizoid Personality Disorder; Schizotypal Personality Disorder; Antisocial Personality Disorder; Borderline Personality Disorder; Histrionic Personality Disorder; Narcissitic Personality Disorder; Avoidant Personality Disorder; Dependent Personality Disorder; Obsessive-Compulsive Personality Disorder; Suicide
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CONTRIBUTORS
SHAWNA WALL, MD Department of Obstetric and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Hyperemesis Gravidarum
KENNETH WASHBURN, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Liver Transplantation
IAN WEDMORE, MD, FACEP, LTC, MC, USA Assistant Chief, Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 06. Altitude-Related Conditions; Hypothermia
RYAN WELLS, MD Willford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas Chapters 01.Cholelithiasis and Cholecystitis; 15. Asthma
ALLEN WHITFORD, DO, LTC, MC, USA (RET) Assistant Professor, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 16. Airway Management; Shock
CLAUDIO F. ZEBALLOS, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 04. Anorectal Disorders; 07. Rabies; 19. Epididymitis
DAVID ZINSMEISTER, PA-C Assistant Professor, Department of Orthopedics, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 12. Acute Compartment Syndrome; Open Fractures
Preface When I first walked into an “Emergency Room” in 1987, as a young PA student, CTs were just coming into general use. MRIs were an experimental radiological test, tPA and Streptolinase-plasminogen were still “voodoo” medicine and cardiac catheterization labs were not yet in general use. We had to “practice” medicine! Back then we still examined patients. We had to! We did not have the radiological or laboratory tests we had today. We talked to patients and listened to them. Patients told us what was wrong with them. You didn't have to have three specialty consults before you could get someone admitted. No one got sued! Patients and insurance companies paid their bills. Patient's respected doctors and PAs; we respected patients and their beliefs. We asked about their families. We were able to talk about fishing! Emergency Medicine wasn't yet a business. With that said, things have gotten better. If you diagnosed someone with HIV/AIDS in 1987, it was a death sentence. With the four drug therapies of today, the life expectancy of someone with HIV is normal. Cardiac catheterization and stents save thousands of lives yearly. We have orthopedic replacement parts for just about every joint! On the horizon, stem cell research will “cure” many diseases in our lifetime. Gene splicing will prevent future human beings from ever developing the diseases that kill us today. We will develop a vaccine for HIV. Emergency Medicine will change and evolve just like all other medical specialties. But we will always be the “safety net” of society. Emergency Medicine and the “emergency room” will always be the last refuge of the sick, injured, tired, and lonely. We will still see and treat all comers no matter what their insurance is or what side of town they live on. They probably won't pay us. If they think we messed up, they will find a lawyer on TV and sue us. We will still listen and console. We will be social worker, chaplain, big brother, and the giver of hope at 3 AM. We will still see that one last patient 5 minutes before our shift change, and we will always leave late. This book is a continuum of the evolution of Emergency Medicine. I spent 4 years in the 2nd Armored Calvary Regiment in Germany. I am a veteran of Desert Storm I. I have practiced a lot of emergency medicine during my time in the Army in a tracked vehicle and a tent. Whether in a tent or a modern emergency center, the principles of emergency medicine are the same; care for the individual’s body, save lives, and never forget to care about the person.
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xx PREFACE
The 2nd Calvary Regiment is the longest continuous active-duty unit in the U.S. Army (1832). During WWI in France, the regiment obtained the regimental motto of Toujours Pret (always ready). If Emergency Medicine ever had a motto I believe it would also be Toujours Pret. Steven W. Salyer, PA-C
Introduction This is my second book on Emergency Medicine. I wrote the first book in its entirety. This is not a second edition of the first book. I selected the best emergency medicine physician assistants and emergency medicine physicians in the country to contribute to this book. Many of the chapter's authors were or are faculty at Emergency Medicine residencies. These are the best emergency medicine minds I could find. I also sought the best non-emergency medicine minds to write the complementary chapters to the book. There is no better an example of the quality of their writing than in the transplant chapters. I have expanded the transplant chapter to include topics on heart, lung, liver and kidney transplants. These topics are written by some of the best transplant practitioners in the country. This is a unique book in that the contributing chapter authors are Physician Assistants, Nurse Practitioners and physicians. It is edited by a Physician Assistant. This collaboration of different practitioners is unique in the medical publishing community. The evolution of the “team process” is evident in collaboration in the production of this book. With the business concern over billing and reimbursement, we have added ICD codes to the beginning of each chapter. This addition will help with identification of the illness or disease and hopefully will increase reimbursement. We have also added “Key Points” and “Emergency Actions” at the beginning of each topic. In a busy emergency department, the “Key Points” section will serve as a quick reference to give the practitioner the key points of knowledge about the illness or condition. The “Emergency Actions” section of each topic will act as a quick reference for the practitioner to refer to what emergency actions need to be taken immediately. This book is designed to be used, not to sit on a shelf. In a year's time, its corners should be bent and its pages worn. Please enjoy and use this book.
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Chapter 1
Acute Surgical Abdominal Emergencies Abdominal Aortic Aneurysm (AAA) MARC L. DAYMUDE
ICD Code: 441.4
Key Points/Quick Reference Abdominal aortic aneurysm (AAA) is diagnosed in most patients as an incidental finding on examination or radiologic procedure for another reason. Most patients who present with ruptured AAA, a life-threatening condition, are unaware that they have an AAA. Ruptured AAA should be suspected in all patients at risk who report abdominal pain, back or flank pain, or symptoms of hypotension such as syncope, even if transient. ! Emergency Actions ! If an AAA is suspected, two large-bore intravenous (IV) lines should be started, a cardiac monitor should be placed, emergent abdominal ultrasound and computed tomography (CT) scans should be performed, and an emergent surgical consult should be obtained.
DEFINITION An aneurysm is a permanent, focal dilation of an artery to greater than 1.5 times its expected diameter, involving all layers of the arterial wall (i.e., intima, media, and adventitia). Although any artery can develop an aneurysm, it is most commonly found in the infrarenal aorta. An infrarenal aortic diameter of 3 cm or greater is defining. This is a different entity from dissection, in which blood flows through a tear in the intima, resulting in a false lumen and dilation of the artery. Pseudoaneurysms are localized arterial wall ruptures that are contained by the adventitia and fibrous reaction and result in focal arterial wall expansion. They commonly result from trauma, infection, or previous surgical intervention of the arterial wall.
EPIDEMIOLOGY AAA is a disease primarily of the elderly. Risk factors include atherosclerotic disease, age older than 50 years, and hypertension. Smoking is the most important risk factor. Men are affected twice as often as women. AAA in first-degree relatives represents an 11.6-fold increased risk. Patients with connective tissue disorders such as Ehlers-Danlos or 1
2 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Marfan syndromes may develop AAA at an earlier age. Incidence in the United States is estimated at 2%–4% in patients older than 50 years and increases to 5%–10% in men over the age of 65 years. The majority of AAAs occur distal to the renal arteries. Two percent extend proximally to include the renals and thoracic portion of the aorta. Forty percent extend distally to involve the iliac arteries. The natural progression of AAA is to gradually expand, then rupture, resulting in fatal hemorrhage. The average rate of enlargement is 0.4 cm/yr. The risk of rupture increases with diameter. AAAs less than 4 cm in diameter have very low risk of rupture, whereas the risk for 4- to 5-cm AAAs is 1%–3%/yr, for those 5–7 cm is 6%–11%/yr, and for those greater than 7 cm is 20%/yr. The mortality rate for ruptured AAA is 78%–94%, with only half of patients surviving the journey to the hospital. The operative mortality rate for ruptured AAA is approximately 50%. Ruptured AAA accounts for an estimated 15,000 deaths per year in the United States and is the tenth leading cause of death. Seventy-five percent of patients presenting to the hospital with a ruptured AAA are unaware that they have an AAA. AAA management is aimed at prevention of rupture and usually involves elective surgical repair. Elective surgical mortality is less than 5%. Patients who survive repair have an excellent prognosis, with life expectancy similar to nonaffected cohorts. The cause of death in these patients is usually from cardiac causes.
CLINICAL PRESENTATION Most patients are diagnosed with AAA as an incidental finding during physical examination or radiographic procedure performed for another reason; most patients are asymptomatic at the time of presentation. The triad of abdominal pain, palpable pulsatile abdominal mass, and hypotension is present in only 30%–50% of patients with ruptured AAA. Patients often present with atypical complaints. The majority of ruptures are left retroperitoneal and may result in left lower quadrant pain and tenderness. Flank pain mimicking renal colic is common, and ureterolithiasis is misdiagnosed in 10% of patients with AAA. Expansion of a retroperitoneal hematoma may result in compression of nerve roots, most commonly femoral and obturator. Five percent of patients report neurologic problems, including anterior thigh pain and numbness with hip flexor weakness. Syncope, diaphoresis, nausea, and vomiting may be the only symptoms related to transient hypotension. Twelve percent of AAAs are initially diagnosed as diverticulitis. Five percent present with peripheral microemboli resulting in “blue toe syndrome.” Hypotension and shock may dominate the presentation. Retroperitoneal ruptures may tamponade and have delayed presentations of days to weeks. Free intraperitoneal ruptures that occur in 10%–30% result in rapid exsanguination, and these patients rarely survive long enough to make it to the hospital. The
Abdominal Aortic Aneurysm (AAA)
3
expanding mass of the AAA may erode into adjacent structures. Aortoenteric fistula results from erosion into the duodenum (most common) and can present as massive upper gastrointestinal tract bleeding. Erosion into the inferior vena cava results in aortocaval shunting and high-output heart failure manifested as dyspnea, jugular venous distention, venous distention, and pulmonary edema.
EXAMINATION Physical examination is not a reliable method to exclude AAA in the patients at risk. A pulsatile abdominal mass—especially if it extends to the right of midline—is suggestive. However, only 30% of AAAs 3–4 cm in diameter, 50% of AAAs 4–5 cm, and 75% of AAAs greater than 5 cm are palpable. Abdominal bruits are present in only 5%–10% and may indicate atherosclerotic occlusive disease of other vessels. Femoral pulses usually are normal.
LABORATORY FINDINGS Laboratory findings are not helpful in establishing the diagnosis of AAA and may be misleading. Hematuria may result from compression of the ureters and is common in aortocaval fistula due to increased renal vein pressure. This, in the face of reports of flank pain, may suggest ureterolithiasis.
DIAGNOSIS Ruptured AAA should be in the differential diagnosis of any patient over the age of 50 years who presents with flank or abdominal pain, hypotension, or syncope. In a patient whose condition is unstable, a palpable, pulsatile abdominal mass is all that is needed to obtain emergent surgical consultation for immediate surgery. In other patients, ultrasound or CT scans may be necessary to establish the diagnosis.
RADIOGRAPHS Plain radiography of the abdomen may reveal the “eggshell” appearance of a calcified AAA, but it is not helpful in excluding AAA from the differential diagnosis in patients who are at risk. Multiple studies have demonstrated that ultrasound is 100% sensitive in the detection of AAA and that this can be done at the bedside in the emergency department (ED) by emergency physicians using portable ultrasound devices with the same accuracy. ED bedside ultrasound for AAA has been demonstrated to significantly decrease time to diagnosis and disposition. Obesity and bowel
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gas may limit visualization of the aorta in some patients, making diagnosis difficult. All patients who are at risk for AAA should have bedside ultrasound scanning performed in the ED. Stable patients can undergo a formal ultrasound or CT scan. The advantages of CT over ultrasound are that CT can better define the extent of disease, identify retroperitoneal hemorrhage or rupture, or identify alternative diagnoses in the setting of a normal aorta. The major disadvantage is that the patient must leave the ED to go to receive the CT scan, and resuscitation is often difficult in that setting. Aortography is helpful for preoperative planning in elective repairs but is not indicated for diagnosis in the ED.
TREATMENT AND OUTCOME For patients whose AAA is found incidentally and is truly asymptomatic, outpatient referral to surgery for elective repair is appropriate. These patients should be cautioned to return for any symptoms potentially referable to AAA. Patients who have suspected rupture of AAA require access via two large-bore IV lines. Blood samples should be drawn for baseline complete blood count (CBC), blood urea nitrogen (BUN)/creatinine and electrolyte measurements, coagulation studies, and type and cross-match for 10 units of blood. Definitive treatment requires operative repair. An emergency surgical consultation should be made as soon as the diagnosis of ruptured AAA is suspected. Preoperative hypotension is the most important prognosticator of mortality. Patients whose conditions are unstable require aggressive fluid/blood product resuscitation to maintain a systolic blood pressure of 90–100 mmHg or adequate cerebral (i.e., normal mental status) and cardiac (no ischemic chest pain/electrocardiographic changes) perfusion.
Bibliography Barkin AZ, Rosen CL: Ultrasound detection of abdominal aortic aneurysm, Emerg Med Clin North Am 2004;22(3):675–682. Bessen HA: Abdominal aortic aneurysm. In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1176–1186. Lin PH, Bush RL, McCoy SA, et al: A prospective study of a hand-held ultrasound device in abdominal aortic aneurysm evaluation, Am J Surg 2003;186(5):455–459. Rogers RL, McCormack R: Aortic disasters, Emerg Med Clin North Am 2004; 22(4):887–908. Salen P, Mclanson S, Buro D: ED screening to identify abdominal aortic aneurysm in asymptomatic geriatric patients, Am J Emerg Med 2003;21(2):133–135. Zarins CK, Heikkinen MA, Hill BB: Aneurysmal vascular disease. In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1969–1981.
Appendicitis
5
Appendicitis MARC L. DAYMUDE
ICD Code: 541
Key Points/Quick Reference Classically acute appendicitis develops as diffuse, periumbilical pain followed by nausea, vomiting, low-grade fever, and anorexia. Over the course of 12^18 hours, the pain localizes to the right lower quadrant with evidence of local peritoneal irritation on examination. The CBC and differential that usually show an elevated white blood cell count (WBC) with a left shift and normal urinalysis results are the most relevant laboratory findings. Diagnosis may be made purely on the basis of history and physical examination in classic cases, or it may require an ultrasound or CT scan in conjunction with surgical consultation. Treatment is primarily surgical. ! Emergency Actions ! Patients who present having experienced 12–18 hours of abdominal pain and the above symptoms should have their fluids replenished; should be treated for their pain, nausea, and vomiting; and should undergo an emergent abdominal CT scan. If an acute appendicitis is present, an emergent surgical consult should be obtained.
DEFINITION The appendix is an appendage off the base of the cecum of uncertain function. It contains lymphoid and mucus-producing tissues. In an adult, its length averages 9 cm but may range from 2 to 22 cm. The location of the tip varies from retrocecal, intraperitoneal in 65% to pelvic in 30% and retroperitoneal in 2%. Acute appendicitis is an inflammatory process of the appendix, usually precipitated by luminal obstruction caused by lymphoid hyperplasia, appendicolith, fecal material, or other foreign body resulting in bacterial overgrowth.
EPIDEMIOLOGY Normal appendiceal lymphoid tissue gradually increases through adolescence then slowly decreases after the third decade, corresponding to peak incidence of appendicitis in the late teens to 20s. The lifetime risk of acute appendicitis is 8.6% in men and 6.7% in women, with a general
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population perforation rate of 17%–20% and a mortality rate of 0.25%. Although appendicitis is less common in young children and elderly persons, perforation rates are as high as 30%–65% in children and 70% in patients older than 60 years. Children also have a higher rate of general peritonitis. The mortality rate in elderly persons is 4%–8%, and the risk of complications and mortality increase with perforation. Annually, 250,000 appendectomies are performed in the United States. Historically, attempts were made to balance the risk of perforation with its higher incidence of complications and mortality in patients with unrecognized appendicitis with the removal of normal appendices. Negative appendectomy rates were accepted at 15%–20% to decrease the chances of missing a case of appendicitis that would go on to perforate.
CLINICAL PRESENTATION The typical history of appendicitis is of generalized abdominal pain followed by nausea and anorexia. Pain is initially most prominent in the epigastrium, then migrating to the periumbilical region, and over a period of hours localizing in the right lower quadrant. Pain typically precedes the onset of nausea and vomiting. As the pain becomes localized, patients may report that activities that jar the abdomen such as jumping, bumps in the road while driving, or coughing exacerbate the pain. Diarrhea is uncommon except in children. Low-grade fever may be present. Because of the varied location of the tip of the appendix, atypical presentations are not uncommon and occur in 20%–33% of affected patients. Atypical presentations are more likely in elderly persons and in young children. The location of the appendix is also affected by pregnancy, with its position becoming more cephalad and lateral as the gravid uterus displaces abdominal contents with the progression of pregnancy; this alters the site of pain, as well. Eighty-three percent of patients present in the first 48 hours of the inflammatory process. Patients who present beyond that time are more likely to have a perforated appendix, fever, and evidence of peritonitis.
EXAMINATION Examination of the abdomen may reveal diminished bowel sounds and localized tenderness in the right lower quadrant. With the progression of inflammation, abdominal muscle spasm may progress from voluntary in response to pain to involuntary guarding. Rebound tenderness may also develop. Signs of peritoneal irritation are often present but are not specific for appendicitis. Psoas sign is elicited by having the patient lie on his or her left side while the right thigh is flexed backward. Pain may indicate an inflamed appendix overlying the psoas muscle. Rovsing sign is pain
Appendicitis
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referred to the right lower quadrant when the left lower quadrant is palpated. A positive obturator sign is pain that is elicited in a supine patient by internally and externally rotating the flexed right hip. Rectal examination may reveal right rectal tenderness or an inflammatory mass. Women require pelvic examination to identify possible gynecologic sources of their pain. With perforation, abdominal pain, tenderness, and guarding may be more pronounced and diffuse.
LABORATORY FINDINGS The total leukocyte count is elevated over 10,000 in 88% of patients with appendicitis. An elevation of the percentage of neutrophils (left shift) is important even in the setting of a normal total WBC. A completely normal WBC and differential is uncommon. The C-reactive protein level may be elevated but is not specific. Urinalysis may reveal pyuria due to the proximity of the ureter to the appendix. Other laboratory tests are neither specific nor helpful in establishing the diagnosis, except to exclude other possible diagnoses. A pregnancy test should be performed on all women of childbearing age.
DIAGNOSIS The diagnosis of appendicitis is made primarily based on history and the results of a physical examination. Corroborative evidence includes elevation of the WBC or left shift. In patients who do not have a typical presentation or physical findings or in whom alternative diagnoses cannot be excluded, radiologic studies can help establish the diagnosis.
RADIOGRAPHY Plain radiographs may reveal an appendicolith but are generally not useful. Ultrasound scanning using graded compression has been shown in multiple studies to have greater than 85% sensitivity and 90% specificity. Sonographic criteria for the diagnosis of acute appendicitis are noncompressible appendix greater than 7 mm in diameter, the presence of an appendicolith, submucosal incontinuity, or periappendiceal fluid or mass. It is less sensitive for perforated appendicitis. Sonography is operator dependent, and patient body habitus can affect performance. CT has essentially supplanted ultrasound scanning, except in specific patient populations such as pregnant women or persons with contrast allergy. The sensitivity and specificity of CT for appendicitis are both around 90%, depending on the clinical study and the use of oral, IV, and rectal contrast. CT criteria for diagnosing appendicitis are an appendix greater than 5–7 mm in diameter, a “target” sign of
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circumferential thickening, and periappendiceal inflammation. CT in conjunction with serial examinations and clinical observation in patients who have atypical presentations or equivocal findings or who are at high risk have lowered the negative appendectomy rate to 2% in some studies without increasing the rate of perforation.
TREATMENT AND OUTCOME When the diagnosis of appendicitis is suspected, urgent surgical consultation is required. Vomiting and anorexia can result in dehydration. Patients should receive replenishing fluids and not receive anything by mouth before possible surgery. Narcotic pain medications have been shown not to significantly change physical examination findings. The patient’s pain should be addressed. If perforation is suspected, treatment with broadspectrum antibiotics that cover coliform and anaerobic bacteria should be initiated. Definitive treatment requires surgical removal of the inflamed appendix, either laparoscopically or by open technique, as determined by the consultant.
Bibliography Cydulka RK: Meta-analysis of the clinical and laboratory diagnosis of appendicitis [abstract], Ann Emerg Med 2005;45(1):105. Jones K, Pena AA, Dunn EL, et al: Are negative appendectomies still acceptable? Am J Surg 2004;188(6):748–754. Lally KP, Cox CS, Andrassy RJ: Appendix, In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004. Lin CJ, Chen JD, Tiu CM, et al: Can ruptured appendicitis be detected preoperatively in the ED? Am J Emerg Med 2005;23(1):60–66. McCollough M, Sharieff GQ: Abdominal surgical emergencies in infants and young children, Emerg Med Clin North Am 2003;21:909–935. Morris KT, Kavanagh M, Hansen P, et al: The rational use of computed tomography scans in the diagnosis of appendicitis, Am J Surg 2002;183(5):547–550. Storm-Dickerson TL, Horattas MC: What have we learned over the past 20 years about appendicitis in the elderly? Am J Surg 2003;185(3):198–201. Wolfe JM, Smithline HA, Phipen S, et al: Does morphine change the physical examination in patients with acute appendicitis? Am J Emerg Med 2004;22(4):280–285.
Cholelithiasis and Cholecystitis
9
Cholelithiasis and Cholecystitis RYAN WELLS
ICD Codes: Calculus of gallbladder with acute cholecystitis 574.0, Calculus of gallbladder with other cholecystitis 574.1, Acute cholecystitis 575.0, Other cholecystitis (without mention of calculus) 575.1
Key Points Cholelithiasis (gallstones) is a very common presenting feature in obese, fertile female patients. Cholecystitis causes prolonged pain in the upper abdomen.The diagnosis of cholelithiasis should be entertained in any diabetic patient with right upper quadrant pain, fever, nausea, and vomiting. ! Emergency Actions ! Any patient who presents with fever, sepsis, and cholelithiasis should be administered IV fluids and antibiotics, and an immediate right upper quadrant ultrasound scan should be performed. An immediate surgical consultation should be sought.
DEFINITION Gallstones are crystalline structures formed from both normal and abnormal bile components. Bile is a pigmented, isotonic fluid that is composed of primarily water and bile acids. Bile is formed in the hepatocytes and is required for the breakdown and absorption of fats in the intestines. The biliary tract consists of the gallbladder, the hepatic bile canaliculi, the intrahepatic bile ducts, the extrahepatic bile ducts, the cystic duct, and the common bile duct. Bile is manufactured in and secreted from hepatocytes before being transported via portions of the biliary tract to the gallbladder for storage. While in the gallbladder, stored bile is concentrated and acidified. Cholelithiasis is the formation of gallstones in any part of the biliary tract. Seventy percent of gallstones are cholesterol stones, and the remainders are pigment stones. The principal cause of biliary tract disorders is related to the formation of gallstones. Gallstones can be asymptomatic, or they can lead to obstruction of the gallbladder and bile ducts, resulting in symptomatic cholelithiasis, cholecystitis, pancreatitis, or cholangitis. Cholecystitis is an acute inflammation of the gallbladder typically caused by gallstone obstruction of the neck of the gallbladder
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or at the cystic duct. However, between 5% and 10% of cholecystitis is acalculous (without gallstones).
EPIDEMIOLOGY An estimated 10%–20% of Americans have gallstones, and as many as one third will develop cholecystitis. Risk factors for the development of cholelithiasis and subsequent cholecystitis include increasing age, obesity, female sex, rapid weight loss, pregnancy, oral contraceptives, medications, chronic intravascular hemolysis, and multiparity. There is also an increased familial tendency for the formation of gallstones. There is an increased incidence in Pima Indians and persons of Scandinavian heritage. Cholelithiasis is less common in children, yet the condition does occur in this age group. Diseases involving hemolytic anemia (e.g., spherocytosis and sickle cell anemia) increase the likelihood of developing gallstones. It is important to note that even patients without classic risk factors develop gallstones and cholecystitis. Therefore, a high index of suspicion should be maintained for anyone presenting with symptoms consistent with gallbladder disease.
PATHOPHYSIOLOGY Bile is formed in the hepatocytes and is transported via the biliary tree to the gallbladder. The gallbladder stores approximately 50 ml of bile at any one time. When the stomach receives food (especially fatty food), both vagal responses and secretion of cholecystokinin cause the gall bladder to contract. Bile is released into the duodenum for digestion of a meal. The purpose of the gallbladder is to concentrate and acidify the bile. When this process is increased or rapidly reproduced and when rising cholesterol levels are present, lecithin and bile acids act to solubilize cholesterol. While cholesterol levels rise and lecithin and bile acids decline, cholesterol comes out of solution and forms crystals or stones. Gallstones can consist of three types: cholesterol, pigmented, and mixed. Between 70% and 80% of gallstones are cholesterol stones. Pigmented gallstones come in two types: brown and black. Black gallstones occur in the gallbladder and contain high concentrations of calcium bilirubinate. Black gallstones are found more often in elderly persons and in those with sickle cell disease and hereditary spherocytosis. Brown gallstones are found in the gallbladder, intrahepatic duct, and extrahepatic duct. Brown gallstones are more often associated with infection. Gallstones may migrate into either the cystic or common bile duct and become lodged, leading to symptomatic cholelithiasis. The consequent obstruction leads to increased intraluminal pressure and distention of the gallbladder, causing pain in the right upper quadrant or epigastric region of the abdomen, nausea, and vomiting.
Cholelithiasis and Cholecystitis
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If the obstruction persists, acute cholecystitis may develop. This often occurs when a gallstone is lodged in either the cystic duct or the infundibulum of the gallbladder. Gallstones are found in 95% of the patients with cholecystitis. Duct obstruction can also occur from external causes such as tumor, parasites, fibrosis, or kinking of the duct. The inflammatory response may be complicated by infection and bacterial organisms can be isolated in 50%–75% of patients with a diagnosis of cholecystitis. The infection is often polymicrobial, but the most common individual pathogens include Escherichia coli and Klebsiella species. Although bacteria are often isolated from inflamed gallbladders, it is unclear what role infection plays in cholecystitis. The small amount of cholecystitis not associated with gallstones is called acalculous cholecystitis. Acalculous cholecystitis makes up approximately 5%–10% of cases of cholecystitis. Conditions associated with acalculous cholecystitis include major surgery, severe trauma, debilitation, sepsis, long-term total parenteral nutrition, prolonged fasting, sickle cell disease, Salmonella infections, cardiac events, and other microbial infections in patients with acquired immunodeficiency syndrome. A very small percentage of patients will develop serious complications associated with cholecystitis, including gallbladder empyema and emphysematous (i.e., gangrenous) cholecystitis. These patients are often elderly and diabetic. The patient typically presents in extremis with fever, septic shock, and right upper quadrant pain.
CLINICAL PRESENTATION Gallbladder disease can produce a wide range of symptoms. Patients may have asymptomatic cholelithiasis or they may experience biliary colic (i.e., symptomatic cholelithiasis) or acute cholecystitis. Biliary colic is the right upper quadrant or epigastric abdominal pain associated with gallstones. The classic presentation for symptomatic cholelithiasis or cholecystitis is biliary colic associated with nausea and vomiting. This often follows ingestion of foods (typically fatty foods) by about 30–60 minutes. However, it is important to note that gallstone pain is not related to meals in at least one third of patients. This pain is typically present in the right upper quadrant and may initially be colicky but often becomes constant. The pain may radiate to the right shoulder or scapula. The patient may be in severe discomfort and diaphoretic. Patients with cholecystitis may also have fever. If the patient has known gallstones or a history of similar episodes, this will aid in diagnosis. Differentiating the clinical presentation of symptomatic cholelithiasis from cholecystitis may be difficult, especially early in the presentation. Cholecystitis is more likely if the symptoms persist longer than 4–6 hours or if fever is present.
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EXAMINATION Patients with biliary colic may be in severe discomfort. On examination, they may be tachycardic and diaphoretic. Abdominal examination reveals tenderness in the right upper quadrant or epigastric region. If the patient has cholecystitis, he or she may have fever and a Murphy’s sign. Murphy’s sign is the inspiratory arrest that occurs upon palpation of the right upper quadrant during a deep breath. Fever makes the diagnosis of acute cholecystitis much more likely than simple biliary colic. However, in a retrospective chart review by Gruber et al, 71% of patients with pathologically diagnosed cases of acute nongangrenous cholecystitis were afebrile. Physicians should be cautious in considering lack of fever a comforting finding in a patient with possible cholecystitis.
LABORATORY FINDINGS Unfortunately, no single laboratory test or combination of tests will catch all cases of acute cholecystitis. Laboratory test values are expected to be normal with cholelithiasis and are often normal in cholecystitis. Nonetheless, a multitude of laboratory tests are often ordered for these patients. A CBC, urinalysis, urine pregnancy test, and measurements of electrolytes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, international normalized ratio, alkaline phosphatase, and lipase may be ordered. The most important lab tests—clinically and diagnostically— are the urine pregnancy test and the lipase analysis. With cholecystitis, one may find an elevated CBC, AST, ALT, and alkaline phosphatase depending on the location of the gallstone in the biliary tract and the disease progression. If the lipase is elevated, the patient likely has pancreatitis. Of note, however, no lab test will make or break the diagnosis of cholecystitis.
DIAGNOSIS A diagnosis is made using a history, physical examination, and imaging study. Ultrasound, CT, and hepatobiliary scintigraphy (hepatobiliary iminodiacetic acid [HIDA] scans) are imaging options. Symptomatic cholelithiasis is differentiated from cholecystitis by complete resolution of symptoms and an ultrasound scan that reveals no evidence of cholecystitis. The differential diagnosis of gallbladder pain includes pancreatitis, cholangitis, gastritis, peptic ulcer disease, hepatitis, hepatic abscess, pyelonephritis, renal colic, right lower lobe pneumonia, pleural effusion, appendicitis, atypical myocardial infarction, pelvic inflammatory disease, and ectopic pregnancy.
Cholelithiasis and Cholecystitis
13
RADIOGRAPHS Plain radiographs can be useful if one is looking for another cause of the pain. In general, plain radiographic films will not help one to diagnose gallbladder problems. Ultrasound has become the imaging modality of choice in the ED. Ultrasound provides greater than 95% sensitivity and specificity for the diagnosis of gallstones more than 2 mm in diameter. Ultrasound is also 90%–95% sensitive for cholecystitis. Ultrasound findings consistent with acute cholecystitis include gallstones, sonographic Murphy’s sign, thickened gallbladder wall, and pericholecystic fluid. HIDA has been found to have a sensitivity approaching 100% and a specificity of 90% for diagnosing acute cholecystitis. Many believe that the HIDA scan is the gold standard imaging study. However, it is a difficult study to attain from most EDs. CT and magnetic resonance imaging (MRI) have recently been advocated for diagnosing gallbladder pathology. There are reports of significantly improving capabilities in diagnosing gallbladder disease in newergeneration CT scanners. CT is preferred over MRI in the ED because it is much quicker and more accessible than MRI. CT has an advantage over ultrasound in that it can make other diagnoses if the gallbladder is not the cause of the symptoms.
TREATMENTS AND OUTCOMES Some patients may be quite ill, especially elderly persons. The ABCs of life support (i.e., airway, breathing, and circulation) must be evaluated and treated. Oxygen administration and cardiac monitoring should be used at least until a cardiac cause is ruled out. The treatment of biliary colic consists of the administration of IV fluids, analgesics, and antiemetics and, rarely, nasogastric suctioning for intractable vomiting. Analgesia can be accomplished with ketorolac or ibuprofen (if tolerating oral) and narcotics. Some practitioners prefer meperidine over morphine because it is thought to cause less spasm to the sphincter of Oddi. However, many authorities feel this is not clinically relevant. Antiemetics include promethazine (Phenergan), prochlorperazine (Compazine), metoclopramide (Reglan), or ondansetron (Zofran). Treatment and time will cause symptoms of symptomatic cholelithiasis/biliary colic to resolve, usually within 4–6 hours. If symptoms are initially thought to be due to symptomatic cholelithiasis but they do not resolve, early acute cholecystitis should be considered. Treatment of acute cholecystitis consists of all of the above plus antibiotic coverage and immediate surgical evaluation. Ampicillin/sulbactam, ticarcillin/clavulanic acid, or piperacillin/tazobactam is a good option. One may also use clindamycin with gentamicin in a penicillin-allergic
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patient. If intra-abdominal sepsis is a concern, a regimen of ampicillin, gentamycin, and metronidazole can be used. All patients with cholecystitis should be admitted to the hospital. Their definitive care will require surgery and a cholecystectomy. The timing of surgery is not universally accepted, however. Some surgeons perform the cholecystectomy on the same day, whereas others wait 24–72 hours for the gallbladder to “cool off.” Patients with acalculous cholecystitis tend to have a more aggressive course with a mortality rate as high as 41%. Emphysematous cholecystitis is a rare form of cholecystitis. Gas-producing organisms likely invade the mucosa, and gas will be found in the gallbladder wall. Treatment in the ED is the same, but surgery is performed emergently.
DISPOSITION Patients with symptomatic cholelithiasis who have complete resolution of symptoms can be discharged home. They should have close follow-up with a surgeon because definitive care for gallstone-related pain is surgery. Other less common options include medical dissolution therapy and gallstone lithotripsy. Patients may be discharged with a prescription for ibuprofen and oral narcotics to treat further episodes of biliary colic. The patient should be instructed to return to the ED immediately if fever or worsening or persistent pain (greater than 2–3 hours) occurs, if the patient is unable to tolerate food or liquids, or if a change in his or her symptoms occurs. If a patient with gallstones has persisting symptoms, he or she should not be discharged without a surgical evaluation. This is true even if the laboratory test results are all normal and possibly even if an ultrasound scan has shown gallstones, as long as no evidence of acute cholecystitis exists. Remember that none of our diagnostic studies are 100% sensitive. All patients with acute cholecystitis should be admitted to the hospital.
Bibliography Aufderheide TP, Brady WJ, Tintinalli JE: Cholecystitis and biliary colic, In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 576–580. Gladden D, Clinton B, Wolf J, et al: Cholecystitis Emedicine online journal. August 2004. Available at www.emedicine.com. Gruber PJ, Silverman RA, Gottesfeld S, Flaster E: Presence of fever and leukocytosis in acute cholecystitis, Ann Emerg Med 1996;28(3):273–277. Guss DA: Cholelithiasis and cholecystitis, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1265–1272. Riviello RJ, Brady WJ: Presentation and management of acute biliary tract disorders in the emergency department: Optimizing assessment and treatment of cholelithiasis and cholecystitis, Emergency Medicine Reports 2002 Aug 12:23(17). Rosen P, Barkin RM, Braen GR, et al: Cholelithiasis and cholecystitis, In Schaider J, Hayden SR, Wolfe R, et al (eds): The 5 Minute Emergency Medicine Consult. Lippincott, Williams & Wilkins: Philadelphia, 1999, pp 226–229.
Hernias
15
Shea JA, Berlin JA, Escarce JJ, et al: Revised estimates of diagnostic test sensitivity and specificity in suspected biliary tract disease, Arch Intern Med 1994;154(22):2573–2581. Singer AJ, McCracken G, Henry MC, et al: Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis, Ann Emerg Med 1996;28(3):267–272.
Hernias MARC L. DAYMUDE
ICD Codes: Femoral 553, Inguinal 550.9, Umbilical 553.1, Incisional 553.21
Key Points/Quick Reference A hernia represents an abnormal protrusion of an organ or tissue through a defect in its surrounding wall. A hernia that cannot be reduced, an incarcerated hernia, is a surgical urgency because of its contents risk loss of blood flow, which is known as a strangulated hernia. ! Emergency Actions ! Any hernia that is suspected to be incarcerated or strangulated and cannot be reduced should be considered a medical emergency. Two large-gauge IV lines should be placed, the patient’s fluids should be replenished, an emergent CT scan should be obtained, and an emergent surgical consult should be sought.
DEFINITION The most common hernias involve the abdominal wall and are inguinal, femoral, umbilical, and incisional. Inguinal hernias occur in the groin superior to the inguinal ligament through a defect in processus vaginalis. A direct inguinal hernia protrudes through the muscle and fascia of the abdominal wall, whereas an indirect inguinal hernia protrudes through the internal inguinal ring into the inguinal canal. Femoral hernias protrude inferior to the inguinal ligament through a defect in the transversalis fascia into the femoral canal. Umbilical hernias pass through the fibromuscular ring of the umbilicus and can be present at birth or acquired in adulthood due to increased abdominal pressure from obesity, ascites, or
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pregnancy. Incisional hernias protrude through areas of postincisional weakness after abdominal surgery. A hernia is considered reducible if, when the abdominal muscles are relaxed and the patient is supine, the hernia contents either spontaneously or under gentle pressure return to an intra-abdominal position. An incarcerated hernia does not reduce with the above measures. A strangulated hernia is an incarcerated hernia in which the blood supply to the hernia contents is compromised by the narrow hernia defect and/or swelling. This can lead to ischemia, bowel obstruction, or perforation.
EPIDEMIOLOGY The lifetime risk of developing a hernia is 5% for males and 2% for females. Approximately 75% of all hernias are inguinal, and two thirds of these are indirect. Incisional hernias account for 15%–20% of hernias. Ten percent are ventral or umbilical, and 5% are femoral. Men are 25 times more likely to have an inguinal hernia, though this is still the most common hernia in women. Women are 10 times more likely to have a femoral hernia and twice as likely to have an incisional hernia. Femoral hernias have the highest rate of strangulation at 15%–20%. Strangulation is more common at either extreme of age.
CLINICAL PRESENTATION Asymptomatic hernias present as a painless lump or bulge at the site. Less commonly, pain may be part of the reported symptoms caused by the compression of local nerves or the hernia defect by the contents as it slides in and out. Incarcerated hernias present with progressive pain and swelling, often at the site of a known hernia. A strangulated hernia may involve features suggestive of bowel obstruction with pain, swelling, nausea, vomiting, and obstipation. The strangulated hernia may become blue or purple and have significant tenderness. There may also be clinical evidence of perforation with fever, shock, and peritoneal tenderness.
EXAMINATION A complete examination must include examination of the suspected hernia in positions that place it both dependent and not dependent to the pull of gravity. For most abdominal hernias, this could be the standing position in which gravity would pull hernia contents through the defect and the supine position, which would allow gravity to pull the hernia contents back into the intraperitoneal cavity. These can be augmented by having the patient perform a Valsalva maneuver to increase intra-abdominal pressure and thereby demonstrate the hernia. Direct palpation over the areas of
Hernias
17
concern during position changes and resultant changes in the hernia mass help to differentiate hernias from other causes of a “lump” and may demonstrate the actual abdominal wall defect.
LABORATORY FINDINGS In hernias found to be uncomplicated by examination, laboratory testing is not necessary. In patients with suspected incarcerated or strangulated hernias, CBC, electrolyte measurements, and renal function tests may reveal an elevated WBC with left shift and evidence of volume depletion. In patients in whom the diagnosis is not clearly hernia, laboratory values may help differentiate other causes of a lump, especially in the inguinal region where adenopathy or genital pathology may mimic a hernia.
DIAGNOSIS The diagnosis of hernias is primarily clinical, with the demonstration on examination of a mass that protrudes when under increased pressure, such as with gravity or a Valsalva maneuver, and recedes when the pressure is decreased or with gentle palpation. Incarcerated or strangulated hernias or “bulges” that are not clearly hernias may require radiologic evaluation.
RADIOGRAPHS Plain supine and upright films of the abdomen may demonstrate free air from perforation or evidence of bowel obstruction in cases of suspected incarceration or strangulation, but these are generally not useful in the evaluation of hernias. Ultrasound is highly sensitive and specific in the diagnosis of inguinal and femoral hernias. CT may be useful in detecting less common hernias and in identifying ischemic hernia contents.
TREATMENT AND OUTCOME Patients with hernias that are easily reduced in the ED may be discharged home with outpatient surgical consultation and precautions to return if they experience increased pain, fever, nausea and vomiting, or irreducibility of the hernia mass. Reduction of hernias may require adequate pain management to relax the abdominal wall and putting the patient into Trendelenburg’s position and applying gentle pressure. Hernias should not be forced back in because of the risk of reducing necrotic bowel into the peritoneal cavity and inducing diffuse peritonitis. Patients with
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suspected incarcerated or strangulated hernias require urgent surgical evaluation in the ED. If there is evidence of strangulation and bowel obstruction or perforation, fluid resuscitation and treatment with broadspectrum antibiotics should be initiated while surgical consultation is awaited.
Bibliography Blaivas M: Ultrasound-guided reduction of a Spigelian hernia in a difficult case: An unusual use of bedside emergency ultrasonography, Am J Emerg Med 2002;20(1):59–61. Fitzgibbons RJ, Jonasson O, Gibbs J: The development of a clinical trial to determine if watchful waiting is an acceptable alternative to routine herniorrhaphy for patients with minimal or no hernia symptoms, J Am Coll Surg 2003;196(5):737–742. Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin 2002;31(3):777–799. Malangoni MA, Gagliardi RJ, Hernias. In Townsend CM: Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1199–1217. Manthey DE: Abdominal hernia reduction. In Roberts JR, Hedges JR: Clinical Procedures in Emergency Medicine, ed 4. Elsevier: St Louis, 2004, pp 860–866. Perrott CA: Inguinal hernias: Room for a better understanding, Am J Emerg Med 2004;22 (1):8–50.
Intestinal Obstruction MARC L. DAYMUDE
ICD Code: 560.9
Key Points/Quick Reference In adults the most common cause of small bowel obstruction (60%^75%) are adhesions from previous abdominal surgery. Malignancy, from primary or secondary metastatic lesions, is the second most common cause of obstructions in adults. In infants aged 2^3 weeks, pyloric stenosis is the most likely cause of obstruction. In children aged 3 months to 6 years, intussusception is the most likely cause of bowel obstruction. ! Emergency Actions ! Any patient who is suspected to have an intestinal bowel obstruction should have two large-gauge IV lines placed, and aggressive fluid resuscitation should be started. Upright and flat plain radiographs should be obtained. If an intestinal bowel obstruction is suspected, an abdominal CT scan and an emergent surgical consult should be obtained.
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DEFINITION Bowel obstruction represents a mechanical interruption in the flow of intraluminal intestinal contents. The etiology and treatment of the obstruction vary widely depending on whether the interruption occurs in the small or large bowel. The terms pseudo-obstruction, ileus, or Ogilvie's syndrome represent a functional decrease in bowel motility and progressive dilation that is thought to result from autonomic imbalance from multiple causes.
EPIDEMIOLOGY In adults, the most common cause of small bowel obstruction (60%–75%) is adhesion after abdominal surgery, especially lower abdominal and pelvic surgeries such as appendectomy, hysterectomy, and colectomy. Malignancy, primarily metastatic with peritoneal implants, account for approximately 20%. The third most common cause of small bowel obstruction in adults, representing 10%, is incarcerated hernia, most commonly inguinal or ventral. Crohn’s disease accounts for 5% either by acute inflammation or chronic scarring and strictures. The remaining 2%–3% are from intraluminal obstruction from intussusception, gallstones that pass through a cholecystoduodenal fistula, enteroliths, foreign bodies, and bezoars. Rarely, intra-abdominal inflammatory masses such as from diverticulitis can cause small bowel obstruction. Large bowel obstruction in adults is predominantly caused by primary malignancy, representing 60% of obstructions. Volvulus (sigmoid 60% and cecal 40%) make up 10%–13% of large bowel obstruction. Sigmoid volvulus usually occurs in an elderly patient with debilitating diseases or in patients with severe psychiatric or neurologic diseases. A common history is of long-standing constipation. Diverticular disease with inflammatory masses or chronic scarring accounts for almost all other cases of large bowel obstruction in the United States. In children, the most common causes of bowel obstruction are age dependent. In the first 2–3 weeks of life, pyloric stenosis causes gastric outlet obstruction in 1 in 150 males and 1 in 750 females. From 3 months to about 6 years, the most common cause of small bowel obstruction is intussusception. The second most frequent cause is incarcerated hernias, especially in the younger age group. Less common causes are postsurgical adhesions, sigmoid volvulus, and Meckel’s diverticula. Pseudo-obstruction or ileus has multiple etiologies to include common medications, intra-abdominal processes, or severe stresses to the body. Common precipitants include narcotic medications, medications with anticholinergic effects, withdrawal of laxative abuse, intra-abdominal surgeries, sepsis, severe burns, pelvic or lumbar trauma or surgeries, spinal cord injuries, and retroperitoneal hematomas.
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CLINICAL PRESENTATION The classic symptoms of bowel obstruction are progressive abdominal distention, colicky abdominal pain, nausea and vomiting, and obstipation or inability to pass flatus or stool. Vomiting is a more prominent symptom the more proximal the obstruction. The crampy abdominal pain tends to occur in paroxysms 4–5 minutes apart as the bowel peristalses against the obstruction. Obstipation is a late finding. The early course may actually be marked by diarrhea due to the increased peristaltic activity both proximal and distal to the obstruction. Later in the course of obstruction, the vomitus may become feculent due to bacterial overgrowth of pooled intestinal contents proximal to the obstruction. Bowel obstruction causes the loss of absorptive properties of the bowel, leading to accumulation of fluids in the lumen, bowel wall edema with third-space fluid losses, and marked intravascular depletion. This can progress to hypotension and shock.
EXAMINATION The patient’s vital signs may reflect the severity of volume depletion with tachycardia and hypotension. Tachypnea may reveal an attempt to compensate a metabolic acidosis. Fever may suggest bowel strangulation and perforation. The abdominal examination typically reveals diffuse distention, tenderness, and tympany to percussion. Early in the course of obstruction, bowel sounds are high pitched and hyperactive with “rushes” and “tinkles.” As the obstruction progresses and the bowel becomes more distended, the abdomen may become quiet. A complete physical examination is essential to identify possible causes of the obstruction. In adults, the abdomen likely will reveal surgical scars from previous surgeries. Incarcerated hernias should be sought, especially inguinal, femoral, or incisional. A rectal examination may reveal an obstructing mass of colon cancer. Similarly, a bimanual pelvic examination may identify ovarian masses. Infants may have an epigastric “olive” of pyloric stenosis or the “sausage” mass of intussusception. “Current jelly” stools of intussusception are a late finding indicative of bowel mucosal sloughing. Focal tenderness or peritoneal signs suggest bowel strangulation, necrosis, or perforation.
LABORATORY FINDINGS Laboratory findings in bowel obstruction are nonspecific and not helpful with the diagnosis. There often will be an elevated WBC with left shift. Elevation of BUN and creatinine levels give evidence of volume depletion. Electrolyte level abnormalities—especially hypokalemia, hypochloremia, and metabolic alkalosis from vomiting—are not uncommon. Lactic acidosis may be present.
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DIAGNOSIS Diagnosis is made primarily based on history and physical examination with the support of plain upright and supine abdominal radiographs. The diagnostic accuracy of plain radiographs for small bowel obstruction is 60%. Characteristic findings include dilated loops of small bowel without colonic gas. Upright radiographs reveal multiple layers of air-fluid levels that resemble stacked coins. Cecal volvulus may have a dilated kidney-bean–shaped dilated loop of colon in the left upper quadrant. Radiographs in sigmoid volvulus reveal dilated sigmoid colon with a tapered end pointing to right upper quadrant resembling a bent inner tube. On equivocal cases, CT is 90% sensitive and specific in the diagnosis of small bowel obstruction and helpful in identifying extrinsic causes of obstruction such as internal hernias, tumors, or inflammatory masses. Barium enema may be both diagnostic and therapeutic for intussusception and sigmoid volvulus. Enteroclysis, in which contrast is instilled directly into the small bowel by a nasogastric tube then followed fluoroscopically through the bowel, may be necessary to diagnose partial or intermittent obstruction.
RADIOGRAPHS For most cases of bowel obstruction, supine and upright radiographs are the only radiographs needed to establish the diagnosis. These may also reveal some causes of obstruction such as foreign bodies or gallstones. CT, barium enema, and enteroclysis increase the diagnostic accuracy in less certain cases or in cases of partial or intermittent obstruction.
TREATMENT AND OUTCOME Emergency management hinges on establishment of the diagnosis, volume resuscitation, and prevention of further distention of the bowel. In the case of small bowel obstruction more so than large bowel obstruction, third-space fluid losses can be substantial and patients will require isotonic crystalloid fluid boluses to restore intravascular volume. Correction of electrolyte abnormalities should be initiated. A urinary catheter may aid in managing fluid resuscitation. All patients should have a nasogastric tube placed at low, intermittent suction to decompress the bowel and prevent further accumulation of fluids and swallowed air. Antibiotics are indicated for patients who have evidence of bowel strangulation, necrosis, or perforation. All patients will require surgical consultation and admission. Many patients with ileus or partial obstruction may be managed conservatively with fluid resuscitation, bowel decompression, and rest. Patients with complete obstruction or evidence of strangulation, necrosis, or perforation will require operative management.
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Bibliography Bitterman R, Peterson M: Large intestine, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1327–1342. Evers BM: Small intestine. In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1323–1375. Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin North Am 2002; 31(3):777–799. Garcia EA: Intestinal obstruction in infants and children, Center Pediatr Emerg Med 2002;3(1):14–21. Kahi CJ, Rex DK: Bowel obstruction and pseudo-obstruction, Gastroenterol Clin North Am 2003;32(4):1229–1247. Nagle A, Ujiki M, Denham W, et al: Laparoscopic adhesiolysis for small bowel obstruction, Am J Surg 2004;187(4):464–470.
Thoracic Aortic Dissection MARC L. DAYMUDE
ICD Code: 441.01 (thoracic)
Key Points/Quick Reference Aortic dissection represents a splitting between the three layers of the aortic arterial wall: the intima, media, and adventitia. This separation of the media allows blood to flow through a false lumen and can result in rupture of the weakened arterial wall.The most common symptom is sudden, sharp chest pain that radiates to the back. Dissection, a potentially lethal condition, should be on the differential diagnosis of any patient with chest or upper back pain. ! Emergency Actions ! Any patient suspected of having an aortic dissection should immediately have two large-gauge IV lines placed, should be placed on the cardiac monitor, and should have an immediate CT angiogram and blood pressure control. If an aortic dissection is present, immediate surgical consult should be obtained.
DEFINITION Aortic dissection is a separation between the layers of the aorta caused by the shear forces of blood flow. This results from a weakening or
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degeneration of the middle layer of the aorta (i.e., the media). A tear in the arterial lining (i.e., the intima) allows blood to flow between the layers of the wall of the aorta, creating a false lumen. The weakened aortic wall can dilate and rupture. The dissection may involve arterial branches off the aorta, resulting in decreased blood flow distal to the involved area and causing additional symptoms due to ischemia. The dissection may propagate both distally and proximally from the intimal tear. Dissection is termed acute if it is diagnosed within 14 days of symptom onset and chronic if diagnosed after 14 days. Aortic dissection is distinctly different in pathogenesis, prognosis, and management from aortic aneurism, which represents a diffuse expansion of all three layers of the aortic wall to 50% or more than the normal diameter. There are two major classification systems based on the site of dissection that correlate with prognosis and guide treatment decisions: Stanford and DeBakey.
Stanford A: Involves the ascending aorta Stanford B: Does not involve the ascending aorta DeBakey I: Involves the ascending and descending thoracic aorta DeBakey II: Involves only the ascending aorta DeBakey IIIA: Does not involve the ascending aorta and is proximal to the diaphragm DeBakey IIIB: Does not involve the ascending aorta and extends distal to the diaphragm
EPIDEMIOLOGY Acute aortic dissection is the most common aortic disaster. It occurs more commonly in men and the incidence increases with age, rarely occurring before the age of 40 years. Mortality rates from dissection are 1 to 5/100,000 per year. Seventy-five percent of untreated patients with dissection die within 2 weeks of symptom onset. The most common risk factor is hypertension. Atherosclerosis is not a contributing factor in most cases. Connective tissue disorders and congenital heart syndromes such as Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, giantcell arteritis, polycystic kidney disease, bicuspid aortic valve, and coarctation of the aorta contribute to increased risk of dissection at an earlier age. Pathophysiology is theorized to be due to degeneration of the media as part of the aging process that is exacerbated by hypertension. Accumulated stresses from the shear forces of blood flow and flexion of the aorta with every contraction of the heart induce a tear in the intima that allows blood to flow into the medial layer. The depth and distance of dissection is related to the degree of medial degeneration and magnitude of shear forces caused by hypertension. Dissections involving the ascending aorta are more lethal and are more often associated with complications of the aortic branch arteries than those confined to the descending aorta.
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CLINICAL PRESENTATION Pain is the most common symptom named at presentation and is present in 90% of patients with dissection. It is typically described as sharp and of sudden onset, with maximal pain from the start. The pain is sometimes described as tearing or ripping. It may involve the anterior chest with or without radiation to the neck and jaw, the interscapular region of the back, or the lumbar and abdominal areas; alternatively, it may migrate through those regions with progression of the dissection from the ascending to descending aorta. Vagal symptoms of nausea and vomiting, diaphoresis, lightheadedness, and anxiety are commonly associated. Syncope, representing acute hemorrhage and hypotension, rupture into the pericardium and tamponade or involvement of the carotid arteries interrupting cerebral blood flow occurs in 9%. Involvement of the carotid arteries may also result in stroke-like neurologic symptoms in 6%. The coronary arteries, most commonly the right coronary artery, may be occluded by the dissection and result in acute myocardial infarction, most commonly an inferoposterior myocardial infarction, when the right coronary artery is involved.
EXAMINATION Most patients will appear apprehensive, pale, and diaphoretic. Patients may be hypertensive from acute catecholamine release or hypotensive due to rupture, tamponade, or impaired blood flow through the subclavian arteries (pseudohypotension). With ascending dissections, involvement of the subclavian arteries may result in pulse deficits and blood pressure discrepancies between the upper extremities. This is evident in 24% of patients with ascending dissection. Involvement of the carotid arteries can result in cerebral ischemia and stroke-like findings of hemiparesis and altered mental status. Ascending dissections can propagate proximally, resulting in aortic valve regurgitation or rupture into the pericardium. Aortic regurgitation (occurs in 18%–50%) is evidenced by a loud pansystolic murmur and can result in congestive heart failure. Rupture into the pericardium can result in cardiac tamponade with muffled heart sounds, distended neck veins, and hypotension. Extension of dissection distally can cause spinal paraparesis, mesenteric ischemia, renal failure, femoral pulse deficits, and lower extremity ischemia.
LABORATORY FINDINGS Laboratory testing is not helpful in establishing the diagnosis of aortic dissection. However, sending blood samples for CBC, electrolyte panel, BUN/creatinine measurement, cardiac enzyme analysis if indicated by presentation, and type and cross-match for 6–10 units packed red blood cells and fresh frozen plasma will aid in management.
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DIAGNOSIS Thoracic aortic dissection must be included in the differential diagnosis of all patients presenting with chest pain, upper back pain, or ischemic symptoms. Confirmation is made with radiography.
RADIOGRAPHS The findings on chest radiograph are abnormal in 80%–90% of patients with aortic dissection, with findings of widened mediastinum (75%), localized bulge in the aorta, obliteration of the aortic knob, displacement of the trachea or nasogastric tube to the right, inferior displacement of the right main bronchus, or calcium sign. Calcium sign is a collection of aortic calcium deposits that are separated from the outer wall of the aorta by more than 5 mm. Transesophageal echocardiography (TEE) is highly sensitive for diagnosing dissection and is helpful in detecting aortic regurgitation and pericardial effusion. The advantage of TEE is that it can be performed at the bedside in the ED, thought it may not be available at every institution. CT angiography is the diagnostic method of choice in most institutions. This method can identify an intimal flap, true and false lumens, and associated dilation of the aorta. Aortography, once the gold standard, has largely been supplanted by TEE and CT. MRI is highly specific and diagnostic, but it may be more appropriate in monitoring chronic, nonoperative dissections rather than making an initial diagnosis.
TREATMENT AND OUTCOME Emergency management revolves around resuscitation, limiting the extension of dissection, and securing emergent surgical consultation. Patients with suspected aortic dissection require two large-bore IV lines with isotonic crystalloid, continuous cardiac and blood pressure monitoring, and oxygen. An arterial line for continuous blood pressure monitoring optimizes control. Pain control with opiates will help decrease catecholamine release. Control of blood pressure and the rate of arterial pulse rise with each heartbeat will decrease the shear forces in the dissection. This is best accomplished initially with beta blockers. Labetalol 20 mg IV can be administered as a bolus every 5–10 minutes, increasing to 80-mg boluses to a target blood pressure of 100–120 systolic and pulse rate 60–80 beats/min or total of 300 mg. This can be followed by 1- to 2-mg/hr continuous drip. Alternatively, esmolol can be titrated with 500 mg/kg boluses every 5 minutes and an initial drip rate of 50 mg/kg/min up to 200 mg/kg/min. If additional blood pressure control is required, nitroprusside can be added and titrated at 0.3–5.0 mg/kg/min. Definitive management of ascending thoracic aortic dissections requires operative repair. Descending dissections often are managed medically with blood pressure control. Twenty
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percent of descending dissections will require operative management for persistent pain, uncontrolled hypertension, occlusion of major arterial branches, aortic leaking or rupture, or localized dilation. New methods of endovascular stenting are being tested and may provide an alternative to medical management for patients at high surgical risk of mortality due to comorbidities. All patients diagnosed with dissection in the ED will require admission to an intensive care unit. Long-term survival rates in treated patients at 1, 5, 10, and 15 years are 56%, 48%, 29%, and 11%, respectively.
Bibliography Ankel F: Aortic dissection, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002; pp 1171–1176. Huyah T, Estrera A, Miller C, et al: Thoracic vasculature (with emphasis on thoracic aorta), In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004; pp 1905–1929. Lee JT, White RA: Current status of thoracic aortic endograft repair, Surg Clin North Am 2004;84(5):1295–1318. Nienaber CA, Zannetti S, Barbieri B, et al: Investigation of stent grafts in patients with type B aortic dissection: Design of the INSTAD trial—a prospective, multicenter, European randomized trial, Am Heart J 2005;149(4):592–599. Rogers RL, McCormack R: Aortic disasters, Emerg Med Clin North Am 2004;22 (4):887–908.
Wound Management CARL MENCKHOFF
ICD or CPT Code: See particular wounds for codes
Key Points/Quick Reference All wounds should be evaluated for infection, potential for infection, bleeding with threat of loss of limb or life, retained foreign bodies, and viability of soft tissue with consideration for underlying bony structures of organ injury and viability.
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EPIDEMIOLOGY Over 12 million traumatic wounds are treated each year in U.S. EDs. The most commonly affected group is young males aged 15–44 years, and the most commonly affected areas are the head (face and scalp) and the upper extremities (hands and fingers). The most common mechanism of injury is blunt trauma, although other causes include glass, sharp implements, wooden objects, and mammalian bites.
WOUND HEALING Wound healing can be divided into five stages: coagulation, inflammation, collagen synthesis, wound contraction, and epithelialization. Coagulation starts immediately after the injury, along with smooth muscle contraction to control bleeding. Inflammation is stimulated by factors released from platelets and by the complement cascade. Vascular permeability is increased with the influx of neutrophils and monocytes, which act as scavengers of debris and bacteria. Monocytes change into macrophages, which provide wound defense and also release chemotactic substances and stimulate fibroblast replication and neovascularization. Collagen synthesis starts as early as 48 hours after the injury and peaks at day 7 as tensile strength increases. The wound has its greatest mass at 3 weeks but only 20% of its tensile strength. The wound then remodels itself over the next 6–12 months. Collagen fibers are unable to form without ascorbic acid and oxygen. Wound contraction is the movement of full-thickness skin toward the center of the wound. Immediately after the injury, the skin edges retract. Over the next 3–4 days, the wound edges move toward the center (independent of epithelialization). The wound then continues to remodel itself over the next 6–12 months. Epithelialization is the process of epithelial cells migrating across the wound. In a repaired laceration, epithelialization will bridge the defect in 48 hours.
MEDICAL HISTORY Because a wound is usually visually obvious, a good history is sometimes overlooked and can lead to serious complications. There are several pieces of information that need to be ascertained to determine the risk of infection and the best way to approach wound repair. The time that has passed since the injury has occurred will influence the decision whether to close a wound primarily, with the risk of infection increasing as the time from injury to closure increases. Most wounds should be closed within 8–12 hours of injury, though some authors
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advocate closure of low-risk wounds on the face up to 24 hours after the injury. Other factors that increase the risk of infection include crush injury, retained foreign body, dirty wound (e.g., saliva, feces, organic material), and puncture or deep penetrating wounds Lastly, one needs to determine the immunocompetence and general health of the patient, any allergies to anesthetics, latex, or antibiotics, and tetanus vaccination status.
PHYSICAL EXAMINATION The physical examination should begin with an assessment of the neurologic, sensory, and motor function distal to the laceration. The wound should then be explored to look for injured structures and foreign bodies. In most cases, anesthesia will be required for adequate wound exploration. In wounds over tendons, the tendon should be examined in its full range of motion. For example, a laceration sustained in flexion during a fistfight may not be readily apparent when the fingers are extended.
ANESTHESIA After an appropriate physical examination, the area can be anesthetized (neurologic exam should always be performed before anesthesia). This can be accomplished by systemic, regional, or local anesthesia. Systemic analgesia may be necessary for some large wounds or in some children. It can be accomplished with a number of different agents, including ketamine, benzodiazepines, narcotics, or etomidate. Regional anesthesia is preferred when applicable because it usually requires less anesthetic, can cover multiple wounds in the same area, and does not distort the wound. However, local anesthesia is simple to perform and appropriate for many wounds. Anesthetic agents can be divided into two classes—the amides and the esters. There is no cross-reactivity between the groups, so an allergy to an amide does not mean an allergy to an ester. Examples of the amides are lidocaine, mepivacaine, and bupivacaine. The esters include procaine, tetracaine, and benzocaine. The two most commonly available local anesthetics in the United States are lidocaine and bupivacaine. Both come with and without epinephrine. Epinephrine causes vasoconstriction, which helps control bleeding and decreases the speed of systemic absorption (thereby allowing for higher doses to be administered). Epinephrine has also been shown to delay healing and increase the risk of infection and, because of the small risk of necrosis, it should not be used where there are distal-end arteries such as in the fingers, nose, penis, and toes. Those looking for alternative local anesthetics may want to consider aqueous Benadryl 1%, LET (lidocaine, epinephrine, tetracaine), or EMLA
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(lidocaine and prilocaine). Aqueous Benadryl is diluted to 1% solution and injected locally. In some studies, it has been found to be equivalent to lidocaine as a local anesthetic. LET is used in gel form and is placed over the wound, then covered with an occlusive dressing. It should not be used near mucous membranes or distal-end arteries due to its epinephrine component. EMLA is also used as a gel and placed over the wound with an occlusive dressing. Both lidocaine and bupivacaine can be toxic, especially when used to close large lacerations on patients with less body mass. Lidocaine toxicity can cause a metallic taste, dizziness, tinnitus, disorientation, dysarthria, seizures, coma, and death. The toxic dose of lidocaine (or bupivacaine) should always be calculated before usage (Table 1-1).
WOUND PREPARATION Hemostasis can be accomplished most of the time with direct pressure alone. Other techniques to assist include gravity, vasoconstriction (epinephrine, ice), completion of partial incisions (so vessels can contract), cautery, tourniquets (maximum time, 30 minutes on the fingers and 1 hour elsewhere), and suture ligature of a bleeding vessel. Skin disinfection can be accomplished with povidone-iodine (Betadine), which is effective against gram-positive bacteria, gram-negative bacteria, fungi, and viruses. However, it is toxic to wound defenses and may increase wound infection, so care should be taken not to spill it into the wound itself. Hair can be prepared with Betadine and should not be shaved because surgical studies show that this increases wound infection by exposing wounded follicles to bacteria. If visualization of the wound is difficult, hair can be clipped short without damaging the follicle. Irrigation is one of the most important determinants of wound prognosis. Three questions should be answered to determine effective irrigation: Table 1-1 Calculating Toxic Dosage of Lidocaine and Bupivacaine TOXIC DOSE
Lidocaine Bupivacaine
ONSET
DURATION
NO EPI
EPI
Seconds to minutes Seconds to minutes
½–1 hr >6 hr
5 mg/kg 2 mg/kg
7 mg/kg 3 mg/kg
Epi, Epinephrine. Example: A 1-year-old boy (weight, 10 kg) presents to the ED with 25 cm of lacerations to the right thigh. How much lidocaine can be used? 1% lidocaine equals 1 g/100 ml ¼ 1000 mg/100 ml ¼ 10 mg/ml 10-kg boy 7 mg/kg (with epi) ¼ maximum dose of 70 mg of lidocaine with epi 70-mg maximum dose/10 mg/ml ¼ 7 ml of lidocaine One can see that 7 ml of lidocaine is not very much for 25 cm of lacerations, and regional or systemic anesthesia may be necessary.
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how much pressure do I need, what solution should I use, and how much volume do I need? Irrigating with pressures of about 8 psi is recommended. This can be accomplished with a 19-gauge Angiocath catheter (or equivalent) and a 60-ml syringe. Low pressures are not as effective at cleaning out debris and bacteria, whereas very high pressures can cause tissue damage. Normal saline is the recommended irrigant. Studies have been done looking at other more expensive solutions but have not shown them to be superior. One study examined the use of tap water, which appeared to be as effective as normal saline. The volume of irrigant that should be used has not been well established. Some authors recommend 50–60 ml/cm of wound. Others recommend that the wound should be irrigated until clean (with a minimum of 200 ml). Debridement of devitalized tissue is important to decrease the risk of infection and to improve overall wound healing. Only devitalized tissue should be debrided. Jagged edges should be preserved when possible because this increases the surface area of the wound and decreases the skin tension.
WOUND CLOSURE The first decision to be made is how the wound should be closed. Primary closure is the traditional immediate closure. In secondary closure, the wound is left open and heals on its own. Cosmetic outcome is the worst with secondary closure. In tertiary (delayed primary) closure, the wound is prepared as with primary closure but then is packed open. If not infected, the wound can be closed 4 days after injury with the same cosmetic outcome as primary closure. Closing a wound loosely is never indicated. Loose closure allows the wound to seal itself within 48 hours without the cosmetic advantage of primary or tertiary closure. Skin tape is quick and inexpensive and has a low rate of infection, but it also has low tensile strength and a higher rate of wound dehiscence. It may be useful in small, linear superficial lacerations without tension. Benzoin should be used on the surrounding skin to help with adhesion. Tissue adhesives are quick and comfortable and do not require removal, but they also do not have the tensile strength of sutures. The octylcyanoacrylates are the most flexible and strongest of the group, and a study comparing octyl-cyanoacrylate to sutures found the cosmetic outcomes to be comparable after 3 months and a year. Tissue adhesives are best used in uncomplicated lacerations in low-tension areas, but they can also be used in combination with subcutaneous sutures. Staples are quick to apply but do not permit a closure quite as accurate, and they are somewhat less comfortable for the patient. Sutures enable the most cosmetic closure of all the techniques. However, a large closure can take time and, with the introduction of foreign
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material, sutures have the greatest amount of tissue reactivity. If sutures are to be used, the next questions to be answered are as follows: what type, what size, and what needle? Suture types can be divided into absorbable and nonabsorbable, defined by whether the tensile strength is maintained for less than or greater than 60 days (Table 1-2). Nonabsorbable sutures are usually used for cutaneous closures and tendon repairs, whereas absorbable sutures are used for deep structures such as fascia and dermis. For cutaneous closures, nylon and polypropylene (Prolene) sutures are the most commonly used and have good strength and low infectivity. Fast-absorbing plain gut or polyglactin (Vicryl Rapide) sutures may be considered for closures requiring tensile strength for a week or less or in cases in which suture removal is difficult (e.g., on a child’s face) or may be doubtful (e.g., in a homeless patient). Silk is comfortable and may be preferred around the lips or nipples. For deep sutures, Vicryl has low reactivity and good strength and is an appropriate choice for most uses. Suture size should be tailored to the amount of tension and the need for cosmesis (Table 1-3). In general, the face should be closed with 6–0 and the body with 5–0. One size larger may be used for deep layers and one size larger should be used for areas of increased tension. For example, this means that deep fascia over the knee can be closed Table 1-2 Suture Type NONABSORBABLE
BRAID (B) VS MONO (M) DURABILITY
Silk
B
Mersilene Nylon
B M
Prolene
M
Ethibond
B
Staples/steel
M
Absorbable Fast-absorbing plain gut Vicryl Rapide
M
3–5 days
B
5–7 days
Plain gut
M
7 days
Chromic gut Vicryl
M B
10–14 days 30 days
Polydioxanone (PDS)
M
45–60 days
COMMENTS Comfortable; use around lips, nose, nipples Use for fascia and tendons Common, strong, low infectivity, tendons Common, strong, low infectivity, tendons Costly, more comfortable, easier workability Fast, low infectivity, strong, uncomfortable, poor cosmesis Can be handy for children's faces; no removal necessary Handy when no removal is desired Rarely used; consider in homeless patients Primarily used intraorally Good for subcutaneous suturing and in mucous membranes Synthetic
32 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 1-3 Suture Size ANATOMICAL LOCATION Face Body
SIZE FOR SKIN SUTURE
SIZE FOR DEEP SUTURE
6–0 skin 5–0 skin
5–0 deep 4–0 deep
Sutures one size larger should be used for increased tension (e.g., over joints).
with 3–0, deep fascia on the forearm with 4–0, skin on the thigh with 5–0, and skin on the face with 6–0. Needles are available in a wide variety of shapes and sizes. Most wounds in the ED can be closed using a conventional cutting needle. The main exception is closure of fascia and repair of tendons, which should be done with a tapered needle
Suture Techniques Several suture techniques can be used to optimize cosmetic outcome (Fig. 1-1). Wound tension should be minimized by undermining the wound edges or by placing subcutaneous sutures. Wound edges should be everted so that the germinating layers of the skin will be in contact with one another. This can be accomplished by ensuring that the needle enters and exits the skin perpendicularly. The suture should be tied just tightly enough to bring the wound edges together. With uneven wounds, care should be taken that the depth of bite should be the same on both sides of the wound. Jagged margins of a wound should be preserved if viable. A better scar will result due to increased surface area and therefore decreased tension. Simple interrupted percutaneous sutures are the most common method of laceration repair in the ED. The needle enters the skin perpendicularly on one side of the wound and crosses subdermally to the other side, where it exits perpendicularly and the knot is tied. Continuous percutaneous sutures are useful in linear lacerations with low tension. They are placed like the interrupted sutures above except that after the first knot is tied, the suture is not cut and the needle is reintroduced on the opposite side of the wound. Inverted intradermal sutures are used primarily to reduce tension on the wound edges. They are placed by introducing the needle deep in the wound and emerging just below the skin’s surface. The needle then enters (at the same level) just below the skin surface on the other side and exits deep in the wound, where the knot is tied. Horizontal mattress sutures are used primarily in areas of tension to help disperse the tension. This author also finds them useful in some elderly patients with paper-thin skin, where simple interrupted sutures may tear through. These begin like a simple interrupted suture, but rather than tying the knot, the needle reenters the skin on the same side
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Needle holder rolled
33
More tissue in depth than at surface Skin edge retracted
Direction of needle Simple interrupted percutaneous
Dermis Subcutaneous layer Grasp this loop and pull through to form knot
Inverted intradermal Continuous percutaneous
A Figure 1-1. Suture techniques. A, Simple interrupted percutaneous, continuous percutaneous, and inverted internal techniques.
(Continued)
of the wound approximately 0.5 cm adjacent to where it emerged. It then exits on the other side of the wound about 0.5 cm from where the stitch began, and the ends are tied. Vertical mattress sutures are useful for forced wound edge eversion as well as for closing deep and superficial layers with one stitch. The needle is introduced and a large bite is taken through to the other side of the wound. The direction of the needle is then reversed and a smaller bite is taken in the reverse direction. Half-buried horizontal mattress sutures (flap stitch) are ideal for closing the tips of wound flaps because they minimize suture-induced ischemia to an already tenuous area. The needle is inserted through the skin on one side of the wound level with the apex of the flap corner. The needle then passes intradermally through the tip of the flap and out through the skin on the other side of the wound. Care should be taken that the needle enters and exits at the same level on each bite so that the flap is not drawn deeper into the wound, causing an uneven scar to develop.
34 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Only a small bite of the skin edge taken here
Horizontal mattress
Begin here with deep bite of tissue
Vertical mattress
1
2
B Half-buried horizontal mattress (flap stitch)
Figure 1-1. cont’d, Suture techniques. B, Horizontal, vertical, and half-buried horizontal mattress techniques.
DRESSINGS The ideal dressing should be nonadherent and gas permeable, should keep the wound from getting too moist or too dry, and should be impermeable to bacteria and dirt. An adequate dressing for the majority of lacerations is antibiotic ointment applied over the wound and covered with a microporous
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35
dressing. Antibiotic ointment should not be used over tissue adhesives because it will loosen the adhesive.
ANTIBIOTIC PROPHYLAXIS Irrigation and debridement are the biggest factors in decreasing wound infection. Routine antibiotic use for lacerations is not recommended, and prophylaxis should be tailored to the individual patient and based on the risk of infection. Some wounds that are considered higher risk, and therefore candidates for antibiotics, are crush injuries, those with gross contamination, those in immunocompromised patients (e.g., persons with diabetes, transplant recipients, HIV-positive persons), puncture wounds, wounds with retained foreign bodies, cat or human bites, dog bites (on the hand or if difficult to clean), open fractures, and exposed joints or tendons. A first-generation cephalosporin such as cephalexin or an antistaphylococcal penicillin such as dicloxacillin is appropriate for most wounds. Penicillin can be used for oral wounds. Alternatively, amoxicillin-clavulanate can be used for oral wounds or mammalian bites. The usual antibiotic course is 5 days.
TETANUS IMMUNIZATION Tetanus toxoid should be given to all patients who received their last dose more than 5 years previous, with the exception of clean minor wounds. Tetanus toxoid should be given even for clean minor wounds if the patient’s last dose was received more than 10 years previous. Passive immunization with tetanus immune globulin (immunoglobulin G) as well as active immunization with tetanus toxoid is recommended for those without a history of primary tetanus vaccination (series of three injections).
DISPOSITION Patients should be discharged with adequate pain control as well as explicit instructions for wound care and signs of infection. The wound should be kept dry for about 8 hours, after which the patient should cleanse it daily. Showering is a sufficient method, but submersion (e.g., in a bath, hot tub, or lake) is not. Patients should return immediately if they experience any redness, swelling, pus, fever, red streaks, or increasing pain. Wound checks should be done after 48 hours for high-risk wounds, and patients should return in 5–14 days for suture removal (Table 1-4).
36 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 1-4 Suture Removal ANATOMICAL LOCATION Face Scalp/trunk Arms/legs Joints
DURATION OF USE 3–5 days 7–10 days 10–14 days 14 days
RADIOGRAPHS Radiography may sometimes be required to rule out fractures or retained foreign bodies. Fluoroscopy may also be used to locate foreign bodies, and ultrasound has been used to detect tendon injuries or retained foreign bodies. CT may be used for foreign bodies that are difficult to visualize.
Bibliography Bowman MJ: Animal bites in infants and children: An approach to diagnosis and treatment, Emergency Medicine Reports 1999;4(6)53–62. Capellan O: Management of lacerations in the emergency department, Emerg Med Clin North Am 2003;21(1):205–231. Freeman L: Update on wound management: Evidence-based strategies for optimizing outcomes, Emergency Medicine Reports 2002;23(26):315–328. Hals G: The facial trauma patient in the emergency department: Review of diagnosis and management, part II, Emergency Medicine Reports 2004;25(28):217–232. Hollander JE, Singer AJ: Laceration management [review], Ann Emerg Med 1999; 34(3):356–367. Lionelli GT: Wound dressings, Surg Clin North Am 2003;83(3):617–638. Marx JA, Hockberger RS, Walls RM, eds: In Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 737–751. Pearson AS: Management of skin trauma, Prim Care 2000;27(2):475–492. Roberts JR, Hedges JR: Clinical Procedures in Emergency Medicine, ed 4. Saunders; Philadelphia, 2004, pp 655–693. Singer AJ, Hollander JE, Quinn JV: Current concepts: Evaluation and management of traumatic lacerations, N Engl J Med 1997;337(16):1142–1148. Sells L: Topical anesthetics and tissue adhesives: A new generation in pediatric wound, Pediatric Emergency Medicine Reports 1999. Tintinalli JE, Kelen GD, Stapczynski JS, eds: In Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 287–331.
Chapter 2
Cardiology Acute Pericarditis LEN GRUPPO
ICD Code: 420
Key Points Chest pain is positional; it is worse when a patient is supine and diminished or relived when he or she is sitting or leaning forward. A friction rub is common and very helpful diagnostically, but it is frequently difficult to appreciate. Life-threatening causes of chest pain and life-threatening etiologies of pericarditis should be ruled out before idiopathic or presumptive viral pericarditis are diagnosed. ! Emergency Actions ! If a cardiac tamponade is suspected and the patient’s condition is rapidly decompensating, an urgent pericardiocentesis should be performed. If fever or persistent tachycardia disproportionate to the fever are present, myocarditis should be considered and the suspected underlying etiology treated.
DEFINITION Pericarditis is an inflammation of the pericardium, the fibrous sack surrounding the heart. It is frequently idiopathic and benign, but several pathologic conditions can be associated with this condition.
EPIDEMIOLOGY Cardiac tamponade is more common in males than in females. It is most common in adolescents and young adults. Cardiac tamponade occurs in up to 20% of patients after acute myocardial infarction (AMI). Myocarditis is frequently associated with pericarditis; however, the reverse is not as common. Common causes include the following:
Idiopathic Infectious, viral, bacterial, fungal Malignancy Drug-induced 37
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Systemic rheumatic disease Radiation AMI (2–4 days post-AMI) Dressler’s syndrome (2–10 weeks post-AMI) Uremia Myxedema Traumatic (occurring in the posttraumatic period)
CLINICAL PRESENTATION Patients present with precordial or retrosternal chest pain. The pain will be positional in nature; it tends to be worse when the patient is supine and diminished or relived when the patient sits or leans forward. The pain will frequently be sharp or stabbing but may be described as pressure or squeezing. The pain can be gradual or sudden onset and aggravated by inspiration, movement, or exertion. Patients will often have a low-grade fever, but this symptom may be intermittent. Patients can present with dyspnea resulting from increased pain with inspiration and dysphagia resulting from esophageal irritation.
EXAMINATION Patients will present with a pericardial friction rub. This is best heard at lower left sternal border or the apex of the heart. It is frequently audible only during certain phases of respiration. The rub is frequently intermittent— there now, but not in the next hour.
ELECTROCARDIOGRAPHIC FINDINGS Electrocardiographic (ECG) findings in a patient with acute pericarditis include the following:
In V5, V6, or I, calculate the ratio of ST-segment elevation (i.e., baseline to J point) to the height of the T wave. Suspect pericarditis if this measurement is >0.25; the condition is unlikely if it is <0.25 (rather, benign early repolarization is likely). There may also be PR-segment elevation in aVR and ST-segment depression in V1 (as a reciprocal change from V5 and V6 ST-segment elevation). Findings can include low-voltage QRS complexes and electrical alternans, if an effusion is present. The stages, by abnormality, include the following: 1. ST-segment elevation, especially V5 and V6, with decreased RR interval; ST-segment depression can be found in II, aVF, and V4–V6 2. Normal ECG
Acute Pericarditis
39
3. T-wave inversions 4. Resolution of abnormalities ECG
LABORATORY FINDINGS Laboratory tests to be performed in a patient suspected of having acute pericarditis include the following:
Complete blood count (CBC) to screen for infection and leukemia Blood urea nitrogen (BUN) measurement; level will be elevated with uremic pericarditis Streptococcal serological testing (e.g., antistreptolysin O, anti-DNAse, antihyaluronidase) important in patients with a history of rheumatic heart disease or pharyngitis Blood cultures if a bacterial etiology is suspected Serological studies (e.g., antinuclear antibodies, anti-DNA titers, or rheumatoid factor) in patients with systemic symptoms Erythrocyte sedimentation rate (ESR) to establish a baseline; ESR should be monitored to assess the response to treatment Acute and convalescent viral antibody titers Thyroid function tests
RADIOGRAPHS A chest roentgenogram showing an enlarged cardiac silhouette suggests that pericardial effusion will be present. An echocardiogram is recommended to further evaluate suspected pericardial effusion and to assess the extent of hemodynamic compromise.
DIAGNOSIS Often, the diagnosis of a cardiac tamponade is difficult to make at the first presentation. A cardiac tamponade is frequently a diagnosis of exclusion, except in clear-cut cases. The diagnosis of cardiac tamponade is made easier by taking a history and performing physical examination, echocardiogram, and an ECG. Serial ECGs, performed over weeks, are helpful in following the progression and resolution of a cardiac tamponade.
TREATMENT Nonsteroidal anti-inflammatory drugs are effective treatment for idiopathic or presumptive viral pericarditis; this treatment should last for 1–3 weeks. If a specific etiology can be identified, treatment should be directed against that disease. An urgent pericardiocentesis should be preformed if a patient is hemodynamically unstable.
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Bibliography Acute pericarditis. Emergency-Medicine.info. Available at: http://www.emergencymedicine.info/articles/pericarditis.html. Accessed July 4, 2005. Niemann JT: The cardiomyopathies, myocarditis and pericardial disease. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, McGraw-Hill: New York, 2004, pp 343–352.
Automatic Implantable Cardioverter-Defibrillators CHRISTOPHER R. MCNEIL
CPT Code: 93640
Key Points Patients who have received an automatic implantable cardioverterdefibrillator (AICD) within the past 30 days should be evaluated for wound site infection bacteremia and acute thrombophlebitis. The major event with a patient with an AICD is malfunction. A patient will report increased shocks if the device is oversensing. If it is undersensing, the ventricular arrhythmia will not be providing the needed cardioversion or pacing, and the patient will present with syncope, light-headedness, dizziness, and palpitations. ! Emergency Actions ! If a patient is in ventricular tachycardia (VT) or ventricular fibrillation (VF), emergency defibrillation should be performed. If patient is bradycardiac, emergency cardiac passing should be performed.
DEFINITION Automatic implantable cardioverter-defibrillators are implanted in patients who are at a high risk of sudden cardiac death from fatal ventricular arrhythmias. Patients who are at significant risk of developing VT or VF have improved survival with AICDs versus medical antiarrhythmic therapy. The majority of these devices are now placed percutaneously through a transvenous electrode system. The device consists of a lithium battery power source (5- to 10-year life), electronic circuitry, and a lead
Automatic Implantable Cardioverter-Defibrillators
41
system that is typically positioned in contact with the endocardium of the right ventricle. The device is implanted in either the right or left anterior chest wall. Most of today’s AICDs are also capable of ventricular pacing, and many have other pacemaker enhancements. The right ventricular lead is used for sensing, pacing, and delivering biphasic waveform shocks at around 8–10 J. When the device senses VT, it first attempts antitachycardiac pacing or overdrive pacing. It attempts to break the ventricular reentrant circuit by pacing the ventricle at a rate above the VT rate. If this maneuver fails, the device then charges to give successive shocks to cardiovert. When the device senses VF, it immediately charges to give successive shocks to defibrillate. Complications arising shortly after AICD placement include localized wound infection, lead infection, bacteremia, acute thrombophlebitis, and chronic thrombosis of the subclavian or jugular venous system. The other main complication is related to AICD malfunction.
EPIDEMIOLOGY The AICD was first introduced in 1980. It is estimated that more than 80,000 AICDs are implanted annually. There still remains approximately a 2% annual incidence of asystolic arrest in these patients. There is also a 2% risk of localized wound infections and about 1% risk for bacteremia and sepsis.
CLINICAL PRESENTATION Patients who visit the emergency department (ED) with AICD problems have symptoms of either infection, thrombosis, or AICD malfunction. Patients with infection will report weakness, fevers, redness, swelling, or drainage around their wound. In the case of thrombosis, patients will present with edema, pain, and venous engorgement of the arm ipsilateral to the site of lead insertion. Patients with AICD malfunction will commonly present with reports of increasing frequency of shocks. Some patients may have an AICD that is undersensing their ventricular arrhythmia and not providing the needed cardioversion. These patients will present with syncope, light-headedness, dizziness, and palpitations.
EXAMINATION The patient should be given a complete physical examination. Examination of the implant site is required to identify any evidence of cellulites, abscess, or purulent drainage. A complete cardiac examination is required to identify any new murmur. An ECG, rhythm strip, and continuous
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telemetry should also be included in the basic examination of a patient with an AICD.
LABORATORY FINDINGS If the patient presents with symptoms or evidence of infection, a CBC, blood cultures, and wound cultures should be performed. If the patient presents with symptoms or evidence of thrombosis, a CBC and coagulation panel should be ordered. If the concern is for AICD malfunction, electrolyte analyses including potassium and magnesium should be performed. Hypokalemia and hypomagnesemia commonly cause increased frequency of VT and VF. If there is concern for ischemia, cardiac enzymes should also be measured. If the patient takes digoxin, the level of this glycoside must be checked.
DIAGNOSIS The diagnosis of infection is based on the physical examination findings, fever, white blood cell count, and blood and wound culture results. The diagnosis of thrombosis is based on the physical examination findings and usually requires duplex sonography of the internal jugular venous system or contrast-enhanced computed tomography. The diagnosis of AICD malfunction is based on patient history and presentation. AICD malfunction is difficult to diagnose or exclude in the ED in a patient with transient symptoms. Often, there is no evidence of malfunction on telemetry during patient evaluation. Electrolyte and cardiac enzyme measurements are helpful to diagnose metabolic abnormalities or myocardial infarction. Ultimately, the patient needs cardiology consultation and formal AICD interrogation.
RADIOGRAPHS Chest radiography should be performed in all patients who present with AICD problems to identify evidence of lead displacement, lead fracture, or congestive heart failure CHF.
TREATMENT Localized infection, bacteremia, or sepsis needs to be treated with intravenous antibiotics. Staphylococcus aureus and Staphylococcus epidermidis are the organisms identified in 60% to 70% of the cultures, respectively. Vancomycin should be included until culture and sensitivity tests are complete.
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Persons with thrombosis should be admitted to the hospital with appropriate anticoagulation. AICD malfunction treatment includes electrolyte replacement, treating ongoing myocardial ischemia, and standard advanced cardiovascular life support (ACLS). Consultation with a cardiologist is necessary for AICD interrogation. Interrogation allows for assessment of the device’s function and identification of the preceding dysrhythmias. In almost all instances, admission to a telemetry unit is required for observation.
SPECIFIC TREATMENT ACLS should be performed in accordance with current recommendations in patients with AICDs. When defibrillation or cardioversion is necessary, the sternal electrode or paddle should be placed 10 cm from the device. If the device is implanted in the left deltopectoral region, this safety distance is usually exceeded. If the AICD discharges during chest compressions, the rescuer may feel a small shock, but it will not cause injury. The AICD can be deactivated during resuscitation or for treatment of inappropriate shocks by placing a magnet directly over the device. Inappropriate shocks from sensing malfunction occur when the device senses and interprets another rhythm as VT (e.g., supraventricular tachycardia [SVT], nonsustained ventricular tachycardia, or the T wave as a second QRS complex). When a magnet is applied, the antitachycardiac pacing, cardioversion, and defibrillation features will be disabled; however, the bradycardic pacing and sensing will continue to function as programmed.
Bibliography The Anti-arrhythmics Versus Implantable Defibrillators (AVID) Investigators: A comparison of antiarrhythmic therapy with implantable defibrillators, N Engl J Med 1997;337: 1576–1583. Gregaratos G, Cheitlin MD, Conill A, et al: ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices, J Am Cull Cardiol 1998;31(5): 1175–1209. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Shah CP, Thakur RK, Xie B, Hoon VK: Implantable cardioverter defibrillators, Emerg Med Clin North Am 1998;16(2):463–489. Truong JH, Rosen P: Current concepts in electrical defibrillation, J Emerg Med 1997;15 (3):331–338.
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Cardiac Arrhythmias CHRISTOPHER R. MCNEIL
ICD Codes: Sinus tachycardia 427.89, Premature atrial contractions 427.61, Premature ventricular contractions 427.69, Supraventricular tachycardia 427.89, Multi-focal atrial tachycardia 427.89, Atrial fibrillation 427.31, Atrial flutter 427.32, Ventricular tachycardia 427.69, Ventricular fibrillation 427.41, Torsades de pointes 427.9, Accelerated idioventricular rhythm 427.9, Sinus bradycardia 427.81, First-degree atrioventricular (AV) block 427.11, Second-degree AV block, type I (Wenckebach) 427.13, Second-degree AV block, type II 427.12, Third-degree AV block 426.0, Bundle branch blocks 426.2, 426.3, 426.4, Hypocalcemia 427.9, Hypercalcemia 427.9, Hypokalemia 427.9, Hyperkalemia 427.9, Pulmonary embolism 427.9, Wolff-Parkinson-White syndrome 427.7
Key Points Any patient who is believed to be having a cardiac arrhythmia should be placed immediately on a cardiac monitor, and an emergent ECG should be obtained. ! Emergency Actions ! The first action should be to maintain and secure airway, breathing, and circulation (i.e., the ABCs). ACLS protocols should be followed. If the patient has an unstable condition and a tachycardia that is not sinus, immediate sedation and cardioversion should be considered. If the patient’s condition is unstable and he or she has a bradycardia, the patient should consider treatment with atropine, dopamine, external or transvenous electrical ventricular pacing, epinephrine, or isoproterenol.
DEFINITION Arrhythmias and conduction disturbances are typically classified and defined by the rate of conduction, the electrophysiological origin, and the appearance of P waves and QRS complexes on ECG. Multiple classification systems and algorithms exist to assist the healthcare provider in
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the identification of specific arrhythmias and conduction disturbances. The two fundamental categories that exist include the tachycardias and bradycardias. Tachydysrhythmias occur as a result of three basic mechanisms: increased automaticity, reentry, and afterdepolarizations. Bradydysrhythmias occur as a result of suppressed sinus nodal activity or conduction system blocks.
CLINICAL PRESENTATION Patients with tachycardias may present with palpitations, chest pain, dyspnea, light-headedness, syncope, and anxiety. Patients with bradycardias may present with chest pain, dyspnea, light-headedness, syncope, weakness, and malaise.
EXAMINATION A 12-lead ECG and rhythm strip is required to identify the specific dysrhythmia and direct therapy. Patients who present with arrhythmias must first be categorized as having either a stable or unstable condition. Unstable patients demonstrate evidence of decreased end-organ perfusion. Cardiac output is a product of ventricular contraction rate and stroke volume. Tachycardias may lead to decreased cardiac output from lack of sufficient ventricular filling time and a reduced stroke volume. Bradycardias may cause decreased cardiac output simply from the decreased ventricular contraction rate. Evidence of reduced cardiac output and end-organ hypoperfusion include hypotension, chest pain suggesting myocardial ischemia, pulmonary edema, and altered mental status. Unstable patients require rapid pharmacological or electrical therapy after an initial focused primary survey. Stable patients deserve a more detailed history and physical examination.
LABORATORY FINDINGS A chemistry panel with calcium, magnesium, and phosphorus is required. A CBC, coagulation panel, and cardiac enzymes should be considered for any patient for whom cardiac ischemia is suspected as the etiology or consequence of the arrhythmia. Other useful laboratory data may include thyroid function test results and an infectious etiology workup, including urinalysis and blood culture.
RADIOGRAPHS A chest radiograph is necessary to identify any evidence of cardiomegaly, pulmonary edema, pneumothorax, or pneumonia.
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TACHYCARDIA Sinus Tachycardia Sinus tachycardia occurs with accelerated sinus node discharge at a rate higher than 100 beats/min. There is a normal P wave, PR interval, and QRS complex. Causes include pain, fear, anxiety, exertion, fever, hypovolemia, pulmonary embolism, hyperthyroidism, CHF, myocardial ischemia, sepsis, alcohol, nicotine, caffeine, catecholamines, atropine, anticholinergic toxicity, and herbal weight loss preparations. Treatment is focused on the underlying cause of the tachycardia. Beta blockers and calcium-channel blockers will suppress sinus node and atrioventricular (AV) node activity.
Premature Atrial Contractions Premature atrial contractions (PACs) arise from ectopic pacemakers located in the atrium. An abnormal P wave occurs earlier than expected in the cardiac cycle. This P wave may or may not be conducted through the AV node. PACs are one of the most common causes of pauses on the rhythm strip (Fig. 2-1). Usually the QRS complex will appear normal. PACs are fairly common in all ages. Causes include stress, fatigue, alcohol, caffeine, nicotine, catecholamines, chronic obstructive pulmonary disease (COPD), theophylline, and digoxin toxicity. PACs rarely require treatment beyond removal of the precipitating agent or treatment of the underlying disease. Beta blockers and calcium-channel blockers may be effective in reducing the frequency of PACs in a symptomatic patient.
Premature Ventricular Contractions Premature ventricular contractions (PVCs) arise from ectopic foci within the ventricular myocardium. The QRS complex occurs earlier than expected in the cardiac cycle. The PVC is abnormal in shape, is not preceded by a P wave, and has a duration of more than 120 msec (Fig. 2-2). The T wave is large and occurs in the opposite direction of the QRS complex. PVCs may occur alone, in pairs called couplets, or as three in succession, called triplets. Bigeminy indicates a regular QRS complex followed by a PVC that occurs regularly, as in Figure 2-3. Trigeminy is a regular pattern that consists of a regular QRS complex followed by two PVCs that
Figure 2-1. Rhythm strip showing an ECG pattern of premature atrial contractions.
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Figure 2-2. Rhythm strip showing an ECG pattern of premature ventricular contractions.
Figure 2-3. Rhythm strip showing an ECG pattern of a regular QRS complex followed by two premature ventricular contractions.
occurs regularly. Causes include stress, caffeine, nicotine, catecholamines, electrolyte abnormalities, myocardial ischemia, structural heart disease, and digoxin toxicity. Most patients require no pharmacological treatment. Treatment includes removing any precipitating drug or toxin and evaluating the patient for structural heart disease. The first-line treatment for symptomatic PVCs or PVCs in the setting of acute coronary syndrome is beta blockers. Antiarrhythmics show no mortality benefit.
Supraventricular Tachycardia SVTs arise from an ectopic pacemaker or reentry above the bifurcation of the bundle of His. Most SVTs are AV nodal reentrant tachycardias. The ECG typically exhibits regular, narrow QRS complexes (Figs. 2-4 and 2-5). P waves are often absent. The causes of SVT include myocardial
Figure 2-4. Rhythm strip showing a typical ECG pattern of supraventricular tachycardia.
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Figure 2-5. Rhythm strip showing another ECG pattern of supraventricular tachycardia (see Fig. 2-4).
ischemia, catecholamines, COPD, digoxin toxicity, rheumatic heart disease, mitral valve prolapse (MVP), alcohol, electrolyte abnormalities, and accessory pathways such as Wolff-Parkinson-White syndrome (WPW). Most patients with SVT have no evidence of structural heart disease. Treatment is aimed at suppressing the ectopic foci or disrupting the reentry circuit. Management may include carotid massage, adenosine, beta blockers, calcium-channel blockers, amiodarone, procainamide, and synchronized cardioversion. If the patient’s condition is unstable, immediate sedation and synchronized cardioversion are indicated. Synchronized cardioversion for SVT is usually effective between 0.5 and 1 J/kg.
Multifocal Atrial Tachycardia Multifocal atrial tachycardia (MFAT) is an irregular rhythm caused by three or more different P waves with varying PP and PR intervals (Fig. 2-6). MFAT is usually seen in elderly patients with COPD or other chronic lung diseases. It may also occur with CHF, sepsis, theophylline
Figure 2-6. Rhythm strip showing an ECG pattern of multifocal atrial tachycardia.
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toxicity, electrolyte abnormalities, and hypoxia. Treatment is focused on the underlying condition. Beta blockers, calcium-channel blockers, and magnesium may be useful in the treatment of MFAT if tachycardia persists despite correction of the underlying cause. Caution should be exercised with beta blockers because they may worsen bronchospasm.
Atrial Fibrillation Atrial fibrillation arises from multiple areas of atrial myocardium continuously discharging and contracting. The atrial rate is between 400 and 600 beats/min, and the ventricular rate is variable depending on the refractory period of the AV node (Fig. 2-7). As a result, the RR interval is irregular. When the ventricular contraction rate is higher than 100 beats/min, it is termed atrial fibrillation with rapid ventricular response (atrial fibrillation with RVR). Atrial fibrillation may be constant or may occur in a paroxysmal manner. Causes of atrial fibrillation include hypertension, rheumatic heart disease, coronary artery disease (CAD), hyperthyroidism, COPD, CHF, and alcohol intoxication. Atrial fibrillation predisposes patients to atrial thrombus formation and subsequent systemic arterial emboli. Patients are frequently administered aspirin or systemic anticoagulation. Treatment is focused on controlling the ventricular rate. Calcium-channel blockers and beta blockers are first-line agents; digoxin may also be considered. If the duration of atrial fibrillation is less than 48 hours or no thrombus is present on transesophageal echocardiography, chemical or electrical cardioversion may be considered. If the patient’s condition is unstable, immediate sedation and synchronized cardioversion is indicated (100–200 J is usually effective).
Atrial Flutter Atrial flutter arises from a localized area of ectopy in the atrium. On ECG there is a regular atrial rate between 250 and 350 beats/min, creating the classical “sawtooth” pattern (Fig. 2-8). The degree of AV block is usually 2:1 but may be greater. Atrial flutter is associated with CAD and AMI. It is also caused by CHF, pulmonary embolus, myocarditis, and digoxin toxicity. Atrial flutter is often the transition between sinus
Figure 2-7. Rhythm strip showing an ECG pattern of atrial fibrillation.
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Figure 2-8. Rhythm strip showing an ECG pattern of atrial flutter.
rhythm and atrial fibrillation. Treatment is directed at controlling the ventricular rate. Calcium-channel blockers and beta blocker are first-line agents. Chemical and electrical cardioversion may also be considered. If the patient’s condition is unstable, immediate sedation and synchronized cardioversion is indicated (0.5–1 J/kg is usually effective).
Ventricular Tachycardia VT occurs when more than three depolarizations occur from a ventricular focus. VT less than 30 seconds duration is termed nonsustained ventricular tachycardia. The QRS complex is generally wide and regular with a rate higher than 100 beats/min (usually 150–200) (Fig. 2-9). The most common causes of VT are ischemic heart disease and AMI. Other less common causes include MVP, hypertrophic obstructive cardiomyopathy, hypoxia, electrolyte abnormalities, Brugada syndrome, and arrhythmogenic right ventricular dysplasia. Treatment is administered according to ACLS guidelines. Amiodarone and lidocaine are first-line agents for stable VT. Magnesium, procainamide, and bicarbonate can also be considered for refractory VT. If the patient’s condition is unstable, immediate sedation and synchronized cardioversion are indicated.
Ventricular Fibrillation VF arises when there are no organized depolarizations or contractions of the ventricles. The “quivering” myocardium does not exhibit discernible P waves or QRS complexes (Fig. 2-10). Treatment is administered according to ACLS guidelines.
Figure 2-9. Rhythm strip showing an ECG pattern of ventricular tachycardia.
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Figure 2-10. Rhythm strip showing an ECG pattern of ventricular fibrillation.
Torsades de Pointes Torsades de pointes is an atypical VT when the QRS axis swings from a positive to a negative direction (i.e., “twisting of the points”) (Fig. 2-11). This condition arises from a prolonged QT interval and early afterdepolarizations. Causes include multiple medications and toxins, electrolyte disorders, CAD, and several congenital conditions. Treatment consists of intravenous magnesium, overdrive pacing, and care according to ACLS guidelines.
Accelerated Idioventricular Rhythm Accelerated idioventricular rhythm (AIVR) is an ectopic ventricular rhythm occurring at a rate of 60–100 beats/min (Fig. 2-12). The QRS complex is wide and most often occurs in short runs of 3–30 beats. AIVR occurs in the setting of AMI and appears during administration of thrombolytics. This rhythm requires no treatment.
Figure 2-11. Rhythm strip showing an ECG pattern of torsades de pointes.
Figure 2-12. Rhythm strip showing an ECG pattern of accelerated idioventricular rhythm.
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BRADYCARDIA Sinus Bradycardia Sinus bradycardia arises from suppression of the sinus node. There are normal P waves, a normal PR interval, normal QRS complexes, and a rate above 60 beats/min (Fig. 2-13). Sinus bradycardia occurs in wellconditioned athletes, during sleep, and as a result of hypothyroidism, vagal stimulation, AMI, and certain medications (e.g., narcotics, beta blockers, calcium-channel blockers, digoxin, and antiarrhythmics). Sinus bradycardia usually requires no treatment. There is generally adequate response to atropine.
First-Degree AV Block First-degree AV block consists of a PR interval greater than 200 msec (Fig. 2-14). This condition requires no treatment.
Second-Degree AV Block, Type I (Wenckebach) Wenckebach block consists of progressive prolongation of the PR interval until a nonconducted P wave occurs (Fig. 2-15). This condition is associated with an acute inferior myocardial infarction or digoxin toxicity. There is generally no treatment required for patients with this condition.
Second-Degree AV Block, Type II In this rhythm, the PR interval remains constant with intermittent conduction of atrial impulses (Fig. 2-16). This rhythm implies a conduction block
Figure 2-13. Rhythm strip showing an ECG pattern of sinus bradycardia.
Figure 2-14. Rhythm strip showing an ECG pattern of first-degree atrioventricular block.
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Figure 2-15. Rhythm strip showing an ECG pattern of second-degree atrioventricular block, type I (Wenckebach).
Figure 2-16. Rhythm strip showing an ECG pattern of second-degree atrioventricular block, type II.
below the AV node. This rhythm may degrade into complete heart block at any time. An adequate safety net must be established for these patients, with a temporary transvenous pacer standing by. Most patients will require permanent pacemaker placement.
Third-Degree AV Block Complete heart block occurs when there is no AV conduction. P waves and QRS complexes exist independently of each other (Fig. 2-17). The ventricular escape beats typically occur at a rate of about 40 beats/min. These patients require transvenous pacer placement for stabilization.
OTHER ABNORMALITIES Bundle Branch Blocks Bundle branch blocks are represented by a QRS complex greater than 120 msec (Fig. 2-18).
Figure 2-17. Rhythm strip showing an ECG pattern of third-degree atrioventricular block.
54 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER V6
V1
Normal
R
R⬘ R RBBB T S
q S
LBBB
T
Figure 2-18. ECG patterns of bundle branch blocks. RBBB, Right bundle branch block; LBBB, left bundle branch block.
Hypocalcemia Hypocalcemia is exhibited on ECG by QT prolongation (Fig. 2-19).
Hypercalcemia A short QT interval identifies hypercalcemia (Fig. 2-20).
Hypokalemia Flat T waves and U waves on ECG are features of hypokalemia (Fig. 2-21).
Hyperkalemia Hyperkalemia is identified on ECG by peaked T waves, increased PR and QT intervals, flat P waves, and wide QRS complexes (Fig. 2-22).
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Figure 2-19. Rhythm strip showing an ECG pattern of hypocalcemia.
Figure 2-20. Rhythm strip showing an ECG pattern of hypercalcemia.
Figure 2-21. Rhythm strip showing an ECG pattern of hypokalemia.
Figure 2-22. Rhythm strip showing an ECG pattern of hyperkalemia.
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Pulmonary Embolism Pulmonary embolism on ECG sometimes displays classically described “S1QT3,” though this only applies to approximately 10% of pulmonary embolisms. More commonly, the features present are sinus tachycardia, ST depressions, and transient right bundle branch block—all evidence of right heart strain (Fig. 2-23).
Wolff-Parkinson-White Syndrome WPW is a preexcitation syndrome in which an accessory pathway connects the atria to the ventricles in addition to the AV node. This syndrome consists of a short PR interval (<120 msec), a wide QRS complex (>100 msec), and a slurred upstroke of the QRS (delta wave) (Fig. 2-24). This condition
Figure 2-23. Rhythm strip showing an ECG pattern of pulmonary embolism.
Figure 2-24. Rhythm strip showing an ECG pattern of Wolff-Parkinson-White syndrome.
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is prone to reentrant SVTs. The SVT may appear as a narrow- or widecomplex QRS, depending on AV node involvement and the direction of the reentry circuit. All AV nodal blocking medications (e.g., adenosine, calcium-channel blockers, beta blockers) should be used with caution in these patients when treating an irregular or wide-complex SVT. Use of these agents may potentiate a more rapid ventricular response from an unopposed accessory pathway. Procainamide or amiodarone are the drugs of choice in irregular or wide-complex WPW tachycardias.
Bibliography The American Heart Association in collaboration with the International Liaison Committee on Resuscitation, Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: Advanced cardiovascular life support; 7D: The tachycardia algorithms, Circulation 2000;102:I158. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al: ACC/AHA/ESC Guidelines for the Management of Patients with Supraventricular Arrhythmias—executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines, Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias, Circulation 2003;108:1871. Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Ferguson JD, DiMarco JP: Contemporary management of paroxysmal supraventricular tachycardia, Circulation 2003;107:1096. Ganz LI, Friedman PL: Supraventricular tachycardia, N Engl J Med 1995;332:162. Gupta AK, Thakur RK: Wide QRS complex tachycardias, Med Clin North Am 2001;85:245. Kastor JA: Multifocal atrial tachycardia, N Engl J Med 1990;322:1713. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Orejarena LA, Vidaillet H Jr, DeStefano F, et al: Paroxysmal supraventricular tachycardia in the general population, J Am Coll Cardiol 1998;31:150. Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000. Trohman RG: Supraventricular tachycardia: Implications for the intensivist, Crit Care Med 2000;28:N129.
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Cardiac Examination LEN GRUPPO
ICD Code: 70.0
Key Points/Quick Reference A rapid focused examination is critical. The goal is to support the primary diagnosis and rule out the differential diagnosis to bring the proper treatment to bear expeditiously. ! Emergency Actions ! When appropriate, the ABC emergency actions should be addressed (i.e., airway, breathing, and circulation).
DEFINITION The cardiac evaluation includes: 1. Formulation of a differential diagnosis. 2. Directed physical examination, to address the concerns of the differential diagnosis in an emergency setting. 3. Stabilization of the patient’s condition based on cardiac examination and EKG. 4. Complete cardiac and physical examination after the patient is stabilized.
CLINICAL PRESENTATION The differential diagnosis of cardiac chest discomfort includes ischemia, infarction, pericarditis, contusion, MVP, aortic dissection (Stanford classification A), tamponade, myocarditis, and endocarditis. Additional cardiac diagnoses include CHF, papillary muscle rupture, MVP, atrial fibrillation, various other arrhythmias, various conduction defects, left ventricular hypertrophy, cardiomyopathy, and cardiogenic shock. These diagnoses can occur as a result of other conditions and can be complicated by a variety of comorbidities.
EXAMINATION
Heart sounds S1 and S2 are often diminished due to poor cardiac contractility.
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S3 (also known as “gallop”) is present in 15%–20% of patients with an AMI. S4 is frequently found in patients with long-standing hypertension or cardiac dysfunction. New murmur is worrisome and can indicate papillary muscle rupture, MVP, or ventricular septal defect. If friction rub is present, pericarditis should be considered. Lung If lungs are clear in the setting of chest discomfort, consider right ventricular MI. If rales are present, CHF may be present. If breath sounds are unequal or unilaterally absent, pneumonia and pneumothorax should be considered. Vascular system Carotid bruits may indicate atherosclerotic disease. If unequal radial and femoral pulses are present, thoracic aortic or abdominal aortic dissection, respectively, should be considered. Jugular venous distention (JVD) after deep inspiration may indicate right-sided MI. Skin The skin of a patient with chest discomfort will likely be diaphoretic. A sympathomimetic response may occur in conjunction with a variety of conditions, including pain and hypotension. Abdomen A pulsatile mass or aortic bruit suggests abdominal aortic aneurysm. Hepatojugular reflux may indicate CHF. Extremities Dependent edema may indicate the presence of CHF. Rectum Rule out active gastrointestinal (GI) tract bleeding; this can exacerbate tenuous CAD, causing ischemia. Active GI tract bleeding also must be ruled out before lytics and heparin are administered. Malodorous, black tarry stool strongly suggests an active GI tract bleed. Heme-positive brown stool may be indicative of an active GI tract bleed.
LABORATORY FINDINGS Pertinent laboratory examination results are required for diagnosis.
RADIOGRAPHS Radiographs should be directed in regard to the differential diagnosis and physical examination.
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TREATMENT AND OUTCOME The cardiac examination will assist the practitioner in evaluating the patient. The cardiac examination is a part of the entire evaluation for a patient suspected of having cardiac disease. The ability to perform cardiac examination is essential to the development of a differential diagnosis, the ordering of laboratory and radiographs test, and the definitive diagnosis and treatment of a patient.
Bibliography Hollander JE: Acute coronary syndromes: Acute myocardial infarction and unstable angina. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 343–352.
Cardiac Tamponade CHRISTOPHER R. MCNEIL
ICD Code: 423.9
Key Points Symptoms of cardiac tamponade are nonspecific. Patients may present with dyspnea, cough, or chest pain. Examination may reveal the classic Beck’s triad: hypotension,distendedneck veins,andmuffledheart sounds. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines, providing oxygen and IV fluid boluses. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. Patients who do not respond to aggressive IV fluid boluses may require inotropic support. Pericardiocentesis should be performed as soon as possible under controlled conditions.
DEFINITION Cardiac tamponade is a physiological condition that occurs when pericardial fluid accumulates under high pressure. As fluid accumulates, the pressure generated compresses the cardiac chambers, resulting in decreased preload, decreased ventricular filling, decreased myocardial
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compliance, and ultimately reduced cardiac output. The amount of pericardial fluid required to produce cardiac tamponade depends on how quickly it accumulates. Trauma can produce tamponade physiology with as little as 20–30 ml of fluid. Nontraumatic pericardial effusions occur more gradually and may require several hundred milliliters of fluid before the pressure in the pericardial sac begins to compress the myocardium.
EPIDEMIOLOGY The incidence of cardiac tamponade in patients with penetrating trauma to the chest and upper abdomen is approximately 2% and rarely occurs after blunt trauma. Medical or nontraumatic causes of tamponade occur much more frequently. Uremia is one of the most common causes. Nearly 10% of all patients with malignancy develop cardiac tamponade during their illness.
ETIOLOGY
Trauma Malignancy Acute viral or idiopathic pericarditis Uremia Bacterial or tuberculous pericarditis Hemorrhagic (e.g., anticoagulation) Systemic lupus erythematosus, rheumatoid arthritis, other connective tissue diseases Postradiation
CLINICAL PRESENTATION Symptoms of cardiac tamponade are nonspecific. Patients may present with dyspnea, cough, or chest pain. Additional symptoms may be present as a result of the underlying disease. Patients may report weakness, exercise intolerance, fevers, weight loss, edema, and ascites. Patients will usually present with hypotension, tachycardia, or tachypnea and may appear extremely anxious.
EXAMINATION Examination may reveal the classic Beck’s triad: hypotension, distended neck veins, and muffled heart sounds. A pericardial friction rub can often be heard. Pulses paradoxus in excess of 10 mmHg is the hallmark of advanced cardiac tamponade. (Pulsus paradoxus is performed by taking
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the blood pressure; as the patient breathes quietly, lower the cuff pressure to the systolic level. At that point, note the pressure, then lower the pressure until the systolic sound can be heard throughout the respiratory cycle. There should be no difference in these two levels of sound greater than 3 or 4 mmHg.) These examination findings may not be present if tamponade develops quickly.
LABORATORY FINDINGS A CBC, chemistry panel, coagulation panel, cardiac enzymes, liver function tests, blood cultures, and a blood type and cross for packed red blood cells and fresh frozen plasma should be performed.
DIAGNOSIS A diagnosis is made on the basis of clinical presentation, physical examination, chest radiography, ECG, and echocardiography. The chest radiograph may show an enlarged cardiac silhouette (Fig. 2-25). The ECG classically has diffuse low-voltage QRS complexes and electrical alternans (Fig. 2-26).
Figure 2-25. Chest x-ray showing enlarged cardiac silhouette in cardiac tamponade.
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Figure 2-26. Rhythm strip showing classic ECG pattern of diffuse low-voltage QRS complexes and electrical alternans in cardiac tamponade.
TREATMENT Initial resuscitative treatment includes establishing adequate intravenous access and providing oxygen and intravenous fluid boluses. Patients who do not respond to aggressive intravenous fluid boluses may require inotropic support. Pericardiocentesis should be performed in the cardiac catheterization laboratory under ultrasound guidance. Many patients with cardiac tamponade will ultimately require a pericardotomy.
Bibliography Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Fowler NO, Gabel M: The hemodynamic effects of cardiac tamponade: Mainly the result of atrial, not ventricular, compression, Circulation 1985;71:154. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Reddy PS, Curtiss EI, Uretsky BF: Spectrum of hemodynamic changes in cardiac tamponade, Am J Cardiol 1990;66:1487–1491. Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000.
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Congestive Heart Failure MARTIN A. DOCHERTY
ICD Code: 428.0
Key Points A history of exertional dyspnea and paroxysmal nocturnal dyspnea, with symptoms exacerbated by lying flat in bed, are commonly associated with CHF. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines and providing oxygen. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. An immediate chest radiograph should be performed.
DEFINITION CHF can be classified into the following categories: (1) systolic failure, due to impaired cardiac contractility; (2) diastolic failure, caused by impaired ventricular relaxation; (3) right heart failure (most commonly due to left heart failure) manifesting as extremity edema, JVD, and hepatic congestion; or (4) high-output or hyperkinetic failure, as seen in thyroid storm, severe sepsis, severe anemia, and beriberi, where cardiac output is unable to keep up with the demands for tissue perfusion. Myocardial ischemia, hypertension, and valvular heart disease are the most common causes of decompensated CHF. Cardiomyopathies, infiltrative cardiac disorders, and pericardial restrictive conditions may also result in CHF.
EPIDEMIOLOGY Approximately 5 million people in the United States have CHF. One million admissions to hospitals annually are due to CHF and its complications.
PATHOPHYSIOLOGY An increase in right ventricular volume and pressure translates into a rise in pulmonary capillary pressure. This causes a subsequent fluid transudate to accumulate in the lung interstitium and alveolar spaces. The effects of this on lung compliance and diffusing capacity lead to the familiar
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presentation of dyspnea and hypoxia. Subsequent activation of the reninangiotensin and sympathetic nervous systems result in tachycardia, increased systemic vascular resistance, and further decreases in myocardial function. This leads to decompensation. This decompensation may be gradual, as seen in chronic CHF, or relatively sudden, as seen in socalled flash pulmonary edema. The above cascade may be precipitated by the following: 1. Acute myocardial ischemia or infarction 2. Acute aortic or mitral valve insufficiency 3. Mitral stenosis complicated by conditions leading to significant tachycardia (such as heavy exercise or atrial fibrillation with a rapid ventricular response) 4. Use of negative inotropic medications such as beta and calciumchannel blockers 5. Significant increase in sodium intake 6. Severe hypertension 7. Overexertion in susceptible patients Other precipitating factors include high fever, sepsis, thyroid storm, and severe anemia (as mentioned previously under high-output failure).
CLINICAL PRESENTATION AND HISTORICAL FINDINGS A history of exertional dyspnea and paroxysmal nocturnal dyspnea, with symptoms exacerbated by lying flat in bed, are common complaints. It is important to determine whether chest pain is an associated symptom because this may point to ischemia as a precipitating factor. Palpitations can indicate atrial fibrillation or other dysrhythmias. A history of increasing fluid retention may be present.
EXAMINATION 1. Obtain vital signs looking for hypertension, hypotension, tachycardia, or profound bradycardia. Also look for hypothermia or hyperthermia. 2. Evaluate for the presence of JVD and hepatojugular reflux (an increase in neck vein distension when the examiner exerts steady pressure over the liver). 3. Observe heart sounds, monitoring for new or significant murmurs, S3 gallop, and muffled heart sounds. 4. Perform lung auscultation to detect crackles (i.e., rales) or wheezes and decreased or absent breath sounds. It may also be helpful to perform percussion to detect the presence of any pleural effusion in cases of decreased breath sounds.
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5. Examine the extremities to determine the presence of edema. Presence of unilateral leg edema in the presence of dyspnea should raise suspicion for deep vein thrombosis and pulmonary embolus.
LABORATORY FINDINGS CBC and serum chemistries should be performed to evaluate for anemia and renal function. Cardiac enzyme analyses may be helpful if ischemia is a concern. B-natriuretic peptide (BNP) levels can be very useful in distinguishing CHF from other causes of dyspnea. They can also provide a baseline level on which to gauge treatment efficacy. Arterial blood gas analyses may be helpful in identifying CO2 retention or O2 saturation in cases where the pulse oximeter reading is not reliable. An ECG should be performed to look for the presence of ischemic changes or dysrhythmias. Lastly, an ED bedside echocardiogram, where available, may aid in the diagnosis of significant pericardial effusion.
RADIOGRAPHS A chest radiograph can show presence of cardiomegaly, pulmonary vascular congestion or frank pulmonary edema, pleural effusions, or focal infiltrates. The size of the mediastinum should be noted, as should the presence of a “water bottle cardiac outline” seen in the presence of pericardial effusion.
TREATMENT The ABCs (i.e., airway, breathing, circulation) should be addressed. If the patient presents in extremis, rapid intubation is often required. It is also reasonable to consider a trial of bilevel positive airway pressure in cases of moderate respiratory failure occurring while other therapy is being instituted. Intravenous access should be initiated (making sure not to overlook the distended external jugular veins as a potential intravenous access site), high-flow oxygen should be started, and observation of the patient with a cardiac monitor and pulse oximeter should be started. A Foley catheter is a viable consideration. Nitrates and diuretics are the mainstay of drug treatment for CHF. 1. Furosemide (Lasix), 20–40 mg, can be given intravenously. If a patient is taking oral Lasix, he or she should receive twice the daily dose as an intravenous bolus. The clinician should watch for hypotension. 2. Nitroglycerin can be given as a spray, sublingually, transcutaneously, or as an intravenous infusion. If an intravenous dose is used, the dosage should start at 0.5 mg/kg/min and titrate up as need. The systolic
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6.
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blood pressure should be kept above 100 mmHg, and clinician should watch for prolonged hypotension. The frequent headache accompanying nitrate use can be treated with acetaminophen. If the patient is taking sildenafil (Viagra) or similar medications, profound hypotension can result when combined with nitrates; caution should be exercised. Morphine in 2–4 mg intravenous boluses may help reduce anxiety and provide some preload reduction. The clinician should watch for hypotension and respiratory depression. Nitroprusside at a dose of 0.1–0.2 mg/kg/min may be useful in cases of severe, refractory hypertension. However, a possibility of cyanide toxicity exists with extended use. Nesiritide, a form of BNP, may be indicated in patients with borderline blood pressure and in those in whom therapeutic doses of other diuretics have failed to produce reasonable urine output. It is given as a 2-mg/kg bolus and then as an infusion of 0.01 mg/kg/min. Dopamine and dobutamine may be used in patients presenting in cardiogenic shock. Dobutamine increases cardiac output and causes a decrease in peripheral vascular resistance. The starting dose is 5 mg/ kg/min and can be titrated up to 20 mg/kg/min. Dopamine at doses of 3–10 mg/kg/min increases stroke volume and cardiac output.
Bibliography Cotter G, Metzkor E, Kaluski E, et al: Randomised trial of high dose isosorbide dinitrate plus low dose furosemide versus high dose furosemide plus low dose isosorbide dinitrate in severe pulmonary edema, Lancet 1998;351:389. Loh E.: Maximizing management of patients with decompensated heart failure, Clin Cardiol 2000;23(Suppl III):1. Morrison LK, Harrison A, Krishnaswamy P, et al: Utility of a rapid B-natriuretic peptide assay in differentiating congestive heart failure from lung disease in patients presenting with dyspnea, J Am Coll Cardiol 2002;39:202. Williams JF, Bristow MR, Fowler MB, et al: Guidelines for the evaluation and management of heart failure: Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Circulation 1995;92:2764.
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Evaluation of Cardiac Chest Pain LEN GRUPPO
ICD Code: 410
Key Points/Quick Reference The differential diagnosis for chest pain is extensive.‘‘Pain’’ or ‘‘discomfort’’ is usually mechanical, inflammatory, infectious, or ischemic in origin. A diagnosis of cardiac chest pain can be difficult to make and often requires a high index of suspicion. Cardiac chest pain can include ischemia, infarction, pericarditis, contusion, MVP, aortic dissection (Stanford classification A), tamponade, myocarditis, and endocarditis. These conditions occur as a result of other conditions and are complicated by a variety of comorbidities. ! Emergency Actions following:
!
Appropriate emergency actions include the
Address the ABCs (i.e., airway, breathing, and circulation). Consider life-threatening diagnoses. Perform an ECG within 10 minutes of presentation. Establish a “safety net”: two large-bore intravenous lines, O2 NC 2–4 L/ min, cardiac/blood pressure/SO2 monitor. Initiate ACLS protocols, if applicable, as soon as possible. Use the acronym and aphorism: “MONA greets all patients.” This stands for the administration of morphine, oxygen, nitroglycerin, and aspirin. Purposefully initiate other appropriate treatments and studies. Consult with a cardiologist or transfer to the patient a facility with cardiac catheterization capabilities.
DEFINITION Myocardial ischemia occurs when a portion of the myocardium receives insufficient oxygen. This is frequently due to inadequate blood supply from a partial or complete blockage of a coronary artery. When the myocardial oxygen supply is completely disrupted, cell death, or infarction, occurs. Blockages usually occur from one of two sources: a fixed atherosclerotic plaque or a ruptured atherosclerotic plaque with subsequent fibrin clot formation. Other causes of ischemia include hypotension, coronary artery spasm, tachycardia in the presence of underlying significant
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cardiovascular disease, cocaine use, methamphetamine use, and hypertrophic cardiomyopathy.
EPIDEMIOLOGY The epidemiology of cardiac chest pain is as follows:
Approximately 5% of all U.S. ED visits—4 to 5 million patients—are evaluated for chest pain each year. Two million have acute coronary syndrome. One and one half million have AMI. One half million have unstable angina. One half million patients with AMI die each year. Fifty percent of deaths occur in the first hour after a cardiac event. Thirty-four percent die during the patient’s first prolonged attack. For 17%, pain is their first, last, and only symptom. Primary risk factors (Note: Risk factors are poor predictors of cardiac risk for acute coronary syndrome and AMI in the ED setting. They are primarily useful in the risk stratification of asymptomatic patients. Despite this, they remain a valuable risk management tool for the provider.) Hypertension Diabetes Cigarette smoking Hypercholesterolemia Immediate family history of CAD or AMI Personal history of CAD or AMI
CLINICAL PRESENTATION Any patient with chest pain or discomfort of any kind; unexplained pain in the neck, jaw, shoulder or arm; or unexplained fatigue, syncope or near syncope, shortness of breath, or dyspnea on exertion is suspect of having a cardiac origin for his or her chest pain. This is a continuum of disease that includes stable and unstable angina, non–Q-wave and Q-wave infarction. Symptoms of acute myocardial infarction include the following:
Chest pain radiating to the shoulder, neck, jaw, or arm lasting more than 15–20 minutes (70%–80%) Pressure, squeezing, ache, dull (32%) Sharp (20%) Pain that patient cannot describe (42%) Feeling described as “indigestion” (43%) Shortness of breath Dyspnea on exertion Tachypnea
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Diaphoresis Dizzy, light-headed, presyncope, syncope Nausea, vomiting Feeling of stress, anxiety, or impending doom Vague, nonspecific complaints are usually seen in the following patients: Persons with diabetes (ketoacidosis should also be ruled out) Elderly persons Women Hypotension or hypertension Tachycardia or bradycardia Signs of CHF (e.g., pulmonary edema, JVD, peripheral edema)
EXAMINATION The examination of a patient with cardiac chest pain should include the following points:
Listen for heart sounds. S1 and S2 are often diminished due to poor cardiac contractility. S3 (i.e., “gallop”) is present in 15%–20% of patients with an AMI. S4 is frequently found in patients with long-standing hypertension or cardiac dysfunction. New murmur is worrisome and can indicate papillary muscle rupture, MVP, or ventricular septal defect. When a friction rub is present, pericarditis should be considered. Examine the lung. If clear, right ventricular MI might be present. If there are rales, CHF might be present. Unequal or unilateral absent breath sounds could indicate pneumonia or pneumothorax. Examine the vascular system. The presence of carotid bruits could indicate atherosclerotic disease. Unequal radial and femoral pulses might be an indicator of thoracic aortic or abdominal aortic dissection, respectively. If there is JVD after deep inspiration, consider right-sided MI. An examination of the skin might reveal a diaphoretic or sympathomimetic response to a variety of conditions, including pain, hypotension, and others. Perform an abdominal examination. A pulsatile mass or aortic bruit could mean an abdominal aortic aneurysm is present. Hepatojugular reflux may indicate the presence of CHF. If an examination of the extremities reveals dependent edema, consider CHF.
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During a rectal examination, it is important to rule out active GI bleeding.
This condition can exacerbate tenuous CAD causing ischemia, and it also must be ruled out before lytics and heparin are administered. Malodorous, black tarry stool strongly suggests active GI bleeding. Heme-positive brown stool may be indicative of active GI bleeding.
ECG FINDINGS ECG findings of note are as follows:
A 12-lead ECG abnormality of concern is ischemia (Fig. 2-27): ST-segment elevation or depression with or without reciprocal lead changes, 1 mm, in two anatomically contiguous leads Flat or inverted symmetrical T waves Poor R-wave progression New left bundle branch block ST-segment elevation in V4R (Always check V4R when inferior MI is suspected. See right-sided MI in later text.) Reciprocal changes, anatomically opposite ECG changes Infarction (Fig. 2-28): Q waves >0.04 sec or > one third the height of the QRS complex Large R wave in V1 (consider as a Q wave from the posterior myocardium)
Figure 2-27. Rhythm strip showing ECG abnormalities in cardiac chest pain: ischemia.
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Figure 2-28. Rhythm strip showing ECG abnormalities in cardiac chest pain: infarction.
Nonspecific ST- or T-wave changes Arrhythmias Serial ECGs very helpful
LABORATORY FINDINGS Useful laboratory test results include the following:
Cardiac enzymes Helpful for patients with nondiagnostic ECG findings. Perform serial cardiac enzyme measurements; repeat every 6 hours for three times (i.e., initial, plus two more). These tests are essential to be reasonably certain that an AMI has not occurred. Troponin I: This test is 90%–100% sensitive and 83%–96% specific. Troponin I rises in 2–4 hours, has a maximum sensitivity in 8–12 hours, and remains elevated for 7–10 days. Creatine kinaseMB isoenzyme: This test of a component of total CK is 71%–86% sensitive and 95%–97% specific. Creatine kinaseMB rises in 3–4 hours, has a maximum sensitivity in 8–12 hours, and remains elevated for 2–4 days. Myoglobin: This test is 80%–94% sensitive and 80%–92% specific. The level rises in 1–2 hours, has a maximum sensitivity in 4–8 hours, and remains elevated 0.5–1 day. BNP: This test is helpful in diagnosing CHF. BNP is a hormone produced by the heart that is increased in the blood when the heart workload increases.
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CBC: This test assists in recognition of bleeding disorders and infection. Chemistries: Electrolyte imbalances can cause arrhythmias, MI can precipitate diabetic ketoacidosis, and hypoglycemia/hyperglycemia can complicate management. Lipid profile: This test helps risk-stratify ambiguous cases and aids cardiologists with in-hospital and discharge management.
RADIOGRAPHS Portable chest x-ray helps to rule out other causes of chest pain and dyspnea. Radiographs can also assist with the identification of cardiomegaly, calcified heart valves, CHF, pneumonia, pneumothorax, pulmonary embolism, and aortic dissection. If chest radiography is available, it should be performed before lytics or heparin are given to rule out aortic dissection.
DIAGNOSIS History is frequently most important component of diagnosis. Symptoms of more than 15 minutes’ duration are concerning and may signify acute coronary syndrome or AMI. Physical examination provides valuable clues. An ECG is critical to the determination of which treatment pathway to take. Cardiac enzyme analyses can also be helpful in ambiguous cases.
TREATMENT AND OUTCOME Appropriate treatment is as follows:
Use the acronym and aphorism: “‘MONA’ greets all patients.” This stands for the administration of morphine, oxygen, nitroglycerin, and aspirin. Administer sublingual nitroglycerin unless the diastolic blood pressure is less than 60 mmHg or the heart rate is less than 60 or greater than 120 beats/min. Consider a diagnosis of right-sided MI if marked hypotension occurs. Always establish the minimum of one intravenous line to deliver NS before administration of nitroglycerin in the event the nitroglycerin causes hypotension. Provide analgesia with morphine: 3–5 mg given intravenously every 5 minutes as needed to control pain. If systolic blood pressure falls to less than 90 mmHg or the heart rate falls below 60 beats/min, discontinue morphine use. Administer aspirin (162.5–325 mg PO).
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If there is ST segment elevation of 1 millivolt (1 mV) or more, in two anatomically contiguous leads, or if there is a newly confirmed left bundle branch block, consider emergent fibrinolysis or percutaneous coronary intervention (PCI). Treatment will be dependent on the availability of an interventional cardiologist at your institution. The goal from the time the patient is received at the emergency department door to the time the patient is receiving PCI is 30 to 60 minutes. Administer beta blockers: metoprolol (Lopressor) at a loading dose of 5 mg intravenous every 5 minutes (3) if systolic blood pressure is greater than 90 mmHg and the heart rate is greater than 60 beats/ min; then give 50 mg PO. Low-molecular-weight heparin (Lovenox) should be given at 1 mg/kg subcutaneously once, unless the patient’s condition meets criteria for lytics or PCI; in that case, use unfractionated heparin. A heparin loading dose of 60 IU/kg up to 4000 IU should be given, followed by 12 IU/kg/hr up to 1000 IU/hr. If CHF is present, a diuretic agent should be given. If the patient is in shock, consider using an intra-aortic balloon pump and catheter with PCI or coronary artery bypass graft. The administration of angiotensin-converting enzyme (ACE) inhibitors is generally not started in the ED. However, this treatment should be initiated within 24 hours. Aspirin and beta blockers are the only class I agents used. (Class I indicates that studies show definite benefit of the agents.)
Fibrinolytic and Unfractionated Heparin Contraindications
Absolute contraindications include the following: Active internal bleeding Suspected aortic dissection Known intracranial neoplasm History of any hemorrhagic cerebrovascular accident (i.e., stroke) ever occurring, or history of other cerebrovascular event within the past year Relative contraindications include the following: Severe hypertension on presentation (blood pressure >180/110 mmHg) History of chronic severe hypertension History of prior cerebrovascular accident or other intracranial pathology Recent major trauma (in the past 2–4 weeks) or major surgery (in the past 3 weeks) Prolonged or traumatic cardiopulmonary resuscitation (lasting >10 minutes)
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Noncompressible vascular punctures Recent internal bleeding (in the past 2–4 weeks) For prior exposure or allergy to anisoylated plasminogen-streptokinase activator complex drugs (APSAC), use tissue plasminogen activator or Tenecteplase. APSAC drugs include Abbokinase (urokinase), Abbokinase Open-Cath (urokinase), Activase (recombinant alteplase), Eminase (anistreplase), Retavase (recombinant reteplase), and Streptase (streptokinase) Known bleeding diathesis or current international normalized ratio greater than 2–3
Special Considerations
Right ventricular MI should be considered as a diagnosis. Suspect right-sided ventricular MI in patients with hypotension, shock, clear breath sounds, or JVD. Right ventricular preload is essential to maintain blood pressure. A right-sided MI rarely occurs as an isolated event. Right-sided MI can be associated up to 30% of the time with an inferior MI. There will be ST-segment elevation in the inferior leads and leads II, III, and AVF. If an acute right-sided MI is suspected, perform an ECG. If a rightsided MI is present, it will show ST-segment elevation in V4R. This is 90% sensitive. ECG shows ST-segment elevation in V4R. This is 90% sensitive (move only the V4 lead to its mirror position, placing on the right and repeat the ECG). Fifty percent of posterior MIs have some degree of right ventricular involvement. Look for ST-segments depression in V1, V2, or V3. Treatment includes the following: Maintain right ventricular preload. Administer fluids (e.g., normal saline) and inotropic agents (e.g., norepinephrine or dobutamine) if the patient is hypotensive. Use nitroglycerin and morphine with extreme caution! These may cause profound hypotension.
Bibliography Hazinski MF, Cummins RO, Field JM, (eds): 2000 Handbook of Emergency Cardiovascular Care for Healthcare Providers, ed 4. American Heart Association: Dallas, 2000. Hollander JE: Acute coronary syndromes: Acute myocardial infarction and unstable angina, In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 343–352. The Merck Manual of Diagnosis and Therapy, ed 2 online, 16.202. Available at: http://www.merck.com/mrkshared/mmanual/section16/chapter202/202d.jsp. Accessed on: July 4, 2005.
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Hypertensive Emergencies MARTIN A. DOUCHERTY
ICD Codes: 401–405
Key Points It is very important to evaluate the patient’s underlying cause of his or her hypertension. The healthcare provider must establish whether the hypertension is constituted by persistent elevated blood pressure, hypertensive emergency, or hypertensive urgency. It is dangerous to lower the blood pressure too fast. A goal of 20% decrease in the mean arterial pressure is safe. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines and providing oxygen. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. An immediate chest radiograph should be performed.
DEFINITIONS Hypertension is defined as a persistently elevated blood pressure. The term hypertensive emergency defines a condition in which an elevated blood pressure leads to a rapid deterioration of end-organ function. Hypertensive urgency defines a condition in which a patient may be in danger of developing end-organ damage as a result of his or her elevated blood pressure. It should be noted that though blood pressure readings of 180/ 110 mmHg have been used in the past to mandate treatment, no good evidence exists to support a rapid reduction of blood pressure in patients who are otherwise asymptomatic and showing no evidence of end-organ damage. The “at-risk” organs affected by markedly elevated blood pressure are the brain, heart, and kidneys. Physical examination, history, and tests should be directed toward evaluating organ function to guide ED therapy.
EPIDEMIOLOGY
Hypertensive encephalopathy: This entity results from a loss of normal vascular autoregulation in the brain resulting from severe hypertension. The most common presenting history is headache, seen in 85% of patients. Altered mental status, nausea and vomiting, and confusion or
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lethargy may be reported. Physical examination findings may include neurological deficits, papilledema, retinal hemorrhages, and exudates. Hypertensive cardiac disease: Patients may present with chest pain associated with markedly elevated blood pressure. Myocardial ischemia is the most common cause; however, the possibility of an aortic dissection should always be considered. In addition, signs and symptoms of CHF should be noted because therapy may differ. Hypertensive renal disease: This is a laboratory diagnosis for the most part. Findings include azotemia, hematuria, and proteinuria.
EXAMINATION A comprehensive history should be obtained, with emphasis on signs and symptoms of acute end-organ damage. In addition, a past medical history of CHF, angina, renal insufficiency, or poorly controlled hypertension should alert the practitioner to patients at higher risk of developing endorgan damage. The use of recreational drugs, stimulants, or monoamine oxidase inhibitors should also be noted.
PHYSICAL EXAMINATION The physical examination should proceed as follows: 1. Measure blood pressure initially and every 5–15 minutes. Check blood pressure in both arms. 2. Evaluate the patient’s mental status for signs of confusion or encephalopathy. 3. Perform a funduscopic examination to look for papilledema or retinal exudates. 4. Check for carotid bruits, distended neck veins, or a goiter. 5. Evaluate for pulses in all extremities and signs of edema. 6. Perform a cardiac examination to look for tachycardia, murmurs, cardiomegaly, and extra heart sounds. 7. Perform a pulmonary examination to evaluate for rales and wheezes. 8. Perform an abdominal examination to evaluate for bruits and pulsatile aortic masses. 9. Perform a neurological examination to evaluate for deficits.
LABORATORY FINDINGS 1. Order a urinalysis to look for proteinuria, hematuria, or casts. 2. Measure serum electrolytes and BUN/creatinine levels to evaluate renal function. 3. Analyze cardiac enzymes and BNP in patients with signs of CHF or angina.
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4. Perform a CBC to evaluate for microangiopathic hemolytic anemia. 5. Use an ECG to evaluate for signs of infarction, ischemia, or ventricular hypertrophy.
RADIOGRAPHS A chest radiograph can be used to evaluate for CHF and a widened mediastinum associated with thoracic aortic dissection. CT of the brain should be undertaken in patients with any signs or symptoms of encephalopathy.
TREATMENT Hypertensive Emergency The presence of end-organ damage constitutes a hypertensive emergency. Most guidelines recommend treatment to drop the mean arterial pressure by 20% over the course of 1 hour. Several agents are available; the most commonly used are as follows:
Sodium nitroprusside 1. Sodium nitroprusside is a rapidly acting agent that reduces preload by venous dilation and afterload by arteriolar dilation. 2. This agent may produce tachycardia and can increase myocardial contractility and oxygen demand. It should be used in conjunction with a beta blocker in cases of aortic dissection. 3. The recommended starting dose is 0.25–0.5 mg/kg/min and can be titrated for effect up to a dose of 10 mg/kg/min. 4. Prolonged use can lead to cyanide and thiocyanate toxicity, especially in patients with underlying renal insufficiency. Labetalol: 1. Labetalol is a combination alpha and beta blocker. 2. This agent decreases heart rate and is a venous and arterial dilator. 3. It should be avoided in patients with CHF, reactive airways disease, and significant bradycardia. 4. Labetalol can be given as an intravenous bolus of 20–80 mg every 10 minutes to a total dose of 300 mg. Alternatively, an infusion of 0.5–2 mg/min may be used. 5. The onset of action is approximately 15 minutes. Nitroglycerin 1. Nitroglycerin is a more potent venodilator than arterial dilator. 2. This is the drug of choice in patients with myocardial ischemia complicated by severe hypertension. 3. Headache, hypotension, and reflex tachycardia are the main adverse effects. 4. The starting dose is 5 mg/min with titration for effect up to 200 mg/min.
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Esmolol 1. Esmolol is a short-acting cardioselective beta-1 blocker. 2. This drug has a rapid onset of action. 3. It is most useful in the treatment of hypertension in perioperative patients. 4. Esmolol is also useful in patients with myocardial ischemia. 5. Use of this drug should be avoided in patients with CHF or reactive airways disease. 6. Appropriate dosage is 200–500 mg/kg bolus over 1 minute and an infusion of 50–300 mg/kg/min. Hydralazine 1. Hydralazine acts as a direct arteriolar vasodilator. 2. This agent can cause reflex sympathetic stimulation. 3. It is contraindicated in patients with angina, myocardial infarction, and aortic dissection. 4. Safe in pregnant patients, hydralazine is considered a drug of choice for treatment of pregnancy-related hypertension. 5. The appropriate dosage is 10 mg given as an intravenous bolus up to a maximum of 20 mg.
Hypertensive Urgency Patients who have asymptomatic hypertension without evidence of endorgan damage should be treated with care. Ischemic complications have been reported with overzealous treatment of such patients. Treatment in the ED should be reserved for those patients at risk for complications of hypertension due to serious comorbid conditions. Selected oral medications for treatment of hypertensive urgencies include the following:
Clonidine 1. Clonidine is an alpha-2 blocker. 2. The appropriate dosage is 0.05–0.2 mg PO. 3. Sedation and orthostatic hypotension are the most common side effects. Labetalol 1. Labetalol is a combined alpha and beta blocker. 2. Dosage is 300 mg PO. 3. Avoid use of this agent in the presence of CHF, reactive airways disease, and significant bradycardia. Nifedipine 1. Nifedipine is a calcium-channel blocker. 2. The appropriate dosage is 5–10 mg PO. 3. Reflex tachycardia, angina, and profound hypotension are side effects.
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Captopril 1. Captopril is an ACE inhibitor. 2. Dosage is 25 mg PO. 3. Adverse effects include angioedema, and use of this drug should be avoided in patients with known renal artery stenosis.
Bibliography Chiang WK, Jamshahi B: Asymptomatic hypertension in the ED, Am J Emerg Med 1998;16:701. Kaplan NM: Management of hypertensive emergencies, Lancet 1994;344:1335. Varon J, Marik P: The diagnosis and management of hypertensive crises, Chest 2000;118:214. Zanchetti A: Impact of hypertension and antihypertensive treatment on organ damage, Am J Cardiol 1999;84:18.
Mitral Valve Prolapse ALICIA NASIR AND STEVE DURNING
ICD Code: 424.0
Key Points/Quick Reference MVP is usually seen in young women and is usually easily managed. MVP is a diagnosis of exclusion. A simple echocardiogram can diagnose or exclude the condition.
DEFINITION Mitral valve prolapse is the billowing of one or both of the mitral valve leaflets into the left atrium during ventricular systole.
EPIDEMIOLOGY MVP is the most common valvular heart disease, affecting approximately 2%–6% of the U.S. population. The high prevalence of MVP reported in the past among asymptomatic young women may be due to inappropriate echocardiographic diagnoses. Although MVP typically occurs with little or no mitral regurgitation, it is the leading cause mitral regurgitation in
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the United States. MVP can be familial or associated with connective tissue disorders or with bony abnormalities of the thoracic cavity (i.e., pectus excavatum, a straight thoracic spine, or scoliosis).
PATHOLOGY The term mitral valve prolapse is typically used to characterize primary myxomatous degeneration of one or both leaflets of the mitral valve. The pathogenesis of MVP is not known, but changes in valvular tissue can usually be seen under histological examination. Functional prolapse can also occur in patients with anatomically normal valves in several conditions: ischemic injury to papillary muscles, rheumatic heart disease, conditions that cause stretching of the mitral annulus (e.g., dilated cardiomyopathy), or diseases causing a small left ventricular cavity (e.g., hypertrophic cardiomyopathy, atrial septal defect, or volume depletion). The term mitral valve prolapse, however, usually refers only to primary myxomatous degeneration and not these causes of functional prolapse.
CLINICAL PRESENTATION Most patients with MVP are asymptomatic. Patients with MVP may also present with palpitations, atypical chest pain, fatigue, and dyspnea unrelated to exertion. Some studies have shown that these symptoms are no more prevalent in MVP than in the rest of the population.
PHYSICAL EXAMINATION The most important auscultatory finding in MVP is a mid to late (nonejection) systolic slick. This is likely generated by the sudden tensing of the chordae tendineae. There may be multiple clicks, and it may be followed by a high-pitched late systolic crescendo-decrescendo murmur heard best at the apex of the heart. The click or murmur occurs earlier in systole with maneuvers that decrease venous return to the heart (e.g., standing or Valsalva); the click or murmur will occur later or even disappear with maneuvers that increase venous return to the heart (e.g., squatting or isometric exercise). Bony abnormalities of the thoracic wall, as described earlier, may also be detected in a patient with MVP.
DIAGNOSIS The diagnosis of MVP is usually made by cardiac auscultation in asymptomatic patients or as an incidental finding on an echocardiogram. Patients with MVP or suspected MVP should receive an echocardiogram. This allows risk stratification and identification of patients who will require antibiotic prophylaxis with procedures.
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LABORATORY AND ANCILLARY FINDINGS No routine laboratory tests or studies are needed for the workup of MVP in the ED. An ECG is frequently obtained in patients presenting with MVP symptoms and typically appears normal. The ECG can also show nonspecific ST-T wave changes, T-wave inversion, U waves, or prolongation of the QT interval. Chest radiographs are also frequently obtained and occasionally show bony abnormalities such as pectus excavatum, a straight thoracic spine, or scoliosis, as mentioned previously. Echocardiography should be performed on an outpatient basis.
TREATMENT The treatment for most patients with asymptomatic MVP is reassurance. Most patients with a definitive diagnosis of MVP will require antibiotic prophylaxis for infective endocarditis before certain procedures. Patients who present with symptoms such as palpitations or chest pain can have resolution of their symptoms with the cessation of use of cigarettes, caffeine, and alcohol. Beta blockers are also effective treatments for this type of chest pain. In patients experiencing focal neurological events, anticoagulation with aspirin therapy or warfarin therapy is indicated.
Bibliography ACC/AHA Practice Guidelines for Management of Patients with Valvular Heart Disease, J Am Coll Cardiol 1998;32:1486–1588. Braunwald E: Valvular heart disease, In Harrison’s Principles of Internal Medicine, ed 15. McGraw-Hill: New York, 2001, pp 1348–1349. Ling LH, Enriquez-Sarano M, Seward JB, et al: Clinical outcome of mitral regurgitation due to flail leaflet, N Engl J Med 1996;335:1417–1423. Cline DM, Valvular emergencies. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, p 375. Winkle RA, Lopes MG, Goodman DJ, et al: Propranolol for patients with mitral valve prolapse, Am Heart J 1977;93:422–427.
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Permanent Pacemakers JIMMY COOPER
ICD Code: 996.01
Key Points/Quick Reference Pacemaker complications can be categorized as failure to pace, failure to capture, failure to sense, and inappropriate rate (tachyarrhythmias). Failure to sense is the most common cause of pacemaker malfunction. Failure to pace is usually due to oversensing. Magnet application converts the pacemaker to a fixed rate pacing mode (‘‘magnet rate’’); it does not turn off the pacemaker. Indications to use the magnet include failure to pace, pacemaker-mediated tachycardia, and the runaway pacemaker. Defibrillation is safe in patients with pacemakers. It should be placed at least 10 cm away from the device (or in the anterior-posterior position). ! Emergency Actions ! The runaway pacemaker is a true potential pacemaker emergency that may require acute intervention. Magnet application can be lifesaving in these patients. Pacemaker-mediated tachycardias can also be terminated by magnet application. Unstable bradycardias may improve with magnet application if the problem is failure to pace and oversensing. It may not improve with the failure to sense or capture patients.
DEFINITION Electrical cardiac pacing has been used since the 1950s. These early devices used external power sources. The first implantable permanent pacemaker was clinically used in 1958. Through the years, advances in technology have allowed pacemakers to become individualized to the person. The modern day pacemaker is a microcomputer with multiple programmable features enabling adjustments to activity level. Despite the increasing complexity of programmable features, the pacemaker is composed of three basic components: the pulse generator, the lead system, and the programming or circuitry. Emergency providers must understand these components to manage related complications. The pulse generator consists of the battery, the reed switch, and the radiopaque marker. Most pacemakers use a lithium battery, which has a slow and steady decay rate. The life of the lithium battery is 4 to 10 years. Voltage output is gradually lost, so that abrupt failure is rare. The reed switch is used to assess pacemaker function. It is activated when placed
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under a magnetic field, which results in inhibition of the sensing circuit. This turns the pacemaker into a fixed-rate pacing mode, also known as the magnet rate. This mechanism is critical to both assessing and managing pacemaker complications. Radiopaque markers are visible with standard chest radiographs. Most patients carry identification cards; however, if they are not available, these markers will identify the pacemaker manufacturer and model. Most pacemakers use endocardial leads that are transvenously placed into the right ventricle, right atrium, or both (dual-chamber devices). Leads can also be implanted on the epicardium during open-heart surgery. Complications associated with leads include infection, thrombosis, cardiac perforation, dislodgement, and lead fracture. Lead fracture is estimated to be 2% per patient-year. Lead displacement is 2%–5% for endocardial leads. There are many different types of pacemaker circuitry. The North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group have developed a five-letter code scheme to describe them (Table 2-1). The first three letters are most useful in understanding the type of pacemaker. Pacemakers are usually inhibited by intrinsic cardiac depolarization (VVI or DDD). Using the pacemaker code and the patient’s ECG, the provider can determine whether there is a malfunction in the circuitry. Programming complications include failure to pace, failure to capture, failure to sense, and inappropriate rates.
EPIDEMIOLOGY Approximately 200,000 pacemakers are placed or replaced in the United States each year, and about 1 million Americans have pacemakers. Indications include symptomatic bradycardias, heart blocks, syncope, heart failure, cardiomyopathies, and congenital heart malformations. The widespread use of pacemakers guarantees that emergency providers will encounter them and their malfunctions. Pacemaker complications are infrequent, occurring in fewer than 6% of patients. They most commonly occur in the first few months after implantation. Most are due to failure to sense, which accounts for 32%–57% pacemaker problems.
CLINICAL PRESENTATION Patients with pacemaker malfunctions can present with chest pain, dyspnea, syncope, near syncope, orthostasis, palpitations, light-headedness, weakness, or fatigue. These may be similar to the patient’s index
Table 2-1 Five-Letter Pacemaker Code LETTER 1
LETTER 2
LETTER 3
LETTER 4
LETTER 5
CHAMBER PACED
CHAMBER SENSED
SENSING RESPONSE
PROGRAMMABILITY
ANTITACHYCARDIA FUNCTIONS
A ¼ atrium V ¼ ventricle D ¼ dual
A ¼ atrium V ¼ ventricle D ¼ dual
P ¼ simple M ¼ multiprogrammable R ¼ rate adaptive
P ¼ pacing S ¼ shock D ¼ dual (shock þ pace)
O ¼ none
O ¼ none
T ¼ triggered* I ¼ inhibited D ¼ dual (A and V inhibited) O ¼ none
C ¼ communicating O ¼ none
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From Niemann JT: Implantable cardiac devices. In Marx JA (ed): Rosen's Emergency Medicine, ed 5. Mosby: St Louis, 2002, p 1100. * In the triggered response mode, the pacemaker discharges or fires when it recognizes an intrinsic depolarization. As a result, pacemaker spikes occur during inscription of the QRS complex. Because this mode results in high-energy consumption and a shortened battery life, and because the sensing response can be misinterpreted as pacemaker malfunction, this sensing mode is not used with modern pacemakers.
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symptoms before pacemaker placement. Loss of pacemaker function leaves the patient with his or her underlying condition, which is usually a bradydysrhythmia. Fortunately, this is rarely immediately life threatening. Patients with pacemakers can also present with tachydysrhythmias, as in the case of pacemaker-mediated tachycardia or a “runaway” pacemaker. This may present emergently with profound hypotension and cardiovascular collapse. Runaway pacemaker is a rare complication caused by an extreme inappropriate increase in the pacing rate. Pacemakermediated tachycardia is seen in conjunction with dual-chamber devices, usually from an endless-loop reentry tachycardia. Retrograde conduction through the AV node is sensed as atrial depolarization, causing repeated pacing of the ventricle. Infectious complications should be considered in patients with pacemakers who present with fever of unclear etiology. These may be localized to the skin or pockets, but they may also be more complicated, involving leads or endocarditis. Initial treatment consists of broadspectrum antibiotics to cover Staphylococcus aureus. The pacemaker often needs to be removed.
EXAMINATION The pacemaker identification card should be obtained. It will provide information on the pacing modality and the indication for the pacemaker. Pulses less than 60 or greater than 100 beats/min are suggestive of altered pacing parameters. Pacemakers are usually programmed with a rate between 60 and 80 beats/min. Hypotension may be present. The general appearance is dependent on the patient’s intrinsic heart rhythm and stability. There may be signs of shock and CHF. The chest wall should be inspected for signs of infection. Cardiac examination may reveal a new murmur suggestive of infective endocarditis.
ECG FINDINGS An appropriately paced ECG will have a left bundle branch pattern because the pacing lead is in the right ventricle. Using the pacemaker code and the patient’s ECG, the provider can determine whether there is a malfunction in the circuitry. Pacemaker malfunctions can be separated into three categories: 1. Failure to pace: The ECG shows a complete absence of pacemaker spikes in a patient whose intrinsic rhythm is slower than the programmed rate. This is most commonly due to oversensing. The pacemaker detects electrical activity other than atrial and ventricular depolarizations that suppresses impulse generation. Other etiologies (rarely) include wire fracture and battery depletion.
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2. Failure to capture: Pacemaker spikes are appropriately present, but without associated QRS complexes. Causes include lead dislodgement, battery depletion, and exit block (e.g., fibrosis, infarction, hyperkalemia, antiarrhythmia drugs). 3. Failure to sense (undersensing): The ECG shows constant pacemaker spikes despite intrinsic cardiac activity. Pacemaker spikes occur at inappropriate times due to the inability to sense the patient’s intrinsic cardiac depolarization. They typically occur earlier than the programmed rate. A paced complex may or may not follow, depending on the cardiac refractory period. This is most common after right ventricular infarctions and with the fibrosis of cardiomyopathies. Lead dislodgment and maturation can also cause undersensing. ECGs may also show tachydysrhythmias as previously described in pacemaker-mediated tachycardia.
RADIOGRAPHS Standard chest radiographs should be obtained and compared with old films. Pacemaker type can be ascertained by radiopaque markers. Lead wires should be examined for fracture, displacement, and perforation.
TREATMENT The approach to pacemaker complications is similar to that of other cardiac symptoms. This basic evaluation includes history, examination, ECG, and chest x-ray, as outlined previously. Key historical information should include the pacemaker identification card, which explains the pacing modality and the reason why the pacemaker was placed. Laboratory studies (i.e., chemistry) need to be performed to assess for metabolic abnormalities. All of these patients should be receiving cardiac monitoring and oxygen administration and should have intravenous access. By analyzing the ECG, the pacemaker complication can usually be identified. Failure to sense and failure to capture requires only the basic evaluation and then “pacemaker interrogation” by cardiology. There is usually no ED intervention for these patients. They have pacemaker activity, although it is inappropriate or without effect. Unless battery depletion is suspected, magnet application is usually not necessary. Battery depletion is a rare cause of pacemaker failure and is diagnosed with a lower than programmed rate with magnet application. Failure to pace problems can further be evaluated with magnet testing to determine whether the malfunction is oversensing, component failure, or battery depletion. Standard ring magnets are typically used for this procedure. Some pacemakers may require specific magnets. Place the magnet directly on the chest wall over the pacemaker. This closes the reed switch
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and converts the pacemaker to an asynchronous or fixed-rate pacing mode. Expect the pacemaker to pace at the programmed rate (60–80 beats/min). If this occurs, then the problem was oversensing and the pacemaker was inappropriately inhibited. Causes of oversensing include atrial depolarizations, muscle activity, and external electrical interference. Component failure should be suspected if there are no spikes on magnet application. Battery depletion is indicated by the presence of a pacemaker rate less than the program med rate. All of these conditions require further evaluation by cardiology. The magnet should be left in place if it corrects the underlying bradydysrhythmia. Certain pacemaker complications require acute interventions. Pacemakermediated tachycardia can present with cardiovascular collapse. A magnet should be applied to terminate the arrhythmia, and it should be left in place if it is successful. If this fails, then isometric pectoral exercises should be attempted. The cooperative patient can flex the pectoral muscles surrounding the pacemaker generator. Alternatively, a transcutaneous pacemaker can be applied to stimulate the pectoral muscle. Low outputs in the range of 5–20 mA should be used. The muscle activity may be interpreted as ventricular activity and inhibit the pacemaker. If the patient is unstable, the healthcare provider should consider delivering a precordial thump. The last resort for an unstable patient is to sterilely cut the pacer leads and connect them to an external temporary pacemaker. Pacemakers are complicated devices, and most emergency providers do not have the expertise to fully evaluate them. If pacemaker malfunction is suspected, the patient’s cardiologist should be consulted. These patients will usually be admitted to a monitored setting for further “interrogation.”
Bibliography Bernstein AD, Camm AJ, Fletcher RD, et al: The NASPE/BPEG generic pacemaker code for antibradyarrhythmia and adaptive-rate pacing and antitachyarrhythmia devices, Pacing Clin Electrophysiol 1987;10:794. Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Copeland LL, Mace SE: Pacemaker emergencies, Crit Decis Emerg Med 2005;19(7): 13–21. Greenberg RM, Greenspon AJ, Bridenbaugh A, Brest AN: Pacemaker-mediated tachycardia: A complication of atrioventricular universal (DDD) pacemakers, Arch Intern Med 1984;144:1061. Hayes DL, Vliestra RE: Pacemaker malfunction, Ann Intern Med 1993;119:828. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Mickley H, Anderson C, Nielsen IH: Runaway pacemaker: A still existing complication and therapeutic guidelines, Clin Cardiol 1989;12:412–416. Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004.
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Prosthetic Heart Valve Dysfunction CHRISTOPHER R. MCNEIL
ICD Code: 394
Key Points/Quick Reference Prosthetic heart valves are classified into two general groups: mechanical and bioprosthetic. Complications of prosthetic heart valves include thrombosis, embolic events, endocarditis, hemolytic anemia, and primary valve failure.Thromboembolic events are the most common complication of prosthetic heart valves. Prosthetic valve endocarditis must be considered in any patient who presents with a fever of unknown origin, sepsis, a change in the murmur, or evidence of peripheral emboli. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines and providing oxygen. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. An immediate chest radiograph should be performed.
DEFINITION Prosthetic heart valves are classified into two general groups: mechanical and bioprosthetic. Most mechanical valves consist of three basic designs: the ball and cage, the tilting disk, and the bileaflet hinged disk. Mechanical valves carry a large risk of thrombosis and the ensuing embolic events, thus requiring lifelong anticoagulation. Risks associated with anticoagulation led the way for development of bioprosthetic valves. These most commonly consist of porcine valves or are synthesized from pericardial tissue. Although the need of long-term anticoagulation is unnecessary, bioprosthetic valves are less durable and usually require replacement after 10 years. Complications of prosthetic heart valves include thrombosis, embolic events, endocarditis, hemolytic anemia, and primary valve failure. Thromboembolic events are the most common complication of prosthetic heart valves. Thrombosis can result in improper valve function, obstruction of valve outlet, or systemic emboli. Valve thrombosis can present acutely with CHF, hypotension, and loss of the metallic valvular click on examination. Patients with chronic thrombosis may develop gradually worsening weakness, shortness of breath, and exercise intolerance. These conditions occur more commonly in mechanical valves
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than in bioprosthetic ones. Typically, thrombosis results from inadequate anticoagulation. Prosthetic valve endocarditis must be considered in any patient who presents with a fever of unknown origin, sepsis, a change in the murmur, or evidence of peripheral emboli. Within the first 2 months after valve replacement, the predominant infecting organisms are Staphylococcus epidermidis and other hospital-acquired organisms. After 2 months, the causative organism mimics those that cause native valve endocarditis. Chronic hemolytic anemia is caused by trauma to the turbulent blood flow through the valve. Severe or acute hemolytic events should raise the suspicion for a paravalvular leak. Valve failure occurs much more commonly in bioprosthetic valves. Failure results from cusp tears, perforations, and calcifications of leaflets. Rarely, artificial valves have also been reported to fail. Fracture of the strut mechanism in certain Björk-Shiley valves have led to embolization of the tilting disk. Although most of these have been replaced, there is still a significant population with these valves in place. Mechanical valves are not void of failure.
EPIDEMIOLOGY Prosthetic heart valves are implanted in nearly 400,000 patients annually. Embolic events occur at a rate of approximately 1% per year among patients taking warfarin. Emboli and thrombosis are more common on the mitral valve. The incidence of bacterial endocarditis in patients with prosthetic valves is approximately 0.5% per patient-year. The 5-year mortality for prosthetic valve endocarditis is 20%–60%.
CLINICAL PRESENTATION The patient may present with a variety of symptoms, depending on the complication he or she is experiencing. Thrombosis can present with hypotension, shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and chest pain. Systemic emboli may present as acute stroke, seizure, or vision loss, or with dermatological findings. Endocarditis presents with fever, weakness, malaise, and with evidence of systemic emboli, as well. Hemolytic anemia presents with weakness and dark-colored urine.
EXAMINATION A complete physical examination should be performed. The healthcare provider should look for signs of pulmonary edema, peripheral edema, and JVD as evidence of CHF. Heart sounds should be auscultated to identify the mechanical click of the valve and any evidence of a diastolic or other new murmur. A funduscopic examination should be performed to
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identify hemorrhages and Roth’s spots. A complete skin examination should be performed to identify petechia, Osler’s nodes, Janeway lesions, and peripheral embolic phenomenon.
LABORATORY FINDINGS A CBC, urine analysis, and lactate dehydrogenase measurement may be required to evaluate for hemolysis. A coagulation panel is necessary to evaluate the patient’s anticoagulation status. A sedimentation rate and multiple blood culture results are useful to diagnose endocarditis.
DIAGNOSIS The diagnosis of prosthetic valve dysfunction is based on a thorough history, physical examination results, and high clinical suspicion. Echocardiography is used to diagnose valve thrombosis, paravalvular leaks, and vegetations (Box 2-1).
RADIOGRAPHS Chest radiography is useful in determining the position of the prosthetic heart valve and in identifying any evidence of pulmonary edema.
TREATMENT Thromboembolic complications require immediate anticoagulation. Patients will also require echocardiography to ultimately diagnose their Box 2-1 Duke Criteria Must meet two major criteria, or one major and three minor criteria, or five minor criteria. Major Criteria: At least two positive blood cultures Endocardial vegetation by echocardiography Paravalvular abscess by echocardiography New partial dehiscence of prosthetic valve by echocardiography New valvular regurgitation by echocardiography Minor Criteria: Predisposition: predisposing heart condition or IV drug use Fever Vascular phenomenon: arterial emboli, septic pulmonary infarction, mycotic aneurysms, conjunctival hemorrhages, Janeway lesions Immunological phenomenon: Osler's nodes, Roth's spots, rheumatoid factor Microbiological evidence: single positive blood culture Echocardiographic findings: consistent with endocarditis but does not meet criteria
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condition. These patients may require surgical thrombectomy or valve replacement. There is a new surge in the use of thrombolytics for the treatment of prosthetic thrombus, but these should be reserved for the intensive care setting. Endocarditis requires intravenous antibiotic therapy. Either vancomycin plus gentamycin or ceftriaxone plus gentamycin is appropriate to administer initially while culture results and sensitivity results are pending. Rarely do these patients require acute valve replacement. Patients with primary valve failure typically experience acute and dramatic onset of CHF and hypotension. These patients require emergent cardiology and cardiothoracic surgery consultation. Their hypotension may not tolerate nitrates or afterload reduction. They may require intubation and positive-pressure ventilation for their pulmonary edema as well as inotropic support. Chronic hemolytic anemia generally responds well to iron replacement. Acute or severe hemolysis may necessitate blood transfusion and requires echocardiography to identify a possible paravalvular leak. Prosthetic heart valves require antibiotic prophylaxis against endocarditis for procedures with high risk for bacteremia. The following common procedures require prophylaxis:
Prophylactic cleaning of teeth Bronchoscopy (with rigid bronchoscope only) Endoscopic retrograde cholangiopancreatography Cystoscopy Urethral dilation
Bibliography Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Cannegieter SC, Rosendaal FR, Wintzen AR, et al: Optimal oral anticoagulant therapy in patients with mechanical heart valves, N Engl J Med 1995;333:11–17. Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis: Recommendations by the American Heart Association, Circulation 1997;96:358–366. Gherli T, Colli A, Fragnito C, et al: Comparing warfarin with aspirin after biological aortic valve replacement: a prospective study, Circulation 2004;110:496–500. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Stein PD, Alpert JS, Bussey HI, et al: Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves [erratum appears in Chest;120(3):1044], Chest 2001;119:220S–227S. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000.
Heart Transplant
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Heart Transplant CHRISTOPHER R. MCNEIL
ICD Code: Heart transplant V42.1
Key Points The surgical procedure causes denervation of their vagus nerve, rendering it void of parasympathetic stimulation. Baseline tachycardia is common and even expected after transplant, with a basal rate of 100^ 110 beats/min. ! Emergency Actions ! Any heart transplant recipient presenting with sepsis, CHF, fever, shortness of breath, hypoxia, hypotension, poorly controlled hypertension, or new dysrhythmia should be admitted to the hospital.
DEFINITION Human heart transplantation was first successfully performed in 1967, and currently more than 2000 transplants are done each year in the United States. Advances in immunosuppressive therapy have established transplantation as an accepted treatment for end-stage heart disease over the last 20 years. Patients are typically discharged from the hospital within 2–3 weeks, and nearly 40% make at least one visit to the ED over the next 3 years. Heart transplant recipients have a 60% ED admission rate after transplant due to an appropriately high concern for rejection or localized or systemic infections. Several important factors must be considered when heart transplant recipients present for medical treatment. The surgical procedure causes denervation of the vagus nerve, rendering patients void of parasympathetic stimulation. Baseline tachycardia is common and expected after transplant with a basal rate of 100–110 beats/min. The ECG typically demonstrates two distinct p waves. The native sinoatrial node remains intact in the posterior wall of the right atrium with the vena caval connections. The donor heart also has a sinoatrial node and maintains action potential conduction to the ventricles as usual. The myocardium upregulates adrenergic receptors in the graft and has an enhanced response to endogenous and exogenous catecholamines. Cardioactive medications have similar effects in the posttransplant heart, with the exception of atropine because of the denervation. The denervation also renders the patient
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void of the typical anginal symptoms that other patients experience. Finally, immunosuppressive agents that heart transplant recipients are prescribed have the potential for significant drug toxicities as well as the increased incidence for both typical and opportunistic infections.
EPIDEMIOLOGY Currently, more than 2000 heart transplants are performed annually in the United States. The 5-year survival rate for adults is now as high as 70%. Acute rejection occurs in 75%–85% within the first 3 months after transplant. Patients experience an annual rate of infection of nearly 20% after the first 3 months. Almost 25% of deaths after transplant result from an infection.
CLINICAL PRESENTATION The most common presenting symptoms are fever, shortness of breath, GI symptoms, and chest pain. Chest pain is rarely related to cardiac ischemia because of the denervation. Infection, rejection, and drug toxicity are the leading causes of morbidity and mortality in the first year after transplant. These conditions need to be strongly considered in the differential diagnosis.
EXAMINATION All patients should be given a complete physical examination to identify any focus of infection. Any evidence of CHF, new murmur, a new S3 heart sound, or dysrhythmia should prompt concerns for rejection and graft CAD.
LABORATORY FINDINGS A CBC, chemistry panel, coagulation panel, liver function tests, cardiac enzymes, BNP, blood cultures, viral cultures, stool cultures, and lumbar puncture should be considered for all patients.
DIAGNOSIS Infection Although many patients will have a major infection in the first year after transplant, life-threatening infections are rare after the first year. All heart transplant recipients with fever should have an aggressive diagnostic workup performed. Typical infections include pneumonia and urinary tract infections. Skin problems typically manifest as herpes zoster. Pneumocystis carinii
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pneumonia and cytomegalovirus (CMV) infection are common pulmonary complications. GI tract symptoms include CMV infection, and abdominal pain may result from diverticulitis. Central nervous system symptoms may include headache, meningitis, or infection with Listeria, Cryptococcus, Toxoplasma, Nocardia, or Aspergillus species.
Rejection Manifestations of rejection include decreased QRS voltage on ECG, a new S3 heart sound, CHF, atrial dysrhythmias, hypotension, and syncope. Most episodes of mild rejection are asymptomatic. Accelerated atherosclerosis of the graft vessels is the hallmark of chronic rejection; however, ischemia presents as congestive heart failure (CHF), ventricular tachycardia (VT) hypotension, and sudden cardiac death (SCD). Patients with these conditions need admission for consideration of myocardial biopsy and increased immunosuppressive therapy.
Drug Toxicity Complications stemming from drug toxicity include the following:
Cyclosporine: nephrotoxicity, hypertension, hyperlipidemia, gout Tacrolimus: nephrotoxicity, neurotoxicity, hyperglycemia, hyperkalemia, not compatible with macrolides Azathioprine: neutropenia, hepatic dysfunction, GI tract disturbance Prednisone: osteoporosis, cataracts, GI tract bleeding, hyperglycemia, adrenal suppression Mycophenolate mofetil: thrombocytopenia, GI tract disturbance OKT3 (muromonab-CD3): increased risk of CMV and opportunistic pathogens, lymphoproliferative disease
RADIOGRAPHS All patients should undergo a chest x-ray to identify evidence of CHF or pneumonia. Patients with abdominal pain should be considered for a CT of the abdomen and pelvis. Patients with headache or CNS symptoms should be considered for a CT scan of the head, with the aim of looking for evidence of infection or brain abscess.
TREATMENT Any heart transplant recipient presenting with sepsis, CHF, fever, shortness of breath, hypoxia, hypotension, poorly controlled hypertension, or new dysrhythmia should be admitted to the hospital.
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SPECIAL TREATMENT Heart transplant recipients are at risk for endocarditis. They require antibiotic prophylaxis for invasive procedures likely to cause bacteremia such as abscess incision and drainage and dental procedures. Varicella-zoster virus immune globulin is recommended for those patients who have had exposure to chickenpox or herpes zoster.
Bibliography Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Deng MC: Orthotopic heart transplantation: Highlights and limitations, Surg Clin North Am 2004;84(1):243–255. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Shanewise J: Cardiac transplantation, Anesthesiol Clin North Am 2004;22(4):753–765.
Chapter 3
Acute Dermatologic Emergencies Erythema Multiforme RICHARD J. SPITZ
ICD Code: 695.1
Key Points Patients present with a symmetrical skin lesion that has a target appearance.
DEFINITION Erythema multiforme (EM) is a mild, self-limited skin disorder that tends to have abrupt onset and is sometimes recurrent. It is recognized by its characteristic target or iris lesion and is usually associated with infection, particularly with herpes simplex virus infection. Previously, EM was grouped with two other skin disorders: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Current thinking separates EM from these other two disorders, which have a distinctly different histopathology. In contrast to the relatively mild nature of EM characterized by target lesions and associated with infection, SJS and TEN are severe, have a poor prognosis, and are associated with drug exposures. Some authors feel that, in actuality, both SJS and TEN are a continuum of the same disorder, with TEN being the more widespread and severe form.
EPIDEMIOLOGY The true occurrence of the disease is unknown due to overlap with other diseases, its benign self-limited nature, and lack of adherence to a uniform definition.
PATHOLOGY Disease is theorized to result from deposition of immune complexes in skin and oral mucous membranes.
CLINICAL PRESENTATION Patients present with a symmetrical skin lesion that has the appearance of a target. The rash is most common on the hands, feet, and extensor 97
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aspects of the forearms and legs, though severe cases can progress to involvement the trunk.
EXAMINATION The patient should be examined to distinguish EM from more severe diseases such as Kawasaki disease, SJS, TEN, meningococcemia, secondary syphilis, toxic shock syndrome, collagen vascular disease, septic emboli in bacterial endocarditis, and Rocky Mountain spotted fever.
DIAGNOSIS A patient is diagnosed by the presence of the classic target lesion in a nontoxic-appearing patient. Skin biopsies would show mononuclear infiltrate, but due to the benign course of the disease, these are not performed.
LABORATORY FINDINGS There are no laboratory findings suggestive of the skin lesions themselves.
TREATMENT The disease is usually self-limited with lesions resolving within several weeks without any residual manifestations. Recurrent episodes can be treated with herpes simplex virus medication (e.g., valacyclovir, acyclovir, or famciclovir). Other agents such as nonsteroidal anti-inflammatory drugs, steroids, and antihistamines do not appear to affect the disease course.
Bibliography Assier H, Bastuji-Garin S, Revuz J, Roujeau JC: Erythema multiforme with mucous membrane involvement and Stevens-Johnson syndrome are clinically different disorders with distinct causes, Arch Dermatol 1995;131:539. Bastuji-Garin S, Rzany B, Stern RS, et al: Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme, Arch Dermatol 1993;129:92. Behrman RE, Kliegman RM, Jenson HB: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Ferri FF: Practical Guide to the Care of the Medical Patient, ed 7. Mosby: St Louis, 2007. Habif TP: Clinical Dermatology, ed 4. Mosby: St Louis, 2004. Leaute-Labreze C, Lamireau T, Chawki D, et al: Diagnosis, classification, and management of erythema multiforme and Stevens-Johnson syndrome, Arch Dis Child 2000;83:347. Long SS, Pickering LK, Prober CG: Principles and Practice of Pediatric Infectious Diseases, ed 2. Churchill Livingstone: New York, 2003.
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Mandell GL, Bennett J, Dolin R: Principles and Practice of Infectious Diseases, ed 5. Churchill Livingstone: New York, 2000. Marx J, Hockberger R, Walls R (eds): In Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Noble J: Textbook of Primary Care Medicine, ed 3. Mosby: St Louis, 2001. Paquet P, Pierard GE: Erythema multiforme and toxic epidermal necrolysis: A comparative study, Am J Dermatopathol 1997;19:127. Rakel RE: Conn’s Current Therapy, ed 57. WB Saunders: Philadelphia, 2005. Roujeau JC, Revuz J: Toxic epidermal necrolysis: an expanding field of knowledge, J Am Acad Dermatol 1994;31:301. Roujeau JC, Stern RS: Severe adverse cutaneous reactions to drugs, N Engl J Med 1994;331:1272. Schofield JK, Tatnall FM, Leigh IM: Recurrent erythema multiforme: Clinical features and treatment in a large series of patients, Br J Dermatol 1993;128:542. Weston WL, Morelli JG: Herpes simplex virus-associated erythema multiforme in prepubertal children, Arch Pediatr Adolesc Med 1997;151:1014. Weston WL, Morelli JG, Rogers M: Target lesions on the lips: Childhood herpes simplex associated with erythema multiforme mimics Stevens-Johnson syndrome, J Am Acad Dermatol 1997;37:848.
Exfoliative Dermatitis BENJAMIN H.TAYLOR
ICD Code: Exfoliative dermatitis 695.89
Key Points Exfoliative dermatitis is usually caused by an underlying disease or illness or is drug induced. ! Emergency Actions ! Any patient suspected to have exfoliative dermatitis should be admitted to a surgical intensive care unit (SICU) or a burn center for evaluation and treatment.
DEFINITION Exfoliative dermatitis and erythroderma are synonymous terms used to define a common clinical syndrome characterized by widespread scaling, often with itching (i.e., pruritus), skin redness with desquamation (i.e., erythroderma), and hair loss.
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EPIDEMIOLOGY Exfoliative dermatitis occurs in all races and accounts for about 1% of all hospital admissions for dermatological conditions. Although the disease affects both men and women, it is more common in men, with an average male-to-female ratio of 2:1. The average age at onset is older than 40 years, although it may occur at any time.
PATHOLOGY Exfoliative dermatitis may occur in response to drug therapy, systemic disease, or an idiopathic entity (Box 3-1). More than half of all cases are due to aggravation of a preexisting skin disease that often has diagnostic findings. Approximately 10% of cases are the result of drug reactions (more than 60 drugs have been implicated), and 40% of all cases are caused by some underlying systemic disease. The remaining cases are idiopathic. Malignancies are a major cause of exfoliative dermatitis. Reticuloendothelial neoplasms, as well as internal visceral malignancies, can produce erythroderma, with the former being the more predominant cause. Cutaneous T-cell lymphomas are the lymphomas most commonly associated with exfoliative dermatitis. The most notable member of this group is mycosis fungoides. Acute and chronic leukemia may also cause exfoliative dermatitis. The relative risk of leukemia inducing exfoliative dermatitis is highly variable, ranging from 11% to 50%.
CLINICAL PRESENTATION The general clinical presentation may be altered according to the nature of the underlying disease and the patient’s general physical condition. Patients often present with generalized erythema in the first stage of the disorder, beginning as single or multiple pruritic patches and involving the head, trunk, and genital region. These patches tend to spread for days, and they may last for weeks when most of the skin surface
Box 3–1 RED MAN: A Mnemonic for Identifying Possible Causes of Exfoliative Dermatitis Radiation (sunburn) or photosensitive eczema Eczema, atopic dermatitis, psoriasis, and other inflammatory skin disorders Drugs Malignancy (most commonly lymphoma, such as mycosis fungoides) AIDS No known cause (idiopathic)
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becomes covered with an erythematous, pruritic eruption. Pruritus commonly results in excoriations and present in varying stages of healing. In some cases, the palms of the hands, the soles of the feet, and the mucous membranes are spared. Exfoliative dermatitis may persist for weeks and becomes a chronic entity. Patients’ hair may shed and their nails may become ridged and thickened. Periorbital skin may be inflamed and edematous, resulting in ectropion (with consequent epiphora). Pigmentary disturbances (especially in darker-complexion patients, resembling vitiligo) has become commonplace. Other signs and symptoms with which patients may present include any of the following:
Gynecomastia is a common finding in almost all patients with a chronic history of exfoliative dermatitis. It is believed to result from hyperestrogenism, but the precise mechanism is unknown. Patients may present tachycardic and febrile, with temperatures higher than 38 C. Lymphadenopathy, referred to as dermatopathic lymphadenitis, is common. Hepatomegaly and splenomegaly is present in approximately 30% of patients and may represent lymphoma. Steatorrhea may develop and tends to resolve when exfoliative dermatitis clears. Patients with exfoliative dermatitis have increased cutaneous blood flow, transcutaneous fluid losses, and radiation and convective heat losses. Hypothermia has been reported in some patients. Cardiac output is increased as a result of fluid shifts causing dyspnea, dependent edema, and, in some patients, cardiac failure. Prostate or thyroid glands may be enlarged or nodular.
EXAMINATION A complete physical examination should include a cardiac examination as well as skin biopsy of representative areas.
DIAGNOSIS AND LABORATORY FINDINGS A detailed history of the sequence of events leading to the development of exfoliative dermatitis is required in all patients. Laboratory evaluation of patients with exfoliative dermatitis is generally not very helpful in determining a specific diagnosis. Typical laboratory values to be obtained include mild anemia, leukocytosis, eosinophilia, elevated erythrocyte
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sedimentation rate, abnormal serum protein electrophoresis with a polyclonal elevation in the gamma globulin region, and elevated immunoglobulin E levels when the condition is caused by atopic dermatitis or drug reactions. Blood counts and bone marrow studies may reveal an underlying leukemia. Analysis for circulating Sézary cells may be helpful—but, only if the Sézary cells are identified in unequivocally large numbers. In most patients, skin biopsies show nonspecific histopathologic features, such as hyperkeratosis, parakeratosis, acanthosis, and a chronic perivascular inflammatory infiltrate, with or without eosinophils. Even patients with clear histories of preexisting dermatoses tend to have biopsy results that are not diagnostic.
TREATMENT Every attempt must be made to determine the underlying cause of exfoliative dermatitis. A history or signs of a primary dermatitis may be helpful. All patients who present with acute exfoliative dermatitis must be hospitalized in the intensive care unit or burn center for supportive care, fluid replacement, laboratory studies, and contact isolation for protection against secondary bacterial and fungal infections. Dermatological consultation is indicated in most cases to ensure that the necessary cutaneous, laboratory, and radiological investigations and monitoring are performed. The administration of all drugs should be stopped or, if essential, should be changed to chemically dissimilar medications. In the acute phase of exfoliative dermatitis, before determination of the etiology, treatment consists of measures to soothe the inflamed skin, including bed rest, lukewarm soaks or baths, bland emollients, and oral antihistamines for pruritus. Petrolatum applied after tap-water baths gives temporary relief. A high-protein diet with folic acid supplementation is required since protein losses may be increased as much as 30% above normal. Exfoliative dermatitis commonly resists therapy until the underlying disease is treated. The outcome is unpredictable, and the course is usually marked by multiple exacerbations. Prolonged glucocorticoid therapy is often necessary. Appropriate inpatient/outpatient medications are influenced by the underlying etiology. Systemic steroids may be helpful in some cases but should be avoided in suspected cases of psoriasis and staphylococcal scalded skin syndrome.
Bibliography Fitzpatrick TB, Johnson RA, Wolff K: Exfoliative dermatitis. In Color Atlas and Synopsis of Clinical Dermatology, ed 4. McGraw-Hill: New York, 2001, pp 152–157. Freeberg IM: Exfoliative dermatitis, In Fitzpatrick TB, Eisen AZ, Wolff K, (et al): Dermatology in General Medicine, ed 4. McGraw-Hill: New York, 1993, pp 527–530.
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Papadakis MA, McPhee SJ: Exfoliative dermatitis. In Current Consult Medicine. McGraw-Hill, 2005, pp 302–303. Sehgal IN, Srivastava G, Sardana K: Erythroderma/exfoliative dermatitis: A synopsis, Inter J Dermatol 2004;43(1):39–52. Thestrup-Pederson K, Sorenson HC, Sogaard H: The red man syndrome: Exfoliative dermatitis of unknown origin. A description and follow-up of 38 patients, J Am Acad Dermatol 1988;18:1307–1312.
Toxic Epidermal Necrolysis GUYON J. HILL
ICD Code: 695.1
Key Points Toxic epidermal necrolysis is a rare skin disorder resulting from a severe hypersensitivity reaction. Up to 100% of the epidermis may separate from the dermis and be shed in sheets. The precipitating factors are usually medications. The disease has a high mortality rate, and patients should be treated in similar fashion to burn patients and transferred to a dedicated burn unit. ! Emergency Actions ! The patient should be stabilized and resuscitated following current advanced cardiac life support guidelines. Use of adhesives should be avoided while intravenous lines are being placed, if possible. Intubation and mechanical ventilation may be necessary if the upper airway or the pulmonary tree is involved. Any sources of skin trauma should be avoided, as should central lines, if possible, due to the risk for infection.
DEFINITION Toxic epidermal necrolysis is a severe hypersensitivity reaction frequently precipitated by medications. The process is thought to be a combination of type III and IV hypersensitivity reactions and can result in a loss of up to 100% of the full thickness of the epidermis. TEN is in the same family of disorders as EM and SJS. Although it is generally accepted that SJS is a more severe form of EM, debate exists as to whether TEN is a further
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point on this spectrum or its own clinical entity. What is known is that the precipitating factors for all three disorders are similar. Medications can be implicated in up to 77% of cases. Common offending medications that are implicated in the etiology of this disorder include sulfa drugs, nonsteroidal anti-inflammatory drugs, and phenytoin and other convulsants. Other possible inciting drugs are allopurinol, penicillins, and barbiturates. A relationship has also been found between the disease and patients with either human immunodeficiency virus (HIV) infection or active malignancy. The rate is also higher in elderly persons (who are often taking more medications) and bone marrow transplant recipients. TEN has occurred after immunization for smallpox, tetanus, diphtheria, measles, and poliomyelitis. Often the etiology is unknown. No association has been found with viral illness.
EPIDEMIOLOGY TEN is an extremely rare condition and accounts for only 1.3% of cutaneous drug eruptions. It occurs in 0.2 cases per million users of penicillins and 4.5 cases per million users of sulfonamides. The overall frequency in the United States is 0.22–1.23 cases per 100,000. There is a female predominance, with the gender ratio of 1.6:1 for infection.
CLINICAL PRESENTATION Early in the course of the disease, patients with TEN usually present with a nonspecific prodrome that may include fever, malaise, arthralgias, anorexia, conjunctivitis, and symptoms of an upper respiratory tract infection. These symptoms occur before skin involvement. As a general rule, mucous membrane involvement precedes skin involvement. Initially affected organs include the eyes, nose, and mouth. The genitalia may also be involved. The painful rash usually begins on the face but may also start on the upper trunk. Blisters form and become confluent, resulting in the sloughing of sheets of epidermis similar to that which occurs in the case of thermal burns. The reaction of the body includes shedding of up to 100% of the epidermis in sheets. This results in substantial fluid loss and a greatly increased risk of secondary bacterial infection. The average onset from exposure to symptoms is 2 weeks, and the range is 1–3 weeks.
EXAMINATION Nikolsky’s sign is present (i.e., gentle traction placed on a blister or rubbing will result in lateral expansion, implying separation of the epidermis from the dermis). The pigment is lost, a phenomenon that does not
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occur with staphylococcal scalded skin syndrome. Other systems such as gastrointestinal, ocular, pulmonary, and renal systems may be involved to varying degrees.
LABORATORY FINDINGS Useful laboratory studies include a complete blood count and electrolyte analysis. Blood and urine cultures should be performed if there is suspicion for a secondary infection.
DIAGNOSIS The diagnosis is primary made on the basis of clinical presentation and an exposure to an offending agent. There is no direct confirmatory test, and the definitive diagnosis is made from a skin biopsy. The differential diagnosis of TEN includes toxic shock syndrome, staphylococcal scalded skin syndrome (although TEN is usually in adults), other exfoliative drug eruptions, Kawasaki syndrome, and primary blistering disorders such as pemphigus or pemphigoid.
TREATMENT AND OUTCOME The cornerstone of treatment is supportive care. This, combined with prevention of secondary infection and proper wound care, will have the greatest impact on survival. Patients with TEN should be treated as burn patients would, with admission to a dedicated burn center. Laboratory results and fluid status should be monitored, and any electrolyte abnormalities should be corrected. Sufficient potassium may be lost from the skin to cause significant hypokalemia. To monitor urine output, a Foley catheter should be placed. The provide should discontinue any newly instituted medications or other medications that may be responsible for the condition. No tests can be used to identify the precipitant, so any nonessential medications should be stopped. TEN is an extremely painful condition, and pain should be treated appropriately. The use of corticosteroids is controversial because there is little effect on the disease and their use may interfere with the early diagnosis of sepsis. Plasmapheresis is experimental. The administration of intravenous immunoglobulin should be considered, in consultation with a dermatologist. Antibiotics should be withheld if there is no suspicion for secondary infection. The condition carries up to a 50% overall mortality rate, with the major source being sepsis from either Staphylococcus aureus or Pseudomonas aeruginosa. Survival is primarily dependent on treatment at a burn center. The next likely cause of death is hypovolemia with associated electrolyte
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disorders. Mortality may be as low as 4% if this occurs within 7 days but as high as 8% if greater than 7 days. Blindness may result from ocular sequelae such as purulent conjunctivitis and erosions. Ocular involvement often portends permanent disability to some degree.
Bibliography Mangione S: Physical Diagnosis Secrets, Hanley and Belfus: Philadelphia, 2000, pp 54–56. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1643, 1729. Salyer S: The Emergency Medicine Physician Assistant Handbook, WB Saunders: Philadelphia, 1997, pp 62–64. Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 1140–1141. Stone C, Humphries RL (eds): Current Emergency Diagnosis and Treatment, ed 5. Lange Medical Books/McGraw-Hill: New York, 2004, p 1014. Tierney LM (eds): Current Medical Diagnosis and Treatment, Lange Medical Books/ McGraw-Hill: New York, 2003, pp 144, 1544. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1595–1596.
Toxicodendron Dermatitis SIMEON W. ASHWORTH AND BENJAMIN P. HARRISON
ICD Code: 696.6
Key Points Toxicodendron dermatitis is the most common cause of contact dermatitis in the United States.
DEFINITION Poison ivy, oak, and sumac, members of the plant genus Toxicodendron, cause an allergic contact dermatitis (i.e., allergic phytodermatitis) that occurs from direct exposure to the plants and their oils. This type of contact dermatitis is often called “Rhus.”
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DEMOGRAPHICS AND EPIDEMIOLOGY Toxicodendron dermatitis is the most common cause of contact dermatitis in the United States. Toxicodendron species are found in every state except for Alaska and Hawaii and in all regions except for the desert areas and the higher elevations. Poison oak is most common west of the Rocky Mountains, poison ivy to the east, and poison sumac in the southeast. Approximately 70% of the U.S. population is susceptible, with 15% of the population being extremely sensitive. There is no clear gender or racial difference in susceptibility, but elderly persons appear to have reduced sensitivity.
NOMENCLATURE AND PLANT IDENTIFICATION Poison ivy and oak have eastern (Atlantic) and western (Pacific) variations: Toxicodendron radicans and Toxicodendron rydbergii for the ivy variations and Toxicodendron pubescens and Toxicodendron diversilobum oak variations, respectively. Poison sumac comes in a single and rarer species of Toxicodendron vernix Kuntze. The leaves of poison oak and ivy are alternate, with trifoliate leaflets. The leaves are shiny green in the spring and turn yellow and deep red in the fall. The flowers grow in axillary panicles and are yellow-green. The fruit is globe shaped, resembling small pumpkins, and turns yellow or light brown when mature. Poison sumac has 7–13 leaflets per leaf, bearing the same kind of fruit as poison oak and ivy.
PATHOPHYSIOLOGY The allergic reaction is to the oil, not the plant itself, so one can react by touching objects that have come in contact with the plant such as tools, pets, and footwear. A delayed type IV hypersensitivity reaction occurs from the antigenic oleoresins that are found in the Toxicodendron species. When the oleoresin evaporates, the solvent—urushiol—remains and produces a dermatitis. Other urushiol-containing plants include the cashew nut tree, mango tree, and ginkgo tree. More resin is contained in younger plants; therefore, exposure to these often causes a more severe reaction. Exposure can come from the roots and other parts of the plant, not exclusively from the leaves, and may even cause a more severe reaction due to higher concentrations of the oleoresins.
CLINICAL PRESENTATION Within 48 hours of exposure to the resin, the reaction occurs in those who are sensitive and can last up to 3 weeks. The integument is primarily
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affected; however, the airway, eyes, and lungs can be involved if exposed to smoke produced from burning plants. Patients can develop erythema, papules, vesicles, bullae, pruritus, and redness, and the lesions often present in crusty, weeping linear configurations. In severe cases, edema, induration, and thickening of the dermis may occur. The dermatitis is usually self-limited and disappears without scarring. Occasionally hyperpigmentation remains and, in severe cases, EM can develop. The dermatitis is not spread by ruptured vesicles. The fluid in the vesicles contains no antigen; thus, the dermatitis cannot be spread by the rupturing of vesicles.
DIAGNOSIS Diagnosis is made primarily based on history and physical examination findings.
LABORATORY FINDINGS AND TESTING Laboratory testing is not needed for diagnosis. Allergenic patch testing is generally discouraged for toxicodendron dermatitis because it might sensitize an unsensitized person.
TREATMENT Treatment is based on the level of severity, the location of the eruption, and the presence of rare secondary infection. Removal of urushiol before it binds to membrane lipids (within 20 minutes) can prevent reaction. This is best performed with copious water irrigation. Soaps may spread the urushiol oil around the skin and worsen the dermatitis, so washcloths should be used with soap, and this washing should be followed by copious irrigation of all contacted skin. Domeboro, calamine, oatmeal baths, and Burrow’s solution (aluminum acetate) are topical solutions that have been proven to reduce the irritation in toxicodendron dermatitis. Recently Zanfel, an over-the-counter topical scrub, has been released for the treatment and prevention of dermatitis after exposure. The manufacturer’s claim that it binds the urushiol resin and clears mild cases of dermatitis, however, is unproven. Systemic steroids are beneficial in the treatment of moderate to severe toxicodendron dermatitis. These can be given orally (e.g., prednisone or methylprednisolone) or intramuscularly (e.g., dexamethasone). Oral medications are most reliable and should be tapered off for at least 10–14 days, with a warning to the patient that early withdrawal might cause the dermatitis to recur. Pre-made dose packs of steroids often have inadequate initial doses or too short of a course of prednisone. Ideally, a
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good starting dose is approximately 1 mg/kg of prednisone tapered over a 10- to 14-day period. Low-dose steroids and topical antihistamines have not been shown to have any beneficial effect but may be used in mild, localized cases. Oral antihistamines are helpful in relieving pruritus. Oral analgesics are occasionally required for pain relief in very severe cases. Oral antibiotics are indicated for secondary infections only. Initial treatment of toxicodendron dermatitis includes education and prevention using barriers to prevent exposure and washing the affected area soon after exposure. Vinyl gloves will not absorb the urushiol as readily as fabric gloves and should be used by patients with a history of severe reactions. Patients should be instructed to clean their clothes and any other objects that might have been in contact with the oils, including pets. Copious irrigation and cleansing of exposed skin should occur immediately after exposure.
Bibliography Davila A, Laurora M, Fulton J: A new topical agent, Zanfel, ameliorates urushiol-induced toxicodendron allergic contact dermatitis, [abstract no 364], Ann Emerg Med 2003;42 (4 suppl 1):s98. Isnar H: Plant poisoning, resins. Available at http://www.emedicine.com. Accessed on May 24, 2005. Stephanides S: Plant poisoning: toxicodendron. Available at http://www.emedicine.com. Accessed on May 19, 2005.
Urticaria DAVID W. KUHNS
ICD Codes: Urticaria 708.9, Angioedema 995.1
Key Points/Quick Reference Urticaria may be minor or can rapidly progress to a life-threatening condition. Rapid progression should prompt early and aggressive treatment. ! Emergency Actions ! Early administration of epinephrine and institution of intravenous access may be lifesaving for patients with urticaria. H1 and H2 blockers are generally recommended. Steroids are also frequently used in the treatment of this disorder.
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DEFINITION Urticaria (also known as hives) and a related condition, angioedema, are the cutaneous manifestations of the release of histamine and other mediators by mast (and other) cells in response to various stimuli. Most frequently, urticaria is self-limited in nature or responds readily to simple therapy. Occasionally, the activation of mast cells can proceed systemically to cause the life-threatening syndrome of anaphylaxis, manifested by hypotension, wheezing, and throat swelling. It is critical to recognize when simple urticaria may be progressing to a more serious condition. Anaphylaxis is dealt with in Chapter 16.
ETIOLOGY Cutaneous mast cells are located primarily around capillaries, lymphatics, and nerves in the skin. Erythema occurs due to vasodilation, the wheal is caused by fluid leakage, and the pruritus is caused by activation of dendritic itch receptors on nonmyelinated C fibers in the epidermis. Urticaria due solely to histamine typically resolves within an hour. Urticaria lasting longer than 1 hour is generally caused by the activity of additional mediators. Angioedema is a result of mediator release in the deeper dermis and leads to swelling that is most frequently nonpruritic. Angiotensin-converting enzyme inhibitor usage is one of the more common causes of angioedema, with an incidence of between 0.1% and 0.7%. Angioedema causing swelling in airway tissues necessitates aggressive treatment. Simple angioedema can be treated similarly to urticaria.
EPIDEMIOLOGY Between 15% and 23% of the population will experience urticaria sometime in their lifetimes. The majority of patients with urticaria do not have increased numbers of mast cells, but instead have mast cells that are more easily triggered to release their mediators. One exception is the clinical entity known as mastocytosis, in which there is a transient increase in the number of mast cells as well as a tendency for these to be easily triggered.
PATHOPHYSIOLOGY The primary cause of urticaria is the release of histamine—and less commonly, other mediators—by activated mast cells and other cells. Other mediators that can be responsible for hives include prostaglandin D2, bradykinin, various leukotrienes, and platelet-activating factor. Urticaria may be a response to exposures such as dust, molds, animal dander, and foods. Urticaria may also occur due to recent viral illnesses, amebiasis, malaria, diabetes, chronic renal insufficiency, primary biliary
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cirrhosis, systemic lupus erythematosus, rheumatoid arthritis, polymyositis, amyloidosis, polycythemia vera, carcinoma and lymphoma, fungal infections, mycoplasma, HIV infection, and pregnancy. Urticaria may also occur as a response to cold, exercise, or vibration.
CLINICAL PRESENTATION Angioedema usually affects the genitals, eyelids, lips, ear lobes, and mucous membranes. The affected area is not ecchymotic, is minimally tender, and is less pruritic than urticaria. Angioedema is often asymmetrical. Hereditary angioedema is a variant that is caused by a deficiency in C1 esterase inhibitor. This type of angioedema is more likely to affect airway tissues.
EXAMINATION The characteristic lesion of hives is a raised, erythematous, pruritic lesion known as a wheal. These lesions may coalesce to become giant wheals. They are often migratory and evanescent.
DIAGNOSIS Diagnosis is based on an appropriate history of exposure to an offending agent and by the presence of the characteristic lesions.
LABORATORY FINDINGS Laboratory evaluation is not generally useful in the emergency department (ED) evaluation of hives. Laboratory evaluation to look for the specific clinical conditions mentioned previously may be helpful in individual circumstances but rarely changes the ED treatment.
TREATMENT Aggressiveness of treatment is based on the severity of the urticaria, the rapidity of progression, and the presence or absence of systemic symptoms. In all cases, further exposure to the offending agent should be avoided. Hypotension, severe respiratory distress, and altered mental status should be treated as anaphylaxis. Any explosive, generalized urticaria should be treated with aqueous epinephrine 0.2 ml of 1:1000 SQ (not IV, because IV epinephrine is a 1:10,000 concentration and this can be a deadly mistake). An intravenous line should be started with preparation for the potential development of anaphylaxis. Intravenous Benadryl should be administered in a dose of
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1 mg/kg. If there is any delay in obtaining intravenous Benadryl, oral Benadryl elixir in the same dose is absorbed almost as rapidly. H2 blockers can be given intravenously as well. Zantac (ranitidine hydrochloride) can be given intravenously, 0.5 mg/kg over the course of 5 minutes. Cimetidine is given intravenously as a dose of 4–8 mg/kg. Intravenous Solu-Medrol (methylprednisolone) in a dose of 1–2 mg/kg up to 125 mg should also be given. Hydrocortisone can be given intravenously in a dose of 5–10 mg/kg up to a maximum dose of 500 mg. Patients with any severe reaction should be admitted to the hospital or at least should undergo prolonged observation in the ED until their conditions are clearly improved and stable. Patients with a severe or progressive episode of urticaria and a history of known hereditary angioedema frequently require C1 esterase inhibitor concentrate. Fresh frozen plasma can be used when C1 esterase inhibitor is unavailable. Mild urticaria (and non–life-threatening angioedema) can be treated with oral antihistamines. Oral Benadryl elixir is frequently given at triage in a dose of 0.5–1.0 mg/kg. Hydroxyzine (0.5–1 mg/kg) can be used as an alternative. Failure of the condition to resolve within an hour should prompt the addition of an H2 blocker and a steroid to the treatment regimen. Commonly used H2 blockers are ranitidine (Zantac) and cimetidine (Tagamet). In mild urticaria, these may be given orally. The oral dose of ranitidine is 1–2 mg/kg every 12 hours. The oral dose of cimetidine is 5–10 mg/kg/day divided twice or three times per day. If these are given for the treatment of the urticaria, they should be continued after discharge. Steroids are not believed to be effective in preventing degranulation of cutaneous mast cells in acute urticaria. They have, however, been shown to prevent a biphasic reaction that may occur 4–8 hours later in 20% of persons. The fact that this reaction cannot be predicted at the initial presentation prompts many ED providers to give steroids to prevent “bounce-backs.” Prednisone is given in an oral dose of 1–2 mg/kg daily. Intravenous steroids have little advantage over oral steroids in terms of effect or time of onset. Patients with minor urticarial eruptions are frequently sent home with a prescription for oral antihistamines. Traditionally, Benadryl or hydroxyzine were used. Newer, less-sedating agents have been developed that deliver various degrees of antihistaminic activity. Some clinicians use a regimen that includes a nonsedating agent during the day and a more sedating agent at bedtime. Various options include the following:
Benadryl 1 mg/kg taken every 6 hours for 4 days may be used in children for whom sedation is less of an issue. Zyrtec (cetirizine) 10 mg daily can be given to adults, 2.5 mg of syrup can be given to children aged 2–5 years, and 5-mg tablets or syrup can be given to children 6–11 years old. (This is less sedating.) Many other agents are available.
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As discussed previously, patients who have been treated with H2 blockers or steroids in the ED should also be sent home with a prescription for these agents. Since leukotrienes have been shown to be partially responsible for persistent or delayed urticaria, leukotriene antagonists have been used with some anecdotal success. These agents are not yet recommended in the treatment of urticaria. Patients with a significant urticarial reaction may be at risk for a more serious reaction in the future. Consideration should be given to providing them with a prescription for an EpiPen (epinephrine) autoinjector for use in case of future attacks that prove to be serious. These patients should be given instructions for administration and should be told to present to the ED if this therapy is required.
Bibliography Beltrani VS: Urticaria and angioedema, Dermatol Clin 1996;14(1):171–198. Beltrani VS: Urticaria, angioedema, and anaphylaxis, ACP Medicine 2003; Ch 6 (Immunology) XIII:1–6. Bensch G, Borish L: Leukotriene modifiers in chronic urticaria, Ann Allergy Asthma Immunol 1999;83(4):348. Heymann WR: Chronic urticaria and angioedema associated with thyroid autoimmunity: Review and therapeutic implications, J Am Acad Dermatol 1999;40(2 Pt 1):229–232. Joint Task Force on Practice Parameters, The diagnosis and management of urticaria: A practice parameter. Part I: Acute urticaria/angioedema. Part II: Chronic urticaria/ angioedema, Ann Allergy Asthma Immunol 2000;85(6 Pt 2):521–544. Tharp MD: Chronic urticaria: Pathophysiology and treatment approaches, J Allergy Clin Immunol 1996;98(6 Pt 3):S325–S330.
Chapter 4
Acute Gastrointestinal Emergencies Anorectal Disorders CLAUDIO F. ZEBALLOS
ICD or CPT Codes: Hemorrhoids 455.0, Anorectal abscess 566.0, Pilonidal 685.0, Proctalgia fugax 546.6, Pruritus ani 698.0, Rectal prolapse 569.1
Key Points/Quick Reference Anorectal disorders include hemorrhoids, anal fissures, anorectal abscesses and fistulas, pilonidal disease, proctalgia fugax, pruritus ani, and rectal prolapse. ! Emergency Actions ! Any patient who has diabetes, fever, chills, an elevated glucose level, and an anal disorder should be thoroughly evaluated for sepsis along with the anorectal disorder.
DEFINITIONS Hemorrhoids are varicosities of the veins of the hemorrhoidal plexus that can become inflamed, thrombose, and bleed. External hemorrhoids are located below the dentate line and are covered by squamous epithelium. Internal hemorrhoids are located above the dentate line. Anal fissures are superficial linear tears in the anal canal that can develop into a chronic ulcer. Anorectal abscess is a localized collection of pus that develops due to an infected anal crypt gland in the intersphincteric space. An anorectal fistula is a communication between the anal canal and, usually, perianal skin that can drain. Pilonidal disease is an acute or recurrent chronic abscess that drains from sinuses located in the midline sacrococcygeal area in the gluteal fold. Hidradenitis suppurativa is a localized infection of the apocrine sweat glands that develops a network of sinus tracts and is associated with hair follicles found along the perineum, groin, or axillae. Proctalgia fugax is a severe painful spasm of the muscles of the pelvic floor and rectal area that can occur spontaneously and usually lasts less than 30 minutes. Rectal prolapse (i.e., procidentia) is a condition in which the rectum protrudes through the anus. Pruritus ani is defined as anal and perianal itching. 114
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EPIDEMIOLOGY Hemorrhoids are common, affect both sexes, and have a 4.4% incidence in the U.S. population with a peak prevalence between the ages of 45 and 65 years and increased incidence among persons with higher socioeconomic status. Anal fissures are most common in persons 30–50 years of age. This is also the most common anorectal problem encountered in infants. Anorectal abscesses and fistulas most commonly affect males aged 30–50 years. Prevalence in the general population is likely higher than is seen in clinical practice because the majority of patients do not seek medical care. Anorectal fistulas develop in 30%–60% of patients with anorectal abscesses. Rectal prolapse tends to affect persons at the extremes of age and has a higher incidence in women with a history of excessive straining. Pilonidal disease usually affects young hirsute males and is associated with obesity. It is rarely found past the fourth decade of life. Pruritus ani is more common in older men and during the summer months, with exacerbation of symptoms at night.
PATHOLOGY Hemorrhoids Hemorrhoids are vascular cushions in the anal submucosa that normally become engorged during defecation to protect the anal canal. With aging and stressors the muscle layer, muscularis submucosa breaks down and the vascular cushions become overdistended with venous blood. These overdistended vascular cushions are prone to bleed, thrombose, or ulcerate. External hemorrhoids are located below the dentate line, whereas internal hemorrhoids are located above.
Anal Fissures An anal fissure is a tear in the lining of the anal canal, usually in the posterior midline, caused by local trauma such as passage of large hard stool. Anal fissures can also be seen in patients with Crohn’s disease, tuberculosis, and leukemia. The tear can reoccur with subsequent bowel movements. The exposed internal sphincter muscle—below the fissure— spasms, pulling apart the edges of the fissure and preventing healing. This cycle leads to the development of a chronic anal fissure.
Anorectal Abscesses and Fistulas Anal glands that are located circumferentially within the anal canal at the level of dentate line become blocked and infected develop into abscesses.
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These can progress into fistulas. Because these glands are located in several different planes, four different kinds of abscesses can present clinically. The four types are perianal (40%–45%), ischiorectal (20%–25%), intersphincteric (2%–5%), and supralevator (>5%). Anorectal fistulas usually develop after either surgical or spontaneous drainage of a chronic perianal abscess, but they can also result from trauma/postoperative and chronic anal fissure, radiation, and leukemia.
Rectal Prolapse Rectal prolapse is caused by weakening of the pelvic floor muscles, creating a laxity in the pelvic structures and may be seen with uterine prolapse.
Pilonidal Disease Debate surrounding the etiology of pilonidal disease centered on the theory that a pilonidal sinus develops in the gluteal fold during embryogenesis. This is in contrast to the concept that disease is caused by a simple bacterial infection of sterile hair follicle that occludes drainage, forming an ever-enlarging cavity that invades the subcutaneous fat and developing an epithelium-lined tract to the skin.
Pruritus Ani Pruritus ani can have many causes, but most commonly carries the benign etiology of poor hygiene and fecal irritation. Other etiologies include pinworms, hemorrhoids, anal fissure or fistulas, and systemic disease such as iron or vitamin deficiencies, psoriasis, lichen simplex, and sexually transmitted diseases. Contact dermatitis can also cause this condition as a result of the use of a new cream or toiletry item.
CLINICAL PRESENTATION Hemorrhoids Because most patients use the term hemorrhoid loosely to describe a myriad of anorectal problems, a thorough patient history should be obtained, including symptoms, bleeding and its association to defecation, pain, itching, protrusion, discharge, color of stool, systemic disease such as human immunodeficiency virus (HIV) infection or Crohn’s disease, polyps, cancer, and anal sexual intercourse. A patient with hemorrhoids most commonly present reporting of rectal bleeding particularly with defecation, and the bleeding described as bright red. Bright red blood seen on toilet paper suggests anal fissure or external hemorrhoids. Drops of blood in the toilet bowl suggest internal
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hemorrhoids. Both internal and external hemorrhoids are usually painless unless the hemorrhoid is thrombosed, at which point it becomes painful. A prolapsed or thrombosed hemorrhoid can present as a gradual-onset, persistent pain.
Anal Fissures Anal fissures commonly present with acute-onset, tearing, intense pain associated with rectal bleeding during bowel movements. The blood is usually bright red and found on surface of stool but not mixed with stool. The pain lasts several hours and subsides until the next bowel movement.
Anorectal Abscesses and Fistulas A patient with an anorectal abscess usually reports severe rectal pain that is constant and not associated with bowel movements. He or she may also report rectal drainage and fever. In the case of anorectal fistulas, the patient will report recurrent perianal intermittent discharge, which is usually painless unless the fistula becomes occluded.
Rectal Prolapse A patient with rectal prolapse will present reporting a painless protruding anal mass or fullness with Valsalva maneuver, walking, or standing. Rectal bleeding may occasionally occur, and incontinence is frequent.
Pilonidal Disease A patient with pilonidal disease reports tender fluctuant nodule midline in the gluteal fold region of sacrococcygeal area.
Pruritus Ani Patients with pruritus ani report uncontrollable anal itching. A thorough history should be obtained, including diet, systemic diseases, use of topical agents, and sexual practices.
EXAMINATION Hemorrhoids Hemorrhoids are usually visualized by performing anoscopy to assess the type and degree. It is useful to have the patient perform the Valsalva maneuver during the examination. Internal hemorrhoids are classified as
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first-degree if they protrude into the anal canal but do not prolapse and can present as a feeling of fullness, whereas second-degree hemorrhoids prolapse with stress but spontaneously reduce. Third-degree hemorrhoids prolapse but require manual reduction, and fourth-degree are not reducible and require surgery. External hemorrhoids usually do not cause any symptoms unless they become thrombosed/clotted. Thrombosed external hemorrhoids presents as a firm bluish-purple and are painful with palpation and defecation.
Anal Fissure Usually found in the posterior midline, anal fissure can also be seen in the anterior midline in women. Fissures found in other areas should make the practitioner consider Crohn’s disease, leukemia, HIV infection, or tuberculosis. Chronic fissure may exhibit the triad of a deep ulcer, an external skin tag (i.e., sentinel pile) at the lower end, and a papillae at the superior end. Rectal examination during an acute painful episode can be difficult because of sphincter spasm and pain.
Anorectal Abscesses and Fistulas In the presence of anorectal abscess or fistula, a fluctuant or indurated mass may be palpated. Purulent drainage may be visualized. Perianal abscess is the most common form and will be visualized and palpated in the perineum. Ischiorectal abscess may present as a fluctuant mass within the buttock. Intersphincteric abscess can be seen as fluctuant mass protruding in the lumen and can be confused with thrombosed internal hemorrhoid. Supralevator abscess usually has no external evidence of disease, which makes the diagnosis difficult. Patients will report buttock pain, fever, and sometimes urinary retention. Computed tomography (CT) scan may aid in this diagnosis. A fistula will often be visualized as a secondary cordlike tract in the perineum. Practitioner should avoid probing the tract because this may create other fistulas.
Rectal Prolapse The patient should be examined while in a standing position or while performing a Valsalva maneuver. A moist reddish protruding mass will often be visualized extruding the anal canal.
Pilonidal Cysts Pilonidal cysts are tender fluctuant nodules midline in the gluteal fold region of sacrococcygeal area.
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Pruritus Ani In examining for pruritus ani, the healthcare provider should carefully examine the anus for tears, lesions, hygiene, excoriations, masses, or any evidence of abscesses. Pinworms can be identified by using transparent tape on the anus then transferring the specimen to glass slide to be viewed for eggs under the microscope at 10 magnification.
LABORATORY FINDINGS A complete blood count (CBC) may be useful if the practitioner is concerned about the amount bleeding or is looking for leukocytosis. Clotting studies can be helpful if the patient is taking Coumadin (warfarin) or has a bleeding disorder. A digital rectal examination should be performed to document the color, quality, and hemoccult status of stool.
DIAGNOSIS Careful history and physical examination with an anoscope is necessary to make a diagnosis.
IMAGING STUDIES, RADIOGRAPHS, AND GRAPHS The American Gastroenterology Society recommends that all patients with bright red rectal bleeding should have an anoscopy, at minimum, and should be scheduled for flexible sigmoidoscopy. CT scanning may aid in the diagnosis of supralevator abscess.
TREATMENT AND OUTCOMES Hemorrhoids Hemorrhoid treatment varies with degree. First-, second-, and most thirddegree nonthrombosed hemorrhoids can be managed with “WASH” regimen consisting of warm water/sitz baths, analgesia (oral), stool softeners, and a high-fiber diet. The use of topical steroids, anesthetics, and suppositories remain controversial for the treatment of hemorrhoids; however, all of these are readily available over the counter. There are data to support the theory that long-term topical steroids use can cause tissue atrophy. Patients with third-degree hemorrhoids will need referral for surgery, whereas acute, gangrenous, or fourth-degree hemorrhoids will require emergent hemorrhoidectomy. Thrombosed external hemorrhoids can be excised within the first 48 hours to provide relief of symptoms. An
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elliptical excision with evacuation of the blood clot should be cautiously performed only by experienced practitioners with prior experience.
Anal Fissures Anal fissures often respond to conservative measure, including “WASH” regimen of warm sitz bath post-defecation for 15 minutes, analgesia (i.e., topical anesthetic cream), stool softeners (e.g., Fiberall or Metamucil), and a high-fiber diet. A topical agent like glycerin trinitrate ointment or nifedipine 0.2% gel given twice a day aid in lubricating the anal canal and decreasing sphincter tone. Steroid suppositories have not been shown to be useful and can actually hinder healing. Most anal fissures will resolve in 2–4 weeks. Cases of chronic anal fissure should be referred to a surgeon.
Anorectal Abscesses and Fistulas Abscesses should be drained in a timely manner in consultation with a surgeon. Antibiotics should be given if perianal abscess involves evidence of cellulitis, if the patient has diabetes, and for all other types of abscesses. Patients with anorectal fistula should be referred to a surgeon for operative repair.
Rectal Prolapse Rectal prolapse should be manually reduced immediately as prolonged prolapse can cause tissue necrosis. Stool softeners should be administered after reduction, along with surgical referral. If the practitioner is unable to reduce the prolapse, the condition becomes an emergent surgical issue.
Pilonidal Disease Pilonidal disease management involves drainage via a lateral incision off midline. Recurrence is common, and definite treatment will often involve surgical consultation.
Pruritus Ani Treatment should be aimed at underlying cause. Appropriate anodermal hygiene is recommended if fecal irritation is identified as the cause. The anus area should be kept clean and dry, and excessive wiping of the anus should be avoided. After defecation, the patient should bathe and pat dry the area. Hydrocortisone cream 1% should be applied twice a day for 1 week; this can help relieve symptoms and promote healing. Oral
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antihistamine such as diphenhydramine can help ease symptoms. Pinworms can be treated with mebendazole 1 g taken once PO. Scabies are treated with lindane 1% or permethrin 5% lotion. Lindane is not recommended in children because it can cause seizures in epileptics or, if overused or misused in children, there is an increased risk of seizures. Lindane is contraindicated for use in infants. If the pruritus is related to sexually transmitted disease, the condition should be treated with appropriate antibiotics. Irritants should be avoided.
Bibliography American Gastroenterology Society, Diagnosis and care of patients with anal fissure, Gastroenterology 2003;124:233. American Gastroenterology Society, Diagnosis and treatment of hemorrhoids, Gastroenterology 2004;126:1461. Barnett JL, Raper SE: Anorectal diseases, In Yamada T, Alpers D, Qwayng C, et al (eds): Yamada Textbook of Gastroenterology, ed 2. JB Lippincott: Philadelphia, 1995, p 2027. Beers MH, Berkow R (eds): Gastrointestinal disorders. Anorectal Disorders, Online Medical Library, www.merck.com. Merck Research Laboratories DIVISION OF Merck & Co, Whitehouse Station, NJ. Breen E, Bleday R: Anal fissures 2005. Available at: http://www.uptodate.com. Burgess BE, Bouzoukis JK: Anorectal disorders. In Tintinalli JE: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Gorfine SR: Topical nitroglycerin therapy for anal fissures and ulcers [letter], N Engl J Med 1995;333:1156. Johanson JF, Sonnenberg A: The prevalence of hemorrhoids and chronic constipation: An epidemiologic study, Gastroenterology 1990;98(2):380–386. Lund JN, Scholefield JH: A randomised, prospective, double-blind, placebo-controlled trial of glyceryl trinitrate ointment in treatment of anal fissure, Lancet 1997;349 (9044):11–14. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Noble J (ed): Textbook of Primary Care Medicine, ed 3. Mosby: St Louis, 2001. Ramanujam P, Venkatesh KS: Fibrin glue application in the treatment of recurrent anorectal fistulas, Dis Colon Rectum 1999;42:1136. The role of endoscopy in the patient with lower gastrointestinal bleeding, Guidelines for clinical application, Gastrointest Endosc 1988;34:23S. Smith LE, Henrichs D, McCullah RD: Prospective studies on the etiology and treatment of pruritus ani, Dis Colon Rectum 1982;25:358. The Society for Surgery of the Alimentary Tract: Surgical management of hemorrhoids. Available at: http://www.ssat.com/cgi-bin/hemorr.cgi. Accessed on August 11, 2003.
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Diverticulosis and Diverticulitis SHAWN M.VARNEY
ICD Codes: Diverticulosis 562.10, Diverticulitis 562.11, Diverticular hemorrhage 562.12
Key Points/Quick Reference Diverticulitis and lower gastrointestinal (GI) bleeding resulting from diverticulosis are clinically important complications of diverticular disease. ! Emergency Actions ! Volume resuscitation and broad-spectrum antibiotics address the emergent complications of diverticulitis and diverticulosis.
DEFINITION Diverticulosis refers to small outpouchings from the colonic lumen formed by herniation of the mucosa and submucosa at sites of vascular penetration. The sigmoid colon is affected most commonly (90%–98%), with the right colon involved only about 15% of the time. Nevertheless, diverticula may affect any portion of the GI tract from the duodenum to the sigmoid and may be solitary or multiple, numbering in the hundreds. Symptomatic diverticular disease is diverticulosis with clinical symptoms (e.g., abdominal pain or change in bowel habits) but no signs of inflammation (e.g., fever, leukocytosis, or peritoneal signs). Diverticulitis is diverticulosis with clinical symptoms and evidence of inflammation.
EPIDEMIOLOGY Diverticular disease is largely an ailment of industrialized Western societies and is found equally in males and females. In the United States, diverticular disease is uncommon (<10%) in persons younger than 40 years, whereas it develops in 30% of the population by the age of 45 years, and 50%–65% by the age of 80 years. Ethnic and cultural differences exist. For example, Asians tend to have more right-sided disease. Between 10% and 25% of patients experience complications, namely diverticulitis and lower GI tract bleeding. Many patients will have
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recurrent attacks. In patients younger than 40 years of age with diverticulitis, 25% will experience recurrence in 1 year and will require emergency surgery.
PATHOPHYSIOLOGY Diverticula result from a combination of high intraluminal pressures and weak colonic walls at sites where arteries (e.g., vasa recta) penetrate the muscularis. Other contributing factors include bowel segmentation from contracted taenia coli, abnormal colonic motility, narrowing of the lumen, thickening of the muscularis, excess elastin deposition, structural collagen changes, and low-fiber diets. Despite these findings, the bowel wall does not hypertrophy. The law of Laplace states that the wall tension (T) of a hollow cylinder is proportional to the pressure (P) within the cylinder multiplied by the radius (R) of the cylinder (T ¼ PR). The anatomy of the colon further contributes to the development of diverticula because the sigmoid has the narrowest lumen and, hence, the greatest pressure. The sigmoid colon thus houses the most diverticula. Diverticular disease is usually discovered incidentally. Most (75%–80%) remain asymptomatic and require no further evaluation or treatment. Diverticulitis is inflammation resulting from inspissated fecal material or food particles in the neck of a diverticulum, exacerbated by increased intraluminal pressure. Erosion of the diverticular wall leads to inflammation, ischemia, focal necrosis, and perforation. Microscopic or macroscopic perforations result in bacterial overgrowth and adjacent peridiverticulitis. Localized abscesses, fistulas, obstruction, or free peritoneal rupture may result. Common organisms include aerobes (e.g., Enterobacter species and Escherichia coli) and anaerobes (e.g., Clostridium species, Peptostreptococcus species, and Bacteroides fragilis). Another problematic complication is diverticular hemorrhage, which develops in 5%–15% of patients with diverticulosis. The vasa recta perforate the colon wall, leading to diverticula. The exposed vessels become abraded, rupture into the lumen, and bleed. Diverticular hemorrhage usually originates from the right colon, is abrupt and painless, and accounts for more than 40% of lower GI tract bleeds. Up to 50% of patients report intermittent maroon stools or hematochezia, and about 5% present with massive bleeding and hypovolemia.
CLINICAL PRESENTATION Diverticulosis Patients with uncomplicated diverticulosis are generally asymptomatic and do well without treatment or follow-up. When symptoms do appear,
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patients report nonspecific, crampy, left-sided lower abdominal pain. Patients are afebrile and have a normal white blood cell (WBC) count. Other common symptoms include bloating and constipation. Eating exacerbates the pain, whereas defecation or flatus decreases discomfort.
Diverticulitis Acute diverticulitis develops in 15%–25% of patients with diverticulosis and presents as a spectrum of disease with occasional life-threatening complications. Microscopic diverticular perforations lead to inflammation and left lower quadrant pain (70%) for several days. Nausea and vomiting are common (20%–60%), along with constipation (50%), diarrhea (25%– 35%), and urinary difficulties (10%–15%). In Western countries, rightsided diverticulitis is uncommon (1.5%), in contrast to Asia, where 75% of persons have diverticulitis. Right-sided disease may mimic appendicitis. The classic presentation of acute diverticulitis involves intermittent or constant left lower quadrant pain of a few days’ duration, anorexia, nausea, vomiting, a change in bowel habits (i.e., diarrhea or constipation), and fever with a temperature over 100.4 F (38 C). Less commonly, patients may present with complicated diverticulitis. (See Examination section.)
EXAMINATION Diverticulosis Physical examination findings for diverticulosis include mild left lower quadrant tenderness or fullness. Either gross or guaiac-positive blood may be present in the stool but should not be attributed to diverticulosis without further evaluation.
Diverticular Hemorrhage Diverticular bleeding begins abruptly and painlessly. The large amount of red blood and clots or maroon stool causes rectal urgency. Melena may be present.
Acute Diverticulitis Physical findings include left lower quadrant tenderness (voluntary guarding or localized rebound tenderness), fever, occasionally a palpable mass, and usually decreased bowel sounds. Right-sided pain is uncommon but may represent a redundant sigmoid colon overlying the appendix. Female patients should receive a pelvic examination to rule out gynecological pathology.
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Complicated Diverticulitis Complicated diverticulitis may manifest as abscesses, fistulas, or obstruction. Abscesses may start as microscopic collections and become phlegmons, and then spread to become localized abscesses or even frank peritonitis. A palpable, tender mass may be present, along with an unrelenting fever despite antibiotics. CT scans detect abscesses well. Fistulas form when abscesses rupture into adjacent organs and form communicating tracks. Colovesicular fistulas are most common and cause pneumaturia and fecaluria. Colovaginal fistulas rank second and produce feces or flatus from the vagina, along with frequent vaginal infections and discharge. Surgery is the treatment of choice. Partial large bowel obstructions may result from inflammation or extraluminal compression by an abscess. Small bowel may be affected if a loop is trapped in the inflammatory mass. Typical symptoms and signs of bowel obstruction predominate with nausea, vomiting, abdominal pain, and distention. Symptoms generally decrease with conservative therapy (e.g., antibiotics and bowel rest). Surgery is the alternative. Recurrent bouts of diverticulitis may lead to progressive narrowing and stricture formation. Endoscopy and dilation with subsequent metal stent placement may offer alternatives to surgery.
LABORATORY FINDINGS Laboratory study results in diverticulosis are normal. The hematocrit measurement has potential utility if bleeding has occurred. A type and cross match for blood and coagulation studies should be considered. Clinical practice guidelines of the American Society of Colon and Rectal Surgeons recommend a CBC and urinalysis, along with flat and upright abdominal radiographs and CT scan for suspected diverticulitis. Leukocytosis and/or a left shift are present less than half the time. Many providers also order electrolyte, blood urea nitrogen (BUN; elevated if blood is present in the GI tract), creatinine (to check hydration status), liver function (to rule out other etiologies), amylase, and lipase tests, as well as a pregnancy test if the patient is of childbearing years. Blood cultures may prove useful in diagnosing complicated diverticulitis before empirical antibiotic administration.
DIFFERENTIAL DIAGNOSIS In any patient older than 40 years presenting with abdominal pain, change in bowel habits, and bloody stool, the differential diagnosis should include diverticulitis, ulcerative colitis, Crohn’s disease, ischemic colitis, irritable bowl syndrome, carcinoma, and appendicitis.
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Ulcerative Colitis Ulcerative colitis usually presents in patients younger than 30 years and peaks again in the sixth decade of life. These patients have frequent loose stools, rectal bleeding, and no abdominal tenderness. Ulcerative colitis starts in the distal colon and progresses proximally. Surgery cures the disease.
Crohn’s Disease Crohn’s disease can occur from the mouth to the anus. It can cause a transmural fistula or an abscess that can be difficult to differentiate from diverticulitis. Patients with Crohn’s disease present with mucus in the stool, diarrhea, and rectal pain. They often have rectal skin tags, fissures, fistulas, and extraintestinal findings such as cholelithiasis, ureterolithiasis, arthritis, and conjunctivitis. These patients need a sigmoidoscopy with a tissue biopsy and subsequent medical therapy. Surgery is postponed as long as possible because of the ability of Crohn’s disease to recur anywhere in the intestinal system.
Ischemic Colitis Ischemic colitis manifests as sudden onset of left abdominal pain and bleeding with pain out of proportion to examination findings. Patients usually have a history of a myocardial infarction, occlusive disease (e.g., thrombosis or emboli), or low flow states (e.g., congestive heart failure or shock). The bleeding is usually self-limited. Bowel rest, a nasogastric tube, and treating the etiology aid in recovery.
Irritable Bowel Syndrome Irritable bowel syndrome is a diagnosis of exclusion and is caused by food or emotional upset. Patients with irritable bowel syndrome present with crampy pain and experience alternating bouts of constipation and diarrhea. Passage of flatus relieves symptoms. Patients are afebrile and manifest a palpable cord-like mass (the sigmoid colon) in the lower abdomen.
Cancer Cancer causes a luminal narrowing of the colon or a small bowel obstruction resulting in a decreased stool caliber. Patients can have diarrhea or constipation, bloody stools, and weight loss. A nontender mass can usually be felt on rectal or abdominal examination. Patients with cancer often have anemia without an elevated WBC count.
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Diverticulitis in Special Situations Diverticulitis in males younger than 40 years experience a more virulent disease process and require surgery 66%–88% of the time during their first episode. Another risk factor for complications in young persons is obesity. Immunocompromised patients with diverticulitis manifest subtle symptoms and signs. The delay in diagnosis leads to more advanced disease processes, higher rates of perforation, greater need for surgery, and more postoperative complications.
RADIOGRAPHS Diverticulosis Although barium enema was the diagnostic modality of choice for diverticulosis and could identify the number and location of diverticula, it does not correlate with the clinical relevance, underestimates the extent of inflammatory process, is inaccurate in one third of cases, and may be fraught with potential complications from contrast (e.g., peritonitis). Presently, colonoscopy is the preferred diagnostic study. CT scanning is also useful and has a sensitivity of 97% for identifying diverticular disease, compared with 92% for a water-soluble contrast enema.
Diverticulitis Studies from the late 1980s suggest that plain abdominal radiographs may demonstrate abnormal findings (e.g., small or large bowel dilatation/ileus, pneumoperitoneum, obstruction, or abscesses) in 30%–50% of patients. CT scans have replaced plain radiographs and contrast enemas. CT scanning technology has advanced in recent years to multidetector helical scanners and is now the radiological examination of choice in the case of suspected diverticulitis. Numerous studies since 1997 have demonstrated sensitivities from 91% to 98% and specificities from 77% to 100% (most often, 100%) with oral and intravenous contrast. In addition, rectally administered water-soluble contrast and air are used in some institutions. Other advantages to CT scans are that they evaluate the extent of disease, assist with medical and surgical intervention, and offer alternative diagnoses. CT findings for diverticulitis include an inflamed diverticulum, pericolonic inflammation, abscess formation, adjacent colonic wall thickening, and intramural sinus tracts.
TREATMENT AND OUTCOME Diverticulosis Treatment for simple diverticulosis entails antispasmodic medications, a fiber-rich diet, and a follow-up sigmoidoscopy.
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Diverticular Hemorrhage Diverticular bleeding is arterial in origin and stops spontaneously in 70%–80% of patients. Diverticula account for more than 40% of lower GI tract bleeding and result in massive hemorrhage (requiring a transfusion) in 3%–5%. Rebleeding occurs in 22% of patients. For unstable patients with diverticular hemorrhage, treatment should proceed as with other GI tract bleeding. An airway should be established as needed, oxygen should be given, two large-bore intravenous lines should be introduced, and fluid resuscitation should be provided in the form of 2 L of normal saline or lactated Ringer’s solution. In severe cases, the healthcare provide should transfuse two units of packed red blood cells, a six-pack of platelets, and two units of fresh frozen plasma, as required. A nasogastric tube should be placed to rule out an upper GI tract source of bleeding and a urinary catheter to monitor resuscitation. Once the patient is stabilized, the practitioner should search for the etiology. Colonoscopy or sigmoidoscopy is diagnostic 50% of the time. When the bleeding source cannot be determined, selective arterial catheterization can be diagnostic and therapeutic. Arteriography can identify vessels if there is active bleeding of at least 1 ml/min (the equivalent of 2 units of packed red blood cells a day). A technetium-99m–tagged red blood cell scan may detect even slower rates or intermittent bleeding. Once the site is located, embolization or intra-arterial vasopressin (0.2 units/min for 6–12 hr) can be given. A consultation with a surgeon or gastroenterologist should be sought promptly, and the monitored patient should be admitted.
Diverticulitis Diverticulitis covers a spectrum of disease and can be divided into complicated and uncomplicated disease. Complicated diverticulitis refers to the presence of perforation, obstruction, abscess, or fistula formation and accounts for 25% of patients with their first bout of acute diverticulitis. Most (90%–95%) require surgical intervention, and a few (2%–11%) experience a recurrence. For the 75% of patients with uncomplicated diverticulitis, the majority (85%) will respond to conservative therapy. Of these, 30%–40% will remain asymptomatic, 30%–40% will have episodic cramps without diverticulitis, and 30% will suffer a second attack. Approximately 15% will require surgery for their first episode of diverticulitis. ACUTE (UNCOMPLICATED) DIVERTICULITIS Patients with uncomplicated diverticulitis should be treated with oral hydration, bowel rest, and oral broad-spectrum antibiotics. Most of the common gram-negative rods (e.g., E. coli, Enterobacteriaceae) and anaerobic organisms (e.g., Bacteroides species) can be treated with a
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quinolone plus metronidazole or amoxicillin-clavulanate, or trimethoprim-sulfamethoxazole plus metronidazole for 10 days. Patients who have mild symptoms, live in a supportive social situation, and tolerate oral intake may be discharged. Patients manifesting systemic signs of infection and requiring hospitalization should receive intravenous clindamycin or metronidazole plus either a quinolone or third-generation cephalosporin for 5–7 days. Another alternative is single-agent coverage with a beta-lactamase inhibitor (e.g., ampicillin-sulbactam, piperacillin-tazobactam, or ticarcillin-clavulanate). COMPLICATED DIVERTICULITIS Patients experiencing sequelae such as abscesses, obstruction, or fistulas should be admitted to the hospital. Patients with peritonitis will require intravenous fluids, broad-spectrum intravenous antibiotics, and surgery. Recommended antibiotic regimens include triple coverage with metronidazole or clindamycin (500 mg IV every 8 hr), an aminoglycoside (gentamicin 1.5–2 mg/kg IV every 8 hr), and ampicillin (2 g IV every 6 hr). An alternative is single-agent coverage with imipenem-cilastin (500 mg IV every 6 hr) or piperacillin-tazobactam (3.375 mg IV every 6 hr). Patients experiencing an initial attack of complicated diverticulitis or a second bout of uncomplicated diverticulitis should undergo elective resection of the involved colon. Recurrence leads to greater complications, morbidity, and mortality.
Bibliography Diverticular disease. Emedicine, Last updated December 20, 2004. Available at: http:// www.emedicine.com. Farrell RJ, Farrell JJ, Morrin MM: Diverticular disease in the elderly, Gastroenterology Clin North Am 2001;30(2):475–496. Kazzi AA, Kazzi Z: Diverticular disease. Emedicine, Available at: http://www.emedicine. com. Last updated December 20, 2004. Accessed on May 27, 2005. Lawrimore T, Rhea JT: Computed tomography evaluation of diverticulitis, J Intensive Care Med 2004;19:194–204. Stollman N, Raskin JB: Diverticular disease of the colon, Lancet 2004;363:631–639. Whetstone D, Hazey J, Pafahl WE, et al: Current management of diverticulitis, Curr Surg 2004;61(4):361–365. Young-Fadok T, Pemberton JH: Clinical manifestations and diagnosis of colonic diverticular disease, UpToDate, version 13.1. Topic last updated September 4, 2003. Available at: http://www.uptodate.com. Accessed on June 9, 2005. Young-Fadok T, Pemberton JH: Epidemiology and pathophysiology of colonic diverticular disease, UpToDate, version 13.1. Topic last updated June 26, 2003. Available at: http://www.uptodate.com. Accessed on June 9, 2005. Young-Fadok T, Pemberton JH: Treatment of acute diverticulitis, UpToDate, version 13.1. Topic last updated December 10, 2004. Available at: http://www.uptodate.com. Accessed on June 9, 2005.
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Gastrointestinal Bleeding DAVID A. HNATOW
ICD or CPT Code: Gastrointestinal bleeding 578.9
Key Points All GI tract bleeding should be treated as life threatening until the source of the bleeding is defined.The many causes of GI tract bleeding are classified into upper or lower, depending on their location in the GI tract. Mortality from GI tract bleeding is approximately 10%. Lower GI tract bleedings are more common in children than adults. A carefully performed patient history can often point to the source of bleeding. The monitoring of vital signs is very important in a patient with acute GI tract bleeding. A review of pertinent laboratory data is an essential step during resuscitation to assess the need for blood product transfusion. Upper endoscopy is the diagnostic modality of choice for acute upper GI tract bleeding, and colonoscopy is used when a lower GI tract bleed is suspected. ! Emergency Actions ! The evaluation, diagnosis, resuscitation, and stabilization phases are usually performed simultaneously in the case of acute GI tract bleeding. A patient with suspected GI tract bleeding should have two large-gauge intravenous lines placed and oxygen administered. The patient’s vital signs should be monitored every 5 minutes until the patient’s condition has stabilized. All patients with hemodynamic instability or active bleeding should be admitted to an intensive care unit for resuscitation and close observation. Adequate resuscitation and stabilization are essential before endoscopy to minimize treatment-associated complications.
DEFINITION The many causes of GI tract bleeding are classified into upper or lower, depending on their location in the GI tract. Upper GI tract bleeding can originate in the esophagus, stomach, or duodenum. The most common upper GI tract bleeding is caused by peptic ulcer disease (45%). The other 55% consist of gastric erosions, varices, Mallory-Weiss tears, esophagitis, and duodenitis. Lower GI tract bleeding originates from the large intestine, rectum, or anus. Bleeding is most often caused by diverticular disease (30%–50%), angiodysplasia, polyps, hemorrhoids, or anal fissures. Blood in the stool can also result from inflammatory bowel disease, cancer, or infectious diarrhea.
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EPIDEMIOLOGY Upper GI tract bleeding occurs in 50–150/100,000 persons per year. It is more common in males and in persons older than 50 years. Mortality from GI tract bleeding is approximately 10%. Morality rates approach 23% in persons who require emergency surgery for GI tract bleeding. The mortality rate has not changed in the past four decades for GI tract bleeding, despite better diagnostic capabilities and treatment modalities. Lower GI tract bleeding is more common in children than adults and has a lower rate of hospitalization than upper GI bleeding.
CLINICAL PRESENTATION Symptoms associated with GI tract bleeding can include fatigue, weakness, shortness of breath, abdominal pain, angina, syncope, or confusion. Even patients in cardiac arrest may harbor occult GI tract hemorrhage. Long-term GI tract bleeding may go unnoticed or may cause fatigue, anemia, black stools, or a positive test result for occult blood. A carefully performed patient history can often point to the source of bleeding. Acute upper GI tract bleeding will appear first as vomiting of blood (blood may look like “coffee grounds”), bloody bowel movements, or black, tarry stools. Lower GI tract bleeding is usually suspected when the patient reports hematochezia (i.e., passage of maroon or bright red blood or blood clots per the rectum). Symptoms that suggest an anorectal source include spots of blood seen on the toilet paper or blood dripping into the toilet after defecation. Anal pain, during or after defecation, is usually due to anal fissures. Systemic symptoms such as night sweats, fever, or weight loss may suggest malignancy, chronic infection, or bowel inflammation. Diarrhea preceding or accompanying passage of blood suggests colitis, whereas tenesmus can be present with proctitis. Lastly, a change in the frequency or caliber of stools is an historical feature suggestive of colonic malignancy. Past medical history should include information regarding previous GI tract bleeding events and studies. A surgical history should always include prior resected colon cancer or polyps. The practitioner should inquire specifically about aortic graft placement because an aortoenteric fistula could be the cause of the bleeding. Finally, a history of inflammatory bowel disease is important because these patients are at increased risk of colonic neoplasm. Numerous drugs, including nonsteroidal anti-inflammatory drugs (NSAIDs), salicylates, anticoagulants, and corticosteroids, have been associated with GI tract bleeding. Peptic ulcer disease, esophageal varices, and erosive gastritis have been associated with the ingestion of alcohol.
EXAMINATION The monitoring of vital signs is very important in a patient with acute GI tract bleeding. There will be no change in vital signs until there is a 15%
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blood loss (10 ml/kg) or greater. A patient with GI tract bleeding will often be pale, clammy, hypothermic, hypotensive, and tachycardic. The patient will often be hyperventilating on presentation. Remember, the foremost cause of anxiety in the emergency department is hypoxia. If the patient is very anxious, his or her oxygen-carrying capacity is compromised because of a lack of red blood cells. A capillary refill time greater than 2 seconds is a quick test of distal perfusion. Examine the entire patient including a complete check of the eyes, ears, nose, and throat. Posterior nasal bleeding can simulate an upper GI tract bleeding as a result of the patient swallowing blood. The skin can be cool and clammy in patients who are hypotensive and tachycardiac. The practitioner should look for jaundice, palmar erythema, spider angiomata, and gynecomastia, which are all signs of chronic liver disease. Petechiae and purpura are signs of underlying coagulopathy or may represent manifestations of Gardner’s syndrome, Peutz-Jeghers syndrome, or Rendu-Osler-Weber syndrome. A rectal examination should be performed to check the color of the stool and for the presence of blood. Bright red blood usually means lower GI tract bleeding in the extreme distal portion of the colon; melena signifies a more proximal bleed. Bright red blood expelled from the rectum is usually from lower GI tract bleeding; however, if massive upper GI tract bleeding is present, an upper GI source of bright red blood per rectum can give the examiner a false sense of security.
LABORATORY FINDINGS Every patient with suspected GI tract bleeding should undergo a CBC, prothrombin time (PT)/international normalized ratio (INR) measurement, liver function tests including amylase and lipase, electrolyte analyses including BUN and creatinine, and urinalysis. If the patient is hemodynamically unstable or is having increased bleeding, a blood type and cross-match for 4–6 units of blood should be performed. It is important to remember that, in cases of acute blood loss, the hematocrit level may be normal. An elevated PT is indicative of vitamin K deficiency, warfarin therapy, liver disease, or consumptive coagulopathy. Patients with a BUN level greater than 100 mg/dl have an 80% mortality rate. A review of pertinent laboratory data is an essential step during resuscitation to assess the need for blood product transfusion. The ideal hematocrit level depends on the patient’s age, the rate of bleeding, and the presence of comorbid conditions such as coronary artery disease, emphysema, or cirrhosis. For example, a hematocrit of 20%–25% may be acceptable for a young patient without other significant medical problems but could be catastrophic for an elderly patient with coronary artery disease. A coagulopathy (PT INR >1.5) or thrombocytopenia (<50,000/ml) should be corrected, if possible, with fresh frozen plasma and platelet transfusions, respectively.
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DIAGNOSIS Diagnosis of upper GI tract bleeding is made by placement of a nasogastric tube with gastric lavage or endoscopy. A gastric lavage that yields blood or coffee-ground-like material confirms upper GI tract bleeding; however, lavage results may not be positive if bleeding has ceased or arises beyond a closed pylorus. Upper endoscopy is the diagnostic modality of choice for acute upper GI tract bleeding. Endoscopy is highly sensitive and specific for locating and identifying bleeding lesions in the upper GI tract. Practice guidelines concerning the evaluation of the patient with presumed lower GI tract bleeding have been issued by the American College of Gastroenterology and approved by the American Gastroenterological Association and the American Society for Gastrointestinal Endoscopy. Once the bleeding is suspected to be coming from a lower GI tract source, colonoscopy is the initial examination of choice for diagnosis and treatment. These recommendations are based on expert opinion and the characteristics of the individual tests; no large controlled clinical trials have demonstrated a clear advantage of any particular strategy. Other diagnostic procedures that may be useful include radionuclide imaging and mesenteric angiography. When available, anoscopy or proctoscopy should be carried out in patients excreting acute bright red blood per rectum because these are simple maneuvers that do not require bowel preparation, and because the yield of these tests is highest when performed during a bleeding episode.
RADIOGRAPHS Radiographic studies of the chest and abdomen should be performed if perforation or obstruction is suspected. Plain abdominal radiographs may also reveal thumbprinting suggestive of transmural injury from advanced ischemic or infectious colitis. Barium studies have no role in the evaluation of acute lower GI tract bleeding.
TREATMENT All patients with suspected GI tract bleeding should be monitored with pulse oximetry and a cardiac monitor and should have two large-gauge (14- or 16-gauge) intravenous lines started. Vital signs should be recorded every 5 minutes. Crystalloid solutions should be used in the resuscitation of the patient. Fluid should be given in 5- to 20-ml/kg boluses, and the patient’s vital signs should be reevaluated after each bolus of fluid until 50 ml/kg has been given. A Foley catheter should be placed, and a urine output goal of 30 ml/hr (for an adult) should be met. After 50 ml/kg of fluid has been administered, blood products should be given. Patients with impending cardiopulmonary arrest from hemorrhagic shock should be
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given O-negative blood immediately, but type and cross-matched blood is preferred. Fresh frozen plasma should be used to correct coagulopathies resulting from liver failure or warfarin therapy. A nasogastric tube should be placed. Gastric lavage should be performed on every patient. It should be remembered that a negative lavage does not rule out acute bleeding, and iced solutions have no proven benefit over solutions at room temperature. Several studies have examined the role of acid suppression given before or after endoscopy. In the setting of active upper GI tract bleeding, acid suppressive therapy with H2 receptor antagonists have not been shown to significantly lower the rate of ulcer rebleeding. On the other hand, high-dose anti-secretory therapy with an intravenous infusion of proton pump inhibitor (PPI) significantly reduced the rate of rebleeding compared with standard treatment in patients with bleeding ulcers. Oral and intravenous PPI therapy also decreases the length of hospital stay, the rebleeding rate, and the need for blood transfusion in persons with high-risk ulcer bleeding who are treated with endoscopic therapy. Somatostatin, or its analog octreotide, have been best studied in the treatment of variceal bleeding but may also reduce the risk bleeding due to nonvariceal causes. It can be used as adjunctive therapy before endoscopy or when endoscopy is unsuccessful, contraindicated, or unavailable. In the case of severe esophageal variceal bleeds, the SengstakenBlakemore or Linton tubes can be used to stop a variceal bleed. These tubes act by tamponading the variceal bleeding in a patient who is exsanguinating. Endoscopy is the most accurate diagnostic tool for detection of upper GI tract bleeds. It can identify a lesion in 78%–95% of cases. If the bleeding is variceal in origin, sclerotherapy can be performed by a gastroenterologist. Colonoscopy is used when lower GI tract bleeding is suspected. It is usually performed 48–72 hours after presentation, after the bowel has been prepared. Colonoscopy is better than barium enema in the evaluation of lower GI tract bleeding. All patients with unstable vital signs at time of admission, hemodynamic instability, serious comorbid diseases, true melena, age greater than 70 years, a large drop in hematocrit, persistent bleeding, the need for multiple blood transfusions, or evidence of an acute abdomen should be promptly resuscitated and hospitalized. A gastroenterologist and general surgeon should be involved early in the hospital course of persons at high risk. Surgery is indicated in patients whose conditions are hemodynamically unstable, who have failed medical therapy, and who are actively bleeding.
Bibliography Aljebreen AM, Fallone CA, Barkun AN: Nasogastric aspirate predicts high-risk endoscopic lesions in patients with acute upper-GI bleeding, Gastrointest Endosc 2004;59:172.
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Baradarian R, Ramdhaney S, Chapalamadugu R, et al: Early intensive resuscitation of patients with upper gastrointestinal bleeding decreases mortality, Am J Gastroenterol 2004;99:619. Gisbert JP, Gonzalez L, Calvert X, et al: Proton pump inhibitors versus H2-antagonists: A meta-analysis of their efficacy in treating bleeding peptic ulcer, Aliment Pharmacol Ther 2001;15:917. Jutabha R, Jenson DM: Management of severe upper gastrointestinal bleeding in the patient with liver disease, Med Clin North Am 1996;80:1035. Kollef MH, O’Brien JD, Zuckerman GR, Shannon W: BLEED: A classification tool to predict outcomes in patients with acute upper and lower gastrointestinal hemorrhage, Crit Care Med 1997;25:1125. Lieberman D: Gastrointestinal bleeding: Initial management, Gastroenterol Clin North Am 1992;22:723. McGuire HH Jr: Bleeding colonic diverticula: A reappraisal of natural history and management, Ann Surg 1994;220:653. Rockey DC: Occult gastrointestinal bleeding, N Engl J Med 1999;341:38. Strate LL, Orav EJ, Syngal S: Early predictors of severity in acute lower intestinal tract bleeding, Arch Intern Med 2003;163:838. Zuccaro G: Management of the adult patient with acute lower gastrointestinal bleeding, Am J Gastroenterol 1998;93:1202. Zuckerman GR, Prakash C: Acute lower intestinal bleeding, Part II: Etiology, therapy, and outcomes, Gastroinest Endoc 1999;49:228.
Jaundice and Hepatitis MARY ANN BROWNING
ICD or CPT Codes: Jaundice (unspecified) 782.4, Viral hepatitis 070.9
Key Points The clinical presentation of viral hepatitis varies from person to person, with a significant number of cases being asymptomatic. The sudden appearance of jaundice in an otherwise healthy young adult, especially if associated with prodrome of fever, malaise, and GI distress, is likely caused by viral hepatitis.The laboratory workup for jaundice should begin with a urine test for bilirubin and, if the result is positive, conjugated hyperbilirubinemia is likely present. Viral hepatitis is a public health concern, and an attempt to identify the type of virus should begin in the emergency department. Hospital admission for patients with fulminant hepatitis as evidenced by encephalopathy or increased INR will need to be considered.
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DEFINITION Jaundice refers to a yellowing of the skin. If the sclera is yellow, the condition is known as icterus. Jaundice results from hyperbilirubinemia and can usually be recognized when the serum bilirubin level exceeds 2.5 mg/dl. A brief summary of bilirubin metabolism will help the clinician understand the workup involved when a patient arrives at the emergency department with acute onset of jaundice. Bilirubin is formed when red blood cells or other heme products are broken down. This process occurs within the reticuloendothelial system. Bilirubin is then released into the bloodstream bound to albumin and is transported to the liver cells, where it is conjugated to form bilirubin diglucuronide. This is water soluble and excreted into the small intestine through the biliary tract. It passes to the colon, where it is broken down to urobilinogen and other pigments that give feces its typical color. A small amount is excreted into the urine. Jaundice may occur if there is a breakdown at any point in this pathway. There can be an overproduction of bilirubin, a failure of the liver cells to uptake bilirubin, a failure to conjugate bilirubin, or an obstruction of biliary excretion into the small intestine. Hyperbilirubinemia can be classified into two major categories:
Unconjugated (indirect) hyperbilirubinemia may result from overproduction of bilirubin (such as with hemolysis), impaired bilirubin uptake by the liver, or abnormalities of bilirubin conjugation. Conjugated (direct) hyperbilirubinemia may result from impaired excretion of bilirubin due to hepatocellular disease, drugs, sepsis, hereditary disorders, or biliary obstruction.
Jaundice is a common clinical problem encountered in the emergency department. Many diseases can be associated with jaundice. However, in this chapter, we will limit our discussion to viral hepatitis. A patient with viral hepatitis may present with jaundice due to liver cell dysfunction resulting in elevated levels of conjugated bilirubin. Hepatitis is a general term and refers to inflammation of the liver. Viruses are the most common cause of acute hepatitis. The most important and clinically significant cases of viral hepatitis are caused by hepatitis A (HAV), hepatitis B (HBV), and hepatitis C virus (HCV).
EPIDEMIOLOGY In 2000, there were approximately 25,000 cases of acute viral hepatitis reported in the United States. This includes 14,000 cases of hepatitis A and 8000 cases of hepatitis B. In addition, 1.25 million persons are chronically infected with HBV, and 2.7 million are chronically infected with HCV.
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Hepatitis A Virus HAV is an RNA virus spread by the fecal-oral route through contaminated water or food. Transmission via contact with blood is thought to be possible but is rare. Close personal contact is the most common mode of transmission; this can include household contact, sexual transmission, and child day care centers. The typical incubation period for hepatitis A is 30 days (range, 15–45 days) (Fig. 4-1). The 2 weeks before the onset of jaundice is the period of greatest viremia (see Fig. 4-1). Fecal shedding of the virus in the stool diminishes by the time the icteric phase begins. HAV is not associated with a chronic carrier state. Protective antibodies develop in response to infection and confer lifelong immunity. In the United States, the incidence of hepatitis A has dramatically declined due to the availability of the hepatitis A vaccine.
Hepatitis B Virus HBV is a partially double-stranded DNA virus with an inner core protein (hepatitis B core antigen [HBcAg]) and an outer surface coat (hepatitis B surface antigen [HBsAg]). HBV is spread by the parenteral route, including exposure to contaminated needles and syringes, infected secretions, sexual contacts, and perinatal contact.
Symptoms
Total anti-HAV
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2
3
4
5
6
12
24
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Figure 4-1. Typical incubation period for hepatitis A virus (HAV). ALT, Alanine aminotransferase; IgM, immunoglobulin M. (Data from slide sets available to the public on the National Center for Infectious Diseases, Centers for Disease Control and Prevention website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/ index.htm.)
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Incubation is approximately 45–160 days (Fig. 4-2). During this phase, the virus is present in nearly all body fluid including blood, saliva, semen, and vaginal secretions. Therefore, infection can be transmitted before symptoms are apparent. In the United States, the incidence of hepatitis B has declined by 70% since the late 1980s due to the use of the hepatitis B vaccine. Fulminant hepatitis is rare (<1%) but carries a mortality rate of up to 60%. HBV persists in 1%–2% of immunocompromised adults, and these persons are at increased risk of cirrhosis and hepatocellular carcinoma.
Hepatitis C Virus HCV is a single-stranded RNA virus. It is the most common chronic blood-borne infection in the United States. An estimated 3.9 million Americans are infected with HCV. The incubation period ranges from 6 to 7 weeks (Fig. 4-3), but about 75% of persons may not be aware of their infection because they are asymptomatic. They may be a source of transmission to others and are at risk for chronic liver disease or other related illnesses. The highest incidence is among the 20- to 39-year-old age group. More than 50% of cases are a result of intravenous drug use. Healthcare workers with accidental blood exposure are also at risk. Neonatal transmission is
Symptoms HBeAg
Anti-HBe
Titer
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IgM anti-HBc
HBsAg
0
4
8
12 16 20 24 28 32 36
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100
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Figure 4-2. Incubation period for hepatitis B virus. HBeAg, Hepatitis B e antigen; HBc, hepatitis B core; HBsAg, hepatitis B surface antigen; HBs, hepatitis B surface; IgM, immunoglobulin M. (Data from slide sets available to the public on the National Center for Infectious Diseases, Centers for Disease Control and Prevention website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/index.htm.)
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Anti-HCV
Titer
HCV RNA
ALT Normal 0
1
2
3
4
5
6
1
2
3
4
Months Years Time after exposure
Figure 4-3. The incubation period of hepatitis C virus (HCV). ALT, Alanine aminotransferase. (Data from slide sets available to the public on the National Center for Infectious Diseases, Centers for Disease Control and Prevention website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/index.htm.)
considered to be low, as is sexual transmission. Having multiple sexual partners may increase the risk. Transmission during breast-feeding has not been documented. HAV, HBV, and HCV are the causative agents of more than 95% of acute viral hepatitis. A small percentage of patients may be infected with other viruses. Hepatitis D virus (HDV) or delta virus is a defective RNA virus that requires the help of HBV to replicate. In the United States, the incidence is between 4% and 30% of patients with chronic HBV. Hepatitis E is rare in the United States but may be associated with travel to an endemic area. Hepatitis G may occur by parenteral transmission but does not appear to be associated with significant liver disease.
CLINICAL PRESENTATION AND EXAMINATION The clinical features of acute disease caused by the hepatitis viruses are similar. However, they may vary from person to person. A significant number of cases are asymptomatic. Signs and symptoms may be divided into phases. During the prodromal phase, the patient may report fatigue, myalgias, arthralgias, loss of appetite, fever, nausea, vomiting, and diarrhea. The patient may present to the emergency department with signs of dehydration due to GI problems Mild abdominal pain along with liver and splenic enlargement may be noted. The patient may think he or she has the “flu,” and, indeed, the symptoms usually appear to be
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nonspecific. These symptoms typically last 3–4 days but may linger for 2–3 weeks. The icteric phase begins with the onset of jaundice (usually after 5–10 days) along with “dark” urine, which may lead the patient to seek advice from a medical provider. Symptoms may worsen at this time, followed by gradual clinical improvement. Physical findings, however, are variable and most patients may never experience jaundice. It should be noted that the presentation of jaundice may be subtle in patients of African–American descent. Sublingual or subungual yellowing may be noted in these patients. Obvious onset of jaundice should lead the clinician to perform laboratory screening. During the convalescent phase, the patient’s condition will steadily improve, appetite will return, jaundice will disappear, and general good health will return. A patient with hepatitis A will usually completely recover within 9 weeks. A patient with hepatitis B will take approximately 16 weeks to completely recuperate. Fewer than 1% of patients will have a fulminant course, which is most often encountered with HBV and HDV.
LABORATORY FINDINGS The initial workup should begin with an evaluation of the serum bilirubin level (both total and direct). The indirect fraction can be calculated by subtracting the direct fraction from the total. Also, serum liver aminotransferase levels, alkaline phosphatase, urinalysis, CBC, serum albumin, and INR should be included. Other tests may be considered, as guided by the physical examination; for example, basic electrolytes and/or lipase measurements may be indicated. A simple urine dip may assist the clinician in determining whether the patient has conjugated or unconjugated hyperbilirubinemia. Only conjugated bilirubin is water soluble. Thus, a positive urine dipstick result for bilirubin signifies the presence of conjugated bilirubin. Elevated transaminase levels are the first laboratory abnormalities associated with viral hepatitis. The serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels have usually reached their peak by the time clinical symptoms have appeared. Levels may exceed 1000 U/L. The ALT level is generally more elevated than that of AST. Bilirubin levels may be moderately elevated but rarely exceed 20 mg/dl. A predominantly conjugated hyperbilirubinemia is said to exist when 30% or more of the serum bilirubin is in the conjugated (direct) form. Alkaline phosphatase levels may be elevated but rarely to more than two to three times normal. Hypoalbuminemia and increased INR may signify more severe liver disease, and admission to the hospital may need to be considered.
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If the initial laboratory test results suggest hepatocellular disease and the clinical history suggests viral hepatitis, then serological studies for viral hepatitis should be done. These include:
Hepatitis A (immunoglobulin M [IgM] anti-HAV) Hepatitis B (HBsAg and IgM anti-HBc) Hepatitis C (anti-HCV)
Refer to Figure 4-1 for the serological and symptomatic course of hepatitis A. ALT levels begin to rise just before the onset of symptoms. Fecal shedding has already peaked and is starting to subside. During the symptomatic period, about 4–5 weeks after exposure, IgM antibodies to HAV (IgM anti-HAV) begin to rise. Acute HAV is therefore diagnosed by the presence of IgM HAV antibody. Prior infection is determined by the IgG antibody and remains detectable for life. The serological and symptomatic course of hepatitis B is portrayed in Figure 4-2. The first marker to appear is HBsAg. Although HBsAg usually precedes IgM anti-HBc, both are typically present at the time of the appearance of symptoms. By chance, some patients may be tested during the “window” period, in which the presence of IgM anti-HBc may be the only marker for recent infection. Therefore, the clinician can only rule out acute hepatitis B if the patient tests negative for both HBsAg and IgM anti-HBc. Another marker that may elevate early in the course is the hepatitis B early antigen (HBeAg). However, measurement of this viral marker and other antibodies adds little to the diagnosis of acute hepatitis B viral infection. Anti-HBsAg antibody levels rise when symptoms decline, ALT returns to normal levels, and immunity to HBV is signified. Anti-HBsAg antibody is the best marker for immunity to HBV. Anti-HCV testing can detect 80%–90% cases of acute hepatitis C. If the test results are negative and infection is suspected, the clinician can repeat the test 4–6 weeks later, during which time the patient’s test result may convert from negative to positive. Or, the clinician may choose to test for HCV RNA, which may be the earliest marker for acute HCV infection. The exact cause of acute hepatitis will probably not be known during the patient’s initial presentation to the emergency department. The practitioner’s primary responsibility will be to initiate the workup to identify possible exposure and diminish the public health risk.
RADIOGRAPHS Imaging studies are usually not indicated for patients who present with acute onset of jaundice and are suspected to have viral hepatitis. However, in a patient with right upper quadrant abdominal pain, biliary disease with
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obstruction may need to be ruled out. Ultrasound is often preferred due to its lower cost and sensitivity for detecting biliary stones. CT scanning can provide more information about liver and pancreatic disease.
DIAGNOSIS In this chapter, we have concentrated on the patient who presents to the emergency department with acute onset of jaundice related to viral hepatitis. It should be kept in mind, however, that jaundice in an adult patient may have a variety of causes. It is important to realize that hyperbilirubinemia may occur with any breakdown along the pathway of bilirubin metabolism (see previous Definition section). The laboratory workup begins by determining whether the patient has conjugated or unconjugated hyperbilirubinemia. Prehepatic causes of jaundice include hemolysis and hematoma resorption, which lead to elevated levels of unconjugated (indirect) bilirubin. Intrahepatic disorders can lead to unconjugated or conjugated hyperbilirubinemia. Elevated conjugated (direct) bilirubin is often caused by alcohol, viral hepatitis, drug reactions, and autoimmune disorders. Gallstone formation is a common cause of biliary tract obstruction leading to an elevated conjugated hyperbilirubinemia. More serious conditions to consider are biliary tract infection, pancreatitis, and malignancy.
TREATMENT Patients with acute viral hepatitis may present to the emergency department with signs of dehydration due to nausea, vomiting, or excess diarrhea. Treatment consists of fluid and electrolyte replacement and antiemetic administration. Patients able to tolerate oral fluid may avoid admission to the hospital. Medications requiring hepatic metabolism generally do not need to be discontinued unless there is a suspicion of severe hepatocellular disease as evidenced by an increased INR. The patient should be advised to completely discontinue alcohol use until signs of liver injury resolve. Hospital admission is rarely needed unless the patient is severely dehydrated and unable to tolerate oral fluid. Patients unable to care for themselves at home may need to be admitted for observation. Obviously, patients with mental status changes or fulminant hepatic failure require hospital admission. Patients with acute viral hepatitis who are discharged should be prescribed antiemetics and instructed to maintain fluid and caloric intake. They should be given strict instructions to return for refractory vomiting or change in mental status. The patient may limit physical activity as needed. It is not necessary for the patient to exclude himself or herself from school or work, although the importance of personal hygiene should
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be emphasized. Patients should follow up with their primary care providers or gastroenterologists within a few days, when serological results are expected. Patients with an elevated INR should be considered for hospital admission. If discharged, however, they should be seen the next day for reevaluation. Serological test results will usually not be available to the emergency department provider at the time of patient discharge. Therefore, patients with possible HAV should be advised to practice meticulous personal hygiene and avoid sexual contact. Family members or close personal contacts may consider short-term protection by receiving immune globulin, as a single intramuscular injection 0.02–0.06 ml/kg IM as soon as possible within 2 weeks after exposure. Hepatitis A vaccine should be encouraged for long-term immunity. Protection against hepatitis A begins 4 weeks after the first dose of hepatitis A vaccine. Although serologies may be unknown at the initial presentation to the emergency department, HBV or HCV may be suspected in patients who have risk factors. Patients and their close contacts should be counseled in regard to preventing the spread of hepatitis. If sexual contacts of persons with hepatitis B are not already immunized, postexposure prophylaxis for hepatitis B is indicated. Prophylaxis is also indicated after percutaneous exposure to hepatitis B–positive blood. Treatment is with intramuscular hepatitis B immune globulin, 0.06 ml/kg. Administration of the vaccine is begun at the same time. This should be completed within 5–7 days of exposure. At this time, postexposure prophylaxis is not recommended for patients exposed to hepatitis C. Viral hepatitis is a reportable disease, and the appropriate forms should be completed by the emergency department healthcare provider and sent to the local public health authorities.
Bibliography Ault M, Geiderman J: Hepatitis. In Wolfson A (ed): Harwood-Nuss’ Clinical Practice of Emergency Medicine, ed 4. Lippincott, Williams & Wilkins: Philadelphia, 2005, pp 365–373. Centers for Disease Control and Prevention, Guidelines for Viral Hepatitis Surveillance and Case Management. CDC: Atlanta, 2005. Cohen A: Liver diseases. In Copstead L, Banasik J (eds): Pathophysiology: Biological and Behavioral Perspectives, ed 2. WB Saunders: Philadelphia, 2000, pp 850–877. Desai S: Clinician’s Guide to Laboratory Medicine, ed 3. Lexi-Comp, Inc: Hudson, OH, 2004. Guss D: Liver and biliary tract. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1251–1272. Heilpern K, Quest T: Jaundice. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 214–219.
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Acute and Chronic Pancreatitis DAVID A. HNATOW
ICD or CPT Codes: Acute pancreatitis 577.0, Chronic pancreatitis 577.1
Key Points Pancreatitis is an inflammatory process of the pancreas that is classified as either acute or chronic. Acute pancreatitis can be suspected clinically but requires laboratory and radiological evidence to confirm the diagnosis. Chronic pancreatitis results in permanent structural changes in the pancreas that lead to impairment of exocrine and endocrine function. Lipase measurement is more specific than serum amylase in diagnostic accuracy.The sensitivity of serum lipase for the diagnosis of acute pancreatitis ranges from 80% to 100% according to various reports. Patients with features of pancreatitis whose conditions do not improve with initial conservative therapy or who are suspected of having complications should undergo CTscanning of the abdomen. ! Emergency Actions ! Fluid resuscitation and pain relief are the mainstay of treatment of acute pancreatitis.
DEFINITION Pancreatitis is an inflammatory process of the pancreas. Pancreatitis is classified as either acute or chronic and is characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood. Chronic pancreatitis results in permanent structural changes in the pancreas, which leads to impairment of exocrine and endocrine function.
EPIDEMIOLOGY The pathogenesis of acute pancreatitis is not fully understood. Nevertheless, a number of conditions are known to induce this disorder. Biliary tract disease and alcoholism account for more than 80% of hospital admissions for acute pancreatitis. Acute gallstone pancreatitis occurs more often in women, whereas alcoholic pancreatitis occurs more often in men. The diagnosis of gallstone pancreatitis should be suspected if the patient has a prior history of biliary colic. In biliary tract disease, pancreatitis is
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caused by temporary impaction of a gallstone in the sphincter of Oddi before it passes into the duodenum. Other conditions causing obstruction of the ampulla that have been associated with pancreatitis include biliary ascariasis, periampullary diverticula, and pancreatic and periampullary tumors. The remaining 20% of cases of acute pancreatitis are attributed to primary hypertriglyceridemia, effects of endoscopic retrograde cholangiopancreatography (ERCP), blunt or penetrating trauma, hypercalcemia, hyperparathyroidism, pregnancy, medications, or infectious agents.
MEDICATIONS Medical treatment for pancreatitis includes the following:
AIDS therapy: didanosine, pentamidine Antimicrobial agents: metronidazole, sulfonamide, tetracycline Diuretics: furosemide, thiazides Neuropsychiatric agents: valproic acid Anti-inflammatory drugs: salicylates, sulindac, 5-aminosalicylic acid, sulphasalazine
INFECTIOUS AGENTS Possible causes of pancreatitis include the following infectious agents:
Viruses: mumps, coxsackievirus, HBV, HIV Bacteria: mycoplasma, legionella, leptospira, salmonella Fungi: aspergillus Parasites: toxoplasma, cryptosporidium, ascaris
In the United States, alcohol abuse accounts for 70%–80% of cases of chronic pancreatitis. Hereditary pancreatitis accounts for a small subset of all cases of chronic pancreatitis.
CLINICAL PRESENTATION Pancreatitis is an important cause of acute upper abdominal pain. Because its clinical features are similar to a number of other acute illnesses, it is difficult to base a diagnosis only on symptoms and signs. The pain of pancreatitis is usually severe enough to require an emergency department visit and hospital admission. Almost all patients with acute pancreatitis have acute upper abdominal pain at the onset, typically associated with nausea and vomiting. The pain is steady and may be in the mid epigastrium, right upper quadrant, diffuse, or left flank. The pain can last for days. Biliary colic may occur postprandially, whereas alcohol-induced pancreatitis frequently occurs 1–3 days after a binge or cessation of drinking. The abdominal pain is typically accompanied by nausea and vomiting.
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The two primary clinical manifestations of chronic pancreatitis are abdominal pain and pancreatic insufficiency. Patients with chronic pancreatitis can have difficulty digesting fats contained in foods leading to weight loss and sometimes diarrhea. In severe cases, the pancreas can also lose its ability to produce adequate amounts of insulin, leading to diabetes mellitus.
EXAMINATION Physical findings can vary. Patients are often tachycardiac and tachypneic resulting from pain and vomiting. Patients with severe attacks may present in shock or coma and often exhibit abdominal distention. Ecchymotic discoloration of the flanks (i.e., Turner’s sign) or periumbilical region (i.e., Cullen’s sign) are due to retroperitoneal bleeding in patients with pancreatic necrosis. Obstruction of the common bile duct due to gallstones or pancreatic head edema can lead to jaundice. There may also be findings indicative of underlying disorders such as hepatomegaly in alcoholic pancreatitis, xanthomas in hyperlipidemic pancreatitis, and parotid swelling associated with mumps.
LABORATORY FINDINGS Since no clinical features are pathognomonic for acute pancreatitis, the diagnosis must often rest on the presence of abnormal laboratory test results. During acute pancreatitis, enzymes that normally flow from the pancreas into the digestive tract leak out of the pancreas and into the bloodstream. Marked increase (i.e., more than three times the upper limit of normal) in the levels of amylase strongly suggest the diagnosis of acute pancreatitis. Levels of amylase in the blood rise within 6–12 hours after the acute attack begins and remains elevated for 3–5 days in uncomplicated attacks. Tissues other than the pancreas also produce amylase. Elevated serum lipase levels help to confirm the pancreatic origin of elevated serum amylase levels. The sensitivity of serum lipase for the diagnosis of acute pancreatitis ranges from 85% to 100% in various reports. Serum triglyceride concentrations above 1000 mg/dl can precipitate attacks of acute pancreatitis, although the pathogenesis of inflammation in this setting is unclear. As with most inflammatory conditions, leukocytosis is usually present but rarely exceeds 20,000 cells/ml. Low calcium levels may be detected on laboratory analysis. Persistent hypocalcemia, less than 7 mg/100 ml, is associated with a poor prognosis. Serum concentrations of amylase and lipase may be slightly elevated in patients with chronic pancreatitis but are more commonly normal.
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DIAGNOSIS The diagnosis of acute pancreatitis can be challenging because the signs and symptoms of other medical conditions can mimic those of pancreatitis. The diagnosis is based on the patient’s medical history, physical findings, and the results of specific diagnostic test. The diagnosis of chronic pancreatitis is confirmed if there are calcifications within the pancreas, an abnormal pancreatogram revealing beading of the main pancreatic duct or ecstatic side branches, or an abnormal secretin pancreatic function test result.
RADIOGRAPHS Imaging tests provide information about the structure of the pancreas, the ducts that drain the pancreas and gallbladder, and the tissues surrounding the pancreas. All patients with a first episode of pancreatitis should undergo an abdominal ultrasound scan to search for gallstones or signs of extrahepatic biliary tract obstruction. In the setting of acute abdominal pain, an abdominal plain radiograph helps to exclude other causes of abdominal pain such as obstruction and bowel perforation. Patients with acute pancreatitis who show evidence of ileus and air trapped in the small bowel near the inflamed pancreas have been described as having a sentinel loop. Calcifications within the pancreatic duct may be associated with chronic pancreatitis. CT, magnetic resonance imaging (MRI), and ultrasound may show calcifications, ductal dilatation, enlargement of the pancreas, and fluid collections (i.e., pseudocysts). Imaging studies that may be useful in chronic pancreatitis include abdominal plain radiographs, ultrasound, CT scan, MRI, ERCP, and endoscopic ultrasound.
TREATMENT AND OUTCOME Acute pancreatitis is a self-limiting disease under most circumstances. The treatment of acute pancreatitis is aimed at correcting any underlying predisposing factors and providing supportive care. This includes ERCP in patients with gallstone pancreatitis who have obstructive jaundice, reversal of hypercalcemia, cessation of possible causative drugs, and the administration of insulin to a patient with poorly controlled diabetes and marked hypertriglyceridemia. Supportive care includes pain control, intravenous fluids, and nothing by mouth. Recognition that profound shock may result from high-volume fluid sequestration in the retroperitoneum has lowered morbidity as resuscitation and monitoring techniques have improved. Although the use of the nasogastric tube is widely accepted, no controlled clinical trial has shown its value in altering the
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course of the disease. Most attacks of acute pancreatitis are mild, with recovery occurring within 5–7 days. Several systems for predicting the course of pancreatitis continue to be developed, including those based on clinical assessment, scoring systems, serum markers, and CT scanning. Unfortunately, none has yet proved to be a consistently accurate predictor for the clinical course. A small number of patients may develop a severe systemic illness, complicated by acidosis, renal failure, severe hypocalcemia, and respiratory failure. In severe pancreatitis, intensive care monitoring and support of pulmonary, renal, circulatory, and hepatobiliary function may minimize systemic sequelae. If a patient’s condition is not improving, a peritoneal lavage should be considered. Peritoneal lavage can dilute or remove the toxic substances released by the pancreatic necrosis. If the patient’s condition has not improved in 7 days, another cause should be considered, such as a pancreatic abscess, pseudocyst, or pancreatic ascites. If the diagnosis of gallstone pancreatitis is made, cholecystectomy with cholangiography is recommended during the same hospitalization. ERCP is performed after laparoscopic cholecystectomy if a common duct stone is found and not removed at surgery. Acute pancreatitis is not a bacterial disease in its early stages, and the initial use of antibiotics is unwarranted. Sepsis, when it occurs, results from secondary infections and is usually encountered late in the course of the disease. The care of patients with chronic pancreatitis principally involves management of pain.
Bibliography Akhrass R, Yaffe MB, Brandt CP, et al: Pancreatic trauma: A ten-year multi-institutional experience, Am Surg 1997;63:598. Butler J: Serum amylase and acute pancreatitis, Emerg Med J 2003;20:550. Frank B, Gottlieb K: Amylase normal, lipase elevated: is it pancreatitis? Am J Gastrol 1999;94:463. Moreau JA, Zinsmeister AR, Melton LJ, et al: Gallstone pancreatitis and the effect of cholecystectomy, Mayo Clin Proc 1988;63:466. Naruse S, Kitagawa M, Ishiguro H, et al: Chronic pancreatitis: Overview of medical aspects, Pancreas 1998;16:323. Pitchumoni CS: Chronic pancreatitis: Pathogenesis and management of pain, J Clin Gastrol 1998;279:101. Pitchumoni CS, Agarwal N, Jain NK: Systemic complications of acute pancreatitis, Am J Gastroenterol 1988;83:597. Powell JJ, Miles R, Siriwardena AK: Antibiotic prophylaxis in the initial management of severe acute pancreatitis, Br J Surg 1988;85:582. Robert JH, Frossard JL, Mermillod B, et al: Early prediction of acute pancreatitis: Prospective study comparing computed tomography scans, Ranson, Glasgow, Acute Physiology and Chronic Health Evaluation II scores, and various serum markers, World J Surg 2002;26:612. Watanabe S: Acute pancreatitis: Overview of medial aspects, Pancreas 1998;16:307. Yadav D, Agarwal N, Pitchumoni CS: A critical evaluation of laboratory tests in acute pancreatitis, Am J Gastroenterol 2002;97:1309.
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Peptic Ulcer Disease JOHN T. KODOSKY
ICD Codes: Peptic acid disease 536.8, Peptic ulcer 533.9
Key Points Ulcers are formed when acid production exceeds the rate of mucosal protection. ! Emergency Actions ! Hemorrhage is potentially life threatening and patients may have melena, hematochezia, hematemesis, with epigastric pain. If the patient’s condition is unstable, two large-gauge intravenous lines providing normal saline should be introduced. The patient should be placed on the cardiac monitor and given oxygen, and a blood type and cross-match for 4 units of blood. If the patient’s condition is unstable, “crash” blood should be given.
DEFINITION Peptic ulcer disease (PUD) is defined as a mucosal break larger than 3 mm in depth in the stomach or duodenum. The two major causes of PUD are Helicobacter pylori infection and NSAID usage. Less common causes are severe physiological stress (e.g., severe illness, burns, or surgery) or hypersecretory states (e.g., Zollinger-Ellison syndrome). Contributing factors include smoking, ethanol, bile acids, aspirin, corticosteroids, and stress. Ulcers are formed when acid production exceeds the rate of mucosal protection. Consequently, treatment is based on reduction of acid formation and/or by increasing mucosal protection. The mucosa protects itself with a layer of bicarbonate, which can be suppressed by the use of NSAIDs and aspirin. The bacterial culprit, H. pylori, has been found to increase acid production and decrease mucosal thickness. Diagnosis and treatment is essential in patients with PUD since recurrence rates are relatively low after treatment has been completed. Resolution of ulceration has been found as high as 96% in patients who complete the regimen.
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EPIDEMIOLOGY PUD affects millions of persons each year and is responsible for 10% of the medical costs for digestive diseases in the United States. The scope of PUD prognosis ranges from resolution without intervention to the development of complications with potentially significant morbidity and mortality. Duodenal ulcers are more common than gastric ulcers and are usually seen more in men than in women.
CLINICAL PRESENTATION Patients who have symptomatic PUD present to the emergency department reporting epigastric pain with or without nausea, vomiting, belching, chest pain, black or bloody stools, or hematemesis. It is important to realize that dyspepsia is not specific because only 20%–25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer. Important questions to ask a patient with suspected PUD include an extensive discussion about chest pain, shortness of breath, diaphoresis, and shoulder pain. Other important points in the history include nausea, vomiting, fever, diarrhea, preprandial or postprandial pain, NSAID use, frequency and duration of pain, family history (cardiac and GI), and previous surgeries. A thorough subjective and objective assessment is imperative at this junction.
EXAMINATION In an uncomplicated presentation of PUD, the objective findings on physical examination are few and very nonspecific. Patients may have tenderness at the epigastrium and may possibly have fecal occult blood as a result of occult bleeding from the ulcer. It is important to include an extensive cardiopulmonary examination as well as an abdominal exam and a fecal occult blood test to rule out other causes of symptoms. Patients with accompanying chronic illnesses require an electrocardiogram to assist in ruling out myocardial infarction. The major complications of PUD are gastric outlet obstruction, perforation, and bleeding. Patients with perforation will present with severe abdominal pain, and the abdomen may feel firm and distended. The patient may also be exhibiting guarding and rebound tenderness. Some of these patients will develop pneumoperitoneum that can be seen on upright chest radiograph. Perforation is a surgical emergency, and an emergent surgical consult is required. Hemorrhage is potentially life threatening, and patients may have melena, hematochezia, hematemesis, with epigastric pain. Hemorrhage can be caused by a severe bleeding ulcer or by esophageal varices
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commonly seen in patients who abuse ethanol. Nasogastric tube placement to low wall suction will aid in the diagnosis by direct visualization of bright red blood or by “coffee ground” appearance, which results from partially digested blood. These patients require endoscopy to discover the cause of the bleed. The severity of the bleeding and the stability of the patient’s condition will determine whether endoscopy must be done emergently or urgently. Gastric outlet obstruction occurs when scarring occurs from repeated ulcerations. It is often associated with abdominal distention and abdominal discomfort and should be suspected in patients who have relief with vomiting. On upright radiograph of the kidneys, ureters, and bladder, an enlarged gastric bubble will be present. Emergent treatment involves gastric decompression with low wall suction via nasogastric tube and fluid resuscitation, and surgical consult may be indicated to dilate the gastric opening. A differential diagnosis is difficult to compile because the symptoms can be very vague and seemingly affect multiple organ systems. Understanding and interpreting the diagnosis of PUD in the emergency setting can be challenging as well because the differential diagnosis includes many potentially life-threatening problems:
Biliary colic Cholecystitis Cholelithiasis Gastritis, acute or chronic Gastroesophageal reflux disease Mesenteric artery ischemia Myocardial ischemia Abdominal aortic aneurysm Gastroparesis Pancreatitis, acute or chronic Drug-induced dyspepsia Duodenitis Functional (nonulcerous) dyspepsia Gastric infections Infiltrative diseases of the stomach
LABORATORY FINDINGS Specimens to check for the presence of H. pylori should be drawn. A CBC, chemistry 13, magnesium, phosphorus, partial thrombin time, INR, amylase, lipase, and albumin levels should be evaluated. If the patient’s condition is unstable and he or she has acute GI tract bleeding, cardiac enzymes should be drawn, an electrocardiogram should be performed, and blood type and cross-match of 4 units of blood should be done.
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RADIOGRAPHS Direct visualization via endoscopy is the gold standard of radiographic evaluation. Biopsy specimens of tissue should be taken to test for H. pylori. The diagnosis of PUD cannot be made clinically and must be made by either visualizing directly through endoscopy or barium swallow, or by performing a blood examination or string test for H. pylori.
TREATMENT Treatment of PUD depends on the cause and severity of the disease. In uncomplicated circumstances, it may resolve spontaneously or through the removal of the irritant (e.g., NSAID, ethanol, diet, tobacco, aspirin). In other, more severe cases, surgical intervention may be required. In patients with PUD caused by H. pylori, dual antibiotic therapy coupled with a PPI for 1–2 weeks can result in resolution of signs and symptoms along with eradication. Uncomplicated PUD in patients who do not receive relief spontaneously or by lifestyle modification requires initiation of prescription medication. The length of time a patient is taking a medication before the treatment is considered “failed” is unique to each patient and must be determined on a case-by-case basis. Medication therapy initiation traditionally involves histamine receptor antagonists—H2 blockers. This class of medications is typically inexpensive and has relatively few adverse effects, making it excellent first-line therapy. These medicines work by competitively inhibiting histamine at the receptors of gastric parietal cells, thereby lowering gastric secretion. If a patient’s condition has failed to respond to H2 blockers and H. pylori test results are negative, the next-line therapy involves a PPI. This type of medication blocks gastric acid secretion at the proton pump, the final common pathway of secretion. Surgery as an elective procedure for PUD treatment is becoming less popular as oral medications and endoscopy become able to resolve most ulcers. The risks of a surgical procedure will, most times, outweigh the benefits of the outcome. Statistically, this increases the morbidity and mortality of surgery for PUD since most operations are done emergently.
Bibliography Fantry G: Peptic ulcer disease, 2005. Available at: http://www.emedicine.com/med/ topic1776.htm. Harwood-Nuss A, Wolfson A: Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2005. Schwartz S, Shires GT, Spencer FC, Husser WC (eds): Principles of Surgery, ed 6. McGraw-Hill: New York, 1994.
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Soll A: Overview of the natural history and treatment of peptic ulcer disease, Up to Date. Updated August 23, 2004. Available at: http://www.utdol.com/application/topic.asp? file¼acidpep/7085&type¼A&selectedTitle¼1~63. Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGrawHill: New York, 2004.
Chapter 5
Maxillofacial and Dental Emergencies Dental Emergencies JAMES A. PFAFF
ICD Codes: Loss of teeth due to trauma 525.11, Loss of teeth due to dental caries 523.13, Disorders of the teeth and supporting structures 525.9, Acute gingivitis 523.0, Acute periodontitis 523.3, Stomatitis 528.0
Key Points Dental pain can be caused by dental caries, trauma, or medical problems that can cause disease or illness of the oral mucosal or gingival mucosa. Many different illnesses can be diagnosed by examining the oral mucosa. ! Emergency Actions ! The correct diagnosis must be obtained before the correct treatment can be initiated. Any avulsed tooth should be placed back into its socket as soon as possible.
DEFINITION A tooth has a number of components. The pulp is at the center of the tooth and includes the tooth’s neurovascular supply. The pulp produces dentin, an off-yellow material composed of microtubular structures that hydrates and cushions the tooth. The tooth is covered by a hard, hydroxyapatite containing material known as enamel, which is the hardest substance in the human body. The root of the tooth extends into the alveolar bone, is covered by a layer of cementum, and is attached by the periodontal ligament. The dental unit is maintained by the attachment apparatus or periodontium, which is broken down into a periodontal and gingival component. The gingival component consists of the junctional epithelium, gingival tissue, and fibers. The periodontal component includes the periodontal ligament, the alveolar bone, and the cementum. There are primary and permanent teeth. The primary teeth begin eruption at age 6 months and, all 20 primary teeth should be in place by 3–4 years of age. The permanent teeth begin erupting around 6 years 154
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of age. The adult mouth consists of 32 teeth and are divided into 8 incisors, 4 canines, 8 premolars, and 12 molars.
EPIDEMIOLOGY Dental pain is a very common presenting symptom in the emergency department.
CLINICAL PRESENTATION The primary symptom in patients with dental problems is pain. In addition, there may be associated swelling, redness, bleeding, and difficulty opening the mouth (i.e., trismus).
EXAMINATION When performing the examination, the practitioner should look for evidence of facial asymmetry as a result of swelling. He or she should palpate for evidence of lymphadenopathy. When examining the mouth, a tongue blade (preferred) or a gloved hand should be used. The soft tissue should be inspected for evidence of erosions, erythema, or abscesses. The healthcare practitioner should inspect, percuss, and move the teeth to identify areas of inflammation or decay. A thorough ear, nose, and throat (ENT) examination will help to identify any causes of referred pain.
LABORATORY FINDINGS There is little use for laboratory tests in addressing most dental symptoms.
RADIOGRAPHS Dental radiographs will help to determine specific tooth pathology, but most physicians’ offices and hospitals do not have dental and Panorex radiographic capability.
DIAGNOSIS AND TREATMENT Pain as a result of dental caries is probably the most common reason patients present to an acute dental care setting. The dentin is often exposed, and this is the direct cause of the pain. The tooth will be sensitive to hot or cold sensations. The treatment is pain control, if there is no evidence of infection. Dental caries most commonly occur in the occlusal surfaces or gingival margins.
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If a dental caries is left untreated, a resulting pulpitis may occur, which will be identified by increasing pain. This can extend into the alveolar ridge, causing a periapical abscess. The treatment for this is drainage, pain control, and antibiotics. The multiple flora in the mouth are sensitive to penicillin, and this should be given at 250–500 mg four times a day. Erythromycin is a reasonable alternative in patients who are allergic to penicillin. Patients who have had a dental extraction 24–48 hours before presentation may present with periosteitis, which is a general inflammation and responds to pain control. Patients, who present 3–4 days after extraction will have alveolar osteitis, also known as a dry socket. This results when the postextraction clot is either dislodged or dissolved, exposing the alveolar bone. Treatment involves packing with gauze soaked in eugenol and pain control. Periodontal disease refers to infection of the gingiva or periodontal ligament and is initially painless. As it progresses, however, there may be gingival bleeding or tenderness. Gingivitis is an inflammation of the gingiva and results from the accumulation of bacterial plaque along the gingival margins with subsequent inflammation. As the inflammation progresses, there will be extension into alveolar bone that results in periodontitis. Resultant bone loss can result in tooth mobility and tooth loss. Treatment of periodontal disease involves dental referral for removal of plague and antibiotics. Patients who present with periodontal abscesses will need antibiotics such as Pen VK (penicillin V) or erythromycin and saline rinses. Large abscesses may require drainage in the emergency department. When bacteria invade the surrounding gingiva, acute necrotizing ulcerative gingivitis may develop. This condition is often called Vincent disease or trench mouth. This is thought to be an opportunistic infection caused predominantly by anaerobes such as Fusobacteria and Treponema species. It has been associated with immunocompromised hosts, fatigue, stress, and smoking. The patient will present with pain, ulcerated lesions, and gingival bleeding. The patient may also have fever, malaise, and lymphadenopathy. Treatment involves antibiotics, dilute hydrogen peroxide rinses, and early dental referral. Pericoronitis is an inflammatory condition of the gingiva that occurs over erupting teeth, most commonly the third molars (i.e., wisdom teeth). This condition can be extremely painful, and treatment includes pain control, hydrogen peroxide rinses, and possibly antibiotics. There are additional conditions that can cause local inflammation of the gingiva, including drugs such as phenytoin (in about 50% of cases), cyclosporine, and calcium-channel blockers. This gingival hyperplasia ranges from slight enlargement of the interdental papillae to massive enlargement of the gingiva, which may cover the teeth. Treatment involves removal of local irritants and surgical incision of the surrounding tissue. There are a multitude of lesions that involve the oral cavity. Some of the more common ones are oral candidiasis, aphthous stomatitis, and herpes
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simplex. Oral candida generally presents with white, curd-like plagues that can be scraped off with a tongue blade. There are a number of risk factors, including extremes of age, malnourished states, antibiotic use, and immunocompromised states. Treatment involves oral nystatin suspension, 500,000 units four times a day, or systemic fluconazole. Aphthous stomatitis is a very common disorder affecting as much as 20% of the population and may be related to stress, oral trauma, and hormonal changes. The ulcers are usually 2–3 mm in size and painful. They can coalesce to form larger lesions. They usually resolve in 10–14 days but may resolve sooner with treatment. Symptomatic treatment includes hydrogen peroxide rinses and steroid antibiotic ointment such as Kenalog (triamcinolone) in Orabase paste or fluocinonide 0.05% topical gel. Herpes simplex can infect the oral cavity and presents as acute, painful ulcerations of the gingiva and mucosa. Patients may have fever and lymphadenopathy. The patient may present with a prodrome of pain and burning of 1–2 days, after which the onset of lesions will resolve in 6–10 days. Antiviral treatment with acyclovir, 400 mg three times daily, or valacyclovir, 500 mg twice daily, may help in earlier resolution. There are several medical conditions that may have oral manifestations. These include diabetes, tuberculosis, collagen vascular diseases such as lupus, and blood dyscrasias such as leukemia and thrombocytopenic purpura. Not all facial pain is dental related. Two of the more common causes of face pain include temporal mandibular joint (TMJ) syndrome and trigeminal neuralgia. TMJ syndrome results from anatomical disharmony and occlusal disturbances. Patients report dull pain in the region of the TMJ and the pain is usually unilateral. This condition may be very difficult to treat and includes a soft diet, nonsteroidal anti-inflammatory drugs, and muscle relaxants. Trigeminal neuralgia, also known as Tic douloureux, is the most common cranial neuralgia. The disease is most common in persons aged 30–60 years and predominantly affects women. The pain is sharp, brief, and excruciating and unilateral and follows the distribution of the fifth cranial nerve. The diagnosis is clinical but should exclude organic causes. The symptoms may be reproduced on physical examination by tapping specific areas of the face. Treatment is usually medical with carbamazepine (initially, 100 mg twice daily, increasing to 1200 mg/day). Surgical ablation may be necessary if the patient is unresponsive to medical management.
Bibliography Amsterdam J: Oral medicine. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 892–897.
158 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Beaudreau RW: Oral and dental emergencies. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1482–1494. Hodgon A: Toothache and common periodontal problems. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 75–78.
Maxillofacial Injuries JAMES A. PFAFF
ICD Codes: Mandible fracture 802.0, Nasal bones 802.0, Malar and maxillary bones (closed) 802.4, (open) 802.5, Facial bones orbit 802.8
Key Points Complete evaluation of all possibly injured maxillofacial injuries should be performed, including the eye, ear, lacrimal ducts, and oral mucosal. ! Emergency Actions ! The ABCs of resuscitation (i.e., airway, breathing, and circulation) should always be performed before specific attention is paid to any maxillofacial wound or fracture.
DEFINITION Head and neck wounds are a common occurrence and involve both lacerations and facial fractures. They may be associated with a number of other injuries including brain trauma, cervical spine injury, basilar skull fractures, chest injuries, abdominal injuries, and extremity injuries. Having a high index of suspicion for other injuries is critical. Lacerations to the face are very common, and they should be evaluated for the possibility of underlying muscle involvement or lacrimal duct injuries. Orbital fracture may involve either the orbital floor or the rim. There should be a heightened suspicion of globe injury. The nose is the most commonly fractured bone in the face. It comprises both a bony proximal portion that is connected to the frontal bone and the primarily cartilaginous lower portion. Septal hematomas may accompany nasal injuries. They present as a discolored, swollen area of the septum. Since the septal cartilage is
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dependent on blood supply from the perichondrium, an unrecognized hematoma can result in significant cosmetic deformity. Maxillary fractures are commonly identified by the Le Fort classification. Le Fort I fracture is a horizontal fracture across the alveolar ridge. It is identified by grasping the upper teeth and pulling out. The resulting anterior movement identifies the fracture. Le Fort II fracture is a pyramidal fracture of the face that is identified by grasping the teeth and having the nose and alveolar ridge move, but no movement of the orbits occurs. Le Fort III injuries are also known as craniofacial dysplasia with notable fractures of the maxilla, zygoma, nasal, and ethmoid bones. These result when the face separates from the skull. There are two types of zygoma fractures. The arch is commonly fractured because it is fairly prominent. The tripod fracture is a combination of an infraorbital rim fracture, diastasis of the zygomaticofrontal suture, and disruption of the zygomaticotemporal junction of the arch. The mandible may be the second most commonly fractured bone of the face. The condyle is the most frequent injury, followed by the body and angle. The ear is sometimes injured by either laceration or contusion resulting in a subperichondrial hematoma. Like the nose, the ear is dependent on the perichondrium for vascular supply. Failure to recognize and treat this may result in a “cauliflower ear.” Mandibles can dislocate with or without trauma. This injury is primarily bilateral but can occur in a unilateral fashion. Inciting events include yawning, laughing, or dental extraction, among other things.
EPIDEMIOLOGY Facial trauma is very common and is seen in emergency departments on a daily basis. There are almost 6 million head and neck wounds seen in the United States annually. It has been estimated that 54%–70% of all motor vehicle collisions sustain facial injuries, accounting for anywhere from 300,000 to 3 million maxillofacial injuries per year. The most frequently injured facial bones are the nose, zygoma, mandible, and maxilla.
CLINICAL PRESENTATION The patient may present with significant facial swelling. The patient may have eye pain, diplopia facial anesthesia, decreased extraocular movement, malocclusion, and trismus.
EXAMINATION Although facial injuries may be dramatic, they should not distract the provider from the normal resuscitative measure of airway, breathing,
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circulation, and other life-threatening injuries. Once the patient’s condition has been stabilized, evaluating for specific facial injuries can take place. The injuries should be inspected and palpated for pain, swelling, lacerations, and crepitus. An ophthalmological examination for evidence of corneal injury, hyphema, and globe injury should also be performed. The ears should be inspected for lacerations and evidence of subperichondrial hematoma. The nose should be inspected for swelling and the presence of a septal hematoma. Be suspicious for cerebrospinal fluid leaks if there is a clear discharge coming from the nose. The use of a tongue blade may help in determining mandible fractures. The examiner will try to twist a tongue blade after a patient bites down. The inability to do this should heighten the examiner’s concern for a mandible fracture.
LABORATORY FINDINGS There is little use for laboratory tests in addressing most maxillofacial symptoms.
DIAGNOSIS The diagnosis of facial fractures is a combination of clinical and radiographic findings. Nasal fractures are a clinical diagnosis given the significance large amount of cartilage. The physical finding should heighten one’s suspicion and direct the necessary imaging.
RADIOGRAPHS The water or occipital-mental view is considered the best radiograph for diagnosing fractures of the face. Although plain film radiography is adequate in many facial fractures, computed tomography (CT) is probably the best modality to define facial trauma. It will define not only the bones, but underlying structural injury as well.
TREATMENT The patient’s condition should be stabilized before investigation of any specific injuries. Lacerations should be repaired with the normal wound care techniques, though high-pressure irrigation may not be required. Septal hematomas and ear subperichondrial hematomas should be identified and evacuated. In the case of many facial fractures, patients can be sent home with good consultant follow-up, but contact should be made with a consultant before discharge.
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SPECIFIC TREATMENT If one is comfortable or experienced in hematoma evacuation, both septal and subperichondrial hematomas can be evacuated. If not, then consultation should be obtained. Relocating a mandible is something that can be performed by most practitioners. After appropriate pain medications or anxiolytics are administered to the patient, the examiner should wrap both thumbs with gauze and place them in the vicinity of the third molars. The examiner should place downward and backward pressure to reduce the mandible.
Bibliography Cantrill SV: Face, In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 314–329. Carlin CB, Ruff CS, Caravalho G, et al: Facial fractures and related injuries: A 10-year retrospective analysis, J Craniomaxillovac Trauma 1988;4:44–48. Hasan N, Colucciello SA: Maxillofacial trauma, In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1583–1590. Hollander JE, Richman PB, Werblud M, et al: Irrigation in facial and scalp irrigations: Does it alter outcome? Ann Emerg Med 1998;31:73–77. Scherer M, Sullivan WG, Smith DJ, et al: An analysis of 1423 facial fractures in 788 patients at an urban trauma center, J Trauma 1989;29:388. Shepherd SM, Reyes IM: Maxillofacial injuries. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 465–475. Singer AJ, Hollander JE, Quinn JV: Evaluation and management of traumatic lacerations. N Engl J Med 1997;337:1142–1148.
Ophthalmological Emergencies JAMES A. PFAFF
ICD Codes: Hordeolum 373.11, Chalazions 373.2, Welder’s keratitis 364.3, Orbital cellulites 376.01, Herpes simplex 053.20, Hyphema 364.61, Corneal abrasion and globe rupture 918.1, Conjunctivitis 372.00, Temporal arteritis or Giant cell arteritis 446.5, Corneal foreign bodies 930.0, Central retinal artery 593.81, Subconjunctival hemorrhages 372.72, Vein occlusion 362.30, Retinal detachment 361.9, Acute narrow angle glaucoma 365.22
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Key Points Ophthalmological emergencies can result from trauma, disease of the eye, or diseases that affect the eye. A visual acuity test should always be performed before any treatment is instigated. ! Emergency Actions ! The key to any alkaline or acidic eye exposure is copious irrigation with water. Central retinal artery or vein occlusion, retinal attachment, acute narrow angle glaucoma, globe rupture, or temporal arteritis warrant an immediate ophthalmological referral.
DEFINITION Infectious etiologies of the lids and soft tissue include hordeolum, chalazions, and preseptal and orbital cellulites. Inflammations of the cornea include conjunctivitis, welder’s keratitis, corneal ulcers, and herpes simplex infections. Acute causes of visual loss include central retinal artery and vein occlusion, retinal detachment, and acute narrow-angle glaucoma. All parts of the eye can be involved in trauma and some of the more common ones are hyphema, corneal abrasion, and globe rupture.
EPIDEMIOLOGY Up to 2% of visits to emergency departments involve eye problems, and the vast majority of these can be treated without ophthalmological consultation.
CLINICAL PRESENTATION The patient may present with reports of vision loss, pain, eye discharge or tearing, photophobia, or redness and swelling.
EXAMINATION Everyone with an eye problem should have visual acuity tested and documented. Distance or near cards can be used. Visual acuity should be measured with correction. If the patient does not have his or her glasses, a pinhole can be used to reduce the refractive error. The lids and periorbital skin can be examined for signs of swelling, redness, or crepitus. If there is a concern for foreign bodies, the eyelids should be everted. The pupils should be examined for symmetry (approximately 10% of the population will have unequal pupils, a condition known as anisocoria) and reactivity. A common nomenclature is PERRLA (pupils equal and reactive to light and accommodation). Unless accommodation is always tested, it is best to leave the “A” out of the nomenclature.
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Ocular motility should be checked to ensure cranial nerves III, IV, and VI are functioning properly. Ocular motility is impaired in a number of conditions, including blowout fractures and cranial nerve palsies. Visual fields by confrontation should also be examined for evidence of hemianopsia, which may help locate the ocular lesion. The anterior chamber should be examined for evidence of blood (in the case of hyphema), white cells (hypopyon), as well as flare and cells. This is best accomplished with the use of a slit lamp, which can also evaluate the cornea, conjunctiva, iris, and lens. The use of fluorescein stain also helps to evaluate the presence of corneal abrasions as well as perforations. The funduscopic examination can review the optic nerve, macula, and retina. Unless the patient has a history of acute narrow-angle glaucoma, this examination can be facilitated by the use of a mydriatic agent. All patients who present with eye pain or redness should have their intraocular pressure measured. Methods available include applanation, a Tono-Pen, or Schi tz tonometer. The cornea should be anesthetized before the use of this instrument.
LABORATORY FINDING There is little use for laboratory tests in addressing most ophthalmological symptoms.
DIAGNOSIS A thorough eye examination will lead the healthcare provider to the correct diagnosis.
RADIOGRAPHS When there is concern for an intraocular foreign body or globe injury, a CT scan is probably the modality of choice.
DIAGNOSIS AND TREATMENT An external hordeolum or stye is an infection of the glands lining the eyelid and appears as a small pustule. An internal hordeolum or chalazion is an inflammation that results from occlusion of the meibomian gland in the lid. Both of these can be treated with topical antibiotics, warm compresses, and ophthalmology referral if no improvement. A preseptal or periorbital cellulitis is an infection that is outside of the orbital septum, involving connective tissue of the orbital periosteum, that is reflected into the upper and lower eyelids and thus does not involve the eye itself. It is usually caused by Staphylococcus aureus and can generally be treated in an outpatient capacity.
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At times, it is difficult to distinguish a periorbital from an orbital cellulitis. Orbital cellulitis is a potentially eyesight- and even life-threatening illness that is caused primarily by S. aureus infection, though a multitude of other organisms such as Haemophilus influenzae and Streptococcus pneumoniae that cause it as well. CT scanning will help distinguish this from a periorbital infection. Treatment involves admission to the hospital, intravenous antibiotics, and possibly an ophthalmological referral. Conjunctivitis is, by definition, an inflammation of the conjunctiva and has a number of causes. The patient will often present with an irritated red eye, and both eyes may be involved. The patient may experience a foreign body sensation and may have a discharge that is usually worse in the morning. Visual acuity and ocular pressures will be normal. The cornea should be stained to avoid missing herpes keratitis. Bacterial conjunctivitis will present with a mucopurulent discharge, and the patient may have preauricular lymphadenopathy. The treatment is topical erythromycin ointment four times a day. Patients who wear contact lenses can experience conjunctivitis caused by pseudomonas, and these persons are treated with fluoroquinolone ointment. Viral conjunctivitis often follows a viral illness and may initially involve a watery mucous discharge. It may be difficult to distinguish viral conjunctivitis from bacterial infection, and topical antibiotics are often prescribed. Additional treatment may include ocular antihistamines or artificial tears. Allergic conjunctivitis will often present with itching, bilateral eye redness, and a watery discharge. Physical examination will reveal redness and swelling of the conjunctiva, also known as chemosis. Treatment consists of cool compresses and antihistamine/decongestant eyedrops. In any case of red eye, the cornea should be stained to avoid missing herpes simplex, a potentially eyesight-threatening form of conjunctivitis. Fluorescein staining will reveal uptake in a dendritic fashion that appears as if it is branching. Patients with this condition will be treated with topical antiviral agents as well as oral acyclovir or its derivatives. These patients need prompt ophthalmological referral. Corneal ulcers are a break in the epithelium of the cornea that can occur from trauma or corneal desiccation resulting from an inability to close the lid in peripheral seventh nerve palsy and is common in contact lens wearers. The patient will present with pain, redness, and photophobia. Ocular examination reveals a corneal defect and white infiltrate. There may be a collection of white cells called a hypopyon. Corneal ulcers are eyesight threatening and need aggressive treatment, including fluoroquinolone antibiotic eyedrops, eye cycloplegics, and ophthalmological follow-up. The eye should not be patched. Patients may present with sudden vision loss that may be painful or painless. The acute onset of painful vision loss is most commonly caused by acute narrow-angle closure glaucoma. It occurs in patients who have
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a congenital narrowing of the anterior chamber angle. When the pupil becomes dilated and touches the anterior iris, a subsequent obstruction occurs. This prevents the flow of aqueous humor from the posterior chamber (where it is produced) to the anterior chamber, where it normally is filtered out of the eye. The increasing intraocular pressure causes the cornea to become cloudy and less transparent. Increased intraocular pressure can result in pain, blurred vision, and halos. On examination, the pupil will be mid dilated and nonreactive. The intraocular pressure is usually greater than 50 mmHg. Treatment is aimed at pressure reduction. Decreasing aqueous humor production is accomplished with topical beta blockers such as Timoptic (timolol) and alpha agonists such as Iopidine (apraclonidine), as well as carbonic inhibitors such as acetazolamide. Intravenous mannitol is excellent at decreasing intraocular pressure. Topical steroids such as Pred Forte should also be given. Once the patient’s pressure is decreasing, topical pilocarpine should be given to make the pupil miotic, subsequently pulling the peripheral iris away from the angle. Patients may also have primary or open-angle glaucoma, the most common form of glaucoma and the leading cause of blindness in the United States. The incidence increases with aging and is three times more common in persons with diabetes than the rest of the population. The patient experiences gradual visual loss, initially at the periphery, that may gradually become more central. Funduscopic examination reveals disk pallor and cupping. The eye pressures are usually greater than 50 mmHg. Treatment involves topical beta blockers, miotic agents, carbonic anhydrase inhibitors, topical steroids, and surgery. Patients may also present with painless vision loss; the primary causes are central retinal artery or vein occlusion and retinal detachment. Central retinal artery occlusion causes an ischemic stroke of the retina and is most common in persons between the ages of 50 and 70 years. Patients report acute visual loss over seconds. Funduscopic examination reveals an edematous pale gray-white–appearing retina with macula that appears as a “cherry red” spot. Expeditious treatment is critical since the patient will sustain irreversible vision loss within 90 minutes. Treatment involves ocular message in an attempt to dislodge the clot, hyperventilation in an attempt to cause vasodilation, pressure-lowering agents such as acetazolamide, and topical beta blockers. An ophthalmologist should be immediately consulted to evaluate the need for paracentesis. Central retinal vein occlusion results in edema, hemorrhage, and vascular leakage of the retinal vein. Risk factors include hypertension, hypercoagulable disorders, vasculitis, and glaucoma. The patient will experience loss of vision, and funduscopic examination may reveal dilated veins, retinal hemorrhages, and disk edema. Treatment is complex and involves ophthalmological referral, topical steroids, and photocoagulation. The posterior segment of the eye is a large cavity filled with vitreous gel. This gel may contract as the patient ages, and this contraction away
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from the retina may cause a “flashing light appearance.” If a complete separation occurs, the patient will perceive “floaters.” Both of these are manifestations of vitreous hemorrhage. Besides aging, conditions that predispose patients to this condition are diabetes, trauma, malignancy, and thrombocytopenia. Definitive therapy is directed at the underlying cause. The retina has two layers that can be separated by fluid accumulations. If this retinal separation occurs, the patient may experience flashes of light and a subsequent filmy, cloudy, or curtain-like appearance. The patient may describe a “curtain being pulled” across the field of vision. If the patient presents with unilateral vision loss, visual acuity tests and dilated funduscopic examination should be performed. A large detachment will be seen as undilated gray area, but detachment may be difficult for a non-ophthalmologist to see, and consultation should be obtained. Optic neuritis is an inflammation of the optic nerve that may cause visual loss over the span of several days. It generally occurs between the ages of 20 and 40 years, affects women more often than men, and is caused by a variety of etiologies to include multiple sclerosis, systemic lupus erythematosus, viral infections, collagen vascular diseases, and idiopathic causes. The majority of patients have pain on eye movement. Color vision is affected more commonly than visual acuity, and funduscopic examination may reveal an elevated, swollen optic disk (i.e., papillitis). Steroids are the treatment of choice, and consultation should be made with an ophthalmologist about timing. Temporal arteritis or giant cell arteritis is a vasculitis of the medium to large vessels in the carotid circulation that can cause painless vision loss and, if left untreated, can affect the contralateral eye as well. It is rare in patients younger than 50 years of age and typically affects patient older than 60 years. The condition is also three times more common in women. Patients may present with a unilateral temporal headache, jaw claudication, myalgias, fever, and anorexia and is frequently seen in patients with polymyalgia rheumatica. A patient’s erythrocyte sedimentation rate (ESR) is greater than 50, and the diagnosis is confirmed with temporal artery biopsy. Steroids are the treatment of choice, and, if there is a high index of suspicion for the condition, this treatment should be initiated, usually in consultation with a specialist. There a number of traumatic eye injuries with which emergency medicine providers should be familiar. Corneal abrasions are fairly common and are corneal defects that can occur with trauma, vegetative matter, and contact lens use, among other things. The patient will present with pain, photophobia, redness, and tearing. The corneal defect is identified by fluorescein stain and a cobalt-blue light. Once identified, a thorough examination should be done, including lid eversion, to ensure that the foreign body is no longer present. The condition may be extremely painful as a result of the ciliary’s spasm.
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One possible treatment is the use of cycloplegics such as 1% cyclopentolate three times a day. The examination is facilitated by the use of an ocular anesthetic agent such as proparacaine. This provides significant relief, but continuous use will retard corneal healing and this drug should never be prescribed for home use. Antibiotic ointment is also used, and erythromycin is a reasonable choice. If the corneal abrasion is a result of vegetative matter, the incidence of pseudomonas infection is high and these patients should receive fluoroquinolone. Eye patching may help with pain relief but has no effect on the ultimate healing. The affected eye should never be patched if the abrasion was caused by vegetative matter or contact lens wear. Corneal abrasions warrant 24-hour follow-up. Patient with corneal foreign bodies may present with pain and photophobia. A thorough history is critical in evaluating these patients. If the cause is from a high-velocity injury from metal work, there should be a heightened suspicion for intraocular foreign body. CT scanning may help to rule this out. After the application of topical anesthesia, superficial foreign bodies may be removed with a small-gauge needle under a slit lamp. Metal foreign bodies may leave a rust ring after removal. If the provider is comfortable with the use of an ocular burr, removal may be attempted. However, rust rings may soften over several days, and the patient can be sent to an ophthalmologist for removal. The abrasion that results after removal should be treated in the usual manner. Subconjunctival hemorrhage can be very traumatic for the patient and is a result of the conjunctival vessels rupturing spontaneously or from trauma or hypertension. Appropriate treatment is reassurance to the patient; the condition will resolve spontaneously in 10–14 days. Chemical injury to the eye is a result of either an acid or alkaline substance. Any exposure should immediately be irrigated with copious amounts of saline. The amount of irrigation can be guided by checking the pH of the tears. Acid usually involves a coagulation necrosis with a limited degree of penetration. Alkali burns, however, cause a liquefaction injury that continues to penetrate through the ocular tissues. Treatment involves cycloplegic agents, antibiotic ointment, and ophthalmological referral. Ultraviolet keratitis or welder’s flash occurs generally when a patient is exposed to welding or tanning equipment without protective eyewear. The patient will present with pain and photophobia 6–12 hours after the exposure. The patient will present with multiple punctuate lesions on the cornea under fluorescein stain and cobalt lights. Treatment involves cycloplegia, antibiotic ointments, pain medications, and ophthalmological referral. Blunt trauma to the eye has the potential for significant injury. The eye may be swollen shut, and it may be difficult to evaluate the structures. The examination should be like any other, with attention paid to visual acuity. An attempt should be made to check ocular pressures
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and do a slit-lamp examination. There may also be associated lacerations or abrasions to the soft tissue. A hyphema is defined as bleeding into the anterior chamber of the eye. It is usually a result of bleeding from the ciliary’s body or iris and can range from a minimal amount to complete occlusion of the eye. It is usually of traumatic origin but can result from spontaneous bleeding, usually from sickle cell disease. The patient may present with pain, photophobia, and decreased vision. These patients need to be seen by an ophthalmologist. Initial treatment involves elevating the patient’s head. If the globe is intact, measure the intraocular pressure. Additional treatments may include cycloplegics, steroids, ocular beta blockers, and acetazolamide. Blowout fractures are another common eye injury. The eye is usually struck by blunt force, and the orbit will fracture in the medial wall or inferior wall into the maxillary sinus. The patient may have diplopia as a result of entrapment of the inferior rectus muscle. CT scanning will identify the extent of injury. Up to one third of blowout fractures will involve additional ocular injuries such as abrasion, hyphema, or retinal tear. Patients with blowout fractures (even with ocular entrapment) do not need immediate surgery and can usually be referred for ophthalmological evaluation. Probably the most significant complication of trauma is a ruptured globe. It can occur with blunt trauma but is most common with penetrating traumas. On physical examination, the eyelid may be significantly softer than the unaffected eye. Additional findings may include a hyphema, decreased visual acuity, and an irregular pupil. Radiography may help the practitioner to locate foreign bodies. When a ruptured globe is suspected, the eye should be covered with a metal shield and ophthalmological consultation should be obtained.
Bibliography Broocker G: The ophthalmic examination. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 42–47. Brunette DD: Ophthalmology. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 908–928. Clayton GC: Optic neuritis. In Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5 Minute Emergency Medicine Consultant. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 764–765. Mitchell JD: Ocular emergencies. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1449–1464. Porter R: Acute eye infections. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 47–53. Reichman E: Glaucoma. In Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5 Minute Emergency Medicine Consultant. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 456–457. Shoff WH, Shepard SM: Eye trauma. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 480–486.
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Otolaryngological Emergencies JAMES A. PFAFF
ICD Codes: Otitis media 382.9, Otitis externa 380.10, Malignant (necrotizing) external otitis 380.14, Epistaxis 784.7
Key Points Diabetic patients should have close follow-up for otitis media, otitis externa,and malignant otitis.Samples should be drawn for complete blood count (CBC) and measurement of partial thromboplastin time (PTT) and international normalized ratio (INR) for patients taking Plavix (clopidogrel bisulfate),Lovenox (enoxaparin sodium), aspirin,or Coumadin (warfarin). ! Emergency Actions ! Any patient with diabetes, bleeding problems, or underlying disease should be evaluated thoroughly, and close followup should be arranged. Patients with fever, diabetes, or high white blood cell count should be of special concern.
DEFINITIONS Otitis Media Otitis media is the most common diagnosis made in children younger than 15 years of age. Otitis media is broadly defined as inflammation of the inner ear. Acute otitis media (AOM) involves signs and symptoms of infection with evidence of effusion. Otitis media with effusion has the presence of effusion without infection. Eustachian tube dysfunction is the central theme of AOM pathogenesis. The dysfunction results in transudation of fluid into the middle ear, which combines with nasopharyngeal secretions and bacteria and the subsequent inflammation. The predominant organisms are S. pneumoniae, H. influenzae, and Moraxella catarrhalis, as well as a multitude of viral etiologies. The symptoms of disease are nonspecific and may include ear pain, fever, cough, diarrhea, vomiting, poor appetite, and ear pulling. The tympanic membrane is usually bulging with decreased mobility. Otitis media with effusion will have a retracted tympanic membrane. The diagnosis is made by a history of acute onset, signs of middle ear effusion, and inflammation. Bullous myringitis is a form of AOM that may involve bullous lesions on the tympanic membrane. It is caused by the same organisms as AOM.
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Treatment starts with amoxicillin. In penicillin-allergic patients, macrolides and cephalosporins should be used in the case of type 1 hypersensitivities. Local anesthetic drops or oral pain medications such as acetaminophen are another option.
Otitis Externa Otitis externa is inflammation of the external auditory canal that occurs when the protective squamous epithelial layer breaks down, resulting in the introduction of bacteria. The most commonly involved organisms are Pseudomonas aeruginosa, S. aureus, and Staphylococcus epidermidis. Fungal infections can also occur and may be the cause of otitis externa in up to 10% of cases. Herpes zoster oticus, also known as Ramsay Hunt syndrome, is a viral inflammation affecting the auricle that can result in facial paralysis and multiple cranial nerve abnormalities. A localized abscess of the ear canal is a furuncle. On physical examination, the canal will be erythematous and swollen. There will be pain to palpation of the tragus or auricle. Vesicular lesions may be present in herpes zoster oticus. The treatment of otitis externa consists of cleansing of the canal and administering local antibiotic drops such as neomycin, polymyxin B-hydrocortisone, or fluoroquinolone drops.
Malignant (Necrotizing) External Otitis If otitis externa persists in an elderly person or a person with diabetes, concern for necrotizing external otitis should arise. This may spread to the base of the skull, resulting in a skull-based osteomyelitis. P. aeruginosa is the predominant causal organism. Clinical symptoms may include pain, tenderness, headache, and otorrhea. CT may help define the extent of the disease. Treatment includes a semisynthetic penicillin and an aminoglycoside or fluoroquinolone.
Sudden Hearing Loss Sudden hearing loss is defined by the gradual or sudden loss of hearing over a 3-day period. This is considered an otolaryngological emergency. There are a myriad of causes, including infections such as measles or mumps, vascular factors, and metabolic phenomena. In addition, medications such as aminoglycosides, conductive causes such as cerumen impaction, and infections and neoplasms can all be causative. Physical examination should include inspection of the external ear canal for evidence of occlusion and evaluation of the tympanic membrane
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for perforations. The use of the Weber and Rinne tests to help distinguish sensorineural from conductive causes. CT or magnetic resonance imaging may be necessary to define anatomical causes. The treatment is directed at the underlying cause.
Epistaxis Epistaxis is a common problem, with 15 people in 10,000 requiring a physician’s care. Most cases occur in persons younger than 10 years. There are a multitude of causes, including trauma, infectious elements, environmental factors, iatrogenic agents, and blood disorders. Contrary to popular belief, epistaxis is not caused by hypertension. The causes of epistaxis are divided into anterior and posterior etiologies. Anterior nose bleeds are the cause in more than 90% of the cases and usually are from the anterior septum in an area called Kiesselbach’s area, which is a confluence of vessels. Anterior epistaxis can also originate from the anterior ethmoidal artery, a branch of the internal carotid artery. The cause of posterior bleeding is most commonly from the sphenopalatine artery, a branch of the internal carotid. The presentation of epistaxis can vary from local oozing to copious amounts of blood from the nose. Depending on the situation, the patient may need resuscitation before examination. After the patient’s condition is stable, the examiner can evaluate the patient with appropriate light, a nasal speculum, and suction. The source may be visible on the nasal septum. If there is too much bleeding, the use of oxymetazoline or cocaine on a gauze pledget may facilitate the examination. For most patients, there is no requirement for laboratory testing. If there is a concern regarding significant blood loss or if the patient is taking a blood-thinning agent, a CBC and coagulation tests may be appropriate. If there is a source visible, the septum can be cauterized with a silver nitrate stick. The provider should avoid both prolonged contact on the septum and using it on both sides of the septum, since this can result in septal perforation. If this procedure is unsuccessful and the bleeding appears anterior, the use of absorbable material such as Gelfoam or surgical suture placement may facilitate relief of bleeding. If this is unsuccessful, the use of a commercially available nasal tampon with or without a balloon should be effective. These patients can be discharged but should be prescribed prophylactic antibiotics such as a cephalosporin to prevent the possibility of toxic shock. If these methods are not successful, or if the patient has identified posterior bleeding, a posterior pack should be placed. The advent of balloon catheters has significantly improved the management of posterior bleeding. The patient may need pain control before placement. After determining that the balloons are working, the catheter should be placed with the
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use of a lubricant. The posterior balloon should then be filled with water (to avoid necrosis) and pulled back. The anterior balloon should then be filled. Patients with posterior pack require hospitalization.
LABORATORY FINDINGS If signs of infection or bleeding are present, a CBC, PTT, INR, Chem-7, and directed laboratory tests should be performed.
RADIOGRAPHS Directed radiographs should be obtained for individual conditions.
Bibliography American Academy of Pediatrics: Subcommittee on Management of Acute Otitis Media: Diagnosis and management of acute otitis media, Pediatrics 2004;20041451–1465. Hodgon A: Toothache and common periodontal problems. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 75–78. Pfaff JA, Moore GE: Otolaryngology. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 928–938. Waters TA, Peacock TA: Nasal emergencies and sinusitis. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1476–1482.
Pharyngitis JAMES A. PFAFF
ICD Code: 462 DEFINITION Pharyngitis is defined as an inflammation from the bacterial or viral infection of the pharynx.
EPIDEMIOLOGY Pharyngitis is the third most common reason that people see a doctor. It is caused by both bacterial and viral causes. The most common cause
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of pharyngitis in adults is viral infection. Rhinoviruses, adenoviruses, and Epstein Barr viruses are common viral etiologies. Group A betahemolytic streptococci (GAHBS) is the most common bacterial cause and is responsible for 5%–15% of causes in adults. Other causes include Neisseria gonorrhea, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Corynebacterium diphtheriae. Anaerobic and fungal causes are uncommon.
CLINICAL PRESENTATION Patients usually present with throat pain, pain on swallowing, and possibly fever, cough, myalgias, headache, rhinorrhea, nausea, vomiting, and, in the case of group A streptococcus, abdominal pain.
EXAMINATION Patients with pharyngitis may have pharyngeal erythema, edema, uvular edema, and palatal petechiae. They may also have anterior cervical neck adenopathy and, in the case of group A streptococcal infection, may present with a scarlatiniform rash that can be present in any area of the body, including the hands and soles of the feet.
LABORATORY FINDINGS The throat culture is considered the definitive diagnostic test. It cannot, however, distinguish acute disease from carrier states, and it may take 24–48 hours for the results. Rapid streptococcal testing has both sensitivity and specificity, but there is debate regarding whether a formal culture is needed to confirm the diagnosis.
DIAGNOSIS It is very difficult to distinguish bacterial from viral forms of pharyngitis. The presence of cough and rhinorrhea suggest a viral etiology. There have been a number of scoring systems developed to try to define bacterial causes. One of the most common scoring systems is the use of the Centor criteria. They consist of fever or history of fever, absence of cough, anterior cervical lymphadenopathy, and tonsillar exudates. There are a number of suggested strategies based on the number of findings a patient exhibits, but even with all four criteria the patient may only have 50% chance of having GAHBS pharyngitis. Given the difficulty in making a clinical diagnosis, laboratory testing may be the only way to make a definitive diagnosis.
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RADIOGRAPHS No radiographs are needed to evaluate pharyngitis, although a CT is the test of choice for the potential complication or other diseases in the differential such peritonsillar abscess, epiglottis, or deep space neck infections.
TREATMENT The treatment for viral pharyngitis is supportive care. The treatment of choice for GABHS infection is penicillin, taken either orally or by injection. This only improves the symptoms by about 24 hours, but it does prevent one of the most common sequelae—rheumatic fever. Of note, it has no effect on post-streptococcal glomerulonephritis. Steroids my improve symptoms.
SPECIFIC TREATMENT In cases of GAHBS infection, oral or intramuscular penicillin is the treatment of choice. In adults, the standard oral dose of penicillin is PenVK 500 mg four times a day for 10 days or 1.2 million units of penicillin IM. Decadron, 10 mg given intramuscularly, will also help with symptomatic relief. Oral erythromycin 250–500 mg orally can be used for persons who are allergic to penicillin.
Bibliography Broder JS, Browne BJ: Pharyngitis. In Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5 Minute Emergency Medicine Consultant. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 844–854. Levin W, Wilson GR: Acute infection of the adult pharynx and laryngitis. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 94–98. Melio FR: Upper respiratory tract infections. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 969–985. Shores CG: Infections and disorders of the neck and upper airway: Oral and dental emergencies. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1494–1501.
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Sialolithiasis JAMES A. PFAFF
ICD Code: Sialolithiasis 527.5
Key Points Sialolithiasis is usually a self-limiting condition that is treated with warm compress and lemon drops. ! Emergency Actions ! If diabetic patient has a fever, an elevated white blood cell count, and elevated glucose levels, the healthcare practitioner should consider admitting the patient to the hospital and calling in an ENT consult.
DEFINITION Sialolithiasis is a blocked salivary gland. It occurs when a calcium stone occludes either Wharton’s duct, blocking the submandibular gland, or Stensen’s gland, with resulting obstruction of the parotid gland. This occlusion results in pain and swelling.
EPIDEMIOLOGY Sialolithiasis occurs primarily in persons between the ages of 30 and 50 years but can occur at any age. The submandibular gland is affected 80%–95% of the time, with the remainder in the parotid gland. Stones of the salivary gland occur in 1% of the population.
CLINICAL PRESENTATION A patient with sialolithiasis will present with pain and swelling of the cheek or jaw. The symptoms are often exacerbated after eating, chewing, or talking.
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EXAMINATION There may be some facial swelling, and the gland will be tender to palpation. There may be purulent discharge from the duct, and the stone may be palpable on physical examination.
LABORATORY FINDING No particular laboratory examinations can diagnosis sialolithiasis. If the patient has a fever or diabetes, a CBC and chemistry panel should be performed.
DIAGNOSIS The diagnosis is clinical, with pain, swelling, and tenderness all hallmarks of the inflammation.
RADIOGRAPHS Ultrasonography and CT may both be helpful but not emergently. A therapeutic trial is generally appropriate before any further testing.
TREATMENT Treatment consists of moist heat, massage, analgesics, sialogogues (e.g., tart candy such as lemon drops to promote secretions), and antibiotics to cover penicillinase-resistant organisms. Complications include recurrent obstruction, strictures, infection, and gland atrophy. If the patient’s glands are infected and he or she has diabetes with an elevated white blood cell count and fever, the practitioner should consider admission to the hospital and consultation with an ENT specialist.
Bibliography Haddon R, Peacock WF: Face and jaw emergencies. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1471–1476. Pfaff JA, Moore GE: Otolaryngology. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 928–938. Pollack CV, Severance HW: Sialolithiasis: Case studies and review, J Emerg Med 1990;8:561. Williams MF: Sialolithiasis, Otolaryngol Clin North Am 1999;32:819.
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Sinusitis JAMES A. PFAFF
ICD Code: 473.9
Key Points Most sinus infections are viral. Particular attention should be paid to patients who might have bacterial sinusitis and who have diabetes, human immunodeficiency virus (HIV) infection, or underlying disease. ! Emergency Actions ! Any patient who presents with sinusitis and has periorbital cellulitis or is immunocompromised should be considered for admission to the hospital or, at least, an ENT specialist should be consulted.
DEFINITION Sinusitis is an inflammation of the paranasal sinuses. Given that it involves and is continuous with the nasal passages, the term rhinosinusitis is more appropriate. The paranasal sinuses include the frontal, maxillary, ethmoid, and sphenoid sinuses. These are all lined by ciliated pseudostratified columnar epithelia that act to clear secretions through their respective ostia. When they become obstructed, this mechanism is impaired and there is an increase in carbon dioxide, an environment resulting in proliferation of bacteria. Although viral disease is significantly more common than bacterial disease, the bacterial organisms most commonly involved include S. pneumoniae, H. influenzae, and M. catarrhalis. The infection is polymicrobial in one third of cases. The disease is defined as acute if the infection lasts 3–4 weeks, subacute if the symptoms last from 3 weeks to 3 months, and chronic if it lasts more than 3 months.
EPIDEMIOLOGY Rhinosinusitis is one of the most common reasons for visits in the acute care setting and may affect as many as 31 million patients. From 1992 to 1999, 7–12 of all antibiotic prescriptions written were for rhinosinusitis. It is estimated that more than $3 billion a year is spent on rhinosinusitis and its treatment.
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CLINICAL PRESENTATION Patients with rhinosinusitis usually have a preceding upper respiratory infection. They may have a headache, teeth pain, fever, mucopurulent discharge, and a poor response to nasal decongestants or antihistamines. The pain is usually unilateral. The headache these patients have is usually increased when they are in an upright position in the case of maxillary sinusitis, but is relieved in the upright position in the case of frontal, ethmoid, and sphenoid sinusitis.
EXAMINATION The physical examination may reveal a purulent nasal discharge. Sinus tenderness is suggestive but not specific for the diseases. Transillumination of the sinuses requires some degree of expertise and is generally not helpful to the primary practitioner.
LABORATORY FINDINGS Laboratory tests are usually not helpful in the diagnosis of sinusitis. If a patient has a high fever, diabetes, HIV infection, or any underlying disease, then a CBC and Chem-7 could be helpful in management.
DIAGNOSIS The diagnosis of sinusitis is often made clinically. The patient should have had symptoms of sinusitis for 7–10 days before the diagnosis of sinusitis is made. Additional predictors for bacterial sinusitis include maxillary toothache, a poor response to nasal decongestants, unilateral facial pain, and purulent nasal discharge.
RADIOGRAPHS There is little utility in plain radiographs because they give little information about the sinus structure. If imaging is used, CT scan is the desired modality. It identifies the anatomy of the nasal cavity and paranasal sinuses and will identify most complications.
TREATMENT Antibiotic treatment of sinusitis should be directed at the offending organisms. Appropriate first-line agents include amoxicillin, amoxicillin/clavulanate, cefuroxime, cefdinir, azithromycin, and trimethoprim/
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sulfamethoxazole. The fluoroquinolones such as levofloxacin and moxifloxacin can also be used. The course of treatment is usually 10 days long. Additional modalities for the treatment include decongestants, nasal saline, and nasal steroids. Complications of sinusitis include meningitis, brain abscess, epidural or subdural empyemas, orbital cellulitis, cavernous sinus thrombosis, and osteomyelitis.
Bibliography Boie E: Sinusitis. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott Williams & Wilkins: Philadelphia, 2001, pp 99–102. Melio FR: Upper respiratory tract infections. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 969–985. Shockley L: Sinusitis. In Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5 Minute Emergency Medicine Consultant. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 844–854. Waters TA, Peacock TA: Nasal emergencies and sinusitis. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1476–1482. Williams JW, Simel DL: Does this patient have sinusitis? JAMA 1993;270:1242.
Dental Trauma JAMES A. PFAFF
ICD Code: Broken tooth 873.73
Key Points The best place for an avulsed tooth is in the mouth, in milk, or in wet gauze. ! Emergency Actions ! Any avulsed tooth should be placed back into the tooth’s socket as soon as possible.
DEFINITION Dental injuries are common events in the emergency department and involve teeth fractures, subluxations/displacement, and avulsions, in addition to soft tissue injuries and lacerations. Subluxated teeth are loosened teeth that may be mobile to palpation, and the patient may have
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some degree of malocclusion. Avulsed teeth involve complete displacement from the socket and are a true dental emergency. The tooth’s viability is directly related to its replacement in the socket. A general rule is that the chances of success decrease by 1% for each minute it is out of the socket. Dental fractures are described by the Ellis classification. An Ellis class I fracture involves chipping of the superficial enamel; these fractures are painless to percussion. Ellis class II fractures involve the enamel and dentin and will have an ivory white or pale yellow appearance. These fractures will have sensitivity to heat, cold, and air. Ellis class III fractures involve the enamel, dentin, and pulp. Examination will involve a red or pinkish coloration within the dentin, and there may be blood from the exposed pulp. These injuries are very painful with extreme sensitivity. Lacerations may involve the lips, oral mucosa, and tongue and are at risk for foreign matter and cosmetic deformity if not repaired.
EPIDEMIOLOGY Dental injuries affect all age groups. Toddlers and younger children are victims of falls. Adolescents have trauma from sporting events and physical altercations. Adults may be affected by altercations or motor vehicle trauma. Domestic and child abuse should be included in the differential diagnosis.
CLINICAL PRESENTATION Patients will often have pain as a result of the laceration or dental injuries. The patient may present with malocclusion, swelling, redness, or bleeding. The mechanism of injury should be elicited.
EXAMINATION Airway patency should be assessed. The teeth should be percussed for pain and evaluated for laxity. The teeth mucosa, tongue, and palate should be visually inspected for evidence of lacerations or trauma. The examiner should attempt to locate any missing teeth, especially because they can be aspirated.
LABORATORY FINDINGS No laboratory tests are usually needed to evaluate dental trauma, unless the patient is taking a blood thinner.
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DIAGNOSIS The diagnosis will depend on the results of the physical examination and the accompanying radiographs.
RADIOGRAPHS Plain film radiographs may identify Ellis class III fractures. If available, a Panorex is the best radiograph to evaluate fractures or teeth displacement.
TREATMENT Ellis class I fractures generally are not painful but require dental referral. Ellis class II fractures should be covered with dry gauze, aluminum foil, or calcium hydroxide paste. Pain control should be initiated, and dental referral should occur within 24 hours. Ellis class III fractures require immediate dental referral. If that is not possible, the tooth can be covered with moist gauze and then foil until a dentist can be located. Patients who have minimally subluxated teeth should be fed a soft diet and given dental referral. Teeth that have a higher degree of subluxation may need splinting, preferably by a dentist. Teeth that are intruded also require early dental referral. The treatment of tooth avulsions depends on the age group involved. If a primary tooth is involved, the tooth is usually not replaced but the child should be referred to a dentist. Teeth that are intruded in the gums also need referral. Permanent teeth that are avulsed require immediate dental care. The teeth can be replanted at the scene after gentle tap water irrigation. The healthcare provider should avoid touching the root of the tooth and should only touch the crown. If the provider is unable to replant the tooth, it should be placed in milk, saliva, or a commercially available balance salt solution. If the procedure is successful, the tooth should be splinted. Many small lacerations do not require repair, but the patients should be cautioned to rinse after eating to avoid particulate matter interfering with wound healing. Injuries of the buccal mucosa can be repaired with absorbable suture, but attention should be paid to the possibility of a ductal injury. Tongue lacerations that are longer than 1 cm should probably be repaired with absorbable suture to avoid the accumulation of particulate matter in the wounds. Lip lacerations should be repaired with meticulous detail, especially if the laceration crosses the vermillion border. A discrepancy of even 1 mm can result in significant cosmetic deformity. Through-and-through laceration should involve a layered closure to ensure that the muscle layer is closed. Lip lacerations are generally repaired with nonabsorbable suture.
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All patients should have pain control and antibiotics on a case-bycase basis. Because many intraoral lesion involves anaerobes, penicillin is an excellent choice.
Bibliography Amsterdam J: Oral medicine. In Marx J (ed): Emergency Medicine: Concepts and Clinical Practice. Mosby: St Louis, 2002, pp 892–897. Beaudreau RW: Oral and dental emergencies. In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York, 2004, pp 1482–1494. Hodgon A: Toothache and common periodontal problems. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 75–78.
Chapter 6
Environmental Emergencies Altitude-Related Conditions JOHN MCMANUS AND IAN WEDMORE
ICD Code: Acute mountain sickness 993.2
Key Points Altitude illness can affect anyone exposed to altitudes over 1500 m (4921 feet) in elevation. ! Emergency Actions ! Descent of 500–1000 m usually relieves symptoms of altitude-related conditions. If descent is not possible or if patients are presenting with moderate to severe symptoms, medical therapy may be necessary. Place patient on oxygen and descend as soon as possible.
DEFINITIONS As the number of persons who venture into the mountains for hiking, climbing, skiing, and other outdoor pursuits increases, the incidence of altitude-related illness is also likely to increase. It is essential that medical providers be well versed in the recognition, evaluation, and treatment of illness resulting from altitude. Altitude illness can affect anyone exposed to altitudes over 1500 m (4921 feet) in elevation. Although high altitude can cause and exacerbate many underlying medical conditions, the term high-altitude illness is most often used to describe acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE). Preexisting medical conditions exacerbated by altitude are often referred to as altitude-exacerbated conditions, whereas other conditions arising from altitude exposure are termed altitude-related illnesses (Box 6-1).
EPIDEMIOLOGY More than 30 million people traverse terrain above 2285 m yearly, and almost 25% of those who travel above an elevation of 2590 m (8500 feet) develop some manifestations of high-altitude illness. Of note, in North America all ski areas in Utah and Colorado are at elevations above 8000 183
184 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Box 6-1 Medical Illness Secondary to Altitude High-Altitude Illness Acute mountain sickness (AMS) High-altitude pulmonary edema (HAPE) High-altitude cerebral edema (HACE) High-Altitude–Related Illness (examples) Peripheral edema Chronic mountain sickness Cold weather injuries High-altitude retinopathy High-altitude pharyngitis and bronchitis High-altitude global amnesia Subacute mountain sickness High-Altitude–Exacerbated Illness (examples) Primary and secondary cardiopulmonary disorders Sickle cell disease and trait Obstructive sleep apnea
feet, placing millions of snow riders at risk for altitude illness. Furthermore, of the many recreational and professional climbers who attempt to summit mountain peaks each year, many will develop some form of altitude-related illness. The incidence of altitude illness is related not only to the absolute altitude obtained but also the rate of ascent to altitude. The faster one travels to a higher altitude, the more likely one is to become ill. For example, a rapid ascent to the summit of Mt. Everest over the span of a few hours will result in coma or death, yet with adequate time for acclimatization it can be climbed without supplemental oxygen. Likewise, a typical 36-hour ascent to the summit of Mt. Rainier in the Cascade mountain range in Washington State results in almost a 70% incidence of altitude illness. If the same ascent is carried out over a 5-day period instead, the incidence of altitude illness is reduced to 5%. Altitude causes its main effects through the decreased partial pressure of oxygen. It should be remembered that the percentage of oxygen is 21% and the barometric pressure is 760 mmHg at sea level. Although the concentration of oxygen remains constant as altitude increases, the barometric pressure drops, reducing the number of oxygen molecules per breath. Also, other factors such as previous altitude illness, temperature, dehydration, and hypobaria have also been linked to high-altitude illness. The initial physiological response to the hypobaric hypoxia of altitude is an increase in a person’s respiratory rate, which occurs at approximately 1525 m (5000 feet) in elevation. By hyperventilating, a person blows off carbon dioxide and, in exchange, can hold onto more oxygen. This hyperventilation causes a respiratory alkalosis, which would inevitably lead to the slowing of one’s breathing if the body did not somehow compensate for it. The body compensates by having the kidneys excrete bicarbonate,
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thus inducing a metabolic acidosis in response to the respiratory alkalosis, normalizing the body’s pH and allowing hyperventilation to continue. As an example, the respiratory rate of a climber on the summit of Mt. Everest is “normally” 40–50 breaths/min. Exposure to hypobaric hypoxia also induces secretion of erythropoietin and production of increased red blood cell mass. However, this process takes time, and the hemoglobin rise initially noted in the first few days of the altitude exposure is actually due to dehydration caused by the excretion of bicarbonate described previously. This also causes increased urination the first few days spent at higher altitude. This adaptation by the human body to altitude that helps to minimize hypoxemia and maintain cellular function is termed acclimatization.
CLINICAL PRESENTATION Acute Mountain Sickness AMS is the most common form of high-altitude illness. It is also the initial medical condition in the spectrum of high-altitude illness that can culminate with the development of HACE. AMS occurs shortly after arrival at an altitude typically over 2286 m (7500 feet) and usually occurs 6–10 hours after ascent, with a peak at 24–72 hours. The incidence of AMS varies from 20% in the general population to as high as 90% in climbers. The predominant symptom of AMS is a headache that is usually described as throbbing and global in nature. It is often worse in the morning on waking from sleep. Accompanying the headache is one or more of the following symptoms: anorexia, nausea, or emesis; weakness or fatigue; dizziness or light-headedness; insomnia. AMS is often described as similar to a “bad hangover” or “bad flu”–like illness.
High-Altitude Cerebral Edema HACE is a neurological syndrome that represents the end stage of AMS and is potentially fatal. The diagnosis of HACE is clinical, and in the presence of AMS, any person exhibiting change in mental status or ataxia during an ascent of altitude is diagnostic of HACE. HACE can run a rapid fulminate course, with death from brain herniation occurring as early as within 12 hours of onset. Although HACE has occurred at elevations of as low as 2590 m (8500 feet) it is most commonly seen at elevations greater than 3658 m (12,000 feet), and the incidence reportedly increases with elevation by 0.01%–31%. The typical onset for HACE is approximately 5 days after arrival at a new elevation.
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HACE is a clinical diagnosis and is a progression from AMS with typical symptoms and signs seen in patients with cerebral edema. Ataxia may begin as a swaying of the upper body, particularly when walking, and progressing to include an ataxic gait. The individual may appear to be “intoxicated.” Behavior and mental status changes may also develop to include extreme lassitude, confusion, disorientation, drowsiness, impaired mentation, obtundation, and coma. Also, symptoms and signs of cerebral edema may be observed to include papilledema, cranial nerve deficits, hearing and speech abnormalities, abnormal limb tone and/or reflexes, and urinary retention and incontinence. HAPE (see below) often coexists with HACE, and hypoxia and cyanosis may also be observed.
High-Altitude Pulmonary Edema HAPE is the most lethal high-altitude illness and has been reported in 0.1% of tourists and as many as 15.5% of climbers involved in a rapid ascent. HAPE is also seen in approximately 5%–10% of climbers with AMS. Although HAPE has a high mortality if untreated, with appropriate descent and therapy it can be just as easily reversed. HAPE typically occurs 2–3 days and rarely after 4 days after arrival at a new altitude and particularly occurs at night, possibly due to the desaturations that occur with periodic breathing at altitude. HAPE is most typically seen at elevations over 2440 m (8000 feet) and is more common in children and younger adults than other populations. HAPE is a noncardiogenic pulmonary edema caused by a breakdown in the alveolar/vascular lining and leak of fluid into the alveoli resulting from markedly elevated pulmonary arterial pressures. Therefore, treatment is aimed at reducing pulmonary artery pressures, improving oxygenation, and increasing fluid removal from the alveoli. Initial symptoms of HAPE are a dry cough, chest tightness, decreased exercise tolerance, and dyspnea at rest (Box 6-2). Anyone with dyspnea at rest and a cough should be considered to have the onset of HAPE and should be treated as such. On examination, one may also note tachypnea, tachycardia, crackles, and a relative cyanosis or decreased oxygen saturation compared with other healthy team members. As HAPE progresses, dyspnea at rest worsens; the cough increases and becomes frothy and later may become blood tinged. With lung auscultation, rales and wheezing develop initially in the right axilla and may progress to being diffuse and audible, possibly without the use of a stethoscope. The person can then become progressively more hypoxic and cyanotic. Mental status can worsen with increasing hypoxemia, ranging from initial anxiety to possible obtundation and even coma. Low-grade fever is not uncommon because HAPE induces an inflammatory response in the lungs.
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Box 6-2 Signs and Symptoms of High-Altitude Illness Acute Mountain Sickness (AMS) Headache and one of the following: Dizziness or light-headedness Insomnia Weakness or fatigue Gastrointestinal symptoms (nausea, vomiting, or anorexia) High-Altitude Cerebral Edema (HACE) Ataxia and mental status changes without AMS or AMS and one of the following: Ataxia Mental status changes High-Altitude Pulmonary Edema (HAPE) At least two of the following signs: Tachycardia Crackles or wheeze in a lung field Central cyanosis Tachypnea and At least two of the following symptoms: Chest tightness or congestion Weakness or decrease in exertion ability Cough Dyspnea at rest
EXAMINATION AND LABORATORY FINDINGS For high-altitude illness, there are no typical examination or laboratory findings. Laboratory workup may be necessary if other diagnoses are suspected or need to be ruled out. An arterial blood gas analysis may need to be obtained for persons with hypoxia or for those suspected of having HAPE. Unless indicated clinically or because of underlying disease processes, routine laboratory tests are generally unnecessary.
DIAGNOSIS The diagnoses for all the high-altitude illnesses are based on clinical findings as described in Box 6-2. For AMS, if symptoms occur after 72 hours at high altitude or persist despite treatment, another diagnosis must be considered. The differential diagnosis of AMS includes HACE, subarachnoid hemorrhage, substance abuse, carbon monoxide poisoning, gastroenteritis, dehydration, exhaustion, and viral syndrome, to name a few.
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With HACE, any rapid onset of neurological symptoms, associated trauma or fever, or continued neurological symptoms despite therapy or ascent arrest should raise concern for the possibility of another diagnosis. The differential diagnosis of HACE is very broad and often requires extensive laboratory and radiographic testing. Carbon monoxide poisoning, cerebral vascular accident, metabolic disorder, toxic ingestion, migraine headache, and seizure disorder are some of the diseases that may mimic HACE. Finally, other diagnosis should be entertained besides HAPE, especially if signs or symptoms of pulmonary distress occur after 4 days at high altitude or if the signs and symptoms persist or worsen despite descent or proper therapy.
RADIOGRAPHS Radiographic testing should be guided by clinical findings. All persons who present with pulmonary symptoms or hypoxia should undergo a chest radiograph. The typical finding for HAPE on a chest radiograph is a noncardiogenic pulmonary edema pattern. The radiograph will have patchy infiltrates without Kerley’s B lines or cardiomegaly. For persons who are suspected of having HACE or who are exhibiting signs or symptoms of increased intracranial pressure, a head computed tomography (CT) scan should be performed. However, a T2-weighted magnetic resonance imaging (MRI) scan is most specific for detecting cerebral edema.
TREATMENT Acute Mountain Sickness Although the development of AMS does not mandate descent, the person should not progress to a higher altitude at that time, particularly for the sleeping elevation. However, descent of 500–1000 m usually relieves symptoms. If descent is not possible or if patients are presenting with moderate to severe symptoms, medical therapy may be necessary. The majority of cases of AMS can be treated symptomatically. For headaches, aspirin, ibuprofen, and acetaminophen have all been used effectively. Antiemetics are indicated for nausea and emesis. Prochlorperazine has been recommended by some because it is one of the few antiemetic medications that is also a respiratory stimulant. Low-dose oxygen given by nasal cannula and short-duration treatment in a portable hyperbaric chamber can also be used to improve symptoms rapidly. Also, 125–250 mg twice daily of acetazolamide (Diamox), a carbonic anhydrase inhibitor with weak diuretic properties, has been shown to be effective in the treatment of AMS. In sulfa-allergic persons who cannot take acetazolamide, dexamethasone may be used in a dose of 2–4 mg every 6 hours.
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High-Altitude Cerebral Edema Definitive treatment of HACE is immediate descent, and the greater the amount of descent the better the outcome of the patient. Descent of more than 1000 feet is recommended, and descents to altitudes of less than 8000 feet are optimal. Dexamethasone and oxygen are adjunctive treatments that should also be used in conjunction with descent. Oxygen should be administered to all subjects with suspected HACE to maintain saturation above 90% SaO2. Dexamethasone is also recommended and should be administered as an initial 8-mg dose by any available route (e.g., oral, rectal, intravenously, or intramuscularly) followed by 4 mg every 6 hours. In cases in which descent cannot be undertaken for whatever reason, treatment in a portable hyperbaric chamber (e.g., Gamow bag, Chamberlite bag) should be used in addition to the administration of oxygen and dexamethasone. Loop diuretics and osmotic diuretic agents (such as mannitol, urea, and glycerol) have been suggested for use in HACE, but there is little experience with them in this role. Careful attention to blood pressure and cerebral perfusion pressure should be maintained, especially if the patient requires intubation or concomitant treatment for HAPE. Persons who develop HACE should not re-ascend for at least several days after complete resolution of symptoms, and, at a minimum, they should ascend at a much slower rate than previously.
High-Altitude Pulmonary Edema The mainstay for treatment of HAPE is descent. This should be initiated once HAPE is suspected and before the person becomes incapacitated and unable to assist in his or her descent. Descent of 1000 feet is recommended and can be lifesaving. Oxygen should always be administered, if available. Nifedipine is a pulmonary vasodilator that will reduce pulmonary arterial pressure. For HAPE treatment, nifedipine may be administered sublingually in a 10-mg dose, repeated in 10–15 minutes, if required, or orally in a 20-mg dose followed by 30 mg given orally three times daily. Salmeterol has been shown to be effective in reducing the incidence of HAPE. Salmeterol bronchodilates closed airways and increases the effect of alveolar/vascular sodium pumps, which in turn increases fluid clearance from the alveoli. Albuterol has not been similarly studied but may also be efficacious. Positive end-expiratory pressure may also be used to improve gas exchange. Because HAPE does not involve fluid overload, treatment with morphine and loop diuretics is of minimal benefit and in some cases may be harmful. As such, these medications are currently not recommended for use in HAPE treatment. Finally, if for some reason descent is impossible,
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treatment in a portable hyperbaric chamber, in addition to the previous adjuncts, is recommended.
OTHER ALTITUDE-RELATED ILLNESS High-Altitude Pharyngitis and Bronchitis High-altitude pharyngitis and bronchitis are common conditions that occur frequently in persons spending a prolonged time at high altitude. This combination typically occurs after 2–3 weeks at high altitude and is due to prolonged environmental exposure to cold, dry air, dehydration, or rapid ventilation rather than to any actual effect of high altitude. Symptoms consist of sore throat and chronic, predominantly dry cough. There is not typically an infectious component. This condition is differentiated from HAPE by the historical feature of occurrence after a prolonged time at high altitude as well as by the lack of dyspnea at rest, which is present in HAPE. Treatment is symptomatic, with lozenges, decongestant nasal sprays, and, if coughing spasms are severe, a cough suppressant. Albuterol can be helpful in selected cases. Breathing through a porous mask or balaclava can also be helpful.
High-Altitude Peripheral Edema High-altitude peripheral edema is altitude-related edema of the hands and face. It is not specifically related to the AMS–HACE spectrum of illness but can be seen with all forms of AMS. It tends to be recurrent on repeated high-altitude exposure and is more common in women. Although treatment is not typically required, diuretic agents may be administered.
High-Altitude Retinopathy A common condition related to hypoxia, high-altitude retinopathy typically occurs at altitudes above 12,000 feet. Funduscopic examination reveals areas of retinal hemorrhage, dilation of retinal veins, disk hyperemia, and retinal edema. Unless a hemorrhagic area falls on the central ocular axis, this condition is usually asymptomatic. There is no specific treatment, and the condition resolves several weeks after descent.
Ultraviolet Keratitis Ultraviolet keratitis is an altitude-related condition often referred to as snow blindness. Ultraviolet light may burn the cornea more easily at high altitudes and usually causes pain, photophobia, tearing chemosis, and
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foreign body sensation. Symptoms typically occur between 1 and 6 hours after exposure and usually resolve spontaneously. Sunglasses or polarizing lenses may help reduce the risk. Treatment of ultraviolet keratitis involves cold compress, oral analgesics, and possibly patching for comfort.
Sleep Disorders Insomnia and sleep disorders are common at high altitudes; CheyneStokes respirations are seen in almost all persons. The associated apneic periods cause both broken sleep as well as potentiate the development of AMS and pulmonary edema. Sleep aids should be used with extreme caution, if at all. Acetazolamide has been shown to improve sleep and decrease the length of apneic episodes during periodic breathing. If medication is required for sleep, zolpidem is the agent of choice because it does not suppress respiration.
SUMMARY High-altitude illness is a disease process that spans a spectrum from the discomfort of AMS to the life-threatening conditions of HAPE and HACE. In all cases, high-altitude illness results from ascending to an altitude too quickly for the human body to acclimatize. All forms of high-altitude illness improve with expeditious descent, but this is only mandatory for HAPE and HACE. It is important as an emergency medical provider to be familiar with the pathophysiology, recognition, evaluation, and treatment of altitude-related medical conditions.
Bibliography Bartsch P: High altitude pulmonary edema, Med Sci Sports Exerc 1999;31(1 Suppl): S23–S27. Bezruchka S: High altitude medicine, Med Clin North Am 1992;76:1481–1497. Gallagher SA, Hackett PH: High-altitude illness, Emerg Med Clin North Am 2004;22(2): 329–355viii. Gertsch JH, Seto TB, Mor J, Onopa J: Ginkgo biloba for the prevention of severe acute mountain sickness (AMS) starting one day before rapid ascent, High Alt Med Biol 2002;3(1):29–37. Grissom CK, Roach RC, Sarnquist FH, Hackett PH: Acetazolamide in the treatment of acute mountain sickness: Clinical efficacy and effect on gas exchange, Ann Intern Med 1992;116(6):461–465. Hackett PH, Oelz O: The Lake Louise consensus on the definition and quantification of altitude illness. In Sutton JR, Coates G, Houston CS (eds): Advances in the Biosciences— Hypoxia and Mountain Medicine, Oxford Press: New York, 1992, pp 327–330. Hackett PH, Roach RC: High altitude cerebral edema, High Altitude Med Biol 2004; 5(2):136–146. Hackett PH, Roach RC: High-altitude illness, N Engl J Med 2001;345(2):107–114.
192 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Harris MD, Terrio J, Miser WF, Yetter JF: High-altitude medicine, Am Fam Physician 1998;57(8):1907–1914, 1924–1926. Honigman B, Theis MK, Koziol-McLain J, et al: Acute mountain sickness in a general tourist population at moderate altitudes, Ann Intern Med 1993;118(8):587–592. Hou S, Lin A, Wang T: Clinical aspects of high-altitude illness, Ann Disaster Med 2004; 2(2 Suppl):S53–S60. Keller HR, Maggiorini M, Bärtsch P, Oelz O: Simulated descent v dexamethasone in treatment of acute mountain sickness: A randomised trial, BMJ 1995;310(6989):1232–1235. Maggiorini M, Buhler B, Walter M, Oelz O: Prevalence of acute mountain sickness in the Swiss Alps, BMJ 1990;301(6756):853–855. Montgomery AB, Mills J, Luce JM: Incidence of acute mountain sickness at intermediate altitude, JAMA 1989;261(5):732–734. Roach RC, Bartsch P, Oelz O, Hackett P: Lake Louise AMS Scoring Consensus Committee: The Lake Louise acute mountain sickness scoring system. In Sutton JR, Houston CS, Coates G (eds): Hypoxia and Molecular Medicine, Charles S. Houston: Burlington, VT, 1993, pp 272–274. Sartori C, Allemann Y, Duplain H, et al: Salmeterol for the prevention of high-altitude pulmonary edema, N Engl J Med 2002;346(21):1631–1636. Sophocles AM: High-altitude pulmonary edema in Vail, Colorado, 1975–1982, West J Med 1986;144(5):569–573.
Thermal Burns GERALD DEPOLD
CPT Code: Burns 949.0 (See specific site and percentage of burn)
Key Points Assess the ABCs, initiate fluid resuscitation, calculate total body surface area (TBSA) burned, and identify airway injuries and all associated injuries. Early referral to a burn center is essential to treatment. ! Emergency Actions ! Follow Advanced Burn Life Support guidelines for the initial evaluation. Pay particular attention to stopping the burning process, addressing airway injuries, providing fluid resuscitation, and preventing infection. Once the patient’s condition has stabilized, evaluate the type, location, and extent (TBSA) of the burn and identify any associated injuries and medical comorbidity. Make a decision on whether to refer to a burn center as early as possible.
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DEFINITION A burn is an injury caused by heat, chemicals, electricity, or radiation. This chapter will focus on thermal injuries.
EPIDEMIOLOGY More than 500,000 burns are treated in the United States each year, of which 4000 are fatal. Most deaths due to burns occur before the patient reaches the hospital. Over half of all patients who are hospitalized for burns are admitted to a burn center; 86% of burns are thermal, and 43% of burns occur in the home.
CLINICAL PRESENTATION Patient presentation will vary according to the type and depth of the burn and associated injuries. First-degree burns are painful, superficial injuries involving the epidermis. Second-degree (partial-thickness) burns extend down to the dermis and are associated with blistering. These burns can be further classified as superficial or deep. Third-degree (full-thickness) burns are painless injuries that extend through the dermis.
EXAMINATION Airway injury from smoke inhalation, a major contributor to fire-related deaths, must be considered in all patients with burns. Singed nasal hairs, difficulty swallowing, carbonaceous sputum, chest pain, and shortness of breath are suggestive of airway injury. Stridor is indicative of upper airway injury; laryngoscopy should be used to examine for edema and soot. Wheezes and crackles suggest lower airway involvement. The Rule of Nines is the most common tool used to assess the extent of burn injuries in adults. Infants require a modified formula due to their large head and trunk (Fig. 6-1). The American Burn Association classifies burns as major, moderate, or minor. Major burns are defined as follows: (1) partial-thickness burns greater than 25% BSA in the 10- to 50-year-old age group, (2) partial-thickness burns greater than 20% BSA in children younger than 10 years or adults older than 50 years, (3) full-thickness burns of greater than 10% BSA in anyone, (4) burns involving the hands, face, feet, or perineum, (5) burns crossing major joints, (6) circumferential burns of an extremity, (7) burns complicated by an inhalation injury, (8) electrical burns, (9) burns complicated by fractures or other trauma, (10) burns in infants and elderly persons, or (11) burns in at-risk patients. Any circumferential burns of
194 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER 9%
9%
18%
18% 9%
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1% 18% 18%
18% 18%
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Head and neck 21% Abdomen or Back 13% Genital area 1%
Each arm 10% Buttocks 5% Each leg 13.5%
Figure 6-1. Rule of Nines for adults and infants. The Rule of Nines is the most commonly used tool in the assessment of the extent of burn injuries in adults. Infants require a modified formulate due to their large heads and trunks.
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the limbs or chest may affect distal circulation or breathing. These burns should be evaluated for immediate escharotomy. Moderate burns are defined as follows: (1) partial-thickness burns of 15%–25% BSA in the 10- to 50-year old age group, (2) partial-thickness burns of 10%–20% BSA in children younger than 10 years or adults older than 50 years, (3) full-thickness burns of the hands, face, feet, or perineum or circumferential burns of an extremity are excluded. Minor burns include the following: (1) partial-thickness burns of less than 15% BSA in the 10- to 50-year-old age group, (2) partial-thickness burns of less than 10% BSA in children younger than 10 years or adults older than 50 years, (3) full-thickness burns of less than 2% BSA in anyone, with associated injuries. Note any circumferential burns of the limbs and chest that may affect distal circulation or breathing. An injury that appears to be second degree can later convert to a third-degree burn, making diagnosis, treatment, and referral decisions complicated. Always seek the opinion of a provider experienced with burn evaluation when formulating your treatment plan. Perform a full secondary survey to identify any other injuries.
LABORATORY FINDINGS Baseline laboratory tests include a complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, glucose, prothrombin time and partial thromboplastin time (PT/PTT), and hepatic enzymes. Respiratory status is monitored with pulse oximetry, arterial blood gas analysis, and peak flow measurements. A carboxyhemoglobin sample is drawn in cases of suspected smoke-inhalation injuries. Plasma lactate levels are elevated with cyanide toxicity from burning acrylics. Myoglobin and creatine kinase levels are elevated with rhabdomyolysis. Elderly patients require an electrocardiogram (ECG).
DIAGNOSIS The diagnosis of burn injuries is based on clinical presentation and examination. The type of burn, depth of the burn, and percentage of the burn area will direct care.
RADIOGRAPHS Radiographs may be required to assess associated injuries. CT scan of the head, chest, and abdomen are recommended. Initial chest radiographs may be normal despite airway burns and should be performed to confirm endotracheal tube placement. Chest x-ray should be repeated serially to rule out adult respiratory distress syndrome in the first 24–48 hours.
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TREATMENT ABCs, fluid resuscitation, and accurate burn assessment are the basic strategy for burn patient care. The provider should give 100% oxygen to all patients and be ready to intubate, if necessary. Consider tracheostomy if mechanical ventilation may be required. Suspect cyanide poisoning in patients who do not respond to oxygen therapy. Start two large-bore IVs with lactated Ringer’s solution and titrate according to the Parkland formula (Box 6-3). Remember, the first 24 hours starts when the patient was burned, not when he or she arrived at the hospital. The Parkland formula does not guarantee adequate fluid resuscitation. Use urine output (0.5–1 ml/kg/hr), vital signs, mental status, base deficit, and gastric tonometry as tools for perfusion endpoint monitoring. Excessive fluid administration may cause intra-abdominal hypertension and abdominal compartment syndrome. Reduce the incidence of infection with careful glucose monitoring and regulation with insulin, and pay careful attention to aseptic technique with all invasive precautions. Use gown and gloves with all direct patient contact. Cool burns to limit burn depth and inflammation without inducing hypothermia. Titer intravenous analgesics according to patient pain levels. Administer appropriate tetanus prophylaxis. Escharotomy may be required with circumferential burns. Consult a surgeon for wound excision. Minor burns are treated on an outpatient basis with wound debridement and topical antibiotics. Research has shown that povidone iodine/neomycin/polymyxin/bacitracin and silver sulfadiazine/cerium nitrate combinations are better than silver sulfadiazine alone. All other burns should be covered with a sterile drape pending referral to a burn center (Box 6-4).
Box 6-3 Parkland Formula
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Box 6-4 Burn Unit Referral Criteria
From American Burn Association; www.ameriburn.org.
Bibliography Ahrns KS: Trends in burn resuscitation: Shifting the focus from fluids to adequate endpoint monitoring, edema control, and adjuvant therapies, Crit Care Nurs Clin North Am 2004;16:75–98. American Burn Association: Burn Incidence and Treatment in the US: 2007 Fact Sheet. Available at: http://www.ameriburn.org/resources_factsheet.php. Accessed on March 28, 2007. Appelgren P, Bjornhagen V, Bragderyd K, et al: A prospective study of infections in burn patients, Burns 2002;28:39–46. Muehlberger T, Kuner D, Munster A: Efficacy of fibreoptic laryngoscopy in the diagnosis of inhalation injuries, Arch Otolaryngol Head Neck Surg 1998;124:1003–1007. Rabanowitz PM, Siegel MD: Acute inhalation injury, Clin Chest Med 2002;23(4):707–715. Saffle JR: What’s new in general surgery: Burns and metabolism, J Am Coll Surg 2003; 196(2):267–289. Span CT, Taylor SC, Weinberg JM: Topical antimicrobial agents in dermatology, Clin Dermatol 2003;21:70–77. Work Loss Data Institute: In Burns. Work Loss Data Institute: Corpus Christi, TX, 2004, p 48.
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Chemical Burns DAVID A. HNATOW
CPT Code: Burns (Chemical) 940-949
Key Points Chemical burns are divided primarily into two groups: acid and alkali. As with most environmental or toxicological exposures, knowing the specifics of the offending agent is key. Although a careful physical examination is important, a thorough history identifying the offending agent usually determines how a patient should be treated. Appropriate evaluation requires knowledge of the offending agent, type of exposure, duration of exposure, and other events or injuries associated with the burn.Chemical burns are treated similarly to thermal burns and require consultation with a burn specialist. ! Emergency Actions ! Appropriate evaluation requires a complete assessment of the offending agent (i.e., composition, acid or alkali, concentration), type of exposure (e.g., inhalation, cutaneous, ocular, gastrointestinal [GI]), and duration of exposure. Knowledge of other events or injuries associated with the burn (e.g., explosion, fall, trauma) are also crucial.
Airway Patients with oral or inhalation injury may experience significant edema or difficulty maintaining their airway and often require intubation. Particular attention should be paid to the presence of drooling, stridor, hoarseness, and oral swelling.
Breathing Respiratory symptoms may range from discomfort and mild wheezing to respiratory failure. Patients may develop wheezing and labored breathing as a result of an inhalation exposure. If the condition progresses to respiratory failure, artificial ventilation would be required.
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Circulation Assess circulation for appropriate heart rate and end-organ perfusion. Attention should be paid to the patient’s body temperature. As in the case of many environmental injuries, patients with chemical burn may be at risk for becoming hypothermic, with associated increased morbidity and mortality. Hydrotherapy is the cornerstone of initial treatment for chemical burns with few exceptions. Preventing further injury is also important. Wet or contaminated clothing should be removed as soon as possible, and the patient should be kept warm and dry.
DEFINITION Most chemicals that cause burns are either strong acids or strong bases. Acids produce coagulation necrosis by denaturing proteins upon tissue contact. An area of coagulation is formed and limits extension of injury. An exception is hydrofluoric acid, which produces a liquefaction necrosis similar to alkalis. Alkalis cause a liquefaction necrosis, which is potentially much more dangerous than acid burns. Alkali agents liquefy tissue by denaturation of proteins and saponification of fats. In contrast to acids, whose tissue penetration is limited by the formation of a coagulum, alkalis can continue to penetrate very deeply into tissue. Because not all chemicals causing burns can be considered acid or alkali, a useful classification from C. Jelenko groups chemicals into six types according to the manner in which they damage protein (Box 6-5).
EPIDEMIOLOGY In the United States, approximately 25,000–100,000 chemical burns are reported every year. Chemical burns can occur in the home, at school, on the farm, in laboratories, or in the workplace. Most chemical burns
Box 6-5 Six Types of Chemical Burns Vesicants produce blisters. Reducing agents cause the binding of free electrons in tissue protein. Corrosives cause protein denaturation, causing eschars and indolent ulcers. Oxidizing agents cause damage when the agent comes in contact with the skin, and often a toxic moiety is released. 5. Desiccants cause cellular dehydration and thermal injuries by an exothermic reaction. 6. Protoplasmic poisons cause protein denaturation by salt formation or by metabolic competition or inhibition.
1. 2. 3. 4.
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occur on the face, eyes, arms, and legs. Usually a chemical burn will be relatively small and will require only outpatient treatment. However, chemical burns can be deceiving, causing deep tissue damage not readily apparent. In the United States, approximately 40% of all occupational injuries involve the skin, 25% of which are chemical burns. Chemical burns result in approximately 20 deaths per year, with a mortality rate of less than 1%. Children and adults have similar exposure rates, but younger children tend to be exposed accidentally because of inadequate childproofing. Young adults may be exposed because of impetuous behavior or experimentation. More than 30,000 products sold in the United States can cause chemical burns. In addition to the occupational hazards associated with industrialstrength product use in the workplace, a plethora of products are available and used by the general public. Some of the more common chemical burns are caused by hair dye and hair-treatment products.
CLINICAL PRESENTATION Symptoms present immediately after a chemical burn injury may include pain, burning, numbness of the affected area, confusion, and shortness of breath. Patients may report pain or swelling of the mouth or eyes, along with visual changes. In addition to determining the offending substance, the provider should determine the location of the exposure (e.g., cutaneous, oral, GI, ocular, or inhalation), the time and duration of the exposure, decontamination or lifesaving measures provided at the scene, and other possible injuries resulting from a fall, explosion, or fire. It is not enough to rely solely on patient history. To determine the offending substance, the provider should obtain the substance’s container, call the manufacturer, use a computerized poison index, and/or call a regional poison control center. It should be determined whether the substance is acid, alkali, or chemical in composition, and the concentration should be ascertained. Absorption of an agent is determined by the area of the body that is exposed, the integrity of the skin, the nature of the chemical agent, and the presence of garments. There is a higher absorption rate for agents that are highly lipid soluble and have a high pH.
EXAMINATION A careful physical examination is important. Patients need to be completely undressed for a thorough examination to be performed. The presence, size, and depth of cutaneous burns should be sought and documented. Depths of burn classifications are superficial partial thickness,
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deep partial thickness, and full thickness. Depth determination involves describing the affected area’s color, texture, and sensation. A superficial burn is a first-degree burn. Patients with this type of injury present with pruritus, burning, and pain. Redness without change in texture or sensation is seen. A deeper partial-thickness burn is a second-degree burn. The patient will have blister formation with or without denuding and pink to mildly pale tissue with intact sensation. In a full-thickness or third-degree burn, affected areas are white, leathery, and insensate. Determining extent of involvement requires an estimate of the affected body surface area (BSA). BSA can be estimated by using a standard chart with the Rule of Nines. However, the Lund and Browder chart provides a more accurate estimate in children. Most small injuries can be approximated using the size of the patient’s palm. The entire palm, including the fingers, represents approximately 1% of TBSA. Appropriate evaluation also requires a complete assessment of other injuries associated with the burn.
LABORATORY FINDINGS In the case of mild burns, no laboratory studies are indicated for most patients. Severe burns, basic screening with a CBC, electrolytes, creatine phosphokinase (CPK), and coagulation studies should be considered. In the case of hydrofluoric or oxalic acid burns, screening levels of calcium, magnesium, and phosphorus may be useful. However, the degree to which these levels contribute to treatment is uncertain.
DIAGNOSIS A diagnosis of chemical burn is made by determining the following: 1. 2. 3. 4. 5. 6.
The The The The The The
mechanism of action—acid or alkali manner of contact with the agent concentration of the agent involved quantity of the agent involved duration of contact with the agent extent of penetration by the agent
Direct visualization (endoscopy) of the posterior pharynx, airway, esophagus, and upper GI tract is the method of choice for evaluation of injury.
RADIOGRAPHS Chest radiography is indicated for patients with inhalation injury or respiratory distress. When evaluating for perforation of the upper GI tract,
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direct visualization with endoscopy is preferred, although abdominal CT with oral and intravenous contrast is also very useful.
TREATMENT Medical care begins with removal of the patient from the source of the injury. All products should be handled as potentially hazardous material. Decontamination should be provided at the scene of contact to avoid spreading the material to the transport vehicles and ED. Preventing further injury is also important. Wet or contaminated clothing should be removed as soon as possible, and the patient should be kept warm and dry. Hydrotherapy is the cornerstone of initial treatment for chemical burns with few exceptions. Any burn, whether acid or alkali, should be irrigated immediately with copious amounts of water. This irrigation should continue for a minimum of 30 minutes. Dilution is the solution to decontamination. Attempts should never be made to neutralize the offending agent because it may result in an exothermic reaction that could worsen the burn or cause explosion. If the chemical is dry, the healthcare provider should brush off as much as possible before applying irrigation. Exceptions to these rules are sodium metals or related compounds, which should be covered with mineral oil or excised as soon as possible. Water can cause a severe exothermic reaction. Water on phenol (carbolic acid) can enhance penetration, thus treatment should include phenol with a 2:1 combination of polyethylene glycol 300 (PEG 300) and industrial methylated spirits (IMS). This should not only reduce the extent of cutaneous corrosion but also decrease systemic toxicity. Affected eyes should be rinsed with copious amounts of isotonic saline. A specialized ocular irrigation cup or Morgan lens may be used. The pH of the eye should be checked after each 30 minutes of irrigation and continued until the pH has normalized (i.e., pH, 7–8). Alkali burns can be disastrous to the eye. The higher the pH, the more damage can occur. Alkali can penetrate the cornea, anterior chamber, and retina. Patients with oral or inhalational exposures should have continuous pulse oximetry monitoring and receive supplemental oxygen as indicated. Patients with inhalation injuries may experience acute bronchospasm and wheezing, for which beta-agonist bronchodilators are indicated. Patients sustaining chemical burns require the same aggressive fluid replacement as those with thermal burns to maintain adequate perfusion to the tissues. External warming devices should be used early in the course of care, if indicated, because hypothermia has particularly deleterious effects on persons who have been burned. Burns are considered tetanus prone, and all patients should be immunized. Wounds should be cleaned and bandaged with medicated creams and sterile wraps, as needed. Antibiotic creams such as silver sulfadiazine can be used for covering
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cutaneous parts of the body, with the exception of the face. Bacitracin ointment can be used on the face. Prophylactic oral antibiotics are not indicated. Chemical burns are treated similarly to thermal burns and require consultation with a burn specialist. The practitioner should consider transferring patients with burns involving the hand, face, eye, or genitals to a burn unit. Patients with severe burns (i.e., full thickness or >30% BSA) should be transferred once their conditions have stabilized. A regional poison control center should always be consulted to determine the offending substance. All but the most trivial of ocular injuries require consultation with an ophthalmologist. Strong alkali substances have the worse prognosis, particularly with ocular exposures. Prognosis depends on the extent of injury and the nature of the exposure. The usual patient with limited injury has a favorable prognosis if care is provided promptly.
SPECIAL SITUATIONS Phenol (carbolic acid) is a corrosive organic acid used in medicine and in industry that can cause chemical burns. Phenol burns cause coagulation necrosis and can become trapped under the eschar. The main treatment is copious irrigation with PEG 300 and IMS in a 2:1 concentration. Isopropyl alcohol can also be used to decontaminate phenol instead of a mixture of PEG and IMS. Hydrofluoric acid is used in fire-proofing material, high-octane fuels, frosting and etching glass, microelectronics, microinstruments, and the semiconductor industry. It is a protoplasmic poison that causes progressive tissue loss, including bone destruction. Hydrofluoric acid penetrates the skin, dissociates, and causes the release of fluoride ions. Fluoride ions cause the immobilization of intracellular magnesium and calcium and can poison the cellular enzyme reactions. Fluoride ions also cause the spontaneous depolarization of nerve tissue, causing pain as a result of the increased permeability of potassium. A patient who has been exposed to hydrofluoric acid presents with both systemic and localized reactions. Hypomagnesemia, hypocalcemia, and hyperkalemia are hallmarks of hydrofluoric acid poisoning. The stronger the solution, the faster symptoms will occur. For solutions of less than 20%, it might take 12–24 hours before symptoms occur. Treatment of hydrofluoric acid poisoning consists of two phases. The first phase is immediate treatment of the contaminated area with copious irrigation with water for 30 minutes. The second phase is the detoxification stage, which can be achieved by giving the patient calcium gluconate by subcutaneous or intradermal injection, topical application, or intra-arterial infusion. Calcium gluconate can be applied to the area after it is mixed with
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Surgilube lubricating jelly or dimethyl sulfoxide (DMSO). This gel mixture will cause binding of hydrofluoric acid to the gel. The drawback to this therapy is that calcium is not very permeable in the skin. Subcutaneous or intradermal injection of a 10% calcium gluconate solution through a 30-gauge needle into the affected area of skin is the best treatment. The maximum dose of 0.5 ml/cm2 of skin is recommended for treatment. After the administration of calcium, pain is almost immediately abated. Extinction of pain is a good guide to the correct amount of calcium therapy. Intra-arterial infusion of calcium gluconate can be used to prevent tissue necrosis and to stop pain in large burns caused by hydrofluoric acid. This treatment must be performed with an intra-arterial catheter in the appropriate vascular supply of the burned extremity and with a threeway stopcock that is attached to arterial pressure monitoring device. Ten milliliters of a 10% calcium gluconate solution in 40 ml of 5% dextrose should be infused over 2–4 hours.
Bibliography Bertolini JC: Hydrofluoric acid: A review of toxicity, J Emerg Med 1992;10:163. Broto J, Asensio M, Jorro CS, et al: Conservative treatment of caustic esophageal injuries in children: 20 years of experience, Pediatr Surg Int 1999;15:323. Buntain WL, Cain WC: Caustic injuries to the esophagus: a pediatric overview, South Med J 1981;74:590. Dalton ML Jr, Bricker DL: Anhydrous ammonia burn of the respiratory tract, Tex Med 1978;74:51. Friedman EM, Lovejoy FH Jr: The emergency management of caustic ingestions, Emerg Clin North Am 1984;2:77. Heimback DM, Waeckerle JF: Inhalation injuries, Ann Emerg Med 1988;17:1316. Herr RD, White GL Jr, Bernhisel K, et al: Clinical comparison of ocular irrigation fluids following chemical injury, Am J Emerg Med 1991;9:228. Jelenko C: Chemicals that “burn,” J Trauma 1974;14:65. Vance MV, Curry SC, Kundel DB, et al: Digital hydrofluoric acid burns: Treatment with intraarterial calcium infusion, Ann Emerg Med 1986;15:890.
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Diving Injuries CAPTAIN SEAN MICHAEL SILER
ICD/CPT Codes: Carbon monoxide poisoning 986, Decompression sickness 993.3, Arterial gas embolism 958.0, 999.1, Physician attendance or supervision of hyperbaric oxygen therapy 991.83
Key Points Diagnoses of most diving injuries are clinically based. Physical examination will often reveal subtle findings suggestive of multisystem involvement. Historical elements are important in diagnosing dive injuries. ! Emergency Actions ! The first point of action is to secure and maintain an airway. Adequate ventilation should be established with supplemental oxygen. Arrhythmias or shock should be treated. Cervical spine immobilization is appropriate when trauma is suspected, rapid transport to a recompression chamber should be ensured.
DEFINITION There are several disorders that encompass the majority of injuries encountered by divers. Initial presentation of diving injuries can vary widely, depending on the severity and speed of symptom onset. Barotrauma refers to the microtrauma caused while a person is ascending or descending underwater by both environmental pressure differences and expanding or contracting gases. Decompression sickness (DCS) is a multisystem disorder that results from the formation of inert gas bubbles in supersaturated liquids and tissues in response to rapidly declining partial pressures. Arterial gas embolism is a result of pulmonary overinflation and alveolar rupture, which allows the introduction of gas bubbles into the pulmonary capillary bed and subsequently leads to systemic arterial circulation. Nitrogen narcosis is the anesthetic effect observed when a person breathes higher than normal partial pressures of nitrogen at depth. Oxygen toxicity is observed when a person breathes higher than normal concentrations of oxygen at depth.
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EPIDEMIOLOGY There are between 3 and 5 million registered divers, with as many as 900,000 new divers trained each year worldwide. Between 10 and 37 injuries or deaths occur for every 10,000 dives. Most accidents are a result either of equipment malfunctions or diver inexperience.
CLINICAL PRESENTATION As divers descend, all gases in the body are compressed and ambient pressure in any enclosed space increases. The body is usually able to equalize pressures between the environment and these spaces, but when an obstruction occurs, pressures can elevate to the point of tissue injury. The same equilibration happens on ascent, and any trapped gas from depth will exponentially expand as the ambient pressure decreases toward the surface. These expansion and contraction forces cause localized tissue trauma, vascular engorgement, edema, and hemorrhage.
BAROTRAUMA Pulmonary overpressurization syndrome (POPS) occurs when a diver takes a breath of compressed air at a given depth and then ascends without allowing the expanding gases to exit the lungs. The result is microalveolar trauma and dissection of gas into surrounding tissue. The degree of injury is dependent on both the amount of dissected gas and the depth at which it occurred. The changes in pressure closer to the surface are much larger than those at deeper depths, thus the closer to the surface the diver is, the higher the risk of POPS. An unconscious diver is unable to exhale on ascent, and providers should have a high index of suspicion for POPS. These patients are at higher risk for a pneumothorax. This will present as it usually does, with decreased or absent breath sounds on the affected side. With barotrauma from an uncontrolled ascent, patients can develop bilateral pneumothoraces, which can be mistaken for soft breath sounds in a loud environment. Any degree of hypotension or desaturation should raise the possibility of a tension pneumothorax. Divers with POPS may also present with hoarseness, substernal chest pain, and neck fullness. On examination, there may be subcutaneous emphysema or mediastinal emphysema visible on chest radiography. Aural barotrauma can present as an external ear squeeze or barotitis externa. When cerumen, earplugs, or a diving hood obstructs the external auditory canal, water cannot enter and balance the tympanic membrane pressure from the middle ear. The result is ear pain and tympanic membrane rupture. Examination findings include perforation, hemorrhage, petechiae, or blood-filled blebs in the ear canal.
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Barotitis media results from the failure to equalize pressures in the middle ear. This is usually caused by eustachian tube dysfunction and will present with pain, decreased hearing from tympanic membrane rupture, and hemorrhage. Inner ear barotrauma presents with vertigo, tinnitus, and hearing loss. These symptoms represent damage to the cochleovestibular system from acute pressure changes and often are permanently disabling. Other signs and symptoms include nausea, vomiting, nystagmus, and ataxia. Alternobaric vertigo is the inability to equalize middle ear pressures during ascent, usually due to eustachian tube dysfunction. It is usually unilateral and induces transient vertigo, nausea, and vomiting, all of which are self-limiting and spontaneously resolve after a few hours. An external ear squeeze usually occurs on descent when a diver is unable to equalize pressures between, most commonly, the inner ear and the sinuses. Alternately, a reverse squeeze is the inability to equalize pressures with the same cavities on ascent. Known as a “tooth squeeze,” barodontalgia occurs when air is trapped either under a tooth or under a recent or damaged filling. It is self-limiting and requires no specific treatment. Aerogastria is commonly reported by inexperienced divers who consume carbonated beverages or heavy meals before a dive. Gas accumulates in the GI tract and expands on ascent. Most divers will experience belching or flatulence, which decompresses the GI tract; however, rarely gases can cause perforations that will present with pain, distention, and fever, appearing as any other bowel perforation.
DECOMPRESSION SICKNESS Henry’s law states that the amount of gas dissolved in a liquid at a given temperature is a function of the partial pressure of the gas in contact with the liquid and the solubility coefficient of the gas in that particular liquid. As a diver is exposed to higher pressures at depth, a greater amount of gas is dissolved into the blood. As the diver returns to the surface, the pressure decreases, and gases diffuse out of tissues and into the blood. When ascent is slow and controlled, the body is able to maintain a balance between the newly diffusing gases and their elimination, mostly through respiration. When ascent is too rapid and the elimination pathways are overwhelmed, dissolved gases reform bubbles in the blood and tissue. The result is mechanical obstruction of vascular and lymphatic vessels and subsequent ischemia and infarction of distal regions. The gas bubbles also are viewed by the immune system as foreign bodies. An immune response triggers the Hageman factor, activating the intrinsic clotting system and complement cascade. This causes platelet activation and clumping, increased vascular permeability, microvascular sludging, and interstitial edema. The end result is decreased tissue perfusion and tissue ischemia.
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Clinical manifestations can present in any organ system or tissue type; however, DCS is commonly described as either musculoskeletal (type I) or neurological (type II). Most patients will become symptomatic within the first hour of surfacing, and 97% will have symptoms within 6 hours. The remaining 1%–2% may not become symptomatic for 24–48 hours after surfacing. DCS type I is commonly known as “the bends.” The signs and symptoms include joint pain or dysesthesia, tenderness to palpation, temporary relief of pain with local pressure from a blood pressure cuff, and worsening pain with movement of the joint. Also included with DCS type I are cutaneous and lymphatic effects, which can present with intense pruritus, skin mottling or hyperemia, or marbled skin (i.e., cutis marmorata). Alternatively, there may be no visible outward signs. DCS type II affects the central nervous system (CNS), with either brain or spinal cord involvement. Symptoms for spinal involvement include back pain, abdominal pain, extremity heaviness or weakness, paralysis or paresthesias, fecal incontinence, or urinary incontinence. Signs include hyperesthesia or hypoesthesia, weakness, and urinary bladder distention or anal sphincter weakness. Lower thoracic and lumbar regions as well as lower extremities are more commonly involved. Brain involvement will present with visual changes, headache, dysphagia, confusion, and altered mental status. Brain involvement can be very difficult to differentiate from arterial gas embolism (AGE). Also included in type II DCS is pulmonary DCS, also known as “the chokes.” This is an uncommon but very serious form of DCS that consists of venous gas emboli causing mechanical obstruction of at least 10% of the pulmonary vascular bed. Patients will have burning substernal chest pain, cyanosis, dyspnea, and cough. Clinically, they may resemble a patient with a pulmonary embolism.
ARTERIAL GAS EMBOLISM AGE is a result of pulmonary overinflation, alveolar rupture, and introduction of gas emboli into the pulmonary capillary circulation. It is often difficult to initially differentiate between DCS and AGE. However, almost all AGE symptoms will develop within 10 minutes of surfacing, whereas DCS often takes longer to present. Any unconscious diver should be presumed to have suffered an AGE until proven otherwise. Seizures, confusion, visual changes, hemiplegia, or paraplegia can occur and appear similar to the signs associated with an acute stroke. Hemoptysis, chest pain, and ECG changes suggestive of coronary ischemia or infarction may also be seen. Peripheral emboli will cause localized pain. An insensitive but very specific sign is the presence of bubbles in the retinal arteries on funduscopic examination, called Liebermeister’s sign.
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NITROGEN NARCOSIS Nitrogen narcosis describes the anesthetic effect of increased nitrogen levels that typically occurs in divers at depths below 70 feet of sea water (fsw). Symptoms include light-headedness, euphoria, and loss of fine motor coordination. At depths of 150 fsw, symptoms progress to intoxication, increasingly worsening judgment, and slowed reflexes. Below 300 fsw, coma may be induced. Patients will usually present as a result of other problems such as an uncontrolled ascent, a blackout, or underwater trauma. Patients with nitrogen narcosis will appear intoxicated, but symptoms will clear rapidly when they return to the surface.
CONTAMINATED GASES Divers can be exposed to toxic levels of gases through contaminated air at depth. Carbon monoxide and oxygen are the most commonly found exposures; however, increased concentrations of carbon dioxide and nitrogen will potentiate their effects at depth. Carbon monoxide exposure will present in the same fashion as non-diving exposure. Oxygen toxicity presents with the mnemonic VENTIDC (i.e., visual symptoms, ear symptoms, nausea, twitching and tingling, irritability, dizziness, and convulsions). Breathing oxygen at partial pressures above 1.6 ATA will induce these symptoms and below 1.4 ATA will rarely be toxic.
EXAMINATION Barotrauma Vestibular and ear-related barotrauma can present with hemotympanum, gross bleeding, vertigo, and pain. Air trapped under poorly filled cavities can cause tooth pain. Pneumothorax from POPS is possible and will appear as any pneumothorax, with decreased breath sounds, dyspnea, and possibly hypotension, hypoxia, and shifting of anatomical structures (i.e., tension pneumothorax). Subcutaneous emphysema may be present, as well as mediastinal emphysema with POPS. Hemoptysis may be present with alveolar hemorrhage, as well as rales and rhonchi. Examination for DCS will manifest itself based on where the gas emboli are lodged. Cutaneous DCS will present with the signs listed previously. Any abnormalities in the neurological examination results should lead the examiner to consider type I DCS. A complete neurological examination consists of muscle strength in all major muscle groups, complete dermatome examination, including two-point discrimination, sharp/dull/ warm and cold differentiation, gait and cerebellar testing, and mental status examination.
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LABORATORY FINDINGS Laboratory testing should be directed toward the presenting signs and symptoms; however, such testing is rarely helpful and often delays transport to or initiating hyperbaric treatment. CT or MRI scanning for neurological problems can be done after hyperbaric treatment.
DIAGNOSIS The diagnoses of most diving injuries are clinically based. Physical examination will often reveal subtle findings suggestive of multisystem involvement. Historical elements are important in diagnosing dive injuries (Box 6-6).
RADIOGRAPHS Most radiographs will not be helpful in patients with DCS or barotrauma. Patients with clinical signs of pneumothorax may show one on chest radiograph; however, these patients should not have treatment delayed in order to obtain one.
TREATMENT All patients with type I and II DCS, AGE, and exposure to contaminated gases must be referred immediately to a hyperbaric treatment facility. Treatment before and during transport should be directed toward stabilization and supportive care. One hundred percent oxygen should be
Box 6-6 Focused Diving History 1. What was the length and depth of the dive (i.e., dive profile)? 2. Was a dive computer used, and did the dive exceed decompression limits? 3. Did the diver perform any other dives in the 48 previous hours? If so, what were the surface intervals, depth, and duration of those dives? 4. Did the diver engage in any air travel since the dive? 5. During the dive, were there any problems equilizing, and did it occur on descent or ascent? 6. Were there any equipment malfunctions on the dive? 7. Are any dive partners feeling ill or having symptoms? 8. Was any alcohol consumed before or after the dive? Was the diver dehydrated? Has the diver engaged in any strenuous work after the dive? 9. Does the diver have a history of previous decompression sickness, asthma or chronic obstructive pulmonary disease, coronary artery disease, patent foramen ovale, or other neurological process?
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provided, if possible, by an aviator-type or fully sealing facemask, and intravenous access should be obtained. Isotonic intravenous fluids should be administered to maintain urine output at 1–2 ml/kg/hr. A urinary catheter may be required if there is urinary retention. Persistent vertigo may be treated with diazepam. If hyperbaric treatment is required and a chamber is not locally available, the Divers Alert Network at Duke University can provide a referral at 1–800–446–2671 or 1–919–684–8111. The Divers Alert Network coordinates a network of decompression chambers around the world and provides 24-hour medical consultation. Ground transport is preferred, but if air transport is required then every effort should be made to minimize the altitude flown, and a pressurized aircraft should be used if possible. AGE is treated similarly to DCS, with the definitive treatment being rapid recompression. One hundred percent oxygen should be provided. Historically, patients with AGE were maintained in the Trendelenburg position. Recent studies have shown that Trendelenburg positioning has no benefit over supine positioning. It is now believed that prolonged Trendelenburg positioning may worsen cerebral edema and hinder patient oxygenation. Steroids have not been shown to decrease cerebral edema. Intravenous access should be obtained and isotonic intravenous fluids should be administered to maintain urine output at 1–2 ml/kg/hr. Uncomplicated lung barotrauma and POPS should be treated with supplemental oxygen, rest, and observation until the patient becomes asymptomatic. Pneumothoraces from POPS should have tube thoracostomy performed. Barotitis externa is treated by removing all ear canal obstructions and administering analgesics and antibiotics, if necessary. Barotitis media requires long-acting decongestants, antihistamines, analgesics, and antibiotics if there is tympanic membrane rupture. Inner ear barotrauma may require diazepam or meclizine for vertigo symptoms. Sinus barotrauma may require antibiotics and topical vasoconstrictors. Barodontalgia is self-limiting and can be treated with analgesics and a routine referral to a dentist.
Bibliography Auerbach PS: Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Jaffee MS: The neurology of aviation, underwater, and space environments, Neurol Clin 2005;23(2):541–552. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Moon RE: Bubbles in the brain: What to do for arterial gas embolism? Crit Care Med 2005;33(4):909. U.S. Navy, Diving Manual, Revision 4 Change A. Naval Sea Systems Command: Washington, DC. January 20, 1999.
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Electrical Injuries JULIE ANN MORGAN
ICD Code: Electrocution 994.8
Key Points High voltage is usually defined as greater than 1000 volts, although there is evidence that the risk for serious and fatal electrical injuries increases significantly with voltages above 600 volts. All electrocutions should initiate a through evaluation, no matter what the voltage of the electrocution was. ! Emergency Actions ! For any patient who has been electrocuted, the practitioner should initiate two large-gauge intravenous lines, begin cardiac monitoring of the patient, perform ECG, provide oxygen, and completely undress the patient. A head-to-toe examination should be preformed, looking for burns and entrance and exit wounds from high-voltage electrocutions.
DEFINITION Electricity is the flow of electrons (i.e., the negatively charged outer particles of an atom) through a conductor. An object that collects electrons becomes negatively charged, and when the electrons flow away from this object through a conductor, they create an electrical current that is measured in amperes. The force that causes the electrons to flow is the voltage, which is measured in volts. Anything that impedes the flow of electrons through a conductor creates resistance, which is measured in ohms. Electrical current can be either continuous in one directions (direct current [DC]) or with periodic reversal in the direction of current flow (alternating current [AC]). AC current is found in the electricity supplied to homes or businesses. The frequency of AC electricity is the number of complete cycles (from positive through negative back to positive) made in 1 second. In the United States, most AC is 60 Hz (cycles per second). Most electronics and many medical devices use DC that is supplied by batteries or power supplies that convert AC supplied from an electrical socket to DC for use in the device.
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High voltage is usually defined as greater than 1000 volts, although there is evidence that the risk for serious and fatal electrical injuries increases significantly with voltages above 600 volts. Power lines in U.S. residential areas are typically 7620 volts, which is stepped down by transformers to 220 volts. Although high voltage is more dangerous, the general population has much greater access to low-voltage sources, and these low-voltage sources account for about half of all electrical injuries and deaths.
EPIDEMIOLOGY Despite significant improvements in product safety, electrical injury is still the cause of many fatalities and of considerable morbidity. Electrical injures are responsible for more than 500 deaths per year in the United States. Three distinct populations are at risk for electrical injury, each accounting for approximately 20%–25% of electrical injuries. These include toddlers who sustain electrical injuries from household electrical sockets and cords, adolescents who engage in risk behavior around electrical power lines, and electrical utility workers, who have an annual death rate from electrical incidences of approximately 1 per 10,000 in the United States.
CLINICAL PRESENTATION The severity of injury depends on the voltage, the amount of current, the type of current (i.e., direct versus alternating), the body’s resistance to the current, the current’s path through the body, and the length of time the current remains in contact with the patient. Symptoms can vary from a tingling sensation from household current to respiratory arrest from thoracic muscle tetany or ventricular fibrillation or asystole. The current pathway will determine the nature of injuries and complications. Skin is the primary resistor to the flow of current into the body. Once surface resistance is overcome, low-voltage current follows the path of least resistance. Thus, nerves, designed to carry electrical signals, and muscles and blood vessels, with their high water content, are good conductors. Bone, tendon, and fat have a very high resistance and tend to heat up and coagulate. Muscle is intermittent in resistance. High-voltage current follows a direct course to ground and flows through the tissues indiscriminately, regardless of tissue type and resistance, thus treating the body as a volume conductor, with potential damage to all tissue in the current’s path. Current passing thought the heart, as in the case of a hand-to-hand or hand-to-foot flow, can result in sinus tachycardia, premature ventricular contractions, atrial fibrillation, or ventricular fibrillation, which is the most common cause of death and is usually induced by alternating current at levels greater than 50 Hz. Asystole can result from direct current. ECG
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usually does not show the standard ischemic injury patterns associated with myocardial infarction. The head is a common point of contact for high-voltage injuries, and acute neurological symptoms may include altered mental status, seizures, quadriplegia, localized paresis, coma, and fracture or ligamentous disruption of the cervical, thoracic, or lumbar spine. Delayed symptoms, which may appear years after the exposure, may have a poor prognosis. These include ascending paralysis, amyotrophic lateral sclerosis, and transverse myelitis. Electrical injuries can also result in compartment syndromes, corneal burns, thermal burns, intraocular hemorrhage, venous thrombosis, fractures of long bones, posterior and anterior shoulder dislocations, and cataract formation, usually more than 4 months after the injury.
LABORATORY FINDINGS The nature of the injury determines the ancillary tests needed, and for most exposures to household current no testing is indicated. However, all patients who exhibit possible conductive electrical injury should be regarded as potentially having sustained multiple crush-type traumatic injures. Thus, it is important to perform a CBC; liver function tests, arterial blood gas analysis, and measurements of electrolyte levels, serum CPK, BUN, serum creatine, serum glucose, platelet count, and cardiac enzymes. More severely injured patients who require surgery may need blood typing or crossmatching and measurements of PT and activated PTT studies. Suspicion of conductive injury also requires cardiac monitoring and 12-lead ECG. If the patient exhibits altered mental status, a CT scan without contrast should be performed to rule out intracranial hemorrhage. If blunt trauma to the musculoskeletal system resulted or if spinal trauma is suspected, appropriate radiographs should be obtained.
TREATMENT On arrival to the ED, all patients who have sustained electrical injury should have a detailed history obtained, including tetanus status. The ED physician should also perform a head-to-toe physical examination and check vital signs, including blood pressure, pulse, respiratory rate, temperature, and pulse oximetry reading. After an observation period, if the evaluation determines that the electrical injury was a minor and of low voltage with no associated injuries, discharge can be performed. However, if any evidence of conductive injury, skin burns, blunt trauma, history of loss of consciousness, chest pain, shortness of breath, altered mental status, or seizures is exhibited, the patient should be approached in the same way as a person who has sustained blunt trauma with a crush
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injury. Fluids should administered to maintain a urine output of 1–2 ml/ kg/hr, and accurate measurements may require a Foley catheter placement. Radiographs of the cervical spine, chest, pelvis, and extremities may be necessary, depending on the results of the physical examination. Resuscitative efforts should concentrate on diagnosis and treatment of cardiac arrhythmias, renal failure, hyperkalemia, intracranial hemorrhage, compartment syndrome, acidosis, burns, rhabdomyolysis, and fractures. All pregnant patients should be referred to the obstetrical service for a period of fetal monitoring if this service is not available in the ED. Children who sustained oral commissure burns as a result of biting an electrical cord may have delayed bleeding form the labial artery and significant contractures that require reconstructive surgery.
Bibliography Auerbach PS, Halstead BW: Injuries from nonvenomous aquatic animals. In Auerbach PS (ed): Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Isbister GK, Caldicott DG: Trauma and envenomations from marine fauna. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Otten EJ, Blomkalns AL: Venomous animal injuries. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Weisman RS: Marine envenomations. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002.
Frostbite JOHN MCMANUS
ICD Codes: Frostbite 991.3, Frostbite, face 991.0, Frostbite, foot 991.2, Frostbite, hand 991.1
Key Points Frostbite injuries have been classified by degrees of severity (first through fourth degree) or by merely classifying an injury as superficial (first and second degree) or deep (third and fourth degree).
216 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! All patients should be assessed and treated for comorbid and coexisting conditions. The possibility of hypothermia should be considered in all cases of frostbite. The treatment of frostbite occurs in three phases: (1) the prehospital phase, (2) the immediate hospital (i.e., ED) phase, and (3) the post-thaw care phase.
DEFINITION There are many forms of localized cold-related injuries, and they are classified by their degree of injury and clinical presentation. Frostbite, the most severe form, is a cold-related injury characterized by freezing and destruction of local tissue. Frostnip is the earliest manifestation of frostbite and in general is a reversible condition. Other milder forms (nonfreezing) of local cold-related injuries include pernio (i.e., chilblain) and trench foot. This chapter will focus on the discussion of frostbite, which is the most serious form of localized cold-related injury.
EPIDEMIOLOGY Although most cases of frostbite are classified as accidental, they can result from recreational, occupational, social, or iatrogenic causes. The majority of cases in the past were attributed to military operations. However, cold injuries are now more prevalent in the civilian populations. Some of the factors that increase the risk for developing cold-related injuries include winter recreation, smoking, alcohol consumption, extremes of age, immobilization, high altitude, chronic medical illness (e.g., diabetes, atherosclerosis), and previous cold-related injuries. Frostbite occurs more commonly in males, and affected patients are usually between 30 and 49 years of age. The extremities are the most commonly affected areas, followed by nose, ears, cheeks, and male genitalia.
PATHOPHYSIOLOGY Humans attempt to maintain a constant body temperature, which is 38 C rectally and approximately 32 C at the skin. As skin temperature drops and is unable to be maintained through the body’s normal thermoregulation mechanisms, local tissue injury and destruction can occur. Frostbite injuries range from reversible injury after rewarming to irreversible tissue destruction. Tissue destruction is usually caused by immediate cellular death at the time of exposure and by progressive cellular ischemia. As the skin cools, peripheral circulation slows down until it stops completely, producing a cold-induced vasospasm. Arterioles constrict to protect any residual heat that is present, and capillary shunting occurs with arteriole-to-venule vasoconstriction and vasodilatation. This process is referred
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to as the “hunting response.” The vasodilatation can lead to thawing of previous frozen tissue and contribute to cellular damage through increased viscosity and thrombosis formation. Furthermore, direct cellular damage will begin to occur as the tissue begins to freeze. Actual ice crystals form in the extracellular and intracellular tissue resulting in cell membrane damage, dehydration, and possible death. The progression of frostbite injury from early ischemia to eventual cellular necrosis is similar to that seen with thermal injuries such as extent, depth, and localization. Inflammatory mediators such as histamine, bradykinin, and prostaglandins are released and contribute to cellular dysfunction and death. Endothelial injury causes loss of vascular integrity as well as thromboses. Rewarming and vasodilatation can also lead to hemoconcentration and both platelet and coagulation-cascade dysfunction, resulting in local bleeding.
CLINICAL PRESENTATION AND PHYSICAL EXAMINATION Frostbite injuries have been classified by degrees of severity, first through fourth degree, or by classifying injury as superficial or deep. However, these classification systems are applied only after rewarming and are used more to predict outcome rather than to determine initial treatment. In general, superficial frostbite involves the skin and subcutaneous tissues. Patients initially report extreme cold, numbness, and pain locally. Mild edema may be present, and the skin usually becomes pale in color with possible clear blister development. The skin usually remains pliable and soft beneath the injury in the case of superficial frostbite. In contrast, deep frostbite injury affects structures below the subcutaneous tissue such as bone, joints, and tendons. Initial pain and numbness may progress to hyperesthesia and loss of cold sensation. The skin often becomes dark and is described as hard and “woody” to palpation, with possible formation of hemorrhagic blisters. Although no prognostic features are predictive of morbidity, favorable prognostic indicators that suggest superficial injury include retained sensation, clear blisters, normal skin color, and the ability to deform skin with pressure. Dark skin color, cyanosis, hemorrhagic blisters, and firm skin are associated with deep injury and a poorer prognosis. Finally, a discrepancy line may be seen between viable and nonviable tissue. However, the presence of this demarcation may take weeks to months to develop.
DIAGNOSIS The diagnosis of frostbite is initially made from history and physical examination findings, as described previously. To determine the extent
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of injury and underlying tissue damage, some have advocated the use of various radiographic modalities. Although some of these radiographic tests have proved to determine viability of tissue, currently no single study has been accurate enough to guide surgical intervention. Some of the radiographic modalities that have been used include MRI, radioisotope scanning (i.e., technetium-99), angiography, and plain radiography.
LABORATORY FINDINGS Although specific laboratory testing is not available to confirm the diagnosis of frostbite, patients with deep frostbite or evidence of comorbidity may benefit from testing. Possible abnormal laboratory findings include hemoconcentration, thrombocytopenia, and coagulation abnormalities.
TREATMENT All patients should be assessed and treated for comorbid conditions. The possibility of hypothermia should be considered in all cases of frostbite. The treatment of frostbite occurs in three phases, as described previously. All life-threatening conditions should be addressed initially. In the prehospital phase, rewarming should begin as soon as possible. However, local rewarming should occur only if refreezing will not occur and severe hypothermia is not present due to the increased potential of tissue injury. All wet, nonadherent clothing should be removed and replaced with dry clothing. Rewarming with skin-to-skin contact and blankets should be the initial treatment. Use of rubbing the affected area with snow or hands or use of a heat source to rewarm frozen areas have all been shown to increase the likelihood of tissue damage. Injured extremities may benefit from splinting and elevation, which has shown to decrease pain and edema and to promote tissue perfusion. Analgesia should also be initiated, if possible. If the patient is also hypothermic, the patient should be handled gently because stimulation and movement have been shown to exacerbate cardiac arrhythmias. Finally, all comorbid conditions should be treated. The second phase, the immediate hospital phase, is directed at reducing the progression of tissue destruction and can be divided into three stages. During the first stage, prethaw, providers should protect the tissue and not allow rough movement or friction. The core temperature of the patient should be addressed and stabilized to prevent “core temperature afterdrop.” Also, all comorbid medical conditions should be addressed and treated. During the next stage, thaw, appropriate analgesia and tetanus status should be addressed. To rewarm the tissue, circulating warm water is recommended at a temperature of 98 –104 F (37 –40 C). Other regimens that may be considered include antiplatelet therapy (e.g., nonsteroidal
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anti-inflammatory medications and low-molecular-weight heparin), smooth muscle inhibitors (e.g., calcium-channel blockers), vasoconstrictor inhibitors (e.g., phenoxybenzamine), topical creams (e.g., aloe vera), and prophylactic antibiotics (e.g., penicillin G). Blister treatment remains controversial. Some advocate removal of clear blisters to decrease the local concentration of prostaglandins and thromboxanes. However, some literature states that the removal of blisters, especially hemorrhagic, results in increased risk of tissue desiccation. Blister treatment should be done in conjunction with a consultant to the subspecialist managing wounds at the institution. The final stage of the hospital phase is also the last stage of care, post-thaw. In this stage, continued wound therapy and protection of the affected area occurs. Active range of motion of the affected area is encouraged as soon as possible. Patients should be discouraged from alcohol intake and smoking. Patients may require surgery and escharotomy. Long-term effects from frostbite include amputation, chronic pain, osteoarthritis, sensory loss, and hyperhidrosis. All patients with a diagnosis of frostbite should have a subspecialty follow-up, and persons exhibiting signs and symptoms of a deep injury admitted to the hospital.
SUMMARY Treatment of cold-related injuries is crucial for emergency providers in both urban and rural settings. Improved rewarming techniques as well as advanced radiological assessment for tissue viability have resulted in better diagnosis, management, and outcome for patients with frostbite injuries. Remember, general therapy should be directed at hypothermia and comorbid conditions. However, the most effective treatment for all cold-related injuries is proper education and prevention.
Bibliography Bracker MD: Environmental and thermal injury, Clin Sports Med 1992;11:419–436. Britt LD, Dascombe WH, Rodriguez A: New horizons in management of hypothermia and frostbite injury [abstract], Surg Clin North Am 1991;71:345–370. Greenwald D, Cooper B, Gottlieb BL: An algorithm for early aggressive treatment of frostbite with limb salvage directed by triple phase bone scanning, Plast Reconstr Surg 1998;102:1069–1074. Heggers JP, Robson MC, Manavalen K, et al: Experimental and clinical observations on frostbite, Ann Emerg Med 1987;16:1056–1062. Murphy JV, Banwell PE, Roberts AH, McGrouther DA: Frostbite: Pathogenesis and treatment, J Trauma 2000;48:171–178. Petrone P, Kuncir EJ, Asensio JA: Surgical management and strategies in the treatment of hypothermia and cold injury, Emerg Med Clin North Am 2003;21(4):1165–1178. Reamy BV: Frostbite: Review and current concepts, J Am Board Fam Pract 1998;11:34–40. Robson MC, Heggers JP: Evaluation of hand frostbite blister fluid as a clue to pathogenesis, J Hand Surg 1981;6:43–47.
220 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Su CW, Lohman R, Gottlieb LJ: Frostbite of the upper extremity, Hand Clin 2000;16:235–247. Urschel JD: Frostbite: Predisposing factors and predictors of poor outcome, J Trauma 1990;30:340–342. Valnicek SM, Chasmar LR, Clapson JB: Frostbite in the prairies: A 12-year review, Plast Reconstr Surg 1993;92:633–641.
Heat Injuries SUMERU GHANSHYAM MEHTA
ICD Codes: Heat stroke 992.0, Heat syncope 992.1, Heat cramps 992.2, Heat exhaustion 992.3, 002.4, 992.5, Heat edema 992.7
Key Points In all patients with suspected heat injuries, cooling should not be delayed. ! Emergency Actions ! Once heat stroke is suspected, efforts to lower the body temperature must be initiated immediately by whatever means available, whether in the prehospital or ED setting.
DEFINITION Patients can present with a variety of heat-related illnesses, including heat cramps, heat edema, heat syncope, prickly heat, heat exhaustion, and heat stroke. They are all the result of the body’s inability to respond to environmental heat conditions. Body temperature increases when the rate of heat production exceeds the rate of heat dissipation. Hyperthermia occurs when thermoregulatory mechanisms are overwhelmed by excessive metabolic production of heat, excessive environmental heat, or impaired heat dissipation.
EPIDEMIOLOGY Between 1979 and 1995, there were 6651 deaths in the United States related to the effects of heat and excessive heat exposure. Heat injuries
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often affect those at the extremes of age—the very young and the very old. The annual rate of death is highest among elderly persons with an incidence of 5 per million in the over-85-year age group. The incidence rates in the age group younger than 4 years of age is six times higher than in those older than 4 years. Heat-related illness is the second leading cause of death among young athletes. Heat-related illness and deaths are clearly related to high environmental temperature, and increased numbers have been seen during urban heat waves all around the world. Although heatrelated illness occurs in healthy persons exposed to extremes of heat and humidity, it is especially dangerous for those impaired by chronic illness, drugs, and age.
CLINICAL PRESENTATION Heat-related illnesses are usually divided into minor syndromes (i.e., heat cramps, heat edema, heat syncope, prickly heat, and heat exhaustion) and major syndromes (heat stroke).
Heat Cramps Heat cramps are painful, involuntary, spasmodic contractions of the skeletal muscles, usually involving the calves. They usually occur in persons who are sweating liberally, and treatment involves replacement of fluid loss with water or other hypotonic solutions. The cramps may occur during exercise or after a latent period of several hours.
Heat Edema Heat edema is a self-limited process manifested by mild swelling and tightening of the hands and feet that appears in the first few days of exposure to a hot environment. It is usually seen in nonacclimatized persons, especially elderly persons, who encounter hot climatic stresses. The edema is usually minimal and not accompanied by a significant impairment in function. It is presumed to be due to cutaneous dilation and orthostatic pooling of interstitial fluid in the extremities.
Heat Syncope Heat syncope is a variant of postural hypotension resulting from the effect of peripheral vasodilation, decreased motor tone, and relative volume depletion. It may occur in nonacclimatized persons during the early states of heat exposure. Elderly persons seem to have a special predilection for this disorder.
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Prickly Heat Prickly heat is also known as miliaria rubra, lichen tropicus, and heat rash. It is an acute inflammatory disorder of the skin caused by blockage of sweat pores that occurs in warm, tropical climates. The blockage causes the ducts to become dilated under pressure and subsequently rupture, producing superficial vesicles on the skin. Clinically, intensely pruritic vesicles on an erythematous base are the predominant feature. The rash is confined to clothed areas, and the affected area is often completely anhydrotic. Over the next few weeks, a deeper obstruction of the sweat gland arises, producing a deeper vesicle within the dermis. This rash resembles the white papules of piloerection and is not pruritic.
Heat Exhaustion Heat exhaustion is an obscure syndrome that is characterized by a combination of salt and water depletion that occurs under conditions of heat stress. Signs and symptoms associated with heat exhaustion include nonspecific symptoms such as dizziness, malaise, weakness, light-headedness, fatigue, vertigo, nausea, vomiting, headache, and myalgias. Clinical manifestations include syncope, orthostatic hypotension, tachypnea, diaphoresis, tachycardia, and hyperthermia. The core temperature is variable but is usually less than 40 C (104 F). Mental status remains normal in these patients.
Heat Stroke Heat stroke is the catastrophic life-threatening emergency that occurs when homeostatic thermoregulatory mechanism fails. It is classically defined as the triad of a core temperature greater than 40.5 C (104.9 F), CNS dysfunction, and anhidrosis. However, anhidrosis may or may not be present and is not considered to be an absolute diagnostic criterion. The CNS, however, is particularly vulnerable and can manifest itself with such symptoms as irritability, bizarre behavior, combativeness, hallucinations, seizures, or coma. Therefore, anyone with hyperpyrexia and CNS dysfunction should be considered to have heat stroke, which has multiple organ system involvement and a high mortality rate.
EXAMINATION Initial attention must be paid to the ABCs (i.e., airway, breathing, circulation), with initiation of high-flow oxygen and continuous cardiac monitoring. Of paramount importance is the serial monitoring of the patient’s core temperature obtained by means of a rectal probe. Another option, in intubated patients, is the use of an esophageal thermometer. A complete examination must be performed, including a check of the patient’s skin
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for sweating and color. A baseline neurological examination should be performed, followed by serial neurological examinations.
LABORATORY FINDINGS Any suspicion of heat exhaustion or heat stroke should prompt a diagnostic workup, which should include a CBC, comprehensive metabolic panel, hepatic panel, coagulation profile, creatine kinase measurement, urinalysis, toxicological screen, and ECG. Electrolyte abnormalities associated with heat injuries include hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia.
DIAGNOSIS The diagnosis of heat injuries is made by clinical presentation, core rectal temperature, laboratory studies, and neurological status of the patient at the time of the presentation. Only after initial assessment and treatment have begun should attention be directed to the differential diagnosis. Other etiologies that should be considered in the differential diagnosis include infection (e.g., meningitis, malaria, typhus, or encephalitis), thyroid storm, drug-induced etiology (e.g., anticholinergic poisoning), and delirium tremens.
RADIOGRAPHS A chest radiograph should be ordered in all patients with moderate heat injury. A CT scan of the head may also be indicated as part of the evaluation of altered mental status encountered in heat stroke.
TREATMENT All of the minor heat illnesses except for severe heat exhaustion can be managed in the ED, and patients can be discharged with prevention tips and close follow-up. Heat stroke and heat exhaustion are reasons for admission to the hospital in patients at the extremes of age and in those with comorbid disease, severe dehydration, or evidence of end-organ damage. Serious heat-related illness is predictable and preventable. The incidence of heat-related injuries can be reduced by paying attention to environmental conditions, ensuring acclimatization for persons who work in hot, adverse environments, providing social services like access to airconditioning for persons at risk (e.g., elderly persons), and ensuring adequate hydration.
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Heat Cramps Heat cramps are usually rapidly relieved by salt solutions. Mild cases without concurrent dehydration may be treated with oral 0.1%–0.2% salt solution. Severe cases respond rapidly to intravenous isotonic saline.
Heat Edema Heat edema is treated with simple leg elevation or thigh-high support hose. In most persons, the problem resolves through adequate acclimatization.
Heat Syncope Heat syncope is self-limited because assumption of a horizontal position is the cure. Persons at risk for heat syncope should be warned to move often, flex leg muscles when stationary, avoid protracted periods of standing when in hot environments, and assume a sitting, horizontal position when prodromal warning signs occur.
Prickly Heat Prickly heat can be prevented if the patient wears clean, light, and loosefitting clothes and avoids situations producing profuse sweating. Chlorhexidine in a light cream is the treatment of choice in the acute phase. Salicylic acid, 1%, can be applied to localized affected areas to assist in desquamation. The application of salicylic acid over large areas may cause salicylic toxicity. For diffuse or pustular rashes, erythromycin or dicloxacillin can be administered orally.
Heat Exhaustion Heat exhaustion is primarily a volume-depletion problem, and therefore fluid administration leads to rapid recovery. Decisions regarding the types of fluid and electrolyte replacements to be administered should be based on electrolyte measurements and hydration status. In mild cases, rest in a cool environment and hydration with an oral electrolyte solution may be sufficient. Patients with significant volume depletion or electrolyte abnormalities require intravenous hydration. Young, otherwise healthy patients with no significant electrolyte abnormalities who are responsive to treatment do not require hospitalization. Older patients, especially those with cardiovascular disease, will require a more cautious fluid and electrolyte replacement and are best managed as inpatients.
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Heat Stroke Heat stroke requires a rapid reduction of core temperature to 40 C (104 F), which is accomplished by physical cooling techniques. Immersion and evaporative (e.g., spray bottle and a standing fan) cooling are the most widely used cooling methods. When the body temperature reaches 40 C, cooling measures should be discontinued to avoid hypothermic overshoot. Other adjunctive cooling methods include cooling blankets, cardiopulmonary bypass, peritoneal dialysis, and gastric/bladder lavage. Hypotension, caused by peripheral vasodilation, is common in heat stroke. Blood pressure usually rises with cooling and intravenous fluid administration. Airway management is critical in the resuscitation of any critically ill patients. Common early complications of heat stroke include seizures, rhabdomyolysis, hypokalemia, hypocalcemia, and shivering. All patients with heat stroke should be admitted for close observation and management.
Bibliography Bouchama A, Knochel JP: Heat stroke, N Engl J Med 2002;346:1978–1988. Khosla R, Guntapalli KK: Heat-related illness, Crit Care Clin 1999;15:251. Tek D, Olshaker JS: Heat illness, Emerg Med Clin North Am 1992;10:299. Walker JS, Barnes SB: Heat emergencies. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1235–1242. Yarbrough B, Bradham A: Heat illness. In Rosen P, Barkin R (eds): Emergency Medicine Concepts and Clinical Practice, ed 4. Mosby: St Louis, 1998, pp 986–1002.
Hypothermia JOHN MCMANUS AND IAN WEDMORE
ICD Code: Hypothermia 991.6
Key Points Mortality can approach 50% for persons with hypothermia and comorbid illness. Important risk factors that increase the incidence of cold-related injury include extremes of age, intoxication, poor nutrition, certain medications, and the presence of comorbid conditions.
226 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! As with all patients who present with serious illness, the general treatment of hypothermia should begin with addressing all life-threatening conditions (the “ABCs”: airway, breathing, and circulation) and monitoring the patients’ vital signs to include ECG activity.
DEFINITION Cold-related injuries have been documented for centuries beginning with Hippocrates and Aristotle and have resulted in devastating losses throughout history. In fact, Hannibal lost more than half of his army to coldrelated injuries while crossing the Pyrenees Alps. Although humans attempt to maintain a constant body temperature (38 C rectally and approximately 32 C at the skin), in many circumstances this can be difficult—especially when exposed to wilderness conditions, high altitude, and substances that inhibit thermoregulation. Hypothermia is defined as a core body temperature of less than 35 C (95 F) and occurs in mild, moderate, and severe forms. Prevention, recognition, and treatment are essential in reducing the morbidity and mortality associated with hypothermia.
EPIDEMIOLOGY Hypothermia accounts for approximately 700 deaths in the United States per year and is one of the leading causes of death during outdoor recreation. Mortality can approach 50% for persons with comorbid illness. Although the time of exposure and ambient temperature are responsible for the greatest risk for developing hypothermia, there are several factors that predispose persons for developing hypothermia. Important risk factors that increase the incidence of cold-related injury include extremes of age, intoxication, poor nutrition, certain medications, and the presence of comorbid conditions.
PATHOPHYSIOLOGY Humans lose heat into the environment through respiration, evaporation, convection, conduction, and radiation. Respiration and evaporation involve releasing heat through water droplets. Convection is the process whereby heat is lost through movement of heat from the body into the environment by movement of air (i.e., wind chill) or liquids over the body surface. Conduction involves the actual transfer of heat from the body with direct contact of a cooler object. Radiation causes heat loss through infrared heat emission into the cooler, surrounding environment.
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The hypothalamus is the thermoregulatory gland for the body that attempts to maintain body temperature through release of substances causing vasoconstriction and increased metabolic rate in conjunction with the endocrine system. The body’s thermoregulation system has allowed humans to survive temperature ranges from 50 C (58 F) to 100 C (212 F). Furthermore, heat is generated through the increase in metabolic rate and shivering. The metabolic rate declines by approximately 6% for every 1 C decrease in core body temperature, which results in decreased thermogenesis. The body’s ability to compensate is lost somewhere between 30 C (86 F) and 32 C (90 F). As vasoconstriction increases and the body’s metabolic rate decreases, poor perfusion, hypovolemia, and blood sludging occur and can lead to eventual cardiovascular collapse.
CLINICAL PRESENTATION A patient’s clinical presentation usually correlates with his or her core temperature. Hypothermia occurs in three different forms: mild, moderate, and severe. Mild hypothermia is defined as a temperature of 32.2 –35 C (90 –95 F). Patients with this form typically present with shivering, tachycardia, tachypnea, apathy, fatigue, decreased concentration, and mild hypovolemia. Moderate hypothermia, defined as 28 –32.2 C (82.4 –90 F), is the stage at which the body generally begins to lose the ability to compensate. The shivering usually stops in this stage, and the patient experiences diminished level of consciousness. Also in moderate hypothermia, the heart becomes bradycardic and J waves (Osborn waves) may be seen on the ECG. The final stage, severe hypothermia, is defined as a core temperature of less than 28 C (82.4 F). Patients with severe hypothermia are unresponsive and in a coma. The patient appears clinically dead. Patients in this stage have various dysrhythmias, apnea, and loss of reflexes.
PHYSICAL EXAMINATION As described previously, the physical examination findings of a patient with hypothermia are dependent on his or her core body temperatures and represent a continuum of metabolic dysfunction. Comorbid illness should be assessed and considered because hypothermia may mask serious symptoms and signs. Furthermore, early signs and symptoms of hypothermia may be ignored or misdiagnosed.
DIAGNOSIS The diagnosis of hypothermia is based on a patient’s core temperature and clinical findings. However, thermometers that measure peripheral
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temperatures are often inaccurate and may give healthcare providers a false sense of reassurance. Furthermore, many standard thermometers used in the emergency setting are limited to a low recorded temperature of 34.4 C (94 F). All patients suspected of having hypothermia should have a core temperature taken.
LABORATORY FINDINGS There are no specific laboratory tests used to confirm or exclude a diagnosis of hypothermia. However, routine laboratory tests are recommended for all patients presenting with moderate to severe hypothermia. Abnormal laboratory values that may be seen in patients with hypothermia include electrolyte dysfunction, hemoconcentration, and coagulopathies. Laboratory testing should be also guided by specific comorbid illnesses that may be present (e.g., thyroid function tests, toxicology screening, blood cultures).
TREATMENT The treatment of hypothermia is based on the location of patient, available assets, and the patient’s clinical condition. As with all patients who present with serious illness, the general treatment of patients with hypothermia should begin with addressing all life-threatening conditions first and monitoring the patients’ vital signs to include ECG activity. Management for patients who initially have no cardiac activity or who have evidence of dysrhythmias on the ECG is discussed later. Initially, patients with hypothermia should be removed from the cold environment, and all wet clothing should be removed and replaced with warm blankets. Glucose abnormalities should be addressed, and empiric administration of naloxone and thiamine should be considered. Responsive patients with mild to moderate hypothermia usually respond well to passive external rewarming. Patients should be encouraged to drink warm fluids containing sugar and should be asked to limit exertional activity until rewarmed. If active external warming is used, most experts recommend using a heating blanket or a system that warms the core such as the Bair Hugger. Heating just the peripheral areas of hypothermic patients before the core area is discouraged and may result in possible core temperature “afterdrop.” Afterdrop is a term used to describe the returning of cooler peripheral blood to the body’s core area, causing possible cardiac irritability and dysrhythmias. Direct skin contact to heated items should also be avoided. Treatment for severe hypothermia in patients with a pulse and normal cardiac activity should proceed as outlined previously, but with more aggressive rewarming and monitoring. Active internal rewarming can be achieved through warmed oxygen administered via face mask or endotracheal tube,
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warmed gastric lavage, warmed bladder lavage, warmed peritoneal lavage, or warmed pleural lavage. Furthermore, extracorporeal blood warming can be accomplished through hemodialysis, arteriovenous rewarming, venovenous rewarming, or cardiopulmonary bypass. Patients with severe hypothermia who have evidence of cardiac dysfunction or no pulse should be managed according to the American Heart Association Basic and Advanced Cardiac Life Support (ACLS) guidelines. Management of persons who have experienced cardiac arrest in the setting of hypothermia is different than in normothermic arrest. Initial treatment focuses on active core rewarming as described above. There are documented survival cases for both pediatric and adult patients with severe hypothermia and initially no cardiac activity with extremely low temperatures below 58 C. Resuscitation should be attempted and should not be discontinued in patients with hypothermia until core temperature is above 32 C (89.6 F). All patients should be handled gently because numerous physical manipulations and vigorous activity has been shown to precipitate cardiac dysrhythmias. If a patient has a pulse, no matter how slow, do not initiate cardiopulmonary resuscitation (CPR). However, providers should assess breathing and pulse for 30–45 seconds to determine the presence or absence of these signs. If breathing and pulse are absent, general ACLS management should begin with the ABCs of resuscitation, including endotracheal intubation. Rescuers should then begin CPR, attempt defibrillation once, establish intravenous access, and provide active warming techniques. Intravenous medications and repeated defibrillation should be withheld until the core temperature reaches 30 C (86 F). Management of cardiac arrhythmias, electrolyte disorders, and medication delivery should be based on current ACLS guidelines.
SUMMARY Treatment of cold-related injuries is crucial for emergency providers in both the urban and rural setting. Improving rewarming techniques as well as increasing the education and training of emergency medical providers has all resulted in better diagnosis, management, and improved outcome for patients with hypothermia. Remember, general therapy should be directed toward rewarming and treating any comorbid conditions. However, the most effective treatment for all cold-related injuries is proper education and prevention.
Bibliography Danzl DF, Pozos RF: Accidental hypothermia, N Engl J Med 1994;331:1756–1760. Gilbert M, Busund R, Skagseth A, et al: Resuscitation from accidental hypothermia of 13.7 C with circulatory arrest, Lancet 2000;355:375–376.
230 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Petrone P, Kuncir EJ, Asensio JA: Surgical management and strategies in the treatment of hypothermia and cold injury, Emerg Med Clin North Am 2003;21(4):1165–1178. Silfvast T, Pettila V: Outcome from severe accidental hypothermia in Southern Finland— A 10-year review, Resuscitation 2003;59:285–290. Stoner J, Martin G, O’Mara K, et al: Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model, Acad Emerg Med 2003;10(3):187–191. Ulrich A, Rathlev N: Hypothermia and localized cold injuries, Emerg Med Clin North Amer 2004;22:281–298.
Hymenoptera Stings CLIFFORD C. LUTZ
ICD Codes: Sting 989.5, Anaphylactic shock or reaction 989.5
Key Points Hymenoptera envenomation is the result of the bodys reaction to the complex toxins that varies from species to species. Primarily, these toxins are composed of proteins, alkaloids, peptides, amines, phospholipase A, and hyaluronidase. ! Emergency Actions ! The systemic reaction to Hymenoptera envenomation represents a true medical emergency and should always be treated as such. Persons with this condition must be placed on a monitor, receive oxygen, and undergo the placement of two large-bore intravenous lines. They should all receive intravenous doses of antihistamine (diphenhydramine 50 mg) and corticosteroid (prednisone 50 mg PO or methylprednisolone 125 mg given intravenously).
DEFINITION Hymenoptera is the order of arthropods to which bees, vespids (e.g., wasps, yellow jackets, and hornets), and fire ants belong. These insects all possess a modified ovipositor that protrudes from the back of the abdomen and acts like a hypodermic needle, injecting the venom. Bees
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possess a barbed ovipositor and sting only once, leaving the ovipositor and venom sac attached to their victim. Vespids have an unbarbed tail and are capable of repeated stings. Ants usually bite onto their victim then sting repeatedly, in a circle.
EPIDEMIOLOGY Hymenoptera stings are the second most common type of human envenomation, preceded only by coelenterate (e.g., jelly fish, anemone). There are an estimated 9 million fire ant stings and 1 million other hymenopter stings per year in the United States. Only about 1%–2% of stings cause generalized reactions. Up to 50% of persons will get a local reaction. Hymenoptera is, however, the leading cause of death due to envenomation in the United States. The ratio of males to females is 2:1, likely due to environmental exposure. There is no difference among races. Fire ants are really the only ants of concern. It is believed that they were introduced to the United States in Mobile, Alabama, from a Brazilian freighter in the not too distant past. In a short time, they have essentially eradicated all other ants and are now found throughout Texas and most of the southeastern United States. Africanized or “killer” honey bees were introduced to Brazil from Africa. It was thought that they would produce more honey and thrive in the tropical environment. Not only do they produce less honey, but also they drive their European cousins out of competing regions. They reached Texas in 1990 and are now believed to have reached the northern edge of their habitat somewhere between North Carolina and Virginia.
PATHOPHYSIOLOGY Hymenoptera envenomation is the result of the body’s reaction to the complex toxins that vary from species to species. Primarily, these are composed of proteins, alkaloids, peptides, amines, phospholipase A, and hyaluronidase. The venom both has a direct toxic effect and starts a cascade of inflammatory and immunological mediators to include acetylcholine, bradykinin, histamine, serotonin, and dopamine. The body’s response is immunoglobulin E mediated and primarily involves the skin, respiratory tract, and vascular system. The acute histamine release can cause varying severities of urticaria, vasodilation and hypotension, bronchospasm, and angioedema.
CLINICAL PRESENTATION There are essentially three types of reactions: local, diffuse, and systemic. The local reaction starts with immediate pain, pruritus, and usually local
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swelling (up to 10 cm), often with some paresthesias. Symptoms usually resolve in less than 1 hour, and there are no sequelae. However, a retained barb can lead to granuloma or infection. The generalized reaction is somewhat more significant in that the swelling and urticaria become spread over the entire body. There are no systemic symptoms except occasional nausea, vomiting, or diarrhea, and the patient usually does well. Medical treatment is often required for symptomatic resolution. The systemic or anaphylactic reaction is the most severe form and the only reaction that often leads to death. There is usually some sensitization from a prior sting; however, an anaphylactoid reaction can occur from the initial sting. The severity of the course in usually more severe with a shorter interval between stings. The onset of symptoms is very rapid. Fifty percent of deaths occur in the first 30 minutes. Patients having a systemic or anaphylactic reaction can have profound shock and hypotension due to vasodilation and loss of vascular tone. They are also in eminent danger of airway compromise because of marked bronchospasm and angioedema of the lips, tongue, soft palate, epiglottis, etc. Other possible serious complications include acute myocardial infarction, syncope, acute renal failure, disseminated intravascular coagulation (DIC), and cerebral edema.
DIAGNOSIS The diagnosis of hymenoptera stings is generally evident after a good history and physical examination have been performed. Laboratory studies are not usually indicated; the exception is a severe systemic reaction. In that case, it would be prudent to check a CBC, coagulation and DIC panels, electrolyte levels, BUN and creatinine levels, and urinalysis. Chest radiographs may be of some help in patients with severe respiratory compromise.
TREATMENT Local reactions can usually be treated with just ice. They may also require some mild oral analgesia and an antihistamine. Generalized reactions are most often treated with intramuscular injection of antihistamine (diphenhydramine, 50 mg). This medication can be given intravenously, but this is not usually required. These persons are also given an oral corticosteroid such as prednisone, 50 mg. They should be watched in the ED until the signs and symptoms are almost resolved. The antihistamines and steroids are generally given for 5 additional days after discharge. A systemic reaction represents a true medical emergency and should always be treated as such. These persons need to be placed on a monitor,
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receive oxygen, and undergo placement of two large-bore intravenous lines. They should all receive intravenous doses of antihistamine (diphenhydramine, 50 mg) and corticosteroid (prednisone, 50 mg PO or methylprednisolone, 125 mg, given intravenously). There is no evidence to support the theory that intravenous steroids work faster than those administered orally. Therefore, intravenous steroids should be reserved for persons who cannot swallow pills. There is also a paucity of supporting evidence for the use of H2 blockers; however, they are very safe and regularly given to these patients (cimetidine, 300 mg, given intravenously). Any patient with hypotension or airway compromise should be given epinephrine immediately. This should first be given as 0.3 ml of 1:1000 solution administered subcutaneously. If this is ineffective, the patient should receive 0.1 ml of 1:10,000 epinephrine given intravenously. Any impending airway compromise should be prophylactically intubated. The conditions of these patients deteriorate rapidly, and the intubation becomes increasingly more difficult as the airway angioedema ensues. An inhaled beta agonist such as albuterol may also be helpful to combat the bronchoconstriction. Intravenous crystalloid should be the treatment of choice for hypotension. Hypotension that does not resolve with 2 L of normal saline may require intravenous dopamine started at 5 mg/kg/min and titrated up to 20 mg/kg/min to achieve the desired blood pressure. All patients with systemic reactions require admission for observation. Any patient with a reaction other than a local reaction should leave the hospital with an EpiPen (epinephrine) auto-injector or an AnaKit anaphylaxis emergency treatment kit. Patients should also be advised to wear a medic alert tag.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Lightning Injuries GUYON J. HILL
ICD Code: 994.0
Key Points/Quick Reference Lightning injuries are one of main causes of death from natural phenomena. Triage priorities should go to any unconscious patients, as they can benefit most from immediate care and ventilatory assistance. Numerous organ systems can be affected by lightning, and thorough primary and secondary surveys are necessary to avoid overlooking injuries. ! Emergency Actions ! Immediate care in the field should be directed first to those persons who are unconscious. Patients may regain automaticity after asystolic cardiac arrest but may still be in respiratory arrest. Providing ventilation to these patients can prevent fatal arrhythmias developing as a result of hypoxia. Patients who are conscious have a low risk of imminent death. The patient should be stabilized and resuscitated following current ACLS guidelines. Immobilize the cervical spine and any injured extremity, as appropriate. Remove the patient from the scene of the injury to reduce the chance of repeat strike. Manage hypotension as appropriate with intravenous fluid administration and vasopressors.
DEFINITION Lightning is an electrical discharge that occurs between two areas of oppositely charged energy in and around a thunderstorm. The potential builds from water and ice particles moving around, and a lightning bolt results when the charge is large enough. Lightning cannot be strictly classified as either AC or DC and is perhaps better described as a massive unidirectional current. The primary differentiation between lightning injury and high-voltage injuries is the time of current exposure. Cloud-to-ground lightning is the most dangerous to humans and occurs from the negatively charged bottom of a cloud to the positively charged earth. It will often strike the highest point in that general area, resulting in direct strikes for victims caught in the open. Being attached to or carrying a metal object (e.g., radio antenna, umbrella, or golf club) may increase the risk of injury. Often, there is a cohort of patients affected by a single strike due to either a spreading of current through the ground, persons being in contact with an
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object, or “side splash” from an object to a person or person to person. Most current “flashes over” the outside of the person who is struck. Rarely does this cause cardiac or respiratory compromise. The extent of injury from lightning is often difficult to predict due to the rapid rise and fall of the energy involved.
EPIDEMIOLOGY Lightning is consistently one of the primary causes of death due to natural phenomena, second only to flash floods. The estimate for annual deaths from lightning injury in the United States ranges between 50 and 300. The true incidence is not known because the majority of potential patients do not seek treatment. Approximately 20%–25% of total injuries are lethal. Approximately 74% of survivors have some permanent injury. Commonly, persons struck by lightning include athletes and outdoor enthusiasts. A significant number of injuries are also work related. Indoor victims are commonly using the telephone or another appliance. Most mortality results from direct strikes.
CLINICAL PRESENTATION Due to the short period of time that the body is exposed to the current, cardiac and pulmonary arrest are more common than extensive burns or renal failure from myoglobinuria. Cardiac asystole may occur due to direct current injury; however, the heart’s intrinsic automaticity may restore rhythm. Respiratory arrest can occur due to the paralysis of the medullary respiratory center. This can persist and lead to arrhythmias such as ventricular fibrillation due to hypoxia. Other common injuries include autonomic instability and various neurological injuries. Acute myocardial infarction is a rare finding. Patients may develop neurogenic shock as a result of spinal cord injury or hypovolemic shock secondary to trauma.
EXAMINATION Lightning injuries can affect any organ system, and thorough primary and secondary surveys are necessary to avoid overlooking sequelae. The examiner should maintain a high level of suspicion for possible cardiac involvement if entrance/exit wounds are on the superior and inferior aspects of the body. Also, the clinician should be wary of a patient’s loss of consciousness at any time. Neurological problems are common and range from mild confusion to paralysis. More than 70% of patients have some altered level of consciousness. Paralysis may be permanent or a
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temporary flaccid paralysis of the lower extremities known as keraunoparalysis. The patient’s condition should be fully treated as an acute spinal cord injury if any deficit is noted. Other neurological abnormalities may include seizures or fixed dilated pupils occurring as a result of autonomic dysfunction or serious head injury. Ruptured tympanic membranes are also common and occur in as many as 50% of persons struck by lightning. Traumatic injuries may include any assortment of fractures or dislocation. Special attention should be paid to inspecting the patient for signs of secondary injury. This may occur either from a fall, debris, or burns from metal portions of clothing or jewelry. Burns may result from the evaporation of water on skin or from the heating of clothing and its attachments or objects attached to the patient. They may also occur at the flexor surfaces as the current causes flexion and moisture in the crease causes an arc. The pathognomonic fernlike burns seen in persons struck by lightning are known as Lichtenberg figures. These form as a result of the cutaneous imprinting of electron showers flowing over the skin, and they quickly resolve. An index of suspicion must also be maintained for compartment syndrome, although fasciotomy is seldom needed. Various ocular injuries can occur after lightning injuries. These may include retinal detachment, intraocular hemorrhage, cataracts, or various corneal disruptions. Cataracts seldom occur immediately and may form up to years after the initial injury.
LABORATORY FINDINGS The following laboratory tests should be performed: CBC with differential, liver function panel, cardiac enzyme measurements such as troponin and creatine kinase, and urinalysis. The physician may also consider a metabolic panel and arterial blood gas analysis, if necessary, to check electrolyte levels and acid-base status. A coagulation profile can also be ordered, although coagulopathy and DIC are rare. ECG should be performed. Acute myocardial infarction is rare, although nonspecific ST-segment changes are common.
DIAGNOSIS The physician should look for entrance or exit wounds, skin manifestations, or other signs of injury if a patient are brought in without a witness to the lightning strike. A history should be obtained from bystanders or emergency medical services (EMS) personnel as to the condition of the scene. The diagnosis of lightning strike should be considered in the case of unexplained loss of consciousness or coma.
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RADIOGRAPHS Specific radiographic studies may be necessary based on a patient’s presentation and any traumatic injuries. A low threshold should be maintained for obtaining a chest radiograph, cervical spine radiograph, or CT can of the head without contrast in the case of either trauma or altered mental status.
TREATMENT AND OUTCOME The treating physician should manage the airway, obtain intravenous access, provide supportive care, and treat cardiac arrhythmias if they are present. If hyperthermia is present, the patient should be warmed. Any burned areas should be cleaned and treated, and tetanus prophylaxis should be updated if not current. Observation on telemetry is warranted if there is a significant clinical suspicion. If the urinalysis results are positive for myoglobin, treatment should include alkalinizing the urine with bicarbonate, and urine output should be maintained with the administration of fluids. The patient should be admitted for any serious injury or if cardiopulmonary arrest occurs at any time. Also, the patient should be admitted for observation in the case of any ECG changes or dysrhythmias.
Bibliography Diaz S: In Blackwell’s Primary Care Essentials: Emergency Medicine. Blackwell Science: London, 2002, pp 62–64. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2010–2019. Salyer S: In The Emergency Medicine Physician Assistant Handbook. WB Saunders: Philadelphia, 1997, pp 141–143. Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5 Minute Emergency Medicine Consultant. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 642–643. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1298–1302.
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Marine Fauna Envenomations JAMES ALAN MORGAN AND JULIE ANN MORGAN
ICD Code: 989.5
Key Points Hundreds of thousands of marine injuries occur in the United States each year. Fortunately, few injuries prove fatal. ! Emergency Actions ! All marine injuries are subject to infections with gram-negative rods. Even minor cuts caused by coral should be treated with antibiotics.
DEFINITION With 71% of the earth’s surface composed of ocean and approximately 80% of the world’s population inhabiting costal regions, it is not surprising that more than 50,000 marine envenomations occur worldwide each year. Therefore, healthcare providers must be prepared to treat patients with a variety of marine-related symptoms ranging from pruritus, paresthesias, bronchospasm, ascending paralysis, seizures, respiratory failure, and arrhythmias. The types of injuries can be divided into those caused by shock, stinging, trauma, and ingestion of poison. These injuries can cause hemorrhage, lacerations, infections, envenomations, or infection from foreign bodies.
EPIDEMIOLOGY Hundreds of thousands of marine injuries occur in the United States each year. Fortunately, few injuries prove fatal. Severe bites from sharks and barracudas have a high mortality and morbidity rate. Approximately 50–100 shark attacks occur annually worldwide. The biting force of some sharks can reach 18 tons per square inch. Between 10% and 20% of all shark bites prove fatal. There are more than 4000 species of sponges that can inflict pain from horny elastic skeletons. Over 9000 species of coelenterates exist, and more than 100 species are dangerous to humans. Coelenterates are divided into three groups: hydrozoans (e.g., Portuguese man-of-war), scyphozoans (e.g., jellyfish), and anthozoa (e.g., anemones). Coelenterates possess
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venom-charged stinging cells called nematocysts. The stinging nematocysts are located on single organelles on the surfaces of the tentacles, and they are triggered by contact with the victim. The Atlantic Portuguese man-of-war (Physalia physalis) is a floating sail that inhabits the surface of the ocean. It has multiple nematocystbearing tentacles that can measure up to 30 m in length. These tentacles can break off, and they are often found on the beach. These animals have the ability to discharge venom for months after breaking off. Jellyfish (Chironex fleckeri) are scyphozoan animals that have some of the most potent venoms in existence. There is a 15%–20% mortality rate from box jellyfish stings, which can kill within 30 seconds.
PATHOLOGY Specialized glands of marine fauna produce crinotoxins. These toxins are usually gastric secretions or slimes and are administered without the aid of traumatogenic devices. Bacterial toxins are products of decomposition that are eaten and are called oral toxins. Venoms that are produced in specialized glands and delivered by special traumatogenic devices are called parenteral toxins. Most marine bacteria are halophilic, motile, and heterotropic and are gram-negative rod forms. Protozoa, yeasts, croalgae, and viruses are present in sea water, marine life, and marine sediments. Bites from sharks and barracudas cause massive tissue loss and destruction. The two major concerns regarding shark-attack injuries are massive tissue injury with hemorrhagic shock and an extremely high incidence of atypical microorganisms that produce wound infections. Sponges have spicules made up of silicon dioxide and calcium carbonate, which can cause a severe dermatitis or “sponge diver’s disease.” Sponges also produce crinotoxins, which are direct thermal irritants in the form of okadaic acid, halitoxin, and subcritine.
CLINICAL PRESENTATION AND EXAMINATION Cuts caused by coral present are accompanied by erythema, stinging pain, and pruritus. Erythema occurs within minutes after the person is cut. If the cut is not treated, cellulitis and ulceration with sloughing of the tissue can occur. These wounds heal very slowly (usually 3–6 weeks). Wound necrosis, reactive bursitis, local ulceration, and deep cellulitis with lymphangitis can develop. A person who comes in contact with a sponge presents with a pruritic dermatitis in the first few hours. After a few hours, an itching and burning
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sensation ensues and can progress to localized joint edema, soft tissue edema, joint stiffness, and vesiculation. The skin may become purpuric and mottled. Mild symptoms usually resolve in 3–7 days without treatment. If a patient’s skin comes in contact with a large sponge, this envenomation can cause cramps, and the areas of contact can become bullous and purulent over several hours. An anaphylactoid reaction or systemic erythema multiforme reaction can develop 7–14 days after exposure to a large sponge. Calcium carbonate can cause an irritant dermatitis. Surface desquamation can occur 10 days to 2 months after contact. Contact with a coelenterate produces an itching, burning, and urticarial reaction. Mild contact causes a mild erythematous reaction. Severe envenomation can cause a delayed, hemorrhagic, or zoster form of reaction within 4–12 hours after contact. The fire coral (Millepora species) can cause severe, intense, painful burning and itching within seconds after contact. Within 30 minutes, warmth, redness, and pruritus ensue. The lesions usually resolve in 3–7 days, but hyperpigmentation can remain for 4–8 weeks. Jellyfish stings can present with hypotension, muscle spasms, respiratory and muscle paralysis, and death. A patient with this condition presents with immediate intense pain. The person collapses within minutes of the sting, and wheals, vesicles, and a dark reddish-brown or purple whip-like flare pattern with stripes occur within 8–10 minutes of envenomation. Blisters can occur within 6 hours, and a superficial necrosis can occur in 12–18 hours. On occasion, a “frosted” pathognomonic, transverse cross-hatch pattern presents as the sting site.
DIAGNOSIS A diagnosis of envenomation caused by marine fauna is made by taking a history of exposure and evaluating the clinical presentation.
LABORATORY FINDINGS There are no specific laboratory tests for marine fauna envenomations. If cellulitis or sepsis is suspected, a CBC, blood cultures, and electrolyte tests should be performed.
TREATMENT All marine injuries are subject to infections with gram-negative rods. Even minor cuts caused by coral should be treated with antibiotics. The patient should be treated with trimethoprim-sulfamethoxazole or ciprofloxacin. Culture specimens should be taken from all wounds. If rapidly
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progressive cellulitis or myositis develops, the patient should be treated for Vibrio parahaemolyticus or Vibrio vulnificus infection. If a wound has the classic erysipeloid reaction, the patient should be treated for Erysipelothrix rhusiopathiae infection. Cephalexin, penicillin, or erythromycin can be used to treat most of these infections. The Vibrio species can be treated with third-generation cephalosporins. If intravenous antibiotics are required, tobramycin, mezlocillin, azlocillin, tetracycline, gentamicin, chloramphenicol, piperacillin, trimethoprim-sulfamethoxazole, or ciprofloxacin should be given. Bites are subject to infection, crush injury, and lacerations. Clostridia are a major infective organism in bites. All bite injuries should receive intramuscular tetanus, 0.5 ml, and intramuscular tetanus immune globulin, 250–500 mg. All bites should be imaged to check for foreign bodies, teeth, coral fragments, or fractures resulting from crush injury. An orthopedic or general surgery consultation is needed if fractures or a large tissue loss is present. Cuts caused by coral are treated with antibiotic therapy. If stinging is severe, rinse the cut site with diluted acetic acid (vinegar) or isopropyl alcohol 20%. Always obtain a radiography of the wound to check whether a fragment of coral was left behind. All wounds should be examined thoroughly for foreign bodies. If the wound is deep, do not close the wound with sutures; rather, close the wound with adhesive tape and debride the wound again in 3–4 days. The wound should be dressed with a sterile wet-to-dry dressing and should be cleaned twice daily with normal saline or a dilute povidone-iodine solution 1%–5%. Bacitracin or polymyxin B-bacitracin-neomycin ointment can be used if the patient is allergic to povidone or iodine. Radiographs should be obtained of all injuries caused by sponges, especially if the interphalangeal or metacarpophalangeal joints are involved. Broken pieces of sponge are often retained by the skin, and frequently they are not radiolucent. The skin should be dried very gently, and any spicules should be removed carefully. Adhesive tape can be used to remove the spicules, and facial peel can be used for large areas. There is no treatment for the irritant dermatitis or desquamation of skin caused by contact with calcium carbonate particles in the sponge. Pain can be treated with acetic acid (vinegar) 5% or isopropyl alcohol 40%–70%. The site should be soaked for 10–30 minutes up to four times a day. Topical steroids should not be applied because they will worsen the primary reaction if applied before acetic acid. If erythema multiforme occurs, the patient should be given systemic corticosteroids (e.g., prednisone, 60–100 mg, PO for 2–3 weeks). After acetic acid has been applied and decontamination is complete, topical steroids can be applied to reduce itching. If severe pruritus is present, antihistamines can be given. The treatment of large or severe jellyfish stings includes supportive care, airway ventilation assistance, and hemodynamic support. All victims
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who are stung by coelenterates should be observed for at least 8 hours. All stings should be rinsed immediately with saltwater, not freshwater. The wound should not be rubbed. The tentacles should be removed with forceps and a well-gloved hand to prevent self-envenomation of the clinician. Ice packs should be applied to the sting site. Apply acetic acid (vinegar) 5% or isopropyl alcohol 40%–70% to the sting site for at least 30 minutes to decontaminate the area. The remaining nematocysts can be removed by applying shaving cream or a paste of baking soda, flour, or talc, and then shaving the area with a razor. Tetanus should be given and antibiotic therapy should be started. Local anesthetic or mild steroid lotions can be applied and oral antihistamines taken to stop any itching. If left untreated, symptoms resolve in 1–2 weeks.
Bibliography Auerbach PS, Halstead BW: Injuries from nonvenomous aquatic animals. In Auerbach PS (ed): Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Isbister GK, Caldicott DG: Trauma and envenomations from marine fauna. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Otten EJ, Blomkalns AL: Venomous animal injuries. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Weisman RS: Marine envenomations. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002.
Submersion Incidents JUSTIN MADILL
ICD Code: Drowning Nonfatal Submersion 994.1
Key Points/Quick Reference Submersion incidents primarily affect males, toddlers, teens, and elderly persons. Hypoxia is the key pathophysiological insult. Primary treatment is adequate oxygenation and ventilation. Early extrication and resuscitation is critical. In almost all cases, an attempt should be made to resuscitate persons who have undergone a submersion incident.
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! Emergency Actions ! Rapid extrication and early resuscitation are the most important factors influencing morbidity and mortality. The patient should be extricated with cervical spine immobilization if the circumstances suggest cervical spine injury. If the airway is not patent, the patient should be intubated. Adequate ventilation should be ensured and high-flow oxygen should be administered to all symptomatic persons who have undergone submersion incidents. The patient’s circulatory status can be addressed by monitoring vital signs, gaining intravenous access, and obtaining an ECG. CPR should be performed immediately upon extrication if the patient is pulseless. The patient should be kept warm and dry, and other injuries should be addressed as needed. Important history such as submersion time, medical history, and precipitating events should be obtained. Lastly, the patient should be transported via EMS to the ED, where focused assessment and management is performed.
DEFINITIONS Drowning is death resulting from suffocation and hypoxia after submersion in any liquid, usually water. Near drowning is survival after a submersion incident. Submersion incident is a general term including both drowning and near drowning, and it does not involve prognosis. Secondary drowning, previously used to describe the delayed deterioration of a well-appearing patient after a submersion incident, causes confusion and should be avoided. Immersion syndrome is sudden death after cold water submersion due to vagally induced dysrhythmias. Wet drowning occurs with aspiration of liquid. Dry drowning, the absence of aspiration resulting from laryngospasm, occurs in 10%–15% of cases.
EPIDEMIOLOGY Drowning is the fourth leading cause of accidental death, accounting for 4500 deaths per year in the United States. Drowning is second only to motor vehicle accidents as the most common cause of accidental death in children younger than 15 years. The incidence of near drowning is unknown but is several times greater than the incidence of drowning. There is a trimodal distribution of submersion incidents. The first peak occurs in toddlers and young children, most often in a residential swimming pool, followed by the bathtub. The most common factor in toddler drowning is inadequate supervision. Toddlers younger than 1 year have the highest drowning rate. The second peak occurs in adolescents and young adults, most often in lakes, rivers, and saltwater bodies. Teenaged males have the second highest drowning rate; alcohol and drug use may be involved. The third peak occurs in elderly persons, who have an increased risk of bathtub drowning and often have preexisting medical conditions.
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Rates of incident are higher for males of all ages and higher for black persons than for whites. Seizures, syncope, cardiac arrest, or stroke while swimming, diving and boating accidents, drug or chemical intoxication, hyperventilation before underwater swimming, cerebral air embolus in scuba divers, inability to swim, preexisting medical problems, exhaustion, hypothermia, nonaccidental childhood trauma, homicide, or suicide all may play a role.
PATHOPHYSIOLOGY Unexpected submersion causes voluntary apnea and panic. Involuntary breathing occurs at a certain PaO2 and PaCO2, causing aspiration and possibly laryngospasm. Water floods the alveoli, causing diffusion impairment and surfactant lost, leading to atelectasis, decreased compliance, and ventilation-perfusion mismatch. Aspiration of particulate matter and emesis may exacerbate pulmonary injury. These insults may lead to noncardiogenic pulmonary edema. The final common pathway is hypoxia. Initially there is respiratory acidosis, followed by a metabolic acidosis. Cardiovascular dysfunction, dysrhythmias, and neurological dysfunction result from hypoxia, acidosis, and ischemia. Differences between freshwater and saltwater aspiration have been noted in animal studies; however, most victims who survive do not aspirate enough volume to give rise to clinically important differences in serum electrolytes or blood volume. Renal failure, hemolysis, and DIC are rare. The concern for respiratory deterioration after an initially stable presentation, or “secondary drowning,” is unwarranted. This probably represents evolution of preexisting lung injury, and symptoms should be evident within 4–6 hours of the injury. The parasympathetic activation of the diving reflex may occur with cold-water submersion. This results in peripheral vasoconstriction, shunting blood to the heart and brain, apnea, and bradycardia. Theoretically, this allows prolonged cold-water submersion with delayed CNS damage. However, this reflex may not be present or strong enough to be protective, as once was thought. In addition to the diving reflex, cold-water submersion results in hypothermia. This decreases metabolic demands, theoretically delaying cerebral hypoxia. The development of hypothermia may be more important than the diving reflex in protecting against CNS damage. However, cold-water submersion itself may have the negative consequences of immersion syndrome (i.e., induction of lethal arrhythmias), exhaustion, and altered consciousness. Severe hypothermia indicates prolonged submersion and is a poor prognostic sign. Despite this, individuals have survived after prolonged cold-water submersion.
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CLINICAL PRESENTATION Patients who have experienced a submersion incident may present anywhere along the spectrum, from alert and oriented to comatose and in cardiac arrest. The clinician should observe for signs and symptoms of pulmonary insufficiency, hemodynamic instability, neurological injury, and hypothermia. An adequate history should be obtained, including assessment of submersion time; fluid type and temperature; events of the incident; level of patient consciousness and vital signs at the scene; signs, symptoms, and treatment before arrival; and any pertinent medical history.
PHYSICAL EXAMINATION The physical examination should be focused on vital signs, cardiopulmonary status, and neurological examination. Core temperature should be measured with a low-reading rectal thermometer. Hypothermia may be present in the case of cool, pale, and cyanotic skin. With severe hypoxia, vital signs may be decreased or absent. The healthcare provide should inspect the oropharynx for water, emesis, or foreign matter. He or she should auscultate for wheezing, rales, or rhonchi on pulmonary examination, although the chest may remain normal to auscultation in the presence of aspiration. Patients may be hemodynamically unstable due to hypothermia and hypovolemia, with associated arrhythmias. An ECG may reveal sinus bradycardia or atrial fibrillation, the most common initial arrhythmias. Atrial fibrillation is especially common in patients with hypothermia. Evidence of ischemia, sinus tachycardia, ventricular ectopy, or asystole may also be seen. Serial neurological examinations should be performed. Neurological injury may be manifested as altered mental status, decorticate or decerebrate posturing, nonreactive pupils, or absent reflexes. Cervical spine injuries and head trauma should be suspected in all unwitnessed incidents. A CT scan of the head should be performed and cervical spine precautions maintained if the history includes trauma or if no history available.
LABORATORY FINDINGS Laboratory values usually will not affect management and are often normal. However, it is routine to perform an arterial blood gas analysis, CBC, serum chemistry and electrolyte measurements, coagulation panel, and urinalysis. Cardiac enzyme levels should be checked for victims who require CPR, have dysrhythmias, or have ECG evidence of ischemia. Arterial blood gas analysis usually shows a respiratory and metabolic acidosis, hypoxia, and hypercapnia. Serum chemistry results are usually normal, except for a decrease in serum bicarbonate, indicating hypoxia. CBC results are usually normal but may show leukocytosis.
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DIAGNOSIS A diagnosis is made primarily on the basis of history, supplemented by physical examination results that support fluid submersion. Laboratory and radiographic studies may support the diagnosis, although these often show no abnormalities and are not required to make the diagnosis.
RADIOGRAPHS Chest radiography should be performed on any symptomatic patient. The chest radiograph may reveal diffuse or isolated patchy infiltrates or pulmonary edema. However, it may be entirely normal, even in a symptomatic patient. An initially normal chest radiograph may be followed by another that displays these patterns, if the process is repeated later. Chest radiographs do not correlate with PaO2.
TREATMENT AND OUTCOME Pre-ED management begins with rapid, cautious removal of the person from the water (Box 6-7). In water, CPR is ineffective and dangerous for both the patient and the rescuer. Spinal precautions should be implemented if a traumatic mechanism is suggested. A patent airway should be maintained and ventilation ensured. Endotracheal intubation should be performed if the patient is not spontaneously breathing or if the patient is unable to protect his or her own airway. All patients in such situations should be given supplemental oxygen. CPR should be immediately
Box 6-7 Prognostic Indicators in Submersion Incidents Good The patient is alert on admission. Hypothermia is present. The patient is an older child or adult. Submersion time was brief. On-scene basic or advanced life support is available. The patient exhibits good response to initial resuscitation measures. Poor The patient is aged less than 3 years. Severe hypothermia is present, with core temperature lower than 33 C. The patient exhibits fixed, dilated pupils upon arrival at the ED. The patient was submerged longer than 5 minutes. No resuscitation attempts were made for more than 10 minutes after the incident. There is preexisting chronic disease. The patient's arterial pH is <7.10. CPR or asystole was required on arrival to the ED. The patient was comatose on admission to the ED.
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initiated in a pulseless patient. Abdominal thrusts and postural drainage do not affect the ability to oxygenate because humans aspirate small quantities of water. These delay definitive care and should only be done when there is evidence of obstruction. Normal body temperature should be maintained. Resuscitation should nearly always be started in the field because witnesses’ estimates of submersion time are often inaccurate, the clinical picture of hypothermia can mimic death, and there are case reports of survival after prolonged submersion. Any patient who has experienced a significant episode, including those asymptomatic at the scene, should be transported to the ED for evaluation. ED personnel manage resuscitation, treatment of respiratory failure, evaluation and treatment of injuries, contact of consultants, and disposition. Resuscitation should be emphasized, even though survival with poor neurological outcome is possible. A patent airway must be ensured, and oxygen, pulse oximetry, cardiac monitoring, and intravenous access must be provided. Laboratory studies, including an arterial blood gas analysis and chest radiographs, should be undertaken for all symptomatic patients. The cervical spine should be immobilized unless its integrity can be confirmed. A spontaneously breathing patient’s degree of respiratory distress and ability to protect the airway and the presence of associated injuries dictate when endotracheal intubation is required. If the PaO2 is below 50 mmHg or the PaCO2 is above 50 mmHg on 100% oxygen by mask, intubation should be introduced. A nasogastric tube should be placed to avoid aspiration. Mechanically ventilated patients should receive positive end-expiratory pressure or continuous positive airway pressure to overcome atelectasis, decreased compliance, and pulmonary shunting. An accurate core temperature should be obtained with a low-reading thermometer; resuscitation is impossible if hypothermia is not treated. Patients with hypothermia should be warmed to at least 30 –32.5 C before resuscitation efforts are stopped; hence the maxim, “You aren’t dead until you are warm and dead.” Hypothermia, hypoxia, hypotension, hypovolemia, bronchospasm, electrolyte abnormalities, seizures, and arrhythmias should be addressed with standard treatment. Neither antibiotics nor steroids alter the course of aspiration pneumonia or pulmonary edema and should not be used prophylactically. Sodium bicarbonate has the potential disadvantages of increasing sodium and fluid load and, paradoxically, increasing lactate, thereby increasing CO2 and worsening acidosis. Cardiac irritability and acidosis respond more favorably to correction of hypoxia. Rapid extrication, prehospital response, and early resuscitation are widely recognized as the most important factors influencing morbidity and mortality in a person who has undergone a submersion incident. The protective role of the diving reflex and hypothermia is unclear, but a combination of preferential shunting of blood to the brain, heart, and
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lungs, along with a generalized slowing of metabolism, may play a role in improved neurological outcome in select cases. However, severe hypothermia often indicates prolonged submersion and is a poor prognostic sign. Despite this, there are case reports of normal neurological outcomes after long periods of submersion, up to 66 minutes.
Bibliography Auerbach PS: Wilderness Medicine, ed 4. Mosby: St Louis, 2001, pp 1340–1365. Bolte RG, Black PG, Bowers RS, et al: The use of extracorporeal rewarming in a child submerged for 66 minutes, JAMA 1988;260:377. Chandy D, Weinhouse GL: Submersion injuries. Available at: http://www.uptodate.com/. Chochinov AH: Recovery of a 62-year-old man from prolonged cold water submersion, Ann Emerg Med 1998;31:127. Cummings P, Quan L: Trends in unintentional drowning: The role of alcohol and medical care, JAMA 1999;281:2198. Harwood-Nuss A, Wolfson AB, Linden CH, et al (eds): The Clinical Practice of Emergency Medicine, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 1694–1696. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2050–2054. Modell JH: Drown versus near-drown: A discussion of definitions, Crit Care Med 1981;9:351. Modell JH, Idris AH, Pineda JA, Silverstein JH: Survival after prolonged submersion in freshwater Florida, Chest 2004;125:5. Orlowski JP: Prognostic factors in drowning and near-drowning, J Am Coll Emerg Phys 1979;8:176. Quan L, Cummings P: Characteristics of drowning by different age groups, Inj Prev 2003;9:163–168. Siebke H, Rod T, Breivik H, Link B: Survival after 40 minutes: Submersion without cerebral sequelae, Lancet 1975;1(7919):1275. Tintinalli JE, Kelen GD, Stapczynski JS, et al (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1278–1281. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Snakebite Injuries JENNY E. DUNLAVY
ICD Code: Venomous E905.0, Nonvenomous E902.2, Sea E905.0
Key Points The quantity, lethality, and composition of snake venom vary with the age and species of the snake, the time of year, the geographical location, and the snake’s diet. ! Emergency Actions ! Prehospital care for a person with a snakebite includes immobilization of the injured area in a functional position below the level of the heart, administration of oxygen, establishment of intravenous access on the contralateral side, and transportation of the patient to the nearest medical facility. Tourniquets, incision and suction, and cryotherapy are no longer recommended and are strongly discouraged.
DEFINITION There are a total of 14 families of snakes, five of which contain venomous species: Colubridae, Hydrophidae, Elapidae, Viperidae, and Crotalidae. Roughly 20 of the 120 snake species indigenous to the United States are venomous and are members of either the Crotalidae or Elapidae family. The Crotalidae, often considered a subfamily of the Viperidae, are otherwise known as the pit vipers. They include the most prevalent North American venomous snakes: true rattlesnakes (Crotalus species), copperheads and water moccasins (Agkistrodon species), and pygmy and massasauga rattlesnakes (Sistrurus species). Pit vipers, native to every state except Maine, Alaska, and Hawaii, are named for their heat-sensitive foramen located between each eye and nostril, allowing for the location of warm-blooded prey or predators. It is the only 100% consistent characteristic of pit vipers used for identification. In addition, pit vipers have elliptical pupils, a triangular head, and a single row of scales on the anal plate, helping to differentiate them from other, harmless species of snakes. The cardinal characteristic of the rattlesnake is the tail rattle. The number and size of the rattles do not tell the age of the rattlesnake. The eastern (Crotalus adamanteus) and western (Crotalus atrox) diamondback rattlesnakes account for the most fatalities. The water moccasin or
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“cottonmouth” (Agkistrodon piscivorus), native to the southeastern and south-central United States, is semiaquatic and named for its pale white oral mucosa, highly visible when fully opened and contrasted by its dark olive to black coloring. The copperhead (Agkistrodon contortrix) is indigenous to the eastern two thirds of the country and is identified by hourglass markings on the body and a copper-colored head. Though not as toxic as rattlesnake and cottonmouth bites, severe envenomations from the copperhead, if left untreated, can result in death. There are two species of the Elapidae family of coral snakes found in the United States. The eastern coral snake (Micrurus fulvius) is found in North Carolina, South Carolina, Florida, Louisiana, Mississippi, Georgia, and Texas. The western or Sonoran (Micruroides euryxanthus) coral snake is native to Arizona and New Mexico. Coral snakes in the United States can be identified by characteristic broad red and black bands separated by yellow or cream bands on their body. The rhyme “red on yellow will kill a fellow; red on black venom lack,” based on the pattern of the snakes’ colored stripes, can be used to identify venomous coral snakes within the United States. In addition, they have black snouts, round pupils, and lack facial pits. These snakes are shy and nocturnal, accounting for relatively few snakebites per year.
EPIDEMIOLOGY Worldwide, approximately 3 million snakebites and 150,000 deaths occur each year. Within the United States, there are an estimated 45,000 bites each year, 8000 from venomous species, resulting in 5–10 deaths per year. Historically, North Carolina, Arkansas, Texas, and Georgia had the highest incidence of snakebites in the United States. However, the prevalence of snake envenomations has shifted in recent decades toward the southwestern United States due to migration of the population westward. Males are bitten nine times more frequently than females and deaths are most common in children, elderly persons, and persons who do not receive prompt treatment. More than 95% of bites occur on the extremities, occurring most frequently in July and August when snakes and their victims are most active. Due to the rising popularity of raising deadly venomous snakes, bites from captive native and nonnative snakes are becoming more common.
PATHOLOGY The severity of any venomous snakebite depends on the species and size of the snake, the amount and toxicity of the venom injected, the location of the bite, first aid treatment performed, the timing of definitive treatment, comorbid conditions, and the patient’s unique susceptibility to the venom.
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Snake venoms are comprised of a chemically complex mixture of proteins, many with enzymatic properties. Quantity, lethality, and composition vary with the age and species of the snake, the time of year, the geographical location, and the snake’s diet. Venom proteins include transaminase, hyaluronidase, phospholipase, phosphodiesterase, and endonucleases. These proteins damage capillary endothelium, resulting in blebs, dilation of the perinuclear space, and plasma membrane destruction. Plasma and erythrocytes leak into the tissues, resulting in massive accumulation of fluid in intracellular spaces, manifested as edema and erythema or ecchymoses. Plasma loss reduces the circulating blood volume and can lead to hypovolemic shock, hemoconcentration, and lactic acidosis. The peptides of snake venom appear to bind to multiple receptor sites in the prey. Crotalidae venom components have the most deleterious effects on the cardiovascular, hematological, respiratory, and nervous systems. Consequently, attempting to label a venom as a “neurotoxin,” “cardiotoxin,” “myotoxin,” or “hemotoxin” is misleading.
CLINICAL PRESENTATION Pit viper envenomations commonly include one or more fang marks, localized burning pain usually occurring within 5 minutes, and early progressive edema around the bite site shortly thereafter. Most clinical finds after a pit viper bite emerge within 30–60 minutes. Local tissue injury may progress to bullae, lymphangitis, erythema, and ecchymoses within 3–6 hours. Systemic manifestations usually include nausea, vomiting, perioral paresthesia, tingling of fingertips and toes, fasciculations, lethargy, and weakness. Patients may also note a rubbery, minty, or metallic taste after being bitten by a larger rattlesnake. Severe systemic effects include tachycardia, respiratory distress, hypotension, and altered mental status. Coagulopathy often occurs after a rattlesnake bite. Pit viper venom also alters capillary membrane and red blood cell membrane permeability, ultimately manifesting as hypovolemic shock, acidosis, and multiorgan failure. In contrast to pit viper envenomations, coral snake envenomations produce relatively few local effects. There may, however, be marked salivation, tremors, drowsiness, euphoria, and cranial nerve palsies. Death is ultimately caused by respiratory muscle paralysis. The onset of signs and symptoms may be delayed up to 12 hours after the snakebite. Once evident, the prevention of neurotoxicity may no longer be possible. Thus, prompt intervention is mandatory when there is any suspicion of a coral snakebite.
EXAMINATION The area around the bite should be examined for pain, erythema, and edema. One may also be able to judge the size of the snake based on
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the distance between fang marks. Greater than 15 mm likely indicates a very large snake, whereas less than 8 mm is consistent with a smaller snake.
DIAGNOSIS Positive identification of the snake as well as clinical manifestations of the envenomation are essential to the diagnosis. In the absence of positive identification, the focus of diagnosis become the history of a snakebite, location of the bite, area in the United States in which the bite took place, and objective symptoms and signs of an envenomation.
LABORATORY FINDINGS Baseline laboratory studies for all patients include CBC; coagulation profile; measurement of electrolytes, BUN, creatinine, magnesium, phosphorus, and calcium; liver function tests; cardiac tests; and blood type and cross-match.
TREATMENT Prehospital care includes immobilization of the injured area in a functional position below the level of the heart, administration of oxygen, establishment of intravenous access on the contralateral side, and transportation of the patient to the nearest medical facility. Tourniquets, incision and suction, and cryotherapy are no longer recommended and are strongly discouraged. ED treatment continues with advanced life support and prompt administration of antivenom. Antivenin Polyvalent (AVP), produced by Wyeth Laboratories since 1954, is derived from equine serum and developed for the treatment of pit viper envenomations. In October 2000, Crotalidae Polyvalent Immune Fab (FabAV/CroFab), developed by Savage Laboratories, was approved by the U.S. Food and Drug Administration (FDA), replacing the once widely used AVP. FabAV dissolves into solution quickly and does not require skin testing. It is administered under the principle of initial control and maintenance therapy. Four to six vials are initially administered to stop the progression of local effects, systemic effects, and coagulopathy. The initial dose may be repeated as necessary to establish initial control, followed by an additional two-vial maintenance dose at 6, 12, and 18 hours to prevent local recurrence. After reconstitution, each vial is diluted in 250 ml of crystalloid. The total volume, but not number of vials, may be reduced for use in small children. Clinical trials have demonstrated the effectiveness and improved safely profile of FabAV compared with AVP. However, if an acute reaction does
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occur, the infusion should be stopped and antihistamines administered. Epinephrine infusion may be necessary, depending on the severity of symptoms. Serum sickness, manifested as fever, rash, arthralgias, and lymphadenopathy, might be seen 7–21 days after treatment. It responds well to a tapering dose of prednisone. Pertinent history on presentation includes time of bite, general description of the snake, first aid measures undertaken, comorbid medical conditions, allergies, and history of snakebites in the past. A complete physical examination is important and includes careful examination of the bite site for evidence of fang marks and local reaction. Continuous observation for evidence of local and systemic progression of symptoms is critical. Baseline circumferential measurements at several points above and below the bite site should be documented every 15–30 minutes, and any advancing edge of swelling should be marked along with the time it was noted. Additional doses of FabAV may be needed if the patient’s condition deteriorates. In general, coral snakebites are treated in much the same way as pit viper bites. In addition, a pressure dressing is placed on suspected coral snake envenomations to delay absorption of venom from the bite site. When coral snake envenomations are suspected, five vials of Wyeth coral snake antivenom should be administered immediately. Between 10 and 15 vials might be necessary if symptoms develop. Children should receive the same amount. All snakebite victims receive tetanus immunization unless they are already up-to-date. Pain is usually managed with opioids, and mild sedation with benzodiazepines may be indicated for severe envenomations. Opioids and benzodiazepines should be avoided in suspected coral snake as well as Mojave and eastern diamondback rattlesnake envenomations due to their potent neurotoxic effects. Wound infections of pit viper bites are rare, and antibiotics are recommended only when there is evidence of wound infection. Local reaction to severe snakebite envenomations may include marked swelling, tenderness, tenseness, hypesthesia, and pain—mimicking true compartment syndrome. A clinical diagnosis of compartment syndrome requires compartment pressure greater than 30 mmHg. If elevated, conservative management includes limb elevation in conjunction with the administration of mannitol and an additional four to six vials of FabAV given over 1 hour. The additional antivenom should effectively neutralize the venom components thought to contribute to the myonecrosis leading to compartment elevation. If these measures fail and there is evidence of circulatory compromise within the next hour, surgical fasciotomy may be required to lower pressures. Because the onset of symptoms and signs can be delayed, all patients with pit viper snakebites should be observed in the ED for a minimum of 8 hours. Any mild envenomation syndrome at 1 hour may
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progress to severe within several hours and lead to death without appropriate treatment. Persons who have been bitten by a coral snake should be admitted for 24–48 hours of observation with frequent monitoring and aggressive respiratory care. Intensive care monitoring is indicated for any patient receiving antivenom.
Bibliography Dart RC, McNally J: Efficacy, safety, and use of snake antivenoms in the United States, Ann Emerg Med 2001;37:181–188. Dart RC, Seifert SA, Boyer LV, et al: A randomized multicenter trial of crotalinae polyvalent immune Fab (ovine) antivenom for the treatment of crotaline snakebite in the United States, Arch Intern Med 2001;161:2030–2036. Garfin SR, Castilionia RR: The effect of antivenin on intramuscular pressure elevations induced by rattlesnake venom, Toxicon 1985;23:677–680. Gold BS, Barish RA, Dart RC: North American snake envenomation: Diagnosis, treatment, and management, Emerg Med Clin Nam 2004;22:423–443. Gold BS, Barish RA, Dart RC, et al: Resolution of compartment syndrome after rattlesnake envenomation utilizing non-invasive measures, J Emerg Med 2003;24:285–288. Gold BS, Dart RC, Barish RA: Bites of venomous snakes, N Engl J Med 2002;347 (5):347–356. Gold BS, Wingert WA: Snake venom poisoning in the United States: A review of therapeutic practice, South Med J 1994;87:579–589. Hall EL: Role of surgical intervention in the management of crotaline snake envenomations, Ann Emerg Med 2001;37:175–180. Kitchens CS, Van Mierop LHS: Envenomation by the eastern coral snake (Micrurus fulvius fulvius): A study of 39 victims, JAMA 1987;258:1615–1618. Klauber LM: Rattlesnakes: Their Habits, Life Histories, and Influence on Mankind University of California Press: Berkeley, CA, 1956. Langley RL, Morrow WE: Deaths resulting from animal attacks in the United States, Wilderness Environ Med 1997;8:8. Malasit P, Warrell DA, Chanthavanich P, et al: Prediction, prevention, and mechanism of early (anaphylactic) antivenom reactions in victims of snake bites, Br Med J [Clin Res Ed] 1986;292:17–20. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Ownby C: Pathology of rattlesnake envenomation, In Tu AT (ed): Rattlesnake Venoms. Marcel Dekker: New York, 1982, pp 163–209. Parrish HM: Incidence of treated snakebites in the United States, Public Health Rep 1966;81:269–276. Rowland SA: Fasciotomy: The treatment of compartment syndrome. In Green DP, Hotchkiss RH, Pederson WD (eds): Green's Operative Hand Surgery, ed 4. Churchill Livingstone: New York, 1999. Ruha A-M, Curry SC, Beuhler M: Initial postmarketing experience with Crotalidae Polyvalent Immune Fab for treatment of rattlesnake envenomation, Ann Emerg Med 2002;39:609. Russell FE: Snake Venom Poisoning. Scholium International: Great Neck, NY, 1983, p 163. Russell FE: Snake venom poisoning in the US, Annu Rev Med 1980;31:247–259. Russell FE, Dart RC: Toxic effects of animal toxins. In Amdur MO, Doull J, Klaasen CD (eds): Casarett and Doull’s Toxicology: The Basic Science of Poisons. MacMillan: New York, 1990, pp 104–136.
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Russell FE, Eventor J: Lethality of crude and lyophilized Crotalus venom, Toxicon 1964;2:81–84. Steinberg EA, Russell FE, Underman AE: Preliminary clinical observations with prophylactic cyproheptadine hydrochloride in potential serum reactions to antivenins. In Rosenberg P (ed): Toxin: Animal, Plant and Microbial. Pergamon Press: Oxford, England, 1978, pp 489–493. Stocker KF: Composition of snake venoms. In Stocker KW (ed): Medical Use of Snake Venom Proteins. CRC Press: Boca Raton, FL, 1990, pp 33–56. White J: Bites and stings from venomous animals: A global overview, Ther Drug Monit 2000;22:65. Wingert WA, Chan L: Rattlesnake bites in southern California and rationale for recommended treatment, West J Med 1988;148:37–44.
Spider Bites and Scorpion Stings BARBARA A.CARR
ICD Codes: Spider 905.1, Scorpion sting 905.0
Key Points There will be initial localized redness and edema at the site of a spider bite or scorpion sting. Person bitten by a brown recluse will present with localized tissue necrosis and malaise and flu-like symptoms. Black widow bites will elicit diffuse crampy pain and hypertension. Persons with scorpion stings will present with severe localized pain and rare systemic symptoms. ! Emergency Actions ! Treatment for a scorpion sting or spider bite involves applying ice to the site and transporting the patient to the hospital.
DEFINITION Spiders and scorpions are members of the Arachnida class. There are approximately 30,000 species of venomous spiders and 1400 species of venomous scorpions; however, most are not harmful to humans. Only 50 species of arachnids pose a threat to inhabitants of the United
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States, primarily because most species do not possess stingers or fangs long enough to penetrate human skin. Venomous species of spiders that live in the United States include the black widow and brown recluse. The bark scorpion (Centruroides exilicauda) is the only potentially dangerous venomous scorpion in the United States.
EPIDEMIOLOGY Scorpion Scorpions are found throughout the world. In the United States, scorpions are found mostly in the southwest. However, only one species, C. exilicauda, is particularly dangerous. At one time it was found only in Arizona, though more recently it has also been spotted in California, New Mexico, Nevada, and Texas. This species has been known by several different names, including Centruroides sculpturans. It is commonly known as the bark scorpion and is typically found on or near trees. The venom apparatus of a scorpion is found on its tail and consists of a stinger and two venom glands. The toxicity of scorpion venom varies widely from species to species. The venom of C. exilicauda is predominantly a neurotoxin that causes or enhances repetitive firing of axons by activation of sodium channels. Despite its effects, no deaths have been reported from C. exilicauda envenomation in the United States since 1968.
Black Widow Spider The black widow spider (Latrodectus mactans) is found throughout the United States (except Alaska) and in southern Canada. It is glossy black with a bright red marking on the abdomen (often resembling an hourglass) and occasionally has bright red stripes. The Latrodectus hesperus spider is closely related to the black widow, and its bite is treated in the same manner. Black widow females are about twice as large as males, with a total length of 1½ inches (including the legs). It is typically found under rocks, in woodpiles, and in outhouses and stables. Females are usually aggressive only when guarding their eggs. Black widow spiders inject a controlled amount of venom through fangs. The venom consists of protein and nonprotein compounds and serves to paralyze and digest prey. In humans, the venom acts as a neurotoxin, causing depletion of acetylcholine at the presynaptic nerve terminal.
Brown Recluse Spider The brown recluse spider (Loxosceles reclusa) is found primarily in the south-central United States. Many species of Loxosceles are venomous
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to humans, and at least five are inhabitants of the United States. Brown recluse coloration is typically tan to dark brown, and its classic distinguishing mark is a violin-shaped darker area found on the cephalothorax. Its total length is 1 inch (including legs). As its name implies, this spider is not known to be aggressive. It is usually found under rocks, in woodpiles, and occasionally in attics and closets. The venom apparatus of a brown recluse is similar to that of most spiders. Its venom composition has not been completely determined but one primary enzyme, sphingomyelinase D, has been isolated. It causes localized tissue destruction via hemolysis and severe vasoconstriction. The systemic symptoms of envenomation are thought to be caused by an allergic reaction.
CLINICAL PRESENTATION Scorpion Scorpion stings present with immediate pain and stinging at the sting site. Localized redness and edema occur shortly thereafter. Envenomation by C. exilicauda may cause heightened sensitivity to touch in the area of the sting or local numbness and weakness. Systemic symptoms can occur within 30 minutes of envenomation and include nausea, vomiting, sweating, blurred vision, excessive salivation, itching of the nose and throat, anxiety, restlessness, hyperthermia, muscle spasms, hypertension, hemiplegia, syncope, pseudoseizures, cardiac arrhythmia, and respiratory failure.
Black Widow Spider The classic manifestation of a black widow spider bite is an initial pinprick sensation followed by minimal localized redness and swelling. Two small fang marks may be noted under close examination of the bite. If the victim is otherwise preoccupied, he or she may not feel the bite at all. Systemic symptoms begin 15–60 minutes later with dull crampy pain developing in the area of the bite and spreading to the rest of the body. Bites to the upper extremities tend to cause more pain in the chest, whereas bites to the lower extremities usually cause pain around the abdomen. The patient may present with a board-like abdomen, and his or her symptoms may mimic those of pancreatitis, acute appendicitis, or a peptic ulcer, though abdominal tenderness to palpation is usually minimal. Headache, vomiting, weakness, ptosis, difficulty speaking, dyspnea, conjunctivitis, anxiety, and crampy pain in all muscle groups may be present. The patient may also be hypertensive and will sometimes have elevated cerebrospinal fluid pressure. ECG changes may be present and usually
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mimic digitalis toxicity. Young children who have been bitten may not survive due to the much smaller volume of distribution of venom.
Brown Recluse Spider Brown recluse spider bites are often not felt initially but may also cause acute burning pain at the site. Over the next 3–4 hours a white ring of vasoconstriction is noted around the site, and pain increases. A bleb then forms over the center with a ring of erythema at the periphery; the bite at this stage often resembles a bull’s-eye. The bleb darkens, necroses over the next several hours to days, and spreads to the surrounding tissue, involving both the skin and subcutaneous fat. Necrotic lesions occur in only 10% of victims. Systemic symptoms of brown recluse envenomation include chills, fever, rash, nausea, vomiting, weakness, malaise, and petechiae. In the case of severe envenomation, the patient may present with thrombocytopenia, hemolysis, jaundice, acute renal failure, pulmonary edema, and shock. As with black widow spider bites, children are at greatest risk of mortality from a brown recluse bite.
EXAMINATION Physical examination of both spider bites and scorpion stings should include complete respiratory, cardiovascular, abdominal, and neurological examinations and close inspection of the suspected site of envenomation. The margins of any erythema or swelling should be marked and followed up for documentation of migration.
LABORATORY FINDINGS A CBC, urinalysis, and measurement of PT, PTT, C-reactive protein (CRP), erythrocyte sedimentation rate, electrolytes, BUN, and creatinine should be performed.
DIAGNOSIS The diagnosis of a spider bites and scorpion stings is often difficult due to inability of the patient to identify the offending arachnid. If the specimen has been secured, an attempt should be made to identify it using the assistance of a local entomologist, if necessary. The physician should obtain a history of the circumstances surrounding the bite or sting, the time elapsed from incident to presentation, and any past history of allergic reactions, medications, or medical problems. Physical examination and close attention to vital signs and laboratory analysis will aid in making a diagnosis.
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TREATMENT AND OUTCOME Scorpion Treatment for a scorpion sting involves applying ice to the site and transporting the patient to the hospital. C. exilicauda scorpion antivenin is available from the Antivenin Production Laboratory of Arizona State University. However, the antivenin is not FDA approved and quantities are limited. Antivenin is generally recommended in cases of severe envenomations. All victims of scorpion envenomation should be observed for 24 hours, and children should be admitted to the hospital and monitored closely. Narcotic analgesics and barbiturates have been reported to increase the toxic effects of the venom and should not be used. Intravenous diazepam may be used for muscle spasms and myoclonus. Ventilatory assistance may be required in children.
Black Widow Spider The initial treatment for a black widow spider bite consists of applying ice packs to the site, providing supportive care, and monitoring the patient for symptoms of hypertension. An ECG should be performed as part of the initial workup. The wound should be cleansed with soap and water, and a tetanus immunization should be given to all persons bitten by spiders if immunizations are not up-to-date. If the patient does not experience symptoms and the spider was not positively identified as a black widow, the patient may be discharged with instructions to return if any symptoms develop. In otherwise healthy adults, the signs and symptoms of a black widow spider bite usually disappear within 2–3 days. If pain is severe, calcium gluconate (10 ml of a 10% solution) infused intravenously over 20 minutes has been shown to alleviate symptoms. Serum calcium levels should be watched and cardiac monitoring should be initiated. Severe hypertension (i.e., diastolic pressure greater than 120 mmHg) should be treated with sodium nitroprusside, and the patient should be admitted to the hospital. Muscle spasms can be treated with dantrolene sodium, diazepam, or other benzodiazepines. Patients younger than 12 years or older than 65 years may be given Latrodectus antivenin (Merck). Because this antivenin is derived from horse serum, patients should be tested for horse serum sensitivity, and allergic reaction precautions should be taken before administration. Antivenin should be given to patients with severe envenomation, pregnant women, and patients not able to tolerate the stress of envenomation.
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Brown Recluse Spider Treatments for the bite of a brown recluse spider have been varied and controversial. Conservative treatment with cold compresses, elevation of the affected extremity, simple analgesics, and tetanus immunization are preferred for uncomplicated envenomations. If tissue breakdown occurs or if the bite appears in a site that is difficult to keep clean, prophylactic antibiotics such as cephalosporins or erythromycin may be used to reduce the risk of a superimposed cellulitis. Dapsone, 50–200 mg/day PO, has been shown to be helpful in preventing the local effects of the venom. Patients receiving dapsone therapy should be monitored for development of methemoglobinemia or hemolysis (in patients with glucose-6-phosphate dehydrogenase deficiency). Systemic steroids may be used in patients with systemic symptoms from Loxosceles envenomation. These patients should be admitted to the hospital and their urine output should be monitored for signs of acute renal failure. Dialysis may be necessary if acute renal failure occurs. Surgical consultation for evaluation of the wound is helpful; however, surgical debridement in the acute stage has been shown to prolong wound healing and to increase localized tissue destruction.
Other Species Several other species of spiders have been imported either intentionally or as stowaways on cargo ships and in luggage, including tarantulas. Tarantulas are popular pets in the United States and are unusual in that the abdominal hairs can be thrown by the spider, embedding in human skin and eyes. These hairs can cause conjunctivitis and severe allergic reactions and must be removed. ED care of tarantula bites is mostly supportive.
Bibliography Castells MC: Spider bites. Available at: http://www.uptodate.com. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Rivers CS, Dorfman T: Preparing for the Written Board Exam in Emergency Medicine, ed 4. Emergency Medicine Educational Enterprises: Milford, OH, 2003. Stibich AS: Brown recluse spider bite. Available at: http://www.emedicine.com. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2003.
Chapter 7
Infectious Disease Emergencies Diphtheria REX L. HOBBS, JR.
ICD Code NOS: 032.9
Key Points/Quick Reference Streptococcal infections or mononucleosis infections are often the presumptive diagnosis when diphtheria is present. When these tests fail to show these processes, especially in the face of worsening health and the presence of the pharyngeal membranes, the practitioner must consider diphtheria. ! Emergency Actions ! Rapid diagnosis and treatment with antibiotics and the diphtheria antitoxin, along with good respiratory support, is crucial when diphtheria is diagnosed.
DEFINITION As recently as the early 1900s, the respiratory infection caused by Corynebacterium diphtheriae resulted in hundreds of thousands of cases in the United States, with a mortality rate of as much as 10%. Most of its victims were children, who initially experienced cold symptoms that progressed into the formation of membranous structures in the throat that could eventually block the airways. Since the discovery of an antitoxin, the rise in availability of antibiotics, and the advent of the standard requirement of childhood immunization, the occurrence rate has dropped to fewer than five U.S. cases per year. However, human reservoirs of the disease are still found worldwide, with occasional epidemics punctuating the need to remain vigilantly watchful.
EPIDEMIOLOGY The epidemiology of diphtheria is as follows:
In the United States, 0.001 cases occur per 100,000 persons. The mortality rate is less than 10% overall but as high as 20% in persons younger than 5 years of age and in those older than 40 years. Humans are the only reservoir for the disease; person-to-person spread usually occurs by inhalation of respiratory droplets. 261
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Infection most commonly occurs in the winter and spring. The vaccine is 99% effective at preventing the disease if initial immunization and follow-up boosters are received. The infecting organism has both toxin-producing and non–toxinproducing strains.
PATHOLOGY C. diphtheriae is a gram-positive aerobic bacillus that has both toxinproducing and non–toxin-producing forms. It is the toxin-producing form that results in the most feared presentation, after being inhaled and deposited in the nasopharynx. The toxin results in local tissue destruction via protein synthesis inhibition, resulting locally in the formation of membranous structures in the nasal passages or, more commonly, in the throat. In the throat, they may reach a size that may occlude the airway. The toxin, which is readily absorbed into the bloodstream, may also cause myocarditis and, very rarely, a local motor neuritis that can spread to involve the limbs and respiratory musculature. Because of the wide-reaching effects of the toxin, both antibiotics aimed at the organism and antitoxin are necessary in the treatment of this infection.
CLINICAL PRESENTATION The initial presenting symptoms can very easily be attributed to the common cold, with such symptoms as fever, chills, sore throat, rhinorrhea, and cervical lymphadenopathy. These symptoms invariably worsen over 2–3 days, with the increased toxin activity resulting in white to green membranes forming along the tonsils and pharyngeal mucosa. These immovable membranes may become large in size and number and result in difficulty swallowing, stridor, or cough. Untreated, increased fever, cervical edema, pallor, tachycardia, and even coma are possible. Diphtheria may also result in cutaneous lesions that have a scaly to ulcerative look. Most of these cases occur in the homeless population.
EXAMINATION Because of the vagueness of early presenting symptoms, a complete examination of the head, ears, eyes, nose, throat, lymphatics, lungs, abdomen, and skin should be performed and repeated if symptoms persist or worsen. This is especially true if an exudative throat and tonsils are noted.
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Streptococcal and Epstein-Barr virus (EBV) infections may give similar signs and symptoms. A culture, antibody studies, or both should be considered to aid in the differentiation of these similar-appearing processes, especially if the condition is considered severe or progressive.
DIAGNOSIS Because of the rarity of diphtheria in the U.S. population, diagnosis is generally approached from the standpoint of ruling in more common problems such as streptococcal infections or mononucleosis with rapid screens, cultures, or serology testing. However, when these tests fail to show these processes, especially in the face of worsening health and the presence of the pharyngeal membranes, one must consider the use of a Gram stain (looking for gram-positive, club-shaped bacteria), culture with tellurite-infused medium, and toxin screening from serum using the polymerase chain reaction method. Depending on the severity of illness and other symptoms, drawing samples for a complete blood count (CBC), chemistry panel, and cardiac enzyme tests may be needed, along with electrography and chest x-ray.
TREATMENT If the index of suspicion for diphtheria is high, then treatment for the condition should be started without delay and continued once the diagnosis has been solidified. In addition to close supportive care, including selective intubation for those at risk, treatment involves a two-pronged attack aimed at the bacteria and the toxin. Erythromycin given intravenously or orally at 40 mg/kg every 12 hours for no less than 7 days is generally suggested; however, procaine penicillin G dosed intramuscularly at 600,000 units/day for persons weighing more than 10 kg may also be used. The antitoxin that will neutralize circulating toxin is available only from the Centers for Disease Control and Prevention (CDC; 1–404–639– 2889) and is administered intravenously after the patient has been tested for sensitivity to the equine-produced substance. It is advisable to perform posttreatment cultures to ensure complete clearance of the infection. In addition, household members and other close contacts should be treated with antibiotics, as mentioned previously, with antitoxin used only for symptomatic patients. Finally, it is also very important to alert the local health department because this is a reportable disease. The most important aspect of this disease is that it is, for the most part, a preventable one—thanks to the advent of routine pediatric immunizations (DTaP) and routine boosters (Td), which should be received every 10 years throughout life.
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Bibliography Centers for Disease Control and Prevention, Division of Bacterial and Mycotic Diseases. Diphtheria. Available at http://ww.cdc.gov. MacGregor RR: Corynebacterium diphtheriae. In Principles and Practice of Infectious Diseases, ed 4. Churchill Livingstone: Philadelphia, 1995, 1865–1871. Phelan D, et al: Current adult and pediatric vaccine recommendations, Infect Med 2001;18 (8s):FV6–FV14. Singh MK: Diphtheria. Topic 138. Aug. 16, 2004. Available at http://www.eMedicine.com.
Foodborne and Waterborne Infections JENNIFER JAMUL
ICD Code: Other food poisoning (bacterial) food poisoning unspecified D005.9
Key Points Ingestion of contaminated foods and beverages and the drinking of recreational water result in various clinical illnesses, predominantly related to the gastrointestinal (GI) tract. ! Emergency Actions ! Aggressive airway management is required in the case of a few toxin ingestions. The mainstay of treatment is assessing and maintaining circulatory volume.
DEFINITION The CDC defines foodborne disease as two or more cases of similar GI illness from ingestion of a common source. Etiological agents can include bacteria, viruses, parasites, toxins, and poisonous chemicals. Waterborne illness is defined by the CDC as illness that occurs after consumption or use of water intended for drinking (potable) or the ingestion or use of recreational water. Recreational water includes pools, spas, water park water, and fresh and marine surface waters. Dysentery is the passage of small-volume stools with gross blood and mucus with tenesmus (i.e., straining without passing stool) and fecal urgency (i.e., inability to delay stool evacuation by 15 minutes).
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EPIDEMIOLOGY In the United States, foodborne illness affects 76 million persons per year, more than 300,000 of whom require hospitalization. Annually, 5000 deaths from this cause are reported to the CDC. The actual numbers may be much greater because most cases go unreported because of the self-limited nature of many organisms. Any patient with foodborne illness may be the sentinel case of a major outbreak. Biological terrorism, through intentional contamination of a food or water supply, should be considered in any major outbreak of dysentery. Contamination occurs through multiple processes. Irrigation water can be contaminated with manure or sewage. In an urban setting, drinking water contamination can result from a water main break. Cross-contamination can occur via utensils, human food-handlers, and slaughter of animals through intestine content contamination with uncooked food. Improper storage, refrigeration, handling, or cooking increases the risk of foodborne disease. Special groups of patients who are more susceptible to disease may present with severe dysentery; these include infants, elderly persons, pregnant women, persons with liver disease, and immunocompromised persons. Patients taking medications that alter gastric pH have an increased risk of infection. Attendants and workers at day care centers, mentally impaired residents of custodial institutions, and travelers (especially outside the United States) all have an increased risk of contact with foodborne or waterborne pathogens.
CLINICAL PRESENTATION The clinical presentation of foodborne or waterborne illness is highly variable, depending on the infectious organism and the patient’s underlying illness (Table 7-1). Symptoms are predominantly GI related. Toxin poisoning can also include respiratory and neurological presentations. Historical information should include place of residence (e.g., custodial institutions), whether the patient has lived on or visited a farm, day care attendance, pet contact, travel, camping, sick contacts (especially in the same household), recent antibiotic use, and medications that alter gastric pH and GI motility. Recent ingestions of raw or poorly cooked foods (e.g., eggs, meats, shellfish, fish), unpasteurized milk or juices, and home canned goods should be inquired of the patient. Diarrhea is defined as three or more stools per day. Bacterial pathogens usually are six or more stools per day, fever, and symptoms lasting longer than 24 hours but less than 1 week. (Continued on page 272)
BACTERIAL ORGANISM (BACTERIAL)
TRANSMISSION/ INCUBATION
Bacillus cereus
1–6 hr
Campylobacter jejuni
Poultry; 2–7 days
Clostridium botulinum
Children/adults 12– 72 hr; improperly canned foods
Fecal/oral route; selfEscherichia coli, enterohemorrhagic limited (0157-H7) Salmonella Non-typhoid 8–48 hr; Typhoid 1–2 weeks
SIGNS AND SYMPTOMS
DIAGNOSTIC STUDIES
Sudden onset N/V; diarrhea Clinical diagnosis; may be present stool culture/toxin identification Fever/malaise; watery Positive fecal leuks; progressing to bloody stool/blood diarrhea cultures; CSF (in children) V/D, blurred vision, Contact State Health diplopia, dysphagia, Dept/CDC; send descending paralysis stool, serum, and food for toxin evaluation Fever ; copious bloody Fecal leuks and PCR/ assays diarrhea with fecal mucus Positive fecal leuks; N/V, malaise, HA, fever, abdominal cramps, stool cultures; blood cultures diarrhea foul/green brown to watery/bloody
TREATMENT
COMPLICATIONS/ SEQUELAE
Self-limited (24 hr); supportive care Supportive care; self- Organisms shed in stool limited (1 week) 3–5 weeks after resolution; antibiotics may shorten Antitoxin; ICU Prolonged recovery supportive care with mechanical ventilation Supportive care; fluoroquinolones
Hemolytic uremic syndrome
Supportive care; fluoroquinolones; third-generation cephalosporins
Chronic carrier state in typhoid infection
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Table 7-1 Foodborne and Waterborne Illnesses
Shigella
Fecal/oral,1–3 days
Staphylococcus aureus
Preformed enterotoxin Sudden onset of N/V, Clinical diagnosis; Supportive care; self from improperly abdominal cramps; fever stool culture, if limited (24–48 hr) refrigerated foods; and diarrhea may be indicated onset, 1–6 hr present 2 days (range, 1–5 Progression to translucent Stool culture; Aggressive fluid 50% mortality without days); water, fecal/ grey watery “rice water” darkfield replacement is the treatment oral, seafood stools 1 L/hr; shock microscopy; mainstay; negative fecal leuks fluoroquinolones; doxycycline 24–48 hr; waterborne, Fever, N/V/D, abdominal Stool, vomitus, blood Supportive care; self- Beta thalassemia increases limited (1 week); risk for acquisition; cultures; positive pain, may have undercooked pork, fluoroquinolones stool excretion can fecal leuks, positive scarlintiform rash unpasteurized milk or TCN persist for months after heme resolution; erythema nodosum, septicemia, mesenteric adenitis
Vibrio cholerae
Yersinia
Dysentery 20–30 stools/ day; fever
Positive fecal leuks; stool/blood cultures; biopsy
Supportive care; fluoroquinolones; antimotility drugs only with antibiotics
Severe anemia; convulsions (in children); pneumonitis; hemolytic uremic syndrome; Reiter’s septicemia; chronic carrier None
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VIRAL ORGANISM (VIRAL) Hepatitis A
Norwalk/Norwalklike viruses Rotavirus
TRANSMISSION/ INCUBATION 15–50 days; fecal/ oral, waterborne, shellfish, infected food-handlers Food/water contamination; 24–48 hr 24–72 hr; fecal/oral; winter months; most common in children
SIGNS AND SYMPTOMS
DIAGNOSTIC STUDIES
Diarrhea, dark urine, Elevated LFT results; jaundice, fever, malaise, positive IgM and N/V, abdominal pain anti-hepatitis A antibodies Abrupt V; abdominal Negative fecal leuks; cramps; watery diarrhea; PCR; F, respiratory symptoms immunoassays Vomiting then diarrhea Negative fecal leuks with abdominal cramps; low-grade fever
TREATMENT
COMPLICATIONS/ SEQUELAE
Supportive care, good 10% can have prolonged/ hygiene relapsing illness up to 9 months Supportive care; self- Malabsorption of fats and limited (2 days) disaccharides after illness Supportive care; self- None limited (1 week); vomiting resolves first, then diarrhea
PROTOZOA ORGANISM (PROTOZOA) Cryptosporidium
TRANSMISSION/ INCUBATION
SIGNS AND SYMPTOMS
5–28 days; Can be asymptomatic; veterinarians and watery diarrhea with farmers secondary cramps, flatulence: V, to animal low-grade fever reservoirs; water/ food contamination
DIAGNOSTIC STUDIES Enterotest; biopsy (small bowel); Giemsa stain
TREATMENT Self-limited (mean, 5–6 days; range, 2–26 days); immunocompromised; paromomycin; azithromycin
COMPLICATIONS/ SEQUELAE Immunocompromised patients: chronic malabsorption; respiratory involvement often fatal; can develop cholangitis
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Table 7-1 Foodborne and Waterborne Illnesses—Cont’d
Entamoeba histolytica
1–4 months; fecal/oral Fluctuation between Direct stool colonic inflammation examination for without dysentery to cysts/trophozoites; stools with mucus/ PCR blood, weight loss, N, anorexia 1–2 weeks; mean, 9 Widely variant; abrupt to Direct stool days; fecal/oral; insidious; explosive examination for waterborne watery diarrhea with cysts/trophozoites; cramping, foul flatus, V, string test; enzyme low-grade fever immunoassay transitioning to subacute (anorexia, fatigue, weight loss); erythema multiforme; urticaria Fecal/oral Mild transient diarrhea Oocysts in stool; with cramps to profuse Ziehl-Neelsen watery diarrhea, stain; biopsy of flatulence, anorexia, jejunum; string weight loss, fever, and test; eosinophilia malabsorption
Giardia lamblia
Isospora belli
Direct stool studies; acid-fast staining
Duration, 7 weeks or more; worse in immunocompromised persons; TMP/ SMX Metronidazole with iodoquinol (tissue amebicide with luminal agent)
Chronic suppressive therapy in patients with AIDS
Perforation with acute abdomen; toxic megacolon; ameboma; abscess (liver, brain, lung); carrier
Duration, 3–10 Carrier, malabsorption weeks; syndrome spontaneous clinical recovery common with or without disappearance of organism; metronidazole Self-limited in Persistent with recurrence: immunocompetent acalculous cholecystitis; host (2–3 chronic suppressive weeks); in therapy in patients with immunoAIDS compromised persons, TMP/ SMX or pyrimethamine (Continued)
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Fecal/oral; waterborne Abrupt onset of diarrhea (via raspberries)
Foodborne and Waterborne Infections
Cyclospora
SEAFOOD TOXIDROMES ORGANISM (SEAFOOD TOXIDROMES) Ciguatera fish poisoning
Clupeotoxin fish poisoning
TRANSMISSION/ INCUBATION
SIGNS AND SYMPTOMS
DIAGNOSTIC STUDIES
TREATMENT
Onset, minutes up to N/V/D with abdominal General studies; send Aggressive 24 hr; most within cramps; neurological food for evaluation supportive care; 2–6 hr; warm water symptoms mimic atropine, reef fish barracuda, organophosphate vasopressors snapper jack, poisoning, usually grouper develop after GI symptoms Violent onset within Metallic taste; xerostomia; General studies; send Aggressive 30–60 min; N/V/D; abdominal pain; food for evaluation supportive ICU herrings, sardines, severe paresthesias; care, gastric anchovies muscle cramps; vertigo; emptying delirium; hypotension
COMPLICATIONS/ SEQUELAE Death secondary to respiratory paralysis (low incidence); during recovery patients should avoid eating fish, shellfish, ETOH, nuts/ nut oils Death secondary to cardiovascular collapse
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Table 7-1 Foodborne and Waterborne Illnesses—Cont’d
Paralytic shellfish poisoning
Rapid onset, 30– 60 min; associated with “red tides,” shellfish
N, Nausea; V, vomiting; leuks, leukocytes; CSF, cerebrospinal fluid; D, diarrhea; CDC, Centers for Disease Control and Prevention; ICU, intensive care unit; N/V, nausea/ vomiting; HA, headache; TCN, tetracycline; LFT, liver function test; IgM, immunoglobulin M; PCR, polymerase chain reaction; TMP/SMX, trimethoprim-sulfamethoxazole; AIDS, acquired immunodeficiency syndrome; GI, gastrointestinal; ETOH, ethyl alcohol.
Foodborne and Waterborne Infections
Initial: paresthesias (facial), General studies; send Aggressive ICU care, Death secondary to numbness, vertigo, food for evaluation activated charcoal, respiratory failure; cranial nerve avoid atropine prolonged recovery; dysfunction progressive avoid ETOH to respiratory failure via diaphragm and chest wall paralysis, lack of GI symptoms Report to local health Scombroid poisoning Onset, minutes; Metallic peppery taste, HA; General studies; send Self-limited (8– department ingestion of dizziness; flushing; food for evaluation 12 hr); H1 and H2 blockers; bacterial urticaria; pruritus; supportive care decomposition or hypotension; seafood (scombroid arrhythmias; N/V/D and nonscombroid) Tetrodotoxin fish Rapid onset, 10 min HA; lethargy; weakness; General studies; send Aggressive airway Death can occur in less poisoning or delayed 4 hr, paresthesias of lips, food for evaluation management; than 20 min after usually 30 min tongue followed by supportive care; ingestion after ingestion hypersalivation,ataxia, atropine; charcoal Fugu (puffer fish) tremor blowfish, sunfish
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Organisms that have preformed toxins (e.g., Staphylococcus aureus, Bacillus cereus) usually will present with symptoms less than 7 hours. An enteropathogen that must first infect the intestine will usually present after more than 8 hours.
EXAMINATION The patient’s volume status and level of hydration should be assessed. Useful vital signs include orthostatic capability, mental status, skin turgor, moisture of mucous membranes, and urine output. Special attention should be given to the abdominal examination. The majority of foodborne and waterborne illnesses do not yield evidence of peritoneal infection. An exception would be an abscess produced by Entamoeba histolytica. If peritoneal signs are found, surgical consultation should be initiated. The rectal examination is to be performed for assessment of tenderness and to evaluate the stool for blood (i.e., heme). The neurological examination should include evaluation for paresthesias, motor weakness, or cranial nerve palsies. Botulism will present with a descending flaccid paralysis. Guillain-Barré can be a sequelae of Campylobacter jejuni infection. Guillain-Barré presents with ascending paralysis.
LABORATORY FINDINGS Laboratory examinations should include a CBC, chemistry studies, liver function studies, a b-human chorionic gonadotropin test (for female patients), and a urinalysis. Fecal leukocyte tests should be performed for any patient presenting with the possibility of foodborne illness. Bloody diarrhea with or without severe illness should be stool cultured. Immunocompromised patients and patients with evidence of bacteremia or sepsis require stool and blood cultures.
DIAGNOSIS A diagnosis is made on the basis of history, clinical presentation, laboratory findings, and the presence of fecal leukocytes. Diagnosis is confirmed by stool studies and cultures.
RADIOGRAPHS No specific radiographs are required for the diagnosis of foodborne or waterborne illness. A patient presenting with fever and respiratory symptoms should receive a chest radiograph. If perforation or acute abdomen is
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of concern, a chest radiograph along with a flat and upright radiograph of the kidneys, ureters, and bladder (KUB) should be obtained, along with surgical consultation. Computed tomography (CT) of the abdomen will aid in defining suspected abscesses or colon involvement, especially in the case of parasitic infections.
TREATMENT Treatment is largely supportive because the etiological agent is often not known during initial assessment. The practitioner should remember to treat the illness, not the infection. Intravenous fluids progressing to oral rehydration is the key of treatment. Soft drinks, sport drinks, fruit juice taken with saltine crackers, the oral rehydration solution recommended by the World Health Organization (WHO) or prepared commercial solutions such as Pedialyte can be used for oral rehydration. If vomiting is the predominant symptom, antiemetic agents should be administered as seen in the treatment of viral agents and preformed toxins of S. aureus and B. cereus. Antimotility medications such as loperamide should be avoided in febrile or dysenteric patients unless concurrent antibiotics are given. Antisecretory agents such as bismuth subsalicylate primarily blocks the effects of enterotoxin on intestinal mucosa. This agent also has antimicrobial and anti-inflammatory properties. Antimicrobial treatment is indicated if a bacterial agent is suspected, if the patient is immunocompromised, or if the course of illness would be greatly reduced. There has been increasing resistance of bacterial agents to antibiotics. In adults fluoroquinolones are recommended; usual treatment ranges from 1 to 5 days. In children, trimethoprim-sulfamethoxazole plus a macrolide (e.g., azithromycin) are used in place of a fluoroquinolone. Antibiotic treatment should not be continued if there is worsening or persistent diarrhea. If botulism is suspected, the botulinum antitoxin should be given as soon as possible to prevent further progression of neurological symptoms. The local health department should be contacted regarding reportable communicable diseases. Aftercare instructions for discharged patients include a clear liquid diet until vomiting is resolved for 24 hours and no dairy or red meat until diarrhea is resolved for 48–72 hours. The patient should avoid caffeine, alcohol, high fiber, and fatty foods. Staple foods such as cereals, toast, bananas, crackers, and potatoes should be eaten. Pregnant female patients can be treated with promethazine for vomiting and attapulgite for diarrhea. Bismuth subsalicylate and antibiotics such as tetracycline and fluoroquinolones should be avoided. Referral to an infectious disease or GI specialist for sigmoidoscopy or colonoscopy is recommended for persons with persistent diarrhea
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(lasting longer than 14 days), homosexual males, and immunocompromised patients. There are several systems in place to protect the consumer from foodborne disease. Surveillance for foodborne and waterborne pathogens in the United States takes place through FoodNet. The CDC, the U.S. Department of Agriculture, and the U.S. Food and Drug Administration collaborate to form the foodborne disease active surveillance network. Technological advances such as implementation of food irradiation in the future would greatly reduce the number of cases and deaths associated with foodborne illness. Through proper food-handling, storing, refrigeration, and cooking, patients can greatly reduce their future risk. Separating cooked and uncooked items aids in prevention of crosscontamination. Cleaning items such as utensils, food for preparation, and cutting boards will also reduce risk. The WHO and the CDC both post information on their Web sites to aid consumers in safe food-handling. When traveling, patients should be instructed to avoid local tap water and ice, unpasteurized products, and raw foods. Foods considered to be safer are steamed hot foods, dry foods, foods high in sugar content, and fruits that have been peeled by the consumer.
Bibliography Auerbach PS: Wilderness Medicine. Mosby: Philadelphia, 2001. Foodborne Illness Primer Work Group: Foodborne illness primer for physicians and other health care professionals, Nutr Clin Care 2004;7(4):134–140. Osterholm MT: Foodborne disease: The more things change, the more they stay the same, Clin Infect Dis 2004;39(1):8–10. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2003.
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Herpes Virus RICHARD L. DAGROSA
ICD Codes: Herpes simplex 054, Genital herpes 054.1, Herpetic gingivostomatitis 054.2, Herpetic meningoencephalitis 054.3, Herpes simplex with ophthalmic complications 054.4, Herpes simplex meningitis 054.72, Herpes simplex with other specified complications 054.79
Key Points Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) can affect many parts of the body.This family of viruses can cause blindness, encephalitis, and death in immunocompromised patients. ! Emergency Actions ! The early clinical diagnosis of herpes virus infection of the eye, a painful rash in an immunocompromised patient or in a neonate, can save sight and lives. A high index of suspicion for a herpes virus infection should always be elicited when a patient presents with unexplained pain, with or without a rash, with a viral prodrome.
DEFINITION Herpes viruses lead to a wide array of infections involving mucocutaneous surfaces, the central nervous system (CNS), and occasionally visceral organs. The herpes viruses all have the ability to dwell in the host as a lifelong latent infection and may cause clinical disease or recurrent disease at a time distant from primary infection. As a class, the herpes viruses are transmitted by close contact and are unable to penetrate intact skin.
Herpes Simplex Viruses 1 and 2 HSV-1 primarily causes oral lesions, whereas HSV-2 causes genital lesions. A prodrome of myalgias, fevers, malaise, and tender adenopathy may precede the lesions. The lesions are shallow painful ulcers that usually crust over within 7–10 days. Treatment is with acyclovir, valacyclovir, or famciclovir.
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Ocular HSV In ocular HSV infection, a prodrome of malaise, low-grade fever, and myalgias may precede a forehead rash. The classic lesion is a dendritic pattern seen after staining the eye with fluorescein dye. These lesions warrant prompt referral to an ophthalmologist because they can cause debilitating pain and blindness.
Bell’s Palsy The classic presentation of Bell’s palsy is hemiplegia or hemiparesis of the face with no forehead sparing. One must rule out stroke and look for ear lesions as a sign of Ramsay Hunt syndrome. Treatment is prednisone, acyclovir, and eye lubrication/protection.
Herpetic Whitlow Commonly seen in healthcare workers, herpetic whitlow most often affects fingers and is misdiagnosed as a felon. Tingling and burning sensations around the lesion site are frequently felt. The disease is self-limited and should be managed conservatively with local wound care. Incision and drainage is contraindicated because it will lead to the spread of infection, will delay healing, and may cause a superinfection to occur.
Herpes Zoster: Chickenpox Classically, herpes zoster is a disease of children. The lesions are described as “dewdrops on a rose petal” and are commonly seen in different stages of healing. A prodrome of malaise, fatigue, and low-grade fever may precede the rash by 48 hours. The lesions start centrally and progress to the extremities. The disease is self-limited. Local wound care and symptomatic relief are the treatments.
Herpes Zoster: Shingles The lesions of zoster are identical to those of chickenpox but only occur in a single dermatomal distribution, usually T3–L3. Patients report a sensation of burning and pruritus. The most debilitating consequence of shingles is postherpetic neuralgia, which leads to debilitating pain long after the lesions heal. Treatment should begin within 48 hours of rash onset and consists of acyclovir or valacyclovir. This shortens the course of the disease and decreases the risk of postherpetic neuralgia.
Epstein-Barr Virus A prodrome of myalgias, weakness, and low-grade fever may precede the posterior cervical lymphadenopathy and exudative pharyngitis of Epstein-Barr virus infection. A palpable spleen is often felt in patients
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infected with this virus. Treatment is primarily supportive, with rest and spleen protection for 4 weeks.
Cytomegalovirus In immunocompetent persons, cytomegalovirus (CMV) infection resembles an EBV infection without the exudative pharyngitis or cervical adenopathy. In pregnant women, CMV may cause intrauterine fetal demise or significant birth defects. The classic triad of petechia, jaundice, and hepatosplenomegaly is seen in 60%–80% of neonatal cases. In immunosuppressed patients or persons with human immunodeficiency virus (HIV) infection, CMV may cause retinitis which leads to blindness as well as a host of other end-stage organ damage. Treatment for immunosuppressed persons is ganciclovir or foscarnet. Neither medication cures CMV, but they do suppress the acute disease process.
EPIDEMIOLOGY Herpes Simplex Viruses 1 and 2 More than 90% of adults have antibodies to HSV-1 by the fifth decade of life. In populations of low socioeconomic status, most infected persons acquire HSV-1 before the third decade of life. As of 2001, nearly 22% of the U.S. population has antibodies to HSV-2—a number that is increasing. Many persons with HSV-2 antibodies do not have a history of genital lesions. Within 12 months of an initial HSV-2 outbreak, 90% of patients will have had at least one recurrence and 40% will have six or more recurrences. Susceptible women have a higher likelihood of contracting genital herpes from an infected man than vice versa. Coinfection with HSV and HIV frequently occurs.
Varicella Zoster Before the use of the varicella vaccine, 90% of primary infection occurred among children aged 10 years or younger, with the majority of children younger than 3 years old. Only 10% of persons older than 15 years remain susceptible to varicella zoster virus. Chickenpox occurs year-round with annual epidemics in late winter and early spring. After exposure, attack rates are close to 80% among susceptible household contacts.
Herpes Zoster: Shingles There is a lifetime incidence of almost 20%, with the majority of cases among elderly persons. It occurs only in persons who have had chickenpox
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or who have been vaccinated with the varicella vaccine. After a single occurrence, there is a 4% likelihood of a recurrence. Twenty percent of persons older than 50 years still experience pain for 6 months after rash onset. Increasing age and immunosuppression are risk factors for the disease. Furthermore, severe rash (>50 lesions) is correlated with older age, severe pain, and greater number of affected dermatomes. Severe rash also is a risk factor for prolonged pain and postherpetic neuralgia. Herpes zoster ophthalmicus represents 10%–25% of all cases of zoster.
Epstein-Barr Virus Between 90% and 95% of the adult population has developed antibodies to EBV. Approximately half of the population will seroconvert as young children, with a second peak incidence during the teen and young adult years. The virus is spread by contact with oral secretions.
Cytomegalovirus CMV is present in approximately 1% of newborns and in 40%–100% of adults. There are two peaks of seroconversion: the first occurs in the perinatal period and the second during young adulthood, presumably due to sexual contact. CMV is transmitted through milk, saliva, urine, semen, and cervical secretions. Virus may be present in milk, saliva, blood, or urine. The virus is not spread by casual contact but rather by prolonged exposure.
CLINICAL PRESENTATION There are a variety of infections associated with herpes viruses. The clinical manifestations of each type are listed later; however, human herpes viruses 6 and 7, both of which cause roseola, and human herpes virus 8, implicated in Kaposi sarcoma, will not be discussed here.
Oral HSV Both HSV-1 and HSV-2 can cause identical oral lesions. HSV-1 is a more common cause of oral lesions than HSV-2. The primary lesion of HSV-1 is often mild. In young children, it may present solely as a pharyngitis or gingivostomatitis and have associated fever or cervical adenopathy. For primary outbreaks, gingivostomatitis and pharyngitis are the most common presenting symptoms, and herpes labialis is most commonly seen in recurrent outbreaks. Lesions are typically distributed throughout the mouth. Primary lesions last 1–2 weeks, on average. Recurrent oral lesions occur in 60%–90% of infected persons, are usually milder, and generally occur
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on the lower vermillion border of the lip. Recurrences may be triggered by local trauma, sunburn, or stress. Prodromal symptoms of local adenopathy, pain, or tingling may precede the outbreaks. The lesions usually present within 48 hours of the prodrome and may last up to 10 days but typically crust over within the first 48 hours. Immunocompromised persons may present with friable, bleeding lips and ulcerations that have penetrated deep cutaneous layers, thus causing debilitating wounds.
Genital HSV HSV-1 and HSV-2 cause identical genital lesions; however, HSV-2 causes the majority of genital lesions. The disease usually presents with painful genital papules that progress to vesicles and then shallow ulcerations. Often, a prodrome of myalgias, fatigue, fever, and tender inguinal lymphadenopathy is present at the time of the first outbreak. Dysuria, pruritus, and vaginal and urethral discharge are also common findings. In some cases, urethritis in the absence of lesions may be the only presenting symptom of HSV infection. When lesions do occur, they typically crust over and reepithelialize within 7–10 days.
Ocular HSV HSV infection of the eye may lead to blindness. Classically, a prodromal phase consists of fatigue, low-grade fever, and malaise may last as long as 1 week. Soon after, the patient will present with acute onset of eye pain, chemosis, conjunctivitis, and blurry vision. An ulcerative keratitis is the most common manifestation. Along with the classic dendritic pattern on the eye, herpetic vesicles may be seen on the conjunctiva or on the lid margin. Furthermore, patients may develop blepharitis and edema of the eye associated with the inflammation. Recurrent ocular infections may include chronic ocular inflammation, loss of vision, and excruciating pain.
Encephalitis There may be a preceding viral-like illness before encephalitis occurs, or the onset may be sudden. Often headache, fever, and altered mental status indicated by focal seizures or speech disturbances may exist. Commonly, there is no cutaneous manifestation of HSV encephalitis.
Bell’s Palsy The clinical features of Bell’s palsy include facial hemiplegia or hemiparesis, taste disturbance, decreased blinking, dry eyes or increased tearing, jaw or face pain, and numbness of the face and or neck. Typically, the
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forehead is not spared in Bell’s palsy, though it is spared in the case of more central lesions. Attempting to close the eye on the affected side will commonly result in an upward gaze by the patient (i.e., Bell’s phenomenon). Paralysis of the stapedius muscle on the affected side will lead to hyperacusis.
Herpetic Whitlow The disease is usually limited to a single digit. It is marked by abrupt onset of digit pain, edema, erythema, tingling, burning, and vesicles on an erythematous base. Often, axillary adenopathy accompanies the rash. The prototypical vesicle of herpetic whitlow appears to contain pus when, in actuality, the vesicles are filled with necrotic epithelial cells. Herpetic whitlow is often misdiagnosed as a paronychia and incised, which leads to a delay in healing and allows a secondary infection to occur. When incised, no pus is expressed from the wound.
Immunocompromise Immunocompromised patients afflicted with herpes virus are at increased risk of disseminated infection, which can cause devastating infections of the esophagus, colon, lungs, and brain.
Herpes Zoster: Chickenpox In children, a prodrome of fever and malaise precedes the classic lesions on the face and trunk by approximately 48 hours. The lesions initially appear maculopapular and then turn to clear fluid-filled vesicles. As the lesions age, they begin to scab over. The rash starts centrally and then spreads to the extremities. The hallmark of chickenpox is lesions in different stages of healing. Systemic symptoms accompanying the lesions are fever, malaise, pruritus, and anorexia. Varicella encephalitis is characterized by chickenpox accompanied by altered level of consciousness, fever, vomiting, seizures, and headaches.
Herpes Zoster: Shingles The lesions of zoster are identical to those of chickenpox but are limited to a single dermatome in distribution. The most common dermatomes are those of the thoracic and lumbar region, specifically in the T3–L3 region. The cranial nerves may be affected as well, with the complications of Ramsay Hunt syndrome and herpes zoster ophthalmicus often seen. The Hutchinson sign, which is a lesion on the tip of the nose, may be noticed before ocular involvement is seen but is not necessary to make the diagnosis of herpes zoster ophthalmicus. The disease begins with a
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prodrome of pain in the affected area lasting 1–3 days before the outbreak of a maculopapular rash that quickly progresses to a vesicular rash. Ocular involvement can be seen in the presence of only a slight rash on the forehead. Often, there is facial pain, regional adenopathy, and occasionally a red eye preceding the appearance of the rash. A dendritiform corneal ulcer can often be identified with fluorescein staining. The skin rash helps differentiate herpes zoster ophthalmicus from ocular HSV. If the seventh cranial nerve is affected, intraoral lesions may occur or Ramsay Hunt syndrome, which is clinically similar to Bell’s palsy, may ensue. Findings associated with Ramsay Hunt syndrome include a unilateral facial motor weakness, loss of taste on the anterior two thirds of the tongue, and vesicles in the ear canal or on the tympanic membrane. The most common complication of shingles is postherpetic neuralgia, which increases in frequency with age. Immunocompromised patients afflicted with zoster may present with disseminated disease. They may have the classic rash involving multiple dermatomes or a rash that crosses the midline. They may also have diffuse organ involvement.
Epstein-Barr Virus A prodrome of fever, malaise, and myalgia may last for up to 2 weeks before the classic presentation of exudative pharyngitis, posterior anterior cervical lymphadenopathy, and splenomegaly begins. Infants and young children may be asymptomatic. Hepatomegaly and jaundice may be clinical manifestations in older adults. The most common presenting symptom is a severe sore throat with the presence of bilateral exudative tonsillitis/pharyngitis along with bilateral tender cervical lymphadenopathy, classically affecting the posterior chain. Approximately half of afflicted patients will have a palpable spleen during the course of their illness (most prominent during the second week of illness). If ampicillin is given to these patients, there is a 95% chance of a rash developing. Although neurological complications of EBV infection are rare, they may include encephalitis, meningitis, cranial nerve palsies, and Guillain-Barré syndrome. In immunocompromised patients, EBV infection may lead to B-cell lymphomas and other lymphoproliferative syndromes. Patients infected with HIV may develop hairy leukoplakia.
Cytomegalovirus CMV is capable of causing intrauterine infections. If a neonate is affected, he or she will show involvement of multiple organs, including jaundice, hepatosplenomegaly, microcephaly, petechiae, and inner ear problems, as well as CNS defects. The triad of petechiae, hepatosplenomegaly, and jaundice are seen in approximately 60%–80% of cases. Newborns may acquire CMV at the time of delivery by traveling through an infected
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birth canal or within the first month of life by drinking infected maternal milk. In the majority of cases, the child remains asymptomatic; however, CMV pneumonitis is a deadly complication that may occur. In healthy immunocompetent children and adults, CMV infection is usually asymptomatic. When CMV does cause disease in these persons, it typically resembles EBV mononucleosis. Presentations include fever, chills, myalgia, headache, lymphadenopathy, and splenomegaly. In CMV mononucleosis, unlike EBV mononucleosis, exudative pharyngitis and cervical adenopathy are rare. In HIV-positive patients, CMV infections can be deadly. CMV usually has its worst effects on those with low CD4 counts or in advanced stages of acquired immunodeficiency syndrome (AIDS). The most common illness is CMV retinitis. Patients may report only floaters or decreased vision. In immunocompromised patients, CMV may affect the liver, lungs, adrenal glands, colon, and CNS.
EXAMINATION Herpes Simplex Viruses 1 and 2 If HSV infection is suspected, the patient would be given a complete examination to include oral cavities, genitalia, and rectum with the aim to locate any painful, shallow ulcerations. Special attention should be paid to regional lymph nodes for enlargement and sensitivity. The posterior oropharynx should be inspected, looking for pharyngitis or tonsillitis. A full ophthalmological examination should be performed on patients suspected of ocular HSV, looking for herpetic vesicles on the conjunctiva or lid margins. Fluorescein staining should be initiated to examine for classic dendritic ulcerations of the cornea. In any patient presenting with altered mental status, fever, headache, focal seizures, or speech disturbances, a complete neurological examination should be performed. Special attention should be paid to any deficit of the seventh cranial nerve, which could be a harbinger of Bell’s palsy. Specifically, one should note facial hemiplegia or hemiparesis, taste disturbances, dry eyes, decreased blinking, or hyperacusis. The examiner should note whether forehead sparing is present which, when present, is more indicative of a central lesion rather than the peripheral lesion of Bell’s palsy. The rest of the cranial nerves along with the ears, tympanic membranes, mastoids, and parotid glands should be unaffected to make the diagnosis of Bell’s palsy. For herpetic whitlow, each digit should be inspected individually. Furthermore, careful attention should be paid to the axillary lymph nodes, looking for axillary adenopathy.
Herpes Zoster: Chickenpox A patient suspected of having chickenpox should be undressed so that a full skin examination can be accomplished. The examiner should look
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for lesions in different stages of healing. The classic lesion of chickenpox starts as a maculopapular rash and becomes a fluid-filled vesicle described by some as “dew drops on a rose petal.” In any patient suspected of varicella encephalitis, a full neurological examination should be performed, with special attention paid to the cerebellum to determine the presence or absence of cerebellar ataxia.
Herpes Zoster: Shingles Any patient suspected of having shingles should be undressed for a full skin examination; the practitioner should look specifically for rashes in dermatomal distributions. If there is a rash of the face, a careful ophthalmological examination should be done to look for herpes zoster ophthalmicus. A complete examination of the regional lymph nodes should also be performed. A thorough check of both ear canals should be accomplished, with the practitioner looking for lesions consistent with Ramsay Hunt syndrome.
Epstein-Barr Virus A complete physical examination should be performed for any patient suspected of having EBV infection, with special attention paid to the posterior oropharynx and tonsils in a search for exudates. The lymph nodes of the cervical chain should be palpated for enlargement and tenderness. A complete abdominal examination with palpation of the liver and spleen should be performed, looking for enlargement.
Cytomegalovirus If there is concern over a neonate with intrauterine exposure to CMV, an examination including head circumference measurements checking for microcephaly, abdominal examination palpating for hepatosplenomegaly, and skin examination looking for jaundice should be performed, at minimum. Furthermore, a neurological examination checking appropriate reflexes should also be done. In immunocompromised persons or patients with AIDS, a complete physical examination with emphasis on a funduscopic examination to look for retinal hemorrhages and exudates should be accomplished. Careful auscultation of the lungs to listen for signs of pneumonia should also be performed.
LABORATORY FINDINGS For oral, genital, and ocular herpes, the diagnosis is clinical. It can take weeks to get results from viral cultures, which in effect makes them useless
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for emergency department (ED) treatment and management. If confirmation is needed, staining of scrapings at the base of lesions with Wright’s, Giemsa, or Papanicolaou’s stain will show giant intranuclear inclusion bodies. Besides the lesions themselves, the virus may be obtained from samples of the cerebrospinal fluid (CSF), stool, urine, throat, nasopharynx, conjunctivae, cervix, or cornea. For HSV encephalitis, CT, magnetic resonance imaging, and electroencephalographic findings may include temporal abnormalities; however, these findings are not always present. CSF findings are nonspecific and usually show an elevated white blood cell count with mononuclear predominance. Conclusive diagnosis is made by biopsy with either culture or direct antibody testing with polymerase chain reaction of the CSF being the most sensitive way to isolate the virus. Again, these results can take weeks to obtain. The diagnosis of Bell’s palsy is largely clinical. If there are any atypical features, imaging should be considered to rule out stroke or tumor. Herpetic whitlow is a clinical diagnosis. For herpes zoster (chickenpox and shingles), the diagnosis is clinical. If confirmation is necessary for the diagnosis of herpes zoster, a variety of serological tools may be used, including the fluorescent antibody to membrane antigen test and the enzyme-linked immunosorbent assay. In the case of EBV, the diagnosis is largely clinical. EBV-specific antibody tests do exist, although they generally do not offer same-day results. A complete blood cell count should be drawn looking for elevations in lymphocytes and monocytes. A peripheral smear will commonly show a large percentage of atypical lymphocytes. Liver function tests may be a helpful adjunct. Tests for heterophile antibodies can be performed to help confirm the diagnosis. Most young children (younger than 4 years) will not produce heterophile antibodies, and false negatives in all patients are common in the first week of illness. In patients with a clinical picture compatible with EBV infection but a negative heterophile antibody test result, CMV infection should be considered. To make a diagnosis of CMV, a conversion from seronegative to seropositive must occur or an acute rise in antibody titer should be seen. Viral cultures can be drawn as well, although results are not readily available. In immunocompromised patients, a biopsy of the affected organ should be done. Emergently, the diagnosis is based on clinical grounds alone because definitive diagnosis is not available in a timely manner.
DIAGNOSIS In the case of oral, genital, and ocular herpes, the diagnosis is made based on clinical presentation. For HSV encephalitis, clinical presentation is the mainstay of diagnosis, with brain imaging and lumbar puncture being useful adjuncts. The diagnosis is clinical in the case of Bell’s palsy, herpetic
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whitlow, and herpes zoster. For EBV infection, clinical presentation is the key to diagnosis, and CBC, peripheral smear, liver function tests, and heterophile antibody tests serve as confirmatory adjuncts. CMV infection is a difficult diagnosis to be made on the basis of clinical examination alone. However, in the ED, appropriate confirmatory tests are not readily available, and results take too long to dictate treatment.
RADIOGRAPHS No specific radiographs are required of herpes viruses. Radiographs should be directed as needed. A patient with a fever and cough should receive a chest radiograph.
TREATMENT Oral and Genital HSV The treatment of recurrent oral and genital herpes is oral acyclovir, valacyclovir, or famciclovir. These medications shorten the course of illness but do not cure herpes. Taken daily, oral acyclovir has been shown to reduce outbreaks by 50%–75%. Furthermore, many recent studies suggest that acyclovir is safe to take during pregnancy. Topical penciclovir taken every 2 hours for 4 days has been proved to reduce the symptoms of oral herpes. Counseling is an important part of treatment of any herpes outbreak to reduce the spread of the disease. Patients should be warned that transmission of the virus is possible during asymptomatic shedding and that having sex while an outbreak is present is dangerous. In fact, up to 70% of HSV transmission occurs during viral shedding in the absence of clinical disease. Due to the high transmission rates of HSV, the use of condoms should be encouraged. Areas of the skin that remain uncovered by condoms are still at risk of infection.
Ocular HSV In the case of ocular HSV infection, immediate consultation with an ophthalmologist is mandated because there is a high risk of vision loss. The administration of intravenous acyclovir should be started immediately. As with oral and genital HSV infections, oral acyclovir can be taken to reduce recurrences.
HSV Encephalitis Due to the high mortality associated with untreated HSV encephalitis, intravenous acyclovir should be started immediately. Due to the poor
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penetration of intravenous acyclovir in to the CNS (30%–50% of plasma levels), the dose should be double that used to treat visceral or cutaneous infections.
Bell’s Palsy The treatment of Bell’s palsy is aimed at reducing the inflammation associated with the illness. Oral prednisone and acyclovir should be started. Follow-up should be set up with either a neurologist or an ear, nose, and throat specialist. Because of the inability to blink associated with the disease, eye care is very important. Artificial tears should be used liberally, and nighttime eye ointment with or without a patch should be applied. Special instructions should be given to the patient regarding eye safety because the eyelid will not provide its normal defense until the symptoms have subsided.
Herpetic Whitlow There is no specific treatment for herpetic whitlow. Patients should be advised to keep the area covered until symptoms resolve so as not to auto-inoculate or spread the disease to others. Local pain control and analgesics are appropriate.
Herpes Zoster: Chickenpox For children under the age of 12 years, treatment is symptomatic and may include skin care, bathing, and the administration of antipruritic agents. Oral acyclovir is indicated for children older than 12 years of age, persons with chronic illnesses, or persons receiving chronic aspirin therapy. The medication should be started within 24 hours of the outbreak of the rash for maximal effect. Any patient presenting with varicella encephalitis or pneumonia should immediately start receiving intravenous acyclovir to reduce mortality and should be admitted to the hospital. Pregnant or peripartum women with chickenpox should discuss treatment plans with a primary care physician or obstetrician and may need to start receiving intravenous acyclovir. Neonates who develop chickenpox or who have postpartum mothers with chickenpox should be admitted for the administration of intravenous acyclovir. Immunocompromised patients with chickenpox should also be admitted for intravenous acyclovir. Varicella zoster immune globulin should be given to any neonate with chickenpox or any neonate born to a mother who developed chickenpox within 5 days before delivery or 48 hours after delivery, regardless of symptoms.
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Herpes Zoster: Shingles The primary goal of the treatment of shingles is to reduce the incidence of postherpetic neuralgia. Studies have shown that antiviral agents such as acyclovir, famciclovir, and valacyclovir shorten the duration of postherpetic neuralgia but do not prevent it. For maximal benefit, the administration of antiviral drugs should be started within 72 hours of symptom onset. A long corticosteroid taper should be initiated in patients older than 50 years to reduce the inflammation associated with shingles. Systemic analgesics are the mainstay of therapy for shingles. If first-line analgesics and narcotics fail to ameliorate symptoms, carbamazepine or amitriptyline should be considered. Furthermore, amitriptyline given nightly in small doses may also reduce the incidence of postherpetic neuralgia by 50%. Immunocompromised patients with disseminated shingles should start receiving intravenous acyclovir and should be admitted to the hospital. Patients with herpes zoster ophthalmicus should have emergent ophthalmological consultation due to the threat of vision loss.
Epstein-Barr Virus In the absence of complications, the treatment of EBV infection is primarily supportive and includes rest and analgesia. The patient should be instructed to limit physical activity for the first month after infection to reduce the risk of splenic rupture. In the event of any airway compromise from tonsillar hypertrophy, prednisone should be given.
Cytomegalovirus There is no cure for CMV infection, but there are medications available for the suppression of the acute disease process. Ganciclovir should be used for AIDS-related CMV retinitis and for the prevention of CMV infection in transplant patients. In patients with CMV retinitis, ganciclovir is given in high doses for 2–3 weeks and then as lifetime suppressive therapy. In other cases, ganciclovir is given for 2–3 weeks and then stopped. Foscarnet is given to patients with resistant CMV infections or in the case of an inability to tolerate ganciclovir.
Bibliography Barker LR, Burton JR, Zieve PD (eds): Principles of Ambulatory Medicine, ed 6. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 478–480. Braunwald E, Fauci AS, Kasper DL, et al (eds): Harrison’s Principles of Internal Medicine, ed 15. McGraw-Hill: New York, 2001, pp 1100–1114. Jung BF, Johnson RW, Griffin DRJ, Dworkin RH: Risk factors for postherpetic neuralgia in patients with herpes zoster, Neurology 2004;62:1545–1551.
288 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Lautenschlager S, Eichmann A: Urethritis: An underestimated clinical variant of genital herpes in men? J Am Acad Dermatol 2002;46:307–308. Nagasako EM, Johnson RW, Griffin DRJ, Dworkin RH: Rash severity in herpes zoster: Correlates and relationship to postherpetic neuralgia, J Am Acad Dermatol 2002;46:834–839. Rimsza ME: Sexually transmitted infections: New guidelines for an old problem on the college campus, Pediatr Clin North Am 2005;52:217–228. Shaikh S, Ta CN: Evaluation and management of herpes zoster ophthalmicus, Am Fam Phys 2002;66:1723–1730. Thomas SL, Hall AJ: What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis 2004;4:26–33. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1050–1055. Yeung-Yue KA, Brentjens MH, Lee PC, Tyring SK: Herpes simplex viruses 1 and 2, Dermatol Clin 2002;20:249–266.
HIV Infections MARTIN A. DOCHERTY
ICD Code: HIV 079.53
Key Points In the ED evaluation of HIV-positive patients, the most important information to obtain is the CD4 count or viral load. Patients with CD4 counts between 200 and 500 cells/mm3 are at increased risk for opportunistic infections. ! Emergency Actions ! In patients for whom the CD4 count is unknown, careful examination for signs of cachexia, oral thrush or hairy leukoplakia, the purple lesions associated with Kaposi sarcoma, diffuse dermatitis, or signs of HSV infection can be a guide to the level of immunosuppression. Patients with altered mental status should be assumed to have toxoplasmosis, Cryptococcus infection, or both; these are the most common causative agents in CNS infection.
DEFINITIONS Human immunodeficiency virus is the retrovirus responsible for infection. Acquired immunodeficiency syndrome refers to the complex of opportunistic infections that occurs in patients who have developed immunosuppression as a result of infection with HIV.
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EPIDEMIOLOGY The first recognized cases of HIV infection in the United States date back to 1981. As of 2005, about 1 million persons in the United States were infected with HIV, and 40,000 new cases are reported each year. In some inner-city hospitals, about 10% of the population is HIV positive. Risk factors for infection include homosexual sex, intravenous drug use, sexual contact with at-risk persons, exposure to bodily fluids from at-risk persons, prostitution, blood transfusions received before 1985, and maternal-toneonatal transmission.
PATHOPHYSIOLOGY After infection, the virus binds to the CD4 receptor site of T-helper lymphocytes. The viral load increases exponentially during the first 6 weeks and becomes widely disseminated. During this time, many patients experience acute viral symptoms and lymphadenopathy. Eventually, an immune response develops, and the virus enters a period of latency that may last up to 10 years, although this is variable. Eventually, as CD4 cell counts decline, most patients develop AIDS. In the ED evaluation of HIV-positive patients, the most important information to obtain is the CD4 cell count or viral load. Patients with CD4 counts between 200 and 500 cells/mm3 are at increased risk for the following:
Oral thrush and oral hairy leukoplakia Mycobacterium tuberculosis Kaposi sarcoma Idiopathic thrombocytopenic purpura
With CD4 counts below 200 cells/mm3, there is increasing risk of infection with the following:
Pneumocystis carinii pneumonia (PCP) Toxoplasmosis and histoplasmosis Cryptococcus organisms Cryptosporidium organisms
In those patients with severe immunocompromise and CD4 counts less than 50 cells/mm3, Mycobacterium avium complex and CMV infection become more prevalent.
CLINICAL PRESENTATION Patients with HIV infection may visit the ED with fever or with symptoms specific to particular organ systems. As previously mentioned, the most important first step is to determine a patient’s CD4 cell count. Patients with CD4 counts greater than 500 cells/mm3 rarely arrive at the ED with symptoms of opportunistic infections. In patients whose counts are
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unknown, careful examination for signs of cachexia, oral thrush or hairy leukoplakia, the purple lesions associated with Kaposi sarcoma, diffuse dermatitis, or signs of HSV infection can be a guide as to the level of immunosuppression.
SPECIFIC SYMPTOMS Pulmonary System Respiratory symptoms are common in patients with AIDS. Such persons are at high risk for “typical” bacterial pneumonia due to Pneumococcus species or Haemophilus influenzae. In addition, tuberculosis and P. carinii infections need to be strongly considered. In patients with PCP, dyspnea on exertion is a hallmark finding. With tuberculosis, night sweats and bloody sputum may be present. Physical examination findings may be subtle, so, in addition to routine laboratory testing and pulse oximetry, chest radiography must be performed. Findings typical for PCP include a diffuse interstitial infiltrate. Tuberculosis infections may show up as hilar lymphadenopathy or, rarely, as cavitary lesions. Communityacquired pneumonia is most often associated with lobar infiltrates. It must be stressed, however, that there is significant overlap and the chest x-ray findings are by no means definitive regarding the causative agent. Intravenous trimethoprim (TMP)–sulfamethoxazole (SMX) is the recommended treatment for PCP. TMP/SMX is given at a dose of 20 mg/kg/day in three or four divided doses (dose is based on TMP). Because of the high prevalence of community-acquired pneumonia, most practitioners also add coverage of this condition with ceftriaxone plus a macrolide, or a newer fluoroquinolone. Treatment for tuberculosis need not be started in the ED, but respiratory isolation should be strongly considered pending definitive diagnosis. In patients with hypoxia and a PaO2 of less than 70 mmHg, prednisone at a dose of 40 mg twice daily should be added.
Gastrointestinal System Dysphagia is commonly due to candidal or herpes esophagitis. It is reasonable to treat for presumed candida with fluconazole or nystatin and reserve endoscopic examination for nonresponders. In patients presenting with abdominal pain, typical causes such as appendicitis, pelvic inflammatory disease, or bowel obstruction should always be considered. AIDS-specific causes may be related to lymphoma, CMV colitis, AIDS cholangiopathy, or medication-related pancreatitis (especially in patients taking the antiretroviral medication ddI). Evaluation and treatment depend on the cause. It is reasonable to order routine CBC and chemistry panels, including liver
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function tests and lipase. CT scanning and ultrasound may be needed in selected cases. Diarrhea is a common sign in patients with AIDS. Chronic diarrhea is usually due to parasitic infections such as Giardia and Cryptosporidium. Bacterial infection due to Shigella, Salmonella, and Campylobacter organisms should be considered in patients with new, acute diarrhea, or in persons with significant worsening of their chronic diarrhea. Clostridium difficile infection should always be considered if chronic antibiotic use is noted.
Central Nervous System CNS infections and neoplasms may have very subtle presentations. The neurological examination results are often normal, and the only relevant symptom may be of headache, with or without accompanying fever. A CT scan of the brain, followed by a lumbar puncture, should be performed in all patients with HIV/AIDS who present with a headache or any CNS symptoms. Toxoplasma and Cryptococcus organisms are the most common causative agents in CNS infections. Multiple brain lesions, found on CT scan, are typical with toxoplasmosis. Diagnosing cryptococcal meningitis requires a lumbar puncture. Opening pressures are often high in cryptococcal meningitis. CSF samples should be sent for routine studies, WBC and RBC counts, protein, and glucose. In HIV/AIDS patients an India ink fungal stain cryptococcal antigen, fungal cultures, and acid-fast bacillus stains should also be performed. The appropriate treatment for toxoplasmosis is with pyrimethamine 100 mg/day and sulfadiazine 100 mg/kg/day for 3–6 weeks. Cryptococcal infection is treated with intravenous amphotericin.
Ophthalmological System Gradual vision loss in patients with AIDS may be due to CMV retinitis. Although it may be possible to see the fluffy, whitish retinal lesions on funduscopic examination, early presentations may be missed. All new ocular symptoms in patients with HIV should mandate very early ophthalmological follow-up. Treatment is usually accomplished with ganciclovir.
Cutaneous System Chronic candidal infections can be treated with topical antifungal drugs such as clotrimazole or oral fluconazole. Diffuse scabies infections respond to treatment with lindane or permethrin. Hospitalization should be considered for patients with overwhelming HSV or varicella zoster infections. Treatment is with acyclovir, 10 mg/kg, given intravenously every
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8 hours. Be alert for the possibility of varicella pneumonia or herpes zoster ophthalmicus affecting the eyes.
POSTEXPOSURE PROPHYLAXIS Postexposure prophylaxis is an evolving field with treatment updates being proposed by the CDC, most recently with recommendations to provide HIV prophylaxis to victims of sexual assault. Most facilities have a protocol governing prophylaxis from inadvertent needle sticks or bodily fluid exposure. In general, a person experiencing a low-risk exposure is prescribed a three- to four-drug regimen of zidovudine and 3TC (lamivudine). Persons experiencing more significant exposures are treated with a three-drug regimen of zidovudine, 3TC, and indinavir. Follow-up for further testing and treatment should be part of the protocol.
Bibliography Hirschtick RE, Glassroth J, Jordan MC, et al: Bacterial pneumonia in persons affected with the human immunodeficiency virus, N Engl J Med 1995;333(13):845. Parente F, Cernushi M, Antinori S, et al: Severe abdominal pain in patients with AIDS: Frequency, clinical aspects, causes and outcome, Scand J Gastroenterol 1994;29:511. Quinn TC: The epidemiology of the acquired immunodeficiency syndrome in the 1990s, Emerg Med Clin North Am 1995;13:1. Simpson DM, Berger JR: Neurologic manifestations of HIV infection, Med Clin North Am 1996;80(6):1363. Weller IV, Williams IG: ABC of AIDS: Treatment of infections, BMJ 2001;322:1350.
Influenza AMY K. DITZEL
ICD Codes: Influenza 487, Influenza with other respiratory manifestations 487.1, Influenza with other manifestations 487.8
Key Points Influenza is a common seasonal viral illness. Complications are common with secondary infections.
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! Emergency Actions ! Any patient who presents to the emergency center with the diagnosis of influenza and shortness of breath should be administered oxygen. Dehydrated patients should be treated with vigorous fluid resuscitation. If the patient is in the extremes of age, very young, very old, or immunocompromised, admission to the hospital should be considered. Any patient with the diagnosis of influenza, who is experiencing any respiratory problems, and is not on oxygen should be admitted to the hospital.
DEFINITION Influenza involves acute, self-limited viral disease often accompanied by pulmonary complications. It occurs seasonally (late fall to winter) in epidemics.
EPIDEMIOLOGY Influenza viruses belong to the class Orthomyxoviridae. Although types A, B, and C exist, type A is the one responsible for the yearly outbreaks of influenza. The entire population is affected by influenza, with the very young most susceptible to infection and the very old most prone to death from complications associated with influenza. Additionally, certain conditions put patients at risk for developing complications, including cardiovascular disease, pulmonary disease (including asthma), hepatic or renal failure, hemoglobinopathies, asplenia, immunodeficiency, and diabetes. A local epidemic will last 5–6 weeks, peaking mid way through and generally affecting young children first. It is expected that 10%–20% of the local population will be affected at that time.
CLINICAL PRESENTATION Sudden onset of fever, chills, headache, and myalgia signals the onset of an influenza infection. These symptoms, along with malaise, anorexia, and ocular tearing and burning will predominate for about 3 days. As the fever decreases, respiratory symptoms (specifically, a dry cough, nasal drainage, and pharyngitis) will begin to appear. The severity and extent of symptoms can vary widely, with elderly persons possibly only displaying fever, confusion, and malaise. It is not uncommon for the convalescent period to extend to 2 weeks before full recovery. Although uncomplicated influenza is self-limited, it easily becomes complicated with the presence of bronchiolitis, croup, pneumonia, or acute exacerbation of chronic bronchitis. The clinician should investigate for the presence of secondary infection in all patients with influenza. Nonpulmonary complications rarely occur but include myositis, Guillain-Barré syndrome, toxic shock syndrome, pericarditis, and Reye’s syndrome.
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EXAMINATION A patient with uncomplicated influenza will often present febrile and tachycardic with watery, red eyes. He or she may be coughing but will generally not be dyspneic. The cervical lymph nodes will be enlarged and tender, and the pharynx will appear hyperemic. Lung sounds will generally be clear, but an occasional rhonchus may be heard.
LABORATORY FINDINGS Rapid, point-of-care testing should yield positive result for influenza A. Viral cultures of nasal secretions will yield positive results but are not appropriate for ED management.
DIAGNOSIS The diagnosis of influenza is generally made on the basis of history and examination within the context of a localized epidemic. Point-of-care testing can provide confirmation of diagnosis. If the patient is acutely ill, a CBC and chemistry panel should be performed.
RADIOGRAPHS Chest radiography may be useful to rule out pneumonia, if it is suspected.
TREATMENT Antiviral therapy is the treatment of choice for limiting the duration and severity of the course of the infection. If treatment is started within 48 hours of symptom onset, oseltamivir (75 mg twice daily, or 75 mg daily if creatine clearance <30 ml/min) can be effective. Amantidine (100 mg twice daily) can also be used for treatment and prophylaxis. Patients should be encouraged to remain well hydrated and rested. Complications (e.g., pneumonia, sinusitis) should be treated appropriately with antibacterial therapy. The annual influenza vaccination should be made available to everyone, especially very young and very old persons or anyone who is immunocompromised, at the direction of their healthcare providers.
Bibliography Kasper DL, Facuci AS, Longo DL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Marx JA (ed): Rosen’s Emergency Medicine, ed 5. Mosby: St Louis, 2002. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Malaria BROOKE VEALE
ICD Code: Malaria 084.0
Key Points Malaria presents with flu-like symptoms. Recent travel to Central America, South America, Haiti, the Dominican Republic, Africa, Asia, Eastern Europe, and the South Pacific should heighten the index of suspicion for malaria. ! Emergency Actions ! Malaria should be treated early based on the patient’s history of recent travel to an endemic area and flu-like symptoms.
DEFINITION Malaria is an infection transmitted by the female Anopheles mosquitoes. The malaria parasites have four species: Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. Although P. falciparum and P. vivax cause the two most common types of infection, P. falciparum is the dreaded form that causes potentially fatal disease. Malaria has been eradicated in the United States, but cases are still seen due to travel to the endemic areas named previously.
EPIDEMIOLOGY About 1300 cases of malaria were confirmed in the United States in 2002. Of these, fewer than 10 were fatal cases, and almost every case was imported from malaria-endemic countries. However, this disease has much higher implications worldwide, with more than 40% of the world’s population living in areas where malaria is transmitted. The statistics are staggering, with an estimated two deaths per minute in some areas of Africa. In 2002, malaria caused about 10% of pediatric fatalities in developing countries, making it the fourth most common cause of death. The mosquito that carries the malaria parasite bites at night; therefore, those persons exposed to the outdoors from dusk to dawn are more likely to get malaria. Also, higher rates of transmission occur during seasons of more rainfall and higher temperatures.
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CLINICAL PRESENTATION Depending on the infecting agent, the incubation period ranges from 7 to 30 days. P. falciparum tends to have a shorter incubation time, whereas the longer incubation period is usually observed with P. malariae. The presentation of malaria can vary from asymptomatic infections to severe complications, depending on the infecting agent and the person’s immunity status. The classic presentation includes fever, chills, diaphoresis, headaches, and myalgia. Symptoms appear every 3 days with P. malariae and every 2 days with P. falciparum, P. vivax, and P. ovale. Severe malaria involves serious organ failure or hematological abnormalities. This may involve cerebral malaria, which manifests with altered level of consciousness, seizures, or coma. Other possibilities are acute respiratory syndrome, thrombocytopenia, severe anemia, hemoglobinuria, acute kidney failure, metabolic acidosis, cardiovascular shock and collapse, and death.
EXAMINATION Upon physical examination, patients with malaria will be febrile and diaphoretic and appear fatigued. Patients often exhibit tachypnea, tachycardia, and jaundice. Hepatosplenomegaly may be appreciated during the abdominal examination or on a CT scan.
LABORATORY FINDINGS A definitive diagnosis of malaria requires detection of malaria parasites on a blood smear with Giemsa stain. However, due to the lack of experience with malaria in the United States, laboratorians might fail to detect the parasites. If initial thick and thin smears have negative results, healthcare providers must repeat the blood smears every 12 hours for 2 days. A CBC may reveal normochromic, normocytic anemia. Inflammation is present, as indicated by an elevated erythrocyte sedimentation rate and C-reactive protein. With P. falciparum, laboratory values may also indicate hypoglycemia, thrombocytopenia, bilirubinemia, elevated levels on liver function tests, albuminuria, and urinary casts.
DIAGNOSIS To prevent complications or spread of the infection, malaria must be diagnosed early. The initial diagnosis and treatment should be done based on the patient’s history and clinical presentation. Therefore, malaria should be considered and treated in persons with recent travel to malaria-endemic areas reporting flu-like symptoms.
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TREATMENT The most effective treatment for malaria is prevention (Table 7-2). Prophylactic medications, such as Malarone (atovaquone and proguanil hydrochloride) or Lariam (mefloquine hydrochloride), should be given to travelers from the United States. Other precautions, such as sleeping beneath permethrin-treated bed nets, wearing long sleeves and pants, and using insecticide with N,N-diethyl-m-toluamide (DEET), must be discussed with travelers. Pregnant women should be encouraged not to travel to malaria-endemic areas. However, gravid females who must travel to these areas should be given mefloquine, chloroquine, or hydroxychloroquine sulfate. Children may be given Malarone, doxycycline, mefloquine, chloroquine, or hydroxychloroquine sulfate at doses adjusted to their weight. Treatment should be given to any person suspected to be infected with malaria (Table 7-3). Instruct patients to take medications with food to decrease possible adverse effects, specifically nausea. Chloroquine is no longer first-line treatment due to the growing incidence of resistance, and primaquine is only used if the patient is unable to take the other medications. If left untreated, a malaria infection can persist throughout a person’s lifetime.
Bibliography Centers for Disease Control and Prevention. Available at http://www.cdc.gov. Accessed June 2005. Kasper DL, Facuci AS, Longo DL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005, pp 1218–1232.
DRUG
ADULT DOSAGE
Malarone (atovaquone 250 mg/proguanil 100 mg)
One tablet daily
Fansidar (pyrimethamine 25/ sulfadoxine 500)
Doxycycline 100 mg
PEDIATRIC DOSAGE
11–20 kg: 62.5/25 mg daily; 21–30 kg: 125/50 mg daily; 31–40 kg: 187.5/ 75 mg daily; >40 kg: 250/ 100 mg daily One tablet weekly 2–11 months: 1/ 8 tablet weekly; 1–3 yr: ¼ tablet weekly; 4–8 yr: ½ tablet weekly; 9–14 yr: 3/4 tablet weekly; >14 yr: 1 tablet weekly One tablet daily >8 years old: 2.2 mg/kg daily
BEGIN TREATMENT FINISH TREATMENT
COMMON SIDE EFFECTS
2 days before travel
7 days after return from travel
Nausea, vomiting, headache
1 week before travel
4–6 weeks after return Nausea, vomiting, from travel gastritis, headache, photosensitivity
2 days before travel
4 weeks after return from travel
Sun sensitivity, nausea, vaginal candidiasis
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Table 7-2 Malaria Prevention
Lariam (mefloquine) 250 mg
One tablet weekly >3 months 5–20 kg: ¼ tablet weekly; 21–30 kg: ½ tablet weekly; 31–45 kg: 3 /4 tablet weekly; >45 kg: 1 tablet weekly
1 week before travel
4 weeks after return from travel
Primaquine 15 mg
Two tablets daily
2 days before travel
7 days after return from travel
Aralen (chloroquine phosphate) 500 mg
One tablet weekly 5-mg base/kg weekly; 500 mg phosphate ¼ 300-mg base
1 week before travel
4 weeks after return from travel
Plaquenil (hydroxychloroquine sulfate) 400 mg
One tablet weekly 5 mg/kg weekly
1 week before travel
4 weeks after return from travel
0.6 mg/kg daily
Avoid use in patients with abnormality of cardiac conduction. Headache, nausea, insomnia, anxiety/depression, seizures Avoid use in G6PDdeficient patients due to potentially fatal effect. Nausea, vomiting Nausea, vomiting, headache, dizziness, blurred vision, increases psoriasis Nausea, vomiting, headache, dizziness, blurred vision, increases psoriasis
G6PD, Glucose-6-phosphate dehydrogenase.
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MEDICATION
ADULT DOSAGE
Malarone (atovaquone 4 tablets daily for 3 days 250 mg/proguanil 100 mg) Fansidar (pyrimethamine 25/ 2–3 tablets once sulfadoxine 500) Doxycycline 100 mg Lariam (mefloquine) 250 mg Primaquine 15 mg Aralen (chloroquine phosphate) 500 mg Plaquenil (hydroxychloroquine sulfate) 400 mg
1 5 2 2
tablet twice daily tablets once tablets daily tablets once, then 1 tablet in 6 hr, then 1 tablet daily for 2 days 2 tablets once, then 1 tablet in 8 hr, then 1 tablet daily for 2 days
PEDIATRIC DOSAGE 5–8 kg: 125/50 mg daily; 9–10 kg: 187.5/75 mg daily; 11–20 kg: 250/100 mg daily; 21–30 kg: 500/200 mg daily; 31–40 kg: 750/300 mg daily; >40 kg: 1000/400 daily 2–11 month: ¼ tablet once: 1–3 yr: ½ tablet once: 4–8 yr: 1 tablet once: 9–14 yr: 2 tablets once: >14 yr: 2–3 tablets once Must be >8 r 20–25 mg/kg once 0.6 mg/kg daily 10-mg base/kg once, then 5 mg/kg in 6 hr, then 5 mg/kg daily for 2 days 10 mg/kg once, then 5 mg/kg in 8 hr, then 5 mg/kg daily for 2 days
DURATION OF TREATMENT 3 days
One dose 2 weeks One dose 2 weeks 2 days 2 days
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Table 7-3 Treatment of Malaria
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Rabies CLAUDIO F. ZEBALLOS
ICD Code: Rabies 071
Key Points Rabies is a viral disease of the CNS usually transmitted by saliva of an animal bite. If left untreated, this disease is usually fatal. ! Emergency Actions ! Immediate thorough wound cleansing, rabies vaccine (RabAvert or Imovax), and human rabies immunoglobulin (HRIG) should be administered postexposure for any routine contact with animals at risk.
DEFINITIONS Exposure is defined as a scratch or bite from an animal that may have the risk of carrying rabies virus. Human rabies immunoglobulin consists of human antibodies and provides passive immunization that neutralize the rabies virus. Rabies vaccines can be either Imovax (human diploid cell vaccine) or RabAvert (purified chick embryo cell vaccine), both of which provide active immunization with inactivated virus. Pre-exposure prophylaxis is rabies vaccine given to persons who work in close contact with potentially infected animals and is given prior to any known exposure. Postexposure prophylaxis includes HRIG and vaccine (Imovax or RabAvert) and is given after a known exposure with a high risk of rabies transmission.
EPIDEMIOLOGY Rabies is a global disease that poses its greatest threat to public health in developing countries. The WHO estimates 30,000–70,000 deaths per year worldwide, mostly in developing countries as a result of inadequate control of the disease in domesticated animals. In the United States rabies is extremely rare, largely due to efforts in 1940s to vaccinate domestic animals. There has been an average of three U.S. cases per year since 1980. In developing nations, dogs are the most commonly infected animal causing transmission to humans. In the United States, however, wild
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animals account for the majority of transmissions. The particular wild animal varies with geography, but the four major animal reservoirs identified are raccoons, skunks, foxes, and bats. Raccoons are the most frequently infected wild animal in the United States. Silver-haired bats account for more than half of U.S. human transmissions since 1980. The majority of bat-to-human transmissions occurred without a known bite; in these cases, the method of transmission is unclear but unrecognized scratches, bites, or aerosolization of viral particles have all been postulated. Therefore, postexposure prophylaxis should be administered. Infected animals become sick and die usually within 3–9 days from when they begin secreting the virus in their saliva and are therefore at their most infectious stage—thus the rationale for a quarantine period for a domestic animal suspected of having rabies. Behavior that suggests an infected rabid animal includes staggering gait, overaggressive behavior, salivation, anorexia, or irritability in an animal that may display convulsions, paralysis, or a change in its usual behavior. In wild animals, a change in instinctual behavior can include a nocturnal or reclusive animal found ambulating in a densely populated neighborhood in broad daylight exhibiting an unwarranted or unprovoked attack.
PATHOLOGY Rabies virus belongs to family Rhabdoviridae and is a bullet-shaped ribonucleic acid virus that is usually transmitted via bite wound from a rabid animal or when the virus is introduced into open skin cuts or mucous membranes, with one documented case of transmission via scratch to mucous membrane. A rare method of rabies virus transmission through human tissue transplantation from an unrecognized infected donor has been documented. Once the virus infects the nervous system, it ascends peripheral nerves at a rate of 8–20 mm/day to reach the spinal cord and the brain, where massive replication and dissemination occurs; at this point, immunization is no longer effective. The incubation period from bite to disease in humans ranges from 30 to 90 days. The risk of developing rabies after a bite ranges from 5% to 80% without treatment and varies with the incidence in endemic species, skin penetration, the amount of salivary contamination, host immunity, degree of innervation at the site of exposure, and proximity to the CNS. Once active rabies develops, it is almost universally fatal; therefore, postexposure prophylaxis is key in the emergent setting.
CLINICAL PRESENTATION Patients will often visit a healthcare provider after an animal attack or animal exposure exhibiting no other medical symptoms. Healthcare
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providers should asses the exposure risk and make a decision either to treat or withhold treatment. Once human infection has occurred, rabies progresses over a period of 7–14 days. The mean time between initial presentation and death is 16.2 days. In the prodromal stage, fevers, pharyngitis, myalgia, and headache or accompanying nausea and vomiting are often earliest findings. This nonspecific prodromal period may last from 2 to 10 days. Paresthesia or pain at the site of the bite or scratch is one of earliest neurological manifestation and should raise suspicion. Back pain and spasms are also common symptoms. The neurological stage of the course of rabies can be either encephalitic (i.e., furious) or, less commonly, paralytic (i.e., dumb) rabies and can last 2–7 days. Encephalitic rabies is the most common form of rabies, manifesting as agitation, irritability, hyperactivity and esophageal and accessory respiratory muscle spasms when exposed to water (i.e., hydrophobia) or air (i.e., aerophobia). Approximately 80% of patients with classic rabies have the encephalitic form. Paralytic rabies can present with quadriparesis; sphincter involvement often mimics Guillain-Barré syndrome. Consciousness is often spared until late in the disease. Late in the course of the disease, hypotension, cardiac arrhythmias, coma, cardiac arrest, and disseminated intravascular coagulation may be seen.
EXAMINATION Most patients with rabies present to the ED after an animal exposure or bite. The healthcare provider should examine the wound and assess and clarify the exposure, including an assessment of risk of transmission and decision to treat. Once human rabies infection has occurred, the disease course begins. Persons with early rabies infection will present with high fevers, myoclonus, anxiety, agitation, hypersalivation or increased lacrimation, and rapidly progressing encephalitis or altered mental status.
LABORATORY FINDINGS For a patient seeking care for animal exposure, no laboratory studies are required. For a patient with suspected active rabies infection, a lumbar puncture and CT scan of the head are warranted. CSF studies may yield normal results but will usually have an elevated protein level and a modest elevated WBC (range, 5–30 cells/ml). A lumbar puncture will often not differentiate between rabies and other encephalitides. The virus can usually be isolated from CSF, saliva, or CNS tissue.
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DIAGNOSIS For a patient seeking care for an animal exposure, no diagnostic tests are required. A patient with suspected rabies should have a collection of samples for diagnosis drawn only in consultation with the state health department or with CDC. Saliva should be collected along with CSF and serum samples for antibody tests. A 5-mm neck biopsy specimen can be taken from the region of the hairline to obtain nerves surrounding hair follicles; this can be sent for direct fluorescent antibody for assistance in diagnosis. A brain biopsy performed postmortem may show Negri bodies along with perivascular inflammation of gray matter.
RADIOGRAPHS No imaging studies are required for asymptomatic patients seeking care for exposure. For a patient with suspected active rabies, a CT scan of the brain is usually performed during the workup for neurological symptoms.
TREATMENT AND OUTCOMES Pre-exposure immunization can be given to persons whose careers place them at risk for exposure such as veterinarians, animal handlers, taxidermists, or wildlife biologists. Imovax or RabAvert vaccine can be given intramuscularly in the deltoid on days 0, 7, and 21 Postexposure treatment consists of immediate thorough wound cleaning and prompt immunization with HRIG and vaccination with Imovax or RabAvert. There is no treatment for symptomatic disease. For treatment with antiserum HRIG 20 IU/kg, it is now recommended that the full dose or as much as possible be infiltrated at or around the wound site. The remainder can be given intramuscularly at a distant site. Treatment with active Imovax or RabAvert vaccine should be given intramuscularly in the deltoid at baseline and on days 3, 7, 14, and 28. It takes 7–12 days to induce immunity that lasts 2 years. Immunization is safe during pregnancy. If a person has been previously immunized, a booster can be given at baseline and on day 3. The risk of exposure is affected by the amount of skin penetration and the amount of saliva or CSF secreted. Open wounds or mucous membranes with deeper wounds and larger inoculums have the greatest risk of infection.
QUARANTINE The local health department should always be notified and guidance sought for individual cases of rabies. Domestic animals that may have been infected should be quarantined for 10 days and observed for any
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neurological symptoms or death. During that time, treatment can be started and discontinued if no symptoms occur. If a domestic animal has been vaccinated during the appropriate timeframe the likelihood of rabies is reduced, but the physician should inquire about any recent bites or fights with wild animals. Wild animals with rabies should be killed immediately to send the brain for diagnostic studies because the period of infectivity in wild animals is not always known. If the wild animal is not available for slaughter (as is usually the case) treatment should be based on the exposure. Small rodents, including mice, rats, gerbils, hamsters, guinea pigs, squirrels, and rabbits, rarely contract rabies and are considered to be at low risk, although exceptional cases have been documented. Treatment for these animals can usually be withheld. The local health department can be contacted for information regarding epidemiology in a particular region. Exposure to woodchucks, beavers, skunks, foxes, jackals, wolves, mongooses, and especially raccoons and bats should be considered a high risk and treated immediately. Dog bites near United States–Mexico border or nondomestic dog bites should be treated as high risk. Significant transmission has been found with bat exposure, and treatment is recommended even in the absence of bites in the setting of a person finding himself or herself in an enclosed space with a bat.
Bibliography Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG: Human rabies in the United States, 1960 to 1979: Epidemiology, diagnosis, and prevention, Ann Intern Med 1984;100 (5):728–735. Auerbach PS: Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Centers for Disease Control and Prevention: First human death associated with raccoon rabies—Virginia, 2003, MMWR Morb Mortal Wkly Rep 2003;52(45):1102. Centers for Disease Control and Prevention: Human death associated with bat rabies— California, 2003, MMWR Morb Mortal Wkly Rep 2004;53(2):33–35. Centers for Disease Control and Prevention: Human rabies—California, 1987, MMWR Morb Mortal Wkly Rep 1988;37:305. Centers for Disease Control and Prevention: Current recommendations for diagnosis of rabies, MMWR Morb Mortal Wkly Rep 1996;46:27–28. Centers for Disease Control and Prevention: Human rabies—California, 1995, MMWR Morb Mortal Wkly Rep 1996;45(17):353–356. Centers for Disease Control and Prevention: Human rabies—California, 2002, MMWR Morb Mortal Wkly Rep 2002;51(31):686–688. Centers for Disease Control and Prevention: Human rabies—Iowa, 2002, MMWR Morb Mortal Wkly Rep 2003;52(3):47–48. Centers for Disease Control and Prevention: Human rabies—Tennessee, 2002, MMWR Morb Mortal Wkly Rep 2002;51(37):828–829. Centers for Disease Control and Prevention: Human rabies—Texas and New Jersey, 1997, MMWR Morb Mortal Wkly Rep 1998;46:1. Centers for Disease Control and Prevention: Human rabies—Washington, MMWR Morb Mortal Wkly Rep 1995;44:625.
306 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Centers for Disease Control and Prevention: Human rabies—West Virginia, 1994, MMWR Morb Mortal Wkly Rep 1995;44:86. Centers for Disease Control and Prevention: Investigation of rabies infections in organ donor and transplant recipients—Alabama, Arkansas, Oklahoma, and Texas, 2004, MMWR Morb Mortal Wkly Rep 2004;53(26):586–589. Centers for Disease Control and Prevention: Rabies. Available at: http://www.cdc.gov/ncidod/ dvrd/rabies. Centers for Disease Control and Prevention: Update: Investigation of rabies infections in organ donor and transplant recipients—Alabama, Arkansas, Oklahoma, and Texas, 2004, MMWR Morb Mortal Wkly Rep 2004;53(27):615–616. Fishbein D, Robinson L: Rabies, N Engl J Med 1993;329:1632. Fisher DJ: Resurgence of rabies: A historical perspective on rabies in children, Arch Pediatr Adolesc Med 1995;149:306. Human rabies prevention—United States, 1999. Recommendations of the Advisory Committee Immunization Practices (ACIP), MMWR Morb Mortal Wkly Rep 1999;48:1. Krebs JW, Wheeling JT, Childs JE: Rabies surveillance in the United States during 2002, J Am Vet Med Assoc 2003;223(12):1736–1748. Krebs J, Rupprecht CE, Childs JE: Rabies surveillance in the United States during 1999, J Am Vet Med Assoc 2000;217:1799. Lentz TL, Burrage TG, Smith AL, et al: Is the acetylcholine receptor a rabies virus receptor? Science 1982;215(4529):182–184. Messenger SL, Smith JS, Rupprecht CE: Emerging epidemiology of bat-associated cryptic cases of rabies in humans in the United States, Clin Infect Dis 2002;35(6):738–747. Noah DL, Drenzek CL, Smith JS, et al: Epidemiology of human rabies in the United States, 1980 to 1996, Ann Intern Med 1998;128:922. Smith JS, Fishbein DB, Rupprecht CD, Clark K: Unexplained rabies in three immigrants in the United States: A virologic investigation, N Engl J Med 1991;324:205. Udwadia Z, Udwadia F, Katrak S: Human rabies: Clinical features, diagnosis, complications, and management, Crit Care Med 1989;17:834. Warrell D, Warrell M: Human rabies and its prevention: an overview, Rev Infect Dis 1988;10:S726.
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Tetanus ROGER MATTHEW BAUTISTA
ICD Code: Tetanus 037
Key Points Elderly persons are at highest risk for the development of tetanus, with a recent study finding that only 30% of tested persons older than 70 years had adequate antibody levels. Increased central muscle tone with superimposed generalized spasms and relative sparing of the hands and feet strongly suggests tetanus. ! Emergency Actions ! Acute treatment includes aggressive supportive care, administration of antitoxin, elimination of toxin production, and active immunization. Respiratory and cardiac status must be monitored closely in an intensive care unit.
DEFINITION Tetanus is a toxin-mediated (tetanospasmin from Clostridium tetani) disease causing severe, uncontrolled skeletal muscle spasms. It can occur in four forms: generalized, cephalic, localized, and neonatal. Spasms of the respiratory muscles can lead to hypoxia and death.
EPIDEMIOLOGY Although tetanus is uncommon in the United States, the worldwide incidence is approximately 500,000 to 1 million cases per year, with a mortality rate ranging from 20% to 50%. It is more common in developing countries. The majority of cases in the United States, fewer than 100 per year, occurs in temperate areas such as California, Florida, and Texas and has a mortality rate of about 11%. Most patients have an inadequate immunization history. The disease is predominant in neonates and young children in countries with inadequate immunization standards and poor hygiene. Elderly populations are at highest risk for the development of tetanus, with a recent study finding that only 30% of tested persons older than 70 years had adequate antibody levels.
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ETIOLOGY C. tetani is an anaerobic, motile, spore-forming, gram-positive, rodshaped organism. The organism is found in soil, dust, and the feces of animals and humans. Neurotoxins are produced by the vegetative forms, which are highly susceptible to adverse environmental conditions. The spores, however, can survive in soil for years and are resistant to heating and chemical disinfectants.
PATHOPHYSIOLOGY Because C. tetani is a noninvasive organism, most cases occur after an acute break in the skin, such as a laceration, puncture wound, or abrasion. The injury could range from major to so minor that medical attention is not sought. Tetanus is also associated with burns, surgery, abortion, childbirth, frostbite, body piercing, and drug abuse. In some cases, no injury could be identified. The presence of damaged or devitalized tissue, foreign bodies, or other bacteria reduces the oxidation-reduction potential of the tissue and allows spores to convert to the vegetative form of the bacteria. In the vegetative form, three exotoxins are produced: tetanospasmin, tetanolysin, and nonconvulsive neurotoxin. Tetanospasmin is responsible for the clinical manifestations of tetanus. When tetanospasmin is released in the wound, it binds to peripheral motor neuron terminals, enters the axon, and is transported to the nerve-cell body in the brainstem and spinal cord by retrograde intraneuronal transport. In generalized tetanus, it enters the lymphatics and bloodstream, spreading widely to distant nerve terminals. In localized tetanus, only the nerves supplying the affected muscles are involved. It interferes with the release of inhibitory neurotransmitters, causes disinhibition of motor groups, and results in excessive, uncontrolled muscle activity. It may also cause autonomic nervous system dysfunction by its effects on the brainstem and autonomic interneurons.
CLINICAL PRESENTATION The incubation period of tetanus is usually between 3 and 14 days but can range from 1 day to several months. A shorter incubation period usually means a worse prognosis. The four clinical types are generalized, cephalic, localized, and neonatal. Generalized tetanus is the most common and severe form. It is the fully developed state of skeletal muscle hypertonicity. Trismus or lockjaw, caused by increased masseter muscle tone, is usually the presenting symptom. When other facial muscles become affected, the characteristic sardonic smile (i.e., risus sardonicus) develops. Other symptoms include myalgia, muscle cramps, dysphagia, hydrophobia, drooling, weakness, and irritability. At its most severe form, muscle rigidity becomes generalized and reflex muscle spasms
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may be precipitated by external stimuli (e.g., noise, light, touch) or spontaneously. Because the posterior trunk and extremities are stronger than the anterior muscle groups, opisthotonos develops. Laryngeal and respiratory muscle spasms can cause respiratory failure and death. Autonomic dysfunction is exhibited by tachycardia, hypertension, hyperthermia, cardiac dysrhythmias, peripheral vasoconstriction, and diaphoresis. Mentation is unimpaired. The illness usually progresses with an increase in clinical manifestations for the first 3 days, persistence for 5–7 more days, and reduction of spasms after 10 days. Recovery is complete in at least 4 weeks, if the patient survives. Mortality ranges from 0% to 50%. Cephalic tetanus is rare, exhibited by trismus with cranial nerve palsies. It usually occurs after facial or head trauma or otitis media and has associated ipsilateral cranial nerve palsies, with the facial nerve being the most common. It has a short incubation period. Two thirds of the cases progress to generalized tetanus, and the remaining one third completely resolve. The mortality rate of this form of tetanus is high. Localized tetanus is exhibited by persistent muscle spasms, mild or severe, in the area of inoculation. It may progress to the generalized form, but the majority of cases, after weeks to months, completely resolve. Neonatal tetanus is a generalized form primarily affecting persons in underdeveloped countries as a result of inadequate maternal immunization and contamination of umbilical cords. There is a short incubation period with symptoms of weakness, irritability, and poor sucking and swallowing appearing during the first 2 weeks of life. The prognosis is poor if the condition is left untreated. The main complication is acute respiratory failure; others include cardiovascular complications, fractures and dislocations, rhabdomyolysis, renal failure, infection, pulmonary embolism, and GI complications.
LABORATORY FINDINGS A CBC and chemistry panel to include calcium should be performed. No laboratory test exists to diagnose tetanus, but serum antitoxin titers greater than 0.01–0.015 IU/ml are considered protective. Wound cultures for C. tetani should be performed even though only about one third yield positive results. A CT scan of the brain can exclude intracranial pathology. A lumbar puncture can exclude meningitis. An electromyogram may assist in the diagnosis of cephalic or localized tetanus.
DIAGNOSIS Tetanus is clinically diagnosed. Increased central muscle tone with superimposed generalized spasms and relative sparing of the hands and feet strongly suggests tetanus. If a reliable history demonstrates the completion
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of a primary vaccination series with appropriate booster immunizations, tetanus is unlikely. The differential diagnosis includes alveolar abscess, dystonic reaction, hypocalcemia, strychnine poisoning, meningitis/ encephalitis, rabies, and an acute abdomen.
TREATMENT Acute treatment of tetanus includes aggressive supportive care, administration of antitoxin, elimination of toxin production, and active immunization. The patient’s respiratory and cardiac status must be monitored closely in an intensive care setting. The patient must be intubated for any signs of airway compromise. Gentle handling of patients and minimization of environmental stimuli must be ensured to minimize reflex muscle spasm. Benzodiazepines can help to reduce muscle spasms and anxiety and to assist in sedating patients for comfort. Nondepolarizing neuromuscularblocking agents, propofol, and dantrolene can also be used. Sympathetic overactivity from autonomic instability can be treated with labetalol. Bradydysrhythmias should be treated with temporary pacing. Hypertension can be treated with nitroprusside. Magnesium sulfate, narcotics, and spinal anesthesia can be used for autonomic instability. Human tetanus immunoglobulin (TIG) and tetanus toxoid should be given to all patients. TIG neutralizes any circulating toxin or toxin at the wound site and reduces mortality. TIG, 3000–8000 U, should be given intramuscularly at separate sites from the toxoid. Repeated doses are not needed because the half-life of TIG is 25 days. Only after TIG and toxoid are given should antibiotics and wound care be started to counteract the possible transient release of tetanospasmin. Penicillin G (10–24 million U/day given intravenously in divided doses for adults, or 100,000 U/kg/day in divided doses for children), metronidazole (500 mg taken orally every 6 hours), and doxycycline (100 mg given intravenously every 12 hours) have been described to be effective against C. tetani. Clindamycin and erythromycin are alternatives for patients who are allergic to penicillin. The wound should be debrided, foreign bodies removed, and the wound cleansed.
Bibliography Abrutyn E: Tetanus. In Kasper DL, Facuci AS, Longo DL (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Carden DL: Tetanus. In Tintinalli. JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Cook TM, Protheroe RT, Handel JM: Tetanus: A review of the literature, Br J Anaesth 2001;87:477–487. Farrar JJ, Yen LM, Cook T, et al: Tetanus, J Neurol Neurosurg Psych 2000;69:292–301. Fernandez-Frackelton M, Turbiak TW: Bacteria. In Marx JA (ed): Rosen’s Emergency Medicine, Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
Chapter 8
Medical Emergencies Acid–Base Problems BARBARA M. FISHMAN
ICD Codes: Metabolic acidosis 276.2, Metabolic alkalosis 276.3, Respiratory acidosis 276.2, Respiratory alkalosis 276.3
Key Points 1. Acid^base homeostasis is achieved as follows: (1) chemical buffering by intracellular and extracellular buffers, (2) changes in renal Hþ excretion, and (3) changes in the rate of alveolar ventilation for the excretion of carbon dioxide (CO2). 2. The bicarbonate (HCO3)/CO2 buffering system is key to the body’s maintenance of acid^base balance because CO2 and HCO3 can both be regulated independently. CO2 is regulated by alveolar ventilation via the lungs and HCO3 concentration is regulated by Hþ excretion via the kidney. 3. In any acid^base disturbance, there will be compensatory mechanisms that return the pH toward but not completely to normal (i.e., there is no overcompensation). 4. Metabolic acidosis results from endogenous production of acid, decreasedrenal excretion of acid,or HCO3 loss.The conditionis divided into two categories: high anion gap and normal anion gap (hyperchloremic acidosis). If a patient’s primary disorder is metabolic acidosis, the pH and HCO3 must be decreased. HCO3 therapy in metabolic acidosis is caused by the generation of endogenous organic acids (i.e., diabetic ketoacidosis [DKA] and lactic acidosis due to sepsis). 5. If a patient’s primary disorder is metabolic alkalosis, pH and HCO3 must be increased.To maintain the metabolic alkalosis there must also be impairment in renal HCO3 excretion. This usually occurs because of volume depletion or potassium (K) depletion. Metabolic alkalosis is divided into saline-responsive alkalosis and saline-resistant alkalosis. Treatment is aimed at increasing the renal excretion of HCO3. For this to occur,volume,Cland Kþ depletion must be corrected.
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312 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER 6. The presence of an acid pH and elevated PCO2 (>45 mmHg) establish the diagnosis of primary respiratory acidosis. Anxiety in these patients may be a sign of elevated PCO2; sedatives should be avoided because they will worsen the respiratory depression. Metabolic compensation for respiratory acidosis takes 3^5 days to develop. 7. Primary respiratory alkalosis is characterized by low PCO2 and elevated pH. Once the diagnosis of primary respiratory alkalosis has been established, the etiology should be sought. 8. The healthcare provider must determine whether the disturbance is simple or mixed. He or she must check the pH, arterial blood gas (ABG), and electrolyte levels to calculate the anion gap and check for appropriate compensation. Compensation returns the pH toward normal but not to normal. The degree of compensation is predictable; lack of appropriate compensation is a sign of a mixed disorder. In a simple acid^base disturbance that produces an elevated anion gap, the increase in anion gap from baseline should equal the decrease in serum HCO3. If the change in anion gap is greater or less than the change in HCO3, a mixed picture is present (i.e., metabolic alkalosis plus acidosis or anion gap acidosis plus non^anion gap acidosis).
DEFINITION Many diseases become evident through acid–base disorders. The acidity of a solution is based on its hydrogen ion activity. The level of activity of hydrogen ions in a solution is equal to the ratio of activity of the acid to its corresponding base, multiplied by its dissociation constant. Like other components of extracellular fluid (ECF), Hþ concentration [Hþ] must be maintained within narrow limits. The pH of any solution is the concentration of hydrogen ions expressed as a negative logarithm. The pH is computed by the HendersonHasselbalch equation: pH ¼ pKa þ log
protein acceptor ðbaseÞ protein donor ðacidÞ
In humans and animals, the pH (and [Hþ]) must remain fairly constant. This is achieved as follows: (1) chemical buffering by intracellular and extracellular buffers, (2) changes in renal Hþ excretion, and (3) changes in the rate of alveolar ventilation for the excretion of CO2, a volatile acid. Chemical buffers in the body are weak acids and can take up or release Hþ. The main extracellular buffer is HCO 3 ; plasma proteins are also buffers. Intracellular buffers are phosphate and protein, and in the red blood cell (RBC), hemoglobin. Bone is also an important buffer. Anemia, decreased muscle mass, and low protein levels all affect the
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body’s ability to buffer hydrogen ions. Patients with anemia, low protein levels, or decreased muscle mass are at a higher risk of severe acidosis.
Renal H+ Excretion and HCO3– Absorption The kidneys contribute to acid–base balance by absorbing filtered HCO 3 and excreting acid. Ammonia represents the majority of renal acid excretion. It is produced in the distal tubule from glutamine and other precursors. Acid is excreted with urine buffers by the phosphate þ (HPO2 4 /H2PO4 ) buffering system. Finally, H can be excreted directly, though a very small amount of acid is excreted in this manner. All of the filtered HCO 3 must be absorbed for the kidney to be able to excrete a daily acid load. The clinician should remember that loss of HCO 3 in the urine is the equivalent to a gain in Hþ to the body. Net renal acid excretion ¼ Acid buffered þ NHþ 4 urine HCO3
Numerous factors affect renal acid excretion. Extracellular pH is the primary regulator of renal acid excretion, but it is also affected by volume status, aldosterone, and plasma Kþ. These other factors will affect renal acid excretion in pathologic states independent of the pH. Ninety percent of filtered HCO 3 is absorbed in the proximal tubule. The sodium (Naþ)-hydrogen (Hþ) exchange in the proximal tubule results in Naþ resorption and Hþ excretion into the lumen. Distal urine acidification involves Hþ-Kþ exchange, Cl secretion, and (Cl)-(HCO 3) exchange. Dehydration or volume depletion will cause increased sodium and HCO 3 absorption in the proximal tubule. This becomes clinically important in dehydrated patients, in whom volume is maintained at the expense of an inability to excrete HCO 3 and resultant metabolic alkalosis. In volume overload, less sodium and HCO 3 will be absorbed. In states of hyperaldosteronism, there is an increase in sodium and chloride absorption in the distal nephron and excretion of K. Hþ is also excreted in response to aldosterone.
Respiratory Excretion of Volatile Acid CO2 is a by-product of the body’s metabolism of proteins, fats, and carbohydrates. It is excreted mainly by the lungs. CO2 is transported from tissues to lungs by plasma HCO 3 and hemoglobin. CO2 is present as carbonic acid in the arterial blood at a PCO2 of 40 mmHg.
Clinical Evaluation of Acid–Base Balance Acid–base balance is usually clinically evaluated in terms of the HCO 3/ CO2 buffer system.
314 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Dissolved CO2 þ H2 O > H2 CO3 > Hþ þ HCO 3
The concentration of carbonic acid is usually so low that it can be ignored. The HCO 3 /CO2 buffering system is key to the body’s maintenance of acid–base balance because CO2 and HCO 3 can both be regulated independently. CO2 is regulated by alveolar ventilation via the lungs, and þ HCO 3 concentration is regulated by H excretion via the kidney. The Henderson-Hasselbalch equation for the HCO 3 /CO2 buffer system becomes: pH ¼ pKa þ log
ðHCO 3Þ ðH2 CO3 Þ
This shows the interrelationship between pH, HCO 3 (the base) and carbonic acid (H2CO3). This can be further derived to the more simplified Kassirer-Bleich equation, which is more clinically useful: ½Hþ ¼ 24
ðPCO2 Þ ðHCO 3Þ
This shows the interrelationship between Hþ concentration (and therefore pH), HCO 3 , and PCO2.
Liver The liver also has a role in acid–base homeostasis. Hepatic conversion of ammonia to urea consumes HCO 3 , though the role of this in acid–base regulation in humans is not fully understood. Nitrogen metabolism by the liver and by the kidney are connected by glutamine, which links renal ammonia production and hepatic urea synthesis to systemic acid–base regulation.
Base Deficit and Base Excess Base deficit or base excess is the measure of change of buffer base from normal. Base deficit (i.e., negative base excess) equals the amount of HCO 3 in mEq/L that is required to restore the total buffer base of ECF to a pH of 7.40. At a pH of 7.15 and HCO 3 of 24 mEq/L, the base deficit will be 6. At a pH of 7.47 with the same HCO 3 of 24, the base deficit will be 1 (i.e., negative base deficit ¼ metabolic alkalosis). Potassium has an inverse relationship with the pH due to intracellular fluid (ICF) shifts. Normal arterial values are as follows:
pH ¼ 7.40 0.03 PCO2 ¼ 40 mmHg Venous HCO 3 ¼ 25 mEq/L 2
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Anion Gap The unmeasured anion concentration is known as the anion gap. The anion gap is based on the principle that plasma is electrically neutral. Measured cations þ unmeasured cations ¼ measured anions þ unmeasured anions
Therefore, Measured cations Measured anions ¼ Unmeasured anions Unmeasured cations ¼ Anion gap
The predominant measured cation is sodium. Measured anions in plasma are chloride and HCO 3 . Unmeasured anions are serum proteins, phosphate, sulfate, and organic anions. Unmeasured cations include calcium (Caþ) and magnesium (Mgþ). The formula becomes: Anion gap ¼ Naþ ðCl þ HCO 3Þ
A normal anion gap is 12 4 but may be lower due to high chloride concentrations measured with newer autoanalyzers. Knowing the normal range for a specific laboratory value is necessary to interpret the anion gap correctly. The most common cause of an elevated anion gap is metabolic acidosis (i.e., increase in organic acids), but it can also be seen in hypocalcemia or hypomagnesemia where there is a fall in unmeasured cations. Decreased or negative anion gap can be seen when there is an increase in unmeasured cations, as in lithium toxicity, bromide, or the positively charged proteins of multiple myeloma. Hypoalbuminemic states like nephrotic syndrome or cirrhosis can cause a false decrease in the anion gap, so increased anion gap in these patients may be missed. In a simple acid–base disturbance that produces an elevated anion gap, the increase in anion gap from baseline should equal the decrease in serum HCO 3 . If the serum HCO3 change is greater or less than the change in anion gap, a coexistent non–anion gap metabolic acidosis or mixed acid–base disorder should be suspected.
METABOLIC ACIDOSIS Definition Metabolic acidosis is defined as a decrease in pH, elevated Hþ concentration, and decreased HCO 3 concentration. The respiratory compensation is hyperventilation, causing a decrease in PCO2.
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Epidemiology Metabolic acidosis results from endogenous production of acid, decreased renal excretion of acid, or HCO 3 loss. It is divided into high anion gap and normal anion gap (i.e., hyperchloremic acidosis). In high anion gap metabolic acidosis, there is increased production of organic acids. The most common causes are ketoacidosis (e.g., diabetic, starvation, and alcoholic), lactic acidosis (seen in persons who have experienced trauma and in critically ill patients), renal failure, and ingestions. The mnemonic MUDPILES can be used to help remember the causes of anion gap metabolic acidosis:
Methanol Uremia DKA Paraldehyde Ingestions, iron, INH Lactate Ethylene glycol Salicylates
It should be noted that many ingestions (i.e., cyanide, biguanides, iron) cause their toxicity by the generation of a lactic acidosis and that ethanol does not cause a significant metabolic acidosis. In non–anion gap metabolic acidosis, HCO 3 is replaced on an equimolar basis by chloride. The anion gap is normal, but there is a rise in the serum chloride concentration. Non–anion gap metabolic acidosis is caused by renal or gastrointestinal (GI) loss of HCO 3, inability of the kidney to excrete Hþ, or Hþ administration. This can be seen with severe diarrhea, ureterosigmoidostomy, intestinal fistulas, renal tubular acidosis (RTA) type 1, 2, or 4, hypoaldosteronism, and infusion or ingestion of HCl-containing compounds (e.g., NH4Cl, lysine-HCl).
Clinical Presentation and Examination In severe acidosis, decreases are evident in cardiac contractility, systemic blood pressure, and hepatic and renal perfusion. Fatal ventricular arrhythmias can occur. Neurological effects from lethargy to coma have been reported. Patients with severe metabolic acidosis may have an increased respiratory rate and may report dyspnea yet have a normal PO2 and lung examination results. This is due to the respiratory compensation for the metabolic acidosis. History is helpful in determining the etiology of the acidosis; possible causes include renal disease, diabetes mellitus, diarrhea, ingestions, and alcohol abuse.
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Laboratory Findings and Diagnosis pH and HCO 3 must be decreased if the primary disorder is metabolic acidosis. Electrolyte measurements and ABG analysis should be performed. Decreased pH with decreased HCO 3 (<25 mEq/L) signifies metabolic acidosis. Next, the anion gap should be calculated to decide whether the patient has high anion gap or normal anion gap metabolic acidosis. The practitioner should know the normal anion gap for relevant laboratory values. If it is determined that the patient has an elevated anion gap acidosis of unknown etiology, it may be useful to calculate an osmolal gap, which will be elevated in methanol and ethylene glycol ingestions. The respiratory compensation for metabolic acidosis involves a decrease in PCO2 of 1.2 mmHg for every 1.0 mEq/L decrease in HCO 3, or PCO2 ¼ 1.5 (HCO ) þ 8. 3
Treatment and Outcome Treatment and outcome vary with the underlying disorder. Treatment emphasizes tissue perfusion and ventilation, correction of the underlying cause, and in some cases, administration of HCO 3 . Bicarbonate is usually not indicated in metabolic acidosis caused by generation of organic acids such as DKA and lactate. In these disorders, the metabolism of the ketones and lactate regenerates HCO 3 . Bicarbonate therapy results in generation of CO2 and may cause paradoxical worsening of acidosis and worsening of respiratory failure. Hypokalemia and fluid overload can also occur. Bicarbonate therapy may be indicated in patients with a HCO 3 level greater than 4 mEq/L, a pH lower than 7.2, with shock or myocardial irritability that does not rapidly respond to other measures. Newer buffers are being studied but are not widely available in the United States. Bicarbonate therapy is used in the treatment of ingestions such as salicylates, methanol, and ethylene glycol and to correct the acidosis caused by diarrhea in non–anion gap metabolic acidosis.
METABOLIC ALKALOSIS Definition Metabolic alkalosis is the elevation of the plasma HCO 3 concentration in the presence of a high pH (i.e., low Hþ concentration).
Epidemiology þ An elevation in HCO 3 can be due to H loss, intracellular movement of þ H , alkali administration, or contraction alkalosis. These factors will
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cause patients to become alkalotic, but to maintain the metabolic alkalosis there must also be impairment in renal HCO 3 excretion. This is usually due to volume depletion or K depletion.
Gastrointestinal H+ Loss Each milliequivalent of Hþ lost generates 1 mEq of HCO 3 . Vomiting (including self induced) and diarrhea are the most common causes of gastric loss; other causes include nasogastric tube, chloride-losing diarrheas due to villous adenoma, or laxative abuse.
Renal H+ Loss Renal Hþ loss can occur from primary mineralocorticoid excess (i.e., renal absorption of sodium and HCO 3 with loss of hydrogen, chloride, and K), loop or thiazide diuretics, posthypercapnic alkalosis (i.e., rapid lowering of chronically elevated PCO2), hypercalcemia including milk alkali syndrome, and low chloride intake in infants given formula high in Naþ but low in Cl.
Intracellular Shifts Hypokalemia causes Kþ to leave cells, and hydrogen enters to maintain electroneutrality.
Alkali Administration If large amounts of HCO 3 are given acutely, as in the treatment of DKA or lactic acidosis, a postcorrection metabolic alkalosis can be induced. Sodium bicarbonate ingestion or the administration of large quantities of citrate, as with the transfusion of many units of banked blood, can result in metabolic alkalosis.
Contraction Alkalosis Contraction alkalosis occurs when there is the loss of a relatively large amount of HCO 3 -free fluid. This causes contraction of the extracellular volume around a constant amount of extracellular HCO 3 . The most common cause is ingestion of loop diuretics. This condition is also seen in gastric losses in patients with achlorhydria, sweat loss in cystic fibrosis, and congenital chloridorrhea.
Clinical Presentation Patients with metabolic alkalosis may be asymptomatic or may present with symptoms of volume depletion (e.g., postural light-headedness, weakness) or hypokalemia (e.g., muscle weakness, polyuria).
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Examination Examination of a patient with metabolic alkalosis may show signs of volume depletion or self-induced vomiting.
Laboratory Findings/Diagnosis For a primary disorder of metabolic alkalosis, the pH and HCO 3 must be increased to the following levels: pH>7.45, HCO 3 >25 mEq/L. Hypokalemia and hypochloremia are usually present. Magnesium and Caþ are also decreased. The etiology is often obtained from the history. If there is no pertinent history, surreptitious vomiting, diuretic use, or a mineralocorticoid excess state should be suspected. Electrolyte measurements and ABG analysis should be performed. A check of the urine chloride level may be helpful in differentiating the etiology and determining treatment. In metabolic alkalosis, the urine chloride may be a better indication of volume status than urine sodium. The urine chloride level is typically less than 20 mEq/L in the presence of vomiting, nasogastric suction, chronic diuretic use, chloride-wasting diarrheas (i.e., laxative abuse) and cystic fibrosis and after hypercapnia. The urine chloride level is greater than 20 mEq/L in primary mineralocorticoid excess states and in the presence of alkali loads and severe hypokalemia (Kþ<2.0 mEq/L). Metabolic alkalosis causes a compensatory hypoventilation that will raise the PCO2 in an attempt to return the pH toward normal levels. PCO2 rises 0.7 mmHg for every 1.0-mEq/L rise in plasma HCO 3 concentration.
Treatment Treatment is aimed at increasing the renal excretion of HCO 3 . For this to occur, volume, Cl and K depletion must be corrected. Treatment is also aimed at the underlying disease and prevention of further Hþ loss. Metabolic alkalosis is divided into saline-responsive alkalosis and saline-resistant alkalosis. Saline-responsive alkalosis includes conditions resulting from vomiting, nasogastric suction, diuretic use, posthypercapnia, and low chloride intake. Unless the patient is hypotensive or has severe electrolyte disturbances, saline-responsive alkalosis is treated with fluid replacement with normal saline or ½ normal saline at 50–100 ml/hr in excess of the totals of urine output, insensible losses (30–50 ml/hr), and any other losses present (e.g., nasogastric drainage, diarrhea). Kþ deficits should be corrected with administration of KCl. This reverses the contraction component, removes the stimulus to renal Na retention, permits the renal excretion of NaHCO3, and increases Cl delivery to the distal nephron, which promotes HCO 3 secretion.
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Vomiting should be treated with antiemetic drugs. If nasogastric suction is ongoing, the acidity of gastric secretions can be decreased with a proton pump inhibitor. Saline-resistant alkalosis includes edematous states occurring after diuretic therapy, mineralocorticoid excess, severe hypokalemia, and renal failure. Treatment of metabolic alkalosis in edematous states (e.g., congestive heart failure [CHF], nephrotic syndrome, cirrhosis) consists of withholding diuretics, if possible, administering acetazolamide, infusing HCl (with consultation from a renal specialist), or providing dialysis. Severe hypokalemia (i.e., Kþ<2.0 mEq/L) is treated initially with Kþ repletion. When the severe Kþ deficit is partially repleted, the metabolic alkalosis will become saline responsive. Primary mineralocorticoid excess states are treated by surgical removal of an adrenal adenoma or a Kþ-sparing diuretic agent.
RESPIRATORY ACIDOSIS Definition Respiratory acidosis is due to decreased effective alveolar ventilation with resultant decreased pulmonary excretion of CO2 and a rise in PCO2.
Epidemiology Respiratory acidosis can be caused by inhibition of the central respiratory center, weakness of respiratory muscles and chest wall, upper airway obstruction, or abnormal gas exchange across the pulmonary capillary. Common causes are head trauma, chest trauma, parenchymal lung disease like chronic obstructive pulmonary disease (COPD), excess sedation, sleep apnea, and mechanical ventilation. In severely obese patients, chronic hypoventilation is referred to as obesity hypoventilation syndrome.
Clinical Presentation Manifestations vary depending on the underlying disorder and the rate of development of the hypercapnia. Acute respiratory acidosis causes multiple neurological symptoms. The presence of an acid pH and an elevated PCO2 (>45 mmHg) establish the diagnosis of primary respiratory acidosis. Symptoms include headache, restlessness, and anxiety. These can progress to tremors, somnolence, and delirium. The neurological abnormalities are experienced as a result of cerebrospinal fluid pH changes, and similar findings are not seen in metabolic acidosis. Arrhythmias, peripheral vasodilation,
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and hypotension can occur with pH less than 7.10. A rise in PCO2 stimulates the brain’s respiratory center to increase minute ventilation and respiratory rate. In patients with COPD, the PCO2 can rise to 60–70 mmHg and depress the respiratory center. As a result, hypoxia becomes the main stimulus for respiration. Oxygen given to a patient with COPD without careful monitoring can cause respiratory depression and apnea.
Examination Examination may give a clue to the etiology of the respiratory acidosis. Patients may have pneumonia; stridor of upper airway obstruction; the physical findings associated with COPD; the obesity, plethoric facies, and short thick neck seen in obesity hypoventilation syndrome; or the neurological findings associated with myasthenia gravis or Guillain syndrome. Cyanosis may be seen if hypoxia is also present. BarrE In addition to neurological and cardiac abnormalities seen in acute respiratory acidosis, patients with chronic respiratory acidosis often have cor pulmonale and pedal edema.
Laboratory Findings In simple respiratory acidosis, the pH will be less than 7.39 and PCO2 will be greater than 45 mmHg. Electrolyte levels in chronic respiratory acidosis will often show an increased HCO 3 , hypokalemia, and hypochloremia. If K and Cl levels are high or normal, then the patient usually has acute respiratory acidosis. A chest radiograph should be obtained to help determine the presence or absence of pulmonary disease as a cause of the respiratory acidosis. Head computed tomography (CT) may be needed if a central cause of hypoventilation is suspected.
Diagnosis The presence of an acidic pH and elevated PCO2 (>45 mmHg) establish the diagnosis of respiratory acidosis. Diagnosis can often be made on the basis of the history. The metabolic compensation for respiratory acidosis differs for acute versus chronic respiratory acidosis. The renal response of renal Hþ excretion takes time to develop. Initial buffers are the intracellular buffers hemoglobin and proteins. In acute respiratory acidosis, for every 10-mmHg rise in PCO2, there is a 1.0-mEq/L increase in plasma HCO 3 . In chronic hypercapnia, there is a compensatory renal response of Hþ secretion, with a resultant addition of HCO 3 to the ECF. This takes 3–5 days to develop. In chronic
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respiratory acidosis, for every 10-mmHg increase in PCO2, there is a 3.5-mEq/L increase in plasma HCO 3.
Treatment and Outcome The goal of treatment of respiratory acidosis is to improve alveolar ventilation and increase minute ventilation. If minute ventilation is doubled, PCO2 will be decreased by 50%. Treatment of the underlying lung disease, oxygen, bronchodilators, steroids, reversal of sedation, and intubation/mechanical ventilation may be needed. Sedatives should be avoided because they can contribute further to respiratory depression. Diuretics and chronic low-flow oxygen may benefit patients with cor pulmonale. Chronic respiratory acidosis should not be corrected too quickly if mechanical ventilation is needed. A rapid lowering of PCO2 to “normal” levels can cause overshoot alkalemia (there is already renal compensation with increased plasma HCO 3 in these patients) and arrhythmias. The sudden increase of central nervous system (CNS) pH can result in seizures and coma.
RESPIRATORY ALKALOSIS Definition Primary respiratory alkalosis is characterized by low PCO2 and elevated pH. Respiratory alkalosis is due to increased effective alveolar ventilation beyond that needed to eliminate the daily load of metabolically produced CO2, with resultant increased pulmonary excretion of CO2 and a fall in PCO2. It is the most common acid–base abnormality in critically ill patients.
Etiology Respiratory alkalosis can be caused by hypoxia, pulmonary disease, direct stimulation of the respiratory center in the brainstem, and mechanical ventilation. Common causes of hypoxia include pneumonia, CHF, pulmonary embolism, parenchymal lung diseases, and severe anemia. Central respiratory stimulation can be due to pain, hyperventilation/anxiety, CNS lesions or strokes, liver failure, sepsis, salicylate toxicity, and pregnancy.
Clinical Presentation and Examination Many patients experiencing respiratory alkalosis will have tachypnea and will be hyperventilating. Tachycardia is frequent. Cyanosis may be present if the patient is hypoxic. Tinnitus may be present in the case
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of salicylate toxicity. Physical examination may yield a clue to underlying pulmonary or neurological disease. An acute decrease in PCO2 causes a decrease in Hþ concentration, resulting in protein binding of Caþ with a decrease in ionized Caþ. Symptomatic hypocalcemia can occur, including light-headedness, circumoral and extremity paresthesias, carpopedal spasm, and syncope. A variety of cardiac arrhythmias may also occur. In addition, respiratory alkalosis causes cerebral vasoconstriction and a leftward shift in the oxygen-hemoglobin dissociation curve, resulting in decreased tissue oxygen delivery.
Laboratory Findings In a simple respiratory alkalosis, pH will be greater than 7.40 and PCO2 will be less than 35 mmHg. An ABG analysis and Chem 7 test should be performed to help establish whether the respiratory alkalosis is primary or compensatory to a metabolic acidosis, and to look for hypoxia. A chest radiograph should be obtained if pulmonary disease is suspected. A head CT scan may be indicated if a central cause is suspected.
Diagnosis Alkaline pH and hypocapnia are diagnostic of respiratory alkalosis. Tachypnea may be an important clue to the presence of decreased PCO2. Once the diagnosis of primary respiratory alkalosis has been established, the etiology should be sought. Respiratory alkalosis may be the first sign of gram-negative sepsis or salicylate toxicity. Critically ill patients can present with hyperventilation; it should not be assumed that all hyperventilation is secondary to hysteria. As in respiratory acidosis, the metabolic responses to acute and chronic respiratory alkalosis that attempt to return the pH toward normal are different. The initial response in acute respiratory alkalosis is from intracellular buffers. The decrease in renal Hþ secretion that is seen with chronic respiratory alkalosis takes 2–3 days to be complete. In acute respiratory alkalosis, for each 10-mmHg decrease in the PCO2, the HCO 3 decreases by 2.0 mEq/L. In chronic respiratory alkalosis, for each 10-mmHg decrease in the PCO2, the HCO 3 decreases by 4 mEq/L.
Treatment and Outcome The treatment of alkalosis per se is not indicated but is directed at the identification and therapy of the underlying cause.
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APPROACH TO PATIENTS WITH AN ACID–BASE DISORDER The patient may have a single acid–base disturbance or a combination of abnormalities. For example, a patient with DKA and severe nausea and vomiting may have both a metabolic acidosis and a metabolic alkalosis. A patient with COPD and sepsis may have respiratory acidosis and metabolic acidosis. The only disturbance that cannot coexist is respiratory acidosis/alkalosis. A patient can hypoventilate or hyperventilate, but he or she cannot do both simultaneously. Compensation returns the pH toward normal but not to normal. The degree of compensation is predictable; the lack of appropriate compensation is a sign of a mixed disorder. Patient evaluation begins with a history and physical examination, including information regarding medications and ingestions, with attention to sources of acid or alkali gain or loss and renal and pulmonary disease. ABG analysis and electrolyte measurements should be performed. Once this is accomplished, the healthcare provider should take the following actions: 1. Look at the pH. If it is decreased, the primary disturbance is acidosis. If it is increased, the primary disturbance is alkalosis. 2. If the pH indicates acidosis, check the HCO 3 level. If the patient has a low pH and the HCO is low, a primary metabolic acidosis is present. 3 Calculate the anion gap. If the HCO 3 is increased, the metabolic acidosis is an anion gap type. If the anion gap is not elevated, the primary metabolic acidosis is of the non–anion gap (hyperchloremic) type. 3. If there is an anion gap acidosis, establish how the change in anion gap is related to the change in HCO 3: If the increase in anion gap is equal to the decrease in HCO3 , pure anion gap acidosis is present. If the increase in anion gap is greater than the decrease in HCO3 , concomitant metabolic alkalosis is present. If the increase in anion gap is less than the decrease in HCO3 , non–anion gap acidosis is present. 4. Check for the appropriate degree of respiratory compensation for the metabolic acidosis using the formula given on page 314. If the decrease in PCO2 is more than expected, a respiratory alkalosis is also present. If the decrease in PCO2 is less than expected, a concomitant respiratory acidosis exists. 5. If the pH indicates acidosis but the HCO 3 is not decreased and the PCO2 is elevated, a primary respiratory acidosis is present. Now check to see whether the metabolic compensation is appropriate. Apply the formula for metabolic compensation with acute or chronic respiratory acidosis. If the increase in HCO 3 is more than expected, a concurrent metabolic alkalosis is present. If the increase in HCO 3 is less than expected, a metabolic acidosis is present.
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6. If the pH indicates alkalosis, check the HCO 3 . If the HCO3 is elevated, there is a primary metabolic alkalosis. Check for the appropriate degree of respiratory compensation using the formula for expected PCO2 increase in primary metabolic alkalosis. If the PCO2 is lower than expected, a concurrent respiratory alkalosis is also present. If the PCO2 is higher than expected, a respiratory acidosis is also present. 7. If the HCO 3 level is normal and the PCO2 is decreased, primary respiratory alkalosis is present. Use the formula for expected change in HCO 3 to determine whether the compensation is appropriate.
Bibliography Nicolaou DD, Kelen GD: Acid–base disorders. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Post TW, Rose BD: Approach to the adult with metabolic acidosis. In Rose BD (ed): UpToDate. Wellesley, MA, 2005. Rose BD: Simple and mixed acid–base disorders. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD, Post TW: Clinical Physiology of Acid–Base and Electrolyte Disorders, ed 5. McGraw-Hill: New York, 2001. Whittier FC, Rutecki GW: Fluids and Electrolytes: A Guide to Everyday Practice. The Little Yellow Book. Anadem: Columbus, OH, 2000.
Acute Ethanol Withdrawal ROBERT D. GRAYDON
ICD Code: Alcohol withdrawal 291.81
Key Points Hypoglycemia is common in the setting of ethanol use, especially in children, and may be a delayed effect. Chronic drinkers are often in a poorly fed, glycogen-depleted state and have multiple other nutritional deficiencies that can worsen this effect.
326 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! All patients with withdrawal should receive intravenous thiamine (100 mg), folate (1 mg), and multivitamins in the first liter of normal saline. Hypoglycemia should be treated with an intravenous push consisting of 25 mg of dextrose, followed by frequent blood sugar determinations.
DEFINITION Ethanol is a small, weakly polar, aliphatic hydrocarbon molecule that is both water and lipid soluble. It is a CNS depressant and is a widely used social stimulant.
EPIDEMIOLOGY Surveys of the U.S. general population show that approximately 65% of adults use alcoholic beverages, and many will experience problems due to their drinking. The prevalence of alcohol abuse and dependence is estimated to be between 7% and 10%. The cost to society is more than $200 billion per year in treatment costs and alcohol-related economic losses. The prevalence of alcohol use disorders in medical settings is estimated to be between 15% and 40%.
PATHOPHYSIOLOGY AND PHARMACOLOGY Ethanol is rapidly absorbed in the GI tract, with approximately 20% of the dose absorbed in the stomach and the remainder in the small intestine. Absorption is delayed by coingestion of foods/drugs and medical conditions that delay gastric emptying. Ethanol has a volume of distribution of 0.56–0.72 L/kg. Ethanol distributes throughout body fluids and tissues, easily crossing the blood–brain barrier and placenta. The metabolism of ethanol begins in the GI cells. Alcohol dehydrogenase is formed in the gastric mucosa. This enzymatic activity is decreased if the person is female, has atrophic gastritis, or has taken drugs such as aspirin and H2 blockers. This process results in increased ethanol levels. Most metabolism occurs through two hepatic enzymes systems: 1. Alcohol dehydrogenase is generally the predominant system. The alcohol dehydrogenase system uses alcohol dehydrogenase to oxidize ethanol to acetaldehyde and then acetaldehyde dehydrogenase to oxidize acetaldehyde to acetate, which ultimately becomes acetyl coenzyme A and either enters the Krebs cycle or undergoes ketone body formation or fatty acid synthesis. Acetate is also converted to acetone. During this process, nicotinamide adenine dinucleotide
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(NAD) is reduced, changing the reduced alcohol dehydrogenase– NADþ ratio. Changes in this ratio impair cellular oxidative processes, such as conversion of lactate to pyruvate and gluconeogenesis. Because gluconeogenesis is critical to maintaining serum glucose homeostasis, profound metabolic abnormalities such as hypoglycemia, acidosis, and other electrolyte disturbances may occur. Dehydrogenase enzymes have variable activity in different persons depending on genetic makeup, gender, and other factors. 2. The microsomal ethanol oxidizing system (MEOS), a cytochrome P450-dependent system, is usually a minor metabolic pathway. This enzyme system is inducible and allows chronic drinkers to degrade ethanol at high rates. Induction of this system can be responsible for multiple drug interactions for other drugs normally metabolized by this system, including increased production of the toxic metabolites of acetaminophen. Ethanol approximates Michaelis-Menten kinetics. At high ethanol levels, saturation of the alcohol dehydrogenase and MEOS enzyme systems occur, and the elimination half-life prolongs as metabolism shifts from concentration-dependent first-order kinetics to time-dependent zero-order kinetics. Ethanol is metabolized at rates of 100–200 mg/kg/ hr or more. Chronic exposure and high levels cause induction of the MEOS system, which accounts for the significant increase in metabolism and clearance seen in chronic drinkers. Other factors that influence the rate of ethanol clearance include continued absorption, liver disease, drug inhibition of the MEOS system, and genetic variation. Approximately 10% is excreted unchanged through the lungs and kidneys. Ethanol is a CNS depressant but may have variable effects on individuals. Early in intoxication, a paradoxical stimulatory effect with euphoria, giddiness, and loss of inhibitions may predominate. As intoxication worsens (levels of approximately 150/dl in the casual drinker), CNS depression becomes generalized, leading to ataxia, slurred speech, and sedation. At serum levels greater than 200 mg/dl, progression to coma, loss of protective reflexes, and autonomic dysfunction occur. Death often occurs at levels of 400 mg/dl. Blood ethanol levels do not always correlate precisely with the degree of intoxication. Persons with a history of chronic ethanol abuse and dependence can exhibit little clinical evidence of intoxication, even with levels approaching 400 mg/dl. Ethanol intoxication is poorly understood and is probably multifactorial. Hypoglycemia is common in the setting of ethanol use, especially in children, and may be a delayed effect. Chronic drinkers are often in a poorly fed, glycogen-depleted state and have multiple other nutritional deficiencies that can worsen this effect. Ethanol-induced hypoglycemia should always be suspected in these patients. Profound hypomagnesemia is a subtle but common and life-threatening complication of chronic
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ethanol ingestion. Low Mg states occur due to poor dietary intake, decreased GI absorption, and ethanol-induced increase in urinary excretion. Because the majority of Mg is stored in bone, serum levels may not reveal the extent of the loss. Many chronic drinkers have profound intracellular Mg losses despite normal serum levels. Thiamine deficiency can produce Wernicke’s encephalopathy. In addition, chronic ethanol abuse affects most of the hypothalamic-pituitary axis, leading to decreased testosterone production in men and amenorrhea in women. Elevated glucocorticoid levels may be seen, and many drinkers have physical manifestations resembling Cushing’s syndrome. Neurological manifestations include seizures (both during intoxication and withdrawal states), auditory hallucinations, and peripheral neuropathy. Dilated cardiomyopathy, atrial fibrillation, and other non–Mg-deficiency arrhythmias may occur. High-output congestive failure may be seen with thiamine deficiency. Other disorders seen in chronic ethanol abusers include skeletal muscle myopathy, thrombocytopenia, and coagulopathies. Because ethanol is a multisystem toxin, chronic use is associated with a host of medical illnesses, leading to acute complications such as esophageal variceal hemorrhage, hemorrhagic gastritis, pancreatitis, Mallory-Weiss tears, and Boerhaave’s syndrome. Hepatic disease can range from mild steatosis to cirrhosis with hepatic encephalopathy. Chronic alcohol consumption affects central a-adrenergic receptors, central b-adrenergic receptors, the inhibitory neurotransmitter g-aminobutyric acid (GABA), and dopamine turnover. Alcohol withdrawal occurs when an ethanol-dependent person reduces or ceases ethanol use. The classic study by Isbell in 1955 showed the relationship between alcohol and the withdrawal syndrome. This study also demonstrated that the severity of withdrawal was dependent on both the dose and duration of ethanol consumption. Withdrawal is triggered by a reduction in blood alcohol level. It is characterized by autonomic hyperactivity. Alcohol withdrawal is multifactorial and incompletely understood.
CLINICAL PRESENTATION Alcohol withdrawal develops 6–24 hours after cessation or reduction of alcohol use and lasts from 2 to 7 days. The severity of alcohol withdrawal ranges from mild irritability and insomnia to fever, hallucinations, diaphoresis, and disorientation. Minor alcohol withdrawal begins as early as 6 hours and peaks at 24–36 hours after cessation or reduction in alcohol intake. Minor withdrawal is characterized by mild autonomic hyperactivity manifested by nausea, anorexia, coarse tremor, tachycardia, hypertension, hyperreflexia, anxiety, and sleep disturbances.
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Major alcohol withdrawal occurs after more than 24 hours and usually peaks at 50 hours, but occasionally takes up to 120 hours after cessation. Manifestations of major withdrawal include worsening anxiety, insomnia, irritability, tremor, anorexia, tachycardia, hyperreflexia, hypertension, fever, decreased seizure threshold, auditory and visual hallucinations, and finally delirium. Delirium tremens is manifested by gross tremor, profound confusion, fever, incontinence, visual hallucinations, and mydriasis. It is seldom seen before the third day of abstinence. One of the most common causes of adult-onset seizures is alcohol withdrawal, with seizures occurring 6–48 hours after cessation of ethanol intake.
EXAMINATION Patients can present in any stage of withdrawal, experiencing symptoms from mild tremors to full-blown delirium. Patient history is often unreliable, and more reliable data can sometimes be obtained from paramedics, police officers, and family members. Accurate recording of vital signs is mandatory, as is frequent monitoring of vital signs. Hypothermia, hyperthermia, tachypnea, tachycardia may be indicators of serious underlying diseases such as sepsis, drug ingestion, intracranial hemorrhage, hypoglycemia, or diabetes. A rapid but thorough physical examination should be performed with attention paid to the level of consciousness, signs of hepatic failure, coagulopathy, occult trauma, and the cardiovascular, respiratory, digestive, and neurological systems. Vital signs and level of consciousness evaluation should be repeated at frequent intervals.
LABORATORY FINDINGS The healthcare provider should perform a complete blood count (CBC), coagulation studies, serum chemistries, urinalysis, urine drug screen, liver function studies, and measurements of blood urea nitrogen (BUN), creatine, Mg, phosphorus, and blood alcohol level. A rapid bedside glucose determination should also be performed, as should fecal occult blood testing.
RADIOLOGY A chest x-ray is mandatory for patients with fever or tachypnea. Blood and urine cultures should be considered in all febrile patients. CT scans of the head and lumbar puncture should also be considered, especially in patients with new-onset seizures or an unclear history. In cases of moderate-to-severe withdrawal, an electrocardiograph (ECG) should be obtained.
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TREATMENT The patient should be completely undressed and placed on a monitor with frequent reassessment of vital signs. Intravenous access should be obtained. A full physical examination should be performed and key components repeated at frequent intervals. The previously noted laboratory and radiological studies should be performed, as guided by history and physical examination. All patients experiencing withdrawal should receive intravenous thiamine (100 mg), folate (1 mg), and multivitamins in the first liter of normal saline. Hypoglycemia should be treated with an intravenous push of dextrose (25 g), followed by frequent blood sugar determinations. Benzodiazepines are the mainstay of treatment for alcohol withdrawal. By interacting with the GABA receptors, benzodiazepines substitute for the GABA-potentiating effect of ethanol and reduce signs and symptoms of withdrawal; they also have excellent anticonvulsant properties. Lorazepam is the preferred drug due to its relatively short half-life, good intramuscular absorption, and the absence of active metabolites. All benzodiazepines involve the complications of excessive sedation, confusion, and hypotension at high doses. The dosage of benzodiazepines required to treat alcohol withdrawal is highly individual and variable. A starting dose of 1–4 mg of lorazepam should be given intravenously, and then repeated at 15- to 30-minute intervals for patients in severe withdrawal. The dosage should be titrated to control the patient’s agitation. Patients with severe delirium tremens may require massive doses of benzodiazepines. Restraints may be required to prevent self-injury or injury to staff. Alcohol-related seizures should be treated with benzodiazepines. Volume depletion should be corrected with normal saline. Underlying electrolyte and metabolic disorders should be corrected. A careful search for underlying medical conditions and other causes of delirium should be sought.
DISPOSITION Patients with signs of major withdrawal—extreme agitation, fever, confusion, or hallucinations—always require admission. Patients with mild withdrawal should be observed in the emergency department (ED) for 6–8 hours and treated appropriately. If, after a period of observation and treatment, an alert, oriented patient with normal vital signs, physical examination, and normal laboratory study results may be released with an oral tapering dose of lorazepam (initially 6 mg/day in divided doses, tapering 1–2 mg/day over 4–6 days). This should be reserved for patients who are motivated to stop drinking and are reliable, or who can be
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supervised by a responsible, sober adult. All patients experiencing ethanol withdrawal should be offered treatment and referral for alcohol dependence.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil’s Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Isbell H, Fraser HF, Wikler A, et al: An experimental study of the etiology of rum fits and delirium tremens, Q J Study Alcohol 1955;16:1–33. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000. Watson W, Litovitz TL, Rodgers GC Jr, et al: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2004;22(5):335–404.
Adrenal Insufficiency BENJAMIN P. HARRISON
ICD Codes: Addison’s disease 255.4, Adrenal crisis 255.4, Adrenal insufficiency 255.4, Sheehan’s syndrome 253.2
Key Points Classically, chronic adrenal insufficiency is associated with Addison’s disease,which develops over months to years and has primary symptoms of weakness, fatigue, anorexia,weight loss, and hyperpigmentation. ! Emergency Actions ! A rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands’ ability to respond immediately.
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DEFINITION Adrenal insufficiency is an acute or chronic decreased or absent level of circulating aldosterone and cortisol. Classically, chronic adrenal insufficiency is associated with Addison’s disease, which develops over months to years and features primary symptoms including weakness, fatigue, anorexia, weight loss, and hyperpigmentation. Persons with chronic adrenal insufficiency can develop adrenal crisis. However, by definition, an acute adrenal crisis involves subphysiological levels of adrenal hormones that result in patients presenting with vomiting, abdominal pain, and hypovolemic shock.
EPIDEMIOLOGY The epidemiology of adrenal insufficiency is as follows:
Approximately 6 million people in the United States are considered to have undiagnosed adrenal insufficiency, which is clinically significant only during times of physiological stress. Critically ill patients with septic shock demonstrate a de novo (i.e., a matter anew, as though it was being tried for the first time) incidence ranging from 19% to 54%. Secondary adrenal insufficiency has been demonstrated in 31% of patients admitted to a critical care unit.
PATHOPHYSIOLOGY The adrenal gland consists of two parts: the cortex and the medulla. The cortex produces three steroid hormones: glucocorticoids (cortisol), mineralocorticoids (11-deoxycorticosterone and aldosterone), and androgens. Their secretion occurs under the control of the hypothalamicpituitary axis through the release of corticotropin-releasing factor and subsequently the activation of adrenocorticotropic hormone (ACTH). In contrast to aldosterone, 11-deoxycorticosterone is a weak mineralocorticoid. The hormones of importance in acute adrenal crisis are cortisol and aldosterone. The medulla secretes catecholamines (e.g., epinephrine and norepinephrine). Their secretion is under neural control. Cortisol has the following basic effects in the body:
Stimulates gluconeogenesis (i.e., glucose production) and decreases cellular glucose use Mobilizes amino acids and fatty acids Inhibits the effects of insulin Gives rise to ketone bodies in metabolism (i.e., ketogenesis) Elevates RBC and platelet levels
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Exhibits anti-inflammatory effects Diminishes cell-mediated immunity (destroying intracellular bacteria, eliminating viral infections, and destroying tumor cells) Enhances the pressor effects of catecholamines on the heart muscles and arterioles Facilitates free water clearance, enhances appetite, and suppresses ACTH synthesis (i.e., feedback inhibition to the hypothalamicpituitary axis)
Aldosterone is released in response to angiotensin II stimulation, hyperkalemia, hyponatremia, and dopamine antagonists. Its effect is on the kidney (the target organ) to promote reabsorption of sodium and secretion of K and hydrogen. Its release is regulated via negative feedback by the renin-angiotensin system and serum K concentration. Increased K stimulates aldosterone production, and decreased K inhibits production. The net effect is to increase intravascular volume. Primary adrenocortical insufficiency is the failure of the adrenal glands to release adequate amounts of these hormones to meet physiological needs, despite release of ACTH from the pituitary gland. The most common causes are infiltrative or autoimmune disorders (80% in the United States), but adrenal exhaustion from severe chronic illness can also occur. Secondary adrenal insufficiency can be caused by hypopituitarism due to the following:
Hypothalamic-pituitary disease (e.g., Sheehan’s syndrome, pituitary apoplexy) Suppression of the hypothalamic-pituitary axis by exogenous steroids (overall, the most common etiology of adrenal insufficiency) or endogenous steroids (e.g., tumor)
A rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands’ ability to respond immediately. Bilateral massive adrenal hemorrhage (BMAH) occurs under severe physiological stress (e.g., septic shock, complicated pregnancy, myocardial infarction) or with concomitant coagulopathy or thromboembolic disorders. Surgery, burns, trauma, convulsions, and adrenal vein thrombosis can all precipitate adrenal hemorrhage. In a child or infant, BMAH can be precipitated by septicemia usually as a result of Pneumococcus, Meningococcus, Staphylococcus, Haemophilus, and gram-negative organisms. This classically occurs in WaterhouseFriderichsen syndrome, which is an overwhelming septicemia resulting from meningococcemia.
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CLINICAL PRESENTATION The clinical presentation of adrenal insufficiency consists of the following:
Prior steroid use Severe physiological stress (e.g., sepsis, trauma, burns, surgery), organisms associated with adrenal crisis (e.g., Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae, fungi), meningococcemia Azotemia (i.e., presence of BUN in the blood) Anticoagulants, hemorrhagic diathesis Neonate; complicated pregnancy Adrenocorticotropin therapy, known primary or secondary adrenocortical insufficiency Acquired immunodeficiency syndrome (AIDS); fatigue is most common presenting symptom Invasive or infiltrative disorders (e.g., sarcoidosis, amyloidosis, neoplastic) Tuberculosis In bilateral adrenal hemorrhage and infarction, signs and symptoms in descending order are as follows: hypotension/shock (>90%); abdominal, flank, back, or lower chest pain (86%); fever (66%); anorexia, nausea, or vomiting (47%); neuropsychiatric symptoms such as confusion or disorientation (42%); abdominal rigidity or rebound tenderness (22%).
EXAMINATION The examination of a patient with adrenal insufficiency will reveal the following:
Unexplained shock, usually refractory to fluid and pressor resuscitation Nausea, vomiting, and abdominal or flank pain Hyperthermia or hypothermia Calcification of auricular cartilage (chronic insufficiency) Hyperpigmentation (most conspicuous in the face, neck, and backs of hands)
ETIOLOGY Possible causes of adrenal insufficiency include the following:
Drug use or abuse Rapid withdrawal of long-term steroid therapy Ketoconazole Phenytoin Rifampin Anesthesia (e.g., etomidate)
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Anticoagulant therapy (between 3rd and 18th day) Mitotane (chemotherapeutic agent used in the treatment in Cushing’s syndrome) Metastatic breast or prostate cancer Sarcoidosis, amyloidosis, neoplastic disease In BMAH: surgery, burns, pregnancy, trauma, convulsions, adrenal vein thrombosis Head trauma
DIFFERENTIAL DIAGNOSIS The differential diagnosis of adrenal insufficiency includes the following:
Shock from any source Septic shock Acute abdomen Anorexia nervosa Hypopituitarism Hypothyroidism and myxedema coma
LABORATORY FINDINGS Common laboratory tests to be performed in a patient with adrenal insufficiency include the following:
Serum chemistry panel results are as follows: Abnormalities are present in as many as 56% of patients. Hyponatremia is common (though not diagnostic). Hypoglycemia (67% occurrence) Hyponatremia (88%) Hyperkalemia (64%) Hypercalcemia (6%–33%) Serum cortisol: Less than 20 mg/dl in severe stress is indicative of adrenal insufficiency. ACTH test (diagnostic) The practitioner should determine the baseline serum cortisol level, then administer ACTH (250 mg intravenous push), and then draw serum cortisol 30 and 60 minutes after ACTH administration. An increase of less than 7 mg/dl is considered diagnostic of adrenal insufficiency. CBC: Anemia (mild and nonspecific), lymphocytosis, and eosinophilia (highly suggestive) may be present. Serum thyroid function tests: These should assess for autoimmune, infiltrative, or multiple endocrine disorders. Cultures: Blood, urine, and other cultures should be performed, as clinically indicated. Infection is a common precipitant of acute adrenal crisis. ABG analysis: Acidemia and hypoxia (neither sensitive nor specific) may be present.
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RADIOGRAPHS A chest radiograph should assess for tuberculosis, histoplasmosis, malignant disease, sarcoid, and lymphoma. It may also show a narrow cardiac silhouette resulting from decreased vascular volume. An abdominal CT scan should visualize adrenal glands for hemorrhage, atrophy, infiltrative disorders, and metastatic disease. Adrenal hemorrhage appears as hyperdense, bilaterally enlarged adrenal glands.
OTHER TESTS Other tests to be undertaken include ECG. Prolongation of the QT interval can induce ventricular arrhythmias. Elevated peaked T waves may indicate hyperkalemia, and deep negative T waves have been described in acute adrenal crisis.
TREATMENT Treatment for chronic adrenal insufficiency should include the following:
Cortisol, 15–20 mg every morning and 10 mg in the evening Fludrocortisone (Florinef), 0.05–0.1 mg every morning Halotestin or depot-testosterone Patent education and administration of an identification card or bracelet Stress dose cortisol (to prevent adrenal crisis) The usual oral dose should be doubled for stressful illnesses or injuries. Hydrocortisone 100 mg should be given intravenously every 8 hours, for at least the first 24 hours after major surgery, trauma, or infection. Treatment for adrenal crisis should proceed as follows:
Administer supplemental oxygen. Engage in coma protocol (i.e., glucose, thiamine, naloxone); administer glucagon if the patient is hypoglycemic and intravenous access cannot be obtained. Administer glucocorticoids in supraphysiological or stress doses (the only definitive therapy). The drug of choice is dexamethasone or a soluble form of cortisol (such as 100 mg hydrocortisone sodium succinate). Dexamethasone sodium phosphate 4 mg should be given intravenously. Dexamethasone is preferred for two reasons: it is long acting (12–24 hours) and it does not interfere with serum cortisol assay.
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However, because dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement is necessary. A short ACTH stimulation test may be performed during resuscitation. Once completed, hydrocortisone (100 mg intravenous every 6 hours) is the preferred treatment to provide mineralocorticoid support. Delaying glucocorticoid replacement therapy while awaiting the results of the ACTH stimulation test is inappropriate and dangerous. Aggressively replace fluids (2–3 L) with 5% or 10% intravenous dextrose and saline solutions. Administer empirical antibiotics, if indicated; seek and resolve precipitating stressors to include infections. Correct electrolyte abnormalities, especially hyperkalemia. Perform reverse coagulopathy with fresh frozen plasma. Correct hyperthermia or hypothermia by initiating cooling/warming measures. Administer pressors (e.g., dopamine, norepinephrine) to combat hypotension if it is present and unresponsive to intravenous crystalloid boluses. Mineralocorticoid therapy is not needed in the ED for initial treatment.
Admission Criteria All patients with acute adrenal crisis should be admitted to the hospital. ICU admission should be considered for unstable or potentially unstable patients.
Consultations Care for patients with adrenal insufficiency should include consultations with the following specialists:
Endocrinologist Infectious disease specialist Critical care physician for ICU admission Cardiologist, if acute coronary syndrome is suspected Surgeon for BMAH or acute abdomen
Bibliography Aono J, Mamiya K, Ueda W: Abrupt onset of adrenal crisis during routine preoperative examination in a patient with unknown Addison’s disease, Anesthesiology 1999;90 (1):313–314. Chin R: Adrenal crisis, Crit Care Clin 1991;7(1):23–42. Iga K, Hori K, Gen H: Deep negative T waves associated with reversible left ventricular dysfunction in acute adrenal crisis, Heart Vessels 1992;7(2):107–111.
338 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Klauer K: Adrenal insufficiency and adrenal crisis, eMedicine. Last updated April 18, 2005. http://www.emedicine.com/emerg/topic16.htm. Kirkland L Adrenal crisis, eMedicine. Updated May 8, 2003. Available at: http://www. emedicine.com/med/topic65.htm. Koo DJ, Jackman D, Chaudry IH: Adrenal insufficiency during the late stage of polymicrobial sepsis, Crit Care Med 2001;29(3):618–622. Obenour RA, Ross S: Hospital Formulary of the University of Tennessee Medical Center. Knoxville, Tennessee, 1999. Passmore JM: Adrenal cortex. In Geehoed GW, Chernow B (eds): Endocrine Aspects of Acute Illness. Churchill-Livingstone: New York, 1985, pp 97–134. Rao RH: Bilateral massive adrenal hemorrhage, Med Clin North Am 1995;79(1):107–129. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Schroeder S, Wichers M, Klingmuller D: The hypothalamic-pituitary-adrenal axis of patients with severe sepsis: Altered response to corticotropin-releasing hormone, Crit Care Med 2001;29(2):310–361. Vella A, Nippoldt TB, Morris JC 3rd: Adrenal hemorrhage: A 25-year experience at the Mayo Clinic, Mayo Clin Proc 2001;76(2):161–168. Williams GH, Dluhy RG: Disease of the adrenal cortex. In Braunwald E, Fauci AS, Kasper DL (eds): Harrison’s Principles of Internal Medicine, ed 13. McGraw-Hill: New York, 1994, pp 1953–1976. Xarli VP, Steele AA, Davis PJ: Adrenal hemorrhage in the adult, Medicine (Baltimore) 1978;57(3):211–221. Zaloga GP, Zaloga G, MacGregor D (eds): The Critical Care Drug Handbook. Mosby– Year Book: St Louis, 1991.
Alcoholic Ketoacidosis RICHARD J. SPITZ
ICD Codes: Ketoacidosis 276.2, Alcoholic withdrawal 291.81, Alcoholism 303.9
Key Points For any alcoholic patient who presents with altered mental status, an acute intracerebral hemorrhage should be included in the differential diagnosis. ! Emergency Actions ! Any patient suspected to be experiencing alcohol withdrawal or alcoholic ketoacidosis (AKA) should have his or her withdrawal symptoms treated aggressively. Alcoholics are particularly disposed to intracerebral hemorrhage due to several physiological and anatomical factors present in alcoholism.
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DEFINITION Alcoholic ketoacidosis is defined as an anion gap acidosis associated with abrupt cessation or relative decrease in alcohol consumption.
EPIDEMIOLOGY AKA tends to occur in chronic alcoholics.
PATHOLOGY The pathology of AKA is multifactorial and complex. The patient’s chronic alcohol use and poor nutritional status deplete glycogen reserves and the ability of the liver to perform gluconeogenesis (Fig. 8-1). The patients are volume depleted as a result of poor oral intake and vomiting. As a stress response, catecholamines are released, which leads to the burning of fat and the release of free fatty acids. The increased generation of free fatty acids ultimately leads to increased ketone formation, predominately b-hydroxybutyrate, which the body in its volume-depleted and stressed state is unable to adequately clear. This is further worsened by the continued burning of fat and ketone body formation (Fig. 8-2).
CLINICAL PRESENTATION The typical presentation of AKA includes abrupt cessation of heavy alcohol consumption and decreased food intake with associated nausea, vomiting, and abdominal pain in a chronic heavy drinker. The patients appear to be ill—showing signs of dehydration, tachycardia, and tachypnea—and feel generalized abdominal pain. The patient may manifest other signs and symptoms of the precipitating illness that initially led them to stop drinking, such as acute GI tract Dietary intake 1 Decreased Glycogen
2 Consumed
Glucose 3 Blocked Pyruvate
Increased
Lactate
Figure 8-1. Ethanol causes hypoglycemia through (1) decreased intake of glucose, (2) depletion of glycogen, and (3) blockade of gluconeogenesis. (From Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001.)
340 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Decreased insulin Increased: Catecholamines Glucagon Glucocorticoids
Lipolysis
Decreased KB metabolism by peripheral tissues
Volume depletion
Free fatty acid release
Ethanol
Acetate
Vomiting and ethanol blockage of ADH secretion
Acetyl CoA
Serum ketones
Tricarboxylic acid cycle
Decreased food intake
Decreased ketone elimination
Figure 8-2. Factors causing ketonemia in alcoholic ketoacidosis. KB, Ketone body; ADH, antidiuretic hormone; CoA, coenzyme. The tricarboxylic acid cycle is significantly slowed owing to intermediates being used for gluconeogenesis. (From Kleinschmidt KC, Delaney KA: Ethanol. In Haddad LM, Shannon MW, Winchester JF [eds]: Clinical Management of Poisoning and Drug Overdose, ed 3. WB Saunders: Philadelphia, 1998.)
bleeding, pancreatitis, hepatic encephalopathy, acute myocardial infarction, or infection.
EXAMINATION The examination of a patient who is suspected to be experiencing AKA should begin with the ABCs (i.e., airway, breathing, and circulation). Stabilization should occur contemporaneously during the initial assessment of the ABCs, with the practitioner keeping in mind that the patient may have a grave medical condition that led to his or her decrease or cessation of alcohol consumption.
Airway and Breathing Airway and breathing may be affected by factors that lead to a decreased mentation: hepatic encephalopathy and infections such as meningitis or encephalitis. Likewise, the patient’s ability to ventilate effectively may be encumbered by physical barriers to efficient respiration, such as lung infections or large pleural effusions.
Circulation Patients are usually volume depleted due to vomiting and poor Intake. They may be intravascularly depleted secondarily to the third spacing
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of fluid seen in patients with liver disease who, with their poor nutrition status, are unable to synthesize serum proteins and have a resulting low intravascular oncotic pressure. This is further worsened by concomitant portal hypertension. A patient with AKA can present in a state of shock and may be unable to provide sufficient tissue perfusion. These patients are at high risk for blood loss from GI tract bleeding (which can lead to hypovolemic shock), a myocardial infarction (which can progress to cardiogenic shock), or septic shock from an overwhelming infection.
Disability A patient with AKA may be obtunded secondarily to infections, head injury, metabolic derangement such as hypoglycemia, or hepatic encephalopathy. Patients with alcoholism are prone to falling down and may sustain an intracerebral hemorrhage. These patients are particularly disposed to intracerebral hemorrhage for several physiological and anatomical factors, as well. Patients with alcoholism may have insufficient clotting factors, ineffective or low platelet counts, and brain atrophy, which creates a greater potential space for bleeding and allows for a greater sheering affect of vessels in the subdural space. Therefore, a high index of suspicion for head trauma and a low threshold to perform C-spine protection should be used during the primary survey.
Exposure The patient should have all clothes removed to facilitate a full examination, otherwise signs of things such as underlying coagulopathy or concomitant trauma may be missed.
Secondary Survey A thorough head-to-toe examination should be performed.
LABORATORY FINDINGS A full panel of laboratory tests should be performed, including CBC, electrolyte panel, BUN and glucose measurements, liver profile, alcohol level test, lipase analysis, serum osmolarity test, urinalysis, blood gas analysis, and an ECG. On a case-by-case basis, blood cultures and an ammonia level test should be performed. Patients will have anion gap metabolic acidosis. The anion gap is usually in the 30- to 35-mEq/L range. Patients may have only small serum
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ketones because the sodium nitroprusside laboratory test used to detect ketones also tests for acetoacetate. A higher percentage of the ketones of a patient with AKA are in the form of b-hydroxybutyrate, not acetoacetate (6:10), compared with a patient with DKA (3:1). Anytime that a patient with AKA has an osmolar gap, the healthcare provider should consider the possibility of a toxic ingestant (e.g., methanol, ethylene glycol, isopropyl alcohol); these have a higher prevalence in this population. Serum osmolality is calculated as follows: ð½Naþ 2Þ þ ð½glucose 18Þ þ ð½BUN 2:8Þ þ ð½ethanol 4:6Þ
DIAGNOSIS Soffer and Hamburger’s criteria for the diagnosis of AKA include a serum glucose level less than 300, a recent history of alcohol intake or a relative or absolute decline in alcohol consumption in the past 24–72 hours before the visit, vomiting, and an otherwise unexplained metabolic acidosis.
TREATMENT The treatment strategy for a patient with AKA is rehydration with intravenous fluids, correction of electrolyte abnormalities (most commonly, low Mg, K, and phosphate), repletion of vitamins (i.e., multivitamins, thiamine, and folate), intravenous glucose administration, and admission to the hospital. Underlying precipitating illnesses should be evaluated and appropriately treated. There is no place for the administration of insulin or sodium bicarbonate in the treatment of AKA, unless the Ph is severely low. An elevated glucose level warrants consideration and treatment as DKA. The practitioner should remain vigilant for the development of alcohol withdrawal and delirium tremens. The patient’s condition typically normalizes within 12–24 hours.
Bibliography Brenner BM: Brenner & Rector’s The Kidney, ed 7. Elsevier: Philadelphia, 2004. Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Halperin ML, Hammeke M, Josse RG, Jungas RL: Metabolic acidosis in the alcoholic: A pathophysiologic approach, Metabolism 1983;32:308. Hojer J: Severe metabolic acidosis in the alcoholic: Differential diagnosis and management, Hum Exp Toxicol 1996;15:482. Larsen PR, Kronenberg HM, Melmed S, Polonsky KS: Williams Textbook of Endocrinology, ed 10. Elsevier: Philadelphia, 2003.
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Levy LJ, Duga J, Girgis M, Gordon EE: Ketoacidosis associated with alcoholism in nondiabetic subjects, Ann Intern Med 1973;78:213. Machiels JP, Dive A, Donckier J, Installe E: Reversible myocardial dysfunction in a patient with alcoholic ketoacidosis: A role for hypophosphatemia, Am J Emerg Med 1998;16(4):371–373. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. St Louis: Mosby, 2002. Mason RJ, Broaddus VC, Murray JF, Nadel JA: Murray & Nadel’s Textbook of Respiratory Medicine, ed 4. WB Saunders: Philadelphia, 2005. Narins RG, Jones ER, Stom MC, et al: Diagnostic strategies in disorders of fluid, electrolyte and acid–base homeostasis, Am J Med 1982;72:496. Reichard GA Jr, Owen OE, Haff AC, et al: Ketone-body production and oxidation in fasting obese humans, J Clin Invest 1974;53:508. Rose BD, Post TW: Clinical Physiology of Acid–Base and Electrolyte Disorders, ed 5. McGraw-Hill: New York, 2001, pp 801–803. Schelling JR, Howard RL, Winter SD, Linas SL: Increased osmolal gap in alcoholic ketoacidosis and lactic acidosis, Ann Intern Med 1990;113:580. Wrenn KD, Slovis CM, Minion GE, Rutkowski R: The syndrome of alcoholic ketoacidosis, Am J Med 1991;91:119.
Diabetic Ketoacidosis JONATHON ALLEN
ICD Code: Diabetic ketoacidosis 250.1
Key Points Approximately 25% of episodes of DKA occur in patients with undiagnosed diabetes. ! Emergency Actions ! Aggressive intravenous fluid rehydration is the mainstay of treatment.
DEFINITION Diabetic ketoacidosis is a disease state in which insulin deficiency and glucagon excess combine to cause hyperglycemia, dehydration, ketoacidosis, and significant electrolyte imbalance.
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EPIDEMIOLOGY DKA most often occurs in persons with type 1 diabetes and is associated with inadequate insulin administration, infection and/or sepsis, or myocardial infarction. DKA can also occur in persons with type 2 diabetes and can be induced by any type of physical or emotional stress. Approximately 25% of episodes of DKA occur in patients with undiagnosed diabetes.
PATHOPHYSIOLOGY DKA is a result of a constellation of effects directly related to insulin deficiency and glucagon excess. The inadequate insulin level decreases glucose uptake by the cells, producing hyperglycemia. This hyperglycemia is further potentiated by increased levels of free fatty acids and amino acids in plasma, which stimulate gluconeogenesis. As plasma glucose levels continue to rise, the renal threshold for glucose reuptake is met, resulting in glycosuria. This produces a resulting osmotic diuresis and ion loss. Coupled with poor oral intake and frequent vomiting, the net result is a profound dehydration and electrolyte imbalance. DKA slows the uptake of lipids from circulation by adipose cells. The insulin deficiency results in the activation of an inducible lipase. The resulting lipolysis increases the levels of free fatty acids. These long-chain free fatty acids are partially oxidized and converted in the liver to acetoacetate and b-hydroxybutyrate. However, as cells are unable to extract glucose from the plasma, they begin to act as though the body is in a state of starvation. Amino acid uptake is decreased, as is the use of ketones as fuel by peripheral tissue. This decreased ketone use, combined with increased production, leads to ketoacidosis. The normal cellular response to starvation is to release the counterregulatory (with regard to insulin use) hormones epinephrine, glucagons, cortisol, and somatostatin. The degree of ketosis is directly related to the magnitude of release of these hormones. They are all catabolic, directly increasing rates of gluconeogenesis and glycogenolysis. Glucagon is frequently elevated four- to five-fold in DKA and is the most influential ketogenic hormone. Other hormones have been shown to indirectly affect ketogenesis through stimulation of lipolysis. As shown, all derangements of DKA are interrelated and are further induced by one another.
CLINICAL PRESENTATION Most patients in DKA will present with a recent history of polydipsia, polyuria, polyphagia, general body weakness, and nausea/vomiting. Up to one half of patients may report abdominal pain. In children, this pain typically decreases as the metabolic derangements are corrected.
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In adults, however, the presence of abdominal pain often signifies true abdominal pathology.
EXAMINATION Vital signs are of the utmost importance in assessing DKA. Peripheral vasodilation and vascular collapse can rapidly develop as the acidosis worsens. Patients can initially present with normal or altered mental status. Their neurological status should be monitored closely because this can deteriorate quickly. Typical other physical examination findings include tachypnea with Kussmaul’s respiratory pattern of deep and rapid breathing, tachycardia, frank hypotension or orthostatic hypotension, and the odor of acetone on the breath. An elevated temperature is rarely associated with DKA but should prompt a close look for a source of infection.
LABORATORY FINDINGS Initial laboratory studies should be directed at confirming the diagnosis of DKA and initiating emergent therapies. These should include a capillary blood glucose level, dipstick urinalysis including urinary ketones, electrolyte measurements, and arterial or venous blood gas (ABG/VBG) analysis. Recent studies have indicated that venous pH is not significantly different from arterial pH in patients with DKA and is much easier to obtain than repeated arterial samples. If an immediate K level is not available, a 12-lead ECG should be obtained to rule out significant hyperkalemia or myocardial infarction. Despite initially normal or high K levels, the total body K deficit may be several hundred milliequivalents. Acidosis and dehydration artificially increase the level due to acid-induced shifts and hypovolemic concentration. True serum K can be approximated by subtracting 0.6 mEq/L from the laboratory value for each 0.1-unit decrease in pH. The reported sodium level can also be misleading in DKA. Hyperglycemia can artificially decrease the reported value. True serum sodium levels can be approximated by adding 1.5 mEq/L to the reported level for each 100 mg/dl above the normal glucose level. Anion gap metabolic acidosis is primarily due to the increased plasma levels of ketones, although lactate, free fatty acids, and volume depletion could contribute to the gap as well. Subsequent tests should be aimed at determining the degree of dehydration, acidosis, and electrolyte imbalance and finding the precipitating factor of DKA. These include CBC with differential, complete urinalysis, chest x-ray, serum osmolarity, and measurements of BUN, creatinine, phosphorus, Caþ, Mg, lactate, and serum lipase levels. Leukocytosis may be present on CBC, but it may more closely indicate ketosis than presence of infection. Only bandemia can reliably demonstrate infection in a patient with DKA. Elevated urine-specific gravity,
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BUN, and hematocrit suggest volume contraction. Microscopic urinalysis and a chest x-ray can help eliminate urinary tract infection and pneumonia as precipitating sources. Serum lipase indicates the presence or absence of pancreatitis.
TREATMENT The care for a critically ill patient with DKA is identical as that for any other patient. The airway must be assessed and protected as the patient’s mental status dictates, especially if the patient is vomiting. Every patient should be placed on a cardiac monitor, and two large-bore intravenous lines should be established. Aggressive intravenous fluid rehydration is the mainstay of treatment. Although hypovolemic shock is the most common, other types of shock, including septic, should be ruled out. In patients with a history of cardiac or renal failure who may not tolerate such aggressive fluid therapy, a central venous pressure line can help to assess their intravascular volume. The severely dehydrated patient with DKA often has a fluid deficit of between 3 and 5 L with a sodium deficit of 450–500 mEq. With hypovolemic shock, 0.9% (normal) saline should be given as rapidly as possible in adults and in 20-ml/kg boluses in children until systolic blood pressure improves. Electrolyte levels should be periodically rechecked. As the serum sodium level approaches 155, adults should begin receiving hypotonic fluids, such as 0.45% (half-normal) saline. In the absence of shock, adults should generally receive 2 L of normal saline over the first 2 hours, followed by a slower continuous infusion. Children should receive constant normal saline infusion adjusted to achieve urine output of approximately 1–2 ml/kg/hr. Normal saline is preferred in children because hypotonic fluids may too rapidly decrease the serum hyperosmolarity of DKA, potentially precipitating cerebral edema. Fluid resuscitation alone may help to lower elevated blood sugar levels by as much as 18%. Acidosis also improves after rehydration, as increased tissue perfusion lowers lactate production and renal perfusion enhances hydrogen ion loss. DKA cannot be reversed without exogenous administration of insulin. Current recommendations suggest a 10-unit bolus of regular insulin followed by a continuous infusion of regular insulin at 0.1 U/kg/hr. This rate can be titrated as capillary blood glucose levels require. Because the half-life of regular insulin is 3–10 minutes, a continuous infusion produces more predictable results than repeated boluses. Should intravenous access be difficult or unobtainable, an intramuscular dose of 10–20 U/hr of regular insulin may also be given. Once blood glucose reaches 250– 300 mg/dl, the administration of dextrose-containing fluids should be started to avoid iatrogenic hypoglycemia and cerebral edema. As glucose levels continue to drop and ketones clear, the administration of
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subcutaneous insulin may be started. There should be an overlap between starting subcutaneous insulin and discontinuing the intravenous infusion. Potassium replacement is always necessary in DKA. Although initial levels are often normal or elevated, levels often sharply drop with correction of acidosis and dehydration and with administration of insulin. Initially, low levels indicate a potentially life-threatening hypokalemia, leading to respiratory paralysis, cardiac arrhythmias, or paralytic ileus. Potassium should be administered with fluids while the level is in the upper half of the normal range. Renal function should be monitored and the dosing adjusted accordingly. Patients experiencing DKA can require 100–200 mEq of K in the first 12–24 hours of treatment. Administration of K should be guided by serial chemistries drawn every 2 hours until the patient is out of DKA. Phosphate replacement is controversial in DKA. Phosphate levels can drop nearly four-fold in the first 12 hours of therapy. This may result in decreased production of 2,3-diphosphoglycerate (2,3-DPG), leading to poor oxygen transfer to erythrocytes (i.e., RBCs). Hypophosphatemia can also cause decreased myocardial and respiratory muscle performance, hemolysis, platelet dysfunction, and altered mental status. Despite its theoretical benefits, studies have shown no significant clinical benefit from the administration of phosphate in DKA. Bicarbonate therapy is indicated only for critically ill patients with a serum pH less than 7.0. In patients with less acidic pH, HCO 3 can antagonize other therapeutic measures. Alkalinizing serum results in decreased release of oxygen from already 2,3-DPG–depleted RBCs. Bicarbonate also increases the K requirement by driving K back into the intracellular space. The overaggressive use of HCO 3 may actually cause alkalosis, inducing cardiac dysrhythmias through the redistribution of various electrolytes. When HCO 3 therapy is clinically indicated, pH should not be corrected above 7.1.
DISPOSITION Nearly all patients experiencing DKA will require admission to the hospital. Most patients will be best suited for care in an ICU. Some patients with mild DKA, a pH greater than 7.35, and HCO 3 greater than 20 who show resolution of symptoms within 3–4 hours may be discharged home provided (1) the patient or caregiver is reliable, (2) the precipitating cause of DKA does not warrant admission, and (3) close follow-up is available.
Bibliography Brandenburg MA, Dire DJ: Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis, Ann Emerg Med 1998;31(4):459–465.
348 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Chansky ME, Lubkin CL: Diabetic ketoacidosis. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Ipp E, Westhoff TL: Diabetes mellitus and the critically ill patient. In Bongard F, Sue D (eds): Current Critical Care Diagnosis and Treatment, ed 2. McGraw-Hill: Montreal, 2002.
Disseminated Intravascular Coagulation MICHAEL K. SHAFE
ICD Code: 286.6
Key Points For a patient to survive disseminated intravascular coagulation (DIC) the underlying cause of DIC must be corrected. Otherwise, DIC will progress, causing death. ! Emergency Actions ! Initial therapy should address the underlying cause of the DIC. Good ventilator support is imperative.
DEFINITION Disseminated intravascular coagulation is a systemic deregulation of the coagulation and fibrinolytic systems that eventually depletes clotting factors and results in uncontrolled hemorrhage. DIC is usually triggered by disease states (e.g., trauma, septic shock or malignancies) that release large amounts of tissue factor (factor III) sufficient to consume the clotting and fibrinolytic intravascular protein stores.
PATHOLOGY Understanding DIC requires a basic understanding of coagulation and fibrinolytic systems. When tissue injury occurs, platelets attach to the exposed injured endothelium, forming a primary hemostatic plug. The platelets and injured endothelial cells release tissue factor, which stimulates the clotting cascades to deposit thrombin over the platelets catalyzing fibrin to cross-link into insoluble clot, forming a secondary hemostatic plug. The fibrinolytic system normally keeps the clotting
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system under control. Plasminogen is part of the fibrinolytic system that lyses the preformed clot, releasing fibrin fragments (D and E dimers) into the bloodstream. DIC occurs under a number of clinical circumstances where there is either a large amount of endothelial injury, a large release of tissue factor into the bloodstream, or both. When the clotting system is overstimulated by either of these events, microclots and microemboli begin to form and lodge in organ capillary beds, forming fibrin plugs and mesh-like screens. RBC membranes are damaged as they pass through these screens and become fragmented RBCs, or schistocytes, seen on peripheral blood smears. Eventually, blood will not be able to pass through the organ capillary beds, creating an ischemic environment and organ dysfunction. Eventually, the platelet, coagulation, and fibrinolytic systems are depleted, resulting in diffuse hemorrhaging into the organs and skin.
CLINICAL PRESENTATION Patients with DIC are invariably toxically ill and present with new petechiae or purpura, which may progress into ecchymosis. Patients may also begin to bleed from wounds that were once hemostatic. It is not uncommon for new hemorrhaging to occur around intravenous lines and in mucous membranes. The proximate cause of the DIC is usually clinically evident at the time of presentation. These include trauma (especially traumatic brain injury), massive hemorrhage, sepsis and septic shock, placental abruption, amniotic fluid embolism, and malignancies.
EXAMINATION A detailed skin examination looking for petechiae, purpura, or ecchymosis should be performed on any patient who is toxically ill, unstable, or has an unusual bleeding presentation. Retinal examination may demonstrate evidence of hemorrhage before formation of skin petechiae. Intravenous lines and oral mucosa should be examined for evidence of hemorrhage. Most importantly, serial examinations should be performed on patients at risk for DIC.
DIAGNOSIS The diagnosis is suspected on the basis of physical exam findings and a history of illness involving a high risk to develop DIC. The diagnosis is suspected clinically and confirmed by laboratory testing. The following laboratory tests should be performed for any patient in whom DIC is suspected: CBC, electrolyte measurements including Caþ and BUN/ creatine, prothrombin time (PT), partial thromboplastin time (PTT),
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international normalized ratio, measurements of fibrinogen level and fibrin split products, and D-dimer test. Request a manual differential on the CBC, and ask the laboratory personnel to specifically look for schistocytes and fragmented RBCs. Fluid cultures, radiographic studies, and chemistry testing should be directed by the patient’s clinical presentation.
LABORATORY FINDINGS The laboratory findings for DIC occur progressively. Initially the platelet count will decrease, followed by the fibrinogen level. The PT will rise before the PTT. The formation of thrombus will initiate the fibrinolytic system and release fibrin split products (e.g., D and E dimers). A rising or elevated D-dimer level in the face of low platelet counts, along with low or decreasing fibrinogen levels in a toxically ill patient with petechiae or purpura, confirms the diagnosis of DIC. As DIC progresses, there will be evidence of organ damage due to microemboli and tissue infarction. Note that the fibrinogen level in pregnant patients is 1.5–2 times that of nonpregnant patients. So, a “normal” fibrinogen level in a pregnant patient should be concerning in the clinical setting of possible DIC.
TREATMENT Initial therapy should focus on the underlying cause of the DIC. If the problem is placental abruption, an emergency cesarean section should be performed. If the patient is a septic, antibiotics and pressor agents should be administered and ventilation and oxygenation should be maximized. If DIC is present, platelets and clotting factors should be replaced simultaneously with multiple lines. Fresh frozen plasma contains all of the clotting proteins needed. Cryoprecipitate has high concentrations of fibrinogen and should be considered if the fibrinogen level is low. If anemia or active hemorrhaging is present, the administration of packed red cells should be initiated as well.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 200, pp 2169–2182. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1697–1698.
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Fluid and Electrolyte Emergencies BARBARA M. FISHMAN AND C. GORDON KING
ICD Codes: Hyponatremia 276.1, Hypernatremia 276.0, Hypokalemia 276.8, Hyperkalemia 276.7, Hypercalciuria 275.42, Hypocalciuria 275.41, Hypomagnesemia 275.2, Hypophosphatemia 275.3, Hypochloremia 276.9, Hyperchloremia 276.9
Key Points In general, fluid and electrolyte emergencies are diagnosed on the basis of laboratory test results. The history, physical examination, and radiographic studies, although useful, are not a substitute for accurate laboratory results. History, physical examination, and further laboratory tests will be useful in determining the cause and appropriate treatment. ! Emergency Actions ! Electrolyte disorders are usually not mutually exclusive. If one electrolyte is out of normal range, a reciprocal abnormal electrolyte is usually also out of range. The practitioner should always look for other electrolyte disorders if one is out of range. Often, one electrolyte cannot be corrected without addressing other electrolyte levels. In general, all electrolyte levels should not be corrected rapidly but, instead, over hours.
SODIUM Sodium is the main extracellular cation (positively charged ion). Ninetyeight percent of total body Naþ is in the ECF. The normal serum sodium level is between 135 and 145 mmol/L.
Key Points Hyponatremia is a serum Naþ level less than 135 mmol/L. Patients with hyponatremia may be hypovolemic, hypervolemic, or euvolemic, corresponding to varying degrees of total body Naþ. The treatment of hyponatremia depends on the time course, severity, and underlying cause of the disorder. Emergency treatment is warranted only for those
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with acute (duration <36–48 hours), severe (>115 mmol/L), symptomatic hyponatremia. The change in serum sodium can be calculated and the sodium “deficit” can be replaced slowly. In a patient with symptomatic chronic hyponatremia, the serum sodium level should not be corrected to greater than 125 mmol/L. Severe neurological complications can occur if the serum sodium level is corrected too rapidly.
Hyponatremia The definitions of hyponatremia are as follows:
Hyponatremia: serum Naþ less than 135 mmol/L Severe hyponatremia: less than 115 mmol/L Acute hyponatremia: less than 36–48 hours’ duration
EPIDEMIOLOGY Hyponatremia can be classified into the following categories: 1. Pseudohyponatremia is associated with normal or elevated plasma tonicity, caused by hyperglycemia, mannitol, glycerol, radiographic contrast media, or any hyperoncotic substance that is confined to the ECF. The resultant movement of water from the intracellular to the intravascular compartment dilutes the serum Naþ. Marked hyperlipidemia was a cause of pseudohyponatremia with older flame photometers but is not a problem with newer analyzers that use ion-selective electrodes. 2. Hypovolemic hyponatremia is associated with low total body Naþ, low total body volume, low intravascular volume, and decreased ability of the kidney to excrete the excess water because of decreased volume status. Causes include protracted vomiting, bulimia nervosa, diarrhea, laxative abuse, blood loss, loop diuretic treatment, osmotic diuresis from hyperglycemia, excessive sweating, renal disease with defective concentrating ability, and fluid sequestration in a “third space” (e.g., severe pancreatitis). These patients get thirsty, drink water, cannot excrete the water load, retain the water, and become hyponatremic. 3. Hypervolemic hyponatremia is associated with high total body Naþ, high total body volume, high intravascular volume, and decreased ability of the kidney to excrete the excess water because of any of a variety of factors. These include decreased filtration capacity of the kidneys and therefore decreased capacity to excrete a water load; decreased cardiac output relative to body needs; inappropriate peripheral vasodilation, including a secondary excess of antidiuretic hormone (ADH); or a combination of these factors. Causes include CHF, cirrhosis, and nephrotic syndrome.
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4. Euvolemic hyponatremia is associated with essentially normal volumes of sodium in the ECF. Causes include syndrome of inappropriate antidiuretic hormone (SIADH), thiazide diuretic therapy, psychogenic polydipsia, pure glucocorticoid deficiency, thyroid hormone deficiency, “tea and toast diet,” and “beer drinkers’ potomania.” SIADH can be caused by cancers, especially oat cell carcinoma of the lung; CNS disorders, including mass lesions, hemorrhage, stroke, and trauma; pulmonary disorders, including pneumonias, respiratory failure, and positive-pressure ventilation; pain; nausea; the postoperative state; infection with the human immunodeficiency virus; and various drugs, including oxytocin, nicotine, selective serotonin reuptake inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), opiates, phenothiazines, carbamazepine, cyclophosphamide, vincristine, and 3,4-methylenedioxymethamphetamine (MDMA). “Tea and toast diet” and “beer drinkers’ potomania” hyponatremia occur when patients do not eat food and drink dilute fluid in large amounts, and this overwhelms the kidneys’ ability to excrete a water load. Persons with healthy kidneys can decrease their urine osmolality to perhaps 50 mOsm/kg, but not to zero. The body’s ability to excrete a water load is therefore related to solute excretion. PRESENTATION Symptoms are dependent more on the rate of decrease than on the absolute serum sodium concentration, though levels less than 115 mmol/L are more likely to be associated with CNS symptoms. Not infrequently, patients with chronic hyponatremia can be asymptomatic with a serum sodium level as low as 105–110 mmol/L (!). Symptoms of hyponatremia include anorexia, nausea, vomiting, weakness, muscle cramps, headache, and difficulty concentrating. Severe symptoms include confusion, hallucinations, urinary and fecal incontinence, respiratory insufficiency, coma, seizures, and respiratory arrest. EXAMINATION Findings on examination will vary depending on the underlying condition. Most importantly, the patient’s volume status should be evaluated using standard criteria and classified as low, normal, or high volume based on the results of the bedside examination. A patient with hyponatremia can be hypovolemic, hypervolemic, or euvolemic. LABORATORY STUDIES In addition to routine ED studies, plasma osmolality, spot urine osmolality, spot urine Naþ, and spot urine creatinine tests should be performed. Urine sodium and osmolality tests will help classify the hyponatremia as renal or extrarenal losses. Other studies should be considered as well,
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including serum cortisol and thyroid-stimulating hormone (TSH) measurements, chest radiography, and CT/magnetic resonance scanning (to look for cancer associated with SIADH). Laboratory samples should be collected before treatment is begun. DIAGNOSIS The serum sodium level does not yield information about the patient’s volume status or about the etiology of the hyponatremia (Table 8-1). The history, examination, and screening laboratory studies mentioned previously will be sufficient to classify more than 90% of the patients and therefore guide therapy. In true hyponatremia, the osmolality is decreased (<275 mmol/L.) In pseudohyponatremia, the plasma osmolality is normal or increased. The criteria for SIADH include hyponatremia with low serum osmolality, euvolemia, inappropriately concentrated urine (>100 mOsm/kg), and normal cardiac, renal, adrenal, hepatic, and thyroid function. Of note, patients with SIADH can generally conserve and excrete sodium normally, and the spot urine Naþ or fractional excretion of Naþ (FENa) should not be part of the diagnostic criteria for SIADH. A low spot urine Naþ level may be helpful to confirm a hypovolemic state, but patients with volume overload (e.g., CHF) also commonly have a low spot Table 8-1 Hyponatremia Etiologies Factitious hyponatremia—normal or elevated serum osmolality Redistributive hyponatremia—elevated serum osmolality hyperglycemia, mannitol, glycerol infusions (for each 100-mg/dl increase in glucose, sodium falls 1.6 mEq/L) Hyponatremia with low serum osmolality Hypovolemic hyponatremia—loss of both sodium and water, more replacement of free water, low total body Naþ level Renal Losses Diuretics, salt-wasting nephropathy, osmotic diuresis, aldosterone deficiency Extrarenal Losses Gastrointestinal (e.g., diarrhea, vomiting) Sweating, cystic fibrosis Third-space losses (e.g., pancreatitis, peritonitis) Euvolemic hyponatremia—normal to slightly increased ECF, no edema, normal total body Naþ level SIADH Glucocorticoid deficiency Pain Drugs Chronic renal failure Primary polydipsia Hypervolemic hyponatremia—increase in ECF and total body sodium, water retention in excess of sodium retention Cirrhosis, CHF, nephrotic syndrome, acute or chronic renal failure SIADH, Syndrome of inappropriate antidiuretic hormone; CHF, congestive heart failure.
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urine Na and generally this test is not helpful in the confirm of a diagnosis. Patients with SIADH commonly have a low serum uric acid level. TREATMENT The treatment of hyponatremia depends on the time course, severity, and underlying cause of the disorder. Hypovolemia Hypovolemic patients with impaired peripheral perfusion (e.g., hypotension, metabolic acidosis, decreased renal function) can be treated with normal saline to restore adequate volume status, then given free water restriction. Hypervolemia Patients with hypervolemic hyponatremia are treated with free water restriction and treatment of the underlying cause (e.g., CHF). Diuretics or dialysis may also be required. Euvolemia Euvolemic hyponatremia is treated with free water restriction and correction of the underlying cause. Emergency treatment is warranted only for those with acute, severe, symptomatic hyponatremia. These patients are at risk of cerebral edema with resultant neurological damage. The most severe consequences of acute hyponatremia are seen in children and in premenopausal women. These patients should be corrected “rapidly,” but the change in serum sodium should not exceed 25 mmol/ L in the first 24 hours. The change in serum sodium can be calculated and the sodium “deficit” can be replaced slowly with 3%–5% saline with furosemide. Furosemide is given to prevent volume overload and to help increase free water loss by the kidney. Consultation with a renal specialist should be obtained if hypertonic saline is considered. In hypovolemic hyponatremia, Estimation of the Naþ deficit in mEq=L ¼ TBWðdesired Naþ current Naþ Þ
where TBW is total body water. Use the following formula to help estimate the initial change in serum Naþ per each liter of Naþ- or Kþ-containing fluids infused: Change in serum sodium ¼
ðinfusate Naþ þ infusate Kþ Þ serum Naþ ðTBW þ 1Þ
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Naþ and Kþ contents of some intravenous solutions are as follows:
Normal saline (0.9% NaCl) ¼ 154 mmol/L of Naþ ½ normal saline ¼ 77 mmol/L of Naþ Ringer’s lactated solution ¼ 130 mmol Naþ/L and 4 mmol Kþ/L 3% NaCl ¼ 513 mmol Naþ/L 5% saline ¼ 855 mmol Naþ/L
TBW is equal to approximately 60% of ideal body weight in males and to approximately 50% of ideal body weight in females and older males. Normal saline will only raise the Na concentration by 1–2 mEq/L for each liter of normal saline administered. By replenishing volume, however, the hypovolemic stimulus to ADH is removed and free water eventually will be excreted. Serial Na measurements are necessary during treatment to assess the adequacy of treatment and to ensure that the Naþ is not being corrected too rapidly. It remains unclear whether patients with chronic asymptomatic hyponatremia should be treated at all. Most of them will be refractory to treatment, perhaps because they have a “reset osmostat” and will therefore defend their low serum sodium concentration by appropriately concentrating or diluting their urine in response to water restriction or water load. In a patient with symptomatic chronic hyponatremia, the serum sodium concentration should not be corrected any faster than 0.5–1.0 mmol/L/hr. The total correction should not exceed 8–12 mmol/L/day. The serum sodium level should not be corrected to greater than 125 mmol/L. Severe neurological complications can occur if the serum sodium deficit is corrected too rapidly. Hyponatremia causes water to move into neurons. The swollen neurons compensate by losing electrolytes and other substances so that within a few days, the brain returns to its normal size. It is these adaptive changes that make the brain susceptible to damage during too-rapid correction of the hyponatremia. Rapid correction of hyponatremia can cause neuronal injury, possibly leading to osmotic demyelination syndrome or central pontine myelinolysis, a potentially devastating and usually avoidable neurological complication that may involve paralysis or other severe sequelae.
Hypernatremia KEY POINTS Hypernatremia represents a deficit of water in relation to the body’s Naþ stores and can result from a net water loss or a hypertonic Naþ gain. Hypernatremia is unusual in adults if thirst is intact and if the patient has access to water.
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Volume status and total body Naþ vary with the cause of the hypernatremia. Signs and symptoms of hypernatremia are caused by dehydration of brain cells and are most prominent when the serum Naþ increase is large or occurs rapidly. If the patient is significantly volume depleted—that is, volume depletion is sufficient to cause hemodynamic compromise, decreased tissue perfusion, and impairment of metabolism—then volume expansion with normal saline sufficient to restore tissue perfusion to normal is appropriate. For all other patients, treatment of hypernatremia is best accomplished with hypotonic fluid. Too-rapid rehydration and lowering of serum Naþ can cause brain cell swelling, cerebral edema, permanent neurological sequelae, and death. DEFINITION Hypernatremia is defined as a serum Naþ concentration greater than 150 mmol/L. EPIDEMIOLOGY Hypernatremia represents a deficit of water in relation to the body’s Naþ stores and can result from a net water loss or a hypertonic Naþ gain. Normal defenses against hypernatremia are thirst and the secretion of ADH. ADH causes the urine to become concentrated, that is, the kidney retains water. Hypernatremia is unusual in adults if thirst is intact and the patient has access to water. An altered level of consciousness with an inability to drink usually precedes the hypernatremia. Infants may easily become dehydrated through gastroenteritis or insensible water losses. REDUCED WATER INTAKE The reduced intake of water is seen in those patients with change in thirst, altered mental status, or immobility and in patients with unreplaced insensible losses, both dermal and respiratory. INCREASED WATER LOSS Renal or extrarenal losses of Naþ and water may occur, with loss of more water than Naþ, such as in the case of loop diuretic use, osmotic diuresis (e.g., hyperglycemia), recovery phase of acute renal failure, intrinsic renal disease with a concentrating defect, vomiting, nasogastric suction, diarrhea, and use of cathartic laxatives. Diabetes insipidus results in a lack of concentrating ability in the distal nephron. Diabetes insipidus can be central (ADH is inappropriately low) or nephrogenic (the kidney does not respond to ADH) and should be suspected when the urine volume is greater than 3 L/day. Most
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patients with diabetes insipidus have intact thirst and do not present with hypernatremia. SODIUM GAIN Patient with hypernatremia may have experienced a net gain of Naþ in an excess of water by Naþ intake or renal Naþ absorption. Common etiologies include iatrogenic administration of sodium bicarbonate (e.g., during a code), improper preparation of infant formula or tube feedings, ingestion of salt tablets, sea water ingestion, use of a hypernatremic dialysis bath, primary hyperaldosteronism, and Cushing’s syndrome. PRESENTATION The signs and symptoms of hypernatremia are caused by dehydration of brain cells and are most prominent when the serum Naþ increase is large or occurs rapidly. Thrombosis and multiple small or even massive brain hemorrhages can occur from brain shrinkage and the tearing of cerebral blood vessels. The level of consciousness is correlated with the severity of marked hypernatremia. Common symptoms in infants include hyperpnea, restlessness, muscle weakness, a characteristic high-pitched cry, insomnia, lethargy, and even coma. Sixteen percent of infants and children with serum sodium levels between 160 and 165 mmol/L will develop chronic neurological deficits. Adults are not usually symptomatic, aside from thirst, until the serum Naþ concentration exceeds 160 mmol/L. Intense thirst can be present initially but decreases as the serum Naþ level exceeds 160 mmol/L and is absent in patients with hypodipsia. Adults can be irritable and restless, and symptoms can progress to tremulousness and ataxia. Seizures and death can occur at serum osmolality greater than 430 mOsm/kg. EXAMINATION Findings on examination will vary, depending on the underlying condition. Most importantly, the patient’s volume status should be evaluated, using standard criteria, and should be classified as low, normal, or high volume based on the results of the bedside examination, not on the serum sodium concentration. LABORATORY FINDINGS Serum osmolarity and spot urine tests for Naþ, creatinine, calculated FENaþ, and osmolarity may prove helpful in confirming a diagnosis,
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but these are not usually necessary. They may, however, be useful in determining the cause and appropriate treatment. DIAGNOSIS Diabetes insipidus can present with hypernatremia, but the patients’ main signs will be polydipsia and polyuria (Table 8-2). There is loss of dilute urine, usually greater than 3 L/day, with urine osm typically 200–300 mOsm/L. Diabetes insipidus can be central (caused by a failure of ADH secretion) or nephrogenic (caused by renal unresponsiveness to ADH). Approximately 70% of central diabetes insipidus is secondary to surgery, trauma, or neoplasms, which destroy or replace the posterior pituitary and decrease ADH release. Approximately 30% is idiopathic.
Table 8-2 Hypernatremia Etiologies Reduced Water Intake Disorders of thirst perception Inability to obtain water—altered mentation, immobile Increased Water Loss/Increased Sodium Retention/Concentration Gastrointestinal Vomiting, diarrhea Nasogastric suction Third spacing Renal Tubular concentrating defects Osmotic diuresis—hyperglycemia, mannitol Diabetes insipidus—central or nephrogenic Post–urinary obstruction Skin Sweating Burns Hyperventilation (in intubated patient) Drugs Lactulose, charcoal/sorbitol Lithium, foscarnet, amphotericin B, cidofovir (nephrogenic diabetes insipidus) Sodium Gain Sodium Intake Na+ bicarbonate Hypertonic saline, enteral or parenteral nutritional fluids Salt tablets Improper infant formula preparation Salt water drowning Peritoneal dialysis Increased Sodium Resorption—mineralocorticoid or glucocorticoid excess Hyperaldosteronism, congenital adrenal hyperplasia Cushing’s disease, ectopic ACTH Exogenous corticosteroids ACTH, Adrenocorticotropic hormone.
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Nephrogenic and central diabetes insipidus can be differentiated by noting serum and urine osmolality after water deprivation and after administration of nasal, subcutaneous, or intravenous desmopressin (dDAVP). Failure of serum osmolality to rise to more than 295 mOsm/ L during water deprivation is diagnostic of diabetes insipidus but does not differentiate a central from a nephrogenic origin. In central diabetes insipidus the urine osmolality will be greater than 400–600 mOsm/L after the administration of dDAVP. Nephrogenic diabetes insipidus will not respond to dDAVP. Diabetes insipidus can result from many medications. TREATMENT If a patient is significantly volume depleted—that is, volume depletion is sufficient to cause hemodynamic compromise, decreased tissue perfusion, and impairment of metabolism—then volume expansion with normal saline sufficient to restore tissue perfusion to normal is appropriate. For all other patients, treatment of hypernatremia is best accomplished with hypotonic fluid, preferably administered orally. If the oral route is not feasible, then hypotonic fluid, preferably 5% dextrose in water (D5W), should be given intravenously. The total body free water deficit should be calculated. One half of the deficit should be replaced over 24 hours, then the remainder over the next 1–2 days. The serum Naþ concentration should not be reduced by more than 10–15 mEq/day. Estimation of the free water deficit in liters ¼ CBW
ðCurrent Na 1Þ 140
where CBW is current body water, which is about 10% less than TBW in patients who are water depleted. For women and elderly men, the CBW is the “ideal” body weight multiplied by 0.4, and for men the CBW is 0.5 times the ideal body weight. The Naþ and Kþ contents of some intravenous solutions are as follows:
Normal saline (0.9% NaCl): 154 mmol/L Naþ D5W: 0 Naþ/L 0.2% saline in D5W: 34 mmol Naþ/L ½ saline: 77 mmol/L Naþ Lactated Ringer’s solution: 130 mmol Naþ/L and 4 mmol Kþ/L 3% NaCl: 513 mmol Naþ/L 5% saline: 855 mmol Naþ/L
The following formula can be used to help estimate the change in serum Naþ per each liter of Naþ or Kþ containing fluids infused.
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ðinfusate Naþ þ infusate Kþ Þ serum Naþ ðTBW þ 1Þ
where TBW for men is 0.6 total ideal body mass, and TBW for women and for elderly men is 0.5 total ideal body mass. This formula estimates the amount of water deficit necessary to return the serum Naþ concentration to 140 mEq/L and does not include any additional iso-osmotic fluid deficit or ongoing insensible losses, which should be included in replacement fluids. In general, each liter of water deficit will result in a rise in the serum sodium of 3–5 mEq/L. In patients with CHF, rehydration should be undertaken more slowly with central monitoring. Dialysis should be considered in the case of severe hypernatremia (180–200 mEq/L). Central diabetes insipidus is treated with vasopressin or DDAVP. The Na level should be monitored closely during treatment. If the hypernatremia has persisted for more than several days, the brain cells have accumulated idiogenic osmoles, a protective mechanism to restore cell volume. Too-rapid rehydration and lowering of serum Naþ concentration can cause brain cell swelling, cerebral edema, permanent neurological sequelae, and death.
POTASSIUM Potassium is the primary intracellular cation. The normal daily Kþ intake is 50–150 mEq/day. Total body Kþ is approximately 50–55 mEq/L or about 3500 mEq in the normal 70-kg man. More than 95% of total body Kþ is located intracellularly, with 75% located in muscle. The serum Kþ concentration is normally 3.5–5 mEq/L, whereas the intracellular Kþ concentration is 110–150 mEq/L. Importantly, the relationship between total body Kþ and serum Kþ is not linear but instead follows an exponential curve. When the serum Kþ is mildly decreased at 3.0 mEq/L, the total body Kþ deficit is approximately 150–175 mEq. When the serum Kþ has dropped to 2.0 mEq/L, the total body Kþ deficit has increased to greater than 350–400 mEq. More than 90% of the daily K þload is excreted renally, with some losses in stool and sweat.
Hypokalemia KEY POINTS Potassium is the primary intracellular cation. Hypokalemia is defined as a serum Kþ concentration less than 3.5 mEq/L. Hypokalemia is usually caused by a shift of Kþ from the extracellular to the intracellular compartment or by increased Kþ losses from the kidney.
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In the case of excess vomiting and nasogastric suction, most of the Kþ is actually lost in the urine. In general, spot urinary Kþ values of greater than 20 mEq/L and/or transtubular Kþ gradient (TTKG) values of more than 2 in the presence of significant serum hypokalemia imply “inappropriate” renal Kþ wasting. The etiology of hypokalemia can often be obtained from the history. Hypokalemia causes arrhythmias and potentiates digoxin toxicity. Treatment is directed toward Kþ repletion and prevention of further Kþ loss with correction of the underlying disorder. Intravenous potassium chloride (KCl) should be given, not faster than 10–20 mEq/hr. No more than 40 mEq of Kþ should ever be put into a single bag of intravenous fluid. DEFINITION Hypokalemia is defined as a serum Kþ concentration less than 3.5 mEq/L. EPIDEMIOLOGY Hypokalemia is usually caused by a shift of Kþ from the extracellular to the intracellular compartment or by increased Kþ losses from the kidney. INTRACELLULAR SHIFTS Hypokalemia is frequently seen in the presence of metabolic alkalosis or correction of acidosis. For every rise in pH of 0.10, the serum Kþ concentration will fall by 0.5 as Kþ shifts into cells in exchange for hydrogen ions. ED patients who are NPO and receive dextrose in their intravenous line commonly become mildly hypokalemic. The decrease in Kþ does not usually exceed 1 mEq/L and is usually of no clinical significance. b2-adrenergic agonist therapy of asthma, if it results in marked hypokalemia, can cause muscle weakness and worsen CO2 retention. Hyperthyroid patients, usually those who have Graves’ disease, can become hypokalemic for the same reason: adrenergic-mediated cellular Kþ uptake. Patients with DKA are commonly Kþ depleted because of urinary losses. Insulin therapy causes Kþ to shift into cells. Severe hypokalemia can result. It is customary to replace Kþ early in these patients. Other conditions to be considered are hypokalemic periodic paralysis, acute increases in cell production causing Kþ uptake by bone marrow cells (e.g., vitamin B12 or folate therapy of megaloblastic anemias and granulocyte-macrophage colony-stimulating factor therapy), and barium salt intoxication (causes an “exit block” from cells).
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ETIOLOGY Gastrointestinal Losses GI tract losses of Kþ can occur through diarrhea, vomiting, nasogastric suction, intestinal fistulas, villous adenomas, or laxative abuse. In excess vomiting and nasogastric suction, most of the Kþ is actually lost in the urine. The loss of Hþ and the resultant metabolic alkalosis causes volume depletion, elevated renin, elevated aldosterone, and increased renal Kþ loss from Naþ/Kþ exchange in the distal nephron. Renal Losses Hyperaldosteronism causes the kidney to excrete Kþ and Hþ ions and retain sodium. Hyperaldosteronism can be primary (e.g., adrenal adenoma, carcinoma, or bilateral adrenal hyperplasia) or secondary (e.g., renovascular hypertension from renal artery stenosis). Other causes of excess renal loss of Kþare tobacco chewing, licorice ingestion, Bartter or Liddle syndromes, diuretic therapy, type I or II renal tubular acidosis, osmotic and postobstructive diuresis, and polyuric states. Drugs and Toxins Diuretics (especially loop diuretics in the presence of increased Naþ intake), amphotericin B, lithium, platinum-based chemotherapy, and aminoglycoside antibiotics can all cause renal Kþ wasting. Other Causes Other etiologies of hypokalemia can include inadequate intake (usually elderly or alcoholic patients), alcohol (causes renal Kþ and Mgþ wasting), hypomagnesemia (if severe, will interfere with the full correction of hypokalemia and hypocalcemia), hypercalcemia (increases renal Kþ and Mgþ wasting), excess sweat loss, and acute leukemia (certain types can cause renal Kþ wasting). CLINICAL PRESENTATION Patients with hypokalemia present with symptoms related to their serum K levels. At levels below 2–2.5 mEq/L, muscle weakness, ileus, and polyuria occur. At levels of 1.5–2 mEq/L, respiratory paralysis and arrhythmia are likely. EXAMINATION Volume status and blood pressure should be determined for these patients. Patients with mineralocorticoid excess may be hypertensive but are not usually edematous. Patients with renal or GI losses may be hypotensive and volume depleted. The muscle weakness associated with hypokalemia will be more proximal. Reflexes and sensation are usually intact. A variety of arrhythmias can be seen, from
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sinus bradycardia to ventricular fibrillation. ECG findings with a serum Kþ concentration of less than 3.0 mEq/L include depressed ST segments, flattened T waves, presence of U waves, and prolonged QT intervals. With more severe Kþ depletion, P wave prominence, PR prolongation, and widening of the QRS complex can occur. Patients with significant hypokalemia and ECG changes should be placed on a cardiac monitor. LABORATORY FINDINGS A serum Kþ concentration of less than 3.5 mEq/L is diagnostic of hypokalemia. In addition to routine chemistries, a check of the acid– base status with ABG (if HCO 3 is abnormal) should be performed, and serum Mgþ, serum Caþ, spot urine Kþ, spot urine Naþ, and spot urine osmolarity should be analyzed. The TTKG can be calculated as follows. (The normal range is 2–6.) TTKG ¼
ðspot urine Kþ serum osmolalityÞ ðspot urine osm serum Kþ Þ
In general, spot urinary Kþ values greater than 20 mEq/L and/or TTKG values of more than 2 in the presence of significant serum hypokalemia imply “inappropriate” renal Kþ wasting. The TTKG formula is not useful if the urine is hypo-osmolar with respect to plasma. Patients who are in a “maintenance” phase of contraction alkalosis and hypokalemia from vomiting or nasogastric suction will generally have a spot urine Cl concentration of less than 20 mEq/L. Conversely, patients with excess mineralocorticoid syndromes will generally have a spot urine Cl of greater than 20 mEq/L. DIAGNOSIS The etiology of hypokalemia can often be obtained from the history— for example, vomiting, diarrhea, or diuretic use may have occurred. If none of those are present in the history, a mineralocorticoid excess state may be present. The various forms of primary hyperaldosteronism present with hypertension, hypokalemia, and metabolic alkalosis. On the other hand, Bartter syndrome presents with hypokalemia and metabolic alkalosis but no hypertension. Patients with Bartter syndrome have elevated renin, aldosterone, and urine Cl levels. In children presenting with metabolic alkalosis, hypokalemia, and sodium and HCO 3 retention without hypertension or edema, Bartter syndrome should be considered. Of all adult patients suspected of having Bartter syndrome, most will turn out to have surreptitious loop-diuretic abuse. Gitelman’s syndrome presents in a similar manner to Bartter syndrome but is associated with hypocalciuria. Liddle syndrome is a rare familial
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form of pseudohyperaldosteronism, with hypertension, salt sensitivity, a tendency for hypokalemia to develop, decreased aldosterone levels, and decreased renin levels. TREATMENT The treatment of hypokalemia is directed toward Kþ repletion and prevention of further Kþ loss with correction of the underlying disorder. Kþ can be given orally to stable patients who can tolerate oral intake, or it can be given intravenously to patients with more severe hypokalemia. The usual oral dose is 20 mEq Kþ every 1–2 hours until the Kþ concentration is improved. Intravenous KCl should be given, though not faster than 10–20 mEq/hr. When receiving intravenous Kþ, the patient should ideally be on a cardiac monitor. No more than 40 mEq of Kþ should ever be put into a single bag of intravenous fluid. The rapid administration of intravenous Kþ is potentially life threatening. The usual dose of intravenous KCl is 10 mEq/hr or 40 mEq/L intravenous fluid over 4 hours. Depending on the patient’s acid–base status and ongoing losses, it may take 100–200 mEq of supplemental Kþ to raise the serum Kþ by 1 mEq. In patients who are being treated for metabolic acidosis or hyperglycemia, the practitioner should anticipate that the Kþ concentration will fall as the acidosis is corrected or as insulin is given and Kþ is driven into the cells. To determine the correct total body K deficit, one should look at the corrected pH level for the serum Kþ level (a rise in pH of 0.10 will lower Kþ by 0.5 mEq/L) and correlate these two values to determine the correct K loss.
Hyperkalemia KEY POINTS Hyperkalemia is defined by a serum Kþ concentration greater than 5.5 mEq/L. The most common cause is hemolysis during blood draw, or pseudohyperkalemia. ECG findings include tall and peaked precordial T waves. The initial evaluation of a patient with hyperkalemia should include a history of renal disease and any use of Kþ-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, NSAIDs, Kþ supplements, and salt substitutes. Emergent treatment of hyperkalemia has three parts: membrane stabilization, shifting Kþ into the cells, and removing excess Kþ from the body. Cardiac monitoring should be performed during treatment. Immediate treatment should be initiated for severe hyperkalemia (Kþ >7–7.5 mEq/L), ECG changes resulting from hyperkalemia, or severe muscle weakness.
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The practitioner must not forget to correct the underlying cause, if possible. Remedies might include decreasing the dietary Kþ intake; stopping administration of the Kþ-sparing diuretic, ACE inhibitor, NSAID, or other offending medication; and arranging for hemodialysis if the patient has renal failure. DEFINITION Hyperkalemia is defined by a serum Kþ concentration greater than 5.5 mEq/L. EPIDEMIOLOGY Hyperkalemia can be divided into the following categories: “factitious” (i.e., pseudohyperkalemia), extracellular Kþ shifts, increased Kþ ingestion or endogenous load, and decreased renal excretion. FACTITIOUS The most common cause of hyperkalemia is hemolysis during blood draw, or pseudohyperkalemia. Other causes of pseudohyperkalemia are prolonged tourniquet use, leukocytosis, and thrombocytosis. If the blood specimen is not analyzed within 30 minutes of being drawn, this can cause a factitious increase in Kþ. EXTRACELLULAR SHIFTS Shifts of Kþ from the ICF to ECF are seen in acidosis, insulin deficiency, use of beta blockers, succinylcholine, and hyperkalemic periodic paralysis. INCREASED POTASSIUM LOAD Increased Kþ load can occur with ingestion of Kþ supplements (usually in the setting of renal insufficiency or taken with drugs that impair Kþ excretion, especially Kþ-sparing diuretics), blood transfusions, intravenous KCl or K3PO4, various Kþ-containing medications, rhabdomyolysis, tissue necrosis, crush injury, and post-chemotherapy tumor lysis syndrome. DECREASED RENAL EXCRETION Decreased renal excretion can occur with acute and chronic renal failure, Kþ-sparing diuretics, ACE inhibitors, NSAIDs, mineralocorticoid deficiency (e.g., Addison’s disease, hypoaldosteronism), and selective defects in renal Kþ excretion (e.g., diabetics with type IV RTA).
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CLINICAL PRESENTATION Hyperkalemia can cause skeletal and smooth muscle weakness, decreased myocardial performance, delays in cardiac conduction, and arrhythmias. In severe hyperkalemia, respiratory failure with CO2 retention can occur as a result of respiratory muscle weakness. Hyperkalemia should always be investigated as a possible cause of the above complications, especially in patients with tissue breakdown, decreased renal function, severe hemolysis, and in those taking Kþ-sparing diuretics, ACE inhibitors, or NSAIDs. EXAMINATION The first thing to do when examining a patient with reported or suspected hyperkalemia is to go to the bedside and perform a brief history and physical examination. Is the patient weak? Does the patient have an ileus? Does the patient have an obvious arrhythmia? If the diagnosis of hyperkalemia is suspected, an ECG should be obtained. The report of significant hyperkalemia in a patient with a normal ECG usually reflects laboratory error or factitious hyperkalemia. With true hyperkalemia, precordial T waves become tall and peaked as the Kþ reaches 5.6–6 mEq/L. At levels of 6–6.5 mEq/L, impulse conduction decreases, the QT interval is shortened, and the PR interval is prolonged. At 6.5–7.0 mEq/L, the P wave diminishes and the ST segment becomes depressed. At levels above 7 mEq/L, atrioventricular conduction is delayed and idioventricular rhythms occur. At levels above 7.5–8 mEq/L, the P wave disappears, the QRS complex widens, ST and T waves merge, and the ventricular rhythm becomes irregular. At levels greater than 10–12 mEq/L, the classic sine wave is seen. At this point, patients die of ventricular fibrillation or diastolic arrest. LABORATORY FINDINGS If pseudohyperkalemia is suspected, the Kþ measurement should be repeated. Cardiac monitoring should be initiated and an ECG should be obtained. Draw Chem 7 to assess renal function and Caþ concentration. The serum Kþ should be correlated with the pH. Acidosis is almost always present with hyperkalemia. Hypocalcemia and hypermagnesemia potentiate hyperkalemic cardiac toxicity. DIAGNOSIS The initial evaluation of a patient with hyperkalemia should include checking the history for any renal disease or use of Kþ sparing diuretics, ACE inhibitors, NSAIDs, Kþ supplements, or salt substitutes, which often contain KCl. In a patient with chronic hyperkalemia, normal renal function, and no other apparent etiology for the elevated Kþ, workup for one of the causes of hypoaldosteronism should be started.
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TREATMENT Emergent treatment of hyperkalemia has three parts: membrane stabilization, shifting Kþ into the cells, and removing excess Kþ from the body. Cardiac monitoring should be undertaken during treatment. Immediate treatment should be initiated for severe hyperkalemia (Kþ >7–7.5 mEq/L), ECG changes resulting from hyperkalemia, or severe muscle weakness. The practitioner should not forget to correct the underlying cause, if possible. Remedies might include decreasing the dietary Kþ intake; stopping administration of the Kþ-sparing diuretic, ACE inhibitor, NSAID, or other offending medication; and arranging for hemodialysis if the patient has renal failure. For mild hyperkalemia (serum Kþ, 5.5–6.5 mEq/L), a common treatment is to start the administration of normal saline at 125–200 ml/hr plus furosemide (40–80 mg given intravenously every 4–6 hours) to increase renal loss of Kþ, along with Kayexalate (sodium polystyrene; 25–50 g) with 50 ml of a 20% sorbitol solution every 4–6 hours orally to increase GI loss of Kþ. Along with Kþ, the previously described therapy will also increase urinary losses of Caþ and Mgþ. Patients with advanced age, renal insufficiency, CHF, cirrhosis, nephrotic syndrome, or other volume overload states will probably not be able to handle the extra volume or will require more than the usual amount of furosemide to establish an effective diuresis, and these factors should be taken into consideration when the initial orders are determined. Kayexalate can also be given rectally, as a 20-g dose with 20% sorbitol every 4 hours. Each gram of Kayexalate will eliminate 1 mEq of Kþ. Caution should be used in patients with impaired cardiac function, because the sodium in Kayexalate can cause acute water retention and CHF. Intestinal necrosis is another potential complication of this medication. For moderately severe hyperkalemia (serum Kþ, >6.5 mEq/L), albuterol should be given at 2.5 mg in 4 ml of normal saline nebulized over 20 minutes, 1 amp of D50W should be given as a slow intravenous push, 10 units of regular insulin should be given in by intravenous push, and D10W should be administered at a rate of 50–100 ml/hr. Albuterol, dextrose, and insulin will cause cellular Kþ uptake, but the effect is minimal and the effect is delayed for several minutes. D50W should not be administered rapidly; the slight increase in plasma osmolarity from the dextrose will cause cellular Kþ release and actually increase the serum Kþ slightly. A D10W drip is necessary to prevent hypoglycemia from insulin, a complication that occurs in approximately 40% of nondiabetic patients. If the ECG shows pronounced peaking of the T waves or widening of the QRS complex, 10 ml (one ampule) of a calcium gluconate 10% solution should be given intravenously, slowly over 2–3 minutes.
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Immediate treatment should be initiated for severe hyperkalemia (serum Kþ, >7–7.5 mEq/L), ECG changes occurring as a result of hyperkalemia, or severe muscle weakness. For severe hyperkalemia, the emphasis is on antagonizing the membrane effects of hyperkalemia by giving Ca, and on arranging for hemodialysis to remove the excess K from the body. Calcium gluconate 10% solution 10 ml (one ampule), slowly over 2–3 minutes, or calcium chloride 10% 5–10 ml can be given intravenously every 5–10 minutes until the most marked cardiac effects of hyperkalemia have subsided. The practitioner should use caution when giving Ca to patients who are taking digoxin. Hypercalcemia can potentiate the toxic effects of digoxin on the heart. If Ca is to be given to a hyperkalemic patient who is taking digoxin, it should be infused very slowly over 20–30 minutes. 1 ampule of NaHCO3 given by slow intravenous push can be considered to correct acidosis and thereby increase intracellular Kþ uptake, but NaHCO3 has been shown to be effective only in patients with azotemia and metabolic acidosis, and rapid administration of NaHCO3 can actually transiently increase the serum Kþ. The measures listed previously, including normal saline, furosemide, dextrose, insulin, and albuterol, can also be implemented. DIALYSIS Hemodialysis using a low Kþ bath is usually indicated for patients with severe hyperkalemia, for those who do not respond to the previously described measures, for those with ongoing tissue destruction and release of Kþ from intracellular stores, and for patients with significant azotemia. If the patient presents with severe hyperkalemia and is in renal failure, a renal consultation should be obtained for the initiation of hemodialysis.
CALCIUM More than 98% of calcium is stored in bone as hydroxyapatite. Calcium is found in three forms in the blood: 40% protein bound, 15% complexed, and 45% ionized, or free. Total plasma Ca ranges from 8.5 to 10.5 mg/dl. The ionized form is physiologically active form. Ionized Ca can be measured directly using a Ca-sensitive electrode. The common practice of “correcting” the serum Ca using the serum albumin, while generally producing linear results when compared with direct determination of ionized Ca, is in error when the serum pH or serum albumin are markedly abnormal. Calcium homeostasis is under the direct control of the parathyroid gland, parathyroid hormone (PTH), calcitonin, and calcitriol, which is a vitamin D metabolite. The parathyroid gland secretes PTH when ionized Ca levels are low. Calcium levels are increased by PTH, which increases bone resorption and renal Caþ
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uptake and stimulates synthesis of active vitamin D. Activated vitamin D increases intestinal and renal Caþ uptake and acts on bone to increase Caþ release. Vitamin D is absorbed directly from the GI tract or can be produced nonenzymatically by ultraviolet light acting on vitamin D precursors. Calcitonin, on the other hand, decreases the release of Ca from bone by inhibiting the activity of the osteoclasts (Caþ moves into bone) and stimulating renal Caþ excretion, lowering the serum Ca levels. Calcium is essential for muscle depolarization, neurotransmitter release in the CNS and peripheral nervous system, and for the function of the clotting cascade. It is also necessary for platelet aggregation and granule release. It acts as a membrane stabilizer and is needed for neutrophil chemotaxis and lymphocyte activation.
Hypocalcemia KEY POINTS The ionized form of hypocalcemia is the physiologically active form. Calcium homeostasis is under the direct control of the parathyroid gland, PTH, calcitonin, and calcitriol, which is a vitamin D metabolite. Hypocalcemia is defined as an ionized Caþ concentration less than 2.0 mg/dl or a serum Caþ concentration less than 8.5 mg/dl. Hypocalcemia can be the cause or the result of critical illness. Hypomagnesemia can cause or potentiate hypocalcemia. Tetany, seizures, hypotension, neuromuscular irritability, or ECG changes warrant emergent treatment. Hypomagnesemia should be treated concurrently, or it will be difficult to correct the Ca. DEFINITION Hypocalcemia is defined as an ionized Caþ concentration less than 2.0 mg/dl or a serum Caþ concentration less than 8.5 mg/dl. EPIDEMIOLOGY Hypocalcemia can be the cause or the result of critical illness. Common causes are renal failure, pancreatitis, shock, sepsis, hepatic failure, malabsorption, hypomagnesemia, drug use, and hypoparathyroidism. Hypocalcemia is seen in renal failure as a result of hyperphosphatemia (ionized Ca binds phosphate) and decreased production of vitamin D in the kidney, which decreases the intestinal absorption of Ca. Acute trauma, hyperpyrexia, and rhabdomyolysis can all cause acute hyperphosphatemia, which can lead to acute hypocalcemia. HYPOMAGNESEMIA Hypomagnesemia lowers secretion of PTH and impairs peripheral action of PTH, which decreases serum Ca. This is usually seen in the presence of alcoholism, malnutrition, and diuretic use.
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HYPOPARATHYROIDISM The most common cause of idiopathic hypoparathyroidism is polyglandular autoimmune syndrome type I, a familial disorder that manifests in childhood and is associated with mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency. The most common cause of acquired hypoparathyroidism is surgical, usually iatrogenic parathyroidectomy during thyroidectomy. Hungry bone syndrome can be seen after parathyroidectomy, with hypocalcemia and hypophosphatemia resulting from rapid remineralization of the skeleton after the parathyroid adenoma has been removed. These patients typically require very large amounts of Caþ, phosphate, Mgþ, and vitamin D postoperatively and will usually require supplemental Ca and vitamin D supplementation for life. PSEUDOHYPOPARATHYROIDISM Familial x-linked dominant disorder manifests by decreased end-organ responsiveness to PTH. Patients with this condition have hyperphosphatemia, hypocalcemia, and increased PTH. RICKETS OR VITAMIN D DEFICIENCY Vitamin D deficiency (i.e., rickets) is rare in the United States. Breastfeeding without adequate sun exposure can cause infantile rickets because breast milk is low in vitamin D. CLINICAL PRESENTATION Hypocalcemia can cause neuromuscular, respiratory, and cardiac complications. Patients may present with fatigue, weakness, paresthesia, tetany, mental status changes, or seizures. The most characteristic initial symptom after parathyroidectomy in patients who become hypocalcemic is paresthesia around the mouth and fingertips. Patients are often irritable with hyperactive reflexes; seizures may occur years after surgery. EXAMINATION Trousseau’s sign is carpal spasm when a blood pressure cuff is applied to the upper arm and maintained above systolic pressure for 3 minutes. If the test result is positive, the fingers will extend at the interphalangeal joints, the fingers will flex at the metacarpophalangeal joints, the wrist will be flexed, and the forearm will be pronated. Chvostek’s sign is a twitch at the corner of the mouth when the examiner taps over the facial nerve in front of the ear. This sign can be present in 10%–30% of healthy patients. Patients with pseudohypoparathyroidism typically have short round facies, brachycephaly, pudgy fingers and toes, growth failure of the fourth and fifth metacarpals, seizures, and mental retardation.
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LABORATORY FINDINGS Laboratory tests should include tests of Chem 7, albumin, Mgþ, phosphorus, and Caþ. Alkalosis lowers the ionized Caþ, though the total serum Caþ concentration will be normal. Each rise of 0.1 in the arterial pH will lower ionized Caþ by 3%–8%. Hypomagnesemia can cause or potentiate hypocalcemia. ECG findings when serum Caþ concentration is less than 6.0 mg/dl include prolonged QT interval, T wave of normal width, and a prolonged ST segment. Radiographs of skull and long bones may show characteristic changes of rickets. DIAGNOSIS When a patient’s Caþ concentration is less than 8.9 mg/dl, the presence of Chvostek’s and/or Trousseau’s signs supports the diagnosis of hypocalcemia. TREATMENT The treatment of hypocalcemia is based on replacing Ca and treating the underlying cause of the deficit. Oral Oral Ca with or without vitamin D can be used to treat an asymptomatic patient. Calcium is available in many oral preparations. Milk is a poor source of Ca in these patients because of its high phosphate content. Patients with hypocalcemia in the setting of chronic renal failure are treated with phosphate binders, oral Ca, and vitamin D (usually as calcitriol or another similar derivative). Emergent Treatment Parenteral treatment is needed in the case of severe acute hypocalcemia (ionized Caþ <1.3 mg/dl). Tetany, seizures, hypotension, neuromuscular irritability, or ECG changes warrant emergent treatment. Parenteral treatment options include CaCl or Ca gluconate. CaCl 10% contains 272 mg of elemental Ca per 10 ml. Ca gluconate 10% contains 90 mg of elemental Ca per 10 ml. Initial emergent treatment is 10 ml of 10% CaCl (or 10–30 ml of 10% Ca gluconate) over 10–20 minutes, followed by continuous intravenous infusion of 10% CaCl at 0.02–0.08 ml/kg/hr. The patient should be on a cardiac monitor during infusion, which must be done slowly. Rapid Ca infusions can cause bradycardia and asystole. Concentrated Ca is irritating to veins and should be diluted in D5W or normal saline. CaCl is more likely to cause tissue necrosis if extravasated. Calcium should not be given in intravenous solutions containing Na bicarbonate or phosphate because they can form insoluble salts with
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Caþ and precipitate. Extreme caution should be used in patients taking digoxin; Ca can potentiate digoxin toxicity. Hypomagnesemia should be treated concurrently, or it will be difficult to correct the Ca because hypomagnesemia causes PTH resistance and decreases PTH secretion. Patients who are receiving massive blood transfusions (more than 1 unit every 5 minutes) will also require Ca because citrate used as an anticoagulant in banked blood binds ionized Caþ. Ten milliliters of 10% CaCl can be given after every 4–6 units of blood. Rickets is treated with daily vitamin D at 5000–10,000 IU until electrolyte and bone changes have been corrected.
Hypercalcemia KEY POINTS Calcium homeostasis is under the direct control of the parathyroid gland, PTH, calcitonin, and calcitriol, which is a vitamin D metabolite. The ionized form is the physiologically active form. Hypercalcemia is defined as an ionized Caþ concentration greater than 2.7 mEq/L or a total serum Caþ concentration greater than 10.5 mg/ dl. The most common causes are metastatic malignancy and hyperparathyroidism. The mnemonic stones, bones, psychic moans, and abdominal groans is used to remember the signs and symptoms of hypercalcemia. Treatment for hypercalcemia should be initiated in symptomatic patients, those with dehydration, or asymptomatic patients with a Caþ concentration greater than 12 mg/dl. Initial treatment is volume repletion. Medications to decrease mobilization of Ca from bone may be considered in the ED setting if the Caþ concentration is greater than 14 mg/dl or the patient is symptomatic. Glucocorticoids are used in certain cases. DEFINITION Hypercalcemia is defined as an ionized Caþ concentration greater than 2.7 mEq/L or a total serum Caþ concentration greater than 10.5 mg/dl. ETIOLOGY The most common causes are metastatic malignancy and hyperparathyroidism. Other causes include drugs, immobilization, and granulomatous disease. MALIGNANCIES The most common malignancies that cause hypercalcemia include lung, breast, and renal cancer; multiple myeloma; and leukemia. Calcium levels over 14 mg/dl are often a result of malignancy.
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ENDOCRINOPATHIES The second most common cause of hypercalcemia is primary hyperparathyroidism. This usually results from a parathyroid adenoma (80%) and parathyroid hyperplasia (20%). Hypercalcemia can also be associated with hyperthyroidism, adrenal insufficiency, pheochromocytoma, and acromegaly. Hyperparathyroidism is seldom caused by parathyroid carcinoma. Several endocrine adenomas can cause hypercalcemia. These include Werner’s syndrome, multiple endocrine neoplasia type I, and Sipple’s syndrome (i.e., pheochromocytoma and medullary cell carcinoma of the thyroid). DRUGS Patients taking thiazide diuretics often present with hypercalcemia resulting from increased renal tubular reabsorption of Ca and decreased plasma volume. Other types of diuretics can increase Ca excretion and lead to hypocalcemia. Lithium, hormonal therapy for breast cancer, and hypervitaminosis D and A are also associated with hypercalcemia. GRANULOMATOUS DISEASES The granulomas of sarcoidosis, tuberculosis, histoplasmosis, and coccidiomycosis can change the inactive form of vitamin D to the active form, with resultant increased GI Caþ absorption, hypercalciuria, and, sometimes, hypercalcemia. Steroids (e.g., prednisone) block the action of vitamin D on the GI tract and usually correct the hypercalcemia. REDISTRIBUTION Patients who are immobilized as a result of trauma or illness can develop hypercalcemia because of suppression of the parathyroid– vitamin D axis. This causes Ca to leave the bones, causing transient hypercalcemia. Patients with Paget’s disease (a high bone turn-over state with poorly mineralized bones) who are on bed rest for chronic pain can also develop hypercalcemia. Other causes include milk alkali syndrome and recovery from severe rhabdomyolysis or necrotizing pancreatitis. CLINICAL PRESENTATION The effects of hypercalcemia are seen in the neurological, skeletal, cardiac, GI, and renal systems. Patients can present with malaise, weakness, abdominal pain, nausea, vomiting, constipation, and mental status changes. Renal concentrating ability is decreased, which causes polyuria. Nephrolithiasis can occur because of the increased filtered load of Ca. Long-term hypercalcemia can cause microscopic renal Ca deposits, which can progress to renal insufficiency. The heart’s conduction
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rate is slowed, and the refractory period is decreased. Hypercalcemia increases cardiac sensitivity to digoxin. Gastric motility is decreased and gastric acid secretion is increased in response to increased gastrin levels. Patients with Ca levels less than 12 mg/dl may be asymptomatic or have polyuria, polydipsia, and dehydration. Patients with Ca levels above 14–15 mg/dl may be lethargic with muscle weakness and confusion or coma. Patients with levels above 15 mg/dl can present with somnolence, stupor, and coma. EXAMINATION The mnemonic stones, bones, psychic moans, and abdominal groans is used to remember signs and symptoms of hypercalcemia:
Stones: renal calculi Bones: osteolysis Psychic moans: psychiatric disorders Abdominal groans: abdominal pain, peptic ulcer disease, pancreatitis Hyporeflexia, hypotonia, and metastatic calcifications can be seen.
LABORATORY FINDINGS Samples should be drawn for Chem 7, Mgþ, PO4, and PTH (intact or mid-molecule) tests, and a urinalysis should be performed. Hypokalemia and hypomagnesemia are commonly seen with hypercalcemia. The serum PTH will not be used in emergency treatment but will be useful later in the diagnostic workup. ECG FINDINGS ECG findings in a patient with hypercalcemia may include a depressed ST segment, a widened T wave, and shortened ST and QT intervals. Bradyarrhythmias, bundle branch blocks progressing to second-degree blocks, and complete heart block can be seen as the Ca level increases. Cardiac arrest occurs when levels exceed 20 mg/dl. DIAGNOSIS The diagnosis of hypercalcemia can be made if the total Ca concentration is greater than 10.5 mg/dl corrected for albumin or if the ionized Ca concentration is greater than 2.7 mEq/L. The ionized Ca level will be affected by systemic pH. Alkalemia shifts hydrogen ions from plasma proteins, leaving more protein unbound. More of the ionized Ca will then be protein bound, causing a decrease in the ionized fraction. The opposite occurs with acidosis. Hypercalcemia should be suspected in patients with cancer who have bone metastases, or in patients with combinations of clinical problems like nephrolithiasis, peptic ulcer disease, and pancreatitis.
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TREATMENT Treatment must be aimed at lowering the serum Ca but also at alleviating the underlying disease. Treatment for hypercalcemia should be initiated in symptomatic patients, in persons with dehydration, or in asymptomatic patients with Ca levels greater than 12 mg/dl. Volume Repletion with Normal Saline Patients are usually dehydrated and have decreased TBW as a result of high Ca level interfering with ADH excretion. Vigorous volume repletion (200–300 ml/hr of normal saline) is required, but caution should be exercised especially in patients with CHF or renal disease to avoid volume overload. If the patient has severe cardiac or renal disease, dialysis may be required. Furosemide or loop diuretics to enhance urine Ca excretion may be used in patients who cannot tolerate a saline load or in those who are fluid overloaded at presentation (renal disease or CHF). Furosemide treatment for hypercalcemia is not as widely used now due to the availability of other drugs and volume and electrolyte complications. Thiazide diuretics should not be used because these decrease renal Ca excretion. Decreased Mobilization of Calcium from Bone The following medications may be considered in the ED setting if the Caþ concentration is greater than 14 mg/dl or if the patient is symptomatic. Calcitonin Calcitonin is used in patients with metastatic bone disease. This agent inhibits osteoclasts and is less toxic than mithramycin, but its use is limited by tachyphylaxis. The dose is 4 IU/kg given subcutaneously or intramuscularly every 12 hours. The action is prolonged when given with corticosteroids. Mithramycin is the antitumor antibiotic plicamycin. It is rarely used now for hypercalcemia due to the toxicity and the availability of newer drugs. Bisphosphonates Bisphosphonates is used in patients with hypercalcemia of malignancy. They inhibit Caþ release from bone by interfering with the metabolic activity of osteoclasts and are also cytotoxic to osteoclasts. Zoledronic acid is the drug of choice for hypercalcemia due to malignancy; it should be administered at a dose of 4 mg given intravenously over 15 minutes. Pamidronate 60–90 mg given intravenously over 2 hours can also be used. Bisphosphonates are more potent than saline and calcitonin, but their maximum effect will not occur for 2–4 days.
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Glucocorticoids Glucocorticoids inhibit the gastrointestinal resorption of Ca. They are used in patients with multiple myeloma, leukemia, sarcoidosis, vitamin A or D intoxication, and breast cancer. Dosing is as follows: hydrocortisone given 3 mg/kg/day in divided doses, or the equivalent in prednisone, prednisolone, or dexamethasone. Gallium Nitrite Gallium nitrite acts by decreasing the solubility of bone mineral crystals. It must be given by continuous intravenous infusion over 5 days. Gallium potentiates nephropathy and must be avoided in patients with renal disease. Surgery or Radiation Surgery or radiation is required for PTH-producing neoplasms.
MAGNESIUM The normal serum Mg concentration is 1.8–2.4 mg/dl. Total body Mgþ content is 2000 mEq, with 50%–70% in bone. Less than 1% is in the ECF. The remaining Mgþ is found in the ICF, with a distribution similar to Kþ. It is the second most abundant intracellular cation. Magnesium is needed for the metabolism of many enzymes and is necessary for the generation of adenosine triphosphate (ATP).
Hypomagnesemia KEY POINTS Plasma levels do not reflect total body Mgþ levels. When evaluating hypomagnesemia, the practitioner should remember that hypokalemia, hypophosphatemia, and hypocalcemia will often also be present. Hypomagnesemia should be anticipated in patients with alcoholism, cirrhosis, malnutrition, and hyperalimentation and during treatment for DKA. DEFINITION Hypomagnesemia is defined as a serum Mgþ concentration less than 1.5 mg/dl. EPIDEMIOLOGY Hypomagnesemia can be seen in many different illnesses. It is most commonly seen in adults with alcoholism, malnutrition, diarrhea, cirrhosis, and pancreatitis.
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NONRENAL MG+ LOSSES Nonrenal Mgþ losses are seen in lactation, burns, sweating, sepsis, GI tract fistulas, and diarrhea. DECREASED MG+ INTAKE Decreased Mgþ intake occurs in alcoholism, malnutrition, and malabsorption. INCREASED RENAL MG+ LOSSES Increased renal Mgþ losses occur with many drugs, including loop diuretics, aminoglycosides, cisplatin, amphotericin B, pentamidine, and alcohol. Endocrine disorders such as hyperparathyroidism, DKA, aldosteronism, and hyperthyroidism also cause hypomagnesemia by renal losses. REDISTRIBUTION FROM ECF TO ICF Magnesium is redistributed from the ECF to the ICF with intravenous glucose or hyperalimentation, insulin ingestion, and after parathyroidectomy hungry bone syndrome. CLINICAL PRESENTATION Patients present with neuromuscular irritability and CNS symptoms of vertigo, ataxia, and seizures. Hypomagnesemia can contribute to delirium tremens in alcoholics and arrhythmias in patients taking digoxin. EXAMINATION Patients can present with hyperreflexia, tremors, tetany, and Chvostek’s or Trousseau’s signs. If Ca levels are normal, this should suggest hypomagnesemia. LABORATORY FINDINGS Measurements of Caþ, Mgþ, PO4, and Chem 7 should be performed. The plasma level of Mg is an unreliable gauge to diagnose hypomagnesemia or hypermagnesemia. Plasma levels do not reflect total body Mg levels. When evaluating hypomagnesemia, the practitioner should remember that hypokalemia, hypophosphatemia, and hypocalcemia will often also be present. ELECTROCARDIOGRAPHY In a patient with hypomagnesemia, the PR and QT intervals can be prolonged and the QRS complex widened with ST segment depression and T wave inversion.
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DIAGNOSIS Hypomagnesemia should be anticipated in patients with alcoholism, cirrhosis, malnutrition, and hyperalimentation and during treatment for DKA. TREATMENT Treatment is Mg repletion administered orally, intramuscularly, or intravenously. Magnesium can be given orally as 6 g/day of MgSO4. In alcoholics or patients with delirium tremens, up to 8–12 g/day can be given intramuscularly or intravenously. The first 1.5–2 g of MgSO4 can be given intravenously over 1–2 hours, then intravenously at 4–6 g/day. Magnesium can be given to patients on hyperalimentation at 12–16 mEq (1.5–2 g) a day. Half the given Mgþ dose will be lost in the urine.
Hypermagnesemia KEY POINTS Hypermagnesemia is usually seen in patients with renal failure who have been ingesting Mgþ-containing antacids. It is also seen in pregnant persons and neonates due to treatment of eclampsia with magnesium sulfate. The diagnosis should be considered in patients with hyperkalemia, hypercalcemia, or renal failure. Treatment consists of immediate cessation of the ingested or parenteral Mgþ plus intravenous fluids (if no renal failure is present) and furosemide. DEFINITION Hypermagnesemia is defined as a Mgþ concentration greater than 2.5 mEq/L. EPIDEMIOLOGY Hypermagnesemia occurs rarely and is usually seen in patients with renal failure who have been ingesting Mgþ-containing antacids. It is also seen in pregnant persons and neonates due to treatment of eclampsia with magnesium sulfate. Other causes include lithium, overuse of Mg cathartics or enemas, rhabdomyolysis, tumor lysis, hyperparathyroidism, and hypothyroidism. CLINICAL PRESENTATION Patients with hypermagnesemia are often asymptomatic. Muscular weakness, loss of deep tendon reflexes (DTRs), nausea, flushing, and headache occur at Mgþ concentrations greater than 4 mEq/L. At levels between 5 and 6 mEq/L, severe respiratory depression can occur. At
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8–10 mEq/L, cardiac conduction abnormalities and neuromuscular paralysis with hypotension, respiratory failure, and death can occur. DIAGNOSIS Hypermagnesemia can be diagnosed when Mg concentrations are greater than 2.5 mEq/L. It should be considered in patients with hyperkalemia, hypercalcemia, or renal failure. TREATMENT Treatment of hypermagnesemia consists of immediate cessation of the ingested or parenteral Mgþ plus intravenous fluids (if no renal failure is present) and furosemide. Severe symptomatic hypermagnesemia can be treated with Ca 5 ml of 10% calcium chloride given intravenously over 5 minutes or 10 ml of 10% calcium gluconate. Patients with renal failure may need dialysis.
PHOSPHORUS Phosphorus is an essential mineral needed for energy metabolism in its phosphate and phosphocreatine forms. Total body phosphorus is 700 g; 80% of this occurs in bone as hydroxyapatite, 10% –15% is intracellular, and less than 1% is in the ECF. Normal serum levels are 2.5–5 mg/dl in adults and 4–7 mg/dl in infants. Serum phosphorus and Ca levels are inversely proportional. 1 mmol of phosphate ¼ 31 mg of elemental phosphorus
Hypophosphatemia KEY POINTS Serum phosphorus levels may not accurately represent total body phosphorus levels because less than 1% of phosphorus is in the ECF. Hypophosphatemia is usually caused by intracellular shift of phosphate, decreased GI absorption, or increased renal loss. Hypophosphatemia should be suspected in alcoholics, patients on hyperalimentation, and those being treated for DKA. The etiology of hypophosphatemia is often made according to the history. Replacement is usually oral. Intravenous phosphorous can be given for severe hypophosphatemia. PO4 should be given more slowly in patients with renal insufficiency or hypercalcemia. DEFINITION Hypophosphatemia is defined as a serum phosphate level less than 2.5 mg/dl.
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EPIDEMIOLOGY Hypophosphatemia is usually caused by intracellular shift of phosphate, decreased GI absorption, or increased renal loss. ECF to ICF shifts are seen with respiratory or metabolic alkalosis (e.g., COPD, bicarbonate infusions). Other clinical settings with hypophosphatemia include hyperalimentation, DKA, hyperparathyroidism, renal tubular defects, Fanconi syndrome, renal transplant, chronic diarrhea, malabsorption, alcoholism, vitamin D deficiency, hypercalcemia, and use of phosphate-binding antacids, steroids, and diuretics. Hypophosphatemia can occur during nutritional recovery, glucose infusions, or treatment of DKA, as glucose moves into cells and phosphorus is consumed during phosphorylation. CLINICAL PRESENTATION/EXAMINATION Symptoms are rare at phosphorus levels greater than 2.0 mg/dl. Hypophosphatemia causes depletion of adenosine triphosphate in platelets, RBCs, and white blood cells. This causes impaired platelet aggregation and increased bleeding. RBCs become rigid spherocytes and impair capillary perfusion. 2,3-DPG decreases and increases the affinity of hemoglobin to oxygen, reducing the oxygen available to tissues. Resistance to infection is decreased due to impaired macrophage chemotaxis, intracellular killing, and phagocytosis. Patients with hypophosphatemia can also present with CNS symptoms of circumoral and fingertip paresthesias and areflexia. Hyperventilation, anorexia, and altered mental status are common at low levels. Both skeletal and smooth muscles are affected. Proximal myopathy and rhabdomyolysis can occur. Patients may become very weak with respiratory depression requiring ventilator support. Cardiac function is depressed, and CHF and cardiac arrest can occur. LABORATORY FINDINGS Serum phosphorus levels may not accurately represent total body phosphorus levels because less than 1% of phosphorus is in the ECF. DIAGNOSIS Suspect hypophosphatemia in alcoholics, patients on hyperalimentation, and those being treated for DKA. The etiology of hypophosphatemia is often made according to the history. TREATMENT Patients need 7–9 mmol/day of phosphate. Replacement is usually oral, 1200–1500 mg/day. Milk is a good source of oral phosphate. In cases of more severe depletion, 2.5–3.5 g/day (80–110 mmol/day) in three to four divided doses may be needed. Intravenous phosphorus can be given for severe hypophosphatemia (<1 mg/dl) or cardiac or respiratory
382 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 8-3 Oral Phosphate Supplements PREPARATION
DOSE
K-Phos Neutral Neutra Phos
IV KPhos
1 capsule 1 capsule or 75 ml 1 capsule or 75 ml 1 ml
IV NaPhos
1 ml
Neutra Phos Kþ
PHOSPHORUS
SODIUM
250 mg PO4 250 mg PO4
13 mEq 7.1 mEq
250 mg PO4 93 mg ¼ 3 mmol PO4 93 mg ¼ 3 mmol PO4
POTASSIUM 1.1 mEq 7.1 mEq 14.2 mEq 4.4 mEq
4 mEq
1 mmol of phosphate (PO4) ¼ 31 mg of elemental phosphorus.
symptoms. The appropriate dose is 2.5–5 mg/kg (0.08–0.16 mmol/kg) given intravenously over 6 hours. Monitor the phosphate level every 6 hours, and switch to oral supplements when the phosphate level is 2.0– 2.5 mg/dl (Table 8-3). Intravenous phosphate can cause hypocalcemia, arrhythmias, and renal failure. PO4 should be given more slowly in patients with renal insufficiency or hypercalcemia. 1 mmol of phosphate ¼ 31 mg of elemental phosphorus
Hyperphosphatemia KEY POINTS Hyperphosphatemia alone is not a problem unless the calcium-phosphate product is greater than 60, at which point metastatic or ectopic calcification can occur. The main complication of hyperphosphatemia is hypocalcemia. Hyperphosphatemia is usually seen in patients with renal disease and is due to reduced renal excretion. It can be seen when there is a high phosphate load due to cell breakdown. Suspect hyperphosphatemia in patients with renal failure and in those with hypocalcemia, hypomagnesemia, or rhabdomyolysis. Therapy is directed at treatment of the underlying cause of hyperphosphatemia. DEFINITION Hyperphosphatemia in adults is defined as a serum phosphorus level greater than 5.0 mg/dl. EPIDEMIOLOGY Hyperphosphatemia is usually seen in patients with renal disease and is due to reduced renal excretion. It can also be seen in conditions that cause movement of phosphate out of the cells and into the ECF (acidosis). It can be seen with rhabdomyolysis and tumor lysis syndrome when there
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is a high phosphate load due to cell breakdown plus accompanying renal failure. Other etiologies are hypoparathyroidism, other conditions that cause hypocalcemia or hypomagnesemia, and increased vitamin D intake or phosphate intake, as in the ingestion of large amounts of phosphoruscontaining laxatives. CLINICAL PRESENTATION Hyperphosphatemia alone is not a problem, unless the calcium-phosphate product is greater than 60, at which point metastatic or ectopic calcification can occur. It is the associated renal failure, along with the hypocalcemia and hypomagnesemia, that are usually the main issue. The main complication of hyperphosphatemia is hypocalcemia. LABORATORY FINDINGS Measurements of Chem 7, Mgþ, and Caþ should be taken. Hypomagnesemia and hypocalcemia are usually seen together with the high phosphorus level. DIAGNOSIS Suspect hyperphosphatemia in patients with renal failure and in those with hypocalcemia hypomagnesemia or rhabdomyolysis. TREATMENT AND OUTCOME Therapy is directed at treatment of the underlying cause of hyperphosphatemia. Calcium phosphate should be restricted to less than 200 mg/day. Patients with normal renal function can be given normal saline (1–2 L every 4–6 hours) and acetazolamide (500 mg every 6 hours). Aluminum oral phosphate binders (e.g., aluminum hydroxide or aluminum carbonate; 30–45 ml/day) can be used to decrease GI phosphate absorption. Dialysis may be needed in patients with renal failure.
CHLORIDE Chloride is an essential extracellular anion that is important in maintaining ECF volume, normal anion gap, and acid–base and K balance. Chloride also maintains urine output and concentrations in the renal countercurrent mechanism. The normal serum chloride is 96–108 mEq/L. Chloride is 90% excreted in the urine and is also excreted in stool and sweat. Chloride is transported actively and passively with either HCO 3 or sodium. It is absorbed in both the small and large intestine. There is a normal Cl-HCO 3 exchange in the small bowel. Parietal cells in the stomach secrete chloride plus hydrogen ions into gastric fluid. Chloride’s main function is to concentrate urine in the kidney. Reabsorption of chloride occurs passively with sodium in the renal
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tubule and actively in the loop of Henle. This active transportation establishes a transport gradient that is needed for the “countercurrent” urine concentrating mechanism. When ADH is absent, this “countercurrent” mechanism allows the kidney to absorb solute without water in the collecting ducts, which allows urine to be more dilute if needed. There are reciprocal changes in chloride and HCO 3 in the plasma, helping to maintain acid–base balance.
Hypochloremia DEFINITION Hypochloremia is defined as a chloride level less than 95 mEq/L. EPIDEMIOLOGY Hypochloremia is usually caused by excess use of loop diuretics, nasogastric suction, or vomiting. Metabolic alkalosis is usually present with hypochloremia. Vomiting causes loss of hydrochloric acid. In the presence of ECF volume contraction, there is an increase in Na and HCO 3 resorption in the kidney, which helps to maintain the alkalosis. Aldosterone accelerates the retention of sodium and HCO 3 at the expense of hydrogen, K, and chloride. CLINICAL PRESENTATION There are no specific signs or symptoms of hypochloremia. LABORATORY FINDINGS A Chem 7 test should be performed, then urine chloride should be analyzed to determine whether chloride-responsive alkalosis is present. DIAGNOSIS The diagnosis of hypochloremia is made based on the patient’s history of diuretic therapy, vomiting, or nasogastric suctioning along with the assessment of chloride values in the presence of metabolic alkalosis. If urine chloride is less than 10 mEq/L, then hypochloremia is due to chloride responsive alkalosis. If greater than 40 mEq/L, hypochloremia is due to volume overload or dilution. These patients usually have a metabolic alkalosis due to excess mineralocorticoid or glucocorticoid. TREATMENT Treatment is aimed at therapy for the underlying disorder. Chlorideresponsive alkalosis is treated with normal saline. Chloride-resistant metabolic alkalosis requires IV normal saline plus K. Give one fourth as KCl and three fourths as NaCl.
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Hyperchloremia DEFINITION Hyperchloremia is defined as a chloride level greater than 108 mEq/L. EPIDEMIOLOGY Hyperchloremia usually occurs as a result of dehydration or excess administration of sodium or other chlorides. It can present as a normal anion gap (“hyperchloremic”) metabolic acidosis. This is often seen in patients with þ þ severe diarrhea or ureteral diversion. HCO 3 and K are excreted while H and Cl are absorbed. Patients on hyperalimentation can develop hyperchloremic metabolic acidosis as a result of the amino acids that are given as chlorides. Hypermagnesemia, hypercalcemia, lithium overdose, RTA, and multiple myeloma can present with hyperchloremia. CLINICAL PRESENTATION The clinical presentation is not specific for hyperchloremia; it depends on the underlying disease and hydration. LABORATORY FINDINGS Samples should be drawn for Chem 7, Caþ, Mgþ, and PO 4 tests. A normal anion gap “hyperchloremic” metabolic acidosis or metabolic alkalosis is often present. DIAGNOSIS When sodium and chloride levels are both elevated, this usually means the patient is dehydrated. When chloride is elevated and the sodium level is normal or low, then there has been an excess loss of HCO 3 from the body or too much chloride (e.g., CaCl therapy or amino acids as hydrochlorides) has been given. A patient with an anion gap of less than 10 mEq/L in the presence of hyperchloremia will often have nephrotic syndrome, hypoalbuminemia, or cirrhosis. TREATMENT If hyperchloremia is due to dehydration, then isotonic intravenous fluids should be given slowly without chloride. Hypotonic fluids, especially if given too quickly, can cause cerebral edema. Underlying disorders can be corrected, causing HCO 3 loss.
Bibliography Adrogue HJ, Madias NE: Hypernatremia, N Engl J Med 2000;342:1493. Adrogue HJ, Madias NE: Hyponatremia, N Engl J Med 2000;342:1581. Agus ZS: Causes and treatment of hyperphosphatemia. In Rose BD (ed): UpToDate. Wellesley, MA, 2005. Agus ZS: Clinical manifestations of hypercalcemia: Etiology of hypercalcemia: In Rose BD (ed): UpToDate. Wellesley, MA, 2005.
386 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Agus ZS: Clinical manifestations of hypocalcemia: Etiology of hypocalcemia in adults. Treatment of hypocalcemia. In Rose BD (ed): UpToDate. Wellesley, MA, 2005. Agus ZS: Diagnosis and treatment of hypophosphatemia: Causes of hypophosphatemia. Phosphate concentration in plasma and phosphate supplements. In Rose BD (ed): UpToDate. Wellesley, MA, 2005. Agus ZS, Savarese D, Berenson JR: Treatment of hypercalcemia. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Gibbs MA, Wolfson AB, Tayal VS: Electrolyte disturbances. In Marx JA, Hockberger RS, Walls RW, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Gross P: Treatment of severe hyponatremia, Kidney Int 2001;60:2417. Gross P: Treatment of severe hyponatremia: Conventional and novel aspects, J Am Soc Nephrol 2001;12(S10–S14):510. Londner M, Hammer D, Kelen GD: Fluid and electrolyte problems. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Rose BD: Causes of hyperkalemia, Treatment of hyperkalemia. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD: Causes of hypokalemia, Treatment of hypokalemia. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD: Causes of hyponatremia, Symptoms of hyponatremia and hypernatremia, Diagnosis of hyponatremia, Treatment of hyponatremia. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD: Diagnosis of hypernatremia. Causes of hypernatremia Treatment of hypernatremia. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD, Post TW: Clinical Physiology of Acid–Base and Electrolyte Disorders, ed 5. McGraw-Hill: New York, 2001. Whittier FC, Rutecki GW: Fluids and Electrolytes: A Guide to Everyday Practice. The Little Yellow Book. Anadem: Columbus, OH, 2000. Yates KE: Salt and water: A simple approach to hyponatremia, CMAJ 2004;170:365.
Geriatric Emergencies MARTIN A. DOCHERTY
ICD Codes: ICD codes are particular to the individual disease ! Emergency Actions ! Vital signs are the most important part of any geriatric examination. Any abnormal vital sign in any geriatric patient must be addressed, as should any mental status or cognitive change. Often, mental status changes in the geriatric population result from electrolyte disorders or infections. The source of any fever in a geriatric patient should be aggressively pursued.
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DEFINITION Anyone older than 65 years is classified as geriatric.
EPIDEMIOLOGY Approximately 15% of the U.S. population is over the age of 65 years. The fasting growing group of patients in the United States are those older than 85 years of age. About 15% of all ED visits are made by older patients, and 45% of all hospital admissions involve patients over the age of 65 years. In the nursing home population, 25% of residents are sent to the ED for care each year.
CLINICAL PRESENTATIONS Age-Specific Concerns INFECTION Because of decreasing antibody titers and lower levels of cell-mediated immunity, elderly patients are at an increased risk for infection and sepsis. In addition, the risk of neoplasm is greatly increased. Neoplasm is the second leading cause of hospital admission and death in the elderly population. CARDIOVASCULAR DISEASE Higher rates of hypertension, peripheral vascular disease, and atherosclerosis are seen. This results in cardiovascular disease being the leading cause of hospitalization and death in this population. ORTHOPEDIC PROBLEMS Arthritis due to “wear and tear” and obesity is a common problem. In addition, fractures are the fifth leading cause of admission to the hospital. This is especially problematic in older women because of the higher rates of osteoporosis. FALLS The leading cause of falls in elderly persons is side effects from prescription medication. Healthcare providers in the ED should be wary about adding yet another medication without a discussion of the riskbenefit ratio with the patient’s primary care physician. An age-related loss of muscle mass is also responsible for an increase in falls.
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EXAMINATION AND HISTORY History Due to cognitive and physical defects in elderly patients, the history is often difficult to obtain. This requires a greater reliance on the family and primary healthcare provider input. Judicious use of old records is often necessary. In the case of patients transferred from nursing homes, the nursing home “transfer sheet” may be the sole source of information regarding the reason for transfer and previous history and often is not complete.
Physical Examination Because of the prominence of “vague complaints” in this population, the physical examination often needs to be more thorough. In particular, vital signs may be deceptive. A “normal” blood pressure may actually signal hypotension in a normally hypertensive patient. Use of medications such as beta blockers can also blunt a physiological tachycardic response. In addition, up to 30% of elderly patients may have a blunted or absent febrile response, even in the face of serious infections. Rectal temperatures should be obtained if any doubt exists. Over 90% of the time, a fever in an elderly patient is due to a bacterial, not viral, infection.
SPECIFIC DISEASE PRESENTATIONS Myocardial Infarction It is important to realize that atypical presentations of acute myocardial infarction in elderly patients are very common. Often, only the presence of associated symptoms may give a clue as to a myocardial infarction. These may manifest as dyspnea, nausea and vomiting, unexplained weakness, or vague mental status changes. Therefore, a very low threshold should exist for evaluating such patients for acute myocardial infarction.
Pneumonia Pneumonia is in the top 10 of causes of hospitalization and death in elderly persons. Pneumococcal pneumonia is still the most common, followed by gram-negative pneumonia. Reactivation of previous tuberculosis is also a growing concern and should be considered in the appropriate setting.
Urinary Tract Infections A high incidence of urinary tract infection occurs in older patients. Bacteriuria is seen in 20% of men and women aged 70 years. Almost 50% of females over 80 years of age have had bacteriuria at one time.
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A higher incidence of infection is seen in patients with indwelling Foley catheters. Because of this, it is important to avoid the “convenience Foley” if at all possible.
Abdominal Pain The underlying cause of abdominal pain is often difficult to diagnose. Vague reports of symptoms and relatively benign examination results may mask a catastrophic problem. More than 60% of presentations are surgical cases, and the mortality is 10 times that of younger patients. The most common causes are cholecystitis seen in 10% – 40% of patients, appendicitis in 5% –15%, and obstruction in 7% –14%. Nonspecific causes may be found in up to 25% of elderly patients. Practitioners should be liberal in the use of laboratory tests and imaging studies such as ultrasound, CT scanning, radionuclide studies, and angiography, where indicated. There should be a very low threshold for admission and prolonged observation.
Trauma Major trauma is less common in elderly persons, comprising about 10% of cases. As expected, the morbidity and mortality in this group is much higher. This is partly due to the presence of comorbid factors and less physiological reserve. It is important to realize that an underlying medical problem, such as dysrhythmia, syncope, myocardial infarction, or cerebrovascular accident may have led to the trauma, and these may need to be treated at the same time as traumatic injuries. Certain injuries seen more commonly in elderly persons include subdural hematoma, seemingly minor head trauma, spinal fractures due to osteoporosis, thoracic rib and pulmonary injuries, as well as extremity fractures. In addition, skin breakdown is more rapid, so patients should be taken off backboards as soon as possible.
Psychiatric Illness Depression is common in elderly persons and often manifests as somatic symptoms or severe agitation. Underlying medical causes such as thyroid disease may also present in this fashion and should be considered. Alcohol dependence is seen in 15% of elderly ED patients and can lead to devastating falls. Practitioners should be suspicious of psychiatric illness when patients present with a history of frequent falls.
SUMMARY Elderly patients may present differently than their younger counterparts. Even potentially catastrophic illnesses may have a vague and atypical
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ED presentation. The practitioner should have a low threshold for diagnostic testing and should look for the unexpected.
Bibliography Bugliosi TF, Meloy TD, Vukov LF: Acute abdominal pain in the elderly, Ann Emerg Med 1990;19:1383. Marco CA, Schoenfeld CN, Hansen KN, et al: Fever in geriatric emergency patients: Clinical features associated with serious illness, Ann Emerg Med 1995;26:18. Solomon CG, Lee TH, Cook EF, et al: Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients, Am Cardiol 1989;63:772. Strange GR, Chen EH: Use of emergency departments by elder patients: A five year follow up study, Acad Emerg Med 1998;5:1157. Zietlow SP, Capizzi PJ, Bannon MP, et al: Multisystem geriatric trauma, J Trauma 1994;37:985.
Hyperglycemic Hyperosmolar Nonketotic Coma JONATHON ALLEN
ICD Codes: Hyperosmolality 276.0, Hyperglycemic 790.6
Key Points Hyperglycemic hyperosmolar nonketotic coma (HHNC) is most common in elderly patients with type 2 diabetes and is much less common than DKA. It is often the initial diagnostic event to occur in adult-onset diabetes. ! Emergency Actions ! Rapid administration of 0.9% (normal) saline is the mainstay of treatment of HHNC.
DEFINITION Hyperglycemic hyperosmolar nonketotic coma is a syndrome of acutely decompensated diabetes. Hyperglycemia, hyperosmolarity, and profound dehydration are found in the absence of serum ketones. This syndrome is at the opposite end of the lipid metabolism spectrum compared with DKA.
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EPIDEMIOLOGY HHNC is most common in elderly patients with type 2 diabetes and is much less common than DKA. It is often the initial diagnostic event in adult-onset diabetes. HHNC can also be found in nondiabetic patients, particularly after severe burns, administration of extended parenteral nutrition, or dialysis.
PATHOPHYSIOLOGY HHNC is the result of severe dehydration resulting from a sustained hyperglycemic diuresis in which the patient is unable to compensate for urinary losses with oral intake. As with DKA, there is a decreased action of insulin that results in glycogenolysis, gluconeogenesis, and decreased cellular uptake of glucose. Initially, the hyperglycemia osmotically pulls fluid back into the intravascular compartment. This temporarily maintains adequate tissue perfusion. Shortly thereafter, a profound osmotic diuresis ensues, as the renal threshold for glucose reuptake is surpassed. This produces severely hypotonic urine, with sodium concentrations of 50–70 mEq/L, approximately one half of the serum sodium concentration. Initially, the diuresis is antagonized by ADH produced by the pituitary gland. However, this effect is quickly overcome, and diuresis continues until limited by frank hypotension and renal hypoperfusion with subsequent drop in glomerular filtration rate. The hypotonic diuresis results in worsening hyperglycemia, hypernatremia, and hyperosmolarity. Patients can quickly lose between 8 and 12 L of free water. The reason for the absence of serum ketones in NNHC is not clearly understood. Free fatty acid levels are lower in NNHC than DKA, limiting the availability of ketogenic substrates. In addition, levels of the insulin counter-regulatory hormones, epinephrine, glucagon, somatostatin, and cortisol, are much lower in NNHC. One explanation is that these patients continue to secrete a very small amount of insulin, significant enough to inhibit ketogenesis and counter-regulatory hormone release. Ketosis may also be limited by a relatively higher level of portal vein insulin, thus preventing partial oxidation of the incoming free fatty acids to ketones.
CLINICAL PRESENTATION The onset of NNHC is much longer in duration than that of DKA. These patients will generally have a recent history of a major illness, including pneumonia, myocardial infarction, GI tract bleeding, cerebrovascular accident, or acute pancreatitis. Certain medications can also predispose patients to developing NNHC. These include phenytoin, corticosteroids, thiazide diuretics, or carbonic anhydrase inhibitors.
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Although only 10% of patients present in frank coma, most will present with some level of neurological deficit. Fifteen percent will exhibit seizure activity. The degree of altered mental status is directly correlated with increasing hyperosmolarity. Patients will also show signs of severe dehydration, including orthostatic hypotension or frank vascular collapse and tachycardia. If awake, patients may report polydipsia, polyuria, oliguria, fever, or thirst.
DIAGNOSIS A diagnosis of HHNC is made on the basis of blood glucose levels greater than 800 mg/dl, serum osmolarity greater than 350 mOsm/L, and negative serum ketones.
LABORATORY FINDINGS Initial laboratory studies should be similar to those drawn in patients with suspected DKA, including CBC and measurements of electrolytes, BUN, creatinine, serum ketones, serum osmoles, and arterial or venous blood gases. Typical findings include blood glucose level greater than 600 mg/dl and serum osmolarity greater than 350 mOsm/L. The serum BUN level will always be elevated due to severe dehydration. Although serum ketones will be absent, patients with HHNC may have a metabolic acidosis due to starvation, increased tissue lactate production, or decreased renal clearance of inorganic acids due to hypoperfusion. The electrolyte disturbances in HHNC are usually more severe than those found in DKA. The K deficit can be between 400 and 1000 mEq, causing a potentially life-threatening hypokalemia. Initial serum sodium readings will be inaccurate measurements of true serum sodium due to hyperglycemia. To approximate true serum sodium concentration, subtract 1.6 mEq/L for every 100-mg/dl increase in glucose above normal levels.
TREATMENT All patients with altered mental status should receive cardiac monitoring and supplemental oxygen. In addition, two large-bore intravenous lines should be started. The initial resuscitation steps in HHNC are similar to those of DKA. Early therapy is directed at decreasing blood glucose levels to less than 300 mg/dl, serum osmolarity to less than 350 mOsm/L, and urine output to 50 ml/hr within 36 hours. Rapid administration of normal saline is the mainstay of treatment. Once the clinical status improves, hypotonic fluids should be administered. As in DKA, correction of serum hyperosmolarity that occurs too rapidly may precipitate cerebral edema, especially in children. Approximately 50% of the
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free water deficit—as much as 8–12 L—should be replaced in the first 12 hours, with the remainder infused over the following 24 hours. In patients with known cardiac or renal failure, sterile water has been administered through a central venous line without clinically significant hemolysis. As in DKA, glucose should be added to fluids when glucose levels reach 300 mg/dl. The regimens for administration of K, Mg, HCO 3 , and insulin are similar to those undertaken in the treatment of DKA. Potassium should be replaced at a rate of 20 mEq/L of fluids. Patients should continue to receive cardiac monitoring during all electrolyte infusions. Insulin should initially be started as a continuous infusion of 0.1 U/kg/hr and titrated as glucose levels indicate. As serum glucose levels begin to normalize, subcutaneous insulin may be started. There should be an overlap between starting subcutaneous insulin and discontinuing the intravenous infusion. Phosphate administration is controversial as in DKA. No studies have shown clinical benefit in hyperglycemic states. These patients are rarely significantly academic to warrant the administration of HCO 3. The neurological status should be closely monitored in patients with HHNC. Dilantin is contraindicated for seizures in these patients because it is often ineffective and may impair endogenous insulin release. Lowdose subcutaneous heparin or enoxaparin (Lovenox) may be necessary to decrease the risk of spontaneous thrombosis due to hyperviscosity, hypotension, and associated bed rest.
DISPOSITION All patients with HHNC should be admitted to the hospital, preferably to the ICU. The mortality of treated HHNC patients is now reported to be between 8% and 25%, improved from 40%–70% in the past.
Bibliography Graffeo CS: Hyperosmolar hyperglycemic state. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Ipp E, Westhoff TL: Diabetes mellitus and the critically ill patient. In Bongard F, Sue D (eds): Current Critical Care Diagnosis and Treatment, ed 2. McGraw-Hill: Montreal, 2002. Matz R: Management of the hyperosmolar hyperglycemic syndrome, Am Fam Physician 1999;60(5):1468–1476. Stoner GD: Hyperosmolar hyperglycemic state, Am Fam Physician 2005;71(9):1723–1730.
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Hyperthyroidism and Thyroid Storm (Thyrotoxicosis) ADAM CLAY KOERTNER
ICD Code: 242.9
Key Points Hyperthyroidism can be seen in 0.5% of the adult population. At a minimum, all patients with hyperthyroidism require close follow-up due to significant risk of development of atrial fibrillation. Most patients present with signs and symptoms of sympathetic hyperactivity. Elderly patients may have a more subtle or ‘‘apathetic’’ presentation. Thyroid storm is a rare but serious complication of hyperthyroidism. It is typically precipitated by a physiological stressor such as infection, surgery, vascular events, or trauma. ! Emergency Actions ! Supportive care for hyperthyroidism and thyroid storm should be instituted immediately. Beta blockers, carefully titrated in small incremental doses, form the cornerstone of ED therapy. Precipitating factors should be aggressively sought and treated.
DEFINITION Hyperthyroidism is a condition of excessive thyroid hormones. It is typically the result of hyperactivity of the thyroid gland but may result from consumption of exogenous thyroid hormone or from accidental release of stored hormone by mechanical or inflammatory disruption of the gland. It presents as a spectrum of disease from asymptomatic to severe life-threatening illness. Thyrotoxicosis can be thought of as symptomatic hyperthyroidism. Thyroid storm refers to severe hyperthyroidism that causes cardiovascular, neurological, constitutional, and GI dysfunction. It is a clinical diagnosis based on the degree of dysfunction present in a patient with hyperthyroidism.
EPIDEMIOLOGY Hyperthyroidism occurs in the adult population with an annual incidence of 0.5%. Graves’ disease is the most common cause of hyperthyroidism, followed by thyroid adenomas and multinodular goiters. Women are affected eight times more frequently than men.
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Thyroid storm typically occurs in patients with a long-standing history of hyperthyroidism that may or may not have been previously diagnosed. Thyroid storm is usually precipitated by a physiological stressor but may result from an iodine load or medication effect. Storm occurs infrequently, complicating the clinical course of about 1% of all patients with hyperthyroidism, but it should be sought and treated because it carries up to a 20% mortality rate even with treatment.
PATHOLOGY Although the exact pathophysiology of hyperthyroidism and thyroid storm are not well understood, it is generally agreed that they represent a state of adrenergic hyperactivity accompanied by elevations of thyroid hormones and/or hypersensitivity to thyroid hormones. It is also known that catecholamine levels and catecholamine sensitivity are not altered in hyperthyroidism or storm. However, antiadrenergic therapy is effective and is the major focus of emergency treatment in thyroid storm. Atrial fibrillation is a common complication of hyperthyroidism. The incidence increases with age, and even asymptomatic patients with hyperthyroidism have a 15%–25% risk of experiencing atrial fibrillation.
CLINICAL PRESENTATION Patients may present with minimal or no symptoms and may simply have laboratory values consistent with hyperthyroidism. Patients presenting with thyroid storm typically have had uncomplicated hyperthyroidism for months or years, though they may have not yet been diagnosed with hyperthyroidism. Alternatively, patients may present with thyroid storm after significant ingestion of thyroid hormone, after thyroid trauma, or after exposure to an iodine load. A precipitating event should be aggressively sought and can usually be found. Surgery, infection, vascular events, drugs and iodinated contrast agents, DKA, trauma, and preeclampsia are well-known precipitants of storm. A typical patient with thyrotoxicosis or thyroid storm presents with symptoms such as palpitations, nervousness, weight loss despite increased caloric intake, tremor, sweating, chest or abdominal pain, and dyspnea. Clinical signs include fever, tachycardia out of proportion to the fever, atrial fibrillation, thyromegaly, widened pulse pressure, lid lag/stare, fine resting tremor, and mental status changes. Exophthalmos, pretibial myxedema, and thyroid bruit may also be present and are fairly specific for Graves’ disease.
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A subset of patients will present in an “apathetic” fashion. Apathetic thyrotoxicosis may be seen at any age but is much more common in elderly populations, making up one third of all thyrotoxicosis presentations in persons older than 70 years. It is frequently missed due to nonspecific signs and symptoms or masked due to concern for predominating symptoms such as atrial fibrillation. Lid lag and tremor are often absent but weight loss, proximal muscle weakness, and apathetic depression are typically very pronounced.
EXAMINATION The physical examination should focus on the identification of precipitating factors, with particular focus on identification of infection. The eyes should be examined for evidence of Graves’ disease. The thyroid should be palpated and the neck examined for surgical scar. The lungs should be auscultated for signs of infection or heart failure. The heart should be auscultated for arrhythmias. The back should be percussed for costovertebral angle (CVA) tenderness. The abdomen should be palpated for localized infection. The skin should be examined for evidence of cellulitis, hyperhidrosis, and edema. The neurological examination should include a check for tremor, weakness, tremor, focal neurological deficits, and evidence of CNS infection.
DIAGNOSIS Hyperthyroidism is diagnosed by a low serum TSH and/or elevated levels of free thyroid hormone. Most often free thyroxine (T4) is elevated; however, triiodothyronine (T3) thyrotoxicosis has been observed and is associated with low or normal free T4. The diagnosis of thyroid storm is based on the level of clinical dysfunction present in a patient with hyperthyroidism. Several scoring systems have been proposed but are of limited use in the emergency setting and will not affect the emergent therapy or workup. It is important to note that this is a clinical diagnosis and is in no way dependent on the numerical degree of TSH suppression or thyroid hormone elevation.
LABORATORY FINDINGS A CBC, liver function tests, chest radiograph, ECG, urinalysis with pregnancy test, and measurements of electrolytes, BUN, creatinine, glucose, cardiac enzymes, T3, T4, TSH, and serum cortisol levels should be performed for patients with suspected thyroid storm. Most laboratory abnormalities in thyroid storm are nonspecific, but the serum TSH level
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is almost always abnormal. T3 and T4 levels are typically not readily available in the ED but will be useful for guiding additional therapy and workup.
TREATMENT Hyperthyroidism in a patient with minimal or no symptoms does not require immediate medical intervention. Close outpatient follow-up is necessary due to the aforementioned risk of atrial fibrillation in these persons. Thyroid storm is a clinical diagnosis that must be recognized early and treated aggressively. Treatment is divided into five areas: (1) general supportive care, (2) inhibition of thyroid hormone synthesis and peripheral conversion, (3) retardation of thyroid hormone release, (4) blockade of peripheral thyroid hormone effects, and (5) identification and treatment of precipitating events. Treatment for thyroid storm should proceed as follows: 1. Intravenous fluid and electrolyte replacement is essential in the treatment. Treat the patient’s fever with antipyretics and active cooling as needed. Acetaminophen is preferred over aspirin because salicylates can increase free T3 and T4 levels due to disruption of protein binding of these hormones. CHF should be treated with diuretics and digitalis. Hydrocortisone at a dose of 100 mg every 8 hours should be administered at least until adrenal insufficiency is ruled out. 2. The antithyroid drugs propylthiouracil (PTU) and methimazole block the synthesis of thyroid hormone by inhibiting the organification of tyrosine residues. The full therapeutic effects of these medications are not achieved for several weeks. PTU is started with a loading dose of 600 mg PO followed by 150–200 mg PO every 4–6 hours and adjusted as necessary for control of hormone levels. Methimazole is started at 20–40 mg PO every 8 hours and again adjusted as needed. Urgent thyroidectomy is usually reserved for patients whose conditions do not improve or are worsening after 24–48 hours of aggressive treatment. Surgery should be undertaken carefully because manipulation of the thyroid gland may cause additional release of hormone and may exacerbate the condition. Removal of circulating thyroid hormone with hemofiltration, hemoperfusion, or plasma exchange has also been shown to be effective; but again, this is typically reserved for the most severe or recalcitrant cases. Peripheral conversion of thyroid hormone can be achieved with dexamethasone in a dose of 2 mg given intravenously every 6 hours. 3. Iodide (Lugol’s, SSKI, sodium iodide) decreases thyroid hormone release when used approximately 1 hour after administration of PTU or methimazole. The rationale for this treatment is that
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additional iodide, when present, can be used in thyroid hormone synthesis, if not previously blocked. Most authors recommend that iodide be administered orally in the form of 10 drops of Lugol’s solution given every 8 hours or 3–5 drops of SSKI given every 8 hours. Intravenous sodium iodide is given at a dose of 1 g every 8 hours. Radiocontrast agents such as iopanoic acid and sodium ipodate can be used to both block release and inhibit peripheral conversion of thyroid hormone. The usual dose is 0.5 g given orally every 12 hours. 4. The peripheral blockade of thyroid hormone activity is achieved by use of beta blockers and should be considered the cornerstone of ED therapy. Propranolol has historically been the beta blocker of choice, in part due to its ability to decrease peripheral conversion of thyroid hormone. This effect, however, is modest in comparison to other available modalities and should be given little, if any, consideration in selecting appropriate beta blockade. Specific beta1 antagonists such as atenolol, metoprolol, or esmolol may be used in cases where reactive airways are a concern. Propranolol is administered at a dose of 1–2 mg given intravenously every 10 minutes and titrated to effect to a maximum of 10 mg. This may be repeated every 4–6 hours, or oral therapy may be initiated at 20 mg PO every 6 hours and titrated to effect. Other beta blockers are dosed and titrated in the usual fashion. Diltiazem given at 0.25–0.35 mg/kg in an intravenous bolus followed by oral therapy or infusion is an alternative for those who cannot take beta blockers. Although complete oral therapy with beta blockers or diltiazem is acceptable, initiating therapy via the intravenous route followed by oral maintenance is typical and prudent in the case of thyroid storm. 5. Precipitating events should be thoroughly sought and treated. This includes collection of appropriate cultures followed by broad-spectrum antibiotic therapy targeting the most likely sources of infection, especially pulmonary and urinary pathogens. Trauma, vascular events, and DKA should be aggressively managed in the usual fashion.
Bibliography Burch H, Wartofsky L: Life-threatening thyrotoxicosis, Thyrotoxic storm, Endocrinol Metab Clin North Am 1993;2:263–277. Floyd JL: eMedicine (website): Thyrotoxicosis. Available at: http://www.emedicine.com/ radio/topic315.htm. Madhusmita M, Singhal A, Campbell, DE: eMedicine (website): Thyroid storm. Available at: http://www.emedicine.com/ped/topic2247.htm. Mohandas M, Gupta KL: Managing thyroid dysfunction in the elderly, Postgrad Med 2003;113(5):54–68100. Available at: http://www.postgradmed.com/issues/2003/05_03/ mohandas1.htm.
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Thyroid disorders. The Merck Manual of Diagnosis and Therapy. Merck 2005. Available at:http://www.merck.com/mrkshared/mmanual/section2/chapter8/8a.jsp. Wogan J: Selected endocrine disorders: hyperthyroidism. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1770–1774.
Hypoglycemia SHAWN M.VARNEY
ICD Code: 251.2
Key Points/Quick Reference Hypoglycemia (i.e., low blood sugar) leads to symptoms of CNS depression and reflex sympathetic nervous system stimulation. Patients with diabetes mellitus are most commonly affected, although hypoglycemia may result from multiple causes. ! Emergency Actions ! A rapid finger-stick glucose level should be checked. Symptomatic adult patients should be given oral glucose if they are protecting the airway and tolerating oral intake; alternatively, 1 ampule of 50% dextrose should be administered intravenously. The healthcare provider should look for a medical alert bracelet.
DEFINITION Hypoglycemia is defined as a serum glucose level of less than 50 mg/dl in adults and 40 mg/dl in children and neonates. Alternatively, hypoglycemia may be defined as a drop in serum glucose with concomitant symptoms and signs (altered mental status or sympathomimetic manifestations). Clinically, hypoglycemia may be diagnosed and defined by three key features known as Whipple’s triad: (1) symptoms of hypoglycemia, (2) a low serum glucose level, and (3) symptomatic relief after receiving glucose. The CNS uses glucose as its primary energy source but can function on ketones during periods of fasting or starvation.
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Organs that produce bioactive agents to maintain glucose control include the pancreas (insulin, glucagon), liver, adrenal glands (glucocorticoids, catecholamines), and pituitary gland (growth hormone). Glucose homeostasis (i.e., preventing hypoglycemia) is controlled by balancing glycogenolysis (i.e., glycogen metabolism) in the immediate postprandial period with gluconeogenesis (i.e., creating glucose from the breakdown of muscle) several hours after meals. In response to hyperglycemia, insulin stores glucose in the liver as glycogen (the major source of stored fuels), inhibits glycogenolysis and gluconeogenesis, and decreases lipogenesis (i.e., fat deposition). Glucagon has the opposite effect and releases glucose from the liver by glycogenolysis when serum levels are depleted. Cortisol and glucagon mediate proteolysis (protein breakdown for gluconeogenesis). Triglycerides serve as the major source of glucose from stored fat tissue. Lipolysis results from low insulin levels along with the presence of growth hormone and epinephrine.
EPIDEMIOLOGY A 2003 Centers for Disease Control and Prevention report stated that 13.8 million Americans had diabetes mellitus. Diabetes mellitus and diabetic medications account for most hypoglycemic episodes, especially when patients maintain tight glucose control. Up to 25% of diabetics experience hypoglycemia regularly. Approximately 7% of ED patients with altered mental status have hypoglycemia. Hypoglycemia is found predominantly in persons with diabetes, older adults, and women. Diseases such as diabetes mellitus and liver disease, along with toxic ingestions, sepsis, and iatrogenic interventions, interfere with glucose homeostasis and may lead to adverse events.
CLINICAL PRESENTATION Patients with hypoglycemia present with a spectrum of findings from vague light-headedness to coma. Symptoms of hypoglycemia reflect the rapidity of onset; patients with precipitous hypoglycemia usually have a more prominent adrenergic response. Sympathetic symptoms and signs include pallor, tremulousness, diaphoresis, palpitations, tachycardia, weakness, and light-headedness. CNS manifestations present as headache, fatigue, vision disturbances, confusion, disorientation, memory loss, depression, altered mental status, focal neurological deficits, catatonia, seizures, and coma. Neuroglycopenic CNS effects may be irreversible if hypoglycemia is unrecognized and untreated. Hypoglycemia commonly results from diabetes. However, hypoglycemia may arise from decreased caloric intake, increased energy
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expenditure, excess insulin or oral hypoglycemic medication, drug interaction, infection, or idiopathic causes. The differential diagnosis also includes medical disorders such as pancreatic tumors (e.g., insulinomas), large tumors (e.g., mesenchymal, epithelial, or endothelial), liver disease, pregnancy, adrenal insufficiency, hypopituitarism, and factitious disorders. A patient with early diabetes can experience hypoglycemia 3–5 hours after a meal with typical adrenergic and CNS manifestations. The initial episode lasts 15–20 minutes and may be the first sign of non–insulindependent diabetes mellitus. Fasting hypoglycemia is common and often forebodes serious underlying organic disease. It occurs 5–6 hours after the last meal, and the patient is difficult to arouse after a 24-hour or overnight fast. A patient with idiopathic hypoglycemia can present 2–4 hours after a meal or after change in meal times. A patient with an insulinoma (from an islet cell tumor of the pancreas) will present with confusion or abnormal behavior 80% of the time. The tumor is usually a single small tumor. Ten percent of patients present with multiple tumors or multiple endocrine neoplasia type I, and 10% present with metastatic malignant insulinomas. Insulinomas usually present in women aged 40–70 years and cause palpitations, sweating, weakness, blurred vision, and diplopia. Presenting symptoms include confusion, seizures, and amnesia or coma. Symptoms are episodic, irregular, often induced by exercise, and generally occur in the late afternoon or early morning before breakfast. These patients are often misdiagnosed before the insulinoma is found. Treatment involves excision of the tumor. Mesenchymal tumors are the most common nonpancreatic tumors that cause hypoglycemia and often present in the thoracic or retroperitoneal areas (usually fibrosarcomas or mesotheliomas). The tumors grow very slowly and can weigh more than 20 kg. Presenting symptoms include weight loss, CNS depression, and intrathoracic or intraabdominal masses. Epithelial tumors of the liver and adrenal glands may cause hypoglycemia. Hepatic carcinomas are present in a 4:1 ratio of men to women. Carcinoid tumors are slow-growing tumors that develop from the amine precursor uptake and decarboxylation series and develop from various locations. They consist of a variety of active biological substances. When 80%–85% of liver function is impaired, gluconeogenesis and glycogenolysis are hindered, leading to hypoglycemia. The HELLP syndrome (i.e., hemolysis, elevated liver enzyme levels, and low platelet count) in preeclampsia or pregnancy can cause hypoglycemia. In children, kwashiorkor, meningitis, or sepsis can cause hypoglycemia. Many endocrine disorders cause hypoglycemia, emphasizing the role of hormones and steroids in the metabolism of carbohydrates and
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proteins. Deficiencies in growth hormone, glucagon, and glucocorticoids can all produce hypoglycemia. Both primary and secondary adrenal insufficiency can cause hypoglycemia. Hypopituitarism can also lead to hypoglycemia by inducing secondary adrenal insufficiency, a deficiency in growth hormone and glucocorticoid. Furthermore, severe thyroid hormone deficiency can result in myxedema coma and hypoglycemia. Induced hypoglycemia usually results from ingestion of salicylates, alcohol, sulfonylureas, or insulin. In children younger than 2 years of age, hypoglycemia is usually due to an acute drug intoxication of a sulfonylurea. In adults, hypoglycemia-induced coma results from intoxication or adverse drug events related to insulin and sulfonylureas (prolonged half-life). Renal or hepatic disease and restricted carbohydrate intake are predisposing factors for hypoglycemia. Renal disease decreases the clearance of insulin and sulfonylureas, and hepatic disease decreases metabolism of sulfonylureas and insulin. In a patient with insulin-dependent diabetes, causes of hypoglycemia include late or absent meals, emotional stress, exercise, low carbohydrate intake, alcohol ingestion, or dosing errors in diabetic medications. Rarely, patients with insulin-dependent diabetes may develop the Somogyi phenomenon in which nocturnal hypoglycemia may lead to rebound morning hyperglycemia, mistakenly attributed to insufficient insulin therapy. Increasing the nighttime insulin dose exacerbates the problem. Both diabetics and nondiabetics can experience a “dawn phenomenon.” Serum glucose levels rise between 5:00 AM and 9:00 AM to provide energy to start the day. Occasionally, the syndrome results in hyperglycemia, insulin release, and resultant hypoglycemia. Distinguishing between the dawn phenomenon and Somogyi syndrome is important because the treatment differs—administering a neutral protamine hagedorn (NPH) insulin dose later in the evening or decreasing the insulin dose is appropriate for the Somogyi phenomenon, in contrast to increasing the dose of insulin to prevent early morning hyperglycemia and rebound hypoglycemia with the “dawn phenomenon.” Sulfonylureas are the most common medications that cause hypoglycemia. These agents stimulate the release of insulin from the pancreas. Chlorpropamide, a first-generation sulfonylurea, has a very long halflife (36 hours) and duration of effect. Glipizide and glyburide are commonly associated with hypoglycemia. Any patient with a sulfonylurea intoxication or hypoglycemia from a sulfonylurea should be admitted to the hospital. Not only can hypoglycemia be delayed after intoxication, but it may persist for 12–24 hours after ingestion. Ethanol intoxication can also cause hypoglycemia, especially in young children and malnourished adults who typically have low glycogen stores. Salicylate intoxication can rarely cause hypoglycemia. Beta blockers can mask the cardinal sympathetic response (e.g., tachycardia, nervousness,
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shakiness) from hypoglycemia. Infants and children with hypoglycemia may present with increased irritability, convulsions, abnormal crying, bradycardia, apnea, limpness, or coma. Many other medications can induce hypoglycemia; thus, a history of chronic or acute medication use should be noted.
EXAMINATION The vital signs often demonstrate the autonomic manifestations of hypoglycemia such as hypertension, tachycardia (bradycardia in neonates), tachypnea, and hypothermia. Although physical findings are usually nonspecific, a complete examination emphasizing the neurological components should be performed. Up to 5% of patients with hypoglycemia may present with focal neurological deficits, mimicking an ischemic or hemorrhagic cerebrovascular accident. The practitioner should look for signs of other causes of altered mental status like photophobia, meningismus, confusion, and fever signaling meningitis. He or she should search for clinical signs of intracranial hemorrhage from trauma (e.g., altered mental status, focal neurological deficits, and abnormal breathing patterns), sepsis (e.g., warm skin, diaphoretic, hypotension, and altered mental status), and hypothyroidism/myxedema coma (e.g., nonpitting edema, ataxia, prolonged deep tendon reflexes, depressed mental status, and cool, dry, waxy skin).
LABORATORY FINDINGS The blood glucose level should be measured. Whole blood glucose levels are 15% lower than serum glucose levels because of the relatively low glucose levels in RBCs. Therefore, a serum glucose level should be obtained for comparison if the whole blood level does not correlate with the clinical presentation. BUN, creatinine, and electrolytes should be measured to rule out metabolic causes of altered mental status and to assess for ability to eliminate insulin. If the patient’s presentation suggests sepsis, the practitioner should consider a CBC, blood cultures, urinalysis, chest x-ray, and lumbar puncture. Hepatic enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), gammaglutamyl transferase (GGT) may be useful. Cortisol and thyroid tests can be used to diagnose endocrine causes of hypoglycemia. Acetaminophen and salicylate levels should be obtained in acute intoxication. Pseudohypoglycemia may occur when the leukocyte count is elevated over 60,000 mm3, in leukemia, in refrigerated blood samples, and with the addition of antiglycolytic agents (e.g., sodium fluoride) in blood products. Adults with alcohol-induced hypoglycemia present
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with an elevated blood alcohol level, mild acidosis, and ketonuria without glycosuria. Self-induced hypoglycemia with exogenous insulin can be detected by low C-peptide levels. C-peptide is the terminal portion of the endogenous proinsulin molecule that is absent in exogenous insulin.
DIAGNOSIS A diagnosis of hypoglycemia is made on the basis of a rapid Dextrostix test or when the serum glucose level is measured to be below 50 mg/dl. The patient should be questioned about a history of insulin- or non– insulin-dependent diabetes, ethanol use, ingestion of sulfonylurea, injection of insulin, or use of other diabetic medications.
TREATMENT AND OUTCOME The initial assessment should include an evaluation of the patient’s airway, breathing, and circulation. For an unstable patient, the healthcare provider should establish a “safety net” of oxygen, intravenous access with 0.9% saline, cardiac monitor, and vital signs. Hypoglycemia should always be considered in any patient with altered mental status or coma. A D-stick blood glucose level should be obtained. If the patient is hypoglycemic, 1 ampule of D50W (50 ml of 50% dextrose, or 25 g) should be administered in the adult. For pediatric patients, a 3-ml/kg altered mental status or intraosseous bolus of D10W should be administered. To maintain euglycemia, a continuous infusion of D10W should be given in 0.45% normal saline at weight-appropriate doses. As always, cervical spine immobilization is imperative in patients with altered mental status and possible trauma or fall. If the patient has a history of alcohol ingestion or abuse, the altered mental status should not be attributed solely to alcohol or hypoglycemia. Persons with alcoholism may be intoxicated but may also develop hypoglycemia, fall, and sustain intracranial trauma. Evaluation for a possible intracranial hemorrhage (e.g., subdural hematoma, traumatic subarachnoid hemorrhage, or intraparenchymal bleed) with a noncontrast head CT scan should be considered for these patients. Patients with a sulfonylurea intoxication have prolonged hypoglycemia due to the drug’s prolonged duration of effect. The practitioner should not rely solely on boluses of D50W in a patient with a functioning pancreas. The repeated boluses work briefly but are followed by rebound hypoglycemia from insulin release. Historically, diazoxide 3–8 mg/kg/day divided every 8–12 hours, maximum dose 10–15 mg/ kg/day has been used, but it can cause hypotension. The treatment of choice for refractory hypoglycemia is octreotide, a somatostatin analog. Octreotide suppresses insulin secretion resulting from the sulfonylurea
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and the dextrose therapy. One method of administration is a 1-mg/kg bolus given intravenously or subcutaneously followed by 1 mg/kg every 8–12 hours. Consultation with a poison center or medical toxicologist is recommended. These patients must be admitted to a critical care setting for serial glucose measurements. Eating will help attenuate hypoglycemia. If the patient is awake and protecting his or her airway, eating a meal may be helpful. However, this should not supplant exogenous glucose. If hypoglycemia persists, an infusion of a 5%, 10%, or 20% glucose solution should be administered until glucose levels normalize or are at least 100 mg/dl. The higher-concentration glucose solutions are hyperosmolar and should be placed through a central line to prevent sclerosing of the peripheral vein. After the infusion is turned off, glucose levels should be checked for 8–12 hours for recrudescence of hypoglycemia. If a patient still has hypoglycemia after 1 liter of glucose solution has been given, 100 mg of hydrocortisone and 1 mg of glucagon should be added to each liter of D5W or D10W solution. Glucagon can be given intravenously or subcutaneously in a dose of 0.5–2 mg. If glucagon is given intravenously, it should be given as a continuous infusion due to its short half-life.
Bibliography Banarer S, Cryer PE: Hypoglycemia in type 2 diabetes, Med Clin North Am 2004; 88(4):1107–1116, xii–xiii. Brady WJ, Harrigan RA: Hypoglycemia. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1283–1287. Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion. National diabetes surveillance system Updated May 10, 2005. Available at: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed May 29, 2005. Cooperman M: Somogyi phenomenon. Updated June 3, 2004. Available at: http://www. emedicine.com/med/topic2098.htm. Accessed May 27, 2005. Cranmer H, Shannon M: Pediatric hypoglycemia. Updated March 15, 2005. Available at: http://www.emedicine.com/emerg/topic384.htm. Accessed May 27, 2005. Octreotide for refractory hypoglycemia. Updated July 9, 2003. Available at: http://www. emedhome.com. Accessed May 27, 2005. Smeeks F: Hypoglycemia. Updated April 27, 2005. Available at: http://www.emedicine. com/emerg/topic272.htm. Accessed May 27, 2005. Stryer L: Integration of metabolism. In Stryer L (ed): Biochemistry, ed 3. W.H. Freeman: New York, 1988, pp 634–635. Young G: Hypoglycemia. In Harwood-Nuss A (ed): The Clinical Practice of Emergency Medicine, ed 2. Lippincott-Raven: Philadelphia, 1996, pp 732–734.
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Hypothyroidism and Myxedema Coma ADAM CLAY KOERTNER
ICD Code: 244.9
Key Points/Quick Reference Hypothyroidism is a common condition that causes slowing of the body’s physiological processes. Myxedema coma is a clinical diagnosis defined by significant mental status, respiratory, and cardiovascular abnormalities. Myxedema coma is typically precipitated by physiological stressors in a patient with hypothyroidism. ! Emergency Actions ! Uncomplicated hypothyroidism can typically be managed with close outpatient follow-up. Myxedema coma is a potentially fatal condition requiring immediate institution of supportive therapy and thyroid hormone replacement. All patients being treated for myxedema coma should receive stress-dose hydrocortisone until concomitant adrenal insufficiency has been ruled out. Precipitating conditions should be aggressively sought and treated.
DEFINITION Hypothyroidism is a condition in which the thyroid gland fails to produce enough thyroid hormone. It exists as a spectrum of disease ranging from subclinical with abnormal laboratory values to myxedema coma. Symptoms of hypothyroidism are attributable to generalized slowing of the body’s physiological processes. Myxedema coma is a life-threatening manifestation of hypothyroidism that is characterized by altered mental status, hypoventilation, and hypothermia. Myxedema coma is a clinical diagnosis in a patient with hypothyroidism based on the severity of symptoms and is not dependent on the degree of abnormality on thyroid function test results. It is typically precipitated by an inciting event such as infection, trauma, surgery, vascular thromboembolic disease, or certain medications such as amiodarone, lithium, and iodinated radiocontrast agents.
EPIDEMIOLOGY The exact incidence of hypothyroidism is unknown. Epidemiological studies have found rates of 2%–10% in adult populations. Hypothyroidism
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becomes more prevalent with increasing age, and women are affected 3–10 times more frequently than men. The increased frequency in women is thought to be related to the generally increased rate of autoimmune disease in this group.
PATHOLOGY Normal thyroid function is regulated via the hypothalamic-pituitarythyroid axis. The hypothalamus detects the level of circulating thyroid hormones and releases an inverse quantity of thyrotropin-releasing hormone. Thyrotropin-releasing hormone stimulates the anterior pituitary gland to release TSH. TSH triggers the release of the thyroid hormones T4 and T3 from the thyroid gland, which thus closes the feedback loop and maintains euthyroidism. The primary failure of the thyroid gland is by far the most frequent cause of hypothyroidism. Worldwide, hypothyroidism is most commonly caused by iodine deficiency. In the United States, the most common cause is autoimmune destruction of the thyroid gland, a condition known as Hashimoto’s thyroiditis. Long-standing Graves’ disease may cause hypothyroidism through eventual “burn-out” of the hyperactive thyroid gland. More commonly, treatment for Graves’ disease with medications, radioiodine, or surgery may cause hypothyroidism. Secondary hypothyroidism results from pituitary failure to provide TSH to stimulate the thyroid gland. Pituitary failure may come as the result of vascular compromise, pituitary tumor growth, or infiltrative/destructive processes such as sarcoidosis, hemachromatosis, and Wilson’s disease.
CLINICAL PRESENTATION AND EXAMINATION Clinically hypothyroid patients present with symptoms such as paresthesias, menstrual irregularities, physical and mental fatigue, cold intolerance, weakness, constipation, and weight gain. A physical examination finding of hypothyroidism is deep-tendon reflexes with a prolonged relaxation phase (i.e., pseudomyotonic reflexes), hypothermia, facial puffiness, hoarse voice, enlarged tongue, dry skin with dependent edema, and hair loss at the eyebrows and axillary and pubic regions. The neck should be examined for evidence of a surgical scar or thyroid goiter. The chest radiograph may show an enlarged cardiac silhouette and possibly evidence of CHF. The ECG may demonstrate sinus bradycardia with T-wave flattening or inversion and PR-interval prolongation.
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Patients with myxedema coma often have hypoventilation, hypotension, and mental status changes along with signs and symptoms of hypothyroidism. Mental status changes may range from cognitive slowing to hallucinations and frank psychosis. History and physical examination evidence of infection or other precipitating factors should be sought aggressively.
DIAGNOSIS Hypothyroidism is diagnosed on the basis of clinical presentation and TSH with or without free T4. Myxedema coma remains a clinical diagnosis in a patient with hypothyroidism.
LABORATORY FINDINGS Samples for a CBC, blood and urine cultures, urinalysis, and measurements of electrolytes, BUN, creatinine, cortisol level, cardiac enzymes, and TSH should be drawn. Patients with an abnormal TSH level and/or myxedema coma should have a sample drawn for free T4, as well.
TREATMENT The treatment of hypothyroidism and myxedema coma involves hormone replacement. Cases of hypothyroidism not requiring hospitalization do not necessarily require ED treatment as long as adequate follow-up is ensured. If treatment is initiated from the ED, a low dose of liothyronine (T3) 12.5–25 mg/day PO should be started. More severe cases, requiring hospitalization, will require substantial doses of thyroid hormone. The most severe cases (i.e., myxedema coma) will require ICU admission and possibly mechanical ventilation. Levothyroxine (T4) is administered at a loading dose of 500 mg IV or PO followed by 100 mg/day. T3 (12.5–25 mg every 6–8 hours) may be used in place of or in addition to levothyroxine. However, because this medication is much more arrhythmogenic and allows for no autoregulation, its use should be directed by an experienced endocrinologist. The clinical condition should be monitored closely, and the minimal effective dose of T4 and/or T3 should be used to prevent complications such as cardiac ischemia or tachydysrhythmia. The mental status changes observed in myxedema coma may be exacerbated by hypoventilation because both hypoxic and hypercapnia respiratory drive are suppressed. Hypoglycemia may be observed in severe hypothyroidism. It is usually mild and is reversed by administration of D5W solution. Hyponatremia is frequently seen in myxedema coma. Most authors believe it is due to SIADH. It is typically mild
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and responsive to fluid restriction. More severe hyponatremia may require hypertonic saline therapy. Hypotension requiring vasopressor therapy may be present. It will often be resistant to pressors until thyroid hormone is administered. Hydrocortisone (100 mg intravenous every 8 hours) should be given at least until adrenal insufficiency is ruled out. Initiating thyroid hormone replacement therapy without hydrocortisone will cause adrenal crisis and subsequent cardiovascular collapse in susceptible persons. Hypothermia should be corrected, preferably with passive external rewarming. Active core rewarming may have utility but has not been adequately studied. Active external rewarming may cause peripheral vasodilation and cardiovascular collapse. Precipitating events such as infection and CHF should be sought and aggressively treated. Broad-spectrum antibiotics—particularly covering pulmonary and urinary pathogens—should be administered after appropriate culture specimens are obtained. CHF should be treated in the usual fashion.
Bibliography Mohandas M, Gupta KL: Managing thyroid dysfunction in the elderly, Postgrad Med 2003;113(5):54–68, 100. Available at: http://www.postgradmed.com/issues/2003/05_03/ mohandas1.htm. Orlander PR: Hypothyroidism. Available at: http://www.emedicine.com/MED/topic1145. htm. Schraga ED, Manifold CA: Hypothyroidism and myxedema coma. Available at: http:// www.emedicine.com/EMERG/topic280.htm. Thyroid disorders, The Merck Manual of Diagnosis and Therapy. Merck: 2005. Available at: http://www.merck.com/mrkshared/mmanual/section2/chapter8/8a.jsp. Wall CR: Myxedema coma: Diagnosis and treatment, Am Fam Physician 2000; 62(11):2485–2490. Available at: http://www.aafp.org/afp/20001201/2485.html. Wogan J: Selected endocrine disorders: Hypothyroidism. In Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1774–1779.
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Lactic Acidosis TERRY EMANUEL
ICD Code: 276.2
Key Points Lactic acid is a by-product of glucose metabolism. Hypoxia is the leading cause of lactic acidosis. ! Emergency Actions ! The goal of treatment is reversal of the underlying condition causing the acidosis.
EPIDEMIOLOGY Lactic acidosis is common among critically ill patients and is the most common from of metabolic acidosis. The 6-month mortality rate of critically ill patients with a blood lactate level greater than 5 mmol and arterial pH less than 7.35 is 75%.
DEFINITION Lactic acid is a by-product of glucose metabolism. Glucose is the food that drives energy production. Demands for energy increase with anything that causes an increase in basal metabolism: exercise, infection, disease, or toxins. Glucose is broken down into pyruvate and the pyruvate is further broken via aerobic and anaerobic pathways. Both take place simultaneously, and under normal circumstances a tremendous amount of lactate is created on a daily basis—15–25 mEq/kg/day, or roughly 1400 mEq/day for a 70-kg man. Oxygen debt does not allow for the breakdown of pyruvate within the mitochondria in an aerobic manner, and there is a subsequent increase in pyruvate in the cytosol. This pyruvate is converted into lactic acid. Lactic acid is therefore a by-product of energy production in the anaerobic state. Anything that upsets oxygen delivery to the cells upsets this fine balance because the aerobic pathway for pyruvate does not yield lactic acid. The same is true for any process that directly increases production or decreases uptake of lactic acid or reduces the amount of available HCO 3 , the primary buffer that converts lactic acid to lactate. Lactic
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acidosis consequently leads to an increased anion gap. Lactic acidosis results when the body’s buffer systems are overwhelmed. This most often occurs when tissue oxygenation is inadequate either because of hypoperfusion or hypoxia. Hypoxia is far and away the leading cause of lactic acidosis. In the liver lactate is metabolized back to pyruvate, which is then converted into either CO2 and water or glucose. Both of these processes result in the regeneration of the HCO 3 lost in the initial buffering of lactic acid. This balancing act, which incorporates the breakdown of glucose (i.e., glycolysis) and the buildup of glucose (i.e., gluconeogenesis) under normal circumstances, leaves the serum lactate levels at approximately 1–2 mEq/L. The muscles, brain, skin, and RBCs produce most of the lactate in the body. In turn, lactate is extracted predominantly by the liver and, to a lesser extent, by the kidney. In hypoxic states, almost all tissues can release lactate. Even the liver can be converted into a producer of lactate. Historical classifications divide the types of lactic acidosis into two types: A (associated with clinical evidence of poor tissue perfusion) and B, which has three subtypes (Table 8-4). These classifications have a great deal of overlap and have given way to more recent classification
Table 8-4 Two Types of Lactic Acidosis TYPE A IMPAIRED TISSUE OXYGENATION Impaired tissue oxygenation Shock Severe hypoxemia Generalized convulsions Vigorous exercise Exertional heat stroke Hypothermic shivering Massive pulmonary emboli Severe heart failure
TYPE B DISEASES AND CONDITIONS Thiamine deficiency Alkaloses Renal failure Hepatic failure Severe infections Pheochromocytoma Mesenteric ischemia Iron deficiency D-lactic acidosis Congenital enzyme deficiency Profound anemia Unknown Causes Malignancies Diabetes mellitus AIDS Hypoglycemia Idiopathic
DRUGS AND TOXINS Epinephrine Norepinephrine Salicylates Ethanol Methanol Ethylene glycol Biguanides Fructose, sorbitol Nitroprusside Streptozotocin Isoniazid Zidovudine Papaverine Cyanide poisoning Acetaminophen Carbon monoxide Nalidixic acid
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systems that divide lactic acidosis into hypoxic nonhypoxic types and those resulting from increased production or decreased clearance. The findings of systemic hypoperfusion are not apparent in type B lactic acidosis. Among the mechanisms that may be involved is a toxin-induced impairment of cellular metabolism or regional areas of ischemia. D-Lactic acidosis is a form of lactic acidosis that occurs in patients with short bowel syndrome, usually from jejunoileal bypass. Glucose and starch are usually metabolized in the small bowel but in the setting of short bowel syndrome are passed on to the colon where they are metabolized in part into D-lactic acid. D-lactate is not recognized by L-lactate dehydrogenase, the catalyst for the conversion of L-lactate back into pyruvate. So, D-lactic acidosis will persist much longer than A or B types. Furthermore, carbohydrate loading in these patients may result in CNS disturbances, chiefly altered mental status, slurred speech, ataxia, and weakness.
TREATMENT Bicarbonate Therapy in Cardiopulmonary Resuscitation Intuitively, one might think that the infusion of sodium bicarbonate would provide a remedy for the body’s overwhelmed buffering systems. However, sodium bicarbonate therapy can lead to a variety of problems in patients with lactic acidosis, including volume overload, a postrecovery metabolic alkalosis (as the excess lactate is converted back to HCO 3 ), and hypernatremia (because sodium bicarbonate is the standard form of delivery). The CO2 by-product of alkali therapy may slow the respiratory rate as well. For these reasons, bicarbonate should generally not be used in cardiopulmonary resuscitation. It is possible that the rise in PCO2 may then exacerbate the intracellular acidosis, leading to impairment in both hepatic lactate use and cardiac contractility. Severe metabolic acidosis with an arterial pH of less than 7.20 is associated with impaired cardiac contractility that in turn exacerbates hypoperfusion. Also, elevated serum lactate depresses contractility independent of pH. Acidosis also causes an altered response to exogenous catecholamines. There is at present no evidence that alkali therapy is beneficial during cardiopulmonary resuscitation. The administration of HCO 3 can also prevent an improvement in cardiac function by inducing a fall in the plasma ionized (unbound) Ca concentration due to increased protein binding, because Ca is required for normal cardiac contractility. However, cautious administration of Ca may become necessary in some patients.
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Treatment with Bicarbonate Therapy in Septic Shock The reversible reaction that demonstrates CO2 as a by-product of alkali therapy is as follows: þ CO2 þ H2 O > HCO 3 þH
Initial studies of patients with septic shock lactic acidosis have not shown any benefit with the acute delivery of alkali treatment. There is a difference in the pH and PCO2 in mixed venous and arterial blood in the face of septic shock acidosis, suggesting that mixed venous pH and PCO2 is more reflective of the oxygen deficiencies that exist at the cellular level. Although cardiac output is generally higher in sepsis, for a variety of reasons output is still not meeting tissue demands. There is, however, no evidence that sodium bicarbonate improves hemodynamics in this setting. In healthy animal subjects, a markedly increased load of exogenous lactic acid is readily tolerated, and pH remains in the normal range.
SUMMARY The appropriate use of HCO 3 therapy in hypoperfusion or hypoxic states resulting in lactic acidosis is unclear. The goal of treatment is reversal of the underlying condition causing the acidosis. Treatment with sodium bicarbonate is marginally indicated, only for acute control of the acidemia, and probably only in a patient who is breathing well or ventilated at an increased rate. The use of sodium bicarbonate, if it results in an increase in intracellular pH, may increase the rate of recovery by inducing better myocardial contractility (oxygenation and perfusion), normalizing ionized Ca levels, and increasing the response to catecholamines. Most physicians would limit the use of sodium bicarbonate to patients with severe metabolic acidemia (i.e., arterial pH <7.10–7.15), with the aim being to maintain the pH above 7.15 until the primary process can be reversed. Because alkali therapy is limited and no alternatives to HCO 3 therapy as yet have been found to be efficacious, treatment revolves around treating the underlying process. This means restoring cardiovascular integrity, treating disease, eliminating drugs that can induce acidosis, and treating infection aggressively.
Bibliography Adrogue H, Madias N: Disorders of acid–base balance. In Schrier RW (ed): Atlas of Diseases of the Kidney. Vol 1, Current Medicine: Philadelphia, 1998, pp 6.12–6.13.
414 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Borron SW, Maegarbane B: Lactic acidosis. 2005. E-medicine. Rose BD, Post TW, Narins RG: Causes of lactic acidosis. 2005. Uptodate. Tintinalli JE, Kelen GD, Staphczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw Hill: New York, 2004.
Rhabdomyolysis CHRIS R. MCNEIL
ICD Code: 728.88
Key Points It is estimated that up to 33% of patients with rhabdomyolysis will develop acute renal failure. ! Emergency Actions ! The most important therapy for rhabdomyolysis is aggressive intravenous fluid administration to prevent renal failure.
DEFINITION Rhabdomyolysis is a condition caused by injury to skeletal muscles. Damage to the sarcolemma results in loss of its intrinsic function, an influx of Ca, activation of intracellular proteases, and release of intracellular contents into the circulation. These contents include myoglobin, creatine phosphokinase, aldolase, lactate dehydrogenase, aspartate transaminase, and K. The complications of rhabdomyolysis include acute renal failure, metabolic abnormalities, and DIC. Common causes include trauma, prolonged exertion, hyperthermia, infections, electrolyte abnormalities, electrical current injury, drugs or toxins, and conditions that cause tissue hypoxia.
EPIDEMIOLOGY The cause of rhabdomyolysis is determined on the basis of an accurate patient history and evaluation of laboratory values. It is estimated that up to 33% of patients with rhabdomyolysis will develop acute renal failure.
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CLINICAL PRESENTATION Patients with rhabdomyolysis may present with a variety of chief symptoms, trauma, hyperthermia, drug overdose, and febrile illness. Symptoms are generally acute in onset and include muscle weakness, muscle tenderness, stiffness, muscle swelling or discoloration, low-grade fever, and dark urine. Acute rhabdomyolysis may also present without any of these signs or symptoms, and the diagnosis may seem elusive. Patients may develop four general types of complications related to acute rhabdomyolysis: 1. Acute renal failure: The main complication of rhabdomyolysis is acute renal failure. Renal failure results from decreased urine output, acidosis, tubular obstruction, and the direct nephrotoxic effects of myoglobin. Neither the presence of myoglobinuria nor the degree of creatine phosphokinase (CK) elevation is predictive of which patients are at risk for developing acute renal failure. 2. Compartment syndrome: Ischemic changes take place within a few hours and may lead to increased compartmental pressures. The swelling and increased pressure may not be present until after aggressive intravenous fluids have been administered. Typical symptoms include pain, paresthesias, paralysis, pallor, and pulselessness. If the compartmental pressure exceeds 30–35 mmHg, consultation with an orthopedic specialist and fasciotomy should be considered. 3. DIC: A patient with DIC will have evidence of thrombocytopenia, prolonged PT, increased fibrin split products, and hypofibrinogenemia. DIC usually resolves spontaneously over several days. Specific treatment depends on whether hemorrhagic or thrombotic manifestations are present. 4. Metabolic abnormalities: Hypocalcemia is the most common electrolyte abnormality. It may be due to Ca deposition in necrotic muscle tissue. Hyperkalemia, hypophosphatemia, and hyperuricemia are also common.
EXAMINATION The patient should be given a complete physical examination. All extremities need to be examined for evidence of compartment syndrome.
LABORATORY FINDINGS A CBC, urinalysis, chemistry panel, coagulation panel, liver function tests, and measurements of creatine phosphokinase, myoglobin, and lactate dehydrogenase should be performed on all patients. A urine drug screen may also be helpful.
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Myoglobin: Serum and urine myoglobin levels may be elevated. Myoglobin is rapidly cleared by the kidneys and may be completely resolved in as little as 6 hours. The absence of serum or urine myoglobin does not exclude the diagnosis of rhabdomyolysis. Urine: A urine dipstick test may be helpful in the diagnosis of rhabdomyolysis. Myoglobin contains heme and enters the urine when the plasma concentration exceeds 1.5 mg/dl. The dipstick does not differentiate between blood and myoglobinuria. Therefore, myoglobinuria should be suspected when the urine dipstick test result is positive for blood but no RBCs are present on microscopic examination. CK: The serum CK level is more sensitive in the diagnosis of rhabdomyolysis. A patient is considered to have rhabdomyolysis if the serum CK level is five times the normal value. The serum CK peaks in 24–72 hours and declines at a relatively constant rate of 39% of the previous day’s value. Hypocalcemia: This is the most common electrolyte abnormality and results from deposition in necrotic tissue. Correction of serum Ca levels is rarely needed and may promote further cellular injury. Hyperkalemia: This results from myonecrosis and leakage of intracellular K into the circulation. Hyperkalemia may be compounded if any evidence of acute renal failure is present. Hypophosphatemia: Critically low serum phosphate levels seen in malnourished patients and persons with chronic alcoholism may instigate rhabdomyolysis. Phosphate is used in ATP as well as 2,3-DPG, which causes RBCs to unload oxygen to tissues. Hyperphosphatemia: Hyperphosphatemia may be present and results from leakage from injured muscle.
DIAGNOSIS A diagnosis of rhabdomyolysis is made by obtaining an accurate patient history, performing a thorough physical examination, and obtaining a proper laboratory evaluation. An elevated CK level is the most sensitive and reliable indicator of rhabdomyolysis. A CK value of five times the normal level is a requirement for the diagnosis. A careful search for the common complications of rhabdomyolysis is also paramount.
TREATMENT The most important therapy for rhabdomyolysis is aggressive intravenous fluid administration to prevent renal failure. High volumes of normal saline increases renal tubular flow to excrete both the toxic metabolites as well as substances that obstruct the tubules. The goal is to maintain urine output at 2 ml/kg or 200–300 ml/hr. Placement of a Foley catheter is usually necessary to adequately monitor urine output.
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Urine alkalinization may help with myoglobin clearance. Myoglobin is broken down to ferrihemate, which is responsible for the direct toxic effects on the renal tubules. This effect appears to occur only in the presence of aciduria and hypovolemia. It is recommended to maintain the urine pH at 6.5 or higher with a sodium bicarbonate infusion. This can be achieved by placing 3 ampules of sodium bicarbonate in a liter of D5W. To assist in diuresis, mannitol is commonly recommended. This should only be considered if adequate urine output cannot be achieved despite aggressive crystalloid infusion. Furosemide has been used in the past to assist with diuresis but should have a very limited role. Furosemide, unlike mannitol (osmotic diuretic), is a loop diuretic. It enhances diuresis after the proximal renal tubule. Most of the damage from rhabdomyolysis occurs in the proximal tubule. Furosemide may actually decrease the flow in this area and worsen the problem. It may be useful in patients with oliguria in which intravenous fluid resuscitation has resulted in pulmonary edema. Ultimately, patients with oliguria in acute renal failure may require dialysis. There is no recommended standardized approach to the disposition of patients with rhabdomyolysis. The risk of developing acute renal failure demands close monitoring of renal function, electrolytes, and hydration. Most patients require admission for treatment, prevention of complications, and determination of the underlying etiology.
Bibliography Fernandez WG: Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis, Am J Emerg Med 2005;23(1):1–7. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Malinoski DJ: Crush injury and rhabdomyolysis, Crit Care Clin 2004;20(1):171–192. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Sauret JM: Rhabdomyolysis, Am Fam Physician 2002;65(5):907–912. Tintinalli JM, Kelen JM, Stapczynski JM: Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2005.
Chapter 9
Neurological Emergencies Ataxia, Dizziness, and Vertigo STEVEN W. SALYER
ICD Codes: Vertigo 780.4, Benign paroxysmal positional 386.11, Labyrinthine 300.11, Me´nie`re’s disease 386.00, Peripheral vertigo 386.10, Vestibular neuronitis 386.12
Key Points The brain regulates the sensory input from the proprioceptors in the cerebellum, brainstem, vestibular nuclei, medial longitudinal fasciculus, basal ganglia, red nuclei, cerebral cortex, and temporal and parietal lobes.Vertigo can occur when one or all of the processes of these systems are interrupted. Metabolic, toxic, vascular, neuronal, or psychogenic changes can also affect these systems and thus cause vertigo. ! Emergency Actions ! A computed tomography (CT) or magnetic resonance imaging (MRI) scan is required if any focal neurological abnormality is found on examination. A lumbar puncture will be required to rule out meningitis or a subarachnoid hemorrhage (SAH). All mass lesions, hemorrhage, and neoplasms will require referral to a neurosurgeon. Any patient with a metabolic cause of vertigo should be admitted to the hospital until the electrolyte abnormality is corrected.
DEFINITION Dizziness is the term used to describe vertigo. Vertigo is the illusion of motion. Patients describe vertigo or dizziness as a whirling or spinning sensation. Syncope is the transient loss of consciousness with a rapid return to normal. Near syncope is often used to describe the impending loss of consciousness. Vertigo is described as central or peripheral.
PATHOLOGY The pathology of vertigo involves spatial orientation. Spatial orientation is regulated by the interaction among visual, labyrinthine, and proprioceptive systems. If any one of these systems is interrupted, the patient will report a disorder of sensation of position, spatial orientation, or motion. 418
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The visual system interacts between the visual cortex, optic pathway, and the eyes, which are all part of the visual-spatial orientation. The labyrinthine system is made up of the otoliths and the semicircular canals. The labyrinthine system is driven by changes in the movement of the head, which causes a change in the afferent vestibular nerve impulses. When there is an alteration of input from one of these systems, a perception of motion is noted. There are also proprioceptors in the joints and muscles of the limbs that regulate the body’s sense of position. The brain regulates the sensory input from the proprioceptors in the cerebellum, brainstem, vestibular nuclei, medial longitudinal fasciculus, basal ganglia, red nuclei, cerebral cortex, and temporal and parietal lobes. Vertigo can occur when one or all of the processes of these systems are interrupted. Metabolic, toxic, vascular, neuronal, or psychogenic changes can also affect these systems and thus cause vertigo. As humans grow older, diminishment occurs in labyrinthine hair cells, labyrinthine nerve fibers, visual acuity, proprioceptive sensations, and auditory sensations, and the diminished integrative abilities of these systems follow.
CLINICAL PRESENTATION A patient with peripheral vertigo presents with an intense vertiginous or whirling feeling. Associated presenting symptoms include nausea, vomiting, sweating, diarrhea, alteration of blood pressure and pulse, and pallor. These symptoms are usually abrupt in onset, and the feeling of propulsion is very intense. In peripheral vertigo, the vertigo is influenced by changes in position and is made worse by certain positions more than others. Tinnitus is often present, and the nystagmus is fatigable. With peripheral vertigo, nystagmus is inhibited by ocular fixation. Common causes of peripheral vertigo are vestibular neuronitis, labyrinthitis, and medications. Patients with vestibular neuronitis present with positional nystagmus and fullness in the affected ear or tinnitus. No hearing loss is present. Caloric vestibular testing is usually present in the affected ear. The exact site of the lesion is unknown but is suspected to be of viral origin. The symptoms are of acute onset, and the vertigo is made worse by certain head movements. Vestibular neuronitis can last for days or weeks. True labyrinthitis is peripheral vertigo with hearing loss. Labyrinthitis is usually caused by a viral infection, but there are cases of bacterial labyrinthitis. If labyrinthitis is caused by a perilymphatic fistula, the patient will experience positional vertigo that is exacerbated by sneezing, coughing, or staining, as with a bowl movement, with fluctuating hearing loss. Hennebert’s sign is diagnostic for a perilymphatic fistula.
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The test for this sign is performed with a pneumatic otoscope. If subjective vertigo and nystagmus occur when air is blown on the tympanic membrane, the finding is positive. A common type of labyrinthitis is Ménière’s disease. Ménière’s disease presents with severe exacerbations of nausea, vomiting, prostration, and progressive deafness and tinnitus. Attacks of Ménière’s disease run in clusters over time, during which successive attacks of vertigo are less severe, but the deafness is progressive. The attacks progress over several minutes and last 30 minutes to 1 hour with profound diaphoresis. The attacks are believed to be caused by gross dilatation of the endolymphatic system of the inner ear. Ménière’s disease presents equally in men and women in middle age. Eighth nerve lesions also produce vertigo. They usually occur as a result of acoustic schwannomas or meningiomas. The onset of vertigo is gradual and is usually preceded by hearing loss. Often, the patient has an unsteady gait or ataxia to involvement of the cerebellopontine angle. Benign positional vertigo is a syndrome of symptoms that is usually brought on by a sudden change in posture or position. There is no associated hearing loss or tinnitus. It is more common in elderly persons and usually lasts for seconds to minutes. Benign positional vertigo is thought to be caused by calcium carbonate crystals that have detached from the otoconia of the utricle and have fallen against the cupula of the posterior semicircular canal. Numerous drugs can cause vertigo. Aspirin and aminoglycosides can produce vestibular symptoms. Diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), anticonvulsants, and cytotoxic agents can all cause vertigo. Children younger than 3 years of age can develop benign paroxysmal vertigo. It occurs abruptly, is paroxysmal and self-limiting, and can resolve spontaneously within months or years. The etiology is unknown. Posttraumatic positional vertigo occurs after cerebral concussion. There are two types: acute posttraumatic vertigo and posttraumatic positional vertigo. Acute posttraumatic vertigo occurs as a result of direct trauma to the labyrinthine system and presents with nausea, vomiting, and vertigo. Symptoms improve gradually and resolve in a few weeks. Posttraumatic positional vertigo occurs days or weeks after the initial head injury and is precipitated by changes in head position. This type of vertigo resolves over months and is usually completely gone within 2 years of the injury. A patient with central vertigo presents very differently than does a patient with peripheral vertigo. Symptoms of central vertigo are slow in onset and are not exacerbated by motion or by specific positional changes. There is no nausea, vomiting, diaphoresis, or pallor. The feeling of vertigo
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is less intense than in peripheral vertigo. Central vertigo is caused by disease of the cerebellum and brainstem. A patient with central vertigo presents with signs of other brainstem pathology. Ataxia, dysphagia, dysarthria, facial numbness, diplopia, bilateral limb weakness, or bilateral visual blurring and oscillopsia are often present. The patient’s hearing is unaffected, and tinnitus is absent. The usual presentation is an acute onset of ataxia and vertigo, with or without nausea and vomiting or an acute headache. Sixth nerve palsy may be present with conjugated eye deviation to the side opposite to that of the hemorrhage. A patient with this condition are often unable to sit up, but the findings of a neurological examination with the patient in the supine position will be normal. The patient will describe the vertigo as occurring from side to side or from front to back. Wallenberg’s syndrome is a lateral medullary infarction that causes vertigo, ipsilateral paralysis of the soft palate, larynx, and pharynx, dysphonia, dysphagia, ipsilateral facial numbness and loss of corneal, reflexes, ipsilateral, Horner’s syndrome, ipsilateral cerebellar asynergy, and hypotonia. Hiccups, nystagmus, nausea, and vomiting have been reported in sixth, seventh, and eighth nerve lesions. If present, there is contralateral loss of pain and temperature on the limbs and trunk. Ependymomas of the fourth ventricle can cause brainstem symptoms. Multiple sclerosis (MS) can produce brainstem dysfunction and vertigo as a presenting symptom. Psychogenic vertigo presents as a long-standing vertiginous feeling that is not caused by position or motion and presents without nausea and vomiting. Anxiety can produce vertigo characterized by disequilibrium. Disequilibrium is vertigo caused by a multiple sensory mismatch. Symptoms of disequilibrium syndrome can be increased at night because of decreased ambient light sources. Symptoms can be increased by unfamiliar situations or by the environment. Sedatives can also exaggerate or precipitate symptoms or disequilibrium syndrome. Near syncope is dizziness and the feeling of impending syncope. All of the conditions that can cause syncope can cause near syncope. There are very few truly life-threatening causes of syncope. Syncope caused by an arrhythmia is cause for concern because of the likelihood of a recurrence of the arrhythmia.
EXAMINATION Nystagmus is a to-and-fro movement of the eyes caused by injury to the vestibular system. It is described by the direction of the fast movement of the eyes. In peripheral vertigo, vestibular nystagmus or the “rapid beating phase” is away from the affected ear. A patient with peripheral vertigo
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will describe the spinning sensation in the direction of the fast component of the eye examination. The three main causes of life-threatening syncope are arrhythmias, lack of glucose to the brain, and lack of oxygen to the brain. The physical examination, electrocardiography (ECG), and laboratory examinations should be aimed at uncovering or eliminating these three causes of syncope.
DIAGNOSIS A diagnosis of syncope and vertigo is made on the basis of clinical presentation, history, and physical examination along with the results of radiological tests, ECG, and laboratory tests.
LABORATORY FINDINGS A rapid glucose check should be performed at the patient’s bedside. A complete blood count (CBC), chemistry, drug screen, and measurement of cardiac enzyme levels should be performed on all patients with syncope.
RADIOGRAPHS A CT scan or MRI is required if any focal neurological abnormality is found on examination. A lumbar puncture will be required to rule out meningitis or an SAH. All mass lesions, hemorrhages, and neoplasms will require referral to a neurosurgeon. Any patient with a metabolic cause of vertigo should be admitted to the hospital until the electrolyte abnormality is corrected. The practitioner should ensure a good follow-up plan for a patient discharged with the diagnosis of peripheral or central vertigo.
TREATMENT For all patients who present to the emergency department (ED) with vertigo, dizziness, near syncope, syncope, or altered mental status, an intravenous line should be placed, administration of normal saline should be initiated, and cardiac monitoring should be engaged. The patient should be given 2 L of oxygen and should have the aforementioned laboratory tests performed, along with an ECG. Antihistamines have been used for 40 years in the control of vertigo and dizziness. Antihistamines with anticholinergics properties work best on peripheral vertigo. Antihistamines work at the brainstem level, peripherally,
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centrally, and within the labyrinthine apparatus. Diphenhydramine, meclizine, promethazine, cyclizine, dimenhydrinate, atropine, and scopolamine can all be used in the treatment of vertigo from a peripheral origin. The antiemetic agents hydroxyzine and promethazine can also be used in the treatment of vertigo. Diazepam, which is a sedative, works well on Ménière’s disease. Chlordiazepoxide also works on peripheral vertigo. The practitioner should remember that all medications that are used to control peripheral vertigo will worsen the symptoms of a patient with disequilibrium syndrome or ill-defined light-headedness.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Bell’s Palsy REX L. HOBBS, JR.
ICD Code: 351.0
Key Points/Quick Reference When there is a sudden onset of unilateral facial weakness and/or paralysis, alterations of taste and inner ear pain, with ipsilateral hypersensitivity to noise and eyelid ‘‘drooping,’’a diagnosis of Bell’s palsy should be considered. The rapid assessment of forehead involvement can determine whether a patient presents with Bell’s palsy or an acute stroke syndrome. Other names for Bell’s palsy are idiopathic facial paralysis and acute peripheral facial palsy. ! Emergency Actions ! No emergency actions are warranted in the treatment of Bell’s palsy.
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DEFINITION Bell’s palsy is a swelling and secondary compression of the seventh cranial nerve, resulting in a unilateral weakness to complete paralysis of the facial musculature. The condition generally occurs with sudden onset.
EPIDEMIOLOGY The epidemiology of Bell’s palsy is as follows:
This condition is the cause for 60%–70% of all unilateral facial palsies. It occurs with equal male and female occurrence. The left and right sides of the face share equal incidence of involvement. The lowest incidence is in persons younger than 10 years (4 cases per 100,000). The highest incidence is in persons older than 70 years (53 cases per 100,000).
PATHOLOGY The seventh cranial nerve originates from the pontomedullary junction of the brainstem, from which it radiates to the muscles of facial expression/ movement by passing through the temporal bone close to the inner ear structures. Even though its main function is motor innervation, this nerve also provides sensory function to the posterior and inner ear and to the anterior two thirds of the tongue for taste. Swelling of the motor fibers in the narrow passage taken through the temporal bone leads to compression of the nerve and decreased signal transmission to the facial musculature, giving the obvious unilateral facial weakness or even “drooping” on presentation. The swelling, long thought to be idiopathic, may actually occur due to involvement of the herpes virus. In some cases the sensory fibers for this nerve may also become involved, resulting in posterior auricular pain, hyperacusis (i.e., painful sensitivity to sound), or unilateral loss of taste, all of which can portend a more difficult recovery. The diagnosis of Bell’s palsy has been overused to describe many less common causes for unilateral facial weakness, including stroke, trauma, tumors, and central nervous system (CNS) infections that have an obvious cause. This misuse of the term has thereby given rise to such new terms as idiopathic facial paralysis and acute peripheral facial palsy to better clarify the exact diagnosis.
RISK FACTORS There are no strong risk factors for the development of Bell’s palsy even though pregnancy, diabetes, and recent viral illness have been shown to
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put one at a slightly increased risk. Most affected persons are otherwise healthy, with no predisposing event or conditions.
CLINICAL PRESENTATION When it occurs in the absence of other neurological signs and symptoms, sudden onset of unilateral facial weakness that may progress to paralysis, reaching its apex in 48 hours, is strongly characteristic for Bell’s palsy. Motor symptoms may be preceded by alterations of taste and inner ear or retroauricular pain by as many as 1–2 days, in some cases. After the onset of motor dysfunction, an ipsilateral hypersensitivity to noise may occur; however, there should be no other sensory or motor dysfunctions present. Symptoms of vision alterations, hearing loss, difficulty swallowing, extremity numbness/weakness, headaches, elevated temperature, or a history of recent head trauma should prompt an in-depth investigation looking for secondary causes. Some patients may have only a noticeable weakness, though many progress to a paralysis that may result in drying of the cornea due to inability to completely close the eyelids and drooling or a “pulling” sensation from the still active and now dominant unaffected side of the face. Historically, only a small percentage of persons will have had a previous occurrence.
EXAMINATION A report of facial weakness would most certainly prompt a complete neurological examination to include sensory, motor, cerebellar, and deep tendon reflexes of the extremities. In the case of Bell’s palsy, the results of the neurological examination as well as those of an evaluation of mental status should be completely normal. It is in the cranial nerve examination results where the abnormalities will lie, and this should enable the examiner to determine whether the cause is a peripheral lesion (i.e., Bell’s palsy) or a central lesion, as in a stroke or tumor. The practitioner should have the patient raise his or her eyebrows, looking for symmetrical movement and the expected wrinkling of the forehead. Next, the patient should be asked to close his or her eyes tightly. Noting any incomplete closure or ptosis, the practitioner should ask the patient to keep them closed as the practitioner gently pushes on the upper lids in a gentle fashion, observing for any inability to maintain closed lids. Finally, the patient should be asked to smile broadly, showing his or her teeth, as the practitioner looks for asymmetry in the lip movement and facial creasing. Findings of normal movement and strength of the brow and eye closure but weak mouth movement unilaterally is indicative of a central lesion and should be followed with an MRI with contrast to localize an area of stroke or mass lesion, which will probably lie in the posterior fossa. Only a complete,
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unilateral facial weakness with a normal remaining cranial nerve and neurological examination results should be attributed to Bell’s palsy without immediate further workup. New symptoms evolving at follow-up visits should also prompt further evaluation or even reevaluation.
DIAGNOSIS In a true Bell’s palsy, there are no diagnostic laboratory tests or radiological studies (except for some possible enhancement of the proximal portions of cranial nerve VII on gadolinium-enhanced MRI) that will directly confirm or solidify the diagnosis. Further evaluation is only required when the diagnosis is in question or when patient risk factors such as advanced age, long-standing hypertension, or diabetes or other symptoms raise the concern of a secondary process (Table 9-1). Some theories suggest that Bell’s palsy is not idiopathic but is actually due to a herpetic infection of the facial nerve; this has raised some question as to whether antibody titers should be drawn in these cases. Thus far, most studies of antibody levels measured from the saliva and serum have not been conclusive enough to warrant their being part of a routine workup. In addition, positive or negative findings on such testing would not change most current treatment regimens. Finally, electrodiagnostic studies are sometimes performed to assess the degree of nerve dysfunction
Table 9-1 Diagnostic Testing for the Differential Diagnosis of Bell’s Palsy ASSOCIATED SYMPTOMS OR FINDINGS Recent head trauma Hearing loss, vertigo, tinnitus Bilateral facial weakness Lymph node swelling, cough Palpable lateral facial mass
POSSIBLE CAUSES Temporal fracture, subdural/ epidural hematoma Cholesteatoma, acoustic neuromas Myasthenia gravis, central lesion or mass Sarcoidosis Parotid tumor
Elevated temperature, nuchal Meningitis, HIV infection, rigidity brain abscess Other sensory or motor deficits CVA, brain tumor, multiple sclerosis History of recurring/resolving Multiple sclerosis deficits
ADDITIONAL DIAGNOSTIC TESTING Radiographs, CT, MRI MRI of the head Head MRI, Tensilon test, anti-ACH antibody screen Chest x-ray, ACE level Biopsy, ENT consult for excision CBC, CSF culture and analysis CT or MRI of the brain Gadolinium contrast MRI, CSF analysis
CT, Computed tomography; MRI, magnetic resonance imaging; ACH, acetylcholine receptor; ACE, angiotensin-converting enzyme; ENT, ear, nose and throat; HIV, human immunodeficiency virus; CBC, complete blood count; CSF, cerebrospinal fluid; CVA, cerebrovascular accident.
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and to differentiate the present disease from demyelinating processes that may present similarly. These tests are also used to aid in determining the need for surgical intervention.
LABORATORY FINDINGS As mentioned previously, in a pure case of Bell’s palsy there should not be any abnormal laboratory tests directly attributed to this disorder. In an effort to rule out other possible causes for a facial palsy, making an assessment of a CBC, and tests for glucose level, thyroid-stimulating hormone (TSH), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), human immunodeficiency virus (HIV), and compliment levels will be helpful in an initial narrowing of the differential. A spinal tap for cerebrospinal fluid (CSF) analysis directed at looking for signs of infection or demyelinating diseases like MS may also be advisable pending patient history and concomitant symptoms.
TREATMENT Numerous studies on the treatment for Bell’s palsy have been varied in their approaches, treatment regimens, and clarity of results. The findings on all are made confusing by the fact that over 70% of patients will have a complete recovery with no treatment whatsoever over time. Current treatment recommendations have therefore been made based more on the rapidity of improvement and attempting to increase the percentage of patients who have no lasting deficits. The most commonly used direct treatment has been a tapering dose of steroids, usually oral prednisone at a dosage of 1 mg/kg/day, over a 7to 14-day course. Preexisting conditions such as diabetes, peptic ulcer disease, and pregnancy must be considered when deciding whether to use a steroid and, if so, at what dose and duration. Due to the ever-increasing body of evidence for a viral etiology to this disorder, studies have looked at a combined regimen of prednisone and an antiviral agent. The administration of antivirals like acyclovir (adult dose, 800 mg five times daily for 7 days) and valacyclovir (adult dose, 1000 mg twice daily for 7 days) should be initiated as early as possible after symptom onset. Antiviral agents prescribed as monotherapy have not been shown to be overly beneficial. It is important to have follow-up visits frequently at first and to counsel the patient that, even under ideal circumstances, symptoms may take several weeks or longer to resolve completely. Indirect treatments such as taping the affected eyelid closed to avoid corneal drying can be instituted, as needed. Surgical intervention to decompress the nerve, though rarely performed, should be considered if facial paralysis remains completely unaffected by medical management after 1 week and electrodiagnostic studies
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indicate a significant signal blockage. Complications from this type of surgery include complete deafness.
Bibliography Axelsson S, Lindberg S, Stjernquist-Desatnik A, et al: Outcome of treatments with valacyclovir and prednisone in patients with Bell’s palsy, Ann Otol Rhinol Laryngol 2003;112 (3):197–201. Becilli R, Perugini M, Carboni A, Renzi G: Diagnosis of Bell palsy with gadolinium magnetic resonance imaging, J Craniofacial Surg 2003;14(1):51–54. Gilbert SG: Bell’s palsy and herpesviruses, Herpes 2002;9:3. Gilden DH: Bell’s palsy, N Engl J Med 2004;351:1323–1331. Gillman GS, Schaitkin BM, May M, Klein SR: Bell’s palsy in pregnancy: A study of recovery outcomes, Otolaryngol Head Neck Surg 2002;126(1):26–30. Kasper DL, Braunwald E, Fauci AS, Hauser SL (eds): Bell’s palsy. In Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005, pp 2436–2437. Lagalla G, Logullo F, Di Bella P, et al: Influence of early high-dose steroid treatment on Bell’s palsy evolution, Neurol Sci 2002;23(3):107–112.
Botulism REX L. HOBBS, JR.
ICD Code: 005.1
Key Points/Quick Reference Any patient who presents with a worsening cranial nerve motor weakness followed by weakness and paralysis that progresses inferiorly through the upper then lower extremities should be considered to have botulism. ! Emergency Actions ! Early elective intubation and administration of the botulism antitoxin is necessary for recovery in patients presenting with rapidly progressing symptoms.
DEFINITION Botulism, typified by a descending paralysis that may become severe enough to result in respiratory failure, is induced by a bacterial toxin that blocks the release of acetylcholine at the neuromuscular junction.
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Classically induced after the ingestion of Clostridium botulinum and/or its toxin, other forms of the disease do exist.
EPIDEMIOLOGY Occurrence of this historically well-known disease varies around the world and, to a certain degree, in the United States as well. Overall in the United States, there is an occurrence of 0.1 case per million persons, resulting in an average of 24 cases per year. The majority of these are classified as infantile botulism and occur from the ingestion of contaminated foods. This gram-positive, anaerobic bacterium is highly prominent in the soil and can form very resilient spores requiring sustained temperatures of greater than 120 C (248 F) to destroy. The botulism toxin is classified by the Centers for Disease Control and Prevention (CDC) as a category A bioterrorism weapon along with the likes of anthrax and smallpox.
PATHOLOGY There are several types of toxin that can be ingested or produced by ingested bacteria or spores. There are currently eight known forms of the toxin (i.e., A, B, C1, C2, D, E, F, and G), with type A resulting in the most prolonged recovery periods. These toxins are considered to be the most deadly on the planet, with only 0.05 mg required to result in a human death. It is because of this extreme toxicity that its use for cosmetic and medicinal purposes is a historical turn of events. After the toxin is absorbed from the gastrointestinal tract or other membrane, it passes readily into the motor nerve terminals and permanently blocks the release of acetylcholine at the neuromuscular junctions. Without the acetylcholine stimulation, the muscle(s) is (are) paralyzed. The toxin does not affect the sensory portion of the nervous system but can result in dry mouth due to involvement of the autonomic nervous system. As mentioned, the blockade is permanent, but recovery is possible due to the formation of new branches of the blockaded nerve terminal.
RISK FACTORS Risk factors for contracting botulism include the following:
Consumption of poorly prepared foods containing toxin, bacteria, or spores (e.g., fermented seafood, home canned foods, undercooked foods) Contaminated honey, especially when consumed by children younger than 1 year of age Deep wounds, heavily contaminated by soil Laboratory exposure to spores or toxin
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Injectable heroin usage, especially if tract abscess exists Exposure to aerosolized toxin in a terrorist act
CLINICAL PRESENTATION The classical presentation of botulism begins with worsening cranial nerve motor weakness followed by weakness and paralysis that progress inferiorly through the upper then lower extremities. The most feared complication is respiratory muscle involvement resulting in respiratory failure. Hypohidrosis and dry mouth may also occur in varying degrees. No sensory abnormalities, such as numbness or paresthesia, are noted through this process. Infant botulism, which occurs after ingested spores germinate and toxin is absorbed, typically presents with constipation followed by generalized weakness, weak cry, and decreased head control.
EXAMINATION In addition to a routine physical, a full neurological examination is required. Assessing all of the cranial nerves along with a complete sensory, muscle strength, and reflex examination is a must. Expected findings would include a symmetrical facial and extremity weakness with a normal sensory examination. Unless there is severe paralysis, deep tendon reflexes should still be present. Higher cognitive function will also be intact, even though speech may be impeded as a result of vocal musculature weakness. It is important to ascertain respiratory function status at baseline and repeatedly thereafter. One way to achieve this is via serial measurements of the forced expiratory volume in 1 second, observing for decreased readings over time that may indicate the need for an elective intubation.
DIAGNOSIS The diagnosis of botulism can be strongly suspected based on historical and physical examination findings, but it is important to consider a differential diagnosis, including myasthenia gravis (MG), GuillainBarré syndrome, poliomyelitis, and tick paralysis. MG has predominately facial muscular weakness that worsens with repetitive activity and at least partially resolves after rest. The weakness and loss of deep tendon reflexes seen in Guillain-Barré syndrome occurs in a distal-toproximal fashion (the reverse of botulism) but may also cause respiratory failure. Electrophysiological testing can provide the differentiating information, as can the detection of botulinum toxin on serum or stool immunoassay results.
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LABORATORY FINDINGS Laboratory tests should be performed to confirm the diagnosis of botulism and to rule out similar processes. With this in mind, a baseline CBC, Chem 20, and TSH should be performed, along with a toxicology screen. Serum and stool samples should be cultured and immunoassay performed to test for the presence and type of toxin. These tests, however, will rarely be confirmatory if symptoms have been ongoing longer than 2–3 days. CSF culture/analysis, muscle biopsy, and autoantibody examinations may also be necessary pending case presentation and progression of symptoms.
TREATMENT Early diagnosis of the disease is the best treatment because it allows for early initiation of aggressive respiratory and supportive care. Indeed, those patients intubated after respiratory failure fair more poorly than those who are electively intubated due to declining function. With this level of support recovery is common, though it may take many weeks or even months. Antitoxin is available through the local health department/ CDC and is used in some cases. Steroids, plasmapheresis, and human immune globulin have been used with limited success. Future modalities include oligoclonal antibodies to aid in toxin neutralization, if given early in the course, and an inhaled vaccination for the disease.
Bibliography Centers for Disease Control and Prevention: Infant botulism—New York City, 2001–2002, MMWR Morb Mortal Wkly Rep 2003;52:21–24. Centers for Disease Control and Prevention: Outbreak of botulism type E associated with eating a beached whale—Western Alaska, July 2002, MMWR Morb Mortal Wkly Rep 2003;52:24–26. Centers for Disease Control and Prevention: Wound botulism among black tar heroin users—Washington, 2003, MMWR Morb Mortal Wkly Rep 2003;52:885–886. Cherington M: Botulism: Update and review, Semin Neurol 2004;24(2):155–163. Park JB, Simpson LL: Progress toward development of an inhalation vaccine against botulinum toxin, Expert Rev Vaccines 2004;3(4):477–487. Sobel J, Tucker N, Sulka A, et al: Foodborne botulism in the United States, 1990–2000, Emerg Infec Dis 2004;10(9):1606–1611.
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Headaches STEVEN W. SALYER
ICD Codes: Classic migraines 349.9, Common migraines 349.9, Ophthalmoplegic migraines 349.9, Hemiplegic migraines 349.9, Cluster headaches 346.2, Toxic metabolic headaches 349.9, Subarachnoid hemorrhage 430, Pseudotumor cerebri 348.2, Subdural hemorrhage 432.1, Tension headache 307.81, Traction headaches (vascular) 784.0, Post–lumbar puncture headaches 349.0, Temporal arteritis 446.5, Trigeminal neuralgia 350.1, Epidural hematomas 432.0
Key Points For a patient who presents to the ED with a headache, it must be assessed whether he or she has a life-threatening cause of headache. Three types of patients visit the ED with headaches: (1) the patient with chronic headaches (like migraines) who requires pain control, (2) the patient who has never had a severe headache like this one before, and (3) the patient who has had headaches in the past and present with a headache that differs from his or her usual headache. ! Emergency Actions ! Any patient with a headache resulting from a suspected mass lesion requires a CT scan or MRI and an immediate referral to a neurosurgeon. An SAH is treated by lowering the intracranial pressure (ICP) and cerebral edema by hyperventilation and elevation of the head of the bed by 30 degrees. Some neurosurgeons recommend the use of nimodipine to reduce arterial spasm. An urgent neurosurgical consultation is required.
DEFINITION Headaches can be caused by trauma, increased ICP resulting from a subdural or epidural hematoma, sentinel bleed, aneurysm, meningitis, viral or hepatic encephalitis, vascular causes, migraine, tension, sinusitis, temporal arteritis (i.e., giant cell arteritis), brain abscess, pseudotumor cerebri, traction headache, postconcussive headache, trigeminal neuralgia, or idiopathic cranial neuralgia.
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EPIDEMIOLOGY Forty percent of the population has a significant headache at some point in their lifetime. Ten percent will have chronic headaches.
PATHOLOGY Pain from the area of the brain that causes an acute headache can come from sensors in the blood vessels, fat, muscle, skin, periosteum, dural arteries, falx cerebri, and the large arteries of the brain’s connective tissue. The practitioner should remember that the arachnoid, dura, and pia mater are incapable of producing painful stimuli. Pain from the neck area is caused by dilation, distention, tension, inflammation, or traction processes. The underlying cause of migraines is the onset of vasoconstriction of the intracranial arteries, which reduces cerebral blood flow. Vasoconstriction causes an aura that is system dependent and based on where the vasoconstriction occurs. The vasoconstriction causes increased serotonin release, which increases interaction with the tyramine, histamine, free fatty acids, prostaglandins, and bradykinin to produce a sterile perivascular inflammation. The serotonin levels are rapidly depleted and then a rebound vasodilation occurs, thus causing the headache resulting from the inflammation and distention. Vascular headaches are often caused by a precipitating cause, such as air pollution, fatigue, oversleeping, stress, or the ingestion of chocolate, cheese, nuts, alcohol, perfumes, vasodilators, or monosodium glutamate. In menstruating women, onset of their menstrual period can be a precipitating event to a migraine, sometimes a hemiplegic migraine. Classic migraines present with a sharply defined prodrome or aura. Fifteen percent of all migraine headaches are of this type. The prodrome or aura can last for up to 60 minutes before the onset of the headache. The aura is usually visual with scotomas, homonymous hemianopsia, or photophobia. The patient also presents with nausea, vomiting, and tingling in hands, feet, lips, mouth, or face as a prodrome. Mild aphasia can occur. Common migraines are not preceded by any sharply defined aura before the onset of the headache. These patients usually present with nausea, vomiting, and throbbing unilateral pain. There is usually a family history of common migraines. Ophthalmoplegic migraines are rare and present in young adults. They usually involve the third, fourth, or sixth cranial nerve. Ophthalmoplegic migraines present with intense unilateral pain with a dilated pupil and the eye outwardly deviated with ptosis. Hemiplegic migraines are rare. These patients present with unilateral motor or sensory symptoms of hemiparesis or hemiplegia. The symptoms can last longer than the headache, and this finding is the diagnosis of exclusion.
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Cluster headaches are a form of vascular headaches seen predominantly in adult males. These headaches come in clusters of severe ocular and retro-ocular pain, which lasts less than 2 hours and occurs several times a day in clusters for weeks to months. The patient with a cluster headache presents with unilateral rhinorrhea, conjunctival injection, flushing of the forehead, and sweating. Horner’s syndrome is often present. At presentation, the patient will likely be holding the side of the head that is affected and will be rocking or pacing. Toxic metabolic headaches are caused by vasodilation of pain-sensitive arteries. A lowered pain threshold is brought about by toxic substances. Food containing ripe cheeses, tyramine, monosodium glutamate, and sodium can precipitate these headaches. These headaches can also occur when there is food or beverage withdrawal such as with coffee, tea, or cola withdrawal or alcohol hangover. Hypoglycemia, hypoxia, hypercapnia, indomethacin, oral contraceptives, and nitroglycerin are all causes of toxic metabolic headaches. Ascent to an altitude greater than 12,000 feet can also cause a headache. The most common cause of a toxic headache is a fever greater than 102 F. Hypertension with a diastolic pressure greater than 130 mmHg can cause a throbbing headache. The control of the blood pressure will resolve this type of headache. Traction headaches are produced by traction, displacement of painsensitive structures, and direct pressure, usually on blood vessels. Traction headache can be divided into categories according to the cause: mass lesion, SAH, post–lumbar puncture, postconcussive headaches, brain abscess, and pseudotumor cerebri. Mass headaches are caused by subdural or epidural bleeding. Subdural hemorrhage can be acute, such as with head trauma, or chronic, as in elderly persons. Patients with an acute subdural hematoma present obtunded and often cannot report the headache. In elderly persons, the traumatic event is often not remembered, and the cause may be atraumatic. Epidural hematomas present with a history of trauma with a brief period of unconsciousness, then consciousness with an onset of a headache. A patient will often present with a unilateral dilated pupil resulting from uncal herniation and a fracture through the middle meningeal groove with laceration of the middle meningeal artery. Brain tumors will present with two different pain patterns. Tumors above the tentorium present with referred pain to the frontal region or vertex. Subtentorial lesions cause pain in the occipital area. Often the pain awakes the patient from sleep, and pain can be made worse by the Valsalva maneuver. Nausea and vomiting can be present, and focal neurological changes may or may not be present. Subarachnoid hemorrhage is caused by bleeding from an intracranial aneurysm. These patients present with the “worst headache of my life,” and loss of consciousness may occur. In the younger age group, the bleeding
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is usually from an arteriovenous malformation. On examination, meningismus may be present with the onset of vomiting, which is a sign of increased ICP. A CT scan should be performed, and, if no bleeding is noted, a lumbar puncture should be performed to check for blood in the CSF. Pseudotumor cerebri (i.e., benign intracranial hypertension) is present in obese young females who have amenorrhea or irregular menstrual periods. This patient will report nonspecific visual symptoms with a severe headache. Papilledema will be present. On CT examination, slit-like ventricles are present without a mass effect. Post–lumbar puncture headaches are caused by leaking CSF. The patients present with a bicranial, pulsatile, frontal headache that is made worse by standing up. Temporal arteritis (i.e., giant cell arteritis) is a disease of inflammation. It involves the branches of the external carotid artery. The artery becomes infiltrated with lymphocytes, multinucleated giant cells, and plasma cells. It is often seen in women more than men in a 4:1 ratio. The women are often older than 50 years. Often these women have polymyalgia rheumatica. They report a severe piercing or burning pain, which can be bilateral or unilateral and usually occurs at night. The inflammatory is enlarged, pulseless, and tender. A CBC and an ESR or CRP test should be performed. The ESR is usually greater than 50 mm/hr. A diagnosis is made using a piece of biopsied artery. The major complication of temporal arteritis is blindness. Trigeminal neuralgia is idiopathic neuralgia. It occurs more often in women than in men in a 2:1 ratio. These women are usually older than 50 years. Patients with trigeminal neuralgia present with unilateral, right-sided face pain in the third and second branches of the fifth cranial nerve. The pain is often of sudden onset and brief in duration, lasting for seconds or minutes and often severe and lancing. Often there are trigger points that exacerbate an episode. The upper eyelid, nasal labial fold, lips, certain facial movements, shaving in males, teeth brushing, or eating or drinking fluids can cause an acute attack. Acute narrow-angle glaucoma can cause a piercing pain in and around the orbit of the affected eye. Nausea and vomiting are often present with acute narrow-angle glaucoma. The intraocular pressure will be elevated, the cornea will be edematous, and the pupil will be in the midposition. Decreased visual acuity will present. Other causes of headache include referred pain from the temporomandibular joint, iritis, optic neuritis, and eye strain.
CLINICAL PRESENTATION A patient who presents to the ED with a headache must be assessed regarding whether he or she has a life-threatening cause of headache. Three types of patients present to the ED with headaches include the following: (1) patients with chronic headaches (like migraines) who present for pain
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control, (2) patients who have never had a severe headache like this one before, and (3) patient who have had headaches in the past and present with a headache that differs from the usual type of headache. The practitioner should always ask the patient whether this is the worst headache this patient has ever had in his or her life. An easy way to determine this is to ask the patient how bad the headache is based on a scale of 1 to 10, with 10 being the worst headache he or she has ever experienced. It is important to determine the time of onset, location, and quality of the headache. A sudden severe onset of a headache in a person who never has headaches is indicative of a serious anatomical process such as an SAH. A history of headaches just before the onset of sexual intercourse or a physical exercise is indicative of an SAH. A history of any preceding events or changes in diet, drugs, or menstrual cycle is often helpful in determining the cause. The location of the headache is also important. A headache that is gradual in onset at the same location and does not go away is suggestive of a mass lesion. Migraines are usually unilateral, and tension headaches are bilateral and circumferential in presentation. The healthcare provider should obtain a history of the quality of the headache. The patient should always be asked whether the pain is shock-like, deep, or piercing. Throbbing headaches are usually vascular in nature, like migraine headaches. Shock-like pain is seen in trigeminal neuralgia and fifth cranial nerve lesions. Deep, piercing, very intense, unilateral pain of rapid onset is seen in cluster headaches. Patients with vascular headaches present with nausea, vomiting, and anorexia.
EXAMINATION A complete physical, mental, and neurological examination should be performed on all patients who present with headaches. Vital signs are a great help in differentiating the types and severity of pain and headache. Tachycardia will be seen with severe pain, and hypertension is usually seen with SAH. The patient’s temperature should always be noted; fever is seen with meningitis, encephalitis, and brain abscess. The examiner should always assess the patient’s cranial nerves and perform a funduscopic examination on every patient. On the funduscopic examination, the physician should assess for papilledema, preretinal hemorrhages, exudates, and subhyaloid hemorrhages. Hypertensive encephalopathy will present with preretinal or subhyaloid hemorrhages. Increased ICP will cause papilledema. The sinus and the scalp in the temporal areas should always be percussed and palpated. Tenderness over the temporal areas is indicative of temporal arteritis. Tenderness over the sinus area is indicative of sinusitis. If the patient says that palpation of the scalp area on examination makes the pain better, this is indicative of a tension or muscle traction headache.
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LABORATORY FINDINGS There are no specific tests to rule in or out headaches. If temporal arteritis is suspected, an ESR or CRP test can be performed. CBC and blood cultures should be performed if meningitis is suspected. A lumbar puncture can be performed to evaluate for infection of the CSF, to rule out an SAH, or to monitor CSF pressure.
RADIOLOGY A CT scan can locate a mass lesion and is only 90% diagnostic in subarachnoid bleeding. An MRI is better for assessing anatomical lesions.
TREATMENT The treatment for migraine headache is divided into four categories: general, abortive, acute, and preventive measures. In the ED, it is generally the acute headache that is treated. There are numerous treatments for acute migraines. You can give prochlorperazine (Compazine) at an intravenous dose of 10 mg to control nausea and vomiting. Often, therapy with prochlorperazine alone will stop the headache. For treatment of the pain of the headache, 0.5–1.0 mg of dihydroergotamine can be given every 30 minutes for two doses. Meperidine hydrochloride (Demerol; 25 mg intravenous or 50–75 mg intramuscular) or butorphanol tartrate (Stadol; 1–2 mg intravenous) can also be used for pain relief. Butorphanol tartrate also comes in the nasal form, which can be used to abort the headache or treat the onset of the headache. Ketorolac tromethamine (Toradol) is an NSAID that can be given as a 60-mg intramuscular dose or a 30-mg intravenous dose for the treatment of pain. For the acute exacerbation of cluster headaches, the patient should be given 100% oxygen. Also, 5%–10% cocaine solution or 4% lidocaine solution can be placed into the ipsilateral nostril to abort the acute cluster headache. The treatment of toxic metabolic headaches is the removal of the toxic substance and analgesia for pain. Any patient with a headache resulting from a suspected mass lesion requires a CT scan or MRI and an immediate referral to a neurosurgeon. An SAH is treated by lowering the ICP and cerebral edema through hyperventilation and elevation of the head of the bed by 30 degrees. Some neurosurgeons recommend the use of nimodipine to reduce arterial spasm. An urgent neurosurgical consultation is required in this situation. Patients with suspected temporal arteritis should be treated at the time of clinical presentation. A biopsy should not delay treatment. Treatment consists of long-term treatment with prednisone, an NSAID, and analgesia.
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Pseudotumor cerebri is treated with steroids and repetitive lumbar punctures to relieve pressure. Post–lumbar puncture headache can be treated with intravenous fluids, 500 mg of caffeine delivered intravenously, analgesics, or blood patch by anesthesiology. Often, a short burst of prednisone (60 mg/day for 5 days) will help to reduce the pain. Postconcussion headaches are treated with NSAID, and they are usually self-limiting. Trigeminal neuralgia is treated with analgesic medications. Outpatient therapy is treated with carbamazepine (100–200 mg three times a day). If this treatment fails, neurosurgical consultation is advised for progressive sectioning of the sensory nerve roots.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Multiple Sclerosis REX L. HOBBS, JR.
ICD Code: 340
Key Points/Quick Reference Optic neuritis, weakness, and sensory loss are the most common symptoms at the time of an initial episode of MS, whereas paresthesias, diplopia, ataxia, and vertigo occur less commonly, all lasting at least 24 hours. Any increase in symptom severity with heat exposure or exerciseçfor example, the transient monocular blurred vision called Uhthoff’s symptomçis also a strong indicator of MS. Lhermitte’s symptom, a painful or stinging sensation into the upper or lower extremities with neck movement, is a nonspecific indicator of potential multiple sclerotic spinal cord disease.
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! Emergency Actions ! The initial attack of MS is addressed with high-dose methylprednisolone given intravenously.
DEFINITION Multiple sclerosis is an autoimmune disorder in which the CNS is the main target. It is characterized by a varying course of waxing and waning neurological symptoms induced by focal areas of inflammation and demyelination as well as generalized cortical atrophy, with nearly all patients developing some degree of disability over years to decades.
EPIDEMIOLOGY Approximately 350,000 people in the United States have MS, and women with the disorder outnumber men by nearly a 2:1 ratio. After trauma, it is the most common cause of disability in young adults in the northern hemisphere, with a steady increase in incidence from the late teens to age 35. No population with a high risk for MS exists between latitudes 40 N and 40 S. In fact, the diagnosis rate in the Japanese is only 2 per 100,000, and it is virtually unheard of in black Africans. The highest occurrence is in persons of northern European lineage demonstrated by the residents of the Orkney Islands, north of Scotland, having a rate of 250 per 100,000. Family history of the disease in a first-, second-, or third-degree relative carries the same lifetime concordance rate of a dizygotic twin at 2%–5%, whereas the same rate is 25%–30% in monozygotic twins.
PATHOLOGY In addition to neurons, a great variety of other cell types are present in the CNS that are collectively called supporting cells or neuroglia. These neuroglia are nine times more numerous than neurons and, unlike neurons, which are amitotic, are able to reproduce themselves throughout a person’s lifetime. Microglia are relatively small and play a role in phagocytizing invading microorganisms and cellular debris, whereas ependymal cells, found throughout the brain and spinal cord but especially in large amounts in the choroids plexus, produce and circulate CSF. The neuroglia most often involved in the evolution of MS are the oligodendrocytes and astrocytes. Oligodendrocytes produce extensions that wrap themselves around as many as 60 different axons of the CNS neurons, providing insulation from other axons but also speeding transmission of electrical impulses. These white, phospholipid-based myelin sheaths not only lend to the term white matter of the brain (versus the poorly to non-insulated gray matter) but also can help produce axonal transmission speeds of 150 m/sec. This is especially important considering that 99% of
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the neurons in the CNS are functionally classified as associated neurons (i.e., interneurons), which form the bridge between afferent (i.e., sensory) and efferent (i.e., motor) neurons, thereby making rapid processing of stimuli and response possible. Astrocytes act to brace and provide form to the neural tissue as well as connecting neurons to their supplying capillaries. It is these same cells that will cause gliosis, or scarring, in the CNS by increased proliferation when damage or death occurs to the oligodendrocytes and their myelin sheaths by a given process. This interferes with the formation of guiding channels by which healing axonal extensions would normally occur, as in the mechanism used by Schwann cells that insulate, protect, and help regenerate neurons in the peripheral nervous system. The development of MS is currently thought to involve a series of events in genetically susceptible persons. Inheritance is believed to be polygenic with suspect regions on chromosomes 6, 7, 18, and 19 concerning MHC formation and T-cell receptor chains. This “susceptibility” is to the induction of autoantibodies to myelin basic protein (MBP) and oligodendrocytes by several suspect viruses, including measles, rubella, influenza C, Epstein-Barr (EBV), and parainfluenza, all of with which higher antibody levels have been found in the serum and CSF of patients with MS. Most recently, the human herpes virus type 6 has been found to share an identical peptide sequence with that of MBP. This identical area can then act as an autoantigen, instigating the production of sensitized T cells to MBP that, when activated, will increase the permeability of the vascular endothelium and increase adhesion molecule expression via release of cytokines, including interleukin 1, tumor necrosis factor, and interferon (IFN) gamma. A second wave of attack then occurs with increased migration of more cytotoxic T cells, natural killer cells, and autoantibodies that begin the inflammation and destruction of the myelin sheaths and oligodendrocytes. The majority of these attacks occur in the white matter of the brain and/or spinal cord where, stripped of their insulating cover, the axonal function is disrupted by ectopic impulses, slowed or blocked conduction, and, finally, gliosis. This scarring occurs in multiple areas initially or over time, hence it is given the name of this disorder. Even though MS has historically been thought to be purely a demyelinating disease, recent studies have found that the development of axonal destruction and cortical atrophy not only take place, but also occur even during symptomfree phases. This and other factors have resulted in large changes in the approach to diagnosing and treating this process.
RISK FACTORS Being a female in late adolescence to her 20s with a northern European lineage is the current cumulative “risk factor.” Other research is ongoing to prove more definitive predictive connections in those having a previous
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herpes family virus infection (e.g., human herpes virus type 6, EpsteinBarr virus). Family history does not play a big role in determining future risk.
CLINICAL PRESENTATION Clinical presentation for MS can be a conglomeration of nebulous functional, sensory, and cognitive symptoms that may lead to an abrupt diagnosis of conversion reaction. However, a careful history, noting the fine details, can help unclutter the picture somewhat. A very important point to elucidate is a previous history of similar occurrence because this is not a monophasic disease. Two or more events separated by time, location, or both are a very strong diagnostic clue. Optic neuritis, weakness, and sensory loss are the most common symptoms at the time of the initial episode, whereas paresthesias, diplopia, ataxia, and vertigo occur less commonly, all lasting at least 24 hours. Bowel, bladder, and sexual dysfunction and decreased cognitive function are rare with initial onset, but they are possible. Any increase in symptom severity with heat exposure or exercise—for example, the transient monocular blurred vision called Uhthoff’s symptom—is also a strong indicator of MS. Lhermitte’s symptom, a painful or stinging sensation into the upper or lower extremities with neck movement, is a nonspecific indicator of potential multiple sclerotic spinal cord disease. Finally, inquiring about personal history of trauma (to the head or spine), travel outside the country, recent immunizations, sexually transmitted disease exposure, animal or tick bites, current medications, including herbal agents, and concomitant disorders (e.g., diabetes mellitus, hypertension), and family history of neurological, metabolic, or rheumatological disease will be important to include in narrowing the differential.
EXAMINATION Abnormalities in physical examination results may be more difficult to locate than a patient’s history would indicate. Assessments of visual fields and acuity, pupillary reflexes, presence of nystagmus, and facial or extremity musculature for weakness should all be done. Incoordination, ataxia, hyperreflexia, ankle clonus, dysarthria, and loss of abdominal muscle reflexes can be present in a patient with MS. This information not only aids in gathering criteria for the final diagnosis of MS, but it also helps in discerning against similar diseases such as the distal to proximal spread of weakness and lack of deep tendon reflexes in Guillain-Barré syndrome, the presence of ipsilateral loss of taste and retroaural pain found in Bell’s palsy, or the prominent dermatomal pattern of a hyperparesthesia due to spinal nerve compression or early varicella zoster development.
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DIAGNOSIS AND LABORATORY FINDINGS The laboratory workup for MS includes a variety of tests to help rule out diseases with similar symptom presentation. Such examinations include a CBC and serum vitamin B12 test for pernicious anemia, rapid plasma reagent for tertiary syphilis, serum protein electrophoresis and urinalysis for Bence Jones proteins in multiple myeloma, and angiotensin-converting enzyme for sarcoidosis. Rheumatological disorders, such as systemic lupus erythematosus, can be ruled out with antinuclear antibody assay, ESR and CRP test, and rheumatoid factor analysis. Metabolic panels for blood glucose, electrolytes, and kidney and liver function should also be taken. Infectious causes need to be considered by running HIV testing for acquired immunodeficiency syndrome dementia, Lyme borreliosis antibodies, and the less common human T-lymphotropic virus (HTLV) types 1 and 2, with analysis of serum or CSF. Epstein-Barr virus and Pasteurella multocida antibody titers can be checked for chronic fatigue syndrome and cat scratch disease, respectively. Finally, serum levels of the heavy metals, like mercury, and “therapeutic window drugs,” such as anticonvulsants, digoxin, and antipsychotics, should be obtained to assess for toxicity. Spinal tap for CSF analysis may be used to assess for mild lymphocytic pleocytosis, elevated immunoglobulin (Ig) G levels and oligoclonal bands, which are produced in the autoimmune attack. Two or more oligoclonal bands are found in 75%–90% of patients with MS, and 80% also have elevated IgG levels due to selective production. A normal total protein and glucose level are usually found in MS, whereas severe pleocytosis or the presence of polymorphonuclear leukocytes generally correlate with an infectious cause of symptoms or a more rapidly advancing demyelinating disease such as acute disseminated encephalomyelitis. Of prognostic value is the presence of intrathecal IgM synthesis which, early in the disease process, predicts a poor prognosis with regard to functional disability deterioration. Through computer averaging, a neurophysiological means has been developed to compare the latencies between stimulus and “response” for myelinated versus demyelinated axon transmission. These so-called evoked potentials, though adding to the suspicion of CNS disease and conduction anomalies, are not very sensitive and have no specificity to any pathophysiological process. More than 90% of persons with symptomatic criteria for MS have changes noted on T2-weighted MRI. The use of MRI with gadolinium contrast (DTPA), which is able to pass the blood-brain barrier where the vascular endothelium has been compromised due to an inflammatory response, has become the most sensitive measure of disease presence. Criteria that strongly support the diagnosis of MS in persons younger than 50 years of age include four or more lesions of equal to or greater
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than 3 mm in diameter, or three lesions, one or more of which is periventricular in location. For those older than 50 years of age, the same criteria apply, but with two of the following as well: (1) lesion diameter greater than 5 mm, (2) presence of lesions abutting the lateral ventricles, or (3) the presence of lesions in the posterior fossa. Though not part of the aforementioned criteria, lesions of the corpus callosum occur commonly in MS but not in other vascular processes. However, even with lesion location, number, and cumulative volumes, it remains a poor indicator of actual neurological impairment and prognosis. This is believed to be due to the fact that current scanning is unable to differentiate reversible edema and inflammation from actual demyelination or axonal loss. Responsiveness to therapy can still be measured with serial scans and clinical response and is commonly used as a marker for studying new medications. New technologies, such as proton magnetic resonance spectroscopic imaging, promise to better fill the objective gaps in determining treatment and prognosis.
TREATMENT Once diagnostic criteria have been met for definite or probable MS, the patient may be assigned to a clinical course defined by the symptom or impairment progression or resolution over time. This course determines the use of medications and planning of adequate and timely follow-up, and is therefore very important. Relapsing-remitting MS (RRMS), which composes nearly 85% of cases initially diagnosed, is typified by courses of relapsing symptoms that completely or nearly completely resolve with time. Some relapses may be spaced by months to several years. Within 10 years, 50% of patients with RRMS will convert to secondary progressive MS, which is constituted by a slow decline in neurological function in between relapses that never in and of themselves completely remit. Only 15% of persons are diagnosed with primary progressive MS, which has no improvement in symptoms whatsoever from the onset, but only a steady decline in function and worsening neurological deficits. Long-term studies, including all courses, show that 20% of patients have no functional limitation at 15 years, whereas 70%–75% have some degree of inability and are not employed. The treatment for MS is aimed at modifying the underlying autoimmune and inflammatory process and, dependent on neurological deficit, severity, and duration, specific symptom treatment as well. The initial attack is addressed with high-dose methylprednisolone given intravenously, generally 1 g daily for 3 days, followed by outpatient oral prednisone tapering down from 60 mg over 10–14 days if MRI findings are suggestive and/or functional impairment is present. RRMS, as defined previously, is then treated with IFNb-lb (Betaseron), IFNb-la (Avonex, Rebif), or glatiramer acetate (Copaxone), all approved in the United
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States, each with a 30% reduction in relapse rate. Each of these agents also decreases the number of new enhancing lesions on MRI, but only IFNb-la has shown to considerably delay onset of sustained progression of disability. Because of this factor and its once-weekly intramuscular dosing, as opposed to every other day or every day with IFNb-lb and Copaxone, respectively, Avonex has become the most commonly used. Even though the exact mechanism of action is not completely understood with these medications, the downregulation of proinflammatory cytokines, decreased MHC molecules on the surface of antigen-processing cells, and decreased vascular endothelial expression of adhesion molecules is thought to be the most likely mechanism, whereas Copaxone aids in increased T suppressor cell function. Due to the formation of neutralizing antibodies, these benefits are variable in their duration; recent studies show no proven effect beyond 1 year. Even a newer agent such as natalizumab, which reduces lymphocytes’ and monocytes’ ability to bind to the vascular endothelium and migrate into the parenchyma, is not immune to the formation of these binding antibodies, but having a 90% reduction in new lesions in preliminary studies still holds promise. Interestingly, some studies using mouse models have shown some degree of decreased nervous system inflammation with atorvastatin. It is important to note that suppressive therapy will not completely avoid disease exacerbations, which, depending on severity and type of relapsing symptoms, will require either repeat steroid therapy similar to doses given in initial therapy or symptomatic treatment. These episodes need to be distinguished from pseudoexacerbations, which are actually aggravated old symptoms brought on by illness, stress, or heat and are short-lived, usually lasting less than 48 hours. Most patients with relapsing MS have an average of one relapse a year. Patients whose MS advances to the secondary progressive type and who are having frequent relapses may continue with the IFN regimens as long as benefits are shown. For less frequent attacks, or for those who have lost observable benefits from IFNb or Copaxone, methotrexate administered in weekly oral doses, along with regular folic acid supplementation, may be used. The avoidance of alcohol and NSAIDs is a must to avoid the present, but low, occurrence of hepatotoxicity. Contraception must be discussed with the patient, and regular laboratory tests to monitor renal, hepatic, and bone marrow function are required. Recalcitrant cases can have the election of bimonthly methylprednisolone tapers added along with the methotrexate. Other medications such as mitoxantrone, cladribine, cytoxan, and azathioprine are also available, but studies are still ongoing on these more expensive and more toxic immunosuppressive drugs. Primary progressive MS has no approved, well-studied treatment and is addressed primarily with symptomatic and supportive care. Complications of MS are wide and varied and can require the involvement of
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urologists, pain management centers, psychologists, physical therapists, occupational therapists, and social workers. A variety of pain syndromes, including tonic spasms, chronic dysesthesias, and musculoskeletal pain, occurs, requiring treatment with overthe-counter anti-inflammatory agents or narcotic analgesics. Tricyclic anti-depressants (e.g., Elavil) and antiseizure medications, including Keppra, alone or in combination, can be helpful. Home and supervised physical activity are generally useful, especially swimming, which gives buoyant support and hypothermia. Associated spasticity triggered by lack of inhibition of the anterior horn cells in the brain or spinal cord is best treated with baclofen at a starting dose of 5 mg/day, advancing as needed and tolerated. On the other hand, some patients benefit from a certain degree of spasticity, especially in the lower extremities, to ambulate due to weakened hip flexor musculature. Additional medications as monotherapy or in combination include diazepam, clonidine, or tizanidine dosed according to the usual dosing guidelines. In extremely select cases, invasive procedures may be used, such as motor-point blocks or neurectomy of a specific muscle or groups of muscles. These must be used with caution so as not to produce a wasting syndrome and the resulting weakness. Depression and fatigue, which are common in patients with MS, are due to anxiety over the disease and its effects on the associated social groups. Bilateral disruption of the subcortical pathways may also cause inappropriate laughter or crying. Medications, including selective serotonin reuptake inhibitors, bimodal drugs (e.g., venlafaxine), and other antidepressants, are generally helpful. Symmetrel (100 mg twice daily) or Cylert (pemoline; 37.5 mg twice daily) can be used to combat severe fatigue along with scheduled naps and early work times. Meetings with a psychologist or support group have also been shown to be advisable and likely able to lessen the high incidence of suicides associated with this process. Social workers can be helpful in dealing with the occupational or financial hardships frequently experienced by both the patient and family. MS causes urinary symptoms in up to 80% of patients. The underlying problem should be assessed with urinary dynamic studies; these are most commonly performed by a urologist. Problems can arise from spasticity of the detrusor muscle, giving frequency and urgency, from dyssynergia of the internal and external sphincter, giving urinary retention or hesitation, or a combination of these two. Oxybutynin chloride 2.5–5.0 mg PO bid–tid, maximum dose 5 mg PO qid, can be used for persons voiding less than 200 ml, and with residual volumes less than 100 ml, because this is likely due to detrusor spasticity. Hyoscyamine sulfate, propantheline bromide, and tolterodine, which has fewer anticholinergic adverse effects, are alternatives. Persons who void more than 500 ml, and have postvoid residuals less than 100 ml, have hypotonic detrusor activity, whereas those with postvoid residuals greater than 100 ml likely have superimposed sphincter dyssynergia. This second group will
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benefit most from oxybutynin chloride, Credé’s maneuver, and/or intermittent self-catheterization. For those with functional disabilities that would make self-catheterization difficult or impossible, a trial of terazosin hydrochloride at a dose of 1–5 mg at bedtime may be used, keeping in mind that by lessening dyssynergia incontinence may occur. Finally, because this disease predominately affects young females during their childbearing years, it should be noted that the choice whether to have children after the diagnosis of MS is one that should be decided based on present symptom and functional severity and the availability of strong family and social support. Typically, relapses occur less commonly during gestation but increase in the 3–4 months postpartum. It is believed this is due to the rise in prolactin levels during this period and its immune-stimulatory effect. However, the net effect over this period compared with that occurring in a nonpregnant patient is equal in magnitude with no increased disease progression noted.
Bibliography Ackerman KD, Heyman R, Rabin BS, et al: Multiple sclerosis flare ups due to stress, Pain & Central Nervous System Weekly. December 30, 2002;14. Bernd CK, Hans-Peter H: Current disease-modifying therapies in multiple sclerosis, Semin Neurol 2003;23(2):133–145. Filippini G, Munari L, Incorvai B, et al: Interferons in relapsing remitting multiple sclerosis: A systematic review, Lancet 2003;361(9357):545. Finlayson M, Denend TV, Hudson E: Aging with multiple sclerosis. American Association of Neuroscience Nurses, J Neurosci Nurs 2004;36(5):245–251, 259. Hauser SL, Goodkin DE: Multiple sclerosis and other demyelinating diseases. In Kasper DL, Braunwald E, Fauci AS, Hauser SL (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: St. Louis, 2005, pp 2461–2471. Humes HD: Demyelinating diseases, In Kelley’s Essentials of Internal Medicine, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 1994, pp 832–833. Kita M, Goodkin DE: Multiple sclerosis. In Conn’s Current Therapy. WB Saunders: Philadelphia, 2000, pp 896–902. Marieb E: Nervous system organization. In Human Anatomy and Physiology. Benjamin/ Cummings Publishing: Redwood City, CA, 1989, pp 333–358. Miller DH, Khan OA, Sheremata WA, et al: Natalizumab’s use in multiple sclerosis, N Engl J Med 2003;348:15–23. Sawsan Y, Olaf S, Patarroyo JC, et al: The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease, Nature 2002;420:78–84. Schroeder SA, Krupp MA: Multiple sclerosis. In Current Medical Diagnosis and Treatment. Appleton & Lange: East Norwalk, CT, 1990, pp 671–673. Tejada-Simon MV, Zang YC, Hong J, et al: Cross-reactivity with myelin basic protein and human herpes virus-6 in multiple sclerosis, Ann Neurol 2003;53(2):189–197. Toran RE: Multiple sclerosis. In Medicine for the Practicing Physician, ed 4. Appleton and Lange: Stamford, CT, 1996, pp 1841–1844. UCB Pharm, Inc: Keppra in combination with conventional treatments for multiple sclerosis, Pain & Central Nervous System Weekly. April 14, 2003;26. Villar LM: Intrathecal IgM synthesis is a prognostic factor in multiple sclerosis, Ann Neurol 2003;53(2):222–226. Wingerchuk DM, Carter JL: Practical consultations: Multiple sclerosis, Semin Neurol 2003;23(3):253–264.
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Myasthenia Gravis REX L. HOBBS, JR.
ICD Codes: Myasthenia gravis 358.00, Exacerbation of myasthenia gravis 358.01
Key Points/Quick Reference The classical presentation of MG is weakness of the facial and the extraocular muscles resulting in diplopia, ptosis, and ‘‘incomplete’’ facial expressions, all of which worsen with increased use of these muscle groups. If the extremities are involved, reflexes are preserved. ! Emergency Action ! Good airway control for persons with MG who are “in crisis” is of the utmost importance.
DEFINITION Myasthenia gravis is an autoimmune disorder in which antibodies are produced that block acetylcholine receptor sites on muscles, thereby blocking the transmission of activating nerve impulses resulting in weakness. This weakness is made worse by repetitive use and improves, at least somewhat, with rest. Most cases involve the facial and proximal musculature; however, certain forms of the disease will involve muscles of the extremities as the primary presentation. In either case, complications, including death, can occur if the respiratory muscles become involved, and this can happen acutely.
EPIDEMIOLOGY The incidence of MG has increased over the last 50 years due to the aging populace and improved methods of diagnosing the disease. Even so, its prevalence is no more than 20 per 100,000, or about 60,000 cases in the United States. Women with the disease tend to outnumber men at a ratio of 3:2. As recently as the 1960s, the mortality rate ranged between 70% and 80%, but with advances in critical care management this number has dropped to less than 5%.
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PATHOLOGY Normal muscle activation takes place at the neuromuscular junction, which consists of the presynaptic motor nerve terminal, the synaptic cleft, and the acetylcholine receptor on the muscle-based postsynaptic end plate. As an action potential approaches the terminus of the presynaptic nerve, it results in an influx of calcium, causing acetylcholine-containing vesicles to release their contents into the synaptic cleft. At approximately 50 nm, the synaptic cleft is rapidly bridged by the acetylcholine binding to its receptor on the muscle surface, resulting in muscular contraction. Several other substances are involved in aiding this action as well. There are some differences in the makeup of neuromuscular junctions in various parts of the body, such as those related to the extraocular muscle groups. The pathophysiological mechanism in MG is the blockade of the acetylcholine receptor by autoantibodies thereby limiting the muscle-activating capability of acetylcholine. Over time, the presence of these antibodies results in the activation of complement and destruction of the receptors and decreases the overall surface area of the muscle-receptive end plate. The production of these antibodies is known to be T-cell mediated and a probable result of loss of immunomodulatory effects of the thymus and the general loss that occurs with age, but the exact mechanism is not fully known. The eventual outcome of this autoimmune blockade is muscle weakness that worsens with increased usage and repetitive activity.
CLINICAL PRESENTATION The classical presentation occurs with weakness of the facial and extraocular muscles, resulting in diplopia, ptosis, and “incomplete” facial expressions, all of which worsen with increased use of these muscle groups. In some cases, weakness of the tongue or decreased soft palate elevation will cause a nasal or slurred speech with swallowing difficulties such as nasal regurgitation also possible. Rest will generally improve these symptoms, at least transiently. Extremity muscle involvement, which is a more uncommon form, generally involves the proximal extremity muscles and has the same pattern of worsening with use. It is interesting to note that in most cases of extremity muscle involvement deep tendon reflexes are intact. This is helpful in differentiating other processes like Guillain-Barré syndrome, in which deep tendon reflexes are completely lost as the disease progresses. The most dreaded presentation is when the respiratory muscles become involved, at which time the patient is said to be “in crisis.” This sort of process occurs in 20% of patients, in many cases within the first few years of diagnosis. When in crisis, the patient may present with either upper or lower respiratory muscle involvement, resulting in difficulty in swallowing one’s own saliva or an inability to speak without becoming short of breath. These symptoms
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will progress toward a more rapid and shallow breathing, use of abdominal accessory muscles, and stridor which, if left untreated, will result in respiratory failure and death. Advancements in diagnosis, treatment, and critical care capabilities have helped to greatly reduce the mortality associated with such events over the last 50 years.
EXAMINATION As with any report of muscular weakness or diplopia, a full neurological examination is needed to not only quantify muscular weakness but also, in the case of MG, to make sure that sensory function, cognition, and deep tendon reflexes are intact. This will aid in ruling out such differential diagnoses as Guillain-Barré syndrome, botulism, or even CNS lesion. Observing for tremor, muscular fasciculations, and muscular atrophy are important to determine the presence of any upper motor neuron disease or primary muscle disorder. Because patients may present early with visual symptoms only caused by extraocular muscle involvement, the examination results may be completely normal. However, these patients may still have visible ptosis or onset of double vision if repetitive movements are performed such as rapid blinking or a sustained lateral gaze. If respiratory symptoms are of concern, a cardiopulmonary examination is mandated, with the aim of checking for respiratory effort, presence of cyanosis, and use of abdominal accessory muscles. An O2 saturation and measurements of vital capacity and inspiratory/expiratory peak flows will also be helpful, especially if done in a serial fashion.
DIAGNOSIS If history and physical examination results seem to point to MG as the culprit, other tests can aid in confirming the diagnosis. The Tensilon test, first used in the early 1950s, makes use of edrophonium chloride, which inhibits the breakdown of acetylcholine by acetylcholinesterase in a rapid but short-lived manner resulting in a sudden if not complete improvement in symptoms. This test is rather specific for MG, and this is the reason it is generally so helpful. Electrophysiological testing using repetitive nerve stimulation can also be helpful because it provides an objective measurement of degrading muscular responses to stimuli. However, it can not be used for some muscle groups and is not very sensitive in others. Serological testing is available to detect the presence of antibodies to the acetylcholine receptor; however, the presence and level of these autoantibodies can be highly variable from patient to patient and may even have a negative result in persons with ocular symptoms only. In addition, those with generalized MG symptoms may need testing for IgG to musclespecific tyrosine receptor kinase to properly diagnose the disease if
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acetylcholine receptors are negative in the presence of convincing signs and symptoms. Because an enlarged thymus is found in many patients with MG, a CT scan of the chest may also be helpful; however, this test is not specific enough to rely on for determining disease presence or absence.
TREATMENT First-line treatment for MG involves the use of acetylcholinesterase inhibitors that prolong the presence of acetylcholine in the synapse. Such drugs as Mestinon (pyridostigmine bromide) and Prostigmin (neostigmine bromide) are examples of this drug class. These oral agents provide excellent control for mild disease but need to be dosed three to four times daily and can cause cholinergic symptoms and weakness themselves at higher doses. Some patients will require immunomodulating medications such as prednisone, or less often, Imuran (azathioprine), Sandimmune (cyclosporine), or Cytoxan (cyclophosphamide), to reduce the level of offending antibody levels. These are also used when the patient is in crisis. The effects of these drugs must be monitored because they can frequently cause leucopenia, secondary infections, and other related effects. Plasmapheresis is rarely used, except in the acute setting where it can reduce antibody levels quickly, but it requires a central line to maintain. The final measure is surgical involvement for a thymectomy. Even when an enlarged thymus is noted on diagnostic evaluation, its removal does not always result in cure or even regression of the disease.
Bibliography Hughes BW: Pathophysiology of myasthenia gravis, Semin Neurol 2004;24(1):21–30. Juel VC: Myasthenia gravis: Management of myasthenic crisis and perioperative care, Semin Neurol 2004;24(1):75–81. Kasper DL, Braunwald E, Fauci AS, Hauser SL (eds): Myasthenia gravis and other diseases of the neuromuscular junction. In Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005, pp 2518–2523. Meriggioli MN, Sanders PB: Myasthenia gravis: Diagnosis, Semin Neurol 2004;24 (1):31–39. Phillips LH II: The epidemiology of myasthenia gravis, Semin Neurol 2004;24(1):17–20. Saperstein DS, Baron RJ: Management of myasthenia gravis, Semin Neurol 2004;24 (1):41–48. Tintinalli JE, Kelen GD, Stapczynski JS: (eds): Myasthenia gravis. In Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1424–1426.
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Neurological Examination REX L. HOBBS, JR. The approach to the patient with neurological symptoms is multifaceted, but taken in a systematic way it can yield much in the way of the selection of diagnostic studies, and in many cases, it can help to provide a solid diagnosis. Historically, the neurological examination is not new. Early Greek physicians and Renaissance scholars postulated the functional aspects of the brain and the “cords” that spread from it. Such ideas as the cerebellum containing a storehouse of animal spirits are most certainly incorrect but nonetheless entertaining conclusions. It was not until the late 1800s and into the early 1900s that the modern examination was completed from the compiled works of such great physicians as Holmes, Charcot, and Babinski. The indications for a partial or complete neurological examination are numerous, with some of the more common ones listed in Table 9-2. In some cases, a complete examination is performed to screen for subtle disease processes as in a Department of Transportation (DOT) physical, whereas only certain components may be needed in a more focused problem such as blurred vision. The type of examination performed is based on symptom history and is modified pending abnormalities within examination results. The complete history of the symptom, as in all areas of medicine, is of paramount importance in guiding the examination and in establishing a more narrow differential diagnosis. Such factors as onset, progression, associated symptoms, and aggravators and alleviators are only a few of these symptom characteristics. For example, a severe headache of new onset in a patient older than 50 years is much more worrisome than a similar patient who is having a recurring headache that is unchanged in its character or frequency. After obtaining this information, consideration can also be given to the underlying functional neuroanatomy to better establish the location in the nervous system of the problem.
Table 9-2 Indications for a Neurological Examination
Weakness or fatigue Sensory changes Dizziness Headache Seizures
Loss of coordination Memory loss Confusion
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ANATOMICAL CONSIDERATIONS The first factor of any symptom is to consider the potentially involved anatomy. In this case, breaking the nervous system into the central and peripheral sections is important. The CNS includes the brain and spinal cord and is the main processor of incoming sensory information and outgoing responses to stimuli as well as enacting orders from the conscious mind. The brain itself is broken up into numerous functional sections with varying degrees of overlap and redundancy. These sections, or regions, regulate emotions and memories, coordinate movements (both voluntary and involuntary), and maintain basic life functions such as respirations and heart rate (Table 9-3). The peripheral nervous system is made up of the 31 pairs of spinal nerves that exit the cervical, thoracic, lumbar, and coccygeal portions of the spinal column and then split into several different patterns of both motor and sensory function. These patterns are roughly the same from person to person and create specific superficial sensory “bands” across the body called dermatomes, and the motor portions control specific muscle groups. This allows for some spinal nerve root problems to be identified based on examination results alone as in a sciatic pattern of pain in a patient with a herniated lumbar disk at L5–S1. In a similar way, lack of muscle strength in a given group may also elucidate the diagnosis. The cranial nerves are also considered by many, but not all, to be part of the peripheral nervous system. These nerves originate directly from the ventral surface of the brain and include sensory and motor nerves. The bulk of their activity occurs around the facial and neck area but includes higher sensory function such as vision, taste, and hearing. Finally, the peripheral nervous system includes the neuromuscular junction, where motor commands from the nervous system are translated into action by the muscles. These junctions, occurring throughout the body, use neurotransmitters (mainly acetylcholine) to cross the synapse and bind with
Table 9-3 Central Nervous System Anatomy and Function ANATOMY Frontal lobe Parietal lobe Temporal lobe Occipital lobe Basal ganglia Thalamus Hypothalamus Cerebellum Brainstem Spinal cord
FUNCTION Voluntary movement, personality, thought, insight, judgment Primary sensory cortex Memory, hearing Primary visual cortex Automated movements (walking) Primary sensory relay Temperature, sleep, emotion, pituitary function Balance, coordination of voluntary movements Cardiorespiratory center Conduit for ascending and descending nerve tracts, reflex activity
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an activating receptor, thereby resulting in muscle activity. It is here that such diseases as MG exert their effect by blocking this muscular stimulation via autoantibodies, thereby resulting in weakness. In addition to anatomy, an understanding of normal function of the nervous system is key. Normal function will have certain bounds of variability due to factors such as age, activity level, current medications, and general health. It is also important to remember that a fully cognizant and compliant patient who is able to follow instructions is required for many examinations to garner high-quality, reliable information—even in the face of excellent examination technique.
GLOBAL ASSESSMENT The initial neurological assessment begins when the practitioner enters the room and observes the patient’s posture, body positioning, grooming, and alertness (or level of consciousness). Such factors can be very helpful in establishing a diagnosis in the emergent to the chronic patient. There are numerous objective grading tools available to quantify and summarize this information beyond simple notations. One of the most well known is the Glasgow Coma Scale (Table 9-4) used to assess level of consciousness. This objective measure based on established criteria is used for initial assessment and to follow response to therapy and infer prognosis. Total scores of less than six are generally classified as a state of coma, with higher scores given titles such as obtunded, stuporous, and normal. Orientation is a product of memory and attention and is usually assessed by determining awareness to person, place, and time. Questioning should begin with specific questions (e.g., full name, name of clinic, approximate clock time) to more general (e.g., partial name, name of town, month of the year) as needed, pending the patient’s correct answers. Normal findings are many times noted as “oriented times three,” whereas the observation of an abnormality might be written as “oriented to self only,” for example. A patient’s affect is represented by the facial reactions, tone of voice, and demeanor that are observable from moment to moment, whereas the patient’s mood is the dominant emotion carried by the patient the majority of the time. An example of this difference might be the withdrawn and sullen mood of a depressed patient that is roused to a brief smile by a joke that would represent a change in affect. “Appropriate mood and affect” might be noted in an otherwise normal patient. Other basic mental functions and higher cognitive functions can also be evaluated with a variety of tools on an as-needed basis. The minimental status examination is commonly used to provide an overall appraisal of these factors in any setting where normal mental function
454 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 9-4 Glasgow Coma Scale Eye Opening: Spontaneous To voice To pain None Best Verbal Response: Oriented Confused Inappropriate words Incomprehensive None Best Motor Response: Obeys commands Localizes pain Withdraws Flexion Extension None TOTAL:
4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
is in question. It can also be used to follow response to therapies with diagnoses such as Alzheimer’s disease.
SENSORY EXAMINATION Sensory function of the peripheral nervous system is divided by function, specific sensation, type of receptor, and the spinal tract by which the information is sent to the brain for processing. For clinical assessment purposes we will concentrate on the spinothalamic tract, which carries pain and temperature, and the posterior columns, which carry vibration. Both of these tracts ferry signals for light touch, which will also be discussed. The tracts are separated in a right/left fashion and should be comparatively tested whether it is an extremity, the face, or the trunk, being mindful of dermatome or spinal root distribution. Many sensory problems begin with distal involvement and progress proximally, making it thereby necessary to perform the examination in a similar fashion so that if a deficit is noted the extent might also be noted. Vibration sense, the first to be lost in diabetic peripheral neuropathy, is typically tested over the joints and boney prominences. For testing, the clinician should use a 128- or 256-Hz tuning fork. The patient should be asked to close his or her eyes while the stem of the active tuning fork is lightly placed over the dorsal aspect of the great toe’s metatarsophalangeal joint; the patient is then asked to tell the physician when the vibration is felt. This can be further assessed by deactivating the fork with the other
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hand without moving the stem; the patient is asked whether the vibration is still felt. This can be repeated bilaterally, advancing proximally (lateral malleolus ! anterior tibial plateau ! trochanter) as needed until normal sensation is noted. This process can also be performed on the upper extremities in a similar fashion. Pain sensation is defined, for the purposes of testing, as the ability to identify a sharp versus a dull stimulus. Pain is mediated by numerous other receptors, tracts, and areas within the brain, but a gross level of function is what would be determined in this case of the peripheral nerve, spinal tract, and associated regions of the brain. Reasons for testing might include ruling out a severed nerve in a finger laceration or determining lumbar nerve root involvement in someone reporting leg numbness. A common technique for this testing might involve the use of an opened safety pin; the skin is gently touched with the sharp end in a right-to-left comparative fashion, progressing in a distal-to-proximal pattern, while the patient’s eyes are closed. The patient is asked to report when he or she feels the sharp sensation. Some clinicians will also occasionally alternate use of the dull end to determine whether the patient is actually feeling sharpness or just reporting the pressure. Being mindful of areas of deficit may reveal a specific nerve distribution. It is also, of course, important to use the safety pin only once to avoid inadvertent spread of infection. Proper technique for light touch assessment is done using a wisp of cotton and following the same pattern as that used to test for pain sensation.
MOTOR EXAMINATION The assessment of the motor function begins with a general survey of the symmetry, size, and bulk of all the muscle groups comparing bilaterally. Involuntary movements such as tics and tremors should be observed with notation of their location, frequency, and severity noted, if present. Some of these involuntary movements may occur at rest or only with activity, so any aggravators should also be noted. Muscle strength is also compared bilaterally using the same muscular groups for comparison, with levels of normalcy based on age, training level, and short versus long types of muscle. While asking the patient to move a particular area (i.e., flex, extend, abduction, adduction, rotation) the practitioner should be mindful of the nerve root that innervates for that activity or muscle(s). As the patient performs these movements, the physician should provide a steady amount of resistance. The amount of resistance used will vary from person to person; it is important to not “overpower” the patient. If weakness is noted, the level of resistance should be lessened to the point where the patient is only working against gravity. Muscular strength is graded on a scale with abnormal results originating from a long list of differential
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diagnoses, including such areas as trauma, neurological, electrolyte, and metabolic factors (Table 9-5).
CRANIAL NERVE EXAMINATION The physicians of Alexander the Great were some of the first to identify the cranial nerves, but their importance or functions were not identified until much later. Early writings reveal a variety of numbering schemes that range from 7 to 10. It was not until the early 1800s that the modern numbering scheme of 12 paired nerves was established. Each paired nerve may have a motor, sensory, or mixed function that can be readily assessed and, because they connect directly with the brain, can aid in the diagnosis of such intracranial pathology as a stroke. The general approach needs to be a systematic one that compares function bilaterally. Many clinicians will do this examination as either a separate examination or will integrate it into their head, ears, eyes, nose, and throat (HEENT) examination.
Cranial Nerve I (Olfactory) The ability to smell is attributed to cranial nerve I, the olfactory nerve, which penetrates the cribriform plate at the base of the ethmoid bone and covers the ceiling of the nasal cavity. Normal function can be disturbed by nasal membrane swelling or obstruction, as from infection or atopic disease, as well as from structural issues like a deviated septum. Thus, checking for bilateral nasal patency is important before nerve testing. The olfactory nerves’ function is done by using familiar substances such as coffee or lemon sealed in opaque containers. Noxious substances like ammonia actually stimulate the fifth cranial nerve and thereby should not be used. While having the patient close his or her eyes and occlude one nostril, the examiner should waft one of the open containers under the opposite nostril, asking whether any scent is noted and, if so, asking the patient to identify it. This process should be repeated on the opposite
Table 9-5 Muscle Strength Grading Scale 0 1 2 3 4 5
! ! ! ! ! !
No muscular contraction Trace of muscular contraction Active movement with gravity eliminated Active movement against gravity Active movement against gravity and some resistance Active movement against full resistance (normal)
-paresis: impaired strength -plegia: absence of strength (paralysis)
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side using a different substance. Such common processes such as smoking can result in anosmia, or the inability to smell.
Cranial Nerve II (Optic) Vision is attributed to the function of cranial nerve II (the optic nerve), which radiates from the visual cortex in the occipital lobe to the receptive fibers that make up the retina in each eye. Medial fibers cross over at the optic chiasm located above the pituitary gland. Assessment includes a funduscopic examination to visualize the retina directly, looking for any abnormalities such as papilledema, which is seen as a blurring of the optic disk and usually represents an intracranial mass or increased pressure. (Papilledema should always be addressed as a medical emergency.) Next, visual acuity, which is mitigated by other ocular structures such as the lens, still reflects gross nerve function. This is most commonly achieved by use of either a wall-mounted Snellen chart (at 20 feet) or a handheld Rosenbaum chart (at 14 inches). In both cases, the patient is asked to read the smallest print possible with each eye solely and then together. Lastly, visual fields are checked to make certain there is no loss of peripheral vision, which most commonly occurs in the lateral fields. A lesion or stroke of the optic chiasm or posterior cerebral artery to would result in partial vision loss, whereas a lesion of the optic nerve would result in complete, unilateral vision loss. To test, the practitioner should have the patient maintain his or her gaze directly into the practitioner’s eyes at a distance of about 2 feet. The patient should be instructed to point when he or she sees the physician’s fingers, or the erasure end of a pencil, move into the field of vision as the physician moves his or her fingers from lateral positions and moves them slowly together. Both should be seen at the same time. This should be repeated in the upper and lower visual fields, as well.
Cranial Nerves III, IV, VI (Oculomotor, Trochlear, Abducens) Cranial nerves III, IV, and VI (the oculomotor, trochlear, and abducens nerves, respectively) share a common motor function in that they all innervate the muscles responsible for extraocular movements. The oculomotor nerve also regulates lens and papillary responses. None of these nerves has a sensory component. The functional layout of the extraocular movements and innervations is shown in Figure 9-1. It is important to systematically assess each of these movements. Many problems with deficient extraocular movements lie in central lesions involving the nerves themselves, and some reasons for abnormalities in movements or orientation of the globe at rest can involve muscular entrapment, as in an orbital blowout fracture.
458 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER SR 3
IO 3
SR 3
LR 6
LR 6
3 IR
4 SO SR IO LR MR IR SO
Superior rectus m. Inferior oblique m. Lateral rectus m. Medial rectus m. Inferior rectus m. Superior oblique m.
Eye Deviation
Name
Upward Downward Outward Inward
Hypertropia Hypertropia Exotropia Exotropia
Figure 9-1. The functional layout of extraocular movements and innervations.
To test for this, the practitioner should have the patient follow the end of the former’s finger with his or her eyes only, not turning the head. The practitioner should observe both eyes, noting any inequalities in their movement. Then the patient should be asked to follow the end of the practitioner’s finger inward toward the patient’s nose, causing a crosseyed appearance. The clinician should watch not only for symmetrical movement but also for bilateral pupillary constriction. Next, the clinician should check for direct (when light is shown in to the eye) and consensual (light shown into opposite eye) pupillary constriction by shining a pen light into one eye momentarily then by switching eyes and repeating. The pupils should respond equally to either stimulus.
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Cranial Nerve V (Trigeminal) Assessment of both the motor and sensory components of cranial nerve V (the trigeminal nerve) is important. Originating from the pons, the trigeminal nerve’s motor portion innervates the temporalis and masseter muscles as well as other muscles of the scalp, and the sensory branch splits into three divisions: the temporalis (I), maxillary (II), and mandibular (III), that serve the face and anterior scalp. These divisions are illustrated in Figure 9-2.
Figure 9-2. Three divisions of the sensory nerve branch: the temporalis (I), maxillary (II), and mandibular (III).
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For motor testing, the patient should be asked to clench his or her jaw, and the practitioner should observe and palpate for muscular contraction, especially over the masseter and temporalis muscles. The response should be equal bilaterally and without signs of atrophy. Sensory testing involves checking for light touch and sharp/dull discrimination, as described in the sensory testing section of this discussion. As always, this test should be performed with the patient’s eyes closed and portions of each branch should be compared bilaterally. Weakness and numbness commonly occur due to stroke, whereas increased sensitivity may occur with facial shingles, certain migraine phenomena, and trigeminal neuralgia (also called tic douloureux).
Cranial Nerve VII (Facial) Cranial nerve VII, also known as the facial nerve, has both a sensory and motor function. Part of this nerve’s sensory function involves the sense of taste over the anterior two thirds of the tongue, and cranial nerves IX and X carry the posterior third. This function is generally not tested but if performed needs to be done one side at a time using an applicator soaked in a sweet, salty, or bitter tasting substance. As in the test of the sense of smell, the ability to determine a flavor is present and properly identifying the flavor are both needed. The more commonly known, and tested, function is this nerve’s motor innervations of the muscles of facial expression. A complete motor function assessment becomes especially important when symptoms of facial weakness are described or if facial drooping (usually unilateral) is noted. Such weakness can be caused by a central lesion, as in a stroke, or a peripheral lesion, as with Bell’s palsy. Distinguishing between the two of these potential causes becomes obviously important. This is sometimes easily achieved by the presence of other sensory or motor deficits, such as aphasia or extremity weakness, which would point to a central lesion. However, a small, localized area of central ischemia may not lend itself so easily to diagnosis. This can still be determined by a complete examination. The patient should be asked to raise his or her eyebrows, and the clinician should look for symmetrical movement and forehead wrinkling. Next, the patient should be asked to close both eyes tightly and resist the clinician’s attempts to gently open them by applying upward pressure on the upper eyelid. Subtle, unilateral weakness may be found this way if the patient is unable to maintain closure. Moving on to lower facial muscles, the examiner should have the patient bare his or her teeth, as in a big smile, and should look for bilateral movement of the lips and the presence of facial creases. For more subtle muscle weakness in this area, the patient should be asked to puff out his or her cheeks and maintain this for 10–15 seconds, during which time there should be no air leakage from the lips, even with light pressure applied to both cheeks. A complete, unilateral facial weakness is indicative of a peripheral lesion,
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whereas a unilateral weakness of the lower facial muscles indicates a central lesion.
Cranial Nerve VIII (Vestibulocochlear) Cranial nerve VIII (the vestibulocochlear nerve) is responsible for the sense of hearing and is grossly assessed with the patient’s ability to comprehend and respond to questions during the history-taking portion of the visit. The volume of the responses and the presence of any speech deficits should be noted. However, a more definitive evaluation is recommended when loss of hearing is suspected. Initially, the patient should be asked to occlude one ear as the clinician whispers a simple phrase (e.g., “1, 2, 3”) into the other ear at a distance of about 6 inches; the patient should be asked to repeat the phrase back. The examiner should switch ears and repeat the process with a different phrase. Hearing loss can occur from such things as cerumen impaction, tympanic membrane perforation, inner ear infections, and, in some instances, simply advanced age. More formal audiometric testing may be needed for some patients to determine the needed intervention.
Cranial Nerves IX and X (Glossopharyngeal and Vagus) Both cranial nerves IX and X (the glossopharyngeal and vagus nerves, respectively) share many common functions and are commonly tested simultaneously. The parasympathetic function of the glossopharyngeal nerve and the extensive innervations and interaction of the vagus nerve with the respiratory, circulatory, and digestive systems goes beyond the scope of this text. Like the facial nerve, these nerves have a sensory role by serving taste sensation over the posterior third of the tongue and proprioception in the pharynx to aid in swallowing. But it is also the motor portion of these nerves that is more commonly assessed. To test these nerves, the patient should be asked to open his or her mouth widely and say “ah.” There should be a symmetrical elevation of the soft palate and uvula. Next, using a tongue blade, the examiner should touch the posterior of the tongue. This should result in the symmetrical, medial movement of bilateral tonsillar pillars and soft palate elevation, giving the typical “gag” reflex. Ideally, both sides of the tongue should be stimulated to rule out the presence of a unilateral lesion. Other signs of a deficit in either nerve would be numbness in the throat or a hoarse or nasal quality to the voice.
Cranial Nerve XI (Spinous Accessory) The sternocleidomastoid (SCM) and trapezius muscles, which aid in stabilization and movement of the cervical spine and shoulders, receive
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their innervation from the eleventh cranial nerve (the spinous accessory nerve). This nerve actually originates in the upper cervical spine but ascends into the cranium before descending back to its muscular connections, thereby making either cervical or intracranial sites locations for lesions that might result in weakness. Testing involves the patient shrugging his or her shoulders while the clinician looks for symmetrical movement and effort. The patient’s upper extremities should be otherwise relaxed. Then, this position should be maintained as a moderate amount of downward pressure is applied over the shoulders to test for subtle loss in muscle strength. Next, with the patient’s head in a level, neutral position, the clinician should have him or her rotate the head to either shoulder while the clinician places gentle resistance to the opposite side of the face. The examiner should observe for the more pronounced appearance of the sternocleidomastoid muscle on both sides with this maneuver and should grade muscular strength on the usual objective scale (i.e., 0–5).
Cranial Nerve XII (Hypoglossal) Motor function of the tongue is achieved through cranial nerve XII (the hypoglossal nerve), and therefore it plays a role in speech and swallowing. Testing involves having the patient stick the tongue straight out and then move it from side to side. The tongue itself should be symmetrical without signs of atrophy, and its movements should be equal in degree. A more subtle weakness of the tongue can be tested by asking the patient to push the tongue against one side of the buccal mucosa, causing the cheek to protrude outward. The clinician should gently push against the cheek, having the patient maintain the tongue’s position. This should be repeated on both sides.
DEEP TENDON REFLEXES To be elicited, reflexes require an intact afferent (sensory) nerve, interneuron junction in the spinal cord, an efferent (motor) nerve, neuromuscular junction, and muscle. Lesions in any one of these areas can result in poor to absent reflexes as in spinal cord injury, spinal nerve root compression, or severed muscle. Hyperactive reflexes usually involve an upper motor neuron problem, as in hyperthyroidism. There are many different reflexes that occur throughout the body, including the cremasteric, anal, and glabellar; however, this discussion will center around the more commonly tested deep tendon reflexes. Each one of these involves a specific skeletal muscle and spinal nerve root, thereby allowing testing to assess the reflex arc and, somewhat indirectly, its component parts (Table 9-6).
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Table 9-6 Deep Tendon Reflexes MUSCLE/REFLEX Biceps Brachioradialis Triceps Knee Plantar Ankle
SPINAL NERVE ROOT C5 and C6 C5 and C6 C6 and C7 L2, L3, and L4 L5 and S1 S1
Deep tendon reflex responses are graded on an objective scale that allows for comparison from one side to the other as well as for observing for response to therapy. Determining “normal” responses requires time and exposure to this examination, allowing for more uniform grading (Table 9-7). Proper technique begins with a relaxed, and, if necessary, distracted patient. Next, the extremity being tested needs to be in a neutral to partially flexed position and supported to avoid voluntary muscular contraction. Regardless of the type of reflex hammer used, it should be held loosely in the hand using wrist movement, not upper arm, to strike the appropriate tendon. The examiner should make sure that the patient’s clothing, examination table, and his or her own technique do not inhibit muscular responses. The physician should observe for movement distal or muscular contraction proximal to the tendon strike. The result should be a single, brisk, and unilateral response. For those examinations in which the reflex is weak, reinforcement techniques can be used to accentuate reflexes. This is accomplished by asking the patient to perform isometric muscle contraction in a group other than that being tested. Examples would include clenching the jaw while assessing the upper extremity reflexes and gripping the hands in front of the chest while pulling away from each other while doing the lower extremity reflexes. The Babinski reflex, or Babinski response, is elicited differently in that the bare sole of a foot is “scratched” with the handle tip of the reflex hammer in a single motion from the heel across the ball of the foot. A normal response would be plantar flexion of all the toes. A fanning of the toes, however, can indicate an upper motor neuron disease or a drug or alcohol intoxication. Finally, hyperactive Table 9-7 Scale for Grading Deep Tendon Reflexes 5þ 4þ 3þ 2þ 1þ 0
Jerk-like response that spreads bilaterally Very brisk; clonus is possible Brisker than average Average or normal response Somewhat diminished No response
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reflexes, grades þ3 to 5, should be further assessed by checking for clonus. This is done by supporting the patient’s relaxed leg in a knee-flexed position while repeatedly plantar and dorsiflexing the ankle, then suddenly holding the foot gently in a dorsiflexed position. Rhythmic oscillations of the foot, observed or felt, indicates the presence of clonus and confirms an upper motor neuron disease.
CEREBELLAR EXAMINATION The cerebellum, which is part of the brainstem, acts functionally to aid in the coordination of both conscious and unconscious motor activity. The smoothness, fluidity, accuracy, and speed at which all activities occur are fine-tuned by this region of the CNS. Balance is also a function of this region of the brain, along with several other areas as well. Alcohol, which exerts a powerful inhibitory effect on cerebellar function, when ingested acutely causes the typical symptoms seen in most cerebellar diseases that may include tremor and involuntary movements. Assessment includes many of the techniques used by law enforcement for sobriety testing. Rapid alternating movements are performed in the upper and lower extremities. First, the patient should rapidly pronate and supinate both forearms simultaneously; then, he or she should tap the ball of the foot against the examiner’s hand, bending at the ankle, one at a time. The clinician should observe for slow, irregular, and clumsy movements indicative of dysdiadochokinesia. Upper and lower extremity assessments are also done in point-to-point testing. Using the tip of the index finger, the patient should touch the end of his or her nose, then the end of the clinician’s finger, repeatedly. After several successful attempts, the examiner should alter the position of his or her finger. For the legs, the patient should be asked to run the heel of one foot down the anterior leg from the knee to the tip of the toes, then repeat with the opposite side. Again, the actions should be smooth and accurate. An inability to regulate the speed and direction of the movements is termed dysmetria. Testing for balance and position sense is done via the Romberg test. In this examination, the patient should stand with his or her feet together, maintaining an upright posture for 30 seconds. If successful, he or she should continue to hold this position for another 30 seconds with eyes closed. A person is said to have a positive Romberg result when balance is lost upon closing the eyes, indicative of a loss of position sense. An inability to maintain this posture with eyes opened is termed a cerebellar ataxia.
SPECIAL EXAMINATIONS Special examinations abound for the neurological system, with a certain amount of carryover into the musculoskeletal examination. Two that will
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be discussed here are the Kernig and Brudzinski signs, both of which aid in the diagnosis of meningeal irritation from such processes as meningitis or an intracranial bleed. A positive Kernig sign occurs when pain occurs in the lower back and/or there is resistance to elevating a straightened leg while in the supine position. While the patient is still supine, the clinician should flex the patient’s neck and observe for flexion of the hips and knees. This is a positive Brudzinski sign. It should be noted that both of these examinations are somewhat weak predictors of the presence of meningitis and should always be considered along with other clinical information.
Bibliography Fine EJ, Ionita CC, Lohr L, et al: The history of the development of the cerebellar examination, Semin Neurol 2002;22(4):375–384. Freeman C, Okun MS: Origins of the sensory examination in neurology, Semin Neurol 2002;22(4):399–488. Nolan MF: Introduction to the Neurologic Examination FA Davis: Philadelphia, 1996. Seidel HM, Ball JW, Daines JE, et al: Mosby’s Guide to Physical Examination, ed 3. Mosby–Year Book: St Louis, 1995. Steinberg DA: Scientific neurology and the history of the clinical examination of selected motor cranial nerves, Semin Neurol 2002;22(4):349–356.
Seizures and Status Epilepticus GARY W. DUFRESNE
ICD Codes: Seizure 780.3, Status epilepticus 345.7
Key Points Seizures are an abnormal repetitive electrical discharge by a group of neurons in the cerebrum. Status epilepticus is a true emergency, traditionally defined as one seizure lasting more than 30 minutes or multiple seizures without return to baseline level of consciousness in between seizures. Recently, experts in the field have suggested that providers should consider a patient in status epilepticus if he or she has a seizure lasting more than 5 minutes. The healthcare provider’s first priority is to stop the seizure and support the ABCs (i.e., airway, breathing, circulation).
466 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! Emergency actions include assessment and support of the ABCs, establishment of a safety net, stopping the seizure, and then render supportive care. The first-line medication for seizures is lorazepam. Lorazepam should be given at 0.02–0.2 mg/kg via intravenous push. In adults, dosing should start with 2 mg and be repeated every 2 minutes until maximum of 0.2 mg/kg is reached. See Table 9-8 for subsequent medication.
DEFINITION Seizures are an abnormal repetitive electrical discharge by a group of neurons in the cerebrum. These abnormal discharges will have somatic manifestations such as repetitive motor activity or changes in the patient’s level of consciousness. Epilepsy is a condition in which there is recurrent seizure activity. Seizures that are idiopathic and for which no underlying cause is found are considered primary. Secondary seizures have an identifiable etiology such as tumor, hypoglycemia, or drug overdose. There are two major classifications of seizures: generalized and partial. Generalized seizures involve generalized abnormal neuronal discharges of both cerebral hemispheres. Just as the word suggests, partial seizures only affect “part” of the brain. Partial seizures are isolated to one hemisphere and used to be known as focal seizures. There are also subcategories of partial seizures—simple partial and complex partial. Status epilepticus is a true emergency. Status epilepticus is traditionally defined as one seizure lasting more than 30 minutes or multiple seizures without return to baseline level of consciousness in between seizures. Recently, experts in the field have suggested that providers should consider a patient in status epilepticus if he or she has a seizure lasting more
Table 9-8 Antiepileptic Drugs for Status Epilepticus Lorazepam, 0.02–0.2 mg/kg IVP. In adults, start with 2 mg and repeat every 2 minutes until a maximum of 0.2 mg/kg is reached.* Phenytoin, 20 mg/kg IV, no faster than 50 mg/min (due to the preservative propylene glycol, faster rates my cause cardiovascular collapse) or fosphenytoin, 20 PE/kg IV, at 100–150 PE/min or IM. Phenobarbital, 20 mg/kg IV, at 50 mg/min.{ At this point, one should be considering general anesthesia. Before inhalation anesthetic, valproic acid, propofol, and/or pentobarbital can be given while anesthesia support is being arranged. Valproate sodium, 20 mg/kg IV, at 200–300 mg/min Propofol, 1–2.5 mg/kg IVP loading dose, then maintenance drip at 0.1–1 mg/kg/min. Pentobarbital, 10 mg/kg IV, at 100 mg/min IVP, Intravenous push; IV, intravenous; PE, phenytoin equivalents; IM, intramuscular. *Lorazepam has been shown in several studies to be the superior benzodiazepam in seizures. {Phenobarbital is very sedating; the clinician should be aware that many patients require intubation because of hypoventilation and hypoxia at this point.
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than 5 minutes because of the morbidity associated with prolonged seizure activity and the inability to predict how long a seizure may last. Status epilepticus refers to both generalized and partial seizures, but generalized carries the highest morbidity and mortality.
EPIDEMIOLOGY Seizures or epilepsy affects 1%–2% of the population. Ten percent of the population will experience a seizure at least once in their lifetime. In the United States, there are approximately 100,000–200,000 episodes of status epilepticus each year. Children younger than 10 years and adults older than 60 years are at greatest risk for developing status epilepticus. The mortality rate of status epilepticus is as high as 20%. Patients with generalized tonic-clonic seizures for a 10-year period lose, on average, 10 IQ points, the same loss suffered after only a single episode of status epilepticus.
PATHOLOGY Generalized seizures are caused by electrical discharges originating deep in the brain and spread outward until the entire cerebral cortex is simultaneously activated by these discharges. The electrical activity of partial seizures is isolated to one focal area of the cerebral cortex. The anatomical location and its associated function is the determining factor for the outward signs observed by the provider. For example, a focal seizure in the left motor cortex of the frontal lobe will manifest itself as repetitive movement of the right upper or lower extremity. Keep in mind that a partial seizure can propagate to involve the entire cortex and may become a generalized seizure with its associated loss of consciousness. All patients have the capacity for seizure activity. Epilepsy has no known secondary etiology, but there are several factors that will lower a patient’s seizure threshold. The seizure threshold applies to both patients with known epilepsy and those who have never had a seizure. Table 9-9 lists some of the common predisposing factors that lower the seizure threshold.
CLINICAL PRESENTATION Generally, there are three phases to all seizures: preictal, ictal, and postictal. Some patients will experience a prodrome or aura before a seizure (i.e., the preictal phase). The ictal phase refers to the time when the patient is actively seizing, which is usually manifested by motor activity, change in level of consciousness, or change in behavior. The transition from the ictal state back to baseline level of consciousness is referred to
468 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 9-9 Predisposing Factors PREDISPOSING FACTORS FOR KNOWN SEIZURE DISORDER* Medication noncompliance Alcohol use Sleep deprivation
PREDISPOSING FACTORS FOR SECONDARY SEIZURES Hypoglycemia Hypoxia Hyponatremia CNS infection CNS trauma CNS neoplasm Intracranial hemorrhage Alcohol, barbiturate, or benzodiazepine withdrawal Drug overdose (e.g., isoniazid, lidocaine, theophylline) Eclampsia
CNS, Central nervous system. *All the predisposing factors for secondary seizures also apply to known seizure disorder.
as the postictal phase. Postictal patients are usually sleepy and confused. These symptoms can last seconds to minutes to hours. On occasion, patients can have a focal neurological deficit during the postictal period. Classically, this focal deficit comes in the form of paralysis, such as an inability to move one arm (i.e., Todd’s paralysis). This deficit is transient and will resolve by the end of the postictal period. Patients with generalized seizures present with a true abrupt loss of consciousness. Most of the time, patients will have bilateral repetitive motor activity. The motor activity of generalized seizures usually involves all four extremities. The motor function may manifest itself as myoclonic jerks, drop attacks, or clonic jerking of the body or extremities, with or without tonic posturing. Urinary incontinence is usually associated with a generalized seizure. The average generalized seizure will last for approximately 1.5–2 minutes. Witnesses will often report that the seizure lasted much longer. Generalized seizures without outward motor activity can rarely occur and are known as nonconvulsive seizures. Nonconvulsive seizures can only be diagnosed by electroencephalogram (EEG). Partial seizures are focal electrical activity, as discussed earlier. Partial seizures can remain focal or become generalized when the electrical impulses propagate to encompass both hemispheres of the cerebral cortex. There are two subcategories of partial seizures: simple and complex. Simple partial seizures present with focal or unilateral motor activity and no change in the level of consciousness. In contrast, complex partial seizures are also manifested by focal motor activity but involve a change in the level of consciousness ranging from depressed to loss. There are a multitude of specific types of partial seizures, but they are irrelevant to ED
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practitioners because this consideration will not change workup or management. Most relevant is the fact that a partial seizure implies that there is a focal structural CNS abnormality. The clinical presentation most relevant to ED practitioners is determining whether the patient is actively seizing. All patients actively seizing in the ED should be assumed to be in status epilepticus and should be treated aggressively to stop their seizure activity. Again, there is no way to predict the length of any seizure, and the morbidity and mortality associated with status is too great to “wait it out.” If the patient presents postictal, supportive care and diagnostics are the top priority.
EXAMINATION A patient who has had a seizure should be given a complete physical examination, including a comprehensive neurological examination. An examination of the head for trauma should always be performed in a postictal patient. The practitioner should examine the patient’s extremities to rule out fractures or sprains. Oropharynx examination may reveal buccal or lingular laceration. The clinician should pay particular attention to any focal changes, weakness, reflex changes, or sensory changes. Focal changes that do not resolve with the postictal period are very worrisome. A good history should be obtained from family, friends, patients, or paramedics.
DIAGNOSIS The key to diagnosing what type of seizure the patient presents with is the history. Cardiac arrest (i.e., ventricular fibrillation seizure resulting from poor cerebral perfusion), syncope, migraine headaches, narcolepsy, cataplexy, hyperventilation syndrome, fugue states, and transient ischemic attacks (TIAs) can all imitate seizure activity. Questions to ask include the following: Did the patient have a prodrome or aura? Was there a loss or change in level of consciousness? Was there motor activity, and, if so, how or where did it start? Was the patient postictal, and does he or she remember the postictal state? How did the episode start and how did it end? Is there any history of recent trauma? Is there a history of cancer? What medication(s) is the patient taking, and is there any chance that an overdose of any medication may have been taken? A CT scan of the head should be considered in all patients who have had a seizure, but the question of who should undergo a CT scan is controversial in some patients. The American College of Emergency Physicians (ACEP) revised its clinical policy on seizures in 2004 and has issued specific guidelines on neurological imaging based on available evidence. ACEP recommendations on this question receive the rating of “moderate clinical certainty,” which means that available evidence
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was primarily composed of nonrandomized clinical studies with strong design. Patients who do not need emergent head CT include known seizure patients who experience their typical seizure and return to their normal baseline. When feasible, all patients with new-onset seizures should receive emergent neuroimaging. First-line neuroimaging should begin with a noncontrast CT of the head. However, when reliable follow-up is available, neuroimaging can be deferred. MRI of the head can be deferred to outpatient evaluations by a neurologist and is not necessary for emergency management. The EEG is used for definitive diagnosis and evaluation of epilepsy. EEG should be part of the inpatient or outpatient evaluation. It is analogous to the ECG in that it records the electrical patterns of neurons in the cerebrum. The EEG can be helpful in distinguishing between partial and generalized seizures. Every patient in status epilepticus who requires intubation and chemical paralysis needs emergent continuous EEG monitoring. Since the paralyzed patient does not manifest any outward motor signs of seizure, the only way to know whether this patient is still seizing is with continuous EEG monitoring. The other type of patient in whom EEG monitoring should be considered is the patient who has had a nonconvulsive seizure.
LABORATORY FINDINGS There are no particular laboratory tests to predict or prove that an episode was a seizure. The patient with a new-onset seizure who is otherwise healthy should have at least the serum glucose and sodium checked. A pregnancy test should be done for all women of childbearing age, and a lumbar puncture should be done after CT in immunocompromised patients. Depending on the history and physical examination results, the ED provider may consider doing a CBC, basic metabolic panel (BMP) (including blood urea nitrogen [BUN], creatinine, and electrolytes), toxicology screen, and measurements of calcium, magnesium, antiepileptic drug (AED) levels.
TREATMENT Any patient presenting to the ED with a possible seizure or actively seizing should have two intravenous lines started with at least one infusing normal saline, in addition to oxygen started at whatever level necessary to keep oxygen saturation greater than 95%. Continuous cardiac, blood pressure, and oxygen saturation monitoring should be initiated. Along with this typical “safety net,” a rapid bedside glucose test should be performed along with the above-mentioned laboratory tests. If a CT scan of the head is indicated, then it should be done immediately if the
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patient is not seizing and is hemodynamically stable. Padding of side rails of the patient’s bed should be used as regular safety measure to protect the patient from further harm. The first challenge the practitioner faces is stopping any seizure activity as rapidly as possible. The seizing brain can be thought of as analogous to the heart in ventricular fibrillation. The first priority in a ventricular fibrillation arrest is to provide electricity in hopes of converting it to a regular rhythm. Remember, all patients who present actively seizing should be considered to be in status epilepticus. The longer a patient is in status epilepticus, the greater the morbidity and mortality. A patient who presents actively seizing must be treated aggressively. Refractory status epilepticus patients can die of cardiovascular collapse, anoxia, renal failure from rhabdomyolysis, and/or trauma if the seizures are not stopped within 30 minutes to 1 hour. As in all of emergency medicine, airway control is paramount; then, the seizure must be stopped. The medication, dose, and sequence of administration are listed in Table 9-8. If an intravenous line is not readily available, diazepam can be administered rectally and fosphenytoin can be given intramuscularly. When eclampsia is suspected in a female patient, magnesium sulfate, 2–4 g, should be given via intravenous push. The possibility of an isoniazid overdose should be considered in refractory status epilepticus, and the antidote is pyridoxine (i.e., vitamin B6). In adults, the dose is empirical and given intravenously (5 g). Once the seizures stop, or if the patient presents postictal, the provider’s top priorities are to provide supportive care and to attempt to identify the underlying etiology. The differential diagnosis for seizures should include medication noncompliance, hypoglycemia, head trauma, alcohol withdrawal, infection, hyponatremia, drug overdose, and neoplasm. There are many more potential causes of seizures, but these are the most common. Determine whether the patient is taking an AED, and check the serum level if applicable. Table 9-10 lists the common AEDs used today. There are many new AEDs being used for which drug levels are not readily available; this information will be available from supporting laboratories. It should always be determined whether the patient has an established diagnosis of epilepsy or whether this presentation represents a new-onset seizure.
Table 9-10 Common Antiepileptic Drugs Phenytoin (Dilantin) Carbamazepine (Tegretol) Ethosuximide (Zarontin) Lamotrigine (Lamictal) Levetiracetam (Keppra)
Phenobarbital Primidone Topiramate (Topamax) Valproic acid Zonisamide (Zonegran)
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Most patients with a history of a seizure disorder can be sent home with a prescription for the correct dose of their AED. A loading dose of their seizure medication can be given intravenously or orally in the ED, and then the patient can be discharged with scheduled neurology or primary care follow-up. The majority of patients with new-onset generalized seizures can be discharged home if they return to baseline and have negative radiological and laboratory workup results. An AED does not need to be started in patients with new-onset generalized seizures, according to the ACEP. The reoccurrence of seizures in the first 72 hours is approximately 9%. This is why close outpatient follow-up is mandatory, but outpatient AEDs are not necessary. In contrast, patients with partial seizures may benefit from an outpatient AED. The patients who have had seizures who require hospital admission are those with persistent status epilepticus, refractory status epilepticus, structural brain disease, intracranial hemorrhage, and seizures resulting from alcohol withdrawal, drug overdose, eclampsia, or CNS infection. If there is ever doubt about the care or disposition of a seizure patient, a neurologist can be consulted.
Bibliography ACEP Clinical Policies Committee, Clinical Policies Subcommittee of Seizures: Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with seizures, Ann Emerg Med 2004;43:605–625. Alldredge BK, Gelb AM, Isaacs SM, et al: A comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus, N Engl J Med 2001; 345:631–637. Delorenzo RJ, Pellock JM, Towne AR, et al: Epidemiology of status epilepticus, J Clin Neurophysiol 1995;12:316. Delorenzo RJ, Towne AR, Pellick JM, et al: Status epilepticus in children, adults, and the elderly, Epilepsia 1992;33(Suppl 4):S15–S25. Dodrill CB: Rapid evaluation of intelligence in adults with epilepsy, Epilepsia 1980;21:359–367. Lepik IE: Treating status epilepticus: A neurologist’s perspective. In ACEP News Supplement: Calming the Storm: Seizures and Status Epilepticus in the Emergency Department, Elsevier, 2005, pp 4–7. Leppik IE, Derivan AT, Howman RW, et al: Double-blind study of lorazepam and diazepam in status epilepticus, JAMA 1983;249:1452–1454. Pollack CV: Seizures. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Vol 2. Mosby: St. Louis, 2002, pp 1445–1456. Sirven JI, Waterhouse E: Management of status epilepticus, Am Fam Phys 2003;68:3. Tardy B, Lafond P, Convers P, et al: Adult first generalized seizure: Etiology, biological tests, EEG, CT scan in the ED, Am J Emerg Med 1995;13:1–5. Treiman DM, Meyers PD, Walton NY, et al: A comparison of four treatments for generalized convulsive status epilepticus, N Engl J Med 1998;339:792–798.
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Acute Stroke Syndromes RALPH TERPOLILLI
DEFINITION A stroke occurs when cerebral blood flow is disrupted to a focal region of the brain, resulting in a neurological deficit. Strokes or cerebrovascular accidents are ischemic (80%–85%) or hemorrhagic (15%–20%). The acute vascular injury that causes neuronal ischemia may result from two primary causes: (1) blood vessel occlusion from primary vessel thrombosis, emboli, or systemic hypoperfusion; or (2) intracerebral (ICH) or subarachnoid (SAH) blood vessel hemorrhage. Cerebral ischemia initiates a biochemical cascade of neuronal injury that, if severe or prolonged, ultimately results in cell death. ATIA is an ischemic neurological deficit that resolves within 24 hours. Three or more TIAs occurring within 72 hours are termed crescendo TIAs. A reversible ischemic neurological deficit lasts longer than 24 hours but resolves within 3 weeks. A stroke in evolution is an ischemic stroke with progressing neurological deterioration. A completed stroke has a stable neurological deficit. Some authorities do not subdivide ischemic neurological deficits according to duration of symptoms and instead consider them all strokes. TIA, reversible ischemic neurological deficit, and stroke are, in fact, a continuum of one disease process.
EPIDEMIOLOGY Stroke is the third leading cause of death in the United States, resulting in 160,000 deaths annually. It is the leading cause of adult disability. More than 750,000 strokes occur each year, and one third occur in patients younger than 65 years. There are currently more than 4.4 million stroke survivors. The annual stroke cost exceeds $51.3 billion. The overall stroke mortality rate is 20% within the first year. Half die from the primary neurological injury (e.g., transtentorial herniation), and half die from medical complications (e.g., pneumonia, underlying heart disease, sepsis, pulmonary embolism). The mortality rate from hemorrhagic strokes is nearly 60% within 30 days. These strokes occur in a younger patient population than ischemic strokes. Only about 10% of stroke survivors return to normal. Of the remaining 90% of patients, 48% are hemiparetic, 22% are unable to walk, 24%–53% are completely or partially dependent, 12%–18% are aphasic, and 32% are clinically depressed.
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RISK FACTORS Ischemic and hemorrhagic stroke risk factors in general are either modifiable or nonmodifiable. Nonmodifiable risk factors for stroke include age, race, sex, and genetic family history of coronary artery disease, stroke, or TIA. Modifiable or treatable risk factors include a variety of clinical conditions that accelerate atherosclerosis, including hypertension, large and small vessel disease (especially carotid artery disease), coronary artery disease, peripheral vascular disease with claudication, atrial fibrillation, valvular heart disease, cardiac septal defects, prior stroke or TIA, diabetes, thyroiditis, arterial dissection, trauma, infection, hyperlipidemia, cigarette smoking, alcohol abuse, vasoactive drug abuse (especially amphetamines, phenylpropanolamine, and cocaine), anabolic steroid use, sedentary or stressful lifestyle, obesity, and use of birth control pills. Prolonged cerebral vasospasm from a migraine can also result in a stroke. Medical conditions that predispose patients to vascular ischemia and stroke are those that increase blood viscosity or predispose patients to hypercoagulable states such as vasculitis, giant cell arteritis, Takayasu’s aortitis, cancer, sickle cell disease, eclampsia, cerebral fibromuscular dysplasia, polycythemia, protein C or S deficiency, lupus anticoagulant, anticardiolipin antibody, antiphospholipid syndrome, fibromuscular dysplasia, antithrombin III deficiency, polycythemia vera, factor V Leiden, and prothrombin gene mutation G20210A. Less common infectious disease conditions predisposing patients to vessel wall injury and thrombosis include HIV infection, syphilis, tuberculosis, aspergillosis, and trichinosis.
PATHOPHYSIOLOGY An understanding of the brain’s vascular anatomy and physiology is a prerequisite to identifying and treating the various stroke syndromes. The brain is completely dependent on a constant supply of oxygen and glucose for high-energy phosphate metabolism. Any disruption in this blood supply, even momentarily, results in cerebral dysfunction and initiates a biochemical cascade that produces mediators of secondary cell injury. Cerebral edema and mass effect, depending on the stroke etiology, worsens the initial insult. The vascular supply to the brain is autoregulated between an arterial blood pressure range of 50–160 mmHg to provide a constant supply of oxygen and glucose at a cerebral blood flow of 50–60 ml/100 g of brain tissue. Any decrease in cerebral blood flow may result in neuronal dysfunction and clinical stroke symptoms. Cerebral blood flow below 20 ml/100 g of brain tissue in the center of the ischemic region represents the core or non-salvageable area of ischemic brain infarction with
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resultant impairment or loss of vascular autoregulation. Outside this core is a zone of cerebral blood flow ranging between 20 and 50 ml/100 g of brain tissue that represents the penumbra or zone of potentially salvageable brain ischemia. Survival of this zone is dependent on the degree and duration of occlusion and is perfusion dependent. The penumbra is perfused by collateral blood flow from the cerebral circulation. The core zone of cerebral infarction and the outer zone of ischemia are illustrated in Figure 9-3. The extent of stroke injury depends on the location and size of the occluded vessel, the presence and magnitude of collateral blood flow distal to the area of vessel ischemia, the duration of ischemia, and the time frame for vessel reperfusion (Fig. 9-4). There is a 6-hour window of opportunity to restore or improve blood flow to the ischemic penumbra before irreversible neurological damage occurs. The improvement or restoration of ischemic cerebral blood flow is the focus of modern stroke management. Blood supply to the brain is provided by the anterior and posterior circulations. The two circulations are connected by the circle of Willis (Fig. 9-5), which may provide collateral blood flow depending on anatomical variation. Eighty percent of the brain is supplied anteriorly by the carotid arteries, which divide into the internal and external carotids. The internal carotid artery courses intracranially and divides into the anterior and middle cerebral artery. The ophthalmic artery is the first branch off of the internal carotid artery and supplies the optic nerve and retina. Amaurosis fugax
Penumbra (20−50)
Core (0−20)
Figure 9-3. The zones of cerebral infarction and ischemia.
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Infarction
Collateral flow
Penumbra
Thrombus
Figure 9-4. Collateral blood flow to the ischemic penumbra.
or painless transient monocular blindness localizes the stroke to the anterior circulation at a level at or below the ophthalmic artery. The anterior (or external) cerebral artery supplies the basal and medial aspects of the cerebral hemispheres extending to the anterior two thirds of the parietal lobe. Perforators supply the anterior aspect of the internal capsule, putamen, and hypothalamus. The two anterior cerebral arteries are joined by the anterior communicating artery, thereby joining the right and left anterior circulations. The middle cerebral artery supplies the entire lateral surface of the cerebral cortex, extending from the anterior portion of the frontal lobe to the posterolateral occipital lobe. Lenticulostriate branches supply the putamen, internal and external capsules, and lentiform nucleus. The remaining 20% of the brain, including the brainstem, is supplied posteriorly by the vertebrobasilar system, which is formed by the two vertebral arteries as they branch off of the subclavian arteries, ascend through the transverse processes of the cervical vertebra, and enter the cranium through the foramen magnum. The vertebral arteries supply the cerebellum through the posteroinferior cerebellar arteries and then join near the pontomedullary junction to form the basilar, artery which then branches to form the posterior cerebral artery. The posterior system supplies the brainstem, cerebellum, thalamus, auditory and vestibular centers of the ear, medial temporal lobe, and visual occipital cortex.
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Anterior cerebral
Anterior communicating Ophthalmic Middle cerebral Circle
Internal carotid Posterior communicating Posterior cerebral Superior cerebellar
Labyrinthine Basilar Anterior inferior cerebellar Posterior inferior cerebellar Vertebral Anterior spinal
Figure 9-5. The circle of Willis.
The posterior communicating artery joins the anterior and posterior systems to complete the arterial circle of Willis (see Fig. 9-5). The majority of strokes (80%–85%) are caused by ischemia. Most of these ischemic events are due to thrombosis of small (lacunar) or large arteries at the site of an ulcerated atherosclerotic plaque (45%). Embolism from an extracranial source causes 20% of all ischemic strokes and, unlike in thrombotic strokes, the occluded cerebral vessel does not have underlying vascular disease (Fig. 9-6). Most emboli originate proximally from the heart or large vessels, including the aorta, carotid, and vertebral arteries. Cardiac emboli result most commonly from mural thrombi from atrial fibrillation, myocardial infarction, ventricular
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Figure 9-6. Extracranial sources of thromboemboli.
aneurysms, cardiomyopathy, congestive heart failure, or dysrhythmias. Cardiac emboli may originate from valvular vegetations on native or prosthetic cardiac valves, cardiac tumors (myxomas), or paradoxical emboli from atrial or ventricular septal defects. Up to 20% of patients presenting with a new stroke have atrial fibrillation. An artery-to-artery embolus occurs when a clot dislodges proximally from an ulcerated large vessel atherosclerotic plaque (i.e., amaurosis fugax). Other less common causes of embolic strokes include fat emboli, debris from injection drug abuse (especially with a patent right-to-left cardiac shunt), and septic emboli. About 5% of ischemic strokes occur from vessel occlusion due to other causes such as external vessel compression or dissection from trauma (carotid or vertebral arteries), cervical arthritis (vertebral arteries), or localized vessel hemorrhage at the site of a mass lesion. Up to 30% of ischemic strokes are from an unknown cause. TIAs represent focal, sudden, and transient neurological deficits that resolve within 24 hours and have often previously occurred in the same cerebral vascular distribution. Up to 20% of patients with a TIA will develop a stroke within 1 month after the event, and nearly 50% experience a stroke within 5 years. Consequently, these events are important warning symptoms for impending stroke. They may occur in the carotid watershed distribution from extracranial carotid vascular disease and resultant emboli, but half of all carotid distribution TIAs have no demonstrable vascular abnormality. A carotid bruit may correlate with carotid distribution TIAs, but the absence of a carotid bruit does not necessarily rule out significant carotid vascular disease. Nearly two thirds of patients with TIA have abnormal brain CT scan results, and up to 80% show abnormalities on brain MRI scans, thereby supporting the theory that
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TIAs are actually strokes. The risk of future strokes after TIA can be reduced with proper therapy. A minority of strokes (15%–20%) are hemorrhagic, with ICHs representing two thirds and nontraumatic SAHs one third. Injury results from mass effect and cerebral edema causing a progressive rise in ICP, thereby impairing cerebral perfusion and initiating the biochemical cascade of neuronal injury. Hemorrhage is often associated with a precipitating event—such as a Valsalva maneuver, labor, or sexual activity—resulting in a sudden rise in blood pressure. ICH usually occurs as a result of poorly controlled hypertension, but other causes include vascular malformation (especially arteriovenous malformation [AVM]), neoplasms, anticoagulation therapy, thrombolytic therapy, tobacco use, illicit drug use (especially cocaine), bleeding disorders, cerebral amyloid myopathy, and trauma. Risk factors for ICH include advanced age (especially if the patient has hypertension), male sex, and black or Asian descent. SAH occurs most commonly from rupture of berry aneurysms at arterial bifurcations on the circle of Willis or rupture of AVMs. The bleeding occurs outside of the brain parenchyma into the CSF. These hemorrhages, unlike ICH, occur more commonly in women, except there is a unique subset of men younger than 40 years, and children with AVM are at higher risk for SAH.
CLINICAL PRESENTATION The clinical presentations of the various stroke syndromes may be subtle and variable depending on the location, severity, and type of stroke. Ischemia or infarction of the various brain control centers is associated with different constellations of neurological symptoms (Fig. 9-7). The cerebral cortex allocated to the motor and sensory innervation of the face, tongue, and upper extremities is disproportionately represented along a large area of the lateral parietal lobe supplied by the middle cerebral artery. The lower extremities below the knee are innervated by the medial aspect of the cerebral hemispheres, which derives its blood supply from the anterior cerebral artery. Stroke involving the vascular distribution of these vessels can cause a variety of overlapping motor and sensory findings. Figure 9-8 illustrates the homunculus distribution of innervation to these anatomical areas. Most right-handed and 80% of left-handed persons are left-cerebral dominant. Strokes involving the dominant hemispheres usually result in more devastating neurological injury. Understanding the relationship of the vascular distribution to the neurological function helps to pinpoint the lesion in the various stroke syndromes.
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Motor cortex (movement) Frontal lobe (judgement, foresight, and voluntary movement)
Central sulcus Sensory cortex (pain, heat, and other sensations)
Broca’s Area (speech) Frontal lobe (smell)
Parietal lobe (comprehension of language) Temporal lobe (hearing) Occipital lobe (primary visual area)
Temporal lobe (intellectual and emotional functions)
Wernicke’s area (speech comprehension) Cerebellum Brainstem (coordination) (swallowing, breathing, heartbeat, wakefulness center and other involuntary functions)
Figure 9-7. The brain control centers.
Figure 9-8. The homunculus distribution of innervation on the parietal cortex.
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The ischemic stroke syndromes subsequently described may cause any combination or degree of neurological deficits within their respective watershed vascular distributions. Anterior cerebral artery infarction of the frontal lobe may cause alterations in consciousness, contralateral hemiplegia and hemisensory loss (lower extremity greater than upper extremity), apraxic gait, perseverative speech or anarthria, and painless monocular visual loss (i.e., amaurosis fugax). Crossed neurological deficits are not present. Dominant left middle cerebral artery infarction of the parietal lobe (80%) may cause contralateral hemiparesis and hemisensory loss (face and upper extremity greater than lower extremity), aphasia (receptive, expressive, or both), dysphasia, dyslexia, agnosia, left gaze preference, and right visual field deficit (i.e., homonymous hemianopsia). Crossed neurological deficits are not present. Nondominant right middle cerebral artery infarction of the parietal lobe (20%) may cause contralateral hemiparesis and hemisensory loss (face and upper extremity greater than lower extremity), left inattention and neglect, dysarthria (not aphasia), right gaze preference, left visual field deficit (i.e., homonymous hemianopsia), constructional apraxia, and double simultaneous extinction. Crossed neurological deficits are not present. Posterior cerebral artery infarction of the occipital and posterior parietal lobes may cause alterations in consciousness, and crossed neurological deficits, including subtle motor deficits (unaware until tested), sensory deficits (especially light touch and pinprick), cortical blindness, visual agnosia, impaired memory, oculomotor nerve palsy, and hemiballismus. Syncope with nausea and vomiting is a common initial presentation. Vertebrobasilar or posterior circulation infarction of the brainstem (reticular activating system), cerebellum, and visual cortex may cause crossed neurological deficits involving ipsilateral cranial nerve palsies with contralateral hemiparesis or pain and temperature hemiparesthesia, as well as dizziness, vertigo, visual field defects, diplopia, nystagmus, ataxia, and dysphagia. A common initial presentation of cerebellar infarction is a drop attack with syncope, nausea, vomiting, headache, and neck pain associated with an inability to walk or truncal ataxia. Posterior fossa imaging with conventional CT scanning may be inadequate due to occipital bone artifact. Radiographic diagnosis may require an MRI or magnetic resonance angiography (MRA). Cerebral edema may develop after 6–12 hours with subsequent elevation of ICP, declining consciousness, and brainstem herniation. A cerebellar hemorrhage may present similarly. Both clinical conditions may become neurosurgical emergencies because surgical decompression may be required to avoid brainstem herniation. Early neurosurgical consultation is indicated.
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The Wallenberg or lateral medullary syndrome is a specific posterior circulation infarct of the cerebellum involving the distribution of the vertebrobasilar and posteroinferior cerebellar artery. Neurological deficits include ipsilateral loss of facial pain and temperature sensation, contralateral loss of body temperature sensation, gait and limb ataxia, partial ipsilateral loss of cranial nerves V, IX, X, and XI in various combinations, and an ipsilateral Horner’s syndrome (i.e., ptosis, myosis, and anhidrosis). Basilar artery posterior circulation infarction of the brainstem may cause hemiparesis, quadriparesis, quadriplegia, crossed neurological deficits, diplopia, disconjugate gaze, vertigo, tinnitus, nausea, vomiting, hiccups, abnormal respiratory patterns, alterations in consciousness, or coma. The “locked-in syndrome” is a specific infarction of the pontine tectum characterized by coma and complete muscle paralysis except upward gaze. Arterial dissection is a stroke syndrome that may occur spontaneously or after trauma to the head or neck. Blunt trauma to the neck may injure the carotid or vertebral arteries with secondary vessel wall dissection and ischemic stroke. Even minor trauma like suddenly twisting the head and neck spontaneously or during chiropractic manipulation may cause vertebral artery dissection. Headache or neck pain may precede spontaneous dissection, and hypertension is a risk factor. Up to 20% of the ischemic strokes in patients aged 15–50 years are due to arterial dissection. The neurological presentation varies depending on the location of the dissection. Transient global amnesia is a TIA stroke syndrome caused by an acute ischemic event in the area of the hippocampus and amygdaloid. Neurological symptoms may include an abrupt loss of the ability to recall recent events or to record any new memories, but prior memory and speech are usually unaffected and the patient can perform complex tasks. Recovery is usually complete. Lacunar infarction of the small penetrating arteries to the subcortical area, especially the pons and basal ganglia, causes pure motor or sensory deficits of one extremity, especially the hand (“clumsy hand”) or ataxic hemiparesis. These microinfarcts are most common in patients older than 60 years with hypertension and diabetes and are less than 2 cm in size when imaged on CT or MRI scan. The underlying vessels, when specifically imaged by ultrasound or angiography, do not show significant vasculitis, ulcerative plaques, or stenosis. The hemorrhagic stroke syndromes subsequently described may cause variable neurological deficits depending on the size, severity, and location of the hemorrhage and the resulting degree of ischemia or infarction to the surrounding brain tissue. The ICP will progressively rise as the size of the space occupying the hemorrhage increases. The brain will autoregulate cerebral perfusion pressure through a compensatory rise in the mean
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arterial pressure according to the Monro-Kellie doctrine. Ultimately, a point of impending herniation will be reached. The initial hypertensive response to the rise in ICP along this autoregulation curve is the Cushing reflex. Severe ICHs, especially occipital or massive nonhemorrhagic strokes, may present with Cushing’s triad of hypertension, bradycardia, and tachypnea. These are ominous symptoms and imply impending brainstem herniation. ICHs may be clinically indistinguishable from their respective ischemic stroke syndromes previously described. The neurological presentation is variable depending on the location of hemorrhage. They are commonly associated with hypertension, alterations in consciousness, headache, nausea, vomiting, and contralateral motor and sensory neurological deficits. Common ICH locations include the putamen (35%), lobar (30%), thalamic (10%), caudate nucleus (5%), and pons (5%). A midline hemorrhage in the pons will present with sluggish pinpoint pupils, decerebrate posturing, and rapid progression to brain death. An SAH will often present with a sudden onset or thunderclap severe headache (“worst headache of my life”). Patients with chronic headaches will have a new or different headache compared with their baseline. Nausea, vomiting, and alterations in consciousness may be present. The neurological presentation is most commonly nonfocal. A careful history may reveal a sentinel hemorrhage or microbleed. If missed, another episode of bleeding will occur in 5%–30% within the next 3 weeks, especially the first 24 hours. A cerebellar hemorrhage will present with symptoms similar to a posterior circulation or vertebrobasilar ischemic stroke, including sudden onset of occipital headache, nausea, vomiting, dizziness, syncope, truncal ataxia, and inability to walk. Rapid hemorrhage enlargement may occur with ipsilateral compression of the pons and sixth cranial nerve, followed by progression to coma, brainstem herniation, and death. Immediate neurosurgical referral for decompression and hemorrhage may be lifesaving. There are multiple clinical conditions that may be indistinguishable from or resemble a TIA or ischemic stroke (Table 9-11). A rapid, accurate diagnosis is critical to the timely initiation of optimal stroke therapy within 3 hours after symptom onset.
PHYSICAL EXAMINATION The first priority is always stabilization of the ABCs (i.e., airway, breathing, circulation) and protection of the cervical spine when trauma is suspected. Rapid diagnostic testing to determine body temperature, whole blood glucose, and oxygen saturation must be performed. A complete general physical examination, including a targeted neurological examination, should then be performed. Trauma should be promptly ruled out. The
484 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 9-11 The Differential Diagnosis of Stroke Hemorrhage Epidural or subdural Brain tumor, abscess, or AVM Meningoencephalitis Hypoglycemia Postictal Todd's paralysis Complicated migraine Bell's palsy Hypertensive encephalopathy Carotid or vertebral artery dissection Functional hemiplegia Demyelinating disease Multiple sclerosis Dementia Peripheral nerve palsy
Hyperglycemia Diabetic ketoacidosis Hyperosmotic coma Wernicke's encephalopathy Collagen vascular diseases Temporal and giant cell arteritis Polyarteritis nodosa Systemic lupus erythematosus Meniere's disease Labyrinthitis Hyponatremia Drug toxicity Lithium Diphenylhydantoin Carbamazepine Air embolism
AVM, Arteriovenous malformation.
focus of the physical examination in a patient with acute stroke is to rapidly identify possible conditions mimicking stroke so that the most appropriate treatment can be administered in a timely manner. The general appearance and vital signs, especially the blood pressure (e.g., Cushing’s response), body temperature (febrile or hypothermic), and respiratory rate/pattern should be noted. A potential infection should be ruled out if the patient is febrile. A fever may be the cause of the neurological presentation or it may be a complication from the stroke. Blood pressure should be taken in all four extremities, especially if the patient is hypertensive (aortic dissection). The practitioner should look for clinical signs of dehydration and should examine the skin for lesions, including rash (meningococcal meningitis), needle marks (intravenous drug use), cellulitis, petechiae or ecchymosis (bleeding dyscrasia), and Janeway lesions or Osler nodes (emboli from endocarditis). The nails should be checked for splinter hemorrhages (septic emboli), the temporal arteries palpated for tenderness, and the head inspected for acute or remote trauma. The ears should be examined for evidence of trauma (hemotympanum, Battle’s sign), and the neck should be checked for a scar over the carotid area (prior carotid endarterectomy), tenderness, or nuchal rigidity (meningismus). The practitioner should palpate the carotid arteries for symmetry and listen for bruits. He or she should also listen to the lungs for rales and examine the heart for rate, rhythm, murmurs, S3 gallop, and prosthetic valve clicks (atrial fibrillation or valvular disorder). The abdomen should be palpated for pulsatile or tender masses (distended bladder from spinal cord lesion), and the practitioner should listen for bruits. The femoral and distal extremity pulses should be palpated for symmetry (aortic dissection).
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During the neurological examination, the practitioner should attempt to narrow the neurological differential diagnosis and localize the lesion. The level of consciousness and orientation should be determined. One should differentiate decorticate from decerebrate posturing, especially if the patient is unconscious and unresponsive. Speech is noted for dysarthria or dysphasia (receptive versus expressive), and the eyes are examined for pupillary reactivity and symmetry. Extraocular muscles are tested for palsies, gaze patterns, or visual neglect. The eyes will deviate toward a stroke lesion. The visual fields should be determined by confrontation. The fundus should be examined for evidence of chronic hypertension or diabetes (hemorrhages, exudates) or elevation of ICP (loss of spontaneous venous pulsations, blurring of the optic disc, or papilledema). Proximal and distal motor strength is tested, including assessment of pronator drift and gait with heel and toe walking. Sensory functions are tested for deficits and neglect by pinprick, graphesthesia, and double-simultaneous elimination. Cerebellar function is assessed by gait, finger-to-nose, and/or heel-to-shin testing. The cranial nerves are tested individually to identify central brainstem versus peripheral nerve (i.e., Bell’s palsy) lesions. Stroke severity is best assessed using a stroke severity scale. The National Institutes of Health Stroke Severity Scale (NIHSS) is most commonly used and correlates well with stroke severity as determined by the clinical neurological deficit and the amount of brain tissue infarcted on CT scan (Table 9-12). The scale ranges from 0 to 42. Scores greater than 20 are considered very severe. The NIHSS has predictive value regarding the likelihood of hemorrhage after fibrinolytic therapy of acute ischemic stroke and prognosis for functional outcome but may underestimate the volume of infarct in nondominant right-hemispheric strokes.
LABORATORY FINDINGS Appropriate blood tests include a CBC; measurements of electrolytes, BUN, creatinine, and glucose; coagulation studies (e.g., international normalized ratio and partial thromboplastin time), cardiac enzymes/markers, and a urine toxicology screen. A bedside hematocrit analysis or a CBC may indicate a hyperviscosity state as in polycythemia or platelet disorders, which predispose the patient to hemorrhage or thrombosis, Table 9-12 The National Institutes of Health Stroke Severity Scale SCORE 0–5 5–15 15–20 >20
SEVERITY Mild or minor in most patients Moderate Moderately severe Very severe
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respectively. Hypoglycemia is a notorious mimic of stroke and can be rapidly ruled out by bedside glucose testing. A venous blood gas analysis for serum sodium, if available, can quickly identify severe hyponatremia, which is commonly associated with altered mental status. Supratherapeutic anticoagulation with warfarin or heparin may be associated with hemorrhagic stroke. Cardiac enzymes or injury markers may identify acute myocardial infarction. Urine toxicology testing may reveal the presence of cocaine or amphetamines, which are often associated with ischemic or hemorrhagic stroke at a younger age. Liver function tests, measurement of blood alcohol level, pregnancy test, and arterial blood gas analysis may be appropriate in selected patients. When clinically indicated, the CSF sample obtained by lumbar puncture should be examined for evidence of infection or hemorrhage.
DIAGNOSIS A patient presenting with symptoms suspicious for an acute stroke must be rapidly evaluated according to a critical stroke pathway. Identification of a possible stroke begins in the prehospital phase with recognition of stroke symptoms by the patient or a family member followed by timely presentation to the emergency care system. Emergency medical services and triage personnel must be educated to identify stroke symptoms so the emergency care provider and stroke team (if applicable) can be immediately notified. An expedited history must accurately identify the time of neurological symptom onset, which is defined as the last moment the patient was known to be in his or her prior baseline condition. Additional information from family members or other observers who were with the patient may be necessary in unclear circumstances or when the patient is unable to provide a clear history. Stroke symptoms noted on awakening are presumed to have occurred when the patient was last observed without symptoms. ATIA followed by a stroke or stuttering strokes are timed from the stroke onset. Historical circumstances associated with symptom onset that should be noted include seizure or syncope, chronology or frequency of symptoms, and residual deficits, especially cognitive or memory changes. The remaining history addresses prior medical, surgical, and psychiatric conditions; medication use; allergies; social history regarding living circumstances and use of alcohol, tobacco, or illicit drugs; and family history. The core diagnostic strategy in the diagnosis of stroke is to determine the brain tissue status with a noncontrast CT scan of the head. The CT scan is rapid, is almost universally readily available, may show brain ischemia within the first 3 hours, and quickly identifies hemorrhage as well as other nonvascular causes of stroke. The noncontrast CT scan of the head identifies ICH greater than 1 cm in size in nearly 100% and up to 95% of all SAH within the first 12 hours. The categorization
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of stroke into hemorrhagic (Figs. 9-9 and 9-10) versus nonhemorrhagic or ischemic (Figs. 9-11 to 9-13) is the primary diagnostic decision point before the initiation of the screening process for fibrinolytic therapy. Although the use of the CT scan is the currently accepted imaging modality in the diagnosis of acute ischemic stroke, its use as a selection criterion before the initiation of fibrinolytic therapy is controversial. The noncontrast brain CT scan may not be 100% sensitive until 7 days after stroke onset or may be normal in the hyperacute phase, is nonsensitive to lacunar strokes, and may not image posterior fossa strokes due to occipital bone artifact. A contrast-enhanced brain CT scan is not indicated if the noncontrast study results are normal. Newer tests to better define the perfusion status of the ischemic penumbra are under study and limited to specialized stroke centers. The following initial noncontrast brain CT findings may be associated with a higher risk of hemorrhagic complications after thrombolytic therapy of acute ischemic stroke:
Hyperdense middle cerebral artery sign (see Fig. 9-11) Loss of gray-white matter differentiation in the lentiform nucleus or cortical ribbon (see Fig. 9-12)
Figure 9-9. Large right intracerebral hemorrhage.
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Figure 9-10. Subarachnoid hemorrhage.
Sulcal effacement in the territory of the middle cerebral artery (Fig. 9-14) Hypodensity or ischemia (see Fig. 9-13) Hypoattenuation in more than one third of the middle cerebral artery Edema or mass effect
Most acute ischemic strokes will not be visualized by noncontrast CT scan within the first 6 hours, but most will be seen by serial CT imaging within the first 24–48 hours. Other imaging modalities that may increase the acute diagnostic yield include CT angiography, xenon-enhanced cerebral blood flow study, and diffusion- or perfusion-weighted MRI, or MRA. Head and neck angiography is the imaging modality of choice to diagnose large vessel abnormalities such as arterial stenosis, occlusion, or dissection and small vessel abnormalities such as aneurysm or AVM. Angiography is often required to determine the cause of SAH. Carotid duplex ultrasonography may demonstrate high-grade carotid stenosis when neurological deficits are progressive or in crescendo TIAs. Emergency carotid endarterectomy or anticoagulation may be indicated. Echocardiography may identify a mural thrombus, tumor, patent foramen ovale, or valvular vegetation when cardioembolism is suspected.
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Figure 9-11. Hyperdense right middle cerebral artery sign.
ECG should be performed for all patients with acute stroke. Up to 60% of all cardioembolic strokes are associated with atrial fibrillation or acute myocardial infarction. The risk of stroke in untreated atrial fibrillation is 6% per year, and there is a 2.5% risk of stroke the first month after myocardial infarction. A chest x-ray may demonstrate prosthetic valves, pacemaker devices, aortic vascular calcifications, or cardiac enlargement associated with ischemic or hypertensive heart disease. A lumbar puncture may be necessary to diagnose SAH when the clinical history is supportive and the non-enhanced brain CT scan yields negative results. The presence of blood in the CSF throughout all tubes without significant clearing is supportive of acute SAH within the first 6 hours. Xanthochromia may be seen when a CSF sample is obtained after 6 hours. A bloody spinal tap may require hospital admission or observation, followed by a repeated tap in 12 hours. A negative initial CSF result does not completely rule out SAH when a high index of suspicion is present. Brain MRA or cerebral angiography may be necessary. A spinal tap is contraindicated when an intracranial mass lesion associated with elevated ICP is present.
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Figure 9-12. Loss of gray-white matter differentiation on the left.
TREATMENT Once identified, a patient with acute stroke enters an accelerated critical treatment pathway that may involve an acute interventional stroke team. The goal of this pathway is to identify and administer fibrinolytic therapy to eligible patients with acute ischemic stroke within 3 hours of symptom onset. General principles of emergency medical management apply, with top priority given to the ABCs. The patient is given nothing by mouth, and the head of bed should be slightly elevated. At least one intravenous line should be started. Isotonic non–glucose-containing fluids should be given only to resuscitate clinically significant dehydration or hypotension to maintain cerebral blood flow. Dextrose should be given only for documented symptomatic hypoglycemia. Overaggressive fluid administration or dextrose may worsen cerebral edema in the region of brain ischemia. Cardiac, blood pressure, and pulse oximetry monitors should be applied. Two liters of nasal canula oxygen should be given if the oxygen saturation is less than 95%. Excessive oxygen administration may theoretically worsen neurological injury by promoting oxygen free radical formation in the penumbra. Fever increases brain metabolic demands and should
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Figure 9-13. Large area of hypodensity (ischemia) in the right cerebral hemisphere.
be treated with acetaminophen, whereas hypothermia may be neuroprotective. The source of a fever should be determined and antibiotics administered in a timely manner. Thiamine should be administered to alcoholic or malnourished patients. Complications within the first few days of a stroke include aspiration pneumonia, dehydration, hypothermia, and rhabdomyolysis. Samples for laboratory tests, as previously mentioned, should be drawn. An ECG should be performed to rule out concomitant myocardial infarction and a chest x-ray to rule out pneumonia. Seizure activity should be treated with benzodiazepines followed by a loading dose of diphenylhydantoin or fosphenytoin. A noncontrast CT scan of the brain must be performed at the earliest possible time. Hypertension in the context of acute ischemic stroke must be carefully managed depending on eligibility for fibrinolytic therapy. The objective is to reduce the blood pressure by a maximum of 10%–15% when treatment is clinically indicated. Conditions in which patients are not eligible for thrombolytic therapy include the following:
Systolic blood pressure less than 220 mmHg or diastolic blood pressure less than 120 mmHg is observed clinically
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Figure 9-14. Sulcal effacement in the distribution of the left middle cerebral artery.
Systolic blood pressure greater than 220 mmHg or diastolic blood pressure 121–140 mmHg should be treated with intravenous labetalol (10–20 mg) or nicardipine infusion starting at 5 mg/hr, then titrated Diastolic blood pressure greater than 140 mmHg should be treated by nitroprusside infusion starting at 0.5 mg/kg/min
Conditions in which patients are eligible for thrombolytic therapy include the following: Pretreatment Systolic blood pressure greater than 185 mmHg or diastolic blood pressure greater than 110 mmHg should be treated with intravenous labetalol (10–20 mg) or 1–2 inches of transdermal nitroglycerin ointment During and Post-treatment
Diastolic blood pressure greater than 140 mmHg should be treated by nitroprusside infusion starting at 0.5 mg/kg/min For systolic blood pressure greater than 230 mmHg or diastolic blood pressure 121–140 mmHg, labetalol, 10 mg given intravenously, should be followed by repeat or doubled doses up to 300 mg maximum or a continuous infusion at 2–8 mg/min after the initial bolus
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or
Nicardipine infusion starting at 5 mg/hr then titrated Systolic blood pressure 180–230 mmHg or diastolic blood pressure 105–120 mmHg should be treated with labetalol, 10 mg given intravenously, followed by repeat or doubled doses up to 300 mg maximum or a continuous infusion at 2–8 mg/min after the initial bolus
Blood pressure should be frequently monitored to avoid overtreatment, which may reduce cerebral perfusion to the penumbra and worsen the zone of infarction. Consistently elevated blood pressures beyond 185/110 mmHg contraindicate the use of fibrinolytic therapy. Stringent postfibrinolytic management of blood pressure is essential to minimize the hemorrhagic conversion of an ischemic stroke. Fibrinolytic therapy with intravenous tissue plasminogen activator (rtPA or alteplase) was approved in 1996 for the treatment of acute ischemic stroke after publication of the National Institutes of Health/National Institutes of Neurological Disorders and Stroke study. Administration has only been proved to be beneficial when given during the first 3 hours after symptom onset and requires a coordinated, multidisciplinary approach. There are strict inclusion and exclusion criteria regarding the administration of fibrinolytic therapy in acute ischemic stroke (Table 9-13). The total intravenous dose is 0.9 mg/kg up to a maximum of 90 mg. A bolus of 10% of the total dose is given, followed by infusion of the remaining amount over 60 minutes. Neurological checks and blood pressure monitoring is performed at 15-minute intervals for 2 hours after starting the infusion. Aspirin or heparin is not given during the first 24 hours after treatment. Hypertension is aggressively managed according to the previously described criteria. All patients receiving fibrinolytic therapy are admitted to an intensive care setting. An ICH is presumed to be the cause of any deterioration in neurological status and must prompt an immediate repeated CT scan. Intracranial hemorrhage complicating fibrinolytic therapy is primarily associated with more severe strokes (stroke score >20) or where the initial CT scan shows an acute hypodensity or edema with mass effect. However, the potential benefit of fibrinolytic therapy in these devastating strokes may outweigh the potential risk of hemorrhage. A bleeding diathesis workup must be initiated and hemorrhagic symptoms treated by infusion of packed red blood cells, cryoprecipitate, or fresh frozen plasma. Emergency consultations with hematology and neurosurgery are indicated. Continuous transcranial Doppler ultrasonography has been shown to augment the degree of rt-PA–induced arterial recanalization, with a trend toward better stroke outcome. Other fibrinolytic drugs, including streptokinase and ANCROD (a fibrinogen-depleting agent derived from snake venom) have been studied but are not presently approved for use. Intraarterial fibrinolytic therapy with tPA or prourokinase in middle cerebral
494 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 9-13 Criteria for Tissue Plasminogen Activator (tPA) Therapy in Acute Ischemic Stroke Inclusion criteria for tPA therapy: Acute ischemic stroke within 3 hours of symptom onset Measurable deficit on NIH Stroke Scale examination No hemorrhage or nonstroke cause of neurological deficit on noncontrast brain CT scan Age >18 years Exclusion criteria for tPA therapy: Minor or rapidly improving symptoms Seizure at onset of stroke Stroke or serious head trauma within the previous 3 months Major surgery within the past 14 days Known history of ICH Sustained systolic BP >185 mmHg Sustained diastolic BP >110 mmHg Aggressive treatment is necessary to lower the BP Clinical symptoms are suggestive of SAH GI or GU hemorrhage within the past 21 days Arterial puncture at a noncompressible site within the past 7 days Heparin administration within the past 48 hrs with PTT elevation Elevated prothrombin time >15 seconds Platelet count <100,000 ml Serum glucose <50 mg/dl or >400 mg/dl Relative contraindications for tPA therapy: Large stroke with NIH Stroke Scale score >22 Large MCA infarction with CT signs of sulcal effacement or loss of gray-white junction in > one third of the MCA cerebral watershed area NIH, National Institutes of Health; CT, computed tomography; ICH, intracerebral hemorrhage; BP, blood pressure; SAH, subarachnoid hemorrhage; GI, gastrointestinal; GU, genitourinary; PTT, partial thromboplastin time; MCA, middle cerebral artery.
artery (MCA) or basilar artery occlusions after the 3-hour intravenous window has expired remains investigational in selected centers. There have been positive reports of intra-arterial thrombolytic infusions in posterior circulation strokes up to 12 hours after symptom onset. The majority of patients with stroke will not be eligible for fibrinolytic therapy due to the strict criteria and short time window for use. Consequently, antiplatelet therapies with aspirin, dipyridamole, clopidogrel, or ticlopidine are indicated for secondary stroke prevention. There is a risk reduction in mortality and stroke recurrence up to 20%–25% with the use of these drugs. Angiotensin-converting enzyme inhibitors may have vascular benefit beyond blood pressure control and may also be beneficial in reducing the risk and recurrence of stroke. The use of anticoagulation with unfractionated heparin, low-molecularweight heparin, or heparinoids has not been proved to be beneficial in treating acute ischemic stroke, any specific stroke subtype, or TIA. Heparin may increase the risk of ICH. Use of unfractionated heparin infusion, however, is discretionary and may be useful in preventing recurrent embolism
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or preventing thrombus propagation in TIA under the following circumstances: stroke in evolution, known high-grade stenosis in a vessel compatible with the clinical symptoms (especially internal carotid artery), cardioembolism from causes other than infective endocarditis, crescendo TIAs, posterior circulation TIA, and TIA refractory to antiplatelet therapy. Urgent carotid endarterectomy is indicated for TIAs resolving within the first 6 hours associated with carotid stenosis greater than 70%. Selective cerebral angioplasty or stenting of other cerebral vessels are currently investigational. Investigational neuroprotective agents targeted at preventing the neuronal physiological cascade initiated by cerebral ischemia include various antioxidants, calcium-channel blockers, N-methyl-D-aspartate (NMDA) inhibitors, glycine, and glutamate receptor antagonists. There is no benefit from the routine use of corticosteroids or anticonvulsants in acute ischemic stroke. The treatment of ICH, especially when consciousness is altered, is focused on stabilization of the ABCs, identification of other causes for mental status changes, and management of elevated ICP. Hypertension should be restored gradually to pretreatment levels when the initial blood pressure exceeds 220/120 mmHg. Patients with known hypertension should not have their blood pressure reduced beyond an estimate of their usual hypertensive level. The head of bed should be elevated 30 degrees above the horizontal. Elevated ICP should be treated with a loop diuretic (furosemide) or osmotic diuretic (mannitol). Intubation and mechanical hyperventilation to a target PCO2 of 30–35 mmHg should be performed when the Glasgow Coma Scale score is less than 9, when there is progressive neurological deterioration, or in situations where the CT scan shows mass effect, midline shift, or impending herniation. Seizure prophylaxis with diphenylhydantoin or fosphenytoin is indicated. An emergency neurosurgical consultation for placement of an ICP monitor and/or surgical intervention is warranted. Surgical decompression and evacuation of the hematoma is indicated in cerebellar hemorrhages greater than 3 cm size or in those involving the brainstem. Steroids are harmful and should not be used. Investigational treatments include barbiturate coma and hypothermia. The treatment of SAH is focused on avoiding rebleeding, which is greatest within the first 24 hours, and preventing vasospasm, which occurs from 2 days to 3 weeks after aneurysm rupture. Lowering systolic blood pressure to less than 160 mmHg or to prehemorrhage levels is associated with a reduced mortality rates and risk of rebleeding. Nimodipine (a calcium-channel blocker), 60 mg given orally every 4–6 hours, should be started within the first 72 hours in patients who can swallow to reduce the incidence and severity of vasospasm. Pain, nausea, vomiting, and seizures should all be treated appropriately to avoid sudden rises in systemic and intracranial pressure. Neurosurgical
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consultation for angiography and possible surgical intervention is indicated, especially when the Hunt and Hess Clinical Grading Scale score for cerebral aneurysms and SAH is less than 3. Other treatment modalities for aneurysmal SAH include coil or microsphere balloon embolization. All patients with an acute ischemic stroke, regardless of eligibility for fibrinolytic therapy, should be admitted to the hospital telemetry or intermediate care unit for monitoring and observation. A neurology specialist should be consulted. Patients with large hemispheric strokes, cerebellar stroke, or significant posterior circulation symptoms and those treated with fibrinolysis should be admitted to the intensive care unit. Patients with new-onset TIA should be admitted to the hospital for a workup to rule out a possible cardioembolic etiology or high-grade carotid stenosis. Some sources suggest discharge of these patients can be considered when carotid and cardiac imaging can be performed on a timely outpatient basis. This is a potentially dangerous disposition since the risk of stroke is nearly 5% within the subsequent 48 hours after discharge. Patients with TIA who have already undergone an extensive prior workup and do not have highgrade carotid stenosis may be discharged on antiplatelet therapy if the ED evaluation results are negative. Patients with repeated stroke who have been previously and extensively evaluated and present with another TIA or a mild completed stroke days to weeks old may be discharged home if the ED evaluation results are negative and aftercare is closely coordinated with the patient’s physicians and family.
Bibliography American College of Emergency Physicians, Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. American College of Emergency Physicians: Emergency Medicine Manual, ed 6. McGraw-Hill: New York, 2004. American College of Emergency Physicians Use of intravenous tPA for the management of acute stroke in the emergency department. Available at: http://www.acep.org. Cort MA, Kuo D: Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep 25(5):23–31, 2004. Cort MA, Kuo D: Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep 25(6):19–28, 2004. Gavin L, Wright D: Transient ischemic attacks: Transient trouble or action-warranted attacks, Emerg Med Pract 5:10, 2003. Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep February 23, 2004;25(5):. Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep March 8, 2004;25(6):. Personal Correspondence, Ms. Anne D. Leonard, RN, Nursing Coordinator, University Hospital Stroke Program, San Antonio, TX. September, 2005. The Internet Stroke Center at Washington University in St. Louis, Mo. 1997–2005. Available at: http://www.strokecenter.org. Transient ischemic attacks: Transient trouble or action-warranted attacks, Emerg Med Pract Volume 5, Number 10, October 2003. University of Texas Health Science Center Stroke Program: Internal Stroke Physician Education Services.
Chapter 10
Gynecological and Obstetric Emergencies Abruptio Placentae KHIM K. LAM
ICD Code: 641.2
Key Points The severity of fetal distress associated with abruptio placentae correlates with the degree of placental separation. ! Emergency Actions ! Two large-bore intravenous lines should be placed to draw blood for laboratory studies and for aggressive fluid resuscitation. The patient’s vital signs and urinary output should be monitored. Hypotension should be treated. The patient should be monitored for signs of hemorrhagic shock/disseminated intravascular coagulation (DIC) and treated as needed. Fetal heart tracing should be obtained to evaluate for possible fetal distress.
DEFINITION The term abruptio placentae refers to premature separation of the normally implanted placenta from the uterus before delivery of the fetus.
EPIDEMIOLOGY The reported incidence of placental abruption varies from 1 in 86 to 1 in 206 births. Abruption severe enough to kill the fetus is less common (1 in 420 to 1 in 830 births). Approximately 10% of cases of abruptio placentae are considered concealed (i.e., no vaginal bleeding). Perinatal mortality ranges from 15% to 25%, and in infants who survived, up to 14% of them could have serious neurological deficits.
ETIOLOGY The primary etiology of abruptio placentae is unknown, but multiple risk factors have been associated with abruptio placentae. Risk factors include the following:
Maternal hypertension: most common cause of abruption (40%–50% are associated with hypertensive disease of pregnancy) 497
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Maternal trauma (e.g., motor vehicle accidents, assaults, falls) Cocaine use Sudden decompression of the uterus (e.g., premature rupture of membranes, delivery of first twin) Multiple gestations/maternal age/grand multiparity Previous abruption: risk of recurrence ranges from 5.5% to 16% Inherited thrombophilia Retroplacental myoma Idiopathic factors: probable abnormalities of uterine blood vessels and decidua Cigarette smoking
PATHOPHYSIOLOGY Abruptio placentae is caused by bleeding from small arterial blood vessels into the decidua basalis. The resultant hematoma causes separation of the decidua from the uterine wall leading to obliteration of the intervillous space. This compromises the gas and nutrient exchange to the fetus, leading to fetal distress. The severity of fetal distress correlates with the degree of placental separation. Bleeding into the myometrium and extending to the uterine serosa can also occur; this is known as a Couvelaire uterus.
CLINICAL PRESENTATION Patients usually present in the third trimester with vaginal bleeding, abdominal or back pain, uterine tenderness, fetal distress or death, and hypertonic or high-frequency uterine contraction.
LABORATORY TESTS Laboratory tests that should be performed include a complete blood count (CBC) and measurements of partial thromboplastin time (PTT), international normalized ratio (INR), fibrinogen, and electrolyte levels. The patient should be type and cross-matched for 4–6 units of blood.
RADIOGRAPHS Ultrasound should be used to evaluate the placenta, to exclude the presence of placenta previa and to look for the presence of retroplacental clots. Negative findings do not exclude placental abruption.
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DIAGNOSIS The diagnosis of abruptio placentae is made on the basis of history, clinic examination, and ultrasound examination.
TREATMENT An obstetrician/gynecologist (OB/GYN) should be consulted, and the patient should be transferred to the Labor and Delivery department as soon as possible. Two large-bore intravenous lines should be placed to draw blood for laboratory studies and for aggressive fluid resuscitation. The patient’s vital signs and urinary output should be monitored. Hypertension should be treated. The patient should be monitored for signs of hemorrhagic shock/DIC and treated as needed. Fetal heart tracing should be obtained to evaluate for possible fetal distress.
Bibliography Ananth CV, Savitz DA, Williams MA: Placental abruption and its association with hypertension and prolonged rupture of membranes: A methodologic review and meta-analysis, Obstet Gynecol 1996;88:309. Benedetti TM: Obstetric hemorrhage. In Gabbe SG, Niebyl JR, Simpson JL (eds): Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: New York, 2002, pp 510–516. Clark SL: Placenta previa and abruptio placentae. In Creasy RK, Resnik R (eds): Maternal-Fetal Medicine, ed 4. WB Saunders: Philadelphia, 1999, pp 621–629. Cunningham GF, Gant NF, Leveno KJ, et al: Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 621–630. Toivonen S, Heinonen S, Anttila M, et al: Obstetric prognosis after placental abruption, Fetal Diagn Ther 2004;19:336.
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Amniotic Fluid Embolism KHIM K. LAM
ICD Code: 673.1
Key Points Amniotic fluid enters the circulation as a result of a breach in the physiological barrier that normally exists between the maternal and fetal compartment. This may trigger a massive anaphylactic reaction, activation of the complement cascade, or both. ! Emergency Actions ! Treatment should focus on cardiopulmonary resuscitation, providing oxygenation (i.e., 100% oxygenation with ventilator support) and support for the failing heart. Circulatory support and blood component replacement are crucial; aggressive fluid resuscitation should be undertaken.
DEFINITION Amniotic fluid embolism is a rare obstetrical emergency in which amniotic fluid/fetal cells enter the maternal circulation, causing cardiopulmonary collapse.
EPIDEMIOLOGY The reported incidence is between 1 in 8000 to 1 in 80,000 deliveries worldwide; the incidence is about 1 in 20,000 to 1 in 30,000 deliveries in the United States. Despite all these aggressive interventions, maternal prognoses have not been shown to improve with amniotic fluid embolism. Maternal mortality rates can reach as high as 86%. One study found a maternal mortality rate of 61% with only 15% neurologically intact, and with fetuses in utero, only 39% survived.
ETIOLOGY/PATHOGENESIS Amniotic fluid enters the circulation as a result of a breach in the physiological barrier that normally exists between the maternal and fetal compartment. This may trigger a massive anaphylactic reaction, activation
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of the complement cascade, or both. Progression usually occurs in two phases. In phase I, pulmonary artery vasospasm with pulmonary hypertension and elevated right ventricular pressure cause hypoxia. Hypoxia causes myocardial capillary damage and pulmonary capillary damage, left heart failure, and acute respiratory distress syndrome. Women who survive these events may enter phase II. This is a hemorrhagic phase characterized by massive hemorrhage with uterine atony and DIC; however, fatal consumptive coagulopathy may be the initial presentation.
CLINICAL PRESENTATION The major clinical findings are abrupt onset of hypotension (cardiogenic shock), hypoxia and respiratory failure, and consumptive coagulopathy. The onset of symptoms most commonly occurs during labor and delivery, in the immediate postpartum period, or during termination. The clinical presentation of amniotic fluid embolism is similar to that of septic or anaphylactic shock. The patient may report the acute onset of shortness of breath followed by severe hypotension. Other signs and symptoms are dyspnea, seizure, cyanosis, fetal bradycardia, pulmonary edema, cardiac arrest, and uterine atony resulting in postpartum bleeding.
LABORATORY TESTS Appropriate laboratory tests should include CBC; measurements of electrolytes, PTT, INR, and fibrinogen; and type and cross-match for 4–6 units of blood.
RADIOGRAPHS Chest radiography, electrocardiography, and arterial blood gas analysis are other diagnostic tests that should be performed.
TREATMENT Management should be multidisciplinary. An OB/GYN and critical care team should be consulted. Treatment should focus on cardiopulmonary resuscitation, providing oxygenation (i.e., 100% oxygenation with ventilator support) and support for the failing heart. Circulatory support and blood component replacement are crucial; aggressive fluid resuscitation should be undertaken. A Foley catheter should be placed for monitoring of urinary output. The patient should be transferred to the intensive care unit. Consideration of emergency perimortem cesarean delivery should be given in undelivered women with cardiac arrest—especially after 5 minutes of cardiopulmonary resuscitation.
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Bibliography Clark SL, Hankins GD, Dudley DA, et al: Amniotic fluid embolism: Analysis of the national registry, Am J Obstet Gynecol 1995;172:1158. Cunningham GF, Gant NF, Leveno KJ, et al: Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 621–630. Dashow EE, Cotterill R, Benedetti TJ, et al: Amniotic fluid embolism, J Reprod Med 1989;34:660. Killam A: Amniotic fluid embolism, Clin Obstet Gynecol 1985;28:32. Sperry K: Amniotic fluid embolism, JAMA 1986;255:2183.
Breast Abscesses and Mastitis JACQUELYN L. SIMONDS
ICD Codes: Abscess of breast 675.1, Nonpurulent mastitis 675.2
Key Points Breast abscesses and mastitis are infections that must be differentiated. Common skin organisms are the usual cause of both infections. ! Emergency Actions ! Any patient who presents with an elevated white blood cell count, fever, and chills must be considered to have bacteremia. Most patients with breast abscess are not septic, but those patents who present with fever, chills, and hot, red swollen breast and have diabetes, should have blood cultures preformed.
DEFINITION Staphylococcus aureus and streptococcal species are the most common organisms isolated in puerperal breast abscesses. Nonpuerperal abscesses typically contain S. aureus, various Streptococcus species, and anaerobes. In mastitis, S. aureus is the most common cause. Streptococci, enterococci, Staphylococcus epidermidis, and Escherichia coli are less common. In light of the increasing incidence of methicillin-resistant S. aureus (MRSA) nosocomial infection, nursing mothers who develop breast abscesses or mastitis within the first 4 postpartum weeks should be considered to have antibiotic-resistant staphylococcal infections until it is proven otherwise.
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EPIDEMIOLOGY Breast abscesses are more common in nonlactating women and are typically found in the third to eighth decades of life. Postpartum mastitis occurs in 1%–5% of lactating women.
CLINICAL PRESENTATION The patient with a breast abscess typically presents with an edematous, painful, erythematous, and indurated area of the breast. Increased warmth is usual and associated symptoms of fever, chills, vomiting, and drainage from the nipple are common. A mass is commonly found in the subareolar or periareolar regions of the breast. Nipple inversion of recent onset may also be reported. The patient may or may not be actively breast-feeding at the time of onset. Patients with mastitis will report pain and are found on examination to have a warm, erythematous, indurated breast without localized mass. They may have fever.
EXAMINATION The provider should also check for axillary lymphadenopathy, which can be associated with a breast abscess or mastitis.
LABORATORY FINDINGS A CBC with differential may be helpful in assessing a patient with breast abscess. Aerobic and anaerobic cultures, although usually obtained in the operating room for breast abscess, may be helpful in the case of recurrent or nonimproving mastitis. If the patient has diabetes, a chemistry panel should be obtained, and if a fever is present blood cultures should be performed.
RADIOGRAPHS Ultrasound scanning should be performed to differentiate a solid mass from a cystic structure. A direct needle aspiration should be performed if prompt surgical consultation is not an available option. Noncystic structures should be followed up with a mammogram as an outpatient study with surgical follow-up.
TREATMENT Breast Abscess Treatment of breast abscess includes pain control, antibiotic therapy, and prompt surgical consultation. Patients are normally admitted for treatment
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with intravenous antibiotics, pain management, and surgical consultation. Although needle aspiration may be an effective first-line treatment, recurrent aspiration is usually necessary. Definite treatment frequently requires incision and drainage and fistulectomy, and it often necessitates general anesthesia. Aerobic and anaerobic cultures should be obtained to identify organism and to determine sensitivities. Medications in the postpartum female patient may include dicloxacillin, cephalexin, or clindamycin. If it is appropriate to suspect MRSA infection, treatment can include intravenous vancomycin; trimethoprim-sulfamethoxazole (TMP-SMX) given orally or parenterally in a range of 10 mg/kg/day (TMP) and 50 mg/kg/ day (SMX) to 15 mg/kg/day (TMP) and 75 mg/kg/day (SMX) in divided doses at 8- or 12-hour intervals for 2–4 weeks (for adults); rifampin (600 mg/day) given orally or parenterally; or either imipenem-cilastatin (500 mg every 6 hours) or meropenem (0.5–1 g every 8 hours) given parenterally. Nonpuerperal abscesses may be treated with amoxicillin/clavulanate, clindamycin, or a combination of metronidazole and cefadroxil, cefazolin, cephalexin, or dicloxacillin. Depending on the level of discomfort, pain medications may range from nonsteroidal anti-inflammatory drugs to Tylenol (acetaminophen) with oxycodone. All antibiotic regimens should be continued for 14 days. As with any breast mass, mammography and follow-up must be arranged.
Mastitis Mastitis should be treated with antistaphylococcal antibiotics, warm packs, and uninterrupted emptying of the breast by breast-feeding or pumping to reduce chance of breast abscess development. Medication choices include nafcillin, cefazolin, dicloxacillin, cephalexin, or clindamycin, and drug therapy should be continued for 14 days. Pain medication may be necessary, with care taken to ensure that the choice reflects one that is safe with lactation.
Bibliography August DA, Sondak VK: Breast. In Greenfield LJ, Mulholland MW, Oldham KT (eds): Surgery Scientific Principles and Practice, ed 2. Lippincott-Raven: Philadelphia, 1997, pp 1357–1415. Dixon JM: Outpatient treatment of non-lactational breast abscesses, Br J Surg 1992;79 (1):56–57. Maier WP, Au FC, Tang CK: Nonlactational breast infection, Am Surg 1994;60 (4):247–250. Ohara RJ, Dexter SP, Fox JN: Conservative management of infective mastitis and breast abscess after ultrasonographic assessment, Br J Surg 1996;83(10):1412–1414. Walker AP, Edmiston CE, Krepel CJ, et al: A prospective study of the microflora of nonpuerperal breast abscess, Arch Surg 1988;123:908–911.
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Ectopic Pregnancy CULLEN ARCHER
ICD Codes: Ectopic pregnancy ruptured 633.90, Ectopic pregnancy with intrauterine pregnancy 633.1, Tubal pregnancy 633.10
Key Points The most common symptoms of ectopic pregnancy are abdominal pain with a history of amenorrhea and vaginal bleeding. The most common finding in a woman with a symptomatic ectopic pregnancy is abdominal tenderness. ! Emergency Actions ! Intravenous access should be attained quickly with volume resuscitation if the patient is pregnant and hemodynamically unstable. In addition, the patient should be cross-matched for at least 4 units of packed red blood cells. Measurement of urine output can also assist in the assessment of volume status. Emergency consultation with a OB/GYN service is necessitated.
DEFINITION An ectopic pregnancy develops after implantation of the blastocyst anywhere other than the endometrium lining the uterine cavity. An abdominal pregnancy (1.37%) is a pregnancy that develops in any portion of the peritoneal cavity. It usually occurs after secondary implantation of the trophoblast after tubal abortion (i.e., secondary abdominal pregnancy). A primary abdominal pregnancy is one that implants directly into the peritoneal cavity. In a cervical pregnancy (0.15%), ectopic gestational tissue is located in the cervical canal below the level of the internal os. Pregnancy developing in one horn of a bicornuate uterus is called a cornual pregnancy (0.61%). A heterotopic pregnancy (1/6579) occurs when a combined intrauterine and extrauterine pregnancy is present, and an interstitial pregnancy (1.2%) is a pregnancy developing in the interstitial portion of the oviduct. Ovarian pregnancy (0.15%) occurs when pregnancy develops in the ovary. For the diagnosis to be made, the tube on the affected side should be intact, the gestational site must occupy the normal position of the ovary, the gestational site must be connected to the uterus by the
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ovarian ligament, and histologically identified ovarian tissue must be present in the sac wall. A tubal pregnancy (97%) is a pregnancy occurring in the oviduct in either the ampulla (75%–80%), fimbria (5%), or isthmus (10%–15%).
EPIDEMIOLOGY In 1992, ectopic pregnancies accounted for approximately 2% of reported pregnancies, and ectopic pregnancy–related deaths accounted for 9% of all pregnancy-related deaths. The incidence of ectopic pregnancy has been increasing since 1970, when the Centers for Disease Control and Prevention (CDC) first began collecting data, from 4.5 per 1000 reported pregnancies to 19.7 per 1000 pregnancies in 1992. The increased incidence is thought to be due to two factors: (1) the increased incidence of acute salpingitis, due to increased infection with Chlamydia trachomatis, and (2) improved diagnostic techniques, which enable diagnosis of unruptured ectopic pregnancy to be made earlier and with more precision. Other factors that appear to be associated with an increased risk of ectopic pregnancy include prior ectopic pregnancy, cigarette smoking, prior tubal surgery (especially for distal tubal disease), diethylstilbestrol exposure, increasing age, multiparity, and current use of an intrauterine device. The 10-year cumulative probability of ectopic pregnancy for all methods of tubal sterilization combined was shown to be 7.3 per 1000 procedures. Of all pregnancies found in that study after tubal sterilization, 32.9% were ectopic. An operative procedure on the oviducts themselves is a cause of ectopic pregnancy. The incidence of ectopic pregnancy after salpingoplasty or salpingostomy procedures to treat distal tubal disease ranges from 15% to 25%. The rate of ectopic pregnancy after reversal of sterilization procedures is about 4% because the tubes have not been damaged by infection. Women who have had a prior ectopic pregnancy, even if treated by unilateral salpingectomy, are at increased risk for a subsequent ectopic. Of women who conceive after having one ectopic pregnancy, about 25% of subsequent pregnancies are ectopic.
CLINICAL PRESENTATION The most common symptoms of ectopic pregnancy are abdominal pain (90%–100%), a history of amenorrhea (75%–95%), and vaginal bleeding (50%–80%). The most common findings in a woman with a symptomatic ectopic pregnancy is abdominal tenderness (80%–95%), which together with adnexal tenderness (75%–90%) is present in nearly all women with an advanced or ruptured ectopic pregnancy. An adnexal mass is palpable in 50% of the women.
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Many of these classical signs and symptoms are associated with an advanced or ruptured ectopic pregnancy and frequently require surgical intervention. In such cases, intravenous access should be attained quickly with volume resuscitation if the patient is hemodynamically unstable. In addition, the patient should be cross-matched for at least 4 units of packed red blood cells. Measurement of urine output can also assist in the assessment of volume status.
TREATMENT In cases in which the pregnant patient is hemodynamically stable and presents with abdominal or pelvic pain, a transvaginal ultrasound scan is warranted. The identification of an ectopic gestational sac is obviously diagnostic. The sensitivity and specificity of transvaginal ultrasound to detect an ectopic pregnancy are 90.9% and 99.9%, respectively, and positive and negative predictive values of 93.5% and 99.8%, respectively, were noted in the adnexal region when women were diagnosed with an ectopic pregnancy using transvaginal ultrasound if any of the following were present: (1) an inhomogeneous mass or blob sign adjacent to the ovary and moving separately from the ovary; (2) a mass with a hyperechoic ring around the gestational sac or bagel sign; or (3) a gestational sac with a fetal pole with or without cardiac activity. When any adnexal mass other than a simple cyst is used as diagnostic criterion for ectopic pregnancy, the specificity is 98.9%, sensitivity is 84.4%, positive predictive value is 96.3%, and negative predictive value is 94.8%. If an intrauterine pregnancy cannot be identified, a quantitative measurement of b human chorionic gonadotropin (hCG) should be performed (according to the First or Second International Reference Preparation). Transvaginal ultrasound can often detect an intrauterine pregnancy within 5 weeks of the last menstrual period. An intrauterine gestational sac in a healthy uterus can usually be seen with a hCG level between 1000 and 2000 mIU/ml. If the patient’s condition is stable, she may return in 48 hours for another quantitative hCG determination. The mean doubling time for hCG in a normal intrauterine pregnancy is 1.4–2.1 days. However, in patients with an ectopic pregnancy, the hCG will rise at a much slower rate. Based on studies of doubling time, hCG levels should rise by 66% in 48 hours in 85% of normal pregnancies. That is, 15% of normal intrauterine pregnancies will not have a normal doubling time. However, a rise of less than 50% is associated with an abnormal pregnancy 99.9% of the time.
Single-Dose Methotrexate Protocol Classically, uterine dilation and curettage has played an important role in the diagnosis of ectopic pregnancy. The absence of chorionic villi
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on curettage in the presence of an elevated b-hCG level is evidence of a presumptive diagnosis of ectopic pregnancy. Stovall’s protocol used dilation and curettage on day 0 followed by methotrexate 50 mg/m2 given intramuscularly on day 1 after liver and kidney function was verified to be normal. A repeated hCG level determination is performed on days 4 and 7. If the hCG level falls less than 15% between days 4 and 7, a repeat dose of methotrexate was given. If the hCG levels fell more than 15%, then hCG titers were followed weekly until undetectable.
Criteria for Receiving Methotrexate ABSOLUTE INDICATIONS Absolute indications for methotrexate are as follows:
Hemodynamic stability without active bleeding or signs of hemoperitoneum Patient desires future fertility General endotracheal anesthesia (GETA) poses a significant risk Patient is reliable and able to return for follow-up care Patient has no contraindications to methotrexate
RELATIVE INDICATIONS Relative indications for methotrexate are as follows:
Unruptured mass 3.5 cm in greatest dimension No fetal cardiac motion b-hCG level does not exceed a predetermined level (among women with initial hCG concentrations below 15,000 mIU/ml, 93% were successfully treated)
Contraindications to Medical Therapy ABSOLUTE CONTRAINDICATIONS Absolute contraindications for medical therapy include the following:
Breast-feeding Evidence of immunodeficiency Alcoholism or liver disease Preexisting blood dyscrasias Hypersensitivity to methotrexate Active pulmonary disease Peptic ulcer disease Hepatic, renal, or hematological dysfunction
Emergent Pelvic and Abdominal Pain
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RELATIVE CONTRAINDICATIONS Relative contraindications for medical therapy are as follows:
Gestational sac 3.5 cm Fetal cardiac motion
The presence of blood in the pelvis is not considered a contraindication to medical therapy. Approximately 50%–60% of unruptured ectopic pregnancies will have blood in the pelvis on pelvic ultrasound.
Bibliography ACOG Committee on Practice Bulletins: Medical management of tubal pregnancy, ACOG Practice Bulletin. No. 3, December 1998. Goldstein SR, Snyder JR, Watson C, Danon M: Very early detection of pregnancy with transvaginal ultrasound, Obstet Gynecol 1988;72:200–204. Kadar N, Freedman M, Zacher M: Further observation on the doubling time of human chorionic gonadotropin in early asymptomatic pregnancy, Fertil Steril 1980;54:783. Stovall TS, Ling FW: Single dose methotrexate: An expanded clinical trial, Am J Obstet Gynecol 1993;168:1759.
Emergent Pelvic and Abdominal Pain AMY DITZEL
ICD Codes: Pelvic inflammatory disease, female, acute 614.3, Pelvic pain, female 625.9, Ectopic pregnancy, ovarian 633.20, Ectopic pregnancy, tubal 633.10, Tubo-ovarian abscess 614.2
Key Points All female patients of childbearing age with pelvis or abdominal pain are considered pregnant until proven otherwise. Ultrasound and gynecological consult should be obtained. ! Emergency Actions ! Two large-bore intravenous lines with normal saline or lactated Ringer’s solution should be introduced. The patient should be administered oxygen. Laboratory tests, including CBC; measurements of electrolytes, prothrombin time (PT), PTT, and serum quantitative and qualitative hCG; and type and cross-match for 6 units of blood.
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DEFINITION A wide spectrum of conditions involving pelvic and abdominal pain can be categorized as those that pose an immediate threat to the life of the patient (“true emergencies”) and those that do not. These conditions are generally gynecological, obstetrical, or infectious in nature. True emergent causes of pelvic pain include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Ruptured tubo-ovarian abscess Ruptured ectopic pregnancy Ruptured hemorrhagic ovarian cyst Premature rupture of membranes Preeclampsia and eclampsia Preterm labor Uterine perforation or rupture Abruptio placentae Placenta previa Molar pregnancy
Other causes of pelvic pain in women, which are gynecological in nature, include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Pelvic inflammatory disease (PID) Mittelschmerz Dysmenorrhea Endometriosis Adnexal torsion Nonruptured ovarian cysts Ruptured corpus luteum cyst Vaginitis Pelvic neoplasm Foreign bodies Uterine leiomyoma Abortion (threatened, inevitable, or incomplete)
Additional causes of pelvic pain in females, not gynecological in nature, are as follows: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Appendicitis Lower-lobe pneumonia Colitis Diverticulitis Gastroenteritis Sickle cell crisis Myocardial ischemia Aseptic necrosis of the femoral head Gastric or duodenal ulcer Cholecystitis
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Pancreatitis Pyelonephritis Nephrolithiasis Musculoskeletal pain Pulmonary embolism
EPIDEMIOLOGY The epidemiology varies according to the cause of the pain.
CLINICAL PRESENTATION The nature of the pain varies according to the source of the pain. A thorough description of the pain should be obtained, including location, radiation, intensity, quality (throbbing, etc.), aggravating or alleviating symptoms, and length of time the pain has been present. Additionally, a thorough gastrointestinal, gynecological, and sexual history must be obtained. The following are guidelines regarding determining the source of pelvic pain from the patient’s description:
Sudden pain is usually caused by a vascular or ischemic insult or by an acute irritation of the peritoneum by a large amount of blood. Gradual onset of pain is generally caused by a slow vascular leak or an infection. Colicky pain suggests pain from a hollow organ such as the gallbladder or uterus. Dull throbbing pain suggests chronic inflammation. Pain from the pelvic organs can radiate to the upper and lower abdomen, back, shoulder, thighs, buttocks, and perineum.
EXAMINATION A complete physical examination, including pelvic and rectal examination, must be obtained. This will allow for the detection of a gravid or nongravid uterus, adnexal masses or tenderness, possible localization of the pain, and identification of vaginal bleeding or gastrointestinal tract bleeding. Depending on the severity of the illness, the patient may be tachypneic, tachycardiac, hypotensive, and diaphoretic or may be completely stable with only moderate adnexal tenderness.
LABORATORY FINDINGS Laboratory findings vary according to the underlying process. Elevated white blood cell counts should be expected with infectious processes,
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and lowered hemoglobin and hematocrits may be present with hemorrhagic processes. Hemoglobin and hematocrit levels are generally slightly depressed in a gravid patient. Additionally, the hemoglobin and hematocrit are late indicators of internal bleeding.
DIAGNOSIS A diagnosis is made on the basis of history, physical examination results, clinical presentation, laboratory values, and abdominal/pelvic ultrasound. Occasionally, the diagnosis cannot be made until a computed tomography (CT) scan is obtained or until the patient is taken to surgery. While the laboratory values and ultrasound scan are being obtained, a consultation with a gynecology specialist should be sought.
RADIOGRAPHS A pelvic ultrasound scan will provide valuable information and rule out or diagnose many conditions. This procedure is generally safe for gravid patients.
TREATMENT AND OUTCOME Treatment and outcome vary widely depending on the nature of the pain.
Bibliography Marx JA (ed): Rosen’s Emergency Medicine, ed 5. Mosby: St Louis, 2002.
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Genital Herpes AMY K. DITZEL
ICD Codes: Genital herpes, NOS 054.10, Vulval ulceration 054.12, Vulvovaginitis 054.11
Key Points Genital herpes is a viral infection that is usually sexually transmitted. The lesions are painful, and often vesicles are present, with itching and burning. Genital herpes is a lifelong disease, with variable presentation, but antiviral therapy can decrease recurrences. ! Emergency Actions ! The patient should always be asked about underlying immunocompromising disease like human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS). Any immunocompromised patient should undergo a detailed evaluation for other immunocompromise-associated disease.
DEFINITION Genital herpes is a common, viral, sexually transmitted disease (STD) for which effective treatment has been developed, but there is no cure.
EPIDEMIOLOGY Genital herpes is a common viral infection, with over half a million new cases diagnosed each year. Genital herpes is caused by the herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2). HSV-2 is more commonly associated with genital lesions, whereas HSV-1 is more commonly associated with oral lesions. However, oral-genital contact can result in either type accounting for genital lesions.
CLINICAL PRESENTATION Women with genital herpes present with a chief symptom of genital pain and rash or sores. Often, these women experience dysuria and may even
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have secondary urinary retention. Patients may have systemic, flu-like symptoms, including fever, headache, myalgias, and malaise. Often patients have had a new sexual contact recently. Approximately 48 hours to 1 week after exposure to an infected person, a patient will develop the initial episode of genital herpes. This is typically the patient’s worst outbreak, lasting up to 3 weeks if untreated. During this time, crops of lesions will appear, each taking an average of 8 days to resolve. Complications can occur with this seemingly localized disease, including aseptic meningitis, hepatitis, and autonomic nervous system dysfunction. Because there is no cure for genital herpes, it can recur, although generally with milder symptoms and a shorter duration of symptoms. Half of all patients will experience a prodrome before the appearance of lesions, including any of the following: localized burning or itching, tingling or paresthesias, or myalgias. Over time, many patients will begin to recognize their own personal prodromal symptoms.
EXAMINATION The findings on examination may vary depending on when in the course of the genital herpes outbreak the patient presents. Initially erythematous maculae appear, which then develop into vesicles on the erythematous base. Eventually, pustules form and often open, creating ulcers that will crust over. Throughout the majority of the course of the disease the lesions will be painful, often exquisitely so. The lesions can be found on the external genitalia as well as on the perineum, along the vaginal walls, and on the cervix. The extent of the speculum examination may be limited due to the severity of the pain. The initial or primary outbreak generally results in a larger number of lesions, which are present bilaterally, whereas recurrent disease will have more limited, often unilateral lesions. Deep inguinal lymphadenopathy is often present with primary disease.
LABORATORY FINDINGS Viral culture and typing will provide diagnosis confirmation. Additionally, these will identify the causative agent as HSV-1 or HSV-2 and will thereby help to predict recurrence patterns. Culture samples can be taken from the vesicular fluid or ulcers, cervix, or vaginal fluid. The earlier in the course of the outbreak, the more likely the culture will have a positive result. A Tzanck smear can be obtained to confirm the diagnosis more quickly than a culture, but the characteristic multinucleated giant cells are present only 50% of the time. The Tzanck smear is prepared by placing some of the vesicular fluid onto a slide and examining it with a Wright or methylene blue stain.
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DIAGNOSIS The diagnosis of genital herpes is made on the basis of physical examination results, with confirmation by Tzanck smear and culture.
TREATMENT The goals of treatment are to shorten the severity and duration of the outbreak with antiviral preparation and comfort measures. Acyclovir 500 mg PO five times a day for 7–10 days is the standard treatment. If complications are present or if the disease is severe, hospitalization with intravenous acyclovir (5 mg/kg every 8 hours) may be necessary. Treatment ideally should be started within 2 days of symptom onset for the most benefit. Suppressive treatment (acyclovir 400 mg given twice daily or 200 mg given five times a day) is also available for patients with greater than six recurrences in a year. Patients can take acetaminophen, ibuprofen, or aspirin in over-the-counter doses to help control the pain. In addition, sitz baths with lukewarm water, wearing loose clothing, and keeping the genitals clean and dry should help patients to be more comfortable. Patients should be advised to adhere to a strict handwashing protocol to decrease the risk of spreading the lesions and to avoid secondary infection to the lesions.
Bibliography Cohen J, Powderly WG (eds): Cohen and Powderly: Infectious Disease, ed 2. Mosby: London, 2004. Marx JA (ed): Rosen’s Emergency Medicine, ed 5. Mosby: St Louis, 2002.
Hyperemesis Gravidarum SHAWNA WALL
ICD Code: 536.2
Key Points Nausea and vomiting is a complication in up to 70% of all pregnancies. Hyperemesis gravidarum occurs in 0.5%^2% of these pregnancies.
516 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! A bolus of normal saline can be given to increase intravascular volume, followed by 5% dextrose in normal saline or 5% dextrose in ½ normal saline to correct ketosis. Correction of vitamin deficiencies, especially thiamine, should also be considered.
DEFINITION Hyperemesis gravidarum is severe, persistent nausea and vomiting that causes dehydration, weight loss, ketonuria, and electrolyte imbalances in a pregnant patient.
EPIDEMIOLOGY Nausea and vomiting is a complication in up to 70% of all pregnancies. Hyperemesis gravidarum occurs in 0.5%–2% of these pregnancies. Onset can occur at 4–8 weeks of gestation, and nausea and vomiting usually resolve by 14–16 weeks of gestation. Those at higher risk are obese persons, nulliparous women, women with history of prior hyperemesis gravidarum, and women with prior molar pregnancy. Pregnant patients with a history of hyperemesis gravidarum should be encouraged to take a daily multivitamin at the time of conception. Multivitamins will lower the risk of similar symptoms occurring with this pregnancy. There is a loose association of hyperemesis gravidarum with a female fetus, history of motion sickness, or a history of migraine headaches.
ETIOLOGY The cause of hyperemesis gravidarum is unknown. Several hypotheses exist. Psychological predisposition has been cited as either a conversion disorder or a somatization disorder. The conversion and somatization disorders are thought to be caused by the inability to cope with life stressors during pregnancy. The second theory is that of an evolutionary adaptation to protect the fetus from potentially harmful foods. The third theory suggests that the hCG peaks during early pregnancy are associated with the timing of the nausea and vomiting. Estrogen has been noted as a possible contributor. When estradiol levels are increased, vomiting occurs. Smokers are less likely to be affected. Estradiol and hCG levels are lower in smokers.
CLINICAL PRESENTATION The patient with hyperemesis gravidarum will present with severe nausea, vomiting, and dehydration. Patients will be afebrile and will have neither abdominal pain nor central nervous system symptoms.
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EXAMINATION The examination should include a pelvic examination for evaluation of uterine size, adnexal tenderness, or mass and rectal examination.
RADIOGRAPHS Confirmation of intrauterine pregnancy should be performed by transvaginal ultrasound or abdominal ultrasound scan.
DIAGNOSIS Hyperemesis gravidarum is a diagnosis of exclusion. All other causes of nausea and vomiting must be ruled out before the diagnosis of hyperemesis gravidarum is made. Hyperemesis gravidarum is a diagnosis of the first trimester of the pregnancy. After the first trimester of pregnancy, a different diagnosis should be entertained for any pregnant patient with severe, persistent vomiting and dehydration. Pancreatitis, cholecystitis, hepatitis, thyroid disease, gastroenteritis, peptic ulcer disease, fatty liver of pregnancy, appendicitis, diabetic autonomic dysfunction, pyelonephritis, and gestational trophoblastic disease (i.e., complete/partial molar pregnancy) can also mimic hyperemesis gravidarum.
LABORATORY FINDINGS A CBC, Chem-10, urine analysis with culture and sensitivity, liver function tests, and measurements of amylase, lipase, thyroid-stimulating (TSH), triiodothyronine (T3), thyroxine (T4) should be performed, with special attention paid to the electrolytes. Thyroid and liver function study results are commonly elevated in patients with hyperemesis gravidarum. Patients who experience elevated TSH, T3, and T4 levels during pregnancy, as a result of hyperemesis gravidarum and without a history of hyperthyroidism or goiter, can expect to have their TSH, T3 and T4 elevation resolve within 20 weeks of gestation without medical intervention. TSH is consistently suppressed, whereas the T4 level is elevated up to 4–6 times normal and T3 is elevated up to 40% of normal. The ratio of T3/T4 should be less than 20 (greater than 20 is suggestive of Graves’ disease). Liver enzyme levels should not be elevated above 300 and bilirubin above 4 mg/dl. Pancreatic enzymes should not be elevated over five times that of normal. Urine analysis will show elevation in specific gravity and ketonuria
TREATMENT The initial treatment of hyperemesis gravidarum should include intravenous fluids when the patient cannot tolerate oral fluids. A bolus of normal saline can be given to increase intravascular volume, followed by 5%
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dextrose in normal saline or 5% dextrose in ½ normal saline to correct ketosis. Correction of vitamin deficiencies should also be considered, especially thiamine. Patients with severe vomiting should not be given anything by mouth for 24–48 hours to rest the bowel. Intravenous antiemetic therapy with promethazine, prochlorperazine, chlorpromazine, or metoclopramide should be considered. It is not recommended to use both phenothiazine and metoclopramide for risk of extrapyramidal reaction. Electrolytes should be replaced as necessary. When vomiting has resolved, a trial of oral fluids can be attempted. The patient should start with small meals, avoiding spicy or fatty foods and including high-protein snacks and meals. Meals high in protein decrease the occurrence of the nausea and vomiting symptoms. If the patient is taking an iron supplement, its use should be discontinued. Vitamin B6 (25 mg PO three times a day) and foods with ginger have been shown to decrease the episodes of nausea and vomiting. Other therapies noted to have some effect on the vomiting are as follows:
Pressure or electrical stimulation of the P6 point on the wrist has been shown to reduce the episodes of vomiting. Ten mg of vitamin B6 combined with 10 mg of doxylamine has been shown to elicit a 70% reduction in nausea and vomiting. This combination is safe for the fetus. Droperidol has been used for hyperemesis gravidarum. Droperidol in doses over 25 mg increases the risk of prolonged Q-T interval, leading to torsades de pointes. It is not recommended. Methylprednisolone, 16 mg three times a day for 3 days, has been used also. This medication improves symptoms and should be tapered over 2 weeks. Avoid use of steroids before the 10th week of gestation. There is an association with oral clefts with steroids used prior to the 10th week. If persistent weight loss continues along with the inability to tolerate oral intake, parenteral caloric replacement should be considered. Mallory-Weiss tears, esophageal rupture, and a number of cases of Wernicke encephalopathy have resulted from thiamine deficiency.
Bibliography ACOG compendium of selected publications 2005, nausea and vomiting of pregnancy, ACOG Practice Bulletin, April 2004, pp 52:601–612. Cunningham FG, Gant NF, Leveno KJ, et al: Gastrointestinal disorders. In Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 1275–1276. Cunningham FG, Gant NF, Leveno KJ, et al: Prenatal care. In Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, p 242. Gabbe SG, Niebyl JR, Simpson JL: Endocrine diseases in pregnancy. In Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: Philadelphia, pp 1126, 1145–1146. Gabbe SG, Niebyl JR, Simpson JL: Maternal physiology in pregnancy. In Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: Philadelphia, p 80.
Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia)
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Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia) CULLEN ARCHER
ICD Code: 642.7
Key Points The cause of preeclampsia is not known.Chronic hypertension is defined as hypertension that is present and observable before pregnancy or that is diagnosed before the 20th week of gestation. The pregnancy-specific syndrome usually occurs after 20 weeks’ gestation, although it may occur earlier with gestational trophoblastic or collagen vascular disease. It is defined by an increase in blood pressure associated with proteinuria. ! Emergency Actions ! Any therapy for preeclampsia other than delivery must have as its successful end point the reduction of perinatal morbidity and mortality. The cornerstone of obstetrical management of preeclampsia is based on whether the fetus is more likely to survive without significant neonatal complications in utero or in the nursery.
DEFINITION Hypertension is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic.
EPIDEMIOLOGY Hypertensive disorders of pregnancy are the third-leading cause, after embolism and hemorrhage, of maternal mortality in the United States, accounting for up to 16% of deaths. Hypertensive disorders of pregnancy occur in 12%–22% of pregnancies.
PATHOPHYSIOLOGY The cause of preeclampsia is not known. The syndrome is characterized by both maternal and fetal manifestations. The maternal disease is
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characterized by vasospasm, activation of the coagulation system, and perturbations in many humoral and autocoid systems related to volume and blood pressure control. The pathologic features in this disorder are primarily ischemic in nature and affect the placenta, kidney, liver, and brain. Many consider the placenta to be the pathologic focus for all the manifestations of preeclampsia because delivery is the only definitive cure. Early in gestation, the spiral arteries (i.e., terminal branches of the uterine artery) are transformed from thick-walled, muscular vessels to sac-like flaccid vessels, which eventually accommodate a 10-fold rise in uterine blood flow. There is evidence in women destined to become preeclamptic that trophoblastic invasion of the uterine spiral arteries is incomplete, and the vessels remain thick-walled and muscular.
CLASSIFICATION AND DEFINITIONS Chronic Hypertension Chronic hypertension is hypertension that is present and observable before pregnancy or that is diagnosed before the 20th week of gestation. Hypertension is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic. Hypertension that is diagnosed for the first time in pregnancy that does not resolve during the postpartum period is also defined as chronic hypertension.
Preeclampsia The pregnancy-specific syndrome of preeclampsia usually occurs after 20 weeks’ gestation, although it may occur earlier with gestational trophoblastic or collagen vascular disease. It is defined by an increase in blood pressure associated with proteinuria. Blood pressure elevation is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic in a woman who was normotensive prior to 20 weeks’ gestation. In the past, a rise in blood pressure of 30 mmHg systolic or 15 mmHg diastolic was used as a diagnostic criterion even when the absolute values were below 140/90 mmHg. This definition is no longer included because the only available evidence shows that women in this group are not likely to experience increased adverse outcomes. According to the National Heart, Lung, and Blood Institute Working Group, however, women who demonstrate an elevation of more than 30 mmHg systolic or more than 15 mmHg diastolic above baseline “warrant close observation.” Proteinuria is defined as a urinary excretion of 0.3 g of total protein in a 24-hour collection. This quantity usually correlates with a concentration of 30 mg/dl (1þ on dipstick) or greater in a random urine determination and no evidence of urinary tract infection.
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The following findings increase the certainty of the diagnosis of preeclampsia:
Blood pressure of 160 mmHg or greater systolic or 100 mmHg of greater diastolic pressure on two occasions at least 6 hours apart while patient is on bed rest Proteinuria of 2.0 g or more within 24 hours (2þ or 3þ on qualitative urinalysis) Serum creatinine >1.2 mg/dl, unless previously elevated Platelet count <100,000 cells/mm3 or evidence of microangiopathic hemolytic anemia (elevated lactate dehydrogenase [LDH]) Elevated hepatic enzymes (alanine aminotransferase [ALT] or aspartate aminotransferase [AST]) Persistent headache or visual disturbances Persistent epigastric pain Oliguria (<500 ml in 24 hours) Pulmonary edema Fetal growth restriction Convulsions (eclampsia)
Edema occurs in too many normal pregnant women to be discriminate and has been abandoned as a marker in these classification schemes.
Superimposed Preeclampsia on Chronic Hypertension Preeclampsia is more common in women with chronic hypertension and complicates almost 25% of those pregnancies. The diagnosis of superimposed preeclampsia is highly likely with the following findings:
In women with hypertension and no proteinuria early in pregnancy (<20 weeks), new-onset proteinuria, defined as the urinary excretion of 0.3 g of protein or more in a 24-hour collection Sudden increase in proteinuria Sudden increase in blood pressure in a woman whose hypertension was previously well controlled Thrombocytopenia An increase in ALT or AST to abnormal levels
Gestational Hypertension Gestation hypertension is defined as blood pressure elevation detected for the first time after mid pregnancy, without proteinuria. This nonspecific term will include women with preeclampsia who have not yet manifested proteinuria as well as women who will never manifest proteinuria. The
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final diagnosis is only confirmed in the postpartum period when the blood pressure has returned to normal levels by 12 weeks.
TREATMENT Fetal Evaluation Any therapy for preeclampsia other than delivery must have as its successful end point the reduction of perinatal morbidity and mortality. The cornerstone of obstetrical management of preeclampsia is based on whether the fetus is more likely to survive without significant neonatal complications in utero or in the nursery. Nonstress testing, ultrasound assessment of fetal activity and amniotic fluid volume (i.e., biophysical profile), and fetal movement counts are the most common fetal surveillance techniques. For all women with preeclampsia, daily fetal movement assessment is a useful screening assessment. More formal testing (e.g., nonstress testing, biophysical profile) is indicated if movements are not normal.
Maternal Evaluation Antepartum testing has two goals. The first is to recognize preeclampsia early; the second is to observe progression of the condition, both to prevent maternal complications by delivery and to determine whether fetal well-being can be safely monitored with the usual observations. The clinical management of preeclampsia is dictated by overt clinical signs and symptoms. Antepartum hospital management should include daily scrutiny of findings such as headache, visual disturbances, or epigastric pain, weight on admittance and daily thereafter, analysis of proteinuria on admission and every other day, blood pressure readings with an appropriate size cuff in the sitting position every 4 hours, laboratory evaluation for severe disease, determination of fetal size, and amniotic fluid volume. Restricted activity is a usual and reasonable recommendation for women with preeclampsia, although its efficacy is not clearly established. Strict sodium and diuretic therapy appear to have no role in management. Antihypertensive therapy in women with gestational hypertension and preeclampsia does not improve the perinatal outcome. Delivery is the only definitive treatment for preeclampsia and should be considered for all women with this diagnosis at 40 weeks’ gestation. Delivery at term can be initiated when the cervix is favorable for induction. There is general agreement that severe preeclampsia after 34 weeks’ gestation should be managed by delivery or before that time if there is evidence of maternal or fetal distress. If delivery of a preterm infant younger than 34 weeks’ gestational age is anticipated at a level I or II hospital, the mother should be given magnesium sulfate and transferred to a tertiary care center with adequate neonatal intensive
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care facilities. If the fetus is younger than 34 weeks’ gestational age, consideration should be made to giving steroids to promote fetal lung maturity. Between 28 and 34 weeks’ gestation, considerable disagreement exists in regard to the management of severe preeclampsia. Treatment ranges from immediate delivery to expectant management with delivery for worsening maternal status or fetal compromise. Criteria for immediate delivery include attainment of 34 weeks’ gestation, labor or rupture of membranes, or vaginal bleeding. When severe preeclampsia develops between 18 and 27 weeks’ gestation, perinatal mortality has been shown to be 87% and with high maternal morbidity rates. In labor, magnesium sulfate is administered to women with preeclampsia. Magnesium sulfate is loaded intravenously in a dose of 4 g, followed by a continuous maintenance dose at 2 g/hr. Serum magnesium levels should be measured every 6 hours and adjusted to maintain levels between 4 and 7 mEq/L (4.8–8.4 mg/dl). The use of magnesium sulfate during labor in women with gestational hypertension varies from one clinician to another. We recommend that, if magnesium sulfate is not administered to women with gestational hypertension during labor, continuous reassessment for signs and symptoms of neuroirritability be undertaken.
HELLP Syndrome The syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) develops in approximately 1 of 1000 pregnancies overall and in 10%–20% of women with severe preeclampsia and eclampsia. As many as 15%–20% of patients do not have antecedent hypertension or proteinuria. Patients manifesting this syndrome usually are seen before term (i.e., less than 36 weeks’ gestation) reporting malaise (90%), epigastric or right upper quadrant pain (90%), and nausea or vomiting (50%), and some will have nonspecific viral syndrome–like symptoms. Laboratory workup should include a CBC with peripheral smear and liver profile, including measurements of AST, total bilirubin, and LDH. The diagnosis is established on the basis of the presence of the following:
Preeclampsia Platelet counts <100,000 cells/mm3 LDH >600 IU/L or total bilirubin >1.2 mg/dl AST >70 IU/L Microangiopathic hemolytic anemia on peripheral smear
There is general agreement that delivery should be effected for pregnancies at gestation of 34 weeks or more, with nonreassuring fetal testing, and in the presence of severe maternal disease (e.g., multiorgan dysfunction, DIC, liver infarction, renal failure, or abruption).
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Eclampsia Preeclampsia complicated by generalized tonic-clonic convulsions is termed eclampsia when not attributed to another cause. Until other such causes are excluded, all pregnant women with convulsions should be considered to have eclampsia. The tenets of treatment include control of convulsions using an intravenous loading dose of magnesium sulfate (4–6 g in 100 ml intravenous fluid over 15–20 minutes), followed by continuous intravenous infusion of magnesium at 2 g/hr if renal function is not compromised. An intramuscular delivery protocol has also been described. Compelling evidence suggests that magnesium sulfate significantly lowers the rate of recurrent convulsions (compared with diazepam and phenytoin) and maternal mortality (compared with phenytoin) in eclamptic women. Serum magnesium levels should be measured at 4–6 hours and adjusted to maintain levels between 4 and 7 mEq/L (i.e., 4.8–8.4 mg/dl). Magnesium is discontinued 24 hours after delivery. Acute elevations of blood pressure are treated with oral or intravenous medications. Magnesium sulfate is not given to treat hypertension. The patient with eclampsia should be delivered in a timely fashion. Fetal bradycardia frequently occurs during an eclamptic seizure; usually, this can be managed by maternal treatment, and cesarean delivery is not necessary. Once the patient’s condition is stabilized, the mode of delivery should depend, in part, on factors such as gestational age, fetal presentation, and the findings on cervical examination.
Acute Hypertension Intermittent intravenous or oral administration of antihypertensive medication is given when the diastolic pressure is dangerously high. Some clinicians treat at 100–110 mmHg. At our institution, we also treat hypertension when the systolic blood pressure is equal to or greater than 160 mmHg. Hydralazine is the most commonly administered medication, usually given intravenously, but it can be administered intramuscularly. The maximal effect is at 20 minutes, and the duration of action is 6–8 hours. At our institution, we start with 5 mg and give escalating doses every 15 minutes, adding an additional 5 mg until a therapeutic dose is found. The maximum dose is 300 mg in a 24-hour period. Labetalol has also been shown to be effective for the treatment of acute hypertension and can be given as intravenous bolus injections or as a continuous intravenous infusion at 1 mg/kg with the appropriate monitoring. However, beta antagonists should be avoided in the setting of acute congestive heart failure and asthma. Labetalol is given as a 20-mg intravenous bolus followed by 40 mg if not effective within 10 minutes; then, 80 mg every 10 minutes every 10 minutes to a maximum total dose of 220 mg. Oral nifedipine has also been used with success in controlling acute, severe hypertension in
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pregnant women. The immediate release formulation acts rapidly, causing significant reduction in blood pressure within 10–20 minutes. It should be noted, however, that the use of nifedipine for this purpose is not approved by the U.S. Food and Drug Administration and that fatal and adverse cardiac events have occurred in older patients when nifedipine was used for this purpose. Rarely, sodium nitroprusside has been used after failure of the previous agents for acute hypertensive emergency.
Bibliography Reubinoff BE, Schenker JG: HELLP syndrome: A syndrome of hemolysis, elevated liver enzymes and low platelet count—complicating preeclampsia-eclampsia, Int J Gynaecol Obstet 1991;36:95–102. Working Group Report on High Blood Pressure in Pregnancy, Working report of the National High Blood Pressure Education Program of NHLBI, Am J Obstet Gynecol 2000;183:S1–S22.
Miscarriage (Abortion) VINITA GOYAL
ICD Code: 637.9
Key Points Between 15% and 20% of all known pregnancies end in clinically recognized abortion.The actual rate of abortion is significantly higher, given that many pregnancies are not diagnosed. ! Emergency Actions ! Any female patient with vaginal bleeding and abdominal pain who is hemodynamically unstable should have two largegauge intravenous lines placed. Type and cross-match for blood should be performed, and the patient should be assumed to be pregnant until proven otherwise. Aggressive fluid resuscitation should be started to elevate blood pressure. If the patient is pregnant, an OB/GYN consult should be obtained urgently.
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DEFINITION Terms on the topic of miscarriage/abortion are defined as follows:
Abortion: Termination of pregnancy prior to 20 weeks’ gestation or delivery of fetus weighing less than 500 g Early abortion: Termination of pregnancy before 12 weeks’ gestation Late abortion: Termination of pregnancy between 12 and 20 weeks’ gestation Threatened abortion: Uterine bleeding in the presence of closed internal cervical os Inevitable abortion: Uterine bleeding with open internal cervical os but no expulsion of products of conception through cervix Incomplete abortion: Uterine bleeding associated with passage of some products of conception through cervix Complete abortion: Expulsion of all products of conception Missed abortion: Fetal death without expulsion of products of conception Septic abortion: Any type of abortion complicated by uterine infection
EPIDEMIOLOGY Between 15% and 20% of all known pregnancies end in clinically recognized abortion. The actual rate of abortion is significantly higher, given that many pregnancies are not diagnosed. Bleeding before 20 weeks’ gestation complicates 30%–40% of pregnancies, half of which result in spontaneous abortion.
ETIOLOGY Most abortions occur as a result of chromosomal or genetically abnormal pregnancies. The most common type of chromosomal abnormality is autosomal trisomy. Other chromosomal anomalies associated with spontaneous abortion include chromosomal nondisjunction, triploidy, tetraploidy, mosaicism, and translocation. Genetic abnormalities due to single gene mutation or polygenic factors are more common than chromosomal abnormalities. Congenital uterine anomalies such as unicornuate, bicornuate, or septate uterus are associated with high rates of spontaneous abortion. Women exposed to diethylstilbestrol have increased rates of spontaneous abortion because of either uterine anomalies or small endometrial cavities. Cervical incompetence is a condition in which the internal cervical os spontaneously dilates during the second trimester of pregnancy, thus allowing for the expulsion of products of conception. Cervical incompetence may be due to a congenital defect of the cervical tissue or prior surgery of the
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cervix. Uterine fibroids (i.e., leiomyomas) can be a cause of abortion. Intrauterine adhesions (i.e., Asherman’s syndrome) often caused by curettage of the pregnant uterus can also lead to abortion in subsequent pregnancies. If progesterone levels are insufficient to support the pregnancy, abortion may ensue. Poorly controlled diabetes is associated with an increased risk of spontaneous abortion. Antiphospholipid syndrome associated with the presence of lupus anticoagulant or anticardiolipin antibody is associated with increased rates of pregnancy loss. The presence of these antibodies is linked with thrombosis. The factor V Leiden mutation is also associated with pregnancy loss.
EXAMINATION Examination with a speculum allows for assessment of the amount of bleeding and dilation of the internal cervical os. With profuse bleeding and an open internal cervical os, with or without products of conception in the cervix, rapid removal of pregnancy tissue with suction curettage is necessary.
RADIOGRAPHS Transvaginal ultrasound is used to detect the presence of a pregnancy in the uterus. If no gestational sac or fetal pole is seen within the uterine cavity, a quantitative b-hCG level should be measured. If the quantitative b-hCG level is 1500 mIU/ml or less, a gestational sac should be seen by ultrasound. If the quantitative b-hCG level is 5000 mIU/ml or more, a fetal pole with cardiac motion should be seen by ultrasound. If these are not detected, a quantitative b-hCG level measurement should be repeated in 48 hours to evaluate for ectopic pregnancy. Visualization of a gestational sac greater than 17 mm diameter without a fetal pole is consistent with an anembryonic gestation (i.e., blighted ovum).
LABORATORY FINDINGS The blood type should be identified in all pregnant patients with the symptoms of vaginal bleeding. If the patient is Rh D negative, anti-D gamma globulin should be given intramuscularly to prevent isoimmunization in future pregnancies.
TREATMENT When a dead fetus is retained in the uterus beyond 5 weeks, consumptive coagulopathy and hypofibrinogenemia may occur. If anembryonic
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gestation or fetal death is diagnosed by ultrasound, dilation and curettage or medical termination should be performed if the pregnancy is not spontaneously passed within 6 weeks of diagnosis. Uterine infection (i.e., septic abortion) occurs in 1%–2% of spontaneous abortions. Fever, elevated white blood cell count, uterine tenderness, cervical motion tenderness, and foul-smelling discharge are all signs of septic abortion. This is a potentially fatal condition. Evaluation of the CBC, urinalysis, electrolytes, and genital culture should be performed. Blood cultures may be warranted. Treatment with intravenous antibiotics (including coverage for anaerobic bacteria) should be initiated and uterine contents should be evacuated. Patients with threatened abortion may benefit from restriction of strenuous physical activity and avoidance of coitus until bleeding resolves. If bleeding or uterine cramping intensifies, the patient should seek medical help. If cardiac activity is noted on ultrasound scanning, the risk of spontaneous abortion is approximately 5%. Patients with inevitable and incomplete abortion are of special concern. The clinician should measure vital signs, place an 18-gauge intravenous line, and run resuscitative fluids. A CBC should be performed, as should type and cross-match of blood for a possible transfusion. As noted previously, the intrauterine contents should be removed as quickly as possible. After the procedure, the practitioner should monitor for continue uterine bleeding. If bleeding is similar to or less than menses, the patient can be discharged home. If all products of conception have been expelled (i.e., complete abortion), uterine cramps have diminished, and uterine bleeding is similar to or less than menses, the presentation is consistent with a complete abortion. Follow-up with these patients can be undertaken on an outpatient basis.
Bibliography ACOG compendium of selected publications 2005, Management of recurrent early pregnancy loss, The American College of Obstetricians and Gynecologists Compendium of Selected Publications 2005, pp 541–552. ACOG compendium of selected publications 2005, Prevention of RhD alloimmunization, The American College of Obstetricians and Gynecologists Compendium of Selected Publications. 2005, pp 738–745. Stenchever MA: Spontaneous and recurrent abortion, Chapter 16. In Comprehensive Gynecology, ed 4. Mosby: St Louis, 2001.
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Ovarian Cysts ROGER MATTHEW BAUTISTA
ICD Code: 620.2
Key Points In the normal menstrual cycle, follicle-stimulating hormone (FSH) recruits about 20 ovarian follicles to mature and produce estrogen. The rise in estrogen causes a surge in FSH and luteinizing hormone that triggers ovulation and leads to the release of an ovum from the dominant follicle and the regression of the remaining follicles. ! Emergency Actions ! Ectopic pregnancy must be ruled out in patients of childbearing age who present with abdominal pain or vaginal bleeding. Two large-gauge intravenous lines should be established while the workup is being done.
DEFINITION Ovarian cysts commonly cause adnexal enlargement and associated pain. They are mostly functional and common during adolescence, occurring from puberty to menopause. The three types are follicular, corpus luteum, and theca lutein cysts.
PATHOPHYSIOLOGY In the normal menstrual cycle, FSH recruits about 20 ovarian follicles to mature and produce estrogen. The rise in estrogen causes a surge in FSH and luteinizing hormone that triggers ovulation and leads to the release of an ovum from the dominant follicle and the regression of the remaining follicles. After ovulation, a corpus luteum is formed that secretes both estrogen and progesterone. It has a life span of about 12–14 days. If fertilization does not occur, it will involute and cause a decrease in the estrogen and progesterone levels. With the decrease in progesterone, the endometrium is shed, resulting in menstruation. Follicular cysts are common, solitary or multiple, and range from 3 to 15 cm in diameter. They are translucent, thin-walled, and are filled with watery, clear to straw-colored fluid. Normal ovarian follicles grow to
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about 2–2.5 cm before ovulation. Follicular cysts result from either a failure in ovulation of the dominant follicle or from failure of other follicles to undergo normal atresia. The fluid of an incompletely developed follicle is not reabsorbed, producing an enlarged follicular cyst. Corpus luteum (i.e., granulose lutein) cysts are thin-walled, unilocular cysts that range from 3 to 11 cm in diameter. They are less common than follicular cysts but may be seen more frequently because they can grow larger and have a higher likelihood to rupture. After normal ovulation, the granulose cells lining the follicle become luteinized. During vascularization, blood collects in the central cavity, producing the corpus hemorrhagicum. When the blood is resorbed, a small cystic space, the corpus luteum, is formed. It is defined as a cyst when it grows larger than 3 cm in diameter. If hemorrhage is excessive, the cystic space enlarges and stretches the ovarian capsule, causing pain. Theca lutein cysts, the least common type, are produced by elevated levels of chorionic gonadotropin. Their size varies from 1 to 10 cm or larger. They are seen in patients with hydatidiform mole, those with choriocarcinoma, and those receiving fertility therapy (e.g., chorionic gonadotropin or clomiphene) and rarely in normal pregnancy. The cysts are lined by theca cells, luteinized or not, and may or may not have granulosa cells. They are usually bilateral and filled with clear, straw-colored fluid. Complications include torsion or hemorrhage.
CLINICAL PRESENTATION AND EXAMINATION A careful history with documentation of the last menstrual period is important. Pelvic examination of the adnexal may or may not reveal abnormal masses. Follicular cysts are usually asymptomatic and found incidentally on routine pelvic examination or ultrasound. Patients may report a vague, dull sensation or heaviness in the pelvis. Large follicular cysts can cause discomfort from stretching of the ovarian capsule, which may result in pelvic pain, dyspareunia, or abnormal uterine bleeding. They can also be subject to hemorrhage and torsion. Rupture usually causes immediate sharp pain that may resolve rapidly or improve over several days. Peritoneal signs are caused by irritation from cyst fluid or blood. Corpus luteum cysts are usually asymptomatic, but a persistent corpus luteum cyst can cause local pain or tenderness with brief episodes of unilateral, dull, or sharp lower abdominal pain before menses. The associated amenorrhea or delayed menstruation may resemble an ectopic pregnancy. Heavy vaginal bleeding may result from prolonged progesterone production. It may also be associated with an ovarian torsion or hemorrhage from rupture.
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Theca lutein cysts may cause a sense of pelvic heaviness or aching, may involve intraperitoneal bleeding from cyst rupture, or may involve continued signs and symptoms of pregnancy (e.g., hyperemesis and breast paresthesias).
LABORATORY FINDINGS A qualitative pregnancy test (quantitative if known pregnant), CBC, PT and PTT measurement, urinalysis with culture, and blood type and screen with Rh factor should be performed and the results evaluated. A blood type and cross-match should be substituted for a type and screen if a blood transfusion is anticipated.
DIAGNOSIS The diagnosis of ovarian cyst is made on the basis of history, laboratory findings, and ultrasound scan. The differential diagnosis includes adnexal torsion, ectopic pregnancy, appendicitis, PID, threatened miscarriage, ruptured endometrioma, and benign tumor or neoplasm.
TREATMENT Ectopic pregnancy must be ruled out in patients of childbearing age who present with abdominal pain or vaginal bleeding. Two large-gauge intravenous lines should be established while the workup is being done. A gynecologist should be consulted early in the case of suspected ectopic pregnancy or ovarian torsion. A general surgical specialist should be consulted early if surgical abdomen is suspected. Follicular cysts usually resolve spontaneously in 1–3 months without treatment. Oral contraceptive pills have been recommended to help establish a normal menstrual rhythm. The treatment of corpus luteum cysts involves symptomatic therapy unless acute complications develop. Bleeding from rupture is usually self-limited, but in rare patients with anemia, marked or persistent pain, or hypovolemia, admission for observation, serial hematocrit tests, or operative intervention may be indicated. The cysts usually regress after 1 or 2 months, after the cycle is complete in menstruating patients. Oral contraceptive pills have been recommended for treatment of these cysts but are of questionable benefit. Theca lutein cysts resolve spontaneously, though this may take months. Resolution typically occurs after termination of molar pregnancy, treatment of choriocarcinoma, or discontinuation of fertility therapy.
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A persistent ovarian mass must be differentiated from a benign tumor or true neoplasm.
Bibliography Benign gynecologic lesions: Vulva, vagina, cervix, uterus, oviduct, ovary. In Stenchever M, Droegemueller W, Herbst A, Mishell D (eds): Comprehensive Gynecology, ed 4. Mosby: St Louis, 2001. Houry D, Abbott JT: Acute complications of pregnancy. In Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Purcell K, Wheeler JE: Benign disorders of the ovaries and oviducts. In DeCherney AH, Nathan L (eds): Current Obstetric and Gynecologic Diagnosis and Treatment, ed 9. McGraw-Hill: New York, 2003. Sifuentes M: Common genitourinary problems in the pediatric and adolescent female. In Pearlman MD, Tintinalli JE (eds): Emergency Care of the Woman. McGraw-Hill: New York, 1998. Wells EC: Pelvic masses. In Pearlman MD, Tintinalli JE (eds): Emergency Care of the Woman. McGraw-Hill: New York, 1998.
Ovarian Torsion SUMERU GHANSHYAM MEHTA
ICD Code: 620.5
Key Points All patients with suspected ovarian torsion should have emergent gynecological consultation. ! Emergency Actions ! Prompt pelvic ultrasound will assist in the evaluation of ovarian torsion.
DEFINITION Ovarian torsion is a twisting of the ovary on its ligamentous supports, resulting in obstruction of blood flow, necrosis, and subsequent infarction of the ovary.
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EPIDEMIOLOGY In one large series of patients at a metropolitan women’s hospital, ovarian torsion accounted for 2.7% of emergency gynecological surgery. In another 10-year review, torsion accounted for 15% of surgically treated adnexal masses. Although it has been described in all age groups from the fetal/neonatal period to elderly women, 80% of cases occur in women younger than 50 years. Women who are pregnant or undergoing ovarian hyperstimulation during infertility treatment are at increased risk. Women of reproductive age have the highest incidence of ovarian torsion. This is likely related to the higher frequency of physiological and pathologic ovarian neoplasms, infertility therapy, and pregnancy in this age group compared with younger or older females.
CLINICAL PRESENTATION The clinical presentation of ovarian torsion is nonspecific and therefore a challenge for the clinician to recognize and differentiate from multiple other causes. The two most common presenting features are lower abdominal pain (83%) and an adnexal mass (72%). The most common symptom of ovarian torsion is sudden-onset lower abdominal pain, often associated with waves of nausea and vomiting. Most patients seek medical attention within 2 days of the event. Many patients report a history of similar episodes in the past lasting from hours to days, representing spontaneous detorsion. In one series of 87 women with torsion, characteristics and frequency of symptoms were as follows:
Nausea and vomiting (70%) Stabbing pain (70%) Sudden and sharp pain in the lower abdomen (59%) Pain radiating to the back, flank, or groin (51%) Peritoneal signs (3%) Fever (<2%; although an uncommon finding, maybe a marker of necrosis)
Torsion in pregnant women presents in a similar fashion with lower abdominal pain, nausea, vomiting, low-grade fever, leukocytosis, and possibly a palpable mass. Uncommonly, abnormal vaginal bleeding or amenorrhea occurs, suggesting ectopic pregnancy.
EXAMINATION Extreme pain may limit the extent of the physical examination, permitting only a superficial examination. Sedation may be necessary to adequately examine patients who are in pain from adnexal torsion. Generally, the
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abdominal examination varies from slight unilateral lower quadrant tenderness to frank peritonitis. A pelvic examination will usually present with cervical motion and adnexal tenderness. A discrete adnexal mass is present in 90% and may enlarge with time. Some patients may exhibit bilateral adnexal tenderness.
LABORATORY FINDINGS A urinalysis should be performed, but results will be unremarkable in ovarian torsion. A CBC, urine or serum hCG test, and serum electrolyte measurements should be performed in the setting of possible ovarian torsion. Hemorrhage can result in anemia, ovarian necrosis can cause leukocytosis, and persistent vomiting can lead to electrolyte abnormalities. No other laboratory testing is required in the evaluation of suspected adnexal torsion.
DIAGNOSIS The clinical diagnosis of ovarian torsion should be considered in women with the triad of lower abdominal pain, an ovarian cyst/mass, and diminished or absent blood flow in the ovarian vessels, after exclusion of ectopic pregnancy, PID, appendicitis, and leiomyoma-related symptoms. The presence of hemorrhage further suggests the diagnosis, but ovarian hemorrhage frequently occurs in the absence of torsion. Moreover, in some cases of torsion the ovaries continue to have a normal appearance and blood flow. If a clinical diagnosis is uncertain, radiographic evaluation may be used to evaluate patients. Laparoscopy or laparotomy is needed for the final diagnosis and treatment.
RADIOGRAPHS Adnexal lesions, ovarian enlargement, and normal ovaries are readily identified by pelvic ultrasound scanning. However, sonography is less useful in determining whether torsion of these structures has occurred. In children and adults with surgically confirmed ovarian torsion, a cystic or solid adnexal mass will be detected by ultrasound in more than 70% of patients, and free fluid in the cul-de-sac is common. The ovary is commonly enlarged and may be hemorrhagic. However, the presence of normal-appearing ovaries does not rule out the diagnosis because normal ovaries can be subject to torsion. The ability of the clinician to distinguish ovarian torsion from other adnexal pathology or normal adnexa using Doppler ultrasound is controversial. Diminished or absent ovarian vessel flow on two-dimensional, color, and three-dimensional Doppler ultrasound has been proposed as a
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sensitive test for ovarian torsion. Recent studies suggest that diminished or absent flow on Doppler examination is indicative of ovarian torsion; however, the presence of normal flow does not exclude the diagnosis.
Magnetic Resonance Imaging and Computed Tomography Magnetic resonance imaging (MRI) and CT scanning can reliably detect ovarian lesions, but information on their ability to diagnose torsion is limited. Both modalities can identify ovarian edema, which is suggestive of torsion. MRI has also detected hemorrhagic infarction, another finding associated with ovarian torsion. MRI and CT may have limited value when Doppler ultrasound findings are equivocal, but the cost and time required for these imaging studies likely do not justify their routine use. Furthermore, the diagnostic criteria for torsion using these modalities have not been well defined or validated in large studies.
TREATMENT The mainstay of treatment is operative evaluation to preserve ovarian function and prevent infection. Historically, the standard treatment has been removal of the affected ovary. However, studies over the past few years have described procedures for detorsion that lead to ovary preservation with return of normal hormonal function and fertility. Indicated procedures range from detorsion with cystectomy and suture stabilization to salpingo-oophorectomy. The procedure of choice can depend on patient age, desire for fertility, and degree of vascular compromise of the peduncle torsion.
Bibliography Albayram F, Hamper UM: Ovarian and adnexal torsion: Spectrum of sonographic findings with pathologic correlation, J Ultrasound Med 2001;20:1083. Bouguizane S, Bibi H, Farhat Y, et al: Adnexal torsion: A report of 135 casest, J Gynecol Obstet Biol Reprod (Paris) 2003;32:535. Hibbard LT: Adnexal torsion, Am J Obstetr Gynecol 1985;152:456. Morrison L, Spence J: Vaginal bleeding and pelvic pain in the non-pregnant patient. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 677–678. Shalev J, Goldenberg M, Oelsner G, et al: Treatment of twisted ischemic adnexa by simple detorsion, N Engl J Med 1989;321:546. Thach AM, Young GP: Pelvic pain. In Rosen P, Barkin R (eds): Emergency Medicine: Concepts and Clinical Practice, ed 4. Mosby: St Louis, 1998, pp 2295–2297. Whitfield BG, Laufer MR: Ovarian torsion. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Zweizig S, Perron J, Grubb D, Mishell DR Jr: Conservative management of adnexal torsion, Am J Obstet Gynecol 1993;168:1791.
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Pelvic Inflammatory Disease KATHERINE ANNE HARRISON
ICD Codes: Pelvic inflammatory disease 614.9, Acute salpingitis and oophoritis 614.0, Gonorrhea 098.0
Key Points A large portion of ectopic pregnancies are attributable to PID. PID is a polymicrobial disease, originating from usual vaginal flora or from pathogens that ascend from the vagina through the cervical os. ! Emergency Actions ! Any patient who is pregnant; has not responded clinically to oral antimicrobial therapy; cannot tolerate an outpatient oral regimen; or has severe illness, nausea and vomiting, or high fever or a tubo-ovarian abscess should be considered for admission. A consultation with a gynecologist should be obtained.
DEFINITION Pelvic inflammatory disease is a generalized term for infection of the upper female genital tract, caused by multiple pathogens, with a varying level of acuity and presenting symptoms. Salpingitis, endometritis, tubo-ovarian abscess, and pelvic peritonitis all share a common pathophysiology and are included in this discussion. Although sexually transmitted organisms (e.g., Neisseria gonorrhea and C. trachomatis) are often implicated, normal vaginal flora (e.g., anaerobes, Gardnerella vaginalis, Haemophilus influenzae) have also been associated with PID.
EPIDEMIOLOGY The CDC estimates that about 1 million cases of acute PID occur each year in the United States, with more than 100,000 women becoming infertile as a result. It is the most common serious infection in women of childbearing age. A large portion of ectopic pregnancies are attributable to the disease, and more than 150 women die annually from PID. The incidence of PID increases with the number of sexual partners a person has, and barrier methods of birth control decrease that risk.
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PATHOLOGY PID is a polymicrobial disease, originating from usual vaginal flora or from pathogens that ascend from the vagina through the cervical os. Usual pathogens include N. gonorrhea, C. trachomatis, anaerobic bacteria, G. vaginalis, H. influenzae, and others. Normal cervical mucus provides a natural barrier to infection; however, there are several conditions that decrease the effectiveness of this barrier, including menses, surgical cervical procedures, intrauterine devices, and hormonal changes. In addition, N. gonorrhea and C. trachomatis are apparently able to penetrate this barrier even under normal conditions. Oral contraceptives appear to be somewhat protective, as does pregnancy, presumably because of the cervical mucous plug that forms early after implantation. Pathogens ascend through the cervix to the uterus, cause inflammation of the uterine lining, and may proceed to the fallopian tubes and out into the pelvic peritoneum. Peritoneal infection may ascend the right colic gutter to become a perihepatic infection known as Fitz-Hugh-Curtis syndrome. It is the inflammation and subsequent scarring of the fallopian tubes that leads to infertility in this disease.
CLINICAL PRESENTATION PID is diagnosed clinically and providers should maintain a low threshold for diagnosis and treatment. Laparoscopy may be used to obtain a more definitive diagnosis, but it is often not readily available. The presentation almost always includes a report of lower abdominal pain and may include vaginal discharge, dysuria, abnormal vaginal bleeding, nausea and vomiting, and dyspareunia. The CDC suggests that, in the absence of other explanation, diagnosis and treatment for PID should be made in the context of uterine/adnexal tenderness or cervical motion tenderness. Additional CDC criteria that support a diagnosis of PID include the following:
Oral temperature above 101 F (38.3 C) Abnormal cervical or vaginal mucopurulent discharge Presence of white blood cells on saline microscopy of vaginal secretions Elevated erythrocyte sedimentation rate Elevated C-reactive protein Laboratory documentation of cervical infection with N. gonorrhea or C. trachomatis The most specific criteria for diagnosing PID include the following:
Endometrial biopsy with histopathologic evidence of endometritis
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Transvaginal sonography or MRI techniques showing thickened, fluidfilled tubes with or without free pelvic fluid or tubo-ovarian complex Laparoscopic abnormalities consistent with PID
EXAMINATION Elevated temperature is found only in a minority of patients with acute PID, so although it supports the diagnosis, the absence of elevated temperature should not be used to rule it out. Most patients will have pain and tenderness of the lower abdomen, although one side may be more tender than the other. Peritoneal signs indicate a more severe infection and should be taken seriously. Pelvic examination may reveal mucopurulent cervical discharge, bilateral adnexal tenderness, cervical motion tenderness, or adnexal mass. Endocervical cultures, wet preparation (wet prep), and samples for gonorrhea and chlamydia tests should be sent. Pelvic examination findings may be atypical in patients with previous infections, tubal ligation, or ectopic pregnancy. Tubo-ovarian abscess may be palpated as an adnexal mass; however, the sensitivity of this test is low.
DIAGNOSIS Laboratory analysis supports what must be a presumptive diagnosis from the emergency department. Cervical cultures for C. trachomatis and N. gonorrhea should be performed and followed up. Urinalysis and a pregnancy test should also be done. The differential diagnosis includes ectopic pregnancy, appendicitis, ovarian torsion, cyst, and urinary tract infection.
LABORATORY FINDINGS Patients should be evaluated with CBC, electrolyte analysis, blood culture (in febrile patients), urinalysis, and pregnancy test. In addition, a wet prep and Gram stain may reveal gram-negative intracellular diplococci. Chlamydia should be assessed for by enzyme-linked immunosorbent assay antibody detection or DNA probe.
TREATMENT Treatment for PID includes antibiotics and possibly hospital admission for parenteral therapy. The decision of whether to admit the patient rests with the good judgment of the treating provider and may be guided by the following criteria provided by the CDC. According to these guidelines, the patient should be admitted if any of the following is true:
Surgical emergencies (e.g., appendicitis) cannot be excluded. The patient is pregnant.
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The patient does not respond clinically to oral antimicrobial therapy. The patient is unable to follow or tolerate an outpatient oral drug regimen. The patient has severe illness, nausea and vomiting, or high fever. The patient has a tubo-ovarian abscess.
There are several proposed regimens for treatment in both inpatient and outpatient settings. Local antibiotic resistance may affect the efficacy of these regimens, so this factor should be checked before administration.
Inpatient Therapy REGIMEN A Cefotetan 2 g given intravenously every 12 hours or
Cefoxitin 2 g given intravenously every 6 hours plus doxycycline 100 mg given orally or intravenously every 12 hours
REGIMEN B Clindamycin 900 mg given intravenously every 8 hours
and
Gentamicin, loading dose given intravenously or intramuscularly (2 mg/kg of body weight) followed by a maintenance dose (1.5 mg/ kg) every 8 hours; single daily dosing may be substituted
Outpatient Therapy REGIMEN A Ofloxacin 400 mg taken orally twice a day for 14 days or
Levofloxacin 500 mg taken orally once daily for 14 days with or without
Metronidazole 500 mg taken orally twice a day for 14 days
REGIMEN B Ceftriaxone 250 mg given intramuscularly in a single dose
or
Cefoxitin 2 g given intramuscularly in a single dose and probenecid, 1 g orally administered concurrently in a single dose or
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Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime) and
Doxycycline 100 mg taken orally twice a day for 14 days with or without
Metronidazole 500 mg taken orally twice a day for 14 days
Patients sent home prescribed with an outpatient regimen of therapy should be specifically instructed to return to the emergency department if they are unable to tolerate their oral medications or if they experience vomiting, increased abdominal pain, or worsening fever. Patients should see improvement within 48 hours; if they do not, they should be reevaluated for possible admission because of failure of outpatient treatment.
Bibliography Centers for Disease Control and Prevention, Sexually Transmitted Disease Surveillance 2003 Supplement. U.S Department of Health and Human Services: Atlanta, GA, 2004. Centers for Disease Control and Prevention, Sexually Transmitted Diseases Treatment Guidelines, 2006. August 4, 2006;55(RR-11):56–60.
Placenta Previa KRISTEN A. PLASTINO
ICD Code: 641.1
Key Points The classic presentation of placenta previa is painless vaginal bleeding. Onset usually occurs without warning but may result from some inciting disturbance, such as intercourse or vaginal examination. ! Emergency Actions ! Digital vaginal examination should only be done by an experienced obstetrician in a setting prepared for emergent delivery and resuscitation—that is, a “double set-up” in the labor-and-delivery ward or a delivery or operating room.
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DEFINITION Placenta previa is the implantation of the placenta on or near the cervix, obstructing the outlet and posing a significant risk for hemorrhage. Degrees of previa exist, from complete previa, in which the entire internal cervical os is entirely covered, to a marginal previa, where the edge of the placenta abuts the possible zone of effacement, to simply a lowlying placenta that involves the lower uterine segment. A similar condition, vasa previa, occurs when prominent fetal vessels within the fetal membranes traverse the cervix.
EPIDEMIOLOGY The incidence of placenta previa depends on the gestational age. Commonly, a placenta found in early gestation to be low-lying or a previa will “migrate” away from the cervix with increasing gestational age. At term, incidence among large observational studies has ranged from approximately 1 in 200 to 1 in 400. Known risk factors include advancing maternal age, multiparity, previous cesarean section, and smoking. Placenta previa is associated with an increased risk of preterm delivery, fetal growth restriction, fetal anomalies, and perinatal mortality. Previa is responsible for 7% of maternal pregnancy-related deaths due to hemorrhage. In addition, placenta previa is associated with the spectrum of conditions of abnormal implantation of the placenta: placenta accreta, increta, and percreta. In these conditions, the placenta is invasively attached deeply to the myometrium of the uterus or beyond—to the uterine serosa or to adjacent organs such as the bladder or bowel.
PRESENTATION The classic presentation of placenta previa is painless vaginal bleeding. The classic differential diagnosis includes labor, infection, trauma, and placental abruption, as well as less common causes such as coagulation defects. Onset usually occurs without warning but may result from some inciting disturbance, such as intercourse or a vaginal examination. A bleeding previa may present as early or mid trimester spotting or as frank hemorrhage. Bleeding usually ceases spontaneously but recurs episodically and unexpectedly. Rarely is the initial episode of bleeding severe enough to be fatal; however, initial or recurrent episodes may require supportive care, close observation, prolonged hospitalization, and transfusion.
DIAGNOSIS Abdominal ultrasound performed before vaginal examination is essential for determining placental location in any patient who is pregnant
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and bleeding. Blind vaginal examination, including speculum examination, even if done with the best intentions, can incite severe hemorrhage. Although ultrasonography is the examination of choice to rule in or rule out the diagnosis of previa, exact qualification of the location of the placenta with respect to the cervical os usually requires one digital examination of the cervix. Digital vaginal examination should only be done by an experienced obstetrician in a setting prepared for emergent delivery and resuscitation— that is, a “double set-up” in the labor-and-delivery ward or a delivery or operating room.
RADIOGRAPHS Transvaginal ultrasound, in the hands of a professional trained in ultrasonography, has also been used to evaluate the exact location of the placenta in relation to the uterine outlet with increasing accuracy. In addition, others have described transperineal ultrasonography to allow for improved visualization without the hazard of vaginal disturbance. Still others have described the benefit of MRI for the elucidation of exact placental location, especially to determine the degree of invasion in the case of the previously described placenta accreta, increta, and percreta.
LABORATORY FINDINGS Immediate management consists of CBC; measurements of electrolytes, PTT, INR; and tests for blood type (including Rh status for need for RhoGam) and cross-match.
TREATMENT Two large-bore intravenous lines should be placed for fluid resuscitation, and early OB/GYN consultation for ultrasound examination is imperative to save the mother and fetus. The plan for delivery is based on a number of factors, including gestational age, degree of bleeding, and assessment of labor. Resuscitation to exact expectant management is the rule until term, unless hemorrhage (or another obstetrical indication) is so severe as to cause imminent harm to the fetus that outweighs the risk of preterm delivery. Cesarean section is the delivery method of choice.
Bibliography Cunningham FG, Gant NF, Leveno KJ, et al: Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001. Gabbe SG, Niebyl JR, Simpson JL (eds): Obstetrics Normal and Problem Pregnancies, ed 4. Churchill-Livingstone: Philadelphia, 2003.
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Sexual Assault MARK S. FUNK
ICD Codes: Rape, traumatic unspecified site 959.9, Alleged rape, observation or examination V71.5, Physical abuse (rape) V15.42
Key Points Persons who have experienced sexual assault should be evaluated by a trained provider whenever possible, and a prepared protocol should be used. ! Emergency Actions ! Treatment of sexual assault should include any physical or psychological trauma, prophylactic treatment for STDs, including HIV infection, pregnancy prevention, and addressing future safety planning.
DEFINITION Rape is defined as a sexual act performed on a person without his or her consent from the use of force, threat of force, fear, or the victim’s inability to give consent. Three components of a rape include (1) compulsion, (2) carnal knowledge, and (3) nonconsensual coitus. Note that seminal emission is not required for an act to qualify as rape.
EPIDEMIOLOGY One in three females will experience sexual assault in her lifetime. More than 500,000 of these assaults will not be reported. Only 2% of persons charged of an assault will be convicted.
EXAMINATION Persons who experience sexual assault should be evaluated by a trained provider whenever possible. This provider should use a prepared protocol and involve police investigation, social workers, psychologist/psychiatrist, and, if available, a rape crisis center. When properly performed, a thorough examination can increase the opportunity and success of criminal prosecution.
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A complete evaluation should include obtaining specific details and history from the person who has been assaulted. This history should include any specific circumstances, description of the assailant, type of penetration or physical abuse, and risk assessment for trauma or STD transmission. If possible, this information, along with garments, photos, and information regarding bathing, douching, or consensual sexual activity since the time of the assault should be gathered for the forensic collection. A careful physical examination should be performed and meticulous care taken to gather any additional evidence necessary. The collection should include photos of trauma or debris collected from the body of the person who was assaulted. This should not only include a careful inspection of the breasts, external genitalia, vagina, anus, and rectum, and any other injuries of the trunk or extremities, but also the person’s emotional state as well. Specific collection kits are available, including sampling instructions for clothing, collection swabs, combed specimens, and blood and saliva collection. These kits come with specific instructions to ensure accuracy of collection and control of evidence.
LABORATORY FINDINGS Laboratory evaluation should be performed to ensure complete STD testing. Blood samples should be collected to evaluate the baseline presence or absence of syphilis, pregnancy, and HIV infection. Gonorrhea and Chlamydia cultures should also be performed.
TREATMENT Treatment should include therapy for any physical or psychological trauma, prophylactic treatment for STDs, including HIV, pregnancy prevention, and planning for future safety. Follow-up care should also be addressed and should include a physician visit, ongoing psychological support, and repeat testing for STDs and pregnancy. Prophylactic protocols are outlined for the prevention of STD transmission: 1. Ceftriaxone 250 mg given intramuscularly with doxycycline 100 mg PO twice a day for 10–14 days 2. Spectinomycin, 2 g given intramuscularly with doxycycline 100 mg PO twice a day for 10–14 days 3. Ciprofloxacin 500 mg PO in one dose, with doxycycline 100 mg for 10–14 days
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Pregnancy prevention can be addressed with the following postcoital protocols: 1. Norgestrel and ethinyl estradiol (Ovral), two tablets initially and two tablets in 12 hours 2. Diethylstilbestrol in a 25-mg dose twice a day for 5 days 3. Intravenous conjugated estrogen (Premarin) 50 mg once a day for 2 days 4. Conjugated estrogen 30 mg once a day PO for 5 days
Bibliography Glasier A: Emergency postcoital contraception, N Engl J Med 1997;337:1058. Gostin LO, Lazzarini Z, Alexander D, et al: HIV testing, counseling, and prophylaxis after sexual assault, JAMA 1994;271:1436. Koss MP: The women’s mental health research agenda: Violence against women, Am Psychol 1990;45:374. Salyer SW: Sexual abuse. In Gynecologic and Obstetric Emergencies: Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Wiley J, Sugar N, Fine D, Eckert LO: Legal outcomes of sexual assault, Am J Obstet Gynecol 2003;188:1638. Up To Date. Available at: http://www.utdol.com/application/vocab.asp?search¼sexualþ assault&submit¼go. Accessed on October 25, 2005.
Toxic Shock Syndrome KATHERINE ANNE HARRISON
ICD Code: 040.82
Key Points Patients with toxic shock syndrome (TSS) may present with an array of symptoms, including flu-like symptoms, fever, chills, headache, nausea and vomiting, and diarrhea. A major feature of TSS is the classic erythroderma and mucous membrane hyperemia. ! Emergency Actions ! Antibiotic treatment should be prompt and broad spectrum, including beta-lactam antibiotics and clindamycin. In
546 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER addition, because of the increasing incidence of community-acquired MRSA, vancomycin should be considered as well.
DEFINITION Toxic shock syndrome is an acute toxin-mediated illness characterized by fever, hypotension, renal failure, and multisystem organ dysfunction and is associated with a generalized erythroderma, conjunctival erythema, and edema of the face, hands, and feet. The erythematous rash proceeds to desquamation during convalescence. TSS is caused most commonly by S. aureus but may also be caused by group A streptococcus, non–group A b-hemolytic streptococci, viridans streptococci, and Clostridium sordellii.
EPIDEMIOLOGY Staphylococcal TSS (STSS) was first described in 1978 by Todd et al. at the time of an epidemic involving young menstruating women who used tampons. The incidence of TSS has decreased from a height in 1980 (6–12 per 100,000) to an incidence of 1–2 cases per 100,000 in 1986. The current annual incidence of menstrual TSS is 1–2 per 100,000 women (ranging from 15 to 44 years of age), with a 3% case fatality rate. Overall, 93% of all TSS cases reported from 1979 to 1996 were among women. Nonmenstrual cases are reported after surgical procedures (many with nasal or wound packing), postpartum or after abortion, or with focal cutaneous infections. The proportion of all nonmenstrual cases reported increased dramatically from 1979 to 1996. STSS is similar in presentation to TSS but was recognized to be a separate entity in 1989. It is also characterized by fever, hypotension, multisystem organ failure, and a scarlatina-form rash. It is seen in association with minor trauma or skin infection or with viral infections. As with TSS, this syndrome affects young healthy patients as well as those with comorbid conditions. STSS has an incidence of 4 per 100,000 persons but has a higher mortality than TSS, with reported fatality rates of 30%–70%.
PATHOLOGY TSS is the result of production of toxic shock syndrome toxin 1 (TSST-1), which acts as a “superantigen” to produce an inflammatory cascade. Tumor necrosis factor, interleukins, and other cytokines are produced in massive quantity and are responsible for fever, vasodilation, and increased capillary permeability. The toxin presumably enters the bloodstream through
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inflamed or injured mucous membranes. Preexisting antibodies to TSST-1 (produced by 90% of adults) are protective to persons colonized with S. aureus. In nonmenstrual TSS, TSST-1 has been isolated in less than half the strains of S. aureus. TSST-1 and the streptococcal pyrogenic exotoxins produce similar clinical effects. These toxins induce mononuclear cells to produce the cytokines tumor necrosis factor-alpha, interleukin-1beta and interleukin6, which mediate fever, shock, and tissue injury. However, STSS is associated with minor trauma or soft tissue infection rather than tampon use. A variety of primary infections may result in STSS, including myonecrosis, pneumonia, septic joint, and meningitis, as well as less severe soft tissue infections and sites of minor trauma. Unlike patients with STSS, more than half of patients with STSS have positive blood culture results.
CLINICAL PRESENTATION AND EXAMINATION Patients with TSS may present with an array of symptoms, including flulike symptoms, fever, chills, headache, nausea and vomiting, and diarrhea. A major feature of TSS is the classic erythroderma and mucous membrane hyperemia. Criteria for the diagnosis are listed in later text as defined by the CDC. Because of the wide range of organ involvement, patients may present with a variety of symptoms, and clinical suspicion should remain high, especially in young menstruating women. The differential diagnosis includes STSS, Stevens-Johnson syndrome, meningococcemia, Rocky Mountain spotted fever, and gram-negative sepsis. Hypotension is an essential element in the case definition of STSS. Presentation also includes flu-like symptoms, nausea, headache, and diarrhea. Renal dysfunction and acute respiratory distress syndrome are frequently present on initial evaluation. In contrast to TSS, with STSS a rash is infrequent, and although signs of soft tissue infection may be present, they are often less severe than the nature of the underlying infection. Pain out of proportion to the physical findings is a hallmark of STSS, as is pain without significant tenderness. The presence of bullae is a late finding, is usually associated with necrotizing fascitis, and indicates the need for urgent surgical debridement.
DIAGNOSIS The CDC’s case definition for TSS is listed in the next section. Probable cases are defined by five of the six clinical findings, whereas confirmed cases have all six findings, including desquamation, unless the patient dies before desquamation can occur.
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Fever: Temperature greater than or equal to 38.9 C (102 F) Rash: Diffuse macular erythroderma Desquamation: 1–2 weeks after onset of illness, particularly palms and soles Hypotension: Systolic blood pressure less than or equal to 90 mmHg for adults or less than fifth percentile by age for children younger than 16 years of age; orthostatic drop in diastolic blood pressure greater than or equal to 15 mmHg from lying to sitting, orthostatic syncope, or orthostatic dizziness Multisystem involvement: Three or more of the following: 1. Gastrointestinal: Vomiting or diarrhea at onset of illness 2. Muscular: Severe myalgia or creatine phosphokinase level at least twice the upper limit of normal for the laboratory 3. Mucous membrane: Vaginal, oropharyngeal, or conjunctival hyperemia 4. Renal: Blood urea nitrogen or creatinine at least twice the upper limit of normal for the laboratory or urinary sediment with pyuria (5 leukocytes per high-power field) in the absence of urinary tract infection 5. Hepatic: Total bilirubin, serum glutamate oxaloacetate transaminase (SGOT) or serum glutamate pyruvate transaminase (SGPT) at least twice the upper limit of normal for the laboratory 6. Hematological: Platelets >100,000/mm3 7. Central nervous system: Disorientation or alterations in consciousness without focal neurological signs when fever and hypotension are absent Negative results on the following tests, if obtained: 1. Blood, throat, or cerebrospinal fluid cultures (blood culture may be positive for S. aureus) 2. Rise in titer to Rocky Mountain spotted fever, leptospirosis, or measles
The case definition of STSS is defined by the CDC Working Group on Severe Streptococcal Infection. 1. Isolation of group A streptococci a. From a normally sterile site (e.g., blood, cerebrospinal fluid, peritoneal fluid, tissue biopsy) b. From a nonsterile site (e.g., throat, superficial skin lesion) 2. Clinical signs of severity a. Hypotension: Systolic blood pressure less than 90 mmHg in adults or less than the fifth percentile of normal limits in children b. Two or more of the following signs: i. Renal impairment (i.e., creatinine 2 mg/dl or more for adults or more than twice the upper limit of normal for age) ii. Coagulopathy (i.e., platelets less than 100,000 or DIC)
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iii. Liver involvement (SGOT, SGPT, or total bilirubin at least twice the upper limit of normal) iv. Adult respiratory distress syndrome v. A generalized erythematous macular rash that may desquamate vi. Soft tissue necrosis, necrotizing fasciitis, myositis, or gangrene
LABORATORY FINDINGS Laboratory changes are similar in both TSS and STSS and include leukocytosis with a left shift, azotemia, elevated serum creatine kinase level, hypoalbuminemia, hypocalcemia, and thrombocytopenia.
TREATMENT Treatment for TSS includes fluids, antibiotics, aggressive supportive measures for systemic manifestations of shock, and, most importantly, early recognition of the disease state. A thorough examination must be performed, with every effort made to remove any foreign bodies, including tampons or any other sort of packing. Wounds need to be debrided, and, in the case of group A streptococcus necrotizing fasciitis, the surgical debridement may be extreme. A Gram stain and culture should be performed on removed foreign bodies as well as any surgical specimens. Antibiotic treatment should be prompt and broad spectrum, including beta-lactam antibiotics and clindamycin. In addition, because of the increasing incidence of community-acquired MRSA, vancomycin should be considered as well. STSS treatment is similar, with a beta-lactam antibiotic and clindamycin. There is some evidence to suggest that administration of intravenous immunoglobulin G may decrease the incidence of sepsis-related organ failure.
Bibliography Historical Perspectives: Reduced incidence of menstrual toxic-shock syndrome, United States 1980–1990. 2005;39:421–423. Centers for Disease Control and Prevention, Summary of notifiable diseases, MMWR Morb Mortal Wkly Rep 2005;55,1–85. Centers for Disease Control and Prevention, Toxic-shock syndrome, United States, MMWR Morb Mortal Wkly Rep 1990;39:421–424. Darenberg J, Ihendyane N, Sjolin J, et al: Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: A European, randomized, double-blind, placebocontrolled trial, Clin Infect Dis 2003;37:333. Hajjeh RA, Reingold A, Weil A, et al: Toxic shock syndrome in the United States: Surveillance update, 1976–1996, Emerg Infect Dis 1999;5:807–810.
550 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Hoge CW, Schwartz B, Talkington DF, et al: The changing epidemiology of invasive group A streptococcal infections and the emergence of streptococcal toxic shock–like syndrome: A retrospective population-based study, JAMA 1993;269(3):384–389. Reingold AL: Toxic shock syndrome: An update, Am J Obstet Gynecol 1991;165(4): 1236–1239. Stevens DL: Invasive group A streptococcus infections, Clin Infect Dis 1992;14:2–13. Stevens DL: The toxic shock syndromes, Infect Dis Clin North Am 1996;10:4. Stevens DL, Tanner MH, Winship J, et al: Severe group A streptococcal infections associated with a toxic shock–like syndrome and scarlet fever toxin A, N Engl J Med 1989;321:1. Todd J, Fishaut M, Kapral F, Welch T: Toxic-shock syndrome associated with phagegroup-I staphylococci, Lancet 1978;2:1116–1118. The Working Group on Severe Streptococcal Infections, Defining the group A streptococcal toxic shock syndrome: Rationale and consensus definition, JAMA 1993;269(3): 390–391.
Vulvovaginitis KATHERINE ANNE HARRISON
ICD Codes: Vulvovaginitis 616.19, Chlamydial vaginitis 099.53, Gonococcal vaginitis 098.0, Trichomonal vaginitis 131.01
Key Points Candidiasis, trichomoniasis, and bacterial vaginosis are the most commonly diagnosed forms of vulvovaginitis. ! Emergency Actions ! All patients at risk for STDs should be referred for HIV screening and should be counseled regarding safe sex practices.
DEFINITION Vulvovaginitis is an infection or overgrowth of the normal vaginal flora of the lower female reproductive tract causing discharge, discomfort, pruritus, burning, dyspareunia, and dysuria. It has multiple causes, including fungal infection, protozoal infection, and bacterial infection. Vaginitis may also be the result of local irritants such as soaps or cleansing agents, without concomitant overgrowth of vaginal flora.
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EPIDEMIOLOGY Vaginal discharge is the most common gynecological symptom in women of reproductive age and may be seen in the emergency department as well as in primary care offices. Approximately 75% of women experience at least one episode of symptomatic vaginitis during their lifetime. Children and adolescents are also subject to the bacterial vaginitis and are at increased risk of bacterial infection due to a variety of factors, including the proximity of the vaginal introitus to the anus, the lack of estrogen-induced mucosal cornification, and the neutral to alkaline pH of the vagina. Other factors, including antibiotic use, diet, and systemic illness (e.g., diabetes), may also predispose a patient to disruption of the normal vaginal flora.
PATHOLOGY The normal vaginal epithelium contains glycogen and is colonized with lactobacilli, creating an acidic environment with a pH of 3.5–4.1. Low estrogen states (e.g., premenarche, postmenopausal, before and during menses) tend to increase the pH of the vaginal environment and increase susceptibility to overgrowth of pathogenic flora. Chemical irritant vaginitis may occur after the use of feminine hygiene products, douches, or other products not intended for vaginal use. There are three main diseases associated with vaginal discharge. Candidiasis, trichomoniasis, and bacterial vaginosis are most commonly implicated, although the mucopurulent cervical discharge caused by C. trachomatis or N. gonorrhea can also cause symptoms of vaginitis. Vulvovaginal candidiasis is the most common cause of vaginitis, caused by Candida albicans in 80%–90% of cases. Factors that may predispose patients to vulvovaginal candidiasis include antibiotic use, diabetes mellitus, immunosuppressant use (e.g., corticosteroids), or immune suppression (e.g., AIDS, chemotherapy). Candida overgrowth may occur in the context of normal acidity and does not tend to occur at the same time as other bacterial infections. Trichomoniasis is caused by Trichomonas vaginalis and accounts for approximately 25% of vaginal infections. The flagellated protozoa may be found in the vagina, in Skene’s ducts, and in the lower urethra and may be noted on urine microscopy. Trichomoniasis is sexually transmitted, with most men being asymptomatic carriers. It may occur with other bacterial infections, and, because its epidemiology is similar to that of STDs, patients should be screened for other STDs, specifically HIV, and referred for appropriate testing, treatment, and counseling. Bacterial vaginosis is a polymicrobial overgrowth of anaerobic bacteria, predominantly G. vaginalis. It is a common infection with prevalence
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rates of about 5% in college populations and as high as 60% in STD clinics.
CLINICAL PRESENTATION AND EXAMINATION Candidiasis presents with vulvar itching, burning, dyspareunia, and dysuria. Discharge is variable but is typically described as thick, white, and clumpy, with little odor, and often adherent to the vaginal walls. The mucosa is tender and inflamed and may show signs of traumatic excoriation. Trichomoniasis presents with a profuse frothy yellow, green, or gray malodorous discharge. Vulvar erythema and edema are commonly present, but the classic “strawberry cervix” is only seen in a minority of cases. Bacterial vaginosis presents with a profuse, malodorous discharge described as “fishy.” Pruritus is mild, with the thin discharge adherent to the vaginal walls.
DIAGNOSIS AND LABORATORY FINDINGS Patients with signs and symptoms of vaginitis should have a pelvic examination performed, along with Gram stain, cultures for gonorrhea and chlamydia, potassium hydroxide preparation, and wet mount to assess for C. trachomatis and clue cells. The vaginal pH should be checked, and urinalysis should be performed. Candidiasis is diagnosed on the basis of microscopic evaluation of vaginal discharge treated with a 20% potassium hydroxide solution, which dissolves the cellular elements, leaving the hyphae of the Candida species more evident. The sensitivity of this test is about 80%, but, if the clinical picture is highly suggestive, treatment should be instituted despite a negative potassium hydroxide preparation. T. vaginalis infection is diagnosed via microscopic examination of the wet prep of vaginal swabs. The pathogen is described as motile, pear-shaped flagellated protozoa. Bacterial vaginosis is diagnosed on the basis of clinical or Gram-stain criteria. Clinical criteria require three of the following symptoms or signs:
Homogeneous, white, noninflammatory discharge that smoothly coats the vaginal walls Presence of clue cells on microscopic examination pH of vaginal fluid >4.5 Fishy odor of vaginal discharge before or after addition of 10% potassium hydroxide (i.e., the whiff test)
Table 10-1 Treatment of Vaginitis DIAGNOSIS Candidiasis Trichomonas vaginalis Bacterial Vaginosis
RECOMMENDED Butoconazole 2% cream, 5 g intravaginally for 3 days
ALTERNATIVE
PARTNER
Fluconazole, 150-mg oral None recommended tablet for uncomplicated VVC Metronidazole, 2 g orally in a Metronidazole, 500 mg Metronidazole, 2 g single dose twice a day for 7 days orally in a single dose Metronidazole, 500 mg orally, Metronidazole, 2 g orally No treatment twice a day for 7 days or in a single dose or metronidazole gel 0.75%, one clindamycin, 300 mg full applicator (5 g) orally, twice a day for 7 intravaginally, once a day for 5 days days
IN PREGNANCY Topical azole therapy only Metronidazole, 2 g orally in a single dose Metronidazole, 500 mg orally twice a day for 7 days or metronidazole gel 0.75%, one full applicator (5 g) intravaginally, once a day for 5 days
Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines 2002, MMWR Morb Mortal Wkly Rep May 10, 2002;51(RR-6):1–80. VVC, Vulvovaginal candidiasis.
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TREATMENT All patients at risk for STDs should be referred for HIV screening and should be counseled regarding safe sex practices. Treatment as recommended by the CDC is listed in Table 10-1.
Bibliography Brook I: Microbiology and management of polymicrobial female genital tract infections in adolescents, J Pediatr Adolesc Gynecol 2002;15(4):217–226. Burtin P, Taddio A, Ariburnu O, et al: Safety of metronidazole in pregnancy: A metaanalysis, Am J Obstet Gynecol 1995;172:525–529. Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines 2006, MMWR Morb Mortal Wkly Rep Aug 4 2006;55(RR-11):49–55. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Stevens DL: Invasive group A streptococcus infections, Clin Infect Dis 1992;14:2–13. Stevens DL: The toxic shock syndromes, Infect Dis Clin North Am 1996;10:4. Vaginitis. In Harwood-Nuss DL, et al: The Clinical Practice of Emergency Medicine, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 394–396. The Working Group on Severe Streptococcal Infections: Defining the group A streptococcal toxic shock syndrome: Rationale and consensus definition, JAMA 1993;269 (3):390–391.
Chapter 11
Hematologic Emergencies Acute Bleeding Diathesis MICHAEL K. SHAFE ICD Codes: Congenital factor VIII 286, Congenital factor IX 286.1, Congenital factor XI 286.2, Congenital deficiency of other clotting factors 286.3, Von Willebrand’s disease 286.4, Hemorrhagic disorders due to intrinsic circulation anticoagulants 286.5
Key Points Bleeding is caused by failure of either the ‘‘intrinsic’’ or ‘‘extrinsic’’ pathways. The intrinsic pathway is associated with the partial thromboplastin time (PTT) and the extrinsic pathway is associated with the prothrombin time (PT). An understanding of these two pathways leads to the different treatments of bleeding diathesis. ! Emergency Actions ! Rapid assessment of the patient’s vital signs is imperative. A quick history can usually direct the practitioner to the cause of the bleeding.
DEFINITION Excessive hemorrhage can result from the following: (1) platelet disorders, (2) coagulation factor disorders, (3) fibrinolytic disorders, (4) vascular abnormalities, and (5) drug ingestion.
PATHOLOGY Injured tissue releases tissue factor, also termed tissue thromboplastin or factor III. The release of tissue factor stimulates the clotting cascade and exposes collagen for platelet adherence. The formation of a clot is a two-step process. The first step is platelet adherence to the site of vascular injury and formation of a primary hemostatic plug. The second is activation of the clotting cascade with deposition of fibrin and subsequent crosslinking of the fibrin to form an insoluble fibrin clot. Excessive bleeding may be caused by a defect of either process. Platelets are an enucleated discoid-shaped cellular blood component responsible for the initiation of clot formation. Their surfaces contain 555
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several binding proteins that allow platelets to attach to damaged tissue (assisted by von Willebrand’s factor [vWF]). Platelets will also link to each other via GIIb IIIa receptors. Once a platelet attaches to injured tissue, it releases vasoactive substances that recruit other platelets and stimulate the clotting cascade. Platelets contain many clotting and vasoactive substances, including fibrinogen, fibronectin, factors V and VIII, thromboxane A2, serotonin, and fibrinolytic inhibitors. Platelets have a serum half-life of about 9–11 days and are rendered dysfunctional by aspirin, clopidogrel bisulfate (Plavix), and GIIb-IIIa inhibitors. Platelet-induced bleeding abnormalities can be caused by medications, thrombocytopenia, and inherited or acquired platelet disorders. A prolonged bleeding time, with a normal PT and PTT, usually indicates a problem with platelets. Most platelet disorders will present with increased bruising, petechiae, epistaxis, or oral cavity hemorrhage. Coagulation factor disorders will typically present with hemarthrosis, intracranial, or deep muscle hemorrhage. Coagulation factors are proteins formed in the liver and endothelial tissues that, when activated, lead to the deposition and formation of insoluble fibrin. These proteins are called “factors” and are enumerated I, II, III, and so on for the order in which they were discovered (except for vWF). The clotting cascade is initiated by one of two pathways: “intrinsic” and “extrinsic.” Both of these pathways’ final proteins are the same, named the “common pathway.” The intrinsic pathway can be initiated by exposed collagen, platelets, or both. The intrinsic pathway is XII, XI, IX, which initiates the common pathway of X, II, XII, and I. Any defect or deficiency of the intrinsic pathway will cause the PTT to be elevated. Almost all cases of hemophilia will involve an elevated PTT. Heparin therapy is measured by the PTT. It binds antithrombin (i.e., antithrombin III) and inhibits many of the intrinsic and common pathway factors. The extrinsic pathway is initiated by factor III (i.e., tissue thromboplastin) released from damaged tissue, which activates factor VII and subsequently the common pathway. Defective or low levels of factor VII will elevate the PT. Factor VII has the shortest half-life (approximately 4.5 hours) of all the coagulation proteins. Thus, significant tissue damage will deplete factor VII levels and elevate the PT. Sodium warfarin therapy is measured by the elevations of the PT and international normalized ratio (INR). The activation of several factors in both the intrinsic and extrinsic pathways requires calcium as a cofactor. Calcium is a required electrolyte for normal coagulation. In fact, it is so important that it was named factor IV. Abnormal bleeding resulting from fibrinolytic disorders are rare and are caused by overactivation of plasmin, antithrombin (antithrombin III), or thrombomodulin. These proteins make up most of the anticoagulation system and maintain homeostasis with the coagulation proteins.
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Disorders of the fibrinolytic system usually cause a hypercoagulable state as a result of deficiencies of protein c, s, antithrombin, or a genetic mutation of factor V (i.e., Leiden mutation). The Leiden mutation is the most common hypercoagulable disorder, affecting 1 in 20 people. It renders factor V resistant to inactivation by activated protein C and increases the risk of deep venous thrombosis formation. Vascular bleeding is caused by defects in the supportive or connective tissue. There are several inherited disorders leading to defects in vascular wall formation and subsequent hemorrhagic diathesis. Most are induced by systemic inflammatory disorders such as Henoch-Schönlein purpura, Wegener’s granulomatosis, systemic lupus erythematosus, rheumatoid arthritis, and polymyositis. These can present with petechiae, purpura, and ecchymosis. The PT, PTT, platelet count, and bleeding times are all normal. Inflammatory disorders will have an elevated sedimentation rate. Vascular bleeding may also be acquired. Acquired vascular abnormalities include senile tissue, steroid induced atrophy, and scurvy.
CLINICAL PRESENTATION Patients can and will present with varied presentations. Gum bleeding, increased bruising with trivial injury, petechiae, joint edema, and effusions. Patients with central nervous system bleeding can present with altered mental status.
EXAMINATION Patients should have a complete physical examination, including examination of the retina, oral mucosa, and joint function and pain throughout the body.
LABORATORY FINDINGS Laboratory workup should include measurements of PT, PTT, INR, complete blood count (CBC), and bleeding time. If disseminated intravascular coagulopathy is suspected, fibrinogen levels, fibrin split products, and D-dimer should also be analyzed. Chemistry tests to be performed should include calcium. Direct drug-induced bleeding diathesis is most commonly caused by heparin, low-molecular-weight heparin, warfarin, clopidogrel (Plavix), and aspirin therapy. Indirect drug-induced bleeding may result from liver failure or thrombocytopenia resulting from bone marrow suppression.
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DIAGNOSIS Any patient presenting with abnormal bleeding or difficult hemostasis should be evaluated with a detailed history and physical examination. Particular attention should be paid to the location and frequency of the hemorrhage as well as family history.
TREATMENT Treatment should be directed at the underlying proximate cause of the bleeding diathesis. Factor defects or deficiencies will respond to specific factor replacement. In the face of idiopathic bleeding, an elevated PT and PTT should be treated with fresh frozen plasma (FFP). If the PT and PTT are normal and the patient has an elevated bleeding time, platelet transfusion should be considered. If the patient is bleeding and has thrombocytopenia, platelet transfusion will also be necessary. Heparin toxicity should be treated with protamine sulfate, and warfarin toxicity will require vitamin K replacement and possibly FFP. Patients bleeding as a result of antiplatelet toxicity will respond to platelet transfusion and cessation of the medication.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
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Blood Transfusions JOHN ROBERT SCOTT
ICD Code: V59.01
Key Points Whole blood is almost never used for transfusions anymore. The threshold for transfusing red blood cells (RBCs) is now 8 g/dl. Each unit of platelets (random donor platelets; RDP) will raise the platelet count by 5000 to 10,000. In a nonbleeding patient, the threshold for transfusing platelets is 10,000. Transfusion-related acute lung injury can occur with FFP transfusions. Between 4 and 6 units of FFP will increase a patient’s clotting factors by 10% ^20%. Transfuse cryoprecipitate for fibrinogen less than 100 mg/dl. Each unit of cryoprecipitate will raise the fibrinogen level by 5^10 mg/dl. Leukoreduced blood products decrease the risk of human leukocyte antigen (HLA) alloimmunization, cytomegalovirus (CMV) infection, and transfusion-associated graft-versus-host disease (TA-GVHD). Irradiated blood products inactivate T lymphocytes and prevent TA-GVHD. Saline-washed blood products help to prevent allergic transfusion reactions.The universal donor is Oþ in all patients except women of childbearing age (for whom it is O). A massive blood transfusion is 50% ^100% of a patient’s blood volume in a 24-hour period. A hemolytic transfusion reaction is due to the transfusion of ABO-incompatible blood. A delayed hemolytic transfusion reaction is seen days to months later due to an anamnestic antibody response to minor RBC antigens. Febrile transfusion reactions are usually due to antibodies against donor leukocytes, but rarely can be due to bacterial contamination of donor blood products. Urticaria occurs in 3% of transfusions due to antibodies against plasma protein antigens. Anaphylactic transfusion reactions occur most often in immunoglobulin (Ig) A^deficient patients with anti-IgA antibodies (IgE). Hepatitis B infection occurs in approximately 1 in 50,000 units, hepatitis C infection in approximately 1 in 10,000 units, and human immunodeficiency virus (HIV) infection in approximately 1 in 150,000 units.
BLOOD COMPONENTS Blood is made up of noncellular and cellular components. FFP, albumin, and cryoprecipitate are all noncellular components of blood. RBCs, platelets, and white blood cells (WBCs) are cellular components of blood.
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Whole Blood A unit of whole blood contains approximately 450–500 ml of venous blood in 70 ml of a citrate-based anticoagulant solution at an average hematocrit of 40% (range, 36%–44%). A unit of stored whole blood lasts 21–35 days, depending on the citrate-based anticoagulant used. Whole blood is almost never used anymore. It has been replaced by component-specific blood products.
Packed Red Blood Cells Packed RBCs are made by removing 200–250 ml of plasma from whole blood. The typical volume is 250–300 ml per bag. Each bag will raise the patient’s hemoglobin approximately 1 g/dl (hematocrit 3%). Additive solutions are anticoagulant-preservative solutions that contain varying concentrations of adenine, which allow increased storage of RBCs to a maximum of 42 days. Packed RBCs may undergo further processing for specific indications, including leukocyte reduction, irradiation, or saline washing. The generally accepted threshold for transfusion of packed RBCs has recently been changed from a hemoglobin concentration goal of approximately 10 g/dl to a goal of 7 g/dl because of a recent randomized, prospective study. This hemoglobin concentration goal does not apply to trauma patients. RBCs may be frozen to significantly increase storage time. Glycerol penetrates the RBCs and allows them to freeze without causing damage to the cells. This technique is useful for rare blood types, autologous transfusions, and stockpiling reserves.
Platelets Platelet concentrates (RDP) are prepared by the centrifugation of 1 unit of whole blood. The RDP pool size is established by the individual hospital transfusion service. Single donor platelets (SDP) are prepared with an apheresis technique. One RDP unit contains platelets concentrated in 40–70 ml of plasma, and one SDP unit contains platelets concentrated in 200–300 ml of plasma. Between 5 and 6 units of RDP are equivalent to 1 unit of SDP. A provider will often order a “six-pack” of platelets, which means 6 units of RDP. Each unit of RDP will raise the patient’s platelet count 5000–10,000/ml. The standard six-pack of RDP will therefore raise the platelet count 30,000–60,000/ml. A single unit of SDP will raise the patient’s platelet count by the same amount (30,000–60,000/ml). SDP units are primarily used in patients who require long-term transfusions to prevent alloimmunization to HLA (anti-HLA antibodies) or platelet-specific antibodies. This practice, while common, is not supported by the Trial to Reduce Alloimmunization to Platelets (TRAP) Study Group. Because platelets cannot be frozen and must be stored with gentle
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agitation to maintain their activity, the storage time until expiration is only 5 days. Generally, platelet transfusion is indicated for platelet counts below 10,000/ml in the absence of bleeding. The range is 20,000– 50,000/ml, depending on local practice. Transfusion should be performed for counts less than 50,000 per microliter in actively bleeding patients or patients with a planned surgical procedure (100,000/ml for neurosurgery or ophthalmological surgery). Rh-negative patients should receive Rhnegative platelets; this is because of the approximately 0.1 ml of RBC contamination per unit of RDP. Platelets do not have Rh antigens. Alternatively, a standard injection of RhoGam can be given to Rh-negative patients who receive Rh-positive platelets. Be aware that platelets are stored at room temperature and they are therefore more susceptible to bacterial contamination. Pay particular attention to fevers, chills, rigors, and hypotension in patients receiving platelet transfusions because these signs and symptoms could represent a septic transfusion reaction. Beginning March 1, 2004, bacterial testing of platelets was mandated by voluntary standard-setting organizations to help mitigate this risk.
Fresh Frozen Plasma One unit of FFP is prepared by the centrifugation of 1 unit of whole blood. It contains 200–250 ml and has a storage time to expiration of 1 year. FFP contains all the coagulation factors, anti-thrombin III, protein C, protein S, fibrinogen, and albumin. The clinician should be aware of patients who experience shortness of breath or decreasing oxygen saturations while receiving FFP. Transfusion-related acute lung injury (TRALI) occurs during transfusions with plasma. A noncardiogenic pulmonary edema occurs due to alveolar membrane damage and capillary leak. Transfusions of preformed antibodies against the recipient’s leukocytes cross-react with the recipient’s alveolar membrane and cause transfusion-related acute lung injury. This should not be confused with febrile nonhemolytic transfusion reactions, which are caused by recipient antibodies to donor leukocytes. The typical dose of FFP transfused is 4–6 units or 10–20 ml/kg. This dose will increase all of a patient’s coagulation factors by 20%.
Cryoprecipitated Antihemophilic Factor (Cryoprecipitate) Cryoprecipitate is derived from the centrifugation of 1 unit of FFP after it is slowly thawed. The unit of cryoprecipitate is then refrozen with only 10–15 ml of plasma and has a storage time of 1 year. Each unit of cryoprecipitate contains 80–120 units of factor VIII (both factor VIII:C and factor VIII:vWF) and 150–250 mg of fibrinogen and fibronectin. Cryoprecipitate was used to treat patients with hemophilia in the past, but this is no longer necessary due to the development of factor-specific products.
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Cryoprecipitate is now primarily used to replace fibrinogen (below 100 mg/dl). Cryoprecipitate does not need to be type-specific because it has such little plasma. However, hemolysis can occur after large volumes of cryoprecipitate have been given. Each unit of cryoprecipitate will raise the fibrinogen level 5–10 mg/dl. A typical dose is 10 units.
Leukoreduced Blood Products Leukoreduction techniques can be used for RBC and platelet units. The units are filtered before storage or at the bedside. Current third-generation leukocyte filters are capable of removing more than 99.99% (4-log reduction) of leukocytes with less than 10% RBC loss. WBCs have HLA antigens (RBCs and platelets do not). Recipients of blood products form antibodies against these antigens. The antibodies cause transfusion reactions, and it becomes harder and harder to give these patients blood products. CMV is transmitted through the WBCs of a CMV-positive donor to an immunosuppressed CMV-negative recipient. Most persons are CMV-positive and are therefore immune to an acute CMV infection. Active donor WBCs can attack an immunosuppressed recipient, causing TA-GVHD. Leukoreduced blood products decrease the risk of HLA alloimmunization, CMV infection, and TA-GVHD.
Irradiated Blood Products RBC, platelet, and nonfrozen plasma units contain active T lymphocytes that are capable of causing TA-GVHD. These units are exposed to 15– 20 gray of gamma radiation to inactivate T lymphocytes and prevent TA-GVHD.
Saline-Washed Blood Products “Washed” RBC and platelet units are used to remove plasma proteins, antibodies, and electrolytes. The units are washed with normal saline in a standardized fashion. The technique removes 99% of the plasma proteins but also removes 20% of RBCs and 30% of platelets. The washing process also removes 90%–99% of leukocytes (but not enough to prevent HLA alloimmunization). Washed RBCs must be used within 24 hours, and washed platelets must be used within 4 hours. Saline-washed blood products help prevent anaphylactic transfusion reactions in IgA-deficient patients.
TRANSFUSIONS Blood transfusions should be administered through large-gauge intravenous tubing with a Y device so that warmed normal saline can be infused
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at the same time as the blood. Glucose- or calcium-containing solutions should not be used at the same time that the transfusion is being performed. Blood should always be warmed before administration. Cold blood can precipitate hypothermia. Pressure in infusion devices can be used, but they should not be inflated to greater than 300 mmHg. All transfused blood should be type specific and should be crossmatched when possible. In an emergency when blood is required immediately, type O blood can be used. Rh-positive O blood should be given to male patients, and Rh-negative O blood should be given to women of childbearing age. Type-specific, cross-matched RBCs should be given as soon as it is possible. Most military studies have been based on O-positive blood, and most civilian studies have been based on the use of O-negative blood. Autotransfusion is the reinfusion of the patient’s blood by collecting the blood from the thorax or peritoneal cavity after washing and antibiotic administration. A massive blood transfusion is when 50% of the patient’s blood volume is transfused in a 24-hour period or when 50% is transfused at one time. Massive blood transfusions have many complications, including acute respiratory distress syndrome, hypothermia, hypocalcemia, citrate toxicity, and coagulopathies.
TRANSFUSION REACTIONS There are four types of transfusion reactions: hemolytic, delayed hemolytic, febrile, and allergic.
Hemolytic Reactions A hemolytic blood transfusion reaction is due to transfusion of ABOincompatible blood. Most often this is due to a mislabeled blood sample or mislabeled blood products. Rapid destruction of transfused RBCs take place as a result of an antibody-mediated reaction. When RBCs are destroyed there is a release of free hemoglobin, which causes hemoglobinuria, hemoglobinemia, elevation of bilirubin, and depletion of haptoglobin. Anesthetized patients will develop hypotension. Patients who are awake will report low back pain, shortness of breath, fever, chills, and a burning sensation at the site of the blood transfusion. Patients with a hemolytic reaction develop hemoglobin in the urine, free hemoglobin in the blood serum, a direct and indirect Coombs’ test result, and coagulation problems. A red-topped tube and a lavendertopped tube should be sent to the blood bank for testing. A rapid, bedside screening sample for hemolytic reaction is taken to centrifuge in a CBC tube. If the color of the centrifuged blood is pink, it suggests free
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hemoglobin at levels of 50–100 mg/dl. If the centrifuged blood is pale brown, hemoglobin concentration is at a level below 20 mg/dl. The appropriate treatment of a hemolytic reaction is immediate discontinuation of the transfusion. Aggressive supportive care should be initiated, including endotracheal intubation, central venous access, arterial blood pressure monitoring, and vasopressor medications, where indicated. Very large amounts of normal saline should be used to maintain blood pressure and to increase urinary outflow. End points of fluid resuscitation include urine output of 0.5–1 ml/kg/hr or central venous pressure of 8–12 mmHg. Central venous pressure monitoring should be used in the event of anuric renal failure. Furosemide may be helpful in preventing renal failure but will render urine output invalid as an end point of fluid resuscitation.
Delayed Hemolytic Reactions Delayed hemolytic transfusion reactions can be seen several days to months after the transfusion. A decrease in hemoglobin level helps the clinician to make the diagnosis. The patient may report vague symptoms such as chills, myalgia, and low back pain. This reaction occurs as a result of the transfused RBCs becoming coated with antibodies and being removed by the tissue-bound macrophages in the spleen. Patients may have previously been sensitized to minor blood group antigens, but their antibody levels fall below detectable levels during the cross-match process. After transfusion, an anamnestic antibody response occurs, usually within 2 weeks. Only the transfused RBCs are destroyed, but occasionally this is enough to cause renal failure. If a delayed hemolytic reaction is suspected, blood should be sent to the blood bank for testing. Often the antibodies to these minor antigens will subside again, putting the patient at risk for recurrent problems. Treatment is supportive.
Febrile Reactions Febrile transfusion reactions are the most common reactions. Patients develop chills, malaise, and fever. Febrile reactions are frequently seen in multiparous patients and patients with a history of multiple transfusions due to their heavy exposure to foreign leukocytes. Fever usually occurs because of antibodies against donor leukocytes. A rarer cause of febrile reactions is transfusion of blood products contaminated with bacteria. Gram-negative bacteria such as Yersinia species and Pseudomonas species can multiply in refrigerated blood products. The fever seen in these patients is due to infusion of preformed endotoxin. Both donor and patient blood should be sent to the laboratory for culture and Gram stain. Treatment should include antibiotics and aggressive support. Anytime a febrile
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reaction occurs, the transfusion should be stopped and a blood sample from both donor and patient should be sent to the laboratory for analysis. Very rarely, leukocyte antibodies can produce lung injury and noncardiogenic pulmonary edema.
Allergic Reactions (Urticarial and Anaphylactic) Allergic transfusion reactions are of two types: urticarial and anaphylactic. Urticaria is seen in 3% of all transfusions. It is usually due to antibodies against minor donor plasma proteins. The transfusion should be stopped and blood work sent to the laboratory for analysis. The patient should respond to antihistamine therapy such as intravenous diphenhydramine. Anaphylactic transfusion reactions are seen in rapid un–cross-matched blood transfusions. They are usually seen in IgA-deficient recipients with anti-IgA antibodies who have a history of numerous allergies. The antibodies against IgA are IgE-type antibodies. When standard blood products (which contain IgA plasma proteins) are transfused, anaphylaxis occurs. A similar phenomenon occurs in patients deficient in haptoglobin. If an anaphylactic reaction occurs, the transfusion should be stopped immediately. Treatment with intravenous fluids, antihistamines, and epinephrine should be given along with good supportive care.
Hepatitis B and C Hepatitis B and C screening has significantly reduced the risk of transfusion-related infection. The risk of hepatitis B infection is approximately 1 in 50,000 units. The risk of hepatitis C is approximately 1 in 10,000 units.
Human Immunodeficiency Virus The use of voluntary blood donations that are screened by questionnaire and blood testing has dramatically reduced the risk of transfusion-related HIV infection. The risk of HIV infection is approximately 1 in 150,000 units.
Transfusion-Related Hemosiderosis Remember to consider hemosiderosis in patients who receive chronic transfusions. Conditions like thalassemia and sickle cell disease cause destruction of red blood cells, but iron is recycled. Every 1 ml of packed RBCs contains 1 mg of iron. This diagnosis requires a high index of suspicion. Signs and symptoms of liver and heart failure may be seen. Treatment should include deferoxamine.
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Bibliography Fakhry SM, Sheldon GF: Blood administration, risks, and substitutes, Adv Surg 1995;28: 71–92. Gelman M: Transfusion complications. In Schaider J, Hayden SR, Wolfe R, et al: Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003. Herbert PC, Blajchman MA: A multicenter, randomized, controlled clinical trail of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group, N Engl J Med 1999;340:409. Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, pp 2410–2411. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, p 51. Rakel RE: Conn’s Current Therapy 2005, ed 57. Elsevier: Philadelphia, 2005, pp 539–543.
Hemophilia MICHAEL K. SHAFE ICD Codes: Congenital factor VIII disorder 286.0, Congenital factor IX disorder 286.1, Congenital factor XI deficiency 286, von Willebrand’s disease 286.4
Key Points Hemophilia A and B are clinically indistinguishable except for activity of factor VIII and IX, respectively. The PT is normal and the PTT is elevated in both A and B.vWF activity is normal in both. ! Emergency Actions ! Many patients have specific dosing regimens recommended by their hematologists. One unit of factor concentrate per kilogram of body weight will raise the plasma activity level by 2%–2.5%. Dosing should be approximately 10–15 units/kg, which will increase the factor VIII by 20%–30%. Severe bleeding will require a correction to 50%–100% for several days. In a 70-kg person, this will require an initial bolus of 3500 units.
DEFINITION Hemophilia is a disorder involving factor deficiencies in the intrinsic pathways. The three most common types of hemophilia are (1) factor
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VIII deficiency, hemophilia A; (2) factor IX deficiency, hemophilia B; and (3) von Willebrand’s disease, a decrease in vWF activity, a distinctly separate disease process that may present clinically similar to hemophilia A and B.
EPIDEMIOLOGY Hemophilias are x-linked inherited disorders of variable penetrance. Hemophilia A occurs in approximately 1 per 5000 male births and is four to six times as common as hemophilia B, estimated at 1 per 30,000 male births. Hemophilia in females is extremely rare; both parents would have to have hemophilia. Von Willebrand’s disease is an autosomal-dominant disease with variable degrees of severity and presentation, occurring in approximately 1 per 800 persons. There appears to be no racial or ethnic propensity for hemophilia or von Willebrand’s disease.
PATHOPHYSIOLOGY Clotting factors are proteins (except factor IV) within the clotting cascade necessary to form cross-linked fibrin. They were numbered in the order they were discovered. Calcium is factor IV, which is a critical cofactor in the activation of many of the proteins. Hemophilia A and B are sexlinked recessive disorders caused by a deficiency in factor VIII and IX, respectively. The disease is further classified based on the level of factor activity:
Severe: < 2% activity Moderate: 2%–5% activity Mild: 5%–30% activity
Hemophilia A and B are clinically indistinguishable except for activity of factor VIII and IX, respectively. The PT is normal and the PTT is elevated in both A and B. vWF activity is normal in both. vWF assists platelet binding to collagen and serves as a plasma carrier for factor VIII. Low levels of vWF will also be reflected by lower than normal factor VIII levels. Like hemophilia, von Willebrand’s disease has three general categories of mild, moderate, and severe.
CLINICAL PRESENTATION Patients with hemophilia will have a variable presentation of symptoms. Most cases with less than 1% factor activity will be diagnosed within the first year of life. Approximately 50% will sustain excessive bleeding during circumcision. Many will typically present with intra-articular or intramuscular bleeding. Inadequately treated incidents of recurrent joint
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bleeding can result in chronic synovial and intra-articular hemosiderin deposits, which lead to cartilage damage and subchondral bone cyst formation. Moderate hemophilia may not be diagnosed until the age of 2–5 years, with increased incidence of falls and trauma. Mild cases may not be diagnosed until the second or third decades of life; these cases involve easy bruising, heavy menses, recurrent bleeding with mild trauma, increased hemorrhage with minor surgical procedures, or hematuria after exercise. Some patients may present with groin pain after retroperitoneal hemorrhage into the psoas facial planes.
EXAMINATION If a bleeding disorder is suspected, a thorough physical examination must be performed, including rectal, funduscopic examination (looking for retinal hemorrhages), and joint and skin examination for petechiae, purpura, and contusions. Most patients with hemarthrosis will report swelling and pain in the affected joint. Hemarthrosis may not always present with an appreciable effusion.
LABORATORY FINDINGS Any patient with a suspected bleeding disorder should have a CBC, liver function tests, and measurements of electrolytes, calcium, blood urea nitrogen, creatinine, PT, INR, PTT, and bleeding time. Hemophilia A and B will present with an elevated PTT and a normal PT and bleeding time. Bleeding time is the time necessary for two standardized cuts on the forearm of a patient to stop bleeding. The laboratory profile found with von Willebrand’s disease includes a decreased VIII-C, vWF:Ag, and vWF activity. Since vWF affects both circulating factor VIII and platelet adherence, the PTT and bleeding times can be elevated in von Willebrand’s disease. Additionally, the results of analyses of vWF:Ag, vWF activity, factor VII-C, and factor IX will usually confirm the diagnosis. If these last test results are normal, one needs to consider other factor deficiencies.
DIAGNOSIS Family history, combined with a clinical presentation of abnormal bleeding, should alert the clinician to consider confirmatory laboratory testing. Intramuscular and hemarthrosis are more common in hemophilia or severe type III von Willebrand’s disease.
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TREATMENT Most patients with hemophilia have recombinant factor at home and often will bring it with them to the hospital. Many have specific dosing regimens recommended by their hematologists. One unit of factor concentrate per kilogram of body weight will raise the plasma activity level by 2%–2.5%. Dosing should be approximately 10–15 units/kg, which will increase the factor VIII by 20%–30%. Severe bleeding will require a correction to 50%–100% for several days. In a 70-kg person, this will require an initial bolus of 3500 units. If recombinant factor replacement is not available, then cryoprecipitate is a good source of concentrations of fibrinogen, factor VIII, vWF, and fibronectin. Each unit of cryoprecipitate contains 80–100 units of factor VIII. FFP contains only 1 unit of each factor per milliliter. Four units of FFP will increase most factors by approximately 10%. Most surgical procedures may be performed once the INR is reduced to less than 1.5. Desmopressin (DDAVP) is a synthetic agent that can raise factor VIII and vWF up to 300%–400% in 30–90 minutes. It stimulates release from endothelial stores. It is only indicated for raising factor VIII levels and for type I (minor) cases of von Willebrand’s disease. The appropriate dosage is 0.3–0.4 mg/kg. DDAVP is a vasoactive substance that should be used cautiously in elderly persons or patients with a history of coronary artery disease because it may precipitate hypertension. Factor IX deficiency should be treated with recombinant factor IX. The recommended dosing is 25 units/kg for minor bleeding, 35 units/ kg for moderate bleeding, and 45 units/kg for severe bleeding. All patients with hemophilia or von Willebrand’s disease who present with a bleeding problem should have consultation performed with a hematologist, and close follow-up should be undertaken within a few days.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, Chapters 114, 115, and 116. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
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Sickle Cell Anemia MICHAEL K. SHAFE ICD Code: Sickle cell anemia 282.60
Key Points Sickle cell anemia is a disease of painful recurrent vaso-occlusive episodes. The condition can be life threatening when infection is present, since sickle cell patients are functionally asplenic. ! Emergency Actions ! Any patient presenting with sickle cell crisis should be treated aggressively with the administration of fluids and analgesic medications. If fever is present, a search for the source of fever must be undertaken, and appropriate antibiotics should be administered.
DEFINITION Sickle cell anemia is a chronic hemolytic anemia with the cardinal feature of recurrent painful vaso-occlusive episodes resulting from RBC deformation and occlusion of the microvasculature.
EPIDEMIOLOGY Sickle cell trait is an autosomal-dominant gene carried by 8% of the African American population in the United States; 1 in 500 of carriers has the disease state. Persons from the Caribbean and Central and South America carry the trait gene in 4% of the population, and the disease prevalence is 1 in 2000 for this group. Sickle cell disease is also prevalent in persons of Arab, East Indian, Greek, or Italian descent. It is usually diagnosed between the age of 6 months and 15 years. Up to 15% of children born with the disease will die by the age of 20 years. The median life expectancy is 42 years for men and 48 years for women.
PATHOLOGY A single DNA nucleotide mutation causes valine to be substituted for glutamic acid on the sixth position of the hemoglobin beta subunit. This hemoglobin (HbS) has a lower solubility than normal hemoglobin
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(HbA), and when exposed to low-oxygen environments HbS molecules will polymerize into long rods that deform the RBC into a sickle shape. These abnormally shaped cells cannot pass through most capillary beds and cause local occlusion of the microvasculature. This occlusion leads to local ischemia, further hypoxia, tissue infarction, and hemolysis of the RBC. This process can affect every organ, and, when severe, can lead to multisystem organ failure. Recurrent occlusive events render patients functionally asplenic and susceptible to encapsulated bacterial organisms like Streptococcus pneumoniae, salmonella, Haemophilus influenzae, and Neisseria meningitides. Sickle SC (HbSC) is a variant that is detected later in life. Patients with HbSC have fewer but just as severe crisis episodes as patients with HbSS. The former will experience similar organ system dysfunction as HbSS patients, including vaso-occlusive crisis and fat emboli syndrome from infarcted bone marrow. There are other rare variants of sickle cell disease. These include HbSB thalassemia, HbSD, and HbSF fetal persistence. The clinical presentation of these varies from asymptomatic to severe. Sickle cell trait contains one normal and one sickle gene, HbSA. This is a benign condition, which is nothing more than a carrier state. Patients neither develop sickled cells nor any clinical manifestations of sickle disease. The peripheral smear of patients with sickle cell trait is essentially normal. Any patient with sickle cell trait who demonstrates clinical or hematological symptoms should be referred to a hematologist for confirmation of HbSA or presentation of an atypical variant of the carrier state.
CLINICAL PRESENTATION Patients with HbSS will not begin to demonstrate signs and symptoms of the disease process until 6 months of age when their fetal hemoglobin dissipates. African-American children who present with hemolytic anemia symptoms, unexplained bone pain, jaundice, or recurrent right upper quadrant pain should have sickle cell anemia included in their differential diagnosis. Acute pain is the first symptom in 25% of patients with sickle cell disease. Pain is also the most frequent symptom after the age of 2 years and the most frequent reason for seeking medical attention. There are several typical “crisis” in which a patient with sickle cell anemia may present. The first and most common is acute pain crisis (some authors have replaced this term with acute painful episode). Another term for this is vaso-occlusive crisis. Bone marrow infarction and subsequent release of inflammatory mediators is suspected to be the proximate cause of acute pain or vaso-occlusive crisis.
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Splenic sequestration crisis presents similar to an acute pain crisis, except that there is splenic enlargement. Since most adults are functionally asplenic, this crisis usually occurs in children. A patient experiencing an aplastic crisis presents with a decreasing hemoglobin level, low reticulocyte count, and decrease of RBC precursors in the bone marrow. Aplastic crisis is usually precipitated by an infectious event. In children, parvovirus B19 accounts for 68% of aplastic crises in children with sickle cell disease. In adults, S. pneumoniae, salmonellae, and Epstein-Barr virus have been demonstrated to account for transient marrow aplasia. Acute chest syndrome involves chest pain, dyspnea, fever, tachypnea, leukocytosis, and pulmonary infiltrates exhibited on chest x-ray. Infections or pulmonary emboli of a thrombus or fat from the bone marrow may account for this syndrome. This crisis carries a 10% mortality rate. Male patients with sickle cell disease may present with priapism. Some literature reports the incidence as high as 42%. Immediate urological consult is necessitated for these patients.
EXAMINATION The patient should be asked whether this is a typical or severe crisis episode. A thorough history and complete review of systems inquiring about stressful precipitating events, fever, or infectious symptoms should be pursued. A detailed physical examination, including neurological and funduscopic examinations, should be performed. Pediatric patients may present with hepatomegaly and splenomegaly.
LABORATORY FINDINGS A typical crisis in most patients with sickle cell anemia may be worked up with a CBC and reticulocyte count. More severe or “worst crisis” should elicit a more aggressive evaluation, including urine analysis, liver function testing, and measurements of electrolytes, blood urea nitrogen, creatinine, PT, PTT, and INR. If infection is suspected, blood and urine cultures should be performed. If chest pain is a presenting symptom, electrocardiography, cardiac enzyme analysis, and chest radiography should be performed. Sickle cell disease is a hemolytic process. Leukocytosis, thrombocytosis, worsening anemia, and reticulocytosis should be expected. Patients experiencing aplastic crisis will present with a low WBC count, low platelet count, and a normal or low reticulocyte count. The peripheral smear may demonstrate sickled cells. The presence of sickled cells does not
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correlate with the severity of vaso-occlusive crisis or level of pain. An elevated bilirubin level will also be present.
DIAGNOSIS The diagnosis is confirmed by family history and serum electrophoresis. Finding sickled cells on a peripheral blood smear may support the initial diagnosis in the office or emergency department.
TREATMENT Supplemental oxygen should be administered if the patient is hypoxic. If the patient is dehydrated, oral hydration will usually be adequate. If the crisis is severe or if the patient is vomiting, intravenous access should be established and hydration with normal saline initiated. The goal of fluid therapy should be a euvolemic state. Care should be taken not to overload these patients with fluid because they are subject to develop pulmonary edema and heart failure. Analgesic therapy should be pursued aggressively. Nonsteroidal antiinflammatory medications and narcotics should be administered. Most patients will have a tolerance to narcotics and will require much higher doses than the average patient. It is possible for patients to experience pain and still be somnolent. The single best measure of pain control is what the patient reports to the clinician. Transfusion therapy may be indicated if the patient has an acute drop of more than 2 g/dl of hemoglobin or a hemoglobin level of 5–6 g/dl. Liberal use of transfusions is discouraged in light of patients developing resistant antibodies and becoming more difficult to find matching blood in the future. Patients experiencing stroke, acute chest syndrome, or aplastic crisis may require exchange transfusions. Priapism that does not respond to ice compress within 1 hour should prompt urology consultation. If infection is present, broad-spectrum antibiotics should be administrated. The usual organisms causing sepsis in asplenic patients are H. influenzae and S. pneumoniae. Mycoplasma pneumoniae, Salmonella typhimurium, Staphylococcus aureus, and Escherichia coli should also be considered. Patients who have received multiple transfusions and have been treated with the chelating agent deferoxamine for iron overload, secondary to those multiple transfusions, are at risk for infection with Yersinia enterocolitica infection. Hematological consultation and admission are warranted if patients with sickle cell anemia do not achieve adequate pain control after several doses of narcotics or if they require prolonged or more aggressive treatment in the office or emergency department.
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Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, pp 591–601, 605–634. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
Chapter 12
Orthopedic Emergencies Basic Principles of Orthopedic Injuries STEVEN W. SALYER
ICD Codes: See ICD codes by fractured bone
Key Points Fractures in children differ from those in adults.Children’s bones are softer and more resilient than those of adults, and their bones can sustain greater forces and more incomplete fractures. In children, greenstick fractures, or incomplete fractures of long bones, are very common. The long bone bows with incomplete angulation. A torus fracture is an incomplete fracture, or a buckling or wrinkling of a bone cortex. ! Emergency Actions ! With any fracture, a good vascular and neurological examination must be performed and documented. Soft tissue must be examined along with range of motion and strength. A good rule to live by in providing orthopedic care is that pain over a bone implies a fracture until proven otherwise. Early referral to an orthopedic surgeon for every trivial bony deformity should be the norm. When in doubt, consult orthopedics early and often.
DEFINITION Patients can experience bone fractures from falls, direct trauma, and motor vehicle accidents. The age of the patient, the underlying medical problems, and whether the injury is open or closed all determine the therapy. Fractures are described by their location, whether they are open or closed, simple or comminuted, and their position, displacement, and angulation. Valgus denotes a deformity in which the described part is angled away from the midline of the body. Varus denotes a deformity in which the angulation of the body part is toward the midline. Fractures are described as either transverse, oblique, spiral, or comminuted. Fractures in children differ from those in adults. Children’s bones are softer and more resilient than those of adults, and their bones can sustain greater forces and more incomplete fractures. In children, greenstick fractures, or incomplete fractures of long bones, are very common. 575
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The long bone bows with incomplete angulation. A torus fracture is an incomplete fracture, or a buckling or wrinkling of a bone cortex. Of most concern in children with fractures are those involving the epiphyses or cartilaginous centers at or near the end of children’s growing bones. The cartilaginous portion of the epiphysis is not seen on radiographic examination. Injuries to the epiphysis can result from either compressive or shearing forces. In children, epiphyseal injuries are quite common, whereas sprains are rare. It is common for an inexperienced practitioner to label an epiphyseal injury as a sprain. Epiphyseal injuries are commonly classified by the Salter-Harris classification system. In a Salter-Harris type I fracture, there is a slip in the provisional calcification. Often this injury is very subtle and will require comparison views. There are no germinal layer disturbances in type I fractures. Any child with pain, edema, and a negative x-ray result should be treated as having a Salter-Harris type I injury, and the area should be x-rayed in 10 days. Salter-Harris type II fractures involve the metaphysis, and often the epiphyseal plate has also slipped. There is no germinal layer involved, thus there are no growth plate disturbances in type II injuries. Type II fractures involve a slip of the growth plate plus a fracture through the epiphysis involving the articular surface. Type III fractures involve the germinal layer and thus have a potential for growth disturbances. Type IV fractures involve the metaphysis and the growth plate, and these fractures have a high rate of growth disturbances. Type V fractures involve a crush injury to the epiphyseal plate. These injuries are often difficult to diagnose on a plain radiograph. There is usually a growth disturbance involved with type V injuries. All Salter-Harris fractures require a referral to an orthopedic surgeon for treatment and follow-up.
EXAMINATION For any fracture, a good vascular and neurological examination must be performed and documented. Soft tissue must be examined along with range of motion and strength. A good rule to live by in providing orthopedic care is that pain over a bone implies a fracture until proven otherwise. Another rule is to splint the patient where he or she lies. Do not perform a reduction until you have obtained a radiograph, unless there is neurological or vascular compromise. Probably no circular casts should be applied to any sprained or fractures extremity in the ED. If a patient presents to the ED wearing a cast and experiencing pain and neurovascular compromise, the cast should be bivalved or removed entirely.
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Early referral to an orthopedic surgeon, for every trivial bony deformity should be the norm. When in doubt, call early for a consultation to the ED.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Acute Back Pain STEVEN W. SALYER
ICD Codes: Back pain 724.5, Lower back pain 724.2, Intervertebral disk 722.2, Myelopathy 722.71 (see specific disk)
Key Points Any patient with lower lumbar pain should undergo an abdominal examination. If the lower lumbar pain is not easily determined or if pelvic pathology is considered in a female patient, a pelvic examination should be performed. ! Emergency Actions ! Any patient with a history of trauma, especially to the cervical spine, should have a radiograph taken of the spine. If a compression fracture is suspected, radiographs should be taken.
DEFINITION The spine is made up of 7 cervical vertebrae, 12 lumbar vertebrae, and 5 lumbar vertebrae. There are five sacral nerves that exit from the sacrum.
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There are eight paired cervical spinal roots in the cervical spine that exit from intervertebral foramina. The atlas of C1 supports the occipital condyles and the axis of C2. There are seven fascial planes of muscles in the neck. The dorsal nerve is the sensory part of the spinal cord, and the ventral root is the motor root of the spinal cord. Thus, if the ventral root is compressed, then painless weakness will occur. If only the dorsal root is compressed, only pain, without weakness, will occur. The ligament structures of the spine consist of the anterior longitudinal ligament, posterior longitudinal ligament, ligamentum flavum, intraspinal ligament, supraspinal ligaments, intratransverse ligaments, and costotransverse ligaments. Acute back pain can be caused from trauma to the vertebrae, prolapse of the disks, osteoporosis, spurs, nerve entrapments, and numerous other pathologies leading to weakness, pain, and bowel or bladder problems.
CLINICAL PRESENTATION AND EXAMINATION The patient should undress completely for the back examination. It is often very helpful to watch the patient get undressed to evaluate the patient’s range of motion. If possible, the practitioner should watch the patient walk from the waiting room to the examination room; this will give some idea of the patient’s true gait and disability. The patient should always be asked whether there is pain, weakness, numbness, and in what distribution. Are there associated bowel or bladder problems? What was the patient doing when the pain occurred? Is there radicular pain? Has the patient ever had back pain before, and is the distribution the same as before? Are there any associated symptoms (e.g., visual, auditory, pharyngeal-laryngeal symptoms)? Was the onset of pain slow or sudden? Does the pain wake the patient during the night? The healthcare provider should check for flexibility of the neck and the thoracic and lumbar spine. The neck should be checked for pain and range of motion. When there is ipsilateral neck pain that radiates into the shoulder or arm, a radicular component is present (i.e., Spurling’s sign). When the head is moved to one side and there is ipsilateral neck pain on the side of movement, there is zygapophyseal joint irritability. If there is contralateral neck pain with neck movement, then there is probably a ligamentous or muscular source of pain. The thyroid gland should be palpated for enlargement or tenderness, and the carotid and subclavian arteries should be auscultated for bruits. The neck should be examined for lymphadenopathy. The posterior neck should be palpated. The pain of occipital neuralgia can be reproduced by palpating the occipital notch. If occipital neuralgia is present, this will produce scalp numbness and a burning dysesthesia in the occipital nerve distribution.
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The first cervical rib is located directly behind the angle of the mandible, and the transverse process of the atlas is between the angle of the mandible and the mastoid process. The hyoid bone is at the level of C3. The thyroid cartilage is anterior to C4. The patient should always be asked whether he or she has dysphagia or vocal hoarseness. Dysphagia can result from pharyngeal edema or retropharyngeal hematomas. Vocal hoarseness can occur because of the stretching of the larynx, with associated edema of the sternocleidomastoid muscles and carotid sheaths. If the patient reports vertigo, tinnitus, ear and eye pain, visual aberrations, and headache, this is termed Liéou-Barré syndrome. The temporomandibular joint should always be checked when a neck examination is performed. Crepitus over the joint with weakness of the temporalis muscle is indicative of joint dysfunction. The radial and ulnar pulses should always be evaluated with a back examination, especially when upper arm weakness or paresthesia is a presenting symptom. If the radial pulse is reduced with passive shoulder abduction in association with a bruit over the subclavian artery, it suggests thoracic outlet syndrome. A complete neurological examination is necessary for every patient. No back examination is complete without a rectal examination to check for tone or masses. Any patient with lower lumbar pain should have an abdominal examination performed. If the lower lumbar pain is not easily determined or if pelvic pathology is considered in a female patient, a pelvic examination should be performed. Straight leg raises should always be performed. Pelvic tilts should be done, and an examination for a positive Patrick’s sign (i.e., loss of hip internal rotation with medial groin pain) should be performed. The patient should be asked to walk on his or her heels and toes. If the patient cannot walk on his or her heels, this suggests an L5 radiculopathy; the inability to walk on the toes suggests an S1 root involvement. Problems with squatting or rising are indicative of quadriceps weakness and thus L4 compromise. Weak hip flexion suggests L3 involvement. The inability to extend the great toe suggests L5 involvement, and calf pain suggests S1 involvement. A positive straight leg raise test result involves the reproduction of sciatic pain when the hip is flexed and the leg is straightened at the knee (placed in extension). The “strum” sign is performed when the hip and knee are in flexion and the sciatic nerve is plucked behind the knee. If this procedure reproduces pain in the back, this sign is pathognomonic for a herniated disk. The crossed straight leg raise test has a positive result when the contralateral leg is elevated, which produces sciatic pain in the symptomatic leg. A positive crossed straight leg raise test result is suggestive of a herniated disk with an impacted nerve root.
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DIAGNOSIS AND SPECIFIC BACK PAIN ETIOLOGIES Pain bilaterally in the upper extremities usually results from C6 spinal radiculopathies. Biceps tenderness is usually caused by an acute subdeltoid bursitis. A patient with a cervical soft tissue injury often presents with a history of an automobile accident, sports injury, or an accidental fall. The patient often reports “whiplash” with very few objective findings. The new, more correct term for this injury is acceleration flexion-extension neck injury. Head-on injuries with extension of the neck produce ventral tears and hemorrhages in the sternocleidomastoid muscles and ruptures of the anterior longitudinal ligament and ventral parts of the annulus fibrosis. When the patient is rear-ended, this produces injury to the dorsal area of the spine, particularly injury to the annulus fibrosis and hemorrhage to the paraspinal muscles. A patient with an acute cervical disk herniation presents with acute radiculopathy, myelopathy, or both. Neck stiffness, occipital neuralgia, and pain are present. Posterior ruptures of the cervical disk present with cervical radiculopathy. The most common cervical herniation is of C5– C6, C6 nerve root on the right side, and C6–C7, C7 nerve root on the left side. The patient presents with the appropriate dermatome pattern into the correct finger and myotome pain pattern. If long-lasting, the patient will present with the appropriate atrophy and weakness in the innervations muscles (Table 12-1). The patient often presents to the ED for pain management of the chronic degenerative disk disease resulting from cervical spondylosis or osteoarthrosis. Pain is secondary to trauma. The most commonly fractured area of the thoracic spine is the T10–T12 vertebrae. These fractures are usually the result of trauma. The most commonly fractured area of the thoracic spine is the T10–T12 vertebrae. These fractures are usually seen in female patients older than 65 years as a result of osteoporosis. These patients present with severe pain without myelopathy. A metastatic malignancy should always be considered in elderly persons with pathologic fractures without trauma. Thoracic herniated nucleus pulposus (HNP) accounts for fewer than 1% of all HNPs. A patient who presents with acute thoracic pain in a unilateral dermatome radicular pattern should have herpes zoster or diabetic thoracic radiculopathy considered in the differential diagnosis. The most common back-related symptom is lower lumbar pain. Lumbosacral pain can be caused by diverticulitis, a kidney or bladder infection, a disorder of the pancreas, a gallbladder disorder, endometriosis, pregnancy, ectopic pregnancy, gastrointestinal tract bleeding, appendicitis, or chronic pelvic pain other than musculoskeletal pathologies.
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Table 12-1 Nerve Root Motor and Sensory Function NERVE ROOT
DISK SPACE
C1–C2 C5
C1–C2 C4–C5
C6
C5–C6
Biceps and brachioradialis
C7
C6–C7
Triceps
C8
C7–T1
Triceps
L1
L1–L2
Cremasteric
L2
L2–L3
Cremasteric and abductor
L3
L3–L4
Patellar
L4
L4–L5
Patellar, gluteal
L5
L5–S1
Tibial posterior
S1
Sacral foramina
Ankle and hamstring
S2
Sacral foramina
None
S3
Sacral foramina Sacral foramina Sacral foramina Tip of coccyx
Bulbocavernosus
Scalp Thumb and shoulder Biceps, deltoid, pronator Index finger, thumb, Biceps, deltoid, and lateral pronator teres, forearm and wrist extensors Forearm and middle Pronator teres and finger triceps Little finger and Flexor carpi ulnaris, half-ring finger triceps, and hand intrinsic muscles Back to trochanter Hip flexion and the groin Hip flexion and Back and anterior abduction thigh to the level of the knee Back, upper Hip flexion, hip buttocks to abduction, and anterior thigh, knee extension medial lower leg Inner calf to medial Knee extension foot and the first two toes Lateral lower leg, Toe extension and dorsum of the ankle foot, first two dorsiflexion toes Sole, heel, and the Ankle plantar lateral edge of the flexion and knee foot flexion Posterior and medial Ankle plantar upper thigh flexion and toe extension None None
Bulbocavernosus
None
None
Anal
None
None
Anal
None
None
S4 S5 C1
REFLEX TESTED Biceps
SENSORY DISTRIBUTION
MOTOR DISTRIBUTION
Lower lumbar pain that is made worse by ambulation can result from peripheral vascular disease. Parasagittal brain tumors and thoracic root lesions can also cause back pain. Neurofibromata can cause lover lumbar pain because of the compression of a nerve root. Thoracic nerve root lesions are usually worse at night while the patient is reclining and are
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improved when the patient is in the standing position. A patient can also present with an S1, tibial nerve entrapment in the tarsal tunnel, behind the medial ankle malleolus, which can present as lumbosacral pain.
LABORATORY FINDING Laboratory examinations are usually of little help in the diagnosis of back pain. An erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) test and a complete blood count (CBC) may be helpful, along with a rheumatoid factor analysis, in differentiating the cause of back pain. Any female patient with lower lumbar pain should have a urinalysis and a pregnancy test performed if she is in her childbearing years.
RADIOGRAPHS Any patient with a history of trauma, especially to the cervical spine, should undergo radiographs of the spine. If a compression fracture is suspected, radiography should be performed. Without a history of trauma, in most cases, radiographs of the spine are of little help in the diagnosis of acute back pain. Magnetic resonance imaging (MRI), computed tomography (CT), and myelography can be used to determine whether a fracture or HNP is present. Electromyography and nerve conduction velocity are used to evaluate degrees of progressive motor impairment or to determine the level of neural compromise. Cervical spinal evoked potential can be used to determine cervical spinal myelopathies and thoracic outlet syndromes.
TREATMENT The majority of cervical, thoracic, and lumbar pain can be treated with nonsteroidal, anti-inflammatory drugs and pain medications (e.g., indomethacin, naproxen, ibuprofen) on an outpatient basis. Early bed rest with ice and heat applied to the affected area for 24–72 hours is the key to early recovery. Physical therapy is essential for recovery from injuries sustained at work. All patients should receive follow-up in 72 hours to evaluate whether the pain is decreasing and to determine whether further testing is required.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Acute Knee Pain HOWELL J. SMITH III
ICD Codes: Osteoarthritis 715.9, Meniscal tear 836.2, Anterior horn meniscus 836.1, Posterior horn meniscus 836.1, Knee collateral lateral 717.81, Knee collateral medical 717.82, Knee cruciate anterior 717.83, Knee cruciate posterior 717.84, Gout 274.9, Rheumatoid arthritis 710.0, Tibia fracture (closed) 823.80, Tibia fracture (open) 823.92, Fibular fracture (closed) 823.81, Fibular fracture (open) 823.92, Femur fracture (closed) 821.0, Femur fracture (open) 820.11
Key Points The most common diagnoses for adult acute knee pain are osteoarthritis (34%), meniscal injury (9%), ligamentous injury (collateral [7%] and cruciate [4%]), gout (2%), fracture (1.2%), rheumatoid arthritis (0.5%), infectious arthritis (0.3%), and pseudogout (0.2%). ! Emergency Actions ! The neurovascular status should be evaluated first for patients with any extremity traumatic injury. Any neurovascular deficiency is a true medical/surgical emergency.
DEFINITION The knee is the largest articulating joint in the body. It involves three bones: the distal femur, the proximal tibia, and the patella. There are four ligaments involved: the anterior and posterior cruciate ligaments and the medial and lateral collateral ligaments. Additionally, the knee has the medial and lateral menisci.
EPIDEMIOLOGY Knee pain is one of the most common musculoskeletal reasons patients seek medical care. In 2000, more than 12.5 million persons presented for care of knee pain, making knee pain the fifth overall reason for doctor
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visits. The differential causes for knee pain are numerous, including referred pain from the hip or ankle, chronic causes with acute exacerbations, trauma, and inflammatory processes. The most common diagnoses for adult acute knee pain are osteoarthritis (34%), meniscal injury (9%), ligamentous injury (collateral [7%] and cruciate [4%]), gout (2%), fracture (1.2%), rheumatoid arthritis (0.5%), infectious arthritis (0.3%), and pseudogout (0.2%). The remaining causes include sprains and strains. Most acute injuries to the knee occur during sporting, motor vehicle, or occupational accidents. More than 3 million Americans sustain knee injuries annually, and knee trauma is the second leading cause of occupational accidents. The causes for knee pain in children differ from those of adults. Growth plate injuries (Salter-Harris fractures) of the femur, tibia, and fibula are more common than ligamentous fractures in skeletally immature children.
PHYSICAL EXAMINATION The examination of the knee is composed of several components. A detailed medical history and, in the case of trauma, a careful detailed description of the mechanism of injury followed by a meticulous physical examination to include specific knee tests are helpful in formulating a diagnosis and effective treatment plan for the patient. Additionally, as indicated, serum laboratory and imaging studies and arthrocentesis can be performed to give the clinician additional insight that will lead to a presumptive diagnosis. The acutely injured knee should be examined as soon as possible after injury because edema, point tenderness, and discoloration are initially localized over the injured structures. For ambulatory patients, the examination begins by assessing gait. The patient should be dressed to allow full exposure of both lower extremities from the feet to the upper thighs. Both lower extremities should be inspected for symmetry (e.g., quadriceps atrophy or knee effusion), skin should be examined for irregularity (e.g., erythema, ecchymosis, abrasions, wounds), and range of motion should be assessed. The examiner should carefully palpate the bony structures, joint lines, muscles, ligaments, tendons, bursae, and popliteal area, noting areas of tenderness or edema. Generally, range of motion and other specialized tests are performed on the uninjured knee first. Since many of the knee’s contours disappear when the knee is fully extended, more accurate diagnosis can be obtained when the knee is palpated in a flexed position. The patient should sit on the examination with the examiner sitting on a stool, facing the patient. The extensor mechanism should be palpated, proceeding from proximal to distal and including the quadriceps tendon, patella, patellar tendon, and tibia tubercle. The examiner should then proceed to the femoral
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condyles and should palpate the prepatellar and pes anserine bursae. The medial and lateral joint lines should be palpated for defects and tenderness, and the medial and lateral collateral ligaments and the tibial plateaus should also be palpated. The posterior area of the knee should be palpated for the pulse of the popliteal artery. Since it is well protected, injury is rare; however, suspicion of injury to popliteal artery is an emergency that requires immediate orthopedic and/or vascular consultation because damage must be repaired within hours to avoid potential amputation. A thorough neurovascular examination is essential. The popliteal nerve and vessels can be injured with posterior knee dislocation or with a femoral supracondylar fracture. Peroneal nerve injury can occur with lateral knee traumatic injuries. The bulge and patella ballottement tests are commonly used to detect for the presence of an effusion. Both tests are performed with the patient in the supine position with the knee extended and relaxed. The bulge test is performed by the clinician massaging or “milking” the suprapatellar pouch distally, with the examiner looking for a bulge at the medial sulcus. The examiner performs the patella ballottement test by applying downward pressure to the patella, compressing it against the femoral condyle. If an effusion is present, the examiner will appreciate a click. Range of motion is measured with the patient lying supine. The patient should be instructed to raise the entire lower extremity, with the knee fully extended, off the table. The patient is then instructed to flex the knee as far as possible (trying to touch the posterior thigh with the heel of the foot). The patient is then instructed to fully extend the knee. Normal knee range of motion is 0 degrees of extension to 135 degrees of flexion. A multitude of different manual specialized tests have been described to assess for cartilaginous tears and ligamentous injury to the knee. Due to the wide variation of ligamentous laxity among individuals, the uninjured knee should be examined first to establish a baseline. The McMurray test is used to detect tears in either the medial or lateral meniscus. The patient is placed in the supine position, and the knee is passively flexed. To test the medial meniscus, the leg is internally rotated by grasping the ankle with one hand and applying a slight valgus stress to the knee with the other, then slowly bringing the knee to full extension. To test the lateral meniscus, the leg is externally rotated and varus stress is applied. If the clinician appreciates a palpable or audible click at the joint line when the knee approaches full extension, suspicion for meniscus tear is raised. The valgus stress test is performed to assess the integrity of the medial collateral ligament. The patient is examined in the supine or sitting position with the examiner supporting the lower extremity to facilitate complete relaxation of the quadriceps and hamstring muscles. The examiner places one hand on the lateral aspect of the knee and the other hand on the medial ankle. Valgus stress is applied as the examiner pushes medially
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against the knee and pulls laterally at the ankle. The test is then repeated with the knee flexed at 30 degrees. Laxity or significant subjective pain along the medial joint line indicates injury to the medial collateral ligament. Medial collateral ligament injury is more common. The varus stress test is performed in either the supine or sitting position described previously for the valgus stress test. The examiner places a hand on the medical aspect of the patient’s knee and the other hand on the patient’s lateral ankle. Varus stress is applied as the examiner pushes laterally on the knee and medially at the ankle. Tests are performed with the knee at 0 and 30 degrees of flexion. Laxity or significant subjective pain along the lateral joint line indicates lateral collateral injury. The integrity of the anterior cruciate ligament is best assessed by Lachman’s test. The patient is placed in the supine position and the examiner stands next to the injured knee. The examiner then stabilizes the distal femur just above the knee with one hand (which prevents movement and hamstring relaxation) and passively flexes the knee to 15 degrees with slight external rotation. The tibia is then grasped with the other hand just below the knee, and a downward motion is applied to the femur while an upward motion is applied to the tibia. If the anterior cruciate ligament is intact, the degree of tibial translation in relationship to the femur should be equal to that of the uninjured knee. A positive result is when the tibia translates anteriorly (more than 5 mm) on the femur, without a discrete end point. Anterior cruciate ligament injury is relatively common and can occur from a variety of mechanisms. The integrity of the posterior cruciate ligament is assessed by pushing the tibia posteriorly. Posterior movement of the tibia is suggestive of a posterior cruciate ligament tear. Injury to the posterior cruciate ligament is indicative of major injury. Acute atraumatic knee pain can be the result of several etiologies, including septic arthritis, gout, pseudogout, or acute exacerbation of chronic conditions, including degenerative joint disease and rheumatoid arthritis. The knee is the most common site for benign and malignant tumors than any other joint.
RADIOGRAPHS Plain radiographic anteroposterior and lateral views are commonly used to assess for fractures, avulsions, and dislocation of the patella, femoral condyles, tibial tuberosity, and tibial plateau. The Ottawa rules criteria have been suggested to determine when radiography should be performed for patients with acute knee pain after trauma. The criteria dictate that radiographs should be obtained for patients older than 55 years who have clinical tenderness at the head of the fibula or isolated tenderness of the patella; patients unable to flex the knee to 90 degrees; and patients who are unable to bear weight on the extremity for at least four steps.
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An MRI evaluation is not commonly part of the ED workup. MRI is helpful to evaluate the menisci, ligamentous structures, and chondral surfaces; however, many orthopedic surgeons forgo MRI and proceed with knee arthroscopy to further assess internal knee integrity. Arteriography should be performed rapidly if there is a suspicion of injury to the popliteal artery, which may, for example, occur with posterior knee dislocation.
LABORATORY FINDINGS Synovial Fluid Analysis and Serum Laboratory Tests When an effusion is present, knee arthrocentesis is often performed to aid in diagnosis of joint aspirate for blood, crystals, or bacteria. The presence of blood indicates ligamentous or meniscal injury. Fat globules are pathognomonic for fracture. Cloudy or purulent synovial fluid samples should be sent for Gram stain, culture and sensitivity, and analysis of fungi, crystals, glucose, and protein. A silver stain can be performed to assess for Lyme arthritis. Knee sepsis accounts for 50% of all reported cases of septic arthritis. More than 20,000 cases of suppurative arthritis are reported in the United States annually. In young, sexually active adults, Neisseria gonorrhoeae is the most frequent pathogen; otherwise, Staphylococcus aureus is the cause of the vast majority of cases. Serum blood analysis for CBC, ESR, CRP, rheumatoid factor, and uric acid can also aid in diagnosis. An elevated white blood cell count and ESR in a patient with fever, warmth, swelling, and erythema over the knee joint also suggest an infectious process.
TREATMENT The key to successful ED or acute care evaluation of the knee is identification and immediate referral to a facility appropriate for the treatment of injuries with suspected or known neurovascular compromise (including posterior knee dislocation and compartment syndrome), open fractures or penetrating injury into the knee joint, and septic arthritis where urgent surgical intervention is generally indicated. Early referral to an orthopedic specialist for fractures, quadriceps and patellar tendon ruptures, first-time patellar dislocation, and obvious ligamentous injuries (i.e., unstable knee) is essential to reduce morbidity. In addition to prescribing analgesic medication (generally acetaminophen or one of the nonsteroidal anti-inflammatory agents), all knee injuries should be afforded the benefit of the RICE therapy while the patient
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awaits orthopedic evaluation or as treatment for simple strains or sprains. RICE therapy is defined as follows:
R: Rest crutch ambulation (with or without weight bearing) I: Ice (ice application 20 min/hr during the first 72 hours) C: Compression (if indicated with knee immobilizer, brace, or splint) E: Elevation of the knee above the level of the heart.
Bibliography Brusch J: Septic arthritis. eMedicine Available at: http://www.emedicine.com/med/ topic3394.htm. Accessed on November 25, 2005. Fletcher K: Ten most common health complaints. Available at: http://www.forbes.com/ execpicks/2003/07/15/cx_kf_0715health.html. Accessed on August 9, 2005. Jackson J, O’Malley G, Kroenke K: Evaluation of acute knee pain in primary care, Ann Intern Med 2003;139:575–583. Johnson M: Acute knee evaluation: A systemic approach to diagnosis, Available at: http:// www.aafp.org/afp/20000415/2391.html. Accessed on July 29, 2005. Levy D: Knee injury, soft tissue. eMedicine Available at: http://www.emedicine.com/ EMERG/topic288.htm. Accessed on November 25, 2005. Mosier R: Primary Care for Physician Assistants. McGraw-Hill: New York, 1998, pp 391–395.
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Acute Ankle Injuries BARBARA A.CARR
ICD Codes: Ankle fracture malleolus closed 824.8, Bimalleolar 824.4, Open ankle fracture 825.21 and 825.31, Trimalleolar fracture 824.6, Achilles tendon sprain, Ankle sprain deltoid 845.01, Talofibular ankle sprain 845.09
Key Points Every patient with an acute ankle injury should undergo assessment for deformity, swelling and pain, and a check of neurovascular status. Treatment of uncomplicated sprains and strains involves ‘‘RICE’’ therapy (i.e., rest, ice, compression, elevation), crutches, and pain control. Outpatient orthopedic referral for moderate sprains, strains, and simple nondisplaced fractures is appropriate. An orthopedic consultation in the ED is necessary in the treatment of dislocations and displaced or complicated fractures.When in doubt, get an x-ray! ! Emergency Actions ! Immediate evaluation of neurovascular status should be performed in any ankle dislocation or open fracture, and immediate reduction should be undertaken for any neurovascular compromise.
DEFINITION Ankle injuries comprise sprains, strains, dislocations, and fractures and usually occur from inversion or eversion injuries, external forces, or direct trauma. Sports-related injuries occur most frequently, but ankle injuries are also seen in falls, industrial accidents, and automobile accidents.
ANATOMY The ankle joint is a hinge joint that consists of three bones: the talus, the tibia, and the fibula. The talus forms the supporting body for the tibia and fibula, with the talus being wider anteriorly than posteriorly. The stability of the ankle depends on the bony and ligamentous integrity of these articulations. The calcaneus is also important to the motion and stability of the ankle.
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There are three groups of ligaments that connect the bony structures of the ankle. The medial side of the ankle is supported by the deltoid ligament, also known as the medial collateral ligament. This ligament has both deep and superficial fibers that originate from the broad, short, and strong medial malleolus, with the superficial fibers running in a sagittal plane and inserting on the navicular and talus. The deep fibers run horizontally and insert on the medial surface of the talus. The ankle is supported laterally by the anterior talofibular, calcaneofibular, and posterior ligaments. They insert as they are named. The tibia and fibula are held together by the syndesmotic ligaments, which consist of the interosseous ligament, the anterior and posterior tibiofibular ligaments, and the inferior transverse ligament. The muscles of the ankle make up four separate compartments. The anterior compartment is involved in dorsiflexion and consists of the tibialis anterior, extensor digitorum longus, and extensor hallucis longus. The medial compartment consists of the flexor digitorum longus, tibialis posterior, and flexor hallucis longus and contributes to inversion. The posterior compartment, which is involved in plantar flexion, is composed of the soleus and gastrocnemius. The lateral compartment contains the peroneus longus and brevis muscles and contributes to eversion and plantar flexion. Blood is supplied to the ankle and foot by the iliac, femoral, and popliteal arteries. The entire foot is innervated by branches of the sciatic nerve.
CLINICAL PRESENTATION A patient with an acute ankle injury will usually present after a fall or inversion/eversion injury. The patient will often report swelling, painful ambulation (or lack of ambulation), ecchymosis, or gross deformity. A complete history should include a timeline and mechanism of injury and whether or not the patient was able to bear weight immediately.
EXAMINATION The entire leg should be uncovered before the examination so that the joints above and below the injury (i.e., knee and foot) can be visualized and examined. The ankle should be examined for gross deformity, edema, and ecchymosis. The proximal fibular head and entire shaft of the fibula should be palpated for tenderness. The bony landmarks of the ankle and fifth metatarsal head should also be palpated. The ankle should be guided through gentle passive and active range of motion to assess for ligamentous stability and to determine which positions cause and alleviate discomfort. Anterior and posterior drawer testing should also be done.
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A neurological and vascular examination should always be documented during the examination of any extremity. The dorsalis pedis and posterior tibialis pulses should be evaluated, along with two-point discrimination. Weight-bearing ability should also be documented.
LABORATORY FINDINGS There are no specific laboratory tests required in the diagnosis of ankle injuries. However, patients receiving anticoagulant therapy should have their prothrombin time and international normalized ratio (INR) checked if excessive bleeding into the joint or injury site is suspected.
DIAGNOSIS Ankle Sprains The most common type of ankle sprain is a result of laxity of the anterior talofibular ligament. Laxity is assessed using the anterior drawer test, which is performed with the patient seated comfortably and with the knee in 90 degrees of flexion and the ankle in neutral position (i.e., 10 degrees of plantar flexion). The examiner then pulls on the heel with one hand and pushes the leg posteriorly with the other. The test result is positive when the talus displaces anteriorly, a “clunk” is heard, or an anteromedial sulcus over the joint is induced. Stress testing should always be done on the uninjured side for comparison. The talar tilt test evaluates both the anterior talofibular and calcaneofibular (medial collateral) ligaments. It is performed by inverting the heel with the knee in 90 degrees of flexion and the ankle in neutral position. Increased laxity compared with the uninjured side suggests partial or complete ligamentous tear. Distal tibiofibular syndesmotic ligamentous injury is assessed with the external rotation stress test. With the knee held in 90 degrees of flexion and the ankle in neutral position, the foot is rotated externally. Pain at the syndesmosis or the sensation of lateral talar motion suggests a partial or complete tear. This injury usually occurs as a result of hyperdorsiflexion and eversion, and patients may prefer to ambulate on their toes. There is often tenderness over the anterior and posterior ligaments, with some tenderness over the medial malleolus resulting from an associated medial collateral ligament injury. Ankle sprains are classified as grade I, II, or III. A grade I injury involves stretching or microscopic tearing of a ligament, causing local tenderness and minimal swelling. Weight bearing is usually possible, and x-ray findings are normal. A grade II sprain involves a partial tear of the ligament with moderate joint instability, often accompanied by significant localized swelling and pain. In a grade III injury, the ligament
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is completely ruptured. The patient will not be able to bear weight, and there is often an obvious deformity. Plain radiographs may show an abnormal relationship of the talus to the mortise. Grade I and II sprains are treated with RICE therapy and the optional use of crutches for a few days. Analgesics are often needed for shortterm use. Rarely, in severe grade II or III injuries, plaster splinting or casting for up to 3 weeks may be necessary, along with RICE. Follow-up with the patient’s primary care physician is necessary within the first 2 weeks after a minor sprain, whereas a severe sprain may require referral to an outpatient orthopedic specialist.
Tendon Injuries The most common ankle tendon injuries are Achilles tendon rupture and peroneal tendon dissociation or tear. An Achilles tendon rupture usually occurs in middle-aged patients during sporadic or weekend involvement in recreational sports (i.e., “weekend warriors”). This injury is frequently misdiagnosed. Rupture occurs from direct trauma or indirectly transmitted forces, including sudden unexpected dorsiflexion, forced dorsiflexion of a plantar flexed foot, or push-off of the foot with simultaneous knee extension and calf contraction. Factors that predispose patients to Achilles tendon injury include rheumatoid arthritis, gout, hyperparathyroidism, and fluoroquinolone antibiotic therapy. Patients often describe a sudden onset of pain with a loud “pop.” With complete ruptures the pain often subsides immediately after the injury, but weakness in plantar flexion persists. On examination, a visible and palpable tendon defect is usually present. Rupture can also be assessed using the Thompson test, which is performed with the patient prone and the knee flexed to 90 degrees. Squeezing the calf muscles should produce passive plantar flexion of the foot. Absence or weakened response compared with the uninjured side is suggestive of rupture of the tendon. Radiographic evaluation of Achilles tendon injuries can include plain radiographs, which may show evidence of opacification of the fatty space anterior to the tendon, known as Kager’s triangle. MRI or ultrasonography can also be used for evaluation. Treatment of Achilles tendon rupture is controversial. Emergency orthopedic referral is recommended, and the ankle should be splinted. The peroneal tendons are the primary everters and pronators of the foot and are also involved in plantar flexion. Both tendons travel posterior and inferior to the lateral malleolus; the peroneus brevis tendon inserts on the head of the fifth metatarsal, whereas the peroneus longus tendon inserts on the medial cuneiform and base of the first metatarsal. Peroneal tendon rupture can occur with forced dorsiflexion and reflex contraction of the peroneal muscles.
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The patient with a peroneal tendon dislocation reports sudden lateral ankle or foot pain with a snapping sensation. As with Achilles tendon ruptures, the pain often subsides while weakness on eversion persists. Tenderness and swelling will be present posterior to the lateral malleolus, and the dislocated tendons may be palpable in this area. Diagnosis is confirmed if the patient is unable to evert the foot while it is held in dorsiflexion. Plain radiographs may reveal an avulsion fracture of the distal fibula or head of the fifth metatarsal. CT scans or MRI may be helpful if the diagnosis is uncertain. Untreated cases of peroneal tendon rupture rarely resolve spontaneously. Orthopedic referral is necessary, and treatment involves either surgical or nonoperative repair with immobilization.
Ankle Fractures Fractures are caused by forces sufficient to overcome the structural strength of a bone. Ligament rupture can cause chip avulsion fractures where the ligament was attached to bone. Most malleolar fractures are transverse fractures or small avulsion fractures just below the joint line. If the talus shifts during injury, it can strike the opposite malleolus and can cause an oblique fracture, often on the side of the bone that was subjected to the compression force. The management of any acute ankle fracture involves identification, assessment of stability, and reduction with immobilization. The injured ankle should be elevated and iced promptly to minimize swelling and tissue damage. Appropriate analgesia and sedation should be used during fracture reduction, with close monitoring of vital signs if conscious sedation is used. Malleolar fractures account for 30% of all ankle fractures. Medial malleolar fractures typically occur from eversion or external rotation. Tension is exerted on the deltoid ligament, causing an avulsion of the tip of the malleolus or a rupture of the ligament. Medial malleolar fractures are often seen in association with lateral or posterior malleolar disruption. When a medial malleolar fracture is identified on a radiograph, careful evaluation and examination of the fibula (including the fibular head) should be performed to exclude fracture of the proximal fibula. Nondisplaced, isolated medial malleolar fractures can be treated with casting, avoidance of weight bearing, and referral to an orthopedic specialist. Lateral malleolar fractures are the most common ankle fracture. They are classified using the Danis-Weber system, which relates the fracture’s location to the tibiotalar joint. Fractures below this joint rarely disrupt other bony or ligamentous structures, are generally more stable, and can be immobilized and referred to orthopedics for outpatient management. The management of uncomplicated, isolated lateral malleolar fractures
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involves casting and avoidance of weight bearing. Associated fractures of the medial or posterior malleolus and fractures proximal to the tibiotalar joint line require orthopedic consultation in the ED. Posterior malleolar fractures are rarely isolated and are often associated with proximal fibular fractures and medial/lateral collateral ligament sprains. These fractures warrant orthopedic consultation in the ED. Significant fractures often require surgical repair. Bimalleolar and trimalleolar fractures are often caused by adduction or abduction injuries. They are considered to be unstable and require immediate orthopedic consultation. Bimalleolar fractures may be managed with external reduction and immobilization, whereas trimalleolar fractures are often managed with internal reduction. Open ankle fractures can occur with multiple trauma and require immediate surgical consultation. Neurovascular status of the affected extremity must be documented and an attempt must be made to reduce any gross deformity before immobilization. Tetanus status should be updated, and the patient should receive intravenous antibiotics for presumed contamination of the wound. Open fractures require early surgical debridement and irrigation.
Ankle Dislocations The ankle joint can bear five times the body’s weight during ambulation. In active dorsiflexion, the foot and the fibula rotate externally on the oblique outer articular surface of the talus. During weight bearing, the fibula descends and provides stability to the ankle mortise. Dislocation of the talus involves displacement of the talus from the mortise and often occurs in association with a fracture of a component of the mortise. Dislocations are often the result of significant trauma, including falls, motor vehicle accidents, or high-contact sports. Ankle dislocations are described according to the direction of displacement of the talus and foot in relation to the tibia. Medial dislocation is the most common. All ankle dislocations should be immediately reduced after radiographs are taken, unless there is vascular or neurological compromise. Reduction of a dislocation involves flexion of the knee to 90 degrees and downward traction on the foot while force is applied in the direction opposite the injury. After reduction, the neurovascular status is again examined and the ankle is splinted.
RADIOGRAPHS The minimum radiographs for any ankle injury are an anteroposterior view with the ankle in 5–15 degrees of adduction, a true lateral view that
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includes the base of the fifth metatarsal and an internal oblique view at a 45-degree angle. The radiograph taken from an anteroposterior view identifies fractures of the malleoli, distal tibia or fibula, talar dome body and lateral process of the talus, and calcaneus. The lateral view identifies fractures of the anterior and posterior tibial margins, talar neck, posterior talar process, and calcaneus, as well as any anterior or posterior displacement of the talus. The lateral view is also helpful in identifying an ankle effusion, which appears as a teardrop-shaped density displacing the normal fat adjacent to the anterior or posterior margin of the joint capsule. The presence of an effusion suggests the possibility of subtle intra-articular injuries. The mortise view, or internal oblique view, is taken with the ankle in 15–20 degrees of internal rotation. It is necessary for viewing the congruity of the articular surface between the dome of the talus and the mortise (which is formed by the medial and lateral malleolus and the distal, horizontal surface of the tibia). The lines formed between the articular surfaces should be parallel throughout the tibiotalar and talofibular components of the joint. Recently, the Ottawa ankle rules (OAR) were developed to assist healthcare practitioners in deciding whether an ankle injury necessitates ankle or foot radiographs. The OAR state that an ankle radiographic series is required if there is pain in the malleolar region and any of the following findings: 1. Bony tenderness occurs over the posterior edge or tip of the medial or lateral malleolus. 2. The patient is unable to bear weight for at least four steps both immediately after the injury and at the time of initial evaluation. Subtle ankle fractures, syndesmotic injuries, or osteochondral fractures can be missed in an evaluation of plain radiographs. When a patient has plain radiographs that appear to be negative for obvious injury, yet he or she continues to have unexplainable symptoms, other radiographic studies should be considered such as radionuclide bone scanning, CT scan, or MRI. Orthopedic consultation can also be considered for possible arthroscopy of the ankle.
TREATMENT Treatments for specific injuries are discussed previously. Ankle injuries may take weeks to months to completely resolve. Severe swelling or prolonged deformity may contribute to neurological sequelae or compartment syndrome, and failure to perform necessary rehabilitative exercises after an acute injury may result in chronic pain and stiffness.
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Bibliography Arnheim DD, Prentice WE: Arnheim’s Principles of Athletic Training, ed 11. McGrawHill: New York, 2002. Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Rivers CS, Dorfman T: Preparing for the Written Board Exam in Emergency Medicine, ed 4. Emergency Medicine Educational Enterprises: Milford, OH, 2003. Skinner HB: Current Diagnosis and Treatment in Orthopedics, ed 3. McGraw-Hill: New York, 2003. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2003.
Acute Compartment Syndrome DAVID ZINSMEISTER
ICD Codes: Compartment syndrome 958.8
Key Points The majority of cases of acute compartment syndrome are caused by fractures. Acute compartment syndrome results in increased pressure that prevents perfusion within a fascial compartment. Pain, paresthesias, and paralysis are the signs of compartment syndrome. Delay in diagnosis and treatment results in tissue necrosis and Volkmann’s ischemic contracture.Treatment is immediate fasciotomy. ! Emergency Actions ! Immediate surgical consultation is appropriate when a compartment syndrome is suspected.
DEFINITION Acute compartment syndrome is a potentially devastating complication of injury to the extremities. Raised pressure within a closed fascial space reduces capillary perfusion below the level needed for tissue viability. The intracompartmental tissue pressure becomes elevated and produces a secondary elevation in venous pressure that obstructs venous outflow,
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thus resulting in an escalating cycle of continued pressure within the fascial compartment. If left untreated, necrosis of muscle and nerves can occur within a short period of time. Early diagnosis is paramount if severe, permanent disability is to be prevented.
EPIDEMIOLOGY Acute compartment syndrome can result from internal expanding forces or external compressive forces. Common causes due to internal expanding force are fractures, crush injuries, snake bites, extravasation of intravenous fluids, rhabdomyolysis, and hemorrhage within a compartment. External compressive force can result from tightly applied cast and splints, burn eschars, military antishock trousers, and sequential compression devices. The anterior compartment of the leg and flexor compartments of the forearm are most commonly affected. The compartments of the hand, foot, arm, thigh, shoulder, buttocks, and back can also be involved. Any muscle enclosed in fascia is subject to acute compartment syndrome. The initial injury results in swelling in the compartment that leads to local hydrostatic and osmotic pressure increases. Once the hydrostatic pressure exceeds a specific level, compression of the thin-walled venules occurs, resulting in hypertension at the venous end of the capillary beds that eventually causes arteriole compression. The cell wall membranes are then disrupted, leading to cytolysis and release of osmotically active cellular components that draw additional fluid into the compartment. The net effect is a vicious cycle of increasing pressure that compromises circulation. Ischemia of the muscles and nerve tissue then ensues, resulting in muscle infarction and permanent nerve damage. If the area of muscle infarction is significant, loss of the limb, myoglobinuria, renal failure, and death can occur.
CLINICAL PRESENTATION Patients will typically present with a fracture (approximately 45% of all cases of compartment syndrome involve fracture of the tibia). The symptoms are usually rapid in onset. Extremity pain is often the chief symptom, and the degree of pain experienced may appear to be out of proportion to the injury sustained. Paresthesias are commonly present in the extremity and in the distribution of the affected nerve distal to the involved compartment. The patient will be unable to actively move the muscles within the compartment involved. The problem arises in unconscious, traumatized patients who are unable to relate the classic symptoms of pain, paresthesias, and paralysis. The clinician must have a high index of suspicion in patients who are unable to communicate about their extremity fractures and crush injuries.
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EXAMINATION The most important clinical finding is severe pain on stretching of muscles in the involved compartment. Full, passive extension of the fingers and plantar flexion of the toes will stretch the muscles of the flexor compartment of the forearm and anterior compartment of the leg (most commonly involved in compartment syndrome) and elicit extreme pain. An inability to actively move the muscles indicates that paralysis is present and is often a late finding. Even though active contraction and passive stretching of muscles around a fracture is painful, it is usually tolerable. If not, the patient may have compartment syndrome. Sensory changes are a sensitive, reliable sign that compartment syndrome is present, and loss of two-point discrimination is often an early finding. The distribution of the sensory changes is also helpful in identifying the compartment(s) involved. The skin overlying the involved compartment may be erythematous and shiny with excessive sweating in the affected area. Upon palpation, the compartment is tender, tense, and swollen, a condition that is often described as having a “woody” feeling. Pulselessness and pallor indicates arterial trauma—not compartment syndrome—although the two may coexist. Pulses are typically normal in compartment syndrome because the intracompartmental pressure required to halt capillary perfusion rarely exceeds systolic blood pressure. Capillary refill time is also normal.
LABORATORY FINDINGS There is no specific laboratory test of use in diagnosing compartment syndrome. The following tests, however, are useful to determine the presence of muscle damage and its sequela: 1. Serum myoglobin and creatine kinase analysis: These assess muscle necrosis and possible rhabdomyolysis. 2. Potassium measurement: Level is elevated in rhabdomyolysis; severe hyperkalemia may result in arrhythmia. 3. Blood urea nitrogen and creatinine analysis: Elevation occurs in renal failure due to myoglobinuria. 4. CBC and coagulation studies: Anemia worsens muscle ischemia; the clinician should evaluate for disseminated intravascular coagulopathy. 5. Urinalysis: The presence or absence of myoglobin and creatine kinase in the urine should be determined. A urine dip positive for blood without the presence of erythrocytes on microscopic examination indicates myoglobin in the urine.
RADIOGRAPHS Radiographs are obtained to establish the presence of a fracture. There are no specific imaging studies to confirm or exclude compartment syndrome.
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DIAGNOSIS Acute compartment syndrome is a clinical diagnosis based on the signs and symptoms previously described. Compartment pressure measurements are adjunctive, and the only situations in which the diagnosis is established based solely on compartment pressure measurements are a patient with a head injury or an unconscious patient. The two most commonly used devices used to measure compartment pressure are the Whitesides apparatus and the STIC device. The Whitesides apparatus is made of items readily available in most EDs, and the STIC pressure monitor is manufactured by Stryker. The ideal zone for measuring compartment pressure is at the level of the fracture (if present) and within the area 5 cm proximal and distal to the fracture. Compartment pressure significantly decreases beyond this zone, even in the presence of compartment syndrome. Two methods are used to determine compartment pressure. The first involves the absolute pressure, which is established simply by measuring the pressure within the compartment(s). Second, is the delta P method, in which the highest compartment pressure is then subtracted from the mean arterial pressure to establish the differential pressure. It is well established that normal resting compartment pressure is 10 mmHg or less. There is, however, no agreed upon minimum pressure to absolutely confirm or exclude acute compartment syndrome. When using the absolute pressure method, 30 mmHg or above is commonly used to indicate decompression. If the delta P method is used, a differential pressure (i.e., the mean arterial pressure minus the highest compartment pressure) of 40 mmHg or less is commonly cited as the reference to determine that compartment syndrome is present.
TREATMENT Immediate fasciotomy is the appropriate treatment. Elevated compartment pressure for as little as 4–8 hours can result in muscle death, scarring, and shortening, which leaves the patient with clawing of the fingers and toes and little or no residual motion. The wrist and ankle develop contractures, and sensation is permanently impaired. There is no conservative treatment for acute compartment syndrome. Application of ice and elevation may seem like a good idea but actually further decreases perfusion. Considering the consequences, there is little negative risk to fasciotomy except an unsightly scar. However, failure to perform a fasciotomy can result in a lifetime disability for which late reconstructive surgery has little chance of restoring normal function.
Bibliography Blick SS, Brumback RJ, Poka A, et al: Compartment syndrome in open tibial fractures, J Bone Joint Surg Am 1986;68A:1348–1353.
600 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Hamlin C: Compartment syndrome in the upper extremity, Emerg Clin North Am 1985; 3(2):283–291. Heppenstall RB, McCombs PR, DeLaurentis DA: Vascular injuries and acute compartment syndrome. In Bucholtz RW, Heckman JD (eds): Rockwood and Green’s Fractures in Adults, ed 5. Lippincott Williams & Wilkins: Philadelphia, 2001, pp 319–352. Hoover TJ, Siefert JA: Soft tissue complications of orthopedic emergencies, Emerg Med Clin North Am 2000;18(1):115–139. Perron AD, Brady WJ, Keats TE: Orthopedic pitfalls in the ED: Acute compartment syndrome, Am J Emerg Med 2001;19:413–416. Snider RK (ed): Essentials of Musculoskeletal Care. American Academy of Orthopaedic Surgeons: Rosemont, IL, 1997, pp 9–11. Tiwari A, Haq AL, Myint F, Hamilton G: Acute compartment syndrome, Br J Surg 2002;89:397–412.
Elbow Injuries GERALD DEPOLD AND CARRY DEPOLD
CPT Codes: Olecranon 813.01, Supracondylar injury 812.41, Humerus lower end 812.49, Radius 813.81, Radius upper end 813.07, Dislocation elbow anterior (closed) 832.01, Dislocation elbow (open) 832.11, Dislocation posterior (closed) 832.02, Dislocation posterior (open) 832.12
Key Points When elbow injury is present, rapid neurovascular assessment of the elbow and extremity must occur. Immediate corrective action must be taken if neurological or vascular function is compromised. The treatment goal in the case of a dislocated or fractured elbow is the concentrically reduced elbow determined by postreduction stability with reestablishment of neurovascular status. If the ED physician cannot reduce the elbow after two attempts, an orthopedic specialist must be consulted immediately. Severe elbow injuries require substantial force; a complete examination should be performed, based on the patient’s history, to rule out any other injuries. ! Emergency Actions ! Advanced trauma life support guidelines should be followed for the initial evaluation. Distal neurovascular status of the affected limb must be assessed. Distal neurovascular compromise should be treated with rapid reduction of dislocation or fracture, as appropriate. If neurovascular status is not restored after two attempts, an immediate referral to an orthopedic specialist and an arteriogram are required.
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DEFINITION The elbow is a very stable joint. As such, severe injuries to the elbow require a significant amount of force and commonly include dislocations and fractures. Dislocations are classified as simple or complex (with associated fracture or neurovascular injury) and by the direction of the dislocation (i.e., anterior, posterior, lateral, medial, and divergent). Fractures are distal humeral, proximal radial, and proximal ulnar. Radial head fractures are the most common, classified as type I, minimal to no displacement; type II, moderate displacement; type III, complete displacement; and type IV, with associated dislocation.
EPIDEMIOLOGY The radial head is the bone most commonly fractured in the adult elbow. The elbow is the second most common joint to be dislocated, with an incidence of 13 dislocations per 100,000 persons. Posterior dislocations are the most common. Dislocations in young persons are usually a result of a fall on an outstretched hand (FOOSH).
CLINICAL PRESENTATION The clinical presentation of dislocations and fractures varies. Patients with dislocations usually present with obvious deformity and the arm splinted at 45 degrees. Fractures may or may not present with deformity or edema and must be ruled out radiographically. An appropriate history will determine mechanism of injury, hand dominance, and any distal neuropathy.
EXAMINATION First, the patient’s distal neurovascular status must be assessed and documented. The elbow should be examined for deformity and evidence of open injury. Dislocation can be confirmed by inspecting the palpable anatomy and comparing it with the uninjured side. Bony landmarks should be palpated for crepitus and grimace, and range of motion should be measured. The physician should examine the carry angle of the injured elbow (formed by the arm and forearm) and compare it with the uninjured side, checking for malalignment. The examiner should also check for compartment syndrome, which is characterized by (1) pain on passive extension of the fingers and wrist, (2) a tense, swollen, painful extremity, and (3) pain out of proportion to the injury. Lacerations must be evaluated to determine whether the joint capsule is involved. The ipsilateral wrist, forearm, and shoulder should be examined for injuries.
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The elbow extension test can be used as a sensitive clinical screening test for patients with acute injury to the elbow. Patients who can fully extend the affected elbow can be safely treated without radiography.
LABORATORY FINDINGS No specific laboratory tests are helpful in the diagnosis of fractures. If the joint is open or if the patient will undergo surgery, a CBC and measurements of partial thromboplastin time (PTT) and INR should be performed.
DIAGNOSIS All extremities and suspected fractures or dislocations should be x-rayed. Diagnosis is made clinically and radiographically.
RADIOGRAPHS Plain anteroposterior and lateral views are required initially and are sufficient for simple dislocations; three-view radiographs should be obtained as soon as possible. The clinician should pay attention to the radiocapitellar line (i.e., Monteggia’s fracture), anterior humeral line, and any anterior fat pad displacement or posterior fat pad (i.e., occult fracture) that may be present. Radial head fracture is commonly missed. A radial head–capitellar view may be required. Osteochondral injuries are likely despite the absence of radiographic findings, and, if visible, they are usually larger than they appear. CT is used before operative stabilization of complex fractures and to locate osteochondral fragments. MRI is of limited use in the acute setting.
TREATMENT Dislocations Simple dislocations can be treated with reduction in the ED. First, neurovascular status should be assessed (the median and ulnar nerves and brachial artery at a minimum). Adequate analgesia should be established, and the patient should be placed in a supine position. The clinician should avoid hyperextension or use of excessive force. The bones of the elbow should be disengaged with traction to the forearm and counter-traction to upper arm. Any lateral or medial displacement should be corrected. The elbow should be flexed with pressure on the tip of the olecranon. Successful reduction is associated with a palpable “clunk.” The practitioner should check stability through the full range of motion. Reduction that
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cannot be maintained with less than 60% of flexion is an indication for surgical consultation. Neurovascular status should be reassessed, and postreduction radiography should be performed. The arm should be splinted at 90 degrees of flexion with the forearm in pronation, and follow-up should be performed in 24 hours for a neurovascular check. Complex dislocations and dislocation that cannot be reduced require an immediate orthopedic consultation. Dislocations reduced in the ED require routine orthopedic follow-up.
Fractures Fracture treatment depends on the type. The following require orthopedic referral: transcondylar or intracondylar fractures and displaced supracondylar, condylar, capitellar, radial, and olecranon fractures. Nondisplaced supracondylar, condylar, capitellar, radial, and olecranon fractures are immobilized with plaster, with follow-up carried out by an orthopedic specialist. Patients with elbow injuries must be continually reassessed for neurovascular compromise and compartment syndrome. Any significant edema requires regular distal neurovascular monitoring. All elbow injures should be referred to an orthopedic surgeon as soon as possible.
Bibliography Brady WJ: Upper extremity fractures and dislocations, Emerg Med Rep Thomson American Health Consultants. Accessed on May 10, 2005. Available at:http://www.emronline. com/textbooks_index.html. Docherty MA: Can elbow extension be used as a test of clinically significant injury? Ann Emerg Med 2003;41(5):760. Hildebrand KA, Patterson SD, King GJ: Acute elbow dislocations: Simple and complex, Orthop Clin North Am 1999;30(1):63–79. O’Driscoll SW: Difficult elbow fractures: Pearls and pitfalls, Instr Course Lect 2003;52:113–134. Saati AZ, McKee MD: Fracture-dislocation of the elbow: Diagnosis, treatment and prognosis, Hand Clin 2004;20(4):405–414. Sheps DM, Hildebrand KA, Boorman RS: Simple dislocations of the elbow: Evaluation and treatment, Hand Clin 2004;20(4):389–404. Work Loss Data Institute. In Disorders of the Elbow, Work Loss Data Institute: Corpus Christi, TX, 2004, p 110.
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Foot Injuries JENNY E. DUNLAVY
ICD Codes: Calcaneus fracture closed 825.0, Calcaneus fracture open 825.1, Metatarsal bone fracture (closed) 825.25, Metatarsal bone fracture (open) 825.35, Toe fracture (closed) 826.00, Toe fracture (open) 827.1, Puncture wound 892.00
Key Points The foot is divided into three regions. The Chopart’s joint separates the midfoot and hindfoot, and Lisfranc’s joint separates the midfoot and forefoot. ! Emergency Actions ! Any foot trauma presenting to the ED should be evaluated for bony fractures, foreign bodies, compartment syndrome, and infection.
DEFINITION Most injuries to the foot are due to direct or twisting forces resulting in acute soft tissue injury, fracture, or dislocation. As with many musculoskeletal injuries, an adequate patient history often aids in the diagnosis. Twisting forces are usually associated with less severe avulsion-type injuries. A history consistent with an increasing inability to ambulate and worsening pain may suggest a minor sprain or an impending vascular catastrophe. History of a puncture wound also requires special attention.
ANATOMY The foot contains 28 bones and 56 articular surfaces, divided into three regions. Chopart’s joint separates the midfoot and hindfoot, and Lisfranc’s joint separates the midfoot and forefoot. The hindfoot is composed of the talus and the calcaneum. The midfoot contains the cuboid bone, three cuneiform bones, and the navicular bone. The metatarsals and phalanges make up the forefoot. Many ligaments and muscles provide support for the foot.
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PHYSICAL EXAMINATION Essential elements of the physical examination include inspection, palpation, neurovascular assessment, and active and passive range of motion. The Ottawa ankle rules (OAR), as their name implies, are used for assessment of the ankle. The OAR also include criteria for assessing whether a foot radiograph is required for a midfoot injury. The OAR state that a foot radiograph series is required if there is pain in the midfoot region and any of the following: bone tenderness present at the navicular bone, bone tenderness present at the base of the fifth metatarsal, or the inability to bear weight for at least four steps, both immediately after the injury and at the time of evaluation. The OAR have a sensitivity approaching 100% in detecting acute midfoot zone fracture but cannot be applied to the hindfoot or forefoot. Normal findings on the physical examination and the ability to complete several weight transfers essentially rule out a significant injury, and a radiograph is not necessary. As always, clinical judgment should prevail. Any abnormal findings on physical examination or trial of ambulation mandate a three-view foot series. If there is tenderness along the heel, an axial view of the calcaneus should be included. A CT scan of the foot is occasionally performed to exclude a subtle diastasis at Lisfranc’s joint from the differential diagnosis.
HINDFOOT INJURIES Rare dislocations and significant fractures of the talus merit immediate surgical consultation for surgical reduction. Fractures of the calcaneus can be caused by any axial load to the heel, such as a fall from a height. Consequently, such fractures are often associated with spinal injuries, and a complete physical examination is mandatory. Calcaneus fractures may be subtle. Thus, when a calcaneus fracture is suspected despite an unremarkable radiograph, Boehler’s angle should be measured on the lateral view of the foot. Boehler’s angle is formed by the intersection of a straight line extending along the superior cortex of the body of the os calcis with a line extending from the dome to the anterior tubercle. If the angle is less than 20 degrees, a fracture is likely. All calcaneus fractures mandate a consultation with an orthopedic specialist.
MIDFOOT INJURIES Isolated fractures of the tarsal bones are rare and usually treated conservatively. An injury to Lisfranc’s joint should be suspected, with identification of a cuboid or cuneiform fracture. Injuries to the joint are rare and often missed in the ED. A fracture of the base of the second metatarsal is often considered pathognomonic for a disruption of the ligamentous complex. This injury should be suspected when there is point tenderness
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over the midfoot or when there is laxity between the first and second metatarsals. Injuries to Lisfranc’s joint may require open reduction or percutaneous pinning. Long-term morbidity may be significant.
FOREFOOT INJURIES Injuries to the metatarsals are often crush injuries. Most nondisplaced metatarsal shaft fractures can be treated conservatively. A notable exception is a fracture of the first metatarsal shaft, which must be treated with a period of avoidance of weight bearing. Displaced fractures of any of the metatarsal shafts are problematic, requiring avoidance of weight bearing and possibly surgical fixation. Fractures of the fifth metatarsal are the most common metatarsal fractures. Nondisplaced shaft fractures can be treated conservatively, as can avulsions from the proximal pole, often referred to as “pseudo-Jones” fractures. However, a true Jones fracture, a transverse fracture through the base of the fifth metatarsal, is prone to malunion and nonunion complications. Thus, the Jones fracture is treated with a non–weight-bearing cast and close orthopedic follow-up.
Phalangeal Injuries Nondisplaced phalangeal fractures are typically treated conservatively, with “buddy taping” or a cast shoe. Dislocations and displaced fractures may be reduced in the ED by the application of manual traction followed by buddy taping.
EXAMINATION When examining any foot for injury, the healthcare provider should remember that the examination includes the leg from the knee down. The skin, pulses, and neurovascular status of each foot should be examined and any differences noted. The skin temperature and tactile sensation of each foot should be compared. Hair growth, skin changes, and difference in toenail growth between the two feet should all be noted. Often this will lead to a nontraumatic diagnosis. The practitioner should always inquire about past medical history, including a history of diabetes and smoking. Reflexes and strength of each extremity should be noted.
LABORATORY FINDINGS There are no specific laboratory examinations for foot trauma. If the patient has diabetes or a cellulitis overlays the fracture, or if an open fracture is present, a CBC, Chem 7, and ESR and CRP measurements should
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be performed. If gout is suspected, a uric acid level measurement should be obtained.
RADIOGRAPHS Radiographs should be performed for all acute foot traumas. If a bone is fractured, the radiograph should include the bones above and below the fracture because of the relationship of associated fractures secondary to twisting forces of an injury.
DIAGNOSIS Diagnosis is based on clinical examination and radiographic examination. All patients with foot fractures should be referred to a podiatrist or orthopedic surgeon within 72 hours.
TREATMENT Open Fractures An open fracture should be protected from further contamination by the application of a wet, sterile dressing. Tetanus toxoid and tetanus immunoglobulin should be administered as indicated. Initially, the antibiotic of choice is a first-generation cephalosporin, or clindamycin if the patient is allergic to penicillin. If the injury appears to be grossly contaminated, an aminoglycoside can also be added.
Puncture Wounds Puncture wounds of the foot carry the risk of retained foreign body, deep tissue infection, or osteomyelitis. Deep penetration increases the risk of damage to bone and tendons, and penetration through a rubber sole may increase the chance of infection with Pseudomonas species. A normal radiograph does not rule out the possibility of bony injury or retained foreign body. The use of prophylactic antibiotics after a puncture wound is as yet controversial and may be reserved for immunocompromised patients or those who have bone or tendon involvement. Any patient presenting with a delayed puncture wound complicated by infection warrants aggressive treatment with antibiotics, wound opening, and irrigation. The first-generation cephalosporins are generally the first line of treatment. A fluoroquinolone can be added for additional coverage of Pseudomonas. An orthopedic consultation for operative debridement is required for complicated foot infections, gunshot wounds to the foot, and many lawnmower injuries.
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Bibliography Michael J, Stiell I: Foot injuries. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide ed 6. McGraw-Hill: New York, 2004. Stiell IG, McKnight RD, Greenberg GH, et al: Implementation of the Ottawa ankle rules, JAMA 1994;271:827–832. Stiell I, Wells G, Laupacis A, et al: Multicentre trial to introduce the Ottawa ankle rules for use of radiography in acute ankle injuries, BMJ 1995;311:594–597.
Injuries to the Forearm and Wrist BRENDA OSWALD AND CARL MENCKHOFF
ICD Codes: Monteggia’s fracture 813.03, Galeazzi’s fracture 813.42, Colles’ fracture 813.41, Smith’s fracture 813.41, Barton’s fracture 813.42, Hutchinson’s fracture 813.44, Torus fracture 813.45, Scaphoid fracture 814.01, Lunate fracture 814.02, Triquetrum fracture 814.03, Pisiform fracture 814.04, Hamate fracture 814.08, Capitate fracture 814.07, Trapezoid fracture 814.06, Carpal tunnel syndrome 354.0, de Quervain’s fracture 727.04
Key Points Any patient who presents to the ED with a wrist or forearm injury should have the entire arm examined from the shoulder down. All extremity examinations should have the neurovascular status evaluated and documented. ! Emergency Actions ! Any patient with an extremity injury that involves any neurovascular deficit should be immediately referred to an orthopedic surgeon.
DEFINITION Injuries to the wrist and forearm can result from traumas due to falls, lacerations, burns, contusions, crush injuries, or overuse that leads to tendonitis or
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carpal tunnel syndrome. If function is compromised, these injuries can be devastating; therefore, treatment is geared toward restoring as much of the previous function as possible. Most fractures occur as a result of a FOOSH, and osteoporosis causes postmenopausal women to have a higher rate of forearm fractures than other adults. Infants and toddlers have no sex predilection for fractures, but after the age of 2 years, fractures are more common in boys than in girls.
ANATOMY The forearm is composed of the radius and ulna bones, which are connected by a fibrous interosseous membrane. The ulna maintains a relatively fixed position during supination and pronation, while the radius rotates around it. Because of this close association, an injury to one bone generally has a direct impact on the other. The carpal bones are aligned in proximal and distal rows. The proximal carpal row from the radial side consists of the scaphoid, lunate, triquetrum, and pisiform bones. The distal carpal row from the radial side is made up of the trapezium, trapezoid, capitate, and hamate bones. The carpal bones are held together by the interosseous, volar, and dorsal ligaments and a triangular fibrocartilage complex. The dorsal ligaments are weaker than the volar ligaments, making dorsal dislocation more common. The wrist flexor-pronator muscle group is made up of the pronator teres, flexor carpi radialis, palmaris longus, and flexor carpi ulnaris. These four muscles originate from the medial epicondyle as a common tendon, and then split as they travel down the forearm. The pronator quadratus pronates the forearm at the superior and inferior radioulnar joints. The primary forearm supinators are the biceps brachii and the supinator. The wrist extensors, which originate from the lateral epicondyle and its supracondylar line, are the brachioradialis, the extensor carpi radialis longus, and the extensor carpi radialis brevis. The forearm and wrist are innervated by the radial, median, and ulnar nerves and receive their blood supply from the radial and ulnar arteries. The radial nerve provides sensory innervation to the posterior aspect of the hand from the thumb to the radial half of the ring finger and also branches to form the posterior interosseous nerve that controls the muscles that extend the fingers and thumb. The median nerve controls finger flexion, wrist movement, and sensation on the volar aspect of the hand from the thumb to the radial half of the ring finger. The ulnar nerve provides innervation to forearm muscles and controls the intrinsic muscles of the hand. It also provides sensation to the fifth finger and the ulnar half of the ring finger.
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EXAMINATION A thorough history and physical examination helps to elicit information regarding how the injury occurred, which will guide the clinician to the appropriate examination and treatment. It is important to note any previous physical injuries or limitations, to assess whether the patient is rightor left-handed, and to evaluate the joint above and below the area of pain. The physical examination includes palpation of the bones, muscles, ligaments, and radial and ulnar pulses. The forearm should be tested for range of motion with supination and pronation. The wrist should be examined for strength and the ability to flex, extend, and deviate in the radial and ulnar directions. Motor function maneuvers include having the patient make an “OK” sign to test the median nerve, extending the fingers or wrist against resistance to test the radial nerve, and separating the fingers against resistance to test the ulnar nerve. Two-point discrimination is the gold standard for sensory integrity. Tenderness of the anatomical “snuff box” may indicate a scaphoid fracture. Phalen’s maneuver or Tinel’s sign may indicate carpal tunnel syndrome.
CLINICAL PRESENTATION A detailed history, including the position of the limb during the injury, can aid in the diagnosis and appropriate treatment. Traumatic injuries from axial loading with the forearm in supination produces both radial and ulnar fractures, loading in a neutral position results in isolated radial head fractures, and loading in pronation causes radial head fractures with severe tearing of the interosseous membrane. The severity of the radial head injury is related to the percentage of contact within the radiocapitellar joint. The most commonly injured carpal bones are the scaphoid, triquetrum, and lunate. Falls with direct impact on the thenar eminence are more likely to cause injury to the scaphoid, and those on the hypothenar eminence are more likely to cause injury to the triquetrum and pisiform. Anteroposterior and lateral radiographic views of the wrist, forearm, and elbow are required to assess fractures. Immediate reduction of a fracture is necessary when there is vascular compromise, or tenting of the skin. Several anesthesia options exist to reduce fractures in the ED. Axillary blocks provide complete anesthesia and muscle relaxation, but they carry a risk of arterial or nerve damage. Hematoma blocks provide anesthesia and muscle relaxation but carry a risk of osteomyelitis. Intravenous regional anesthesia (Bier block) provides anesthesia and muscle relaxation but may cause lidocaine toxicity. Conscious sedation provides effective anesthesia, muscle relaxation, and amnesia, but it should only be
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performed on patients who are otherwise healthy or have only mild or moderate systemic disease that does not interfere with daily routines. Treatment for minor fractures is generally splinting, rest, elevation, and analgesia. An orthopedic specialist should be consulted for open fractures, operative fractures, and some dislocations.
Forearm Fractures The treatment of most fractures to the forearm requires an orthopedist. The exceptions are a nondisplaced ulnar shaft fracture with less than 10 degrees of angulation (i.e., nightstick fracture), which can be treated with a posterior long-arm splint, and a nondisplaced radial head fracture, which can be treated with a sling and early mobilization. Monteggia’s fracture is defined as a fracture of the proximal one third of the ulna with dislocation of the radial head. It frequently results from a fall on an outstretched hand in forced pronation. The radial head may be palpable in the anterolateral or posterolateral location, and the forearm may appear shortened and angulated. The radiocapitellar line is a line drawn down the center of the radius that should intersect the middle of the capitellum regardless of elbow flexion or extension. Malalignment of this line on an anteroposterior or lateral elbow radiograph indicates radial head displacement. Treatment is immobilization with a long-arm splint, with the elbow flexed at 90 degrees and the forearm in neutral position for children. Adults may require orthopedic consultation and open reduction internal fixation (ORIF). Complications include nonunion, redislocation, infection, compartment syndrome, and injury of the posterior interosseous nerve, which causes weakness or paralysis with extension of the fingers or thumb. Galeazzi’s fracture is defined as a fracture of the distal one third of the radius with dislocation of the distal radioulnar joint. It is a reverse Monteggia’s fracture and is three times more common. The radial fracture is generally obvious on radiograph, but the associated ulnar dislocation is best seen on lateral view. Studies have shown that 90% of patients treated with just immobilization in a long-arm splint had poor outcomes; therefore, the best treatment is referral to an orthopedic specialist and ORIF. If the fracture dislocation is missed initially, the patient may experience progressive subluxation of the distal radioulnar joint, limitation of supination and pronation, chronic pain, and weakness. Colles’ fracture is the most common wrist fracture in adults. It often results from a FOOSH injury causing the distal radius to displace and dorsally angulate. It may be described as a “dinner fork” or “silver fork” deformity. Patients may report palmar paresthesias due to tension or pressure on the median nerve. Stable fractures, those with less than 20 degrees
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of angulation and less than 1 cm of shortening, can be placed in a sugartong splint and have orthopedic follow-up. Unstable fractures require closed reduction and immobilization with orthopedic evaluation and possible ORIF. Complications include malunion, median nerve injuries, triangular fibrocartilage complex injuries, secondary radioulnar and radiocarpal instability patterns, and arthritis. Smith’s fracture is a reverse Colles’ fracture and is sometimes referred to as a “garden spade” deformity. It is a distal metaphyseal fracture with volar displacement and angulation. This injury results from a direct blow on the dorsum of the hand or wrist or from a hyperflexion injury. Treatment is the same as for Colles’ fractures. Barton’s fracture is a dorsal rim fracture of the distal radius. It results from a dorsiflexion and pronation force and may be associated with dislocation of the radiocarpal joint. Treatment is similar to that recommended for a Colles’ fracture. Hutchinson’s (chauffeur’s) fracture is an avulsion fracture of the distal radial styloid that occurs from a force transmitted from the scaphoid to the styloid. This injury is considered unstable because of the associated ligamentous injury, such as scapholunate dissociation and perilunate and lunate dislocation. Treatment is immobilization in a posterior splint and urgent orthopedic referral for percutaneous fixation. Torus fractures (i.e., buckling of the cortex) and greenstick fractures (i.e., cortex is broken on one side only) occur in children with only a moderate degree of trauma and can be managed with a long-arm cast when angulation is less than 10 degrees. However, referral to an orthopedic specialist is required for those with more than 10 degrees of angulation.
Carpal Fractures and Injuries The scaphoid is the most frequently fractured carpal bone. A fracture usually occurs from a fall on an outstretched dorsiflexed hand or by an axial load directed along the thumb’s metacarpal. There is generally pain along the radial side of the wrist and localized tenderness in the anatomical snuffbox. Although standard and scaphoid view radiographs are helpful to identify a fracture, 10% of initial fractures are undetected. High clinical suspicion of a fracture and nondisplaced fractures are treated with a thumb spica splint and orthopedic referral in 7–10 days for reexamination and repeat radiographs. Displaced or unstable fractures should be immediately treated by an orthopedic specialist or a hand surgeon. The more proximal, oblique, or displaced the fracture, the greater the risk of developing avascular necrosis (AVN). Other complications include delayed union, malunion, and early degenerative arthritis. The scapholunate ligament is the most commonly injured ligament of the wrist. It frequently results from a FOOSH injury with impact on the
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thenar eminence. Patients present with pain and swelling of the radial side of the wrist and may have a clicking sensation with wrist movement. Scapholunate dislocation is diagnosed radiographically when the scapholunate distance exceeds 3 mm on the anteroposterior radiograph. This may be increased on the clinched-fist view with the wrist in ulnar deviation and is often referred to as the “Terry Thomas” or “David Letterman” sign in reference to the gap between their front teeth. Scapholunate dissociation may be associated with a rotary subluxation of the scaphoid that will appear as a ring shadow superimposed over the scaphoid bone on anteroposterior radiograph; this is known as the “signet ring sign.” Treatment is a volar splint in neutral position with orthopedic referral for closed reduction or for open reduction with surgical repair of the ligament. Isolated lunate fractures are rare, usually occurring in association with other carpal injuries after a fall on an outstretched hand. Because the other carpal bones overlap the lunate bone, a fracture may be difficult to identify on plain radiographs and may require CT or MRI to confirm. Treatment is thumb spica splint and orthopedic follow-up. Complications include median nerve damage and AVN of the lunate (Kienböck’s disease), which may lead to lunate bone collapse, osteoarthritis, chronic pain, and decreased grip strength. Lunate and perilunate injuries usually occur from a fall on an outstretched upper extremity. The patient presents with a swollen wrist, decreased mobility, and severe pain. A median nerve injury may also be present. The lunate may be displaced either dorsally or volarly. Radiographs will show a triangular shape, often called a “piece-of-pie sign” on anteroposterior view and a “spilled teacup sign” seen on the lateral view. In perilunate injuries, the capitate is displaced. An orthopedic specialist should be consulted for immediate reduction and further care. Easily reducible dislocations may only require closed reduction and long-arm splint immobilization, but open, unstable, or irreducible dislocations may require ORIF. Both perilunate and lunate dislocations usually involve a scaphoid fracture or rotary subluxation of the scaphoid. Complications of perilunate and lunate dislocations include early degenerative arthritis, delayed union, malunion, AVN, and median nerve compression. Triquetrum fractures may be either dorsal avulsion (i.e., chip) fractures or fractures through the body of the bone. They often occur from hyperextension injuries. Perilunate and lunate dislocations may be associated with fractures through the body of the triquetrum and are best seen on the anteroposterior view. These fractures require casting for 6 weeks and orthopedic follow-up. Avulsion fractures are best viewed on the lateral radiograph and may be treated with a wrist splint for 6 weeks. Trapezium injuries are the result of a direct blow to the thumb or from a dorsiflexion and radial deviation force of the hand. A vertical fracture of the bone is rare and may be associated with a Bennett’s fracture, which
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is an intra-articular proximal thumb metacarpal fracture. Presentation is pain with movement of the thumb and tenderness of the apex of the anatomical snuffbox and at the base of the thenar eminence. Treatment for nondisplaced fractures is a thumb spica splint. Displaced fractures require ORIF. The pisiform may be fractured during a fall on the hypothenar eminence. Increased pain will be elicited with palpation of the pisiform bone. Damage may occur to the ulnar nerve and artery, which lie in Guyon’s canal, whose bony walls are formed by the pisiform and the hook of the hamate. Treatment is a compression dressing or a splint in 30 degrees of flexion and ulnar deviation to relax the tension on the flexor carpi ulnaris tendon, which houses the pisiform bone. Hamate fractures may involve the hook of the hamate, the body of the bone, or any of its articular surfaces. Most fractures involve the hook of the hamate and occur from mechanisms such as an interrupted swing with a golf club, bat, or racquet. Hamate body fractures are rare and are usually associated with a fracture or dislocation of the fourth or fifth metacarpal. Treatment is a compression dressing or splint. Complications include nonunion of the fracture and injuries to Guyon’s canal and the ulnar nerve or artery. Capitate fractures usually occur in association with scaphoid fractures during a forceful dorsiflexion of the hand with impact on the radial side. If the neck of the capitate bone is fractured, AVN may develop in the proximal fracture segment because it receives its blood supply from the distal end. Capitate neck fractures are best viewed on lateral view radiographs. Dislocated or displaced bones require orthopedic evaluation for closed or open reduction. Trapezoid fractures account for less than 1% of all carpal bone fractures. They usually occur from an axial load shifting onto the index metacarpal. Because these fractures are difficult to identify on plain radiographs, MRI or CT may be necessary to visualize the fracture. Treatment is placement in a thumb spica splint and orthopedic referral.
Wrist Nerve Entrapment and Overuse Syndromes The wrist is a common site for overuse injuries. Approximately 15% of workers are at risk of experiencing carpal tunnel syndrome. Overuse is defined as the level of repetitive microtrauma sufficient to overwhelm the tissue’s ability to adapt. Microtrauma results from repetitive loading episodes at a force or elongation level well within the physiological range. Fibrosis forms after continued or repeated release of inflammatory products that lead to thick, unyielding, restrictive tendon sheaths or retinacular tunnels.
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Occupational risk factors for developing an overuse injury include repetitive movements, high force, awkward joint posture, direct pressure, vibration, and prolonged constrained posture. Treatment is aimed at preventing fibrosis. The affected area should be rested for 2 weeks, the aggravating causes decreased, and postures or work tools shifted to avoid further injuries. Carpal tunnel syndrome is commonly seen in patients who perform repetitive hand movements, such as typists, cashiers, assembly line workers, and carpenters, but may also result from rheumatoid arthritis, pregnancy, diabetes, or thyroid disease. The transverse carpal ligament is subjected to a repeated mechanical stress that causes subsequent edema and fibrosis that compresses the median nerve. Presenting symptoms are pain and paresthesias over the distribution of the median nerve. In advanced stages, patients may develop impaired dexterity, altered sensation, and thenar weakness causing them to frequently drop items. The pain may radiate up the arm but will spare the fifth finger. Symptoms are generally worse at night and may awaken the patient from sleep because of the increased fluid accumulation in the supine position and the wrist flexion that occurs during sleep. Diagnosis is based on clinical findings. Plain radiographs will only indicate bony abnormalities. MRI and CT are only helpful to visualize any anatomical factors that may cause compression, but are not useful for specifically diagnosing entrapment neuropathy unless a mass or other lesion is found. Conservative treatment is to splint the wrist in neutral position and administer oral anti-inflammatory drugs to treat pain. Corticosteroid injections are occasionally used for transient relief of persistent symptoms. Patients should be cautioned that more than two or three injections may cause local tendon damage, and only 22% of those with minor symptoms are still pain-free 12 months after the injection. Surgical decompression is indicated when conservative treatments have failed, distal median neuropathy is severe, or thenar atrophy develops. The operation releases the transverse carpal ligament via a longitudinal incision from the wrist to the palm. Patients who undergo surgical correction have a good prognosis if the procedure is done before severe axonal loss develops. Ulnar tunnel syndrome occurs when the ulnar nerve is compressed as it passes through Guyon’s canal. Patients present with numbness of the fifth finger and the ulnar half of the fourth finger, with or without weakness of grip. Treatment is similar to that of carpal tunnel syndrome, with initial splinting, reduction of inciting activities, and surgical repair if refractory to conservative treatment. Tendonitis is usually the result of a repetitive motion that causes inflammation of the tendon with associated pain, edema, and tenderness over the affected area. De Quervain’s stenosing tenosynovitis involves the abductor pollicis longus and extensor pollicis brevis muscles. Patients report pain and mild
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edema, with increased pain when the Finkelstein’s test is performed. This test involves holding the thumb in the palm and making a fist, then deviating the wrist in an ulnar direction. Women are affected at a ratio of 10 to 1 compared with men. The tendon may be injected with corticosteroids, but this may cause weakness of the tendon or damage to surrounding tissues. A thumb spica splint may be applied to keep the thumb in neutral position for 3 weeks. A consultation with an orthopedic specialist is indicated if the patient’s pain is refractory to conservative treatment.
Bibliography Halimi KM, Jones TR: Wrist dislocation. Available at: http://www.emedicine.com. Accessed on April 8, 2005. Hoppenfeld S: Physical Examination of the Spine and Extremities Appleton & Lange: New York, 1995. Huang E, Grimes P: Fractures, forearm, Available at: http://www.emedicine.com. Accessed on February 2005. Knoop KJ, Stack LB, Storrow AB: Atlas of Emergency Medicine, ed 2. McGraw-Hill: New York, 2002. McGinley JC, Hopgood BC, Gaughan JP, et al: Forearm and elbow injury: The influence of rotational position, J Bone Joint Surg Am 2003;85A(12):2403–2409. Netter FH: Atlas of Human Anatomy, ed 3. ICON Learning Systems: Teterboro, NJ, 2002. Perron AD, Brady WJ: Evaluation and management of the high-risk orthopedic emergency, Emerg Med Clin North Am 2003;21:159–204. Simon R, Koenigsknecht S: Emergency Orthopedics: The Extremities, ed 3. McGraw-Hill: New York, 2000. Simon RR, Koenignsknecht SJ: Emergency Orthopedics: The Extremities, ed 4. McGrawHill: New York, 2001. Stone CK, Humphries RL: Current Emergency Diagnosis and Treatment, ed 5. Lange Medical Books/McGraw-Hill: New York, 2004. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 1999. Wellik GM: Nerve entrapments of the wrist, J Am Assoc Phys Assist 2005;18(4):18–23.
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Hand Injuries MARK S. SHORT AND BENJAMIN P. HARRISON
ICD Codes: Finger fracture 816.00, Metacarpal bone fracture 817.00, Tendosynovitis finger 727.05, Tendon laceration 848.9, Finger infection 681.00, Nail infection 681.02
Key Points All hand injuries should be evaluated as surgical emergencies. Loss of function of a digit or hand is devastating to a person’s recreational and professional life. Saving and maintaining function is of the utmost importance in treatment of any hand injury. ! Emergency Actions ! During the assessment of hand injuries, the entire upper extremity should be exposed for examination, and dressings applied in the field or in the triage area of the ED should be removed. Hemostasis should be achieved with direct pressure and elevation of bleeding sites. The patient’s neurovascular status should be assessed and treated, if compromised.
ANATOMY The anterior surface of the hand is referred to as palmar or volar, whereas the posterior surface is referred to as dorsal. The proximal and distal palmar creases can easily be identified in their generally horizontal orientation and can be important landmarks when describing injuries to a consultant. The sides of each finger or the sides of the hand itself are referred to as ulnar or radial, depending on which bone of the forearm they face. The joints of the hand are capable of various motions termed flexion, extension, hyperextension, and radial and ulnar deviation.
The Bones The hand skeleton consists of 19 bones: 14 phalanges of the digits and five metacarpals. Numbers 1 through 5, representing the thumb, index finger, middle or long finger, ring finger, and little finger, respectively, refer to each digit. Each finger has three phalanges—distal, middle, and
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proximal—and articulate with one another at the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints. The thumb has two phalanges, distal and proximal, that articulate at the interphalangeal joint (IP). The distal carpals of the wrist articulate with the metacarpals and will not be discussed in this section, except to note the importance of the fixed, much less mobile articulations of the second and third digits, also referred to as the first and second rays of the hand.
Blood Supply The vascular supply to the hand is provided by the radial and ulnar arteries, which form anastomoses named the superficial and deep palmar arches. The superficial arch extends more distally in the hand, and branches from it form the common digital arteries. These arteries bifurcate into the proper digital arteries, which have numerous arcades that nourish the fingers. This redundant blood supply makes it unlikely for a traumatic injury to cause distal hypoperfusion. Accordingly, if such an injury is suspected to have disrupted a major feeding vessel, the lack of distal hypoperfusion should not curtail an appropriate investigation to uncovering it.
Flexor Tendons The flexor digitorum profundus (FDP) and superficialis (FDS) are common to each finger, inserting on the proximal aspect of the distal and middle phalanges, respectively, whereas the thumb has only the flexor pollicus longus inserting on the distal phalanx. Each finger FDS bifurcates just distal to the metacarpophalangeal (MCP) joint into branches known as slips, allowing the FDS to emerge anteriorly between them. Synovial-lined flexor sheaths enclose the flexor tendons just distal to the distal palmar crease and regions of thickening provide a pulley effect, disallowing bowstringing of these tendons as they cross joints. Ulnar and radial collateral ligaments stabilize each of the IP joints of all digits.
Extensor Tendons The extensor system of the hand is composed of six dorsal compartments on the wrist through which the extensor tendons pass. The first compartment is located radially and houses the extensor pollicus brevis and the abductor pollicus longus. The compartments pass under the extensor retinaculum, which roofs the tendons to prevent them bowstringing in hyperextension. Both intrinsic and extrinsic muscle groups mobilize the extensor tendons.
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Sensory and Motor Function The ulnar, median, and radial nerves supply both motor and sensory functions of the hand. The intrinsic muscles of the hand are the thenar, hypothenar, lumbrical, and interosseus groups.
INJURY HISTORY As with most injuries, the patient’s, bystanders’, or paramedics’ history of hand injuries can provide valuable clues regarding particular injuries, and a detailed account of the mechanism of injury should always be obtained. All parties should be asked about any prehospital manipulations or reductions of deformities. The patient’s medical history should be taken, with the practitioner specifically noting prior hand surgeries, medications, and chronic illnesses such as diabetes that may predispose him or her to an immunocompromised state. Prior tetanus immunizations, smoking status, and drug allergies should be documented, as should the patient’s occupation, since these historical aspects may influence management. The time interval between the injurious event and the ED presentation is also important because this may affect wound management.
PHYSICAL EXAMINATION During the assessment of hand injuries, the entire upper extremity should be exposed and dressings applied in the field or in the triage area of the ED should be removed. Hemostasis should be achieved with direct pressure and elevation of bleeding sites. If this fails, a blood pressure cuff can be placed on the forearm and inflated until bleeding stops; however, it should not be left inflated for more than 20-minute intervals. All hand injuries should be assessed for point tenderness, vascular supply, and motor and sensory function. Two-point discrimination should be checked at the fingertips, and the integrity of the extensor and flexor tendons should be assessed. When evaluating the FDP, the practitioner should immobilize the PIP in extension since a disruption of the FDP can easily be missed if this maneuver is not performed. The range of motion of all joints of the hand should be evaluated, noting the presence of rotational deformities that suggest a phalanx or metacarpal fracture. The patient should be asked to make a fist, with the hand in supination, while the practitioner notes any overlapping of digits with this active flexion. It is helpful to also assess the uninjured hand for comparison.
Fractures Fractures of the phalanges and metacarpals are quite common and are classified as either open or closed and either transverse, intra-articular, comminuted, spiral, or oblique. Distal tuft fractures are common and
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involve the fingertips. Of note, subungual hematomas (i.e., blood collection beneath the nail plate) may occur with or without an underlying fracture and can be quite painful. Trephination of the nail plate should be undertaken using a disposable cautery device, or the practitioner can drill with an 18-gauge needle, to drain the hematoma. This can usually be done without analgesia, but occasionally a patient may require a digital block before the procedure. Finger fractures that are intra-articular, displaced, or angulated may require surgical fixation or it will cause significant deformity and dysfunction. Patients with these injuries should be referred to a hand surgeon after a finger splint is placed and/or the affected finger is taped to an adjacent finger (dynamic splint). Metacarpal fractures are also commonly seen by emergency care providers. The following summarizes the management of the four types of metacarpal fractures:
Transverse fractures without rotational deformity are splinted and an orthopedic referral is made, usually for evaluation within 72 hours. Oblique fractures usually have some degree of rotational deformity and require reduction and stabilization by an orthopedic surgeon. As little as 10 degrees of malrotation can result in significant disability. Metacarpal fractures of the second through fifth rays are classified into four anatomical areas: the metacarpal head, neck, base, and shaft. Fracture of the fifth metacarpal neck is the most common metacarpal fracture. It often occurs a result of a punch injury and is thus commonly referred to as a “boxer’s fracture.” These fractures are relatively easy to reduce, and a certain amount of angulation is permissible before splinting. However, referral to an orthopedist within 72 hours is still advised to ensure optimal management and follow-up. Conversely, fractures to the second and third metacarpal necks require near anatomical reduction of angulation before splinting or casting, and if this is unobtainable in the ED, an urgent referral is indicated. Fractures at the base of the fifth metacarpal are often associated with disruption of the metacarpal-hamate articulation and may require surgical reduction. Intra-articular thumb metacarpal base fractures are important to recognize. Bennet’s fractures are through the base of the thumb metacarpal and disrupt the joint at the volar base, with dislocation or subluxation of the carpometacarpal joint. They require ORIF by a surgeon and, despite optimal management, may cause prolonged disability. Likewise, Rolando’s fracture is a comminuted fracture at the thumb metacarpal base that requires thumb spica splinting and orthopedic referral; these fractures have the potential to cause long-term disability.
Dislocations Hand joint dislocations are commonly reported in the ED, and their associated ligamentous injuries range from simple mild sprains to complete
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disruptions with joint instability. Dislocations are frequently sports related and often have been reduced before arrival at the ED by the patient, other players, or trainers. Even a normal-looking hand must undergo meticulous evaluation to uncover such occult and potentially disabling injuries. Significant pain may hamper the patient’s ability to withstand such an examination, and digital block anesthesia can facilitate a thorough evaluation. DIP joint dislocations are almost always dorsally angulated and can usually be reduced easily. Longitudinal traction should be applied to the distal finger with simultaneously applied dorsal pressure to successfully reduce. Postreduction radiographs should be taken to ensure no avulsion fracture exists at the extensor tendon insertion site, then the DIP should be immobilized in a splint in neutral position. Importantly, the PIP should be left free of immobilization with this type of splint to avoid unnecessary stiffness of this joint. The patient should be advised to exercise early active range of motion as tolerance to pain allows. Occasionally, DIP dislocations will be irreducible as a result of intra-articular avulsed bone entrapment and will require operative reduction. Likewise, patients with unstable joints should receive early referral to a hand surgeon. The PIP is the most commonly dislocated finger joint. Due to its complex structures, complications such as persistent pain, flexion deformity, and joint instability are frequent sequelae. Of particular note, the examiner should always evaluate for a boutonniere deformity, which is a complete rupture of the central slip causing extension of the metaphalangeal and DIP joints and flexion of the PIP joint secondary to the unopposed flexors. To evaluate for this injury, the practitioner should have the patient try to extend the PIP against light resistance while held in 90 degrees of flexion. An inability to do so suggests central extensor disruption; however, these injuries are difficult to uncover in the acute setting and are often only discovered after the boutonniere deformity has already developed. MCP joint dislocations and ligamentous injuries are most common at the thumb MCP joint. Dorsal dislocations should be reduced with the wrist and thumb IP in flexion while volarly directed pressure is applied to the dorsum of the base of the proximal phalanx. These reductions may require prereduction ulnar and median nerve regional anesthesia. Postreduction splinting with a thumb spica is required. Irreducible thumb MCP dislocations may indicate dorsal or volar plate entrapment and require urgent referral. The integrity of the thumb ulnar (UCL) and radial collateral ligaments (RCL) should always be assessed. This is best accomplished with radial and ulnar stress applied to a slightly flexed thumb MCP. The degree of laxity, if present, should be compared with the contralateral thumb. UCL laxity, diminished pinch strength, and edematous tenderness at the dorsoulnar aspect of the thumb MCP may represent gamekeeper’s/skier’s thumb. This injury can be acute, chronic, or acute
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on chronic. Stener’s lesion represents trapping of the completely torn UCL proximal to the adductor pollicus aponeurosis, which can lead to significant long-term disability if not operatively repaired. RCL injuries are less common but can also lead to prolonged impairment. UCL/RCL injuries should be secured in a thumb spica splint, and referral should be arranged for further evaluation by an orthopedist.
Tendon Injuries While not uncommon, tendon injuries to the hand can be subtle and difficult to diagnose, whether they present as open or closed wounds after hand trauma. Again, a detailed history of the type of injury, the position of the hand during the injury, time elapsed since the injury, and subjective changes in functional status of the digits are important data to ascertain to lessen the incidence of missed diagnoses. Extensor tendon disruptions usually occur as a result of trauma to the dorsum of the hand, which affords little protection to these structures within the thin skin overlying their superficial position. In most cases, the extensors will be lacerated secondary to open injuries. Most extensor tendon injuries should be repaired by an orthopedist. Extensor tendon injuries over the dorsum of the metacarpals can be repaired by emergency care providers with the knowledge and experience of proper suturing techniques. The tendons here are more superficial and not associated with joint structures. To evaluate for flexor tendon injuries, each flexor tendon should be tested separately (see Dislocation section). Potentially devastating complications include concomitant injuries to the delicate pulley systems of the digits, and all flexor tendon disruptions require evaluation by an orthopedist. ED management includes adequate analgesia, wound irrigation, and splinting with consultation of a hand surgeon in the ED. Operative repair may be delayed for days, and the orthopedist may appropriately request that the skin over the wound be loosely closed before the patient is sent out for follow-up. Although not supported by evidence for uncontaminated wounds, many orthopedists also request oral antibiotics for patients with open flexor tendon lacerations.
Hand Infections Most patients with established hand infections require admission to the hospital and parenteral antibiotics. Exceptions include superficial or localized abscess collections such as paronychia. Simple lacerations should be copiously irrigated with high-pressure normal saline and should be fully
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explored in a well-lighted environment under a bloodless field/tourniquet. Bite wounds require prophylactic antibiotics (e.g., amoxicillin/clavulanate), but simple hand lacerations do not. Dorsal injuries to the metaphalangeal joints should be considered bite wounds until proven otherwise. Usually a result of the patient’s closed fist hitting the teeth of another person, these so-called fight bites require meticulous irrigation, examination through the entire range of motion, and antibiotic therapy. Pain with axial loading suggests septic arthritis, which requires intraoperative joint irrigation by an orthopedist. Often, these infections involve periarticular structures and are associated with open extensor tendon lacerations as well. Radiographs are required to assess for fractures and possible foreign bodies (e.g., teeth). Antibiotics should be administered (ampicillin/sulbactam is a good choice for all bite wound infections), and a hand surgeon should be consulted for further evaluation. A paronychia is an abscess of the medial or lateral nail fold that usually presents as a painfully erythematous and fluctuant swelling. There may or may not be a history of trauma. This type of infection is exquisitely tender on physical examination and, as with most abscesses, the treatment is incision and drainage. A No. 11 scalpel blade should be directed along the transverse diameter of the nail plate and into the point of maximal fluctuation after anesthesia with a digital block (very small, superficial paronychias may not require anesthesia). The practitioner should express the residual pus through the incision and irrigate the wound. Frequent warm tap water soaks for 3 days will allow continued drainage and prevent reaccumulation of purulence. Antistaphylococcal antibiotics should be administered for associated cellulitis or in the case of immunocompromised patients. A felon is an infection of the pulp space of the finger pad. This type of infection is most common on the thumb and index finger of the dominant hand. The pad is classically tender and enlarged, and there may be minimal fluctuation on physical examination. As with acute paronychia, purulence within a felon must be drained before healing can begin. Treatment is undertaken with a unilateral longitudinal incision sparing the midline of the volar aspect of the digit to preserve the sensory capability after digital block anesthesia. If the area of greatest fluctuation is over the midline, the clinician should make a longitudinal incision over this area just large enough to permit drainage. He or she should bluntly dissect the septae through the incision, but ensure the incision does not approach the distal flexor crease or extend to the fingertip. Wound culture samples should be sent for analysis, and the wound should be irrigated. A gauze or surgical wick should be placed to facilitate continued drainage before warm soaks are started in 1–2 days. Complications such as osteomyelitis are possible, and good follow-up is essential.
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Flexor tenosynovitis is a potentially devastating infection that can course within the flexor tendon sheath and requires surgical drainage. It usually results from penetrating trauma to the hand, and mismanagement can lead to loss of function of a digit or the entire hand. Flexed posture of the affected digit at rest, symmetrical edema of the involved digit, tenderness over the flexor tendon sheath, and exquisite pain on passive extension are the four components of the classic physical examination findings (i.e., Kanavel’s signs). Intravenous antibiotic therapy should be initiated in the ED, and a culture of the wound should be performed, if possible. Most cases require immediate drainage in the operating room, although orthopedists may request that patients for whom equivocal findings are available early be admitted to receive parenteral antibiotics and close observation. The emergency care provider should immobilize the hand and consult a hand surgeon immediately for definitive management.
High-Pressure Injection Injuries It is estimated that 100 lb per square inch (psi) is required to breach the skin with pressurized liquid. Industrial equipment can generate thousands of pounds of pressure, and these injection injuries can be limb threatening. The pressure, the amount, the location, and the type of material injected determine injury severity. The affected digit may present similar to a compartment syndrome with pain, pallor, and edema. The use of antibiotics in this situation is controversial but may be recommended by the consultant. Warm water soaks and digital blocks are contraindicated. Administer systemic analgesia and consult an orthopedist for immediate surgical debridement. Amputations are common, and many times patients with these injuries must undergo surgery within several hours of presentation to avoid this. The use of parenteral steroids is controversial; these should be administered only at the request of the hand surgeon.
LABORATORY FINDING There are no specific laboratory tests for hand injuries. Laboratory tests are directed to the specific kind of injury or the patient’s underlying illnesses.
RADIOGRAPHS Radiography is directed to the kind of injury that is suspected. Radiographs should be taken of all hand injuries to examine for fracture or foreign bodies.
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Bibliography Bowman SH, Simon RR: Metacarpal and phalangeal fractures, Emerg Med Clin North Am 1993;11(3):671–702. Harrison BH, Hilliard MW: Emergency department evaluation and treatment of hand injuries, Emerg Med Clin North Am 1999;17(4):793–822. Hart RG, Uehara DT, Kutz JE: Extensor tendon injuries of the hand, Emerg Med Clin North Am 1993;11(3):637–649. Henry M: Fractures and dislocations of the hand. In Rockwood CA, Green DP, Heckman JD, Bucholz RW (eds): Rockwood and Green’s Fractures in Adults, ed 5. Vol 1. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 656–748. Seaberg DC, Angelos WJ, Paris PM: Treatment of subungual hematomas with nail trephination: A prospective study, Am J Emerg Med 1991;9(3):209–210.
Hip Trauma KATHLEEN M. SAMSEY
ICD Codes: Femoral fracture (closed) 821.00, Femur condyle fracture 821.21, Fracture capital 820.01, Femur head 820.01, Femur trochanteric 820.01, Hip dislocations (closed) 835.00, Hip dislocation (anterior) 835.03, Congenital hip dislocations 754.30, Legg-Calve´-Perthes disease 732.1, Slipped capital femoral epiphysis 737.2, Septic hip or septic arthritis 711.0
Key Points Patients with suspected hip injuries should be undressed from the waist down to check for obvious deformities, leg shortening, internal/external rotation, and skin color. The patient should not have range-of-motion examination performed until radiographs have demonstrated no fracture. ! Emergency Actions ! All patients with suspected hip fracture or dislocation should have a “safety net” established. Two large-gauge intravenous lines delivering normal saline should be established, the patient should be administered oxygen, and full cardiac monitoring should be undertaken. The ABCs (i.e., airway, breathing, circulation) take precedence over all other evaluation and treatment.
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DEFINITION The hip is a ball-and-socket joint consisting of the acetabulum, made up of the three bones of the pelvis 5 inches below the iliac crest, and the proximal 4 inches of the femur, including the femoral head and neck. In a growing child, the femoral head may be referred to as the capital epiphysis, the presence of which can cause specific types of injuries. Dislocations can be classified as anterior, posterior, central, and inferior. Hip dislocations and fracture-dislocations are two of the few true orthopedic emergencies.
EPIDEMIOLOGY Approximately 250,000 hip fractures occur annually in the United States, and mortality from a hip fracture approaches 25% at 1 year. Age and sex predispose patients to certain types of hip and femur injuries. Fractures and dislocations in younger adults are often the result of direct trauma such as motor vehicle accidents and assault. In older adults and postmenopausal women (often with preexisting bone disease), falls are often the culprit. Pathologic fractures are often the result of cancer, radiation, and chemotherapy. Femoral neck fractures occur more in men, whereas intertrochanteric fractures occur more in women. Hip injuries in children are often the result of congenital or traumatic causes, and they are more common in boys.
ANATOMY The femur is the strongest and longest bone in the body. The two femurs extend obliquely from the pelvis medial to the knee, where they can best support the body. The hip joint itself is reinforced by a well-developed fibrous capsule, ligaments, and the proximal musculature of the lower extremity. The proximal femur consists of the femoral head, neck, and intertrochanteric region, with the greater trochanter located superolateral and the lesser trochanter located inferomedial. The greater trochanter is typically at the level of the palm of the hands when the arms are resting by the sides. The intertrochanteric line is an oblique line that connects the greater and lesser trochanter, marking the junction of the femoral neck and its shaft. The powerful musculature of the hip and thigh are located in three separate compartments, each containing associated nerves and blood vessels. The muscles are also grouped according to their primary action at the hip. The arterial supply for the hip includes the obturator, medial/lateral femoral circumflex, and the superior/inferior gluteal arteries. Of note, the circumflex arteries that branch off of the deep femoral artery provide
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the tenuous blood supply to the femoral head. The major nerves of the hip are the femoral and sciatic nerves.
EXAMINATION Patients with suspected hip injuries should be undressed from the waist down to check for obvious deformities, leg shortening, internal/external rotation, and color. The patient should not have range-of-motion examinations until radiographs have demonstrated no fracture. The joint itself should be palpated and a thorough neurological and vascular examination performed. Serious hip injuries will demonstrate pain with even mild axial loading (pressing up on the bottom of the foot). According to the old adage to check “one joint above and below” the site of suspected injury, the knee should also be examined and radiographs possibly obtained.
CLINICAL PRESENTATION All patients with suspected hip fracture or dislocation should have a safety net established. Two large-gauge intravenous lines of normal saline should be established, the patient should be administered oxygen, and full cardiac monitoring should be undertaken. The ABCs of resuscitation take precedence over all other evaluation and treatment, and the examiner must always remember that significant blood loss can accompany any femoral fracture. Proximal femoral fractures are generally categorized according to location (e.g., neck, trochanteric, intertrochanteric, and subtrochanteric). There are rare femoral head fractures, associated with dislocations, and an orthopedic surgeon should be consulted to manage these. There are also avulsion fractures, common in young adults and athletes, which often present as thigh pain. These generally occur at the anterior superior iliac spine, the anterior inferior iliac spine, and the ischial tuberosity. They present as a “snapping” or “popping” sensation. The appropriate treatment is rest and consultation with an orthopedic specialist. Femoral neck fractures are generally considered pathologic, due to underlying bone loss. They are classified as displaced or nondisplaced. Patients with nondisplaced fractures present with a history of minor trauma and a painful limp. The appropriate treatment is early ambulation or internal fixation, depending on the stability. Ninety-six percent of cases will heal without complication. If a fracture is suspected, but not evident on radiograph, the hip should be imaged again in 10–14 days. A CT may also be helpful. AVN of the femoral head is the most common complication. Patients with displaced fractures will present with pain and inability to ambulate. The limb will lie externally rotated, abducted, and slightly
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shortened. It will be evident on plain radiographs. Treatment is usually accomplished with closed reduction and internal fixation. Complications included AVN, infection (because the fracture line extends into the joint), and pulmonary embolism. Trochanteric fractures are rare. Greater trochanteric fractures are usually a result of a direct fall or avulsion at the insertion of the gluteus medius. In the young adult population, it is due to a true epiphyseal separation. The patient presents with hip pain when walking and pain upon palpation of the greater trochanter. Treatment is controversial: conservative versus internal fixation. Lesser trochanteric fractures are a result of an avulsion at the insertion of the iliopsoas muscle. Patients with this type of injury usually report pain with hip flexion and internal rotation. Treatment consists of pain control, early mobilization, and a return to weight bearing as tolerated. Intertrochanteric fractures, like most hip fractures, usually occur as a result of high-speed trauma in younger patients and falls in older patients. They will present with swelling and pain with any movement or weight bearing. The extremity may be shortened and externally rotated. These fractures are classified as stable or unstable and also according to the number of separate bone fragments. Caution should be exercised with these patients because the majority of them are often under-resuscitated; they are frequently dehydrated, and up to 3 units of blood may be lost into the fracture site. Most will require urgent, not emergent, internal fixation by an orthopedic specialist. If this is delayed greater than 48 hours, however, there is a 10-fold increase in mortality. It is also imperative to evaluate the patient for other associated fractures of the upper extremities, ribs, and spine. The femoral fracture can distract both the patient and the examiner. Subtrochanteric fractures occur between the lesser trochanter and the proximal 5 cm of the femoral shaft, often associated with an intertrochanteric fracture. The risk for hypovolemic shock from blood loss at the site is significant in these patients, and the injury should be immobilized with splint and the patient resuscitated with fluids. Hip dislocations and fracture-dislocations are two of the few orthopedic emergencies. Often the result of significant trauma, they require considerable forces to be produced. These patients should be evaluated as persons who have experienced major trauma because of the high rate of multisystem injury. Dislocations with associated fractures should not be reduced by an emergency care provider. Isolated dislocations can be reduced, but multiple attempts should be avoided. If reduction proves difficult, it should be performed with the patient under general anesthesia. Anterior dislocations (10%–15% of patients) occur as a result of forceful extension, abduction, and external rotation. As a result, patients with this type of injury present with the hip abducted, slightly flexed, and externally rotated. On radiograph, the femoral head will be inferior and medial
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to the acetabulum, best viewed laterally. Reduction can be achieved by placing the patient supine, applying traction along the long axis with the hip slightly flexed, and gently adducting/internally rotating the leg. This can be attempted in the ED with proper procedural sedation or with the patient under general anesthesia. Posterior dislocations (80%–90% of patients) are almost always due to motor vehicle crashes in which the patient strikes his or her knee on the dashboard. On presentation, the limb is shortened, adducted, and internally rotated. The hip is often mildly flexed. This type of injury will usually be obvious on anteroposterior and lateral radiographs, but another clue is the loss of the lesser trochanter on anteroposterior view, due to internal rotation. Posterior dislocations are particularly at risk of developing AVN, and this condition should be considered a true emergency. Reduction should be attempted quickly in the ED, with the patient under proper sedation. Commonly, the Allis technique is used, in which strong traction is applied along the axis of the femur with the hip and knee each flexed at 60–90 degrees. Assistants hold the pelvis to the bed as the operator applies traction. Gentle internal and external rotation can also be used while traction is applied. Postreduction radiographs should be obtained and the limb stabilized. A thorough prereduction and postreduction neurovascular examination should be performed, focusing on the sciatic nerve and femoral vessels. Sciatic injury occurs in approximately 10% of patients with posterior hip dislocations. Pediatric hip injuries are unique to that age group, and any hip injury has the potential for premature growth arrest. Congenital hip dislocations are more common in girls and in firstborn children. The diagnosis is made based on the results of the Ortolani test where pressure is applied along the axis of the femur with the hips and knees flexed, and the femurs are rotated outward. If the femoral head subluxes or an audible click is heard, orthopedic consultation is required. Traumatic dislocations are evaluated and managed similarly to those in adults. Traumatic pediatric fractures are rare. If one is suspected, however, the classic Salter-Harris system is not used. Rather, the Delbert classification is used, which separates fractures through the physis, transcervical, cervicotrochanteric, and intertrochanteric regions. Legg-Calvé-Perthes disease is idiopathic AVN of the pediatric femoral head. It occurs between ages of 2 and 10 years, with a peak incidence at 6 years of age. It is five times more common in boys. It presents insidiously with a painful limp. On radiograph, there will be necrosis, reabsorption, and regeneration of bone in different stages. Consultation with a pediatric orthopedic surgeon is needed. Slipped capital femoral epiphysis occurs between the ages of 10 and 17 years, with a peak incidence at 13 years for boys and 11 years for girls. It occurs twice as frequently in boys as in girls, and 25% of cases are
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bilateral. It is thought to occur due to structural weakness in the physeal cartilage at the onset of puberty. Risk factors include obesity, previous radiation or chemotherapy, renal osteodystrophy, hypothyroidism, and neglected septic arthritis. Patients present with insidious onset of groin, thigh, or knee discomfort, which develops into hip stiffness and limp. Examination will reveal hip tenderness and decreased range of motion. Initially, anteroposterior, lateral, and frog-leg radiographs should be obtained, and findings may be normal. Comparative bilateral views should be obtained if slipped capital femoral epiphysis is suspected but not obvious on radiograph. One should look for the “scoop slipping off the ice cream cone” as the epiphysis slides off the femoral head. If occult fracture is suspected, CT or MRI should be used. A consultation with an orthopedic surgeon is warranted for traction and fixation. Septic hip or septic arthritis, though not traumatic injuries, should be included in the differential for a pediatric patient with painful hip. Septic arthritis is the most common finding in an infant with a painful hip. Infants will be fussy and febrile, will cry when held, and will likely be feeding poorly. The most common causes are group B Streptococcus, Staphylococcus epidermidis, and Haemophilus influenzae. Older children present with limp or painful weight bearing. On examination, there is decreased or painful range of motion. Blood cultures and ESR test should be performed. If septic hip is suspected, immediate orthopedic consultation is warranted.
RADIOGRAPHS All suspected hip dislocations and fractures should be evaluated with at least a low anteroposterior pelvis view. Lateral films are also helpful if the injury is not obvious from this angle. Trauma patients should not be put in a frog-leg position. If injury is suspected but not obvious, the integrity of Shenton’s line should be evaluated. This line (on anteroposterior view) is a smooth, curved line drawn along the superior border of the obturator foramen and the medial aspect of the femoral metaphysis. If the line is disrupted, femoral neck fracture or hip dislocation is more likely.
LABORATORY EVALUATION All patients with suspected hip fractures should be type and crossmatched for at least 2–4 units of blood. They should undergo a CBC, coagulation panel, serum chemistry test, and a urinalysis.
Bibliography Bedi A, Le T: Subtrochanteric femur fractures, orthopedic, Clin North Am 2004; 35(4):473–483.
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Canale ST: Campbell’s Operative Orthopedics, ed 10. Mosby: St Louis, 2003. Mirza A, Ellis T: Initial management of pelvic and femoral fractures in the multiply injured patient, Crit Care Clin 2004;20(1):159–170. Roberts J, Hedges J: Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004. Rosen P, Marx R: Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Salyer S: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Vlauvelt C, Nelson F: Manual of Orthopaedic Terminology, ed 6. Mosby: St Louis, 1998.
Infections of the Bones and Joints BENJAMIN H.TAYLOR
ICD Codes: Osteoarthrosis 715.9, Osteomyelitis periostitis 730.0, Pyogenic arthritis 711.0
Key Points Osteomyelitis can be either acute or chronic. Septic arthritis usually occurs from hematogenous spread. ! Emergency Actions ! Septic arthritis in children whose growth plates are not closed is a medical emergency and requires evaluation by an orthopedic surgeon.
DEFINITIONS Osteomyelitis Osteomyelitis, inflammation of bone and bone marrow, is the name given to infections of the bone. This condition may present in an acute or chronic stage. The affecting organisms are bacteria, mycobacteria, or fungi.
Septic Arthritis Infectious or septic arthritis is an inflammatory reaction resulting from hematogenous spread, direct inoculation, or direct extension from an adjacent focus of the joint space by pathogenic microorganisms, resulting in
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pain, swelling, redness, limitation of joint motion, and eventually joint destruction and permanent disability, if the condition is left untreated.
EPIDEMIOLOGY Osteomyelitis The overall prevalence of acute hematogenous osteomyelitis is cited as affecting 1% of hospitalized patients and occurring in 1 case per 5000 children. Male children have a modestly greater susceptibility to this disease than do female children, with a male-to-female ratio of 2–3:1. The majority of children diagnosed with osteomyelitis have no previous medical history or risk factors, with the exception of patients with sickle cell disease. Although most children in whom osteomyelitis is diagnosed have no identifiable risk factors, the opposite is true for adults, among whom the majority of cases occur in the chronically ill patients, patients with altered immune states, persons with diabetes, and patients with peripheral vascular occlusive disease. Osteomyelitis after open fracture or orthopedic surgery is the most common form of the disease in adults. Patients of lower socioeconomic status are more prone to present with osteomyelitis. The prevalence of chronic osteomyelitis is 2 cases per 10,000 persons.
Septic Arthritis Septic arthritis occurs in all age groups but is more common in children than adults. Half of all cases of septic arthritis occur in children younger than 3 years of age. Males are usually affected more commonly than females, although in patients with underlying rheumatoid arthritis, females are affected more often. Other groups at high risk include intravenous drug users, patients receiving dialysis, and patients with sickle cell disease, diabetes, and acquired immunodeficiency syndrome. Disseminated gonococcal infection with associated gonococcal infective arthritis is the leading cause of hospital admission in these patients.
PATHOLOGY Osteomyelitis Osteomyelitis causing microorganisms involved in the development of osteomyelitis (e.g., pyogenic bacteria, mycobacteria, fungi) can spread to bone by one of three routes: hematogenous spread, direct extension from a contiguous site of infection or direct introduction, and vascular
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disease. More than 90% of acute osteomyelitis cases are caused by S. aureus, but Streptococcus pyogenes and H. influenzae may also cause acute infection of the bone. Pyogenic bacteria cause almost 90% of bone and joint infections in injection drug users, with S. aureus and Pseudomonas species reported as the most frequent etiology. Gram-negative osteomyelitis may follow gastrointestinal or genitourinary infections. Bacteroides fragilis or pneumococcal osteomyelitis is often preceded by a severe respiratory infection. S. aureus, S. epidermidis, Pseudomonas aeruginosa, Serratia marcescens, and Escherichia coli are typically responsible for persistent osteomyelitis. Acute osteomyelitis can be caused by blood-borne pathogens or infection resulting from injury. Chronic osteomyelitis refers to an untreated exogenous or hematogenous infection or one that has failed treatment. There have been several classification systems proposed for osteomyelitis, yet none have achieved universal acceptance. The most common system continues to be the Waldvogel classification system. Hematogenous osteomyelitis occurs predominately in children before the age of epiphysial closure (<21 years) and typically originates in the metaphysis of long bones. The most common organisms isolated in these cases include S. aureus, Streptococcus pneumoniae, and H. influenzae type b. Hematogenous osteomyelitis in adults rarely involves the long bones but usually occurs in the more vascular vertebrae. Osteomyelitis resulting from a contiguous focus of infection often follows a traumatic bone injury or surgery, or it reaches the bone from an adjacent infected soft tissue. Common predisposing conditions include open fractures, surgical reduction and internal fixation of fractures, and wound infections. Osteomyelitis associated with vascular insufficiency or peripheral vascular disease results from inadequate blood supplies to vulnerable tissues and almost always affects diabetic patients between 50 and 70 years of age with advanced atherosclerosis.
Septic Arthritis The majority of cases of septic arthritis occur as a result of hematogenous spread of infection. In intravenous drug abusers, the causative organism is usually Pseudomonas or other gram-negative organisms. Iatrogenic septic arthritis is usually caused by S. aureus (the most common pathogen in nongonococcal septic arthritis), S. epidermidis, and gram-negative organisms. N. gonorrhoeae is the most common organism seen in nontraumatic acute monoarthritis, especially in young, sexually active persons. Group B streptococcal infections are seen more often in patients with diabetes.
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CLINICAL PRESENTATION Osteomyelitis A patient with an acute presentation may report nonspecific constitutional symptoms such as chills, fevers, palpitations, lethargy, or malaise. Local findings include swelling and warmth, erythema, and point tenderness over affected area. Younger populations manifest systemic signs more frequently than adults and have limited use of the involved extremity. Infants with osteomyelitis are noted for a lack of local or systemic findings. In some cases, several months of nonspecific extremity pain may precede a diagnosis. An antecedent history of infection at another site (e.g., skin or throat) or previous trauma may be noted. Joint range of motion may be reduced, and an effusion may be present. Prolonged infections may produce a draining sinus tract from the infected bone to the overlying skin and are more common in adults. There are no exact criteria existing to define when acute osteomyelitis becomes chronic. Clinically, the first bone infection is considered acute, and relapse of bone infection is labeled chronic. Thus, the hallmark of chronic osteomyelitis is the presence of dead bone (the sequestrum). Involucrum (i.e., reactive bony encasement of the sequestrum), local bone loss, persistent drainage, and sinus tracts are other common features of chronic disease. Patients with chronic osteomyelitis commonly present with chronic pain and sinus formation with purulent drainage. Radiographs will show bone destruction, deformity, or both. Fever is usually low grade or absent.
Septic Arthritis A patient with an acute septic arthritic joint typically reports constitutional symptoms (e.g., fever, chills, nausea/vomiting, and anorexia) but almost invariably, the chief symptoms will be joint pain, swelling, and immobility. To accommodate maximum effusion, the limb is kept with the joints held in the position of ease or maximum relaxation of the capsule of the joint. Passive movements are completely restricted and painful. The degree of erythema and warmth may not be marked if the patients’ symptoms have been of short duration.
LABORATORY FINDINGS Osteomyelitis Laboratory studies are often nonspecific in the diagnosis of osteomyelitis, so results should be correlated with the clinical findings and other available data. White blood cell counts of 16,000/ml or less, mild anemias, and ESRs of 100 mm/hr or less may be present within 24 hours of
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symptom onset. Leukocytosis is more common during acute infections, and ESR elevations are noted more frequently in recurrent ones. CRP should also be measured, since levels rapidly increase after the onset of infection. It can also be used to monitor response to therapy, since it has a shorter half-life than ESR. Blood cultures are an essential part of the workup of suspected osteomyelitis and should be obtained before the administration of antibiotics or at least 48 hours after antibiotic therapy has been discontinued. Blood culture results are positive in 50% of cases of acute osteomyelitis. Once the affected area is localized by careful physical examination and diagnostic imaging studies, bone biopsy (via needle aspiration or surgical biopsy) with histopathologic examination and cultures should be performed for confirmation of the diagnosis of osteomyelitis. Histopathologic features indicating osteomyelitis include necrotic bone with extensive resorption adjacent to an inflammatory exudate. Biopsy techniques are crucial because improperly performed biopsies may interfere with accurate organism identification.
Septic Arthritis Arthrocentesis is required if infection is suspected, although a superimposed cellulitis is a relative contraindication to the procedure. Synovial fluid obtained should be sent for a white blood cell count with differential; this count typically will be elevated with the differential count showing polymorphs. Gram staining and blood cultures should also be obtained. Gram stains yield positive results in about 75% of patients infected with staphylococci and 50% of patients with gram-negative bacilli, but in fewer than 25% of patients with joints infected with gonococci. Blood culture results are positive in about 50% of nongonococcal infections but are rarely positive in gonococcal infections. A throat swab may detect previously undiagnosed bacterial pharyngitis. The ESR is elevated in approximately 90% of the cases of septic arthritis. Likewise, levels of CRP are often increased. The ESR usually rises 3–5 days after initiation of therapy and then slowly returns to normal within about 4 weeks. In contrast, CRP peaks at day 2 of therapy and can normalize within 1 week in uncomplicated cases.
IMAGING Osteomyelitis Diagnostic imaging studies remain the main investigative tests in osteomyelitis. Plain radiographs of the affected area can indicate changes in bone consistent with osteomyelitis, but these do not become apparent
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until 1–2 weeks after the onset of symptoms. Therefore, early in the clinical course, plain radiographs do not show evidence of infection. The earliest sign of osteomyelitis seen on a plain radiograph is adjacent soft tissue swelling followed by a periosteal reaction. Eventually, the infection may lead to bone destruction with the development of lytic lesions and areas of sclerosis. Sequestra formation and bone abscesses are common in chronic osteomyelitis and should be ruled out. In osteomyelitis of the neonate, joint effusions can accompany the bone findings, and plain radiographs can detect bone abnormalities earlier than in older children. If osteomyelitis is suspected and plain radiographs fail to demonstrate signs of the disease, CT scanning or technetium bone scan should be performed.
Septic Arthritis Plain radiographs are seldom useful early in the disease, though they may reveal an effusion with distention of the joint capsule or narrowing of the joint space as articular cartilage is destroyed, followed by evidence of synovial thickening. Comparison of the affected joint with the contralateral joint is helpful to distinguish subtle changes. Joint x-rays may detect osteomyelitis in bones adjacent to the joint. An air density noted in the joint may be a sign of infection with gas-forming organisms or may be the result of a previous joint aspiration.
TREATMENT Osteomyelitis Appropriate therapy for osteomyelitis includes the initiation of antibiotic treatment, drainage of purulent foci, and debridement of necrotic tissue. Antibiotic selection should be based on the most likely pathogen(s), the local antimicrobial resistance patterns, and intrinsic host factors. Appropriate initial empirical therapy consists of parenteral nafcillin, oxacillin, a cephalosporin, or clindamycin. Osteomyelitis that is caused by a contiguous focus of infection is often polymicrobial and should be treated with amoxicillin-clavulanate, clindamycin, piperacillin-tazobactam, or ampicillin-sulbactam. Once culture or biopsy results are available, antibiotic regimens should be adjusted to target the causative organisms. Osteomyelitis may require surgical therapy depending on the extent, location, and longevity of infection. Surgical management in acute osteomyelitis should be performed if the response to antibiotic therapy is not rapid or if any sign of abscess develops. Osteomyelitis recurrence is noted if debridement of all nonviable or infected tissue is not performed.
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Septic Arthritis The keys to the management of septic arthritis include drainage of the purulent synovial fluid and administration of appropriate parenteral antimicrobial therapy. Orthopedic consultation should be sought when a suspected case presents. Antimicrobial therapy should be administered as soon as the diagnosis is suspected and synovial fluid culture samples are obtained. Initial selection should be based on the results of Gram stain of joint fluid or other body fluids or secretions. If no microorganisms are identified, empirical treatment should be given with the patient’s age, risk factors, and clinical picture taken into consideration. Normally, patients should be treated initially for infections with gram-positive organisms, whereas broad-spectrum antibiotics are indicated in debilitated, severely ill, and immunocompromised persons. Once culture results become available, antibiotic therapy can be changed, if indicated. Some authors recommend a 4–6-week treatment period, but good results have been documented with shorter duration and careful monitoring of the patient. Closed-needle aspiration should be accomplished once or twice daily until fluid fails to reaccumulate. Most patients can be treated in this manner, although early surgical drainage is indicated in deep-seated joints like the hip and shoulders. Joint immobilization and elevation is useful for symptomatic relief of pain early in the course of the disease, but early active range-of-motion exercises are beneficial to prevent muscle atrophy and for ultimate functional outcome.
Bibliography Canale ST: Campbell’s Operative Orthopaedics, ed 10. Mosby: St Louis, 2003. Marx JA: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Paluska S: Osteomyelitis, Clin Fam Pract 2004;6(1):127–132. Rakel RE: Textbook of Family Practice, ed 6. WB Saunders: Philadelphia, 2002. Shetty AK, Gedalia A: Management of septic arthritis, Indian J Pediatr 2004;71:819–824. Skinner HB: Current Diagnosis and Treatment in Orthopedics, ed 2. McGraw-Hill: New York, 2000. Stone KC, Humphries RL: Current Emergency Diagnosis and Treatment, ed 5. McGrawHill: New York, 2004.
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Injuries to the Lower Leg BRENDA OSWALD AND CARL MENCKHOFF
ICD Codes: Tibia fracture 823.80, Tibial plateau fractures 823.0, Fibular fractures 823.81, Maisonneuve fracture 823.01, Compartment syndrome 958.8, Achilles tendon rupture 845.09, Osgood-Schlatter 734.4, Achilles tendonitis 726.71
Key Points Any patient who presents to the ED with a lower extremity injury should have the entire leg examined from the hip down. All extremity examination should have the neurovascular status evaluated and documented. ! Emergency Actions ! Any patient with an extremity injury that involves any neurovascular deficit should be immediately referred to an orthopedic surgeon.
DEFINITION The lower leg consists of the fibula, tibia, and four major compartments that are divided by deep fascia. The tibia is the primary weight-bearing bone. It is also the most commonly fractured long bone and the one most likely to sustain an open fracture. Soft tissue and musculoskeletal injuries are common. A thorough history and physical examination are important to properly diagnose and manage lower extremity injuries.
ANATOMY OF THE LOWER EXTREMITY The tibia and fibula are connected by a dense interosseous membrane. The lower leg is divided into four compartments. The anterior compartment is bordered by the tibia medially, the interosseous ligament posteriorly, and the anterior intermuscular septum laterally. It contains the anterior tibial artery and veins, the dorsiflexors of the ankle and toes, and the deep peroneal nerve that provides sensory innervation to the web space of the first and second toes. The lateral compartment is surrounded by the anterior intermuscular septum, the fibula, and the posterior intermuscular septum. It contains the
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superficial peroneal nerve that provides sensory innervation to the lateral dorsum of the foot and motor control for the muscles within the compartment that evert the foot. No major arteries run through this compartment. The superficial posterior compartment houses the gastrocnemius, soleus, and plantaris muscles that plantar flex the ankle. The sural nerve provides sensory innervation to the lateral heel. No major arteries traverse this compartment. The deep posterior compartment contains the muscle groups that plantar flex the toes, namely the tibialis posterior, flexor hallucis longus, and flexor digitorum longus. The tibial nerve runs through this compartment and provides motor control to these muscles and sensation to the sole of the foot. The posterior tibial and peroneal arteries and veins are contained in this compartment.
CLINICAL PRESENTATION AND EXAMINATION A thorough history and physical examination helps to elicit how the injury occurred and will guide the clinician to the appropriate examination and treatment. To evaluate nerve or sensory deficits, the clinician should palpate the lateral heel, the sole of the foot, and the posterior ankle web space. Motor function can be assessed with plantar and dorsal foot flexion and eversion of the foot. The clinician should palpate the muscle groups and along the entire shaft of the tibia and fibula. The popliteal, dorsalis pedis, and posterior tibial pulses should be checked. Absent or decreased pulses may indicate a vascular injury and require urgent fracture reduction. To evaluate for bony abnormalities, anterior-posterior and lateral x-rays of the tibia and fibula should be obtained. Further radiography may be needed for ankle or knee injuries. Treatment such as splinting, wound care, tetanus, medications, and orthopedic referral should be tailored to the specific injury.
LABORATORY FINDINGS There are no specific laboratory examinations helpful in the diagnosis of lower extremity fractures. If a fracture is open, if the patient is going to undergo surgery, or if he or she has an underlying disease process, a CBC, Chem 7, and measurement of PTT and INR should be performed, at minimum.
RADIOGRAPHS Radiographs are directed toward the specific type of injury.
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TREATMENT OF SPECIFIC INJURIES The tibia is the most commonly fractured long bone and usually requires orthopedic evaluation in the ED. Mechanisms such as axial loading (e.g., fall from a height), varus or valgus forces, and rotation of the knee may cause tibial plateau fractures. Violent twisting motions or abductionadduction injuries may cause fractures of the intercondylar eminence. Patients with these injuries usually present with tenderness and edema over the fracture site, instability of the knee with stress testing, and the inability to bear weight. Plain radiographs or CT scan can identify the extent of the fracture. Conservative treatment in the ED involves stabilization of the fracture with a knee-immobilizer or long-leg splint with the leg in 10–20 degrees of flexion, avoidance of weight bearing, and referral to an orthopedic specialist. Tibial plateau fractures depressed or displaced more than 1 cm require ORIF. Open tibial fractures require an update of tetanus status and intravenous antibiotics with a first-generation cephalosporin. Additional gram-negative coverage may be required for patients with severe wound contamination and/or 2 cm of tissue defect. Deep vein thrombosis, compartment syndrome, and injuries of the peroneal nerve and popliteal artery are common complications of tibial fractures. Fibular fractures are usually the result of direct trauma. Proximal fractures are due to external rotation of the ankle. Distal fractures usually result from internal rotations or inversion. Distal stress fractures may be seen in runners as a result of repetitive trauma. Isolated fibular fractures are rare, so it is important to check for possible associated ankle or ligamentous injuries. A Maisonneuve fracture is a fracture of the proximal fibula with an associated tibiofibular syndesmosis disruption (with or without a fracture). It is an unstable ankle injury that requires orthopedic consultation and treatment. If the common peroneal nerve is injured, the patient may have decreased sensation to the dorsal aspect of the foot and may develop “foot drop,” in which the affected foot hangs down due to the loss of ability to evert and to dorsiflex the foot. The appropriate treatment for an isolated, uncomplicated fibula fracture is a splint or compressive dressing for comfort and instructions to advance weight bearing as tolerated. Patients with stress fractures often report a gradual onset of pain over the lateral and anterior tibia that worsens with exertion and is relieved with rest. Peak incidence occurs in persons 18–25 years old with a slightly higher incidence in females, white persons, and military recruits. Many athletes report this pain in the early phases of their training after running on a hard surface. Stress fractures are frequently underdiagnosed in part because they are difficult to identify on plain radiographs. Up to 50% of stress fractures are not seen on radiograph until 2–6 weeks after healing has begun. A bone scan is the diagnostic gold standard because of its sensitivity, but it has a lower specificity and cannot differentiate among a
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fracture, neoplasm, and infection. Treatment consists of reducing the pain, inducing activity for 3–6 weeks, applying ice, and administering analgesic agents to treat the pain. Compartment syndrome is sometimes associated with tibial shaft fractures. It is characterized by the “five Ps”: pain (out of proportion to other findings and worse with passive stretching of the muscle groups), pallor, paresthesia (i.e., tingling or decreased sensation to pinprick, light touch, or two-point discrimination), paralysis, and pulselessness, which is a very late finding. The anterior compartment is most commonly involved. If intercompartmental pressures are elevated more than 30 mmHg, an orthopedic specialist should be consulted to determine the need for an emergency fasciotomy. If not done promptly, increasing pressures can cause significant muscle damage resulting in myoglobinuria, renal failure, metabolic acidosis, hyperkalemia, contracture formation, or loss of the limb. Achilles tendon rupture often occurs in patients who sustain a forceful plantar flexion to their ankle, such as from a motor vehicle collision, fall from a height, or taking off at a run from first base after a winter of inactivity. They frequently hear a popping sound and have difficulty ambulating. Achilles tendon ruptures have been documented in the second through eighth decades of life with a male preponderance. Risk factors include middle age, diabetes mellitus, hypothyroidism, chronic renal insufficiency, obesity, rheumatoid arthritis, lupus erythematosus, and prior injection of the tendon with steroids. The Achilles tendon is usually ruptured 2–6 cm above the attachment to the calcaneus, where it has the poorest vascular supply. A visible deformity or dent is noted, and a gap may be palpated. The Thompson test, which is performed by squeezing the mid portion of the calf, causes the foot to plantar flex in an intact tendon. Partial tears may have a negative Thompson test result. Radiological imaging is usually not necessary in the ED unless the diagnosis is unclear or a fracture is suspected. Ultrasound and MRI have high sensitivity and specificity for Achilles tendon rupture. Treatment consists of a posterior leg splint in plantar flexion for several weeks, crutches for ambulation, and referral to an orthopedist. Surgical repair is sometimes required. The medial head of the gastrocnemius muscle is often injured when the foot is forcefully plantar flexed and the knee is extended, or as the result of a fall on a plantar-flexed foot. Inadequate prior stretching before an activity, history of muscle injury, or advanced age can increase the likelihood of injury. The patient usually reports a sharp pain on the medial aspect of the proximal gastrocnemius muscle with increased pain to ambulate and plantar flex the foot. Examination may reveal a painful, edematous, bruised calf. The patient history is similar to that of Achilles tendon rupture, but the pain and tenderness are generally more proximal and the Thompson test result is negative. Treatment consists of immobilization with posterior leg splint, crutches for ambulation, application of ice, and administration of analgesics for pain.
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Pediatric Injuries Osgood-Schlatter disease is the partial separation of the tibial tuberosity at the insertion of the patellar tendon and is frequently noted in teenagers. They have pain with palpation of the tibial tuberosity. Treatment consists of rest, application of ice, administration of analgesic medications, and follow-up with an orthopedic specialist. Tibial tuberosity fractures in children may occur as a result of contraction of the quadriceps, such as with a leaping motion. They will have pain and tenderness of the tibial tuberosity and possibly an effusion of the knee joint. ED treatment consists of placement in a knee immobilizer, use of crutches, and follow-up with an orthopedic specialist in 1–2 days for operative reduction and fixation. Fractures in toddlers often occur as the result of a twisting motion of the leg such as during a fall when they are learning to walk. They usually will not have a direct history of trauma, will present with pain or a limp on the affected leg, and have tenderness and swelling at the fracture site. The appropriate treatment is application of a long leg cast for 2–4 weeks and consultation with an orthopedic specialist.
Bibliography Brady WJ, Degnan GG, Buchanon LP, et al: Challenging and elusive orthopedic injuries: Diagnostic and treatment strategies for optimizing clinical outcomes. Part II: Lower extremity injuries and pediatric fractures, Emerg Med Rep 1999;20(10). Hals GD, Logan M, Cory J: Management of acute foot and ankle disorders in the emergency department: Part I—The ankle, Emerg Med Rep 2003;24(20):1–13. Knoop KJ, Stack LB, Storrow AB: Atlas of Emergency Medicine, ed 2. McGraw-Hill: New York, 2002. Netter FH: Atlas of Human Anatomy, ed 3. ICON Learning Systems: Teterboro, NJ, 2002. Perron AD, Brady WJ: Evaluation and management of the high-risk orthopedic emergency, Emerg Med Clin North Am 2003;21:159–204. Powers J, Boenau I: Common fractures of the knee and lower leg, Emerg Med 2005; 26:46–53. Simon R, Koenigsknecht S: Emergency Orthopedics: The Extremities, ed 3. McGraw-Hill: New York, 2000. Simon RR, Koenignsknecht SJ: Emergency Orthopedics: The Extremities, ed 4. McGrawHill: New York, 2001. Stone CK, Humphries RL: Current Emergency Diagnosis and Treatment, ed 5. Lange Medical Books/McGraw-Hill: New York, 2004. Tintinalli JE, Kelen GD, Stapczynski JS, et al (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 1999.
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Open Fractures DAVID ZINSMEISTER
ICD Code: Open fractures 829.1
Key Points Open fractures need to be approached in a methodical manner. The Gustilo-Anderson classification of open fractures provides guidance for the initial management in the ED and the operating room. Open fractures are treated after other life-threatening injuries are stabilized. Optimally, open fractures should be treated within 8 hours of the time of injury to reduce the possibility of infection. ! Emergency Actions ! Emergency actions include removal of gross contamination using sterile technique and performance of cultures. The wound should be irrigated with sterile normal saline and covered with sterile dressing if surgery is delayed. If needed, the bone should be realigned and a splint applied. Antibiotic therapy should be based on the Gustilo-Anderson classification.
DEFINITION An open fracture involves a break in the skin that communicates with the fracture or its hematoma.
EPIDEMIOLOGY Common causes of open fractures are motor vehicle accidents, industrial injuries, or falls from great heights.
CLINICAL PRESENTATION The shaft of the tibia is most commonly involved, and the patient will usually have other injuries. Inquiry should be made regarding the environment in which the fracture occurred, since this may alter treatment.
EXAMINATION Any swelling, bruising, bleeding, or deformities should be noted. The skin should be inspected circumferentially. Piercing, inside-out fractures
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of the humerus and femur are commonly missed because the patient is placed in the supine position on the examination table. The extremity should be palpated in its entirety for crepitus and abnormal motion. Vascular status should be assessed, with the clinician looking for pallor, palpating pulses, and checking capillary refill time. Doppler examination of the pulse should be performed if arterial injury is suspected. In the conscious patient, sensory and gross motor function should be documented.
LABORATORY FINDINGS There are no specific laboratory findings useful in the diagnosis of open fractures. Laboratory studies should be directed at complementing underlying disease. If the patient is going to undergo surgery, a CBC, Chem 7 panel, and measurements of PTT and INR should be preformed.
DIAGNOSIS Since its introduction in 1976, the Gustilo-Anderson classification system, with its modifications and recommended treatment of open fractures, has become universally accepted as the standard for treatment of open fractures. Treatment based on proper fracture classification results in a significant reduction in bone infections. The following classifications should be applied once the diagnosis of an open fracture is made:
Type I: The cause is usually a low-energy injury in which the bone spike pierces the skin from the inside outward. Wound size is less then 1 cm, with minimal soft tissue injury. Simple fractures of the bone with minimal comminution are included. The level of bacterial contamination is usually low. Type II: The mechanism of injury is usually penetrating or blunt trauma from the outside in. Wound size is greater than 1 cm but less than 10 cm with moderate soft tissue injury and some muscle damage that is usually confined to one compartment. There is moderate comminution of the fracture. The level of bacterial contamination is moderate. Type III A: This type of injury results from a high-energy, penetrating, blunt trauma or crush injury from the outside to the inside. Wound size is greater then 10 cm. Limited soft tissue stripping from the bone may be present, and the soft tissue envelope around the bone is preserved. More than one compartment can be involved. The fracture is markedly comminuted and displaced. The level of bacterial contamination is high. Type III B: Same as type III A, except with extensive soft tissue stripping from the bone and devitalization of the surrounding muscle. Type III C: Same as type III A or B, except with major vascular injury.
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When classifying open fractures, the obvious wound size is not as important as the degree of damage to the surrounding soft tissue envelope, bone injury, and level of contamination. A fracture with a 10-cm wound caused by a saw is far less devastating than a severe crush injury with a small wound opening. With that in mind, the following types of fractures automatically result in a type III classification: 1. High-velocity gunshot wounds and shotgun wounds 2. Fractures that occur in a highly contaminated environment such as in a barnyard; in the presence of fecal matter or soil; involving water from lakes, rivers, and pools; and gross contamination on inspection 3. Segmental fractures, bone loss, extensive degloving of the skin and fat, and open fractures with compartment syndrome
RADIOGRAPHS Anteroposterior and lateral radiographs of the long bones on the arm, forearm, thigh, and leg and of the elbow and knee should be obtained. Anteroposterior, lateral, and oblique views of the wrist, hand, ankle, and foot should be obtained. Special views may be required such as Judet and inlet and outlet views in the presence of an open pelvic fracture. If pulses are absent, an arteriogram is indicated.
TREATMENT The principles of advanced trauma life support should be applied. Once the initial assessment and resuscitation measures are completed, the open fracture can be addressed. Gross contaminants such as leaves and rocks should be removed with sterile gloves and forceps. Culture samples for aerobic and anaerobic organisms should be obtained. If there will be a long delay before surgery, the wound should be irrigated with 1–2 L of sterile normal saline. The use of povidone-iodine and hydrogen peroxide in the irrigation solution has been shown to markedly decrease osteoblastic function and should not be used in the ED. Probing of the wound or debridement should not be performed in the ED, since it results in deeper seeding of the contaminates and bacteria. Any gross deformity or angulation should be promptly realigned, since this often improves diminished pulses and reduces bleeding and pain. A sterile dressing is then applied and the fracture is stabilized with a splint. Once the wound is dressed and splinted, no further examination of the wound should be done until the patient is in the operating room. The early use of antibiotics is considered therapeutic and not prophylactic, since culture studies have shown open fractures to be contaminated.
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Antibiotics should be administered in the ED based on the initial classification of the fracture. 1. In type I, type II, and all type III open fractures, a first-generation cephalosporin is the drug of choice for gram-positive coverage. One gram of cephazolin should be administered by intravenous piggyback every 8 hours in an adult patient. 2. In addition to cephazolin, all type III fractures should be treated with an aminoglycoside for gram-negative coverage. Adults with normal renal function should receive 360 mg of gentamycin, administered intravenously. 3. In open fractures that are highly contaminated, 2 million units of penicillin should be given by intravenous piggyback every 4 hours. Fractures exposed to soil, organic matter, and nonpotable water are susceptible to infection from anaerobic organisms such as clostridia. Definitive treatment occurs in the operating room. The wound is irrigated with pulse lavage and debrided, and the fracture is stabilized. The “golden period” for the treatment of open fractures is 8 hours from the time of injury until definitive treatment in the operating room is accomplished. Beyond this period, the rate of infection increases.
Bibliography Anglen JO: Comparison of soap and antibiotic solutions for irrigation of lower limb open fracture wounds: A prospective, randomized study, J Bone Joint Surg Am 2005;87-A: 1415–1422. Gopal S, Giannoudis PV, Murray A, et al: The functional outcome of severe, open tibial fractures managed with early fixation and flap coverage, J Bone Joint Surg Br 2004;86-B:861–867. Gustilo RB, Anderson JT: Prevention of infection in the treatment of one thousand and twenty five open fractures of long bones: Retrospective and prospective analysis, J Bone Joint Surg Am 1976;58-A:453–458. Olson SA: Instructional course lecture, the American academy of orthopaedic surgeons— open fractures of the tibial shaft: Current treatment, J Bone Joint Surg Am 1996;78A:1428–1437. Olson SA, Finkemeier CG, Moehring HD: Open fractures. In Bucholz RW, Heckman JD (eds): Rockwood and Green’s Fractures in Adults, ed 5. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 285–317. Spencer J, Smith A, Woods D: The effect of time delay on infection in open long-bone fractures: A 5 year prospective audit from a district general hospital, Ann R Coll Surg Engl 2004;86:108–112. Watson J, Moed BR, Karges DE, Cramer KE: Pilon fractures: Treatment based on severity of soft tissue injury, Clin Orthop Relat Res 2000;375:78–90.
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Shoulder Injuries KATHERINE ANNE HARRISON
ICD Codes: Humeral fracture (open) 812.59, Humeral fracture (neck) 812.01, Humeral fracture (pathologic) 733.11, Humeral fracture (shaft) 812.21, Scapular fractures 811.00, 811.11, Clavicle fractures 810.00, Sternoclavicular joint injury 839.61, Acromioclavicular joint injury 831.04, Shoulder dislocation (anterior) 831.11, Shoulder dislocation (posterior) 831.02, Rotator cuff tear 840.4
Key Points When shoulder dislocation is suspected, a radiograph taken from the scapular Y view should be obtained to confirm anterior or posterior dislocation. Radiography will also help to identify concomitant fractures including the Hill-Sachs compression fracture of the humeral head, greater tuberosity fracture, coracoid fracture, and others. ! Emergency Actions ! Neurovascular status should always be evaluated first when shoulder dislocation or fracture is suspected. If neurovascular status is compromised, an immediate shoulder reduction should be performed or an emergent orthopedic consultation should be obtained.
DEFINITION The shoulder consists of the pectoral girdle (clavicle and scapula), humerus, and three joints: the sternoclavicular, glenohumeral, and acromioclavicular joints.
ANATOMY The clavicle acts as a bony strut, supporting the upper limb away from the chest wall. The medial aspect of the clavicle articulates with the sternum through a synovial joint, which is saddle shaped but functions as a ball-and-socket joint. It is stabilized by the anterior and posterior sternoclavicular ligaments, the interclavicular ligament superiorly, and the costoclavicular ligament inferiorly.
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The acromioclavicular joint is a plane-type synovial joint between the lateral clavicle and medial aspect of the acromion. The joint is stabilized by anterior, posterior, superior, and inferior acromioclavicular ligaments. The scapula is a flat, triangular bone that forms the posterior aspect of the shoulder girdle. The superior and inferior spine of the scapula give rise to the supraspinatus and infraspinatus muscles. The posterior aspect of the scapula gives rise to the teres minor and major, and the anterior aspect of the scapula gives rise to the subscapularis. The coracoid process, at the superior border of the scapula, gives rise to the biceps, coracobrachialis, and pectoralis minor muscles. The glenohumeral joint is a multiaxial ball-and-socket synovial joint. The humeral head articulates with the shallow glenoid cavity of the scapula. The “socket” is enlarged by the glenoid labrum, a fibrocartilaginous rim. A synovial membrane extends from the glenoid fossa to the humeral head and extends to form the subscapularis bursa medially and the synovial sheath of the biceps brachii laterally. The strength of the joint results mainly from the muscles that surround it, especially the rotator cuff muscles (i.e., supraspinatus, infraspinatus, teres minor, and subscapularis).
LABORATORY FINDINGS There are no specific laboratory tests for shoulder injuries. Laboratory tests should be directed to assist in management of underlying diseases.
RADIOGRAPHS Radiographs should be directed toward the type of injury and clinical examination.
CLINICAL PRESENTATION Clavicle fractures account for about half of significant shoulder girdle injuries and are the most common fractures seen in children. The typical mechanism is direct blunt force or falling onto the shoulder. Fractures are seen most commonly in the middle third of the clavicle (80%), followed by the distal clavicle (15%) and the proximal clavicle (5%). Distal third fractures are further classified into three types. Type I are nondisplaced with intact coracoclavicular ligaments. Type II are displaced with ligamentous rupture, and type III involve the articular surface of the acromioclavicular joint. Treatment is accomplished with a figure-of-eight bandage or clavicle strap. Scapular fractures are diagnosed by anteroposterior shoulder radiographs with axillary and scapular views. Scapular fractures are relatively
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uncommon and generally indicate a high-force mechanism of injury. The scapula may be fractured at the body or spine, the acromion process, the coracoid process, the glenoid rim, the neck, or any combination thereof. Associated injuries, including pneumothorax, pulmonary contusion, neurovascular injury, and additional fractures, are present in approximately 80% of scapular fractures. The examination should always include distal neurovascular assessment. Significantly displaced fractures are treated with open reduction and internal fixation, whereas less serious injuries are treated conservatively with sling and swathe. Proximal humerus fractures (those proximal to the surgical neck) account for 4%–5% of all fractures and are commonly seen in elderly persons after a fall. The Neer classification system divides the humerus into four segments: the greater tuberosity, lesser tuberosity, anatomical neck, and surgical neck. Fractures are then classified according to the displacement of one or more parts from the remainder, with displacement defined as separation of greater than 1 cm or angulation of more than 45 degrees. Approximately 80% of proximal humerus fractures only require sling and swathe treatment with referral to an orthopedist for follow-up. Early mobilization of this type of fracture is critical to return of function. More complex fractures may require open reduction and internal fixation for adequate stabilization, and orthopedic consultation is indicated. Humeral shaft fractures are most commonly the result of direct force, usually from a fall or a direct blow. There are four typical injury patterns: transverse, oblique, spiral, and comminuted. The humeral shaft lies in close proximity to the radial nerve, which may be injured or, less commonly, lacerated by a fracture. Neurovascular function, especially including wrist, finger, and thumb extension, should be documented before any manipulation of the arm occurs. Treatment depends on the type of fracture, the amount of displacement, and the associated neurovascular injuries that may be present. Because of the incidence of delayed nonunion, patients with humeral shaft fractures should be referred to an orthopedist. Simple fractures without nerve injury may be treated with a coaptation splint and urgent orthopedic follow-up, whereas more complex, displaced, or angulated fractures require emergent orthopedic referral. Sternoclavicular joint injuries result from high-force mechanisms of injury and may result in significant damage to the neurovascular structures posterior to the injury. Sprain without dislocation is treated with ice, analgesia, and a sling. If dislocation is suspected, CT is the diagnostic test of choice. Sternoclavicular joint dislocation is a rare occurrence and accounts for fewer than 5% of shoulder girdle injuries. The joint may be dislocated anteriorly or, much less frequently, posteriorly. Posterior dislocation places the superior mediastinal structures, including the great vessels, trachea, and esophagus, at risk for compression
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or laceration. Anterior dislocation is treated by positioning a sandbag or towel roll between the shoulder blades and applying direct pressure over the proximal clavicle. The patient may be discharged in a figure-of-eight clavicle harness. Because of the concomitant ligamentous injury, this is often an unstable fracture that may require ORIF. Posterior dislocation may be treated with closed reduction by an orthopedic specialist after vascular injury has been assessed and stabilized. Acromioclavicular (AC) joint injuries result from falls and direct trauma to the shoulder. These injuries are classified into six types with increasing amount of ligamentous damage. Type I is simple sprain of the AC ligament with a normal presentation on radiograph, type II is rupture of the AC ligament with widening of the AC joint visible on radiograph. Type III is rupture of the AC and coracoclavicular ligaments with detachment of the deltoid and trapezius. On radiography, the AC joint appears dislocated 100% and the coracoclavicular space is widened as well. Type IV is rupture of all supporting structures with displacement of the clavicle posteriorly into or through the trapezius. Type V is similar to type IV, but with greater displacement of the clavicle, and type VI is rupture of all supporting structures with inferior displacement of the clavicle. Types IV through VI generally require surgical repair. Types I and II are generally managed conservatively with analgesia and sling, whereas treatment of type III injuries is controversial and may require operative repair. Shoulder dislocations are the most common major joint dislocation. The vast majority (95%) are anterior dislocations, with posterior and inferior (e.g., luxatio erecta) dislocations occurring rarely. A dislocated shoulder is held in slight abduction and external rotation, and the humeral head may be palpable. Axillary nerve injuries are common, and the skin overlying the deltoid should be tested for sensation. Chronic dislocations (greater than 3 incidents) should be referred to an orthopedist for evaluation for surgical repair. Anterior dislocations are caused by the head of the humerus being placed under marked abduction and external rotation, causing the tearing of the anterior capsule and glenoid labrum. The humeral head will rest in a subcoracoid, anterior position on radiograph. When dislocation is suspected, a radiograph taken from the scapular Y view should be obtained to confirm anterior or posterior dislocation. Radiography will also determine concomitant fractures, including the Hill-Sachs compression fracture of the humeral head, greater tuberosity fracture, coracoid fracture, and others. Posterior dislocations are classically described with tonic-clonic seizure and electrocution mechanisms of injury, with high-force internal rotation of the humeral head. An axillary view radiograph is the best way to identify the injury. On examination, the patient will not be able to passively externally rotate the arm; there will be a prominence of the humeral head posteriorly and a relatively flat anterior shoulder.
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There are many techniques for reduction described in the literature. All require adequate analgesia and relaxation for success. In the hanging weight or Stimson method, the patient is placed in a prone position with a weight (10–15 lb) suspended from the wrist. Scapular manipulation is an often successful adjunct to this method. In this technique, the inferior tip of the scapula is grasped and rotated toward the spine, presenting the glenoid fossa to the humeral head. This is an atraumatic approach to reduction of anterior or posterior dislocation. Traction-countertraction may be used for direct reduction of the shoulder. This method is aided by a sheet wrapped around the chest under the affected axilla, with another folded sheet used for traction of the bent affected arm. Reduction is achieved with slow steady pressure and aided by good patient pain control and relaxation. The Hennepin technique uses rotation to achieve reduction with little analgesia. The physician supports the elbow at 90 degrees abduction while slowly externally rotating the patient’s arm to 90 degrees. Rotator cuff tears occur in the context of degenerative changes in the case of elderly persons or repetitive and high-force trauma in the younger population. The rotator cuff comprises the tendinous insertions of the subscapularis, supraspinatus, infraspinatus, and teres minor muscles. These muscles control internal and external rotation and initiate abduction. The drop arm test indicates a significant tear and is performed by passively abducting the arm to 90 degrees, then asking the patient to hold it there while applying light downward pressure. In the case of significant tears, the patient is unable to hold the arm up and it drops precipitously.
Bibliography DeLee JC, Drez D: DeLee and Drez’s Orthopedic Sports Medicine: Principles and Practice, ed 2. WB Saunders: Philadelphia, 2005. Moore KL: Clinically Oriented Anatomy, ed 3. Williams & Wilkins: Baltimore, 1992. Simon RR, Koenigsknecht SJ: Emergency Orthopedics: The Extremities, ed 4. McGrawHill: New York, 2001.
Chapter 13
Pediatric Emergencies A. Emergencies and Resuscitations The Pediatric Patient: An Overview STEVEN W. SALYER The most important realization about pediatric patients is that “they are not just little adults.” Children, especially those younger than 6 months, markedly differ from adults or even from older children; their anatomy and physiology vary from those of older children or adults. Newborns, up to 6 weeks, are very demanding. The child bonds with the mother, father, and other children in the family during these first 6 weeks. At 6 weeks of age, the child responds more to sounds, actions, faces, and light. The child starts to respond to sound in a pleasurable environment. Between 4 and 9 months of age, the infant grows by leaps and bounds. The infant goes from lying to sitting up and even to standing with support. The infant responds to different stimuli with facial expressions and sounds. The infant reaches for objects and must explore everything. The infant also tries to taste and touch every object. The infant starts to say “Dada” and “Mama” by the age of 9 months. At 1 year to 18 months, the infant is on the threshold of walking and thus increased exploring. The infant’s mobility and independence increase. The infant’s vocabulary starts to increase to several single words. From 18 months to 3 years, the child’s mobility increases dramatically. The child learns to climb, ride a tricycle, jump, and kick. The child wants to be part of every activity and enjoys listening to stories. At 4–8 years of age, the child’s performance of complicated tasks improves. He or she learns to balance and to play catch with an improvement in coordination and speed. Language goes from a single word to sentences of multiple words. The child is now very independent and wants to dress himself or herself.
THE APPROACH TO A CHILD IN THE EMERGENCY CARE CENTER The emergency department (ED) can be a very scary place for both children and their parents. The family may have to wait for a long time, and this creates frustration for children and parents alike. People wearing white coats can be very scary to some children who have already had numerous visits to a healthcare provider. White coats represent “pain” or “shots” to many children. 652
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If possible, separate quiet rooms designed for pediatric patients should be available. A calm, caring, concerned attitude toward both the child and the parent should be the norm. It is important to remember that the child is there because someone brought him or her to the ED! It is not the child’s fault that he or she is here. The clinician should listen to what the adult who brought in the child is saying and ask, “What brings you to the emergency department today?” This should be asked in a caring and concerned voice. The practitioner should remember that the family usually does not want to be there. Does the family have a primary care provider? When was the last time that the child was seen by the primary care provider? Has the child received all of his or her immunizations? Was the child born at term, premature, or late? Was the delivery normal? Did the mother have a cesarean section or a vaginal delivery, and did she have a single or multiple deliveries? Is the mother or father present, and is this the first child of the parents? Are any of the other children at home also ill? Who is the primary care provider at home (e.g., grandmother, mother, or father)? What has changed in the last 24 hours in the child’s behavior? Is the child eating and drinking less? Does the person who brought the child to the ED suspect abuse, and if so, why? Has the child lost any weight? The point here is to determine why the child and adult have really come to the ED. The clinician should not judge the answer but should accept the explanation and address the concerns of both the child and the parent as justifiable. The patient’s vital signs should include the pulse, blood pressure, respirations, and rectal temperature, and pulse oximetry should be performed for every child. The practitioner should remember that an infant younger than 3 months of age who has a temperature higher than 100.4 F is septic until proven otherwise. Any allergies, prior hospitalizations, and prior hospital admissions should be noted. If the child was admitted, it should be determined what illness or disease was present at that time. What medications, if any, is (was) the child taking, including over-the-counter medications? Antipyretic medications should be administered to any child who has a temperature higher than 39 C. Acetaminophen 15 mg/kg is the drug of choice. The most commonly reported symptoms among children brought to the ED are as follows: 1. 2. 3. 4. 5. 6.
Feeding problems, spitting up, vomiting Failure to gain weight Crying or irritability Intestinal colic Diarrhea Constipation
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7. 8. 9. 10. 11. 12. 13. 14. 15. 16.
Rapid breathing, cough, or shortness of breath Noisy breathing or stridor Blue spells or stridor Eye problems, discharge, redness, or drainage Diaper rash Thrush Fever Child abuse Ear infections Sore throat
The clinician should be flexible in the examination and should listen to what the child and adult are really trying to communicate. When there is doubt regarding the diagnosis, a consultation with a pediatrician should be sought early and often. No one will ever blame a healthcare provider for setting up an early consultation. If someone does find fault, then that person does not understand the process of disease in children.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Cardiopulmonary Arrest in Children JOHN MCMANUS
ICD Codes: Cardiopulmonary arrest in a newborn 770.89, Cardiac arrest 427.5
Key Point The administration of oxygen is the key to treating a child in cardiopulmonary arrest.
DEFINITION Sudden cardiopulmonary arrest in infants and children is much less common than in adults and usually represents the terminal event of progressive shock or respiratory failure rather than a primary cardiac event. Because the etiology of cardiac arrest in infants and children varies by age, setting, and the underlying health of the child, resuscitation for infants and children requires a different approach from that used for adult patients.
EPIDEMIOLOGY In children, the incidence, precise etiology, and outcome of cardiac arrest and resuscitation are difficult to ascertain because most reports contain insufficient patient numbers or use exclusion criteria or inconsistent definitions that prohibit broad generalization to all children or the recognition of a gold standard for outcome. Only 15% of pediatric patients experiencing arrest in the out-of-hospital setting and 20% in-hospital have been shown to have ventricular tachycardia or fibrillation when rhythm is assessed by first responders. Survival after out-ofhospital cardiopulmonary arrest ranges from 3% to 17% in most studies, and survivors are often neurologically devastated. However, for resuscitation of children with respiratory arrest alone, a neurologically intact survival rate greater than 70% has been reported. In the pediatric age group, resuscitation is most frequently required at the time of birth; 5%–10% of newly born infants require some degree of resuscitation. Worldwide, 1 million neonatal deaths occur annually at birth occur from asphyxia and could be prevented by simple resuscitation techniques. The main causes of pediatric cardiopulmonary arrest after the neonatal period are sudden infant death syndrome (SIDS),
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respiratory disease, airway obstruction, trauma, sepsis, asphyxia, poisoning, and near drowning. Prompt, effective chest compressions and rescue breathing have been shown to improve the return of spontaneous circulation and to increase neurologically intact survival in children with cardiac arrest; however, no other intervention has been definitively shown to improve survival or neurological outcome.
PATHOPHYSIOLOGY Cardiac arrest in children typically represents the terminal event of progressive shock or respiratory failure. Either shock or respiratory failure may include a compensated state from which children can rapidly deteriorate to a decompensated condition, with progression to respiratory or cardiac arrest. Arrest in these instances is characterized by a progression from hypoxia and hypercarbia to respiratory arrest and bradycardia, then asystolic cardiac arrest. Therefore, emergency medical providers must detect and promptly treat early signs of respiratory and circulatory failure to prevent cardiac arrest. In children, early effective bystander cardiopulmonary resuscitation (CPR) has been associated with successful return of spontaneous circulation and neurologically intact survival.
CLINICAL PRESENTATION AND PHYSICAL EXAMINATION As described previously, the causes of pediatric cardiopulmonary arrest are heterogeneous and result in a multitude of possible clinical presentations. The physical examination should focus on determining the underlying cause for the child’s arrest. Early discovery of possible reversible causes of the child’s arrest through physical examination findings has been shown to decrease morbidity and mortality. Also, signs and symptoms of impending arrest (e.g., increased respiratory rate, poor circulation) should be recognized and treated.
LABORATORY FINDINGS Standard resuscitation laboratory tests should be a part of each institution’s quality assurance and improvement program. Other laboratory testing should be focused on determining an underlying etiology for the cardiopulmonary arrest.
TREATMENT The following recommendations for treatment of a pediatric patient in cardiopulmonary arrest are based on the American Heart Association’s
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guidelines published in the winter of 2005. Because resuscitative science is always evolving, healthcare providers should not only incorporate local standards of care but also update resuscitative science based on current literature. For the purpose of these guidelines, a neonate is a newborn infant until discharged from hospital. An infant is defined as younger than 1 year of age, and a child is between 1 year of age and adolescence. This section will discuss resuscitation for infants and children. The clinician should proceed with treatment as follows: 1. Check responsiveness. a. Gently shake the child and assess for trauma or injuries. b. If alone, give five cycles (about 2 minutes) of CPR. One cycle is 30 compressions and two breaths. Then get automatic external defibrillator (AED) or crash cart and alert a “code.” c. If two rescuers are present, one can retrieve the AED and alert additional personnel. d. If trauma is suspected, cervical spine precautions should be maintained. 2. Position the patient in the prone position. 3. Open the airway with head tilt–chin lift or jaw thrust if trauma is suspected. a. Give two breaths if the patient is not breathing. b. Advanced airway adjuncts may be used here by experienced providers (e.g., bag-mask, endotracheal [ET] tube, laryngeal mask airway [LMA]). c. Other airway considerations are: (1) delivery of 100% oxygen, (2) suctioning, (3) use of confirmatory devices (e.g., pulse oximetry, end-tidal carbon dioxide, and (4) backup airway adjuncts. d. If the presence of a foreign body is suspected, deliver five back blows and five chest thrusts (not abdominal) for infants. In children older than 1 year of age, use the subdiaphragmatic abdominal thrust (i.e., Heimlich maneuver) to relieve foreign bodies. Do not perform blind sweeps. 4. Assess circulation with a 10-second pulse check. a. If a pulse is present, assess for signs of perfusion such as mental status, pulse character, capillary refill, and urinary output. b. If no pulse is present, begin chest compressions. i. One rescuer should deliver 30 compressions to two breaths (about 100 compressions per minute). ii. Two rescuers should deliver 15 compressions to two breaths if no advanced airway device is present. If an advanced airway device is present, compression cycles should not be interrupted and should be delivered at 100 compressions/min. Ventilation should be done at a rate of 8–10 breaths/min.
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iii. Chest compressions should be hard (depress the chest one third to one half the anterior-posterior diameter of the chest) and fast (100 compressions/min). Completely allow the chest to recoil between compressions, and minimize interruptions. iv. For an infant, use two fingers or the “two thumb encircling” technique to deliver compressions. For a child use the heel of one hand, or the two-hand technique for larger children. v. Compressions are recommended in all children with a pulse slower than 60 beats/min and continued signs of poor perfusion. c. Place the patient on a monitor and obtain vascular or intraosseous (IO) access. i. If a shockable rhythm is present, deliver 2 J/kg. ii. AEDs can be used in all children older than 1 year of age (with proper pad size). iii. Fluids should be administered to correct shock such as isotonic crystalloids (e.g., lactated Ringer’s solution or normal saline). Glucose should be used only for documented hypoglycemia. A 20-ml/kg bolus dose should be started. 5. Assess for and correct possible contributing factors to the arrest. a. Check for the Hs—hypovolemia, hypoxia, hypothermia, hypoglycemia, hypokalemia/hyperkalemia, and hydrogen ion (acidosis). b. Check for the Ts—toxins, tamponade, trauma, tension pneumothorax, and thrombosis. 6. Assess the rhythm and treat per the appropriate pediatric advanced life support (PALS) algorithm.
Ventricular Fibrillation/Tachycardia Without a Pulse After the previous care is administered, the clinician should undertake the following actions if ventricular fibrillation or tachycardia is present without a pulse. 1. 2. 3. 4.
Continue CPR. Administer a second shock (4 J/kg). Resume CPR. Administer epinephrine (every 3–5 minutes) intravenously (IV) or (IO) at 0.01 mg/kg (1:10,000: 0.1 ml/kg) or via ET tube at 0.1 mg/kg (1:1000: 0.1 ml/kg). 5. Continue CPR (five cycles). 6. Administer another shock (4 J/kg). 7. Consider administering antiarrhythmic medication (e.g., amiodarone IV/IO, 5 mg/kg and repeated up to 15 mg/kg, 300 mg maximum;
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lidocaine IV/IO, 1 mg/kg, 100 mg maximum; magnesium IV/IO, 25–50 mg/kg, 2 g maximum).
Asystole/Pulseless Electrical Activity After the previous care is administered, the clinician should undertake the following actions if asystole or pulseless electrical activity is evident. 1. Continue CPR. 2. Administer epinephrine (every 3–5 minutes) IV/IO at 0.01 mg/kg (1:10,000: 0.1 ml/kg) or via ET tube at 0.1 mg/kg (1:1000: 0.1 ml/kg).
Bradycardia With a Pulse After the previous care is administered, the clinician should undertake the following actions if the patient exhibits bradycardia with a pulse. 1. Continue to support the ABCs of resuscitation (i.e., airway, breathing, and circulation). 2. Perform CPR if the pulse is slower than 60 beats/min and poor perfusion is present. 3. Administer epinephrine (every 3–5 minutes) IV/IO at 0.01 mg/kg (1:10,000: 0.1 ml/kg) or via ET tube at 0.1 mg/kg (1:1000: 0.1 ml/kg). 4. If there is an increased vagal tone or an arteriovenous block, administer atropine IV/IO at 0.02 mg/kg, with a minimum dose of 0.1 mg and a maximum dose of 1 mg.
Unstable Tachycardias With a Pulse SINUS TACHYCARDIA After the previous care is administered, the clinician should undertake the following actions if sinus tachycardia is present. 1. Continue to support the ABCs. 2. Search for and treat the underlying cause(s). SUPRAVENTRICULAR TACHYCARDIA After the previous care is administered, the clinician should undertake the following actions if supraventricular tachycardia is present. 1. Continue to support the ABCs. 2. Consider vagal maneuvers. 3. Administer adenosine (0.1 mg/kg, with a maximum dose of 6 mg), which may be repeated with double the first dose up to a maximum of 2 mg.
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4. Provide synchronized cardioversion (sedate the patient, if possible). Deliver 0.5–1 J/kg and increase to 2 J/kg for subsequent shocks. VENTRICULAR (WIDE-COMPLEX) TACHYCARDIA After the previous care is administered, the clinician should undertake the following actions if ventricular tachycardia is present. 1. Continue to support the ABCs. 2. Provide synchronized cardioversion (sedate the patient, if possible). Deliver 0.5–1 J/kg and increase to 2 J/kg for subsequent shocks. 3. The clinician may attempt adenosine (0.1 mg/kg, with a maximum dose of 6 mg), which may be repeated with double the first dose up to a maximum of 2 mg. 4. Consider the administration of antiarrhythmic medications (e.g., amiodarone IV/IO at 5 mg/kg, 300 mg maximum, over 20–60 minutes; procainamide IV/IO at 15 mg/kg, 17 mg/kg maximum, over 30–60 minutes).
SUMMARY Immediate, correct CPR can improve survival rates in pediatric patients experiencing cardiopulmonary arrest. The use of in-hospital medical emergency teams that respond to all codes and continuous quality improvement monitoring has led to decreased morbidity and mortality rates from pediatric cardiopulmonary arrest. “Best evidence” and local experts should help to guide the emergency care providers in delivering resuscitative medicine.
Bibliography Abella BS, Alvarado JP, Myklebust H, et al: Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest, JAMA 2005;293:305–310. American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 3: Overview of CPR, Circulation, 2005;112:IV12– 18, 156–211. Babbs CF, Nadkarni V: Optimizing chest compression to rescue ventilation ratios during one-rescuer CPR by professionals and lay persons: Children are not just little adults, Resuscitation 2004;61:173–181. Eftestol T, Sunde K, Steen PA: Effects of interrupting precordial compressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest, Circulation 2002;105:2270–2273. Wik L, Kramer-Johansen J, Myklebust H, et al: Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest, JAMA 2005;293:299–304. Young KD, Seidel JS: Pediatric cardiopulmonary resuscitation: A collective review, Ann Emerg Med 1999;33:195–205. Yu T, Weil MH, Tang W, et al: Adverse outcomes of interrupted precordial compression during automated defibrillation, Circulation 2002;106:368–372.
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Pediatric Cardiopulmonary Resuscitation CHRISTOPHER R. MCNEIL DEFINITION CPR in a pediatric patient presents unique challenges to the healthcare provider. First and foremost, establishing emergent vascular access and stabilizing the airway of a child prove to be technically difficult. Second, the dosage of medications given to a 10-kg infant is different than the dosage given to a 40-kg child. Lastly, unlike adults, children usually develop cardiac arrest as a result of respiratory arrest and shock syndromes. Respiratory failure in children is generally caused by hypoxia and airway obstruction. If this condition goes unrecognized or untreated and the child becomes apneic, cardiovascular collapse soon follows. Decreased cardiac output, hypotension, end-organ hypoperfusion, and decreased oxygen delivery to the brain and heart ultimately result in cardiac arrest.
EPIDEMIOLOGY SIDS is the leading cause of out-of-hospital pediatric cardiac arrest, followed by trauma, airway obstruction, and near drowning. Common etiologies of respiratory arrest in children include the following:
Foreign body obstruction Epiglottitis Asthma Sepsis Croup Near drowning Aspiration Pneumonia Drugs/toxins Smoke inhalation Hypoglycemia
The best chance of survival occurs when impending respiratory failure or shock is recognized and someone intervenes to prevent cardiopulmonary arrest. The survival rate without significant neurological deficits in children is only 2% after cardiac arrest. The poor outcome is likely a result of prolonged hypoxia suffered before arrest.
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GOALS OF INITIAL RESUSCITATION (BEYOND BYSTANDER CPR AND BASIC LIFE SUPPORT) Airway Establishing and securing the airway is the first priority. A bag-valve-mask device (BVM) with 100% oxygen should be used initially until intubation is possible. If the clinician is unable to ventilate a child using the BVM technique, an upper airway obstruction must be considered, and direct laryngoscopy must be performed immediately. A Magill forceps may prove useful to remove a foreign body lodged in the upper airway. If both BVM and intubation are unsuccessful, a rescue airway must be supplied. This includes techniques such as a needle cricothyroidotomy or standard cricothyroidotomy, depending on the age and size of the patient. Until the airway has been established and secured, CPR cannot continue.
Breathing Providing adequate oxygenation and ventilation is the second priority. After the airway has been established and secured, the patient’s breathing requires assessment. Bagging on 100% oxygen should be continued, and the patient should be ventilated with tidal volumes of approximately 10 ml/kg. The patient should be examined for equal chest rise, equal breath sounds, chest wall crepitans, and tracheal deviation (signs of tension pneumothorax).
Circulation The absence of a pulse or poor perfusion with a heart rate less than 60 beats/min mandates chest compressions. The goal of external cardiac massage is two-fold. First, it serves to circulate blood through the pulmonary vasculature to bind oxygen. Second, chest compressions maintain coronary and cerebral perfusion pressures. The coronary arteries require a perfusion pressure of 15 mmHg to deliver oxygen to the myocardium. It takes approximately 7–10 sequential chest compressions to produce this pressure. To regain return of spontaneous circulation, the myocardium must be supplied with oxygen-rich blood, and coronary washout must occur. Chest compressions should occur at a rate of approximately 100 per minute. Finally, a cardiac monitor should be used to assess the rhythm and level of cardiac electrical activity.
TREATMENT Intravenous Access A means of delivering drug therapy must be established. After one or two failed attempts at securing a peripheral IV line, an IO catheter
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should be established. The IO needle is inserted perpendicularly into the proximal anterior tibia, midline on the flat surface, and 2–3 cm below the tibial tuberosity. When there is a lack of resistance and the needle stands by itself, bone marrow aspiration should be attempted. If marrow can be aspirated and fluid runs smoothly, medications can safely be given. Central venous catheters can also be inserted.
Medications Medications such as atropine, epinephrine, lidocaine, and naloxone can be administered through the ET tube. The dose should be increased by 10 times for ET tube administration, followed by 1–3 ml of normal saline. The following medications are used in pediatric CPR:
Epinephrine: 0.01 mg/kg IV/IO, or 0.1 mg/kg via ET tube Atropine: 0.02 mg/kg IV/IO/ET tube (minimum dose, 0.1 mg) Amiodarone: 5-mg/kg bolus IV/IO Lidocaine: 1-mg/kg bolus IV/IO Magnesium: 25–50 mg/kg IV/IO (maximum dose, 2 mg) Procainamide: 15 mg/kg IV over 30–60 minutes Adenosine: 0.1 mg/kg IV/IO (maximum first dose, 6 mg) Sodium bicarbonate: 1 mEq/kg IV/IO See Figure 13-1 for the PALS algorithm. Attempt peripheral vascular access; if not successful, proceed based on need for drugs or fluids
Drugs
Fluids
ET tube present?
<3 years of age
Yes Epinephrine, atropine, lidocaine, naloxone
No
No
Yes
Intraosseous cannulation
1. Femoral vein 2. External jugular vein 3. Internal jugular vein 4. Subclavian vein
If operator skilled, cutdown may precede other sites
Figure 13-1. Pediatric advanced life support (PALS) algorithm.
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Reversible Causes Identify and treat the following reversible causes of cardiopulmonary arrest during resuscitation:
Hypoxemia Hypovolemia Hyperthermia Hyperkalemia and metabolic factors
Tamponade Tension pneumothorax Toxins/drugs/poisons Thromboembolism
Neonatal Emergencies RYAN GARNER, KAZUO MIHATA AND LINDA L. LAWRENCE
ICD Codes: These will vary according to the specific illness or injury.
Key Points The many diverse conditions that lead to critical illness in neonates make neonatal emergencies a vast topic of discussion. Any neonatal resuscitation situation will be chaotic. Critically ill children will present to all types of emergency medicine settings; therefore, every provider must be prepared to treat them. For purposes of this discussion, we will focus on neonates up to 1 month of age. In treating a critically ill neonate, the clinician must assume that sepsis is present. Early initiation of antibiotics may be lifesaving. ! Emergency Actions ! Initial stabilization requires skill in the ABCs: airway, breathing, and circulation. The airway should be stabilized, if necessary, with intubation. A 3.0-mm ET tube should suffice for a term newborn, whereas a 2.5-mm ET tube is more appropriate for a premature infant. Breathing should be assessed for rate, depth, and respiratory effort. If respiratory insufficiency or failure is suspected, the infant should be assisted with a BVM delivering 100% oxygen and intubated. The pulse should be assessed for rate, rhythm, and quality. If the pulse is greater than 220 beats/min and is regular and narrow-complex in nature,
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supraventricular tachycardia should be suspected. Initial treatment consists of vagal maneuvers followed, if necessary, by adenosine 0.1 mg/kg followed by a 5-ml saline push. If the patient is unstable, synchronized cardioversion can be used at 0.5–1.0 J/kg. Urine output should also be evaluated. If volume resuscitation is necessary, a bolus with 20 ml/kg of normal saline can be administered. However, if congenital heart disease is suspected and the patient may have congestive heart failure, then a bolus of 10 ml/kg of normal saline is a safer option. After the ABCs have been stabilized, the infant should be evaluated for disability. Increased intracranial pressure (ICP) can be seen in meningitis, intracranial injury, or other metabolic disorders. Altered mental status, hypertension, hyperpnea, bradycardia, and bulging fontanels may be evidence of increased ICP. A rapid determination of glucose level should also be made. Hypoglycemia should be treated with 0.5–1 g/kg of dextrose (2 ml/kg of D10W solution), repeated as necessary.
DEFINITION The topic of neonatal emergencies encompasses a vast variety of emergency conditions. As children mature, they may develop severe illness due to previously unrecognized congenital conditions. Establishing a diagnosis may be difficult, and the differential diagnosis should remain broad during the workup.
CLINICAL PRESENTATION Clinical presentation will vary depending on the systems affected, the health of the infant, and the point in the course of the illness at which the infant is brought to the ED. Prenatal history, gestational age at birth, and birth weight are also important. Most of the time, signs and symptoms will be vague and nonspecific. Some examples of nonspecific signs and symptoms of neonatal illness include fever or hypothermia, abnormal tone, weak suck, difficulty with feeding, jaundice, grunting respirations, cyanosis, or vomiting. Unexplained, excessive crying, also known as inconsolability, may result from a variety of sources. True inconsolability (when the child’s only awake state is crying) is a serious condition, and, if a source workup yields negative results, admission to the hospital is still warranted. Fever in an infant younger than 4 weeks old must be taken seriously. A complete septic workup should be accomplished (i.e., complete blood count [CBC], urinalysis, blood and urine cultures, lumbar puncture with cerebrospinal fluid [CSF] analysis, and culture). A chest radiograph should be ordered if respiratory symptoms are present, and stool
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cultures should be performed if gastrointestinal symptoms are present. Empirical, parenteral antibiotics should include ampicillin (100 mg/kg IV) plus gentamicin (2.5 mg/kg IV) or third-generation cephalosporinlike cefotaxime (50 mg/kg IV) (Table 13-1). As a clinical pearl, it should be noted that a “well-appearing” neonate on clinical examination does not rule out serious infection because signs and symptoms in the neonate can be nonspecific. If congenital heart disease is suspected, consider whether the lesion is left or right sided. A left-sided lesion with a patent ductus arteriosus (PDA)–dependent flow should be considered when the infant has poor distal pulses, an enlarged liver, or abnormal chest radiograph results. Examples of left-sided lesions are coarctation of the aorta, aortic stenosis, or hypoplastic left heart syndrome. Right-sided lesions with a PDAdependent flow usually present early after birth with cyanosis. If a ductaldependent lesion is suspected, prostaglandin E1 should be given and an immediate consultation with a pediatric cardiology specialist is warranted. Onset of action is fairly rapid with prostaglandin E1 and there are serious adverse effects related to the medication, including apnea. When congenital heart disease lesions present in the first 2–3 weeks of life, they are typically ductal-dependent lesions.
Table 13-1 Neonatal and Pediatric Resuscitative Drugs DRUG Adenosine Atropine Epinephrine (1:1000) Labetalol Lidocaine Nitroprusside Diphenhydramine Etomidate Flumazenil Glucose Ketamine Lorazepam Naloxone Phenobarbital Thiopental Ampicillin Ceftriaxone Cefotaxime Gentamicin
DOSE 0.1 mg/kg 0.02 mg/kg (max 0.5 mg) 0.01 ml/kg (max 0.5 ml) IM/SQ 3 q 5 min 0.2–1.0 mg/kg IV over 2 min q 10 min (max 20 mg) 1 mg/kg 1–8 mg/kg/min (max 10 mg/kg/min) 1–2 mg/kg IV/IM (max 50 mg) 0.3 mg/kg 0.01 mg/kg 0.5–1 g/kg (2–4 ml/kg D25 or 1–2 ml/kg D50) 1–2 mg/kg 0.05–1.0 mg/kg (max 4 mg) slow IV 2 0.1 mg/kg 20 mg/kg (max 1 g) IV 4–6 mg/kg 50–100 mg/kg 50 mg/kg 50–100 mg/kg 2–3 mg/kg
Data from Crain EF, Gershel JC: Clinical Manual of Emergency Pediatrics, ed 4. McGraw-Hill: New York, 2003. IM, Intramuscular; SQ, subcutaneous; IV, intravenous; D25, 25% dextrose solution; D50, 50% dextrose solution.
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Gastrointestinal disease may have various presentations, including vomiting or diarrhea. Causes may include malrotation (1/500 live births), volvulus, or Hirschsprung’s disease. An infant with bilious vomiting is likely to have a surgical emergency. Nonbilious vomiting may be due to pyloric stenosis. Necrotizing enterocolitis, more commonly seen in premature infants, is a multifactorial and poorly understood inflammation of the bowel wall that can lead to perforation. Abdominal radiographs may reveal classic signs of pneumatosis intestinalis and hepatic portal air. These infants can be quite ill and require broad-spectrum antibiotics and an urgent pediatric surgery consultation. Seizures are another possible emergency in neonates that has an extensive list of possible etiologies. Some important causes to consider include anoxia, hypoxia, hypoglycemia, electrolyte disturbances, sepsis, inborn errors of metabolism, and drug withdrawal. The presentation can be subtle and sometimes difficult to distinguish from normal neonatal movements/activity and startle reflexes. Two clues in distinguishing seizures from normal activity are that seizures cannot be suppressed by passive restraint and seizures cannot be elicited by motion or startling. The first-line therapy for seizures are benzodiazepines, preferably lorazepam given at a dosage of 0.05–0.1 mg/kg IV. If benzodiazepines are unsuccessful, phenobarbital is second choice—not phenytoin/fosphenytoin, due to its potential depressive myocardial effect.
EXAMINATION General Appearance A critically ill infant may appear pale or gray due to the shunting of blood away from his or her skin to perfuse the vital organs. It is also important to assess the infant’s breathing pattern and work of breathing. Bruising, especially in a neonate, is concerning for nonaccidental trauma.
Vital Signs Even though it is frequently not done, infants can have their blood pressure measured with a cuff of the appropriate size. In neonates in the first month of life, the systolic blood pressure should be at least 60 mmHg. Healthy infants of this age will have a pulse in the range of 140 beats/min. If an infant’s pulse is below 60–80 beats/min, chest compressions should be initiated. The respiratory rate should be between 30 and 60 breaths/min. Neonates should have their temperature measured rectally. A fever is defined as a rectal temperature above 100.4 F.
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Head The fontanelle should be palpated. A sunken fontanelle may indicate hypovolemia, whereas a bulging fontanelle reflects increased ICP, usually from infection, hydrocephalus, or nonaccidental trauma.
Chest The examiner should assess the rate and work of breathing, including retractions or nasal flaring. He or she should auscultate for breath sounds, wheezing, and stridor and auscultate the heart for murmurs. Most asymptomatic neonates with a murmur in the first few days of life have structural heart disease.
Abdomen Distention of the abdomen is very nonspecific. Engorgement of the liver indicates congestive heart failure. A rigid abdomen is very concerning.
Skin A full skin examination should be accomplished. Petechiae and purpura may reflect serious infection. If bruising is present in neonates, a high suspicion for nonaccidental trauma should be held. The clinician should examine the skin for jaundice, bruising, or extensive peeling. Critically ill infants should be placed on continuous monitoring. This should include cardiac monitoring for dysrhythmias and pulse oximetry.
LABORATORY FINDINGS Blood cultures, urine cultures, CBC, electrolyte measurements, liver function tests, coagulation tests, and a urinalysis should be performed. Other tests to consider, depending on the system involved or the patient’s history, would be an arterial blood gas (ABG) analysis (for respiratory and acid–base status), lactate or ammonia measurements, and a toxicology screening (if poisoning is suspected). Imaging based on presentation will vary but may consist of chest or abdominal plain radiographs, a skeletal survey, echocardiogram, or head computed tomography (CT) scan. An ABG analysis can help differentiate a congenital heart disease with decreased pulmonary blood flow from a primary pulmonary problem. This test should be performed after 100% oxygen has been administered for 10 minutes. If there is a primary pulmonary process, the
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PO2 will rise above 150 mmHg, whereas in congenital heart disease, the PO2 will remain below 50.
TREATMENT Fluid administration will likely be necessary. If attempts to secure peripheral IV access are not rapidly successful, the clinician should attempt to place an IO line. If shock is suspected because of sepsis or other reasons, aggressive fluid administration is warranted. If anemia is suspected, the healthcare provider might consider administering 10 ml/kg of packed red blood cells. Foley catheters are usually necessary to assess urinary output as well as to obtain a urinalysis. Bag urines are unacceptable in the evaluation for sepsis. Gastric tubes may be inserted to decompress the stomach. This is important, especially if the infant underwent prolonged ventilation with a BVM. Finally, given the limited physiological reserve of neonates and the broad differential of life-threatening illnesses, all providers should give serious consideration to consultation with a pediatrician earlier rather than later, especially for patients with unstable conditions. If the clinician’s facility does not have a neonatal or pediatric intensive care unit, it is likely the patient will require transfer if he or she is seriously ill.
Bibliography Brown L, Denmark TK, Jones J: The critically ill or comatose infant: An organized approach, Emerg Med Pract 2002;4(10):1–24. Crain EF, Gershel JC: Clinical Manual of Emergency Pediatrics, ed 4. McGraw-Hill: New York, 2003. Ma OJ, Cline DM: Emergency Medicine Manual, ed 6. McGraw-Hill: New York, 2004. Sharieff GQ, McCollough M: The nightmare neonate: Life-threatening events in the first month of life, Emerg Med Pract 2003;5(9):1–20.
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Pediatric Airway Management ROY JOHNSON III AND LINDA L. LAWRENCE
CPT Codes: 315.00, Intubation, endotracheal, emergency procedure
Key Points Pediatric airway compromise is the most common cause of pediatric death. Effective airway management can be lifesaving. BVM ventilation is a critical skill and the first procedure that should be undertaken in emergency situations of respiratory arrest or severe airway compromise. The procedure is similar to airway management in adults, but there exist important anatomical differences in the infant/child that must be considered. ! Emergency Actions ! In the ED, airway management is typically an emergency procedure. During the evaluation of a critically ill or injured child, airway assessment is the highest priority.
DEFINITION Pediatric airway management is an absolutely critical skill in ED healthcare providers. The goal of airway management is to allow for and/or to facilitate proper ventilation and gas exchange in the respiratory system. Pediatric patients have anatomical and pathophysiological airway differences from adults.
EPIDEMIOLOGY In children, a compromised airway is the most common cause of death and severe morbidity. Airway management is the top priority in resuscitation and, when done effectively, saves more lives than any other single intervention. Unlike in adults, in whom cardiac arrest most often has a primary cardiac cause, in children cardiac arrest is usually the result of respiratory arrest.
PATHOLOGY Pediatric airways have a number of differences from those of adults. The child’s head and occiput are proportionally larger, causing the neck
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to flex when the child is lying supine. Instead of placing a towel under the head as often is done in adults, a towel or pad may need to be placed under the shoulders of infants due to the disproportionately large head size. The child thus requires less neck flexion to be in the appropriate “sniffing” position. Pediatric patients have lower muscular resting tone, which contributes to increased passive obstruction by the relatively larger tongue. The airway is located more anterior, increasing the difficulty of visualization. The smaller airway with its decreased diameter has increased resistance to airflow per Poiseuille’s equation. The narrowest part of a pediatric airway is the cricoid ring, which can lead to increased resistance for the ET tube after it has passed the vocal cords. An awareness of these differences will help to minimize difficulties in managing a child’s airway. The causes of respiratory difficulty and failure in children are numerous. Upper airway obstructions that could be seen in an ED are foreign body aspiration, epiglottitis, croup, and anaphylaxis. Obstruction of the lower airway could impede oxygenation and lead to respiratory distress. Causes of lower airway obstruction include acute asthma exacerbation, bronchiolitis, and cystic fibrosis. Parenchymal and alveolar disorders like severe pneumonia, pulmonary edema from a near drowning, and smoke inhalation can lead to ventilation difficulty. Impaired neurological control of ventilation from causes such as head trauma, intracranial hemorrhage, botulism, tetanus, high cervical spine injury, or drug intoxication can lead to respiratory arrest. A child can also experience respiratory distress from the physical fatigue associated with prolonged exertional breathing.
CLINICAL PRESENTATION The pediatric patient with respiratory difficulty can present in a variety of ways based on the cause and duration of the problem. The spectrum at presentation extends from within normal limits to stridorous dyspnea to coma. Children who seem to be doing well but for whom airway obstruction is in the differential diagnosis must be observed closely because they can decompensate rapidly. The history obtained should include the time course of the current presenting episode. Somnolence, agitation, and changes in mental status should be annotated and may signal potential imminent respiratory arrest. Any recent cough, fever, or sore throat should be noted. The clinician should find out whether the patient’s immunizations are up to date. He or she should inquire about any known respiratory disorders such as asthma or cystic fibrosis. Previous airway problems, trauma, foreign object ingestion, and exposure to chemical and medications should be explored. The contents and time of last oral ingestion should be identified.
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EXAMINATION The physical examination should be directed at the evaluation of the degree of respiratory compromise, the cause, and anything that could affect airway management. The patient should be observed for drooling, nasal flaring, use of accessory muscles to aid breathing, retraction of intercostal muscles, the tripod position, tachypnea, audible wheezing, stridor, signs of trauma, cyanosis, and a general appearance of anxiety or distress. The lungs should be percussed and auscultated. A cardiac examination is also warranted. Any physical findings that could affect airway management such as mandibular or maxillary hypoplasia should be noted.
DIAGNOSIS The diagnosis of airway compromise is a clinical one. Indications for the emergent management of an airway include respiratory failure, failure to oxygenate adequately, increased work of breathing, failure to remove carbon dioxide, neuromuscular weakness, cardiac arrest, central nervous system (CNS) failure, and risk for pulmonary aspiration.
LABORATORY FINDINGS Oxygen saturation monitoring is the standard of care for any pediatric patient with breathing difficulty. Cardiac monitoring is a helpful adjunct. An electrolyte panel can be performed, with special attention paid to the potassium level; hyperkalemia is a contraindication for the use of succinylcholine during rapid sequence intubation (RSI), if required. A CBC can be sent to evaluate the hemoglobin level and a head CT scan can aid in the diagnosis of an inflammatory condition such as epiglottitis. A toxicology screen should be considered in older children and adolescents or when there is a historical indication.
TREATMENT The initial management of airway obstruction in a pediatric patient should be undertaken per basic life support, PALS, and advanced pediatric life support protocols. Mechanical repositioning via a head tilt/chin lift maneuver should be attempted before more definitive airway management techniques such as intubation are undertaken.
COMMON PEDIATRIC AIRWAY EQUIPMENT It is extremely important to use properly sized equipment in pediatric airway management. Often, code carts or airway carts are set up by
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weight and are color coded. The Broselow tape is a frequently used color-coding system that allows the provider to measure the length of the child. The tape then identifies the size of resuscitation equipment and appropriate drug dosage for the child according to his or her length.
Oropharyngeal Airway An oropharyngeal airway is a simple device that can be used on an unconscious patient to prevent obstruction of the airway by an atonic tongue. The appropriately sized device should match the patient’s size from the corner of the mouth to the angle of the mandible.
Nasopharyngeal Airway A nasopharyngeal airway is a safe device to use in a conscious patient. In pediatric patients, the lumen is so small it can easily become occluded with mucus or blood. The properly sized nasopharyngeal airway should measure the same as the tip of the patient’s nose to the tragus of the ear.
Bag-Valve-Mask Device A poorly fitting mask is a common reason for inability to ventilate with a BVM. At a flow rate of 15 L/min, oxygen delivery is maximized. It is important to perform a jaw lift or other procedure when using a BVM to reduce the risk of airway occlusion from the tongue. Another caution is to ensure proper tidal volume, which minimizes the risk of barotrauma. A good approach is to start with small tidal volumes and gradually increase them, assessing chest rise and auscultating. Pediatric Ambu-Bags are smaller than adult Ambu-Bags with a 750-ml volume. An adult bag can be used, but the practitioner needs to be very careful to not exceed necessary tidal volume for the patient. BVMs come in multiple sizes and should fit over the nose and mouth and be able to create a seal.
Laryngoscope Blades The two most commonly available types of laryngoscope blades are the straight (Miller) and the curved (Macintosh, Mac). Some data suggest that a Miller blade is superior in children younger than 2 years. A straight blade allows the large floppy epiglottis common in small children and infants to be lifted, providing direct visualization of the vocal cords. The proper size for a straight (Miller) blade size, according to patient age, is as follows: premature, blade size 0; neonate, 0–1; 1 month to 2
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years, 1; 2–6 years, 1–2; 6–12 years, 2; and older than 12 years, 2–3. The appropriate size of a curved (Mac) blade, according to patient age, is as follows: 2–6 years, blade size 2; 6–12 years, 2–3; and older than 12 years, 3.
Laryngeal Mask Airway The LMA has been largely used in the pediatric population. It can be inserted blindly. The LMA prevents supraglottic obstruction, giving it superior protective qualities over a simple mask. However, the LMA is less reliable than an ET tube at preventing aspiration. The proper size of this device can be selected according to patient weight in kilograms: less than 5 kg, LMA size 1; 5–10 kg, 1.5; 10–20 kg, 2; 20–30 kg, 2.5; 30–50 kg, 3; 50–70 kg, 4; and more than 70 kg, 5.
Endotracheal Tube The ET tube can provide adequate ventilation, protection from aspiration, and a route for drug administration. The tube should fit snugly to ensure ease of ventilation, adequate airway protection, and maximum delivery of medications. The tube should be advanced until the second mark is past the vocal cords. Patient age and weight can be used to select the correct size of ET tube. In patients younger than 1 year old, weights and corresponding sizes are as follows: less than 1.5 kg, ET tube diameter 2.5 mm; 1.5–2.5 kg, 3.0 mm; and more than 2.5 kg, 3.5 mm. In patients older than 1 year of age, the ET tube size can be calculated as follows: ET tube size in millimeters ¼ ðpatient’s age in years=4Þ þ 4
It should be noted that resuscitation measuring tapes have been shown to be more accurate than this formula, and the use of cuffed tubes is generally avoided in patients younger than 8 years of age.
RAPID SEQUENCE INTUBATION RSI is the systematic method of ET intubation facilitated by the use of medications for sedation, analgesia, and paralysis. The goal is to obtain an adequate airway with minimal adverse effects. The use of RSI in critically ill pediatric patients has been well described, and it is the first choice of intubation technique in the absence of contraindications. Contraindications include known difficult airway, patients who are too ill to receive induction medications, and cases in which RSI is not
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required for safe, rapid intubation (e.g., a comatose patient). There are multiple ways to organize the steps for RSI; the breakdown that follows comes from Tintinalli et al.’s Emergency Medicine: A Comprehensive Study Guide. The clinician should take the following steps in preparation for RSI:
Preparation
Gather all tools and materials. Establish a functioning IV line. Pre-draw all medications dosages and label syringes. Obtain laryngoscopes of proper size, and check for function and working light. Hook up suction equipment and check for function. Obtain a BVM of proper size, hook it up to oxygen, and check it for function. Obtain an ET tube of estimated appropriate size, and check inserted stylet and cuff for function. Have a second experienced provider on hand to apply cricoid pressure. Establish continuous pulse oximetric monitoring. Have an exhaled carbon dioxide detection device on hand. Have materials for rescue maneuvers handy in case ET intubation fails.
Preoxygenation
Have patient breathe 100% oxygen with a tight fitting mask for 2 minutes.
Premedication
Administer atropine, 0.015–0.20 mg/kg, via IV push. Small children and infants are at greater risk for vasovagal stimulation and bradycardia with intubation, especially with the use of succinylcholine. If the patient is suspected of having increased ICP, administer lidocaine, 1.5 mg/kg, via IV push 1–5 minutes before intubation.
Cricoid Pressure
Apply firm pressure at the cricoid cartilage in an anteroposterior direction. The goal is to occlude the esophagus to reduce the risk of aspiration and to improve visualization. Initiate cricoid pressure just before intubation; do not release until the ET tube is in place.
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Induction of Anesthesia
Choose one of the following induction agents based on the clinical picture. Etomidate is preferred by many due to its cardiostability and short duration of action. If reactive airway disease is the cause of respiratory distress, ketamine is a popular choice because of its bronchodilator effect. 1. Etomidate, 0.3 mg/kg: Positive effects include cardiostability, short duration of action, and effect of decreasing intracranial and intraocular pressure. Adverse effects include pain on injection, myoclonic movements, nausea, and vomiting. 2. Thiopental, 4 mg/kg IV: This drug is favorable because is decreases intraocular pressure, decreases ICP, provides cerebroprotection in intracranial injuries, and has a short duration of action. Adverse effects include hypotension, histamine release, and neuroexcitatory effects such as hiccups, twitching, and cough. 3. Midazolam, 0.1–0.2 mg/kg IV: This drug has the advantages of being cardiostable, reversible with flumazenil, and amnestic. Possible adverse effects include apnea, respiratory distress, and hypotension. 4. Ketamine, 2 mg/kg IV or 4–6 mg/kg intramuscularly (IM): This drug is favorable because it is cardiostable, a bronchodilator, an analgesic, a dissociative, and amnestic. Possible adverse effects include laryngospasm, increased secretions, increased intraocular and intracranial pressure, and emergence reactions.
Neuromuscular Blockade
Inject the neuromuscular blockade (NMB) immediately after the induction of anesthesia. The neuromuscular paralysis allows for the best visualization and relaxation of the vocal cords. Choose one of the following agents: 1. Succinylcholine, 1–2 mg/kg IV (depolarizing NMB): The advantages of this drug are that it is reliable, has a rapid onset, and has a short duration. Side effects include hyperkalemia; malignant hyperthermia; elevated intraocular, intracranial, and intragastric pressures; prolonged blockade; and fasciculations, which can be prevented with preadministration of defasciculating dose (10% of an intubating dose) of a nondepolarizing NMB 2 minutes prior. It should be noted that the U.S. Food and Drug Administration has issued an advisory against routine use of this agent in children due to the association with hyperkalemic arrest. However, it is still approved for emergency airway management. 2. Vecuronium, 0.15–0.4 mg/kg (nondepolarizing NMB): The positive effects of this drug include rapid onset and a lack of hemodynamic effects.
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3. Rocuronium, 0.9–1.2 mg/kg (nondepolarizing NMB): The advantages of this agent are a lack of hemodynamic effects and a faster onset than vecuronium.
Intubation
Visualize the vocal cords. Insert the tube, watching it pass the vocal cords. Advance the tube until the second line passes the cords. Verify tube placement with auscultation and end-tidal carbon dioxide detection. Because of the shortened trachea in infants, it is easy to intubate the right main stem bronchus. Careful auscultation and rapid radiographic confirmation of tube placement are critical. Secure the tube. Continue to monitor the patient’s condition.
Failed Intubation In case of failed intubation, the patient should be ventilated with a BVM until oxygen saturation optimizes. At that point, intubation should be reattempted.
SURGICAL AIRWAY On rare occasions, a surgical airway may be necessary. In patients younger than 11 years, the preferred method is needle cricothyroidotomy with needle jet insufflation. Although this provides oxygenation, it does not allow for adequate ventilation, which can result in hypercarbia. Thus, this is a temporary procedure requiring urgent surgical consultation to provide a definitive surgical airway.
Bibliography Geradi MJ, Sacchetti AD, Cantor RM, et al: Rapid-sequence intubation of the pediatric patient, Ann Emerg Med 1996;28(1):55–74. Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Miller RD: Miller’s Anesthesia, ed 6. Churchill-Livingstone: New York, 2005. Reichman EF, Simon RR (eds): Emergency Medicine Procedures. McGraw-Hill: New York, 2005. Roberts JR, Hedges JR: Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Upper Respiratory Emergencies in Children DAWN F. RONDEAU
ICD Codes: Croup 464.4, Epiglottitis 464.3, Bacterial tracheitis 464.1, Foreign bodies, pharynx/larynx 933, Bronchiolitis 466.1
Key Points Oxygen delivery is the key to treatment of any upper respiratory tract emergency in children. ! Emergency Action ! The stability and safety of the airway should be assessed. Emergency airway measures should then be planned, if needed. The child should be left in a position of comfort with family members. Oxygen should be delivered in whatever method the child will tolerate, and any distressing procedures should be avoided. Emergency airway equipment can be used at bedside. A BVM delivering 100% oxygen should be the initial modality if impending respiratory compromise is evident. For epiglottitis, intubation should occur in a controlled setting with experienced providers.
DEFINITION Croup is a clinical diagnosis characterized by barky cough, hoarseness, inspiratory stridor, and a variable degree of respiratory distress. It is divided into two types: viral laryngotracheobronchitis (LTB) and spasmodic croup. LTB is characterized by infection with parainfluenza viruses types 1, 2, and 3 as well as respiratory syncytial virus (RSV), influenza virus type A, or adenovirus. Anatomically, the subglottic tissues and sometimes the tracheal mucosa become inflamed, leading to a narrowed airway. The supraglottic area is not involved. Spasmodic croup has no defined etiology. It appears to be associated with previous episodes of croup and a family history of asthma or allergies. This presentation may also be a presentation of laryngomalacia, congential subglottic stenosis, vocal cord paralysis, congenital laryngeal webs, and atresia. Epiglottitis is an acute bacterial process that can be life threatening. It involves the swelling of the epiglottis and aryepiglottic folds. The
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glottis and subglottis are unaffected. The swelling is in response to infection by Haemophilus influenzae type B (HIB). Since the introduction of the HIB vaccine, its incidence has markedly dropped; however, particular concern should be granted to children who are not immunized. The onset is that of a rapid fulminant course, potentially leading to full obstruction and arrest. Bacterial tracheitis, also known as pseudomembranous croup, is a relatively uncommon illness in children and generally occurs in those younger than 3 years of age. This infection results in very thick, mucopurulent secretions in the trachea. It often follows LTB and could be considered a bacterial complication of a viral disease. Foreign bodies can also cause symptoms similar to croup. This may present primarily in toddlers, as a cough, wheeze, or choking and upper airway stridor. Dyspnea and fever are less commonly present. Most commonly aspirated items include food (e.g., peanuts, hot dogs, popcorn), and the aspiration of balloons have the highest morbidity and mortality rates.
EPIDEMIOLOGY In croup, there is a 2:1 male-to-female ratio. This condition occurs more in the late fall and early winter. It can occur in all age groups but is particularly prevalent in 2-year-olds. The recurrence rate is 2%. LTB is characterized by infection with parainfluenza viruses types 1, 2, and 3 as well as RSV, influenza virus type A or adenovirus. Occasionally, measles, rhinovirus, enterovirus, and herpes simplex are causes, as well. Metapneumoviruses typically affect the lower respiratory tract but have been seen in the upper tract as well. Finally, Mycoplasma pneumoniae has also been associated with mild cases of croup. Hospital admissions for croup have steadily declined the past few years. In general, patients admitted in afternoon have a longer length of stay than those admitted during the night. Spasmodic croup is not associated with a prevalence related to the time of year. The etiology is uncertain and appears most common in persons with a family history of allergies or asthma or a personal history of croup. There does not appear to be a male or female prevalence in this disease. Epiglottitis incidence is markedly reduced in those countries where the HIB vaccine is dispensed. Incidence in persons younger than 5 years old in the United States decreased to 0.3 cases per 100,000 in 2000.This infection is not seasonal and commonly affects children of school age but can affect persons of all ages, including adults. In fact, as a result of the vaccination of younger
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children, it is now more common in older children and adolescents. The mortality of this disease has also been reduced by early intubation or tracheotomy performed on recognition of the infection. Untreated epiglottitis has reported mortality rates of 6%. This infection generally results from infection by HIB. Bacterial tracheitis is most common in children younger than 3 years of age. With the HIB vaccine reducing epiglottitis, some references indicate that this bacterial infection is now more common than epiglottitis. There has not been documentation of any prevalence in male or female persons. This infection is generally caused by staphylococcal infection, sometimes following a upper respiratory tract infection. The infection is less commonly caused by Moraxella catarrhalis, H. influenzae, Streptococcus pneumoniae, alpha-hemolytic streptococcus, and other Streptococcus organisms. The incidence of foreign body aspiration has not changed through the years. Eighty percent of the children who aspirate are younger than 3 years old. There are fewer than 25 deaths a year, and the majority of those are due to aspiration of balloons. Although the death rate has decreased through the years, aspiration of foreign bodies continues to be present in the toddler population and should be included in the differential diagnosis.
CLINICAL PRESENTATION Barking cough, inspiratory stridor, and a hoarse voice are typical presentations of croup. Symptoms are usually worse at night. There may be mild to moderate respiratory distress. The clinical history includes 2–3 days of coryza with low-grade fever. Because the airway is more narrowed from edema and swelling, the stridor becomes more pronounced, and there may be mild tachypnea and a prolonged inspiratory phase. If the airway obstruction becomes severe, the child will be increasingly restless or anxious and supraclavicular or intercostal retractions may be seen. Agitation increases the narrowing by creating negative pressure in the airway, which can lead to further respiratory distress and agitation. In the worst case scenario, continued progression will lead to respiratory fatigue and distress with hypoxia and decreased ventilation requiring intubation. Dehydration may occur in association with decreased oral intake and fever. In the case of spasmodic croup, there is not generally the history of fever, upper airway symptoms. or any precursor of illness. It occurs most frequently in the evening or nighttime with a sudden onset of croup and possibly coryza and hoarseness. The child is awakened with a barky cough and respiratory distress. After a few hours these symptoms resolve,
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and in the morning the only residual element is a slightly hoarse voice and cough. These symptoms may recur as a cluster of occurrences. Laryngoscopic examination would demonstrate a noninflammatory edema of the tracheal epithelium. Epiglottitis is a potentially life-threatening occurrence that presents with an abrupt onset of sore throat, high fever, and some of the following: dysphagia, drooling, stridor, and dysphonia. These symptoms occur over a 12- to 24-hour period. There is usually no cough, but inspiratory stridor is present. In the classic presentation, patients are sitting in a tripod position with the mandible thrust forward, unwilling to move, drooling, apprehensive, and toxic appearing. This positioning increases the diameter of the upper airway. Their speech is also sometimes described as muffled or a “hot potato voice,” as if there is a hot potato in their mouth. This infection can occur in all age groups. Bacterial tracheitis can also present with croup symptoms. This illness is distinguished from croup by the presence of thick, mucopurulent secretions. These patients may also have the history of 2–3 days of a viral prodrome but then rapidly appear more ill with fever and frequent cough. This patient will tolerate lying flat, does not drool, and does not have any symptoms of sore throat or inability to swallow. Some children present with no prodrome and sudden onset of croup, fever, and toxic appearance. Patients who have aspirated a foreign body primarily present with choking and coughing but may also display wheezing, dyspnea, and fever. These aspirated objects are typically seen in children 3 years old and younger. The history of aspiration may not be obtained from the patient or siblings if it was not witnessed. This presentation of course mirrors other illnesses, and the symptoms are not specific. The key is the sudden onset of symptoms in a toddler.
EXAMINATION In croup, the child will prefer a position of sitting rather than lying down. Supraclavicular and rib retractions may be present. The classic barky cough and hoarseness will be apparent, and nasal flaring, inspiratory stridor, and wheezing may also be present. An examination of the pharynx will reveal normal anatomy. In spasmodic croup, the previously described symptoms are present, but the history is that of an afebrile child with no upper respiratory tract symptoms and a sudden onset of a barky cough usually in the evening or at night. In epiglottitis, patients are sitting in a tripod position with the chin forward, unwilling to move, drooling, apprehensive, and toxic appearing. The degree of respiratory distress is variable. The inability to swallow, drooling, and labored breathing are very pronounced and according
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to the history have rapidly evolved. Fever is present (temperature, 38.8 – 40.0 C). In the progression of symptoms, there is described a period of air hunger and restlessness followed by cyanosis, respiratory arrest, and coma. Stridor is a late finding in this disease process. On laryngoscopy, the epiglottis will appear as “cherry-red.” Bacterial tracheitis has a clinical presentation of viral prodrome for a few days, after which the patient rapidly appears more ill with high fever and signs of upper airway obstruction. These patients are coughing and will lie flat; they do not assume a tripod position. The presence of thick, purulent airway secretions are the most dramatic and clinically important examination finding. The degree of respiratory distress is dependent on the time of presentation in the course of the disease process. With a foreign body aspiration, the physical examination can appear as any of the previously described. Choking and aspiration occur in 90% of patients, stridor in 60%, and wheezing in 50%. The key to this diagnosis is the sudden onset of symptoms and the inclusion of aspiration in the differential diagnosis of a toddler presenting to the ED with respiratory symptoms.
LABORATORY FINDINGS Croup Laboratory tests are not indicated if croup is suspected. A CBC with differential white blood cell count should be performed if a diagnosis other than croup is suspected. RSV washings and influenza testing will help in the determination of the etiology and with the decision whether to place the child in isolation if he or she requires admission to the hospital. Serum chemistry tests do not reveal data specific to croup.
Epiglottitis If epiglottitis is suspected, blood cultures, a metabolic panel, and CBC with differential should be performed, and CSF fluid testing might also be useful, depending on the patient’s presentation. A white blood cell (WBC) count is often higher than 20,000 with increased neutrophils and bands. A culture of the epiglottic surface should be performed during bronchoscopy, if done at all.
Bacterial Tracheitis A child with bacterial tracheitis will appear ill. In most cases, the physician should obtain a basic metabolic panel and CBC with cell differential count. The CBC will likely show an elevated WBC count with
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increased neutrophils as is common in any bacterial illness. In bacterial tracheitis, unless bronchoscopy is performed, culture specimens are not commonly obtained.
Foreign Body Aspiration Specific laboratory tests are not helpful in identifying foreign body aspiration.
DIAGNOSIS In the usual presentation of croup, laboratory and radiological studies are not helpful for this clinical diagnosis. In LTB caused by parainfluenza or influenza virus, the presentation will include stridor and wheezing and could appear as bronchiolitis. Epiglottitis is differentiated by the acute, fulminant process. Unfortunately, vaccination for HIB does not rule out epiglottitis. Patients with Ludwig angina will present with marked anterior swelling of the floor of the mouth that leads to swelling that moves posterior to involve the upper airway. This swelling is visible just under the tongue. Retropharyngeal and peritonsillar abscesses can also be identified with visual inspection of the oral cavity.
Spasmodic Croup Episodes of spasmodic croup occur with or without the history of upper respiratory tract illness and occur primarily at night. The initial presentation may be dramatic with croup symptoms that are relieved by comforting the child and providing cool mist for the patient to breathe. The pronounced wellness between occurrences is most assistive in discriminating this disease from LTB. If a child is presenting with recurrent symptoms, or if the time of year is not correct for the illness, consider unusual causes such as congenital airway anomalies, acquired tracheal stenosis resulting from previous intubations, tracheal hemangiomas, recurrent angioneurotic edema, or congenital heart disease with vascular anomalies.
Epiglottitis Epiglottitis is clearly delineated by a rapid progression of respiratory distress, anxiety, and drooling in a febrile and ill-appearing child. There is not a barky cough as there is in croup, and a child with this infection is markedly ill and toxic in appearance.
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Bacterial Tracheitis A child with bacterial tracheitis will present as ill appearing with a high fever and mucopurulent airway secretions. No findings of epiglottitis will be present.
Foreign Body Aspiration The diagnosis of foreign body aspiration requires suspicion in the toddler age group for this event. The family may or may not inform the examiner of this history. In the evaluation for a foreign body presence, many items will not be radiopaque. Chest radiology is indicated. The definitive diagnostic approach is to perform bronchoscopy, which can be diagnostic and therapeutic. Late findings would include atelectasis and secondary pneumonia.
RADIOGRAPHS Croup Radiographs are not helpful in the diagnosis of croup. For LTB, the steeple sign (in a lateral neck radiograph) may be observed but is not diagnostic by itself. This sign demonstrates narrowing at the subglottic area. The presence or absence of this finding is not indicative of the diagnosis or the severity of affliction.
Epiglottitis For epiglottitis, the clinical course is more important in making a diagnosis, and the stress of a radiograph may exacerbate the patient’s airway issues. If radiography is performed, a lateral neck x-ray will reveal a swollen epiglottis resulting in an radiography with a “thumb sign.” Some centers who have been studying the use of ED ultrasound have completed a trial using volunteers and were able to identify the normalsized epiglottis on radiography.
Bacterial Tracheitis Chest radiography will show patchy infiltrates and possible focal densities when bacterial tracheitis is present. Subglottic narrowing may be visible. Radiology does not assist in diagnosis of this condition.
Foreign Body Aspiration Radiographs are indicated in the diagnosis of foreign body aspiration. Posteroanterior and lateral chest radiographs with inclusion of the upper
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abdomen should be taken. These radiographs are very helpful if the aspirated object is radiolucent. If not, the examiner should consider expiration and inspiration radiographs to assess for hyperventilation in the affected side. The affected lung will experience air trapping during expiration and incomplete emptying of that lung. This is thought to be due to a ball-valve effect wherein the air can pass through into the lung but is then trapped by the foreign body, which prevents exhalation. The affected lung will appear hyperexpanded, with a shift of the mediastinum to the opposite side. Direct bronchoscopy may be required for definitive diagnosis and treatment of a foreign body aspiration.
TREATMENT Assessment and support for a stable airway is always foremost. If an adequate airway is not present, or if the child appears markedly fatigued, the clinician should engage in an emergency airway protocol with BVM and intubation. Because of swelling, an ET tube may be needed that is a one size smaller than would otherwise be used for the patient.
Monitoring Pulse oximetry monitoring will assist in identifying hypoxia. Carbon dioxide monitoring should be considered, if available; this procedure is particularly helpful if the clinician is concerned about fatigue and decreased ventilation.
Oxygen Supplemental oxygen should be provided in a form the child will tolerate. Oxygen saturations should be maintained at 90% or better. Humidified cool air may help to reduce the inflammation and liquefy secretions for ease of expectoration.
Positioning The position of comfort for the child is most important. If the patient is comfortable and calm, there will be decreased work of breathing from any environmental stressors.
Croup The treatment of croup is initiated with the administration of cool mist, unless it aggravates bronchospasm or increased wheezing. Nebulization
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of epinephrine is indicated. Steroids are also indicated and are the standard of care. (However, steroid therapy should not be given to children with varicella or tuberculosis since it will worsen their course.) Treatments with a helium-oxygen mixture have yielded the same results as the use of racemic epinephrine. Antibiotics are not indicated. For children at high risk (e.g., patients with congenital heart disease or chronic lung disease and certain preterm infants), RSV prophylaxis should be considered. The current recommendation is for the use of palivizumab as an IM injection given every month to prevent RSV infection. The dosage for this medication is 15 mg/kg IM once per month for 5 months.
Spasmodic Croup Spasmodic croup should be treated in the same manner as croup. For repetitive courses of infection, an allergic etiology should be explored. If that appears unlikely, the clinician should consider referral for continued evaluation of other upper airway anatomical abnormalities. Antibiotics are not indicated.
Epiglottitis Epiglottitis involves a tenuous airway. The setting and the most controlled environment for ET intubation should be considered. If intubation is not successful, tracheostomy may be needed. IV starts, laboratory draws, and radiology should be delayed until the airway is secure. The patient will decompensate with the stress and agitation and the airway could quickly occlude. If impending respiratory arrest is identified in a child with epiglottitis and access to an operating room is unavailable, the practitioner should use a smaller ET tube with a stylet and should look for an air bubble at the glottic opening while someone else compresses the chest. Nebulization therapy is not indicated. Steroids have not been proved to be effective. Antibiotics are indicated (though there has been some resistance [10%–40%] of HIB to ampicillin). Treatment includes ceftriaxone, 50–75 mg/kg/day up to 2 g divided every 12–24 hours. Resolution will take several days, and the patient can typically be extubated after evaluation is performed with bronchoscopy to evaluate the epiglottic inflammation and readiness for extubation. Family members do not need to be treated for prophylaxis unless there is a child in the home younger than 2 years old who has not completed the HIB vaccination series. In that case, all family members should be treated with rifampin 20 mg/kg orally every day for 4 days. (maximum dose, 600 mg/day).
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The outcome of epiglottitis is usually good, with no increased rate of reoccurrence unless there was delay in treatment or identification of illness. In that case, recovery depends on the sequela associated with those events.
Bacterial Tracheitis Bacterial tracheitis should be treated with antibiotics for staphylococcal coverage. Nebulization therapy can be considered for bronchospasm related to secretions. Steroids are not generally recommended but could be considered if the provider believes this to be a secondary infection with marked stridor. After antibiotic therapy, the illness defervesces in 2–3 days, depending on the timing of the diagnosis and the initiation of treatment. There has been toxic shock associated with this presentation as well.
Foreign Body Aspiration Definitive treatment is removal of the foreign body by bronchoscopy. With early discovery and removal of the object, observation for 24–48 hours is indicated depending on the degree of symptoms. If diagnosis and treatment is delayed, then the course will be prolonged. Appropriate nebulized medications include racemic epinephrine (0.05 ml/kg per dose) of a 2.25% solution diluted in 3 ml of saline and nebulized. l-epinephrine is also effective at 1:1000 0.5 ml/kg to a maximum of 5 ml/dose. If discharge is planned, it is recommended that the patient be held for observation for 2–3 hours after the last nebulization treatment to be sure that rebound and clinical worsening do not occur. For children with moderate- to-severe croup, steroids are now the recommended treatment. For example, Decadron (dexamethasone) 0.15–0.6 mg/kg can be given orally or IM. This drug has a half-life of 54 hours. Recent studies indicate that steroids decrease laryngeal edema, decrease symptoms, and reduce return visits to the ED, as well as decrease the need for admission, nebulization treatments, and lengthy observation times. The efficacy does not appear to vary related to oral or IM dosing. The onset of action is approximately 6 hours.
BRONCHIOLITIS Bronchiolitis appears as a upper respiratory tract process and then progresses to tachypnea, nasal flaring, retractions, increased work of breathing, productive cough, hypoxia, wheezing, and rales. Symptoms are the worst at days 3–5, so it is important to know where the child is in the trajectory of illness. If the clinician is seeing this child at day 2, he or she should recognize that the patient will become more ill in the next few days, and this will affect decisions regarding discharge
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from or admission to the hospital. The symptoms can last as long as 2 weeks. Infants are particularly affected by the burden of secretions in their upper airway, which markedly decreases their ability to feed. Children at higher risk for more serious disease are those who are younger than 3 months of age, those who were premature at birth (less than 35 weeks’ gestation), and those with congenital heart disease, pulmonary hypertension, immunosuppression, or chronic lung disease. Supportive management consists of warmed humidified oxygen therapy, suctioning of upper airways, and nasal secretions. Bronchodilators may be helpful in some children. Steroid treatment may be helpful in critically ill children. Infants have marked difficulty feeding with the occlusion of nasal passages with secretions and may need IV hydration to maintain a euvolemic status.
Emergency Action Emergency actions to be taken when a patient has bronchiolitis are as follows: 1. Check pulse oximetry. This is the most sensitive indicator of disease. 2. Suction the infant’s airway to promote air exchange. Apnea is a common symptom. 3. Keep the infant/child in a position of comfort for as long as possible and avoid agitation. Progressive respiratory distress may require intubation. 4. Administer 100% oxygen with BVM as the initial modality if respiratory compromise is occurring.
Definition Bronchiolitis is a respiratory disease that begins in the upper airways and progresses to the lower airways. It is characterized by inflammation of the bronchiolar epithelium by an acute infection. This inflammatory response leads to necrosis of the epithelium and plugging of airways with resultant distal atelectasis and air trapping. RSV is the most common causal pathogen. There have been two identified subtypes: strains A and B. The A strain is most associated with severe disease. This virus is most common in late fall and through the winter. Parainfluenza, influenza, adenovirus, and rhinoviruses may also cause bronchiolitis. A new group, a type of paramyxovirus called metapneumovirus, can occur in the setting of other viruses.
Epidemiology RSV is the most prevalent and important respiratory virus in children. It is the leading cause of hospitalization. More than 50% of infants will
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acquire the RSV infection during their first season of exposure, and 40% will progress from an upper airway reaction to a lower airway response to this virus. Among children younger less than 1 year of age, 3% will require hospitalization. Infants younger than 2 years old are primarily affected by bronchiolitis in the winter months. Those infants requiring hospital admission have moderate to severe disease and are usually 1–6 months of age. Those at higher risk for severe disease include boys, infants born prematurely, and infants born with congenital heart disease, chronic lung disease, or immune deficiency states.
Clinical Presentation The clinical presentation of a patient with bronchiolitis is variable, depending on the point in course at which the patient presents and the progression of disease. The patient may be a smiling interactive child with mild tachypnea or an infant in severe respiratory distress. The patient’s history will include several days of coryza and congestion representing the upper airway time of the disease. This is followed by a progressive history of increasing tachypnea, cough, increased work of breathing, and decreased ability to feed. Fever is usually present earlier in the disease but is mild to moderate (<38.3 C). Smaller infants may exhibit episodes of apnea, lethargy or irritability, tachypnea, and retractions. RSV in particular seems to cause only a low-grade fever. Higher temperatures may be seen with the other viruses.
Examination Audible expiratory wheezing is present with tachypnea and subcostal and intracostal retractions. The chest may appear hyperexpanded. Patients may have a combination of rales, prolonged inspiration, and crackles. If they have progressed to decreased air movement, then wheezing may not be audible. Pulse oximetry will reveal mild hypoxemia (saturation <95%). These infants are usually not feeding well with early fatigue or vomiting; they will also appear lethargic and hypovolemic. The total course of this disease is 3–10 days. The severity of illness is affected by any history of other comorbid conditions and prematurity at birth. There are tools for illness severity rating; however, none have been universally accepted as helpful. Patients should be admitted to the hospital if they are toxic or appear to be ill, if they are younger than 3 months old, or if they have an oxygen saturation less than 95%, a respiratory rate greater than 70 breaths/ min, and/or atelectasis on chest radiograph.
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Laboratory Findings A CBC is not diagnostic for bronchiolitis but may be helpful to evaluate for other causes of illness. RSV nasal wash for antigen detection is helpful in determining the etiology of the disease, as well as to isolate or cohabitate children with infection of this virus. Rapid antigen tests are available for RSV, parainfluenza, and influenza viruses.
Diagnosis Bronchiolitis is identified by means of a clinical diagnosis. It must be recognized by ruling out other disorders such as pneumonia, foreign body aspiration, asthma, congenital heart disease, heart failure, vascular rings, and chronic lung disease. Several of these can be excluded on the basis of the length of illness. Congenital lesions that compromise the airway such as vascular rings, slings, or teratomas can appear to have an acute onset. Foreign body aspiration should always be included in the differential diagnosis. In addition, bronchiolitis can also be a portion of another yet unrecognized diagnosis such as congenital heart disease with heart failure. The first episode of wheezing in a young child should be considered bronchiolitis. Confusing to parents, this may be the child’s first episode of asthma or reactive airway disease. It is not uncommon for children to have more than one RSV episode. Infants who have had RSV may be more prone to experience further episodes of wheezing. It is unknown whether children who progress to a diagnosis of reactive airway disease had damage as a result of these illnesses or had reactive airway disease that was exacerbated and discoverable as a result of this episode of bronchiolitis.
Radiographs Chest radiography is indicated in a first episode of wheezing and may show hyperinflation or peribronchial thickening. Atelectasis is prevalent in only 10% of children. This study is not definitive for diagnosis, but it does rule out others.
Treatment In the majority of healthy children without other comorbidity, treatment is primarily supportive. The overall treatment is dependent on the clinical appearance of the child. The clinician should evaluate the patient’s respiratory rate, oxygen saturation, work of breathing, accessory muscle use, and air exchange.
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Pulse oximetry is the only objective measure that is most helpful. If the child is in acute respiratory distress, intubation will be necessary. The patient’s hydration state must be assessed according to the appearance of tears, mucous membranes, skin turgor, central and peripheral capillary refill and history of intake, and/or wet diapers. Many children, particularly infants, become dehydrated by the work of feeding and breathing. Recognizing the timing in the progression of the illness is crucial. It appears that early in the course, airway obstruction and inflammation may be reversible, whereas once the disease has progressed to the point at which obstruction has occurred it is not clear whether treatments alter the course. Saline nose drops can be used to liquefy secretions, and bulb or catheter suction can be performed to clear nasal passages. Warmed humidified oxygen should be administered to keep oxygen saturation levels greater than 92%. Carbon dioxide monitoring should be considered, and mechanical ventilation may be required depending on the presence of RSV and the child’s comorbidities. Increased fluid requirements of patients with fever and tachypnea should be addressed, as should decreased oral intake. Plasma ant diuretic hormone is elevated in this disease process, so fluid retention can occur. Intake and output must be monitored. Pulmonary congestion is undesirable. Steroid administration—whether inhaled or given orally or via IV routes—has not been shown to be helpful unless there are other underlying conditions such as chronic underlying lung disease for which steroids are indicated. In children requiring mechanical ventilation, dexamethasone reduced the number of days ventilation and supplemental oxygen were required in some studies. Heliox therapy (i.e., 70% helium and 30% oxygen) has been used and studied in this setting. This technique reduces the oxygen requirement in infants with improved clinical recovery time and decreases patient length of stay in the intensive care unit. However, this modality is cumbersome, may not be available in all facilities, has small benefits in a limited group of infants, and is not recommended by some. Bronchodilators are widely used and studied; however, their efficacy remains uncertain. Some of this uncertainty relates to the clarity of the diagnosis. Since bronchiolitis is identified by clinical diagnosis, it can be present but at times indistinguishable from other diseases that involve wheezing, such as acute viral-triggered asthma. In the clinical setting, many providers believe that some patients do benefit from bronchodilator therapy. Since there are limited adverse effects, what follows is a strategy to see whether this technique helps an individual patient. The clinician should take the following steps, watching for decreased oxygen need, wheezing, or respiratory rate.
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Appropriate nebulized medications include the following:
Albuterol should be administered at a dose of 0.02–0.06 ml/kg of a 0.5% solution diluted with 2.5–3.0 ml of saline, nebulized over 5–15 minutes. Racemic epinephrine should be administered at 0.05 ml/kg/dose of a 2.25% solution diluted in 3 ml of saline and nebulized. L-epinephrine is also effective at 1:1000 0.5 ml/kg to a maximum of 5 ml/dose.
If discharge is planned, it is recommended that the patient be held for 2–3 hours after the last nebulization treatment to be sure that rebound and clinical worsening do not occur. The patient should be admitted to the hospital if any of the following conditions are present:
Oxygen saturation less than 94% with continued oxygen requirement Lethargy, dehydration, and decreased feeding Toxic appearance Respiratory distress; that is, tachypnea (respiration >70 breaths/min) and/or dyspnea, nasal flaring, intercostal retractions, and cyanosis Consolidation or atelectasis identified by chest radiography (if taken) Parent unable to care for child
Bibliography Adams WG, Deaver KA, Cochi SL, et al: Decline in childhood Haemophilus influenzae type b (HIB) in the HIB vaccine era, JAMA 1993;269:221–226. Agency for Healthcare Research and Quality: Management of bronchiolitis in infants and children. U.S. Department of Health and Human Services, Evidence Report/Technology Assessment 2003;69:1–5. Barr FE, Graham BS: Respiratory syncytial virus, UpToDate, Available at: http://www. uptodate.com. September 3, 2005, 1–15. Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, pp 1405–1412. Berstein T, Brilli R, Jacobs B: Is bacterial tracheitis changing? A 14-month experience in a pediatric intensive care unit, Clin Infect Dis 1998;27:458–462. Bittencourt PF, Camargos PA, Scheinmann P, Blic JD: Foreign body aspiration: Clinical, radiological findings and factors associated with its late removal, Int J Pediatr Otorhinolaryngol 2006;70(5):879–884. Committee on Infectious Diseases and Committee on Fetus and Newborn American Academy of Pediatrics: Policy Statement, Revised indications for the use of palivizumab and Respiratory Syncytial Virus Immune Globulin Intravenous for the Prevention of Respiratory Syncytial Virus Infections, Pediatrics 2003;112(6):1442–1446. Horn SD, Smount RJ: Effect of prematurity on respiratory syncytial virus hospital resource use and outcomes, J Pediatr 2003;143:S133–S141. Kellner JD, Ohlssont A, Gadomski AM, Wang E: Efficacy of bronchodilator therapy in bronchiolitis: A meta-analysis, Arch Pediatr Adolesc Med 1996;150:1166. Leader S, Kohihase K: Recent trends in severe respiratory syncytial virus (RSV) among U.S. infants, 1997–2000, J Pediatr 2003;143:S127–S132.
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Ledwith CA, Shea LM, Mauro RD: Safety and efficacy of nebulized racemic epinephrine in conjunction with oral dexamethasone and mist in the outpatient treatment of croup, Ann Emerg Med 1995;25:331–337. Piedra PA, Stark AR: Treatment and prevention of bronchiolitis in children. UpToDate. Available at: http://www.utdol.com/application/topic/print.asp?fileþpedipulm/8346. Accessed on September 3, 2005. Rimell FL, Thome A, Stool S, et al: Characteristics of objects that cause choking in children, JAMA 1995;274:1763–1766. Rogers MC: Textbook of Pediatric Intensive Care. Vol 3. Williams & Wilkins: Baltimore, 1996, pp 69–70. Schuh S, Coates AL, Binnie R, et al: Efficacy of oral dexamethasone in outpatients with acute bronchiolitis, J Pediatr 2002;140:27–32. Shah RK, Roberson DW, Jones DT: Epiglottitis in the Haemophilus influenzae type B vaccine era: Changing trends, Laryngoscope 2004;114(3):557–560. Shaw KN, Bell LM, Sherman NH: Outpatient assessment of infants with bronchiolitis, Am J Dis Child 1991;145:151. Shay DK, Holman RC, Newman RD, et al: Bronchiolitis-associated hospitalizations among US children, 1980–1996, JAMA 1999;282:1440–1446. Van Woensel JB, van Aaldren WM, de Weerd W, et al: Dexamethasone for treatment of patients mechanically ventilated for lower respiratory tract infection caused by respiratory syncytial virus, Thorax 2003;58:383. Werner SL, Jones RA, Emerman CL: Sonographic assessment of the epiglottis, Acad Emerg Med 2004;11(12):1358–1360. Wohl ME, Chernick V: Treatment of acute bronchiolitis, N Engl J Med 2003;349–382. Wolfson AB, Hendey GW, Hendry PL, Linden CH: Harwood-Nuss’ Clinical Practice of Emergency Medicine, Lippincott, Williams & Wilkins: Philadelphia, 2005, pp 1284–1287, 1297–1301, 1332–1335. Woods CR: Epiglottitis, UpToDate. Available at: http://www.uptodate.com. Accessed on May 31, 2005.
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Dehydration in Children MARY ANN BROWNING
ICD Codes: Dehydration 276.5, Dehydration in a newborn 775.5
Key Points In children, severe dehydration represents a medical emergency. Poor perfusion, sunken eyes, dry mucous membranes, and absent tears may be the most sensitive signs of fluid deficit in young infants and children. Most cases of mild-to-moderate dehydration can be managed with oral rehydration therapy (ORT). Presume a 10% fluid deficit in healthy infants and children who appear dehydrated. Serum electrolyte analyses are usually not necessary in most cases of mild-to-moderate dehydration. If IV access is difficult to secure, hydration can be achieved through a nasogastric tube in children. ! Emergency Actions ! In patients with severe dehydration, IV therapy should be initiated starting with 20-ml/kg boluses of normal saline or lactated Ringer’s solution. IV therapy should continue until the pulse, blood pressure, and level of consciousness return to normal. ORT can often be safely introduced when the patient’s condition becomes stable.
DEFINITION Dehydration in children results from any combination of insufficient fluid intake and excessive fluid losses. Diarrhea is a frequent cause of dehydration in children. Worldwide, dehydration due to diarrhea is the leading cause of infant and child mortality. Depletion of extracellular fluid (ECF) volume is termed hypovolemia. It occurs because of abnormal fluid loss from the skin, gastrointestinal system, or renal system. Hypovolemia can also be caused by bleeding, decreased fluid intake, or third spacing of fluid into the tissues. Severe ECF volume depletion can lead to hypovolemic shock. Young children tend to be more susceptible to volume depletion as a result of gastrointestinal losses. Infants are particularly vulnerable to the loss of water and solutes because water makes up a higher percentage of their body weight. Water composes approximately 70% of body weight in infants, 65% in children, and 60% in adults. In addition, infants and young children have a higher metabolic rate and a relatively small
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amount of reserve. Early recognition and intervention are necessary to prevent progression to cardiovascular collapse. Dehydration is often classified according to serum sodium concentration. Isonatremic (isotonic) dehydration is the most common fluid and electrolyte problem encountered in pediatric patients and is usually caused by diarrhea. In this condition, sodium and free water are lost in equal proportion. Thus, the serum sodium concentration remains normal (130–150 mEq/L). Hypernatremic dehydration (>150 mEq/L) occurs when there is an excess loss of free water. It often occurs when patients with gastroenteritis are treated with salt-rich solutions (e.g., broth, baking soda, improperly diluted infant formula). Because the serum sodium level is high, water will shift from the intracellular space to the extracellular space, helping to preserve intravascular volume. The degree of volume depletion is frequently underestimated. Serious CNS effects may occur as a result of structural changes in brain cells caused by this type of dehydration. In hyponatremic dehydration (<130 mEq/L), there is excess sodium loss. Because the serum sodium concentration is low, water shifts into the cells and plasma volume decreases. CNS symptoms can occur in association with cerebral edema, and the child usually appears very ill. Hyponatremic dehydration most commonly occurs when gastrointestinal losses are replaced with tap water. Less common causes include adrenal insufficiency, third-space losses from ascites or pancreatitis, and diuretic use. Dehydration is divided into mild (3%–5%), moderate (7%–10%), and severe (10%–15%) categories. Assessment of the degree of dehydration is an important first step in the management of a dehydrated child. Most cases can be managed with ORT. However, the degree of dehydration indicates the severity of the situation and the need for IV fluid replacement.
EPIDEMIOLOGY Worldwide, dehydration related to acute gastroenteritis is a leading cause of pediatric morbidity and mortality, with 1.5–2.5 million deaths estimated annually among children younger than 5 years old. In the United States, dehydration still remains a major cause of morbidity and mortality. There are approximately 1.5 outpatient visits per year, 200,000 hospitalizations, and about 300 deaths per year. Although the use of ORT has been proved effective in the worldwide management of childhood dehydration, its use has lagged behind in the United States. Current research and recommendations from the Centers for Disease Control and Prevention (CDC), however, advocate the use of ORT to reduce medical cost, hospitalizations, and deaths from dehydration.
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CLINICAL PRESENTATION/ EXAMINATION Infants and young children have a greater risk of compromise with sudden fluid losses. A thorough patient history should focus on the length of illness and the frequency and character of stools or emesis (i.e., bile, blood, mucus). Recent oral intake and urine output should be assessed. Current weight should be measured and compared with the previous weight. Any associated symptoms such as fever or change in mental status need to be noted. Underlying medical problems, history of recent infections, medications, and contact with ill persons all need to be considered. The clinical evaluation should focus on assessing the degree of dehydration, which will help the clinician determine the need for and type of acute intervention. A mildly dehydrated infant or child (3%–5%) may have few clinical signs or symptoms. The vital signs may be normal, and the pulse may be normal or slightly elevated. Urine output may be decreased. A patient with moderate dehydration (7%–10%) may present with tachycardia, decreased urine output, and irritability or fatigue. The eyes and fontanel may be slightly sunken. Tears are decreased, and mucous membranes are “sticky.” The patient’s extremities may be cool and dry along with a delayed capillary refill (1.5–3 sec). A severely dehydrated (10%–15%) infant or child may present in extremis. The pulse may be rapid and weak. Blood pressure may be decreased (a late sign) and extremities cold, dry, and mottled (capillary refill >3 sec). There is no urine output. Tears are absent, and the eyes and fontanels are very sunken. Mucous membranes are parched. A severely dehydrated child will need immediate and aggressive intervention, including IV therapy. Fluid losses are often underestimated in very young infants, and reliable weight comparisons are often difficult to obtain. Physical examination has been demonstrated to provide a reliable estimation of the degree of dehydration. It should be noted, however, that a change in vital signs may not be apparent until the patient is close to shock. Some studies have demonstrated that certain signs such as prolonged capillary refill, sunken eyes, dry mucous membranes, absent tears, and a general appearance of illness may be the most sensitive markers indicating a fluid deficit of at least 5%–10%.
LABORATORY FINDINGS Laboratory studies are usually unnecessary in the assessment of a dehydrated child. Most recent research confirms that frequent clinical evaluation and resolution of signs of dehydration are the best assessment of improvement. In neonates and young infants, it may be practical to evaluate serum electrolytes if there is a history of significant fluid loss.
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With severe dehydration, laboratory studies, including serum electrolytes, may be required. A low serum bicarbonate level may reflect poor tissue perfusion, diarrheal losses, and lactic acid production. Potassium levels may be elevated or low. The blood urea nitrogen (BUN) level usually rises with renal hypoperfusion. Stool cultures are indicated in the case of dysentery but are not usually indicated for acute-onset watery diarrhea in an otherwise healthy child. If the diagnosis is unclear, however, or if the patient is toxic in appearance, then measurement of serum electrolytes, CBC, and urine and blood cultures may be indicated.
TREATMENT ORT has been recognized as a major factor in the worldwide reduction of deaths from diarrheal disease. ORT is now recommended as the most efficient and cost-effective therapy for the management of mild to moderate cases of gastroenteritis in infants and children. Even so, the CDC reports ORT as underused in the United States and other developed countries. ORT consists of two phases of treatment: 1. The rehydration phase, during which fluid is replaced over 3–4 hours 2. The maintenance phase, in which maintenance calories and fluids are administered The technique of delivering ORT is as follows:
If patient is vomiting, 5–10 ml of oral rehydration fluid (commercially prepared solutions such as Pedialyte) should be given every 5–10 minutes. A small amount of vomiting is not an indication to stop oral rehydration. For a child who has mild or moderate dehydration, 50–100 ml of oral rehydration solution per kilogram of body weight should be administered over 2–4 hours to replace fluid deficit. Additional oral rehydration solution should be given to replace ongoing losses: approximately 10 ml/kg (or about 120 ml in older children) for each diarrheal stool. The child should be returned to a regular age-appropriate diet as soon as possible (gut rest is not indicated). Breast-feeding should continue, even early in the course of therapy. Contraindications to ORT include shock, severe dehydration, intractable vomiting, coma, acute abdomen, or absent bowel sounds.
Fluids such as apple juice, soda pop, milk, and broth are generally considered to be inappropriate for ORT. These fluids contain excess
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carbohydrates and low concentrations of sodium and may actually worsen the degree of diarrhea. Once the child is rehydrated, an age-appropriate diet should be followed. The healthcare provider should encourage foods that contain complex carbohydrates such as rice, lean meat, potatoes, bread, cereals, or yogurt. Fatty foods and simple carbohydrates should be avoided. In general, pharmacological agents should not be used to treat acute gastroenteritis. Probiotic agents may shorten the course of diarrhea. Some studies report a link between diarrhea and abnormal zinc levels. Zinc supplementation may improve outcomes in children with acute or chronic diarrhea. If vomiting persists, oral rehydration solution can be administered via nasogastric tube. Rehydration through a nasogastric tube can be well tolerated, cost effective, and associated with few complications. Clinical trials support the use of nasogastric feedings in the ED setting.
INTRAVENOUS THERAPY In severe dehydration, the first phase includes aggressive IV rehydration. Boluses of 20 ml/kg of normal saline or lactated Ringer’s solution are given until mental status, vital signs, and perfusion improve. In patients in shock, this may require three to four boluses. The next phase will focus on deficit replacement, maintenance fluid, and replacement of ongoing losses. It is safe to assume a 10% deficit in healthy infants and children who appear to be dehydrated by physical examination. Fifty percent of the estimated volume deficit should be replaced in the first 8 hours and the remainder over the next 16 hours. Maintenance fluid must be added to the deficit replacement. Ongoing losses of diarrhea stool and emesis must also be replaced, and the child’s condition should be monitored closely. Maintenance fluid should be administered according to patient weight, as follows: <10 kg ¼ 100 ml=kg=day 1020 kg ¼ 1000 þ 50 ml=kg=day for each kilogram over 10 kg >20 kg ¼ 1500 þ 20 ml=kg=day for each kilogram over 20 kg
For example, for a 12-kg infant with an estimated 10% dehydration, the clinician should provide a 20-ml/kg IV bolus of normal saline until there is an improvement in clinical status, then maintenance fluids calculated as follows: 100 ml=kg 10 kg=day ¼ 1000 ml þ 50 ml=kg 2 kg=day ¼ 100 ml Total :1100 ml=day or 46 ml=hr
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The deficit of 10% estimated dehydration ¼ 1.2 kg ¼ 1200 ml 600 ml over the first 8 hours or 75 ml=hr; then 600 ml over 16 hours ¼ 38 ml=hr
Therefore, the total ORT would be calculated as follows: First 8 hours; maintenance þ deficit ¼ 121 ml=hr Next 16 hours; maintenance þ deficit ¼ 84 ml=hr
In addition, ongoing fluid losses should be measured and replaced. Suitable rehydrating fluids for infants include 5% dextrose in 0.2% saline or 5% dextrose in 0.45% saline. In infants, 5% dextrose in 0.2% saline is isotonic for maintenance rehydration in isotonic dehydration. In children, 5% dextrose in 0.45% saline can be used for maintenance rehydration for isotonic dehydration. Potassium (20 mEq/L) may be added once urine output is noted. As the child’s condition improves, ORT can also be used and parenteral therapy can be discontinued. Isonatremic and hyponatremic dehydration can be treated with saline or other isotonic solutions. Hypernatremic dehydration should be corrected more slowly because of the possibility of CNS complications resulting from rapid correction. Full correction of severe sodium abnormalities should continue over 24 hours or longer and require admission to the hospital. In all patients, oral hydration should be encouraged as much as possible. Severely dehydrated infants and children should be admitted to the hospital for rehydration. An inability to tolerate ORT may also warrant hospital admission for nasogastric or IV fluid therapy. A patient can be discharged from the hospital if the child is able to tolerate oral therapy and if family members can be relied on to continue hydration therapy at home. Clear instructions must be provided, and close follow-up is recommended within 24–48 hours.
Bibliography Ahrens W: Fluid and electrolyte therapy. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 843–848. Barkin R, Ward D: Infectious diarrheal disease and dehydration. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002, pp 2316–2320. Centers for Disease Control and Prevention: Managing acute gastroenteritis among children: Oral rehydration, maintenance, and nutritional therapy, MMWR Morb Mortal Wkly Rep 2003;52(RR–16):1–16. Egland A: Pediatrics, dehydration. Available at: http://www.emedicine.com/emerg/topic372. htm. Accessed on February 22, 2005.
700 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Ellsbury D: Dehydration. Available at: http://www.emedicine.com/ped/topic556.htm. Accessed on February 22, 2005. Friedman J, Goldman R, Srivastava R, Parkin P: Development of a clinical dehydration scale for use in children between 1 and 36 months of age, J Pediatr 2004;145 (2):201–207. Gorelick M, Shaw K, Murphy K: Validity and reliability of clinical signs in the diagnosis of dehydration, Pediatrics 1997;99:e6. Nager A: Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration, Pediatrics 2002;109(4):566–572.
Electrolyte and Fluid Management in Pediatric Patients ROBERT L.CLOUTIER
ICD Codes: Dehydration 276.5, Dehydration in the newborn 775.5, Dehydration with hypernatremia 276.00, Dehydration with hyponatremia 276.1
Key Points Management of the ABCs (i.e., airway, breathing, and circulation) and bedside glucose measurement are vital first steps in the assessment of a pediatric patient. The appearance of the eyes, skin turgor, urine output, and capillary refill must be used collectively to be effective as assessment tools in a dehydrated child. ! Emergency Actions ! The initial evaluation of an acutely dehydrated child includes evaluation of the ABCs. After this assessment, a bedside glucose measurement is indicated. Volume resuscitation composed of normal saline boluses (20 ml/kg of body weight given intravenously) repeated up to three times to rapidly expand the patient’s intravascular volume represents the keystone of emergent intervention in a dehydrated pediatric patient.
DEFINITION The management of fluids and electrolytes in pediatrics is vitally important due to the shifting physiological needs of children as they grow and
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mature. Due to the increased incidence of associated illnesses resulting in significant fluid losses due to vomiting or diarrhea, a basic framework for safely and effectively administering IV fluids is indispensable.
CLINICAL PRESENTATION The body seeks homeostasis at all times. We possess a number of redundant biological systems that seek to balance our osmotic environments between various fluid compartments. The human body is composed of 65%–75% water (with infants and children tending toward 75% and adults approaching 65%) and possesses two major fluid compartments: (1) the extracellular space (i.e., ECF), which is divided into two subcompartments the interstitial space (i.e., fluid outside blood vessels and surrounding cells) and the intravascular space (i.e., fluid inside blood vessels), and (2) the intracellular space (i.e., ICF), which includes only fluid within cells. There is a predominance of certain ions within different fluid compartments. Potassium predominates in the ICF and sodium in the ECF. It is interesting to note that the intravascular space (part of the ECF) is the smallest of the fluid spaces (occupying but 5% of the 65%–75% of total body water) but acts as our primary window into the entire fluid balance of the body. In the absence of illness, the body loses fluid daily in the form of urine and water vapor (primarily from the lungs and skin) and accounts for the need for IV maintenance therapy when fluids cannot be taken orally.
Calculation of Maintenance Fluids An IV fluid and electrolyte regimen is composed of three main ingredients: (1) water, (2) electrolytes (specifically, sodium and potassium), and (3) glucose. Daily (24-hour period) water requirements can easily be determined by weight of the patient, assigning 100 ml/kg/day for the first 10 kg of body weight followed by 50 ml/kg for the next 10 kg and 20 ml/kg for each kilogram above 20 kg. Therefore, a 20-kg patient would require 1500 ml of maintenance fluid for a 24-hour period. This would be run at approximately 63 ml/hr as an IV drip. The next ingredients to consider are electrolytes in the form of sodium and potassium. As noted previously, the amounts of sodium are based not on weight but on the daily fluid requirement of the patient. In general, replacement saline containing fluids come in three tonicities: (1) 0.9% normal saline, which contains 154 mEq of sodium/L, (2) 0.045% ½ normal saline, which contains 77 mEq of sodium/L, and (3) 0.025% ¼ normal saline, which contains 38 mEq of sodium/L. To calculate the
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maintenance sodium requirement for our sample 20-kg patient would be as follows: given a 1500-ml fluid requirement, 2–3 mEq per 100 ml of fluid per day would be 15 2–3, resulting in a range of 30–45 mEq/ day across 1500 ml. This amount of sodium correlates most closely to ¼ normal saline and would be considered the fluid of choice in this patient. One-half normal saline generally may be used in children older than 12 months and/or when patient losses are thought to be largely composed of sodium from the ECF. Potassium requirements are calculated in similar fashion, using 2 mEq of potassium per 100 ml of fluid per day. Thus, our 20-kg patient would require 30 mEq of potassium across the 1500 ml of daily fluid. Potassium tends to be added in dose of either 10 or 20 mEq/L of fluid. In this case, 20 mEq/L will result in 30 mEq of total potassium being administered across 1500 ml of fluid. The final ingredient is carbohydrate in the form of dextrose. Dextrose is used in IV fluids to prevent ketosis. A 5% dextrose solution (which translates into 5 g of dextrose per 100 ml of fluid) delivers approximately 20% of a patient’s daily caloric requirements, which is sufficient to prevent ketosis. (It should be noted that one’s daily caloric requirement in kilocalories is equal to one’s daily fluid requirement in milliliters). A 5% dextrose solution will be the maintenance fluid of choice except in the case of true hypoglycemia or hyperglycemia. Therefore, a sample 15-kg patient will require 1500 ml D5 ¼ normal saline with 20 mEq of potassium/L to run at 65 ml/hr for 24 hours to meet his or her maintenance fluid requirements.
Calculation of Deficit Fluids In terms of evaluating patients for deficit therapy, it is important to look at weight to determine the extent of a patient’s deficit. In pediatric patients, weight is a vital sign; the clinician should be sure it is documented. In general, we stratify dehydration in terms of percentage weight loss compared with “well” weight. For example, a normally 20-kg child who presents for care after vomiting for 24 hours and weighs 19 kg has lost 1000 g and has therefore suffered a 5% weight loss. A full 2.0-kg weight loss would imply a 10% weight loss and would correspond with a more severe degree of dehydration. Children who are 10% and 15% dehydrated are much more ill appearing than children with a 5% loss. The vast majority of children experience an approximately 5% weight loss or less. For the purposes of calculation, we frequently use a 5% weight loss as the basis for calculating fluid therapy when a patient’s well weight is unavailable. The delivery of fluids must be separated to first account for maintenance therapy. Once maintenance therapy has been calculated, deficit
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therapy may be added. The deficit therapy in terms of volume is equal in milliliters to the amount of weight loss. Therefore, a 20-kg patient with a 5% weight loss equivalent to 1000 g will equate to 1000 ml of fluid requiring replacement over and above maintenance fluid. The deficit volume is delivered over a 24-hour period, with the first 50% delivered in the first 8 hours and the last 50% delivered over the remaining 16 hours. The fluid used would be the same as the fluid calculated for maintenance fluid, with the hourly rates calculated accordingly and added to the maintenance fluid rate. Our sample 20-kg patient would require an IV fluid rate of 128 ml/hr for 8 hours (65 ml/hr of maintenance fluid plus 63 ml/hr of deficit therapy for 8 hours) followed by a rate of 97 ml/hr for 16 hours (65 ml/hr of maintenance fluid plus 32 ml/hr of deficit therapy for 16 hours). Delivery of this amount of fluid would result in the patient having received his or her maintenance fluids and lost deficit fluids over the course of 24 hours.
EXAMINATION The most important aspect of treatment of dehydrated children is a thoughtful assessment of their clinical appearance. Special attention should be paid to the appearance of the eyes—are they producing tears, or do they appear dry and sunken? Do the mucous membranes appear moist or relatively dry? Do the extremities feel warm or cool? Is the capillary refill less than or greater than 2 seconds? Does the skin of the extremities tent when lightly pinched? If the patient is an infant, is the anterior fontanel sunken or flat? How many times has the patient urinated in the last 8 hours? Each of these components alone is poorly sensitive in terms of detecting significant levels of dehydration. However, when taken together, they are more useful.
LABORATORY FINDINGS Serum electrolyte samples are frequently drawn, but analyses of these are somewhat controversial regarding their utility. A bedside glucose measurement can be extremely important in the evaluation of an ill-appearing child.
DIAGNOSIS A careful clinical examination and assessment are generally more important than results of laboratory tests. Clinical diagnosis is supported by selective use of laboratory studies, including electrolyte measurements with particular attention to serum glucose measurement.
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RADIOGRAPHS Radiographs are not required in the management of fluids and electrolytes of children, except when required for the detection of an underlying cause of dehydration.
TREATMENT More currently, many mildly to moderately dehydrated children may be treated with ORT. What is discussed previously pertains to a child unable to tolerate oral rehydration. Overall, most children have uneventful outcomes after an associated illness and require little to no intervention. However, the small fraction of children requiring medical intervention with IV fluid therapy must be carefully assessed using the patient’s weight coupled with other clinical signs such as eye appearance, skin turgor, mucous membrane appearance, and urine output to appropriately treat them (Table 13-2). In acutely ill children, it is important to assess the airway, breathing, and circulatory status of the patient as well as performing the bedside serum glucose measurement. Once IV access has been established, a fluid bolus in the form of normal saline should be administered. The volume of these boluses should be 20 ml/kg, and they should be administered rapidly to quickly restore intravascular volume; administration of these boluses can be repeated up to three times. A patient who fails to respond to initial bolus
Table 13-2 Calculation of Deficit Fluids Sources of Daily Water Loss Insensible losses 50 ml/100 kcal/day One third via lungs Two thirds via skin (not perspiration) Urine 60–80 ml/100 kcal/day Daily Water Requirement per Kilogram of Body Weight 3–10 kg 100 ml/kg/day 10–20 kg 50 ml/kg/day >20 kg 20 ml/kg/day Daily Electrolyte Requirements Naþ 2–3 mEq/100 ml of fluid/day Kþ 2 mEq/100 ml of fluid/day Daily Glucose Requirement Glucose represents 20% of caloric expenditure, requires replenishment with a 5% dextrose solution to prevent ketosis In 5% dextrose in water, 5 g dextrose per 100 ml of fluid
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therapy is experiencing a state of shock and requires more ongoing aggressive therapy. Patients who have responded well to bolus therapy may then be started on maintenance and deficit therapy, as needed, using the previous instructions as guidelines for composition of the administered fluid. Bolus therapy volumes are not counted toward maintenance or deficit therapy volumes. Many children will likely require up to 24– 48 hours to fully reverse significant fluid and electrolyte deficits—this is particularly true for potassium levels.
Bibliography Fleisher GR, Ludwig S: Textbook of Pediatric Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2005. Gorelick MH, Shaw KN, Murphy KO, et al: Validity and reliability of clinical signs in the diagnosis of dehydration in children, Pediatrics 1997;99:1–6. Spandorfer PR, Alessandrini EA, Joffe M, et al: Oral vs. intravenous rehydration of moderately dehydrated children: A randomized controlled trial, Pediatrics 2005;115:295–301.
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Pediatric Bacteremia, Sepsis, and Meningitis SAMUEL TIMOTHY MCILRATH
ICD Codes: Bacteremia 790.7, Sepsis 995.91, Sepsis in a newborn 771.81, Meningitis 322.9
Key Points The infectious processes of bacteremia, sepsis, and meningitis represent a continuum of disease that may present differently according to the age of the patient. Fever is a common presenting symptom in children with infection but is not necessarily predictive of severity. The majority of fevers in children are due to self-limited viral infections (e.g., upper respiratory tract infection, flu) or minor bacterial infections (e.g., otitis media, sinusitis). Most are benign and resolve spontaneously without medical intervention. In most cases, the diagnosis can be made on the basis of a thorough history and physical examination alone; extensive laboratory testing generally is not helpful or necessary. More serious infections, however, may have significant morbidity and mortality if not treated. A serious bacterial infection (SBI) is a bacterial infection with potential for significant morbidity and mortality if left untreated (e.g., sepsis, meningitis, pyelonephritis, osteomyelitis, cellulitis, peritonitis, pneumonia). Certain factors, such as the patient’s age, clinical findings, degree of fever, and WBC count, can be used to differentiate those children at increased risk for SBI requiring a more extensive evaluation and workup. At times, it may be necessary to take quick and decisive action in resuscitating the unstable pediatric patient and to initiate prompt antibiotic therapy even before a definitive diagnosis is achieved. ! Emergency Actions ! Depending on the severity of illness, initial management may require stabilization of airway and breathing as well as circulatory support. Initially, hypotension is treated with isotonic fluids (e.g., normal saline, lactated Ringer’s solution) in 20-ml/kg boluses. After three such fluid boluses, refractory hypotension should be treated with appropriate vasopressors. When severe infection is suspected, empirical IV antibiotic treatment should be initiated as soon as possible after appropriate culture samples are obtained.
DEFINITION Bacteremia is defined as the recovery of bacteria in a blood culture. This may be a transient phenomenon not associated with any significant
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disease (e.g., after instrumentation of the gastrointestinal or genitourinary tract) or may result from extension of an undiagnosed invasive bacterial infection elsewhere. When a positive bacterial blood culture is obtained from an otherwise healthy-appearing child without a known source of infection, it is termed occult bacteremia. If the child’s immune system is unable to effectively eliminate the bacteria, a systemic inflammatory response may occur. Sepsis is the term used to describe this systemic inflammatory response. If sepsis is not recognized and treated early, it may progress to overwhelming infection, septic shock (i.e., sepsis with hypotension), multiple organ dysfunction syndrome, and death. Severe sepsis is a more advanced sepsis that has progressed to cause failure in multiple organ systems (e.g., brain, kidneys, heart). Septic shock may be recognized by a clinical triad of hyperthermia or hypothermia, altered mental status, and flash capillary refill and bounding pulses (warm shock) or mottled cool extremities and diminished pulses (cold shock). Of note, hypotension is a late finding of septic shock and is not necessary to make the diagnosis. Meningitis is an extension of infection to involve the meninges of the CNS.
EPIDEMIOLOGY The majority of pediatric infectious diseases (50%–60%) are self-limited viral infections primarily affecting the respiratory and gastrointestinal tracts. In addition, there are many minor bacterial diseases (30%) that can be diagnosed by examination alone, with little or no laboratory testing, and treated with antibiotic therapy on an outpatient basis (e.g., otitis media, Streptococcus infection, pharyngitis, impetigo). Fewer than 5% of febrile children have an SBI such as sepsis or meningitis. Infants younger than 3 months of age are most susceptible to SBI because of their immunological immaturity, and an even greater suspicion must be reserved for those younger than 28 days of age. In neonates (<28 days), the bacteria that cause SBI are reflective of maternal flora as well as environmental pathogens. In children 1 year of age or younger with fever without a source, urinary tract infection (UTI) is common and must be considered and ruled out. Children most at risk for occult bacteremia are 3–36 months of age. Occasionally, bacteremia may progress to sepsis. Sepsis may develop as a complication of a localized community-acquired infection or may follow colonization and local mucosal invasion by more virulent pathogens. The organisms responsible for sepsis and meningitis are essentially the same and vary according to the patient’s age (Table 13-3). Sepsis typically occurs in children with underlying chronic illnesses (e.g., neurological and cardiovascular illnesses, cancer, and immunodeficiency). In immunocompromised patients, nosocomial infections are a substantial risk. Neutropenic patients are susceptible to gram-negative sepsis and fungemia. Patients with surgical wounds or IV
708 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 13-3 Common Causative Organisms of Sepsis and Meningitis in Children AGE OF CHILD <1 month 1–23 months 2–18 years
INFECTIOUS ORGANISM Group B streptococcus, Listeria monocytogenes, and gram-negative organisms (e.g., Escherichia coli, Klebsiella species) Streptococcus pneumoniae and Neisseria meningitidis N. meningitidis, S. pneumoniae, and Haemophilus influenzae type b
catheters can become infected by skin pathogens such as Staphylococcus aureus or coagulase-negative staphylococci. Meningitis can be caused by virtually any microbe, with the specific pathogen influenced by the age and immune status of the individual. Although viral infections of the CNS are much more common, bacterial infection is more severe. Fungal and parasitic organisms represent much less common causes of CNS infection. Since the introduction of conjugate vaccines for HIB and S. pneumoniae, the incidence of bacterial meningitis has dropped significantly. The incidence is still higher in younger children, especially neonates, for whom vaccines have not yet been developed. The most common causative organisms vary by patient age (see Table 13-3).
CLINICAL PRESENTATION Fever is the most common presenting symptom of these disease processes in pediatric patients; however, it is neither specific nor predictive of disease severity. By definition, occult bacteremia is said to occur in a child with a positive blood culture result in the absence of any obvious source of infection. Therefore, the child may be febrile but lacks any historical clues or clinical findings that indicate a specific source. In contrast, sepsis is more clinically apparent because the child will have unstable vital signs. The septic child may appear to be more ill and possibly toxic, with symptoms and findings consistent with a source of infection. The body’s inflammatory response to sepsis leads to hypotension and decreased perfusion to vital organ systems that explains the clinical findings and toxic appearance consistent with sepsis. Decreased perfusion of the brain causes mental status changes such as confusion, anxiety, agitation, excitation, lethargy, obtundation, and coma. (Lethargy is an often overused term and, in the true medical sense, refers to an inappropriately decreased response to external stimuli.) As blood flow to the skin and kidneys decreases, the child may become cool and clammy, and urine output may decrease or even
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cease. Underperfusion of the body’s tissues leads to metabolic acidosis and resultant compensatory hyperventilation/tachypnea. Sepsis may have an acute onset, especially in certain populations such as very young or immunocompromised persons but usually represents the progression of a preceding infection such as an upper respiratory tract infection. Meningitis may present differently given the age of the patient. Older children frequently report fever, headache, photophobia, nausea/vomiting, and neck or back pain. Younger children who are unable to verbalize their symptoms may present with lethargy, decreased or increased sleeping, poor appetite, or other changes in behavior from baseline such as inconsolability or irritability. For this reason, it is important to ask parents how their child’s behavior compares with their baseline because this is often an important historical clue. Up to 30% of children with acute bacterial meningitis have seizures on initial presentation. Similar to sepsis, the onset of meningitis has two predominant presentations: a rapidly progressing fulminant form and an insidious form. The fulminant form, while less common, is much more severe and may progress quickly to shock and reduced levels of consciousness, frequently resulting in death within 24 hours. The insidious form is typically preceded by several days of fever accompanying upper respiratory or gastrointestinal symptoms, followed later by the more typical signs of CNS infection.
EXAMINATION On physical examination, children with sepsis are typically ill-appearing and may be lethargic. The early primary signs and symptoms of sepsis and its complications include hyperthermia or hypothermia, rigors, tachycardia (which may be absent in the hypothermic patient), tachypnea, skin lesions (e.g., petechiae, ecchymoses, diffuse erythema), and mental status changes such as confusion, anxiety, agitation, excitation, lethargy, obtundation, and coma. Later manifestations include hypotension, cyanosis, symmetrical peripheral gangrene (purpura fulminans), oliguria or anuria, jaundice, and signs of heart failure. Children with meningitis may have similar clinical presentations and physical findings to those with sepsis. Special attention must be made to evaluate for meningismus and/or focal neurological abnormalities. Meningismus, or meningeal irritation, is manifested as nuchal rigidity, back pain, Kernig’s sign (i.e., flexion of hip to 90 degrees with subsequent pain with extension of the knee), and Brudzinski’s sign (i.e., involuntary flexion of the knees and hips after passive flexion of the neck in the supine position). Meningismus is almost always present in children with bacterial meningitis beyond 13 months of age and generally absent in children younger than 6 months of age.
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LABORATORY FINDINGS By definition, bacteremia implies the presence of a positive blood culture result. Often, there may be an elevated WBC count and/or left shift as well. Laboratory findings in sepsis may be more widespread. Apart from an identifiable source of infection such as a positive culture result or clinical finding, typical laboratory findings in sepsis/septic shock often include increased lactic acid and metabolic acidosis, thrombocytopenia, prolonged prothrombin time (PT)/partial thromboplastin time (PTT), anemia, decreased PaO2 and increased PaCO2, and elevated neutrophil and band counts. In a nonimmunocompromised host, neutropenia can be a sign of overwhelming sepsis. Patients with suspected meningitis warrant further testing, including evaluation of the CSF. This should include culture, cell count and Gram stain, protein and glucose analysis, and possibly other studies depending on the patient’s age and clinical circumstances. An examination of the CSF may demonstrate neutrophils and bacteria. Typical CSF findings are listed in Table 13-4. If a lumbar puncture is performed in the early stages of meningitis, bacteria may be detected in the CSF before the development of an inflammatory response. Approximately 1% of children with bacterial meningitis will have a normal CSF cell count. Due to the risk of cerebral herniation, patients with focal neurological findings should wait for lumbar puncture until a head CT scan has ruled out a space-occupying lesion. Otherwise, a head CT scan is not routinely recommended before lumbar puncture. Thrombocytopenia and overlying cellulitis are contraindications to lumbar puncture.
TREATMENT Occult Bacteremia Many have implemented the use of so-called fever guidelines in directing their management of children 0–36 months of age with fever without source. When the source of fever cannot be identified on the basis of initial history and physical examination, such guidelines can be used
Table 13-4 Typical Cerebrospinal Fluid Findings in Meningitis BACTERIAL WBC/mm3 Protein (mg/dl) Glucose (mg/dl) Gram stain WBC, White blood cell.
>1000 Markedly elevated (>100) Markedly decreased (<40) Bacteria Polymorphonuclear cells
VIRAL <500 Normal (<100) Normal (>40) No bacteria Mononuclear cells
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as a means of identifying and empirically treating those children most at risk for harboring an occult bacteremia that, if left untreated, may progress to an SBI. Some argue that such guidelines are no longer appropriate since the incidence of the two most common pediatric bacterial pathogens, HIB and S. pneumoniae, has been greatly reduced by the introduction of their respective conjugate vaccines. The following is a synopsis of these “fever guidelines.” As a general rule, all toxic-appearing infants and children and all febrile infants younger than 28 days old should undergo a sepsis evaluation, including analysis of blood, urine, and CSF, and should be hospitalized for parenteral antibiotic therapy pending culture results (Table 13-5). Febrile infants 28–90 days old meeting low-risk criteria may be managed as outpatients if close follow-up is ensured. (Low-risk criteria include previously being healthy, having no evidence of focal bacterial examination on physical examination, and having negative laboratory screening results. Negative laboratory screening results includes WBC count of 5000–15,000/mm3, fewer than 1500 bands/mm3, normal urinalysis results, and, when diarrhea is present, fewer than 5 WBC/high-power field in stool.) Well-appearing children older than 3 months of age with a temperature below than 39.0 C without an apparent source of fever need no antibiotics or specific laboratory tests, other than urinalysis/culture in specific cases. Children aged 3–36 months with a temperature of 39.0 C or more and a WBC count of 15,000/mm3 or more should have a blood culture drawn and be treated with antibiotics. Typically, an IM injection of ceftriaxone is administered pending culture results. Parenteral antibiotics are more effective than no or oral antibiotic therapy in reducing the risk of subsequent bacterial meningitis. Children in this group should be reevaluated in 12–24 hours. Urinalysis and culture samples should be obtained from all boys 6 months or younger and all girls 2 years or younger who are treated with antibiotics.
Table 13-5 Suggested Initial Antibiotic Therapy for Children with Sepsis and Meningitis AGE <1 month
>1 month
ANTIBIOTICS (INTRAVENOUS) Ampicillin 50 mg/kg plus Gentamicin 2.5 mg/kg or cefotaxime 50 mg/kg plus Vancomycin if Staphylococcus species or pneumococcus is suspected Ceftriaxone 100 mg/kg or cefotaxime 50 mg/kg plus Vancomycin 15 mg/kg
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Although these fever guidelines are commonly used by some clinicians, there is no replacement for decision making based on the patient’s unique circumstances and the clinician’s sound judgment.
Sepsis In a patient with sepsis, it is necessary to expediently administer broadspectrum antibiotic therapy that is based on the patient’s risk factors. For example, community-acquired illnesses (e.g., Neisseria meningitidis, S. pneumoniae, HIB) can be treated with a third-generation cephalosporin (e.g., ceftriaxone, cefotaxime). Sepsis due to a nosocomial infection can be treated with a third-generation cephalosporin or a penicillin with broad gram-negative coverage (e.g., mezlocillin, piperacillintazobactam) plus an aminoglycoside. If the patient has an indwelling medical device, then vancomycin should be added for improved grampositive coverage. If fungal infection is suspected, as in the case of neutropenic patients receiving chemotherapy, then empirical amphotericin B may be administered. In septic shock, resuscitative efforts must be initiated early as well. Supplemental oxygen should always be given and intubation and mechanical ventilation performed if the patient shows signs of increased work of breathing and early respiratory failure. Fluids should be given in 20-ml/kg boluses. If the liver edge becomes palpable or rales are heard, more fluid is not advised. Shock that is refractory to fluids may require central venous access and dopamine therapy. For septic shock that remains refractory to dopamine, the clinician should titrate epinephrine (cold shock) or norepinephrine (warm shock). For catecholamine-resistant shock, the risk of adrenal insufficiency should be considered, and hydrocortisone should be given if deemed necessary. The practitioner should assess and correct for hypoglycemia and hypocalcemia, and communicate early with a pediatric intensivist regarding patient care and arrangements for transfer to an intensive care unit.
Meningitis If bacterial meningitis is suspected, antibiotics should be administered immediately after collecting samples for blood culture and CSF analysis. Depending on the infecting organism, the yield for CSF culture declines within 1–8 hours of the administration of antibiotics. The choice of antibiotic should be based on the age of the patient, the presence or absence of various risk factors, and the Gram stain results. Suggested empirical antibiotic therapy for various age groups is provided in Table 13-5. Children with CNS hardware such as a ventriculoperitoneal shunt or history of recent head trauma or CNS surgery are more likely to have infection due to Streptococcus or Staphylococcus species and should
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receive vancomycin in addition to standard therapy. Also, vancomycin is recommended as a part of any antibiotic regimen if the presence of penicillin-resistant pneumococcus is suspected. The adjunctive use of dexamethasone in bacterial meningitis remains controversial. Dexamethasone has been recommended in cases of bacterial meningitis due to the belief that it reduced the incidence of hearing loss, especially in persons with meningitis due to HIB. With the introduction of the HIB vaccine and the subsequent dramatic decline in the incidence of disease caused by this organism, the use of dexamethasone is no longer considered the standard of care in the management of bacterial meningitis. Close contacts of patients with infection due to HIB and N. meningitidis should be offered prophylactic therapy to prevent spread of disease. Prophylaxis should be offered to family contacts and close social contacts (e.g., day care or school classmates). Prophylaxis for meningococcus should be offered to all hospital personnel involved in direct contact with the patient, especially those with exposure to the patient’s oral secretions such as in deep-suctioning or intubation. For HIB prophylaxis, oral rifampin 20 mg/kg (maximum dose, 600 mg) is given daily for 4 days. For N. meningitidis, recommended prophylaxis includes rifampin 600 mg every 12 hours for 2 days (5 mg/kg for children younger than 1 month), a single dose of ciprofloxacin 500 mg, or a single dose of ceftriaxone 250 mg IM (125 mg for children younger than 15 years).
Bibliography Baraff LJ, Bass JW, Fleisher GR, et al: Practice guideline for the management of infants and children 0 to 36 months of age with fever without source, Ann Emerg Med 1993;22(7):1198–1210. Stormorken A, Powell KR: Sepsis and shock. In Behrman RE, Kliegman RM, Jenson HB (eds): Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, pp 846–850.
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Asthma STEPHEN A.CRANDALL AND DIANE DEVITA
ICD Code: 493.9
Key Points Asthma is the most common chronic disease of childhood, affecting 9 million children in the United States. The prevalence of asthma among children younger than 18 years of age both in the United States and worldwide has doubled over the last two decades, with similar increases in ED visits, hospitalizations, and deaths related to asthma. ! Emergency Actions ! Oxygen, inhaled beta-2 agonists, systemic corticosteroids, and anticholinergic agents are the mainstays of treatment for acute asthma exacerbations.
DEFINITION Asthma is a complex, multifactorial chronic inflammatory disorder of the airways characterized by airway inflammation, airway hyperresponsiveness, and reversible airway obstruction. Airway inflammation leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing in susceptible persons.
EPIDEMIOLOGY Asthma is the most common chronic disease of childhood, affecting 9 million children in the United States. The prevalence of asthma among children younger than 18 years of age both in the United States and worldwide has doubled over the last two decades, with similar increases in ED visits, hospitalizations, and deaths related to asthma. Of the 9 million diagnosed children in the United States, 4 million have experienced an acute asthma attack over the last year. Pediatric asthma accounted for more than 728,000 ED visits in 2000, with one third of those leading to hospitalization. Asthma is the third ranking cause of hospitalization for children younger than 15 years old. Death rates resulting from asthma among children nearly tripled from 1979 to 1996 (up to 266 from 93). Rates of asthma, exacerbations, hospitalizations, and asthma-related deaths are
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markedly greater among African-American, poor, and inner-city children. Children living in poverty are four times more likely to visit the ED for asthma care than a pediatrician’s office. More than half of all cases of persistent asthma start by the age of 3 years, and nearly 80% of children with persistent asthma develop symptoms before they are 6 years old. Risk factors for developing asthma include early exposure to tobacco smoke and common allergens in the home (such as dust mites and cat dander), family history of atopy, or prior diagnoses of ectopic dermatitis or allergic rhinitis. Approximately 40% of children with a family history of asthma will develop persistent asthma. Although genetics and environmental exposures both play a crucial role in the development of asthma, it is the complex interaction of these combined with individual susceptibilities that influence both the development and severity of asthma.
PATHOPHYSIOLOGY Asthma results from complex interactions among inflammatory cells, inflammatory mediators, and other cells and tissues in the airway. Airway inflammation, airway hyperresponsiveness, and airway obstruction combine to lead to symptoms of wheezing, cough, chest tightness, and breathlessness that are the hallmarks of asthma exacerbations. Exposure to a trigger or antigen leads to immunoglobulin (Ig) E–mediated activation of mast cells, release of preformed mediators (including cytokines, leukotrienes, and histamine), and initiation of a complex inflammatory cascade involving T lymphocytes, macrophages, neutrophils, eosinophils, and other cells that serve to intensify and prolong the inflammation and edema in the airway. Hyperresponsiveness of the airway to a wide variety of stimuli is a major feature of asthma, and the level of response contributes to the severity of asthma. Airway obstruction is caused both by allergen-induced acute bronchoconstriction and airway edema from the inflammatory response. The “early phase” of an acute asthma exacerbation, occurring immediately after exposure and lasting 1–2 hours, is marked by bronchospasm and smooth muscle contraction directly caused by histamine, leukotrienes, prostaglandins, and other mediators released by activated mast cells. The “late phase” of an exacerbation (approximately 4 hours after exposure/trigger) results from the inflammatory response caused by cellular and chemotactic mediators, as noted previously, that leads to recurrent bronchospasm, airway inflammation, airway obstruction, and edema. The late phase can last 12–24 hours or longer in more severe cases. With chronic airway inflammation, airway remodeling can take place with subepithelial alterations and basement membrane thickening that contributes to an irreversible component of airway narrowing and obstruction unresponsive to therapy.
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Viral respiratory infections and allergens are the most common precipitants of asthma exacerbations. Common allergens include dust mites, pollen, molds, animal dander, and cockroaches. Airway irritants such as tobacco smoke and air pollutants, cold air exposure, exercise, stress, sinusitis, and gastroesophageal reflux can also be potent triggers of asthma exacerbations.
PRESENTATION On presentation to the ED, the child’s respiratory status should immediately be assessed to determine the severity of the exacerbation and the possibility of impending respiratory failure. Wheezing, breathlessness, chest tightness, respiratory distress, and cough are the symptoms most commonly associated with acute asthma exacerbations. For some children, persistent cough without wheezing may be the predominant feature. Although a wheezing, dyspneic child with a history of asthma most likely is experiencing an asthma exacerbation, other entities that can cause wheezing should be considered and kept in the differential diagnosis. Upper respiratory tract infections (e.g., rhinitis/sinusitis), choanal atresia, tonsillar enlargement, or foreign bodies can all cause upper airway wheezing and obstruction. Croup, epiglottitis, LTB, vocal cord dysfunction, laryngeal webs, laryngotracheomalacia, tracheoesophageal fistulas, tracheal stenosis, and tracheal foreign bodies should all be considered. Other lower airway conditions that can present with wheezing include pneumonia, cystic fibrosis, bronchiolitis, bronchopulmonary dysplasia, pulmonary edema (due to exacerbation of congenital cardiac disease), inhalation injury, alpha-1 antitrypsin syndrome, Löffler’s syndrome, and aspiration due to gastroesophageal reflux.
EVALUATION A brief and focused history and examination should be performed immediately to assess for complicating factors and to determine the severity of the event. Important items to ask about include the onset, duration, and nature of symptoms; triggering event or exposure; the character, frequency, and duration of prior asthma exacerbations; the relative severity of current event; prior ED visits, hospitalizations, and intensive care unit admissions for asthma; prior intubations or use of continuous or biphasic positive airway pressure for asthma; recent use of corticosteroids and medications; medication allergies; family history of atopy or asthma; and other past medical history, including cardiopulmonary illnesses (e.g., congenital heart conditions, gastroesophageal reflux disease, bronchopulmonary dysplasia) (Table 13-6). The physical examination should be focused on the respiratory status of the child and the determination of the severity of the episode.
Table 13-6 Classifying Severity of Asthma Exacerbations MILD
MODERATE
SEVERE
Symptoms Breathlessness
While walking
While at rest (infant: stops feeding)
Talks in Alertness
Can lie down Sentences May be agitated
While talking (infant: softer, shorter cry; difficulty feeding) Prefers sitting Phrases Usually agitated
Sits upright Words Usually agitated
RESPIRATORY ARREST IMMINENT
Drowsy or confused
Signs Respiratory rate
Increased
Increased
Often >30 breaths/min
Guide to rates of breathing in awake children Age < 2 months 2–12 months 1–5 years 6–8 years Usually not
Commonly
Paradoxical thoracoabdominal movement
(Continued) (continued)
Asthma
Use of accessory muscles; suprasternal retractions
Normal rate <60 breaths/min <50 breaths/min <40 breaths/min <30 breaths/min Usually
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MILD
MODERATE
Wheeze
Moderate, often only end expiratory
Loud; throughout exhalation
Pulse/min
<100 beats/min
100–120 beats/min
SEVERE Usually loud; throughout inhalation and exhalation >120 beats/min
RESPIRATORY ARREST IMMINENT Absence of wheeze Bradycardia
Guide to normal pulse rates in children Age 2–12 months 1–2 years 2–8 years Pulsus paradoxus
Normal rate <60 beats/min
Absent <10 mmHg
May be present 10–25 mmHg
>80%
Approximately 50%–80% or response lasts <2 hr
<120 beats /min <110 beats/min Often present >25 mmHg (adult) 20–40 mmHg (child)
Functional Assessment PEF % predicted or % personal best
<50% predicted or personal best
Absence suggests respiratory muscle fatigue
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Table 13-6 Classifying Severity of Asthma Exacerbations—Cont’d
PaO2 (on air) and/or PCO2
SaO2 (on air) at sea level
Normal (test not usually necessary) <42 mmHg (test not usually necessary) >95% (test not usually necessary) Hypercapnia (hypoventilation) develops more readily in young children than in adults and adolescents.
>60 mmHg (test not usually necessary) <42 mmHg (test not usually necessary) 91%–95%
<60 mmHg: possible cyanosis 42 mmHg: possible respiratory failure <91%
Modified from National Institutes of Health: The National Asthma Education Program Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health Publication 97–4051. NIH: Bethesda, MD, 1997. Note: The presence of several parameters, but not necessarily all, indicates the general classification of the exacerbation. Many of these parameters have not been systematically studied, so they serve only as general guides. PEF, Peak expiratory flow.
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Important features of the examination include respiratory rate, heart rate, degree of dyspnea, work of breathing and the use of accessory respiratory muscles, presence of wheezing, evidence of retractions or nasal flaring, level of alertness, length of inspiratory/expiratory phase, and cyanosis. Patients are often tachypneic and tachycardic, depending on the degree of severity. Dyspnea can be assessed by asking the child his or her name, asking him or her to count, or eliciting a sentence. Accessory muscle use and retractions correlate with decreased peak flow rates and forced expiratory volumes in 1 second (FEV1) and suggest a moderate to severe exacerbation. Wheezing may be absent initially with severe airway obstruction, and decreased air movement may become more prominent with treatment. Increased drowsiness and decreased activity/agitation may suggest fatigue, hypercarbia, and impending respiratory failure. Often, patients will present with an increased expiratory phase. Cyanosis is a late finding with worsening hypoxia. Peak expiratory flow rate (PEFR) tests and oxygen saturation (SaO2) identified by pulse oximetry can be helpful in the assessment of the severity of the asthma episode. A PEFR less than 50% of the predicted or personal best is indicative of a severe exacerbation. SaO2 less than 91% is suggestive of severe airway obstruction and suggests the need for hospitalization if the condition does not improve with treatment. PEFR or FEV1 should be measured on presentation to the ED, after initial therapy, and after subsequent interventions to help gauge response. Infants are at greater risk for respiratory failure due to anatomical differences in their lungs, including greater peripheral airway resistance, less elastic recoil, and the mechanical inefficiency of the diaphragm. Infants are also at greater risk for dehydration due to increased respiratory rate and imperceptible water losses. Close monitoring of this age group is especially important to prevent potentially fatal complications.
LABORATORY TESTS AND RADIOGRAPHS ABG analyses are indicated in patients with moderate to severe respiratory distress who remain refractory to therapy, with impending respiratory failure, with hypoventilation, or with oxygen requirements exceeding 40% FiO2. A CBC may be helpful in patients with fever or purulent sputum. Serum theophylline levels should be measured for patients chronically taking this medication. Chest radiographs are not part of the routine evaluation of asthma exacerbations. They may be considered for a child with fever, impending respiratory failure, or poor response to therapy. Concerns for other complicating features such as pneumothorax, pneumomediastinum, or
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possible presence of a foreign body would also merit a chest x-ray. Lung hyperinflation may be seen with radiography in the case of moderate-to-severe airway obstruction.
TREATMENT Oxygen, inhaled beta-2 agonists, systemic corticosteroids, and anticholinergic agents are the mainstays of treatment for acute asthma exacerbations. Humidified oxygen should be given to maintain arterial saturation (SaO2) above 92% and to prevent further bronchoconstriction and worsening hypoxia. Short-acting inhaled beta-2 adrenergic agonists such as albuterol, levalbuterol, pirbuterol, and bitolterol are the foundation of acute asthma treatment. Beta-adrenergic agonists reverse airway constriction by relaxing bronchial smooth muscle and inhibiting mediator release from inflammatory cells, limiting both the early and late phases of asthma attacks. Intermittent nebulization, continuous nebulization, and metered dose inhaler (MDI) are the preferred modes of delivery. IV and oral preparations have little role in the management of acute exacerbations. Albuterol is the most commonly used beta-agonist. Nebulized albuterol should be given at a dose of 0.15 mg/kg (minimum, 2.5 mg) every 20 minutes for the first hour then 0.15–0.3 mg/kg every 1–4 hours, as needed. Continuous nebulizers at 0.5 mg/kg/hr (maximum, 15 mg/hr) can also be used for moderate/ severe exacerbations. MDI with spacers are comparable to nebulizers in mild-to-moderate exacerbations for children older than 3 years old. Four to eight puffs (90 mg/puff) should be administered every 20 minutes for the first hour, then every 1–4 hours, as needed. A nebulizer with face mask remains the preferred mode of delivery for children younger than 3 years of age. A second hour of treatment every 20 minutes (or by continuous nebulizer) may be necessary depending on the severity of the exacerbation or degree of response. Levalbuterol (Xopenex), the R-enantiomer of racemic albuterol, was initially developed to have increased response and fewer adverse effects than albuterol. However, recent trials have demonstrated a similar efficacy and side effect profile as albuterol. Dosing is half that of racemic albuterol. Systemic glucocorticoids should be given to patients who do not have dramatic response to initial beta-2 agonist therapy (PEFR <80%), those who are chronically treated with or have recently discontinued corticosteroid therapy, those at increased risk for death from asthma, and those requiring hospitalization. Steroids are a potent suppressive agent of the inflammatory process involved in acute and chronic asthma. They prevent the formation of leukotrienes and prostaglandins and inhibit the migration of inflammatory cells involved in the late phase of asthma exacerbations. Their use has been shown to reduce hospitalization rate
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and duration, relapse frequency, need for additional intervention, and overall morbidity. Oral and parenteral routes have equivalent efficacy and time of onset. Inhaled corticosteroids have not been shown to have additional benefit acutely and are not recommended for asthma exacerbations. Prednisone, prednisolone, or methylprednisolone can be given 1 mg/kg every 6 hours for 48 hours then 1–2 mg/kg/day (maximum, 60 mg/day) in two divided doses. Dosing for outpatient therapy for acute exacerbations is 1–2 mg/kg/day in two divided doses for 3–10 days. Inhaled corticosteroids can be added following acute exacerbations to reduce the rate of relapse. Anticholinergic medications, including ipratropium bromide and glycopyrrolate, can provide additional bronchodilation when used with beta-adrenergic agonists. These drugs block parasympathetic acetylcholine receptors and reduce vagal-mediated bronchoconstriction of the airway. There is poor systemic absorption of inhaled agents and few to no anticholinergic side effects. Ipratropium bromide can be administered by nebulizer (0.25 mg) or via MDI (4–8 puffs, 18 mg/puff) in conjunction with albuterol every 20 minutes for the first hour then every 2–4 hours as needed. Terbutaline is a systemic selective beta-2 agonist that can be administered subcutaneously (0.01 mg/kg every 20 minutes for three doses) as an adjunctive therapy to inhaled bronchodilators for a severe asthmatic patient with little air movement. Epinephrine (1:1000) is a nonselective alpha and beta agonist that can be used in acute exacerbations if inhaled beta agonists are not available. It is given subcutaneously (0.01 mg/kg up to 0.5 mg every 20 minutes for three doses) and has substantial beta-1 agonist activity that can cause tachycardia, agitation, and dysrhythmias. Systemic beta-adrenergic agonists, however, lend little additional benefit over inhaled medications. Long-acting beta-2 agonists such as salmeterol and formoterol can be effective in reducing the frequency of nighttime symptoms and are used in chronic asthma management; there is no role for these medications in acute exacerbations. Theophylline and other methylxanthines were frequently used in the past to treat acute bronchospasm. However, the recent literature suggests that methylxanthines with or without beta agonists provide little additional improvement in bronchodilation and have a higher degree of adverse effects. For those patients treated with theophylline, a theophylline level should be measured to check for toxicity. Cromolyn and nedocromil are mast cell stabilizers that help to inhibit the release of inflammatory mediators. Leukotrienes inhibitors such as zafirlukast, montelukast, and zileuton help to decrease asthma symptoms and improve lung function by interfering in the inflammatory cascade. These agents are restricted primarily to the chronic management of asthma, however, and have not been shown to be effective in acute exacerbations.
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Magnesium sulfate administered parenterally (25–70 mg/kg) may be effective in reducing hospitalization rates and improving pulmonary function and clinical symptoms in children with moderate-to-severe asthma exacerbations. The exact mechanism of action is unknown, though it is hypothesized that magnesium interferes with smooth muscle contraction in the airway. Further studies are needed to determine those groups that would particularly benefit from magnesium as an adjunctive therapy. Heliox, a mixture of helium and oxygen (70:30 to 80:20), has been considered for treatment of acute obstructive respiratory disorders. Although there is some literature to suggest that delivery of beta agonists with heliox may be superior to nebulizers with oxygen, more research is needed. Its use is limited to persons requiring less than 30% oxygen, and there is no benefit to administering heliox alone without beta–agonist therapy. Antibiotics are rarely indicated because infectious triggers of exacerbation are almost exclusively viral in origin. Their use should be limited to patients with clear evidence of bacterial infection. Intubation and mechanical ventilation may be necessary if the patient’s condition continues to deteriorate despite maximal management. Decreasing PaO2, increasing PaCO2 (>42 mmHg), increasing fatigue, change in mental status, apnea, and worsening respiratory acidosis are all indications to consider mechanical ventilation. Once the decision to intubate is made, it should not be delayed. Continuous positive airway pressure and biphasic positive airway pressure ventilation may be alternatives to intubation if begun early and if rapid improvement is noted. Patients with a good response to therapy within the first hour (i.e., no shortness of breath or wheezing, oxygen saturation >95%, PEFR >70% of predicted/personal best) can be discharged home with little occurrence of relapse. Patients should be observed for a minimum of 30 minutes after the last beta-agonist nebulizer/MDI treatment. Intensification of home asthma treatment should be initiated with the increased frequency of dosing with nebulizers/MDI or the addition of inhaled corticosteroids. Patients at a higher risk of developing complications should be treated with a 3–10-day course of systemic corticosteroids. Follow-up with their primary physician should be arranged within 48–72 hours. Patients with an incomplete response and continued symptoms after the first hour of therapy require a second hour of intensive therapy. Corticosteroids should be administered, and these patients should be observed closely for improvement or deterioration. Hospitalization should be considered for those with an initial PEFR less than 30%, continued oxygen saturation less than 91%, or inadequate response after 2–4 hours of therapy in the ED. In addition, high-risk patients without complete response within the first hour or two of therapy should be admitted for further beta-agonist therapy, steroids, supplemental oxygen, and observation.
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Bibliography Aligne CA, Auinger P, Byrd RS, Weitzman M: Risk factors for pediatric asthma: Contributions of poverty, race, and urban residence, Am J Respir Crit Care Med 2000;162: 873–877. American Lung Association: Trends in Asthma Morbidity and Mortality. New York: May 2005. Castro-Rodriguez JA, Rodrigo GJ: Beta-agonists through metered-dose inhaler with valved holding chamber versus nebulizer for acute exacerbation of wheezing or asthma in children under 5 years of age: A systematic review with meta-analysis, J Pediatr 2004;145(2):172–177. Centers for Disease Control and Prevention: Asthma’s impact on children and adolescents. November 2005. Available at: http://www.cdc.gov/asthma/children.htm. Centers for Disease Control and Prevention: Measuring childhood asthma prevalence before and after the 1997 redesign of the national health interview survey—United States, MMWR Morb Mortal Wkly Rep 2000;49:908–911. Darr CD, Kirelik S, Russell S, et al: Reactive airways disease and pneumonia, In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Dey AN, Bloom B: Summary health statistics for U.S. children: National Health Interview Survey, 2003, Vital Health Stat 10 2005;10(223):1–78. Eid NS: National Asthma Education and Prevention Program. Update on National Asthma Education and Prevention Program pediatric asthma treatment recommendations, Clin Pediatr (Phila) 2004;43(9):793–802. Kim IK, Phrampus E, Venkataraman S, et al: Helium/oxygen-driven albuterol nebulization in the treatment of children with moderate to severe asthma exacerbations: A randomized, controlled trial, Pediatrics 2005;116(5):1127–1133. National Asthma Education and Prevention Program: Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma Update on Selected Topics—2002, J Allergy Clin Immunol 2002;110(5 Suppl):S141–S19. National Heart, Lung, and Blood Institute: Guidelines for the Diagnosis and Management of Asthma. Expert Panel Report 2. National Institutes of Health Publication 97–4051. National Heart Lung and Blood Institute: Bethesda, MD, 1997. National Heart, Lung, and Blood Institute: Data Fact Sheet: Asthma Statistics National Institutes of Health, National Heart Lung and Blood Institute: Bethesda, MD, 1999. National Institute of Allergy and Infectious Diseases: Asthma: A Concern for Minority Populations. National Institutes of Health, Bethesda, MD: October 2001. Rowe BH, Bretzlaff JA, Bourdon C: Intravenous magnesium sulfate treatment for acute asthma in the emergency department: A systematic review of the literature, Ann Emerg Med 2000;36(3):181–190. Wolfson AB, Hendey GW, Hendry PL (eds): The Clinical Practice of Emergency Medicine, ed 4. Lippincott, Williams & Wilkins: Philadelphia, 2005.
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Bronchiolitis JULIE HUSLEY
ICD or CPT Code: 466.19
Key Points RSV causes the majority of cases of bronchiolitis. The treatment of bronchiolitis is mainly supportive. The peak occurrence is between October and May. ! Emergency Actions ! Infants with bronchiolitis should be monitored with pulse oximetry and cardiac monitoring. Frequent reassessment of the patient for respiratory fatigue is essential so that ventilatory therapy starts at the appropriate stage of treatment in the few infants who will need it.
DEFINITION Bronchiolitis is an infection of the bronchial and bronchiolar epithelial cells, with subsequent inflammation and edema resulting in airway obstruction. The term refers to a clinical syndrome of wheezing, tachypnea, and use of accessory muscles to breathe in children younger than 2 years of age.
EPIDEMIOLOGY Bronchiolitis peaks between late October and early May. It is the most common cause of lower respiratory tract infection in infants younger than 12 months of age and is the most frequent cause of hospitalization in infants younger than 6 months of age. American Indian/Alaska Native children have about twice the incidence of hospitalizations for bronchiolitis than the general population of U.S. children.
PATHOLOGY RSV causes 50%–80% of all cases of bronchiolitis. Other causes include rhinovirus, parainfluenza virus, echovirus, adenovirus, M. pneumoniae, and Chlamydia trachomatis. RSV is highly contagious and can
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survive without a host for up to 6 hours. It can be shed from infected patients for up to 9 days. Immunity to the virus is not acquired by infection, so reinfection can occur. Mucous plugging and widespread airway edema result in air trapping and variable obstruction. It is a self-limiting condition but may progress to life-threatening pneumonia in a few patients, especially those with comorbidities.
CLINICAL PRESENTATION Early symptoms of bronchiolitis include coryza, rhinorrhea, and cough. High fever may also be reported early in the onset. Mild symptoms are then followed by wheezing, increasing respiratory rate, poor feeding, and chest retractions. In infants younger than 6 months of age, parents may report apneic periods. It is important to ask about preexisting conditions, including premature birth, chronic respiratory conditions (e.g., cystic fibrosis), underlying neurological or neuromuscular conditions, cardiac conditions and immunodeficiency, infectious contacts, duration and rate of progression of symptoms, and how well the infant is feeding.
EXAMINATION The clinician should observe the general appearance of the child. The presence of tachypnea (i.e., >60 breaths/min), flushing of the skin, tachycardia, nasal flaring, chest retractions, or apnea should be documented. Some children may present with dehydration, so the mucous membranes and urine output in the diaper should be examined. Feeding attempts and presence of fatigue should be observed. Crepitations on chest auscultation and hypoxemia are the best clinical predictors of the need for hospitalization.
LABORATORY FINDINGS A CBC usually yields normal results with bronchiolitis. If WBC counts are elevated, bacterial pneumonia should be considered. Electrolytes and kidney function values are helpful if the patient needs IV hydration. A blood culture should be performed if the patient’s temperature is above 38.5 C (101.3 F). Nasopharyngeal aspirate samples should be obtained for RSV and viral culture; the results can usually be back from the laboratory within 1 hour. This will help guide the decision whether to admit the child to the hospital.
DIAGNOSIS Bronchiolitis is a clinical diagnosis made on the basis of presentation and physical examination results. It can be difficult to distinguish bronchiolitis
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from other conditions that present with transient early wheezing, such as asthma, since much of the early clinical presentation is the same.
RADIOGRAPHS A chest radiograph may be helpful if diagnosis is uncertain. It may show pulmonary hyperinflation, patchy atelectasis, and peribronchial wall thickening.
TREATMENT During the ED course, infants with bronchiolitis should be monitored with pulse oximetry and cardiac monitoring. Frequent reassessment of the patient for respiratory fatigue is essential so that ventilatory starts at the appropriate stage of treatment in the few infants who will need it. Supplemental humidified oxygen at concentrations of 28%–40% is the most important form of therapy. Also, fluid rehydration with a 20-ml/kg bolus of normal saline improves the outcome for some patients with poor fluid intake and insensible fluid loss. Pharmacological therapy is controversial because studies of adrenaline, bronchodilators, and glucocorticoid use have failed to demonstrate any proven benefit for viral lower respiratory infections. However, if the patient has a history of asthma or has an element of reactive airway disease causing current symptoms, along with or instead of bronchiolitis, then adrenaline, bronchodilators, and glucocorticoids may be of benefit. The use of ribavirin, IV immunoglobulins, and antibiotics have not been proved to benefit the treatment of bronchiolitis. Most cases can be treated on an outpatient basis, as long as the parents are reliable and have good follow-up within 24 hours. However, there are certain cases in which admission is necessary. Admission should be considered in the following cases:
Poor fluid intake with signs of dehydration Respiratory rate faster than 50–60 breaths/min Apneic spells Use of accessory muscles Pulse oximetry less than 90%–93% Underlying comorbidities complicating the illness Risk factors for dying with bronchiolitis include the following:
Very low birth weight and low birth weight infants Increasing birth order Low 5-minute Apgar score Young maternal age Unmarried mother Tobacco use during pregnancy
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Bibliography Black CP: Systematic review of the biology and medical management of respiratory syncytial virus infection, Respir Care 2003;48:209–233. Frey U, Makkonen K, Wellman T, et al: Alterations in airway wall properties in infants with a history of wheezing disorders, Am J Respir Crit Care Med 2000;161:1825–1829. Lowther SA, Shay DK, Holman RC, et al: Bronchiolitis-associated hospitalizations among American Indian and Alaska Native children, Pediatr Infect Dis J 2000;19:11–17. Lozano JM, Wang E: Bronchiolitis, Clin Evid 2002;8:291–303. Martinez FD: Respiratory syncytial virus bronchiolitis and the pathogenesis of childhood asthma, Pediatr Infect Dis J 2003;22(2 Suppl):S76–S82. Martinez FD, Wright AL, Tuassig LM, et al: Asthma and wheezing in the first six years of life. The Group Health Medical Associates, N Engl J Med 1995;332:133–138. Reynolds EOR: The effect of breathing 40 percent oxygen on the arterial blood gas tensions of babies with bronchiolitis, J Pediatr 1963;63:1135–1139. Shay DK, Holman RC, Newman RD, et al: Bronchiolitis-associated hospitalizations among US children, 1980–1996, JAMA 1999;282:1440–1446. Singleton RJ, Petersen KM, Berner JE, et al: Hospitalizations for respiratory syncytial virus infection in Alaska Native children, Pediatr Infect Dis J 1995;14:26–30. Tintinalli J, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 795–797.
Pediatric Pneumonia MELISSA KAGARISE
ICD Code: Pneumonia 486
Key Points Infants 1^24 months of age with pneumonia will most commonly present with a viral etiology, including RSV, parainfluenza virus, influenza virus, or adenovirus. ! Emergency Actions ! Any child with evidence of hypoxia, as directed by a pulse oximetry of less than 93%, should be admitted to the hospital for treatment.
DEFINITION Pneumonia is the inflammation of the lung parenchyma, most commonly a result of bacteria or viruses. Community-acquired pneumonia
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in the pediatric population has an annual incidence of 34–40 cases per 1000 children in North America and Europe. Determination of the etiological pathogen can be linked to the age of the patient as well as vaccination status and the presence of underlying conditions. Bacterial agents, group B Streptococcus, Escherichia coli, and Klebsiella are the predominant pathogens in the newborn age group. Infants aged 1–24 months will most commonly present with a viral etiology, including RSV, parainfluenza virus, influenza virus, or adenovirus. Although a viral etiology remains more common in the preschool-aged child, the incidence of an S. pneumoniae infection increases. Children of school age through adolescence most commonly will present with M. pneumoniae bacterial infections.
EPIDEMIOLOGY Children with asthma, cystic fibrosis, gastroesophageal reflux with aspiration, or neurological disorders, or those who are immunocompromised are at greater risk for the development of pneumonia. Viral infections are more common in the fall and winter and are commonly seen in children up to 2 years of age. An incomplete immunization status may predispose a patient to infection with H. influenzae and S. pneumoniae.
CLINICAL PRESENTATION Children will present with a variety of symptoms dependent on the etiological agent, patient age, and whether there is an underlying disease state. Pneumonia may follow a history of upper respiratory tract infection with cough and rhinitis, although tachypnea can be the only clinical sign of infection. Fever will be present in the patient and is most commonly more severe with bacterial infection. As infection progresses, patients will exhibit signs of respiratory distress. Nonbacterial pneumonia will present with a gradual progression of symptoms with headache, malaise, and a nonproductive cough. Bacterial pneumonias will present with a sudden change in symptoms, usually with a surge in temperature associated with chills as well as pleuritic chest pain and productive cough.
EXAMINATION A general inspection of the child will reveal intercostal, subcostal, and suprasternal retractions as well as accessory muscle use. Cyanosis may be present with severe infection. Respiratory rate must be counted through
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the full minute to obtain an accurate rate revealing any tachypnea. Auscultation of the lungs may reveal decreased breath sounds, rales, and wheezing, which will worsen as infection continues. Keep in mind that auscultatory findings in children may not be reliable.
LABORATORY FINDINGS Any child suspected of having pneumonia must have a two-view chest radiograph to confirm the diagnosis and evaluate for complications. Lobar consolidation is typically associated with pneumococcal infection, whereas interstitial infiltrates is associated with viral infection. Radiographs must be evaluated for signs of pleural effusion and empyema. A WBC count can be used to help differentiate between bacterial and viral infections. A left shift will be noted with bacterial pneumonias. Obtaining sputum samples for Gram stain and culture are difficult in the pediatric population and generally do not yield good results. Cultures should be done in severely ill patients in whom empirical treatment has failed.
DIAGNOSIS The diagnosis of pneumonia is made on the basis of the patient’s clinical history, physical examination, and chest radiographs. Invasive sampling for cultures through ET, percutaneous lung aspiration, and bronchoalveolar lavage should be reserved for critically ill persons.
TREATMENT Treatment is based on the child’s age, clinical findings, and the suspected offending agent. Any child with evidence of hypoxia, as directed by a pulse oximetry of less than 93%, should be admitted for treatment. Outpatient treatment can be initiated if the patient is not critically ill and not in respiratory distress. Empirical treatment should be based on the patient’s age, presentation, and suspected etiological agent. Outpatient treatment for suspected bacterial pneumonia should be amoxicillin 40 mg/kg/day given in three divided doses. Alternatives include cefuroxime axetil or amoxicillin/clavulanate. Worsening of symptoms with these treatments can indicate resistance, which may respond to clindamycin or vancomycin. A 10-day course of treatment is recommended for treatment in the outpatient setting. If a viral cause is suspected, treatment should address symptoms and should include fever control and adequate hydration.
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Documentation of resolution made by chest radiography after 6–8 weeks is indicated for any child treated as an inpatient or for outpatients who have a persistent cough.
Bibliography Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Dershewitz RA: Ambulatory Pediatric Care, ed 3. Lippincott-Raven: Baltimore, 1999. Hay WW, Levin MJ, Sondheimer JM, Dterding RR: Current Pediatric Diagnosis and Treatment, ed 17. McGraw Hill: New York, 2005. Ostapchuk M, Roberts DM, Haddy R: Community acquired pneumonia in infants and children, Am Fam Phys 2004;70(5). Available at: http://www.mdconsult.com. Rudolph AM, Kamei RK, Overby KJ: Rudolph’s Fundamentals of Pediatrics, ed 3. McGraw Hill: New York, 2002. Schwartz WM: The 5-Minute Pediatric Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2000. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
B. Abdominal Problems Abdominal Pain CHRISTOPHER B.CROWELL
ICD Code: Abdominal pain 789.0
Key Points Abdominal pain with vomiting or diarrhea accounts for 20% of pediatric ED visits. Five percent of visits are for abdominal pain alone. Misdiagnoses are more common in the pediatric population, with the highest rates among infants. ! Emergency Actions ! Assessment of vital signs is the first step in the evaluation of pediatric abdominal pain, and any abnormalities must be promptly addressed. It is therefore necessary to know the age-appropriate vital signs for different age groups in pediatrics.
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DEFINITION Abdominal pain is the subjective feeling of discomfort in the area between the thoracic cavity and the pelvic cavity. The intrapelvic region is often included because of the open communication of these two cavities. In a nonverbal patient, the presence of abdominal pain is much more difficult to assess. This subjective symptom must be inferred from inconsolable crying, colic, flexion of legs up against the abdomen, or findings on physical examination. Abdominal pain often occurs as a result of a benign process but can also be the leading presentation of severe infectious, inflammatory, metabolic, endocrine, congenital, or vascular disease. Disease of nearly every organ system can produce abdominal pain.
EPIDEMIOLOGY Abdominal pain with vomiting or diarrhea accounts for 20% of pediatric ED visits. Five percent of visits are for abdominal pain alone. Misdiagnoses are more common in the pediatric population, with the highest rates among infants. These statistics can be attributed to patients’ inability to provide accurate histories, lack of physical findings on examination, and the relative benign presentations of serious diseases. During the first year of life, abdominal pain is difficult to identify because of the nonverbal state of the child. This symptom must be recognized from a history of an inconsolable infant, the raising of the child’s leg against the chest, progressive vomiting, or findings on physical examination. Intussusception is the most common cause of intestinal obstruction in this age group and is caused by the telescoping of a proximal portion of bowel into the distal segment. Malrotation of the intestines with volvulus is a rare but life-threatening cause of intestinal obstruction in the first month of life. Incarcerated hernias will cause severe abdominal pain and vomiting in this age group. Pyloric stenosis must be differentiated from gastroesophageal reflux disease as a cause of colic and postprandial vomiting. Premature infants are at increased risk of developing necrotizing enterocolitis. Hirschsprung’s disease is a rare but pathologic cause of constipation that can have associated abdominal pain. Toddlers frequently present with nonspecific abdominal pain and no clear etiology. Stressors in these children are often manifested as “tummy aches.” Pain can also be referred pain from acute otitis media or lower lobe pneumonia. Gastrointestinal foreign bodies can cause significant pain if they cause intestinal obstruction. Meckel’s diverticulum usually presents with painless rectal bleeding in this age group, but pain can occur with significant inflammation. Finally, constipation with associated abdominal discomfort may be associated with toilet training.
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In the school-aged population, appendicitis is the most common emergent diagnosis of abdominal pain. The highest incidence occurs between the ages of 9 and 12 years but can occur at any age. The risk of perforation is inversely proportional to age, with rates as high as 90% in children younger than 2 years. Diabetic ketoacidosis (DKA) is another emergent diagnosis that frequently presents in patients of this age with abdominal pain and is a common initial presentation of insulindependent diabetes. The incidence of UTI increases with age in females but is usually confined to infancy in males. Peptic ulcer disease is another cause of postprandial abdominal pain. Henoch-Schönlein purpura can cause a recurrent abdominal pain and is associated with a classic purpuric rash over the legs and buttocks. The differential diagnosis for abdominal pain broadens with the onset of sexual maturity. The diagnosis of ectopic pregnancy must be considered with all menstruating females. Intrauterine pregnancies can also present with abdominal pain with vomiting. Sexually transmitted diseases can cause abdominal pain, particularly when they result in pelvic inflammatory disease in females. Gonadal torsion is an emergent cause of abdominal pain in both sexes. Of note, testicular torsion also has another peak incidence in the first days of life. Inflammatory bowel disease (e.g., Crohn’s) often presents in persons of this age group. Other causes of pediatric abdominal pain are not specific for any particular age group. Acute gastroenteritis is the most common diagnosis in children and requires both vomiting and diarrhea as diagnostic criteria. Blunt abdominal trauma can result in lacerations to the liver or spleen, pancreatic injury, or small bowel injury. Penetrating trauma causes a similar injury pattern to those seen in adults. Sickle cell disease, malignancies, porphyria, hyperparathyroidism, pancreatitis, hepatitis, gallstones, and kidney stones can all present with abdominal pain.
CLINICAL PRESENTATION The quality, location, and duration of the abdominal pain are the most important features of the history. Pain that comes and goes or that has drastic variations in intensity is described as colicky. Colicky pain is often benign but is also present with intestinal obstruction (e.g., intussusception, incarcerated hernia, volvulus), gonadal torsion, nephrolithiasis, and cholelithiasis. Constant, gradual worsening pain occurs with appendicitis, peptic ulcer disease, and UTI. Epigastric pain occurs with disease of the stomach, hepatobiliary system, duodenum, and the lower lobes of the lung (in pneumonia). Umbilical pain is present with disease of the small bowel, proximal large bowel (early appendicitis), and the pancreas. Suprapubic pain occurs with disease of the distal large bowel and the genitourinary system.
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Associated symptoms can also aid with the diagnosis of certain conditions. Fever is suggestive of infection or inflammation and can be seen with appendicitis, UTI, gastroenteritis, Crohn’s disease, sexually transmitted disease, and neoplasm. Vomiting is a very nonspecific symptom and is commonly seen with acute gastroenteritis. However, protracted vomiting can be seen with DKA, intestinal obstruction, appendicitis, or nephrolithiasis. Back pain is seen with pancreatitis, as well as kidney and uterine disease. Peritonitis is defined as inflammation of the peritoneum and is highly suggestive of surgical or emergent disease. It is caused by irritation of the peritoneum by blood, air, or serous fluid. Patients will report significantly worsening pain with any movement, such as walking, deep inspiration, or driving over speed bumps. Some diseases that can result in peritonitis include appendicitis, intestinal perforation, and intraabdominal/intrapelvic hemorrhage.
PHYSICAL EXAMINATION The assessment of vital signs is the first step in the evaluation of pediatric abdominal pain, and any abnormalities must be promptly addressed. It is therefore necessary to know the age-appropriate vital signs for different age groups in pediatrics. Fever is suggestive of infection or inflammation. The gold standard method of measurement is to take a rectal temperature, which is more important in infants and young children. Tachycardia can result from pain, fever, or intravascular volume loss, which is why treatment of fever and pain in the ED is both therapeutic and diagnostic. Hypotension is a very late sign of volume loss in pediatrics. Infants and young children can be particularly difficult to examine on presentation to the ED. It is important to distract irritable children with toys, popsicles, or family members while the presence and location of the tenderness is determined. Abdominal distention is suggestive of intestinal obstruction. A rectal examination with hemoccult should be performed if there is concern for Meckel’s diverticulum, gastrointestinal tract bleeding, or invasive gastroenteritis. Signs of peritonitis include pain with movement, involuntary guarding, loss of bowel sounds, and focal/diffuse rebound tenderness. These patients often hold completely still and cannot tolerate slight jarring of the examining table. Any findings of peritonitis on examination should prompt surgical consultation in the ED.
LABORATORY TESTS AND RADIOLOGY In a selected population, laboratory studies are indicated in the evaluation of pediatric abdominal pain. However, these studies rarely make the diagnosis that is not suggested by the history and physical examination.
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CBC can show signs of infection or acute hemorrhage. Liver function tests and lipase abnormalities can suggest hepatobiliary disease or pancreatitis, respectively. Urinalysis can show signs of infection, trauma, or the presence of a kidney stone. Serum glucose levels should be measured when there is any concern for DKA. A qualitative serum beta-human chorionic gonadotropin test should be performed for all menstruating females to rule out ectopic and normal pregnancy. Chest radiography should be performed if there is concern of pneumonia. An acute abdominal series is a sensitive screening method for intestinal obstruction and, perforation. Ultrasound is a useful modality in the assessment of gonadal torsion (in both sexes), pelvic disease, hepatobiliary disease, and, in some centers, appendicitis. Air enemas are both diagnostic and therapeutic in intussusception. CT has become the test of choice for appendicitis, genitourinary tract disease, and intestinal obstruction/perforation. A Meckel’s scan can be performed if there is concern for Meckel’s diverticulum.
TREATMENT The mainstay of treatment of pediatric abdominal pain includes oral/parenteral analgesia, antiemetic medications, fluid and electrolyte replacement, and antipyretic drugs. The diagnosis is often unclear after the first full evaluation. Disposition is dependent on the diagnosis or exclusion of emergent or surgically correctable disease. Any signs or symptoms of peritonitis warrant surgical consultation in the ED. When emergent causes of abdominal pain cannot be ruled out after ED evaluation, admission to an observation unit is appropriate. All patients who are discharged should be given close follow-up, as well as strict return precautions in case of worsening symptoms.
Bibliography Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Wolfson AB, Hendey GW, Hendry PL, Linden CH: Harwood-Nuss’ The Clinical Practice of Emergency Medicine, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001.
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Constipation JULIE HUSLEY
ICD Code: Constipation 564.00–564.9
Key Points Encopresis is the repeated passage of feces in inappropriate places, such as in clothing or in bed. It is a consequence of constipation wherein fecal fluid manages to leak past a fecal bolus and out of the anus. Functional constipation is constipation without evidence of pathology. Childhood constipation can be successfully treated, but this usually takes several months. Successfully treated childhood constipation is subject to a high rate of relapse. ! Emergency Actions ! Constipation is a diagnosis of exclusion, so it is important when evaluating a patient for constipation to consider other more life-threatening causes of similar symptoms, such as appendicitis or bowel obstruction. A definitive diagnosis of constipation is not usually associated with any medical emergencies, but clinicians should keep in mind one very rare but life-threatening consequence of chronic constipation, a condition known as toxic megacolon. When a fecal bolus is retained long enough over a period of time, the distal colon and rectum can become grossly distended. When it ruptures, toxic contents are spilled into the peritoneal cavity, leading to sepsis and shock. A patient with toxic megacolon may present with fever, abdominal pain, distention, decreased bowels sounds, and leukocytosis. The goal of initial treatment is to decompress the colon and prevent any further increases in pressure. Initial treatment of this emergent condition also includes addressing dehydration, sepsis, and shock.
DEFINITION The first issue in approaching treatment of constipation is discerning how constipation is defined to the patient. Because the range of normal bowel movement frequency is rather wide, patients may be unclear as to what constitutes real constipation. In general, infants have roughly four stools per day during the first 7 days, decreasing to one to two stools per day by 2 years of age and then to one stool per day on average by the age of 4 years. It is generally accepted that the term constipation refers
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to fewer than three stools per week, to the painful passage of stool, or to a palpable colonic mass upon examination. Childhood constipation falls into two categories: functional and organic. Up to 95% of cases are functional, also referred to as idiopathic, fecal withholding, and functional fecal retention. A small percentage of cases do have important organic causes that must be ruled out before treatment ensues.
EPIDEMIOLOGY The worldwide prevalence of childhood constipation broadly ranges from 0.3% to 28%, with younger children being affected most often. Boys with constipation outnumber girls with the condition by a ratio of 3:1 by the time they enter school. Higher numbers are seen in patients with low levels of dietary fiber and exercise. Recognition and treatment is important because up to 5% of children aged 4–11 years with acute constipation will go on to develop chronic constipation (lasting more than 6 months). A significant proportion (30%–50%) of children will relapse after being successfully treated for constipation.
PATHOLOGY Functional constipation refers to the voluntary withholding of stool. A painful bowel movement is the most common precipitant to stool withholding. Subsequently, the child attempts to avoid further pain by contracting his sphincter when he feels the sensation to defecate. With repeated episodes of fecal retention, the rectum slowly dilates to accommodate the collecting stool, it loses the ability to contract in response to distention, and it habituates to distention and stretching over time. Eventually, softer stools can “leak out” around this hard stool mass without the child being aware of the process, angering the parents and scaring the child. This is referred to as encopresis and is frequently mistaken by the parents as diarrhea. Organic causes make up about 5% of cases. These include congenital conditions such as Hirschsprung’s disease (aganglionic megacolon), anal atresia, anal stenosis, lichen sclerosis, hypothyroidism, anorectal malformations, and spinal cord disorders. Medications are another organic cause of constipation. The list includes anticholinergics (e.g., antihistamines), opiates, diuretics, nonsteroidal anti-inflammatory drugs, sympathomimetics, and some antihypertensives. Finally, some children benefit from a dietary restriction of cow’s milk protein, reflecting a common childhood food allergy that is often responsible for constipation.
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CLINICAL PRESENTATION Newborns who do not pass meconium within the first 48 hours of life typically have an anatomical anomaly. After this time frame, constipation may arise when infants are first introduced to solid foods or when they are being weaned, either from the bottle or breast. Infants up to 12 months of age may have episodes of irritability, becoming red-faced, grunting, and pulling the knees up to the abdomen in what appears to be an effort to pass stool. The stool itself may be soft. Children older than 12 months may present with a history of decreased frequency in bowel movements, crankiness, decreased appetite, nausea, abdominal pain and bloating, bright red bleeding with stool passage, and a change in character of stool such as dry, hard, or large, painful passage of stool. Fecal retention often occurs during toilet training. Children may hold their breath, clench their fists, become flushed, rock up on their toes, pace, or hide while they try to contract their rectal sphincter. Fever, weight loss, syncope, bloody diarrhea, or poor weight gain could be signs of an organic condition.
EXAMINATION A complete physical examination should be performed. The abdomen may be mildly distended with nonfocal, nonsurgical tenderness. If physical findings are more significant, such as rebound tenderness or rigidity, the clinician needs to assume the child has a surgical pathology until further tests are done. A colonic mass may be palpable in the abdomen. A rectal examination should be performed if the child can tolerate it, and a hard fecal mass may be palpable in the rectal vault. The stool should be evaluated for blood. The anus should also be examined for tone, fissures, hemorrhoids, and scars.
LABORATORY FINDINGS Laboratory tests have limited value in the diagnosis of constipation, except for assessing thyroid function and serum calcium. However, blood work can be helpful in ruling out more emergent causes of abdominal pain. For example, constipation should not cause a leukocytosis, and in the presence of such, the clinician needs to investigate other causes of abdominal pain.
DIAGNOSIS In the emergency care setting, constipation is a diagnosis of exclusion. It should be made after more life-threatening conditions have been ruled out, such as acute appendicitis. If, in the course of treatment, the
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patient’s symptoms are relieved after a bowel movement, the clinician can carefully consider that the symptoms are indeed caused by constipation.
RADIOGRAPHS Radiographs are not necessary in the diagnosis of constipation but are sometimes helpful in the course of evaluation to rule out other conditions. Large amounts of stool are often seen throughout the large bowel in cases of constipation.
TREATMENT Treatment goals in the emergency care setting include evacuating a fecal impaction, if present, by either oral or rectal administration of medication. Osmotic agents in large doses can be given orally, and phosphate soda or mineral oil enemas can be administered rectally. Glycerin suppositories may be used in infants and bisacodyl suppositories in older children. Once the initial evacuation has been successful, or when a child without impaction has been fully evaluated, maintenance treatment can begin. Maintenance therapy involves medication, patient education, diet modification, bowel retraining, and long-term monitoring by parents. Medications include osmotic agents (e.g., MiraLax, lactulose), which cause water to be retained within the stool, stool softeners such as Colace (docusate sodium), and bulking agents such as psyllium. Generally, children should not be given stimulant laxatives and oral mineral oil products because the former may dehydrate the patient and the latter can cause aspiration pneumonia and rectal leakage, as well as deficiencies of vitamins A and D. Educating and counseling parents helps remove their anxiety regarding their child’s health; they need to understand that encopresis is not a purposeful, defiant behavior; that all family interactions regarding the issue be positive; that adequate levels of exercise increase bowel motility; that this condition is subject to relapse and requires patience: and that constipation requires long-term treatment but treatment can be successful. Diet modification is also part of long-term maintenance of healthy bowel habit, but this should not be forced upon the child. Diets that include absorbable carbohydrates like sorbitol, found in prunes, pears, and apples, can soften stools. A diet including grains, fruits, and fiber is recommended, as well as sufficient fluid intake. Bowel retraining is just as important for success. Parents need to ensure a scheduled 5–10 minutes of “toilet time” after every meal for the child, adjusting this frequency to the child’s age and gradual improvement.
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Maintenance interventions should be continued for a period of 6–12 months until the rectal vault has resumed normal size and tone. Subsequently, parents should monitor the frequency of stooling; if 2 or more days pass without a bowel movement, interventions should resume promptly.
Bibliography Baker SS, Liptak GS, Colletti RB, et al: Constipation in infants and children: Evaluation and treatment. Medical position statement of the North American Society for Pediatric Gastroenterology and Nutrition, 1999. Available at: http://www.naspgn.org/. Accessed on September 19, 2005. Borowitz SM, Cox DJ, Tam A, et al: Precipitants of constipation during early childhood, J Am Board Family Pract 2003;16(3):213–218. Brooks RC, Copen RM, Cox DJ, et al: Review of the treatment literature for encopresis, functional constipation, and stool-toileting refusal, Ann Behavioral Med 2000;22:260–267. Castiglia P: Constipation in children, J Pedi Health Care 2001;15(4):200–202. Coughlin EC: Assessment and management of pediatric constipation in primary care, Pediatr Nurs 2003;29(4):296–301. Data requested on safety of laxative ingredients, FDA Consumer 1996;30(8):6. Loening-Baucke V: Fecal incontinence in children, Am Fam Phys 1997;55(6):2229–2235. Price KY, Elliott TM: Stimulant laxatives for constipation and soiling in children, Cochrane Rev Abstracts Updated April 1, 2002. van Ginkel R, Reitsma JB, Buller HA, et al: Childhood constipation: Longitudinal followup beyond puberty, Gastroenterology 2003;125:357–363.
Pediatric Diarrhea SAMUEL TIMOTHY MCILRATH
ICD Code: Diarrhea 787.91
Key Points Pediatric diarrhea is a common presenting symptom. For the most part, it is self-limited and can be managed with appropriate rehydration therapy. It is important to assess and monitor for dehydration and to know what signs and symptoms to look for that may indicate the rare patient who may require additional antibiotic therapy or further evaluation.
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! Emergency Actions ! It is important to quickly assess the degree of dehydration and begin appropriate rehydration therapy. In severe cases, airway and ventilatory management may be necessary. Acute diarrheal illness may be accompanied by other systemic manifestations requiring additional treatment, that is, neurological manifestations such as seizures.
DEFINITION Diarrhea is defined as an acute increase in the frequency and/or water content of the stools. Chronic diarrhea is defined as diarrhea that persists for more than 14 days.
EPIDEMIOLOGY Gastrointestinal infections are caused by a variety of enteropathogens, including viruses, bacteria, and parasites. The major route of transmission is person to person via fecal-oral route or by ingestion of contaminated food or water. Acute infectious diarrhea is divided into two categories: noninflammatory and inflammatory. Noninflammatory diarrhea is caused by enterotoxin-producing bacteria, viral destruction of intestinal villi, adherence by parasites, and adherence and/or translocation of bacteria (e.g., enterotoxigenic E. coli, rotavirus, Giardia lamblia). Inflammatory diarrhea results from bacteria directly invading the intestine or by producing cytotoxins. Bacterial enteropathogens associated with inflammatory diarrhea include Campylobacter jejuni, Clostridium difficile, enteroinvasive E. coli, Shiga toxin–producing E. coli (E. coli O157: H7), Salmonella species, Shigella species, Vibrio parahaemolyticus, and Yersinia enterocolitica. The typical causative organisms in viral gastroenteritis include rotavirus, enteric adenovirus, astrovirus, Norwalk agent–like virus, and calicivirus. Among parasitic causes of diarrhea, G. lamblia is the most common cause in the United States. Chronic diarrhea is characteristic of certain enteropathogens (e.g., G. lamblia, Cryptosporidium parvum, enteroaggregative or enteropathogenic E. coli), but it may also occur with any enteropathogen in an immunocompromised patient. Often it is a residual symptom resulting from intestinal damage. Although most pediatric diarrhea is infectious in nature, there are various other causes as well. Other, noninfectious, causes of diarrhea include anatomical defects (e.g., malrotation, Hirschsprung’s disease), malabsorption (e.g., disaccharidase deficiencies, pancreatic insufficiency in cystic fibrosis), endocrinopathies (e.g., thyrotoxicosis, Addison’s disease), food poisoning (e.g., heavy metals, mushrooms), neoplasms (e.g., neuroblastomas, pheochromocytomas), and others (e.g., Crohn’s disease,
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laxative abuse). In neonates, diarrhea can result from overfeeding or feeding formulas with a high osmotic content. Diarrhea can also be a nonspecific manifestation of a systemic illness, such as UTI.
CLINICAL PRESENTATION Enteric infections usually cause gastrointestinal tract signs and symptoms, but they may cause extraintestinal symptoms as well. Gastrointestinal tract symptoms include diarrhea, abdominal pain and cramping, and sometimes vomiting. Various extraintestinal manifestations include vulvovaginitis, UTI, endocarditis, osteomyelitis, pneumonia, meningitis, peritonitis, hepatitis, chorioamnionitis, soft tissue infection, and septic thrombophlebitis. Neurological manifestations may include paresthesias and muscle weakness. After diarrhea has resolved, immune-mediated extraintestinal manifestations may present as reactive arthritis, GuillainBarré syndrome, glomerulonephritis, IgA nephropathy, erythema nodosum, hemolytic anemia, and hemolytic uremic syndrome. In obtaining a patient history, it is imperative to gather information about frequency and volume of stool output as well as the character of the stool, such as the presence or absence of blood or mucus. Remember that frequent stooling is common in neonates, especially those who are breast-fed. In this population, it may be best to ask about any significant change in the stooling pattern. Oral intake and urinary frequency may help to approximate the degree of dehydration. The presence of concomitant symptoms such as fever or nausea/vomiting should be determined. Other pertinent data to obtain include day care or school attendance, travel to an endemic area, recent antibiotic use, exposure to contacts with similar symptoms, and intake of suspect foods (e.g., contaminated water, uncooked meats, seafood, unwashed vegetables, and unpasteurized milk).
EXAMINATION The physical examination must focus on the general appearance of the child and an assessment of the degree of dehydration. It is important to note blood pressure, pulses, heart rate, temperature, capillary refill, skin turgor, fontanel, mucous membranes, tearing or sunken orbits of the eyes, mental status, and urine output. Often, an elevated heart rate is one of the first signs of dehydration. Decreased blood pressure is most often a late finding that indicates a more severe process and a greater degree of dehydration. Focused abdominal and stool examinations are important as well.
LABORATORY FINDINGS AND DIAGNOSIS Laboratory studies to identify specific diarrheal pathogens are generally not required because most illnesses are self-limited. When ordered,
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stool specimens should be evaluated for blood, mucus, and leukocytes. The presence of fecal leukocytes indicates the presence of an invasive or cytotoxin-producing organism such as those that cause inflammatory diarrhea. If a bacterial cause of diarrhea is suspected, then stool cultures are indicated. Stool cultures should also be performed for patients who are immunocompromised or in whom hemolytic uremic syndrome is suspected. Additionally, stool samples should be cultured during diarrhea outbreaks or if they are bloody or contain fecal leukocytes. During periods of rotavirus epidemics, an enzyme-linked immunosorbent assay may be helpful to confirm the diagnosis. Examination for ova and parasites should be reserved for specific clinical situations, including patients with the following conditions: (1) the patient has a history of recent travel to an endemic area and diarrhea that persists for greater than a week that is otherwise culture-negative for other enteropathogens; (2) the patient is part of a diarrheal outbreak; and (3) the patient is immunocompromised. In children who are severely dehydrated, electrolyte levels should be measured.
TREATMENT Severe (>10%) dehydration is a medical emergency and should be treated with IV fluids in 20-m/kg doses of normal saline or lactated Ringer’s solution. ORT can then be initiated after the patient’s condition is stabilized. Most children with gastroenteritis are not severely dehydrated, and so most do not require IV fluids as part of their management. In children with mild (3%–5%) to moderate (6%–9%) dehydration, ORT is the preferred treatment of hydration. There are a variety of commercially available ORT solutions available (e.g., Pedialyte, Infalyte). Such solutions contain an appropriate ratio of carbohydrates to electrolytes. Other remedies, including decarbonated soda beverages, fruit juices, and sports beverages, are not as suitable because they are hypertonic due to excessive carbohydrate concentrations, which may subsequently worsen diarrhea; low electrolyte concentrations; and inappropriate carbohydrate-to-sodium ratios. The key is to administer small volumes of a glucose-electrolyte solution frequently. In young children, this can be initiated with 5-ml aliquots given every few minutes. The goal is to correct dehydration over a 4-hour period, in addition to replacing any continuing losses from diarrhea or emesis. In mild dehydration, this should be 50-ml/kg ORT over a 4-hour period; in moderate dehydration it is increased to 100-ml/kg ORT. Losses from stool are replaced by giving 10 ml/kg for each stool, and emesis volume is estimated and replaced. The replacement for these continuing losses should be added to the amount of fluid remaining to be given. Reevaluation of hydration status and
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ongoing losses should take place every 1–2 hours, depending on the severity of dehydration. Once rehydration is complete, early refeeding should be initiated while ORT is continued. Early refeeding may reduce the duration of diarrhea by approximately half a day. Certain foods, including complex carbohydrates (e.g., rice, wheat, potatoes, bread, and cereals), lean meats, yogurt, fruits, and vegetables are generally better tolerated than fatty foods or foods high in simple sugars. Antidiarrheal agents are not recommended for use in the pediatric population because of their minimal benefit and potential for adverse effects. Although most infectious diarrhea is self-limited, there are cases in which antimicrobial therapy is warranted. Refer to Table 13-7 for a list of common enteropathogens and their respective therapies.
Table 13-7 Pediatric Diarrhea: Common Enteropathogens, Clinical Features, and Therapies* ORGANISM Bacterial Campylobacter jejuni Clostridium difficile Escherichia coli (enterotoxigenic) E. coli (enteropathogenic) E. coli (enteroinvasive) Salmonella Shigella Vibrio cholerae Parasitic Giardia lamblia
Entamoeba histolytica
CLINICAL FEATURES Watery or bloody diarrhea, fever, abdominal pain; may mimic appendicitis Recent antibiotic use
ANTIMICROBIAL AGENT Erythromycin
Watery diarrhea
Metronidazole or vancomycin TMP/SMX
Watery diarrhea
TMP/SMX
Watery diarrhea
TMP/SMX
Bloody diarrhea, fever
Ceftriaxone or cefotaxime, ampicillin, TMP/SMX Ampicillin or ceftriaxone
Mucoid diarrhea, fever, abdominal pain, headache Rice-water diarrhea Diarrhea, flatulence: exposure to day care centers or unfiltered water Bloody, mucoid stools; hepatic abscess
Doxycycline or tetracycline Metronidazole
Metronidazole followed by iodoquinol
Doses: Ampicillin 50 mg/kg/day divided into four doses; erythromycin 40 mg/kg/day divided into four doses; metronidazole 30 mg/kg/day divided into two doses; trimethoprim and sulfamethoxazole (TMP/ SMX) 8–12 mg/kg/day, based on the TMP component, divided into two doses. *All organisms should be tested for sensitivities.
Hirschsprung’s Disease or Congenital Aganglionic Megacolon
745
It is important to reduce transmission. Healthcare providers should wash their hands before and after every contact with a patient with a diarrheal illness. Patients who attend day care should be excluded from the center or cared for separately until the diarrhea has subsided. Certain diseases (e.g., Clostridium botulinum, E. coli O157:H7, Salmonella species, Shigella species, V. cholerae, Cryptosporidium species, and Cyclospora species should be reported to the local health department.
Bibliography American Academy of Pediatrics, Subcommittee on Acute Gastroenteritis: Practice parameter: The management of acute gastroenteritis in young children, Pediatrics 1996;97 (3):424–435. Pickering LK, Snyder JD: Gastroenteritis. In Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, pp 1272–1276.
Hirschsprung’s Disease or Congenital Aganglionic Megacolon RYAN GARNER, KAZUO MIHATA AND LINDA L. LAWRENCE
ICD Code: Hirschsprung’s disease 751.3
Key Points Hirschsprung’s disease, also known as congenital aganglionic megacolon, is a congenital absence of parasympathetic nerve ganglia in the distal colon. In early infancy, Hirschsprung’s disease accounts for approximately 20% of partial intestinal obstruction cases. It is the most common cause of lower intestinal obstruction in neonates. It most often presents in the nursery with failure to pass meconium, but less severe disease may not be diagnosed until adolescence or early adulthood. It should be considered in the differential in cases of constipation; however, other etiologies of constipation are much more common. ! Emergency Actions ! Adequate fluid and electrolyte status should be ensured. Ill-appearing children with a fever should be evaluated for possible enterocolitis and toxic megacolon. Enterocolitis (often caused by C. difficile) will present with abdominal distention, bloody stools,
746 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER fever, and an elevated WBC count. Enterocolitis is associated with up to 30% mortality. These patients require aggressive resuscitation and broadspectrum IV triple-antibiotic coverage. Five percent of patients with Hirschsprung’s disease will eventually develop enterocolitis, which should be considered life threatening.
DEFINITION Hirschsprung’s disease is a congenital aganglionosis of the colon. It is caused by a genetic defect that leads to the incomplete migration of neural crest cells during development. This creates an absence of ganglion cells of the myenteric plexus in the distal colon. The absence of the ganglion cells prevents the colon’s ability to relax, which creates a functional obstruction. Typically it involves the anus and extends 4–25 cm proximally. The obstruction causes stool to accumulate and produces a dilation of the colon (i.e., megacolon).
EPIDEMIOLOGY Hirschsprung’s disease occurs in 1 in 5000 life births. It is four to five more times common in males. It may be associated with Down syndrome or other congenital abnormalities. Most patients are diagnosed before 1 year of age, but the age of diagnosis correlates with the extent of the disease.
CLINICAL PRESENTATION Infants with Hirschsprung’s disease often present with the failure to pass stool and with a history of constipation and obstipation. Vomiting (which may be bilious) and abdominal distention may also occur. A history of chronic constipation and poor weight gain or failure to thrive should make the provider concerned. The history may include stools consisting of small pellets, or stools may be ribbon-like. Patients may also present with diarrhea. Diarrhea can occur after a period of constipation and is the result of fluid being expelled around the obstruction.
EXAMINATION The abdomen will be distended. The dilated colon, filled with impacted feces, is often palpable. A rectal examination should be performed and will reveal normal rectal tone, no ampullary dilation, and no feces in the rectal vault. This is in contrast to a dilated rectum full of impacted feces, which is seen in acquired megacolon. After the rectal examination, the
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patient may have an explosive bowel movement with foul-smelling feces and gas. This may provide some temporary relief of the patient’s symptoms.
LABORATORY FINDINGS Laboratory studies should consist of a CBC, electrolyte analysis, and blood cultures. CBC results may demonstrate a hypochromic anemia.
DIAGNOSIS Anorectal manometry is used to measure pressure of the internal anal sphincter when the rectum is distended. Normally, rectal distention causes a decrease in internal sphincter pressure. In patients with Hirschsprung’s disease, there will be no drop or even a rise in internal sphincter pressure with rectal distention. This test is 90% accurate; however, the test is difficult to perform in infants. A definitive diagnosis is made with rectal biopsy, which will demonstrate the absence of myenteric ganglia.
RADIOGRAPHS Abdominal plain radiographs may demonstrate impacted fecal material. Proximal to the obstruction there will be a dilated colon with air-fluid levels consistent with obstruction. A funnel-shaped transition zone between the dilated proximal colon and the smaller-caliber obstruction area may be seen. Barium enema will reveal a narrowed segment with proximal dilation, which is suggestive of this disease (Fig. 13-2). Postevacuation radiographs should also be taken at 24 hours; the presence of a significant amount of barium retained in the colon increases suspicion of Hirschsprung’s disease.
TREATMENT Initial resuscitation and stabilization of the patient’s condition should be accomplished first. IV access should be obtained, and fluid and electrolyte abnormalities should be treated. If enterocolitis is suspected, then broad-spectrum, triple-therapy, IV antibiotics should be given. Decompression of the dilated segment may be necessary. This can be accomplished using a rectal tube. A nasogastric tube should also be placed. Consultation with a surgeon should be obtained because the definitive treatment is surgical resection of the aganglionic colon segment. Surgery is curative; however, postoperative patients remain at risk for enterocolitis.
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Figure 13-2. Lateral view of a barium enema in a 3-year-old girl with Hirschsprung’s disease. The aganglionic distal segment is narrow, with distended normal ganglionic bowel above it. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 313.3-2 Copyright # 2004 Elsevier.)
Bibliography Bitterman RA, Peterson MA: Large intestine: Disorders of colonic motility. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Hostetler MA, Bracikowski A: Gastrointestinal disorders. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Wyllie R: Motility disorders and Hirschsprung disease. In Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004.
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Pyloric Stenosis RYAN GARNER, KAZUO MIHATA, AND LINDA L. LAWRENCE
ICD Codes: Acquired hypertrophic pyloric, stenosis 537.00, Congenital hypertrophic pyloric, stenosis 750.5
Key Points Pyloric stenosis is the progressive hypertrophy of the pylorus during infancy, which eventually leads to gastric outlet obstruction. It presents with progressive, nonbilious emesis, which can become projectile and result in significant dehydration. Management involves correction of fluid and electrolyte imbalance and prompt surgical consultation. ! Emergency Actions ! Care should be taken to prevent aspiration of emesis. IV access should be established immediately. Extensive emesis can lead to the loss of hydrogen and chloride ions followed by renal compensation, producing a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis, the classic electrolyte abnormality. Profound hyponatremia can result in lethargy and seizures.
DEFINITION Pyloric stenosis is also referred to as hypertrophic pyloric stenosis or infantile hypertrophic pyloric stenosis. The progressive hypertrophy in the smooth muscle of the gastric antrum and pyloric musculature leads to eventual gastric outlet obstruction.
EPIDEMIOLOGY The etiology of pyloric stenosis is unknown. It is four times more common in males than females with the incidence estimated to be 1:150 males and 1:750 females. It tends to run in families; however, the exact inheritance pattern is not known. Thirty percent are seen in first-born children, with the highest incidence seen in children of a mother who had pyloric stenosis. It is seen in approximately 20% of males and 10% of females of a mother who had the condition. It is most common in white persons of northern European ancestry, is less common in black persons, and is rare in Asians. There is an association between pyloric stenosis and the use of erythromycin in neonates. Erythromycin
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used for pertussis after exposure for prophylaxis, but it is also a motilin agonist. At doses used for the antibiotic properties, it can produce contractions, which may lead to the hypertrophy of the pylorus.
CLINICAL PRESENTATION Infants commonly present with symptoms in the second to sixth week of life but may present as late as 3 months. They present with progressively worsening nonbilious emesis that may become projectile in nature. Vomiting occurs near the end of feeding or immediately after feeding. They maintain their appetite and will aggressively feed, only to regurgitate the entire feeding a short time later. Poor weight gain or weight loss will be noted, and it is important to compare the current weight to the birth weight or other previously measured weights. Jaundice may be present as a result of glucuronyl transferase deficiency. Infants at birth are healthy, with the hypertrophy developing over time. As the hypertrophy advances, there is a progressive outlet obstruction. Emesis ensues, with the child losing both hydrogen and chloride ions. As the emesis continues, the kidney attempts to compensate by retention of hydrogen with the loss of potassium, leading to a hypochloremic, hypokalemic metabolic alkalosis; but this can be a late finding. The emesis continues and the infant becomes malnourished and dehydrated. In severe dehydration, the infant may appear lethargic.
EXAMINATION Infants may have a palpable pylorus. This is commonly referred to as a pathognomonic “olive-mass.” This is best palpated immediately after emesis or after nasogastric tube emptying of the stomach because the “mass” may be obscured by a distended antrum. The mass is firm, mobile, and approximately 2 cm in length, best palpated just lateral to the rectus abdominis muscle in the right upper quadrant of the abdomen. In advanced stages, visible waves of abdominal peristalsis may be seen as the stomach produces intense contractions against the obstruction. Children in advanced stages will show the clinical picture of marasmus, with protein-calorie malnutrition. They may have poor skin turgor, sunken eyes, and may be lethargic. Major differential considerations include gastroesophageal reflux and malrotation. Both of these may begin early in life but can have variable presentations. Therefore, it is important to differentiate these from pyloric stenosis, which usually does not begin until after 2 weeks. Emesis from malrotation may be bilious, whereas emesis in pyloric stenosis will be nonbilious.
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LABORATORY FINDINGS A CBC, chemistry panel, liver-associated enzyme analysis, and blood and urine cultures should be obtained. Blood chemistries may demonstrate a hypochloremic, hypokalemic metabolic alkalosis. This may be a late finding because the severity will depend on the duration of the emesis before presentation. The CBC may demonstrate an elevated hematocrit as a result of hemoconcentration.
DIAGNOSIS The finding of the “olive mass” is pathognomonic. It can be confirmed with ultrasound or upper gastrointestinal tract series.
RADIOGRAPHS Abdominal radiographs are nonspecific but often will demonstrate gastric dilation. In rare cases, gastric perforation can occur and free air may be seen on radiograph. Ultrasonography will reveal a hypertrophic pylorus. A normal pylorus is less than 2 mm in diameter. The criterion for diagnosis is a pyloric thickness greater than 4 mm or an overall pyloric length greater than 14 mm (Fig. 13-3). An upper gastrointestinal tract series will demonstrate a classic “string sign,” the result of
Figure 13-3. A, Transverse sonogram demonstrating a pyloric muscle wall thick-
ness of greater than 4 mm (distance between crosses). B, Horizontal image demonstrating a pyloric channel length greater than 14 mm (wall thickness outlined between crosses) in an infant with pyloric stenosis. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 310.1-2, Copyright # 2004 Elsevier.)
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contrast being able to pass through the hypertrophied pyloric sphincter. The “shoulder sign” may also be seen, which is created by the prepyloric collection of barium (Fig. 13-4). Both ultrasound and upper gastrointestinal tract series have reported accuracies greater than 95%.
TREATMENT The important first steps in the treatment of pyloric stenoses include IV access and nasogastric tube insertion to decompress the stomach. These infants will be admitted to the hospital. Fluid and electrolyte replacement is essential and should be guided by electrolyte values and physical appearance. Fluid resuscitation should be accomplished with an initial 20-ml/kg bolus of normal saline and followed by 5% dextrose in half normal saline at 1.5–2 times the maintenance rate. Additionally, potassium supplementation is often required. Fluid and electrolyte therapy should continue until the infant has appropriate fluid status and serum bicarbonate level is less than 30 mEq/dl (correction of the alkalosis). Antibiotic therapy should be started if signs of sepsis are present.
Figure 13-4. Barium in the stomach of an infant with projectile vomiting. The attenuated pyloric canal is typical of congenital hypertrophic pyloric stenosis. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 310.1-3, Copyright # 2004 Elsevier.)
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Consultation with a surgeon should be promptly obtained. The definitive corrective surgical procedure is the Ramstedt pyloromyotomy; however, laparoscopic pyloromyotomy has become increasingly common. Surgical treatment is curative and has a low mortality rate of between 0 and 0.5%.
Bibliography Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Garcia EA: Pediatric surgical emergencies: Intestinal obstruction in infants and children, Clin Pediatr Emerg Med 2002;3(1):14–21. Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002.
Urinary Tract Infections in Children JAKE ROBERTS
ICD Code: Urinary tract infection 599.0
Key Points The gold standard for diagnosing UTI is a positive urine culture result obtained from a suprapubic aspiration, urethral catheterization, or clean catch. ! Emergency Actions ! No specific emergency actions are required for a child with a UTI. The clinician should ensure that the child is not uroseptic.
DEFINITION Pediatric urinary tract infections are defined as any infection involving the kidneys, ureter, bladder, or urethra. UTIs are a frequent and important cause of pediatric illness. Unrecognized infections can result in systemic infection or permanent renal damage and secondary hypertension.
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EPIDEMIOLOGY The epidemiology of pediatric UTIs is both age and sex dependent. In neonates, males have a higher incidence of UTI than females. After around 2 months, UTIs become much more common in females rather than males. Uncircumcised males run a higher risk of UTI than circumcised males. Approximately 8% of uncircumcised males younger than 1 year presenting with fever have UTIs versus only 1.2% of circumcised males. After 1 year, UTIs in boys are exceedingly uncommon unless the child has an anatomical defect. Overall, approximately 4%–7% of fevers in children aged 2 months to 2 years are the result of UTI. Girls older than 2 years continue to be at risk for UTI, especially sexually active adolescents. Children who have had prior UTIs are much more likely to have recurrence, usually shortly after the initial infection. Neonates with developing immune systems are at increased risk, as are children with immune deficiency disorders such as diabetes or human immunodeficiency virus (HIV) infection.
PATHOLOGY The vast majority of pediatric UTIs result from one of the following mechanisms: retrograde ascent of normal perineal flora, hematogenous spread from an underlying bacteremia, or nosocomial instrumentation. The most common cause is retrograde ascent. For this to occur, the bacteria have to attach to the urinary tract and not be washed out by normal urinary flushing. Patients with depressed immunity or an anatomical pathology resulting in urinary retention or reflux are at increased risk for acquiring infection. Hematogenous spread is less common, except in the neonatal period, and the bacterial etiology are more commonly Staphylococcus or Streptococcus species instead of perineal flora. Nosocomial infections are relatively uncommon, occurring in small minority of patients requiring urinary tract instrumentation.
CLINICAL PRESENTATION Older children and adolescents with UTIs report symptoms similar to those of adults. Common symptoms are dysuria, increased frequency, and suprapubic pain. Physical examination might reveal costovertebral angle tenderness to palpation or percussion. Younger children rarely present with typical symptoms. Often the only clue might be a vague history of fever, “fussiness,” decreased feeding, or some change in the normal bowel and bladder pattern. Of these, fever is the most common. The American Academy of Pediatrics recommends obtaining an adequate urine sample for culture and urinalysis in all febrile girls and uncircumcised boys younger than 2 years and circumcised males younger than
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1 year old. Adolescents need to be questioned about sexual activity. Newly sexually active girls are at a higher risk of UTI. If sexually active, adolescents should be counseled regarding safe sexual practices and tests for sexually transmitted diseases and should be referred for routine gynecological care. Abuse should be considered in younger children and adolescents with sexually transmitted disease.
EXAMINATION Younger children presenting with UTIs will most likely have nonspecific examination results. A genital examination should be performed to rule out trauma or external infections. The differential diagnosis includes sexually transmitted disease as well as parasitic infections such as enterobiasis (from Enterobius vermicularis pinworms). Older children will often have suprapubic or flank tenderness to palpation or percussion. A pelvic examination and testing for sexually transmitted disease should be considered in older, sexually active girls. Children younger than 2 years old who have documented UTI require further imaging studies to rule out correctable, anatomical defects. According to the American Academy of Pediatrics, children who respond appropriately to antibiotics should receive an ultrasound scan followed by voiding cystourethrography or radionuclide cystography at the earliest convenient time. Children who do not respond to antibiotics after 2 days of treatment should receive an ultrasound scan and either voiding cystourethrography or radionuclide cystography immediately. This is a change from previous practice that only required such workup in female children who had recurrent UTIs.
DIAGNOSIS The gold standard for diagnosing UTI is urine culture. The collection method used has a bearing on the diagnostic accuracy. Urethral catheterization and suprapubic aspiration have the highest combined sensitivity and specificity, followed by clean-catch samples. Perineally bagged urine has a very high rate of contamination with normal flora. The result is an unacceptably high false-positive rate (>85%) and thus only negative culture results have clinical significance. Performing urinalysis on bagged urine should be avoided unless there is absolutely no other way to obtain the sample. Suprapubic aspiration is the gold standard; however, aspiration is rarely used in clinical practice. If available, portable ultrasound scan can be used to verify adequate urine volume in the bladder before aspiration. Urinary catheterization is the most common method used in children too young to produce a voluntary sample. Older children should be instructed on proper cleaning and collection before producing a sample. Having the child sit backward on the toilet enhances labial traction and helps to decrease contamination.
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LABORATORY FINDINGS The gold standard for diagnosing UTI is a positive urine culture result obtained from a suprapubic aspiration, urethral catheterization, or clean catch. A positive culture result from a suprapubic tap is any gram-negative growth on the media and any more than a few thousand gram-positive cocci. For female urinary catheterization and clean catch, a culture result is generally considered positive if more than 100,000 colony-forming units of a single organism are isolated. In males, a positive culture result is greater than 1000 colony forming units. Urinary cultures take approximately 24–36 hours to grow and be interpreted. In the meantime, the urinalysis can be used to judge which patients have a higher likelihood of true infection. Leukocyte esterase, nitrate test, and microscopy are all useful. Leukocyte esterase has a high sensitivity but a low specificity (many false positives). The nitrate test is more specific but less sensitive. Identifying bacteria or WBCs on a spun urine sample also has good sensitivity and specificity. Combining the three increases the diagnostic accuracy. Findings suggestive of catheterized UTI are a positive nitrate or leukocyte esterase test, at least 5 WBCs per high-power field, or any bacteria. Although none of these tests are definitively diagnostic, positive findings can be used to select who receives antibiotic treatment before culture results are available.
TREATMENT Treatment of UTIs requires antibiotic therapy (Table 13-8). The following patients should be admitted for inpatient parenteral antibiotics: patients who are systemically ill, dehydrated, have suspected pyelonephritis, are unable to tolerate oral antibiotics, those deemed unlikely to be compliant with the recommended oral regimen, and those younger than 3 months old. Initial choice of oral antibiotics pending urine culture and sensitivity results varies based on the local resistance patterns and practitioner preferences. Options include sulfonamides such as trimethoprim/sulfamethoxazole and cephalosporins. The use of fluoroquinolones has been discouraged in the past because of possible arthrotoxic and cartilage toxicity, although in actuality these medications are probably safe. Administer 7 days of therapy for older children with simple cystitis and 10–14 days of antibiotics for children with fever or other signs of ascending infection or pyelonephritis. Arrange follow-up for repeat urinalysis after completion of the antibiotic regimen to rule out persistent infection. In children younger than 2 years old, consider giving prophylactic antibiotics until imaging studies are completed. Phenazopyridine may be given to help anesthetize the urinary system in older children reporting urinary dysuria, frequency, or urgency. The dose is 12 mg/kg/day PO divided into three doses. Treatment should only be given for 1–2 days.
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Table 13-8 Selected Antibiotics for Treatment of Urinary Tract Infection Trimethoprim-sulfamethoxazole
Oral Antibiotics Give 5 ml of suspension per 10 kg up to a 20-ml/dose twice daily for 7–14 days. Children weighing more than 40 kg can take one DS tablet twice daily for 7–14 days. Administer 15 mg/kg every 12 hours for 7– 14 days. Give 5 mg/kg every 12 hours for 7–14 days.
Cefprozil (second-generation cephalosporin) Cefpodoxime (third-generation cephalosporin) Intravenous (IV) Antibiotics Ceftriaxone (third-generation cephalosporin) Avoid use in children younger than 2 months old.) Cefotaxime (third-generation cephalosporin) (Safe for use in children younger than 2 months old.)
Administer 75 mg/kg IV or intramuscularly every 24 hours. Give 40 mg/kg IV every 6 hours.
DS, Double strength.
Bibliography American Academy of Pediatrics, Subcommittee on Urinary Tract Infection: Practice parameter: Diagnosis, treatment and evaluation of urinary tract infection in infants and young children, Pediatrics 1999;103:843–852. American College of Emergency Physicians Clinical Policies Committee, Clinical Policy for Children Younger Than Three Years Presenting to the Emergency Department With Fever. American College of Emergency Physicians Clinical Policies Subcommittee on Pediatric Fever, Ann Emerg Med 2003;42(4):530–545. Hampel B, Hullman R, Schmidt H: Ciprofloxacin in pediatrics: Worldwide clinical experience based on compassionate use—Safety report, Pediatr Infect Dis J 1997;16(1): 160–162127–129. Hellerstein S: Recurrent urinary tract infections in children, Pediatr Infect Dis 1982; 1:271–281. Hooton TM, Scholes D, Stapleton AE, et al: A prospective study of asymptomatic bacteriuria in sexually active young women, N Engl J Med 2000;343(14):992–997. Ma J, Shortliffe L: Urinary tract infection in children: Etiology and epidemiology, Urol Clin N Am 2004;31:517–526. Shaw KN, Gorelick M, McGowan KL, et al: Prevalence of urinary tract infection in febrile young children in the emergency department, Pediatrics 1998;102:1–5.
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C. Pediatric Problems The Abused Child RYAN GARNER, KAZUO MIHATA, AND LINDA L. LAWRENCE
ICD Codes: Child abuse, unspecified 995.50, Child sexual abuse 995.53, Child physical abuse 995.54
Key Points Child abuse encompasses a broad spectrum of child maltreatment leading to harm to a child. The knowledge of the normal child and childhood development is essential for the provider if he or she is to recognize abuse. Child abuse frequently recurs and will usually intensify without appropriate intervention. ! Emergency Actions ! Life-threatening emergencies should always be treated first. Medical management will be dictated by the type of injury and acuity of the presentation.
DEFINITION Child abuse or nonaccidental trauma is a broad category of maltreatment of a child by parents, guardians, or other caretakers. There are several types of abuse including (1) neglect, (2) emotional abuse, (3) sexual abuse, and (4) physical abuse. Child neglect occurs when the caretaker fails to meet the child’s basic physical and emotional needs. These can include medical care, nutrition, appropriate supervision, and emotional nurture. It can be intentional either with or without intent to harm or, more commonly, unintentional. The cause of neglect is often multifactorial and can include devaluation of the child as well as physical, emotional, or psychological illness in the caretaker. It is most common in children younger than 3 years of age. Victims of neglect can present with failure to thrive syndrome (FTT). Emotional abuse may include intentional verbal or behavioral acts that result in emotional harm to a child. This can include failure to provide a nurturing environment that is essential for normal development. Other emotional maltreatment includes exploiting or corrupting, extensively isolating, or terrorizing the child. Sexual abuse can have multiple presentations. It is most commonly the involvement in sexual activities of children who are developmentally
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immature. The child does not fully comprehend these activities and therefore is unable to provide consent. This may include subjecting the child to incest, rape, fondling, and pornography. The child may not reveal the abuse until a significant time has passed since the event or onset of the abuse. The sexual abuse will be repetitive in 90% of cases and is most often perpetrated by family members or other persons known to the victim. Physical abuse is a leading cause of injury and death in childhood. It encompasses a wide spectrum of intentional trauma with many contributing factors. Younger children are at higher risk; two thirds of the children are younger than 3 years of age. Physical abuse should be considered in any situation where the presenting symptoms are not consistent with the history given by the caretaker, or when the history changes over time. A delayed presentation to the ED should also bring up the possibility of abuse. Munchausen by proxy is a relatively uncommon form of physical abuse wherein a caretaker fabricates or induces an illness so that the caretaker can obtain attention and sympathy from medical providers. These cases will likely be medically difficult to determine and may unnecessarily subject the child to extensive studies as the provider attempts to determine the cause of the child’s illness.
EPIDEMIOLOGY Current estimates are that 11 children per 1000 experience child abuse. Nearly 3 million reports of abuse or neglect occur each year, with one third of these being substantiated. Ten percent of children with injuries presenting to the ED have injuries sustained from abuse. Approximately 2000 deaths occur each year, with approximately half of these from physical abuse and half from neglect. Child abuse accounts for approximately 140,000 serious injuries each year, with 18,000 of these injuries resulting in lifelong disability. There is a strong correlation between child abuse and domestic violence, with abuse of a child occurring in 50% of cases of domestic violence.
CLINICAL PRESENTATION The presentation is varied with the type of abuse sustained. The history is often incompatible with the type or degree of the injury. Additionally, the history may be vague, may change over time, and can be contradictory in nature to the physical findings. Inquiry into the patient’s social situation may reveal important information. Children with single-parent families, those with a “live-in significant other,” or those in a home with known alcohol or drug abuse are at higher risk for abuse. Children in the toilettraining age group are at increased risk for “punishment” after accidents.
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Neglected children may present as malnourished. Hygiene may be poor, and the child may have skin rashes or diaper dermatitis, attributable to infrequent changing. FTT will likely be present, usually affecting children younger than 3 years. The child’s weight and length may both be affected, and commonly the child has a body mass index lower than the 15th percentile. Children with FTT will be difficult to console and will turn away from close eye contact. Sexual abuse victims may present to the ED after disclosure of the abuse to another adult. Sexual abuse should be considered when related physical symptoms such as vaginal/penile/rectal pain or discharge, bruising, erythema, or bleeding are presenting symptoms. Other presentations may include dysuria, enuresis, or encopresis. Fifteen percent of children diagnosed as having sustained sexual abuse present to the ED with other unrelated symptoms. Children who have experienced physical abuse may present with the abuser. Abusers are unlikely to give an accurate history of the abuse and may deny knowledge of how the injury occurred. The stated history may change over time, and it is important for the providers to document changes in the history. Elaborate histories may be made up by the abusers in an attempt to explain the injury; these may be completely unreasonable or may be relatively believable. Any delay in seeking medical treatment should raise suspicion of abuse. Past medical history and family history may also reveal signs of abuse such as previous injuries, injuries or deaths of siblings, and in particular, severe injuries including burns, fractures, or brain injury. It is important to attempt to take the histories from the caregiver and from the child separately and compare the two, noting inconsistencies. If appropriate, ask the child directly what happened. Differing histories between the child and the caretaker may indicate abuse. Any history obtained directly from the child should be documented in the medical record. The interaction between the child and caretaker and the provider can provide clues in suspected abuse cases. Parental behavior in the ED should be observed, as should the level of concern about the injury. Suspicion should be raised if a parent hesitates to share the mechanism of injury, refuses to let diagnostic studies be performed, or is not supportive of the child or the provider. Anger or apathy that is directed toward the child may be subtle or obvious and should raise concerns. Suspicions should also be raised in the case of a caretaker who ignores major injuries while addressing minor concerns. Repeat visits or multiple occurrences of injury should also raise suspicion of abuse. Caretakers who express “losing control” or being overwhelmed by the child’s behavior may be making “cries for help.” Parental anger at the filing of a report of suspected abuse is a natural response. Providers should not be accusatory in their interactions; it is important to advise
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the family that providers are required by law to report any suspicious injuries.
EXAMINATION Bruises and skin lesions are the most frequent indication of physical abuse, seen in 90% of abused children. Therefore, it is important for all children presenting to the ED to be undressed and placed in a gown so a quick skin examination can be performed, regardless of the presenting symptom. An essential component of evaluating child abuse is knowledge of normal childhood developmental stages because they can provide important information about what injuries are real accidents versus abuse. The developmental milestones of rolling over, sitting up, standing, and walking are clearly important for consideration when evaluating the history and mechanism of injury. For example, children learning to walk will normally have numerous bruises on the anterior tibia, extensor surfaces, forearms, and even forehead. A disparity between injuries, possibly based on accidents during normal development and the physical findings, may alert the provider to abuse. Another important factor is the social situation. The caretaker who brought the child to the ED may or may not be the abuser, and he or she may not even be aware of the abuse. Bruises that are linear or uniform raise suspicion because they may be caused by objects such as belts, buckles, light cords, or other instruments (Fig. 13-5). The location of these bruises, especially on the back, buttocks, upper arm, chest, or face is also concerning. If bruising is found in multiple areas of the body in various stages of healing, physical abuse must be considered. Other common injuries include the following: CNS injuries occur in 15% of abused children, 13% have burns, 10% have toxic ingestions, 8% have skeletal injuries, and 2% have abdominal injuries. CNS injuries are the most serious and lethal because children, especially those younger than 2 years old, can have intracranial hemorrhages from being shaken or beaten. Burns may have atypical/unusual patterns that will raise suspicion. Abdominal injuries may present as symptoms of recurrent or persistent vomiting, unexplained abdominal pain, bruising, or tenderness. Skeletal injuries may present as unexplained or asymmetrical swelling or refusal to bear weight or walk. Long bone fractures are most common in abuse, and metaphyseal fractures are most specific for physical abuse. Spiral fractures are caused by a twisting motion. The provider should suspect physical abuse if the stated history is not consistent with a twisting motion when a spiral fracture is found. If abuse is suspected, a complete physical examination is warranted to document any findings of bruises, burns, scars, or other abnormalities. Burns should be evaluated for size and shape, paying close attention to
762 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Marks from instruments Belt buckle
Fly swatter
Bite
Belt
Looped cord
Coat hanger Board or spatula
Sauce pan
Paddles
Stick/whip
Hand/knuckles
Hair brush
Spoon
Figure 13-5. A variety of instruments may be used to inflict injury on a child. Often, the choice of an instrument is a matter of convenience. Marks tend to silhouette or outline the shape of the instrument. The possibility of intentional trauma should prompt a high degree of suspicion when injuries to a child are geometric, paired, mirrored, of various ages or types, or occur on relatively protected parts of the body. Early recognition of intentional trauma is important to provide therapy and prevent escalation to more serious injury. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 35-2, Copyright # 2004 Elsevier.)
margins (Fig. 13-6). Burns with a “glove and stocking” pattern with sharp demarcation of the burn margin can indicate immersion in hot water. Real accidents involving liquid burns are likely to have irregular borders and with areas of “splash.” Cigarette burns will give a characteristic circumferential shape and size. It is important to examine the skin for old scars or marks as well as acute injuries. Oral lacerations, including lacerations of the frenulum or other areas of the oral mucosa, may be present in infants who have been force-fed. If head injury or “shaken-baby” syndrome is suspected, a good funduscopic examination is warranted, looking for signs of retinal hemorrhages (associated with subdural hematomas), hyphema, lens dislocation, or retinal detachment. Physical examination of a sexually abused child can be difficult. These patients should undergo a genital examination that includes careful inspection of the genitalia and perianal region. The “frog-leg” position is normally best for this examination in children. Speculum examinations are not necessary unless the patient is an older adolescent or if vaginal trauma is suspected. The examination should look for acute injuries such as bruises, abrasions, and lacerations, as well as for evidence of forensic material such as semen. Any findings indicative or sexually transmitted infections should be documented.
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Burn marks Hot plate
Light bulb
Curling iron
Car cigarette lighter
Steam iron
Knife
Grid
Cigarette
Forks
Immersion
Figure 13-6. Marks from heated objects cause burns in a pattern that duplicates that of the object. Familiarity with the common heated objects that are used to traumatize children facilitates recognition of possible intentional injuries. The location of the burn is important in determining its cause. Children tend to explore surfaces with the palmar surface of the hand and rarely touch a heated object repeatedly. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 35-3, Copyright # 2004 Elsevier.)
Knowledge of the normal anatomy for age group of the female patient is very important because the female genitalia changes with age. In the prepubescent group, girls will have a thin, small labia minora and a full labia majora. The hymen is reddish-orange and will cover the vagina. In infancy, the hymen is thick. From infancy to puberty, it is thin with smooth edges and is annular or crescent shaped. The hymen should be examined for trauma. An indentation at the 6-o’clock position suggests penetration trauma. White areas or areas of swirling vascularity are signs of scarring. It is important to note that redness is a sign of inflammation or irritation and does not necessarily indicate abuse. Genital examinations in males should consist of inspection of the penis and testicles. In rare cases, there may be bite marks on the genitalia. Bruising, abrasions, scars, and any urethral discharge should be documented. The perianal examination in males and females may show fissures, abrasions, or hematomas. Anal penetration is easier than vaginal penetration in the young female, and therefore this portion of the examination must not be overlooked. Anal tone should be evaluated because it is often decreased when there has been repetitive prior anal penetration. The clinician should look for thickening or thinning in the anal rugae. The healthcare provider should consider orogenital contact in cases of suspected sexual abuse. The mouth and throat should be examined for trauma, including lacerations and bruising. If sexually transmitted infections are suspected, cultures should be taken of the oropharynx, anus, and penis or cervix/vagina.
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LABORATORY FINDINGS Laboratory tests should be directed by the situation, suspected trauma, and physical examination findings. A CBC, PT, PTT, liver associated enzymes, amylase, and lipase should be measured in the setting of suspected abdominal trauma. Basic chemistries, along with calcium, magnesium, and phosphorus analyses, should also be included. Urinalysis should be accomplished to rule out kidney contusions or trauma. If multiple bruises are present, the CBC and coagulation studies will be helpful because the differential diagnosis includes leukemia, aplastic anemia, and thrombocytopenia. In cases of sexual abuse, as previously stated, cultures of the throat, genitals, and rectum should be performed for gonorrhea and chlamydia. Serological studies for syphilis should be accomplished only if there is evidence of history of syphilis. HIV infection should be considered after appropriate counseling, but only if there is a reason to suspect infection.
RADIOGRAPHS CT scan or magnetic resonance imaging (MRI) should be included if head trauma or “shaken child syndrome” is suspected. Plain film radiographs of the long bones should be performed as indicated. If physical abuse is suspected, a skeletal survey should be accomplished, especially in children younger than 2 years. A skeletal survey consists of the following: anteroposterior/lateral skull (with cervical spine), anteroposterior/lateral chest, anteroposterior pelvis, anteroposterior humeri and forearms, posteroanterior hands, anteroposterior femurs/tibias/feet, and lateral lumbar spine. Radiographs may demonstrate multiple periosteal elevations, indicating previous fractures in different stages of healing. In cases of abdominal trauma, an abdominal series should be performed, which may demonstrate the “double-bubble” sign indicative of duodenal hematoma.
TREATMENT Medical emergencies and physical injuries should always be addressed first. Physical findings and ancillary studies should direct medical management. Often children will require hospitalization. Hospitalization will allow a “cooling-off period,” ensure child safety in the short term, and allow time for authorities and social work services to perform the necessary actions to ensure the future safety of the child. Medical documentation may be used in court and should be accurate and complete. Of utmost importance is that providers are aware of state and local laws because they relate to child abuse. All 50 states and the District of Columbia have mandatory reporting laws for suspected child abuse and neglect. The primary responsibility of reporting belongs to
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the medical providers. Providers may be held liable for future abuse if they fail to report even suspicion of abuse. Studies of abused children who are returned to their caretakers without any intervention demonstrate that approximately 5% are subsequently killed, and 25% have subsequent serious injuries. However, with intensive family treatment, 80%–90% of families involved with child abuse can learn to provide adequate care for their children. The ultimate focus and concern in all situations of suspected abuse should be the safety of the child.
Bibliography Barnett TM: Child abuse. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Johnson CF: Abuse and neglect of children. In Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Mace SE: Child physical abuse: A state-of-the-art approach, Pediatr Emerg Med Pract 2004;1(2):1–20.
Sudden Infant Death Syndrome and Apparent Life-Threatening Event Syndrome JULIE HUSLEY
ICD or CPT Code: Sudden infant death syndrome 798.0
Key Points
Crib death: Alternate or traditional name for SIDS Back to Sleep campaign: National effort to educate parents that babies who sleep on their backs are less likely to die from SIDS
! Emergency Actions ! Emergency intervention of a patient who has experienced SIDS or an apparent life-threatening event (ALTE) begins the moment the patient is discovered, usually at home by its caregivers. If noninvasive arousal efforts have failed to resume normal breathing, CPR is required by whoever is at bedside. Transportation to the nearest hospital by ambulance is also required.
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DEFINITION Sudden infant death syndrome is defined as the sudden unexpected death of an apparently healthy infant younger than 1 year of age that remains unexplained after a thorough case investigation. Victims are usually discovered in the crib by the parents, provoking the alternate name of “crib death.” There are more than 70 hypotheses as to what causes SIDS. An apparent life-threatening event refers to the sudden occurrence of a breathing abnormality, color change, or alteration in muscle tone or mental status in an infant, which may require stimulation or resuscitation to arouse the child and to reinitiate regular breathing. Eight to fifteen percent of children with ALTE die of SIDS, although one study that focused on children of nurses reported that 27% of patients who died of SIDS exhibited previous ALTEs.
EPIDEMIOLOGY The Back to Sleep campaign was launched by the National Institute of Child Health and Human Development (NICHD) in June 1994, reflecting the research conclusion that infants who sleep on their stomachs are more likely to succumb to SIDS. Since the introduction of this campaign, the rate of SIDS has dropped by more than 50%, and the numbers of infants put to sleep on their stomachs has dropped from 70% to 15%. However, according to the NICHD, African American babies are still at twice the risk of experiencing SIDS, and American Indian infants are at three times the risk as that of white infants to die from SIDS. The incidence of SIDS deaths is between 0.56 and 2 per 1000 live births worldwide, and at least 2500 babies are still dying from this cause each year in the United States. SIDS is the leading cause of death for babies between the ages of 1 month and 1 year of age, with the highest rate occurring between 2 and 4 months of age. More deaths have occurred in colder months, and boys of all ethnicities are at 1.5 times higher risk than girls. Risk factors for SIDS include the following:
Stomach sleeping Smoking, drinking, or drug use by the mother during pregnancy Poor prenatal care Prematurity or low birth weight Mothers younger than 20 years old Smoke exposure after birth A previous ALTE
Unlike SIDS, there has been no drop in the incidence of ALTEs since the initiation of the Back to Sleep campaign. Regardless, children with ALTEs do have a statistically higher incidence of sudden death. Further studies are needed to clarify this relationship.
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PATHOLOGY Several studies have sought to determine the cause of SIDS, yet no single factor has been identified. Recent literature suggests many possible etiologies for SIDS and ALTE, giving providers useful information for assessment, risk stratification, and prevention in certain subgroups of infants. The central cause of SIDS appears to be prolonged hypoxia, leading to respiratory and cardiac failure. The cause of hypoxia has been studied with a variety of interesting results. For example, congenital anomalies of the cardiorespiratory centers in the brainstem, namely the arcuate nucleus, have been found frequently in autopsies of sudden unexplained infant and perinatal deaths. Other study results have suggested certain predictive factors, such as immunological sensitivities, exposure to cigarette smoke, use of promethazine-containing medications, elevated salivary IgA concentrations, and a decreased heart rate variability (which is used as an index of sympathovagal balance). The most frequent problems associated with an ALTE are digestive (about 50%), neurological (30%), respiratory (20%), cardiovascular (5%), metabolic and endocrine (under 5%), or diverse other problems, including child abuse. Up to 50% of ALTEs remain unexplained. Abusive head injury, a recently recognized cause, occurs frequently enough to obligate its inclusion in the differential diagnosis. An ophthalmological evaluation with dilated fundus examination and cranial imaging should therefore be considered early in the investigation unless another cause becomes apparent soon after admission. A subgroup of infants with ALTE present with a mild facial dysmorphia, which is associated with an abnormal breathing pattern during sleep. This dysmorphia can be so mild as to be overlooked, but it needs to be recognized to initiate appropriate treatment.
CLINICAL PRESENTATION A child presenting with a history of an ALTE can have completely normal examination findings, and a child who has become or ultimately becomes a victim of SIDS may present in cardiac arrest. The parents may report “stiffening” or “jerking” if a seizure preceded what looked like an apneic event; the patient may have had a recent feeding if gastroesophageal reflux is a factor causing apnea; or the patient may have recently taken medications containing promethazine.
EXAMINATION The evaluation of a child who has had an ALTE requires a detailed history of the event, factors leading up to the event, details of the surroundings, the
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child’s position when found, and the measures required to resuscitate the child. A past medical history is also very important, including medications taken. The physical examination must be complete, with particular consideration to the existence of facial dysmorphia, signs of child abuse, a retinal examination for hemorrhages, and complete cardiac, pulmonary, and neurological examinations. Poor muscle tone, slow response to pain, bradycardia, abnormal skin color, and shallow breathing are signs of incomplete resuscitation.
LABORATORY FINDINGS Basic laboratory tests useful in a patient with a normal physical examination may include a CBC (results useful in infection, anemia), serum bicarbonate and lactate (acidosis), urinalysis (infection), pertussis, and RSV infection. However, laboratory evaluation is highly individualized to each case.
DIAGNOSIS The diagnosis of SIDS is made on the basis of autopsy after a thorough investigation of the patient’s medical history, surroundings, and caregiver interviews have been completed. ALTEs should be considered a manifestation of an underlying pathology, and an investigation should ensue to identify the pathology so that appropriate treatment can begin. Patients should be admitted for apnea monitoring until all possible causes of apnea are ruled out. Electrocardiography (ECG), salivary IgA testing, and fetal hemoglobin synthesis determination may be helpful in select patients. In approximately half of these patients, no diagnosis will be made.
RADIOGRAPHS The history and physical examination will help determine which imaging studies are needed. Long bone studies are a good consideration if child abuse is suspected. A chest radiograph may reveal an occult respiratory infection.
TREATMENT The challenges for the provider are to manage the immediate event, discern the underlying cause of the event when possible, educate parents, and determine the need for further monitoring. Infant who appear to be only partially revived by prehospital treatment should be vigorously
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resuscitated. Inpatient workups will help to determine the appropriate treatment for some patients with ALTEs by diagnosing the underlying cause, but 50% of children will remain undiagnosed. Consensus guidelines recommend cardiorespiratory home monitoring for cases in which no clear diagnosis is identified or when a severe ALTE has been experienced. Unfortunately, no currently available home monitoring device is free of false alarms or offers complete protection. Vigilant follow-up care of the infant and immediate institution of home monitoring are recommended, and readmission is warranted in infants with severe or multiple recurrent events.
REDUCING THE RISK The NICHD’s Back to Sleep campaign recommends that, unless there is a medical reason not to do so, infants should be placed on their backs to sleep, on a firm mattress with no blankets or fluffy bedding under or over them. If a blanket is used, it should be placed no higher than the baby’s chest and should be tucked in under the crib mattress. The baby’s sleep area should be free of pillows and stuffed toys, and the temperature in the baby’s room should be kept at a level that feels comfortable for an adult.
Bibliography Altman RL, Brand DA, Forman S, et al: Abusive head injury as a cause of apparent lifethreatening events in infancy, Arch Pediatr Adolesc Med 2003;157(10):1011–1015. Bard H, Cote A, Praud JP, et al: Fetal hemoglobin synthesis determined by gamma-mRNA/ gamma-mRNA þ beta-mRNA quantitation in infants at risk for sudden infant death syndrome being monitored at home for apnea, Pediatrics 2003;112(4):e285. Cote A, Hum C, Brouillette RT, Themens M: Frequency and timing of recurrent events in infants using home cardiorespiratory monitors, J Pediatr 1998;132(5):783–789. Edner A, Katz-Salamon M, Lagercrantz H, et al: Heart rate variability in infants with apparent life-threatening events, Acta Paediatr 2000;89(11):1326–1329. Gleeson M, Clancy RL, Cox AJ, et al: Mucosal immune responses to infections in infants with acute life threatening events classified as ‘near-miss’ sudden infant death syndrome, FEMS Immunol Med Microbiol 2004;42(1):105–118. Gold Y, Goldberg A, Sivan Y: Hyper-releasability of mast cells in family members of infants with sudden infant death syndrome and apparent life-threatening events, J Pediatr 2000;136(4):460–465. Goldhammer EI, Zaid G, Tal V, et al: QT dispersion in infants with apparent life-threatening events syndrome, Pediatr Cardiol 2002;23(6):605–607. Guilleminault C, Pelayo R, Leger D, Philip P: Apparent life-threatening events, facial dysmorphia and sleep-disordered breathing, Eur J Pediatr 2000;159(6):444–449. Hall K, Zalman B: Evaluation and management of apparent life-threatening events in children, Am Fam Phys 2005;71(12):2301–2308. Kahn A: Recommended clinical evaluation of infants with an apparent life-threatening event: Consensus document of the European Society for the Study and Prevention of Infant Death, 2003, Eur J Pediatr 2004;163(2):108–115. Published online December 3, 2003.
770 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Matturri L, Biondo B, Suarez-Mier MP, Rossi L: Brain stem lesions in the sudden infant death syndrome: Variability in the hypoplasia of the arcuate nucleus, Acta Neuropathol (Berl) 2002;194:12–20. McKelvey GM, Post EJ, Wood AK, Jeffery HE: Airway protection following simulated gastro-oesophageal reflux in sedated and sleeping neonatal piglets during active sleep, Clin Exp Pharmacol Physiol 2001;28(7):533–539.
Pediatric Diabetes and Pediatric Diabetic Ketoacidosis CHRISTOPHER R. MCNEIL
ICD Codes: Diabetes 250.0, Diabetes ketoacidosis 250.1
Key Points DKA is a complication syndrome of diabetes mellitus. An insulin deficiency and glucagon excess combine to produce hyperglycemia, dehydration, free circulating ketone bodies, acidosis, and significant electrolyte abnormalities. ! Emergency Actions ! In children with DKA, fluid replacement is the main goal of treatment. Patients should be given an initial bolus of 10–20 ml/kg of normal saline.
DEFINITION There are two basic types of diabetes mellitus. Type I diabetes mellitus or juvenile diabetes occurs at a young age and renders patients insulin dependent. These patients have a deficiency of insulin release from the beta cells of their pancreas. Epstein-Barr virus, rubella, cytomegalovirus, mumps, and Coxsackie virus have all been implicated in the cause of type I diabetes. It is believed to be an autoimmune disease in which circulating isletcell antibodies cause the destruction of the insulin-secreting beta cells. Between 80% and 90% of patients demonstrate evidence of one or more of these antibodies. Type II diabetes mellitus is a disease of insulin resistance. Until recent years, type II diabetes has been a disease of
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adulthood in which patients may remain asymptomatic for years. There is an increasing prevalence of type II diabetes among children, especially among African American, Hispanic, and Native American children; this increase is related to an increased prevalence of childhood obesity. The primary treatment for type II diabetes is diet and exercise rather than exogenous insulin. Diabetic ketoacidosis is a complication syndrome of diabetes mellitus. An insulin deficiency and glucagon excess combine to produce hyperglycemia, dehydration, free circulating ketone bodies, acidosis, and significant electrolyte abnormalities. During states of insulin deficiency and glucagon excess, circulating serum glucose is unable to enter cells and participate in glycolysis. Hyperglycemia causes an increase in serum osmolality and leads to an osmotic diuresis and dehydration. The hepatic processes of gluconeogenesis and glycogenolysis are stimulated. Free fatty acids are released, muscle breakdown occurs, and serum amino acid levels increase. Free fatty acids in circulation are partially oxidized and converted in the liver to the ketone bodies: beta-hydroxybutyrate, acetoacetate, and acetone, thus creating a ketoacidosis. This metabolic acidosis leads to an increased respiratory rate and compensatory respiratory alkalosis. Eventually, if untreated, cardiac depression and circulatory collapse occur as a result of volume depletion and severe acidosis.
EPIDEMIOLOGY The incidence of type I diabetes mellitus affects 1 in 500 school-aged children. Males and females are equally affected, and the condition is more commonly in the summer and winter. Approximately 25% of all episodes of DKA occur in patients whose diabetes was previously undiagnosed. DKA accounts for approximately 14%–31% of all hospital admissions for diabetes. The mortality rate is approximately 15%.
CLINICAL PRESENTATION Most patients with DKA have a recent history of polydipsia, polyuria, hunger, visual blurring, weakness, weight loss, muscle cramps, nausea, vomiting, and abdominal pain. Clinically, a patient’s presentation will depend on the severity of the acidosis. The more severe cases of DKA will present with hyperventilation, fruity (acetone)-smelling breath, and possibly an ill appearance. It is often difficult to differentiate DKA from sepsis in children. DKA in a child with diabetes may be caused by a viral or bacterial infection, emotional or environmental stresses, drugs, changes in diet, trauma, or surgery.
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EXAMINATION The patient should be given a complete physical examination. Special attention should be given to look for evidence of infections. Typical findings include tachypnea with Kussmaul’s respirations, tachycardia, hypotension, acetone odor, and dehydration.
LABORATORY FINDINGS A CBC, chemistry panel, urinalysis, ABG or (preferably) venous blood gas (VBG) analysis, serum ketone measurements, and blood cultures should be performed. Hemoglobin A1c can be a useful measurement of long-term glucose control. The glucose level will be elevated, usually greater than 300–350 mg/dl. Glucosuria will also be present. VBG analysis results will reveal a low pH. Venous pH is not significantly different than arterial pH in patients with DKA and is preferable considering the need for multiple samples. A chemistry panel will reveal a decreased bicarbonate level and evidence of a widened anion gap. The BUN level is usually elevated because of the dehydration. There is usually a total body potassium deficit despite a normal or high serum potassium level. Because of the dehydration, potassium is lost by the kidneys in attempt to reabsorb sodium and bicarbonate to maintain blood volume. The serum potassium level is falsely elevated from the potassium and hydrogen cellular shifts, and the serum potassium will increase 0.6 mEq/L for each decrease of 0.1 in pH. A pseudohyponatremia may result from the hyperglycemia. The true sodium level can be estimated by adding 1.6 to the sodium for every 100 mg/dl of glucose over the norm. The measurement of serum ketones is not of very much clinical value in DKA. The laboratory assay for ketones only measures acetoacetate, not beta-hydroxybutyrate. In an acidotic state, the pKa is such that most of the ketones are in the form of beta-hydroxybutyrate, thus serum ketones in DKA are often negative. As DKA is treated and the serum pH normalizes, the ketone test result will turn positive.
DIAGNOSIS The diagnosis is made on the basis of a thorough patient history, clinical presentation, and laboratory results showing a hyperglycemic, anion gap metabolic acidosis.
RADIOGRAPHS A chest radiograph should be obtained to identify any evidence of infection. CT scanning of abdomen/pelvis can be considered for a DKA
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patient with abdominal pain if clinical suspicion for an intra-abdominal infection is high.
TREATMENT Fluids In children with DKA, fluid replacement is the main goal of treatment. Patients should be given an initial bolus of 10–20 ml/kg of normal saline. If they are hypotensive, a second bolus may be required. Patients experiencing DKA should be assumed to have a 10%–15% total body water deficit, which corresponds to approximately a 100–150-ml/kg fluid deficit. After the initial boluses, this deficit along with maintenance fluids should be administered evenly over 36–48 hours as ½ normal saline. Fluids are administered more slowly in children to prevent cerebral edema.
Potassium Dehydration along with hydrogen and potassium shifts falsely elevates serum potassium. There is generally a total body potassium deficit. Once the potassium falls into the high-normal or normal range, potassium replacement is usually needed.
Insulin A regular insulin drip should be started after the initial fluid bolus. The rate of infusion should be 0.1 units/kg/hr and titrated to slowly lower serum glucose levels 50–100 mg/dl/hr. Once the serum glucose reaches 250 mg/dl, D5 should be added to the IV fluids. This limits the decline of serum glucose and osmolality, thus reducing the risk of developing cerebral edema. The insulin infusion is maintained until the acidosis resolves and the anion gap closes. Patients may then be transitioned over to subcutaneous insulin.
Bicarbonate Bicarbonate therapy may be indicated in severely acidotic patients with pH less than 7.0. The use of bicarbonate is not warranted in less ill patients because of paradoxical CNS acidosis.
Laboratory Studies During treatment, a good rule of thumb is to check blood glucose every hour and to follow VBG and serum chemistry trends every 2 hours.
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Specific Treatment If cerebral edema occurs, it carries a 90% mortality rate. It generally occurs 6–10 hours after the initiation of therapy. Cerebral edema should be suspected in any patient with DKA who lapses into coma after treatment, remains comatose despite treatment, or experiences severe headache, altered mental status, or neurological deficits during treatment. Patients require a mannitol bolus of 0.25–1 g/kg and fluid restriction. A head CT scan should be obtained. These patients may also require intubation.
Bibliography Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 16. WB Saunders: Philadelphia, 2000. Glaser NS: Mechanism of cerebral edema in children with diabetic ketoacidosis, J Pediatr 2004;145(2):164–171. Kreshak A: Arterial blood gas analysis: are its values needed for the management of diabetic ketoacidosis? Ann Emerg Med 2005;45(5):550–551. Lawrence SE: Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis, J Pediatr 2005;146(5);688–692. Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000.
Acute Rheumatic Fever JAVED M. NASIR
ICD Codes: 041.01, 034.0
Key Points Anyone with suspected group A streptococcal (GAS) infection should undergo at least a throat culture. If the culture result is positive for GAS infection, then treatment must be initiated to prevent valvular heart disease.
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DEFINITION Rheumatic fever is a delayed, immunologically mediated sequela of a pharyngeal GAS infection.
EPIDEMIOLOGY In the developed world, the incidence of rheumatic fever has declined significantly since World War II. However, all healthcare providers must remain alert for this disease because several outbreaks have occurred in North America in the last two decades. Acute rheumatic fever (ARF) develops after GAS pharyngitis. It occurs most often in children between 5 and 15 years old but has been reported as late as the fourth or fifth decade of life. Rheumatic fever will develop in approximately 3% of patients with untreated GAS pharyngitis. Inadequately treated AFR is a major cause of acquired valvular disease. This classically occurs decades after the episode of ARF and affects the mitral or aortic valve, or both.
PATHOLOGY Although a beta-hemolytic GAS infection, usually originating from the respiratory tract infection, is the essential trigger that predisposes a person to rheumatic fever, the pathogenesis of ARF remains unclear. It has been proposed that after colonization of the pharynx by GAS, B lymphocytes are sensitized by streptococcal antigens. These lymphocytes then produce antistreptococcal antibodies that cross-react with cardiac and neuronal cells.
CLINICAL PRESENTATION ARF can present in many ways. Although it is always preceded by a GAS pharyngeal infection, not all patients will provide this history. The prevalence of the major criterion has not been precisely defined for all patient populations, but a recent, large study (N ¼ 786) in Brazil showed the prevalence of symptoms as follows: polyarthritis (58%), carditis (50%), chorea (35%), erythema marginatum (2%), and subcutaneous nodules (2%). The symptoms of ARF usually follow the GAS pharyngitis by 2–4 weeks. However, the manifestation of chorea may be delayed.
DIAGNOSIS The diagnosis of ARF requires a high degree of suspicion because there is no single sign, symptom, or test that is diagnostic of AFR. Evidence of a recent streptococcal infection and the presence of two major or one major and two minor Jones criteria indicates a high probability of rheumatic fever.
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Evidence of Antecedent GAS Infection Typically, evidence of an antecedent GAS infection is provided by rapid streptococcal antigen tests, throat culture, and/or streptococcal antigen test results.
Jones Major Criteria 1. Carditis: Rheumatic fever can cause a pancarditis. Clinically, rheumatic carditis is usually associated with a murmur of valvulitis. ARF usually affects the mitral or aortic valves and only rarely affects the right-sided valves. Rheumatic carditis should be suspected in patients without a history of rheumatic heart disease who experience a new murmur of mitral or aortic regurgitation. Early myocarditis can be manifested as a tachycardia. Severe myocarditis can present with signs and symptoms of congestive heart failure. Inflammation of the pericardium can present with distant heart sounds, friction rub, or pleuritic chest pain. Pericarditis and myocarditis are unlikely due to ARF in a patient without valvulitis. 2. Polyarthritis: Pain in multiple joints is the most common symptom of ARF. The arthritis is typically migratory, and the knees, wrists, ankles, and elbows are commonly involved. The affected joints will typically be erythematous, swollen, tender to palpation, and warm to touch. The arthritis typically last for 4 weeks and responds dramatically to treatment with salicylates. 3. Sydenham’s chorea (St. Vitus’ dance): This neurological disorder is characterized by involuntary, rapid, purposeless, nonrhythmic movements of the trunk and/or extremities. Muscle weakness and emotional labiality can also be present. The onset of chorea may be delayed for several months after GAS infection and may cease when the patient is asleep. 4. Erythema marginatum: This transient, migratory rash is a rare manifestation of ARF. The rash will appear erythematous with pale centers and serpiginous or rounded margins. The rash is most commonly found on the trunk and extremities, is blanchable, and is not pruritic or indurated. It may be induced by the application of heat. 5. Subcutaneous nodules (i.e., Aschoff bodies): These nodules are firm and painless. They will most often be seen over the spine, scalp, and extensor surfaces of the wrists, elbows, and knees.
Jones Minor Criteria 1. Arthralgia, pain in one or more joints without evidence of inflammation (no swelling, warmth or tenderness to palpation) 2. Fever (usually at least 39 C [102.2 F])
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3. Prolongation of the PR interval on an ECG 4. Elevated acute-phase reactants (erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP])
LABORATORY FINDINGS Supportive evidence of GAS infection should be sought. Typically, this is done with rapid streptococcal antigen tests, throat culture, and/or streptococcal antigen tests. Acute-phase reactants (e.g., CRP, ESR) should be analyzed. An ECG and chest radiograph should also be obtained to look for evidence of cardiac involvement. A routine CBC and chemistry panel should be performed to rule out infection and renal disorders. If cardiac involvement is suspected, cardiac markers should be followed.
TREATMENT There are three arms of therapy that should be initiated by when a patient presents with ARF: anti-streptococcal antibiotic therapy, therapy for the clinical manifestations of the disease, and long-term streptococcal prophylaxis. All patients with ARF, with or without positive GAS culture, are treated with anti-streptococcal antibiotics. A single dose of 1.2 million units benzathine penicillin G IM (600,000 units IM if patient weighs <27 kg) is effective therapy. Oral penicillin V is also effective, and erythromycin can be used in patients allergic to penicillin. Arthritis of ARF typically responds to 75–100 mg/kg/day of aspirin with serum salicylate levels between 20 and 30 mg/dl for 7 days. This is followed by 50 mg/kg/day for 4–6 additional weeks. In hemodynamically stable patients, significant carditis can be managed with 1–2 mg/ kg of prednisone daily for 2 weeks after symptoms resolve and the ESR returns to normal. The steroid dosage is subsequently tapered over 4–6 weeks. Patients presenting with chorea can be given 0.0025–0.0075 mg/ kg of haloperidol four times per day. All patients with ARF, at a minimum, need prophylaxis against GAS until the age of 21 years and until 5 years have elapsed since their last episode of ARF. However, based on risk stratification, patients may require longer prophylaxis. Benzathine penicillin G (1.2 million units IM monthly) is typically recommended as the first-line therapy in the United States. The frequency can be increased to every 3 weeks in high-risk patients (i.e., residual carditis). Daily oral penicillin V or sulfadiazine is also an acceptable alternative. Erythromycin should be used for prophylaxis in patients who are allergic to penicillin.
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Bibliography Dajani A, Taubert K, Ferrieri P, et al: Treatment of acute streptococcal pharyngitis and prevention of rheumatic fever: A statement for health professionals. Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, the American Heart Association, Pediatrics 1995;96(4 Pt 1):758–764. da Silva CH: Rheumatic fever: A multicenter study in the state of Sao Paulo. Pediatric Committee—Sao Paulo Pediatric Rheumatology Society, Rev Hosp Clin Fac Med Sao Paulo 1999;54(3):85–90. Ferrieri P: Jones Criteria Working Group. Proceedings of the Jones Criteria workshop, Circulation 2002;106(19):2521–2523. Galvin JE, Hemric ME, Ward K, Cunningham MW: Cytotoxic mAb from rheumatic carditis recognizes heart valves and laminin, J Clin Invest 2000;106:217. Kaplan EL: Rheumatic fever. In Harrison’s Principles of Internal Medicine, ed 15. McGraw-Hill: New York, 2001, pp 1340–1343. Kirvan CA, Swedo SE, Heuser JS, Cunningham MW: Mimicry and autoantibodymediated neuronal cell signaling in Sydenham chorea, Nat Med 2003;9:823–825. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Cardiovascular Disease in the Young of the American Heart Association: Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 Update, JAMA 1992;268(15):2069–2073. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Tetralogy of Fallot RYAN GARNER, KAZUO MIHATA, AND LINDA L. LAWRENCE
ICD Code: Tetralogy of Fallot 745.2
Key Points Tetralogy of Fallot is the most common congenital heart deformity. Patients with this condition visit the ED with varying presentations, depending on the degree of right ventricular outflow obstruction. Cyanosis and heart failure may be the presenting signs. Although it is most often diagnosed in the nursery, a widely patent ductus arteriosus may be missed in the nursery and patients may present to the ED at later time when the PDA closes.
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! Emergency Actions ! During a hypoxic spell (commonly referred to as a “tet” spell), supplemental oxygen should be provided immediately. These spells consist of hyperpnea, irritability, crying, and increasing cyanosis. Spells have a peak incidence at between 2 and 4 months of age and need to be treated immediately because they may lead to syncope, convulsions, cerebrovascular accident, or death. Placing the child in the knee-tochest position during hypoxic spells also helps by reducing venous return, increasing systemic vascular resistance (SVR), and decreasing the rightto-left shunt. Morphine sulfate at 0.1–0.2 mg/kg can be given either subcutaneously or IM to suppress the respiratory center and decrease the hyperpnea. Saline boluses at 10 ml/kg are given to augment preload. Acidosis, if present, should be treated with sodium bicarbonate (1 mEq/kg). If the child does not respond to these treatments, other acute treatments can be attempted, such as IV phenylephrine (5–20 mg/kg) to increase SVR, or IV ketamine (1–3 mg/kg) administered over 60 seconds, which works to increase SVR and sedates the infant. If the cyanotic spell occurs close to birth and there is evidence of dependency on a PDA, IV prostaglandins (e.g., PGE1) may be considered at 0.1 mg/kg/min.
DEFINITION Tetralogy of Fallot is the most common congenital cyanotic heart disease. There are four classic components of tetralogy of Fallot: (1) a ventricular septal defect (VSD), (2) right ventricular outflow tract obstruction, (3) right ventricular hypertrophy, and (4) an overriding aorta. Right-to-left shunting leads to decreased pulmonary blood flow and cyanosis. Keeping a PDA patent may be crucial to maintaining perfusion of the pulmonary vasculature.
EPIDEMIOLOGY Tetralogy of Fallot accounts for nearly 10% of all cases of cyanotic heart disease, occurring in nearly 3000 births a year. Tetralogy of Fallot affects males and females equally.
CLINICAL PRESENTATION The clinical presentation of a patient with tetralogy of Fallot is dependent on the degree of the right ventricular outflow obstruction. The right ventricular outflow obstruction (most commonly from infundibular stenosis) and the VSD are the primary defects. This right ventricular outflow obstruction leads to increased right ventricular pressures. This causes a right-to-left shunt of deoxygenated blood from right ventricle to left ventricle bypassing the lungs, altered hemodynamics of the right ventricle, and a decreased pulmonary blood flow. This has several
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manifestations, including cyanosis and dyspnea on exertion. The patient’s parents may convey a history of the child squatting after exertion; squatting increases SVR and decreases the right-to-left shunting. Infants who have mild right ventricular outflow obstruction may present in heart failure. Cyanosis may not be present at birth. However, as the right ventricular hypertrophy develops, the right ventricular pressure becomes closer to the left ventricular pressure, causing an increasing right-to-left shunt and increased cyanosis.
EXAMINATION Cyanosis, tachypnea, and clubbing may be seen. Cyanosis may be most prominent in the lips, mouth, and nail beds. The child may have a palpable right ventricular impulse. Cardiac examination may reveal a systolic thrill best over the left sternal border, a single second heart sound, and a systolic ejection murmur as a result of the right ventricular outflow obstruction. The systolic murmur may be confused or compounded by the holosystolic murmur from the VSD.
LABORATORY FINDINGS CBC, ABG analysis, pulse oximetry, and ECG should be performed. CBC may demonstrate polycythemia from long-standing cyanosis. An ABG analysis would demonstrate hypoxemia, with normal pH and pCO2. ECG most commonly shows right ventricular hypertrophy (right axis deviation >90 degrees, with R wave greater than S wave in the V1 lead) and possibly right atrial enlargement.
DIAGNOSIS Diagnosis is made on the basis of echocardiograph or cardiac catheterization. Tetralogy of Fallot should be suspected in any neonate, infant, or child with cyanosis accompanied by a heart murmur. Primary differential diagnoses include isolated VSD, PDA, aortic stenosis, pulmonary atresia, asthma, or pneumothorax.
RADIOGRAPHS Chest radiographs may show a “boot-shaped heart,” also described as “coeur en sabot” (Fig. 13-7). Right atrial enlargement or right aortic arch may also be present. Hilar areas and lung fields will be relatively clear due to decreased pulmonary blood flow. Echocardiography will demonstrate the VSD with a stenotic right ventricular outflow tract and overriding aorta (Fig. 13-8). Cardiac catheterization may eventually be necessary.
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Figure 13-7. Roentgenogram of an 8-year-old boy with the tetralogy of Fallot. Note the normal heart size, some elevation of the cardiac apex, concavity in the region of the main pulmonary artery, right-sided aortic arch, and diminished pulmonary vascularity. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 423.1-2 Copyright # 2004, Elsevier.)
TREATMENT After emergency actions, adequate hydration and supportive measures should be provided. Cardiology and surgical consults should be obtained. If tetralogy of Fallot is diagnosed, the patient will need referral to a center experienced in surgical treatment and repair. Palliative treatment consists of surgery to increase pulmonary blood flow and reduction of the right-to-left shunting. The Blalock-Taussig shunt is one procedure in which a shunt is created between the subclavian artery and the pulmonary artery. The Waterson shunt attaches the ascending aorta to the right pulmonary artery. The Potts shunt attaches the descending aorta to the left pulmonary artery. Definitive treatment, recommended for nearly every patient with tetralogy of Fallot, consists of closing the VSD with a Dacron patch and relieving the right ventricular outflow obstruction. Fewer than 3% of patients with tetralogy of Fallot will reach the age of 40 years without a surgical procedure, and 85% of patients who have
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Figure 13-8. Echocardiogram in a patient with the tetralogy of Fallot. This shortaxis, subxiphoid, two-dimensional echocardiographic projection demonstrates anterior/superior displacement of the outflow ventricular septum that resulted in stenosis of the subpulmonic right ventricular outflow tract and an associated anterior ventricular septal defect (VSD). RV, Right ventricle; AO, overriding aortic valve; LV, left ventricle. (From Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, Figure 423.1-3 Copyright 2004, Elsevier.)
surgical repair will survive to the age of 36. Complications from surgery can result, mainly in the form of atrial and ventricular tachyarrhythmias and decreased exercise tolerance. Rarely, postoperative shunt obstruction can occur and would present with worsening cyanosis and murmur. If this occurs, heparinization and thrombolytics should be considered and immediate surgical consultation should be sought.
Bibliography Congenital heart disease. Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Practice, ed 5. Mosby: St Louis, 2002. Cyanotic congenital heart lesions: Lesions associated with decreased pulmonary blood flow. In Behrman RE, Kliegman RM, Jenson HF (eds): Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Park MK: Pediatric Cardiology for Practitioners, ed 4. Mosby: St Louis, 2002. Wu W-C, Petropoulos P: Tetralogy of Fallot. In Ferri’s Clinical Advisor: Instant Diagnosis and Treatment. Mosby: St Louis, 2005.
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Seizures and Status Epilepticus STEVEN W. SALYER
ICD Code: Seizure 780.39, (See codes for specific seizure type.)
Key Points Up to 73% of first seizures are idiopathic. Idiopathic seizures recur in 17% of children within 20 months of the first seizure, and 26% of the children will have another seizure within 36 months. ! Emergency Actions ! If a child is actively seizing, then oxygen, dextrose, and anticonvulsant medications should be administered (see p. 787).
DEFINITION A seizure or convulsion is an episodic, paroxysmal disturbance in motor activity, behavior, sensation, or psychic or autonomic function. A seizure is a physiological abnormality that occurs suddenly with excessive electrical discharge or gray matter neurons and that propagates down the white matter neuronal processes and affects end organs. The International Classification of Epileptic Seizures is used to classify seizures types: A. Partial seizures (seizures beginning locally) 1. Partial seizures with elementary symptomatology (generally without impairment of consciousness) a. With motor symptoms (includes Jacksonian seizures) b. With special sensory or somatosensory symptoms c. With autonomic symptoms d. Compound forms 2. Partial seizures with complex symptomatology (generally with impairment of consciousness) a. With impairment of consciousness b. With cognitive symptomatology c. With affective symptomatology d. With “psychosensory” symptomatology e. With “psychomotor” symptomatology 3. Partial seizures secondarily generalized
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B. Generalized seizures (bilaterally symmetrical without local onset) 1. Absence (petit mal) 2. Bilateral massive epileptic myoclonus 3. Infantile spasms 4. Clonic seizures 5. Tonic seizures 6. Tonic-clonic seizures (grand mal) 7. Atonic seizures 8. Akinetic seizures C. Unclassified epileptic seizures Status epilepticus is seizure activity that lasts longer than 30 minutes and is repeated so often or is so prolonged that it creates a fixed and lasting epileptic condition. In a primary generalized grand mal status epilepticus, the seizure can be of a tonic-clonic, myoclonic, or clonic-tonic status. In secondary generalized convulsive status epilepticus, the seizure can be either tonic or tonic-clonic status with partial onset. Both primary and secondary status epilepticus can be continuous or noncontiguous. Status epilepticus can also present as a simple partial status, complex partial, or absence status seizures. Many toxic substances can cause seizures. Aspirin, lead, cocaine withdrawal, theophylline, anticholinergics (e.g., phenothiazine) or tricyclic overdose; carbon monoxide or propoxyphene ingestion; alcohol overuse; and withdrawal of seizure medication can all cause seizures. In children, the most common neoplasm is a glioma. The supratentorial lesion is most likely to cause seizures. Vascular intracranial hematoma, cerebral, subarachnoid, or extradural, can all cause seizures. Embolism, hypertensive encephalopathy, and transient ischemic attacks can also cause seizures in children. Degenerative and deficiency disorders such as Tay-Sachs disease, juvenile Huntington’s chorea, pyridoxine deficiency, and metachromatic leukodystrophy can all present as seizures.
EPIDEMIOLOGY Up to 73% of first seizures are idiopathic. Idiopathic seizures recur in 17% of children within 20 months of the first seizure, and 26% of the children will have another seizure within 36 months. There is an increased occurrence of a recurrence in children who have generalized spike waves evident on electroencephalography.
PATHOLOGY Seizures can have many etiologies. From birth to 6 months, hyperglycemia, hypoglycemia, trauma at birth, hypoxia, drugs, infections, hypocalcemia,
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hypernatremia, inborn error of metabolism, intracranial hemorrhage, pyridoxine deficiency, and illicit drug withdrawal resulting from use by the mother are the main causes of seizure activity. From 6 months to 3 years, febrile seizures, trauma, infection, toxic ingestion, metabolic disorders, cerebral degeneration disorders, and birth injury are the most common causes of seizures activity. In children older than 3 years, infection, trauma, cerebral degeneration, disease, and idiopathic problems are the most common causes of seizure activity. In a child with a fever, febrile seizure, meningitis, encephalitis, and intracranial abscess are the most common causes of seizures. Infectious diarrhea, such as with Shigella infection or pertussis, tetanus, or diphtheria-pertussis-tetanus immunizations can also cause fever and thus seizure activity. Endocrine causes such as phenylketonuria, uremia, and amino and organic acidemias can cause seizure activity. Hypoglycemia or hyperglycemia in any age group, DKA, or a new onset of diabetes can cause seizures. Hyponatremia or hypernatremia caused by the parents giving tap water while trying to hydrate a child who is experiencing vomiting and diarrhea can cause seizures and altered mental status. Infantile spasms occur between 3 and 9 months of age. The onset is sudden. The child will have a very brief spasm of flexion or extension of the head and trunk that lasts for seconds. Spasms will come in bursts of 5–20 spasms. The child will present with a history of regressive development, and mental retardation can be as high as 85%. Spasms will occur after a sudden auditory or physical stimulation or on awaking from sleep. Metabolic disorders, trauma, infection, and vitamin B6 deficiency have all been related to infantile spasms. The electroencephalography results will be abnormal.
CLINICAL PRESENTATION Different kinds of seizures will present with different symptoms. The key to diagnosis is to take a good history from the parent of from someone who witnessed the seizure. Absence (petit mal) seizures usually last only a few seconds. There are very brief lapses in awareness that are often associated with rhythmic eye blinking, head dropping, or just staring ahead. Absence seizures are often noted by the child’s teacher while in the classroom. Complex partial or psychomotor seizures are of two types: (1) temporal lobe seizures that impair consciousness and (2) those that are generalized. In complex partial seizures, there is usually an “aura” before the onset of the seizure. Hallucinations or an alteration in perception can occur. Patients who have partial seizures will have no loss of consciousness and can present in many ways. They may exhibit a Jacksonian march
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presentation. They can present with somatosensory symptoms, such as a different taste in the mouth or a severe headache. They can present with déjà vu, autonomic sweating, rhinorrhea, or flushing. Generalized seizures will present with specific movement patterns. Generalized seizures will present with specific movement patterns. Juvenile myoclonic epilepsy presents with early morning neck, head, and arm myoclonus tonic-clonic or absence of seizure activity. Benign rolandic epilepsy involves hemifacial seizures and a simple partial seizure. Onset occurs in persons aged 3–13 years, and it usually resolves by the age of 16 years.
EXAMINATION All children should be given a complete examination, including a complete neurological examination. Particular attention should be made to ensure that no evidence of trauma is present. Vital signs, including attention to fever, should be taken. The practitioner should look for asymmetry during in the examination and should ask about premature birth history, complications at the time of birth, perinatal asphyxia, or any family history or a history of siblings with seizures or febrile seizures.
DIAGNOSIS A diagnosis is made on the basis of history, physician examination, and ancillary data.
LABORATORY FINDINGS Upon presentation to the ED, a blood glucose determination must be made. A CBC with differential, urinalysis, and complete electrolyte panel of tests with special attention to sodium and potassium levels should be performed. If the child is febrile, a lumbar puncture should be performed to obtain samples for a Gram stain and culture. A blood culture should also be performed. If there is an abnormal neurological finding or a history of trauma, a CT scan of the head should be performed. Aspirin, acetaminophen, phenytoin, valproate, theophylline, lead, cocaine, and toxicological levels should be measured, as indicated.
TREATMENT If the child is actively seizing, oxygen, dextrose, and anticonvulsant medications should be administered. Metabolic abnormalities should be
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addressed as needed. Seizures occurring after trauma require an immediate CT scan of the head and a neurosurgical consultation. If meningitis or infectious etiology is suspected, antibiotics should be administered. If a child presents to the ED in status epilepticus, the following steps should be taken: 1. 2. 3. 4. 5.
6. 7. 8.
9. 10. 11.
Establish an airway and administer oxygen. Obtain IV access. Administer an IV bolus of 25% glucose, 2 ml/kg. Obtain blood samples for a CBC, calcium, electrolytes, blood cultures, BUN, and creatinine measurements. If the child is actively seizing, give the following: a. Diazepam 0.2 mg/kg with a maximum dose of 5 mg for infants up to 2 years of age, and 10 mg for infants over 2 years of age. The dose can be repeated three times. Give 1 mg/min and watch for respiratory depression. Doses of up to 2.6 mg/kg have been established as safe. Diazepam is the drug of choice in status grand mal seizures. Tonic-clonic generalized seizures respond very well to diazepam. Noncontinuous clonic or tonic-clonic seizures are refractory to diazepam, or b. Lorazepam 0.05 mg/kg IV, with a maximum dose of 0.2 mg/kg, can be repeated twice. Give over 2 minutes. Lorazepam has a slower onset of action and has a longer duration than does diazepam. If the child is still seizing after a trial of diazepam or lorazepam, give phenytoin 15 mg/kg at a rate of 25 mg/min. If the child is still in status epilepticus, give phenobarbital 10– 15 mg/kg IV slowly. If the child is still in status after lorazepam, diazepam, phenytoin, and phenobarbital are administered, give paraldehyde 0.3 ml/kg rectally mixed with mineral oil. Paraldehyde should only be administered using glass syringes and rubber tubing because of degradation in toxic formations caused by certain plastics. If the patient is still in status epilepticus, give IV lidocaine 2 mg/kg. Give clonazepam (Klonopin) via and nasogastric tube, 0.2–0.6 mg/ kg as a single dose. If the child is still in status epilepticus, consult an anesthesiologist to administer general anesthesia.
The treatment for infantile spasms is early diagnosis and aggressive treatment with adrenocorticotropic hormone. These children should be admitted to the hospital and should have a pediatric neurologist called in for consultation. Juvenile myoclonic epilepsy is treated with valproate with good results. Benign rolandic epilepsy is treated with phenytoin or carbamazepine. Absence seizures are treated with valproate or ethosuximide.
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Adverse Effects of Seizure Medications Phenytoin has a narrow serum level concentration. Toxicity occurs above 25 mg/ml. Nausea, diplopia, dysarthria, and impaired level of consciousness can occur. Ataxia and lethargy can occur. When phenytoin is given via IV, there can be burning of the limb at the IV site. Chronic phenytoin use can cause folate deficiency, peripheral neuropathy, lupus-like syndrome, myasthenic weakness, and macrocytic anemia. Phenytoin levels are reduced when used with valproic acid. Valproic acid (Depakene) can cause hepatic failure, vomiting, behavioral changes, and increased lethargy. Gastrointestinal side affects are common. Pancreatitis has also been reported. The use of the antibiotic erythromycin with theophylline and carbamazepines can cause a toxic rise in the levels of these medications. Clonazepam and diazepam can cause bladder dysfunction. Choreic movements can occur after use of ethosuximide or carbamazepines. These movements can be relieved by the use of diphenhydramine. If the child is already on anticonvulsive medication and the child has a “breakthrough seizure” because of noncompliance in taking medication, viral or bacterial infections, change in sleep habits, new job, emotional stress, or use of alcohol or illicit drugs, the practitioner should assume that the anticonvulsant level is low. The patient should be given a partial loading dose of the current medications. If the patient is compliant and this fact is verified by the parent, the child should be given his or her daily dose of phenobarbital or phenytoin. If the patient is noncompliant or if blood levels are low, a dose that is twice the normal daily dose should be administered. The normal daily dose should be given if the child seizes, and the second dose should be repeated no matter what the serum level is. Children are usually prescribed anticonvulsant medication for 2 years. If, after this time, the child has been seizure free, an attempt is made to discontinue the medication.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Febrile Seizures REENIE LOPEZ
ICD Code: Febrile seizure 780.31
Key Points Simple febrile seizures are those that last less than 15 minutes, have no focal features, and occur once during a 24-hour period.Febrile seizures lasting longer than 15 minutes, having focal features,or reoccurring within 24 hours are considered complex. ! Emergency Actions ! In the emergency care setting, evaluation and stabilization of the patient’s airway remains the top priority, followed by termination of ongoing seizure activity, stabilization of vitals signs, and prevention of recurrent seizures.
DEFINITION Febrile seizures occur in a febrile child who does not have a defined cause such as an intracranial infection or severe metabolic disturbance; these seizures are classified as either simple or complex. Simple febrile seizures are those that last less than 15 minutes, have no focal features, and occur once during a 24-hour period. Febrile seizures lasting longer than 15 minutes, having focal features, or reoccurring within 24 hours are considered complex. The most common type of seizure is a generalized tonic-clonic. Other types of seizure posturing include staring with stiffness, limpness, or jerking movements without preceding stiffness.
EPIDEMIOLOGY Fever is the most common cause of childhood seizures, with a frequency of 2%–5% and an onset usually between the ages of 3 months and 5 years. Children are considered to be at high risk for the development of febrile seizures if there is a positive family history within the immediate family, a history of delayed development, or male gender.
PATHOLOGY Infections, such as upper respiratory tract, urinary tract, viral, or involving endotoxins such as Shigella or Salmonella species are common causes of
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febrile seizures. Less common but also possible causes include meningitis, encephalitis, and drug exposure or withdrawal.
CLINICAL PRESENTATION Usually, a patient with febrile seizure is no longer seizing at the time of presentation to the ED. The child may still be postictal if the seizure occurred within the past 30 minutes on arrival to the ED.
EXAMINATION The examiner should first look at the child. Does the child appear irritable or lethargic? Has the child returned to his or her baseline level, according to the parents? Does he or she interact with the examiner? Does the child look sick? If the patient appears to be ill or has a prolonged postictal period, a more complete workup is indicated than if the child has returned to baseline status and appears well.
LABORATORY FINDINGS A basic chemistry panel including magnesium and phosphorous measurements should be performed to check for an underlying electrolyte abnormality and renal function. A urinalysis may be done to check for infection or, in the case of a hypoglycemic child, ketones. If the child was seizing on arrival to the ED and did not respond to benzodiazepines, an ABG analysis may be done to evaluate a potential underlying metabolic or hypoxic process. CBC, blood culture, and lumbar punctures may also be done.
RADIOGRAPHS The imaging indicated is dependent on the history provided. A CT scan of the brain is indicated if there is a history of trauma or focal neurological deficits or if the child has a prolonged postictal period. Chest radiography may be done if there is a history of antecedent respiratory symptoms.
TREATMENT In the emergency care setting, evaluation and stabilization of the patient’s airway remain the top priority, followed by termination of ongoing seizure activity, stabilization of vitals signs, and prevention of recurrent seizures.
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During a seizure, while supporting the airway and preparing for intubation, the healthcare provider should administer oxygen, obtain IV access, monitor the vital signs and cardiac function, and get a bedside glucose level measurement. The type of activity including focal movements, direction of gaze and nystagmus, and any alteration in autonomic function should be noted. A first-line anticonvulsant agent should be administered IV—specifically, a benzodiazepine. Lorazepam (Ativan) is preferred over diazepam (Valium) because it has a longer duration, is less likely to cause respiratory depression, and allows for a second dose to be administered after 5 minutes, if needed. The usual dose is 0.05–0.1 mg/kg given slowly via IV over 2 minutes, IO, per rectum, or intrabuccally. The maximum dose is 1–2 mg. IM administration of lorazepam is not recommended because erratic absorption may occur. All patients should be given acetaminophen (15 mg/kg PO or per rectum every 4 hours) or ibuprofen (10 mg/kg PO every 6 hours). After a seizure, providers must obtain a thorough history, including past medical and developmental history, recent illness, and description of the seizure. Alternate etiologies of the seizure should be explored, including hypoglycemia, hypoxia, electrolyte abnormality, or drug ingestion. In the pediatric population, head trauma must also be considered. Meningitis must be ruled out. In younger children, meningitis may present without the typical signs found in older children (such as stiff neck, headaches, or Brudzinski and Kernig’s signs). Consequently, a lumbar puncture must be performed on children younger than 12 months of age if no other identifiable source of fever has been identified. Despite the frequency of the occurrence of febrile seizures, there is no unanimity about therapeutic interventions. Antibiotic and antiviral agents must be considered and tailored to the individual patient. Acute treatment with antipyretic drugs with continued scheduled dosing over the next 24 hours is a generally accepted practice and is usually sufficient to prevent recurrences. It is also important to provide reassurance to parents, who often believe their child is dying during the seizure or will suffer “brain damage” from having had a seizure, when in fact the intelligence and behavior of children with febrile seizures is the same as their unaffected siblings. A patient who has an unusually severe seizure or who required intubation merits a neurological consultation for recommendations regarding treatment with an antiepileptic drug. Indications for admission include status epilepticus, CNS infection, failure to return to baseline status after 2 hours, recurrent seizures, structural lesions, or evidence of increased ICP. A patient who has returned to baseline status may be discharged with instructions to the parents to continue the administration of antipyretic drugs (acetaminophen 15 mg/kg every 4 hours and/or ibuprofen 10 mg/kg every 6 hours) and seek follow-up with their pediatrician within 24 hours. Parents should be instructed to return to the ED if the seizures reoccur and last longer than 15 minutes, if more than three
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seizures occur within 24 hours, if the fever is unrelieved by antipyretic drugs, or if any neurological abnormality occurs.
Bibliography Barata I: Pediatric seizures, Crit Decis Emerg Med 2005;19(6):1–10. Crain EF, Gershel JC:Clin Man Emerg Pediatr 2003;16:470–476. Gordon KE, Dooley JM, Camfield PR, et al: Treatment of febrile seizures: The influence of treatment efficacy and side-effect profile on value to parents, Pediatrics 2001;108 (5):1080–1088. Shneker BF, Fountain NB: Epilepsy, Dis Mon 2003;49(7):426–478.
Kawasaki Disease DAVID W. KUHNS AND JACQUELYN L. SIMONDS
ICD Code: 446.1
Key Points Kawasaki disease should be in the differential diagnosis for any child with a temperature that is higher than 104 F for longer than 5 days, nonpurulent bilateral conjunctivitis, oral mucosal involvement, soft tissue abnormalities of the hands and feet, polymorphous, nonvesicular rash, and cervical adenopathy. ! Emergency Actions Kawasaki disease.
!
No emergency actions are warranted for
DEFINITION Kawasaki disease, first described in 1967 as mucocutaneous lymph node syndrome, causes a vasculitis with fever higher than 104 F for more than 5 days. Although it is usually a self-limiting syndrome, coronary artery involvement can be associated with significant mortality. The disease has three phases, (1) the acute phase, with a febrile illness lasting 7–10
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days, (2) the subacute phase, lasting 10–14 days, and (3) the convalescent phase, lasting 6–8 weeks. The syndrome generally presents in the subacute phase with cardiovascular disease, desquamation, and anorexia. The morbidity and mortality of Kawasaki syndrome (1%–2%) is associated with the development of coronary artery aneurysms, which are generally asymptomatic at the time of formation. Smaller aneurysms resolve on their own 60% of the time. Coronary events may occur many years after the febrile illness. Seventy percent of the deaths will occur within 15–45 days of the onset of fever and usually occur during the subacute and convalescent phases.
ETIOLOGY The etiology is suspected to be infectious in nature. Most of the pathology is caused by a medium-vessel arterial vasculitis.
EPIDEMIOLOGY Kawasaki syndrome affects boys at a ratio of 1.5:1 over girls and occurs in the late winter and early spring. The peak ages for Kawasaki disease are between 18 and 24 months. It is a multisystem illness that generally affects children younger than 5 years. It can, on rare occasions, affect adults. It is most common in persons of Asian descent, intermediate among persons of African descent, and lowest among whites. It is more common in persons from the middle to upper-middle socioeconomic classes.
CLINICAL PRESENTATION The clinical features of Kawasaki disease are dependent on which stage the patient is seen. The acute phase (days 1–11) is characterized by temperature higher than 104 F with irritability, nonexudative bilateral conjunctivitis (90%), lymphadenopathy (75%) (generally a single enlarged node of about 1.5 cm), anterior uveitis (70%), perianal erythema (70%), strawberry tongue, and fissured lips, with acral erythema and edema that impede ambulation. Myocarditis, pericarditis, and hepatic, renal, and gastrointestinal dysfunction can occur. The subacute stage (days 11–30) can lead to persistent irritability, anorexia, and conjunctival injection. The temperature generally falls during this stage to near normal levels. Acral desquamation may occur. The convalescent phase can be characterized by aneurysm expansion and possible myocardial infarction. Kawasaki syndrome can also cause aseptic (lymphocytic) meningitis, obstructive jaundice, distention of the gallbladder with serous fluid, uveitis,
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urethritis, and diarrhea. High spiking fevers may persist for 1–2 weeks, if left untreated.
DIAGNOSIS The following are diagnostic criteria for Kawasaki disease: Persistent fever lasting longer than 5 days, with temperature higher than 104 F (40 C) plus four of the following five criteria: 1. Nonpurulent bilateral conjunctivitis 2. Oral mucosal involvement (e.g., erythematous pharynx, red or fissured lips, strawberry tongue) 3. Soft tissue abnormalities of the hands and feet (e.g., edema/erythema, desquamation) 4. Polymorphous, nonvesicular rash 5. Cervical adenopathy
LABORATORY FINDINGS The WBC count is generally elevated to greater than 20,000 cells/mm3, with a neutrophil predominance. The hematocrit level is generally low. The ESR will be greater than 55 mm/hr, and platelet levels are often higher than 1 million/mm3. A urinalysis will often show sterile pyuria from urethral origin and proteinuria. Serum alanine aminotransferase levels will often be elevated. An ECG is often not helpful in making the diagnosis, but a baseline ECG is recommended to be compared with others 2 and 6 weeks later. Echocardiography may be helpful 7–12 days after the onset of the illness to detect aneurysms.
TREATMENT Treatment should proceed as follows: 1. IV gamma globulin at a dose of 2 g/kg as a single dose over 12 hours. Alternatively, a 4-day regimen of 400 mg/kg/dose over 2 hours can be given. Gamma globulin before day 10 of the illness reduces the incidence of coronary artery aneurysms from 20%–25% to fewer than 5%–10%. 2. Aspirin is recommended to decrease platelet aggregation and to decrease the risk of coronary artery thrombosis. It is given at a dose of 25 mg/kg every 6 hours for 14 days, then 3–5 mg/kg/day for 2–3 months through the convalescent phase. The high doses are needed due to poor absorption. 3. Steroids are not given in the treatment of Kawasaki syndrome, and some authorities believe their use is contraindicated. They may be
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used, however, in resistant cases where the patient’s illness does not respond to IV gamma globulin and aspirin within several days. 4. Antibiotics are not helpful. 5. Patients are admitted to the hospital while receiving IV gamma globulin and until their fever subsides.
Bibliography Barron KS, Shulman ST, Rowley A, et al: Report of the National Institutes of Health workshop on Kawasaki disease, J Rheumatol 1999;26:170–190. Dajani AS, Taubert KA, Gerber MA, et al: Diagnosis and management of Kawasaki disease in children, Circulation 1993;87:1776–1780. Dajani AS, Taubert KA, Takahashi M, et al: Guidelines for long-term management of patients with Kawasaki disease: Report from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association, Circulation 1994;89:916–922. Kato H (ed): Kawasaki Disease: Proceedings of the 5th International Kawasaki Disease Symposium, Fukuoka, Japan. Elsevier: Amsterdam, 1995. Shulman ST, Rowley AH: Etiology and pathogenesis of Kawasaki disease, Prog Pediatr Cardiol 1997;6:187–192. Taubert KA, Shulman ST: Kawasaki disease, Am Fam Phys 1999;57:3093–3102.
Reye’s Syndrome JOHN ROBERT SCOTT
ICD Code: Reye’s syndrome 331.81
Key Points Reye’s syndrome is a poorly understood phenomenon involving a viral syndrome and salicylate use in genetically predisposed children. The age range at onset is 4^11 years. The mortality rate is 30%^35%. The syndrome is marked by severe, refractory vomiting that progresses to coma. Seizures are treated with benzodiazepines and phenytoin. Coagulation abnormalities are treated with fresh frozen plasma and vitamin K. Elevated ICP is treated with mannitol, hyperventilation, and ultimately ET intubation and pentobarbital-induced coma, if necessary. ! Emergency Actions ! All patients with Reye’s syndrome who have a Glasgow Coma Scale score of 8 or less should be intubated.
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EPIDEMIOLOGY Reye’s syndrome was first described in 1963 and is poorly understood. Reye’s syndrome is defined by the Centers for Disease Control and Prevention as an acute, noninflammatory encephalopathy associated with altered levels of consciousness and liver dysfunction. Reye’s syndrome occurs in all ages, seasons, and geographical locations, but it usually affects young children. The average age at onset is 7 years, and the age range is 4–11 years. Fewer than 10% of cases occur in children younger than 1 year old. It often follows a viral syndrome. The use of aspirin or salicylates has been implicated as a precipitating factor in Reye’s syndrome. Epidemiological studies strongly associate three virus infections (i.e., influenza B, influenza A, and varicella-zoster) with Reye’s syndrome, although the mechanism of their involvement with the pathogenesis of the condition is unclear. Overall, the mortality currently is 30%–35%. Often, in survivors, hepatic function returns to normal but neurological sequelae remain. Even among children believed to have full recovery, 34% had measurable deficits in school achievement, visuomotor integration, sequencing, and problem solving.
PATHOLOGY Metabolic disorders, genetic predisposition, and the interaction between toxins and viruses have all been proposed as causes of Reye’s syndrome. A Reye-like syndrome is encountered in children with genetic defects of fatty acid oxidation. A growing body of evidence suggests that Reye’s syndrome may be a multiorgan disease due to diffuse mitochondrial injury of unknown origin. The liver will have microvesicular lipid accumulation without evidence of inflammation or necrosis. These microvesicular lipid accumulations may occur in the skeletal muscle, kidneys, and myocardium. The brain will have ultrastructural abnormalities and cerebral edema. Encephalopathy may occur despite normal or declining ammonia levels.
CLINICAL PRESENTATION AND EXAMINATION The patient will present with refractory nausea and vomiting and altered mental status. Soon after the vomiting starts, the encephalopathic phase occurs. Behavioral changes, delirium, combativeness, disorientation, and hallucinations will occur. Finally, coma will ensue. The five stages that occur are as follows:
Stage 0: Alert and awake Stage 1: Lethargic, follows commands
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Stage 2: Combativeness and inappropriate verbalization, stupor, and conjugate gaze deviation on doll’s eye maneuver Stage 3: Decorticate (flexor) posturing and coma Stage 4: Decerebrate (extensor) posturing and coma Stage 5: Flaccid paralysis, coma, minimal or absent brainstem reflexes
Pancreatitis and hepatitis may be present at any stage. Respiratory failure, cardiac dysrhythmias, and cerebral herniation are common causes of death in children.
DIAGNOSIS Reye’s syndrome is a diagnosis of exclusion. Infection, trauma, metabolic problems, and electrolyte abnormalities must be ruled out. A liver biopsy may demonstrate characteristic changes of Reye’s syndrome.
LABORATORY FINDINGS Regarding blood tests, the liver function tests and the ammonia level are often the most helpful. The aspartate transaminase and alanine aminotransferase are universally elevated to three times the normal level. The ammonia level is usually 1.5–3 times the normal level. Bilirubin levels can be normal or elevated. The international normalized ratio (INR) and PT can also be normal or elevated. Measuring the salicylate and acetaminophen levels is usually not helpful. To meet the diagnosis of Reye’s syndrome, the CSF must have less than 8 WBC/mm3.
IMAGING FINDINGS A CT scan of the head may reveal cerebral edema and is indicated to rule out other causes of altered mental status. A chest x-ray should be performed to rule out concurrent pneumonia.
TREATMENT Generally, the treatment of Reye’s syndrome consists of aggressive supportive care. Seizures may be treated with benzodiazepines, phenytoin, or both in the usual fashion. If the INR and PT are elevated, administer fresh flood frozen plasma and vitamin K as needed. As the patient’s mental status declines and ICP increases, intracranial monitoring may be needed in consultation with a neurosurgeon. The ICP should be kept between 15 and 18 mmHg. Treatment of elevated ICP may include using mannitol 0.25–1 g/kg/dose IV and gentle hyperventilation to
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achieve a pCO2 of 30–35 mmHg. For persistently elevated ICP, the patient should be intubated and a pentobarbital coma should be induced.
Bibliography Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004, p 2027. Centers for Disease Control and Prevention, Reye syndrome surveillance—United States, 1989, MMWR Morb Mortal Wkly Rep 1991;40:88–89. Cohen J, Powderly WG: Infectious Diseases, ed 2. Elsevier: St Louis, 2004, pp 310–311. Euerle B: Reye syndrome. In Barkin RM, Rosen P, Hayden SR, et al: Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Philadelphia: Lippincott, Williams & Wilkins, 2003. Goetz CG: Textbook of Clinical Neurology, ed 2. Elsevier: Philadelphia, 2003, p 656. Kotagal S, Rolfe U, Schwartz KB, Escober W: Locked-in state following Reye’s syndrome, Ann Neurol 1984;15:599–601. Van Coster RN, DeVivo DC, Blake D, et al: Adult Reye’s syndrome: A review with new evidence for a generalized defect in intramitochondrial enzyme processing, Neurology 1991;41:1815–1821.
Otitis Media DANIEL F. MCBRIDE
ICD Code: Otitis 382.9
Key Points Otitis media is an inflammatory process of the middle ear that may be caused by bacterial or viral infection. ! Emergency Action ! Patients presenting with otalgia, otorrhea, or high fever must be evaluated with an expanded differential diagnosis in mind. Pediatric patients with temperature higher than 100.4 F should be assessed following pediatric fever protocols. The history, physical examination, and clinical presentation will guide providers regarding which resuscitative measures may be required.
DEFINITION Otitis media is an inflammatory process of the middle ear that may be caused by bacterial or viral infection. This clinical entity may be subdivided
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into three distinct variants: acute otitis media (AOM), otitis media with effusion (OME), and chronic otitis media (COM). The following definitions are provided to clarify the terminology associated with otitis media.
Middle ear effusion (MEE): The presence of any fluid within the middle ear Myringitis: Erythema of the tympanic membrane (TM) without MEE usually due to fever, crying, viral infection, or early bacterial infections AOM: MEE with rapid onset of one or more of the following: ear pain, fever, ear tugging, otorrhea, anorexia, vomiting, or diarrhea OME: MEE without signs or symptoms of AOM; occurs in both healthy children and also expected to be present after AOM with effusion Chronic OME: Implies an effusion is present for longer than 2–3 months Recurrent AOM: At least three episodes of AOM in the past 6 months, or four episodes in the past 12 months; affects 15%–30% of children; MEE may persist between episodes
EPIDEMIOLOGY Otitis media is the second most common disease of childhood and the most common reason for children to visit the doctor’s office. It is so common that more than one third of children will experience an episode of AOM by the age of 7 years. In addition, it is also the most common diagnosis made in children younger than 15 years old and is commonly seen in the pediatric ED population. Major risk factors for developing otitis media include male sex, day care attendance, parental smoking, a family history of otitis media, Down syndrome, and immunocompromise while breast-feeding may be protective against otitis media.
ETIOLOGY Otitis media may be caused by bacterial or viral infection in association with predisposing eustachian tube dysfunction (ETD). ETD may occur as a result of mucosal edema, neoplasm, or negative intratympanic pressures that disrupt normal host defense mechanisms. Recurrent upper respiratory tract infections may predispose patients to ETD and increase the risk of otitis media. S. pneumoniae, nontypable H. influenzae, and M. catarrhalis are common bacterial pathogens in AOM, and RSV is the most commonly associated viral pathogen. Approximately one third of effusions in OME are sterile.
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CLINICAL PRESENTATION AOM, otherwise known as acute suppurative or purulent otitis media, has a rapid onset of symptoms, including fever, otalgia, otorrhea, anorexia, irritability, vomiting, diarrhea, and decreased TM mobility with pneumatic otoscopy. Other symptoms of a viral upper respiratory tract infection, such as cough and rhinorrhea, often precede or accompany AOM. Although debatable, it is recommended that providers search for another bacterial source of fever for higher temperatures (>103 –104 F), since AOM is unlikely to cause hyperpyrexia.
EXAMINATION Otoscopic examination often shows bulging and erythema of the TM. An MEE is also commonly observed, giving the TM a dull gray or yellow appearance. If the external auditory canal is obstructed with cerumen, attempts at removal with an ear curette or irrigation with 3% hydrogen peroxide may be made. Signs of an effusion may be present in air-fluid levels, bubbles, color change, or opacification. Decreased TM mobility has been found to be the most sensitive indicator of an effusion.
LABORATORY FINDINGS Laboratory evaluation for uncomplicated otitis media is not generally necessary. Children with fever, however, may require further evaluation for occult bacteremia. Cultures of MEE may be taken to assist with antibiotic selection in cases of COM or ruptured TM or in patients with tympanic tubes. Tympanocentesis is not a commonplace ED procedure, and if cultures are required a consultation with an otorhinolaryngologist should be sought.
DIAGNOSIS The diagnosis of otitis media is made clinically on the basis of history and physical examination findings and by direct visualization of the TM.
TREATMENT The initiation of antibiotic treatment for otitis media is controversial; however, it is the most common childhood diagnosis resulting in antibiotic administration. Outpatient versus inpatient treatment depends on the patient’s age, the presence of fever, and the clinical presentation. Children younger than 2 months old with fever should be admitted for further
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evaluation and inpatient treatment. Infants who are 30- to 90-day-old and nonimmunized infants require a more in-depth workup to search for potentially serious bacterial illnesses including sepsis, meningitis, and occult bacteremia. The 2004 American Academy of Pediatrics/American Academy of Family Physicians’ Clinical Practice Guidelines on Acute Otitis Media recommends treating patients with antibiotics when they are younger than 2 years of age with a certain diagnosis of AOM, under the age of 6 months if the diagnosis is uncertain, or of any age if severe symptoms (e.g., temperature >102.2 F or severe otalgia) are present. Initial observation may be used for children with mild AOM if they are older than 2 years or between ages of 6 months and 2 years when the diagnosis is uncertain. Observed patients require reevaluation within 2–3 days after initial evaluation in the ED, and if their symptoms persist or worsen, then antibiotics should be prescribed. This initial observation has not been shown to lead to an increase in complication rates in previous studies. The selective use of antibiotics is controversial because of increasing antimicrobial resistance and low therapeutic value. Antibiotics provide a relatively small benefit for AOM in most children because the majority of cases will resolve spontaneously. Any benefit derived from antibiotic use must be weighed against possible adverse reactions. Antibiotic treatment may play an important role in reducing the risk of mastoiditis and preventing suppurative complications and is the only reason to administer antibiotics. Nevertheless, this treatment has also been questioned, as the rates of mastoiditis are similar in countries that do not routinely treat AOM with antibiotics. Antibacterial treatment may be deferred for selected children for 48– 72 hours while management is limited to the relief of symptoms. The decision whether to observe or treat is based on the child’s age, diagnostic certainty, and illness severity. Trials of antibiotic treatment in AOM over the past 30 years have consistently shown that most children do well without antibacterial therapy. Between 7 and 20 cases must be treated to allow one child to benefit. Symptoms resolve in the majority of children after 24 hours regardless of whether they are treated. Approximately 75% of children will have a complete resolution of symptoms within 1 week. The recommended initial antibiotic choice for AOM is amoxicillin, 80–90 mg/kg/day divided into two daily doses. Ceftriaxone at 50 mg/ kg per day, IV or IM, may be given for 3 days in children with vomiting, although a one-time dose of ceftriaxone is nearly 90% effective in treating AOM. If there is no improvement in the clinical condition after 48–72 hours, untreated patients should receive a course of antibiotics, and treated patients should have the antibiotic changed.
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The complications of AOM include mastoiditis, meningitis, brain abscess, facial nerve paralysis, ETD, TM retraction, permanent hearing loss, ossicular erosion, or retraction pocket formation. Children with recurrent AOM that is not responding to antibiotic treatment or those with complications should be referred to an otorhinolaryngologist for further management.
Bibliography American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media: Diagnosis and management of acute otitis media, Pediatrics 2004;114(3):898–899. Glasziou PP, Del Mar CB, Sanders SL, Hayem M: Antibiotics for acute otitis media in children, Cochrane Database Syst Rev 2004;1CD00219. Karma PH, Penttila MA, Sipilia MM, et al: Otoscopic diagnosis of middle ear effusion in acute and nonacute otitis media: The value of different otoscopic findings, Int J Pediatr Otorhinolaryngol 1989;17:37. Muhammad W, Muhammad A, Jones M, et al: Otitis media. Emedicine. 2007. Available at: http://www.emedicine.com. Accessed on April 9, 2005. Rosenfeld RM: Clinical efficacy of antimicrobial drugs for acute otitis media: meta-analysis of 5400 children from thirty-three randomized trials, J Pediatr 1994;124(3):355–367. Ruuskanen O, Heikkinen T: Otitis media: Etiology and diagnosis, Pediatr Infect Dis J 1994;13:S23. Stool SE, Berg AO, Berman S, et al: Managing otitis media with effusion in young children: Quick reference guide for clinicians, AHCPR Pub 94–0623, Agency for Health Care Policy and Research, Public Health Service, US Dept of Health and Human Services: Rockville, MD, 1994.
Pharyngotonsillitis MELISSA KAGARISE
ICD Code: Pharyngotonsillitis 465.8
Key Points The most common etiology of sore throat is viral. The peak incidence of group A beta-hemolytic Streptococcus (GABHS) infection is seen in children between the ages of 5 and 11 years and is unlikely in children younger than 3 years of age.
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! Emergency Actions ! GABHS must be identified and treated. It can cause nonsuppurative complications such as rheumatic fever and glomerulonephritis.
DEFINITION Sore throat is one of the most common symptoms in the pediatric population. An infectious cause for the sore throat is most often seen. Pharyngotonsillitis is the inflammation of the pharynx and tonsils as a result of infection with viral or bacterial organisms. The most common etiology of sore throat is viral. Viral agents associated with pharyngitis include adenovirus, Epstein-Barr virus, parainfluenza, enteroviruses, and herpes simplex virus (HSV). GABHS is the most frequent bacterial cause of pharyngitis, accounting for 15%–30% of cases. Other less common bacterial agents associated with pharyngitis include group C or G streptococci, Arcanobacterium hemolyticum, Corynebacterium diphtheriae, Francisella tularensis, M. pneumoniae, and Neisseria gonorrhoeae. Identifying the cause of pharyngitis is important to prevent complications associated with GABHS infection. Left untreated, GABHS can cause nonsuppurative complications such as rheumatic fever and glomerulonephritis. Suppurative complications, including cervical adenitis, otitis media, cellulitis, peritonsillar abscess, and septicemia, may also develop.
EPIDEMIOLOGY Pharyngitis occurs more frequently during the colder months of the year, most commonly late winter and early spring. The peak incidence of GABHS infection is seen in children between the ages of 5 and 11 years and is unlikely in children younger than 3 years of age. Viral etiology should be suspected in children aged 3 years and younger. Transmission occurs mostly through hand contact with nasal discharge. The incubation period is 24–72 hours.
CLINICAL PRESENTATION Integrating information from the history as well as physical examination findings will help the clinician determine the etiology of pharyngitis and allow for the most appropriate treatment to prevent complications. A history of streptococcal exposure at home or school will increase the suspicion of infection with GABHS. Symptoms will include an acute onset of sore throat and fever as well as the presence of a headache and gastrointestinal symptoms.
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Symptoms of rhinorrhea, cough, conjunctivitis, and hoarseness, which have developed gradually, indicate a viral cause of the pharyngitis.
PHYSICAL EXAMINATION Patients suspected of having GABHS infection will have physical examination findings of pharyngeal erythema, tonsillar edema and exudates, and lymphadenopathy of the anterior cervical chain. Petechiae of the soft palate or a scarlatiniform rash, if present, are highly indicative of infection with GABHS.
LABORATORY FINDINGS The current “gold standard” for laboratory diagnosis is a throat culture. Studies have shown a 97% sensitivity and 99% specificity for GABHS. Incubation of throat cultures takes 24–48 hours. With a specificity of 98%–100%, the rapid streptococcal antigen detection tests are being used to initiate treatment earlier than are cultures. Although this text is highly specific, the sensitivity can range from 50% to 90%. In a patient with a positive rapid test result, the initiation of treatment should be started without the need to confirm the diagnosis with a throat culture. If a patient has signs and symptoms indicative of GABHS infection and a rapid test result is negative, then a culture can be done to verify presence or absence of infection.
DIAGNOSIS Determination of viral versus bacterial pharyngitis is based on a history of exposure, symptomatology, physical examination findings, and laboratory results. The goal in diagnosing pharyngitis is to identify GABHS in order to treat promptly and avoid complications.
TREATMENT Symptomatic therapies can be instituted in cases of pharyngitis. These include acetaminophen or ibuprofen to relieve fever and sore throat pain, warm salt-water gargles, and throat lozenges or sprays. A positive rapid streptococcal antigen detection test or throat culture result indicates the need for antibiotic treatment. Antibiotic treatment may also be initiated for patients pending culture results when a high index of suspicion exists for infection with GABHS. Goals of treatment for GABHS infection include obtaining a bacteriological cure, preventing nonsuppurative and suppurative complications, hastening clinical recovery by 1–2 days, and reducing the risk of transmission.
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The treatment of choice remains penicillin V (250–500 mg bid for 10 days). Amoxicillin suspension may be substituted at the same dose for patients unable to swallow pills. When compliance with dosing regimen is a concern, ED clinicians can administer penicillin G benzathine IM. Patients weighing 27 kg or less should receive 600,000 units of penicillin G benzathine IM, whereas patients weighing more than 27 kg should receive 1.2 million units. Penicillin-allergic patients should be given erythromycin 40–50 mg/kg/day in two to four divided doses for 10 days. Cephalosporins are an alternative treatment to penicillins. Tetracyclines and sulfonamides should not be used because of the increased risk of resistance.
Bibliography Behrman RE, Kliegman RM, Jenson HF: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Dershewitz RA: Ambulatory Pediatric Care, ed 3. Lippincott-Raven: Baltimore, 1999. Hay WW, Levin MJ, Sondheimer JM, Dterding RR: Current Pediatric Diagnosis and Treatment, ed 17. McGraw Hill: New York, 2005. Rudolph AM, Kamei RK, Overby KJ: Rudolph’s Fundamentals of Pediatrics, ed 3. McGraw Hill: New York, 2002. Schwartz WM: (2000) The 5-Minute Pediatric Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2000. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Vincent MT, Celestin N, Hussain AN Pharyngitis, Am Fam Phys 69(6):1465–1470. Available at:http://www.mdconsult.com. Accessed on June 13, 2005.
Pediatric Analgesia and Sedation ROY JOHNSON III AND LINDA L. LAWRENCE
CPT Codes: Sedation with or without analgesia; IV, IM, or inhaled 99141, Sedation with or without analgesia; PO, per rectum, or intranasal 99142 DEFINITION Appropriate and effective pediatric analgesia and sedation are critical to high-quality ED care. Clear evidence indicates that adequate pain control in the ED setting has been lacking in children. The literature indicates a
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myriad of reasons for pediatric patients not receiving appropriate analgesia including a fear of oversedating the patient, an underestimation of patient needs, and an overall lack of experience and training in pediatric sedation and analgesia. Among these are the ideas that children do not perceive pain at the same level as an adult and the concern of altering physical examination findings, thus leading to a missed diagnosis. The data suggest that both of these are incorrect. There is a growing body of information showing the long-term adverse clinical sequelae of inadequate pediatric pain management. The Joint Commission on Accreditation of Healthcare Organizations has made this an area of intense review. Actively managing pain and anxiety will likely improve the quality of care and patient satisfaction by minimizing patient suffering and facilitating diagnostic and therapeutic procedures. Effective historical and physical assessment of the patient is crucial to safe and efficacious anxiolysis, analgesia, and sedation. Particular attention should be paid to presenting pain level and injuries, respiratory state, current health, recent food intake, and past medical history. It should be kept in mind when evaluating a child’s pain that it is by definition subjective and, the literature shows, often underestimated. The nature and type of injury will also factor in to the type of analgesia and sedation selected. The most serious complication of analgesia and sedation is cardiorespiratory arrest; therefore, careful evaluation of the patient’s respiratory status at presentation is required. Consider any conditions of the current state of health that could affect safe analgesia such as medications or underlying medical conditions, especially respiratory disorders. The timing, amount, and content of the last oral intake must be considered when assessing candidacy. The past medical history obtained should focus on information that could affect analgesia and sedation such as reactive airway disease or adverse reaction to previous sedation. There are no specific prerequisite diagnostic or laboratory tests routinely required. In making decisions related to pediatric analgesia and sedation, one should always be aware of the institutional policies. Recent food intake is not in and of itself a contraindication to procedural sedation. There is no uniform standard for fasting before sedation. No pharmacological agents have been shown to decrease the risk of aspiration for patients who have not fasted, including antacids. Although events of pulmonary aspiration are rare, timing of the last meal must be weighed when considering type and depth of sedation. The depth and level of analgesia and sedation will dictate the required support equipment and type of monitoring. The worst case scenarios of respiratory and cardiopulmonary arrest, airway compromise, allergic reactions, and severe medication adverse effects must be properly anticipated. Appropriate supplies would include, but not necessarily be limited to, advanced life support medication and equipment, oxygen, and reversal
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agents. An IV catheter should be considered in all procedural sedation cases and definitely maintained if this is the route used to deliver the sedatives and analgesics. Monitoring is crucial to maintain the safety and effectiveness of sedation in a pediatric patient. This monitoring must include visual assessment and observation by at least one dedicated person who is trained to recognize sedation complications. Specific components of monitoring are level of consciousness and mental status, respiratory rate, heart rate, blood pressure, oxygen saturation, exhaled carbon dioxide, and cardiac monitoring. Vital signs should be monitored and recorded before, during, and after sedation. Pulse oximetry should be used, but it is not a substitute for continuous clinical assessment. Capnometry can be considered as an adjunct monitor to provide additional information for identifying hypoventilation. If transportation of the patient is required, every effort should be made to maintain the same level of monitoring during transport as within the ED. Complications can occur with sedation and analgesia. The median time for the onset of serious complications is 2 minutes after the administration of the final IV dose of medication, with nearly all events occurring within 25 minutes. All patients who had a serious adverse reaction after the completion of the procedure had a reaction at some time during the procedure. Proper monitoring, training, and preparation will help to avoid long-term negative sequelae. Personnel administering or monitoring pediatric sedation must have an understanding of the medications being used, the ability to recognize adverse reactions, and the skills to intervene during adverse events, especially respiratory and hemodynamic emergencies.
NONPHARMACOLOGICAL ANXIOLYSIS Anxiolysis has been shown to improve procedural outcomes. Not all interventions to relieve anxiety and pain are pharmacological; appropriate discussion with both the parent and the child has been proved to be beneficial. The clinician should give realistic expectations while avoiding anxiety-promoting words such as pain, cut, or shot; instead, words like poking or squeezing should be used. The clinician should avoid discussing adverse possibilities with other healthcare workers or parents in front of the child. Parents should be allowed to stay with the child if they wish. Children overwhelmingly prefer this, and the data show that having parents in the room does not interfere with the provider’s procedure performance. Nonpharmacological anxiolytic techniques are a proven adjunct to medications.
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TOPICAL ANALGESICS The following are examples of some commonly used topical analgesics: 1. LET solution consists of lidocaine 4%, epinephrine 0.1%, and tetracaine 0.5%. The dose is 5 ml delivered topically, and the time to onset is 20–30 minutes. LET can be applied to the affected areas as drops from syringe or soaked on a cotton ball or piece of gauze. The healthcare provider should wear gloves when applying LET to avoid absorption. Because this agent contains epinephrine, contact with and use of it on distal appendages (e.g., distal phalanx, nose, and ears) should be avoided. 2. Eutectic mixture of local anesthetics (EMLA) cream contains lidocaine 2.5% and prilocaine 2.5%. The usual dose is 2 g applied in a thick layer. The time to onset is 1 hour. EMLA is currently not available in a sterile form and is therefore only recommended for use with intact skin and not open wounds. This agent should be used cautiously in children younger than 3 months. Its long onset time often makes use of this cream impractical for use in the ED.
LOCAL ANALGESICS Some commonly used local analgesics include the following: 1. Lidocaine is available in 0.5%, 1%, and 2% solutions with and without epinephrine for injection. The maximum dose of the 1.0% solution is 5 mg/kg and of the 1.0% with epinephrine is 7 mg/kg. The time to onset is 2–5 minutes, and the duration of effect is 15–45 minutes. Lidocaine is contraindicated in persons with a previous adverse reaction to lidocaine. Side effects include CNS toxicity beginning with subjective symptoms of lightheadedness, circumoral numbness, tinnitus, sleepiness, and lethargy with progression to objective excitatory signs of shivering, tremors, and tonic-clonic seizures, with further progression to coma and apnea as well as cardiotoxicity with cardiovascular collapse. To avoid pain with infiltration, lidocaine should be pushed slowly, 30 sec/ml, and the solution should be buffered (9 ml of lidocaine 1% should be buffered with 1 ml sodium bicarbonate 8.4%). If a preparation with epinephrine is chosen, injection into end-arterial fields such as the tips of digits, nose, penis, and pinna should be avoided. If accidental injection into one of these areas occurs, the effects can be reversed with the placement of 1 inch of nitroglycerin paste. Adverse effects with infiltration are rare but can happen if the maximum dose is exceeded. This situation can occur with infants with large lacerations. 2. Bupivacaine is available with and without epinephrine for injection. A concentration 0.25% is most appropriate for local anesthesia. The
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maximum dose of the 0.25% solution is 2 mg/kg; for the 0.25% solution with epinephrine, the maximum dose is 3 mg/kg. Bupivacaine’s time to onset is 3–7 minutes, and the time of duration is 90–360 minutes. Use is contraindicated in persons who have had a previous adverse reaction to bupivacaine. Side effects include CNS toxicity beginning with subjective symptoms of lightheadedness, circumoral numbness, tinnitus, sleepiness, and lethargy with progression to objective excitatory signs of shivering, tremors, and tonic-clonic seizures, with further progression to coma and apnea as well as cardiotoxicity with cardiovascular collapse. Bupivacaine 0.25% is four times as potent as lidocaine 1%. To avoid pain with infiltration, it should be pushed slowly, 30 sec/ml. The addition of sodium bicarbonate can cause precipitation of the bupivacaine. Sodium bicarbonate should only be added if the newly buffered solution would immediately be used. For buffering, the ratio is 29:1 of 0.25% bupivacaine to 8.4% of sodium bicarbonate. As with lidocaine, if a preparation with epinephrine is chosen, injection into end-arterial fields such as tips of digits, nose, penis, and pinna should be avoided. If accidental injection into one of these areas occurs, the effects can be reversed with the placement of 1 inch of nitroglycerin paste.
SYSTEMIC ANALGESIA AND SEDATION There are no high-quality data that show the definitive safety of analgesic and sedative agents in children. Extreme caution should be exercised when sedating children younger than 1 year of age, especially in children younger than 3 months old. Because serious adverse effects are rare, the studies in the literature lack sufficient statistical power to document true safety in the ED or the operating room. The required patient cohorts would need to be in the thousands to have the necessary power. The drugs included in this section are some of the most common and well studied. Their safety is based on the available data. Particular attention should be paid to dosing and dosing calculations. Ideally, a second, qualified person should check dosing amounts for pediatric patients to help ensure safety and proper dosing.
Sedatives Sedatives as a sole pharmacological agent can be used for noninvasive procedures requiring motion control and anxiolysis such as with CT, MRI, ultrasound, and echocardiogram and those associated with a low level of pain but high anxiety such as lumbar puncture, slit-lamp examination, ocular irrigation, or simple foreign body removal.
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Some commonly used sedatives are listed below: 1. Midazolam is an ultra-short-acting benzodiazepine. Dosing is as follows: IV, 0.05–0.1 mg/kg with a maximum dose of 0.4 mg/kg; IM, 0.1–0.15 mg/kg; PO, 0.5–0.75 mg/kg with a maximum dose of 15 mg; intranasal, 0.2–0.5 mg/kg with a maximum dose of 5 mg; per rectum, 0.25–0.5 mg/kg. The time to onset varies by administration: IV, 2–3 minutes; IM/PO/intranasal/per rectum: 10–30 minutes. The duration of effect is 30–120 minutes. Contraindications of midazolam include uncontrolled pain, CNS depression, shock, and hypersensitivity to benzodiazepines, and side effects are respiratory depression, apnea, paradoxical excitement, and hypotension. The reversal agent is flumazenil. Dosing should be reduced when used with an opioid. It produces skeletal muscle relaxation, amnesia, and anxiolysis. Amnesia is both anterograde and retrograde. 2. Etomidate is an ultra-short-acting sedative dosed at 0.1–0.2 mg/kg IV. The time to onset is 1–2 minutes, and the length of duration is 5–10 minutes. Side effects include nausea, vomiting, transient oxygen desaturation, myoclonus (normally lasting less than 1 minute, associated with injection), and adrenal suppression lasting up to 24 hours (but levels remain in the normal range). Etomidate is associated with a favorable hemodynamic profile. It involves decreased ICP with minimal effect on cerebral perfusion and is often used for rapid sequence intubation. 3. Methohexital is a rapid-acting barbiturate administered per rectum at a dose of 25 mg/kg. Its time to onset is 10–15 minutes, and its duration is 60 minutes. Methohexital is contraindicated in persons with CNS depression, hypersensitivity to barbiturates, hepatic impairment, porphyria, or temporal lobe epilepsy. Side effects include hypotension, hypoventilation, and apnea. This agent should be considered for use in diagnostic imaging. It lacks a reversal agent and provides sedation, motor control, and anxiolysis but no analgesia. 4. Thiopental, a rapid-acting barbiturate, is administered per rectum at 25 mg/kg. Its time to onset is 10–15 minutes, and its duration is 60 minutes. Contraindications include CNS depression, hypersensitivity to barbiturates, hepatic impairment, and porphyria, and possible side effects include hypotension, hypoventilation, and apnea. This agent, too, should be considered for diagnostic imaging and lack a reversal agent. Thiopental provides sedation, motor control, and anxiolysis but no analgesia. 5. Pentobarbital is a short-acting barbiturate dosed at 1–6 mg/kg IV (maximum dose, 100 mg), 2–6 mg/kg IM (maximum dose, 100 mg), 3–6 mg/kg per rectum or PO in patients younger than 4 years old (maximum dose, 100 mg), and 1.5–3 mg/kg per rectum or PO in patients older than 4 years (maximum dose, 100 mg). Pentobarbital’s time to
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onset varies according to the route of administration: IV, 3–5 minutes; IM, 10–15 minutes; per rectum/PO, 12–60 minutes. The time of duration is 30–240 minutes, and contraindications include CNS depression, hypersensitivity to barbiturates, hepatic impairment, and porphyria. Side effects are transient respiratory depression, paradoxical hyperactivity, paradoxical inconsolability, severe irritability, combativeness, hypotension, hypoventilation, apnea, emesis, and coughing. If IV pentobarbital is used and the patient is not sedated within 5 minutes, fentanyl 1 mg/kg IV can be added as an adjunct. This agent can be considered for diagnostic imaging, and it lacks a reversal agent. It provides sedation, motor control, and anxiolysis but no analgesia. Best results are seen when used in children younger than 8 years.
Analgesics Opioid analgesics are the mainstay for the pharmacological treatment of severe pain. There are three broad chemical classes for opioids that include the phenanthrene derivatives (e.g., morphine, codeine, hydrocodone, hydromorphone, oxycodone, and oxymorphone), the phenylpiperidine derivatives (e.g., meperidine and fentanyl), and the diphenylheptane derivatives (e.g., propoxyphene and methadone). These three classes do not share allergic cross-sensitivity with agents from the other classes. Examples of analgesic agents include the following: 1. Fentanyl is a fast-acting phenylpiperidine opioid derivative. It is administered IVat 1.0 mg/kg/dose and can be repeated every 3 minutes until the desired effect is reached. The time to onset is 2–3 minutes, and the duration is 30–60 minutes. Side effects include respiratory depression with resultant hypoxia and/or apnea, chest wall rigidity associated with rapid infusion of moderate to large doses, nausea and vomiting, and pruritus. The reversal agent used with fentanyl is naloxone. Fentanyl is 100 times more potent than morphine. The former does not stimulate histamine release and has less associated nausea than other opioids. No allergic cross-sensitivity occurs with phenanthrene opioid derivatives (e.g., morphine, codeine, hydrocodone, hydromorphone, oxycodone, and oxymorphone) or the diphenylheptane opioid derivatives (e.g., propoxyphene and methadone). It is the opiate of choice because of its fast onset, short duration, and reversibility. 2. Morphine is a phenanthrene opioid derivative dosed at 0.05–0.1 mg/kg IV, 0.1–0.2 mg/kg IM/subcutaneous, or 0.3–0.5 mg/kg PO every 4–6 hours. Its time to onset varies according to the route of administration: IV, 5–10 minutes; IM/PO/subcutaneous, 15–30 minutes. Its duration is 120–240 minutes. Contraindications are hypovolemia and asthma, and side effects include respiratory depression, histamine release, hypotension, pruritus, nausea, and vomiting. The associated reversal agent is
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naloxone. Morphine carries no allergic cross-sensitivity with phenylpiperidine opioid derivatives (e.g., meperidine and fentanyl) or the diphenylheptane opioid derivatives (e.g., propoxyphene and methadone).
Analgesia and Sedation Both analgesia and sedation may be required for procedures involving high levels of pain and anxiety. A combination of a sedative with an analgesic agent can meet the procedural requirements. Some data suggest that there is an increased chance for respiratory distress when combining sedatives and analgesics. A common, well-studied, and recommended combination is fentanyl with midazolam because both have a short onset of action and duration. One agent that can be considered is ketamine, an N-methyl-D-aspartate glutamate receptor antagonist with dissociative, sedative, analgesic, and amnesic properties. Dosing is as follows: IV, 1–1.5 mg/kg in an initial dose, 0.5–0.75 mg/kg in repeat doses every 10 minutes as required; IM, 4–5 mg/kg, repeat after 10 minutes as required; PO/per rectum, 10 mg/ kg. The time to onset varies with the route of administration: IV, 1 minute; IM, 3–5 minutes. When administered IV, the dissociation occurs within 15 minutes and recovery takes 60 minutes. When ketamine is given IM, dissociation takes 15–30 minutes and recovery takes 90–150 minutes. Contraindications include age younger than 3 months, history of airway instability, tracheal stenosis, upper respiratory tract infection, asthma, cardiovascular disease, hypertension, increased ICP, poorly controlled seizure disorder, glaucoma or globe injury, psychosis, porphyria, and thyroid disorder. Possible adverse effects are respiratory depression, laryngospasm, emesis, recovery agitation, hallucinations, and “bad dreams.” Ketamine preserves upper airway tone and protective airway reflexes. It should be pushed slowly over 1–2 minutes. Administration with atropine for hypersalivation 0.01 mg/kg for IM/IV and 0.02 mg/kg for PO/per rectum dosing is the current standard, but data suggest that this does not actually decrease secretions. The coadministration of midazolam (0.05 mg/kg; maximum dose, 2 mg IV/IM; 0.5 mg/kg, maximum dose, 15 mg PO/per rectum) to decrease the incidence of emesis. Many practitioners add midazolam for the prevention or blunting of unpleasant hallucinations and emergence reactions; however, studies have shown there is no benefit from addition of midazolam, and the reactions occur at the same frequency.
REVERSAL AGENTS Reversal agents, with doses precalculated, should be kept readily available at the bedside when opiates or benzodiazepines are used. Examples of reversal agents include the following:
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1. Naloxone, an opioid antagonist, is administered IM or IV at 0.1 mg/ kg/dose to a maximum of 2 mg/dose, repeated every 2 minutes as required. The time to onset varies according to the route of administration: IV, 2 minutes; IM, 10–15 minutes. The duration of effect is 20–90 minutes. 2. Flumazenil is a benzodiazepine antagonist. It is given IV at 0.01 mg/ kg/dose with a maximum initial dose of 0.2 mg, repeated every minute until the desired effect is achieved, or to a maximum of 0.05 mg/ kg or 1.0 mg. The time to onset is 1–2 minutes, and the duration is 20–60 minutes. Flumazenil is contraindicated in persons receiving chronic benzodiazepine therapy for seizures, those currently using a medication that has a side-effect profile, including seizures (such as theophylline, bupropion, tricyclic antidepressants, lithium, or isoniazid), and persons with a hypersensitivity to benzodiazepines.
Bibliography American Academy of Pediatrics, Clinical Report: Relief of Pain and Anxiety in Pediatric Patients in Emergency Medical Systems, Pediatrics 2004;114:1348. American College of Emergency Physicians: Clinical Policy: Evidence-Based Approach to Pharmacologic Agents Used in Pediatric Sedation and Analgesia in the Emergency Department, Ann Emerg Med 2004;44:342. Clinical Policy, Procedural Sedation and Analgesia in the Emergency Department, Ann Emerg Med 2005;45:177. Goldfrank LR, Flomenbaum NE, Lewin NA, et al: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Green SM, Krauss B: Clinical practice guideline for emergency department ketamine dissociative sedation in children, Ann Emerg Med 2004;44:460. Krauss B, Green SM: Sedation and analgesia for procedures in children, N Engl J Med 2000;342:938. Proudfoot J, Krug S: Pediatric procedural sedation and analgesia (PSA): Keeping it simple and safe, Ped Emerg Med Reports 2002;7(2):13–24. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Young KD: Pediatric procedural pain, Ann Emerg Med 2005;45:160.
Chapter 14
Psychiatric Emergencies Panic Disorder BROOKE ASHLEY VEALE
ICD Code: Panic disorder without agoraphobia 300.01, Panic disorder with agoraphobia 300.21
Key Points Panic attacks are recurrent and unexpected. Patients with this disorder are concerned about possible future panic attacks. ! Emergency Actions ! In any patient reporting chest pain, an electrocardiogram (ECG) and cardiac enzyme measurements should be performed to rule out myocardial infarction. Pulse oximetry should be also documented. Patients with acute pulmonary embolisms can present similar to a person having a panic attack.
DEFINITION Panic disorder involves recurrent panic attacks and subsequent fear of future attacks. It may occur with agoraphobia, indicating that the patient worries about situations in which escape might be difficult. It can also occur in the absence of agoraphobia.
EPIDEMIOLOGY Studies show that panic disorder occurs in about 2% of the general population. It is more common in females and occurs more often in persons with a family history of panic. About half of the persons with panic disorder will also have major depression. Panic disorder increases the risk of impaired social functioning, substance abuse, and suicide.
CLINICAL PRESENTATION Patients present with a history of recurrent panic attacks, which peak in 10 minutes and last no longer than an hour. The patient describes intense fear but is unable to determine the source of the fear. Oftentimes, anticipatory anxiety occurs between attacks. The examiner taking a patient’s history should inquire about use of stimulating substances (e.g., caffeine), 814
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nicotine, cold medications, alcohol, and illicit drugs. It is also useful to ascertain the patient’s sleeping patterns and his or her stress levels at home and work.
EXAMINATION Patients with panic disorder often have completely normal physical examination results. However, several signs can be detected if they are being examined during an attack. Patients currently experiencing a panic attack often have cold hands and are hypertensive, tachycardic, tachypneic, and diaphoretic. The clinician should be sure to rule out cardiopulmonary disorders, especially in persons who have never had a panic attack before.
LABORATORY FINDINGS A laboratory workup is warranted to rule out other possibilities before a diagnosis of panic disorder is made. All patients must have blood samples drawn for a CBC, Chem 7 (which includes blood urea nitrogen, creatinine, chloride, carbon dioxide, glucose, potassium, and sodium), calcium measurement, liver function tests, and thyroid function tests. Respiratory alkalosis may be revealed on laboratory analysis as a result of hyperventilation. In addition, a urinalysis, ECG, drug screen, and cardiac enzyme analysis should always be considered.
DIAGNOSIS The diagnosis of panic disorder is made on the basis of criteria set forth in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). Patients must meet both of the following criteria: 1. Recurrent panic attacks occur without triggers. 2. The attack is followed by at least 1 month of worrying about additional attacks, the implications of the attack, or a significant change in behavior. Panic attacks are also defined by the DSM-IV. These episodes begin abruptly without triggers and peak in 10 minutes. The attacks are not due to ingestion of a substance, a general medical condition, or another mental disorder. Patients must experience at least four of the following symptoms for the episode to qualify as a panic attack: 1. 2. 3. 4.
Palpitations or tachycardia Diaphoresis Trembling Feelings of dyspnea
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5. 6. 7. 8. 9. 10. 11. 12. 13.
Choking sensation Chest pain or heaviness Nausea Vertigo, lightheadedness, or presyncope Feelings of detachment from self Fear of losing control Fear of dying Paresthesia Chills or hot flashes
If the above criteria are met and the patient does not experience anxiety about situations in which escape might be difficult, the diagnosis of panic disorder without agoraphobia is most appropriate. If the above criteria are met and the patient does experience anxiety about situations in which escape might be difficult, the diagnosis of panic disorder with agoraphobia can be made.
RADIOGRAPHS Chest radiography is appropriate if the patient reports chest pain. Magnetic resonance imaging of the brain will aid in ruling out lesions in patients with atypical neurological symptoms.
TREATMENT There are several pharmacological options for patients diagnosed with panic disorder. Some selective serotonin reuptake inhibitors (SSRIs), including paroxetine (Paxil), sertraline (Zoloft), and fluoxetine (Prozac) are indicated for the use in panic disorder. Although SSRIs are quite effective, these medications may take up to 6 weeks to reach their maximum effect. They also usually require dosing adjustments to reach the therapeutic level for each patient. Alprazolam (Xanax) and clonazepam (Klonopin) are benzodiazepines that may be used on an as-needed basis during the initial phases of treatment. Benzodiazepines should not be used in the long term due to their potential adverse effects and addictive nature. Pharmacological therapy should always be accompanied by psychotherapy. A referral to a psychiatrist or therapist for cognitive therapy, relaxation techniques, breathing exercises to avoid hyperventilation, or desensitization often aids patients in dealing with secondary symptoms.
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Generalized Anxiety Disorder BROOKE ASHLEY VEALE
ICD Code: 300.02
Key Points Patients with generalized anxiety disorder (GAD) have excessive worry about daily events. There is an absence of panic attacks with this condition.
DEFINITION Generalized anxiety disorder is defined as uncontrollable and excessive worry occurring for at least 6 months. Anxiety must be related to several aspects of life to include home, school, work, or social activities. By definition, patients with GAD do not experience anxiety attacks.
EPIDEMIOLOGY It has been estimated that about 5% of the American population will be diagnosed with GAD sometime in life. GAD is twice as prevalent in females than in males. Those at an increased risk for GAD include persons with an increased number of minor stressors, peer victimization, and a family history of anxiety.
CLINICAL PRESENTATION Upon presentation, patients usually have somatic symptoms and seek the advice of a specialist. After further questioning, patients report excessive worry over everyday activities. There are three additional types of symptoms: motor tension, autonomic hyperactivity, and cognitive vigilance. Symptoms of motor tension may include headaches, fatigue, restlessness, and muscle spasms. Autonomic hyperactivity occurs as palpitations, tachycardia, shortness of breath, dry mouth, nausea, diarrhea, sweating, and dizziness. Finally, cognitive vigilance is manifested by irritability, feeling on edge, impaired concentration, and being easily startled.
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EXAMINATION Upon physical examination of the patient, the healthcare provider may note sweating, tachycardia, and tachypnea. However, physical examination results are likely to be normal.
LABORATORY FINDINGS A laboratory workup is warranted to rule out other possibilities before a diagnosis of GAD is made. Blood samples should be drawn from all patients for a Chem 7 panel (which includes blood urea nitrogen, creatinine, chloride, carbon dioxide, glucose, potassium, and sodium) and thyroid function tests. In addition, a urinalysis, ECG, and drug screen should always be considered. Providers must administer the mental status examination to identify any deficits.
DIAGNOSIS The DSM-IV contains diagnostic criteria for GAD. The patient must experience excessive anxiety about several different activities. The anxiety occurs on the majority of days for at least 6 months, and the patient is unable to control it. Only one symptom is required to make the diagnosis in children, but at least three of the following symptoms must be present in adults: 1. 2. 3. 4. 5. 6.
Restlessness or feeling on edge Fatigue occurring easily Difficulty concentrating Irritability Muscle tension Insomnia or restless sleep
To qualify as GAD, these symptoms must not be due to a confined situation, any axis I disorder, ingestion of a substance, or a general medical condition. GAD causes clinically significant distress.
TREATMENT GAD is often a lifelong problem, and spontaneous remission is uncommon. Some studies show that 2 years after diagnosis, about half of the patients diagnosed with GAD will continue to have symptoms. Several antidepressants, including buspirone (BuSpar), imipramine (Tofranil), paroxetine (Paxil), trazodone (Desyrel), or venlafaxine (Effexor),
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have shown effectiveness in the treatment of GAD after 4 weeks of administration. Buspirone continues to have the most convincing data of usefulness in this disorder and is therefore used the most often. The use of benzodiazepines has been a primary treatment in the past despite the lack of evidence that these medications reduce symptoms. The risks of dependence, potential adverse effects, sedation, and possible accidents far outweigh the benefits of their use in GAD. Hydroxyzine (Vistaril) is a safer and nonaddictive medication that can also be used as needed until the buspirone begins to alleviate symptoms. It is recommended that treatment with either hydroxyzine or a benzodiazepine and buspirone simultaneously be initiated at the beginning of therapy. The medication, which is used as needed while the buspirone reaches therapeutic levels, should be discontinued after a few weeks of buspirone. The patient should also be referred to a psychiatrist for cognitive therapy and to learn relaxation techniques.
Bibliography American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, ed 4. American Psychiatric Association: Washington, DC, 1994. American Psychiatric Association Web site. Available at:http://www.psych.org. Gale C, Oakley-Browne M: Generalized anxiety disorder, Am Fam Phys 2003;67(1):135–138. Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry, ed 9. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 591–642.
Conversion Disorder BROOKE ASHLEY VEALE
ICD Code: 300.11
Key Points Conversion disorders convert anxiety to physical symptoms. Neurological symptoms are not caused by a medical condition. Conversion disorder symptomsbeginand worsenwith stress.
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DEFINITION Conversion disorder is defined as one or more neurological symptoms that cause dysfunction and cannot be explained by a medical condition. The symptoms may be motor, visceral, or sensory deficits. Symptoms begin and are aggravated by circumstances the patient perceives as stressful.
EPIDEMIOLOGY Although no definitive study has been completed, it has been estimated that 10–500 persons per 100,000 are affected by conversion disorder. It is more common in females than in males. However, it is increased in males with a history of occupational injury or military combat experience. Although conversion disorder may occur at any age, it is much more likely to affect adolescents and young adults. Those at a higher risk include rural citizens and persons of low educational level or low socioeconomic status.
CLINICAL PRESENTATION The most common presentation of conversion disorder includes paralysis, blindness, or mutism. Other possible symptoms include deafness, tunnel vision, anesthesia, involuntary movements, tics, seizures, syncope, abnormal gait, weakness, falling, vomiting, diarrhea, and urinary retention. Patients with conversion disorder are more likely to experience anxiety and depression, and they are at a higher risk for suicide attempts. This disorder is often associated with some personality disorders, including histrionic, dependent, and antisocial.
EXAMINATION The symptoms of conversion disorder cannot be explained by a medical illness. Therefore, the physical examination results will be unremarkable. For example, patients with seizures will not exhibit the typical presentation for seizures. Usually, patients do not bite their tongues, experience urinary incontinence, or sustain injuries during the course of the seizure. There is no postictal stage, and papillary and gag reflexes are retained.
LABORATORY FINDINGS There will be no abnormal laboratory test results in patients who have a conversion disorder.
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DIAGNOSIS Conversion disorder is diagnosed based on DSM-IV criteria. The criteria are as follows: 1. At least one symptom, either motor or sensory, suggests a neurological deficit or other medical condition. 2. Symptoms are initiated or exacerbated by stressors, including conflict. 3. Symptoms are not intentionally produced by the patient. 4. After investigation, the symptom cannot be explained by a medical condition, ingestion of a substance, or a culturally based experience. 5. Symptoms cause clinically significant distress or impairment. 6. Symptoms are not limited to pain or sexual dysfunction, do not occur only during somatization disorder, and are not better explained by another psychiatric illness.
TREATMENT Conversion disorder usually resolves spontaneously in a short period of time. However, patients often benefit from insight-oriented psychotherapy involving stress management and coping skills. Hypnosis and relaxation techniques can also improve symptoms. In some cases, anxiolytic medications may be necessary. It is not advised to tell patients with conversion disorder that their symptoms are not real because this aggravates the illness.
Bibliography American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, ed 4, text revision. American Psychiatric Association: Washington, DC, 2000. Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry, ed 9. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 647–651. Stoudemire A: Clinical Psychiatry for Medical Students, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 1998, pp 353–357.
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Personality Disorders BROOKE ASHLEY VEALE DEFINITION Overall, personality disorders involve chronic maladaptive traits that interfere with personal and occupational functioning. Their repetitive behaviors cause a strain on interpersonal relationships. There are three clusters of personality disorders, known as clusters A, B, and C. Descriptors for these clusters are “weird,” “wild,” and “worried,” respectively (Table 14-1).
EPIDEMIOLOGY Personality disorders are not uncommon in the United States. It has been determined that almost 15% of Americans are diagnosed with at least one personality disorder. By definition, the onset of personality disorders is in adolescence or early adulthood. In general, personality disorders are more common in persons who are young, have obtained less than a high school education, earn a lower income, and are unmarried.
DIAGNOSIS Although each personality disorder has its own set of DSM-IV criteria, diagnostic criteria for personality disorders in general are outlined in the DSM-IV. For a diagnosis to be made, persons with a persistent pattern of deviated behavior must exhibit a pattern in at least two of the following areas:
Table 14-1 Personality Disorder Classifications CLUSTER
DESCRIPTOR
A
“Weird”
B
“Wild”
C
“Worried”
DISORDERS Paranoid personality disorder Schizoid personality disorder Schizotypal personality disorder Antisocial personality disorder Borderline personality disorder Histrionic personality disorder Narcissistic personality disorder Avoidant personality disorder Dependent personality disorder Obsessive-compulsive personality disorder
Paranoid Personality Disorder
1. 2. 3. 4.
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Cognitive Affective Interpersonal functioning Impulse control
The behavior associated with personality disorders is inflexible and affects social and occupational functioning. This behavior, although stable throughout life, is stressing or impairs functioning in a variety of settings. It is also important for the clinician to rule out other causes of the condition, including general medical illnesses.
TREATMENT AND OUTCOME Treatment for personality disorders always involves therapy with a psychiatrist. The type of therapy will depend on the disorder and the patient. The types of therapy include group, individual, behavioral, and assertiveness training. Pharmacological treatment aims at treating the symptoms; for example, SSRIs are used to treat depressive symptoms.
Paranoid Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.0
Key Points/Quick Reference Paranoid personality disorder is a cluster A disorder. Distrust and suspicion are key features displayed by persons with this condition.
DEFINITION Paranoid personality disorder involves a general distrust of others and a tendency to be suspicious of others’ motives.
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EPIDEMIOLOGY Paranoid personality disorder is present in about 4.4%, or approximately 9.2 million, of the U.S. population. This disorder begins by early adulthood and is more common in women. Persons at an increased risk for this disorder include patients with a family history of schizophrenia, those from an ethnic/racial minority group, and persons with low income, lack of higher education, or history of separation or divorce.
CLINICAL PRESENTATION Patients with paranoid personality disorder rarely present to a healthcare provider on their own. They are most often encouraged by family, friends, or co-workers to seek help.
EXAMINATION Muscle tension and spasms may be evident on physical examination.
DIAGNOSIS To diagnose a patient with paranoid personality disorder, DSM-IV criteria must be met. A patient exhibiting distrust and suspicions that motives are malevolent must meet at least four of the following criteria: 1. Displays suspicion that others are harming them 2. Doubts friends’ trustworthiness 3. Has difficulty confiding in others because of concerns that the information will be used against them 4. Believes innocent remarks are threatening to them 5. Holds grudges 6. Falsely perceives and reacts quickly to attacks on their character 7. Doubts fidelity of spouse or partner These symptoms cannot be explained by schizophrenia, a mood disorder with psychotic features, any other psychotic disorder, or a general medical condition.
TREATMENT AND OUTCOME When a diagnosis of paranoid personality disorder is made, the patient must be referred to a psychiatrist for individual psychotherapy. Actions to build trust and intimacy are especially beneficial for patients. Group and behavioral therapies can be harmful for the patient and should be avoided. Most patients respond with anxiolytic medications, such as diazepam (Valium), which also relieves muscle spasms. Occasionally, haloperidol (Haldol), an antipsychotic, is added to aid in controlling aggression.
Schizoid Personality Disorder
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Schizoid Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.2
Key Points/Quick Reference Schizoid personality disorder is a cluster A disorder. Patients display loneliness and are not sensitive to praise or criticism by others.
DEFINITION Schizoid personality disorder involves a detachment from social relationships and difficulty showing emotion. Patients with this disorder are not concerned with others and usually seek noncompetitive employment.
EPIDEMIOLOGY About 6.3 million Americans, or just over 3%, are diagnosed with schizoid personality disorder. It begins by early adulthood and occurs at equal rates in men and women. This disorder is more common in African Americans, Native Americans, and Hispanics and is less common in the Asian population. Risk factors for this disorder include low income, low level of education, and being unmarried.
CLINICAL PRESENTATION Patients with schizoid personality disorder appear lonely and detached.
EXAMINATION Blunted affect and lack of eye contact may be appreciated during the physical examination.
DIAGNOSIS The diagnosis of schizoid personality disorder can only be made if DSM-IV criteria are met. Patients who are detached and have difficulty expressing emotion must have at least four of the following criteria:
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1. 2. 3. 4. 5. 6. 7.
Does not want or enjoy close relationships Chooses solitary activities Is not interested in sexual relationships Does not find pleasure in many activities Does not have close friends Is not concerned with the opinions of others Seems detached
The symptoms cannot be explained by schizophrenia, a mood disorder with psychotic features, any other psychotic disorder, any developmental disorder, or a general medical condition.
TREATMENT AND OUTCOME The treatment of schizoid personality disorder includes a referral to a psychiatrist for psychotherapy. Although patients are very quiet upon initiation, group therapy has proved to be beneficial for patients with this disorder. Pharmacological treatment usually involves SSRIs and possibly antipsychotic drugs.
Schizotypal Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.22
Key Points/Quick Reference Schizotypal personality disorder is a cluster A disorder. A patient with this condition exhibits magical thinking.
DEFINITION Schizotypal personality disorder is characterized by superstition, odd behavior and speech, and a high sensitivity to others. Schizotypal patients are known to experience decompensation with stress.
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EPIDEMIOLOGY Although no definitive prevalence studies on schizotypal personality disorder have been completed, it has been estimated to occur in about 3% of the population, accounting for approximately 6.2 million cases in the United States. This disorder begins by early adulthood and is equally distributed among men and women. Persons with a family history of schizophrenia are at a higher risk for this disorder.
CLINICAL PRESENTATION It is often very difficult to elicit a history in patients with schizotypal personality disorder due to their odd speech patterns. When under stress, patients with this disorder may exhibit psychosis and signs of severe depression.
EXAMINATION Inappropriate affect and peculiar appearance may be noted during physical examination.
DIAGNOSIS DSM-IV criteria must be met before a diagnosis of schizotypal personality disorder can be made. A patient who is uncomfortable with close relationships, has distorted perceptions, and exhibits eccentric behavior must have at least five of the following: 1. 2. 3. 4. 5. 6. 7. 8. 9.
Ideas of reference Magical thinking affecting behavior Perceptual distortions Odd thought process and speech Suspicious Inappropriate affect Eccentric behavior and appearance Lack of close friends Social anxiety that does not improve with familiarity
The symptoms cannot be explained by schizophrenia, a mood disorder with psychotic features, any other psychotic disorder, or a pervasive developmental disorder.
TREATMENT AND OUTCOME The cornerstone of treatment for schizotypal personality disorder involves a referral to a psychiatrist for psychotherapy. It is vital that the patient not
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feel judged because of his or her beliefs. The use of antidepressants is beneficial if the patient experiences anhedonia or signs of severe depression. Antipsychotic medications are helpful in the management of ideas of reference and illusions. Although some patients are stable with this disorder, schizotypal personality disorder is a known precursor to schizophrenia. It has been estimated that up to 10% of schizotypal patients commit suicide.
Antisocial Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.7
Key Points/Quick Reference Antisocial personality disorder is a cluster B disorder. Patients with this condition are impulsive, commit illegal acts, and show no remorse. They exhibit no irrational thought process.
DEFINITION Antisocial personality disorder may be present in young adults who are aggressive and unable to conform to social norms. They do not experience signs of anxiety, depression, or irrational thoughts.
EPIDEMIOLOGY Antisocial personality disorder affects approximately 7.4 million Americans, accounting for over 3.5% of the population. This disorder is more common in men than in women. Although the patient must be 18 years old for a diagnosis to be made, signs of this disorder must be present before the age of 15 years. Patients with a family history of antisocial personality disorder are at a higher risk for this disorder. Native Americans, persons living in the western United States, and those with a lower income, less education, and single marital status are at higher risk. Asians are at a lower risk for this disorder.
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CLINICAL PRESENTATION Patients with antisocial personality disorder often seem calm and charming on presentation, but manipulative behavior could be evident. Patients are articulate, and appropriate questioning might reveal a disordered life, including multiple fights, substance abuse, and truancy.
DIAGNOSIS The diagnosis of antisocial personality disorder is based on DSM-IV criteria. Patients with a persistent pattern of violating others’ rights since the age of 15 years must have at least three of the following: 1. 2. 3. 4. 5. 6. 7.
Inability to conform to social norms, including unlawful behavior Deceitful nature Impulsive behavior Irritability and aggression Disregard for safety Irresponsibility Lack of remorse
The patient must be at least 18 years old and must have shown evidence of conduct disorder before the age of 15 years. The behavior does not occur only during the course of schizophrenia or mania.
TREATMENT AND OUTCOME Patients with antisocial personality disorder often fail to comply with follow-up for psychotherapy, but they tend to do well with self-help groups. Pharmacological options include methylphenidate (Ritalin) or dextroamphetamine (Adderall) if signs of attention-deficit/hyperactivity disorder are present. Impulsive behavior may respond to antiepileptic medications, such as carbamazepine (Tegretol) or valproate (Depakote). Propranolol is often used to decrease aggressive behavior.
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Borderline Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.83
Key Points/Quick Reference Borderline personality disorder is a cluster B disorder. Patients with this condition have unstable personal relationships and exhibit impulsive behavior.
DEFINITION Borderline personality disorder involves the line between neurosis and psychosis. Patients with this disorder always appear to be in a state of crisis, are impulsive, and go through extraordinary measures to maintain unstable relationships. They believe that people are either all good or all bad.
EPIDEMIOLOGY Although no definitive prevalence studies on borderline personality disorder have been completed, it has been estimated to occur in about 4.2 million of Americans (2%). This disorder begins by early adulthood, and it is more common in women than in men. Persons with a family history of major depressive disorder or substance abuse are at a high risk.
CLINICAL PRESENTATION Mood swings are quite common in patients with borderline personality disorder. Upon questioning, the patient is likely to reveal a history of anxiety and chaotic sexuality.
EXAMINATION Upon physical examination, the practitioner may discover evidence of self-mutilation acts, such as scars on the wrists.
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DIAGNOSIS A diagnosis of borderline personality disorder is made when DSM-IV criteria are met. A patient who has a history of unstable relationships and extensive impulsivity must meet at least five of the following criteria: 1. 2. 3. 4. 5. 6. 7. 8. 9.
Extraordinary efforts to avoid abandonment History of intense and unstable relationships Unstable self-image Impulsive behavior (in areas of the 5 S’s: sex, spending, substance abuse, scary driving, scarfing food) History of suicidal ideation Reactive mood Feelings of emptiness Temper tantrums, physical fights, intense anger Paranoid ideation when under stress
TREATMENT AND OUTCOME The mainstay of treatment for borderline personality disorder is a referral to a psychiatrist for long-term, reality-oriented psychotherapy. This is a difficult process that is often aided by videotaping the patient’s behavior for his or her review. This form of behavioral therapy is proven to aid patients in understanding the effects of their behavior on those around them. Pharmacological options include monoamine oxidase inhibitors, which aid in controlling impulsive behavior; antipsychotics, which help to control anger; anxiolytics to aid in acute anxiety; and SSRIs, which help with depressive symptoms.
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Histrionic Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.5
Key Points/Quick Reference Histrionic personality disorder is a cluster B disorder. Patients with this condition seek attention and display provocative behavior.
DEFINITION Persons with histrionic personality disorder are often described as extroverted, colorful, or “drama queens.” They usually act provocatively to achieve being the center of attention. Others are able to easily persuade them, and they lack the ability to maintain meaningful relationships.
EPIDEMIOLOGY Histrionic personality disorder affects almost 2% of the American population, or approximately 4 million persons. This disorder, which begins by early adulthood, affects men and women equally. There is an increased incidence among African-Americans and persons with lower income, lower education, a history of somatization disorder or alcohol abuse, and single marital status.
CLINICAL PRESENTATION Patients with histrionic personality disorder may exhibit excessive emotions and seductive behavior.
EXAMINATION The provocative style of dress may be the only clue of histrionic personality disorder during the physical examination.
Narcissistic Personality Disorder
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DIAGNOSIS A diagnosis of histrionic personality disorder is made on the basis of DSM-IV criteria. A patient who displays excessive emotions and attention-seeking behavior must meet at least five of the following: 1. 2. 3. 4. 5. 6. 7. 8.
Is uncomfortable if not the center of attention Displays inappropriate seductive behavior Exhibits fast changes in emotions Draws attention by physical appearance Lacks detail in speech Self-dramatizes Is easily influenced by others Believes relationships are more serious than they are
TREATMENT AND OUTCOME The mainstay of treatment for histrionic personality disorder is psychoanalytic-oriented therapy. Whether the patient is involved in group or individual therapy is at the discretion of the psychiatrist and the patient. Occasionally, medications used to treat anxiety and depression are used to target specific symptoms.
Narcissistic Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.81
Key Points/Quick Reference Narcissistic personality disorder is a cluster B disorder. Patients with this condition exhibit grandiose behavior and a need for admiration.
DEFINITION Persons with narcissistic personality disorder believe they are special and not well understood by the general population. They thrive on the praise of others, and they do not handle criticism gracefully.
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EPIDEMIOLOGY Although no definitive prevalence studies on narcissistic personality disorder have been completed, it has been estimated to occur in fewer than 2 million Americans (1%). By definition, signs begin before early adulthood. Persons with a family history of narcissistic personality disorder are more likely to have the disorder themselves.
CLINICAL PRESENTATION During questioning, persons with narcissistic personality disorder will exaggerate their accomplishments. They often mislead others regarding their social and occupational status.
EXAMINATION Often, narcissistic personality disorder encourages persons with the condition to be well groomed.
DIAGNOSIS A diagnosis of narcissistic personality disorder is made on the basis of DSM-IV criteria. A person with a high level of self-importance, who thrives on others’ admiration must meet at least five of the following criteria: 1. 2. 3. 4. 5. 6. 7. 8. 9.
Exhibits exaggerated self-importance Believes in his or her unlimited success and attractiveness Believes he or she is “special” Needs constant admiration Has a sense of entitlement Exploits others Lacks empathy Believes others envy him or her Displays arrogant behavior
TREATMENT AND OUTCOME Referral to a specialist for group therapy might aid in increasing thoughtfulness of others in a patient with narcissistic personality disorder. Lithium can be used if the patient reveals mood swings, and SSRIs can be of use to decrease rejection sensitivity.
Avoidant Personality Disorder
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Avoidant Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.82
Key Points/Quick Reference Avoidant personality disorder is a cluster C disorder. Patients with this condition are socially inhibited, hypersensitive to negative feedback, and shy, although they desire personal relationships.
DEFINITION Avoidant personality disorder involves persons who are socially withdrawn and who avoid criticism. Because of their perceived inferiority, they often take sideline jobs and avoid new situations.
EPIDEMIOLOGY Avoidant personality disorder involves almost 2.4%, or 4.9 million, of the U.S. population. It is more common in females than in males. It occurs in higher incidence among Native Americans, those living in urban areas, and persons of younger ages, lower income, lower level of education, and single marital status.
CLINICAL PRESENTATION Persons with avoidant personality disorder often do not present to healthcare providers. During appropriate questioning, the patient will appear shy and uninvolved.
DIAGNOSIS DSM-IV criteria determine the diagnosis of avoidant personality disorder. A person who is socially withdrawn, feels inadequate, and is hypersensitive to negative feedback must meet at least four of the following criteria: 1. 2. 3. 4.
Avoids interpersonal contact at work due to fear of criticism Avoids social interaction unless certain of approval Shows restraint in intimate relationships Fears criticism in social settings
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5. Feels inadequate 6. Views self as unappealing 7. Avoids risks or new activities due to fear of embarrassment
TREATMENT AND OUTCOME Getting the patient involved in a group for assertiveness training is of the utmost benefit for persons with avoidant personality disorder. SSRIs can be prescribed to aid in decreasing rejection sensitivity.
Dependent Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.6
Key Points/Quick Reference Dependent personality disorder is a cluster C disorder. Patients with this condition feel that they must be taken care of and can experience separation anxiety.
DEFINITION Dependent personality disorder defines persons who rely on others to make their decisions. Their clinging behavior is a direct result of their need to be cared for.
EPIDEMIOLOGY About 0.49% of the U.S. population, or 1 million Americans, are diagnosed with dependent personality disorder. It is more common in women
Dependent Personality Disorder
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than in men. It occurs more commonly in younger age groups and persons of lower income level, lower level of education, and single marital status.
CLINICAL PRESENTATION A patient with dependent personality disorder often presents to a healthcare provider with a supportive friend or family member. It is common for the supportive person to be an active participant in the history portion of the examination. The patient often yields to them for direction or answers. If the patient does present alone, marked distress is often recognized.
EXAMINATION Patients with dependent personality disorder may present with tachycardia and elevated blood pressure, especially if they are alone.
DIAGNOSIS Dependent personality disorder must be diagnosed according to DSMIV criteria. For this diagnosis, the patient must meet at least five of the following criteria: 1. 2. 3. 4. 5. 6. 7. 8.
Is unable to make everyday decisions in the absence of advice Must have others assume responsibility Does not disagree with others due to fear of abandonment Does not work on projects alone Volunteers for unpleasant tasks to obtain support from others Is uncomfortable when alone Frantically searches for a replacement if a relationship ends Focuses on the fear of being left alone
TREATMENT AND OUTCOME Referral to a psychiatrist, who usually involves the patient in behavioral and group therapy, is the mainstay of treatment. Patients with dependent personality disorder will also benefit from assertiveness training. Pharmacological options are available based on the patient’s symptoms. For example, imipramine is helpful if the patient experiences panic attacks, and SSRIs relieve depressive symptoms.
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Obsessive-Compulsive Personality Disorder BROOKE ASHLEY VEALE
ICD Code: 301.4
Key Points/Quick Reference Obsessive-compulsive personality disorder is a cluster C disorder. Patients with this condition are inflexible and preoccupied with perfection and control.
DEFINITION Obsessive-compulsive personality disorder describes a controlling need for perfection and order. Patients with this disorder are unable to control their thoughts (i.e., obsession) and reactions to those thoughts (i.e., compulsions).
EPIDEMIOLOGY Obsessive-compulsive personality disorder is the most common personality disorder, occurring in almost 8% of Americans, or 16.7 million persons. By definition, it occurs before early adulthood. It is equally prevalent in males and females. It is more common in white persons and in younger age groups. There are no differences of incidence among persons of different income levels or marital status.
CLINICAL PRESENTATION Patients with obsessive-compulsive personality disorder are aware of their problems and are likely to seek treatment on their own. During the history portion of the examination, clinicians will detect formality and the need for organization. Patients often lack a sense of humor and are indecisive.
EXAMINATION Persons with obsessive-compulsive personality disorder have a neat and clean appearance.
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DIAGNOSIS The diagnosis of obsessive-compulsive personality disorder is based on DSM-IV criteria. A person who focuses on perfection and control must meet at least four of the following criteria: 1. Loses the major point of an activity due to preoccupation with organization 2. Strives for perfection to the point of interference with task completion 3. Works at the expense of leisure activity 4. Has inflexible morals 5. Is known as a “pack rat” 6. Does not delegate tasks 7. Saves money for future disasters 8. Is rigid and stubborn
TREATMENT AND OUTCOME The mainstay of treatment for obsessive-compulsive disorder is a referral to a psychiatrist for involvement in group and behavioral therapy. Efforts must be made to help the patient reduce compulsive behaviors. Pharmacological treatment often consists of clonazepam (Klonopin) with the addition of clomipramine (Anafranil) for breakthrough symptoms.
Bibliography American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, ed 4, text revision. American Psychiatric Association: Washington, DC, 2000. Grant BF, Hasin DS, Stinson FS, et al: Prevalence, correlates, and disability of personality disorders in the United States: Results from the National Epidemiologic Survey on Alcohol and Related Conditions, J Clin Psychiatry 2004;65(7):948–958. Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry, ed 9. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 800–821. Stoudemire A: Clinical Psychiatry for Medical Students, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 1998, pp 186–241.
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Suicide BROOKE ASHLEY VEALE
ICD Codes: Suicide and self-inflicted injury E950–E959, Suicide and self-inflicted poisoning by solid or liquid substances E950, Suicide and self-inflicted poisoning by gases in domestic use E951, Suicide and self-inflicted poisoning by other gases and vapors E952, Suicide and self-inflicted injury by hanging, strangulation, and suffocation E953, Suicide and self-inflicted injury by submersion (drowning) E954, Suicide and self-inflicted injury by firearms, air guns, and explosives E952, Suicide and self-inflicted poisoning by other gases and vapors E955, Suicide and self-inflicted injury by cutting and piercing instrument E956, Suicide and selfinflicted injuries by jumping from a high place E957, Suicide and self-inflicted injury by other and unspecified means E958, Late effects of selfinflicted injury E959
Key Points If a patient is at risk for suicide, the examiner should ask about any previous suicide attempts or suicidal ideation. ! Emergency Actions ! Any life-threatening injuries should be evaluated and treated. Direct questions should be asked regarding suicidal ideation in persons at risk for suicide.
DEFINITION Suicide is defined as the intentional act of taking one’s own life. Attempted suicide involves the intentional act but does not result in death. Suicidal ideation is the development of an action plan to take one’s own life.
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EPIDEMIOLOGY In the United States, suicide is the eleventh most common cause of death. The incidence of completed suicide has remained stable over the past 25 years, accounting for about 30,000 deaths annually. Women are four times more likely to attempt suicide, but men are four times more likely to commit suicide. This can be explained by the traditional male preference for violent methods, such as the use of firearms, whereas, historically, the female preference was for drug overdosing. However, more recent data reveal that the use of firearms is increasing among women, and firearm usage is currently the most common method for committing suicide in persons of both sexes. The rates of suicide are higher in young and old persons, so concern is greater with those between the ages of 15 and 24 years and older than 70 years. Depressive disorders, schizophrenia, personality disorders, and anxiety disorders are all associated with an increased risk in suicidal behavior. Although these psychiatric illnesses increase the risk of suicide, most patients with psychiatric disorders will never attempt suicide. Other groups at risk include white persons, those belonging to Protestant or Jewish religions or with weak or absent religious affiliation, and persons with single marital status, high social status, alcohol or drug dependence, chronic illness, or a history of abuse. In 2001, almost three fourths of suicide cases were committed by white males.
CLINICAL PRESENTATION Persons who commit suicide are not routinely brought to the emergency department. However, many persons with suicidal ideation and suicidal attempts are evaluated by emergency care providers. It is vital to assess all high-risk patients for suicidal ideation by means of a complete history.
EXAMINATION Upon physical examination, patients may have signs of attempted suicide, including healed scars from past attempts. However, the physical examination results may be normal.
LABORATORY FINDINGS Drug screenings are used to determine a recent history of alcohol and drug use.
DIAGNOSIS The SADPERSONS scale (Table 14-2) was developed to assist in the assessment of possible suicidal ideation. Patients with four or fewer of
842 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 14-2 Sadpersons Scale CHARACTERISTIC S : Sex A: Age D: Depression P : Previous attempt E : Ethanol (alcohol) or drug abuse R: Rational thinking loss S : Separated, widowed, or divorced O: Organized plan N: No social support S : States future intent
RISK FACTOR Male Under 25 or over 45 years Signs and symptoms of major depressive disorder History of attempts or psychiatric inpatient care Chronic addiction or recurrent use Disoriented, irrational, pessimistic, self-critical, loss of concentration, preoccupied with death Recent loss of significant other Detailed plan to include time, method, and place of planned suicide No close family, friends, or religious affiliation Determined to repeat attempt
the characteristics will require outpatient follow-up. However, those with three or four of the listed characteristics will require psychiatric assistance. Steps to protect the patient, including a psychiatric evaluation in the emergency department, should be made with for any patient with five or six characteristics. Any patient with at least seven of the characteristics should be protected and hospitalized.
RADIOGRAPHS Radiographic evaluation should be completed to assess the extent of any injury.
TREATMENT The most effective treatment for suicidal persons is prevention, thus making screening and detection a requirement for healthcare providers. Asking direct questions about thoughts of self-inflicted injury will help to allow the patient to openly discuss his or her history and recent plans to commit suicide. Once a patient is viewed as suicidal, the decision to treat the patient as an outpatient or in an inpatient facility must be made. This decision should be based on the patient’s diagnosis, risk factors, presence of an organized plan to commit suicide, social support, and living environment. Any patient with substance abuse, suicidal plan of action, attempted suicide, or lack of strong support must be hospitalized. This may be done on a voluntary or involuntary basis. Therefore, every provider should be familiar with the state’s laws concerning commitment to a psychiatric facility. If the patient is treated as an outpatient, an action plan must be put in place in the event that the patient becomes suicidal. The patient must
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commit to the action plan, and the clinician must ensure the constant availability of his or her initial contact. It is also vital to obtain accurate personal records for the patient, including home address and phone numbers. Pharmacotherapy often includes antidepressant medications with the possible addition of antipsychotics, when indicated. However, use of antidepressants can be somewhat risky in cases of suicidal depression. During the initial phases of treatment, the patient becomes energized and is able to put suicidal ideations into action. Therefore, extra precautions should be made during the first few weeks of treatment with any antidepressant medication. A referral for supportive psychotherapy is very helpful in the long-term treatment of patients.
Bibliography Mann J: A current perspective of suicide and attempted suicide, Ann Intern Med 2002;136:302–311. National Institute of Mental Health: National strategy for suicide prevention. Available at: http://www.mentalhealth.org/suicideprevention. Patterson HH, Dohn J, Patterson CA: Evaluation of suicidal patients: The SAD PERSONS scale, Psychosomatics, 1983;24:343–349. Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry, ed 9. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 913–922.
Chapter 15
Pulmonary Emergencies The Basics of Ventilator Management in the Emergency Department STACEY BLACK PEARLMAN With the increasing volume of critical care management in the emergency department (ED), mechanical ventilation is often initiated by emergency medicine providers. Additionally, in many facilities, the healthcare provider on duty in the ED is frequently responsible for evaluating ventilated patients who undergo decompensation in the intensive care unit (ICU) when other physicians are not available or after hours. Therefore, it is vital that these providers have a basic understanding of respiratory failure and be able to recognize the need for mechanical ventilatory assistance. Emergency medicine clinicians must also be able to distinguish between negative- versus positive-pressure ventilation, volume versus pressure cycle ventilation, the different modes of ventilation, and when to use noninvasive versus invasive mechanical ventilation. Mechanical ventilation is a vital modality for managing various pathologic compromises leading to acute respiratory failure due to an inability to maintain adequate oxygenation resulting from obstruction, muscle fatigue, or paralysis. Mechanical ventilation is also useful for providing airway protection in comatose or trauma patients who are unable protect their own airways from secretions. The management of every patient with respiratory failure, regardless of the cause, has four essential components. These include the following: (1) establish a patent airway, (2) maintain sufficient ventilation, (3) ensure adequate oxygen delivery to the tissues, and (4) treat the underlying cause of the respiratory failure.
INDICATIONS FOR INITIATION OF MECHANICAL VENTILATORY SUPPORT Recognition and early diagnosis of respiratory failure is essential in the emergency care setting. Respiratory failure refers to the inadequate exchange of gas by the cardiopulmonary system. Respiratory failure can be due to several different mechanisms, including failure of the ventilatory muscles (e.g., in cardiopulmonary disease), decreases in chest wall compliance (e.g., scoliosis, kyphosis, splinting after abdominal or thoracic surgery), neuromuscular disease (e.g., muscular dystrophy, GuillainBarré syndrome, myasthenia gravis), or central nervous system (CNS) dysfunction (e.g., traumatic injury, brainstem infarction or compression, pharmacological depression, drug overdose, electrolyte abnormality). Mechanical ventilation may also prove beneficial to reduce raised 844
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intracranial pressure by manipulation of blood pCO2 levels, decrease systemic or myocardial oxygen consumption, or permit sedation and/or neuromuscular blockade. Once respiratory failure has been recognized, the provider must then decide whether the patient is compensating or in need of assistance via mechanical ventilation. The most frequent indication for mechanical ventilation in the ED is failure of adequate oxygenation or ventilation. The primary goals of mechanical ventilation include improvement of gas exchange and a decrease in the work of breathing, while ensuring patient comfort. The decision to initiate mechanical ventilation is based primarily on the clinical presentation and physical examination, such as the presence of rapid, shallow breathing with use of accessory muscles, inability to speak in complete sentences, or cyanosis. However, there are some physiological abnormalities that may be an adjunct in the decision process. These include the presence of hypoxemia, defined as arterial oxygen partial pressure (PaO2) less than 50 mmHg at room air; hypercapnia, which is defined as arterial carbon dioxide partial pressure (PaCO2) greater than 50 mmHg. and a significant respiratory acidosis with a pH less than 7.25. Arterial blood gas (ABG) analysis, pulse oximetry, chest radiography, and spirometry are tools useful in defining the need for mechanical intervention.
TYPES OF MECHANICAL VENTILATORY SUPPORT All types of mechanical ventilatory support share a common goal: to support respiratory gas exchange as safely and comfortably as possible while the underlying condition responds to therapy or resolves spontaneously. The two types of support systems are negative-pressure ventilators and positive-pressure ventilators.
Negative-Pressure Ventilation Negative-pressure ventilators mimic spontaneous inspiration by facilitating chest expansion and inward flow of air into the lungs by reducing the atmospheric pressure surrounding the thoracic cavity, therefore making the alveolar pressure negative. This is achieved by generating a negative pressure around the chest wall or thorax during inspiration via a garment or device such as the head of an iron lung to substitute for the negative pleural and airway pressures normally created by contraction of the respiratory muscles. Before the mid 1950s, negative-pressure ventilation through the use of iron lungs was the predominant and most widely used method of mechanical ventilation. With the advent of endotracheal intubation in the 1960s, positive-pressure ventilation has
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become the mainstay for both invasive and noninvasive mechanical ventilation in the treatment of respiratory failure.
Positive-Pressure Ventilation Positive-pressure ventilators are characterized by gas delivery under positive pressure into the airways and lungs during inspiration. This pressure overcomes the impedance to flow and the elasticity of the respiratory system by raising the airway pressure above atmospheric pressure, leading to inflation of the alveoli, which provides both ventilation and arterial oxygenation while reducing the work of breathing. Positive-pressure ventilators provide control of all aspects of ventilation, including rate, tidal volume, flow and FiO2. When positive-pressure ventilation is applied to the respiratory system, many physiological changes occur. Normal spontaneous breathing is a process of negative-pressure ventilation. Air is naturally drawn into the airways and lungs via a negative intrapleural pressure created by chest wall expansion and diaphragmatic contraction. Exhaled gas is then moved out of the tracheobronchial tree when the diaphragm and chest wall are relaxed, decreasing the pressure gradient from the environment to the lungs. Positive-pressure ventilation forces air into the thorax against the natural physiological course, affecting mainly the cardiopulmonary system. This pressure acts to increase oxygenation by redistributing extravascular water in the lungs and to increase functional residual capacity by inflating alveoli and recruiting collapsed alveolar units with the use of positive end-expiratory pressure (PEEP). Positive-pressure ventilation may also lead to a decrease in cardiac output. MODES OF POSITIVE-PRESSURE VENTILATION Positive-pressure ventilators are classified into modes of ventilation distinguished by the mechanism to initiate, sustain, and terminate inspiration. The basic goals for the modes of positive-pressure ventilation are ventilation limited by a pressure target and ventilation limited to the delivery of a specified volume. The two most common delivery modes are pressure-cycled and volume-cycled modes of ventilation. Flow-cycle mode is another delivery mode that is less commonly used; this mode delivers gas at a set flow rate. Newer ventilators are now capable of both pressure- and volume-cycled modes of ventilation, classifying them as “dual-control” modes. Pressure-Cycled Mode With pressure-cycled ventilation, inspiration is terminated when a preset peak inspiratory pressure is reached. The delivered volume (i.e., tidal
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volume) with each respiration is dependent on pulmonary and thoracic compliance, airway resistance, and respiratory effort. Flow is delivered in a decelerating pattern, in which inspiratory flow tapers off as the lung inflates and varies from breath to breath. The advantage of this type of ventilation is that it allows for a homogeneous gas distribution throughout the lungs. Studies have suggested that patients are more comfortable breathing spontaneously while receiving ventilation via the pressure-cycled mode. However, because the tidal volume is variable with this mode of ventilation, inconsistent alveolar minute ventilation can occur, resulting in potentially inadequate ventilation. Therefore, pressure-cycled ventilators are less useful than volume-cycled ventilation in critically ill patients with rapidly changing respiratory mechanics. If pulmonary compliance decreases or airway resistance increases, hypoventilation might result. This form of ventilation requires constant and aggressive monitoring of respiratory mechanics and is less favored in the ED setting. Volume-Cycled Mode With volume-cycled ventilation, a preset tidal volume (Vt) is reached, terminating the inspiratory phase and beginning passive expiration. The goal of this strategy is to guarantee a preset minimum minute ventilation, which is usually a function of set tidal volume and set respiratory rate. The gas is delivered with a constant inspiratory flow pattern, resulting in peak pressures applied to the airways that are higher than that required for lung distention. Since the volume delivered is constant, applied airway pressures vary with changing pulmonary compliance (i.e., plateau pressure) and resistance (i.e., peak pressure). Therefore, the disadvantage of volume-cycled ventilation is the potential for barotrauma. Caution should be used in patients with poorly compliant lungs, including persons with cystic fibrosis or restrictive lung disease such as emphysema with blebs. Pressure limits are regularly checked by a respiratory therapist to avoid this complication. Volume-cycled ventilation used in the controlled mandatory ventilation (CMV), assist-control (A/C) ventilation, intermittent mandatory ventilation (IMV), or synchronized intermittent mandatory ventilation (SIMV) modes are the most commonly used forms of ventilation in the ED. SPECIFIC TYPES OF NONINVASIVE POSITIVE-PRESSURE VENTILATION Positive-pressure ventilation can be delivered invasively through an endotracheal tube or noninvasively via a face mask or nose mask. Recent studies demonstrate that noninvasive positive-pressure ventilation may successfully be used via bilevel positive airway pressure (BiPAP) ventilators in patients with hypercapnia as seen in acute exacerbations of
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chronic obstructive pulmonary disease (COPD), acute asthma attacks, and cardiogenic pulmonary edema. Noninvasive ventilation is contraindicated in patients with impending cardiovascular collapse or respiratory arrest, excessive secretions, upper airway obstruction, altered mental status, or any recent facial or upper airway surgery. This type of positive-pressure ventilation requires careful selection of an awake, cooperative patient. In appropriately selected patients, noninvasive positive-pressure ventilation has been proved to reduce the requirement of invasive endotracheal intubation by 50%. BiPAP provides differential preset support of spontaneous inspiration and expiration. Inspiration is set higher than the expiration phase. BiPAP is pressure limited and flow triggered. It senses the initiation of inspiration, which triggers a preset inspiratory positive airway pressure (IPAP), thereby increasing tidal volume with less work of breathing. This pressure is sustained for up to 3 seconds, or until the patient ceases inspiration and begins to exhale. This mode of ventilation has been used historically in nocturnal hypoventilation due to sleep apnea. However, recent studies have proved BiPAP useful in selected patients experiencing respiratory failure caused by COPD, pulmonary edema, pneumonia, and status asthmaticus. Recommended initial settings for BiPAP ventilators in respiratory distress or failure are an IPAP of 8 cm H2O and an expiratory positive airway pressure (EPAP) of 3 cm H2O for a pressure support (IPAP minus EPAP) of 5 cm H2O. BiPAP can be administered via a face mask or nose mask. Oxygen is administered based on pulse oximetry, usually starting at a rate of 2–5 L/min. Adjustments to the BiPAP settings in a patient with hypoxia include adjusting the EPAP in 2-cm increments, with IPAP at a higher fixed interval. Hypercapnic patients can be managed by raising the IPAP in 2-cm H2O steps, with EPAP being increased in a 1:2.5 ratio with IPAP. Because auto-PEEP cannot be measured in patients with noninvasive ventilation, the EPAP should not exceed 10 cm H2O in patients with COPD. Patients treated in the ED with noninvasive positivepressure ventilation generally should not be given sedatives or major analgesics that may affect respiratory drive. Continuous positive airway pressure (CPAP) is not a mode of mechanical ventilation; however, it is often useful as an adjunct to other ventilatory modes. CPAP delivers a constant level of pressure support without regard for the respiratory cycle. CPAP allows spontaneous breathing at an elevated baseline pressure. The patient controls the rate and tidal volume, which are totally dependent on the patient’s inspiratory effort. CPAP is often used in patients with sleep apnea as well as in conjunction with A/C ventilation or SIMV during the weaning process from the ventilator.
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SPECIFIC TYPES OF INVASIVE POSITIVE-PRESSURE VENTILATION Several different machine modes may be used to provide positivepressure mechanical ventilation as described later. Each mode has advantages and disadvantages (Table 15-1). In choosing a mode of ventilation, it is important to consider specific goals. The most important goals of mechanical ventilation are reducing the work of breathing, ensuring patient comfort and synchrony with the ventilator, and providing adequate ventilation and oxygenation. Pressure support ventilation (PSV) is considered a partial ventilatory support system, which provides a set amount of pressure support to each patient-generated breath and acts as an assistant ventilatory method only. The pressure assists the patient to overcome the increased resistance and work of breathing imposed by the underlying disease process or endotracheal tube. In this mode, the patient controls the respiratory Table 15-1 Advantages and Disadvantages of Different Modes of Mechanical Ventilation MODE
ADVANTAGE
DISADVANTAGE
Controlled mechanical ventilation (CMV)
Decreases work of breathing
Assist-control ventilation (A/C)
Patient determines amount of ventilatory support; reduced work of breathing; full Vt regardless of respiratory effort
Synchronized intermittent mandatory ventilation (SIMV) Pressure-support ventilation (PSV)
Less interference with normal cardiovascular function
May require use of paralytic drugs, neuromuscular blockade, or heavy sedation; asynchrony with the ventilation if patient is breathing spontaneously Tachypnea may lead to respiratory alkalosis; poor synchrony between patient and vent may lead to autoPEEP; may lead to inappropriate hyperventilation or barotrauma Increased work of breathing and respiratory muscle fatigue compared with A/C
Bi-level positive airway pressure (BiPAP)
Noninvasive form of ventilation; easily taken on or off
Patient comfort; decreased work of breathing
Vt, Tidal volume; PEEP, positive end-expiratory pressure.
Apnea alarm is only backup; variable effect on patient tolerance; needs careful monitoring to guarantee adequate Vt and minute ventilation Requires an awake, cooperative patient; no airway control
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rate, duration of inspiration, gas flow rate, and tidal volume. The delivered tidal volume varies depending on pulmonary compliance and resistance. The amount of pressure support given is titrated depending on the tidal volume exhaled by the patient. When PSV is used independently, an apneic patient will receive no ventilatory support. A backup ventilation setting is therefore required in case of apnea. PSV is rarely used in the ED. CMV represents the most basic form of positive-pressure ventilation. Breaths are supplied at a constant rate regardless of patient effort. The patient is not able to trigger any additional ventilator breaths outside the preset respiratory rate. This mode should only be used in paralyzed, apneic, or deeply sedated patients. In a patient attempting spontaneous respirations, this type of ventilation causes distress, asynchronous breathing, and increased work of breathing. Therefore, this mode is rarely used independently and is now used in synchrony with A/C ventilation. A/C ventilation is the single most commonly used mode of positivepressure ventilation in the ED setting. The ventilator is set to assist the patient with his or her own spontaneous breaths by ensuring a delivered tidal volume with each breath as well as control ventilation with the delivery of breaths if the patient becomes apneic or begins to breathe at a rate less than the set respiratory rate. A ventilator set in this mode is triggered by the patient’s own inspiratory effort responding with a full tidal volume delivery. In the absence of any such effort, it automatically cycles at a preset minimum background rate. This allows the patient to spontaneously breathe over the baseline set respiratory rate and continue to receive a full tidal volume with each breath. With proper use of A/C ventilatory support, the work of breathing may be significantly decreased. Potential disadvantages include poor tolerance in awake patients and the potential for worsened air trapping in patients with COPD. IMV is a combination of spontaneous ventilation and CMV ventilation. The background CMV rate is set and triggers regardless of any inspiratory effort made by the patient. When the patient breathes spontaneously, warmed humidified gas is supplied to the patient—but not at a set pressure or tidal volume. The disadvantage of this mode is breath stacking. Breath stacking is defined as a mechanical breath being delivered at the same time of the spontaneous breath, which can lead to hyperinflation and barotrauma. Because of this potential complication, IMV is rarely used and has been substituted with SIMV support. SIMV is a combination of spontaneous ventilation and A/C ventilation. This mode delivers a preset tidal volume at a preset number of times each minute. In addition to the preset rate, spontaneous breaths are also supplied despite whatever tidal volume the patient generates on his or her own. If the spontaneous breath occurs at the same time
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as the scheduled preset ventilator breath, the machine will synchronize with the patient. SIMV can be combined with PSV, allowing for pressure support to be added to the spontaneous breaths if desired. However, this mode is usually associated with a greater work of breathing compared with A/C ventilation and is thus less frequently used as an initial ventilator mode.
Bibliography Bone RC, Eubanks DH: The basis and basics of mechanical ventilation, Dis Mon 1991;37 (6):321–406. Calfee SC, Matthay MA: Recent advances in mechanical ventilation, Am J Med 2005;118:584. Chatburn RL, Lough MD: Mechanical ventilation. In Lough MD, Doershuk CF, Stern RC (eds): Pediatric Respiratory Therapy. Year Book: Chicago, 1985. Grabovac MT, Kim K, Quinn TE, et al: Respiratory care. In Miller RD (ed): Miller’s Anesthesia, ed 6. WB Saunders: Philadelphia, 2005. Available at: http://home.mdconsult. com/das/book/48791005–2/view/1255. Accessed on April 8, 2005. Hess RD: The evidence for noninvasive positive-pressure ventilation in the care of patients in acute respiratory failure: A systemic review of the literature, Respir Care 2004; 49(7):810. Hill NS: Noninvasive ventilation: Does it work, for whom, and how? Am Rev Respir Dis 1993;147:1050. Kreit JW, Rogers RM: Approach to the patient with acute respiratory failure. In Shoemaker WC, Ayres SM, Grenvik A, Holbrook PR (eds): Textbook of Critical Care Medicine, ed 3. WB Saunders: Philadelphia, 1995. Lanken PN: Mechanical ventilatory support. In Wilson J, Braunwald E, Isselbacher K , et al (eds): Harrison’s Principles of Internal Medicine, ed 12. McGraw-Hill: New York, 1991. Luce JM: Ventilator management in the intensive care unit. In Cecil RL, Goldman L, Bennett JC (eds): Cecil Textbook of Medicine, ed 21. WB Saunders: San Francisco, 2000. Orebaugh SL: Initiation of mechanical ventilation in the emergency department, Am J Emerg Med 1996;14:59. Pollack CV Jr: Mechanical ventilation and noninvasive ventilatory support. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St. Louis, 2002. Pollack CV, Torres M, Alexander L: A feasibility study of the use of bilevel positive airway pressure for respiratory support in the emergency department, Ann Emerg Med 1996;27:189. Slutsky AS: ACCP Consensus Conference: Mechanical ventilation, Chest 1993;104:1833.
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Acute Respiratory Distress Syndrome JULIE ANN MORGAN AND JAMES ALAN MORGAN
ICD Code: Respiratory distress syndrome (adult) 518.5
Key Points More than 50 different etiologies of acute respiratory distress syndrome (ARDS) have been documented, and all age ranges can be affected. Up to one fifth of mechanically ventilated patients meet the criteria for ARDS. ! Emergency Actions ! The mainstay of treatment is mechanical ventilation with the judicious use of PEEP to improve oxygenation.
DEFINITION Acute respiratory distress syndrome is manifested by noncardiogenic pulmonary edema and acute respiratory failure. It is the result of a wide variety of both direct and indirect insults to the lung parenchyma and is identified by a PaO2-to-FiO2 ratio (ratio of the PaO2 to the inspired fraction of oxygen) of less than 200:1. The end result is fluid leakage across the alveolar-capillary membrane producing alveolar edema and refractory hypoxemia.
EPIDEMIOLOGY More than 50 different etiologies of ARDS have been documented, and all age ranges can be affected. Up to one fifth of mechanically ventilated patients meet the criteria for ARDS. Although the syndrome is thought to be a “pattern of injury,” there is evidence to suggest a more severe course from a direct pulmonary insult (e.g., pneumonia) versus ARDS from a nonpulmonary insult (e.g., sepsis). The most common cause is sepsis, but it is also seen with aspiration events, pneumonia, trauma, near drownings, burns, pancreatitis, and drug overdose.
CLINICAL PRESENTATION The initial symptoms generally reflect the underlying cause of the precipitating condition. Within 1–2 days of the medical or surgical insult, patients
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develop pulmonary symptoms of increasing tachypnea, dyspnea, and hypoxia that is refractory to increasing oxygen supplementation. Patients may experience a dry cough and chest pain. Serial chest radiographs show progressive diffuse bilateral alveolar infiltrates. All patients will require intubation and mechanical ventilation with a clinical course marked by reduced pulmonary compliance and increasing airway pressures.
EXAMINATION Tachypnea, tachycardia, and cyanosis are common. The lung examination typically reveals diffuse crackles in all fields. The pulmonary capillary wedge pressure is less than 18 mmHg.
LABORATORY FINDINGS Laboratory test findings are nonspecific for ARDS but can include leucocytosis, evidence of disseminated intravascular coagulation, and a lactic acidosis. ABG analysis reveals severe hypoxia, with an elevated A-a gradient and respiratory alkalosis. Other laboratory findings relate to the inciting event.
DIAGNOSIS The syndrome is diagnosed on the basis of four criteria:
Acute onset Ratio of PaO2 to FiO2 of 200:1 or less (regardless of the level of PEEP) Bilateral infiltrates on frontal radiograph Pulmonary artery wedge pressure of 18 mmHg or less when measured or no clinical evidence of left atrial hypertension
TREATMENT The mainstay of treatment is mechanical ventilation with the judicious use of PEEP to improve oxygenation. Recent advances in ventilator strategy, including use of smaller tidal volumes and other maneuvers to limit airway pressures, have improved mortality rates. As patients pass through the acute phase, oxygenation improves but they remain dependent on mechanical ventilation with high minute ventilation, exhibit poor compliance, and continue to have hypoxia. The proliferative phase is associated with lung healing, but high minute ventilation requirements and a large dead space fraction are characteristic findings. Mortality remains high (between 35% and 60%) with some improvement noted in the past decade with advances in mechanical ventilation and other aspects of intensive care. Death is often attributed to the underlying insult
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and multiorgan failure. Death from refractory respiratory failure occurs in fewer than 20% of patients. Long-term survivors demonstrate persistent functional disability 1 year after discharge from the ICU with extrapulmonary conditions being most prominent.
Bibliography Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome, N Engl J Med 2000;342:1301–1308. Brower RG, Lanken PN, MacIntyre N, et al: Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome, N Engl J Med 2004;351:327–336. Frutos-Vivar F, Nin N, Esteban A: Epidemiology of acute lung injury and acute respiratory distress syndrome, Curr Opin Crit Care 2004;10:1–6. Herridge MS, Cheung AM, Tansey CM, et al: One-year outcomes in survivors of the acute respiratory distress syndrome, N Engl J Med 2003;348:683–693. Piantadosi CA, Schwartz DA: The acute respiratory distress syndrome, Ann Intern Med 2004;141:460–470.
Asthma RYAN WELLS
ICD Codes: Extrinsic asthma 493.0, Intrinsic asthma 493.1, Asthma, unspecified 493.9
Key Points Asthma is a prevalent disease and is commonly encountered in the ED. Asthma is a chronic inflammatory disease of the lower airways characterized by intermittent exacerbations with varying degrees of bronchospasm. Common presenting symptoms include wheezing, dyspnea, and cough. The mainstay of therapy is beta-2 agonist by nebulizer or metered dose inhaler (MDI). ! Emergency Actions ! Emergency actions should include rapid assessment and administration of supplemental oxygen, beta-2 agonists, and further medications to avoid the need for endotracheal intubation.
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DEFINITION Asthma is a chronic inflammatory disease of the tracheobronchial tree characterized by mild to severe obstruction of airflow. Obstruction of the bronchial airways is due to inflammation of the bronchi and contraction of the bronchial smooth muscle. Hyperresponsiveness causes the classic symptoms of dyspnea, wheezing, and cough with variable airway response. Asthma is a chronic disease with intermittent exacerbations. It has been defined as extrinsic, allergy induced, or intrinsic when no obvious extrinsic causes are found. Asthma can be triggered by a single stimulus or any number of combinations of extrinsic stimuli.
EPIDEMIOLOGY Approximately 15 million persons in the United States have asthma. Fifty percent of cases are in children younger than 10 years of age. It is the most common chronic disease of childhood. In 1999, asthma was responsible for 2 million ED visits, 478,000 hospitalizations with asthma as a primary diagnosis, and 4426 deaths. Since 1995, the rate of outpatient visits and ED visits for asthma increased, whereas the rates of hospitalization and death decreased. The prevalence and mortality of acute asthma are higher in the African American population than in white persons. Prevalence is higher in males in the under-10-years age group, is equal in the teenage years, and greater in adult women than in adult men. Risk factors include a family history of asthma or atopic skin, lower respiratory tract infection from a viral cause during infancy, and environmental exposure to tobacco smoke.
PATHOPHYSIOLOGY The understanding of the pathophysiology of asthma has advanced in the past decade. It is a condition of bronchial hyperactivity with the inflammatory component central to the pathogenesis of symptoms. Asthma is characterized by inflammation of the airways, with an abnormal accumulation of inflammatory cells in the bronchioles. Asthma is associated with increased responsiveness of the tracheobronchial tree from many different stimuli, either singly or in combination with each other. There is increased expiratory resistance as well as bronchospasm, airway inflammation, mucosal edema, and mucus plugging. This leads to air trapping, increased dead space, and hyperinflation. Allergic or extrinsic asthma is frequently associated with a personal or family history of allergic diseases such as eczema, rhinitis, and urticaria. Nonallergic or intrinsic asthma is not associated with a family or personal history of allergy. In intrinsic asthma, no extrinsic cause is
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usually found. Normal serum levels of immunoglobulin E are typically seen in nonallergic asthma. Some of the stimuli or triggers of asthma attacks include viral upper respiratory infections, pollen, dust mites, molds, animal dander, other environmental allergens, occupational chemicals, tobacco smoke, cold air, exercise, gastroesophageal reflux, sinus infections, emotional factors, and drugs such as aspirin, nonsteroidal anti-inflammatory drugs, and beta blockers. There is an early and late response in asthma. A trigger initiates the airway inflammatory response in asthma. After inhalation, these triggers may stimulate resident airway mast cells and cause cross-linking of immunoglobulin E on the mast cell surface. This will result in the release of histamine and will induce the production of prostaglandins, leukotrienes, and other enzymes. Simultaneously, cytokines derived from the mast cell will signal other inflammatory cells and their mediators to the lung. The result is airway inflammation, increased vascular permeability, mucus secretion, bronchospasm, and wheezing. These events are referred to as the early asthmatic response because they occur within minutes. A major component of the early response is bronchospasm. The late asthmatic response is delayed by hours. It is caused by a multitude of inflammatory cells continuing the inflammatory process. Of the inflammatory cells, the T cells play an important role. Antigen presenting cells may present a variety of allergenic antigens to chronically activated T helper cells. These cells then secrete multiple cytokines that maintain and intensify the local inflammatory response. Many other inflammatory cells, including mast cells and eosinophils, will respond to the T cells’ cytokines. These inflammatory cells will produce cytokines, which amplify the cellular response and the inflammatory reaction. There is a migration of inflammatory cells from the circulation into the pulmonary vasculature and the airway submucosa. A central component to the inflammatory process as well as treatment is the arachidonic acid pathway, which leads to the generation of leukotrienes. Understanding the concept of early and late asthma has clinical importance in how asthma is treated. Different therapies may be more effective at different points in the disease process. Beta-2 agonists will stabilize mast cells and are likely to be most effective in the early asthma response. Corticosteroids and leukotriene antagonists with their anti-inflammatory effects are more effective in the late asthmatic response. Asthma is a chronic disease of the airways. If treated inadequately, chronic airway inflammation can result in airway damage, including smooth muscle hypertrophy, epithelial hyperplasia, and airway connective tissue deposition. These airway changes are likely a result of repetitive or chronic airway inflammation.
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When airway obstruction occurs, there is increased airway resistance, decreased maximum expiratory flow, air trapping, increased airway pressure, hypoxemia, hypercarbia, the presence of pulsus paradoxus, and respiratory fatigue and failure.
CLINICAL PRESENTATION Asthma has variable presentations, even in the same person. The most common presenting symptoms are progressive dyspnea, chest tightness, cough, and wheezing. It is important to remember that not all patients with asthma will be wheezing and that “all that wheezes is not asthma.” Conditions that can mimic asthma include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
New-onset congestive heart failure (CHF) Aspiration of a foreign body or gastric contents Upper airway obstruction Pulmonary embolus Pneumonia or bronchitis Bronchiolitis (pediatric) Anaphylaxis COPD Vocal cord dysfunction Panic disorder and hyperventilation syndrome Endobronchial obstruction resulting from bronchogenic carcinoma or sarcoidosis
Aspects of the history that are very important to glean include the duration of symptoms and the precipitating factors. It is also very important to assess the severity risk factors, which include previous intubations, number of ICU admissions, most recent ICU admission, number of ED visits per year, date of most recent ED visit, hospitalizations per year, and time since last hospitalization. It is also important to determine whether this is how previous exacerbations have occurred. If not, what is different, and has another diagnosis become more likely? How long have the symptoms been going on? A duration of more than 2 days makes admission more likely.
EXAMINATION Rapid assessment of the patient’s condition is important. Does the patient look sick? Is the patient using accessory muscles or is he or she in the tripod position (i.e., a hunched-over sitting position with the hands supporting the torso)? Is the patient able to speak in full sentences? If the patient is unable to link at least several words between breaths, he or she is in severe respiratory distress. The patient’s skin color should be examined. Is the patient cyanotic, blue, or diaphoretic?
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The examiner should auscultate the patient’s lungs. Does the patient have wheezing? Most patients with an asthma exacerbation will have wheezing. However, some will be so “tight” that the clinician will not be able to hear wheezing until the patient has had one or two nebulizer treatments. It is important to remember that the severity of wheezing does not always correlate with the severity of the asthma attack. Prolonged expiration is a hallmark of asthma. The practitioner should also evaluate for stridor, subcutaneous emphysema, bilateral breath sounds, or other findings that may help with an alternative diagnosis. A peak expiratory flow rate (PEFR) test or spirometry should be performed on the patient before and after every nebulizer treatment. This will help the clinician objectively gauge how the patient is doing. It will provide a physiological assessment of airflow and the degree of bronchospasm. The PEFR test is commonly performed in the ED because it is inexpensive and portable. Serial measurements will document progress and help in determining whether to admit the patient. Peak flow is limited in that it is effort dependent. Peak flow can be compared with the patient’s asymptomatic baseline PEFR, if it is known. There is also a reference group for the ideal predicted peak flow based on the age, sex, and height of the patient. Unfortunately, the predicted peak flow is often inaccurate for individual patients.
LABORATORY FINDINGS Laboratory testing is rarely indicated in patients with acute asthma exacerbations. If ordered, a complete blood count (CBC) may reveal eosinophilia. A CBC may also show an elevated white blood cell count resulting from stress, steroid use, or another cause. If sputum analysis is performed, eosinophilia is characteristic. Charcot-Leyden crystals (i.e., crystalline structures representing coalescence of free eosinophilic granules), Curschmann’s spirals (i.e., bronchiolar casts of sputum), or Creola bodies (i.e., large compact clusters of sloughed mucosal epithelial cells) can be noted on sputum examination under low power. The theophylline level should be tested if the patient is using theophylline and has signs of toxicity. An ABG analysis is rarely indicated and is rarely useful clinically. A pulse oximetry can give you the information you need in most cases. If ABG is measured, a low PaO2 (correlating with a low pulse oximetry) may be evident, in addition to variable PaCO2. Early in the exacerbation, the PaCO2 is often low because the patient is hyperventilating. As the episode persists, the patient may tire and the PaCO2 will climb. Of note, the decision to intubate a patient is a clinical assessment and should not be dictated by a lab test. Electrocardiography (ECG) should be performed if a cardiac cause is in the differential diagnosis or if the patient has a dysrhythmia. If an ECG is performed in a patient with an
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asthma exacerbation, the results may be normal, may show sinus tachycardia, or may have evidence of right heart strain. Pulse oximetry measurement is desirable in all patients presenting with asthma exacerbation. Pulse oximetry often obviates the need for an ABG analysis. It also helps in assessing the severity of the exacerbation and the need for admission to the hospital.
DIAGNOSIS The diagnosis is made by history and physical examination. Most patients with asthma will tell the clinician they are having an asthma attack. If a patient is known to have asthma, ask him or her about the severity of the attack. Most asthmatics know when they are getting into trouble.
RADIOGRAPHS Chest radiography of a patient with an asthma exacerbation rarely reveals clinically significant findings. Results are usually normal or may show hyperinflation of the lung fields or streaky infiltrates. In general, a chest x-ray is not indicated in most asthma exacerbations. Chest radiography should be performed for a patient’s first attack, if the diagnosis is in doubt, if the patient has had fever (to look for pneumonia), or if the patient has pleuritic chest pain (to look for pneumothorax or pneumomediastinum). A computed tomography (CT) scan of the chest is not indicated for a simple asthma exacerbation. This should only be included if another diagnosis is being considered (e.g., pulmonary embolism [PE]).
TREATMENTS AND OUTCOME There are two main components to asthma: bronchial constriction and inflammation. Both components should be treated. Treatment for a patient with asthma who presents to the ED should proceed as follows: 1. The patient should be rapidly examined. This may take place concomitantly with the first breathing treatment. Initiate pulse oximetry. A PEFR measurement should be obtained, and oxygen should be administered by nasal cannula, starting at 2–4 L/min or higher, if needed. The patient should be monitored if he or she appears to be sick or if another cardiac or pulmonary cause is a concern. Intravenous access should be initiated for patients who appear to be ill. Intravenous fluids should be given to volumedepleted patients.
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2. The mainstay of therapy for an asthma exacerbation in the ED is inhaled beta-2 agonists. Standard treatment is albuterol 2.5–5 mg administered via nebulizer every 20 minutes, as needed. Typically, three doses are given. If needed, the patient can be placed on continuous nebulizer treatment with 10–15 mg of albuterol over approximately 1 hour. For children, use 0.15 mg/kg every 20 minutes for three doses. Continuous nebulizers in children are reserved for severe asthma at an albuterol dose of 0.3–0.5 mg/kg/hr. Many studies have shown that an MDI can be used effectively in place of the nebulizer. The MDI administers a standard 90 mg of drug per inhalation. The dose is 6–10 puffs into the spacer, which is then inhaled by the patient. This can be repeated every 20 minutes as needed. Levalbuterol (Xopenex), the R-isomer of racemic albuterol, is available as a nebulizer solution for prevention and treatment of bronchospasm. It is becoming more common in EDs around the country, and some believe it may have a better therapeutic index than racemic albuterol. However, it has not been shown to be more effective than albuterol in any well-done human clinical trial. 3. Most patients presenting to the ED will also receive ipratropium (Atrovent) 0.5 mg in their nebulizer. Current recommendations are to add inhalation ipratropium to the first three beta-2 agonist nebulizer treatments to treat severe asthma. This medication decreases bronchomotor tone, airway secretions, and airway mucosal edema. This anticholinergic agent has been shown to be beneficial, especially in children and smokers. 4. Most patients presenting to the ED with an asthma exacerbation will also be given steroids. Multiple studies show that oral corticosteroids are equivalent to intravenous corticosteroids in the treatment of asthma. Most patients can tolerate oral medications and thus are given 50–60 mg prednisone orally. If the patient cannot tolerate oral medications, 60–125 mg of methylprednisolone should be given intravenously. Some authors recommend only giving prednisone if the response to the first or second beta-agonist treatment is incomplete. Corticosteroid use decreases the relapse rates of patients with asthma. 5. Magnesium has been shown to be beneficial in severe asthma exacerbations. A meta-analysis by Rowe et al. found magnesium administration in patients with severe asthma attacks reduced hospitalizations and improved PEFR. Magnesium relaxes bronchial smooth muscle in vitro and instigates bronchodilation of asthmatic airways in vitro. Two grams of magnesium is given intravenously at a rate as fast as 1 g/min. 6. After the above have been initiated, if the patient is still experiencing a severe exacerbation, parenteral beta agonists can be administered. Terbutaline 0.25 mg or epinephrine 0.3 mg of a 1:1000 concentration is administered subcutaneously.
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7. Leukotriene antagonist zafirlukast (Accolate) or montelukast (Singulair), given orally, may produce a response in persons with severe asthma. A study by Silverman evaluating 20 or 160 mg of zafirlukast versus placebo showed a strong tendency to decrease admissions to the hospital in the 160-mg group. 8. In all persons with asthma, inhaled beta-2 agonists are the mainstay of therapy. However, in severe asthmatics, many of the previously described drugs will be administered simultaneously to avoid endotracheal intubation. 9. Noninvasive considerations include Heliox, a mixture of helium (60%–80%) and oxygen (20%–40%). It reduces the resistance to air flow and may decrease the work of breathing long enough for other medications to work and thus avoid intubation. Another consideration is a CPAP or BiPAP mask. Unfortunately, there are no controlled studies showing benefit in the treatment of asthma exacerbations with CPAP or BiPAP. 10. Endotracheal intubation is used after other efforts have been exhausted and the patient is near or at respiratory failure. Once the patient has been intubated, care must be taken to avoid causing excessively high auto-PEEP and barotrauma. Oxygenation and ventilation should be maximized while high airway pressures and barotraumas are minimized. The clinician should ensure low tidal volumes (7–8 ml/kg), low ventilation rates (10 breaths/min), and high inspiratory flow rates and provide prolonged time for expiration. Ketamine may be used for sedation because ketamine has the added benefit of causing bronchodilation. 11. Pregnancy is a special consideration. The risks of uncontrolled asthma to both the mother and fetus are higher than typical asthma medications used when treating an attack. Acute asthma exacerbations should be treated maximally.
DISPOSITION The disposition of patients experiencing an asthma exacerbation is based on several factors. The clinician must consider the patient’s appearance, pulse oximetry, vital signs, peak flow, access to medications, and follow-up. Factors that should favor admission (i.e., poor outcome risk factors) include prior intubation, recent ED visit, multiple ED visits or hospitalizations, symptoms lasting more than several days, failure of outpatient therapy, use of steroids, inadequate followup mechanisms, psychiatric illness, or complications of asthma (e.g., pneumothorax, pneumomediastinum, pneumonia, fatigue). Of note, the PEFR is one component of patient evaluation. It is effortdependent and should not be the sole factor for any decision. Nonetheless, it is an objective finding that can assist in appropriate disposition of patients.
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A patient should be admitted to the ICU if his or her symptoms include persistent respiratory distress, PEFR less than 80%, minimal air movement, endotracheal intubation, or concern that the patient may tire soon and require intubation. ICU admission should be considered if the PEFR is less than 50% of the predicted value and respiratory insufficiency is evident. A patient should be admitted to the hospital if the PEFR is less than 50% of the predicted value, if he or she is without subjective improvement, if continued wheeze and diminished air movement are evident, or if the patient exhibits some response to therapy but remains symptomatic. If there is any concern that the patient may tire soon and require intubation, he or she should be admitted to an ICU setting. Patients with PEFR between 50% and 70% of the predicted value, and who are tiring, should be considered for admission as well. Their appearance and admission risk factors should guide the clinician’s decision whether to admit. Patients may be discharged if they exhibit: normal pulse oximetry, significant improvement in symptoms, improved lung findings with good air movement, a PEFR greater than 70% of the predicted value, and adequate follow-up within 48–72 hours. Patients with a PEFR greater than 50% of the predicted value but less than 70% who appear to be well and have no admission risk factors can also be considered for discharge. Of note, all patients should be discharged home with an albuterol MDI and typically a 3- to 5-day course of steroids. Each patient should be aware of the appropriate use of an inhaler and spacer. If the patient is using a beta agonist more than twice per week, a steroid inhaler should be added to the regimen. Good return precautions should be given to the patient. Follow-up should be scheduled for within 48–72 hours.
Bibliography Alter HJ, Koepsell TD, Hilty WM: Intravenous magnesium sulfate as an effective adjunct in acute bronchospasm: A meta-analysis, Acad Emerg Med 1999;6:521–522. Asthma. Schaider JJ, Hayden SR, Wolfe RE, Barkin RM: In The 5-Minute Emergency Medicine Consult., Lippincott, Williams & Wilkins: Philadelphia, 1999, pp 104–107. Barnett PL, Caputo GL, Baskin M, Kuppermann N: Intravenous versus oral corticosteroids in the management of acute asthma in children, Ann Emerg Med 1997;29:212. Becker JM, Arora A, Scarfone RJ, et al: Oral versus intravenous corticosteroids in children hospitalized with asthma, J Allergy Clin Immunol 1999;103:586. Brennan JA: Asthma update. American College of Emergency Physicians website. 2005. Available at: http://www.acep.org. Brenner B: Asthma. eMedicine. 2004. Available at: http://emedicine.com. Cydulka RK, Khandelwal S: Acute asthma in adults. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 476–485. Cydulka RK, Emerman CL, Schrieber D, et al: Acute asthma among pregnant women presenting to the emergency department, Am J Respir Crit Care Med 1999;160:887–892.
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Idris AH, McDermott MF, Raucci JC, et al: Emergency department treatment of severe asthma: Metered dose inhaler plus holding chamber is equivalent in effectiveness to nebulizer, Chest 1993;103:665. Kay AB: Role of T cells in asthma. In MacDonald TT (ed): Mucosal T cells in Chemical Immunology, Karger: Basel, 1998. Mannino DM, Homa DM, Akinbami LJ, et al: Surveillance for asthma—United States, 1980–1999, MMWR Surveill Summ 2002;51:1. National Asthma Education Program Report of the Working Group on Asthma and Pregnancy: Management of Asthma During Pregnancy. NIH Publication No. 93–3279, 1993. National Institutes of Health, National Heart, Lung, and Blood Institute: Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. NIH Publication No. 02–5074, 2002. Newman KB, Milne S, Hamilton C, Hall K: A comparison of albuterol administered by metered-dose inhaler and spacer with albuterol by nebulizer in adults presenting to an urban emergency department with acute asthma, Chest 2002;121:1036–1041. Nowak R, Tokarski G: Asthma. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 938–956. Rowe BH, Spooner CH, Ducharme FM, et al, Corticosteroids for preventing relapse following acute exacerbations of asthma. In Cochrane Review Issue 3, 2001. Rowe BH, Bretzlaff JA, Bourdon C, et al: Intravenous magnesium sulfate in the treatment of severe asthma: A systematic review of the evidence, Ann Emerg Med 1999;43:S85. Silverman RA, Chen Y, Bonuccelli CM, et al: The Zafirlukast Acute Asthma Study Group: Zafirlukast improves emergency department outcomes after an acute asthma episode, Ann Emerg Med 2000;35:S10. Silverman RA, Nowak RM, Korenblat PE, et al: Zafirlukast treatment for acute asthma: evaluation in a randomized, double-blind, multicenter trial, Chest 2004;126:1480–1489.
Adult Bacterial Pneumonias DAVID GLENDENING
ICD Code: Bacterial pneumonia 482.9
Key Points Infectious pneumonias may be locally classified by the population at risk as either community-acquired (CAP) or nosocomial/hospital-acquired pneumonia (HAP). A specific pathogen is not identified in 40%^60% of patients with the diagnosis of pneumonia. ! Emergency Actions ! As with any disease, pneumonias may present with any degree of severity, and the cardinal ABCs of resuscitation (i.e., airway, breathing, and circulation) should never be ignored. Evaluation, stabilization, and initial therapies frequently occur simultaneously.
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DEFINITION Pneumonias are infections of the gas-exchanging portions of the lung—classically occurring with consolidation. Pneumonia was first described by Sir William Osler as “an infectious disease characterized by inflammation of the lungs and constitutional disturbances of varying intensity.” In the broadest sense, pneumonias include any inflammation of the pulmonary parenchyma. Bacterial pneumonias occur by various routes of infection. Patients at the greatest risk are those with immunocompromise, multiple comorbidities, and impaired mucociliary clearance mechanisms.
EPIDEMIOLOGY Infectious pneumonia can be locally classified by the population at risk as either CAP or HAP. HAP arises more than 48 hours after admission and was not incubating at the time of patient admission. Ventilatorassociated pneumonia arises more than 48–72 hours after endotracheal incubation. Healthcare-associated pneumonia is defined as pneumonia in a patient who was hospitalized for 2 or more days within 90 days of the infection; resided in a nursing home or long-term care facility; received recent intravenous antibiotic therapy, chemotherapy, or wound care within 30 days of the infection; or attended a hospital or hemodialysis clinic. CAP is the more common variety in most emergency care settings, with about 4 million cases annually and 1 million hospitalizations in the United States. Pneumonias are the sixth leading cause of death in the United States and the major cause of death due to infectious disease. A specific pathogen is not identified in 40%–60% of patients, but pneumococcus remains the most common single bacterial pathogen involved, accounting for 40%–80% of CAP in adults. It is the most frequent cause of death in persons who die from CAP. CAP due to opportunistic and atypical infections is being recognized with increasing frequency. “Atypical” agents are numerous and include legionella, mycoplasma, chlamydia, Coxiella organisms, Francisella tularensis, and viruses. Legionella is the most common atypical pathogen in hospitalized adults, and mycoplasma is the most common atypical cause of CAP in patients younger than 40 years of age.
PATHOPHYSIOLOGY Pneumonias occur year-round, more commonly in middle aged and elderly persons and with increased mortality at the extremes of age, giving rise to its historical characterization as “the old man’s friend” and “captain of the men of death.”
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Infectious inoculations of the lung may occur via aspirations, inhalation, or hematogenous seeding. Once established, the infection spreads via the bronchial arborizations or the channels of collateral ventilation. Bacterial replication and the host’s inflammatory response may result in exudative filling of air spaces, ventilation-perfusion mismatching, hypoxemia, and radiographic infiltrates. Mortality increases with age, comorbidities, multilabor involvement, leucopenia, hypotension, hypoxemia, and the advent of sepsis.
CLINICAL PRESENTATION The clinical presentation of pneumonia may vary widely and is influenced by its infecting pathogen, the duration of illness, the extent of involvement, and the age and baseline status of the patient. Clinical diagnosis may be difficult due to the variety of symptoms and physical findings. A usual but nonspecific presentation may include any combination of cough, sputum production, fever, chills, dyspnea, and pleuritic chest pain. The classical presentation for pneumococcal pneumonia includes abrupt onset, often with pleuritic pain that may proceed to a single rigor and fever. Cough may be absent, and the chest radiograph may be nondiagnostic. Older patients may present without typical respiratory symptoms manifesting only mental status changes or decline in function. Constitutional symptoms of headache, myalgias, and nausea are common along with signs of fever, tachycardia, tachypnea, and vomiting. There are no clinical or radiographic features that regularly distinguish the pathogens in bacterial pneumonias, and a specific etiology is not identified in a very significant number of patients.
DIAGNOSIS In the ED, the presence of pneumonia is initially suspected based on a variety of presenting signs and symptoms. Vital signs may give important clues, and pulse oximetry is appropriate if respiratory symptoms or tachypnea are present. If pneumonia is a consideration, chest radiography is generally appropriate. Predictors of radiographic pneumonia in adults presenting with acute respiratory symptoms include temperature higher than 37.8 F, pulse faster than 100 beats/min, rales, diminished breath sounds, and the absence of asthma. Radiographic pneumonia is initially absent in one third of patients with serious lower respiratory infections. Approximately two thirds of admitted patients with “suspected pneumonia” initially will have “normal” results on chest radiography. They will exhibit significant radiographic findings within 72 hours.
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LABORATORY FINDINGS Screening laboratory studies may reveal complicating acute or chronic comorbidities that contribute to overall risk and mortality such as leukopenia (<4000), neutropenia (<1000); leukocytosis (>30,000), coagulopathy, renal insufficiency, hepatocellular diseases, or acidosis. Cultures of sputum and blood have very little utility in the initial evaluation and management of pneumonia in the ED. Gram stains of sputum samples are not generally useful and would not identify atypical organisms. Regional or personal preferences vary regarding blood cultures for admitted patients, but the results infrequently cause a change in therapy. The data synthesis from history, laboratory presentation, clinical features, and radiography does not allow a specific etiological diagnosis. The responsible pathogen is not defined in at least half of cases.
DISPOSITION As with any disease, pneumonias may present with any degree of severity, and the cardinal ABCs of resuscitation should never be ignored. Evaluation, stabilization, and initial therapies frequently occur simultaneously. Decisions regarding disposition and therapy are inter-related because recommendations for therapy are influenced by whether the patient is ambulatory or hospitalized. Determining which patients can be safely discharged and which require hospital admission may be difficult and subjective to clinical debate. Major variables influencing disposition decisions must include the severity of illness at presentation, advanced age, and coexisting illness. Various scoring systems have been proposed to codify the disposition dilemma, and careful evaluation of risk factors must influence the decision. Comorbidities and risk factors include age older than 65 years, COPD, diabetes, chronic renal insufficiency, CHF, neoplasm, altered mental status, cerebrovascular accident, alcohol abuse, malnutrition, HIV infection, anemia, splenectomy, multilabor involvement, pleural effusion, neutropenia, hypotension, hypoxemia, hypercarbia, and acidosis. Rather than a rigid reliance on any of several risk severity stratification formulas, decisions regarding disposition may well remain an “arc of medicine.” Risk factors must influence disposition and therapy decisions because, when present (and especially if multiple), they greatly increase the risks of a complicated course of illness and death. Very simply put, any patient with any risk factors who “looks sick” or who lacks a reliable caregiver should be considered for admission to the hospital.
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Table 15-2 Antibiotics in CAP PATIENT Ambulatory
Older than 60 years Hospitalized
FIRST CHOICE Macrolide Azithromycin Clarithromycin Tetracycline Doxycycline Fluoroquinolone Levofloxacin Gatifloxacin Fluoroquinolone Levofloxacin Gatifloxacin Ceftriaxone or cefotaxime plus macrolides Fluoroquinolone Levofloxacin Gatifloxacin
SECOND CHOICE Amoxicillin/clavulanic and 875/ 125 Second-generation cephalosporin Cefdinir Cefprozil Cefprozil Cefuroxime axetil Amoxicillin/clavulanic 875/125 Cefuroxime plus macrolides Beta-lactam/beta-lactamase inhibitor plus macrolide
Antibiotic therapy of adult bacterial pneumonias allows for choices (Table 15-2), and it may be useful to think in terms of “the bug, the drug, and the host.” We want to select the right weapon (drug) to kill the enemy (bug) to save our patient (host) with the least collateral damage. Bacterial susceptibility and antibiotic resistance patterns may vary on local, regional, or international scale and should influence the choice of antibiotics, as must patient allergies and pregnancy status.
Bibliography American Thoracic Society: Guidelines for the initial management of adults with community acquired pneumonia, Am Rev Resp Dis 1993;148:1418–1426. American Thoracic Society, Infections Disease Society of America: Guideline for the management of adults with hospital acquired, ventilator associated and healthcare associated pneumonia, Am J Respir Crit Care Med 2005;171:388–416. Giernsheimer J: Antibiotics in the ED: How to avoid the common mistakes of treating not wisely but too well, Emerg Med Pract 2005;7(4):1–32. Infectious Disease Society of America: Community acquired pneumonia in adults: Guidelines for management, Clin Infect 1998;26:811–838. Mamde LA: Community acquired pneumonia: Etiology, epidemiology and treatment [review], Chest 1995;108:S355–S425.
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Aspiration Pneumonia MELISSA KAGARISE
ICD Codes: Aspiration pneumonia bacterial 482.9, Aspiration pneumonia viral 480.0, Aspiration pneumonia food 507.0, Aspiration pneumonia vomitus 507.00
Key Points Any condition that increases the volume or bacterial count of secretions in a patient with impaired respiratory defense mechanisms can lead to aspiration pneumonia. ! Emergency Actions ! Any patient with suspected aspiration pneumonia should have his or her airway evaluated and 100% oxygen administered. Oxygen saturation should be determined. If oxygen saturation is below 90%, an arterial blood gas should be obtained and treatment directed toward airway maintenance and oxygenation.
DEFINITION Aspiration is defined as inhalation of fluid or foreign body into the lungs. There are three types of syndromes based on the particulate substance that has been aspirated: aspiration or chemical pneumonitis, bronchial obstruction, and aspiration pneumonia. Aspiration or chemical pneumonitis is the inflammatory response within the lungs from the introduction of gastric contents. Bronchial obstruction occurs when a foreign body is lodged within the airway. Aspiration pneumonia is the inflammation and subsequent infection as a result of the aspiration of oropharyngeal contents into the tracheobronchial tree. Aspiration pneumonia occurs as a result of polymicrobial infection by aerobic organisms found within the oropharyngeal secretions. Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae have been found to be the most common etiological organisms in community-acquired cases. Pseudomonas aeruginosa and enteric gram-negative bacilli are commonly found in hospitalized and severely compromised patients. Left untreated, aspiration pneumonia may progress causing lung abscess, necrotizing pneumonia, or empyema.
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EPIDEMIOLOGY During sleep, approximately half of all healthy persons will aspirate minute amounts of oropharyngeal secretions without sequelae. This is termed microaspiration. Aspiration of larger amounts of material leads to the colonization of organisms within the lungs. Any condition that increases the volume or bacterial count of secretions in a patient with impaired respiratory defense mechanisms can lead to aspiration pneumonia. Persons with impaired deglutition due to esophageal disorders, CNS disease (e.g., stroke or seizure), depressed levels of consciousness (from drug use, alcohol use, or general anesthesia), or disruption of the natural airway defenses (e.g., tracheal or nasogastric intubation) are predisposed to the development of aspiration pneumonia.
CLINICAL PRESENTATION The diagnosis of aspiration pneumonia is usually made through a high index of suspicion. Many times the actual episode of aspiration has not been witnessed. A history of an event such as vomiting, coughing while eating, displacement of a feeding tube, or tube feeding on bed clothes will alert the clinician of the likelihood of aspiration. Symptoms of aspiration pneumonia occur over a period of several days. Constitutional symptoms such as fever, loss of appetite, and malaise will be present. Shortness of breath, tachypnea, and a cough with purulent sputum production are characteristic. Symptoms progress as the bacterial agent continues to proliferate, leading to weight loss and copious foul-smelling sputum when a lung abscess has formed. Additionally, necrotizing pneumonia may develop with fevers of 102 –103 F and putrid sputum production.
PHYSICAL EXAMINATION Physical examination findings include coarse rhonchi localized over the dependent lung zones. Signs of consolidation may or may not be present at initial presentation. Additional physical examination findings relative to the underlying illness will be present.
RADIOGRAPHS Any patient suspected of having aspiration pneumonia based on history and physical examination must undergo radiography to demonstrate the consolidation. The location of the pneumonia will depend on the position of the patient when the aspiration occurred. A patient who aspirated while in the recumbent position will have patchy infiltrates in the posterior segment of the upper lobes. Aspiration occurring in an upright or
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semi-recumbent position will have changes in the posterior basal segments of the lower lobes. Development of a lung abscess will show the presence of a cavity with an air-fluid level located in a dependent segment.
LABORATORY FINDINGS Laboratory studies are of limited value when diagnosing a patient suspected of having aspiration pneumonia. A CBC may reveal leukocytosis, and ABG analysis results may reflect hypoxia or hypoventilation. Sputum cultures commonly yield inconclusive results resulting from the increased rate of oropharyngeal contamination. Transthoracic aspiration, thoracentesis, or bronchoscopy are the only procedures that could provide an accurate culture sample.
DIAGNOSIS The diagnosis of aspiration pneumonia is often made on the basis of the patient’s clinical history, physical examination results, and chest radiographs. Invasive sampling for cultures should be used only when empirical treatment is ineffective or when it is imperative to know the offending agent.
TREATMENT Treatment with empirical broad-spectrum antibiotics should be initiated for the treatment of aspiration pneumonia. Levofloxacin 500 mg daily or ceftriaxone 1–2 g/day should be started for patients who present with CAP. Patients residing in long-term care facilities should receive levofloxacin 500 mg/day, piperacillin-tazobactam 3.375 g every 6 hours, or ceftazidime 2 g every 8 hours. Consultation with an infectious disease or pulmonology specialist should be obtained for patients in respiratory distress, for persons receiving ventilatory support, or when necrosis or cavitation is evident on radiography.
Bibliography Cunha B, Rakel R (eds): Conn Current Therapy, ed 57. Elsevier: Philadelphia, 2005, p 290. Ferri F: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment. Mosby: St Louis, 2005. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Isbister GK, Downes F, Sibbritt D, et al: Aspiration pneumonitis in an overdose population: Frequency, predictors, and outcomes, Crit Care Med 2004;32(1):88–93.
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Kasper D, Braunwald E, Fauci A, et al: Harrison’s Principles of Internal Medicine, ed 16. McGraw Hill: New York, 2005. Mandell G: Principles and Practice of Infectious Diseases, ed 5. Churchill Livingstone: New York, 2000. Marik PE: Aspiration pneumonitis and aspiration pneumonia, N Engl J Med 2005;344 (9):665. Marik PE, Kaplan D: Aspiration pneumonia and dysphagia in the elderly, Am Coll Chest Phys 2003;124(1):328–336. Tierney L, McPhee S, Papadakis M: Current Medical Diagnosis and Treatment, ed 44. McGraw-Hill: New York, 2005. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw Hill: New York, 2004.
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Ventilator Settings and Ongoing Monitoring of Critical Patients in the Emergency Department STACEY BLACK PEARLMAN Emergency medicine providers must have a basic understanding of how to manage mechanical ventilation and how to provide the optimal quality of care for critical patients while they are waiting for an ICU bed in the ED. The same is true if an emergency physician is called to the ICU to assist in the management of a ventilator crisis. The provider must be able to initiate appropriate ventilator settings as well as recognize special ventilator needs of patients with obstructive lung disease, asthma, ARDS, pneumonia, or pregnancy. Once the patient is intubated, continuous monitoring and respective ventilator changes are essential. Knowledge of the potential complications from mechanical ventilation and ways to prevent these complications are also very important.
INITIAL VENTILATOR SETTINGS When initiating ventilatory support in adults, the clinician must first select the appropriate mode of ventilation. The mode of the ventilator should be tailored to the needs of the patient. For the apneic or paralyzed patient, CMV, A/C ventilation, or SIMV mode is acceptable. For the patient who has inadequate breathing or hypoventilating, A/C ventilation is the best approach. Overall, A/C ventilation is the most commonly used mode of ventilation in the ED.
RESPIRATORY RATE An appropriate respiratory rate (RR) for the desired minute ventilation should be chosen. Normal minute ventilation (Vt RR) is approximately 7–8 L/min. The minute ventilation should be titrated to produce the PaCO2 level that allows the appropriate acid-base (pH) status for the patient’s clinical condition. If A/C ventilation is used, the rate should be set to about 4 breaths/min lower than that of the patient’s spontaneous breathing. This allows assessment of the patient’s PaCO2 and minute ventilation and prevents a significant decrease in minute ventilation if apnea occurs. An initial respiratory rate set between 8 and 12 breaths/min is usually sufficient for clinically stable patients in acute respiratory failure or in a patient with apnea. If SIMV is used, the rate should be adjusted to achieve at least 80% of the patient’s minute ventilation.
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Tachypnea, defined as a respiratory rate over 20 breaths/min, is a red flag when it occurs before intubation. The etiology of the tachypnea must be addressed to appropriately choose the correct respiratory rate setting. Often in the ED, paralytic drugs are used during the rapidsequence intubation process. In a paralyzed patient, the clinician must remember to treat the patient’s pain and give adequate sedation to reduce anxiety and provide comfort. In a patient who is not paralyzed and continues to be tachypneic, anxiety or undersedation are potential reasons. Sedatives, analgesics, or both may be necessary to aid in the comfort of patients and synchrony with the ventilator, which often lowers the respiratory rate. However, the clinician must distinguish between undersedation or discomfort versus a physiological compensation for a metabolic abnormality. An ABG analysis is a useful adjunct to make this distinction. If the patient is hyperventilating as a result of compensation for a metabolic acidosis, the respiratory rate should be set to mimic the patient’s spontaneous rate prior to intubation or use of paralytic drugs. It should be remembered that when paralytic medications are used, the patient’s ability to compensate is reduced. Therefore, compensation for the metabolic abnormality must be correctly accounted for in the ventilator settings to avoid a potentially catastrophic complication. As the metabolic acidosis is corrected, the ventilator respiratory rate setting should be adjusted appropriately.
TIDAL VOLUME Tidal volume is a measure of the amount of air a person inhales during a normal breath. Traditional preset tidal volumes higher than 10 ml/kg have been proved to be associated with increased risk of pulmonary barotrauma and should be avoided. High tidal volumes also decrease venous return and reduce cardiac output. For patients with no significant lung disease, such as patients who have experienced drug overdose or trauma, a maximum tidal volume of 10 ml/kg should be used for mechanical ventilation. Recent studies have shown decreased mortality with the use of lower tidal volume in patients with acute lung disease. Therefore, patients with an acute lung disease such as pneumonia, ARDS, fibrotic lung disease, or COPD should be ventilated with tidal volumes of 6–8 ml/kg.
FRACTION OF INSPIRED OXYGEN The fraction of inspired oxygen (FiO2) is usually set at 100% at the initiation of mechanical ventilation so that maximal amounts of oxygen are available during the patient’s adjustment to the ventilator and during the
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initial attempts to stabilize the patient’s condition. Attempts should be made to titrate the FiO2 down as rapidly as possible to maintain the SaO2 <90% or PaO2 <60 mmHg. A FiO2 less than 50% is preferable to minimize oxygen toxicity.
Positive End-Expiratory Pressure Positive end-expiratory pressure is defined as an elevation in alveolar pressure above atmospheric pressure at the end of exhalation. Clinically, mechanical ventilators can apply PEEP either invasively via an endotracheal tube or noninvasively via a tight fitting mask. The application of PEEP improves oxygenation and increases functional residual capacity. PEEP acts to distend alveoli so that the surface area between the alveoli and capillary is increased as well as to increase lung compliance by recruiting previously collapsed airways. PEEP enables the clinician to lower the FiO2, thus preventing O2 toxicity. Initially, “physiological” PEEP is set at 3–5 cm H2O to prevent the decrease in functional residual capacity seen in endotracheal intubation. The key is to set the PEEP high enough to inflate or distend the diseased/collapsed alveoli while being careful not to overdistend the healthy, functional alveoli. Studies have shown that PEEP less than 10 cm H2O will probably keep healthy alveoli open at end exhalation but will not be enough to distend diseased airways. During ventilation, these airways will then continually open and collapse. PEEP can be titrated up in increments of 2–3 cm H2O, not to exceed 15 cm H2O if possible. The adverse effects of elevated PEEP include barotrauma resulting in a pneumothorax, hypotension, decreases in cardiac output from reduced venous return to the heart, and an increase in PaCO2.
INHALATION/EXHALATION RATIO The times for inhalation (inspiratory) and exhalation (expiratory) is measured as the inspiratory/expiratory (I/E) ratio. This reflects the duration of machine ventilations and rest periods between them. During spontaneous breathing, the normal I/E ratio is 1:2, indicating that the exhalation time is twice that of the inspiration time. In chronic lung disease, the exhalation time becomes prolonged, resulting in an I/E ratio change of 1 to 2.5–4. These conditions should directly influence the clinician’s ventilator setting selection to avoid air-trapping and autoPEEP (Table 15-3). The I/E ratio is often set by the respiratory therapist unless otherwise specified.
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Table 15-3 Typical Initial Ventilator Settings
SPECIAL CONSIDERATIONS Each patient requiring mechanical ventilation should be managed individually. Some persons require special ventilator settings, as described in Table 15-4.
COPD Exacerbation Patients with an acute exacerbation of COPD may have a respiratory acidosis, a condition that should be corrected gradually over hours. In Table 15-4 Special Ventilator Setting Circumstances
SPECIAL NEEDS COPD exacerbation, respiratory acidosis Status asthmaticus ARDS
MODE CMV, A/C, SIMV *any mode with PHC CMV, A/C, SIMV *any mode with PHC CMV, A/C, SIMV
VT FIO2 (ML/ (%) KG)
RR (BREATHS/ PEEP (CM MIN) H2O)
I/E RATIO
100
5–10
10–12
2.5–10
1:3–1:4
100
5–8
8–12
2.5–10
1:3–1:4
100
5–10
8–12
2.5–10
1:4
100
5–8
6–10
2.5–10
1:4
100
6–8
20–25
2.5–10
1:2
Adapted from Pollack CV Jr: Mechanical ventilation and noninvasive ventilatory support. In Marx JA, Hockberger RS, Walls RM (eds): Rosen's Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. FiO2, Fraction of inspired oxygen; Vt, tidal volume; RR, respiratory rate; PEEP, positive endexpiratory pressure; I/E, inspiratory/expiratory; COPD, chronic obstructive pulmonary disease; CMV, controlled mandatory ventilation; A/C, assist-control ventilation; SIMV, synchronized intermittent mandatory ventilation; ARDS, acute respiratory distress syndrome. *Permissive hypercapnia (PHC) is a ventilatory strategy that can be used in multiple modes.
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these patients, it is important to know the patient’s baseline PaO2, PaCO2, and pH levels, if possible. Overcorrection of hypercapnia and acidosis can lead to metabolic alkalosis, hypokalemia, and hypophosphatemia. Patients with COPD are at increased risk of barotrauma from auto-PEEP. If the auto-PEEP becomes significantly high, the immediate solution is to momentarily disconnect the patient from the ventilator and allow complete exhalation. The rate and tidal volume should be kept as low as possible for patients with COPD. An ARDS Network trial demonstrated a 10% decrease in mortality with lower tidal volume (6 ml/kg) compared with conventional tidal volume (12 ml/kg).
Asthma Exacerbation Similar to the appropriate course in patients with COPD, the tidal volume and respiratory rate should be minimized as much as possible in patients with asthma. If peak pressures are elevated despite conventional ventilator settings, further reductions in tidal volume or respiratory rate leading to increases in PaCO2 to 70–90 are acceptable as well as a pH as low as 7.20. Both patients with asthma and those with COPD often benefit from the clinician allowing the PaCO2 to remain well above 40 mmHg without ventilatory correction, a procedure known as controlled hypoventilation or permissive hypercapnia (PHC). PHC is one way to reduce lung volumes, thereby reducing auto-PEEP and the risk of barotrauma while maintaining adequate oxygenation. PHC should only be initiated in the ED with the support of a pulmonary or critical care consultant.
Acute Respiratory Distress Syndrome ARDS is usually seen in the ICU after the patient has been transferred out of the ED. However, with the longer lengths of stay of critical patients in the ED awaiting beds in the ICU, ARDS is now becoming evident in the ED setting. If suspected, the goal of the ventilator setting should be to keep PEEP and FiO2 as low as possible with small tidal volume (6–8 ml/kg) and rapid respiratory rate (20–25 breaths/min). These patients often require a higher PEEP, which puts them at risk of barotrauma.
Pregnancy Due to the physiological changes that occur with pregnancy, adjustments should be made in the ventilator settings to adjust for increased tidal volume and normal respiratory alkalosis. During the last trimester of pregnancy, the physiological PaCO2 is 30 mmHg.
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MONITORING DURING MECHANICAL VENTILATION Patient Positioning and Complimentary Equipment All patients undergoing mechanical ventilation should be observed via continuous telemetry monitoring with frequent blood pressure and pulse oximetry evaluation. Tachycardia may indicate ventilator intolerance and a need for an increase in sedation or analgesia. Bradycardia and ventricular irritability may indicate hypoxemia. All patients should have the head of the bed elevated above 30 degrees to reduce the risk of pneumonia, unless contraindicated in patients with skeletal trauma or risk of increased intracranial pressures. In invasive positive-pressure ventilation, a portable chest radiograph is necessary to confirm endotracheal tube placement and to rule out a pneumothorax. A nasogastric or orogastric tube is useful to be placed postintubation to decompress the stomach and air or gastric contents reducing the potential complication of aspiration. In patients who need frequent ABG monitoring, an arterial line is helpful to reduce the number of arterial blood sticks, as well as to evaluate continuous blood pressure.
Arterial Blood Gas ABG measurements provide valuable information about the adequacy of oxygenation, ventilation, and acid-base balance. An ABG analysis should be obtained within 15–30 minutes after intubation to evaluate the need for adjustment in ventilator settings. After each change on the ventilator, a new ABG check should be considered to evaluate the effectiveness of the adjustment. The PaO2 should verify the accuracy of the transcutaneous pulse oximetry readings. If the noninvasive pulse oximetry and PaO2 from the ABG correlate, the FiO2 can be adjusted based on the noninvasive pulse oximetry alone. The PaCO2 guides the need for adjustments in minute ventilation.
Oxygenation In most patients, the ideal PaO2 is 60–80 mmHg with a correlating noninvasive pulse oximetry of more than 90%. As previously described, the initial FiO2 setting should be at 1.0 or 100%. After the initial ABG results, the goal is to lower the FiO2 to less than 50% in a timely manner to prevent oxygen toxicity. The FiO2 should never be less than 30%. If more than 50% FiO2 is needed, PEEP should be increased. However, careful monitoring is necessary when increasing PEEP as to not result in barotrauma. Ideally, the maximum PEEP that is considered safe in most
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patients is no more than 10 cm H2O. PEEP is adjusted upward in increments of 2.5–5 cm H2O to allow a reduction in FiO2 to acceptable levels. A pulmonary or critical care consultation is recommended in patients who require the upper limits of FiO2 and increased PEEP.
Ventilation The pH and minute ventilation (Ve) are key components of the monitoring of a ventilated patient. The Ve is calculated by RR Vt. The PaCO2 is directly proportionate to ventilation and the pH. For every 10-mmHg change in the PaCO2, the pH will change by 0.03–0.08 depending on acute versus chronic compensation. Adjustment of the respiratory rate or tidal volume should be aimed at achieving a normal pH (range, 7.35–7.45) and correcting the acid-base abnormality, rather than adjusting PaCO2 levels. A thorough understanding of acid-base abnormalities is essential in ventilatory management (Tables 15-5 and 15-6).
Peak and Plateau Pressures The respiratory therapist plays a vital role in the monitoring of the pulmonary mechanics. This specialist is typically responsible for recording and monitoring the ventilator settings as well as peak and plateau pressures. The peak and plateau pressures should be closely monitored. The peak inspiratory pressure (PIP) is the highest pressure measured during the respiratory cycle and is a function of both the resistance of the airways and the compliance of the respiratory system. Peak pressure is the force required to push air through the airways and to inflate the lungs. The plateau pressure is the pressure recorded during a pause at end-inspiration, which reflects the static compliance of the respiratory system, including the lung parenchyma, chest wall, and abdomen. Plateau pressure is the force required to keep the lung inflated. The goal is to keep the plateau pressures below 30 cm H2O to avoid pulmonary complications such as barotrauma. The PIP can be considered an additional vital sign in the monitoring of a vented patient. A decrease in PIP reflects inadequate volume delivery to the patient, which may in turn be caused by a machine abnormality such as insufficient gas supply to the ventilator, inadvertent change on the ventilator, a leak in the breathing circuit, or unintended extubation or disconnection from the ventilator. An increase in PIP may indicate an endotracheal tube occlusion by secretions or kinking of the tubes, acute bronchospasm, pneumothorax, or development or worsening of pulmonary edema. In patients with asthma or COPD, a decrease in the PIP indicates less airway resistance and improvement in the
Table 15-5 Suggested Basic Ventilator Changes* GOAL
POTENTIAL ABG RESULTS
ACTION TO BE TAKEN
PaO2 >60 mmHg or SaO2 >90%
PaO2 <60 mmHg or SaO2 <90%
pH 7.35–7.45, Ve will increase or decrease PaCO2
Normal pH
Baseline PaCO2{ Low PaCO2{ High PaCO2}
High pH (>7.45)
Baseline PaCO2{
Low PaCO2{ High PaCO2}
Titrate down the FiO2 to obtain the ideal PaO2 of 60–80 mmHg or SaO2 of 90%–100%. *Do not lower beyond 30% FiO2. Increase the FiO2 as needed. If more than 50% FiO2 is needed, then increase the PEEP by 2.5-cm H2O increments, as tolerated. *Do not exceed a PEEP of 10 cm H2O, if possible. A critical care or pulmonary consultation may be needed if the PEEP is over 10 cm H2O. No action is required. Decrease the RR or lower the Vt. Increase the RR to the patient's baseline PaCO2 to blow off CO2. *Limit the respiratory rate increase to 26; watch for auto-PEEP. Decrease the RR or lower the Vt if the acid-base disorder is a primary respiratory alkalosis but is not metabolic. Decrease the RR or lower the Vt. If it is unclear which disorder is present, it may be a mixed respiratory/metabolic disorder. (Continued)
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PaO2 >60 mmHg, SaO2 >90%
879
POTENTIAL ABG RESULTS
Low pH (<7.35)
PIP <50 mmHg, plateau pressure <30 cm H2O
Plateau pressure >30
Baseline PaCO2{
Low PaCO2{
High PaCO2}
ACTION TO BE TAKEN Consultation with a critical care or pulmonary specialist is recommended. Increase the RR or increase the Vt; this may not be effective if the primary disorder is metabolic. The patient is compensating; correct the underlying metabolic acidosis. Increase RR or increase the Vt. Decrease Vt. Reassess PEEP. Switch to pressure-cycled mode.
PaO2, Arterial oxygen partial pressure; SaO2, oxygen saturation in arterial blood; FiO2, fraction of inspired oxygen; PEEP, positive end-expiratory pressure; Ve, minute ventilation; RR, respiratory rate; Vt, tidal volume; PIP, peak inspiratory pressure. *This table should only be used as a basic guideline; the clinician must treat and manage each patient individually based on the underlying etiology. Ventilatory settings are not a treatment for the underlying disease {Baseline PaCO2 refers to the patient's normal PaCO2; for example, an average patient with no prior lung disease should have a baseline PaCO2 of 35–45 mmHg, whereas a patient with a history of obstructive lung disease may have a baseline PaCO2 <45 mmHg. {Low PaCO2 refers to a measured PaCO2 lower than the patient's baseline PaCO2. }High PaCO2 refers to a measured PaCO2 greater than the patient's baseline PaCO2.
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Table 15-5 Suggested Basic Ventilator Changes*—Cont’d GOAL
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Table 15-6 Glossary of Common Pulmonary Ventilatory Acronyms ACRONYM ABG A/C ARDS ARF CMV CPAP ETI ETT FiO2 FRC IBW IMV NPV MV PaCO2 PaO2 PEEP PIP PPV PSV RR SIMV Ve Vt
DEFINITION Arterial blood gas Assist-control ventilation Adult respiratory distress syndrome Acute renal failure Controlled mechanical ventilation Continuous positive airway pressure Endotracheal intubation Endotracheal tube Fraction of inspired oxygen Functional reserve capacity Ideal body weight Intermittent mandatory ventilation Negative-pressure ventilation Minute ventilation Arterial carbon dioxide partial pressure Arterial oxygen partial pressure Positive end-expiratory pressure Peak inspiratory pressure Positive-pressure ventilation Positive support ventilation Respiratory rate Synchronized intermittent mandatory ventilation Minute ventilation Tidal volume
patient’s condition. The expiratory volume should also be assessed periodically by the respiratory therapist to ensure that the set tidal volume is being delivered.
PEEP and Auto-PEEP Careful monitoring of potential auto-PEEP is also very important. AutoPEEP, also known as intrinsic PEEP, is often the result of improper assisted ventilation when adequate time is not allowed between breaths for complete exhalation. This phenomenon is commonly referred to as “breath stacking.” The end-expiratory pressure in the alveoli becomes more positive than the positive pressure in the more proximal airways, resulting in hyperinflation and barotrauma. Auto-PEEP can be directly measured in many of the newer ventilators by the respiratory therapist. Minute ventilation (Ve) greater than 15 L/min creates a high risk for development of auto-PEEP. Reduction in undesirable auto-PEEP is usually accomplished by shortening the inspiratory time, increasing the flow rate or decreasing tidal volume (which reduces minute ventilation), suctioning the airway to remove phlegm, or using bronchodilators to relieve obstruction. Auto-PEEP occurs in a majority of patients with obstructive respiratory failure such as acute COPD or asthma exacerbations.
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ALARMS Modern ventilators are equipped with alarms and monitors, which assist with patient management and adverse event detection. Alarm parameters are usually set by the respiratory therapist when initiating ventilatory support.
POTENTIAL COMPLICATIONS OF MECHANICAL VENTILATION The endotracheal tube itself can lead to damage of the larynx and trachea. Studies have shown that the longer the endotracheal tube is in place, the more likely the development of laryngeal edema, stenosis, or laryngospasm. Barotrauma resulting in a tension pneumothorax is the most lifethreatening complication of positive-pressure ventilation. Mechanically applied gases tend to be diverted toward normal healthy alveoli because of inflammation or lung injury. This results in alveolar overdistention and the potential for a tension pneumothorax. Hypotension may result from reduced preload and dynamic hyperinflation caused by positive-pressure ventilation. This is commonly due to high mean airway pressures that result from the airflow obstruction seen in COPD and asthma. Infectious complications such as ventilator-associated pneumonia are also possible. These infections are usually discovered after multiple days on the ventilator and are rarely discovered in the ED setting.
Bibliography Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome, N Engl J Med 2000;342:1301. Amato MB, Barbas CS, Medeiros DM, et al: Beneficial effect of the ‘open lung approach’ with low distending pressures in acute respiratory distress syndrome, Am J Respir Crit Care Med 1995;152:1835. Bhan U, Hyzy RC: Conventional mechanical ventilation. Available at: http://www.utdol. com. Accessed on April 17, 2005. Bidani A, Tzovanakis AE, Cardena VJ, et al: Permissive hypercapnia in acute respiratory failure, JAMA 1994;272:957. Fitzgerald JM, Hargreave FE: The assessment and management of acute life-threatening asthma, Chest 1989;95:888. Honig EG: Chronic obstructive pulmonary disease and asthma. In Perel A, Stock MC (eds): Handbook of Mechanical Ventilatory Support. Williams & Wilkins: Baltimore, 1991. Irwin RS: A physiologic approach to managing respiratory failure. In Rippe JM, Irwin RS, Alpert JS, Funk MP (eds): Intensive Care Medicine, ed 2. Little Brown: Boston, 1991. Jubran A, Tobin M: Monitoring during mechanical ventilation, Clin Chest Med 1996;17 (3):453. Manning HL: Peak airway pressure: Why the fuss? Chest 1994;105:242.
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Marik PE, Krikorian J: Pressure-controlled ventilation in ARDS: A practical approach, Chest 1997;112:1102. Neufeld JDG: Trauma in pregnancy. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Orebaugh SL: Initiation of mechanical ventilation in the emergency department, Am J Emerg Med 1996;14:59. Pollack CV Jr: Mechanical ventilation and noninvasive ventilatory support. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tobin MJ: Respiratory monitoring, JAMA 1990;264(2):244. Weisman IM, Rinaldo JE, Rogers RM: Positive end-expiratory pressure in adult respiratory failure, N Engl J Med 1982;307:1381.
Chronic Obstructive Pulmonary Disease STEVEN W. SALYER
ICD Code: Emphysema 492.8
Key Points The primary cause of COPD is cigarette smoking. Environmental and industrial air pollution and passive cigarette smoke have also been implicated in COPD. ! Emergency Actions ! A patient with COPD should undergo cardiac monitoring, and pulse oximetry readings and vital signs should be monitored closely every 10 minutes. The patient is placed on a nasal cannula at 1–2 L/min. Bronchodilators should be administered every 10–15 minutes, and the patient’s vital signs and response to treatment should be monitored. Corticosteroids should be administered in the form of intravenous methylprednisolone, 125 mg.
DEFINITION Chronic obstructive pulmonary disease is defined by the American Thoracic Society as two distinct types of disease: 1. Pulmonary emphysema (defined pathologically) is a condition of the lung characterized by abnormal, permanent enlargement of the air
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spaces distal to the terminal bronchiole, accompanied by destruction of their walls. 2. Chronic bronchitis (defined clinically) is a condition of excess mucus secretion in the bronchial tree, occurring on most days for at least 3 months per year for at least 2 consecutive years. Patients who have these conditions are sometimes referred to as “blue bloaters” and “pink puffers” based on the patient’s stature. They usually have a mixture of asthma, bronchitis, and emphysema.
PATHOLOGY The primary cause of COPD is cigarette smoking. Environmental and industrial air pollution and passive cigarette smoke have also been implicated in COPD. This is a disease of chronic air flow obstruction, primarily expiratory air flow. The pathophysiology of COPD can be defined in stages:
Stage A: A patient has no respiratory symptoms, even on exertion, and minimal if any hypoxemia. Stage B: The patient has mild or minimal symptoms and has little disability. There is detectable lung damage and dyspnea only on exertion, with slight hypoxemia. Stage C: This stage marks the onset of ventilatory insufficiency and dyspnea at rest. There is erosion of normal lung function with hypocarbia and hypoxemia. Stage D: The physiological reserve of the lung is exhausted, followed by erosion of the baseline lung function. There is chronic ventilatory failure with the onset of cor pulmonale. Stage E: At this final stage of lung disease, the patient will die without oxygen and ventilatory assistance. Most COPD bronchitis is caused by the following organisms:
H. influenzae Diplococcus pneumoniae Branhamella catarrhalis Mycoplasma species Chlamydia species Bordetella pertussis
CLINICAL PRESENTATION The patient will present in one of two ways: A “blue bloater” is short and obese and a “pink puffer” is thin in stature. A patient with COPD will be tachypneic, will be using accessory respiratory muscles, and will
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be pursing his or her lips upon exhalation. Wheezing can be present on exhalation, coarse crackles can be present, or both can be heard on examination. The long-term chronic disease is that the thorax will be hyperexpanded with increased anteroposterior diameter. Poor dietary intake and weight loss are common in end-stage disease. Confusion resulting from hypercarbia, plethora caused by polycythemia, and cyanosis can all be present.
RADIOGRAPHS Chest radiography is a poor examination for use in determining the severity of COPD. Bronchitis pathology will be shown poorly on the chest x-ray. Emphysematous disease will show signs of hyperaeration with increased anteroposterior diameter, flattened diaphragm, increased parenchymal lucency, and attenuation of pulmonary arterial vascular shadows.
EXAMINATION The most valuable examination or test to determine the severity of the COPD is the pulmonary function test forced expiratory volume in 1 second and the forced vital capacity (FVC); these are the two best measurements of lung disease. In the absence of restrictive ventilatory disease, a reduction in FVC when bronchodilators are given is a sign of emphysema. If the FVC improves with the administration of bronchodilators, the underlying disease is more likely the form of COPD that involves bronchitis.
LABORATORY FINDINGS The ABG levels can be normal or exaggerated. The alveolar-arterial (A-a) gradient is almost always elevated. Usually there is an increase in this gradient of more than 30. The normal PaCO2 is 35–45 mmHg, and less than 35 mmHg represents excessive carbon dioxide elimination or hypoventilation. For every 10-mmHg increase in PaCO2 over 40 mmHg, the pH will decrease by 0.08 units, and for every 10-mmHg decrease below 40 mmHg, the pH will increase by 0.08. Also, for every change in bicarbonate of 10 mmHg, the pH should change by 0.15. A sputum examination in a patient with COPD in the ED is very helpful. Sputum with tiny dark specks that are 1–2 mm in diameter is characteristic of inspissated mucous plugs as seen in patients with asthma or COPD. If the sputum contains polymorphonuclear cells, an infectious agent is probably present. Gram staining is helpful if infection is present.
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An ECG will usually show right ventricular hypertrophy, which suggests cor pulmonale. The finding of “P pulmonale”—peaked Ps in leads II, III, and avF—suggests COPD. The classic triad of a low QRS voltage, poor R wave progression, and clockwise rotation is indicative of COPD on an ECG but it is nonspecific and insensitive to COPD.
TREATMENT Treatment must be directed toward both acute exacerbations and longterm therapy. The most important factor in preventing exacerbations is for the patient to stop smoking if he or she is still smoking and the cessation of exposure to secondary smoke if someone else is smoking in the home. Patients should receive antibiotics for bronchitis exacerbations. Bronchodilators are the main form of treatment for the asthma component of COPD, and corticosteroids are needed in short bursts to treat the inflammatory process of COPD. Oxygen is needed for acute exacerbations in the ED, and home oxygen is required for treatment of end-stage disease. All patients with COPD should receive the pneumococcal 23-valent vaccine and the annual trivalent influenza vaccines to prevent viral infections and thus COPD exacerbations. There is controversy regarding whether theophylline therapy has a place in the treatment of COPD. In theory, oral theophylline helps to keep the large and small airways open. Theophylline is rarely used in the treatment in COPD today. If the patient’s resting room air oxygen saturation is less than 90%, home oxygen is indicated at 1–2 L/min. Antibiotics commonly used to treat bronchitis include trimethoprimsulfamethoxazole (Septra), ciprofloxacin, first-generation cephalosporins, erythromycin (be careful if given with theophylline), ampicillin, and amoxicillin. Most patients with COPD also have left-sided heart failure and are dehydrated at the time of presentation to the ED. Patients with end-stage COPD will have secondary pulmonary hypertension and cor pulmonale. There is a delicate balance in treating these patients. Bronchodilators increase heart rate and thus increase stress on the heart, which can cause the heart to fail. A patient with CHF can have heart failure as a result of rapid intravenous fluid administration if an attempt is made to move the mucous plugs in a dehydrated patient. It is recommended that the patient’s lungs be auscultated after every 250 ml of fluid administration. All patients with COPD should undergo an ECG, especially those receiving theophylline therapy. Patients with COPD can present experiencing atrial fibrillation or multimodal atrial tachycardia. Those patients who also have CHF are sometimes receiving digoxin therapy and should undergo an ECG and testing of digoxin levels.
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Many patients are also taking diuretic agents and have the potential for hypokalemia. Hypokalemia can also promote dysrhythmias. Patients with COPD can have metabolic abnormalities, and all patients with COPD should have a complete set of electrolyte tests along with a determination of theophylline and digoxin levels if the patient is taking these medications. If there is a history or suspicion of CHF or a prior myocardial infarction, cardiac enzyme levels should be measured. Expectorants are sometimes used; however, there is no objective evidence that they improve the expectoration of mucus or improve the quality of life of a patient with COPD.
TREATMENT OF A PATIENT WITH COPD IN THE EMERGENCY DEPARTMENT Emergency treatment of a patient with COPD should include the following: 1. The patient should undergo cardiac monitoring, and pulse oximetry readings and vital signs should be monitored closely every 10 minutes. 2. The patient should be placed on a nasal cannula at 1–2 L/min. 3. Bronchodilators should be administered every 10–15 minutes, and the patient’s vital signs and response to treatment should be monitored. 4. Corticosteroids should be given in the form of intravenous methylprednisolone, 125 mg. 5. The practitioner should perform ECG, chest radiography, CBC, and measurement of electrolytes and cardiac enzymes as needed. The PEFR should be analyzed between treatments. 6. If the patient shows signs of pneumonia, antibiotics should be administered intravenously. If the patient is dehydrated, intravenous fluids should be given very slowly. 7. If the patient shows no improvement or exhibits oxygen desaturation, he or she should be admitted to the hospital.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Hemoptysis JULIE ANN MORGAN AND JAMES ALAN MORGAN
ICD Code: Hemoptysis 786.3
Key Points Bronchial circulation is an important source of hemoptysis. The etiology and evaluation vary depending on the patient’s history, his or her geographical location, and the amount of bleeding present. ! Emergency Actions ! Persons who present with massive hemoptysis require aggressive treatment. The bleeding lung (if known) should be placed in the dependent position to preserve function in the nonbleeding lung. Early consideration for tracheal intubation is warranted, with either selective intubation of the nonbleeding lung or with a dual-lumen endotracheal tube. Early bronchoscopy is indicated to attempt to localize the bleeding site.
DEFINITION Hemoptysis is defined as expectorated blood that originates below the vocal cords. It can range from blood-tinged sputum to voluminous amounts of gross blood. The lungs enjoy a dual circulation from the low-pressure pulmonary system that allows for gas exchange and the high-pressure bronchial circulation that provides the nutritive blood supply to the airways. In general, the bronchial circulation is the more important source of hemoptysis. The etiology and evaluation vary depending on the patient’s history, his or her geographical location, and the amount of bleeding present. Massive hemoptysis is variously defined as 100–600 ml/24 hours and is considered a medical emergency requiring immediate evaluation and intervention.
EPIDEMIOLOGY Hemoptysis can occur in all age ranges. In the United States, the most common causes include bronchitis, bronchogenic carcinoma, and bronchiectasis. In other areas, infectious diseases such as tuberculosis and paragonimiasis (caused by a parasitic lung fluke) are frequent etiologies.
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Massive hemoptysis can result from bronchitis, bronchiectasis, mycetomas, or autoimmune diseases and as a complication of cystic fibrosis and bone marrow transplant. Bronchogenic carcinoma rarely causes massive hemoptysis.
CLINICAL PRESENTATION When patients present coughing up blood, the upper airway and gastrointestinal tract must be excluded as the source. It is important to characterize the duration, amount, and character of hemoptysis because this will influence the direction of the subsequent evaluation. A thorough medical history to include country of origin, travel, medications taken (both prescribed and over-the-counter), tobacco use, and past medical history is essential. Persons presenting with massive hemoptysis are generally anxious, may present with hypoxia, and are at risk of losing an effective airway due to an inability to clear the bronchial tree of blood.
EXAMINATION A check of vital signs, including pulse oximetry, is essential. Fever generally suggests an infectious etiology but can also be seen with a PE or infarction. Localized wheezing may suggest an endobronchial lesion (e.g., carcinoma-bronchogenic or metastatic, carcinoid, bronchial adenoma, or Kaposi sarcoma in a patient with AIDS). Aphthous ulcers suggest Behçet’s syndrome or other autoimmune disease. Multiple telangiectasias may signal pulmonary arteriole-venous malformations. Signs of CHF and a mitral murmur suggest a potential cardiac source. Digital clubbing is seen in chronic lung/cardiac disease as well with some bronchogenic carcinomas. The lower extremities should be examined for signs of a deep venous thrombosis.
LABORATORY FINDINGS Routine laboratory tests to be performed include a CBC; measurement of electrolytes, blood urea nitrogen, and creatinine; liver function tests; coagulation profile; urinalysis; and ABG analysis. Blood should be typed and cross-matched for persons with massive hemoptysis. Abnormal urinalysis results and creatinine levels suggest a pulmonary renal syndrome such as Goodpasture’s syndrome. Other laboratory tests to be performed depend on the clinical situation. Sputum samples for acid-fast bacillus and fungi tests should be obtained in patients with pulmonary infiltrates (especially in the upper lobes) and in those originating from or with travel to endemic tuberculosis areas. Serological studies for Wegener’s granulomatosis (antineutrophilic cytoplasmic antibodies), Goodpasture’s
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syndrome (anti-granulomembranous body antibodies), systemic lupus erythematosus, and Behçet’s syndrome are indicated in the appropriate clinical setting. All patients should undergo chest radiography, which may provide the etiology—a pulmonary mass suggesting tumor, a cavitary lesion with a fungus ball representing an aspergillosis mycetoma, an infiltrate representing infection (tuberculosis until proven otherwise for upper lobe infiltrates), an arteriovenous malformation, foreign body, or bronchiectasis. On the other hand, persons with hemoptysis resulting from bronchitis may have unremarkable study results.
DIAGNOSIS The diagnosis of hemoptysis is often made on the basis of the history, physical examination results, chest radiography, and results of the laboratory tests noted previously. No further evaluation is indicated for the subset of patients with negative chest radiography results, age younger than 40 years, nonsmoking status, and hemoptysis of less than 1 week’s duration. If hemoptysis persists, further evaluation should be pursued. In approximately 30% of patients with this condition, no etiology will be found (i.e., cryptogenic hemoptysis); long-term follow-up suggests that these patients have a favorable outcome. Other patients will require further evaluation with a chest CT scan and bronchoscopy to further define findings seen on the chest radiograph. A chest CT, especially high-resolution HRCT, can reveal bronchiectasis. Bronchoscopy is particularly helpful in the diagnosis of pulmonary carcinomas and to localize the site of bleeding. Bronchoscopy is most effective if performed acutely (within 48 hours of the event) to localize the site of active bleeding but has not been shown to significantly affect clinical outcome in nonmassive hemoptysis. Bronchoscopy in the face of normal chest radiography results rarely reveals an occult endobronchial lesion.
TREATMENT The treatment and outcome depend on the etiology of the hemoptysis. Therapy is directed toward the underlying etiology (i.e., antibiotics for persons with infections, steroids, and immunosuppressive agents for those with autoimmune diseases). Patients who present with massive hemoptysis require aggressive treatment; the bleeding lung (if known) should be placed in the dependent position to preserve function in the nonbleeding lung. Early consideration for tracheal intubation is warranted, with either selective intubation of the nonbleeding lung or with a dual-lumen endotracheal tube. Early bronchoscopy is indicated to
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attempt to localize the bleeding site. Bronchial blockers, laser coagulation, and topical sealants have been described as temporizing therapy. Selected patients will benefit from bronchial artery angiograms with embolization of the offending artery. This procedure is effective in controlling bleeding in 90% of those in whom the procedure can be completed and can serve as both a definitive procedure (for poor surgical candidates) or as a bridge to surgical intervention under less urgent and more controlled conditions. Patients who succumb to hemoptysis do so as a result of asphyxiation and not as a result of exsanguination.
Bibliography Adelman M, Haponik EF, Bleecker ER, et al: Cryptogenic hemoptysis: Clinical features, bronchoscopic findings, and natural history in 67 patients, Ann Intern Med 1985; 102:829. Cahill BC, Ingbar DH: Massive hemoptysis: Assessment and management, Clin Chest Med 1994;15:147. Hirshberg B, Biran I, Glazer M, Kramer MR: Hemoptysis: Etiology, evaluation and outcome in a tertiary referral hospital, Chest 1997;112:440. Jean-Baptiste E: Clinical assessment and management of massive hemoptysis, Crit Care Med 2000;28(5):1642. White RI: Bronchial artery embolotherapy for control of acute hemoptysis: Analysis of outcome, Chest 1999;115:912.
Pneumothorax ROBERT NOLAN
ICD Codes: Pneumothorax, acute 512.8, Pneumothorax, accidental puncture or laceration 512.1, Pneumothorax, tension 512.0, Pneumothorax, traumatic 860.0
Key Points A pneumothorax is a collection of gas that develops in the potential space between the pleura of the lung and the chest wall. It is frequently referred to as a collapsed lung.
892 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! Anyone suspected to have an acute pneumothorax should have 100% nonrebreathing mask place. At least one 18-gauge intravenous line should be started, the patient should be placed on a cardiac monitor, and pulse oximetry should be performed. An emergency chest radiograph should be performed.
DEFINITION A pneumothorax is a collection of gas that develops in the potential space between the pleura of the lung and the chest wall. It is frequently referred to as a collapsed lung. In normal physiology, the lining of the lung, the visceral pleura, lies in contact with the chest wall, the parietal pleura. As the chest wall expands, a vacuum effect draws the visceral pleura out with the expanding chest wall. It is in this potential space that air (in a pneumothorax) or blood (in a hemothorax) can accumulate, causing the lung to “collapse.” The causes of this condition include trauma, which can be blunt, penetrating, or spontaneous. In both blunt and penetrating trauma, the vacuum seal between the two pleural spaces is violated and the lung retracts away from the chest wall. Iatrogenic pneumothorax is a form of penetrating injury that results from diagnostic or therapeutic procedures such as central line placement in the subclavian vein or thoracentesis. A tension pneumothorax is a life-threatening condition caused by air within the pleural space that is under pressure, usually from a one-way leak from the lung into the pleural space. The expanding air volume displaces mediastinal structures and compromises cardiopulmonary function. Spontaneous pneumothorax can occur without any direct trauma to the chest wall. This is frequently caused by damage to the lung tissue in which the lung breaks open and air can escape into the pleural space. Diseases such as COPD, asthma, pneumonia, and cystic fibrosis have caused spontaneous pneumothorax. The management of pneumothorax centers on recognizing and treating the complications of this condition (e.g., tension pneumothorax, hypoxia, and ventilatory failure) while attempting to maximize pleural healing and reducing recurrence. Spontaneous pneumothorax occurs with an incidence of 6–8 cases per 100,000 men per year and roughly 2 cases per 100,000 women per year. An estimated 20,000 cases of spontaneous pneumothorax are estimated per year, and there is evidence suggesting that the incidence may be increasing. Spontaneous pneumothorax is predominantly a condition of tall lanky males with a history of smoking. There is a small genetic component that has been identified, however, and smoking increases the risk for spontaneous pneumothorax by 20 times.
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CLINICAL PRESENTATION The signs and symptoms produced by tension pneumothorax are usually more dramatic than those seen with a simple pneumothorax, and symptoms vary based on the size and extent of pneumothorax. Typically, patients report pleuritic chest pain (90%), dyspnea (80%), anxiety, and a feeling of doom. Physical examination findings may include decreased or absent breath sounds on the affected side of pneumothorax, tachypnea, hyperresonance of the chest wall on percussion, and tachycardia. Findings with tension pneumothorax include distended jugular veins, tracheal deviation away from the affected side, hypotension, shock, and, finally, pulseless electrocardiographic activity.
RADIOGRAPH Anyone who is suspected of having a pneumothorax should undergo a two-view chest x-ray.
LABORATORY FINDINGS An ABG analysis can be obtained to check whether severe hypoxia or acidosis is present. A CBC, Chem 7, and measurement of partial thromboplastin time (PTT) and international normalized ratio should be performed.
DIAGNOSIS Pneumothorax is best diagnosed with a posteroanterior upright radiograph taken at a distance of 6 feet (Fig. 15-1). Evidence of absent vascular markings in the periphery, collapsed lung, or radiolucent line separating the visceral and parietal pleura is most suggestive of a pneumothorax. Another suggestive sign on radiograph is the so-called deep sulcus sign in which the costophrenic angle is unusually deep. Although the initial chest radiograph may show no evidence of pneumothorax, the clinician should consider delayed traumatic pneumothorax development in any penetrating chest wound. Serial chest radiographs should be obtained every 6 hours the first day after injury to rule this out. Air in the pleural cavity, with contralateral deviation of mediastinal structures, is evidence of a tension pneumothorax. CT scanning of the chest wall is a more sensitive and specific study for pneumothorax but is rarely indicated for spontaneous pneumothorax. A CT scan can help to further assess the underlying pathology of the lung tissue or assess other chest structures to determine damage from penetrating or blunt trauma.
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Figure 15-1. This patient presented with shortness of breath, and chest radiography revealed a left superior pneumothorax and loculated pneumothorax of the left costophrenic angle. White arrows outline the pleural line superiorly and inferiorly. This would be classified as a large pneumothorax because apex-cupola distance is greater than 3 cm. CT showed partial collapse of the left lower lobe and lingula.
TREATMENT There is no current consensus on the treatment of pneumothorax. The goals of treatment include patient comfort, elimination of interpleural air, optimization of healing, timely hospital discharge, and prevention of recurrence. Treatment depends on the stability of the patient and the ability to obtain surgical consultation in a timely fashion. For a minor pneumothorax in a stable patient, oxygenation, observation, catheter aspiration, or tube thoracostomy are all acceptable treatments. Vital signs should be checked frequently, and continuous pulse oximetry should be enacted. More aggressive treatments that help prevent recurrence of pneumothorax include pleurodesis, video-assisted thoroscopy,
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and thoracotomy. It should be noted that the natural resolution of 1.25% of interpleural air is expected every 24 hours. Patients whose conditions are stable and who have a small pneumothorax (10%–15% of lung volume) may be monitored in the ED for 6 hours and discharged, if their conditions remain stable, with a repeat chest radiograph confirming no expansion of the pneumothorax. These patients require follow-up within 24 hours with their primary care physician and should have a reliable friend or family member stay with them until follow-up takes place. The one exception to this rule is small traumatic pneumothoraces, often detected incidentally on CT scan. These must be addressed if the patient is intubated or transported via air evacuation to another facility. Patients with larger than 15% pneumothorax, significant comorbidities, or expanding pneumothorax should be treated with either catheter aspiration or tube thoracostomy and a Pleur-Evac chest drainage system after surgical consultation is obtained. In the event that the patient develops any signs or symptoms of tension pneumothorax, needle aspiration or emergent thoracostomy should be performed immediately. A needle aspiration should be performed as follows: 1. Locate puncture site. The second intercostal space in the midclavicular line on the affected side immediately superior to the rib is most commonly recommended site. 2. Prepare the puncture site with Betadine antiseptic and/or alcohol scrubs. 3. Insert a large-bore Angiocath (14-gauge in an adult, 18-gauge or 20-gauge in an infant) into the desired intercostal space over the top of the rib and perpendicular to the chest wall. Listen for a rush of air. 4. Remove the needle. 5. Secure the Angiocath in place, and establish a water seal or flutter valve. 6. Immediately prepare to insert a chest tube. 7. Listen for a rush of air on insertion to confirm the diagnosis of tension pneumothorax. Note this finding on the patient’s chart. In an area with high ambient noise, the escape of air may not be detected. 8. Needle thoracostomy requires follow-up placement of a chest tube. Tube thoracostomy is performed as follows: 1. If the patient is hemodynamically stable, administer procedural analgesia and sedation with careful titration of a short-acting narcotic and benzodiazepine in addition to applying a local anesthetic. 2. Place the patient in a 30- to 60-degree reverse Trendelenburg position and prepare the site with Betadine antiseptic. 3. Make a 3- to 4-cm incision over the fifth or sixth rib in the midaxillary line.
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4. Use a curved hemostat to puncture the intercostal muscles and parietal pleura immediately superior to the rib border, avoiding damage to the underlying lung. Then, slide a finger over the clamp to maintain the formed tract. 5. Perform a digital examination to assess the location and to evaluate any pulmonary adhesions. Sweep the finger in all directions, and feel for the diaphragm and possible intra-abdominal structures. To avoid losing the desired tract, keep the finger in place until the tube is inserted. 6. Insert the chest tube alongside the finger, using a clamp on the tube if desired. 7. Direct the chest tube posteriorly and inferiorly, and insert it until it is at least 5 cm beyond the last hole of the tube. Stop once resistance if felt so as not to damage mediastinal structures or cause bending or kinking of the thoracostomy tube. 8. Attach the tube to a water seal and vacuum device (e.g., Pleur-Evac). Look for respiratory variation and bubbling of air through the water seal. Document the amount of blood or other fluids that may drain. 9. Suture the site and secure the tube. A variety of anchoring and closure techniques exists, all of which are probably equivalent in efficacy. Cover the site with gauze impregnated with petroleum jelly, and apply a suitable dressing.
DISPOSITION A patient who has a stable, small pneumothorax that has not expanded over a 6-hour period in the ED and who has retained stable vital signs can be discharged home with follow-up in 24 hours. All other patients require surgical consultation and inpatient management for observation, continued aspiration of air in sequential fashion, or management of tube thoracostomy. All patients with traumatic pneumothorax require admission and management of their condition. Spontaneous pneumothorax has a frequent recurrence, and therefore referral for definitive treatment is required. It has been estimated that the 1-year recurrence rate approaches 30%, but smoking cessation reduces the risk of recurrence by half.
Bibliography Baumann MH, Strange C: The clinician’s perspective on pneumothorax management, Chest 1997;112(3):822–828. Baumann MH, Noppen M: Pneumothorax, Respirology 2004;9(2):157–164. British Thoracic Society Research Committee: Simple aspiration versus intercostal tube drainage for spontaneous pneumothorax in patients with normal lungs, BMJ 1994;309 (6965):1338–1339. BTS guidelines for the management of spontaneous pneumothorax, Thorax 2003;58 Suppl 2(ii):39–52.
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Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Vol 3. Mosby: St Louis, 2002. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw Hill: New York, 2004. Wakai A: Spontaneous pneumothorax [review], Clin Evid 2004;11:1947–1955. Wolfson AB, Hendey GW, Hendry PL, et al (eds): Harwood-Nuss’ Clinical Practice of Emergency Medicine, ed 4. Lippincott, Williams & Wilkins, Philadelphia, 2005.
Pulmonary Embolism DEREK R. LINKLATER
ICD Codes: Pulmonary embolism 415.19, Pulmonary embolism with infarction 415.1, Iatrogenic pulmonary embolism and infarction 415.11
Key Points Historical factors, risk assessment, physical examination, and ancillary testing may be useful in suggesting PE versus other etiologies of the patient’s condition. Multiple risk-stratification schemes exist, and providers should be comfortable with at least two of them. It is not recommended that inexperienced providers use the‘‘clinical gestalt’’ method for estimating pretest probability of disease. A highly sensitive D-dimer (e.g., enzyme-linked immunosorbent assay [ELISA] or immuno-turbidimetric) of less than 500 ng/dl may be sufficient to exclude the diagnosis in low-risk patients. A combination of radiographic and nuclear medicine studies may be required to exclude the disease in patients at higher risk. If significant time delays are likely in the diagnostic approach, it is recommended to begin immediate anticoagulation with regular or low-molecular-weight heparin pending final diagnostic resolution. ! Emergency Actions ! Upon suspecting the diagnosis of PE, the clinician should do the following:
Obtain immediate noninvasive pulse oximetry. Provide supplemental O2 sufficient to keep the SpO2 greater than 90%. Start at least one large-bore (18-gauge or greater) intravenous line in a large peripheral vein. Administer a bolus of crystalloid for hypotension (mean arterial pressure < 75–80 mmHg) or tachycardia (heart rate <110–120 mmHg).
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Place the patient on continuous cardiac monitoring and measure vital signs frequently. Provide anticoagulation immediately if the patient is at high risk for PE and has no contraindications.
DEFINITION Pulmonary embolism is defined as a sudden occlusion or obstruction of the pulmonary artery, either one of its branches or in its entirety, by material arising from a distant site; this differentiates it from pulmonary thrombosis, in which the obstruction happens in situ. This material is most commonly clotted blood arising from the deep venous system of the lower extremities and pelvis but could include other material, including the following:
Air (e.g., scuba diving, orovaginal insufflation, iatrogenic causes) Amniotic fluid (associated with parturition) Fat (e.g., fracture of large long bones such as the femur and tibia) Foreign body (associated with intravenous drug use)
EPIDEMIOLOGY According to the National Heart, Lung, and Blood Institute, PE is one of the most common causes of death in hospitalized patients, affecting more than 600,000 persons in the United States every year. Mortality rates are substantial; even with treatment 5%–10% of these patients die, with the majority succumbing within 30–60 minutes of symptom onset. Prevalence varies with age, and the risk rises drastically after the age of 60 years, from approximately 100 per 100,000 persons to 600 per 100,000 persons aged 80 years or older.
CLINICAL PRESENTATION Symptoms associated with PE include the following:
Anxiety and apprehension Chest pain (often “pleuritic” in nature) Dizziness/lightheadedness Dyspnea (either at rest or on exertion, often of sudden onset) Palpitations Signs associated with PE include the following:
Dyspnea Hemoptysis Hypotension
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Syncope Tachycardia/ECG changes (S1Q3T3, strain pattern, and other ST/T changes) Tachypnea Wheezing, rales, or rhonchi
RISK FACTORS The diagnosis of PE is often elusive, and the workup is resource intensive and time-consuming. It is important, because of these factors, to embark upon the process with a firm idea of the patient’s actual risk of having the disease. There are three major schemes that have been devised for estimating the patient’s risk of having a pulmonary embolus (also called the “pretest probability”): clinical gestalt, the Wells criteria, and the “Geneva/ Wicki” criteria.
Clinical Gestalt The clinical gestalt represents a practitioner’s best guess regarding the pretest probability based on clinical experience, the patient’s symptom complex, and the presence of risk factors for the disease. These risk factors include the following:
History of deep vein thrombosis/PE Trauma or other vascular injury Prolonged immobilization Recent hospitalization or surgery Known coagulopathy Smoking, obesity, oral contraceptive use, and other lifestyle factors
Incidence data from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) investigation (which used this clinical gestalt model for risk assessment) define the following categories of risk for disease:
High risk: 60%–70% will have a PE Intermediate risk: 15%–25% will have a PE Low risk: 5%–10% will have a PE
Wells Criteria Wells et al. developed a clinical scoring system in an attempt to further quantify the risk of patients having a pulmonary embolus (Table 15-7).
900 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 15-7 Wells Criteria for Assessing Risk of Pulmonary Embolism (PE) Clinical symptoms of DVT PE the most likely diagnosis Heart rate greater than 100 beats/min Immobilization or surgery within past 4 weeks Previous DVT or PE Hemoptysis Malignancy
3 points 3 points 1.5 points 1.5 points 1.5 points 1 point 1 point
Adapted from Wells PS, Anderson DR, Rodger M, et al: Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: Increasing the model utility with the SimpliRED D-dimer, Thromb Haemost 2000;83:418. DVT, Deep vein thrombosis.
Incidence data from several trials using this model for risk assessment define the following categories of risk for disease:
High risk (>6 points): 75%–80% will have a PE Moderate risk (2–6 points): 25%–30% will have a PE Low risk (<2 points): 1%–5% will have a PE
Geneva (Wicki) Criteria Wicki et al. also developed a clinical scoring system to quantify the risk of pulmonary embolus (Table 15-8). This system is somewhat unique in that it incorporates the results of ABG and chest x-ray analyses. Table 15-8 Geneva (Wicki) Criteria for Assessing Risk of Pulmonary Embolism (PE) Previous PE or DVT HR <100 Recent surgery Age ○ 60–79 years ○ 80 years PaCO2 ○ <36 mmHg ○ 36–38.9 mmHg PaO2 ○ <48.7 mmHg ○ 48.7–59.9 mmHg ○ 60.0–71.2 mmHg ○ 71.3–82.4 mmHg Atelectasis Elevated hemidiaphragm
2 points 1 point 3 points 1 point 2 points 2 points 1 point 4 3 2 1 1 1
points points points point point point
Wicki J, Perneger TV, Junod A, et al: Assessing clinical probability of pulmonary embolism in the emergency ward: A simple score, Arch Intern Med 2001;161:92–97. DVT, Deep vein thrombosis; HR, heart rate.
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Incidence data from several trials using this model for risk assessment define the following categories of risk for disease:
High risk (>8 points): 65%–70% will have a PE Intermediate risk (5–8 points): 35%–40% will have a PE Low risk (<5 points): 10%–15% will have a PE
None of these risk assessment models have been shown to be superior in clinical practice. Thus it is left to the provider’s discretion which model to use. Caution should be exercised, however, given that clinical experience with PE is difficult to come by early in a provider’s career. It seems prudent, given the risk of poor outcomes, to use the highest pretest likelihood predicted by the models.
LABORATORY FINDINGS Few laboratory studies are useful in the diagnosis and treatment of PE. Most lack the specificity required to shed any light on the presence or absence of the disease. There are three tests that bear mentioning, however: ABG analysis, prothrombin time/activated PTT, and D-dimer.
Arterial Blood Gas Interpretation Primarily of historical interest, ABG interpretation has long been used as part of the risk-stratification process. Interpretation had centered on the calculation of the so-called A/a gradient. Unfortunately, many disease states (including pneumonia, CHF, ARDS, and others) are more likely to result in an abnormal A-a gradient than is PE, thus making its use questionable at best. Although the ABG itself is of dubious usefulness, its use has been included as part of the Wicki/Geneva criteria; obtaining an ABG analysis is indicated as part of risk stratification using this algorithm.
Prothrombin Time/Activated PTT Obtaining a coagulation profile is recommended by some in an effort to both unmask an unexpected coagulopathy and to establish a “baseline” before initiating anticoagulant therapy. Given the recent shift in the anticoagulation paradigm toward the use of low-molecular-weight heparin (which does not require repeated monitoring of the patient’s coagulation profile) and the infrequency that unexpected abnormalities occur, these tests cannot be routinely recommended. However, assessing the patient’s coagulation status is recommended in all patients known to be taking anticoagulants.
902 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER D-Dimer
A recent addition to the risk-stratification armamentarium is the use of quantitative D-dimer testing. Two types of ultra-sensitive D-dimer assays (i.e., ELISA and immuno-turbidimetric) possess sufficient sensitivity and specificity to be useful in a specific clinical scenario: the low-risk patient. Patients who are determined to be at low risk using either clinical gestalt or one of the clinical scoring systems may be safe for discharge without any further testing if their quantitative D-dimer is less than 500 ng/dl. Care must be taken, however, to ensure that the clinical laboratory is using one of these ultrasensitive D-dimer assays and not an older, less sensitive test.
RADIOGRAPHS Diagnostic Studies Radiographic and nuclear medicine diagnostic testing are the cornerstones of PE diagnosis. Traditionally, ventilation-perfusion (V/Q) scanning has been predominantly used, but, in recent years, CT angiography has become an increasingly viable and useful tool. Other types of studies are often impractical due to patient acuity or because they are too difficult to obtain. Possible studies include the following:
V/Q scanning CT angiography, single-detector CT scan CT angiography, multidetector CT scan CT venography Lower extremity compression ultrasonography Magnetic resonance imaging angiography/venography Transthoracic/transesophageal echocardiography Alveolar dead space measurement
DIAGNOSIS There are many algorithms that have been published in both textbooks and the primary literature describing various diagnostic approaches to PE. The main disadvantage to using these algorithms is that each individual provider’s work environment differs, and an algorithm that is useful at one facility may be impossible to use at another due to variations in test availability. For this reason, algorithmic approaches to the diagnosis of PE are problematic. What follows is a stepwise approach that allows each provider to risk-stratify patients according to his or her practice pattern and the availability of tests at his or her facility.
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1. Determine your threshold for risk of disease. Ask yourself, “At what probability do I feel that the risk to the patient is low enough that he or she can be sent home without further testing?” Suggested ranges for this probability range from 2% to 4%. 2. Determine the pretest likelihood for the patient having the disease. Use whichever clinical scoring system you prefer, and try to be as accurate as possible given the patient’s clinical presentation and risk factors. For example: “The patient has a Wells score of 4.5 and is at moderate risk; based on these data, I believe the patient has a 40% risk for having a PE.” 3. Take this pretest probability and plot it as a dot on the left-hand axis (Pretest Probability %) on Figure 15-2. 4. Perform your diagnostic test of choice on the patient. 5. Look up the negative likelihood ratio for the test you have performed in Table 15-9, and plot the result as a dot on the middle axis (Likelihood Ratio) of Figure 15-2. 6. Draw a straight line connecting the two dots and continuing on to intersect a third point on the right-hand axis (Posttest Probability %) on Figure 15-2. This will give you the probability of the patient having the disease based on your pretest probability and the characteristics of the test you performed. 7. If the posttest probability exceeds your risk threshold, then you must either perform an additional diagnostic test (begin at step #2 and use the current posttest probability as your new pretest probability) or provide anticoagulation and admit the patient to the hospital. 8. If any of the diagnostic radiographic or nuclear medicine studies have positive results for the presence of PE, it is recommended that anticoagulation and admission be arranged immediately. A “positive” D-dimer (i.e., <500 ng/dl) is not sufficient evidence because the test is so sensitive—further testing must be arranged to confirm or exclude the diagnosis.
TREATMENT The treatment of PE includes the following:
High-flow oxygen for patients with documented hypoxia Crystalloid infusion for significant hypotension or tachycardia Opioid analgesics, as necessary, for relief of pain, anxiety, and dyspnea In the presence of confirmed PE, or in patients with a high pretest probability of disease and a diagnostic delay expected, anticoagulation is indicated: Heparin: 70-units/kg bolus then 15 units/kg/hr with titration to keep PTT 1.5–2 times control Low-molecular-weight heparin: 1 mg/kg
904 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER 0.1
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Figure 15-2. Worksheet for stepwise approach to risk assessment for pulmonary embolism.
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Table 15-9 Calculating Negative Likelihood Ratio for Pulmonary Embolism RADIOGRAPHIC OR LABORATORY TEST ELISA or equivalent D-dimer <500 ng/dl V/Q scan, “indeterminate” V/Q scan, “low probability” V/Q scan, “normal” or “near normal” CT angiography (single detector), “negative” CT angiography (multidetector), “negative” Lower extremity ultrasound, “negative” CT venography, “negative” MRI pulmonary angiography, “negative” Transthoracic echocardiography, “negative” Transesophageal echocardiography, “negative” Alveolar dead space measurement, “negative”
NEGATIVE LIKELIHOOD RATIO (LR) LR() LR() LR(1) LR() LR() LR() LR() LR() LR() LR() LR() LR()
¼ ¼ ¼ ¼ ¼ ¼ ¼ ¼ ¼ ¼ ¼ ¼
0.1 1.1 0.4 0.1 0.3 0.1 0.5 0.05 0.3 0.4 0.4 0.1
ELISA, Enzyme-linked immunosorbent assay; V/Q, ventilation-perfusion; CT, computed tomography; MRI, magnetic resonance imaging.
Thrombolytics (should be reserved for hemodynamically unstable and perimortem patients)
Bibliography Kline J, Meek S, Boudrow D, et al: Use of the alveolar dead space fraction (Vd/Vt) and plasma D-dimers to exclude acute pulmonary embolism in ambulatory patients, Acad Emerg Med 1997;4:856–863. National Heart, Lung, and Blood Institute: Pulmonary embolism: What is it? Available at: http://www.nhlbi.nih.gov/health/dci/Diseases/pe/pe_what.html. Accessed on June 22, 2005. Silverstein MD, Heit JA, Mohr DN, et al: Trends in the incidence of deep vein thrombosis and pulmonary embolism: A 25-year population-based study, Arch Intern Med 1998;158:585–593. The PIOPED Investigators: Value of the ventilation/perfusion scan in acute pulmonary embolism diagnosis (PIOPED), JAMA 1990;263(20):2753–2759. Wells PS, Anderson DR, Rodger M, et al: Derivation of a simple clinical model to categorize patients’ probability of pulmonary embolism: Increasing the model utility with the SimpliRED D-dimer, Thromb Haemost 2000;83:418. Wicki J, Perneger TV, Junod A, et al: Assessing clinical probability of pulmonary embolism in the emergency ward: A simple score, Arch Intern Med 2001;161:92–97.
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Sedation and Analgesia in the Intubated Patient STACEY BLACK PEARLMAN All ventilated patients should be administered the appropriate medication management to aid in patient comfort and ventilatory compliance. The placement and location of the endotracheal tube removes the patient’s ability to verbally communicate while intubated. Therefore, careful attention to vital signs, physical signs of agitation or discomfort such as persistent facial grimacing, random motor activity, or coughing may indicate the need for sedation, analgesics, paralytics, or a combination thereof. Other reasons for noncompliance or asynchrony with the ventilation may include inadequate ventilation (hypercapnia), academia, inadequate oxygenation, or CNS dysfunction. The Society for Critical Care Medicine (SCCM) published practice parameters for intravenous sedation and analgesia in critically ill adult patients. These guidelines were originally designed for the ICU; however, they are also useful in the ED for use in a ventilated patient who is waiting for an ICU bed. The suggested sedative, analgesia, and paralytic agents in this chapter are intended for use after the patient has been intubated. These recommendations are only for adult patients older than 12 years of age. Please refer to Chapter 16 on rapid sequence intubation for medications used before intubation.
ANALGESICS Pain in a ventilated patient can lead to clinically significant physiological responses, including tachycardia, increased myocardial oxygen consumption, hypercoagulability, immunosuppression, and persistent catabolism. Therefore, analgesics are vital for pain control. Intravenous opiates are the mainstay for analgesia in intubated patients (Table 15-10). 1. Morphine sulfate is the preferred analgesic agent for hemodynamically stable patients. Morphine sulfate has a half-life of 1.5–2 hours after intravenous administration in the average adult patient. Morphine may induce a histamine response resulting in hypotension. Morphine should be titrated to effect. Typically, therapy is started with a loading dose of 0.05 mg/kg over 5–15 minutes. Most adults require 4–6 mg/hr after receiving an adequate loading dose. Redosing is usually required every 1–2 hours for adequate results. Continuous infusion therapy may be necessary.
Table 15-10 Analgesics for Use in Ventilated Patients ANALGESIC AGENT
ADVANTAGE
DISADVANTAGE
DURATION OF ACTION
Ideal for hemodynamically stable patients
Histamine release resulting in hypotension
1.5–2 hr
Fentanyl
Ideal for hemodynamically unstable patient and those with morphine allergies
May cause bradycardia
30–40 min with single dose
Hydromorphone (Dilaudid)
Substitute for morphine sulfate; higher potency than morphine
Hypotension potential; increases CSF pressure; transient hyperglycemia
1–2 hr
*Increased dosage may be required for some patients.
DOSAGE Loading dose: 0.05 mg/kg over 5–15 min Maintenance dose: 4–6 mg every 1–2 hrs as needed* Loading dose: 1–2 mg/kg Maintenance dose: 1–2 mg/kg/hr drip* Loading dose: 0.5 mg, titrate in 0.5-mg increments Maintenance dose: 1–2 mg every 1–2 hr as needed
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2. Fentanyl (Sublimaze) is the preferred analgesic agent for hemodynamically unstable patients or those with a morphine allergy. Fentanyl is a synthetic opiate with 100 times’ greater potency and 7000 times more lipophilic properties than morphine, resulting in a faster onset of action and effect. Compared with morphine, fentanyl has no histamine release, therefore a reduced frequency of hypotension is seen. The half-life of fentanyl is 30–60 minutes. However, prolonged fentanyl administration leads to accumulation and an increased half-life of 9–16 hours. Due to the short half-life, fentanyl should be administered via a drip at 1–2 mg/kg/hr. One more loading dose of 1–2 mg/kg is recommended when initiating the fentanyl intravenous drip. Caution should be used in patients with bradyarrhythmias because this agent may produce bradycardia. 3. Hydromorphone (Dilaudid) is a semisynthetic morphine derivate and is an acceptable alternative to morphine. It is a more potent analgesic/sedative than morphine with fewer euphoric effects. The dosage is usually initiated at 0.5 mg and titrated by 0.5-mg increments. Most patients require 1–2 mg every 1–2 hours for desired results. Dilaudid should be used with caution in patients with neurological disorders or injury because it increases cerebrospinal fluid pressures. It also can potentially cause transient hyperglycemia in some patients. There are several analgesic agents that are not recommended as the primary analgesic agent in critically ill intubated patients. These include meperidine (Demerol), which may produce CNS excitement; opiate agonist-antagonists such as nalbuphine, butorphanol, or buprenorphine, which may reverse other opiate agents; or nonsteroidal anti-inflammatory agents such as ibuprofen or ketorolac (Toradol) because of potential risks of gastrointestinal bleeding, bleeding secondary to platelet inhibition, and the development of renal insufficiency.
SEDATIVES Sedation is necessary in most ventilated patients to provide comfort and to treat anxiety and agitation (Table 15-11). Sedatives have no analgesic affect; therefore, analgesics are recommended in conjunction with sedation medications. Sedative agents are inappropriate as sole agents in the management of intubated patients. Oftentimes, the analgesic medication alone will be sufficient for analgesia and sedation. Each patient’s circumstances vary and each should be managed individually based on his or her needs. When CNS monitoring is important, short-acting
Table 15-11 Sedatives for Use in Intubated Patients SEDATION AGENT
ADVANTAGE
DISADVANTAGE
DURATION OF ACTION
Rapid onset; short acting; easily turned off for frequent neurological monitoring
High cost
10 min with single dose
Midazolam (Versed)
Rapid onset of action; short acting
Potential for peripheral accumulation
30 min with single dose
Lorazepam (Ativan)
Long acting; ideal for patients for whom >24-hour intubation is required; low cost; intermittent or continuous-infusion dosing
Potential for peripheral accumulation
60–90 min
*Increased dosage may be required for some patients.
Loading dose: 5 mg/kg/min, increase by 5 mg/kg/ min every 5–10 min as needed for effect Maintenance dose: 5–50 mg/kg/min drip Loading dose: 0.03 mg/kg Maintenance dose: 0.03 mg/kg/hr drip Loading dose: 2–3 mg Maintenance dose: 0.44 mg/kg every 2–4 hours or 1- to 2-mg/hr continuous infusion*
Sedation and Analgesia in the Intubated Patient
Propofol (Diprivan)
DOSAGE
909
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benzodiazepines or propofol should be used. The SCCM recommends the followed sedatives for critically ill intubated patients: 1. Propofol or midazolam (Versed) are preferred agents only for the short-term (<24 hours) treatment for anxiety and to provide sedation. These agents not only act in a sedative capacity, but also as a hypnotic, anxiolytic, and some anterograde amnestic effects. Propofol (Diprivan) is an ultra-short-acting sedative/hypnotic agent. It is administered as a continuous drip infusion. The onset of action is 1–2 minutes and has a brief effect of only 10–15 minutes when discontinued. Propofol is administered at an initial infusion rate of 5 mg/kg/min and titrated rapidly upward in increments of 5 mg/kg/ min every 5–10 minutes as needed. Typical maintenance dosages are 5–50 mg/kg/min. Propofol can cause apnea and respiratory depression in higher doses. It may also cause hypotension when given by rapid bolus injections, particularly in patients with hypovolemia or when administered concurrently with other sedative/hypnotic or analgesic agents. Because of the high cost of this medication, some hospitals have protocols that limit the use of propofol. Midazolam (Versed) is a short-acting, water-soluble benzodiazepine that becomes lipophilic in the blood and rapidly penetrates the CNS. The onset of action is 2–3 minutes. Typically, a loading bolus dose of 0.03 mg/kg is required. The maintenance dosage is 0.03 mg/ kg/hr, which can be titrated as needed. There is a potential for peripheral accumulation with this medication; therefore, patients must be monitored so as to avoid prolonged effect. 2. Lorazepam (Ativan) is the preferred agent for the prolonged (>24 hours) treatment of anxiety and to provide sedation. Lorazepam is an intermediate-acting benzodiazepine. One advantage of this medication with its long half-life is the ability to administer the drug with intermittent dosing. A continuous infusion is also an acceptable route for administration. The usual initial starting dose is 0.44 mg/kg every 2–4 hours, as needed. However, the effect varies from patient to patient. Some patients require hourly dosing or a continuous infusion to be effective. Lorazepam has a slightly longer onset of action than propofol or Versed but a longer half-life. Typical continuous infusion rates are 1–2 mg/hr.
Other Sedating Medications Haloperidol (Haldol) is the preferred agent for the treatment of delirium in critically ill adults. Haloperidol is a butyrophenone neuroleptic drug. The U.S. Food and Drug Administration has approved this medication to be administered as an intramuscular injection only. However, it has been reported to be safe and effective when given intravenously. The
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dosing is typically 2–10 mg every 2–4 hours. Delirium is defined as an inappropriate response to external stimuli, such as disorganized thinking, rambling, incoherent/irrelevant speech, decreased level of consciousness, altered sensory perception, and disorientation. Delirium is very difficult to evaluate in an intubated patient; therefore, haloperidol is not commonly used in intubated patients. Diazepam (Valium) is a long-acting lipophilic benzodiazepine that rapidly penetrates the CNS, allowing for a quick onset of action within 2–3 minutes. The typical initial dose is 0.2–0.3 mg/kg. However, this drug is rapidly redistributed into the peripheral tissues, causing frequent repeated dosing for effect. Frequent repeated dosing can lead to saturation of peripheral and central nervous system binding sites, potentially resulting in prolonged oversedation. For this reason, Valium is rarely used as a continuous sedative in intubated patients according to the SCCM practice guidelines. Etomidate (Amidate) is an intravenous anesthetic/hypnotic agent that is often used to provide anesthesia for short procedures. However, it is not recommended for sedation in an intubated patient. Long-term use of etomidate has proved to be associated with adrenal suppression and increased mortality. Ketamine (Ketalar) is another intravenous anesthetic/analgesic agent that is used for short procedures. According to the SCCM practice guidelines, this medication is not recommended for prolonged sedation in an intubated patient because of the potential for increased blood pressure, tachycardia, and increased intracranial pressure. This medication should be used with caution in patients with ischemic heart disease.
NEUROMUSCULAR BLOCKERS (PARALYTICS) Neuromuscular blockade agents should be a last resort rather than a first-line alternative in intubated patients when analgesics in combination with sedatives at maximum dosages are ineffective. Neuromuscular blockade agents have no amnestic, analgesic, or sedative effect; therefore, they must always be used in conjunction with an analgesic and/ or sedative. Paralytic medications are often not necessary in intubated patients when the appropriate combination of analgesia and sedation are used and titrated to effect. When using paralytic drugs, the frequent assessment of vital signs is essential for clues that the patient is experiencing discomfort or undersedation. Paralytic drugs often mask many potential complications; therefore, these should only be used as longterm agents selectively. Paralytic medications are often used as part of the rapid-sequence intubation series while mechanical ventilation is initiated. Depending
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on which paralytic agent and dosage are used, the duration of effect can range from 1 to 3 hours. Prolonged use of paralytics is being used in special circumstances such as with pressure-control ventilation but is not routinely recommended in most intubated patients. Complications of neuromuscular blockers include increased risk of venous thromboembolism, pressure ulcers, corneal ulcers, nerve compression syndromes, and muscle atrophy. Depolarizing neuromuscular-blocking agents are not recommended for sustained paralysis. Nondepolarizing neuromuscular-blocking agents, such as pancuronium and vecuronium, can be used for sustained paralysis when desired. 1. Pancuronium (Pavulon) is the preferred nondepolarizing neuromuscular-blocking agent according to the SCCM practice parameters. It is a long-acting agent that produces effect within 4 minutes after a 0.06–0.08 mg/kg intravenous bolus dose is administered. It generally lasts approximately 75–90 minutes. Repeated dosing increases the duration of effect. The maintenance dosage is typically 0.02–0.03 mg/kg every 1–2 hours. This medication can also be given as a continuous infusion. The typical maintenance dosage when given via continuous infusion is 0.02–0.03 mg/kg/hr. Dosages must be adjusted in patients with liver or renal disease. Use of pancuronium should be avoided in patients with asthma because of its side effect of histamine release and the potential for bronchospasm. 2. Vecuronium (Norcuron) is an intermediate-acting, nondepolarizing, neuromuscular-blocking agent. It is about one third more potent than pancuronium; however, the duration of effect is significantly less than that of pancuronium. It is preferred in patients with cardiac disease or in hemodynamically unstable patients in which tachycardia (commonly seen with pancuronium) may be detrimental. The onset of action is 2.5–3 minutes after a 0.08–0.10 mg/kg intravenous bolus dose (approximately 5–10 mg for the average patient). Additional dosages at approximately 25% of the paralyzing dose are usually given when motor activity is observed. Due to the short duration of action, a continuous infusion is usually required with the maintenance dosage of 0.8–1.2 mg/kg/min. Vecuronium is metabolized via the liver; therefore, caution should be used in patients with hepatic dysfunction.
CONCLUSION Appropriate pharmacotherapy in intubated patients varies depending on the patient and facility. Every facility has specific protocols that must be followed for sedation, analgesia, and paralytic use. Most patients undergoing mechanical ventilation require analgesia, sedation, and, in rare
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instances, neuromuscular paralytic agents. Analgesic medications should be used in all intubated patients to provide comfort. Reduction of pain or discomfort from the endotracheal tube itself has proved to contribute to a faster recovery. The combination of analgesics and sedatives often provides the optimal comfort and compliance with the ventilator. When using a neuromuscular blockade agent, analgesics and/or sedatives should always be used in conjunction with close monitoring.
Bibliography Chudnofsky CR, Lozon MM: Sedation and analgesia for procedures. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Vol 3. Mosby: St Louis, 2002. Cullen DJ, Bigatello LM, DeMonaco HJ: Anesthetic pharmacology and critical care. In Chernow B (ed): The Pharmacologic Approach to the Critically Ill Patient, ed 3. Williams & Wilkins: Baltimore, MD, 1994. Lumb PD, Gallagher TJ: Sedatives and muscle relaxants in the intensive care unit. In Ayres SM, Grenvik A, Holbrook PR, Shoemaker WC (eds): The Textbook of Critical Care, ed 3. WB Saunders: Philadelphia, 1995. Pollack CV Jr: Mechanical ventilation and noninvasive ventilatory support. In Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Vol 1. Mosby: St Louis, 2002. Schneider S: Acute respiratory insufficiency: Overview. In Schwartz GR, Hanke BK, Mayer TA, et al (eds): Principles and Practice of Emergency Medicine, ed 4. Williams & Wilkins: Baltimore, MD, 1999. Shapiro BA, Peruzzi WT: Respiratory care. In Miller RD (ed): Anesthesia, ed 5. Vol 2. Churchill Livingstone: Philadelphia, 2000. Shapiro BA, Warren JW, Egol AB, et al: Practice parameters for intravenous analgesia in sedation for adult patients in the intensive care unit: An executive summary, Crit Care Med 1995;23:1596. Shapiro BA, Warren JW, Egol AB, et al: Practice parameters for sustained neuromuscular blockade in the adult critically ill patient: An executive summary, Crit Care Med 1995;23:1601. Ungar JR, Brandes D, Reinoehl BM, et al: Pain management. In Schwartz GR, Hanke BK, Mayer TA, et al (eds): Principles and Practice of Emergency Medicine, ed 4. Williams & Wilkins: Baltimore, MD, 1999.
Chapter 16
Acute Resuscitation Emergencies Airway Management ALLEN WHITFORD
ICD Codes: Airway compressed, disease 993.3, Airway obstruction not elsewhere classified 519.8, Airway obstruction asthma not elsewhere classified 493.2 DEFINITION Airway management is a common problem encountered on a daily basis in the emergency department (ED). It is the “A” of ABCs of resuscitation. Airway obstruction can be as simple as a tongue fallen back into the airway or as complicated as angioedema, foreign body, or a maxillofacial gunshot wound. Airway obstruction causes hypoxia and hypercapnia resulting in brain death if not addressed within in as little as 5 minutes. Cyanosis occurs when the hemoglobin desaturates to 5 g/100 ml, assuming that there is enough hemoglobin to cause cyanosis. (For a discussion of pediatric airway management, see the section titled Pediatric Airway Management in Chapter 13.)
CLINICAL PRESENTATION Aphonia indicates a complete airway obstruction. Hoarseness is specifically localized to the larynx and is associated with edema and unilateral vocal cord dysfunction. Stridor is a high-pitched squeaking or crowing noise that is indicative of a partial airway obstruction at the larynx or tracheal level. For stridor to occur, the airway must be constricted to less than 4 mm at rest and 4–6 mm on exertion. Patients with pharyngeal obstruction will present with a “snoring” sound. An obstruction at the bronchial level will present as expiratory wheezing. Coughing can be the result of a mechanical, chemical, or thermal stimulus. A croupy “barking” cough is indicative of subglottic pathology such as croup, and a “brassy” cough generally results from tracheobronchial disease.
TREATMENT The management of the failed airway takes precedent over all other resuscitation considerations. Establishment and protection of the airway with maximum oxygenation and ventilation is the hallmark of airway management. Cervical spine stabilization should always be maintained if the 914
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mechanism of injury is unknown. Once the decision to intubate is made, the patient should be administered on 100% oxygen at a rate of 12–20 breaths/min at a volume of 10–15 ml/kg of body weight by bag-valvemask (BVM) until intubation is accomplished. BVM should maintain SaO2 at or above 90%. Endotracheal or nasotracheal intubation is the recommended method of airway control. The Combitube device, which is a dual-lumen, dual-cuff airway, allows ventilation whether placed into the trachea or esophagus. The Combitube is a marked improvement over the old esophageal obturator airway. Indications for endotracheal intubation include airway obstruction, hypoxia, hypercarbia, and the inability of the patient to maintain a patent airway. Another indication would include facilitating computed tomography imaging without motion artifact for further evaluation. The indications for nasotracheal intubation are difficult or impossible direct laryngoscope intubation or long-term ventilation. The contraindications of nasotracheal intubation include apnea, upper airway foreign body, tumor, abscess, central facial fractures, basal skull fracture, coagulopathy, epiglottitis, and prosthetic devices. Nasotracheal intubation can cause epistaxis, bacteremia, turbinate mucosal avulsion, necrosis of the nares, sinusitis, otitis media, and retropharyngeal or piriform sinus perforation. When performing oral intubation, cricoid pressure using the backward, upward, and right pressure (BURP) technique should be applied (Boxes 16-1 to 16-3). This refers to pressure applied to the cricoid cartilage. This will bring the vocal cords into a direct line of sight when looking into the patient’s mouth from the right side. It also helps to prevent aspiration during the intubation procedure. There are two basic types of laryngoscope blades, the Miller (straight blade) and the MacIntosh (curved). Only by constant practice can the clinician learn and become proficient in their use. Whichever blade Box 16-1 Rapid Sequence Induction in an Asthmatic Patient or Patient with Chronic Obstructive Pulmonary Disease Preoxygenate with 100% oxygen delivered via face mask for 3 minutes with cricoid pressure BURP. Pretreatment Options Atropine, 0.02 mg/kg IV (routine, if patient is younger than 10 years of age) Lidocaine, 1.5 mg/kg IV (routine) Induction agent: Ketamine, 0.5–1 mg/kg IV
Paralytic agent: Succinylcholine, 1.5 mg/kg IV BURP, Backward, upward, and right pressure; IV, intravenous.
916 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Box 16-2 Rapid Sequence Induction Preoxygenate the patient with 100% oxygen via bag-valve-mask for 3 minutes with cricoid pressure BURP. Pretreatment Options Atropine, 0.02 mg/kg IV Lidocaine, 1.5 mg/kg IV and/or Vecuronium, 0.01 mg/kg IV defasciculating dose in head injuries
or Fentanyl, 3 mg/kg IV
Wait for 1-3 minutes. Induction and Muscle Relaxation Pick one induction agent: Thiopental, 3–5 mg/kg for hemodynamically stable patients Etomidate, 0.3–0.4 mg/kg IV for hemodynamically stable patients or 0.1–0.2 mg/kg
IV for unstable patients or Methohexital (Brevital) 1–2 mg/kg IV for hemodynamically stable patients
Pick one paralytic agent: Succinylcholine, 1.5 mg/kg IV
or Vecuronium, 0.1–0.3 mg/kg IV BURP, Backward, upward, and right pressure; IV, intravenous.
Box 16-3 Rapid Sequence Induction in a Patient with a Head Injury Preoxygenate with 100% oxygen delivered via face mask for 3 minutes with cricoid pressure. Pretreatment Options Fentanyl, 3 mg/kg IV Induction agent: Etomidate, 0.3 mg/kg IV Thiopental, 3–5 mg/kg IV for hemodynamically stable patients, 0.5–1 mg/kg for
hemodynamically unstable patients Paralytic agent: Succinylcholine, 1.5 mg/kg IV IV, Intravenous.
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the practitioner is most comfortable with is the one he or she should use. Familiarity with all of the types of equipment on the difficult airway cart in one’s own ED is necessary. Each time the clinician picks up an endotracheal tube, he or she must be prepared to pick up a scalpel if all other adjuncts fail. One should be familiar with endotracheal inducers, fiberoptic scope intubations, obturator airways, and esophageal obturator airways. Once a patient has been intubated, he or she can be maintained in a paralyzed and sedated state with 5–7 mg of intravenous vecuronium and 2–3 mg of intravenous Versed every hour until the clinician wishes to wake the patient.
Bibliography Brandenburg RO, Fuster V, Giuliani ER, et al (eds): Cardiology Fundamentals and Practice. Year Book: Chicago, 1987. Braunwald E, Isselbacher KJ, Petersdorl RG, et al (eds): Harrison’s Principles of Internal Medicine, ed 11. McGraw-Hill: New York, 1987. Eagle KA, Harber E, DeSanctis A, Austen WG (eds): The Practice of Cardiology, ed 2. Little, Brown: Boston, 1989. Hamilton CE, Sanders AB, Strange GR, et al (eds): Emergency Medicine: An Approach to Clinical Problem Solving. WB Saunders: Philadelphia, 1991. Hurst JW, Logue RE, Rackley CE (eds): The Heart, ed 6. McGraw-Hill: New York, 1994. Kravis TC, Warner CG, Jacobs LM (eds): Emergency Medicine: A Comprehensive Review, ed 3. Raven Press: New York, 1993. May HL, Aghababian RV, Fleisher GR (eds): Emergency Medicine, ed 2. Little, Brown: Boston, 1992. Rosen P, Barkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby–Year Book: St Louis, 2002. Schwartz GR, Cayton CG, Manglesen MA, et al (eds): Principles and Practice of Emergency Medicine, ed 3. Lea & Febiger: Philadelphia, 1992. Tintinalli JE, Krone RL, Ruiz E (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Walls R (ed): Manual of Emergency Airway Management. Lippincott: Philadelphia, 2000.
918 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Shock ALLEN WHITFORD
ICD Code: Shock 785.50 DEFINITION Shock is the acute reduction of blood flow resulting from diminished cardiac output and misdistribution of output with potential for reversal. Shock causes impairment of the brain, heart, lungs, kidneys, mesentery, muscles, and skin. Patients present in three generalized types of shock: hypovolemic (traumatic or nontraumatic), cardiogenic (traumatic or nontraumatic), and vasogenic (septic, anaphylactic, neurogenic, or pharmacological).
PATHOLOGY As the fluid loss progresses, the venous capacitance is decreased by about 10%–20% before a patient is symptomatic, with an interstitial to intravascular compartment shift of fluid and arteriolar constriction. The central venous pressure (CVP) is decreased, even though there is compensation stroke volume, and urine output decreases. There is decreased skin perfusion and decreased temperature regulation. The central nervous system also has decreased perfusion, which causes altered mental status. There is a decrease in microvascular perfusion and cardiovascular dysfunction. As the process ensues, there is anaerobic metabolism and release of proteolytic enzymes and vasoactive substances. Platelet aggregation and myocardial function is depressed.
CLINICAL PRESENTATION Nontraumatic Hypovolemic Nontraumatic hypovolemic shock occurs as a result of dehydration or hemorrhage, due to decreased fluid volume. Patients with hemorrhage present with bloody stools, hematemesis, hemoptysis, signs of a ruptured aortic aneurysm, or severe epistaxis. An acute ectopic pregnancy should be considered in any female of childbearing years who is hypotensive. Patients with hypovolemia due to dehydration appear very pale and have moist skin as a result of adrenergic stimulation. Patients with traumatic hypovolemic shock present with hypotension or tachycardia that may respond to intravenous fluids and blood.
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Other causes of hypovolemic shock are sedatives, anorexia, bulimia, gastrointestinal obstruction, central nervous system abnormalities, overdiuresis, diabetes, diabetic ketoacidosis, and adrenal insufficiency. Pancreatitis, peritonitis, and ascites can cause sequestration of fluids and hypovolemia.
Cardiogenic Shock Cardiogenic shock is most often seen in patients who have had a myocardial infarction (MI), papillary muscle rupture, or ventricular septal defect. Ventricular septal defect and papillary muscle rupture can be detected by a loud systolic murmur that is louder than the first heart sound (S1). Pericardial tamponade, air embolus, tension pneumothorax, and pulmonary embolus can all cause cardiogenic shock. Dilated, nondilated, restrictive, and hypertropic cardiomyopathies can also cause cardiogenic shock resulting from decreased stroke volume and decreased ejection fraction. Symptoms of cardiogenic shock are the same as those for hypovolemia, including anxiety and obtundation. Tachypnea and tachycardia are often present, unless a heart block is also present, as a result of a new MI. The patient is usually hypotensive. There is elevated jugular venous distention and an S3, resulting from an increase in left ventricular end-diastolic pressure. If a right-sided MI is suspected, a right-sided electrocardiogram should be performed. The clinician should remember that right-sided MIs are fluid dependent.
Traumatic Cardiogenic Shock Traumatic cardiogenic shock results from cardiac tamponade, tension pneumothorax, or myocardial contusion, all of which decrease cardiac output secondary to poor venous return to the heart. Pericardial tamponade can be the result of penetrating trauma to the chest or abdomen. It can occur because of a gunshot wound or a stab wound. It only takes 200 ml of blood to create a hemodynamic compromise. Beck’s triad is the presence of distended neck veins, decreased arterial pressure, and muffled heart sounds resulting from cardiac tamponade. A patient with a tension pneumothorax presents with agitation, dyspnea, cyanosis, hypotension, and tachycardia. Always look for a tracheal shift toward the good lung and away from the pneumothorax. Cardiac contusion rarely causes cardiogenic shock, but if blunt trauma is a factor in the history, myocardial contusion should be considered. Usually, the right atrium and ventricle are affected more than the left atrium and ventricle because of their posterior location to the sternum.
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Vasogenic Shock Vasogenic shock is a result of arteriolar and venous dilatation. Vasogenic shock includes septic, pharmacological, anaphylactic, and neurogenic shock. Septic shock results from infection, usually in compromised patients with underlying disease. The patient can present with chills, hyperthermia, hypothermia, nausea, vomiting, or mental status changes.
Pharmacological Shock Pharmacological shock is a drug-induced shock resulting from sedative hypnotics, narcotics, nitrates, antidepressants, antihypertensives, and anticholinergics.
Anaphylactic Shock Anaphylactic shock occurs because of immunoglobulin E–and immunoglobulin M–mediated hypersensitivity of the immune system. The patient presents with hypotension, bronchial spasm, dyspnea, pruritus, increased vascular permeability, and arteriolar dilation.
Neurogenic Shock Neurogenic shock is a result of a spinal cord injury. The patient presents with hypotension and bradycardia because of a loss of sympathetic tone distal to the level of the spinal cord injury.
LABORATORY FINDINGS A complete blood count, hematocrit and hemoglobin analysis, and measurements of prothrombin time, partial thromboplastin time, and electrolytes should be performed in any patient with shock. If shock occurs as a result of bleeding, type- and cross-matched blood (6–8 units) should be ordered. Type-specific blood should be used if time permits. It usually only takes an extra 5 minutes to determine a blood cross-match from a type and screen. Blood and urine cultures should be obtained if septic shock is considered. Cardiac enzyme levels should be checked if an MI or cardiac injury is suspected. An arterial blood gas analysis should be performed to determine the acid-base status of the patient.
TREATMENT The mainstay of treatment for any kind of shock is to treat or remove the underlying cause of the shock. Treatment goals are to maximize
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oxygenation, correct underlying metabolic abnormalities, and improve hemodynamic dysfunction. To monitor the fluid status of the patient is to monitor the CVP. The CVP is the filling pressure of the right atrium, which is dependent on the right ventricle function, venous tone, intrathoracic pressure, and intravascular volume. The normal values for CVP lie between 0 and 4 mmHg. CVP is elevated in pericardial tamponade, pulmonary embolism, right ventricular failure, and vasogenic causes resulting from left ventricular failure. In nonvasogenic causes, venous tone is low and CVP will be low. CVP will be low in cases of hypovolemic shock and increased in cardiogenic shock. Hypovolemic shock is treated with crystalloid infusions of lactated Ringer’s solution or normal saline. Fluid should be given in boluses, and the patient’s vital signs should be continuously monitored. If feasible, CVP should be monitored. Hemorrhagic shock should be treated with blood after the initial 2 L of crystalloid are given. In most institutions, 2 units of fresh frozen plasma are given for every 10 units of blood. Platelets should be given as needed to keep the platelet count above 100,000 platelets/mm3. Cardiogenic shock treatment is a delicate balancing act. Fluid levels should be monitored by a Swan-Ganz catheter. If the cardiac index is below 2.2 J/min/m2, fluids should be given to obtain a wedge pressure of 15–18 mmHg. Dysrhythmias should be treated aggressively. In the setting of an acute MI, the pain should be treated with oxygen, nitrates, morphine, and beta blockers if the blood pressure is stable. In the setting of cardiogenic shock, the drug of choice is dopamine. The actions of dopamine are dose dependent. At 1–2 mg/kg/min, dopaminergic effects occurs. At this dose, in the first few hours of oliguric renal failure an increase in urine output can be produced. A dose of 3–10 mg/kg/ min predominantly causes beta action. This dose will cause increased cardiac output and peripheral vascular resistance. A 10–20-mg/kg/min dose will give combined alpha and beta effects. At greater than 20 mg/kg/ min, the action is predominantly alpha. At this dose, a generalized vasoconstriction occurs with a greatly increased systemic vascular resistance with the likelihood of ischemia. Dobutamine is the drug of second choice. It is primarily a beta receptor agonist and is a positive inotrope, which means it increases or maintains cardiac output. Dobutamine also lowers the wedge pressure. If the cardiogenic shock occurs as a result of penetrating trauma to the chest and the patient loses his or her pulse within 2 minutes of arrival in the ED, a left anterior thoracotomy should be performed. This procedure increases afterload by decreasing arterial bleeding inferiorly when the aorta is cross-clamped and the pericardium is opened, thus relieving pericardial tamponade. This procedure should only be performed by a qualified physician. If cardiac tamponade is believed to be the cause of the hypotension, then a pericardiocentesis should be performed.
922 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Vasogenic shock due to septic shock is managed by treating the underlying infection. Blood, sputum, and urine culture samples should be obtained, and the patient should be given broad-spectrum antibiotics. Antibiotics should include gram-negative coverage with a third-generation cephalosporin or an aminoglycoside. Penicillin or vancomycin should be added to cover staphylococcal infections. If the patient is neutropenic, antibiotic coverage for Pseudomonas organisms should also be included. Pharmacological shock resulting from use of narcotics should be treated with naloxone, fluids, and vasopressors if necessary. Neurogenic shock is treated with fluids and dopamine or epinephrine. If bradycardia is present, the heart rate should be treated first with atropine or pacing, if required. Neurogenic shock usually resolves in 3–8 days. Anaphylactic shock is treated with epinephrine and fluids. If the patient’s blood pressure is not responding to subcutaneous or intravenous epinephrine, then an epinephrine drip of 2–4 mg/kg/min should be started and titrated until a clinical response is achieved. The patient should also be given intravenous diphenhydramine (50 mg), aerosolized albuterol (0.5 ml in 3 ml of saline), intravenous methylprednisolone (125 mg), and intravenous cimetidine (300 mg). Any patient in shock should be admitted to an intensive care unit once his or her condition has been stabilized. The patient should remain in the ED until adequate resuscitation has been achieved.
Bibliography Brandenburg RO, Fuster V, Giuliani ER, et al (eds): Cardiology Fundamentals and Practice. Year Book: Chicago, 1987. Braunwald E, Isselbacher KJ, Petersdorl RG, et al (eds): Harrison’s Principles of Internal Medicine, ed 11. McGraw-Hill: New York, 1987. Eagle KA, Harber E, DeSanctis A, Austen WG (eds): The Practice of Cardiology, ed 2. Little, Brown: Boston, 1989. Hamilton CE, Sanders AB, Strange GR, et al (eds): Emergency Medicine: An Approach to Clinical Problem Solving. WB Saunders: Philadelphia, 1991. Hurst JW, Logue RE, Rackley CE (eds): The Heart, ed 6. McGraw-Hill: New York, 1994. Kravis TC, Warner CG, Jacobs LM (eds): Emergency Medicine: A Comprehensive Review, ed 3. Raven Press: New York, 1993. May HL, Aghababian RV, Fleisher GR (eds): Emergency Medicine, ed 2. Little, Brown: Boston, 1992. Rosen P, Barkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby–Year Book: St Louis, 2002. Schwartz GR, Cayton CG, Manglesen MA, et al (eds): Principles and Practice of Emergency Medicine, ed 3. Lea & Febiger: Philadelphia, 1992. Tintinalli JE, Krone RL, Ruiz E (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Walls R (ed): Manual of Emergency Airway Management. Lippincott: Philadelphia, 2000.
Chapter 17
Toxicology Emergencies General Principles of the Poisoned Patient ROBERT D. GRAYDON
DEFINITION Numerous words are used to describe a poisoned patient. Inebriation is used to describe the symptoms of alcohol ingestion. Intolerance is used to describe a low sensitivity to a nontoxic substance. Hypersensitivity describes an altered immunological response, independent of the metabolism of the compound. Intoxication is used interchangeably with inebriation, but intoxication can be the result of ingestion of any substance that can cause alcohol-like effects. Idiosyncrasy describes an aberration in host biochemistry that can lead to disease state peculiar to the metabolism or genetic composition of the host. Poisoning describes a dose-dependent reaction that is harmful to the organism.
EPIDEMIOLOGY Accidental and intentional poisonings or drug overdoses constitute a significant source of morbidity, mortality, and healthcare expenditure. An estimated 2–5 million poisonings and drug overdoses occur annually in the United States, although the true incidence may be double this number due to underdiagnosis and underreporting. Although the overall mortality from drug overdose and poison exposure is 0.05%, the mortality rate for hospitalized patients is 1%–2%. Only 6.6% of the 2.5 million exposures reported to poison control centers in 2003 required hospital admission. However, poison exposures account for 5%–10% of emergency department (ED) visits and more than 5% of adult intensive care unit (ICU) admissions.
TOXICOKINETICS AND PHARMACOKINETICS With every poisoning, several questions must be answered about the toxin before appropriate treatment can be given. Important pharmacokinetic questions to be answered include the following: 1. What is the absorption rate of the toxin? 2. Where is the toxin stored in the body? 923
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3. 4. 5. 6.
What is the volume of distribution of the drug/toxin in the body? How is the drug/toxin excreted from the body? How does the body metabolize the drug/toxin? Is the toxin/drug protein bound?
The volume of distribution is the measurement of the amount of drug that is located in a certain part of the body (e.g., blood, fat, or organ tissues). The larger the volume of distribution of the toxin, the greater the concentration of the toxin in the blood. The volume of distribution is required to determine the usefulness of dialysis, hemoperfusion, or exchange transfusions as therapy. The way that a toxin is excreted or eliminated is very important. Often, excretion or elimination can be affected by therapy. The liver, kidneys, and lungs eliminate most toxins in bile, urine, or breath. Elimination is described as zero-order, first order, or Michaelis-Menten order. Zero-order or enzyme kinetics means that a drug is metabolized only to a certain point, usually in the liver; once the liver reaches this fixed point of metabolism, serum levels of the toxin rise dramatically. In zeroorder kinetics, a constant amount of toxin is eliminated over a fixed period of time. In first-order kinetics renal elimination means that the higher the plasma concentration, the greater will be the amount excreted by the kidneys over a fixed period of time. In first-order kinetics, a constant fraction will be eliminated over a fixed period of time. Michaelis-Menten elimination is a combination of both zero-order and first-order kinetics. Often, after the enzyme systems of the liver are saturated, elimination is switched to zero-order kinetics. Elimination can be increased by dialysis, hemoperfusion, diuresis with ion trapping, and multiple doses of activated charcoal.
OVERVIEW OF THE APPROACH TO TREATMENT OF A POISONED PATIENT Clinicians who treat poisoned patients should have a systematic and consistent approach to the evaluation and management. Evaluation involves recognition that poisoning has occurred, identification of the involved agents, assessment of severity, and prediction of toxicity. Management is directed toward the provision of supportive care, prevention of poison absorption, and, when appropriate, the administration of antidotes and the enhancement of the elimination of the toxin. The speed, sequence, methods, and priorities of management are determined by the toxins involved, the presenting and predicted severity of the poisoning, and the presenting phase of the poisoning.
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The preclinical phase follows exposure but precedes the development of symptoms and signs. Management is guided by the history and is aimed at reducing or preventing the predicted toxicity. Decontamination is a priority in this phase. The toxic phase covers the period from onset to the peak of clinical and laboratory manifestations of toxicity. The objectives are to shorten the duration and lessen the severity of toxicity. Treatment is largely guided by the physical examination findings and to a lesser degree by laboratory values. The highest priorities are to stabilize the patient’s airway, breathing, and circulation (i.e., the ABCs) and to administer antidotes when appropriate. The resolution phase runs from the time of peak toxicity to recovery. Management is guided by the patient’s clinical status, with the major goal of shortening the duration of toxicity.
“SAFETY NET” AND INITIAL EVALUATION OF THE POISONED PATIENT The clinician should always establish a safety net for any patient with known or suspected poisoning. In many cases, ingestion can cause clinical deterioration to occur both rapidly and dramatically. Continuous cardiac monitoring and continuous pulse oximetry should be initiated, and vital signs should be noted every 4–5 minutes. At least one large-bore intravenous (IV) line should be placed, and the patient should be administered supplemental oxygen. A brief initial screening examination should be performed on all patients to identify immediate measures required to stabilize and prevent deterioration of the patient’s condition. As noted, vital signs should be assessed as well as mental status and pupil size. Electrocardiography (ECG) should be performed. In-line cervical immobilization is required for patients with suspected occult trauma. The airway should be assessed frequently and endotracheal intubation strongly considered if there is doubt about the patient’s ability to protect the airway and avoid aspiration. Advanced cardiac life support (ACLS) measures must be taken, as required. Altered consciousness requires the rapid IV infusion of 100 mg of thiamine and 25 g of glucose (as 50 ml of a 50% dextrose solution) should be given for possible Wernicke’s encephalopathy and hypoglycemia, respectively; 0.4–2.0 mg of IV naloxone should be administered to patients with signs, symptoms, or a history suggestive of opiate intoxication. Complete exposure and examination of the patient and measurement of core temperature are essential. Patient decontamination should then be initiated (if indicated), and a more detailed diagnostic evaluation can ensue.
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HISTORY A complete history of the event should always be obtained. Although intuitively the source of the most helpful information for identifying the cause of poisoning, the history is often unreliable when provided by a patient after an intentional ingestion. In the pediatric population, ingestions are often not witnessed, and the child is usually a poor historian. The patient’s history should be confirmed whenever possible and correlated with the signs, symptoms, and laboratory data expected from poisoning with the agent(s) implicated by history. A specific overdose history includes how much of the drug was taken, when it was taken, why it was taken, what else was taken, and whether the patient has taken the drug before. It should be kept in mind that many intentional overdoses involve multiple substances. A complete past medical and psychiatric history should be obtained, including a history of prior overdoses or suicide attempts. The past surgical history should include chronic pain or pain medications. The social history should include the use of alcohol, drugs, tobacco, and caffeine. Information on current and past medications should be obtained. A family history should include psychiatric illnesses. Knowledge of drugs prescribed to the patient or to the patient’s family or friend (to which the patient could have had access) may prove to be important. Unknown pills may be identified by consultation with a regional poison center, computerized poison identification system, or product manufacture. Consultation with a poison control center is recommended in all cases.
EXAMINATION The physical examination of symptomatic poisoned patients may provide invaluable clues to the etiological agent involved. All patients should have a complete physical examination, including cardiac, pulmonary, and neurological systems; mental status; rectum; and skin. The mental status, vital signs, and papillary examination findings are the most useful elements and allow classification of the patient into either a state of physiological excitation or depression. Physiological excitation—manifested by central nervous system (CNS) stimulation and increased pulse, blood pressure, respiratory rate and depth, and temperature—is most commonly caused by anticholinergic, sympathomimetic, or central hallucinogenic drugs or by drug-withdrawal states. Physiological depression—manifested by a depressed mental status, blood pressure, pulse, respiratory rate and depth, and temperature—is most commonly caused by cholinergic (parasympathomimetic), sympatholytic, opiate, or sedative-hypnotic agents or alcohol.
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Mixed physiological effects occur in polydrug overdoses or after exposure to certain metabolic poisons (e.g., hypoglycemic agents, salicylates, cyanide), membrane-active agents (e.g., volatile inhalants, antiarrhythmic drugs, local anesthetic agents), heavy metals (e.g., iron, arsenic, mercury, lead), or agents with multiple mechanisms of action (e.g., tricyclic antidepressants). Discrepancies between the physical examination and the history may reflect an inaccurate ingestion history or a brief or a prolonged time interval between exposure and physical examination. The evaluation of mental status and vital signs should be repeated frequently to determine the course of the poisoning and the need for further intervention.
ELECTROCARDIOGRAM ECG abnormalities may provide diagnostic and prognostic information, and an ECG should be performed on all patients who are symptomatic or who have been exposed to potentially cardiotoxic agents.
RADIOGRAPHS Imaging studies are not required in every patient but may be useful in several situations. Plain film radiographs may visualize certain radiopaque toxins. Ingested drug packets in “body packers” may be seen on plain radiographs. Noncardiogenic pulmonary edema or ARDS due to exposure to certain toxic agents may be suggested by the appearance of the chest radiograph.
LABORATORY FINDINGS Certain laboratory abnormalities are characteristic of specific agents. Symptomatic patients or those with unclear histories should, at a minimum, undergo urinalysis, complete blood count (CBC), and measurement of serum electrolytes, blood urea nitrogen (BUN), creatinine, and glucose levels. Liver function tests and measurements of serum osmolality, ketones, creatine kinase, amylase calcium, and magnesium should also be performed in most ill patients. Routine urine pregnancy testing should be performed in all women of childbearing age. Arterial blood gas (ABG) analysis, co-oximetry, and serum lactate measurements may be necessary in patients with acid-base, cardiovascular, neurological, or respiratory disturbances. Co-oximetry can aid in the rapid diagnosis of carbon monoxide poisoning and methemoglobinemia. The presence of an anion gap metabolic acidosis may be the first clue to a toxic ingestion and should prompt the measurement of serum salicylates, ethylene glycol, and methanol, and an examination of the urine for oxalate
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crystals, serum creatinine, glucose, ketones, and lactate should also be undertaken to detect other causes of high anion gap acidosis. The presence of an abnormally high serum creatinine level with a normal BUN concentration may be seen with isopropyl alcohol poisoning. Toxicological screen is rarely necessary when patients with an unintentional ingestion are asymptomatic or have clinical findings consistent with the medical history. Screening for acetaminophen, salicylates, and ethanol is strongly recommended for patients with uncertain history or intentional poisoning; few early signs may be present after lethal doses of these agents are ingested, and specific treatments are available and effective if implemented early. “Drug of abuse” immunoassays detect opiates, benzodiazepines, cocaine metabolites, tricyclic antidepressants, barbiturates, tetrahydrocannabinol, and phencyclidine. Positive and negative drug screening results do not absolutely confirm or refute poisoning diagnosis and may require confirmation.
TREATMENT Optimal treatment of a poisoned patient depends on the specific poison(s) involved, the presenting and predicted severity of the illness, and the elapsed time between exposure and presentation. Treatment variably includes decontamination, supportive care, antidotal therapy, and enhanced elimination techniques.
DECONTAMINATION After initial stabilization, patient decontamination is a priority. The sooner decontamination is begun, the more effective it is in preventing poison absorption. Copious water or saline irrigation for any eye or topical exposures should be performed as soon as possible. The administration of activated charcoal for any toxic ingestion is the preferred method of decontamination. In select circumstances, other methods of gastric decontamination may be indicated, such as gastric lavage, whole-bowel irrigation, dilution, cathartics, and endoscopy.
SUPPORTIVE CARE Supportive care is the most important aspect of treatment and, when coupled with decontamination, is frequently sufficient to effect complete recovery. Supportive care for the poisoned patient is generally similar to that used for other critically ill patients, but certain issues are managed differently. Airway protection with endotracheal intubation should be performed early in poisoned patients with depressed mental status because of the high risk of aspiration and its associated complication, particularly when
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gastric decontamination procedures are required. Endotracheal intubation with mechanical ventilation is also indicated in the presence of severe acid-base disturbances or acute respiratory failure. The management of high-grade physiological stimulation may require sedation or paralysis with mechanical ventilation to limit the extent of complications such as hyperthermia, acidosis, and rhabdomyolysis. Hypotension should initially be managed with IV fluids. Vasopressors may be required when hypotension does not resolve with volume expansion. Direct acting-vasopressors, such as norepinephrine, have been shown to be more effective than indirect-acting agents when tricyclic antidepressants have been ingested. Hypertension in agitated patients is best treated initially with nonspecific sedatives such as a benzodiazepine. When hypertension requires specific therapy due to associated end-organ damage, preferred treatments are verapamil or other calcium-channel blockers (CCBs), labetalol, or nitroprusside. The use of beta blockers alone is not recommended for patients with sympathetic hyperactivity because it may result in unopposed a-adrenergic stimulation and increased vasoconstriction. Ventricular tachycardias are generally treated with standard doses of lidocaine. When ventricular tachycardia occurs in the setting of tricyclic antidepressant intoxication or other membrane active agents, sodium bicarbonate is indicated as first-line therapy. Type IA, IC, and III antiarrhythmic agents are not recommended and are potentially dangerous because they may further impair cardiac contractility. Overdrive pacing with isoproterenol or a temporary pacemaker may be effective in patients with drug-induced torsades de pointes and prolonged QT intervals. Bradyarrhythmias associated with hypotension should be treated with atropine or temporary pacing. In patients with CCB or beta-blocker toxicity, the administration of calcium and glucagons may eliminate the need for other measures. Seizures are generally best treated with benzodiazepines, followed by barbiturates if necessary. Seizures caused by certain agents require specific antidotes for their successful termination (e.g., pyridoxine for isoniazid toxicity, glucose for hypoglycemic agents). Drug-associated agitated behavior is best treated with benzodiazepines, supplemented with high-potency neuroleptic drugs as needed. Agitation associated with anticholinergic syndrome is best treated with physostigmine.
ANTIDOTES Antidote administration is appropriate when there is a poisoning for which an antidote exists, when the actual or predicted severity of the poisoning warrants its use, when expected benefits of therapy outweigh
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its associated risk, and when there are no contraindications. Antidotes dramatically reduce morbidity and mortality in certain intoxications, but they are unavailable for most toxic agents. Antidotes may reverse or reduce poisonous effects by a variety of means. They may prevent absorption, bind and neutralize poisons directly, antagonize end-organ effects, or inhibit conversion to more toxic metabolites. The pharmacokinetics of the intoxicant and the antidote must be considered because toxidromes may recur if the antidote is metabolized more rapidly than the ingested substance, especially if the antidote acts by antagonizing end-organ effects or by inhibiting the conversion to toxic metabolites. In certain situations, it may be necessary to repeat administration of antidotes or provide for continuous infusion. Although a response to empirically administered antidotes can be used to confirm a suspected diagnosis, their indiscriminate use can potentially increase patient morbidity. The administration of flumazenil to comatose patients with suspected benzodiazepine overdose can precipitate seizures and worsen the clinical course if tricyclic antidepressants have been co-ingested.
ENHANCED ELIMINATION TECHNIQUES Procedures to enhance the elimination of poisons include multiple-dose activated charcoal, forced diuresis, urine ion trapping, hemodialysis, hemoperfusion, hemofiltration, and exchange transfusion. Various methods are useful in selected circumstances.
DISPOSITION After initial evaluation, treatment, and a short period of observation, the decision to discharge the patient is made on the basis of the observed and predicted severity of toxicity. Patients who have only mild toxicity and who have only a low predicted severity can be observed in the ED until they are asymptomatic. An observation period of 4–6 hours is usually adequate. Patients with moderate observed toxicity or those who are at risk for such on the basis of history or initial laboratory data should be admitted to an intermediate-care floor or an appropriate observation unit for continued monitoring and treatment. Patients with significant toxicity should be admitted to an ICU. All patients with intentional ingestions require psychiatric evaluation before discharge.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 2. WB Saunders: Philadelphia, 2004.
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Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System 2003, Am J Emerg Med 2003;22(5):335–404.
Acetaminophen Toxicity ANANTHA K. MALLIA
ICD Code: Acetaminophen poisoning 965.4
Key Points The hallmark of acetaminophen (APAP) toxicity is hepatotoxicity. After an acetaminophen overdose patients classically progress through various clinical stages ranging from nonspecific signs and symptoms to fulminant hepatic failure. Most patients who are treated appropriately recover fully without progressing to fulminant liver failure.The key to guiding treatment is measuring the 4-hour (or beyond) postingestion serum acetaminophen level and correlating the level with the time postingestion (or plotting the value on the Rumack-Matthew nomogram if a single acute ingestion occurred). Treatment is indicated if the 4-hour acetaminophen level is 150 mg/ml or greater or at a point above the ‘‘possible toxicity’’ line when plotted on the nomogram. ! Emergency Actions ! Treatment consists of early gastrointestinal (GI) decontamination with 1 g/kg of activated charcoal (unless contraindicated) and oral or IV administration of N-acetylcysteine (NAC), preferably within 8 hours of the ingestion.
DEFINITION Acetaminophen is the most widely used antipyretic and analgesic agent in the United States and is found in many over-the-counter and prescription medications. Though very safe when used in therapeutic doses, overdoses can result in severe toxicity and even death. Acetaminophen overdose is the most common medication overdose and the most common cause of acute liver failure in the United States.
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Acetaminophen exerts its pharmacological effects both centrally and peripherally. Its analgesic effects are the result of inhibition of prostaglandin synthesis in the CNS (as opposed to peripheral inhibition by aspirin and nonsteroidal anti-inflammatory drugs) and the blocking of pain impulse transmission in the peripheral nervous system. It produces antipyresis by directly lowering the set point of the hypothalamic thermostat. The drug is absorbed rapidly from the GI tract, typically reaching peak levels within 30–60 minutes. Metabolism takes place almost exclusively in the liver. When taken in therapeutic doses, up to 90% of the drug is either glucoronidated or sulfated and subsequently cleared renally; less than 5% is excreted unchanged in the urine. The remainder (5%–15%) is oxidized by the hepatic cytochrome P450 (CYP) system to form N-acetyl-p-benzoquinone imine (NAPQI), a highly reactive metabolite, which is rapidly reduced by hepatic glutathione to form a nontoxic mercaptide conjugate. Recommended therapeutic dosages are 10–15 mg/kg/dose in children or 325–1000 mg/dose in adults every 4–6 hours, with maximum daily doses of 80 mg/kg in children and 4 g in adults. Acetaminophen toxicity generally occurs when more than 150 mg/kg is ingested at one time or more than 7.5–10 g (in adults) is taken within a 24-hour period. In the setting of acetaminophen overdose, it is thought that the sulfation and glucuronidation pathways become saturated, causing larger amounts of the drug to be metabolized by the CYP system. This results in the formation of high hepatic concentrations of NAPQI and the eventual depletion of glutathione stores. When glutathione stores decrease to less than 30% of normal, NAPQI remains un-detoxified in the hepatocytes, reacts with cellular proteins, and induces hepatocellular necrosis. Hepatic necrosis develops within 12 hours of an overdose, though clinical manifestations are generally more delayed. The kidneys and pancreas contain smaller amounts of CYP and can also be damaged from NAPQI accumulation, particularly in more severe overdoses. Certain factors affect the likelihood of acetaminophen toxicity. Patients with lower baseline glutathione stores (e.g., persons with alcoholism and persons with AIDS) and patients with upregulation of their CYP pathways (again, persons with alcoholism and those taking CYP-inducing medications like anticonvulsants or antituberculosis agents) may be at greater risk for developing acetaminophen toxicity.
CLINICAL PRESENTATION The signs and symptoms of acetaminophen toxicity have classically been divided into four stages: 1. Stage 1 occurs within 24 hours of a toxic exposure and is characterized by nonspecific symptoms, including nausea/vomiting, malaise, and anorexia.
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2. Stage 2 typically occurs 24–72 hours after exposure, when more specific signs of hepatotoxicity emerge. The patient experiences right upper quadrant pain and tenderness, transaminitis, hyperbilirubinemia, and elevated prothrombin time (PT) and international normalized ratio (INR). Most patients fully recover from this clinical stage without progressing to liver failure. 3. Stage 3 is characterized by fulminant hepatic failure and generally occurs 3–4 days after ingestion in a small percentage of patients. Serum transaminase and bilirubin levels peak (aspartate aminotransferase [AST] >1000 and alanine aminotransferase [ALT] >1000) and patients experience acute renal failure, metabolic acidosis, coagulopathies, and hepatic encephalopathy. Complications during this clinical stage include acute respiratory distress syndrome (ARDS), hemorrhage, cerebral edema, and multiorgan failure. Without proper treatment, 50%–86% die during this stage; those who survive progress to stage 4. 4. Stage 4 is the stage of gradual recovery and normalization of hepatic function.
EXAMINATION During clinical stage 1, physical examination results may be nonspecific. By stage 2, the patient may experience right upper quadrant tenderness, scleral icterus, or jaundice. The physical examination should be targeted to exclude bleeding (e.g., rectal examination, joint examination) and multiorgan dysfunction.
LABORATORY FINDINGS Elevated liver transaminase levels, bilirubin level, and PT/INR as well as elevated BUN and creatinine levels will likely be present. The 4-hour acetaminophen level measurement greater than 150 mg/ml is considered a toxic dose. Toxic doses can be plotted on the Rumack-Matthew nomogram (Fig. 17-1).
DIAGNOSIS To determine the likelihood of hepatotoxicity and, thus, the need for antidotal therapy, serum acetaminophen levels should be correlated with time after ingestion or plotted on the Rumack-Matthew nomogram (see Fig. 17-1). Acetaminophen levels should be obtained at 4 hours after ingestion; if the ingestion occurred more than 4 hours before presentation, a level should be obtained immediately. Levels drawn before 4 hours postingestion are not helpful clinically. If the serum acetaminophen level is
934 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER µg/mL.
Single acute acetaminophen overdose nomogram
300 200
Rumack-Matthew line
150
Acetaminophen plasma concentration
100 90 80 70 60 50 40 30
20
Treatment line 10 9 8 7 6 5 4 3 2
Treatment should be administered if level is above solid line.
4
8
12
16 20 24 Hours postingestion
26
32
36
The nomogram has been developed to estimate the probability of whether a plasma acetaminophen concentration in relation to the interval postingestion will result in hepatotoxicity and, therefore, whether acetylcysteine therapy should be administered. Cautions for use of this chart: 1. Time coordinates refer to time postingestion. 2. Graph relates only to plasma concentrations following a single, acute overdose ingestion. 3. The treatment line is plotted 25% below the Rumack-Matthew line to allow for potential errors in plasma acetaminophen assays and estimated time from ingestion of an overdose.
Figure 17-1. Rumack-Matthew Nomogram for single acute acetaminophen ingestions. (From Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, pp 265–274.)
150 mg/ml or greater at 4 hours (or above the “possible toxicity” line on the Rumack-Matthew nomogram), then hepatotoxicity is possible and antidotal therapy is indicated. Of note, the previous rules apply only in the setting of single, large acetaminophen ingestions. Measurement of transaminase levels, PT/INR, electrolytes, BUN and creatinine, and lipase
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should also be obtained to gauge the degree of hepatic, renal, and pancreatic toxicity.
TREATMENT AND OUTCOME Early recognition and treatment of acetaminophen toxicity are essential to successful management. The mainstays of treatment are early GI tract decontamination with activated charcoal and the administration of NAC. Activated charcoal effectively adsorbs between 75% and 85% of the acetaminophen in the GI tract when given within 2–3 hours of ingestion and reduces serum absorption by 50%–90%. Activated charcoal is the most effective method of GI tract decontamination in the setting of acetaminophen overdose and should be administered as a single dose of 1 g/kg. NAC, the antidote of choice for acetaminophen toxicity, is indicated in patients with any of the following: (1) a serum acetaminophen level 150 mg/ml or greater at 4 hours (or at a point above the “possible toxicity” line on the Rumack-Matthew nomogram), (2) a single ingestion of 150 mg/kg or greater in a patient for whom a serum acetaminophen measurement will not be available within 8 hours, (3) an unknown time of ingestion and a serum acetaminophen level greater than10 mg/ml, (4) a history of excessive acetaminophen ingestion (acute or chronic) and laboratory evidence of hepatic toxicity. The likelihood of preventing serious hepatotoxicity and death is greatest when NAC is administered within 8 hours of acetaminophen ingestion. Oral and IV NAC regimens are equally efficacious, except when therapy is delayed for more than 10 hours after ingestion, in which case the oral regimen is superior. The oral regimen consists of a loading dose of 140 mg/kg followed by 17 more doses of 70 mg/kg every 4 hours. NAC has a foul odor and taste; mixing it with juice or soft drinks and drinking through a straw or co-administering metoclopramide can prevent nausea and vomiting. If vomiting occurs within 1 hour of a dose, the dose should be repeated. The IV regimen is a 20-hour protocol, consisting of a 150-mg/kg loading dose given over 15 minutes, followed by a 50-mg/kg infusion over 4 hours and a 100-mg/kg infusion over the remaining 16 hours. Adverse effects of NAC are uncommon but may include fever, urticaria, diarrhea, flushing, angioedema, and hypotension (which may be rate related). All patients requiring NAC therapy should be admitted to the hospital. Monitored settings are required for those with hemodynamic instability or fulminant hepatic failure. Patients with nonhepatotoxic ingestions of acetaminophen can be toxicologically cleared after appropriate observation and evaluation for co-ingestions or other medical problems.
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Bibliography Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, pp 265–274. Marx JA (ed): In Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2069–2075. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1089–1093. Up to Date: Management of acetaminophen (paracetamol) intoxication. Available at: http://www.utdol.com. Up to Date: Pathophysiology and diagnosis of acetaminophen (paracetamol) intoxication. Available at: http://www.utdol.com.
Amphetamines MICHAEL A. MILLER
ICD Code: Amphetamine poisoning 967.7
Key Points Amphetamines are CNS stimulants. They cause peripheral release of catecholamines, prevent reuptake of catecholamines, and inhibit monoamine oxidase, thus prolonging catecholamine effects. ! Emergency Actions ! Attention to the airway, breathing, circulation, and body temperature is essential. GI tract decontamination may be important in cases where the patient has ingested packets of amphetamine.
DEFINITION Amphetamines and amphetamine derivatives share the common structure of phenylethylamine. Various modifications of this basic molecule have led to an array of amphetamines with somewhat varied effects. Methylenedioxymethamphetamine (MDMA) or “Ecstasy,” among other modified amphetamines, are often said to have more “hallucinogenic” or euphoric properties. However, all amphetamine and amphetamine derivatives share common toxicological presenting features. In the last 5 years, epidemics of “Ice,” a smokeable form of methamphetamine, and MDMA have been frequent in some areas of the United States.
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PATHOLOGY Amphetamines are CNS stimulants. They cause peripheral release of catecholamines, prevent reuptake of catecholamines, and inhibit monoamine oxidase, thus prolonging catecholamine effects. Some of the modified amphetamines such as MDMA are thought to have more effects on serotonergic receptors than other catecholamine receptors, thus accounting for some of the mood-modifying intoxication that occurs more prominently with MDMA. Severe intoxication may include psychosis, agitation, seizures, coma, hyperthermia, and even intracranial hemorrhage.
CLINICAL PRESENTATION The clinical presentation of amphetamine toxicity spans the gamut from mild agitation and euphoria to severe hypertension, psychosis, and seizures. A multitude of clinical presentations are possible, but all revolve around the clinical effects of the sympathomimetic toxidrome. In a sympathomimetic toxidrome, the patient is usually hot or febrile and has moist skin, tachycardia, active bowel sounds, and hypertension. This is contrary to the effects of anticholinergic agents, which usually cause dry skin, absent bowel sounds, and less severe tachycardia and hypertension. Without adequate control of these serious symptoms, resultant hyperthermia, myocardial ischemia, intracranial hemorrhage, or other bad outcomes may occur.
DIAGNOSIS The diagnosis is made by a history of ingestion in conjunction with the presenting toxidrome.
LABORATORY TESTS Urine drug screens analyzing for amphetamines will generally have positive results in recent users of amphetamines and some of the derivatives. Other useful laboratory tests include measurement of creatine kinase to assess for rhabdomyolysis. Other tests should be added based on clinical concern.
TREATMENT As with most intoxications, professional and aggressive supportive care is the mainstay to therapy. Attention to the airway, breathing, circulation, and body temperature is essential. GI tract decontamination may be important in cases where the patient has ingested packets of amphetamine. The key steps to therapy are outlined as follows:
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1. Assess airway, breathing, and circulation. 2. Provide IV hydration and monitor the patient’s temperature, blood pressure, and neurological status. 3. Cool the patient if he or she is hyperthermic. 4. Treat seizures, agitation, hypertension, and psychosis with benzodiazepines. 5. If evidence of end-organ injury is present, consider administering nitroprusside or phentolamine. 6. Consider administering beta blockers to treat tachyarrhythmias. 7. Good supportive care and close monitoring should be provided throughout the course.
Bibliography Logan BK, Fligner CL, Haddix T: Cause and manner of death in fatalities involving methamphetamine, J Forensic Sci 1998;43(1):28–34. Patel M, Belson M, Longwater A, et al: Methylenedioxymethamphetamine (ecstasy)related hyperthermia, J Emerg Med 2005;29(4):451–454. Patel MM, Wright DW, Ratcliff J, et al: Shedding new light on the “safe” club drug: Methylenedioxymethamphetamine (Ecstasy)-related fatalities, Acad Emerg Med 2004;11: 208–210.
Anticholinergics ROBERT D. GRAYDON
ICD Code: Anticholinergic agents 971.1
Key Points Anticholinergics cause thermoregulatory dysfunction by impairment of sweating. This impairment may result in fatal hyperthermia in an agitated or seizing patient with an anticholinergic overdose. Heat stroke fatalities have been reported in heat-exposed or exercising patients taking therapeutic doses of anticholinergic drugs.
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! Emergency Actions ! Hyperthermia may be more life threatening than the anticholinergic overdose itself. Cooling should be initiated for any patient whose temperature is more than 104 F. Aggressive cooling should be accomplished with an ice water bath or evaporative techniques.
DEFINITION Anticholinergics, a large family of drug and plants that encompass the Solanaceae plants and the belladonna alkaloids. Drugs with prominent anticholinergic effects also include antihistamines (H1 antagonists) and the chemically related antiparkinsonian drugs such as benztropine mesylate (Cogentin) and trihexyphenidyl hydrochloride (Artane). Some cyclic antidepressants and some phenothiazines also have anticholinergic effects. The phenothiazine promethazine (Phenergan) and the cyclic cyclobenzaprine (Flexeril) also exhibit predominantly anticholinergic toxicity in the setting of an overdose. The cyclic antidepressants and phenothiazines have toxic cardiac, hemodynamic, and CNS effects that overshadow the effects of anticholinergic toxicity. Scopolamine, which has significant CNS toxicity, is the predominant alkaloid in Jimson weed. Recreational poisonings are commonly reported in groups of adolescents who ingest or smoke Jimson weed to get “high.” Accidental and suicidal overdoses occur with nonprescription antihistamines such as Benadryl, Nytol, and Sominex. Common prescription drugs implicated in serious overdoses include Cogentin, Periactin, Atarax, Flexeril, and Phenergan.
EPIDEMIOLOGY The American Association of Poison Control Centers reports a 1% incidence of serious adverse effects or fatalities related to anticholinergic or antihistamine overdoses. Poisoning with drugs whose toxicity is limited to anticholinergic effects rarely results in death if adequate supportive care is provided. However, the thermoregulatory dysfunction caused by impairment of sweating may result in fatal hyperthermia in an agitated or seizing patient with an anticholinergic overdose. Heat stroke fatalities have been reported in heat-exposed or exercising patients taking therapeutic doses of anticholinergic drugs.
PATHOLOGY Anticholinergic agents have a wide variety of therapeutic uses, including use as mydriatics, cardia drugs, antiparkinson agents, antihistamines, antipsychotic agents, antispasmodic drugs, cyclic antidepressants, ophthalmic products, and skeletal muscle relaxants. They can be absorbed if smoked or if ingested via the GI tract or IV and transdermal routes.
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Absorption from the GI tract is usually rapid. However, with large ingestions, evidence of significant toxicity may be delayed several hours, possibly due to decreased gut motility. The toxic (and many therapeutic) effects of anticholinergic drugs are related to their inhibitory effects on both central and peripheral muscarinic cholinergic receptors. Nicotinic cholinergic receptors in the neuromuscular junction are not affected. Peripheral muscarinic receptors mediate the end-organ effects of the parasympathetic nervous system, which stimulate sweating, secretion from mucosal and salivary glands, papillary constriction, intestinal motility, and bladder contraction. Parasympathetic fibers in the vagus nerve slow heart rate and atrioventricular nodal conduction. Central muscarinic receptors are involved in recent memory, cognition, perception, and some aspects of motor coordination. Blockade of these receptors produces the signs and symptoms of anticholinergic toxicity.
CLINICAL PRESENTATION The classic presentation is described with the following phrases:
Hot as Hades Blind as a bat Dry as a bone Red as a beet Mad as a hatter
Symptoms occur with in a few hours of ingestion but may be delayed with Flexeril ingestions. Inhibition of peripheral muscarinic receptors results in tachycardia, papillary dilation, loss of accommodation, inability to sweat, drying of mucosal surfaces, GI paresis, and urinary retention. These physical signs (i.e., mydriasis; dry mouth and dry, flushed skin; ileus; and bladder distention) constitute the anticholinergic toxidrome and suggest poisoning with an anticholinergic agent. Inhibition of CNS muscarinic receptors causes visual hallucinations, amnesia, delirium, seizures, and coma.
HISTORY A full medical and psychiatric history should be taken, with particular attention given to prescription and nonprescription drug use. It should be determined whether ingestion was accidental or intentional.
EXAMINATION A full physical and neurological examination should be performed, with particular attention paid to vital signs, temperature, mental status, and
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cardiovascular systems. In chronic poisonings, only a few of the classic signs may be present. Patients may present with seizure and coma. Agitated, delirious patients with peripheral anticholinergic signs may develop markedly elevated temperatures that result in the classic manifestations of heat stroke: liver injury, rhabdomyolysis, myoglobinuric renal failure, cerebral edema, and disseminated intravascular coagulation.
ELECTROCARDIOGRAPHY The ECG is a critical test in cases of suspected anticholinergic poisoning. Many drugs that have anticholinergic toxicity also have significant cardiac effects. The finding of conduction disturbances such as ORS complex widening or QT prolongations suggests the presence of a cyclic antidepressant or neuroleptic agent. The demonstration of ECG conduction disturbances helps in the diagnosis of the agent involved and contraindicates the use of physostigmine. Routine laboratory investigations should include CBC, liver function tests, urinalysis and measurements of electrolytes, BUN, and creatinine. This will detect disorders of sodium, calcium, glucose, and uremia as well as infectious etiologies. Elevation of serum creatinine kinase levels with a urine dipstick test that indicates myoglobinuria (positive for blood in the absence of red cells) suggests the presence of rhabdomyolysis. Elevation of the anion gap should prompt the search for the presence of other toxins, salicylate, toxic alcohol or glycol, or an infectious or metabolic disturbance such as sepsis or diabetic ketoacidosis. Further testing should be undertaken to evaluate for the presence of serious infection, including blood cultures and chest radiography should be guided by the clinical setting and physical examination. The liberal use of head computed tomography (CT) scan and lumbar puncture is indicated to exclude structural abnormalities of CNS infection. Toxicological screening is rarely useful in the diagnosis of anticholinergic toxicity but is helpful in ruling out other agents (e.g., cyclic antidepressants).
TREATMENT Cardiac monitoring should be initiated, supplemental oxygen should be administered, and a large-bore IV line should be placed. Institute the safety net described in the section titled “General approach to the poisoned patient.” The previously noted studies should be performed. Most patients with anticholinergic poisoning do well with supportive care. Hyperthermia may be more life threatening than the overdose itself. Cooling should be initiated for any patient whose temperature is higher than 104 F. Aggressive cooling can be accomplished with ice water bath
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or evaporative techniques. Heat production caused by intense muscle activity is best controlled with benzodiazepines titrated to effect. A brisk urine output of 1–2 ml/kg/hr should be maintained to protect the renal tubules from injury by myoglobin. IV benzodiazepines are also indicated for sedation of agitated patients with suspected anticholinergic overdose. These drugs protect against seizures, lack anticholinergic effects, are least likely to cause hypotension, and are the agents of choice for patients whose actual diagnosis is sedative-hypnotic withdrawal or cocaine poisoning. Gastric decontamination with a single dose of activated charcoal is usually sufficient in the majority of cases. Abdominal distention due to ileus is a common problem in patients with significant toxicity. Repetitive doses of cathartic agents should be avoided because they contribute to distention and increase the risk of aspiration. Gastric lavage should be considered in patients who present within 1–2 hours when a life-threatening ingestion is suspected by history. Anticholinergic effects delay gastric emptying so that lavage may be helpful regardless of the time of ingestion in very seriously poisoned patients. Significant agitation is a contraindication to gastric lavage because the risk of injury or aspiration during lavage is high relative to the expected benefit. Physostigmine is a naturally occurring anticholinesterase inhibitor similar to neostigmine. Because it is a tertiary amine, it is the only anticholinesterase inhibitor that crosses the blood-brain barrier. Its routine use as an antidote in anticholinergic poisoning is controversial. The demonstration of conduction abnormalities on ECG is a contraindication to its use. Despite its potential toxicity, physostigmine can be helpful in the management of some patients with pure anticholinergic toxicity. It is indicated in the management of intractable seizures, coma, severe agitation, and symptomatic narrow-complex supraventricular tachycardia. The initial dose is 1–2 mg/kg in adults, or 0.02 mg/kg in children, infused IV over 5 minutes. The effects of a single dose begin to wear off within 1 hour. After that time, with the diagnosis confirmed, the patient’s condition should be managed supportively. Repeat dosing is rarely indicated unless there is a recurrence of a life-threatening condition that responded to initial therapy, in which case the dose may be repeated as necessary. Its use is contraindicated in patients with conduction abnormalities or cyclic antidepressant ingestions. Patients with moderate to severe signs of anticholinergic toxicity or with conduction abnormalities should be admitted to an ICU for monitoring, observation for seizures, and control of agitation and temperature. Some patients may have prolonged clinical courses requiring days of intensive care before anticholinergic effects resolve. Patients with milder symptoms that resolve during ED observation do not require admission. Because the onset of symptoms after antihistamine ingestion occurs within several hours, a 4-hour period of observation is adequate to exclude significant toxicity in an asymptomatic patient. Patients who
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have ingested Flexeril should be observed for 8 hours before discharge. Psychiatric assessment, documentation of a nontoxic acetaminophen level, and pediatric patients’ home situations should be accomplished before discharge.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2003;22(5):335–404.
Arsenic LAURA ANN SPIVAK
ICD Code: Arsenic poisoning 985.1
Key Points Metal alloys exposed to acidic solutions may release arsine and cause unintentional poisoning via inhalation of this gas. ! Emergency Actions ! Patients presenting with acute arsenic intoxication may require prompt cardiovascular stabilization, hemodialysis for renal failure and immediate arsenic clearance from the blood, and initiation of chelation therapy. Arsine gas intoxication resulting in hemolysis requires immediate whole blood exchange transfusion. IV fluids and mannitol should be administered to promote urine output. Hemodialysis should be initiated in the setting of renal failure.
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DEFINITION Arsenic is a naturally occurring metalloid found in soil and groundwater. It is rarely found in its elemental (zero valence) state and is more likely to be encountered as an inorganic salt (arsenite or arsenate) or organic compound (organoarsenical). Nontoxic organic compounds, such as arsenobetaine and arsenosugars, are found in many marine organisms. Due to its lack of identifiable odor or taste and its ability to dissolve in solution, arsenic has been used as a homicidal agent. Arsine (AsH3) is a nonirritating, colorless gas that is released when an inorganic arsenic compound reacts with hydrogen. Metal alloys exposed to acidic solutions may release arsine and cause unintentional poisoning via inhalation of this gas.
EPIDEMIOLOGY Arsenic is recognized as a human carcinogen, although there are no animal studies demonstrating its carcinogenicity. Arsenic-containing compounds are used in industries, such as semiconductor manufacturing, and in medicine, as treatment for acute promyelocytic anemia (arsenic trioxide). Certain regions such as Bangladesh and India contain high levels of groundwater contamination, with resultant poisoning.
CLINICAL PRESENTATION Acute arsenic intoxication presents in several clinical phases. Phase I, occurring within hours of an ingestion, is characterized by the development of GI symptoms, including nausea, vomiting, diarrhea, and abdominal pain. Cardiovascular manifestations, such as tachycardia, arrhythmias, and hypotension leading to shock, are the results of capillary leakage along with fluid depletion resulting from GI distress. Decreased urine output, metabolic acidosis, and rhabdomyolysis may also be seen. CNS manifestations include lethargy, agitation, and seizures. Phase II, occurring 24 hours to 1 week after ingestion, may be characterized by a prolonged QTc interval, arrhythmias, cardiomyopathy, noncardiogenic pulmonary edema, encephalopathy, lowgrade proteinuria, palmar and plantar skin desquamation, and periorbital edema. Phase III, occurring 1–4 weeks after ingestion, may result in pancytopenia, basophilic stippling of erythrocytes, disseminated intravascular coagulation, peripheral neuropathy, and transverse striate leukonychia (i.e., Mees’ lines). Arsenic causes an axonopathy, characterized by symmetrical, diffuse “stocking-glove” sensory and motor loss in an ascending pattern. Quadriplegia may occur, but cranial nerve functions are usually spared. Arsine intoxication results from inadvertent inhalation of the gas resulting in hemolysis, acute tubular necrosis, and renal failure.
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EXAMINATION If a history of inorganic arsenic ingestion is unavailable, the presence of multiple systemic symptoms is one clue to the diagnosis. Acute, subacute, and chronic inorganic arsenic intoxications are almost always characterized by GI derangement and associated cardiovascular, neurological, and hematological abnormalities. Patients should be monitored for cardiovascular compromise, including telemetry and serial ECGs to diagnose arrhythmia, and should have a thorough neurological assessment for evidence of distal sensorimotor deficits. Lower extremities are typically affected first, and sensory deficits precede motor weakness. Proprioception may also be affected. Periorbital edema may be seen. A dermatological assessment may reveal plantar and palmar desquamation, spotted hyperpigmentation, a diffuse maculopapular rash, or the occurrence of herpetic lesions. Transverse white bands (i.e., Mees’ lines) on the nail beds of fingers and toes appear 4–6 weeks after poisoning. Arsine gas inhalation has been reported to cause hemodynamic instability and death within 2 hours of exposure. However, arsine exposure does not always result in immediate symptomatology. Findings may be evident up to 24 hours after exposure and include fevers, chills, GI distress, flank or abdominal pain, dark urine, and decreased urine output.
LABORATORY FINDINGS An elevated anion gap metabolic acidosis may be present. The creatine phosphokinase (CPK) level may be elevated, indicating rhabdomyolysis. The BUN and creatinine concentrations may be increased as a result of shock or rhabdomyolysis. ECG findings may include sinus tachycardia, a prolonged QTc, and nonspecific S and T wave changes. The AST/ALT levels may be mildly to moderately elevated, and moderate hyperbilirubinemia may also be seen. Hematological abnormalities include pancytopenia within 1–2 weeks of an acute ingestion of inorganic arsenic, along with lymphocytopenia and neutropenia. Eosinophilia may also be seen. Basophilic stippling of erythrocytes may be present on a peripheral blood smear. A spot urine or 24-hour urine collection is adequate for the diagnosis of arsenic intoxication. Speciation, or the quantification of inorganic versus organic arsenic compounds present in the urine, may be necessary to differentiate between harmful and benign forms of arsenic. The total urine arsenic concentration should be less than 50 mg/L. Blood levels of arsenic are not useful. Although arsenic is incorporated into hair and nails, there is no way to reliably distinguish between internal versus external contamination. Arsine poisoning commonly results in laboratory evidence of hemolysis. Elevation of the BUN, creatinine, and bilirubin levels may be seen. Blood and urine arsenic levels may be tested, but the diagnosis of arsine
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poisoning is supported by the history, clinical presentation, and laboratory results.
DIAGNOSIS The diagnosis of inorganic arsenic poisoning relies on an accurate history, clinical presentation, and laboratory confirmation. Arsenic’s effects on many organ systems, as well as the variability of intensity, duration, route, and timing of exposures, makes diagnosis a challenge. The differential diagnosis for arsenic poisoning includes gastroenteritis, Guillain-Barré syndrome, thallium poisoning, alcoholic peripheral neuropathy, porphyria, and nutritional deficiencies. The differential diagnosis for arsine poisoning includes paroxysmal nocturnal hemoglobinuria, as well as other chemical and biological agents with hemolytic effects, such as stibine (SbH3) and Plasmodium falciparum.
RADIOGRAPHS Although arsenic is radiopaque, its presence on radiographs is neither sensitive nor specific for arsenic intoxication. Other findings on chest radiographs may include cardiomegaly or pleural effusions.
TREATMENT Patients with suspected arsenic intoxication should be placed on a cardiac monitor and resuscitated with IV crystalloid solutions. Hypotension should be treated with vasopressors, and sodium bicarbonate may be administered to treat severe metabolic acidosis. Seizures should be treated with benzodiazepines or phenobarbital. Gastric lavage can be performed if the patient is not already vomiting, and whole-bowel irrigation is useful, especially if arsenic is seen on radiographs. Activated charcoal is of unknown efficacy for arsenic but may adsorb to co-ingestants. The rapid initiation of hemodialysis in an acute ingestion may be useful in clearing arsenic from the blood before it distributes into the extravascular compartments. The ascending motor neuropathy should be carefully monitored for potential respiratory muscle involvement. Repeated measurements of inspiratory capacity should be recorded. Rapid chelation in acute poisoning is recommended. Dimaval (2,3-dimercaptopropanesulfonic acid [DMPS]) is the recommended first-line agent; the dosing is as follows: 3–5 mg/kg IVevery 4 hours by slow infusion over 20 minutes. Dimercaprol (British anti-lewisite [BAL]) is a second-line agent. Dosing for this agent is 3–5 mg/kg given intramuscularly (IM) every 4–6 hours. The patient may be switched to an oral chelating agent such as succimer (dimercaptosuccinic acid [DMSA]), given 7.5 mg/kg PO every 6 hours,
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or 10 mg/kg every 8 hours. DMPS may also be given orally, 4–8 mg/kg orally every 6 hours. There are animal and human data to support placental transfer of arsenic. As chelation therapy appears to lack adverse effects on the fetus, acutely poisoned pregnant patients should receive chelation therapy with DMPS or DMSA. Arsine gas exposure may result in intravascular hemolysis with resultant renal failure. IV hydration with crystalloid solutions and mannitol are recommended to promote adequate urine output, and whole blood exchange transfusion is recommended if there is evidence of substantial hemolysis. Chelation in the setting of arsine poisoning is of questionable efficacy. Dimercaprol may be given in the first 24 hours, and DMPS (oral or IV) or DMSA may be given subsequently (see doses listed previously).
Bibliography Anthonisen P, Nielsen B, Pedersen K, et al: Clinical picture and treatment in arsine poisoning, Acta Med Scand 1968;496(Suppl):12–22. Concha GC, Vogler D, Lezeano D, et al: Exposure to inorganic arsenic metabolites during early human development, Toxicol Sci 1998;44:185–190. Domingo JL: Developmental toxicity of metal chelating agents, Reprod Toxicol 1998;12:499–510. Domingo JL: Prevention by chelating agents of metal-induced developmental toxicity, Reprod Toxicol 1995;9:105–113. Fanton L, Duperret S, Guillaumee F, et al: Case report: fatal rhabdomyolysis in arsenic trioxide poisoning, Hum Exp Toxicol 1999;18:640–641. Fennell JS, Stacy WK: Brief report: Electrocardiographic changes in acute arsenic poisoning, Irish J Med Sci 1981;150:338–339. Glazener FS, Ellis JG, Johnson PK: Electrocardiographic findings with arsenic poisoning, Calif Med 1968;109:158–162. Hood RD, Vedel-Macrander GC, Zaworotko MJ, et al: Distribution, metabolism, and fetal uptake of pentavalent arsenic in pregnant mice following oral or intraperitoneal administration, Teratology 1987;35:19–25. Kosnett M: Arsenic. In Brent J, Wallace K, Burkhart K (eds): Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. Elsevier: Philadelphia, 2005, pp 799–815. Kyle RA, Pease GL: Hematologic aspects of arsenic intoxication, N Engl J Med 1965;273:18–23. Muehrake RC, Pirani CL: Arsine-induced anemia: A correlative clinicopathological study with electron microscope observations, Ann Intern Med 1968;68:853–866. Pedersen F, Ladefoged J, Winkler K, et al: The renal circulation in acute arsine poisoning, Acta Med Scand 1968;496(Suppl):27–31. Rahman M, Chowdhury U, Mukherjee S, et al: Chronic arsenic toxicity in Bangladesh and West Bengal, India: A review and commentary, Clin Toxicol 2001;39(7):683–700. Sanz P, Corbella J, Nogue S, et al: Rhabdomyolysis in fatal arsenic trioxide poisoning, JAMA 1989;262:3271. Teitelbaum DT, Kier LC: Arsine poisoning: Report of five cases in the petroleum industry and a discussion of the indications for exchange transfusion and hemodialysis, Arch Environ Health 1969;19:133–143.
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Barbiturates DAVE BARRY
ICD Code: Barbiturate overdose 967.0
Key Points Barbiturates are in the sedative-hypnotic class of drugs, generally causing CNS depression. Large overdose can lead to respiratory arrest and hypotension. ! Emergency Actions ! Airway protection and assisting ventilation are the most important interventions.
DEFINITION Barbiturates are a group of drugs in the class known as sedativehypnotics. Barbiturates were first introduced in 1903 and became increasingly popular in the 1960s and 1970s as treatments for anxiety, insomnia, or seizure disorders. The abuse of barbiturates increased in a similar fashion. Barbiturate use and abuse has declined dramatically since the 1970s, primarily due to the advent of the safer benzodiazepines. Barbiturates all have a similar structure (barbituric acid), but differing side chains influence the drug’s potency, duration of effect, and rapidity of symptom onset. Barbiturates are generally divided into four groups based on their duration of effect: ultra-short-acting (e.g., methohexital, thiopental), short-acting (e.g., pentobarbital, secobarbital), intermediate-acting (e.g., amobarbital, butabarbital), and long-acting (e.g., phenobarbital, primidone).
EPIDEMIOLOGY Barbiturates were popular for both legitimate medical use and for abuse in the 1960s, but their use has dramatically declined since the advent of benzodiazepines, which are safer. Today, barbiturate overdose is relatively uncommon compared with that of benzodiazepines. The American Association of Poison Control Centers Toxic Exposure Surveillance System follows exposure rates throughout the United States based on calls reported to the nation’s poison control centers. In 2003, the Toxic
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Exposure Surveillance System reported 2824 barbiturate exposures resulting in 12 (0.4%) deaths, compared with 60,014 benzodiazepine exposures resulting in 180 (0.3%) deaths. The majority of these overdoses occur in adults.
PATHOPHYSIOLOGY Barbiturates can be thought of as general CNS depressants. Their mechanism of action is largely explained by their interaction with the gammaaminobutyric acid (GABA) receptor. GABA is the major inhibitory neurotransmitter in the brain. Stimulation of the GABA receptor causes a chloride channel to open, leading to hyperpolarization of the cell and decreased neuronal firing. Barbiturates bind to GABAA receptors, prolonging the duration the chloride channel remains open and leading to CNS depression, respiratory depression, and in severe poisonings, depression of cardiac contractility. Barbiturates have a narrow toxic to therapeutic index. The dose required to produce therapeutic effects is very close to that which can produce toxic effects. It is this narrow therapeutic index that makes barbiturates relatively more dangerous than other sedative-hypnotics. The usual route of administration of barbiturates is oral, although they can also be administered IM or IV. Barbiturates are rapidly absorbed after an oral dose and are widely distributed throughout the body due to their high lipid solubility. The extent of lipid solubility is generally proportional to their duration of effect, with the ultra-short-acting agents being the most lipid soluble and the long-acting agents less lipid soluble. With the exception of phenobarbital and aprobarbital, barbiturates are metabolized by the liver and the conjugates are renally excreted. A larger proportion of phenobarbital (25%) and aprobarbital (90%) are eliminated unchanged in the urine. Barbiturates can affect the metabolism of other drugs by competing for the same hepatic metabolic enzymes commonly referred to as the cytochrome P450 system. They also have an inducing effect on some P450 enzymes, leading to an increased rate of metabolism for a number of drugs. Chronic use of barbiturates can lead to tolerance (i.e., higher doses are required to produce the same effect) and dependence (i.e., continued use of the drug is needed to maintain normal functioning). Rapid cessation of barbiturates in a dependent person can lead to a withdrawal syndrome similar to that of alcohol withdrawal.
CLINICAL PRESENTATION Barbiturates primarily lead to CNS depression, as one would expect from their sedative-hypnotic classification. In mild doses, barbiturates can cause drowsiness, disinhibition, and mild intoxication. Moderate doses
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can lead to slurred speech, lethargy, and respiratory depression. Large doses may lead to coma, respiratory arrest, hypothermia, and circulatory collapse. Barbiturate withdrawal may present many days after use of the drug is discontinued. The timing of withdrawal symptoms is dependent on the half-life of the barbiturate being used. Barbiturate withdrawal is similar to withdrawal from other GABA agonists such as alcohol or benzodiazepines. Withdrawal can lead to tremor, irritability, tachycardia, hypertension, diaphoresis, seizures, and altered mental status. Death can occur, primarily due to hyperthermia, dehydration, seizures, and cardiovascular collapse.
DIAGNOSIS Barbiturate poisoning and withdrawal are clinical diagnoses. A history of barbiturate use or abuse combined with the typical clinical presentation is more than enough to make the presumptive diagnosis of either barbiturate overdose or barbiturate withdrawal. Although specific laboratory studies are available, the similarity of their results in the presence of barbiturate poisoning to those of other sedative-hypnotic agents makes these studies unlikely to alter the acute treatment of a patient with a classic clinical presentation.
LABORATORY FINDINGS Immunoassay urine drug screens can identify barbiturate metabolites and more specific testing (e.g., thin-layer chromatography, mass spectrometry) can identify individual agents, but these tests vary among institutions in sensitivity, specificity, and threshold standards, limiting their ability to adequately identify many agents. This variability makes these tests unlikely to alter the initial treatment of a patient with symptoms consistent with sedative-hypnotic poisoning or withdrawal. Relying on these tests to direct treatment decisions is a dangerous pitfall that should be avoided. The laboratory testing necessary to adequately evaluate a patient with altered mental status or coma consistent with barbiturate poisoning or sedative-hypnotic poisoning is directed toward excluding other lifethreatening effects or complications and identifying metabolic, infectious, or traumatic etiologies. Depending on history and presenting symptoms, it may be necessary to perform a CT scan of the head, chest x-ray, ECG, ABG analysis, and measurement of serum electrolytes with BUN (including the calculation of the anion gap), creatinine, serum glucose, serum acetaminophen, or other specific drug levels.
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TREATMENT Initial treatment should be directed at protecting the airway and assisting ventilation. Oxygen, airway supportive techniques, endotracheal intubation, or some combination of these may be necessary. Hypotension should be treated with IV fluid boluses or vasopressor agents. Hypothermia should be corrected with controlled rewarming techniques. Decontamination with activated charcoal may decrease the absorption of barbiturates if they are administered quickly after ingestion, but altered mental status or respiratory compromise are considered relative contraindications because of the increased risk of aspiration. There may be some benefit to gastric lavage in massive barbiturate poisoning if the procedure is initiated within 60 minutes of ingestion, but this is controversial and has not been proved. The overwhelming majority of solitary barbiturate overdoses will recover with supportive care and prudent evaluation to exclude co-ingestant or metabolic, infectious, or traumatic diagnoses. Gastric lavage is rarely necessary. Urinary alkalinization and multiple-dose activated charcoal treatment may be helpful to increase the elimination of phenobarbital but not the other barbiturates. Hemodialysis can also increase the elimination halflife of phenobarbital. These interventions are generally unnecessary except in the case of severe or massive barbiturate overdose. Barbiturate withdrawal should be treated with a GABA agonist such as a benzodiazepine or barbiturate agent in doses necessary to control withdrawal symptoms. Gradually tapering doses (10% per day) can avoid severe withdrawal when chronic use of barbiturates is discontinued.
Bibliography Barry JD, Beach CB: Barbiturate abuse. In AAEM Emergency Medical and Family Health Guide [Web-based book on EMedicine.com]. Coupey SM: Barbiturates, Pediatr Rev 1997;18(8):260–264. Lee DL: Sedative-hypnotics agents. In Goldfrank LR, et al (eds): Goldfrank’s Toxicologic Emergencies, ed 6. Appleton & Lange: Stamford, CT, 1998, pp 929–945. Saunders PA, Ho KI: Barbiturates and the GABAA receptor complex, Progress Drug Res 1990;34:261–286.
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Beta-Blocker Overdose LAURA ANN SPIVAK
ICD Code: Overdose or overdosing 977.9
Key Points/Quick Reference Beta-blockers are commonly used by patients for treatment of hypertension, migraine headaches, and post-MI heart rate management. The healthcare provider should inquire about beta-blocker use with any patient who presents with symptomatic bradycardia. ! Emergency Actions ! Hypotensive, bradycardic patients with suspected beta-blocker overdose should be immediately placed on a cardiac monitor, and large-bore IV access should be secured. The airway should be assessed and oxygen administered. An ECG should be obtained. Transcutaneous pacing paddles or pads should be placed on the patient, and pacing should be used to treat symptomatic bradydysrhythmias. Atropine and glucagon should be at the bedside in the event of a patient’s precipitous decline.
DEFINITION Beta-adrenergic blockers block the actions of beta-agonists at betaadrenergic receptors. This results in a decrease of calcium influx across cell membranes and resultant cardiac impairment. They are used in the management of many conditions, including hypertension, cardiac arrhythmias, glaucoma, and thyrotoxicosis. Not all beta blockers possess the same binding affinity for the two beta-adrenergic receptors (beta-1 and beta-2), and certain beta blockers bind selectively to one receptor over the other. Atenolol, metoprolol, and esmolol bind to beta-1 receptors; propranolol and timolol block both beta-1 and beta-2 receptors. Labetalol binds to both beta receptors, as well as the alpha-1 adrenergic receptor. Beta blockers also differ in their lipid solubility, protein binding, intrinsic sympathomimetic activity, and membrane-stabilizing activity. Receptor selectivity may be lost in an overdose.
EPIDEMIOLOGY According to data collected by the American Association of Poison Control Centers, beta blockers and CCBs represent about 40% of cardiovascular
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drug ingestions. These two medications are responsible for more than 65% of the mortality from these exposures.
CLINICAL PRESENTATION Patients with beta-blocker overdose may present with mild symptoms, such as light-headedness or weakness, and may rapidly progress to bradycardia, hypotension, and shock. Sustained-release preparations (e.g., metoprolol and propranolol) may result in a delay of symptoms. However, delays longer than 6 hours have not been reported in association with beta blockers. First-degree atrioventricular block and interventricular conduction delays are the most common ECG finding. Fatal beta-blocker overdoses are most commonly associated with bradydysrhythmias and asystole. Propranolol possesses high membrane stabilizing activity, resulting in a quinidine-like effect in overdose (i.e., QRS prolongation). Highly lipophilic beta blockers, such as propranolol and carvedilol, may cause seizures or CNS depression, even in normotensive patients. Despite beta-2–adrenergic blockade, bronchospasm has not been commonly reported in overdose. If present, it may be treated with a beta-2 agonist (e.g., albuterol).
EXAMINATION Patients with a suspected overdose should have their airway, breathing, and circulation assessed. An ECG should be immediately obtained. Evidence of sinus bradyarrhythmia or conduction delays is a cause for concern because patients can precipitously deteriorate into third-degree heart block or asystole. Transcutaneous pacing pads or paddles should be placed on the patient. Patients should be assessed for evidence of end-organ ischemia resulting from hypotension. Mental status changes, delayed capillary refill, cool extremities, and decreased urine output are all evidence of inadequate perfusion.
LABORATORY FINDINGS Hypoglycemia may be seen, although this is a more common finding in pediatric patients. Hyperglycemia has also been reported. Cardiac enzymes should be checked, as well as CPK, electrolytes, and renal function. Metabolic acidosis may be attributable to lactate production from hypoperfusion or from seizure activity. An elevated lactate level may also signal the advent of mesenteric ischemia, and an elevated creatinine concentration may be the result of renal hypoperfusion or rhabdomyolysis. Drug levels can confirm the presence of a specific beta blocker but do not affect initial management.
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DIAGNOSIS Beta-blocker overdose should be suspected in patients presenting with hypotension and bradycardia. If an overdose cannot be confirmed on the basis of the patient’s history, nontoxicological causes should also be evaluated. The differential toxicological diagnosis for patients presenting with hypotension and bradycardia includes poisoning with CCBs, digoxin, clonidine, opiates and opioids, sedative-hypnotic agents, antidysrhythmic drugs, and organophosphates.
RADIOGRAPHS Chest radiographs may reveal evidence of congestive heart failure and pulmonary edema.
TREATMENT AND OUTCOME Patients should be placed on a cardiac monitor, oxygen should be administered via nasal cannula or mask, and IV access should be obtained. The patient’s airway, breathing, and circulation should be assessed immediately. If the patient needs to be intubated, atropine may be given before insertion of the laryngoscope to attenuate vagally induced bradycardia. Transcutaneous pacer pads or paddles should be placed on the patient. Symptomatic bradydysrhythmias are an indication for pacing (60 beats/ min). Transvenous pacing may need to be initiated. A cardiologist should be notified of the patient’s condition in the event that extracorporeal measures are needed to support cardiac function (e.g., extracorporeal membrane oxygenation, cardiopulmonary bypass, intra-aortic balloon pump). Bedside echocardiography and pulmonary artery catheterization are useful in differentiating hypotension caused by vasodilatation versus cardiogenic shock. An ECG should be obtained with a rhythm strip. If available, prior ECGs on the same patient should be obtained for comparison. Gastric decontamination with activated charcoal (1 g/kg) and gastric lavage are most efficacious within 1–2 hours after ingestion. Multipledose activated charcoal and whole-bowel irrigation are recommended for sustained-release preparations. The patient must be intubated or otherwise able to protect his or her airway and bowel motility needs to be assessed before decontamination measures are started. Due to their lipophilicity and large volumes of distribution, hemodialysis is an ineffective elimination technique for most ingestions of beta blockers. Hemodialysis may be effective in the clearance of atenolol, nadolol, sotalol, and acebutolol. IV normal saline solution in 500- to 1000-ml boluses may be given to correct hypotension. Atropine may be given for bradycardia at 1 mg IV up to a maximum dose of 3 mg. Dopamine may be started at 5 mg/kg/min
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and titrated upward to achieve a systolic blood pressure greater than 90 mmHg. Norepinephrine, phenylephrine, and epinephrine may also be used to treat hypotension. If the patient’s bradycardia and hypotension do not respond to atropine, crystalloid fluid infusions, or catecholamines, glucagon may be administered in a 2- to 10-mg IV bolus. Attention must be given to the patient’s airway because glucagon rapidly induces vomiting. A glucagon infusion may be started at 2–10 mg/hr. Calcium gluconate (0.6 ml/kg) or calcium chloride (0.2 ml/kg) may be administered in boluses or as infusions. Phosphodiesterase inhibitors, such as inamrinone, may also be used. In the event of cardiogenic shock refractory to all of the previous modalities, cardiopulmonary bypass, intra-aortic balloon pump, or extracorporeal membrane oxygenation may be necessary to support cardiac function until the drug’s effect wears off. All patients with known or suspected beta-blocker overdose should be admitted to an ICU.
Bibliography Benowitz NL: Beta-adrenergic blockers. In Olson KR, Anderson IB, Benowitz NL, et al: Poisoning and Drug Overdose, ed 4. Lange Medical Books/McGraw-Hill: New York, 2004, pp 131–133. DeWitt CR, Waksman JC: Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity, Toxicol Rev 2004;23(4):223–238. Frishman W, Jacob H, Eisenberg E, et al: Clinical pharmacology of the new beta-adrenergic blocking drugs: Part 8: Self-poisoning with beta-adrenoceptor blocking agents: Recognition and management, Am Heart J 1979;98(6):798–811. Hesse B, Pederson JT: Hypoglycaemia after propranolol in children, Acta Med Scand 1973;193(6):551–552. Hong CY, Yang WC, Chiang BN: Importance of membrane stabilizing effect in massive overdose of propranolol: Plasma level study in a fatal case, Hum Toxicol 1983;2(3): 511–517. Kerns IIW, Kline J, Ford MD: Beta-blocker and calcium channel blocker toxicity, Emerg Med Clin North Am 1994;12(2):365–390. Love JN, Enlow B, Howell JM, et al: Electrocardiographic changes associated with betablocker toxicity, Ann Emerg Med 2002;40(6):603–610. Love JN, Litovitz TL, Howell JM, et al: Characterization of fatal beta blocker ingestion: A review of the American Association of Poison Control Centers data from 1985 to 1995, J Toxicol Clin Toxicol 1997;35(4):353–359. McBride JT, McBride MC, Viles PH: Hypoglycemia associated with propranolol, Pediatrics 1973;51(6):1085–1087. Reith DM, Dawson AH, Epid D, et al: Relative toxicity of beta blockers in overdose, J Toxicol Clin Toxicol 1996;34(3):273–278. Rooney M, Massey KL, Jamali F, et al: Acebutolol overdose treated with hemodialysis and extracorporeal membrane oxygenation, J Clin Pharmacol 1996;36(8):760–763. Shore ET, Cepin D, Davidson MJ: Metoprolol overdose, Ann Emerg Med 1981;10 (10):524–527. Weinstein RS, Cole S, Knaster HB, et al: Beta blocker overdose with propranolol and with atenolol, Ann Emerg Med 1985;14(2):161–163. Wood AJ: Pharmacologic differences between beta blockers, Am Heart J 1984;108(4 Pt 2): 1070–1077.
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Calcium-Channel Blockers LAURA ANN SPIVAK
ICD Code: Overdose 977.9
Key Points CCB overdose can cause bradydysrhythmias, hypotension, and asystole. Transcutaneous/transvenous pacing, calcium, catecholamines, glucagon, hyperinsulinemia/euglycemia, and inamrinone are all treatments for CCB overdose. ! Emergency Actions ! Hypotensive, bradycardic patients with suspected CCB overdose should be immediately placed on a cardiac monitor, and large-bore IV access should be obtained. The airway should be assessed and oxygen administered. An ECG should be obtained. Transcutaneous pacing paddles or pads should be placed on the patient, and pacing should be used to treat symptomatic bradydysrhythmias. Atropine, glucagon, and catecholamines should be accessible at the bedside in the event of the precipitous decline of a patient’s condition.
DEFINITION Calcium-channel blockers exert their effects via the blockage of calcium flow across cell membranes. CCBs act directly on L-type calcium channels. These calcium channels are located in the heart, vascular system, and pancreas. There are three classes of CCBs: phenylalkylamines (e.g., verapamil), benzodiazepines (e.g., diltiazem), and dihydropyridines (e.g., nifedipine, amlodipine). Verapamil and diltiazem act on cardiac and vascular receptors, whereas the dihydropyridines act primarily on the vasculature. This selectivity may be lost in overdose. CCBs reduce myocardial contractility, depress the sinoatrial node, and slow atrioventricular nodal conduction. CCB are used in the management of hypertension, supraventricular arrhythmias, migraines, coronary spasm, and angina pectoris. Nimodipine is used in the treatment of subarachnoid hemorrhage because it causes cerebral artery vasoconstriction. Therapeutic doses of CCB, especially when used in conjunction with beta-adrenergic blockers, can lead to toxicity. Of note, propranolol inhibits verapamil metabolism.
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EPIDEMIOLOGY According to data collected by the American Association of Poison Control Centers, beta blockers and CCBs represent about 40% of cardiovascular drug ingestions. These two medications are responsible for more than 65% of the mortality from these exposures.
CLINICAL PRESENTATION Patients may present with hypotension and bradydysrhythmias (e.g., sinus bradycardia, second- or third-degree atrioventricular block, sinus arrest with a junctional rhythm). CCBs do not typically affect interventricular conduction. Patients may also present with nausea, vomiting, and altered mental status.
EXAMINATION Patients with a suspected overdose should have their airway, breathing, and circulation assessed. An ECG should be immediately obtained. Evidence of sinus bradyarrhythmia or nodal blockade is a cause for concern because patients can precipitously deteriorate into third-degree heart block or asystole. Transcutaneous pacing pads or paddles should be placed on the patient. Patients should be assessed for evidence of endorgan ischemia resulting from hypotension. Mental status changes, delayed capillary refill, cool extremities, and decreased urine output are all evidence of inadequate perfusion.
LABORATORY FINDINGS Hyperglycemia may result from decreased insulin release resulting from the blockade of calcium channels in the pancreas. Cardiac enzymes should be checked, as well as CPK and electrolyte levels and renal function. Metabolic acidosis may be attributable to lactate production from hypoperfusion. An elevated creatinine concentration may be the result of renal hypoperfusion or rhabdomyolysis. Drug levels can confirm the presence of a specific CCB but do not affect initial management.
DIAGNOSIS CCB overdose should be suspected in patients presenting with hypotension and bradycardia. If an overdose cannot be confirmed on the basis of the patient’s history, nontoxicological causes should also be evaluated. The differential toxicological diagnosis for patients presenting with hypotension and bradycardia includes poisoning with beta-adrenergic
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blockers, digoxin, clonidine, opiates and opioids, sedative-hypnotic agents, antidysrhythmic drugs, and organophosphates.
RADIOGRAPHS Chest radiographs may reveal evidence of congestive heart failure and pulmonary edema.
TREATMENT Patients should be placed on a cardiac monitor, oxygen should be administered via nasal cannula or mask, and IV access should be secured. The patient’s airway, breathing, and circulation should be assessed immediately. If the patient needs to be intubated, atropine can be given before insertion of the laryngoscope to attenuate vagally induced bradycardia. Transcutaneous pacer pads or paddles should be placed on the patient. Symptomatic bradydysrhythmias are an indication for pacing (60 beats/ min). Transvenous pacing may need to be initiated. A cardiologist should be notified of the patient’s condition in the event that extracorporeal measures are needed to support cardiac function (e.g., extracorporeal membrane oxygenation, cardiopulmonary bypass, intra-aortic balloon pump). Bedside echocardiography and pulmonary artery catheterization are useful in differentiating hypotension caused by vasodilatation versus cardiogenic shock. An ECG should be obtained with a rhythm strip. If available, prior ECGs on the same patient should be obtained for comparison. Gastric decontamination, with activated charcoal (1 g/kg) and gastric lavage are most efficacious within 1–2 hours after ingestion. Multipledose activated charcoal and whole-bowel irrigation are recommended for sustained-release preparations. The patient must be intubated or otherwise able to protect his or her airway and bowel motility needs to be assessed before decontamination measures are started. CCBs are extensively protein bound, rendering dialysis ineffective. IV normal saline solution in 500- to 1000-ml boluses can be given to correct hypotension. Atropine may be given for bradycardia at 1 mg IV up to a maximum dose of 3 mg. Dopamine may be started at 5 mg/kg/ min and titrated upward to achieve a systolic blood pressure greater than 90 mmHg. Norepinephrine and epinephrine can also be used to treat hypotension. If the patient’s bradycardia and hypotension do not respond to atropine, crystalloid fluid infusions, or catecholamines, glucagon can be administered in a 2- to 10-mg IV bolus. Attention must be given to the patient’s airway because glucagon rapidly induces vomiting. A glucagon infusion may be started at 2–10 mg/hr. Calcium gluconate (0.6 ml/kg) or calcium chloride (0.2 ml/kg) may be administered in boluses and as
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infusions. High-dose insulin/glucose therapy can be initiated to augment cardiac glucose use and hence cardiac inotropy. The recommended insulin bolus is 0.5 units/kg IV, with an insulin infusion of 0.5–1 unit/kg/hr. This is accompanied by a dextrose infusion of 0.5 g/kg/hour, of either D10W or D25W, to maintain euglycemia (100–200 mg/dl). Solutions with a dextrose concentration greater than 10% should be given via central venous access. Blood glucose levels should be checked every 20 minutes while the infusion is running. Potassium levels should also be monitored. Phosphodiesterase inhibitors, such as inamrinone, may also be used. In the event of cardiogenic shock refractory to all above modalities, cardiopulmonary bypass, intra-aortic balloon pump, or extracorporeal membrane oxygenation may be necessary to support cardiac function until the drug’s effect dissipates. All patients with a known or suspected CCB overdose should be admitted to an ICU.
Bibliography Benowitz NL: Calcium channel blockers. In Olson KR, Anderson IB, Benowitz NL, et al: Poisoning and Drug Overdose, ed 4. Lange Medical Books/McGraw-Hill: New York, 2004, pp 144–147. DeWitt CR, Waksman JC: Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity, Toxicol Rev 2004;23(4):223–238.
Carbon Monoxide JAMES ALAN MORGAN AND JULIE ANN MORGAN
ICD Code: Carbon monoxide poisoning 986
Key Points The signs and symptoms associated with carbon monoxide toxicity are notoriously nonspecific and include headache, dizziness nausea, syncope, seizures, vomiting, altered mental status, chest pain, palpitations, tachycardia, tachypnea, dyspnea, blurred vision, coma, and myocardial ischemia.
960 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! The treatment of the patient with carbon monoxide poisoning begins with initiation of 100% oxygen as soon as possible to treat the hypoxia and accelerate elimination of carbon monoxide from the body.
DEFINITION Carbon monoxide is a colorless, odorless, tasteless, nonirritating gas found naturally in the body as a by-product of hemoglobin degradation. Carbon monoxide is generated externally from incomplete combustion of carbon-containing compounds, such as fossil fuels and house fires, and from methylene chloride, a solvent found in paint remover and aerosol propellants, which is converted in the body after inhalational exposure or absorption through the skin. The concentration of carbon monoxide in the atmosphere is usually less than 0.001%, with the blood carboxyhemoglobin commonly reaching a level of 10%–15% in smokers and 1%–3% in non-smokers.
PATHOPHYSIOLOGY Carbon monoxide competes with oxygen and interacts with deoxyhemoglobin to form carboxyhemoglobin, which cannot carry oxygen. Carbon monoxide binds tightly with hemoglobin, and the affinity of hemoglobin for carbon monoxide is approximately 240 times as great as its affinity for oxygen. Besides carbon monoxide displacing oxygen, it affects cellular oxygen use at the tissue level and interferes with the ability of normal hemoglobin to release its bound oxygen to tissues.
EPIDEMIOLOGY Carbon monoxide is the leading cause of poisoning mortality in the United States.
CLINICAL PRESENTATION The signs and symptoms associated with carbon monoxide toxicity are notoriously nonspecific and include headache, dizziness, nausea, syncope, seizures, vomiting, altered mental status, chest pain, palpitations, tachycardia, tachypnea, dyspnea, blurred vision, coma, and myocardial ischemia. The incidence of carbon monoxide poisoning in symptomatic patients presenting to the ED with flu-like symptoms (e.g., headache, dizziness, and nausea) in the winter ranges up to 24% in some series, making influenza the most common misdiagnosis. Making an accurate diagnosis is dependent on the patient’s history combined with a high
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index of suspicion, especially in the winter months when any illness suggests more than one victim of a group from a common environment. The critical action is to entertain the diagnosis in patients with suggestive symptoms so they get treatment and are not discharged back to the dangerous environment to experience more serious exposures.
LABORATORY FINDINGS A carboxyhemoglobin level is the most useful diagnostic test obtainable in a suspected incident of carbon monoxide poisoning. Obtaining an ABG measurement for identifying carbon monoxide poisoning is not useful except to identify the presence of a metabolic acidosis. Pulse oximetry is also inadequate to detect carbon monoxide poisoning because carboxyhemoglobin can be misinterpreted as oxyhemoglobin. Carboxyhemoglobin levels do not always correlate with the clinical severity, especially in patients with prolonged, low-level exposures that result in extremely high tissue concentrations of carbon monoxide. Therefore, the decision whether to administer hyperbaric oxygen therapy should be made only on the basis of the carboxyhemoglobin levels.
TREATMENT The treatment of a patient with carbon monoxide poisoning begins with initiation of 100% oxygen as soon as possible to treat the hypoxia and accelerate elimination of carbon monoxide from the body. The patient should have continuous cardiac monitoring, and IV access should be secured. If life-threatening dysrhythmias develop, standard ACLS protocols should be followed. Use of hyperbaric oxygen therapy is controversial, but this appears to be the treatment of choice for patients with significant carbon monoxide exposure. Hyperbaric oxygen therapy has been recommended for patients with the following conditions:
Any period of unconsciousness Signs of cardiac ischemia or arrhythmia Seizures Altered mental status History of ischemic heart disease and carboxyhemoglobin level >20% Pregnancy and carboxyhemoglobin level >15% Carboxyhemoglobin level >40% Coma Symptoms that do not resolve with patient breathing 100% oxygen Recurrent symptoms that last for up to 3 weeks
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Any delay in hyperbaric oxygen may decrease its efficacy, and early use of this treatment in appropriately selected exposures is encouraged. The healthcare provider should always call the local poison control center in case of carbon monoxide poisoning. If information is needed on the location of hyperbaric chambers, one should contact the Divers Alert Network at Duke University at 919–684–8111.
Bibliography Ernest A, Zitbak JD: Carbon monoxide poisoning, N Engl J Med 1998;339:1603–1608. Myers RAM, Thomas SR: Carbon monoxide and cyanide poisoning. In Kindwell EP (ed): Hyperbaric Medicine Practice., Best Publishing: Flagstaff, AZ, 1994, p 357. Tomasezewski CA: Carbon monoxide. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002.
Caustic Ingestions LAURA ANN SPIVAK
ICD Code: Overdose or wrong substance given or taken 977.9
Key Points/Quick Reference Alkaline substances cause a liquefactive necrosis, resulting in deep tissue penetration. Acidic substances cause a coagulative necrosis that results in the formation of a coagulum, or eschar, limiting the depth of tissue injury. Other mechanisms of corrosive injury include the denaturation, oxidation, reduction, or alkylation of cellular proteins. ! Emergency Actions ! In a patient with a suspected corrosive injury to the aerodigestive tree, prompt attention must be paid to the airway. Injury occurs within seconds of contact, and care must be taken to avoid vomiting and reinjury to the esophageal, bronchial, and oropharyngeal mucosa. Once the airway is secure, patients with evidence of mucosal ulceration or edema should have esophagogastroduodenoscopy and bronchoscopy performed in the ED or operating room to assess the degree of mucosal injury and to rule out gastric, esophageal, and aortic perforation.
DEFINITION Caustic agents are chemical and physical agents with the potential to cause tissue destruction. Alkaline substances cause a liquefactive
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necrosis, resulting in deep tissue penetration. Acidic substances cause coagulative necrosis that results in the formation of a coagulum, or eschar, limiting the depth of tissue injury. Other mechanisms of corrosive injury include the denaturation, oxidation, reduction, or alkylation of cellular proteins. The nature of tissue injury is dependent on the amount and concentration of the caustic material ingested, as well as the duration of exposure. Agents include button batteries (via leakage of metal salts), chlorine gas, ammonia gas, acetic acid (photography), formaldehyde (embalming agent), hydrofluoric acid (glass etching), phenol (antiseptics), phosphoric acid (toilet bowl cleaner), phosphorous (matches), selenious acid (gun bluing), and sodium hypochlorite (bleach). Household bleach containing less than 6% sodium hypochlorite is not corrosive.
EPIDEMIOLOGY Corrosive agents are encountered in environmental, occupational, and recreational settings, with injury the result of both accidental and intentional exposure.
CLINICAL PRESENTATION Skin exposure to corrosive agents can result in erythema, blistering, and discoloration. Ocular exposure can result in conjunctivitis, corneal injury, and blindness. Inhalation of corrosive gases can lead to varying degrees of respiratory distress, with patients exhibiting cough, stridor, hoarseness, and bronchospasm. Patients may develop pulmonary edema and require mechanical ventilation. The ingestion of caustic agents can lead to mucosa ulceration and edema. Patients may exhibit drooling, dysphagia, odynophagia, hematemesis, and signs of shock.
EXAMINATION Patients need immediate evaluation of airway, breathing, and circulation. In patients with oral injuries, airway patency is an immediate priority. Progressive edema with resultant airway occlusion may occur with burns of the tongue and oral mucosa. Hoarseness and stridor indicate laryngeal edema. Auscultation of the lungs can reveal wheezing or rhonchi. Symptoms of throat, chest, and abdominal pain may indicate perforation with ensuing mediastinitis, peritonitis, and pancreatitis. Hypotension and abdominal rigidity are two other findings suggestive of perforation. The patient should be fully disrobed, and the skin should be examined thoroughly for occult burns. All skin and eye burns should be copiously irrigated with water (sterile saline solution for ophthalmic injuries).
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LABORATORY FINDINGS Systemic complications include metabolic acidosis, hypocalcemia, hypomagnesemia, renal failure, methemoglobinemia, and hepatic injury. Depending on the clinical scenario, the following laboratory tests may be of value: CBC; liver function tests; measurements of electrolytes, BUN, creatinine, and lipase levels; and ABG with co-oximetry.
DIAGNOSIS Diagnosis can be made on the basis of a history of exposure to a corrosive agent(s) or based on examination results consistent with the physical findings described previously.
RADIOGRAPHS Upright chest and abdominal radiographs may show free air (i.e., pneumomediastinum, pneumoperitoneum) in the incidence of esophageal or gastric perforation. Button batteries may be visualized on radiographs. Batteries impacted within the esophagus need to be rapidly removed via endoscopy to avoid perforation. Once a battery reaches the stomach, the patient should be observed until the battery passes through the GI tract.
TREATMENT Once the patient’s airway is assessed, appropriate supportive care should be established (i.e., IVaccess, supplemental oxygen, suctioning for excessive secretions, pain control). Tetanus prophylaxis should be updated in patients with skin and ocular burns. Activated charcoal may interfere with endoscopy and may induce vomiting, with resultant reexposure of the mucosa to the corrosive agent. The patient should be not be given any food or drink by mouth because of the risk of reinjury and aspiration if vomiting ensues. A surgeon and/or ear, nose, and throat specialist should be consulted immediately to evaluate patients with evidence of aerodigestive injury because emergency endoscopy may be warranted. The use of steroids in initial management may be harmful, especially if perforation has not been ruled out. Empirical antibiotics are not warranted. Patients with substantial mucosal injury are at an increased risk for esophageal strictures and esophageal carcinoma.
Bibliography Appelqvist P, Salmo M: Lye corrosion carcinoma of the esophagus: A review of 63 cases, Cancer 1980;45:2655–2658.
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Mullen WH: Caustic and corrosive agents. In Olson KR, Anderson IB, Benowitz NL, et al: Poisoning and Drug Overdose, ed 4. Lange Medical Books/McGraw-Hill: New York, 2004, pp 157–159. Rao RB, Hoffman RS: Caustics and batteries. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al. (eds): Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002, pp 1323–1340.
Clonidine YOKO NAKAMURA AND MOHAMUD DAYA
ICD Code: Clonidine poisoning 972.6
Key Points Clonidine is well absorbed orally with an onset of action of 30^60 minutes.With therapeutic dosing, peak levels are achieved within 1^3 hours and the elimination serum half-life is approximately 12 hours (range, 6^24 hours). ! Emergency Actions ! The mainstay of clonidine overdose management is good supportive care because there is no antidote. Since some features of clonidine poisoning are similar to those of opioid poisoning (e.g., CNS depression, respiratory depression, and miosis), naloxone (0.4–2 mg) may be effective as a reversal agent.
DEFINITION Clonidine, an imidazoline, is a selective alpha-2–adrenergic receptor agonist that is primarily used as a centrally acting antihypertensive agent. It is also used in the treatment of attention-deficit/hyperactivity disorder and menopausal hot flashes and to diminish the symptoms associated with opioid, alcohol, and nicotine withdrawal. Currently available oral forms include 0.1-, 0.2-, and 0.3-mg tablets (Catapres) and combination tablets containing 15 mg of chlorthalidone (Combipres). Clonidine is also available in a patch form known as the transdermal therapeutic system (TTS) that allows continuous drug delivery. Formulations include Catapres
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TTS-1 2.5 mg of clonidine (delivers 0.1 mg/day), TTS-2 5 mg of clonidine (delivers 0.2 mg/day), and TTS-3 7.5 mg of clonidine (delivers 0.3 mg/day). Each patch contains much more drug then is delivered and the amount of residual drug after use ranges from 35% to 70%. Chewing, tasting, and ingesting discarded patches has been associated with toxicity.
EPIDEMIOLOGY In 2003, the American Association of Poison Control Centers Toxic Exposure Surveillance System reported 5402 clonidine exposures of which 3386 were treated at healthcare facilities. Life-threatening effects were reported in 199 exposures with death occurring in 7 cases.
PATHOPHYSIOLOGY Although the exact mechanism of action is not completely understood, clonidine lowers the blood pressure by decreasing the sympathetic outflow from the CNS to the peripheral tissues. Sympathoinhibition results from the activation of presynaptic and postsynaptic alpha-2–adrenergic receptors as well as imidazoline receptors in the cardiovascular control centers of the brain. Modulation of neurotransmitters especially nitric oxide (NO) and GABA is also thought to be important in the clinical effects of clonidine. In very high doses, clonidine can act as a peripheral alpha-2–adrenoreceptor agonist at vascular smooth-muscle sites leading to vasoconstriction, tachycardia, and hypertension. This effect is normally transient because the central antihypertensive effects quickly predominate.
PHARMACOKINETICS Clonidine is well absorbed orally with an onset of action of 30–60 minutes. With therapeutic dosing, peak levels are achieved within 1–3 hours, and the elimination serum half-life is approximately 12 hours (range, 6–24 hours). Clonidine is lipid soluble and 20%–40% protein bound and has an apparent volume of distribution of 3–6 L/kg. Fifty percent of an ingested dose is excreted unchanged in the urine, and the remainder is metabolized through the liver.
CLINICAL PRESENTATION AND EXAMINATION Life-threatening overdoses are characterized primarily by neurological and cardiovascular findings. Neurological features, which usually appear within an hour of ingestion, include altered mental status, miosis, respiratory
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depression, hypotonia, hypothermia, and, rarely, seizures. Cardiovascular signs that appear later include hypotension and bradydysrhythmias, especially sinus bradycardia and varying degrees of atrioventricular block. There is little correlation between the severity of symptoms and the amount ingested. As little as 0.1 mg has produced signs and symptoms of toxicity in children. Most symptoms usually resolve over 12–36 hours.
DIAGNOSIS The diagnosis of clonidine poisoning is clinical and made on the basis of the history and physical examination.
LABORATORY FINDINGS Laboratory tests are of little help in this context. Clonidine is not detected by qualitative urine or serum toxicology assays. Serum levels are not readily available or useful for guiding therapy. No specific laboratory work (e.g., CBC, electrolyte measurements, liver enzyme tests, urinalysis) is needed unless otherwise indicated (e.g., in the case of co-ingestions, or preexisting disease). A 12-lead ECG should be obtained to evaluate the cardiac rhythm and atrioventricular conduction.
TREATMENT The mainstay of clonidine overdose management is good supportive care, since there is no antidote. GI tract decontamination with activated charcoal (1 g/kg) is recommended in patients presenting within 1 hour of ingestion. GI tract decontamination using whole-bowel irrigation is recommended for clonidine patch ingestions. Gastric lavage has limited use, since the drug is rapidly absorbed, and syrup of ipecac is contraindicated because the potential exists for rapid CNS depression. All patients require close observation and frequent monitoring of their vital signs, including cardiac rhythm. Patients who remain asymptomatic after 4–6 hours of observation may be discharged after the administration of appropriate psychiatric evaluation, where necessary. Since some features of clonidine poisoning are similar to those of opioid poisoning (e.g., CNS depression, respiratory depression, and miosis), naloxone (0.4–2 mg) may be effective as a reversal agent. The benefits of naloxone in clonidine poisoning, however, have been inconsistent. If effective, a continuous infusion drip (two thirds of the reversal dose per hour) is indicated due to its short half-life (30–60 minutes). Bedside capillary blood glucose measurements should be taken in all patients with altered mental status. Sinus bradycardia is common but usually mild and does not require therapy. Symptomatic bradycardia generally responds to atropine
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(0.5–1.0 mg), although repeat doses may be necessary. Dopamine should be considered in the treatment of refractory patients. Hypotension should be treated with isotonic IV fluids. If hypotension persists, dopamine or norepinephrine should be considered. Respiratory depression often responds to tactile stimulation, but severe cases require intubation and mechanical ventilation. Seizures should be treated with a benzodiazepine. Clonidine-induced hypothermia is usually mild, responds to passive rewarming, and resolves within 6–8 hours. The management of hypertension after clonidine ingestions should be done cautiously due to the transient nature of the phenomenon; generally, no treatment is necessary. If hypertension is life threatening, sodium nitroprusside is the therapy of choice. Aggressive therapy with hypotensive agents can result in profound and prolonged hypotension. Tolazoline, an a-adrenergic antagonist, has also been recommended as a treatment for clonidine poisoning. It has had variable success and, due to its lack of availability and clinician unfamiliarity with this agent, it is not currently recommended as a first-line agent in the treatment of clonidine poisoning. The adult dose is 5–10 mg given by IV infusion every 15 minutes to a maximum of 40 mg. The abrupt cessation of clonidine in a patient who has been receiving long-term therapy can lead to an acute withdrawal syndrome characterized by excessive sympathetic activity. Symptoms include anxiety, headache, nausea, diaphoresis, tachycardia, and hypertension. Hypertensive encephalopathy, acute myocardial infarction (MI), and ventricular dysrhythmias have been reported after abrupt clonidine withdrawal. Severe hypertension should be treated with sodium nitroprusside. Clonidine therapy should always be tapered gradually.
Bibliography De Roos F: Miscellaneous antihypertensives. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Toxicological Emergencies, ed 7. McGraw-Hill: New York, 2002, pp 775–778. Nichols MH, King WD, James LP: Clonidine poisoning in Jefferson County, Alabama, Ann Emerg Med 1997;29:511–517. Seger DL: Clonidine toxicity revisited, Clin Toxicol 2002;40:145–2002.
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Cocaine BARBARA M. FISHMAN
ICD Code: Cocaine poisoning 970.8
Key Points Any patient who presents with chest pain should be asked about cocaine use. Patients presenting with euphoria, restlessness, excitement, dilated pupils, increased respiratory rate, and increased pulse should be considered to have taken cocaine or another drug. Cocaine psychosis, which resembles paranoid schizophrenia, may occur. ! Emergency Actions ! Patients with more severe toxicity must be treated aggressively to prevent life-threatening complications. These patients should have continuous pulse oximetry measured, along with core temperature by rectal probe. IV normal saline and IV benzodiazepines should be administered.
DEFINITION Cocaine (benzoyl-methyl ecgonine) is obtained from the Erythroxylon coca plant, which grows in Peru, Bolivia, and Colombia. Cocaine has a high abuse potential and can be snorted intranasally, smoked, injected IV, ingested orally, or applied to mucous membranes. Its only medical use is as a topical anesthetic and vasoconstrictor for nasal surgery.
EPIDEMIOLOGY Cocaine is the most abused major stimulant in the United States, where more than 50 million persons have used it at some time. Except for alcohol and tobacco, cocaine is the drug of abuse most often involved in ED visits. Cocaine enters the United States as the hydrochloride salt after South American refinement from the coca leaf. This is the white powder known as “coke.” The most popular use of the powder is snorting of inhaled lines through the nose; the powder can also be dissolved in water and injected or applied to mucous membranes. When combined with heroin for IV injection, the combination is called a “speedball.” Street purity varies;
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common adulterants include local anesthetics, amphetamines and other stimulants, sugars, talc, cornstarch, quinine, lysergic acid diethylamide (LSD), phencyclidine (PCP), and opiates. Crack and freebase are the alkaloid heat-stable forms that are smoked. Crack is very available, inexpensive, and has become an urban epidemic. Smoking crack is often an instant high and an instant addiction.
PATHOLOGY Cocaine is a local anesthetic and a CNS stimulant. Its effects as a local anesthetic are due to its ability to block the rapid sodium influx during peripheral nerve depolarization. Cocaine’s systemic effects are the result of blockage of the presynaptic uptake of norepinephrine (NE), epinephrine, serotonin, and dopamine. This causes a postsynaptic excess of these neurotransmitters and, therefore, increased sympathetic stimulation. Cocaine is rapidly metabolized by the liver and plasma to several active metabolites. Alcohol consumption before cocaine use increases the bioavailability of cocaine and generates cocaethylene (ethylbenzoylecognene), an active metabolite with greater toxicity and longer halflife than cocaine. Urine drug screening results will be positive within minutes of use and will remain positive for up to 72 hours, or longer in chronic users. Blood levels are not clinically useful due to cocaine’s rapid serum half-life.
CLINICAL PRESENTATION AND EXAMINATION Cocaine is a potent sympathomimetic agent. Manifestations of use involve the CNS and autonomic nervous system. Initial symptoms are euphoria, restlessness, and excitement. Pupils are dilated; blood pressure, respiratory rate, and pulse are increased. Patients may become restless as symptoms progress to diaphoresis, tremors, and the tactile and visual pseudohallucinations of “cocaine bugs” and “snow lights.” Cocaine psychosis may occur; this resembles paranoid schizophrenia. Progression from the initial agitation to seizures, status epilepticus, hyperthermia, ventricular arrhythmias, and rapid cardiopulmonary collapse and death can occur within minutes to half an hour after cocaine use. Most users experience only euphoria and self-limited mild to moderate CNS stimulation, but many acute and chronic complications of cocaine use can occur and should be recognized and treated. Cardiovascular complications include acute MI, arrhythmias, aortic dissection, dilated cardiomyopathy, myocarditis, and endocarditis. Acute MI is a well-known complication of cocaine use but is relatively rare. Although cocaine accounts for up to 25% of acute MIs in patients aged
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18–45 years, the actual rate of MI in patients presenting with chest pain after cocaine use is only 6%. Patients with cocaine-related MI can have typical or atypical chest pain, most are male, 75% smoke, and ECGs can appear normal. Symptoms can occur immediately after use to more than 24 hours later. MI, as with most cocaine complications, can occur with first time or chronic use, with any route of use, and with small doses. Many patients with cocaine-induced MI have no coronary disease revealed on cardiac cauterization. Mechanisms for cocaine-associated MI are believed to be increased myocardial oxygen demand, vasospasm of the coronary arteries, enhanced thrombogenesis, and accelerated atherosclerosis seen in cocaine users. A wide variety of atrial and ventricular arrhythmias have been seen and are attributed to the increase in circulating catecholamines, cocaine’s direct quinidine-like effects on the myocardium, QT prolongation, and multiple other problems that occur in this setting such as myocardial ischemia, hypotension, hypoxia, and seizures. Strokes can occur, both ischemic and hemorrhagic. Patients may present with headache, focal signs and symptoms, or seizures. The possibility of an intracranial event should be considered in any cocaine user who presents with headache, altered level of consciousness, seizures, or persistent agitation. Other neurological complications include seizures, altered mental status, migraine like headaches, movement disorders, and cerebral vasculitis. Pulmonary complications are more often seen with the use of crack or freebase. These include spontaneous pneumothorax, pneumomediastinum, inhalation injuries and burns to the respiratory tract, “crack lung” (a form of hypersensitivity pneumonitis), and hemoptysis. Asthma exacerbations, pulmonary edema, pulmonary emboli, pulmonary artery hypertrophy, and cor pulmonale can be seen with other forms of cocaine use as well. Rhabdomyolysis is a well-recognized cocaine complication. It occurs with all forms of use, even in the absence of seizures, hypotension, crush injuries, or other precipitating factors. Hyperthermia is always present with severe cocaine toxicity. GI effects include ischemic injury and infarction in almost every organ, bowel perforation, and perforated ulcers. Renal infarctions, idiopathic thrombocytopenic purpura, and diabetic ketoacidosis can occur. Obstetrical complications of cocaine include placental abruption, spontaneous abortions, and premature births. In addition, IV cocaine users will have all the complications of IV drug abuse, ranging from endocarditis to AIDS. Body packer and body stuffer are terms used to describe a person who ingests cocaine in an attempt to conceal the drug. Body packers are smugglers who ingest many cocaine-filled bags in an attempt to transport the drug through customs. The packets are well wrapped, usually with multiple layers of latex, and often followed by an antimotility agent. However, rupture of even one packet can be fatal because of the large amount of cocaine per packet. Body stuffers are those who hastily down several
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packets to hide the evidence, usually during a traffic stop or drug bust. Stuffers ingest fewer packets, but the packets are not wrapped well for ingestion and the risk of rupture or leak into the GI tract is greater.
DIAGNOSIS Diagnosis of cocaine toxicity is made on the basis of a history of cocaine use (though many patients may deny its use when questioned), presenting symptoms, physical examination, and positive urine drug screen result. Cocaine toxicity should be suspected in a previously healthy young patient who presents with sudden change in behavior, chest pain, seizure(s), arrhythmias, cerebrovascular accident, or a hyperadrenergic state.
LABORATORY FINDINGS All patients with suspected cocaine toxicity should undergo CBC, liver function tests, urinalysis, urine drug screening, and measurements of electrolytes, BUN, creatinine, creatine kinase, cardiac enzymes, including troponin I, INR, and partial thromboplastin time (PTT).
TREATMENT There is no specific antidote for cocaine. Treatment is supportive and aimed at the systems involved. Patients with suspected cocaine toxicity should be placed on a cardiac monitor and oxygen and should have two large-bore IV lines established. They should be placed in a quiet area, if possible, to minimize external stimulation. The above laboratory tests and ECG should be performed. ABG analysis and chest radiography are appropriate if the patient reports dyspnea or chest pain or has abnormal pulmonary or cardiac examination results. Mild agitation and mild to moderate adrenergic symptoms should be treated with IV benzodiazepines (e.g., lorazepam or diazepam). Patients with more severe toxicity must be treated aggressively to prevent life-threatening complications. These patients should have continuous pulse oximetry measured, along with core temperature by rectal probe. The clinician should administer IV normal saline and IV benzodiazepines. Use of phenothiazines should be avoided, if possible, because they can lower the seizure threshold and contribute to hyperthermia. Obtunded patients should be given IV D50 and thiamine, plus naloxone if respiratory depression is occurring. Seizures are first treated with benzodiazepines, then phenobarbital and intubation for status. Dilantin has been ineffective in this setting. Patients with altered mental status, seizures, or neurological signs and symptoms require a head CT scan to rule out intracranial bleed.
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Supraventricular arrhythmias are treated with IV fluids and benzodiazepines, then CCBs or cardioversion. Beta blockers are contraindicated in cocaine toxicity due to an unopposed alpha effect causing paradoxical worsening hypertension and tachycardia. Ventricular arrhythmias in this setting are treated with bicarbonate, lidocaine, and ACLS protocol with correction of underlying metabolic abnormalities. Class Ia agents should be avoided. Hypertension that does not respond to benzodiazepines or in association with other signs and symptoms that constitute a hypertensive emergency should be treated with a nitroprusside infusion or phentolamine, or, in the setting of cardiac ischemia, IV nitroglycerine. Cocaine-associated ischemic chest pain is treated with oxygen, acetylsalicylic acid (ASA), nitrates, and benzodiazepines. Beta blockers are contraindicated. Phentolamine and CCBs may be beneficial in the treatment of refractory chest pain. Cardiac consultation and intracoronary intervention should be considered over thrombolytics for cocaine users with acute MI or refractory ischemic pain. Low-risk patients who present with cocaine-associated chest pain can be dismissed after a 9- to 12-hour period of observation if cardiac enzyme tests are negative and if no ECG changes, dysrhythmias, or recurrent chest pain are present. Rhabdomyolysis should be suspected and screened for in all cocaine users and if present, should be treated with IV fluids and bicarbonate infusion. Hyperthermia must be treated aggressively in the standard way by evaporative cooling. Hypotension should be treated with IV fluids, norepinephrine, or dopamine. An asymptomatic suspected body packer or stuffer should be placed on a cardiac monitor with IV access established. Radiographs of the kidneys, ureters, and bladder and abdominal CT scan may show packets in the body packer, but studies with negative results do not rule this out. Both packers and stuffers should be given oral charcoal and sorbitol, followed by whole-bowel irrigation with a polyethylene glycol electrolyte solution. Endoscopy, colonoscopy, or enemas may cause packet rupture and should be avoided. Patients with bowel obstruction or serious signs and symptoms that imply packet rupture must be treated surgically. Body packers are admitted to the ICU for monitoring and continued bowel irrigation. Stuffers may be observed after decontamination and discharged after several hours if they remain asymptomatic. When the acute episode is over, cocaine users should be referred to a drug treatment center or counselor for help with their addiction.
Bibliography Albertson TE, Dawson A, de Latorre F, et al: TOX-ACLS: Toxicologic-oriented advanced cardiac life support, Ann Emerg Med 2001;37:S78–S90.
974 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Boghadi MS, Henning RJ: Cocaine: Pathophysiology and clinical toxicology, Heart Lung 1997;26:466–485. Brody SL, Slovis CM, Wrenn KD: Cocaine related medical problems: Consecutive series of 233 patients, Am J Med 1990;881:325–331. Erwin MB, Deliagyris EN: Cocaine associated chest pain, Am J Med Sci 2002;324:37–44. Frishman WH, DelVecchio A, Sanal S, et al: Cardiovascular manifestations of substance abuse. Part 1: Cocaine, Heart Dis 2003;5:187–201. Hoffman RS, Smilkstein MJ, Goldfrank LR: Whole bowel irrigation and the cocaine body packer: A new approach to a common problem, Am J Emerg Med 1990;8:523–527. Jones JH: Cocaine associated chest pain, Crit Decis Emerg Med 2003;18(3):448–449. McCarron MM, Wood JO: The cocaine “body packer” syndrome: Diagnosis and treatment, JAMA 1983;250:1417–1420. McMullen MJ: Cocaine, amphetamines, and other stimulants. In Rosen P, Barkin RM (eds): Emergency Medicine: Concepts and Clinical Practice, ed 4. Mosby–Year Book: St Louis, 1998. Roth DR, Alarcon FJ, Fernandez JA, et al: Acute rhabdomyolysis associated with cocaine intoxication, N Engl J Med 1988;319:673–677. Weber JE, Shofer FS, Larkin GL, et al: Validation of a brief observation period for patients with cocaine associated chest pain, N Engl J Med 2003;348:510–517.
Cyanide ROY JOHNSON III AND JASON CAPRA
ICD Codes: Cyanide compounds, salts, pesticides, fumigants poisoning 989.0, Cyanide gas, dust, inhalants poisoning 987.7
Key Points Cyanide is an intracellular poison that works by uncoupling oxidative phosphorylation. A patient exposed to cyanide will present with severe hypoxia without cyanosis because their tissues are unable to use oxygen, though there is sufficient availability. Patients may also present smelling of the classic‘‘bitter almond’’odor.Cyanide has potential use as a weapon of terror, and exposure should be suspected in patients who are found unconscious in building fires. Serum cyanide levels, though available, can take several hours to obtain, so the diagnosis of acute cyanide toxicity is mainly a clinical one.Treatment consisting of a cyanide antidote kit should be started promptly if poisoning is suspected.
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! Emergency Actions ! Proper protective precautions should be taken if cyanide exposure is expected. The healthcare provider should administer 100% oxygen by face mask and give dextrose and naloxone if the patient is unconscious. Laboratory tests should include CBC, electrolyte panel, urinalysis, ABG analysis, and measurement of cyanide, BUN, creatinine, calcium, magnesium, phosphorus, amylase, lipase, and cardiac and liver enzyme levels. Treatment with a cyanide antidote kit should be initiated, and the patient should be monitored and admitted to the ICU.
DEFINITION Found in cherry laurels and bitter almonds, cyanide is one of the oldest known poisons. It is a highly reactive but simple compound made of nitrogen and carbon that acts as a potent cellular poison. The ancient Romans and Greeks used cyanide to execute prisoners, extracting it from peach, cherry, and apricot pits. Cyanide gas was synthesized in 1786. Cyanide can be found in common items such as pits of the Prunus species, nuts, fungi, bacteria, plants, and hypertensive medications such as sodium nitroprusside.
EPIDEMIOLOGY The common routes of accidental cyanide poisoning in the United States are occupational exposure, ingestion of substances such as fruits or nuts that contain cyanide, house fires, and iatrogenic exposure due to prolonged dosing of IV nitroprusside. Occupational exposure to cyanide nitrogen may occur during the manufacture of synthetic fibers, fumigation, and work in the photographic and metallurgic industries. The usefulness of cyanide in these industries is due to its intrinsic affinity for metal. This property is exploited in extraction of ores, in electroplating metal, and in metal polishing. Cyanide is also used in the leather industry to strip hair from hides. Ingestion of cyanide-containing substances is not common in the United States except as cases of accidental pediatric poisoning. However, the ingestion of only 1 mg/kg of hydrogen cyanide can produce death within 15 minutes. Chronic exposure to cyanogenic glycosides occurs in third-world countries such as African nations, where plants containing cyanide compounds are used as sources of carbohydrates. The bitter roots of cassava are a staple food and contain high concentrations of cyanogenic glucosides such as linamarin. Ingestion of these substances produces an upper motor neuron disease known as Konzo or tropical spastic paraparesis that consists of ataxia and goiter. Soaking cassava roots will remove cyanogens, but when water is scarce, this soaking process is limited and outbreaks of Konzo occur.
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Iatrogenic exposure to cyanide occurs during IV administration of sodium nitroprusside. Cyanide is released when solutions of sodium nitroprusside deteriorate in aqueous solutions. Furthermore, infusions of sodium nitroprusside in rates above 2 mg/kg/min may cause cyanide to accumulate to toxic concentrations.
CHEMICAL WARFARE Weapons used for chemical warfare range from military-grade agents to commonly used industrial chemicals. Thus, cyanide has the potential to be used for such purposes. Cyanide, classified as a blood agent, is highly volatile, which means it has a strong tendency to evaporate and form a vapor at usual atmospheric temperature and pressure. Furthermore, unlike the majority of other chemical agents, cyanide is lighter than air. Therefore, after detonation of munitions, cyanide can easily be dispersed over a wide area as a suspension of fine liquid droplets. Persistence is inversely related to volatility. Being weakly persistent, cyanide is unlikely to remain in contact with body surfaces for long periods after exposure and pose a risk of secondary exposure to rescue and medical personnel. However, the clinical effects of cyanide exposure are usually seen within seconds to minutes, even with minimal exposure.
PATHOLOGY Exposure to cyanide results in disruption of aerobic metabolism via inhibition of the function of metal-containing enzymes. Cyanide poisoning causes inhibition of mitochondrial cytochrome A3, which catalyzes the final step in electron transport during oxidative phosphorylation. Due to this disruption, oxygen cannot be reduced to water and body tissues are unable to use oxygen. Cyanide is bound rapidly to enzymes, and only anaerobic metabolism occurs. As cyanide poisoning increases, the inability of oxygen to be extracted from the blood increases, and there is a direct increase in the oxygen content of venous blood.
CLINICAL PRESENTATION Patients with cyanide poisoning present with respiratory distress and normal oxygen saturation. Small amounts of cyanide bind to the ferrous ion on the hemoglobin molecule, which does not interfere with oxygen binding. However, cyanosis can occur as a preterminal event if a large amount of cyanide exposure occurs. Hypoxia in the presence of adequate oxygen occurs due to the inability of mitochondria to use oxygen as the terminal electron acceptor in the electron transport chain. Patients present with mental status changes followed by cardiac symptoms, since
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cyanide first affects the brain, then the heart. The classic history of acute cyanide poisoning given by onlookers is an “inspiratory gasp” that is followed by hyperventilation, severe anxiety, and breathlessness. The presentation of patients who are exposed to large doses of cyanide includes altered mental status, unconsciousness, and possibly coma.
EXAMINATION After securing the patient’s airway, ensuring ventilation, and checking for perfusion, the clinician should proceed with physical examination of a patient with suspected cyanide exposure, including a thorough examination of the patient’s skin. Examination may reveal caustic burns due to cyanide salts. On secondary survey, funduscopic examination may reveal brightly erythematous retinal vessels. Although only a small percentage of the population can smell the characteristic bitter almond odor of cyanide, an evaluation of the patient’s breath should be undertaken to reveal such an odor. The differential diagnosis of an unconscious patient should include exposure to carbon monoxide, hydrogen sulfide, natural gas, methanol, ethylene glycol, iron poisoning, and salicylate poisoning. A clue to occupational exposure to natural gas or hydrogen sulfide is a history of smelling “rotten eggs” before the incident. Careful consideration should be given to cocaine and isoniazid poisoning, which can cause acidosis and seizures that mimic cyanide poisoning.
LABORATORY FINDINGS Every patient with suspected cyanide poisoning should undergo the following laboratory tests: CBC, electrolyte panel, urinalysis, ABG test, and measurement of BUN, creatinine, calcium, magnesium, phosphorus, amylase, lipase, and cardiac and liver enzymes. A carboxyhemoglobin test should be performed with each ABG analysis. Cyanide levels can be measured, but the results will not be readily accessible and treatment should be initiated promptly, without confirmation of exposure. Laboratory findings include severe acidosis on ABG analysis due to lactic acidosis, hypoglycemia if poisoning is slow due to disruption of glycogen and lipid metabolism, and a decrease in the arterial-venous oxygen gradient.
DIAGNOSIS The classic clinical presentation of cyanide poisoning is a patient who is hypoxic without cyanosis, has bright red retinal vessels, and smells of bitter almonds. The correct diagnosis is facilitated by a thorough patient
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history. Occupational exposure should be expected in metal polishers, jewelry makers, or laboratory technicians. A history of nontraditional cancer therapy, ingestion of laetrile or cyanogen-containing preparations, or exposure to burning plastic (e.g., during a house fire) is suggestive of cyanide exposure.
TREATMENT Before the initiation of any treatment, it is imperative to ensure adequate decontamination of the patient and proper protection for treatment providers if the patient is topically contaminated. All patients with suspected cyanide poisoning should be administered 100% oxygen by face mask or should be intubated and given 100% oxygen. Two large-bore IV lines should be secured and normal saline administered, and the patient should be placed on a cardiac monitor. Mouth-to-mouth resuscitation should not be used. The previously mentioned laboratory tests should be performed and serial blood gas samples should be obtained. Ingestion of cyanide should be treated with gastric lavage and activated charcoal that should not impede, restrict, or replace IV therapy with nitrates. The goal of therapy is to provide an alternate source of ferric iron, which restores cellular respiration by freeing the cytochrome oxidase system. This is accomplished via the cyanide antidote kit, which works by two mechanisms: inducing methemoglobinemia via nitrites and providing a sulfur substrate for detoxification. The antidote kit contains sodium nitrate and sodium thiosulfate for IV administration and an ampule of amyl nitrate for inhalation. The adult dosage is 300 mg of sodium nitrate followed by 12.5 g of sodium thiosulfate. Pediatric dosage is 0.33 ml/kg of 10% sodium nitrate solution followed by 1.65 ml/kg of 25% sodium thiosulfate solution. Methemoglobin’s ferric ion will bind cyanide preferentially and restore cellular respiration. Sodium thiosulfate included in the kit provides exogenous sulfur groups that bind to cyanide and form thiocyanate, which is excreted by the kidney. The antidote kit is used as follows: Amyl nitrite inhalant perles are used as a temporizing measure. They can form 2%–5% methemoglobin. This step is omitted if venous access is established. The healthcare provider should alternate 100% oxygen and the inhalant for 30 seconds of each minute. A new perle is used every 3 minutes. An ampule of sodium nitrite is indicated for cyanide exposures, except in cases of residential fires, smoke inhalation, and nitroprusside or acetonitrile poisoning. The ampule is given slowly via IV at 5 ml/min and produces methemoglobin of 20%–30% approximately 50 minutes after administration. The rate of infusion should be decreased if hypotension occurs.
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Sodium thiosulfate is administered IVover 10–20 minutes. This is contraindicated in cases of hydrogen sulfide poisoning but may be useful alone in cases of smoke inhalation, acetonitrile toxicity, and nitroprusside toxicity. Further treatment with the cyanide antidote kit has been proposed for recurrent symptoms. It is suggested to repeat the kit in 30 minutes using half of the initial dose. However, this method lacks efficacy and is controversial at the current time. Careful compliance to the child dosage regimen on the package insert must be ensured. Methemoglobin levels should be measured 1 hour after antidotes are administered to ensure that the levels do not exceed 20%. Methylene blue should not be used to reverse excessive methemoglobin. It has been well documented that even a small amount of methemoglobin therapy can result in rapid reversal of cyanide poisoning and hypoxia. Therefore, it is standard practice to administer at least two doses of sodium nitrate and sodium thiosulfate, even if cardiopulmonary resuscitation has been prolonged and there are no signs of life. Special consideration for cyanide treatment occurs when an unconscious patient arrives in the ED and the history reveals that he or she has been recovered from a burning building. It is often difficult to determine acutely whether the patient’s hypoxic and unconscious state is caused by carbon monoxide inhalation or cyanide inhalation. Empirical nitrate therapy should not be given to these patients because it will cause elevated levels of carboxyhemoglobin, which will further decrease the oxygen-carrying capacity in patients that have inhaled carbon monoxide. If physical examination reveals a presentation suspicious for cyanide poisoning (e.g., hypoxia in the absence of cyanosis), 100% oxygen and sodium thiosulfate should be given. Sodium nitrate should not be given. If a subsequent ABG analysis reveals normal carboxyhemoglobin levels, then cyanide poisoning should be suspected and sodium nitrate can be administered. If the carboxyhemoglobin level is elevated, then carbon monoxide poisoning is likely and the appropriate treatment is 100% oxygen with hyperbaric chamber therapy. Alternate therapy for cyanide poisoning that has recently gained orphan drug approval from the U.S. Food and Drug Administration is hydroxocobalamin, vitamin B12a (Cyanokit), which has been proved effective when given immediately after cyanide exposure. The therapy must be given in large doses—either 50 mg/kg or 50 times the amount of cyanide exposure—and is given with 8 g of sodium thiosulfate. Hydroxocobalamin combines with cyanide to form cyanocobalamin, which is excreted in the urine and bile. Any patient with suspected cyanide poisoning who is treated with an antidote kit should be admitted to the ICU for continued monitoring. Patients who are asymptomatic but have suspected exposure should be observed for a minimum of 3 hours.
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Bibliography Auerbach PS: Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Bryant S, Singer J: Management of toxic exposure in children, Emerg Med Clin N Am 2003;21:101–109. Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, p 705. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, p 2167. Rakel RE: Conn’s Current Therapy 2005, ed 57. Elsevier: Philadelphia, 2005. Shenoi RP, Stewart G, Rosenberg N: Screening for carbon monoxide in children, Pediatr Clin Emerg Med 2002;3(4):275–283.
Cyclic Antidepressant Toxicity ANANTHA K. MALLIA
Key Points The hallmark of cyclic antidepressant toxicity is cardiac toxicity, particularly cardiac conduction delays, most commonly manifested as QRS complex prolongation as exhibited on ECG. Other conduction delays, including QT- and PR-interval prolongation, may also be present. Patients with moderate to severe toxicity may present with altered mental status, ‘‘anticholinergic’’ signs and symptoms, hypotension, seizures, dysrhythmias, or coma. Rapid clinical deterioration is common. ! Emergency Actions ! Given the rapid deterioration often seen with cyclic antidepressant toxicity, intubation and ventilatory support are often required. Two large-bore peripheral IV lines should be established and hypotension treated with crystalloid fluids. Direct-acting alpha agonists (e.g., norepinephrine or phenylephrine) can be used if hypotension does not respond to fluids. Specific therapy for cyclic antidepressant toxicity is to administer 2- to 3-ampule IV boluses of sodium bicarbonate until the QRS complex narrows to less than 100 msec.
DEFINITION Cyclic antidepressants were among the first medications used to treat depression. Their popularity has diminished in recent years because of their low therapeutic index, their high potential for toxicity, and the emergence of new, far less toxic antidepressants (i.e., selective serotonin
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reuptake inhibitors). Cyclic antidepressants are still used to treat refractory depression and also to manage chronic pain, neuropathy, enuresis, GI tract disorders, anxiety, and drug withdrawal syndromes, among others. Furthermore, their use in children and adolescents has increased recently. Cyclic antidepressants commonly used in the United States include amitriptyline, amoxapine, doxepin desipramine, imipramine, maprotiline, and nortriptyline. The muscle relaxant cyclobenzaprine (Flexeril) is structurally similar to cyclic antidepressants but has minimal antidepressant effects. Cyclic antidepressants are thought to work by inhibiting the uptake of biogenic amines like norepinephrine, dopamine, and serotonin in the CNS. The original agents in this class consisted of a three-ring structure (hence the original class name, tricyclic antidepressants); newer agents have structures that have anywhere from one to four rings. Cyclic antidepressants are absorbed rapidly from the GI tract and are metabolized and eliminated hepatically, primarily by the CYP system. Cyclic antidepressants are highly lipophilic and thus readily cross the blood-brain barrier and have a large volume of distribution (tissue levels are typically 10–100 times higher than serum levels). Most of the toxic properties of cyclic antidepressants in the setting of overdose are the result of six physiological effects: 1. 2. 3. 4. 5. 6.
Sodium-channel blockade Potassium-channel blockade a-adrenergic blockade Muscarinic-receptor blockade GABAA-receptor blockade Histamine-receptor blockade
Remembering these six toxic properties of cyclic antidepressants will help one readily remember and recognize the cyclic antidepressant toxidrome. Sodium- and potassium-channel blockade have their primary effects on the heart. Sodium channels in myocardial cells are responsible for membrane depolarization, so blockade of these channels slows depolarization across the myocardium. On ECG, slowed depolarization leads to widening of the QRS complex, which is the hallmark of cyclic antidepressant overdose. Potassium channels in the myocardium are involved in repolarization, so blockade slows myocardial repolarization. This is manifested on ECG by QT-interval prolongation. Blockade of a-adrenergic receptors results in systemic vasodilatation, causing hypotension. Inhibition of muscarinic receptors produces an anticholinergic syndrome, the most prominent aspect of which is sinus tachycardia. Other manifestations include hyperthermia, flushing, agitation, mydriasis, urinary retention, impaired GI tract motility, and decreased salivation, lacrimation, and perspiration.
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Antagonism of GABAA receptors produces seizure activity (though CNS sodium channel and muscarinic blockade likely also contribute to seizure induction). Finally, the antihistaminic properties of cyclic antidepressants cause sedation and, eventually, coma.
CLINICAL PRESENTATION The clinical presentation of cyclic antidepressant overdose is extremely variable. Patients can present alert with normal vital signs or comatose and hypotensive. In any case, rapid onset of symptoms and rapid deterioration are characteristic of cyclic antidepressant overdose. The most common manifestation of cyclic antidepressant overdose is altered mental status. Signs and symptoms of mild to moderate toxicity may include sedation; confusion; decreased salivation, lacrimation, and perspiration; urinary retention; constipation; and sinus tachycardia. As toxicity becomes severe, patients may develop cardiac conduction delays and dysrhythmias, hypotension, respiratory depression, seizures, and coma.
EXAMINATION Concise mental status, neurological, eye, heart/lung, abdominal, and skin examinations should be performed to assess for the aforementioned clinical signs. An ECG should be obtained promptly.
DIAGNOSIS Most patients with moderate to severe cyclic antidepressant toxicity will have characteristic ECG abnormalities (Fig. 17-2). The most common finding is prolongation of the QRS complex; there may be a rightward shift of the terminal 40 msec of the QRS with a characteristic “slurring upstroke” of the s-wave (see Fig. 17-2). (This rightward shift alone, without QRS prolongation, may be present with therapeutic levels of cyclic
Figure 17-2. Characteristic ECG abnormalities in cyclic antidepressant overdose: QRS complex prolongation, right-axis deviation of the terminal 40 msec of the QRS with slurring upstroke of the s-wave. (From Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, pp 265–274.)
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antidepressant on board and is not necessarily an indication of cyclic antidepressant toxicity.) Significant QRS prolongation identifies patients who are at greater risk for developing serious complications, including ventricular dysrhythmias and seizures. PR- and QT-interval prolongation may also be present.
TREATMENT AND OUTCOME Given the rapid deterioration seen in cyclic antidepressant toxicity, patients with this condition often require intubation and ventilatory support. Hypotension should initially be treated with isotonic fluid resuscitation. Direct alpha agonists like norepinephrine or phenylephrine should be used if fluid resuscitation alone fails to correct hypotension. After the ABCs are addressed, gastric decontamination with activated charcoal (1 gm/kg) should be considered. Specific management of cyclic antidepressant toxicity primarily revolves around preventing or limiting the cardiovascular effects of the agent. It has been shown that the sodium-channel blocking effects of cyclic antidepressants are inhibited by alkalemia; the key to managing cardiovascular toxicity of cyclic antidepressants, therefore, is alkalinizing the serum. This is achieved by infusing IV sodium bicarbonate, using the QRS duration as a marker for therapeutic effect. The recommended practice is to infuse 1–2 mEq/kg boluses (2–3 ampules) of bicarbonate of soda (NaHCO3) until the QRS complex narrows to less than 100 msec. If the QRS narrows after bolus therapy, a continuous infusion of NaHCO3 using 132 mEq (3 ampules) in 1 L of D5W may be considered, running the solution at twice the maintenance dose. A patient started on a NaHCO3 drip must be monitored very closely; the limit of infusion therapy is a serum pH of 7.5. NaHCO3 bolus therapy is indicated in patients with cyclic antidepressant overdose and QRS prolongation, refractory hypotension, or cardiac dysrhythmias. It is important to remember that NaHCO3 is the primary treatment of choice for cyclic antidepressant–induced dysrhythmias (e.g., ventricular tachycardia), which are commonly refractory to antidysrhythmic agents. Class Ia (e.g., quinidine, procainamide), Ic (e.g., flecainide), and class III (e.g., amiodarone, sotalol) antidysrhythmic agents should be avoided because they have the same sodium- and potassium-channel blocking properties as cyclic antidepressants and can actually worsen dysrhythmias. If sodium bicarbonate itself does not terminate the dysrhythmia, lidocaine, phenytoin, hypertonic saline, or magnesium sulfate can be considered (though limited data support their use). Because seizures are most likely caused by inhibition of CNS GABAA receptors, GABA agonists like benzodiazepines are first-line therapies; barbiturates can be tried if benzodiazepines are ineffective. If these agents fail, then a neuromuscular-blocking agent can be used to stop the physical
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manifestations of the seizure (and to prevent resultant acidosis and rhabdomyolysis). Paralyzed patients should be monitored on electroencephalography with continued anticonvulsant therapy. Phenytoin is ineffective in controlling cyclic antidepressant–induced seizures. Any patient with suspected cyclic antidepressant overdose should be observed on a cardiac monitor for at least 6 hours. If any signs of toxicity develop, the patient should be admitted to the ICU for further observation and therapy. If the patient does not exhibit suggestive signs or symptoms after 6 hours he or she can be cleared from a toxicology standpoint because cyclic antidepressant toxicity would be expected to manifest itself in some way by that time.
Bibliography Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, pp 515–521. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2088–2093. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1028–1032. Up to Date Online: Tricyclic antidepressant intoxication. Available at: http://www.utdol.com.
Digitalis Glycoside Toxicity ANANTHA K. MALLIA
ICD Code: Digitalis poisoning 972.1
Key Points Digitalis glycoside toxicity may be acute or chronic in nature. Acute toxicity results from a single large ingestion of digoxin or from exposure to a natural source of digitalis. Chronic toxicity is more common and occurs typically in elderly patients from gradual accumulation of digoxin in the serum. Digitalis toxicity should be suspected in any elderly patient taking digoxin if he or she presents with altered mental status. ! Emergency Actions ! Careful attention to the airway is paramount, especially in patients presenting in extremis. Two large-bore peripheral IV lines should be established. Early antidotal therapy with digoxinspecific antigen-binding fragments (Digibind) is indicated for patients with
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digitalis-induced dysrhythmias, hyperkalemia, or cardiovascular collapse. GI tract decontamination with activated charcoal should also be considered (unless contraindicated). Administration of insulin/glucose, NaHCO3, inhaled beta agonists, furosemide and Kayexalate for hyperkalemia and transcutaneous pacing, and phenytoin or lidocaine for dysrhythmias should be considered if Digibind is not available or if its administration may be delayed.
DEFINITION Digitalis (or cardiac) glycosides have been used for centuries for both their therapeutic and toxic properties. They are found naturally in plants such as the foxglove, oleander, and lily of the valley and in the skin secretions of some species of poisonous toads. The most common pharmacological formulation is digoxin, which is used in the management of supraventricular tachydysrhythmias and heart failure. Acute digitalis toxicity tends to occur in younger patients, resulting from a large single ingestion of digoxin or exposure to digitalis-containing plants or animals. Chronic toxicity is more common and generally occurs in elderly persons, particularly those with renal insufficiency or those taking diuretics. It is the result of gradual accumulation of the drug from excessive chronic intake (e.g., dosing error), increased free levels of the drug (e.g., decreased protein binding), or impaired clearance (e.g., renal failure). Digitalis glycosides, including digoxin, have a very narrow therapeutic index. The agents work by binding to and inactivating the sodium/potassium adenosine triphosphatase (ATPase) pump on the myocardial cell membrane. The function of this membrane pump is to transport sodium out of the myocyte and potassium into the myocyte, generating the myocardial resting membrane potential. When this pump is inhibited, sodium accumulates in the myocyte, which is pumped out in exchange for calcium by the still-active Naþ/C3þ-ATPase channel, resulting in increased intracellular concentrations of calcium. This increase in intracellular calcium is thought to be the mechanism behind the positive inotropic effects of digoxin. Digitalis also causes an increase in vagal tone and a decrease in atrioventricular nodal conduction, which makes the drug useful in controlling supraventricular tachydysrhythmias. Digitalis glycosides are rapidly absorbed from the GI tract into the bloodstream, reaching peak serum levels within minutes after an IV dose and 1–2 hours after an oral dose. They are highly protein bound in the serum and have a large volume of distribution; myocardial concentrations are typically 30 times serum levels. Serum levels, therefore, may not accurately reflect total body concentrations. Digitalis is partially metabolized hepatically, and elimination is primarily renal. The elimination halflife of digoxin is approximately 36–48 hours. The drug readily crosses the placenta.
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The toxic properties of digitalis are simply extensions of its therapeutic effects. In therapeutic doses, increased intracellular calcium concentrations enhance contractility; in toxic doses, intracellular calcium overload induces late myocardial depolarizations (or “after-depolarizations”) and increases automaticity and irritability in the atria and ventricles. The result is atrial and/or ventricular ectopy and dysrhythmias. The increase in vagal tone and decrease in atrioventricular nodal (and, less so, sinoatrial nodal) conduction seen with therapeutic doses translate into sinoatrial node depression and atrioventricular nodal blockade in toxic doses. Preexisting medical conditions, including heart disease, renal or hepatic insufficiency, and hypothyroidism, can increase susceptibility to digitalis toxicity, as can electrolyte abnormalities, particularly hypokalemia, hypomagnesemia, and hypercalcemia. Drug interactions with other myocardial depressants (e.g., beta blockers and calcium-channel blockers) and other agents that are highly protein bound (such as warfarin, phenytoin, and sulfonamides) can also potentiate digitalis toxicity.
CLINICAL PRESENTATION Digitalis-toxic patients may present without symptoms, with vague signs and symptoms, or in extremis. Acute overdoses generally begin with an asymptomatic interval followed by a steady onset of symptoms, sometimes several hours later. Chronic toxicity is more common and tends to be more insidious and nonspecific in presentation (e.g., flu-like symptoms), particularly in the early stages. Cardiac dysrhythmias are a prominent feature of digitalis toxicity. A host of various dysrhythmias can occur, but the underlying pattern tends to be increased atrioventricular ectopy combined with sinoatrial/atrioventricular nodal depression. Examples include sinus bradycardia, atrial tachycardia with second- and third-degree atrioventricular block, atrial fibrillation with supraventricular tachycardia, and ventricular tachycardia. The most common disturbance is frequent premature ventricular contractions (PVCs); dysrhythmias most specific for digitalis toxicity are junctional tachycardia and bidirectional ventricular tachycardia (rare, but very specific). Extracardiac signs and symptoms may be vague and nonspecific, though often they precede the cardiac manifestations. CNS symptoms are common and can include confusion/delirium, hallucinations, and visual scotomata (classically, colorful halos around objects or lights). Digitalis toxicity should be suspected in any elderly patient taking digoxin who presents with an altered mental status. The most common laboratory abnormality is hyperkalemia, particularly in acute toxicity (serum potassium level may be normal or low in chronic toxicity). The degree of hyperkalemia can be used as a marker of acute toxicity. The serum digoxin level may be supratherapeutic (>2 ng/ml), but this is neither sensitive nor specific for actual toxicity.
Digitalis Glycoside Toxicity
987
EXAMINATION Concise mental status, neurological, visual, cardiovascular, and abdominal examinations should be performed to assess for the aforementioned clinical signs. An ECG should also be obtained rapidly.
LABORATORY FINDINGS An elevated serum potassium level is common in acute digitalis toxicity; hyperkalemia can be used as a marker of acute toxicity. Potassium levels may be low, normal, or elevated in chronic toxicity. Serum digoxin levels may be elevated (>2 ng/ml).
DIAGNOSIS The diagnosis of digitalis toxicity is a clinical one; though serum digoxin levels may be elevated, they are neither sensitive nor specific for actual toxicity. The presence of dysrhythmias, hyperkalemia, and/or the aforementioned extracardiac manifestations is suggestive of acute digitalis toxicity, particularly if there is a history of digoxin ingestion or natural digitalis exposure. The diagnosis of chronic toxicity requires a higher index of suspicion and, again, should be suspected in any elderly patient taking digoxin who presents with an altered mental status or even nonspecific flu-like symptoms.
TREATMENT AND OUTCOME Careful attention to and timely management of airway, breathing, and circulation are of paramount importance and should include supplemental oxygen, intubation, ventilation if necessary, and the establishment of large-bore IV access. In asymptomatic patients, management revolves around preventing absorption and enhancing elimination of the drug. Digitalis is readily adsorbed by activated charcoal, so the administration of 1 gm/kg of activated charcoal should be considered in patients with acute overdose and patients with chronic toxicity who have ingested their last dose less than 6 hours before arrival. Any measures that increase vagal tone can potentiate the toxic effects of digitalis, so placing orogastric or nasogastric tubes should be done with great care. Specific antidote therapy with digoxin-specific antigen-binding fragments (Digibind) is indicated for patients with digitalis-induced dysrhythmias (bradyarrhythmia or tachyarrhythmia), hyperkalemia (serum hyperkalemia >5.5 mEq/L), and/or cardiovascular collapse. An elevated serum digitalis level alone is not an indication for Digibind. The number
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of vials indicated is calculated by multiplying the serum digoxin level (ng/ ml) by the patient’s weight (kg) and dividing this by 100. If Digibind is not available or if its administration may be delayed, nonspecific therapies may be initiated. For bradydysrhythmias, atropine or transcutaneous cardiac pacing can be attempted. Transvenous pacing should be avoided because it can induce ventricular fibrillation or tachycardia. Digitalis-induced tachydysrhythmias may be refractory to or even exacerbated by conventional ACLS measures. Electrical cardioversion may induce ventricular fibrillation in a digitalis-toxic patient, so it should be used as a last resort, with low energy levels (10–30 joules). Class IA antidysrhythmic drugs (e.g., quinidine and procainamide) may also worsen tachydysrhythmias. Phenytoin both decreases automaticity and increases atrioventricular nodal conduction, so it may be effective in managing digitalis-induced ventricular tachycardias. Lidocaine has also shown efficacy in the treatment of ventricular dysrhythmias. Conventional therapies for hyperkalemia, including IV glucose with insulin, sodium bicarbonate, inhaled beta agonists, furosemide, and Kayexalate can also be initiated. Calcium administration, the other component of hyperkalemia treatment, has the theoretical potential to worsen digitalis cardiotoxicity and is not recommended.
Bibliography Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001, pp 379–390. Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2104–2108. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1102–1105. Up to Date Online: Basic approach to arrhythmias due to digitalis toxicity. Available at: http://www.utdol.com. Up to Date Online: Management of digitalis (cardiac glycoside) intoxication. Available at: http://www.utdol.com.
Ethanol Intoxication
989
Ethanol Intoxication ROBERT D. GRAYDON
ICD Code: Ethanol poisoning 980.0 DEFINITION Ethanol is a small, weakly polar, aliphatic hydrocarbon molecule that is both water and lipid soluble. It is a CNS depressant and a widely used social stimulant.
EPIDEMIOLOGY Ethanol is the most widely ingested toxin throughout the world. The legal manufacturing of beer, wine, and liquor and the wide use of ethanol as a solvent in food and pharmaceuticals make ethanol the most widely available drug in society. It is formulated into numerous household products (e.g., perfume and mouthwash, which may contain up to 70% ethanol). These products are an important source of both intentional and unintentional overdoses. Ethanol’s cost to society is huge; costs are estimated in excess of $200 billion a year in the United States alone. Alcohol-related deaths are estimated at 200,000 per year. It has been estimated that ethanol is related to 40% ED visits and one third of all hospital admissions. Ethanol has been associated with 67% of homicides, sexual assault, drowning, burns as well as 50% of motor vehicle fatalities, and suicides. It is a major contributor to domestic violence. At least 6% of the population can be classified as ethanol dependent, with a much larger proportion of the population classified as problem drinkers.
PATHOPHYSIOLOGY AND PHARMACOLOGY Ethanol is rapidly absorbed in the GI tract, with approximately 20% of the dose absorbed in the stomach and the remainder in the small intestine. Absorption is delayed by co-ingestion of food and drugs and by medical conditions that delay gastric emptying. Ethanol has a volume of distribution of 0.56–0.72 L/kg. Ethanol distributes throughout body fluids and tissues, easily crossing the blood-brain barrier and placenta.
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The metabolism of ethanol begins in the GI cells by gastric alcohol mucosal alcohol dehydrogenase (ADH); this enzymatic activity is decreased in females, in persons with atrophic gastritis, and by drugs such as aspirin and H2 blockers, and this results in increased ethanol levels. Most metabolism occurs through two hepatic enzymes systems: 1. Generally the predominant system, ADH is used to oxidize ethanol to acetaldehyde and then acetaldehyde dehydrogenase to oxidize acetaldehyde to acetate, which ultimately becomes acetyl coenzyme A and either enters the Krebs cycle, undergoes ketone body formation, or initiates fatty acid synthesis. Acetate is also converted to acetone. During this process, nicotinamide adenine dinucleotide (NAD) is reduced to NADH, changing the NADH/NADþ ratio. Changes in this ratio impair cellular oxidative processes, such as conversion of lactate to pyruvate and gluconeogenesis. Because gluconeogenesis is critical to maintaining serum glucose homeostasis, profound metabolic abnormalities, such as hypoglycemia, acidosis, and other electrolyte disturbances may occur. Dehydrogenase enzymes have variable activity in different individuals depending on genetic makeup, sex, and other factors. 2. The microsomal ethanol oxidizing system (MEOS), a CYP-dependent system, is usually a minor metabolic pathway. This enzyme system is inducible and allows chronic drinkers to degrade ethanol at high rates. Induction of this system can be responsible for multiple drug interactions for other drugs normally metabolized by this system, including increased production of the toxic metabolites of acetaminophen. Ethanol approximates Michaelis-Menten kinetics. At high ethanol levels, saturation of the ADH and MEOS enzyme systems occurs, and the elimination half-life prolongs as metabolism shifts from concentration-dependent first-order kinetics to time-dependent zero-order kinetics. Ethanol is metabolized at rates of 100–200 mg/kg/hr or more. Chronic exposure and high levels cause induction of the MEOS system, which accounts for the significant increase in metabolism and clearance seen in chronic drinkers. Other factors that influence the rate of ethanol clearance include continued absorption, liver disease, drug inhibition of the MEOS system, and genetic variation. Approximately 10% is excreted unchanged through the lungs and kidneys. Ethanol is a CNS depressant but may have variable effects on individuals. Early in intoxication, a paradoxical stimulatory effect with euphoria, giddiness, and loss of inhibitions may predominate. As intoxication worsens (i.e., levels of approximately 150/dl in the casual drinker), CNS depression becomes generalized, leading to ataxia, slurred speech, and sedation. At serum levels greater than 200 mg/dl, progression to coma, loss of protective reflexes, and autonomic dysfunction occur. Death often occurs at levels of 400 mg/dl. Blood ethanol levels do not always
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correlate precisely with degree of intoxication. Persons with a history of chronic ethanol abuse and dependence can exhibit little clinical evidence of intoxication, even with levels approaching 400 mg/dl. Ethanol intoxication is poorly understood and is probably multifactorial. Ethanol affects the GABA and N-methyl-D-aspartate (NMDA) receptors. Hypoglycemia is common in the setting of ethanol use, especially in children, and may be a delayed effect. Chronic drinkers are often in a poorly fed, glycogen-depleted state and have multiple other nutritional deficiencies that can worsen this effect. Ethanol-induced hypoglycemia should always be suspected in these patients. Profound hypomagnesemia is a subtle but common and life-threatening complication of chronic ethanol ingestion. Low-magnesium states occur due to poor dietary intake, decreased GI absorption, and an ethanol-induced increase urinary excretion. Since the majority of magnesium is stored in bone, serum levels may not reveal the extent of the loss. Many chronic drinkers have profound intracellular magnesium losses despite normal serum levels. Thiamine deficiency can produce Wernicke’s encephalopathy. Chronic ethanol abuse affects most of the hypothalamic-pituitary axis leading to decreased testosterone production in men and amenorrhea in women. Elevated glucocorticoid levels may be seen, and many drinkers have physical manifestations resembling Cushing’s syndrome. Neurological manifestations include seizures (both during intoxication and withdrawal states), auditory hallucinations, and peripheral neuropathy. Dilated cardiomyopathy, atrial fibrillation, and other non–magnesium-deficiency arrhythmias may occur. High-output congestive heart failure may be seen with thiamine deficiency. Other disorders seen in chronic ethanol abusers include skeletal muscle myopathy, thrombocytopenia, and coagulopathies. As a multisystem toxin, chronic use of ethanol is associated with a host of medical illnesses, leading to acute complications such as esophageal variceal hemorrhage, hemorrhagic gastritis, pancreatitis, MalloryWeiss tears, and Boerhaave’s syndrome. Hepatic disease can range from mild steatosis to cirrhosis with hepatic encephalopathy.
CLINICAL PRESENTATION The clinical presentation of acute ethanol toxicity depends on the patient’s underlying tolerance, since chronic drinkers may tolerate a blood ethanol level that could produce coma or death in a novice drinker. The primary symptoms may be those of altered mental status and CNS depression. A history ingestion should be obtained. Children metabolize ethanol faster than adults but are more susceptible to hypoglycemia and respiratory depression than adults. Pediatric ethanol exposure can occur when children imbibe remnants of drinks from a party or ethanol-containing products such as mouthwash or from deliberate
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administration. Prolonged observation of symptomatic pediatric patients is necessary because hypoglycemia may be prolonged as long as 6 hours after ingestion and does not correlate with ethanol dose. CNS depression can range from euphoria to coma, with respiratory compromise. Nausea, vomiting, drowsiness, ataxia, slurred speech, nystagmus, tachycardia, hypoventilation, hypothermia, hyperthermia, and facial flushing all may occur. The classic triad of oculomotor disturbance, cerebellar ataxia, and mental confusion should lead to the diagnosis of Wernicke’s syndrome. However, few patients present with the classic triad. Korsakoff psychosis may be manifested by antegrade and retrograde amnesia and confabulation.
EXAMINATION The patient should be fully undressed, and a careful physical and neurological examination should be performed. Particular care should be focused on the neurological and mental status examinations. A careful search for occult trauma should be performed. The cardiovascular, respiratory, and GI systems should be examined in detail. The smell of alcohol may be present. A digital rectal examination and fecal occult blood testing should be performed. Patients with alcoholic ketoacidosis present with dehydration, abdominal pain, nausea vomiting, and weakness with an anion gap acidosis.
LABORATORY FINDINGS A CBC; coagulation studies; measurements of electrolytes, BUN, creatinine, blood ethanol, magnesium, and phosphate; liver function tests; urinalysis; and urine toxicology screen for common drugs of abuse should be performed. ABG measurement may be indicated in cases of hypoventilation or anion gap acidosis. Chronic drinkers with fever should be evaluated for infection with blood and urine cultures, lumbar puncture, and cerebrospinal fluid analysis, and chest radiography should be performed as needed to localize the source. A CT scan of the head should be considered when clinical findings are not consistent with the blood ethanol level, when signs of trauma are present, when no clinical improvement occurs after several hours of observation, or when clinical status deteriorates. An anion gap acidosis should prompt a search for other toxic causes or concurrent medical conditions. An ECG should be performed, and ECG abnormalities such as increased PR and QT interval, nonspecific ST segment changes, U waves, and flipped T waves can indicate hypomagnesemia. Ventricular dysrhythmias, particularly torsades de pointes, are potential fatal complications. Recognition of the rhythm and emergency administration of magnesium sulfate can be lifesaving.
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TREATMENT Treatment beings with careful evaluation of the patients level of consciousness, airway patency, and adequacy of ventilation. Patients should be fully undressed and placed on a cardiac monitor with pulse oximetry and automated blood pressure and pulse monitoring. IV access should be obtained. Neurological examination should be repeated frequently. Many other serious conditions cause altered mental status and can masquerade as ethanol intoxication. Head injury, hypoxia, hypercapnia, hypothermia, hypoglycemia, sepsis, meningitis, hepatic encephalopathy, and poisoning from other sedative hypnotics, drugs of abuse, antidepressants, and other alcohols not only resemble acute ethanol intoxication, but also may coexist. The diagnosis of ethanol intoxication is one of exclusion. The clinician should never assume the patient is just “drunk.” Most patients do well with supportive care. In somnolent patients with adequate ventilations, airway patency can be improved with placement of an oropharyngeal or nasopharyngeal airway. The patient should be positioned in the left lateral decubitus position to prevent aspiration. If the gag reflex is absent or if there is evidence of respiratory depression, endotracheal intubation and mechanical ventilation are indicated. A rapid bedside determination of glucose should be made, and hypoglycemia should be corrected. Circulator status should be assessed and IV fluids given with attention to hydration, electrolyte status, and rewarming or cooling, as indicated. Thiamine, folate, multivitamins, and magnesium sulfate should be given to all patients. Gastric decontamination and activated charcoal have a very limited role in ethanol intoxication. Alcoholic ketoacidosis is treated with volume repletion with crystalloids, dextrose, and thiamine. Seizures can be treated with benzodiazepines.
DISPOSITION Most patients with ethanol toxicity are managed in the ED and, once clinical inebriation has resolved and the patient is able to safely ambulate, may be transferred to a detoxification facility or discharged into the care of a responsible adult. Ethanol intoxication can delay the discovery of traumatic injuries. Careful and complete clinical reevaluation should be performed before discharge to avoid missing injuries initially masked by intoxication. Patients who experience severe toxicity, have alcoholic ketoacidosis, or have serious coexisting disease or trauma require hospital admission. Chronic drinkers requesting detoxification should be referred to a source of outpatient substance abuse counseling or admitted for inpatient detoxification.
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Bibliography Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2003;22(5):335–404.
Ethylene Glycol ROBERT D. GRAYDON
ICD Code: Ethylene glycol 982.8
Key Points Ethylene glycol is absorbed rapidly from the GI tract. Hepatic ADH mediates the initial enzymatic conversion of ethylene glycol into a number of toxic metabolites. The two rate-limiting steps in the metabolism are conversion of ethylene glycol to glycoaldehyde and the metabolism of glycolic acid to glyoxylate. ! Emergency Actions ! Treatment consists of supportive care, antidotal therapy with an inhibitor of ADH, and extracorporeal removal when indicated.
DEFINITION Ethylene glycol is a colorless, odorless, sweet-tasting alcohol. It is used in antifreeze, coolants, polishes, paints, deicers, lacquers, detergents, and pharmaceuticals.
Ethylene Glycol
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EPIDEMIOLOGY Ethylene glycol ingestions are either intentional (e.g., suicide attempt or gesture) or accidental. 2003 data from the American Association of Poison Control Centers show more than 5000 exposures with 16 deaths resulting from ethylene glycol ingestion.
PATHOPHYSIOLOGY Ethylene glycol is absorbed rapidly from the GI tract. It rapidly distributes into the total body water with a volume of distribution of 0.54–0.8 L/kg. There is no serum protein binding. Hepatic ADH mediates the initial enzymatic conversion of ethylene glycol into a number of toxic metabolites. The two rate-limiting steps in the metabolism are conversion of ethylene glycol to glycoaldehyde and the metabolism of glycolic acid to glyoxylate. The latter results in the accumulation of glycolate, which is responsible for the anion gap acidosis. These metabolites undergo renal excretion. Fomepizole, ethanol, and hemodialysis, as well as diminished real function, affect the rate of elimination. Target organs include CNS, kidneys, lungs, heart, liver, muscles, and retina. Reported tissue affected includes the following: 1. CNS: cerebral edema, meningoencephalitis, and loss of cerebellar Purkinje cells 2. Kidney: proximal and distal tubular dilation, interstitial edema, and intertubular deposition of calcium oxalate crystals 3. Lung: edema, interstitial pneumonitis, and hemorrhagic bronchopneumonia 4. Other: interstitial myocarditis, hepatic centrilobular fatty infiltration, myositis, and retinal deposition of calcium oxalate crystals
CLINICAL PRESENTATION The onset of toxicity usually develops within 4–12 hours after exposure; concomitant ethanol ingestion can delay the development of toxicity. Depending on the amount ingested and the degree of toxic metabolite production, presentations range from alert and asymptomatic, to coma with severe anion gap metabolic acidosis and incipient renal failure. Vital signs are usually normal or demonstrate mild sympathomimetic effects, with tachycardia and mild elevations of temperature and blood pressure. Hemodynamic stability until the preterminal stage is typical, and clinically significant dysrhythmias are rare. Kussmaul’s respirations are seen in patients with metabolic acidosis.
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Ethylene glycol poisoning initially produces CNS effects similar to those produced by ethanol, such as intoxication, stupor, coma, nausea, and vomiting. As toxicity progresses in untreated patients, cardiovascular and pulmonary signs and symptoms, such as tachycardia, tachypnea, cyanosis, and cardiogenic or noncardiogenic pulmonary edema occur. Metabolic acidosis and elevated levels of serum creatinine and BUN have been reported within 16 hours of ingestion. The metabolic acidosis is relatively refractory to sodium bicarbonate therapy. Frank renal failure is usually present within 48–72 hours. During this time, cerebral edema may manifest as progressive CNS depression, prolonged seizures, or herniation syndrome. Generalized seizures are typical, but focal, and myoclonic seizures can also occur. Pulmonary edema can be both cardiogenic and noncardiogenic in origin, and pneumonia may develop. Muscle tenderness with elevated levels of serum creatine kinase may represent myositis. Transient cranial nerve palsies can occur. Patients should be reexamined frequently to monitor clinical deterioration. Poisoning with ethylene glycol or methanol should be considered in all patients who present with an anion gap metabolic acidosis. The lethal dose of ethylene glycol is 1–1.5 ml/kg of a 100% solution. Any dose of ethylene glycol should be considered toxic and lethal.
LABORATORY FINDINGS All patients with suspected ethylene glycol intoxication should receive a CBC, ECG, and measurement of ABGs, electrolytes, BUN, creatinine, glucose, lactate, ethanol, and specific ethylene glycol levels. A chest radiograph should be obtained in patients with suspected aspiration or pulmonary edema. An increased anion gap correlates directly with glycolate levels. An ionized calcium level and urinalysis for monohydrate calcium crystals should be checked. Early in the course of ethylene glycol toxicity laboratory study results may be normal, but as the toxic metabolites accumulate, anion gap acidosis develops and renal function test results start to rise and ionized calcium levels drop owing to calcium complication with oxalic acid. Nonspecific ST-T wave changes and QTc prolongation may reflect hypocalcemia or hyperkalemia resulting from renal failure. Calcium oxalate crystals occur in two forms: monohydrate and dihydrate. The monohydrate form predominates and is more specific for ethylene glycol. The absence of these crystals does not rule out toxicity, and repeated examinations of the urine might be necessary. A Wood’s lamp examination may detect fluorescence in the urine of a patient who ingested antifreeze containing fluorescein. Ethylene glycol levels should be measured by gas chromatography whenever toxic alcohol ingestion is suspected. A level of 20 mg/dl or more is considered toxic, even in the absence of acidosis. Unfortunately, few hospital laboratories have the capability to run these tests in “real
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time,” and specimens are sent to a reference laboratory with results not available in time to effect clinical management. A CT scan of the head may reveal cerebral edema in severely ill patients. Ethylene glycol toxicity can produce lesions in the basal ganglia, pons, temporal lobe, and cerebellum.
TREATMENT Treatment consists of supportive care, antidotal therapy with an inhibitor of ADH, and extracorporeal removal, when indicated. Supportive care includes appropriate airway management, IV access, cardiac and neurological monitoring, and the necessary laboratory studies. Gastric decontamination via nasogastric suction may be effective in patients who have ingested large volumes, even if performed several hours after ingestion but is unlikely to be helpful in patients who have accidentally ingested small volumes, given rapid GI absorption. Activated charcoal should be administered orally for co-ingestants but is relatively ineffective in adsorbing alcohols. The administration of IV sodium bicarbonate may be necessary for life-threatening acidemia. Seizures should be managed with benzodiazepines and phenobarbital. The occurrence of seizures or coma should prompt an evaluation for cerebral edema. Depending on the severity of cerebral edema, therapies such as intraventricular pressure monitoring, mannitol, and arterial vasopressors may be needed; the patient should be observed for early signs of cerebral herniation. Calcium should be administered to treat symptomatic hypocalcemia. It should not be administered to normalize serum calcium levels, since this may increase the production of calcium oxalate crystals. An inhibitor of ADH should be administered immediately to all patients with known or suspected ethylene glycol poisoning. Some patients present early after exposure; this offers the opportunity to block the metabolism of the toxic alcohol, and therapy should not be withheld until acidosis develops. Fomepizole and ethanol are the two inhibitors available. Both are administered IV, and ethanol can also be administered orally. Fomepizole offers many advantages over ethanol and is the preferred antidote. The advantages include ease of dosing and administration; no CNS depression; no associated hypoglycemia, dilutional hyponatremia, or hyperosmolality; no need for frequent monitoring of drug levels; reduced nursing and pharmacy work; and no risk of subtherapeutic serum levels. Fomepizole is dosed as follows. A loading dose of 15 mg/kg is administered, followed by a maintenance dose of 10 mg/kg every 12 hours for four doses, then 15 mg/kg every 12 hours for all subsequent doses. Hemodialysis enhances the elimination rate of ethylene glycol and is a necessary adjunctive therapy in all cases of ethylene glycol poisoning. It should be instituted as soon as possible in all patients with metabolic
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acidosis, a sign of appreciable accumulation of toxic metabolites. Hemodialysis offers other benefits, including control of acid-base and fluid status. Hemodialysis should be continued until the ethylene glycol is eliminated and the metabolic acidosis has resolved.
DISPOSITION Patients should be admitted for treatment if any of the following is present: suspected intentional ingestion, serum ethylene glycol level of 20 mg/dl or greater, metabolic acidosis, or clinical manifestations of end-organ damage. Most of these patients will require intensive care monitoring and treatment. An exception may be patients with an elevated serum level without metabolic acidosis; these patients can be treated in a less intensive setting. All patients with intentional ingestion should undergo psychiatric evaluation at an appropriate time.
SEQUELA Patients who develop renal failure may require regular hemodialysis for weeks or months. Recovery of renal function is expected, although persistent renal failure has been reported. Patients who experience severe CNS manifestations, including seizure and coma, can recover full neurological function. Cranial nerve palsies typically resolve over weeks to months.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2003;22(5):335–404.
Hallucinogens
999
Hallucinogens DAVE BARRY
ICD Codes: Psychostimulants poisoning 969.7, Intravenous anesthetics poisoning 968.3, Psychodysleptic agent poisoning 969.6
Key Points In general, the mortality rates from hallucinogen toxicity is low. Most morbidity results from complications of abuse or injuries sustained during the altered state. Once complications and nontoxicological etiologies have been excluded, symptomatic care is all that is needed in most cases. ! Emergency Actions ! Symptomatic treatment of potential life threats is the primary focus of treatment interventions. Exclusion of complications and alternate differential diagnoses should be performed with a liberal but directed laboratory evaluation.
DEFINITION Hallucinogens are a poorly defined collection of drugs that are grouped together due to their ability to cause false perceptions, thoughts, or moods (i.e., hallucinations). Many of these drugs have been used for centuries for religious or cultural purposes and are sometimes categorized as entheogens. Since some cause a state resembling psychosis, they have also been called psychedelic drugs. Newer serotonergic club drugs have been coined empathogens or entactogens because they facilitate feelings of empathy and “touching the inner self.” Drugs with a wide range of structures and functions have been termed hallucinogens. This section will discuss the major categories of drugs commonly referred to as hallucinogens: indole alkylamines (including lysergamides), phenylethylamines, phencyclidine, and marijuana.
PATHOPHYSIOLOGY Lysergamides are structurally related to the synthetic ergot alkaloid, LSD-25, commonly known as LSD. LSD is considered by some to be the prototypical hallucinogen. Its hallucinogenic properties were accidentally discovered by Albert Hoffman in 1943 after dermal exposure while researching synthetic variants of a wheat mold called ergot. Its
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hallucinogenic properties are thought to be related to its indole ring structure, which it shares with serotonin. The exact mechanism of action is poorly understood but involves a complex interaction between different neurotransmitters including serotonin and dopamine. Pure LSD is a clear or white water-soluble crystal that is distributed in tablets (i.e., microdots), in thin gelatin squares (i.e., window panes), on sugar cubes, or impregnated on colorful “blotter” paper. A few of the various street names for LSD include acid, alice, battery acid, and names that reflect the design on the sheets of blotter paper. Naturally occurring lysergamides are found in several species of morning glory (Ipomoea species) and the Hawaiian baby wood rose (Ipomoea violacea). Indole alkylamines also have structural similarity to serotonin. Many are tryptamine analogs and are found naturally or synthesized. Psilocybin is found in specific types of mushrooms (Psilocybe, Conocybe, Panaeolus species) commonly abused for their hallucinogenic properties and frequently called magic mushrooms. N,N-Dimethyltryptamine (DMT), known as “businessman’s trip,” can be synthesized or found naturally in some specific South American plants (e.g., Piptadenia peregrine, Virola calophylla). 5-Methoxy-DMT is found in the venom of the Colorado River Toad (Bufo alvarius). Its synthesis and use as a club drug has earned it the street name foxy-methoxy. Ibogaine, derived from the African shrub Tabernanthe iboga, has been used as a religious hallucinogen by some African cults and has been researched for use in the treatment of addiction. There are multiple other tryptamine variants abused as street drugs. Alpha-methyl phenylethylamine (amphetamine) and the amphetamine analogs all share structural similarity in the family of Phenylethylamines. They generally increase the amount of neurotransmitter available in the nerve terminal through a number of mechanisms, including altering vesicle storage and release, reuptake inhibition, and monoamine oxidase inhibition. Side-chain substitutions on the phenylethylamine structure lead to variable affinities for different neurotransmitters and diverse clinical effects. Those with profound serotonergic or dopaminergic effects are sometimes categorized as hallucinogens. Examples include mescaline (the active ingredient in the peyote cactus, Lophophora williamsii), MDMA (commonly referred to as Ecstasy), and multiple others. PCP is categorized as a dissociative anesthetic. Its primary mechanism of action is thought to involve noncompetitive inhibition at a specific type of glutamic acid receptor called the NMDA receptor. Inhibition of this excitatory receptor may be responsible for the dysphoric and anesthetic properties that some describe as hallucinogenic. PCP also has interactions with multiple other neurotransmitter receptors that may contribute to its complex clinical effects. Street names include peace pill, rocket fuel, hog, angel dust, and multiple others. Ketamine (i.e., special K ) and dextromethorphan (i.e., dex or roboshots) share similar actions as
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noncompetitive NMDA antagonists and can share similar clinical effects, although dextromethorphan only causes dysphoric effects in large doses. Marijuana is the common name for the plant parts of Cannabis sativa, the Indian hemp plant. Cannabis contains numerous psychoactive compounds, termed cannabinoids, the most potent being delta-9-tetrahydrocannabinol (THC). The effects of marijuana are mediated by interaction with a family of specific cannabinoid receptors. Marijuana is usually smoked but is frequently mixed into foodstuffs as well.
CLINICAL PRESENTATION There is a substantial variation in the clinical effects and experiences witnessed by users of hallucinogens, and the specific effects experienced by an individual are unpredictable. The blending of sensory perceptions (i.e., synesthesias) such as “feeling colors” or “seeing sounds” is commonly described. Rapid mood alterations can be seen, including psychotic-like symptoms. These effects may be interpreted as pleasurable or as disagreeable and frightening, leading to anxiety or panic. In general, mortality from hallucinogens is low, and most morbidity is due to complications of abuse or injuries sustained during the altered state. The indole alkylamines, exemplified by LSD, cause hallucinatory symptoms similar to those described previously. Mild sympathomimetic effects can be seen including mydriasis, flushing, tremor, hypertension, and tachycardia. Severe intoxication can lead to coma, seizure, and possibly, neuroleptic malignant syndrome. Complications from indole abuse include hyperthermia, rhabdomyolysis, and psychosis. Indole alkylamines, especially LSD, can lead to “flashbacks” days or years later, now more precisely defined in Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM IV), as hallucinogen persisting perception disorder. Hallucinatory phenylethylamines share the effects of the classic amphetamines. Sympathomimetic stimulation causing tachycardia, hypertension, diaphoresis, and hyperthermia are common. Increased neuromuscular activity is frequently described with phenylethylamine use, including jaw clenching, teeth grinding (i.e., bruxism), and vigorous dancing. Some use lollipops or pacifiers to counteract these bothersome effects. Reported complications include hyperthermia, rhabdomyolysis, intracerebral and subarachnoid hemorrhage, cerebral infarction, seizures, cardiac dysrhythmias, and hepatic and renal failure. Severe hyponatremia from profound sweating, free water consumption, and syndrome of inappropriate antidiuretic hormone (SIADH) drug effect is commonly reported with MDMA ingestion. Chronic administration of amphetamines may lead to irreversible destruction of neurons and neurocognitive deficits.
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PCP causes an altered state of mental status with nystagmus, ataxia, and altered gait. Mild sympathomimetic effects can be seen. The delusion of invincibility and superhuman strength leading to unintentional actions or violent behavior is repeatedly described. Some authors consider this a hallmark of PCP toxicity. Hypersalivation and lacrimation can be seen, especially with ketamine. Complications include acute psychosis, hyperthermia, rhabdomyolysis, cerebral hemorrhage, dystonic reactions, convulsions, and coma. Traumatic injuries sustained during the altered state are frequently reported. Marijuana can lead to feelings of euphoria and heightened sensory awareness. Conjunctival injection, increased appetite, tachycardia, orthostatic hypotension, and incoordination are regularly seen. Loss of motor skills and judgment can lead to traumatic injuries and other complications. Acute psychosis is also associated with marijuana use. Smoking marijuana has been implicated in chronic lung disease and cancer and may be more detrimental than tobacco smoking in some ways.
LABORATORY FINDINGS Specific serum levels of the hallucinogens described in this section are not routinely available. In general, qualitative urine screens are associated with from poor sensitivity and/or specificity and do not correlate reliably with the degree of intoxication. These studies are seldom helpful in the emergency evaluation of an altered patient. The extent of laboratory evaluation necessary will be determined by the presenting symptoms and physical examination. Laboratory and radiological evaluation should be directed toward eliminating dangerous differential diagnoses and identifying possible complications. Serum glucose measurement, ECG, chest radiography, CT scan of the head, venous/arterial blood gas analysis, urinalysis, and measurement of electrolytes, BUN, creatinine, total CPK, and serum acetaminophen level should be ordered liberally to ensure exclusion of these possibilities.
DIAGNOSIS AND TREATMENT The diagnosis of ingestion of a particular hallucinogen is difficult to make without definitive historical information. A suspicion of hallucinogen ingestion can be made by incorporating historical elements, presenting symptoms, and physical examination findings. Treatment of presenting symptoms, concentration on potential life threats, appropriate screening for impending complications, and evaluation for dangerous co-ingestions or nontoxicological etiologies are more important than making a specific diagnosis. Benzodiazepines can be used to control agitation and seizures. Active cooling may be necessary to
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control hyperthermia. Laboratory tests and studies to exclude possible complications and alternate diagnoses are necessary. A thorough physical examination to exclude secondary traumatic injuries is essential. There are no specific antidotes for any of the hallucinogens described in this section.
Bibliography Aghajanian GK, Marek GJ: Serotonin and hallucinogens, Neuropsychopharmacology 1999;21(2 Suppl):16S–23S. Caravati EM: Hallucinogenic drugs, In Dart RC (ed): Medical Toxicology, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2004, pp 1103–1111. Halpern JH: Hallucinogens: An update, Curr Psychiatry Rep 2003;5(5):347–354. Halpern JH, Pope HG Jr: Hallucinogen persisting perception disorder: What do we know after 50 years, Drug Alcohol Depend 2003;69(2):109–119. Howlett AC, Breivogel CS, Childers SR, et al: Cannabinoid physiology and pharmacology: 30 years of progress, Neuropharmacology 2004;47(Suppl 1):345–358. Morris BJ, Cochran SM, Pratt JA, et al: PCP: From pharmacology to modelling schizophrenia, Curr Opin Pharmacol 2005;5(1):101–106. Morton J: Ecstasy: Pharmacology and neurotoxicity, Curr Opin Pharmacol 2005;5(1):79–86. Passie T, Seifert J, Schneider U, Emrich HM: The pharmacology of psilocybin, Addict Biol 2002;7(4):357–364. Stafford P: Psychedelic Encyclopedia, expanded ed 3. Ronin: Berkeley, CA, 1992. Tucker JR: Lysergic acid diethylamide and other hallucinogens, In Goldfrank LR: Goldfrank’s Toxicologic Emergencies. Appleton & Lange: Stamford, CT, 1998, pp 1046–1053.
Hydrocarbons GUYON J. HILL
ICD Code: Hydrocarbon poisoning 987.1
Key Points Hydrocarbons are commonly found in household and industrial compounds. They include gasoline, paint thinner, benzene, carbon tetrachloride, and numerous solvents. Ingestion in young children is typically accidental, whereas adults and adolescents may ingest it for the purpose of abuse or as a means for suicide.The primary complication is aspiration, although GI, renal, and hepatic complications are not uncommon.
1004 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! The patient suspected of experiencing a hydrocarbon poisoning should be stabilized and resuscitated according to current ACLS guidelines. Intubation and ventilation may be necessary based on the patient’s level of CNS depression or in the case of concomitant injuries. IV access should be secured, and hypotension should be treated with IV fluids as appropriate. Caution should be exercised when using dopamine and epinephrine because they increase the circulating catecholamine levels and can contribute to arrhythmias. All patients with altered mental status should receive naloxone, thiamine, and glucose, if appropriate.
DEFINITION Exposure to hydrocarbons may occur accidentally, for the purpose of euphoria and abuse, or as a suicide attempt. There are four major classes of hydrocarbons: halogenated hydrocarbons, aliphatic compounds, cyclic or aromatic hydrocarbons, and terpenes. Halogenated hydrocarbons are primarily industrial compounds and include carbon tetrachloride, trichloromethane, and trichloroethylene. These compounds are well absorbed by the GI tract and even small exposures can cause significant toxicity. Hepatic and renal failure are not uncommon complications. The aliphatics are straight-chain compounds and include gasoline, kerosene, paint thinner, and various solvents. The major complication with these compounds is aspiration. The propensity for this is based on their physical properties such as low viscosity and low surface tension. Asphyxiation can occur from the displacement of alveolar oxygen. The more volatile hydrocarbons are more readily inhaled and have increased neurological symptoms resulting from increased systemic absorption. Compounds in the cyclic or aromatic class of hydrocarbons include benzene, toluene, and xylene. This class also includes plastic cements and airplane glues. Death can occur with very small ingestions of benzene. The terpenes, most notably, cause CNS depression. The metabolites of hydrocarbons cause both metabolic acidosis and damage to mitochondria via lipid peroxidation. The metabolites are excreted primarily through the kidneys except for the more volatile hydrocarbons that are primarily excreted through the lungs. Aspiration causes destruction of the pulmonary parenchyma via damage to alveolar and capillary membranes. Damage is not dependent on the volume aspirated, and a significant pneumonitis can occur in children with very small amounts. Methods of abuse include huffing and bagging. The former involves inhaling the intoxicant of choice from a soaked rag, and the latter is the process of inhaling the product after spraying it into a bag.
EPIDEMIOLOGY According to the American Association for Poison Control Centers, in 2003 there were 3035 toxic exposures to hydrocarbons. Of these, 41%
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occurred in children younger than 6 years old, 92% were unintentional, 6% had moderate or major effects, and no fatalities occurred. Exposures to children are usually accidental, whereas exposures in adolescents or adults can also occur from the abuse of volatile substances or suicide attempts.
CLINICAL PRESENTATION Patients may present without symptoms or may have varying degrees of respiratory distress or CNS dysfunction. Patients may be choking, coughing, or gasping for air. The CNS effects could appear as intoxication or euphoria if presenting soon after ingestion, or CNS depression ranging to coma with later presentations. Patients may report GI tract irritation with symptoms of gastritis or diarrhea. They may present with jaundice and right upper quadrant tenderness or with life-threatening arrhythmias such as ventricular tachycardia and ventricular fibrillation.
EXAMINATION Patients who have ingested hydrocarbons may exhibit tachypnea or varying levels of respiratory distress. They may be tachycardic, and chronic abuse of volatile substances has the potential for cardiac dysrhythmias. Patients may also be febrile. Ataxia may be present on neurological examination. Patients may have a “huffer’s rash,” or sores on the face, if they abuse these substances chronically. This appears as local erythema or maculopapular or vesicular skin lesions.
LABORATORY FINDINGS Essential laboratory studies include a CBC, coagulation studies, urinalysis, and measurements of electrolytes and renal and liver function to include gamma-glutamyl transferase. The clinician should consider performing an ABG analysis in the case of respiratory difficulty or abnormal pulse oximetry results. Laboratory studies may show metabolic acidosis, hypokalemia, or hypophosphatemia. Patients who have ingested certain halogenated hydrocarbons may have abnormal liver function test results 24 hours after ingestion. The carboxyhemoglobin level should be measured if possible exposure to methylene chloride has occurred. In addition, a lead level measurement may be helpful in the case of lead-based paint exposure of peripheral neuropathy.
DIAGNOSIS The diagnosis of hydrocarbon poisoning is primarily made on the basis of a history of ingestion as well as physical examination results. The examiner should obtain as much information about the substance ingested
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as possible, including the exact name, manufacturer, and ingredients. Knowledge of the chemical properties such as viscosity, volatility, and surface tension can also be useful. The healthcare provider should view the container, if possible. The patient or witnesses should be asked to estimate the quantity ingested, and an ECG should be obtained for abusers of volatile substances.
RADIOGRAPHS Chest x-ray can be used to investigate the possibility of aspiration, pneumothorax, pneumomediastinum, or pleural effusion. Changes are usually evident on radiographs within 4–6 hours.
TREATMENT IV access should be obtained and supplemental oxygen administered. In addition, the patient should be placed on a cardiac monitor. Hypotension should be treated with IV fluids as appropriate. Intubation and mechanical ventilation may be required based on the patient’s presentation. Albuterol may be beneficial for bronchospasm, although steroids are not indicated. Agitated patients should be provided with a calm environment to avoid increasing symptoms of respiratory distress. The use of epinephrine should be limited to cardiac resuscitation due to the potential for inducing arrhythmias resulting from increased levels of circulating catecholamines. Gastric decontamination is usually not beneficial but is indicated for the ingestion of certain compounds. The mnemonic CHAMP (i.e., camphor, halogenated hydrocarbons, aromatic hydrocarbons, metals, pesticides) may be useful to remember these instances. Charcoal is only indicated in the case of co-ingestants; others do not generally benefit due to the rapid gastric absorption. The major complication associated with hydrocarbon exposure is aspiration. Patients with severe toxicity will die from necrotizing pneumonitis and hemorrhagic pulmonary edema within 24 hours. Most patients who survive this period will experience resolution of symptoms in 2–5 days. Exceptions are patients that develop pneumatoceles or pneumonia, and in these patients symptoms may last for weeks or months. Cardiac arrest has been known to occur from cardiac dysrhythmias as a result of adrenergic stimulation. Certain halogenated hydrocarbons such as carbon tetrachloride and chloroform can be hepatotoxic and cause hepatomas and cirrhosis with chronic abuse. Hemodialysis has been proved helpful in the treatment of carbon tetrachloride. Toluene can cause acute renal tubular acidosis with a non-gap metabolic acidosis, hypokalemia, and hypophosphatemia. Chronic abusers of hydrocarbons can have a chronic constellation of symptoms that includes cerebellar ataxia,
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recurrent headaches, mental status changes, cognitive impairment, and emotional lability. Patients may be discharged after 6 hours of observation if they are asymptomatic with a normal chest radiograph and pulse oximetry. Patients without symptoms but with an abnormal chest x-ray may be discharged if reliable follow-up can be ensured. Patients abusing these substances should be observed or admitted while altered. All symptomatic patients or those with ingestions with a potential for delayed organ toxicity, such as in the case of carbon tetrachloride, should be admitted. Psychiatric consultation should be obtained in all cases of intentional ingestion. The possibility of child neglect should be investigated in the case of accidental child ingestions.
Bibliography Salyer S: The Emergency Medicine Physician Assistant Handbook. New York: WB Saunders, 1997, pp 577–581. Schaider J, Hayden SR, Wolfe RE, Barkin RM (eds): Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 540–541. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005, pp 1162–1168. Watson W, Litovitz T, Klein-Schwartz W, et al: 2003 American Association of Poison Control Centers Annual Report. Available at: http://www.aapcc.org/2003.htm. Accessed June 30, 2005.
Iron Toxicity CARRY DEPOLD
ICD Code: Iron poisoning 964.0
Key Points Iron toxicity can lead to hypotension, metabolic acidosis, and intestinal hemorrhage. Iron poisoning can be fatal without early recognition and adequate and immediate supportive care. The fraction of elemental iron and the size and weight of the patient are important in determining the risk of iron toxicity.
1008 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! The treatment of iron toxicity consists of prompt recognition, initial stabilization using the ABCs, and continuous reevaluation. Shock should be managed aggressively with large-bore IV access, continuous cardiac and pulse oximetry, and the administration of supplemental oxygen.
DEFINITION Iron is widely available by prescription and as an over-the-counter purchase. Many different iron-containing preparations are available. Iron toxicity results from intentional or unintentional iron ingestion. The fraction of elemental iron and the size and weight of the patient are important in determining the risk of iron toxicity. Toxic doses are categorized as moderate or severe. Deaths have been reported with ingestion of 60 mg/kg, commonly from circulatory shock. Iron toxicity should not be underestimated.
EPIDEMIOLOGY The Association of Poison Control Centers reported 3371 cases if acute iron ingestion in 2003, two of which were fatal. Of the reported cases, 58% were children younger than 6 years of age, 12% were aged 6–19 years, and 29% were older than 19 years. Eighty-one percent of poisonings are unintentional, 12% intentional.
CLINICAL PRESENTATION Historically, there are four stages of iron toxicity. Stage one symptoms, 30 minutes to 6 hours after ingestion, can include diffuse abdominal pain, emesis, and hematemesis, diarrhea, melena, and acidosis. This stage can lead to hypovolemic shock resulting from blood and fluid loss. This is also called the GI phase. Stage two, seen up to 24 hours after ingestion, may see the patient’s symptoms improve. This may falsely reassure the provider; the patient may still have high serum iron levels. This is also called the latent phase. Stage three symptoms, which occur up to 4 days after ingestion, include fever, jaundice, elevated liver function test results, and mental status changes resulting from hepatic, renal, and other organ damage. This is also called the metabolic phase. Stage four, 2–8 weeks after ingestion, is characterized by gastric outlet obstruction resulting from pyloric stenosis from mucosal injury. This is also called the delayed phase.
EXAMINATION The patient’s history is critical in evaluating iron overdose. The examiner should inquire about the specific preparation ingested. If the patient
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or caregiver is unsure of the exact substance ingested, the substance should be brought in from the home. The physical examination should focus on signs of poor tissue perfusion.
LABORATORY FINDINGS Essential laboratory tests include CBC, blood type and cross-match, serum iron and serum glucose tests, a comprehensive metabolic panel, and measurements of ALT, AST, gamma-glutamyl transferase, bilirubin, PT, and PTT. Leukocytosis is likely to occur with a large ingestion. Anemia may occur from GI blood loss. An elevated anion gap is seen in metabolic acidosis. Transfusion of red blood cells may be necessary to replace blood loss from the GI tract. Low serum iron levels may be misleading because peak levels will vary depending on the amount of iron ingested and the rate of iron absorption. First serum iron levels should be drawn within 3–5 hours of ingestion and drawn again 6–8 hours after ingestion. Total iron-binding capacity levels are not reliable for assessing toxicity. In the presence of an elevated anion gap, ABG and serum lactate analyses are used to evaluate acidosis. Serum creatinine should be measured to monitor kidney function when deferoxamine (Desferal) treatment is administered.
DIAGNOSIS The diagnosis of iron toxicity is made on the basis of history and clinical presentation and can be confirmed with laboratory tests and radiographic evaluation.
RADIOGRAPHS Plain film abdominal radiograph may show iron tablets in the GI tract.
TREATMENT The treatment of iron toxicity consists of prompt recognition, initial stabilization of the patient’s condition using the ABCs of resuscitation, and continuous reevaluation. Shock should be managed aggressively with largebore IV access, continuous cardiac and pulse oximetry, and supplemental oxygen. Fluid therapy initially consists of crystalloids, but red blood cell transfusion may be required. Gastric lavage should be considered if the patient presents within 2 hours of ingestion and the tablets are small. Wholebowel irrigation with polyethylene glycol is used in the absence of bowel
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obstruction, GI tract bleeding, perforation, and ileus. Syrup of ipecac and activated charcoal are not clinically useful or therapeutic. The clinician should consider metoclopramide or ondansetron for antiemetic therapy. If coagulopathy is present, it should be treated with vitamin K and fresh frozen plasma. Deferoxamine combines with iron and is used in all symptomatic patients. The route of administration depends on the severity of symptoms: IM for euvolemic patients, IV for hypovolemic patients. The healthcare provider should contact the American Association of Poison Control Centers and consider an inpatient toxicology consultation.
Bibliography American Association of Poison Control Centers: 2003 AAPCC TESS Report, Available at: http://www.aapcc.org/2003.htm. Accessed on May 22, 2005. Kronfol R: Acute iron intoxication in children and adolescents, 2004. UpToDate.com. Available at: http://patients.uptodate.com/topic.asp?file¼nutri_ch/2103. Accessed on June 16, 2005. Rella JG, Nelson LS: Iron. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1121–1124. Wang RY, Girard DD: Over-the-counter medications. Toxic effects and adverse reactions: Part II, Emerg Med Rep Available at: http://www.emronline.com/textbooks_index.html. Accessed on May 22, 2005. Wright RO, Wang RY: Poison antidotes, Emerg Med Rep Available at: http://www. emronline.com/textbooks_index.html. Accessed on May 22, 2005.
Isopropanol GUYON J. HILL
ICD Code: Isopropanol poisoning 980.2
Key Points Isopropanol is most commonly found in rubbing alcohol and other household items. Intentional ingestions are usually made by chronic alcoholics or suicidal patients; unintentional ingestions are usually made by children. Most care is supportive, although dialysis does remove isopropanol and its major metabolite acetone. Fatalities are rare.
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! Emergency Actions ! A patient with isopropanol toxicity should be stabilized and resuscitated according to current ACLS guidelines. Intubation and ventilation may be necessary based on the patient’s level of CNS depression or in the case of concomitant injuries. Treat hypotension with IV fluids and vasopressors as appropriate. All patients with altered mental status should receive naloxone, thiamine, and dextrose.
DEFINITION Isopropanol is a clear, colorless, and volatile liquid. It is also commonly known as isopropyl alcohol or 2-propanol. The most common source of exposure is rubbing alcohol, which contains 70%–90% isopropanol or ethanol. Other possible means for exposure include household cleaners, cosmetic products, nail polish removers, paint thinners, disinfectants, and antifreeze. Inhalational and transdermal exposure can be significant, and children have become affected after sponge bathing. Adults may intentionally ingest isopropanol because it has twice the CNS depression as ethanol. Its duration of action is also between two and four times longer. Oral absorption is rapid, with 80% being absorbed within 30 minutes of ingestion. The major metabolite is acetone, which is produced in the liver by the oxidation of isopropanol by ADH. The kidneys primarily excrete acetone, and a minor amount of elimination occurs via the lungs. This accounts for 80% of ingestion. The remaining 20% is excreted unchanged by the kidneys. The half-life of isopropanol (with no co-ingestions) is 6–7 hours. The half-life of acetone is 22–28 hours. The lethal adult dose is between 150–240 ml or 2–4 ml/kg, and the toxic dose is 1 ml/kg. Children are very sensitive to isopropanol and may develop toxicity with much smaller ingestions. In the realm of alcohols, the toxicity of isopropanol falls between ethanol and the more toxic methanol and ethylene glycol.
EPIDEMIOLOGY After ethanol, isopropanol is the most commonly ingested alcohol. According to the American Association for Poison Control Centers, in 2003 there were 7945 exposures. Of these, 60% occurred in children younger than 6 years old, 85% were unintentional, 5% had moderate or major effects, and three fatalities occurred. Fatalities are rare, with the typical patient being an older person with chronic alcoholism and upon presentation displays a mixed ethanol and isopropanol ingestion.
CLINICAL PRESENTATION Patients who have ingested isopropanol may appear drunk while having the odor of acetone rather than ethanol. Neurological symptoms may
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include weakness, dizziness, or headache. Confusion and incoordination may be apparent. GI symptoms may include nausea, vomiting, abdominal pain, or symptoms consistent with gastritis. Patients may experience hemorrhagic gastritis. Coma, respiratory or myocardial depression, and peripheral vasodilation leading to hypotension may occur with large doses. The coma is more prolonged than that associated with ethanol intoxication. Serious cardiac dysrhythmias are rare.
EXAMINATION There are no pathognomonic physical findings for isopropanol ingestion. Sinus tachycardia is a common finding, but arrhythmias are rare and are usually found with coexistent states of shock, hypoxia, or acidosis. Neurological examination may yield a loss of deep tendon reflexes or other reflexes that serve to protect the cornea and the airway. Patients may have a present Babinski sign and usually exhibit nystagmus. They are often hypothermic.
LABORATORY FINDINGS Essential laboratory studies include CBC, ABG analysis, urinalysis, and tests of electrolytes, renal function, glucose, osmolality, serum and urine ketones, and isopropanol and acetone levels. The most common laboratory test result abnormality is the elevation of ketones with little or no acidosis. This occurs as a result of the metabolite acetone because it is uncharged and therefore does not elevate the anion gap. Serum isopropanol levels may be elevated within 15 minutes of ingestion, and excretion in the urine may occur in as soon as 3 hours. Levels peak 30 minutes to 3 hours after ingestion. Patients do not have a metabolic acidosis unless there are confounding factors in the condition. An elevated osmolar gap occurs as a result of both isopropanol and acetone ingestion. An isolated false elevation of creatinine with a normal BUN level may be the result of acetone and acetoacetate confounding the creatinine assay. Other rare sequelae include acute tubular necrosis, hepatic dysfunction, rhabdomyolysis, and hemolytic anemia.
DIAGNOSIS The diagnosis of isopropanol toxicity is typically made on the basis of a history of ingestion, physical examination results, and laboratory values. Patients may have an odor of isopropanol or acetone on their breath. The differential diagnosis includes ethanol, ethylene glycol, methanol, glycerol, or mannitol ingestion.
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RADIOGRAPHS Chest radiography should be performed if aspiration pneumonia is suspected, and a head CT scan should be included if the patient also has a head injury.
TREATMENT Most treatment is supportive. IVaccess should be obtained and the patient should be placed on continuous cardiac monitoring. Chest radiography and ECG should be performed. Administer dextrose, thiamine, and naloxone if indicated. Activated charcoal and gastric lavage are not useful unless there is a significant ingestion or a co-ingestant. If present, hypotension should be managed in the usual fashion with IV fluids or vasopressors, as appropriate. Dialysis may be indicated in recalcitrant hypotension or other clinical deterioration or if the predicted peak isopropanol level is greater than 400 mg/dl. Hemodialysis is effective to remove both isopropanol and acetone. Hemorrhagic gastritis may require transfusion and other therapy for upper GI tract bleeding. Patients whose conditions are stable without coma 6 hours after ingestion are at a low risk of significant effects and will generally not require dialysis. Patients may be discharged if they are asymptomatic for 6 hours after ingestion.
Bibliography Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2133–2135. Salyer S: The Emergency Medicine Physician Assistant Handbook. New York: WB Saunders, 1997, pp 585–586. Schaider J, Hayden SR, Wolfe RE, Barkin RM (eds): Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 616–617. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005, pp 1104 –1105. Watson W, Litovitz T, Klein-Schwartz W, et al: 2003 American Association of Poison Control Centers Annual Report. Available at :http://www.aapcc.org/2003.htm. Accessed on June 30, 2005.
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Lead MICHAEL A. AROCHO
ICD Code: Lead poisoning 984.9
Key Points Blood lead levels greater than 10 mg/dl are diagnostic of lead poisoning. Elevated levels of gamma-aminolevulinic acid (d-ALA) in a patient’s blood and urine, as well as elevated protoporphyrin in the blood, support the diagnosis of lead poisoning. ! Emergency Actions ! The key first step in treating all cases of lead poisoning is the reduction of or removal from the source of lead exposure.
DEFINITION Lead poisoning, also known as plumbism, is a toxic condition produced by the absorption of excessive lead. Lead is a common metal found in many sources, including paints (especially in pre-1978 homes and buildings), insecticides and herbicides, batteries, contaminated seafood, ammunitions, pigments, and some ceramic ware.
EPIDEMIOLOGY Lead is the most common cause of chronic metal poisoning, with approximately 890,000 children between ages 1 and 5 years having a blood lead level of at least 10 mg/dl. Data from the Third National Health and Nutrition Examination Survey (NHANES III) suggest that an estimated 700,000 adults in the United States have levels of 25 mg/dl or greater. Lead exposure occurs through occupational, recreational, or environmental exposure.
PATHOPHYSIOLOGY Lead is absorbed from the lungs or the GI tract, the former being the most significant route of entry in adults and the latter in children. Once
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absorbed, lead is distributed to multiple sites, including erythrocytes, soft tissues, and skeletal tissue. Lead exerts a variety of effects: it affects astrocytes and the microvasculature in the CNS, demyelinates peripheral nerves, disrupts hemoglobin synthesis, and impairs proximal renal tubule function. Additionally, lead interferes with energy and transport systems in cell membranes, which may be responsible for shortened erythrocyte survival time, hemolysis, renal toxicity, and hypertension.
CLINICAL PRESENTATION Lead is a complex toxin that exerts numerous effects on a variety of organ systems, and the manifestation of lead poisoning varies according to systems affected. Lead poisoning should be suspected in patients, especially children, who present with CNS symptoms (e.g., delirium, seizures, cognitive impairment, mood and behavioral changes, altered mental status), GI symptoms (e.g., colicky abdominal pain, constipation, diarrhea), or anemia (hypoproliferative and/or hemolytic). Lead toxicity to the peripheral nervous system can manifest as paresthesias, motor weakness (classic wrist drop), and/or depressed or absent deep tendon reflexes. A bluish discoloration of gingiva may also be present.
DIAGNOSIS The approach to all suspected poisonings must include a thorough history and physical examination. This is especially true in lead poisoning, since most poisonings result from chronic exposure rather than acute exposure. Furthermore, due to its complex nature, a person with lead poisoning can present with multiple, vague signs and symptoms of varying intensity, so knowledge of the clinical features (mentioned previously) and a heightened index of suspicion are necessary for the diagnosis.
LABORATORY Blood lead levels greater than 10 mg/dl are diagnostic of lead poisoning. Elevated d-ALA in the blood and urine, as well as elevated protoporphyrin in the blood, support the diagnosis of lead poisoning. Basophilic stippling on a peripheral blood smear also supports this diagnosis, but it is a rare and nonspecific finding.
RADIOGRAPHS Radiographic evaluation may assist in the diagnosis. Radiographic evidence of lead toxicity includes horizontal metaphyseal bands (“lead lines”) in long bones of children, particularly around the wrist and knee,
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and radiopaque material in the GI tract, representing lead-based paint chips or particles.
TREATMENT The key first step in treating all cases of lead poisoning is the reduction of or removal from the source of lead exposure. For acute lead ingestion (rare), GI tract decontamination with whole-bowel irrigation using a polyethylene glycol solution is indicated. In adults, the rate of administration is 500–2000 ml/hr, and in children the rate is 100–500 ml/hr. Chelation therapy is indicated in all symptomatic patients and in patients with serum lead levels of 70 mg/dl or greater in adults or 45 mg/dl or greater in children. Symptomatic patients, especially encephalopathic patients, should receive dimercaprol (BAL) 3–5 mg/kg IM every 4 hours, followed in 4 hours with calcium EDTA (calcium disodium edetate) 50–75 mg/kg/ day IM or IV. Adults with blood lead levels of 70–100 mg/dl or children with blood lead levels of 45–69 mg/dl with few or no symptoms should receive succimer (DMSA) 10 mg/kg PO every 8 hours for 5 days, then 10 mg/kg PO every 12 hours for 9 days (total treatment period is 14 days). In asymptomatic adults with blood lead levels less than 70 mg/dl, and in asymptomatic children with lead levels less than 45 mg/dl, removal from the exposure is all that is needed. Chelation therapy is not required in these cases. Admission to the hospital is warranted in patients with severe symptoms, in patients requiring parenteral chelation therapy, and in patients who have no choice but to return to the environment producing the lead exposure. Additionally, benzodiazepines and/or barbiturates may be necessary to suppress seizure activity in patients with CNS involvement.
Bibliography Brody DJ, Pirkle JL, Kramer RA, et al: Blood lead levels in the US population: Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III), JAMA 1994;272:277. Goldfrank LR, Flomenbaum NE, Lewin NA, et al: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2003, pp 1200–1221, 1239–1247. Goldman RH, Hu H: Adult lead poisoning. Available at: http://www.uptodate.com. Klaasen CD: Casarett and Doull’s Toxicology: The Basic Science of Poisons, ed 6. McGraw-Hill: New York, 2001, pp 827–837. Ma OJ, Cline DM, Tintinalli JE, Kelen GD: Emergency Medicine: Just the Facts, ed 2. McGraw-Hill: New York, 2004, pp 347–351, 398–399. Marcus S: Toxicity, lead, eMedicine Clinical Knowledge Base, 2004. Available at: http:// www.emedicine.com. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1146–1149, 1151–1153.
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Lithium MICHAEL A. MILLER
ICD Code: Lithium poisoning 985.8
Key Points Lithium poisoning may occur as a result of a single acute overdose, chronic excessive overmedication, or gradual accumulation of lithium in a patient with worsening renal insufficiency. ! Emergency Actions ! Charcoal does not adsorb lithium but should be given if there is a suspicion of co-ingestion in a patient who has intentionally overdosed. Correction of dehydration with IV normal saline is usually necessary, and close monitoring of electrolytes is very important.
DEFINITION Lithium is a monovalent metal cation with physiological actions similar to potassium and sodium. Modern medicinal use of this agent is primarily for bipolar mood disorders, and it gained popularity in the 1970s. Despite the development of newer agents to treat depression and bipolar mood disorders, lithium’s excellent efficacy has led to an estimated 0.1% of the U.S. population taking this agent. The efficacy of lithium as a psychotropic agent has justified its expanded use despite a narrow therapeutic index. Patients undergoing dosing adjustments or patients in whom drug elimination is altered are at risk for toxicity from this agent. Symptoms of toxicity include nausea, polyuria, somnolence, and myoclonic jerking. In severe cases, toxicity has resulted in seizures, dysrhythmias, and death. Usual adult dosing starts at 600 mg daily. The usual effective dose is 900–1800 mg/day. Available formulations include (1) regular-release lithium carbonate tablets and capsules (150, 300, or 600 mg), (2) sustained-release tablets of various types (300–600 mg), and (3) lithium citrate syrup (8 mEq/ 5 ml). Lithium carbonate 300 mg equals approximately 8 mEq of lithium.
PATHOLOGY Acute single ingestions of lithium are less likely to cause significant toxicity, but very large single ingestions are capable of causing symptoms.
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More commonly, therapeutic use can lead to significant toxicity in patients with decreased drug clearance or increased tubular reabsorption such as in the setting of dehydration or renal failure. Therapeutic dosing can also cause nephrogenic diabetes insipidus. There are several proposed mechanisms for lithium’s desired neurological effects. These mechanisms include the ability of lithium to increase serotonin synthesis. These same mechanisms, as well as the ability of lithium to substitute for the cations potassium and sodium, may also account for the diverse neurological manifestations of lithium poisoning.
CLINICAL PRESENTATION Lithium poisoning may occur as a result of a single acute overdose, chronic excessive overmedication, or gradual accumulation of lithium in a patient with worsening renal insufficiency. The latter two circumstances are referred to as chronic intoxication and are much more common. Chronic lithium intoxication often follows a clinical illness leading to dehydration or it may occur as a result of an adverse drug interaction, especially in the setting of dosing changes. The signs and symptoms of lithium toxicity may be present in varied combinations and do not correlate well with serum levels of lithium. As poisoning progresses from mild to severe, a spectrum of symptoms ranging from tremor, mild fatigue, nausea, weakness, and agitation to frank coma, seizures, and death will be seen.
DIAGNOSIS The diagnosis of lithium toxicity is usually not difficult to make in the setting of the appropriate symptoms found in a patient taking lithium. Often there is another intercurrent acute illness such as gastroenteritis that has made a contribution to the negative effects of lithium. The healthcare provider must recognize both of these acute entities and treat each to maximize benefit to the patient.
LABORATORY FINDINGS Therapeutic lithium levels are 0.6–1.2 mEq/L. Signs and symptoms of toxicity may occur at levels as low as 1.5 mEq/L, but it is crucial to recognize that levels at which toxicity occurs may vary widely. Symptoms of severe neurotoxicity may occur at minimally elevated levels in the setting of chronic toxicity. In these patients with chronic intoxication, CNS symptoms provide a better measure of severity than serum levels. Falsely elevated serum levels may result from collection of serum into speckled green–topped tubes, which contain lithium heparin as an anticoagulant.
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TREATMENT In a symptomatic patient, appropriate attention to airway, breathing, and circulation is essential. Correction of dehydration with IV normal saline is usually necessary, and close monitoring of electrolyte levels is very important. Charcoal does not adsorb lithium but should be given if there is a suspicion of co-ingestion in a patient who has intentionally overdosed. Although controversy exists regarding the use of gastric lavage, it may be of benefit if performed in the case of an acute, large ingestion presenting to a medical care facility within an hour of ingestion. Whole-bowel irrigation is an acceptable method of gastric decontamination after ingestion of sustained-release preparations and may also be considered in very large acute overdoses of sustained-release lithium formulations. Since most cases of toxicity involve chronic exposure, gastric decontamination is relatively less important in lithium poisoning. A general approach to lithium poisoning is as follows: 1. Ensure that basic resuscitative measures have occurred, focusing upon support of the patient’s airway, breathing, and circulation. 2. Consider gastric decontamination with lavage for acute ingestions presenting within 1 hour or whole-bowel irrigation for sustainedrelease preparations. 3. Consider other causes of illness, such as infection. 4. Provide supportive care. A. Intravascular fluid repletion with normal saline B. Further circulatory support as necessary with vasoactive agents C. Hemodialysis for severe symptoms such as seizures, coma, increasing alterations in mental status or for moderate symptoms such as lethargy and confusion in the setting of renal failure
Bibliography Favin FD, Oderda GM, Klein-Schwartz W, et al: In vitro study of lithium carbonate adsorption by activated charcoal, J Toxicol Clin Toxicol 1998;26:443–450. Groleau G, Barch R, Tso E, et al: Lithium intoxication: Manifestations and management, Am J Emerg Med 1987;5:527–532. Hansen HE, Amdisen A: Lithium intoxication: Report of 23 cases and review of 100 cases from the literature, Q J Med 1978;186:123–144. Miller MA, Olson KR: Lithium. In Dart RC: Medical Toxicology, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2004.
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Methanol GUYON J. HILL
ICD Code: Methanol poisoning 980.1
Key Points Methanol is a clear, volatile liquid that was originally distilled from wood. It is also known as methyl alcohol or wood alcohol. It is commonly found in many industrial and household products. Ingestion can cause seizures, blindness, or even death. ! Emergency Actions ! The patient’s condition should be stabilized and he or she should be resuscitated according to current ACLS guidelines. Intubation and ventilation may be necessary based on the patient’s level of CNS depression or in the case of concomitant injuries. Hypotension should be treated with IV fluids and vasopressors, as appropriate. All patients with altered mental status should receive naloxone, thiamine, and dextrose, if appropriate.
DEFINITION Methanol is a clear, volatile liquid that was originally produced naturally from the distillation of wood. It is also commonly referred to as wood alcohol or methyl alcohol. Methanol can frequently be found in products such as adhesives, lacquers, antifreeze, windshield washer fluid, carburetor fluid, formalin and embalming fluid, gasohol, and Sterno. Like other alcohols, it is well absorbed by the GI tract and levels peak at between 30 and 90 minutes. Inhalation and transdermal exposure may also cause toxic levels. The major routes of elimination are the liver and the kidney with 90%–95% and 2%–5%, respectively, eliminated by these organs. Formaldehyde and formic acid are both toxic metabolites of methanol. They result from the metabolism by ADH in the liver. Symptoms correlate with the level of formic acid. Formaldehyde is formed in the retina and causes optic papillitis and retinal edema. Blindness can result. Tissue hypoxia results when formate inhibits mitochondrial respiration and lactate is subsequently produced. The oxidation of methanol also stimulates anaerobic glycolysis and further lactate production. The minimal fatal dose is 30 ml of a 40% solution, although death has been reported after the ingestion of half this much.
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EPIDEMIOLOGY According to the American Association for Poison Control Centers, in 2003 there were 1044 toxicological exposures to methanol. Of these, 25% occurred in children younger than 6 years old, 86% were unintentional, 11% had moderate or major effects, and 17 fatalities occurred.
CLINICAL PRESENTATION Patients may appear drunk or have more profound CNS depression to the level of coma. GI symptoms such as abdominal pain, nausea, and vomiting are common but not always present, even in significant ingestions. It is not uncommon for patients to develop pancreatitis. Visual symptoms occur in up to 50% of patients and can include decreased visual acuity, diplopia, blurred vision, or blindness. Patients may also have photophobia and describe “looking into a snow field.” Seizures are possible. Symptoms of ingestion may not be apparent until 12–18 hours, during which time the toxic metabolites are formed.
EXAMINATION Patients may exhibit various levels of CNS depression up to and including coma. Nystagmus or fixed and dilated pupils may be present. Funduscopic examination may show papilledema, retinal edema, and atrophy or hyperemia or the optic disk. Patients with significant ingestions may have hypotension and bradycardia, but these are late findings.
LABORATORY FINDINGS Patients with methanol poisoning have a wide anion gap metabolic acidosis. An increased osmolal gap is usually present as well. A normal methanol level from endogenous sources is 0.05 mg/dl. Patients with levels below 20 mg/dl are usually asymptomatic, whereas levels above 50 mg/dl indicate a significant ingestion and levels of 150–200 mg/dl can be fatal. Ocular manifestations usually occur above 50 mg/dl.
DIAGNOSIS The diagnosis of methanol poisoning is typically made on the basis of a history of ingestion, an elevated osmolal gap, and the presence of a wide anion gap metabolic acidosis. The differential diagnosis includes any other cause of a wide anion gap acidosis. These include carbon monoxide, cyanide, alcoholic ketoacidosis, toluene, uremia, diabetic ketoacidosis, paraldehyde, isoniazid, iron, lactic acidosis, phenformin, or salicylates.
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RADIOGRAPHS A CT scan of the head may show basal ganglia infarcts. Chest radiography should be performed if aspiration pneumonia is suspected.
TREATMENT AND OUTCOME The clinician should obtain IV access, administer supplemental oxygen, and begin cardiac monitoring for the patient. Intubation may be necessary to protect the patient’s airway. The blood glucose should be determined immediately, and dextrose, naloxone, and thiamine should be given, if indicated. Persons with chronic alcoholism can be deficient in folate, which is a cofactor for turning formic acid into carbon dioxide and water. This may cause them to be more vulnerable to its toxic effects. Treatment should begin as soon as an ingestion is suspected and should not be delayed until serum methanol determination is available. Gastric lavage is not useful unless the patient presents rapidly because methanol, like other alcohols, is rapidly absorbed by the GI system. Activated charcoal is not useful unless there are co-ingestants because it binds methanol poorly. The administration of both fomepizole (4-methylpyrazole) and ethanol have been used successfully in the treatment of methanol intoxication. They decrease conversion to toxic metabolites. Fomepizole is a competitive inhibitor of ADH and blocks the metabolism of methanol to its toxic metabolites. Its advantage over ethanol is the avoidance of CNS depression although it will not alleviate a need for dialysis. The current recommended dose is 15 mg/kg given over 30 minutes IV. It may be redosed at 10 mg/kg every 12 hours for four doses. This dose must be increased in patient receiving dialysis to compensate for the removal of the drug involved in that kind of therapy. Ethanol’s affinity for aldehyde dehydrogenase is 10–20 times that of methanol and it has a significant impact of reducing the formation of toxic metabolites. The goal of treatment should be to maintain a level between 100 and 150 to have its intended effect of preventing toxic metabolites from being formed. Alcohol may be given IV, orally, or by nasogastric tube. The method should be selected based on the patient’s condition. IV administration is ideal but may cause a superficial thrombophlebitis. A normal pH improves some of the toxic effects of methanol such as visual impairment. IV ethyl alcohol is given in a preparation of 10% ethyl alcohol in D5W (bolus of 10 ml/kg then 1.6-ml/kg/hr infusion). Also, folate should be given at 50 mg IV every 4 hours. Oral ethanol should be at a level of 20%–30% solution. If loading orally, the dose should be 0.6–0.8 g/kg by mouth or IV with a maintenance dose of 0.11 g/kg/hr. A maintenance infusion of 0.15 g/kg should be used if the patient chronically consumes alcohol. Commercially available ethanol can be
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used if nothing else is available. The following formula should be used to calculate the amount of ethanol in commercial alcohol beverages: ethanol ðgÞ ¼ volume of beverage ðmlÞ 0:9 ðproof =200Þ
Hypoglycemia may result from the administration of ethanol, so both ethanol and blood glucose levels should be monitored closely. The administration of hemodialysis should be considered in the treatment of CNS dysfunction, visual abnormalities, or a methanol level exceeding 25 mg/dl; if severe metabolic acidosis develops regardless of the level; or if there is a suspected ingestion that exceeds 30 ml. Hemodialysis and peritoneal dialysis are both effective treatments for methanol poisoning. Hemodialysis is faster and has a greater elimination of both methanol and its toxic metabolites. Dialysis is effective to remove both methanol and its toxic metabolites. Treatment with fomepizole or ethanol and dialysis should be continued until methanol levels are reduced to zero and the acidosis is resolved. Methanol ingestion can result in neurological dysfunction, permanent blindness, or death. Patients may develop a permanent parkinsonian syndrome. Outcomes relate more to the degree of acidosis than the absolute methanol level, and the development of sequelae is associated with increased morbidity. Patients with hypotension and bradycardia tend to have a poor prognosis. Symptoms generally correlate with the level of formic acid. Blindness may occur with as little as 15 ml of a 40% solution. The patient with a history of significant ingestion or any signs of instability should be admitted to the ICU. Patients should be transferred to facilities capable of providing dialysis if the receiving facility does not have this capability. The patient should be observed for 12–18 hours after ingestion even if he or she is symptom free.
Bibliography Diaz S: Blackwell’s Primary Care Essentials: Emergency Medicine. Blackwell Science: London, 2002, p 281. Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2127–2129, 2132–2133. Salyer S: The Emergency Medicine Physician Assistant Handbook. New York: WB Saunders, 1997, pp 595–597. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005, pp 1062, 1105–1107. Watson W, Litovitz T, Klein-Schwartz W, et al: 2003 American Association of Poison Control Centers Annual Report. Available at: http://www.aapcc.org/2003.htm. Accessed on June 30, 2005.
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Mercury MICHAEL A. AROCHO
ICD Code: Mercury poisoning 985.0
Key Points Mercury occurs in two forms: organic and inorganic. Elemental mercury is found in liquid form and easily vaporizes at room temperature, where it becomes well absorbed through inhalation. As a vapor, elemental mercury is highly lipid soluble and crosses the blood-brain barrier. ! Emergency Actions ! The approach to all patients with suspected mercury poisoning must include a thorough history and physical examination, with particular emphasis on the neurological examination. Attention to airway, breathing, and circulation always takes precedence in managing a poisoned patient. Patients require oxygen and cardiac monitoring, and IV access should be obtained.
DEFINITION Mercury is the only metal that is liquid at room temperature. Mercury occurs in two forms: organic and inorganic. Although mercury poisoning is rare, all forms of mercury are toxic. Inorganic mercury is divided into elemental mercury and mercurous and mercuric salts. Organic mercury is divided into short- and long-chained alkyl and aryl compounds. Of these, the short-chained alkyls in the form of methyl mercury and ethyl mercury are the most toxic to humans.
EPIDEMIOLOGY Exposure to mercury usually results from occupational or accidental exposure to mercury salts.
PATHOPHYSIOLOGY Elemental mercury is found in liquid form and easily vaporizes at room temperature, where it becomes well absorbed through inhalation. As a vapor, elemental mercury is highly lipid soluble and crosses the blood–brain barrier. In the CNS it is ionized and becomes trapped, which
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contributes to its significant toxicity. There is usually very little absorption of elemental mercury by the GI tract (so ingestion of mercury found in thermometers is mildly toxic). Inorganic mercury, found mostly in mercuric salt form (in batteries), is highly toxic and corrosive. It is absorbed orally or percutaneously, and once absorbed, it accumulates primarily in the kidneys causing significant renal toxicity. Organic mercury is more readily absorbed from the GI tract. Once absorbed, the alkyl and aryl compounds are converted to inorganic forms and react similarly to inorganic mercury.
CLINICAL PRESENTATION Short-chained alkyl mercury and elemental mercury produce a constellation of neurological abnormalities collectively referred to as erethism. Erethism includes anxiety, irritability, mania, sleep disturbance, depression, and cognitive deficits. Visual disturbance, hearing loss, paresthesias, and tremor may also be present. In addition to causing CNS abnormalities (i.e., erethism), inhalation of elemental mercury can result in severe pneumonitis, ARDS, and pulmonary fibrosis. The ingestion of mercury salts may result in severe GI symptoms (e.g., abdominal pain, vomiting, diarrhea, and subsequent dehydration resulting from volume loss) and acute tubular necrosis. Mercury salts spare the CNS due to their poor lipid solubility. Children exposed to mercury may experience acrodynia (also known as pink disease), an immune-mediated condition that features fever, generalized rash, splenomegaly, irritability, and poor muscle tone (with specific weakness of the pectoral and pelvic muscles).
DIAGNOSIS The approach to all patients with suspected mercury poisoning must include a thorough history and physical examination, with particular emphasis on the neurological examination. Every attempt should be made to ascertain the number of persons exposed, as well as the timing, type, amount, and route of exposure. Coupled with the clinical features, this information provides the necessary clues to diagnosis. Confirmation of mercury poisoning is made by performing a 24-hour urine test.
LABORATORY FINDINGS An elevated 24-hour urine mercury level greater than 10–15 mg/L (where levels greater than 100 mg/L point to significant exposure) confirms the diagnosis of mercury poisoning from most forms of mercury except the
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short-chained alkyl mercury compounds, which are excreted in the bile, undergo extensive enterohepatic circulation, and accumulate in erythrocytes. An elevated whole blood mercury level must be used to confirm poisoning from these types of mercury compounds. Furthermore, inorganic mercury redistributes readily to other body tissue, so the levels in the blood are only accurate after an acute ingestion.
RADIOGRAPHIC FINDINGS Plain abdominal radiographs may reveal ingested elemental mercury, which is radiopaque. This finding is nonspecific, however, and there are no pathognomonic radiographic features of mercury toxicity.
TREATMENT Attention to airway, breathing, and circulation always takes precedence in managing a patient with mercury poisoning. Patients require oxygen and cardiac monitoring, and IV access must be obtained. In patients with significant exposure and symptoms, treatment should not be delayed while confirmatory laboratory analysis is awaited (which may take several days). Dimercaprol (BAL) is the chelating agent of choice for the treatment of acute toxicity from mercury salts. BAL is given 3–5 mg/kg IM every 4 hours, in addition to initial GI decontamination. Cathartic agents are usually not needed, since diarrhea is often present. BAL may also be given to patients with renal failure. BAL is contraindicated in short-chained alkyl mercury poisoning because it may exacerbate the CNS symptoms. Succimer (DMSA) is the agent of choice in short-chained alkyl mercury poisonings. Succimer is given 10 mg/kg PO every 8 hours for 5 days, followed by 10 mg/kg PO every 12 hours for 14 days. The patient should be well hydrated to prevent toxicity. Hemodialysis is useful when mercury poisoning causes significant renal toxicity. Regular hemodialysis is of limited use due to mercury’s mode of distribution among erythrocytes and plasma. Hemodialysis with L-cysteine compounds is beneficial. Consultation with the regional poison control center or a medical toxicologist is helpful to provide further information and patient care recommendations.
Bibliography Diner B: Toxicity, mercury, eMedicine Clinical Knowledge Base, 2004. Available at: http://www.emedicine.com.
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Goldfrank LR, Flomenbaum NE, Lewin NA, et al: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2003, pp 1200–1221, 1239–1247. Klaasen CD: Casarett and Doull’s Toxicology: The Basic Science of Poisons, ed 6. McGraw-Hill: New York, 2001, pp 827–837. Ma OJ, Cline DM, Tintinalli JE, Kelen GD: Emergency Medicine: Just the Facts, ed 2. McGraw-Hill: New York, 2004, pp 347–351, 398–399. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 1146–1149, 1151–1153.
Opioids ROBERT D. GRAYDON
ICD Code: Opioid poisoning 965.0
Key Points Heroin, codeine, methadone, and meperidine all cross the blood-brain barrier and can affect a newborn child if ingested by or administered to the mother. ! Emergency Actions ! Cardiac monitoring should be initiated for patients with acute opioid intoxication, and two large-bore IV lines should be placed. The patient should receive supplemental oxygen. The treatment of an acute opioid intoxication consists of airway and ventilation support and the administration of naloxone (0.4–2.0 mg in an adult and 0.01 mg/kg in children), which is a pure opioid antagonist.
DEFINITION Opioids are naturally occurring or synthetic drugs that have opium or morphine-like activity. Opioids include morphine, heroin, codeine, methadone, meperidine, fentanyl, oxycodone, and hydrocodone. Heroin and other street drugs are often adulterated with quinine, baking soda, lactose, sucrose, magnesium silicate, and procaine. Co-toxicity and complications of ingesting or injecting these drugs or compounds must be assumed. Opioids are used in antidiarrheal medications, cough medications, and analgesics.
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EPIDEMIOLOGY Opioids continue to be widely used and abused. Approximately 5% of all acute intoxications involve opioids. Mortality rates from overdose of opioids continue to rise in the United States. Morphine, codeine, heroin, and oxycodone are the primary agents of intoxication.
PATHOLOGY Opioids are readily absorbed nasally, parenterally, and from the GI tract and respiratory mucosa. They are usually absorbed within 10 minutes of parenteral injection, within 30 minutes of IM injection, and 60–90 minutes after oral administration. Heroin, codeine, methadone, and meperidine all cross the blood-brain barrier and can affect newborn children if ingested by or administered to the mother. The clinical effects of most opioids last 4–6 hours; however, fentanyl lasts 1 hour and methadone persists for 24–48 hours. Opioids act on opioid receptors in the nervous system with increased concentrations in the areas that involve pain perception and appreciation, mainly in the spinothalamic, limbic, and extrapyramidal system. Hepatic biotransformation is the primary route of metabolism of all opioids. Patients with severe hepatic disease have impaired metabolism and are at increased risk for toxicity due to the accumulation of active metabolites. Elimination primarily occurs renally. Patients with renal disease are at risk of toxicity due to the accumulation of active metabolites. Many opioid users intravenously inject their drugs and are at risk for all of the sequelae of injection drug use. These patients can present with abscesses, cellulites, and thrombophlebitis. They are also at risk for infection with human immunodeficiency virus (HIV) and hepatitis. Noncardiogenic pulmonary edema is associated with certain opioids; parenteral and inhalant use of heroin is particularly associated with pulmonary edema. Other complications of injection include septicemia and endocarditis. The most common causative organisms are penicillinase-producing staphylococci; in endocarditis, the valve most commonly affected is the tricuspid valve. Two other complications of injection drug use are malaria and tetanus. Malaria is seen infrequently in the United States but is associated with injection drug use in less developed countries. Tetanus is seen more frequently in subcutaneous injectors and women. All injection drug users should be questioned about the status of the tetanus immunization status.
CLINICAL PRESENTATION The classic triad of opioid toxicity is CNS depression, respiratory depression, and miosis. However, multiple organ systems may be involved. Patients may be hyporeflexic, hypothermic, or hypotensive or have
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decreased bowel sounds. Less severe or early intoxication produces euphoria, drowsiness, and conjunctival injection. A patient who presents with acute opioid overdose will present with diminished mental status, hypoventilation, and pinpoint pupils. If the patient is hypoxic, the pupils may be midrange or dilated due to CNS hypoxia.
HISTORY A complete history should be obtained, including all drugs ingested. Most drug abusers are polydrug users. Often alcohol, benzodiazepines, and inhalants are used as a substitute when narcotics are unavailable. Police and paramedics are often useful sources of patient history information. It should be determined whether the overdose was intentional or accidental.
EXAMINATION A full set of vital signs should be obtained, including core temperature, heart rate, blood pressure, respiratory rate, and continuous pulse oximetry results. Vital signs should be measured at frequent intervals. The patient should be completely undressed, and the skin should be inspected for “tracks” or sites of injection, including the web spaces of the hands and feet, the popliteal area behind the knees, and the axilla. The pupils should be pinpoint; if dilated, the examiner should suspect co-ingestion or CNS hypoxia. The heart should be examined carefully for murmurs. The lungs should be auscultated for rales and wheezes. The abdomen should be examined for organomegaly and the presence or absence of bowel sounds. A full neurological examination should be completed. The extremities should be examined for evidence of septic emboli ore abscesses. The bones and joints should be evaluated for signs of septic arthritis and osteomyelitis, and any signs of occult trauma should be noted. The pregnancy status of female patients of childbearing age should always be determined; there is a high incidence of toxemia and premature delivery in females who abuse drugs. If this is an emergent delivery of a child born to a drug-using mother, the healthcare provider should be prepared for respiratory depression, arrest, or neonatal withdrawal.
LABORATORY FINDINGS A CBC, electrolyte panel, BUN and creatinine measurement, liver function tests, hepatitis panel, assessment of amylase and lipase, blood cultures, urinalysis, and urine cultures should be performed. A urine drug screening and ethanol samples should be collected. The clinician should discuss HIV status with and offer HIV testing to the patient. An ECG and chest radiograph should be obtained, as well.
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RADIOLOGY Chest radiography should be performed to rule out infection or aspiration.
DIAGNOSIS The diagnosis of opioid poisoning is made on the basis of history, clinical presentation, physical examination, and positive drug screening results. However, a negative drug screen result does not rule out methadone toxicity.
TREATMENT Patients with acute opioid intoxication should be placed on a cardiac monitor, and two large-bore IV lines should be placed. The patient should receive supplemental oxygen. The treatment of an acute opioid intoxication consists of airway and ventilation support and naloxone (0.4–2.0 mg in an adult and 0.01 mg/kg in children), which is a pure opioid antagonist. Naloxone can be give IV, intratracheally, subcutaneous, or IM. In severe cases, it can be given as a continuous infusion at a rate of 0.4 mg/hr. The half-life of naloxone is 1 hour with duration of 2–3 hours. Frequent redosing may be necessary, and patients should be closely monitored. In addition, unconscious or comatose patients should receive glucose and thiamine. Naloxone may precipitate opioid withdrawal; the classic picture of opioid withdrawal is one of lacrimation, piloerection, rhinorrhea, yawning, abdominal cramping, myalgias, nausea, vomiting, and diarrhea.
DISPOSITION All patients with opioid toxicity should be observed in the ED or an appropriate observation unit for 8–12 hours. Patients with noncardiogenic pulmonary edema should be admitted to an ICU. Patients with methadone toxicity should be admitted to an intermediate-level floor for at least 36 hours due to the prolonged half-life of the drug. All patients should be offered drug and alcohol counseling. Patients who have intentionally overdosed must undergo a psychiatric evaluation before discharge.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998.
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Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli J (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2005. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2003;22(5):335–404.
Organophosphorus and Carbamate Insecticides Poisoning MICHAEL A. MILLER
ICD Codes: Organophosphate, carbamate herbicide, and insecticide poisoning 989.3
Key Points Insecticides are widely available and heavily used worldwide. These agents can be absorbed via inhalation, ingestion, and, to some extent, the skin. ! Emergency Actions ! Profound dehydration may occur due to excessive diarrhea, vomiting, and sweating; thus aggressive circulatory support in the form of IV fluids may be necessary for patients with organophosphorus or carbamate insecticide poisoning.
DEFINITION Organophosphorus compounds and carbamates are common chemicals used across the world primarily as insecticides. Their toxicity results from their ability to inhibit the acetylcholinesterase enzyme leading to a cholinergic toxidrome.
EPIDEMIOLOGY Some of the chemical warfare agents known as nerve agents are potent cholinesterase inhibitors. Tabun, sarin, and soman are examples of such agents. Severe poisoning with these agents is relatively infrequent within
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the United States and is much more common in developing and agrarian nations such as Sri Lanka.
PATHOLOGY Due to their efficacy as insecticides, these agents are widely available and heavily used worldwide. These agents can be absorbed via inhalation, ingestion, and, to some extent, the skin. Once absorbed, the agents bind to the acetylcholinesterase enzyme, leading to accumulation of acetylcholine in the CNS and at muscarinic (cholinergic effector cells) and nicotinic receptors (skeletal neuromuscular junctions and autonomic ganglia). This accumulation of acetylcholine accounts for the prominent clinical symptoms seen in poisoning with these agents: diarrhea, vomiting, bronchorrhea, trouble breathing, muscle fasciculations, bronchospasm, and sweating. Organophosphorus agents “age.” This is the formation of a permanent bond between the agent and the cholinesterase enzyme. The use of pralidoxime is aimed at reactivating the cholinesterase enzyme and preventing the permanent aging process. Carbamates do not undergo this process.
CLINICAL PRESENTATION After exposure to the agent, which usually occurs in an agricultural setting or during a suicide attempt, a patient will experience symptoms within 1–2 hours, but occasional delays of up to 8 hours may occur with certain agents that require metabolism before causing symptoms. Symptoms may occur within minutes in cases of very large exposures or intentional ingestions. Muscarinic symptoms are prominent in large exposures. These symptoms include vomiting, diarrhea, abdominal cramping, bronchorrhea, and sweating. Common nicotinic symptoms are muscle fasciculations and weakness. This muscle weakness includes paralysis of the respiratory muscles and may contribute to profound respiratory failure. CNS symptoms include seizures and coma. Various mnemonics have been used to describe cholinesterase inhibitor poisoning clinical presentations. SLUDGe is a very common mnemonic and describes the salivation, lacrimation, urination, defecation, an GI disturbance found in patients poisoned by these agents.
DIAGNOSIS The diagnosis of organophosphorus or carbamate insecticide poisoning should be easily made given a reasonable suspicion, exposure history, and the clinical toxidrome.
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LABORATORY FINDINGS Laboratory evidence of organophosphorous agent poisoning can be obtained by measuring plasma pseudocholinesterase and red blood cell cholinesterase activities, which will be depressed in the setting of large exposures to organophosphorous agents due to the aging process. Other laboratory tests should be performed as needed for clinical management.
TREATMENT These agents have a multiplicity of effects on airway and breathing due to their ability to cause bronchospasm, bronchorrhea, and muscle weakness, and careful attention must be paid to airway and breathing. Additionally, profound dehydration may occur due to excessive diarrhea, vomiting, and sweating; thus, aggressive circulatory support may be necessary in the form of IV fluids. Before treatment, all healthcare workers must ensure that the patient has been externally decontaminated. Providers should also take care when handling body fluids from these patients because these may also cause significant toxicity. After ensuring provider safety, internal decontamination with activated charcoal and consideration of gastric content aspiration via a nasogastric tube for patients presenting within 1–2 hours of ingestion should be considered. Seizures should be treated aggressively with benzodiazepines such as diazepam or lorazepam.
ANTIDOTAL THERAPY Beyond supportive therapy, the use of specific antidotal therapy is vital. This therapy comprises the following actions: 1. Give 1–2 mg of atropine IV initially for patients with significant symptoms. The dose may need to be frequently repeated or escalated and should be titrated to effect as needed. Wheezing and bronchorrhea are the most important clinical effects to treat with atropine. 2. Pralidoxime should be given as soon as possible to reverse muscle weakness and fasciculations. Initial IV bolus of 1–2 g should be given over 10 minutes. This can be followed by an infusion of 250–500 mg/hr for at least 24 hours in clinically ill patients.
Bibliography Eddleston M, Szinicz L, Eyer P, Buckley N: Oximes in acute organophosphorus pesticide poisoning: A systematic review of clinical trials, Q J Med 2002;95(5):275–283. Johnson MK, Jacoben D, Meredith TJ, et al: Evaluation of antidotes for poisoning by organophosphorus pesticides, Emerg Med 2000;12:22–37. Miller MA: Organophosphorus and carbamate insecticides. In Olson KB (ed): Poisoning and Drug Overdose, ed 4. McGraw-Hill: New York, 2004, pp 291–295.
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Phenytoin MOHAMUD DAYA AND YOKO NAKAMURA
ICD Code: Phenytoin poisoning 966.1
Key Points Phenytoin is a type IB antiarrhythmic agent that decreases sinoatrial and ventricular automaticity, increases atrioventricular conduction, and prolongs the effective refractory period. Acute and chronic phenytoin toxicity usually presents with CNS features that progress along a continuum. ! Emergency Actions ! Good supportive care with attention to airway, breathing, and circulation composes the initial treatment of any patient with acute or chronic phenytoin toxicity.
DEFINITION Phenytoin (diphenylhydantoin; Dilantin) is a nonsedating anticonvulsant agent that is effective against generalized tonic-clonic and partial complex seizures. It has also been used as an antidysrhythmic drug. Oral preparations contain either phenytoin acid or phenytoin sodium in promptrelease, extended-release, or suspension formulations. Phenytoin sodium is poorly soluble in water and is available as a parenteral preparation containing 50 mg/ml formulated in 40% propylene glycol and 10% ethanol with the pH adjusted to 12 to maintain stability. Fosphenytoin is an expensive water-soluble phosphate ester prodrug derivative of phenytoin that is also available for parenteral use. Fosphenytoin solutions are freely soluble in water, do not contain propylene glycol, and have an adjusted pH of 6–9.
EPIDEMIOLOGY In 2003, the American Association of Poison Control Centers Toxic Exposure Surveillance System reported 4145 exposures involving phenytoin, of which 2756 were treated at healthcare facilities. Life-threatening effects were reported in 98 exposures, and 10 cases resulted in death.
PATHOPHYSIOLOGY Phenytoin’s mechanism of action involves the suppression of highfrequency firing in neuronal cells by reducing the ability of sodium channels to recover from inactivation. At higher doses, additional mechanisms
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of action, including inhibition of calcium flux and potentiation of GABA, appear to have a role. Phenytoin is also a type IB antiarrhythmic agent that decreases sinoatrial and ventricular automaticity, increases atrioventricular conduction, and prolongs the effective refractory period.
PHARMACOKINETICS The absorption of phenytoin is variable and dependent on the oral formulation. Peak serum levels are attained in 1–3 hours with prompt-release preparations and in 4–12 hours with extended-release preparations. As a result of bioavailability differences, drug interchanges have been associated with therapeutic failure and toxicity. The time to maximal concentration is prolonged after an overdose. Phenytoin is distributed widely and is highly protein bound (90%), mainly to albumin. The apparent volume of distribution ranges from 0.5 to 0.8 L/kg in adults. Since only the free fraction is pharmacologically active, anything that alters plasma protein binding or decreases plasma protein concentration can precipitate toxicity. Plasma protein binding is decreased in overdose, uremia, liver disease and malnourishment, and by displacement from other drugs. Pharmacokinetic parameters for fosphenytoin are similar to those of parenteral phenytoin. Fosphenytoin is rapidly converted to phenytoin by phosphatases found in many tissues, primarily the liver and red blood cells. The conversion half-life to phenytoin is 8–15 minutes. Phenytoin is metabolized in the liver by the CYP enzyme system to inactive metabolites. Phenytoin metabolism follows saturation kinetics. At low serum concentrations (0–10 mg/L), metabolism follows first-order kinetics, and a fixed percentage of drug is metabolized in a given time period. At higher concentrations, metabolic pathways become saturated, leading to zero-order kinetics where a fixed amount of drug is metabolized for a given unit of time. As a result, linear increases in dosage lead to disproportional increases in serum concentration. There is considerable individual variability in metabolism due to genetic and ethnic polymorphisms. Reported therapeutic serum half-lives range from 7 to 42 hours.
CLINICAL PRESENTATION Toxicity from phenytoin can occur from oral ingestion, either acute or chronic, and with parenteral administration. Acute and chronic phenytoin toxicity usually presents with CNS features that progress along a continuum. At low serum concentrations (20–30 mg/L), ocular and vestibulocerebellar abnormalities such as horizontal nystagmus and ataxia predominate. With levels above 40 mg/L, mental status abnormalities such as lethargy, confusion, disorientation, and coma are encountered. Several studies have also documented “paradoxical seizures” with phenytoin toxicity. Movement disorders, including choreoathetosis, ballismus, dystonia, and asterixis, are also described. Psychiatric symptoms more commonly seen in
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chronic intoxication include confusion, depression, and visual, tactile, and auditory hallucinations. Significant cardiotoxicity has not been reported from acute or chronic phenytoin toxicity. Long-term phenytoin therapy is associated with gingival hyperplasia, peripheral neuropathy, facial coarsening, endocrine abnormalities, and megaloblastic anemia. Hematological and hypersensitivity skin reactions have also been reported with phenytoin toxicity. IVadministration of phenytoin has been associated with apnea, hypotension, and serious and occasionally fatal dysrhythmias, including highdegree atrioventricular block. The responsible factor is believed to be the propylene glycol diluent. Elderly persons and those with compromised cardiac function are more susceptible to these adverse effects, which can be avoided by slowing the infusion rate to below 30 mg/min. Extravasation of IV phenytoin has been associated with skin necrosis. IM injection is also not recommended due to risk of tissue injury. IVas well as IM injections of fosphenytoin are free of local tissue corrosive effects.
DIAGNOSIS Diagnosis of phenytoin toxicity is based on clinical features and measurement of total serum phenytoin levels. Precipitating factors such as accidental or intentional overdose, change in dose or formulation, drug-drug interactions, and other underlying conditions (e.g., uremia, liver disease, hypoalbuminemia) should be searched for in all cases.
LABORATORY STUDIES Initially, a CBC and metabolic panel (including liver enzymes and albumin) should be performed and total serum phenytoin should be measured. A baseline 12-lead ECG should be obtained. Other tests should be obtained as needed for suspected co-ingestions. The therapeutic total phenytoin level is 10–20 mg/L. Toxicity has also been described in patients with therapeutic total phenytoin concentrations but elevated free phenytoin concentrations. Free phenytoin concentrations can be measured or calculated if the clinical picture suggests toxicity but does not correlate with total phenytoin concentrations. The normal range for free phenytoin levels is 1–2 mg/L. An albumin corrected total phenytoin level can also be calculated using the following formula: corrected phenytoin ¼ measured phenytoin=½ðalbumin 0:25Þ þ 0:1Þ
TREATMENT Good supportive care with attention to airway, breathing, and circulation composes the initial treatment of any patient with acute or chronic
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phenytoin toxicity. If concurrent opioid intoxication is suspected, naloxone (0.4–2 mg) can be administered IV. Hypoglycemia should be ruled out by rapid bedside glucose determination. Ataxia is common, and patients should be confined to bed or allowed up only with assistance to prevent falls and secondary trauma. GI decontamination with activated charcoal (1 g/kg) is effective even hours after ingestion due to the slow and prolonged absorption. Multiple doses (30–60 g every 4 hr) of activated charcoal increase phenytoin clearance. The potential risks of ileus and pulmonary aspiration should be weighed against the expected benefits when considering multiple-dose activated charcoal. Seizures can be treated with benzodiazepines. There is no proven role for extracorporeal drug removal in the therapy for phenytoin toxicity, and there are no specific antidotes for phenytoin toxicity. Due to slow and delayed absorption, patients should be observed and have serial levels monitored for at least 6–8 hours after an acute overdose. Patients with mildly symptomatic acute and chronic intoxications can be discharged home as long as there is no concern about rising plasma concentrations and after an appropriate psychiatric assessment has been performed. Chronic intoxications require dose adjustments as well as correction of precipitating factors. Patients with significant ataxia, seizures, and CNS depression should be admitted to the hospital. Admission to an ICU may be required for close observation and safety, although cardiac monitoring is not necessary. Slowing or stopping the infusion treats cardiovascular toxicity resulting from propylene glycol during IV phenytoin administration. Symptomatic bradycardia may be treated with atropine sulfate (0.5–2.0 mg) and hypotension with crystalloid infusion. If the hypotension is unresponsive to crystalloid infusion, vasopressors such as dopamine or norepinephrine should be added.
Bibliography Doyon S: Anticonvulsants. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Toxicological Emergencies, ed 7. McGraw-Hill: New York, 2002, pp 614–630. Larsen JL, Larsen LS: Clinical features and management of poisoning due to phenytoin, Med Toxicol Adverse Drug Exp 1989;4:229–245. Mauro LS, Mauro VF, Brown DL, Somani P: Enhancement of phenytoin elimination by multiple-dose activated charcoal, Ann Emerg Med 1987;16:1132–1135. Murphy JM, Motiwala R, Devinsky O: Phenytoin intoxication, South Med J 1991;84: 1199–1204. Wyte CD, Berk WA: Severe oral phenytoin overdose does not cause cardiovascular morbidity, Ann Emerg Med 1991;20:508–512.
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Salicylates MARK STEVENS
ICD Codes: Aspirin and salicylate poisoning 965.1
Key Points Salicylate toxicity can result in severe morbidity and mortality. This section provides evidence-based guidelines that will aid clinicians through the recognition, evaluation, and management of patients presenting with salicylate poisoning.There is no specific antidote for salicylate poisoning. ! Emergency Actions ! There are three main steps in caring for the patient with salicylate poisoning: preventing further absorption, assessing the severity of poisoning, and when appropriate, increasing elimination.
DEFINITION The widespread availability of ASA is found in over 200 over-the-counter medications and prescription drugs. Fiorinal, Percodan, and Darvon all contain ASA. Methyl salicylate is found in oil wintergreen, and sodium salicylate is used as a ketolytic agent. ASA is also found in over-the-counter medications such as Excedrin, Pepto-Bismol, Bayer Decongestant, Dristan, and Sine-Off. The ease with which incremental chronic dosing can cause toxicity makes salicylism a common and sometimes fatal occurrence.
EPIDEMIOLOGY There are three distinct patterns in persons who become poisoned with a salicylate. The first group typically includes the young adult who intentionally overdoses on salicylate products. The second group includes the chronic unintentional overdose by the elderly patients who use large doses of salicylate-containing products and home remedies. The final group represents the accidental poisoning within the pediatric population. Fifty percent of suicide attempts involve ingestion of ASA. Acute salicylate poisoning is associated with a mortality rate of 1% and a morbidity rate of 16%. In chronic salicylate overdose in elderly persons, there is a 25% mortality rate and a 30% morbidity rate. The diagnosis of salicylate poisoning is often missed at the time of admission in an elderly patient and
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should be considered in any patient with unexplained nonfocal neurological and behavioral abnormalities, especially with coexisting acid-base changes. ASA poisoning is the most common poisoning in children younger than 5 years of age. Children younger than 4 years tend to experience metabolic acidosis (pH <7.38), whereas children older than 4 years usually have mixed acid-base disturbances similar to adults.
PATHOLOGY After oral ingestion of salicylic acid, it is rapidly absorbed in the GI tract (primarily the small bowel) in 60 minutes, with peak blood levels in 4–6 hours. After salicylates are absorbed, they are rapidly hydrolyzed to free salicylic acid, which is then protein-bound to albumin. When the albumin-binding sites are saturated, the unbound fraction of salicylate increases. This unbound salicylate in the plasma then enters the body cells. Once all albumin-binding sites are saturated, any increase in salicylate dose increases the levels of unbound salicylate, thus causing an uncoupling of oxidative phosphorylation, and an acute metabolic acidosis occurs. With the inhibition of ATP-dependent reactions, catabolism occurs resulting in the following: 1. 2. 3. 4. 5.
Increased oxygen consumption Increased carbon dioxide production Depletion of hepatic glycogen Increased activity of the glycolytic and lipolytic pathways Hyperpyrexia
At low doses, salicylates are eliminated by first-order kinetics. In higher doses, salicylates are eliminated by zero-order kinetics. The salicylate half-life ranges from 15 to 30 hours in large doses, where concretions can occur. Salicylic acid has a blood pH of 7.4. The level of pH is very important in ASA poisoning. A drop in pH from 7.4 to 7.2 will double the amount of un-ionized ASA that is able to diffuse out of the plasma. Commercial products can have variable rates of absorption as a result of their co-compounds or their enteric coating. If the ASA product is entericcoated, the absorption rate can be as long as 6–12 hours, with complete absorption taking up to 24 hours. Acute salicylate poisoning causes an increase in oxygen consumption. However, in very high doses, it causes decreased oxygen consumption. Very high doses of ASA will cause respiratory depression. ASA also inhibits the synthesis of prostaglandins, which stimulate platelet aggregation and vasoconstriction. A large ingestion of ASA will cause an increased mobilization of inhibitor of glycogen stores and thus hyperglycemia. A salicylate is also a potent inhibitor of gluconeogenesis; thus, an acute ingestion can cause normoglycemia hypoglycemia, or hyperglycemia. Children usually experience
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hypoglycemia. Nephrotoxicity with interstitial nephritis and acute tubular necrosis has been associated with prolonged large doses of ASA.
CLINICAL PRESENTATION A patient with salicylate poisoning presents with a mixed anion gap metabolic acidosis and respiratory alkalosis. A patient will present with acute gastric upset, vomiting, fever, and possibly GI tract bleeding. Renal failure and rhabdomyolysis are rarely reported consequences of an acute poisoning. CNS symptoms consist of lethargy, convulsions, respiratory arrest, coma, and brain death. The decreased production of ATP causes uncoupling of oxidative phosphorylation, acute brain failure, and cerebral edema. Often patients will present with altered mental status as if they have bacterial meningitis. This mental status change is the result of the low glucose concentrations in the cerebrospinal fluid. The glucose levels in the cerebrospinal fluid are often much lower than serum glucose levels; thus, serum glucose levels are a poor determination of actual glucose levels in the brain. Pulmonary symptoms include noncardiogenic pulmonary edema or ARDS. Respiratory complications are more common in adults than in children. Cardiac effects of an acute ASA poisoning include arrhythmias, ventricular premature beats, ventricular fibrillation, and ventricular tachycardia. Cardiac toxicity results from the impairment of ATP production, electrolyte abnormalities, acidosis, and hyperthermia. Unconsciousness, fever, severe acidosis, seizures, and dysrhythmias are all associated with an increased mortality rate.
EXAMINATION All patients should be given a complete examination, including a check of cranial nerves I–XII, vital signs to include a core temperature, and a rectal examination to rule out an acute GI tract bleeding. Patients should be monitored for findings consistent with multiorgan system dysfunction (e.g., Kussmaul’s breathing, oliguria, purpura). The patient’s volume status and cardiopulmonary and neurological status should be evaluated at least every hour until the patient’s condition is fully stabilized.
LABORATORY FINDINGS A CBC, an ABG analysis (metabolic acidosis), and measurements of PT, PTT, electrolytes, BUN, creatinine, serum calcium level, salicylate, and acetaminophen levels (co-ingestions) should be drawn and followed up as clinically indicated. A urinalysis and urine pH should always be performed as well.
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If the first salicylate level is in the normal or safe range, a second level should be drawn in 2 hours. If the second level is greater than the first level, then serial levels should be drawn every hour until the levels are decreasing instead of increasing and the patient’s clinical status stabilizes. A simple test for salicylate overdose is the ferric chloride test. A few drops of 10% ferric chloride solution should be added to a sample of the patient’s urine. If salicylic acid is present in the urine, a violet-to-purple color develops. Reagent sticks (Phenistix) can also react to salicylate acid by turning brown to purple.
DIAGNOSIS A diagnosis of salicylate toxicity is made based on the basis of history of chronic or acute ingestion of ASA products, physical examination, and presenting symptoms. An acute aspirin ingestion of less than 150 mg/kg will generally induce no toxicity to a mild case. An acute ingestion of 150–300 mg/kg will produce mild to moderate toxicity. Symptoms associated with mild to moderate toxicity include vomiting, diaphoresis, tinnitus, and mild acid-base changes. Any acute ingestion greater than 300 mg/ kg is associated with a severe toxicity. A dose over 500 mg/kg is considered lethal. Although widely taught, the Done nomogram typically is misunderstood and often is misused. It can be used only for a single acute ingestion. It cannot be used for chronic ingestion, enteric-coated aspirin ingestion, or if a second dose of ASA has been taken within the previous 24 hours. It is strongly recommended that the patient’s clinical condition and early course, rather than the nomogram, guide clinical decisions. The differential diagnosis of salicylate toxicity includes theophylline toxicity, caffeine overdose, acute iron poisoning, Reye’s syndrome, diabetic ketoacidosis, sepsis, and meningitis.
RADIOGRAPHS Chest and abdominal radiographs, along with a baseline ECG, should be performed. Chest radiographs should be repeated and monitored for any findings of acute pulmonary edema. Risk factors for poor prognosis include the following:
Delayed presentation Unrecognized intoxication Serum salicylate level higher than 70 mg/dl Older age Pulmonary edema Hyperpyrexia Acidemia Coma
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TREATMENT The top emergency care priorities for patients with salicylate toxicity continue to be airway, breathing, and circulation. Any patient with a suspected salicylate overdose should have two large-gauge IV lines initiated and normal saline administered, and they should be given 2 L of oxygen via nasal cannula. Continuous cardiac monitoring with pulse oximetry should be initiated, and baseline laboratory tests, including an ABG analysis, should be obtained. GI tract decontamination can be lifesaving. Gastric lavage should be considered for any patient presenting within 1 hour of an acute ingestion. The patient’s airway should always be protected during lavage. The clinician should administer 1–2 g/kg of activated charcoal to patients who have ingested potentially toxic amounts of salicylate. In contrast, no convincing data support the use of repeated or multiple doses of activated charcoal. Evidence supports the use of whole-bowel irrigation as a more effective means of GI tract decontamination when dealing with entericcoated or sustained-release ASA in the GI tract. A cathartic agent such as sorbitol should be given as a single dose with the first dose of activated charcoal to decrease the risk of obstruction. Most patients who have acutely ingested salicylates are dehydrated. They will usually need several liters of IV normal saline to correct dehydration. Urine output should be targeted at 1–2 ml/kg/hr. Forced diuresis should be avoided due to the potential development of pulmonary edema, which is a major cause of mortality. Concurrent to the primary IV infusion of normal saline, an IV bolus of sodium bicarbonate (1–2 mEq/kg) should be administered, followed by a continuous IV infusion of 1 L of D5W, to which 3 ampules (either 44 or 50 mEq/ampule) of sodium bicarbonate have been added, starting at 1.5–2.0 times the normal maintenance rate and then adjusted to maintain the urine pH above 7.5. Even a small decrease in pH will cause a greater concentration in un-ionized salicylate. ABGs and serum electrolytes should be closely monitored. Arterial pH higher than 7.5, hypokalemia, and hyponatremia should be avoided. The administration of sodium bicarbonate should be stopped when the serum salicylate level is lower than 35 mg/dl. Potassium (40 mEq/L) should be supplemented in the normal saline infusion (may require central line placement) after adequate urine output has been established for significant hypokalemia. A very large dose of bicarbonate and potassium may be needed to alkalinize the urine. Salicylate can be effectively removed from the body by either peritoneal or hemodialysis. Any patient with continued mental deterioration despite supportive care should undergo immediate dialysis for treatment of cerebral edema. Hemodialysis is preferred because it allows concomitant treatment of fluid and electrolyte derangements.
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Hemodialysis should be considered in a patient with any of the following: 1. 2. 3. 4. 5. 6.
A deteriorating condition despite alkaline urine and diuresis Severe acid-base disturbances Acute renal insufficiency/acute renal failure Cardiac toxicity Altered mental status ARDS and salicylate levels that are not dropping
If peritoneal dialysis is performed, 5% albumin should be placed in the peritoneal solution to enhance salicylate clearance through protein binding. Peritoneal dialysis is not as effective as hemodialysis. Hemorrhagic complications are seen rarely in single massive salicylate overdoses. Patients with clinically significant bleeding should be treated with fresh frozen plasma, since the administration of large doses of vitamin K has been proved to be ineffective. Seizure precautions and anticonvulsant therapy should be initiated as needed. The clinician should consider discharging a patient home after adequate GI tract decontamination if there is progressive clinical improvement, no significant acid-base disturbance, and a documented serial decline in serum salicylate levels toward the therapeutic range. All patients with altered mental status, salicylate levels in the mild or greater range, or GI tract bleeding or patients who are in metabolic acidosis or respiratory alkalosis should be admitted to the ICU. In addition, a psychiatric evaluation should be carried out if suicide attempt is suspected. All infants with salicylate toxicity should be admitted to the hospital.
Bibliography Dargan PI, Wallace CJ, Jones AL: An evidence based flow chart to guide the management of acute salicylate (aspirin) overdose, Emerg Med J 2002;19:206–209. Available at: http://emj.bmjjournals.com/cgi/content/full/19/3/206. Accessed April 29, 2005. Greene SL, Jones PI, Jones AL: Acute poisoning: Understanding 90% of cases in a nutshell, Postgrad Med J 2005;81:204–216. Available at: http://pmj.bmjjournals.com/cgi/ contentfull/81/954/204. Accessed April 29, 2005. Kreplick LW: Toxicity, salicylate, Medicine: Instant Access to the Minds of Medicine. Available at: http://www.emedicine.com/EMERG/topic514.htm. Accessed April 29, 2005. Kruse JA, Fink MP, Carlson RW: Saunders Manual of Critical Care. WB Saunders: Philadelphia, 2003. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Theophylline CHRISTOPHER M. KREBS AND ROY JOHNSON III
ICD Code: Theophylline poisoning 974.1
Key Points Theophylline is used primarily in treatment of chronic obstructive pulmonary disease and acts on the respiratory, cardiovascular, nervous, and GI systems. Theophylline overdose typically occurs unintentionally and is more common in adults than children. Overdose should be suspected more in patients with underlying cardiac, liver, or pulmonary disease because these patients are less able to metabolize theophylline. Presentation may include tachycardia, arrhythmia, headache, dizziness, agitation, restlessness, nausea,vomiting, and seizure. ! Emergency Actions ! Airway and breathing should be secured. Cardiovascular status should be checked and any potential for dysrhythmias noted. A “safety net” should be ensured, including two large-bore IV lines, supplemental oxygen, monitors, and ECG. Normal saline should be used for IV fluid rehydration if the patient is hypotensive. In cases of altered mental status, naloxone, thiamine, and D50W should be administered (or blood glucose should be checked immediately). If supraventricular tachyarrhythmia is present, rate control can be obtained with beta blockers or CCBs. It should be noted that theophylline is refractory to treatment with adenosine. If patient have seizures, they should be treated with benzodiazepines.
DEFINITION Theophylline is a methylxanthine related to caffeine. It is a b-adrenergic agonist and exerts its effect through inhibition of phosphodiesterase and induction of catecholamine release. It is used for the treatment of symptoms of reversible airway obstruction secondary to chronic obstructive pulmonary disease, asthma, or chronic bronchitis. Theophylline may be administered orally or IV. It comes in tablet, capsule, oral, and IV solutions. Tablets allow for immediate, timed, extended, or sustained release. Dosing is variable, dependent on patient age and cardiac, respiratory, and liver function. Theophylline has a narrow therapeutic window, with a therapeutic plasma level of 10–15 mg/L and toxicity beginning at 15–20 mg/L. Mild
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toxicity manifests in roughly 30% of patients at concentrations of 15 mg/L. At 25 mg/L, approximately 75%–80% of patients will demonstrate adverse effects, with major toxicity (e.g., seizure, arrhythmia) in about 25%. Bioavailability and half-life of the methylxanthines, including theophylline, are highly variable, and it should be noted that deaths have been reported at levels as low as 20 mg/L. Theophylline is metabolized by the hepatic CYP 450 system, primarily the CYP1A2 isozyme. Factors that enhance theophylline clearance include cigarette smoking, carbamazepine, phenobarbital, phenytoin, primidone, and rifampin. Medications that inhibit clearance include ethanol, ciprofloxacin, erythromycin, verapamil, propranolol, ticlopidine, tacrine, allopurinol, and cimetidine. Additionally, patients with underlying congestive heart failure, liver failure, or pulmonary disease may have decreased clearance of theophylline.
EPIDEMIOLOGY There were 861 reported cases of theophylline exposure in 2003 in the United States, with about 75% of cases in adults older than 19 years old. The majority of cases (about two thirds) were unintentional, and one half of patients required treatment in a healthcare facility. Outcomes included 41 major events and 10 deaths. Of the deaths, five were attributed to therapeutic error, four to suicide, and one to adverse reaction. The lowest plasma theophylline level measured in any of the 10 deaths was 32 mg/ L, except for one case of suicide in which the patient had a theophylline level of 29 mg/L in addition to an acetaminophen level of 69 mg/liter and ingested other unknown substances as well.
CLINICAL PRESENTATION Symptoms of theophylline intoxication are similar to those found with other methylxanthines and include symptoms primarily related to the cardiac, nervous, and GI systems. At low levels (15–25 mg/L), symptoms may include tachycardia, dizziness, restlessness, agitation, tremor, headache, nausea, and abdominal pain. As the level further increases (25–35 mg/L), patients may have vomiting, seizures, arrhythmias, or death.
EXAMINATION Cardiovascular System As a cardiac stimulant, theophylline causes sinus tachycardia almost universally. In toxic doses, dysrhythmias may occur, including supraventricular tachycardia, atrial fibrillation, atrial flutter, multifocal atrial
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tachycardia, ventricular tachycardia, and ventricular fibrillation. Dysrhythmias are more likely in patients who have preexisting cardiac disease and in cases of chronic overdose. In addition to rhythm disturbances, theophylline may also cause hypotension through beta-2 stimulation. Hypotension is more common in acute than chronic overdoses.
Gastrointestinal System In theophylline overdose, nausea and vomiting are common. Emesis is more common in acute cases of overdose and can be very difficult to control even with potent antiemetics. Nausea and vomiting are also prolonged in cases of overdose with sustained-release preparations.
Central Nervous System Theophylline acts as a stimulant, and at low levels patients may demonstrate elevated mood, activity, and alertness. However, at toxic levels, irritability, insomnia, and agitation predominate. Seizures may occur as well and occur more commonly and at lower serum levels in cases of chronic overdose. Seizures are also more common in patients at the extremes of age.
Respiratory System Methylxanthine overdose may result in hyperventilation, respiratory alkalosis, and respiratory arrest.
LABORATORY FINDINGS Pertinent laboratory values include theophylline level, electrolytes, ABG, renal function panel, liver function test results, and results of tests for additional toxins.
Theophylline Serum levels should be tested as soon as overdose is suspected, and follow-up values should be obtained every 2–3 hours to ensure decreasing values. Increasing or stable values indicate higher potential for a poor patient outcome.
Hypokalemia Transient hypokalemia occurs as potassium shifts into cells due to stimulation of sodium/potassium ATPase. Vomiting and renal losses may also cause an actual loss of total body potassium. Care should be taken to avoid hyperkalemia resulting from aggressive repletion of potassium.
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Hyperglycemia Serum glucose levels are often elevated in acute theophylline overdose, typically to approximately 200 mg/dl.
Mixed Acid-Base Disturbance Metabolic acidosis and respiratory alkalosis are common in theophylline overdose. Rhabdomyolysis, which may occur as a result of seizure, can contribute to acidosis and also to decreased renal function.
Liver Function Liver enzyme test results may be useful in assessing a patient’s ability to clear theophylline.
Toxins Patients who have intentionally overdosed on theophylline may have taken additional toxins as well. Urinalysis or other tests to evaluate for these medications can be useful and should be ordered as soon as this possibility is suspected.
DIAGNOSIS The diagnosis of theophylline overdose is based on history and examination as listed previously and confirmed with a measurement of the serum theophylline level.
RADIOGRAPHS Radiographs of the kidneys, ureters, and bladder may reveal undissolved tablets or pharmacobezoars.
TREATMENT The treatment of theophylline overdose is focused on stabilization of the patient’s condition. Emphasis is placed on cardiac and respiratory stabilization and treatment of seizures, as well as maintenance of physiological acid–base status. The ABCs of emergency care (i.e., airway, breathing, and circulation) apply first and foremost. A standard safety
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net, with large-bore IV access (preferably administering normal saline), supplemental oxygen, and monitors, should be initiated. Vital signs should be monitored carefully and an ECG obtained to evaluate for cardiac dysrhythmia. In cases of supraventricular tachyarrhythmia, the initial goal of treatment should be rate control through beta blockers or CCBs, if necessary. Adenosine is generally ineffective in the treatment of theophylline overdose due to theophylline’s antagonism at adenosine receptors. Ventricular dysrhythmias may be treated with lidocaine, cardioversion, or defibrillation. Continued monitoring is important after electrical reversal of dysrhythmia because these dysrhythmias may recur until the serum concentration of theophylline falls below a toxic level. Hypotension should initially be treated with an IV fluid bolus. The fluid of choice is normal saline. In cases refractory to fluids, beta blockers such as propranolol or esmolol may be effective. In the event of seizure, benzodiazepines are the drug class of choice, followed by barbiturates. Phenytoin is contraindicated and has been shown in animal models to decrease the dose of theophylline required to induce cardiac dysrhythmia. Electrolyte disturbances should be treated cautiously. Hypokalemia may occur transiently with theophylline ingestion and typically resolves as the serum theophylline concentration decreases. Beta blockers may be useful in the treatment of hypokalemia but are generally not recommended due to the temporary nature of the condition. Aggressive treatment may result in hyperkalemia. Once the initial life-threatening factors have been treated, decontamination should occur, but this may be complicated by the repeated emesis associated with theophylline overdose. Excessive vomiting should be treated with metoclopramide or ondansetron. Gastric lavage is useful in cases of severe acute overdose presenting within 1 hour of ingestion. Additionally, activated charcoal should be administered in multiple doses until the theophylline level falls below 20 mg/L, and sorbitol should be given with the first dose as a cathartic agent. Whole-bowel irrigation may be performed if sustained-release products were ingested. High levels of theophylline (60–100 mg/L) or rapidly rising levels indicate a need for more expeditious elimination of the toxin through extracorporeal removal (i.e., hemodialysis or hemoperfusion). Patients presenting with theophylline intoxication generally recover well, though death occasionally occurs and many patients require hospitalization. Patients at increased risk for poor outcome include those at the extremes of age and those with significant comorbidities. Patient transfer should be considered early if extracorporeal removal may be required and the facility does not have the capability for hemoperfusion or hemodialysis.
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Patients should be admitted to the hospital if they display any of the following:
Serum theophylline concentration >100 mg/L in acute overdose Serum theophylline concentration >60 mg/L in acute-on-chronic or chronic overdose Rising or stable serum theophylline concentration >30 mg/L by serial measurements Seizure Cardiac dysrhythmia or hypotension refractory to treatment in the ED Imminent threat of self-harm if discharged
Patients should be considered for discharge if they meet the following criteria:
Two consecutive declining serum theophylline concentration measurements taken at least 2 hours apart, with the most recent measurement <30 mg/L Mildly symptomatic or asymptomatic condition without significant comorbidity Serum theophylline level <30 mg/L No evidence of intent to harm self if discharged
Bibliography Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001. Goldfrank LR, Flomenbaum NE, Lewin NA: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Mokhlesi B, Leikin JB, Murray P, Corbridge TC: Adult toxicology in critical care: Part II: Specific poisonings, Chest 2003;123:897–922. Rosen P, Barkin RM, et al: The 5 Minute Emergency Medicine Consult. Lippincott, Williams & Wilkins: Baltimore, MD, 1999. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Watson W, Livovitz T, Rodgers G Jr: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2003;22(5):335–404.
Chapter 18
Care of the Multiple Trauma Patient Trauma Overview JEFF FOXWORTH
DEFINITION Trauma can be defined in the terms of bodily injury severe enough to pose a threat to life or limb. The patient who has suffered injury to multiple systems deserves a level of care that can only be provided by a team of professionals, which includes not only physicians, nurses, and technicians, but also in many modern teaching institutions the expertise of a trauma-trained physician assistant. It is this highly dedicated and skilled group of caring individuals that functions best in the controlled chaos of the trauma/resuscitation rooms of America’s level I trauma centers. Not all trauma patients will require the skills and tools available at a level I trauma center, but the ones in the most critical condition should be transported to these facilities to provide them with the best chance of survival. Modern-day trauma centers are usually found at medical teaching institutions that also have air medical transport capabilities and integrated emergency medical systems that include highly skilled and trained paramedics. These level I centers have all medical and surgical specialties represented 24 hours a day as well as dedicated radiology and operating room personnel in-house.
EPIDEMIOLOGY Approximately 57 million people in the United States alone are traumatically injured every year; of this number, more than 150,000 will succumb to their injuries. Trauma is the leading cause of death in the age range from birth to 44 years. Motor vehicle crashes (MVC), once called motor vehicle accidents (MVAs), account for more deaths than all other causes combined between the ages of 1 to 34. More than 3 million people are injured in MVCs every year, and of these nearly 42,000 die each year. Traumatic brain injury is the number one cause of death in children and young adults. The annual cost of treating traumatically injured patients is well over $244 billion if one accounts for death, disability, lost wages, taxes, medical care, and rehabilitation. In a recent study, 115 people were killed each day in MVCs—that is, one every 13 minutes—and one person died every 94 minutes after being struck by some type of motorized vehicle. 1050
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There is a trimodal distribution of death from trauma. The three modes are defined as follows: (1) Death at the scene, which accounts for half and is mostly caused by severe, irreversible injury to the brain or cardiovascular systems; (2) early death or death occurring within the first few hours caused by major torso or closed head injuries that are treatable at most modern trauma facilities; and (3) late death that is attributed to multiple organ failure in patients who die days to weeks after injury from collapse of multiple internal organ systems, chiefly renal and cardiovascular. Even though these statistics are staggering, traumatic deaths are on the decline in recent years in most parts of the United States. This is due in no small part to the use of helmets by cyclists and more stringent penalties for driving while intoxicated, as well as the enforcement of child safety seat use. However, interpersonal violence has led to a small but notable increase in death from knife and gunshot wounds, mainly in the inner cities among young black and Hispanic males.
PATHOLOGY The vast majority of deaths due to traumatic injury are directly related to the acute and uncontrolled loss of blood and body fluids. This is commonly known as hemorrhagic hypovolemia or simply shock. The term shock has been defined by many in various ways, but for the purposes of this text, shock is the lack of adequate supply of oxygenated blood to the tissues such that those tissues cannot support vital function. Or even more simply, shock is inadequate tissue perfusion. Patients who die from shock not related to volume depletion usually die from cardiovascular or central nervous system collapse.
LABORATORY FINDINGS A patient with a traumatic injury should have the following blood and fluid samples sent as soon as possible: complete blood count (CBC), complete metabolic panel (i.e., sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine, glucose), coagulation studies, including partial thromboplastin time (PTT) and international normalized ratio (INR), and liver function studies, including aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, amylase, lipase, calcium, alkaline phosphatase, total bilirubin, total protein, and troponin I if cardiac involvement is suspected. A 12-lead electrocardiogram (ECG) is also indicated in those patients. A type and screening of blood is mandatory for all patients who present hypotensive or tachycardic or may be suspected of becoming such. It has also been helpful to send a urine sample to screen for the presence of drugs of abuse and alcohol levels in all patients who have been in an MVC. These tests are necessary
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in patients who present with no report of pain or have an altered mental status with little or no identifiable cause.
RADIOGRAPHS Several radiographic studies are indicated in the evaluation of a patient with multiple traumas; however, none should be undertaken until the basics of evaluation and resuscitation have been accomplished. The only immediate radiographic study advocated at most level I trauma centers is the supine chest radiograph because an undiagnosed hemothorax or pneumothorax can be life threatening and is easily and quickly corrected. Up until just a few years ago, most patients who sustained trauma and presented with a positive loss of or alteration in level of consciousness were given the following x-rays: at least three views of the cervical spine, anterior/posterior, lateral and adenoid, anterior/posterior of the chest, and anterior/posterior of the pelvis. These views were sufficient and may still be obtained at centers where high-speed computed tomography (CT) machines are not available. However, due to the ready availability of these devices and the efficiency of the operators, plain radiographs of areas other than the extremities and the chest x-ray mentioned previously are not routinely obtained. A review of the current trauma literature has shown that plain radiographs of the cervical spine may and do miss approximately 50% of cervical spine fractures that were easily found by CT scans. According to some trauma surgeons, 11 separate plain film radiographs were needed to fully evaluate the cervical spine. The use of CT also allows the trauma surgeon or physician assistant to readily evaluate all intracranial as well as intrathoracic, intra-abdominal, and intrapelvic organs that would not be visualized by plain radiographs. Therefore, the standard is moving away from flat plate x-rays to CT. Intra-abdominal ultrasound, also known as focused abdominal sonography for trauma (FAST), has found a place in more and more trauma centers due to its ready availability, ease of use, and noninvasiveness. It should be noted, however, that the use and interpretation of FAST is extremely operator dependent. Angiography and interventional radiology are also being used more often for the evaluation of intra-abdominal and intra-pelvic bleeding, which can be controlled by identification and embolization of the culprit vessels.
CLINICAL PRESENTATION All trauma patients presenting to an emergency department (ED) should have the following established as soon as possible upon arrival if not
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already performed by the prehospital providers: two large-bore (16- or 14gauge) intravenous (IV) access sites by which normal saline or lactated Ringer’s solution is administered, oxygen delivered by non-rebreather mask at 100% or other suitable means to maintain a pulse oximetry of as close to 100% as possible, and cardiac monitoring (ECG) of the 12-lead variety, if available. In obtaining the history of the events that brought the patient to the trauma center, the clinician should never discount the extremely valuable information that can only be provided by the paramedics who transported the patient. These highly dedicated men and women may be the physician’s only source of information related to vehicular damage, scene overview, and initial presenting signs and symptoms as well as any changes en route that the patient may have experienced. The initial response to the patient should begin once the trauma team has been notified of the patient’s pending arrival. This team should be led by the team member with the most experience in dealing with traumatically injured patients. This person should gather the needed resources— nurses and technicians to assist the movement of the patient as well as establishment of the IV lines and drawing of blood samples if needed, placement of the ECG leads, and removal of the patient’s clothing for exposure of injuries. Notification of the blood bank, pharmacy, radiology, and respiratory departments and a call to the anesthesia department if an advanced airway should be needed are all items to be included in the team leader’s first thoughts. Once these resources have been mobilized, the trauma team should be ready to deal with any life-threatening situations.
EXAMINATION Once the patient arrives in the trauma room, the team leader should asses the ABCDEs of the primary survey: 1. A denotes airway. Establish an airway if the patient is not able to maintain his or her own. This may be done by simple jaw-thrust-chin lift, placement of an oral airway, and nasal or endotracheal intubation, if warranted. If these are not available or not accessible, then a cricothyrotomy should be performed. The clinician should remember to always protect the cervical spine as much as possible. 2. B is for breathing. If the patient is breathing on his or her own or if the airway has been secured via an endotracheal tube, the breath sounds should be auscultated on both right and left sides of the chest as well as over the epigastric region. The clinician should inspect for symmetry of chest rise and fall and should place a pulse oximeter probe if not already done. The number per minute and quality of respirations should be noted, and supplemental oxygen or a bag-valve-mask device
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(if the patient is intubated) should be used, as needed. A pulse oximetry reading of greater than 97% should be maintained. 3. C denotes circulation. The clinician should evaluate the carotid, radial, and femoral pulses for strength and regularity. Most trauma texts agree that a strong pulse in each of these locations correlates well with an approximate systolic blood pressure of 60, 70, and 80 mmHg, respectively. If a blood pressure cuff is not readily available or is nonfunctional, it is relatively safe to use the previous numbers as a basic guide. 4. D stands for disability. This is quickly and easily evaluated using the Glasgow Coma Scale (GCS), which is a measurement of the patient’s best response in three areas: eye opening and verbal and motor responses (Table 18-1). Each area is graded and then totaled. A best/normal result is 15. If total is less than 8, intubate! 5. E denotes exposure. The patient should be undressed fully and completely to allow an evaluation of all body areas, including the back. This can be accomplished by “log rolling” the patient, which requires at least three people in addition to the person who will be performing the back examination if the cervical spine is to be properly protected. The patient should be kept warm because even in a warm climate a fully exposed patient will lose body heat rapidly. Once the patient has been fully exposed, the secondary examination can begin, and it is during this time that the old saying “fingers and tubes in every orifice” still holds true. A rectal examination including
Table 18-1 Glasgow Coma Scale for Head Injury Eye Opening Opens eyes spontaneously Opens to command Opens to pain No response Verbal Response Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response Motor Response Obeys commands Localizes pain Withdraws from pain Flexion (decorticate) Extension (decerebrate) No response
4 3 2 1 5 4 3 2 1 6 5 4 3 2 1
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temperature measurement is indicated in all patients with multisystem trauma to check for sphincter tone as well as gross blood. An examination of the external genitalia is also warranted for indications of pelvic hematoma or hematuria, both of which may indicate intrapelvic injury. The clinician should consider placing a Foley catheter if the patient is unable to void on his or her own or if monitoring of urine output is indicated. If the patient is a female of reproductive age and there is a possible or confirmed pregnancy, an obstetrical evaluation is indicated. Placement of a nasogastric or orogastric tube should be done after an evaluation for facial fractures has been conducted. Patients presenting with or suspected of developing hypotension, tachycardia, or other overt signs of shock should receive at least 2 L of normal saline as rapidly as possible for the stabilization of these issues (Table 18-2). If the vital signs do not stabilize or normalize after the administration of this fluid, the recommendation of the Advanced Trauma Life Support (ATLS) guidelines is to administer cross-matched blood, if available. If this is not available, then type O-negative can be used in the meantime. A simple rule to follow when deciding how much crystalloid to administer is that for every 1 ml of blood estimated to have been lost, 3 ml of crystalloid should be infused. Patients with head or spinal cord injuries should not be sedated unless necessary for advanced airway protection to evaluate neurological status or function. In the last several years, many studies have been reported stating that the head-injured patient should not be hyperventilated unless overt signs of herniation are seen; this will be addressed in a separate section. However, it is generally accepted that the head of the bed should be elevated to 30 degrees and blood pressure should be maintained at or slightly above normal to increase cerebral perfusion pressure. An immediate CT scan of the head and spinal cord should be obtained as well as a neurosurgical consultation.
Table 18-2 Transfusion Information COMPONENT RBC FFP Platelets
INDICATION Blood loss >15% Blood loss >50% or INR >1.6 Count <50,000
Cryoprecipitate Fibrinogen <100 mg/dl
DOSE
VOLUME
OUTCOME
1 unit 10–15 ml/kg or 1 unit/20 kg 6 pack
350 ml 200 ml
Increase 1 g/3% Decrease in INR
300 ml
10 units
125 ml
Increase 30,000– 50,000/dose 100 mg/dl increase in fibrinogen
RBC, Red blood cells; FFP, fresh frozen plasma; INR, international normalized ratio.
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Patients with multiple long bone fractures should have splints placed as soon as possible after the secondary survey is complete. A timely orthopedic consultation is also warranted in these patients. One of the most challenging and dangerous patients in any ED is one who is intoxicated either by alcohol or mind-altering drugs, which may be prescription as well as nonprescription. These patients require large amounts of time and resources devoted to them as well as constant reevaluation. As mentioned previously, a urine drug screening should be performed to ascertain the type of substance ingested. An intoxicated patient cannot be discharged from the ED until he or she is sober and has a safe, reliable companion to transport the patient home. Another challenge to the ED team is the pregnant patient. The most critical point to remember is that to save the baby, the mother must be treated quickly and appropriately. During the prehospital phase of care, all pregnant patients should be transported lying on the left side so as to not compromise venous return to the mother’s heart. If venous return is compromised, then blood flow to the fetus will also be in jeopardy. Once these patients arrive at the ED, an immediate consultation with the obstetrical service with ultrasound is indicated.
DIAGNOSIS Before discharge, every patient should receive a complete tertiary survey. This is ideally performed by the person who performed the initial evaluation. If this is not possible, a template should be constructed so that all identified injuries have been documented and redocumented, and any new issues or symptoms have been investigated. It is during this time that all laboratory and radiographic findings should be gone over with the patient so as to inform him or her of the diagnosis and prognosis. A few simple rules to live by in dealing with traumatically injured patients: 1. Listen to those who brought the patient to the facility; they are a wealth of knowledge regarding the initial presentation. 2. Listen to the patient or his or her family; most of the time, these people know what is wrong and what has been done in the past. 3. Always tell the patient what you are going to do to them and why; a little reassurance can go a long way. 4. If you obtain some type of information and are not sure what to do with it, take it to someone with more training/experience than you. Do not keep it to yourself. 5. The one test you do not order is the one you will definitely need the most. 6. Lastly, remember that patients have gone through a horrific experience, and never discount this. It may not be a true emergency to us, but it is to them.
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Bibliography Diaz JJ Jr, Gillman C, Morris JA Jr, et al: Are five-view plain films of the cervical spine unreliable? A prospective evaluation in blunt trauma patients with altered mental status, J Trauma 2003;55(4):658–664. Nwariaku F, Erwin T: Parkland Trauma Handbook, ed 2. Mosby: London, 1999. Peitzman AB, Rhodes M, Schwab CW: The Trauma Manual, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2002. Sayler SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Schenarts PJ, Diaz J, Kaiser C, et al: Prospective comparison of admission computed tomographic scan and plain films of the upper cervical spine in patients with altered mental status, J Trauma 2001;51(4):663–668. Widder S, Doig C, Burrowes P, et al: Prospective evaluation of computed tomographic scanning for the spinal clearance of obtunded trauma patients: Preliminary results, J Trauma 2004;56(6):1179–1184.
Abdominal Trauma CHARLES R. BAUER
ICD Codes: Laceration of spleen 865.09, Laceration of liver 864.05, Laceration of kidney 866.02, Hemorrhage, bowel 578.9
Key Points Abdominal injuries can be caused by both penetrating and blunt forces. Blunt trauma occurs with blows or kicks to the abdomen or with the striking of seat belts, steering wheels, or other objects against the abdomen or lower thorax. Significant injury can be caused by deceleration forces applied to solid organs such as the spleen or liver. ! Emergency Actions ! The initial treatment of a patient with abdominal trauma follows the ABCDE evaluation and resuscitation guidelines of ATLS. The patient is administered high-flow oxygen via a nonrebreather mask and is given warm crystalloid fluids followed by blood replacement, if needed.
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DEFINITION Abdominal injuries can be the result of blunt or penetrating trauma. It can be extremely challenging to recognize intra-abdominal injuries, which can be a major source of occult hemorrhage. Unrecognized abdominal injuries continue to be the cause of many preventable deaths after trauma to the torso.
ANATOMY External The anterior abdominal cavity extends from the nipple line superiorly to the pubic symphysis and the inguinal ligaments and laterally to the anterior axillary lines. The upper area lies beneath the lower thoracic cage, which both protects and makes organs vulnerable to thoracic area injuries. The flanks are the areas between the anterior and posterior axillary lines from the sixth intercostal space to the iliac crests. The area is somewhat protected by the thick musculature compared with the anterior abdominal wall. Posteriorly, injury to the abdomen can occur through the area between the posterior axillary lines from the tip of the scapula to the iliac crests. The thick musculature is somewhat protective.
Internal The abdomen consists of the peritoneal cavity, pelvic cavity, and the retroperitoneal space. The peritoneum lines the peritoneal cavity and wraps all of the contained organs in a continuous sheath. The upper peritoneal cavity beneath the bony thorax contains the diaphragm, spleen, liver, stomach, and transverse colon and the lower peritoneal cavity contains the ascending, descending, and sigmoid colon, small intestine, and in women the internal reproductive organs. The pelvic cavity is surrounded by the bony pelvis and has both retroperitoneal and intraperitoneal spaces containing the rectum, bladder, iliac vessels, and internal reproductive organs. It can be difficult to evaluate due to the confining bony pelvis. The retroperitoneal space is posterior to the peritoneal lining and contains the aorta; the inferior vena cava; much of the duodenum, pancreas, kidneys, and ureters; and the posterior areas of the ascending and descending colon. It also extends down to include the retroperitoneal pelvic structures. This area is remote to direct examination and can be the source of major injuries not recognized by procedures such as a diagnostic peritoneal lavage (DPL) or FAST. If the patient’s condition is stable, CT can help identify retroperitoneal injuries and hemorrhage.
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MECHANISMS OF INJURY Abdominal injuries can be caused by both penetrating and blunt forces. Blunt trauma occurs with blows or kicks to the abdomen or with the striking of seat belts, steering wheels, or other objects against the abdomen or lower thorax. Significant injury can be caused by deceleration forces applied to solid organs such as the spleen or liver. Sheering forces can avulse bowel from the mesentery. Loops of bowel trapped by a seat belt or other structure can cause perforation of the large and small bowel. Penetrating trauma is usually caused by sharp objects such as knives or by gunshot, which can be of high or low velocity. High-velocity missiles transfer significantly more kinetic energy to the tissue, increasing the extent of damage due to cavitation and tumbling. Organ injury is related to the anatomical area and the trajectory of the bullet recognizing the potential to ricochet off bony structures.
CLINICAL PRESENTATION AND EXAMINATION Evaluation of a patient with abdominal trauma must begin with the assurance of adequate airway and ventilation/breathing. Large-bore IV infusion sites must be established and intravascular volume restored. A brief neurological survey is completed along with external examination of the entire body, including log-rolling the patient to observe and palpate his or her back. External marks over the thorax, abdomen, and back indicate energy forces applied to the body. Attention should be directed to look for seat belt marks over the abdomen and thorax as opposed to ecchymotic marks over the anterior iliac crests indicating a properly positioned seat belt. A positive “seat belt mark” is associated with about a 20% intra-abdominal injury rate. Guarding and muscle spasm may be related to deep or abdominal wall injury. The absence of pain, guarding, and rebound does not exclude potential significant injury. Significant blood loss can occur without abdominal distention. The pelvis must be evaluated for fractures. Penetrating wounds must be recognized and after resuscitation may be evaluated by the attending surgeon for peritoneal penetration. Pregnancy must be recognized, when present, and the patient treated appropriately (see the section “Trauma in the Pregnant Patient ”). All of these findings direct the attention to potential abdominal injuries, and additional studies are required to evaluate the patient. If the patient’s condition is unstable, he or she may require immediate transfer to the operating suite for exploratory laparotomy.
DIAGNOSIS The diagnosis of acute abdominal injuries can be difficult and may require serial examinations by persons trained to deal with subtle findings.
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During the placement of the IV lines, blood is drawn for CBC, electrolyte measurements, liver function profile, blood type and cross-match, and measurements of amylase, lipase, lactate, serum beta human gonadotrophic hormone (in women).
RADIOGRAPHS Abdominal and Pelvic Computerized Tomography A hemodynamically stable patient can be subjected to an abdominal/pelvic CT using oral and IV contrast with a high degree of specificity for injury and a sensitivity of 92%–98%. Because of the extra time required for the administration of oral contrast with an increased risk of aspiration, some clinicians will use only the IV contrast. The use of CT has increased significantly as the speed and quality of technology have advanced along with further experience of the trauma and radiology teams. Emergency medicine and trauma surgery physicians are becoming skilled in the use of ultrasonography, commonly referred to as the focused assessment sonography of trauma. The FAST examination is most useful for recognizing intra-abdominal fluid in hemodynamically unstable patients. Sites examined are the subxiphoid for looking for pericardial fluid/blood clot; the right upper quadrant examining for fluid between the diaphragm, liver, and the kidney in Morison’s pouch; the left upper quadrant looking for fluid between the diaphragm and the left kidney; and the suprapubic pouch of Douglas searching for fluid around the bladder and loops of the bowel. It is noninvasive, rapidly completed, repeatable, and does not use nonionizing radiation. The usual criterion suggesting hemoperitoneum is the presence of free fluid within the abdominal cavity. It does not indicate the source of bleeding and does not evaluate the retroperitoneal area.
DIAGNOSTIC PERITONEAL LAVAGE DPL was introduced by Root et al. in 1965 as a way to improve the diagnosis of intraperitoneal injuries. The abdominal cavity is entered in the infraumbilical area using either the open, semiopen, or closed Seldinger technique unless there is concern for a suprapubic hematoma as with a pelvic fracture, in which case it can be entered above the umbilicus. The procedure can be accomplished in the resuscitation or operating room and is usually reserved for patients with blunt injury. Members of the surgical team tasked with caring for the patient should be involved directly or indirectly in the procedure because they will be providing the follow-up care, especially if the study results are positive, leading to a laparotomy. The stomach and the urinary bladder should be decompressed with
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a gastric tube and a Foley catheter to lessen the potential injury. The local infiltration of lidocaine with epinephrine will help decrease false-positive study results. The open technique uses a small vertical incision inferior to the umbilicus with dissection down to the fascia, which is then opened to visualize the peritoneum. The fascia is lifted upward with clamps or forceps away from the underlying structures, and the peritoneum is incised. The catheter can then be inserted with direct visualization into the pelvis. For the closed technique, the skin is penetrated below the umbilicus with an 18-gauge needle and then the catheter introduced over a wire using the Seldinger method. With the semiopen technique, once the fascia is visualized, the Seldinger technique is used. A grossly positive DPL result is the presence of obvious blood or aspiration of 10 ml of blood. If negative, 1 liter of warmed crystalloid is introduced into the pelvis via the catheter. For children, 10 ml/kg is used. After waiting a brief period for the fluid to equilibrate, it is allowed to siphon out via the catheter and fluid is sent to the laboratory for analysis. The criteria for a positive DPL result are as follows: 1. 2. 3. 4.
Grossly positive or aspiration of 10 ml of blood Red blood cell count of >100,000 White blood cell count of >500 The presence of bile, feces, or food materials
Some trauma care providers will obtain a serum amylase analysis. Studies report that a lavage amylase level of 20 IU/L or higher had a sensitivity of 87% and a specificity of 75% for predicting significant intra-abdominal injuries. With modern imaging equipment and techniques, DPL is reserved for patients too unstable to undergo an abdominal/pelvic CT. Relative contraindications for DPL include coagulopathy, advanced cirrhosis, morbid obesity, and previous abdominal operations. In pregnant patients, the open technique is preferred. Complication rates vary between 0.8% and 1% in large series and can include injury to underlying organs such as the bowel, aorta, iliac veins and arteries, and ovaries. False-negative rates are 1%–1.3% of patients with significant abdominal injuries.
TREATMENT The initial treatment of a patient with abdominal trauma follows the ABCDE evaluation and resuscitation guidelines of ATLS. The patient is administered high-flow oxygen via a non-rebreather mask and is given warm crystalloid fluids followed by blood replacement, if needed. The surgical team should be present in consultation to expedite transfer to the operating suite if this action is required. Radiographs of the chest
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and pelvis are taken as the “primary survey and resuscitation” phase is completed. A patient with penetrating trauma or bowel perforation is given broad-spectrum antibiotics in consultation with a surgeon. Additional evaluation of the patient is completed based on the hemodynamic stability of the patient. A gastric tube is placed after evaluation of the patient’s mid face for possible trauma. If present, the gastric tube is placed transorally to prevent further injury such as penetration of the cribriform plate. In a male with a potential pelvic fracture, the genital and rectal areas are examined, looking for blood at the urethral meatus, ecchymosis of the scrotum or perianal area, and on rectal examination, the soft mushy feel of the hematoma associated with a “high-riding prostate” due to a tear of the membranous urethra. If present, the patient should have a retrograde urethrogram to rule out urethral injury before the catheter is placed. Upon catheter placement, gross blood may indicate a bladder or renal injury. These can be further evaluated with a cystogram and CT. It is important to recognize diaphragm injuries. Although these are frequently repaired through an abdominal approach, they are addressed in the section on chest trauma. With modern diagnostic techniques, many patients with injuries to the liver and spleen are observed with frequent serial evaluations in a setting where immediate surgical capabilities are present. This trend started with children, and with continued advances in trauma care it is now common with adults. If there is continued blood loss from an unrecognized source, perforation of a hollow viscus, vascular or retroperitoneal injury, or diaphragmatic injury, the patient should have timely surgical intervention. Delayed intervention remains a major cause of trauma deaths.
Bibliography Abdominal trauma. In Student Course Manual: American College of Surgeons Committee on Trauma, ed 7. 2004, 137–138. Demetriades, Velmahos: Indications for laparotomy. In Moore EE, Feliciano DV, Mattox KL: Trauma, ed 5. McGraw-Hill: New York, 2004, p 598. Hawkins ML, Scofield WM, Carraway RP, et al: Is diagnostic peritoneal lavage for blunt trauma obsolete? Am Surg 1990;56:96. Root HD, Hauser CW, McKinley CR: Diagnostic peritoneal lavage, Surgery 1965;57:633. Shanmuganathan K, Killeen KL: Imaging of abdominal trauma. In Mirvis SE, Shanmuganathan K (eds): Imaging in Trauma and Critical Care, ed 2. WB Saunders: Philadelphia, 2003.
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Genitourinary Tract Trauma STEVEN W. SALYER
ICD Code: Trauma 959.9 (See specific injury for code.)
Key Points Any patient who has microscopic hematuria, has fractures of the transverse process of the lumbar spine or bony pelvis, has a palpable mass in the flank or side of the abdomen, was involved in a high-speed accident, or has been injured by a high-velocity projectile should be considered to have an injury to the genitourinary tract until proven otherwise. ! Emergency Actions ! As with any trauma patient, a “safety net” should be made. Two large-gauge IV lines should be initiated and normal saline or lactated Ringer’s solution administered. The patient should be given 100% oxygen and have cardiac monitoring begun.
DEFINITION If urinary tract trauma is present, there is often other severe trauma present also. Urological trauma should be treated only after the patient’s airway, breathing, and circulation have been treated and other more severe trauma is addressed.
CLINICAL PRESENTATION A patient will present with one of five types of genitourinary trauma: trauma to the kidney, ureter, bladder, urethra, or genital area. Any patient who has microscopic hematuria, has fractures of the transverse process of the lumbar spine or bony pelvis, has a palpable mass in the flank or side of the abdomen, was involved in a high-speed accident, or has been injured by a high-velocity projectile should be considered to have an injury to the genitourinary tract until proven otherwise. A patient with genitourinary tract injury will present with renal contusions, lacerations, ruptures, renal pelvic ruptures, and pedicle injuries. Most penetration renal injuries are the result of gunshot wounds. Gunshot wounds often have other associated injuries. Stab wounds to the kidney are usually not associated with the other organ injuries. Blunt trauma to the kidney usually results from an MVC or a fall.
1064 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Renal contusions are the result of blunt trauma, which causes minor tears of renal tissue and bruises, but the renal capsule is left intact. Ninety-two percent of all renal injuries are renal contusions. Occasionally, there can be a subcapsular hematoma. Renal lacerations account for 5% of all renal injuries. Lacerations cause disruption of the parenchyma with damage to the renal capsule with or without calyceal disruption. Lacerations cause perirenal hematomas and can fill and displace Gerota’s fascia, which can act to tamponade the spread of blood within the flank. There is controversy regarding how to treat renal lacerations. Some authors treat lacerations to the kidney by restricting the patient to bed rest and monitoring the vital signs and hematocrit for signs of hematuria. Other authors suggest surgical intervention as the treatment of choice. Ruptures of the renal pelvis involve extravagation of urine into the perirenal space along the psoas muscle. A patient will present with a high fever and increased abdominal pain. A rupture of the renal pelvis is often mistaken for a renal laceration. The diagnosis is confirmed by a retrograde pyelogram or CT. Renal ruptures are rare and account for fewer than 1% of all renal injuries. The kidney is fragmented or shattered, and this creates a large perirenal hematoma. The patient’s condition becomes clinically unstable within hours. An IV pyelogram (IVP) or CT with contract will show extravasation of contrast into the abdomen. Open surgical treatment is the treatment of choice, often with nephrectomy. Renal pedicle injury is the tearing or occlusion of the renal vein or artery or its branches, which is usually the result of a deceleration, a high-velocity injury, or a penetration injury. An IVP or CT with contrast will show a nonfunctioning kidney, and an arteriogram will show renal artery occlusion or bleeding. These injuries require surgical intervention. Injury to the ureter can occur from blunt or penetrating trauma. An injury can be easily diagnosed early; these patients will present with an increasing fever, toxic appearance, and abdominal pain, and the diagnosis is confirmed by a retrograde pyelogram. Bladder injuries can also be caused by blunt trauma, penetrating trauma, and pelvic fractures. The bladder is an intra-abdominal organ in children but not in adults. In adults, the bladder lies in the bony pelvis, which gives it some protection. If there is a bony pelvic fracture, a large hematoma is usually present that will cause the displacement of the bladder either superiorly or laterally. Intraperitoneal bladder ruptures are usually a result of a deceleration injury to the abdomen when the bladder is full of urine. There is usually a very large amount of urine spilled into the pelvis. A cystogram or contrast CT will show intraperitoneal extravasation of contrast into the abdomen. The treatment is surgical.
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Urethral injuries can occur to the anterior, bulbous, and penile areas or to the posterior area or the posteromembranous area. If a rupture of the urethra is suspected, a urethrogram should be performed. If a rupture is present, there will be extravasation of contrast at the site of the injury and no contrast will pass into the bladder. In a partial urethral rupture, contrast may pass into the bladder slowly. Partial urethral ruptures are managed by passing a catheter into the bladder, and then the partial ruptures are allowed to heal. Complete ruptures will require surgical repair. Posterior urethral injuries are associated with pelvic fractures. Anterior urethral injuries are associated with a direct blow to the pelvis (e.g., kicks). On digital rectal examination, in the case of a posterior urethral injury, the prostate will be riding high or detached. If detached, then the urethra is completely disrupted. The perineum should be visualized. If there is a posterior urethral injury with bleeding, the classic “butterfly rashes” will be present, resulting from a perineal hematoma, limited by the attachments of the fascia lata. Genital injuries can also be caused by penetrating or blunt trauma. The testes should be examined for tenderness, blue scrotal masses, cremaster muscle contraction, hematocele, or hydrocele. A scrotal ultrasound scan can be used to evaluate the testicle for tunica albuginea or tunica vaginalis injury, testicular rupture, or scrotal hematoma. Hematomas must be evacuated because of their high rate of infection and testicular atrophy. All penetrating injuries to the scrotum should be explored to rule out tunica vaginalis perforation. The penis can suffer many injuries, including self-inflicted injuries, such as vacuum cleaner injuries or blunt trauma. Traumatic rupture occurs when the penis is in an erect state. Usually, the penis is forcibly impacted on a hard object, often the sexual partner’s pubis bone or the floor. The patient will state that he heard a “cracking” sound with immediate pain, detumescence, rapid swelling, discoloration, and distortion. Surgical evacuation of the blood clot and repair of the tunica albuginea of the corpus cavernous is required.
EXAMINATION The entire abdomen must be visualized and examined. The patient must be log-rolled to examine the back of the patient. The external meatus should be examined for blood. If present, a retrograde urethrogram should be performed with contrast solution, with 10 ml of radiocontrast solution injected into the urethral meatus. While this is taking place, traction is maintained on the penis, and oblique radiographs of the pelvis are taken.
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A cystogram is performed after the bladder has been catheterized. Fivehundred milliliters (5 ml/kg in children) of contrast is placed into the bladder through the catheter and anteroposterior (AP) radiographs are taken. The bladder is then washed out with saline solution, and another “AP washout” x-ray is taken. An IVP is used to examine the kidneys and ureters. One hundred milliliters of a 60% iodine-containing solution is injected IV, if the patient has no allergies to iodine. Films are taken at 5, 10, and 20 minutes. If extravasation, incomplete filling, or delayed visualization is noted, then a CT scan should be obtained of the abdomen. A renal ultrasound can be used to examine the kidney’s anatomy for hematomas, rupture of the capsule, or lacerations and enlargement of the kidney.
DIAGNOSIS The simple and most inexpensive test for trauma to the genitourinary tract is a dipstick test of the urine. A positive blood test result requires further evaluation. A positive dipstick test result for blood and a negative result on microscopic examination for red blood cells is suggestive of myoglobinuria.
LABORATORY FINDINGS A CBC, analysis of electrolytes and glucose, liver function tests, measurements of amylase and lipase, and a complete urinalysis should be performed on any patient with any abdominal or genitourinary trauma. If bleeding is suspected, 6–8 units of blood should be typed and crossmatched. Blood and urine cultures should also be performed if urine extravasation has occurred.
TREATMENT As with any trauma patient, a safety net should be established. Two largegauge IV lines should be placed with normal saline or lactated Ringer’s solution administered. The patient should be given 100% oxygen and cardiac monitoring. The aforementioned laboratory examinations should be performed, including radiographs of the cervical spine, chest, and pelvis. It should be remembered that basic life support takes precedence over all other evaluations and treatment. Evaluation of trauma to the genitourinary tract is performed by urethrograms, cystograms, IVPs, contrast CT scans, and renal ultrasonography. Early and frequent consultation with a urologist should be standard procedure.
Head and Brain Trauma
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Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Head and Brain Trauma JOHN T. KODOSKY
ICD Codes: Skull fractures 800–803, Hematomas 805–829, Hematomas, Brain traumatic 853.0, Subdural hematoma 432.1, Epidural hematoma 432.0
Key Points Epidural hematomas account for approximately 1% of all head trauma admissions. The typical presentation is a brief loss of consciousness followed by a ‘‘lucid interval,’’ then rapid decompensation of mental status with contralateral hemiparesis, ipsilateral pupil dilation, and decerebrate posture. ! Emergency Actions ! The threshold for ordering a CT scan should be low when an injury occurs in a patient who is obviously intoxicated or elderly or in the case of focal neurological findings including loss of or altered level of consciousness. The most common artery responsible for the bleeding is the middle meningeal artery in 85% of cases.
DEFINITION Head trauma is simply defined as any injury to the structures of the head or brain. It need not involve any loss of consciousness, altered mental status, or focal neurological deficit. The range of injury can be from minor concussion (or closed head injury) to severe structural damage resulting in death. The severity of the injury is determined not only by the modality
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and force inflicted, but by the posttraumatic sequelae found on examination of the patient. Caution must be used with head trauma to elderly patients, children, chronic ethanol abusers, and patients with coagulopathies. It is imperative that a thorough history, physical examination, and appropriate radiological studies be completed in a timely manner to rule out severe complications from the traumatic insult.
PATHOPHYSIOLOGY The skull encapsulates the brain as a protective barrier; however, this protection is rigid and inflexible. When the barrier is broken, the incidence of brain injury rises dramatically. Head injuries are classified by two methods: open or closed and primary or secondary. An open head injury is when there is a communicating pathway from the brain to the area outside the skull. A closed head injury is an injury to the brain occurring while the skull remains intact. Primary head injuries are the result of a direct insult to the head, whereas secondary injuries occur because of hypoxia, ischemia, hemorrhage, hypercarbia, and increased intracranial pressure (ICP). In patients with a head injury, a noncontrast CT scan of the brain may be indicated as soon as possible. Many times, an accurate history is difficult to obtain due to mental status of the patient and a thorough physical examination unobtainable if the patient is intubated or has an altered mental status. A CT scan can be a fast, reliable way to assess brain injury and make an accurate diagnosis. The threshold for ordering a CT scan should be low when an injury occurs in a patient who is obviously intoxicated or elderly or when there are focal neurological findings, including a loss or altered level of consciousness.
SKULL FRACTURES As with any bone in the body, the skull can fracture with traumatic injury. If the skull fracture is depressed toward the brain, there is a likelihood that bony fragments are pushed intracranially, causing further damage. These are potentially life threatening and are especially lethal over the middle meningeal artery or a major dural sinus. Fractures to the petrous portion of the temporal bone or base of the skull are called basilar skull fractures and are life threatening. There are four physical examination findings that must be addressed in a patient with head trauma: 1. 2. 3. 4.
Battle’s sign: hematoma over the mastoid process Raccoon eyes: bilateral periorbital ecchymosis without direct trauma Hemotympanum Clear rhinorrhea
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If any of these findings are present, a CT scan is required and special attention should be noted to the temporal bones. If the base of the skull is poorly visualized, plain radiographs may assist in the diagnosis. Most importantly, do not attempt to pass a nasogastric tube via the nose because there is a risk of the tube passing intracranially. Treatment depends on the severity of the fracture; most require no treatment. If there is persistent rhinorrhea, surgery may be indicated to repair a fistula. Meningitis and cerebral abscesses can occur, especially if the fracture occurs through a sinus. Linear nondepressed skull fractures without overlying scalp lacerations typically do not require treatment.
MINOR HEAD INJURY A concussion is defined as nonpenetrating head trauma resulting in a brief loss of consciousness. There is no definition for the length of a “brief” period, but some experts allow up to 6 hours before consciousness returns. Most important, patients with a concussion will regain normal consciousness and have a normal neurological examination findings and a normal CT scan of the brain. In as many as 30% of patients who experience a concussion, postconcussive syndrome (PCS) will develop. Patients with PCS may have headache, nausea, emesis, memory loss, dizziness, diplopia, blurred vision, emotional lability, or sleep disturbances after a minor head injury. Fixed neurological deficits are not part of PCS, and any patient with a fixed deficit requires careful evaluation. PCS usually lasts 2–4 months. Typically, the symptoms peak 4–6 weeks after the injury. It is important to always look for a contrecoup injury to the brain with any head trauma. Contrecoup injuries occur when a force strikes one side of the head hard enough to shift the brain in the opposite direction of the injury, and inertia then forces the brain to strike the opposite side of the intracranial cavity, thus causing an injury to the opposite side of the brain from the original trauma. Both direct trauma and contrecoup injuries can cause intracerebral and extracerebral bleeding, or both. Intracerebral bleeding, such as cerebral contusion, is caused by the disruption of microvasculature typically within the parenchyma. That disruption can cause the arteries beneath the arachnoid and above the pia to bleed, called a subarachnoid hemorrhage. Nearly half of all patients with minor head injury will have a cerebral contusion visible on CT scan.
HEMATOMAS Epidural hematomas account for approximately 1% of all head trauma admissions. The typical presentation is a brief loss of consciousness followed by a “lucid interval,” then rapid decompensation of mental status
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with contralateral hemiparesis, ipsilateral pupil dilation, and decerebrate posture. The most common artery responsible for the bleeding is the middle meningeal artery in 85% of cases. Physical examination may show hemi-hyperreflexia, upward unilateral Babinski reflex, and bradycardia. A CT scan will show a high-density biconvex (“football”-shaped) lesion between the brain and the skull with or without mass effect on the brain. There is a mortality rate of up to 55% usually from uncal herniation of the brain causing respiratory arrest resulting from damage to the midbrain. Treatment is commonly surgical, with the goal being clot removal in an effort to lower ICP. Also, homeostasis must be obtained to prevent reoccurrence of the bleeding. Subdural hematomas are a much more lethal form of intracranial bleeding because the force of the insult must be so great as to cause damage to the bridging arteries on the surface of the brain. Physical examination findings are very similar to that of a patient with an epidural hematoma. CT scan will show a crescent-shaped lesion between the brain and skull and usually some severe brain damage below the hematoma. Treatment may require rapid surgical intervention via craniotomy. Studies show that if surgery is delayed greater than 4 hours, a 90% mortality rate ensued, versus a 30% mortality rate if evacuation of the clot could be performed with 4 hours. The worst outcome associated with hematomas is herniation. Although this can occur in many places, the most lethal is transtentorial or uncal. In these cases, the temporal lobe is forced through the tentorial hiatus into the space between cerebral peduncle and tentorium. These patients will often have a fixed and dilated ipsilateral pupil with hypertension and bradycardia with breathing irregularities known as Cushing’s triad. ICP monitoring is indicated in most of these cases. Normal ICP is less than 15 mmHg, and greater than 30 mmHg is considered lethal. Treatment of increased ICP includes elevating the head of the bed, reducing jugular vein occlusion, reducing blood pressure, providing hyperventilation if the patient is intubated, and sedating the patient. Mannitol can be given to patients who have a persistent increased ICP. The exact mechanism of action is unknown but it is believed to reduce ICP by an osmotic effect drawing fluid from the parenchyma. Adverse effects can include hyperosmolar nonketotic acidosis when used with steroids and Dilantin (phenytoin), and renal tubular necrosis. Dosages must be tapered off from a continuous infusion to reduce the rate of ICP rebound. No evidence exists that the use of anticonvulsants decreases the incidence of late-onset seizures in patients with closed head injury. One study showed that the routine use of Dilantin in the first week after brain trauma decreases the incidence of seizures in the first 7 days but does not change the incidence of late-onset seizures, and the prevention of early posttraumatic seizures does not improve the outcome. Therefore, the prophylactic use of anticonvulsants is not recommended for more than 7 days after traumatic brain injury and
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is considered optional in the first week after traumatic injury. If increased ICP persists after Mannitol, a burr hole must be placed immediately to remove cerebrospinal fluid, thereby relieving the pressure on the brain.
HISTORY Many times a history is unobtainable from the patient because there may be a loss of consciousness, altered mental status, or the patient may be nonverbal from other injuries. It is very important for first responders to attempt to discover the nature of the injury and assess the severity of the insult on the patient. Key points to inquire are force, loss of consciousness (with duration), type of injury (i.e., penetrating versus nonpenetrating), and presence of a lucid interval.
PHYSICAL EXAMINATION There is no standard physical examination that can be used universally. Each patient and injury are unique and the physical examination must be malleable to each case. The GCS is a fast, easy, and well-known measure to convey the degree of the injury. The criteria for GCS are listed in Table 18-1. An accurate GCS score is crucial to diagnosis, treatment, and prognosis. If a patient has a score of less than 8, intubation should be seriously considered to protect the airway. Patients with a GCS score of 3–5 will have a mortality rate of approximately 60%, and patients with a score of 6–8 have a mortality of 20%. This makes the GCS an excellent tool for first responders to convey the degree of injury to the hospital for a patient who will be receiving treatment, and for healthcare providers to use for treatment, reassessment, and discussion of the case with consultants.
DISPOSITION After a patient has been evaluated in the ED, the patient must either be discharged or admitted to the hospital. A patient who has had a head injury with normal CT scan results; an initial GCS score of 14 or higher; no evidence of intoxication, altered mental status, or focal neurological findings; and who can be observed by friends/family at home with access to return to the ED if necessary can be discharged home. It is important that the patient and family be informed to return if any of the following occur:
Mental status changes Worsening headache Slurred speech Vomiting Focal neurological deficit
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Patients who have had a head injury and display evidence of intoxication, altered mental status, abnormal neurological examination results, vomiting, amnesia, signs of basilar skull fracture, or child abuse should be admitted with a high index of suspicion for intracranial abnormality.
COMPLICATIONS Complications from head injuries are divided into two categories: systemic and neurological. The systemic complications depend on the types of intensive treatments used. Neurological complications include focal neurological deficits, global neurological deficits, seizures, cerebrospinal fluid fistulae, hydrocephalus, vascular injuries, infections, and brain death.
OUTCOME The outcome of the patient with head trauma varies greatly based on numerous factors, including type of trauma, injury sustained, other injuries to the body (both physical and physiological), and any comorbidities of the patient. There are five factors that indicated a poor prognosis: 1. 2. 3. 4. 5.
Age older than 60 years old Initial GCS score of 5 or less Fixed dilated pupils Hypoxia and/or hypotension after the injury Intracranial lesion requiring surgery
Bibliography Brunicardi FC, Anderson DK, Billiar TR, et al: Principles of Surgery, ed 6. McGraw-Hill: New York, 1994. Greenberg M: Handbook of Neurosurgery, ed 4. Greenberg Graphics: Lakeland, FL, 1996. Harwood-Nuss A, Wolfson A: Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins: Philadelphia, 2005. Shepard S: Head trauma. Emedicine.com. August 20, 2004. Available at: http://www.emedicine.com/med/topic2820.htm#top. Tintinalli J, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill Professional: New York, 2003.
Pediatric Trauma
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Pediatric Trauma STEVEN W. SALYER The priorities of assessment and management for the pediatric population are the same as for adults, but there are specific differences in the management of children. The most common cause of trauma in the pediatric population is an MVC. Aggressive management of the airway and cardiopulmonary systems should be the norm. The clinician should assume the most serious diagnosis and treat the patient based on clinical findings. The nature of the accident must be considered in relation to the child’s different anatomy, initial appearance, initial vital signs, and changing vital signs and mental status.
AIRWAY MANAGEMENT The biggest difference in the pediatric population versus the adult population is airway management because of the child’s anatomy. The child’s airway is smaller (Table 18-3). The smaller radius of the nasopharynx causes an increased workload to breathe. If edema or a foreign body is present in the smaller airway of a child versus an adult’s airway, the child will have a larger percentage of obstruction than does an adult. The child’s tongue occupies a larger percentage of oropharynx than an adult’s tongue. The glottis is higher in the neck. The shape of the epiglottis is different in the child than in the adult, and the child has more lymphoid tissue than does the adult in the oropharynx. The chest of a child is also different from that of an adult. It is made up of more cartilage than bone and is more compliant. Therefore, direct trauma will cause fewer fractures in a child than in an adult. A child is also a diaphragmatic breather. Children’s ribs are more horizontal than are those of adults. This limits the child’s respiratory compensation. Children rarely die from cardiac arrest; they die as a result of pulmonary arrest. Pediatric trauma patients need 100% oxygen delivered by a bag-and-mask device if they are not intubated. A child’s airway is also much more compliant than is an adult’s airway; therefore, by using good airway control and a good bag-mouth-mask technique, in many cases the healthcare provider can ventilate a child effectively with an airway obstruction resulting from epiglottitis or foreign body obstruction. If it is impossible to intubate a child, the Seldinger technique can be used in a small child to use transtracheal catheter ventilation. This procedure is carried out as follows:
1074 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 18-3 Pediatric Resuscitation Formulas WEIGHTS Term newborn 6 months 1 year
Weights in Children Younger Than 1 Year of Age 3.5 kg/7.7 lb 7 kg/15.4 lb 10 kg/22 lb
Weights in Children Older Than 1 Year of Age Weight in kg ¼10 þ ðage 1Þ2 Pediatric Endotracheal Tube Size Tube size þ age of child 4in years þ 16 -Use an uncuffed endotracheal tube in patients up to 8 years old. -The distance to the mid trachea in centimeters from the front teeth is three times the size of the tube. (Example: tube size 3.5 mm 7.5 cm þ 10.5 cm ¼ 1.5 cm from the front teeth to the mid trachea) -Endotracheal tube size ¼ size of small finger -Endotracheal tube size ¼ size of the nasal passage -Preterm infant, 2.5 to 3.0 -3-month-old infant to 1 year, 4.0 -2-year-old infant, 4.5 Pediatric Chest Tube Size -Chest tube size ¼ 3 endotracheal tube size (French) Foley Catheter Size -Foley catheter size ¼ 5 þ age in years Pediatric Nasogastric Tube Size Nasogastric tube size ¼ 2 endotracheal tube size Blood Pressure Normal systolic blood pressure for children older than 1 year of age ¼ 80þ2(age in years) The diastolic blood pressure will be 60% of the systolic pressure. Fluid Resuscitation Fluid resuscitation can be accomplished with crystalloid solution (20 ml/kg), lactated Ringer's solution, or normal saline. Do not use dextrose fluids unless hypoglycemia is documented. Hypoglycemia can cause osmotic diuresis.
1. Make a small incision over the cricothyroid membrane. 2. Attach a needle to a syringe, and insert the needle at a 60-degree angle caudad until air is aspirated. 3. Remove the syringe, and place a flexible guidewire into the needle, then remove the needle. 4. Place an 18- to 20-gauge end-hole catheter over the guidewire, withdraw the guidewire, attach the catheter to a syringe, and check to see whether air can be aspirated. 5. Ventilate with 100% oxygen from the wall and an in-line pressurereducing valve. (Wall oxygen is usually 50 psi.) The reducing valve should be set at the lowest effective ventilating pressure.
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There is an increased risk of barotraumas as time goes on using this ventilation system. Cricothyrotomy can be used in a child but is highly discouraged because of the danger of a major surgical error resulting from the child’s smaller anatomy. Induction and intubation of a child are also different from those of an adult trauma patient. A dose of lidocaine (1 mg/kg) before intubation can relieve increased ICP.
CARDIOVASCULAR MANAGEMENT To asses the circulatory status of a child, the clinician should evaluate the skin temperature and capillary refill (< 2 seconds). Capillary refill of 1 to more than 5 seconds over the forehead or trunk will require rapid volume replacement. The quality of peripheral pulses should be checked because good peripheral pulses mean good peripheral circulation. Persistent tachycardia is a sign of hypovolemia. Tachycardia resulting from fear will fluctuate, whereas tachycardia secondary to hypovolemia will stay the same or increase as hypovolemia increases. All of the patient’s vital signs should be checked, and the correct pulse rate and blood pressure for the child’s age should be known. In any trauma patient, multiple IV lines should be secured via peripheral vein, intraosseous, and femoral vessel routes. The initial fluid administered should be isotonic crystalloid fluids, either normal saline or lactated Ringer’s solution. The fluid should be given in a 20-ml/kg bolus and then the patient’s vital signs, pulse, capillary refill, skin color, and blood pressure should be reassessed after each bolus. If shock is persistent after several crystalloid boluses (total of 40– 50 ml/kg) have been given and no response to these fluid boluses has been obtained, then type-specific and cross-matched packed red blood cells should be given. If cross-matched or type-specific blood is not available, O-negative blood should be given.
RENAL PERFUSION ASSESSMENT Urine output is the best monitor for renal status. In children, an output of 0.5 ml/kg/hr is acceptable. No urine output can result from intraabdominal injury or hypovolemia resulting from a lack of renal perfusion.
NEUROLOGICAL EVALUATION The patient’s neurological status is evaluated by assessing the child’s papillary response, verbal response, eye opening, and motor activity. The modified pediatric GCS should be used (Table 18-4). Only one person
1076 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 18-4 Infant and Child Resuscitation Scoring (Modified Pediatric Glasgow Coma Scale) EYE OPENING SCORE
INFANT
CHILD Opens eyes spontaneously Opens eyes to speech Opens eyes to pain No response
5
Opens eyes spontaneously Opens eyes to speech Opens eyes to pain No response Verbal Response Coos, babbles, or cries appropriately
4 3 2
Irritable crying Cries only to pain Moans to pain
1
No response
4 3 2 1
6 5 4 3 2 1 Newborn Older children:
Motor Response Spontaneous movements Withdrawals for touch Withdraws from pain Abnormal flexion Abnormal extension No response Fluid Requirements Day 1: 3 ml/kg/hr D10W Day 2: 4 ml/kg/hr D10/0.25% normal saline 4 ml/kg/hr for the first 10 kg of body weight 2 ml/kg/hr for next 10 kg 1 ml/kg/hr for each kilogram over 20 kg Maintenance fluid: ¼ normal saline þ 20 mEq KCl/L Urine output: 0.5 ml/hr
Oriented with appropriate use of words Confused Inappropriate use of words Incomprehensible use of words No response Obeys commands Localizes (purposeful movement) Withdraws from pain Abnormal flexion Abnormal extension No response
KCl, Potassium chloride.
should speak to the child, in a soft calm voice, to reassure the child, calm his or her fears, and to explain what is going on around him or her. The healthcare provide should not lie to the child because this will violate the child’s trust and he or she may never trust another medical healthcare provider again. The clinician should check the ears and nose for cerebrospinal fluid leakage. In an infant, the fontanelles should be evaluated for bulging. In a child with a head injury, a mild injury can cause transient or no loss of consciousness. The child can have pallor, vomiting, lethargy, or increased irritability or may hold his or her breath. The incidence of
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hematomas visible on CT scan in children also differs from that in adults. Space-occupying lesions are fewer (25–30) in children than in adults (40–50). There is an increased risk of shearing forces in children with high-speed injuries. In treating a child with a head injury, hyperventilation is the most effective method to decrease ICP. The goal of hyperventilation is to keep the PCO2 between 25 and 30 mmHg. The head should be elevated to 30 degrees to facilitate venous drainage from the head. Mannitol should be given rapidly at 1 g/kg IV. Mannitol will initially increase intracranial blood flow. Furosemide 1 mg/kg can also be given IV to reduce brain edema without increasing blood flow to the brain. Any child with a suspected head injury should undergo a CT scan. The child’s skull has a thinner calvarium, and the child is subject to leptomeningeal cyst or “growing skull fractures” after head trauma. The child’s cervical spine must also be evaluated differently from that of an adult. On the child’s lateral cervical spine, the anterior placement of C2 in relationship C3 can give a false appearance of traumatic subluxation. If a line is drawn from the anterior aspect of the spinous process of C3, and the posterior cervical line misses the anterior aspect of C2 spinous process by greater than or equal to 2 mm (1.5 mm is borderline), this finding is suggestive of a hangman’s fracture. The measurement technique should only be used in situations in which C2 is displaced anteriorly on C3. On normal pediatric radiographs that do not exhibit C2 on C3 displacement, the posterior aspect of C2 spinous process may be 2 mm or more. There is also normal anterior wedging of the vertebral bodies. There can also be an increased distance between the odontoid process and the anterior arch of the atlas (predental space). A prevertebral soft tissue mass can vary with the infant’s inspiration. Lordosis is absent in the child’s cervical spine up to the age of 16 years. There is less cervical cord injury in children than in adults (3%-5%); this is because of the laxity of the transverse ligament. In children younger than 8 years of age, this space is more than 3 mm in 20% of children. In adults, a distance greater than 2.5–3 mm is evidence of a torn transverse ligament or subluxation of C1 on C2. In children younger than 8 years of age, a predental space greater than 3.5 mm is considered abnormal. However, a predental space of 5 mm may be normal in some children. The prevertebral soft tissue space in children also differs from that in adults. This space can increase because of soft tissue widening due to edema or hemorrhage. In the pediatric population, the soft tissue density of less than 7 mm anterior to C2 or less than three quarters of the adjacent vertebral body is normal. However, these numbers become more unreliable the younger the child is because of the flexibility of the neck, causing increased flexion. Furthermore, inspiration and expiration can cause a change in prevertebral soft tissue space.
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CHEST EVALUATION The child’s chest is more compliant than that of an adult. Children are also diaphragmatic breathers. They experience fewer fractured ribs than do adults. A child experiences underlying visceral injury without fracture of the bony thorax. Because of the anatomy of the child’s chest, a tension pneumothorax produces more of a lung shift and more respiratory and cardiovascular compromise; thus, hypoxia will be greater in children than in adults. Children need 100% oxygen because of their higher oxygen demand. There is also an increase in aerophagia resulting from increased crying. This causes increased gastric distention and a tense, distended abdomen, which can increase the chances of vomiting an aspiration. Early nasogastric tube placement should be standard procedure.
ABDOMEN EVALUATION Injuries to the liver, spleen, and kidneys are the must common intraabdominal injuries in the pediatric population. A Foley catheter should be placed to evaluate urine output. Decreased urine output is indicative of an intra-abdominal injury. The clinician should look for a pelvic fracture and have an abdominal CT scan performed if injury is suspected.
EVALUATION AND STABILIZATION The evaluation and stabilization of pediatric patients who have sustained traumatic injuries should be carried out as follows:
For airway evaluation and stabilization, give 100% oxygen by face mask or bag-valve-mask device. Incubate, if indicated, by using a rapid sequence of induction. Immobilize the cervical spine with a rigid cervical collar. Assess breathing; treat any pneumothorax; and remember that a pneumothorax is a clinical diagnosis not a radiological diagnosis. Perform a primary survey. Evaluate the patient’s mental status by using the revised pediatric GCS. Assess circulation, capillary refill, skin color, pulse rate, and blood pressure. Obtain a vascular access and a minimum of two IV lines; administer lactated Ringer’s solution or normal saline IV via peripheral vein, intraosseous route, or femoral vein access. If 40–50 ml/kg has been given and vital signs are still deteriorating, consider giving the patient blood. Obtain blood samples for laboratory tests, and type and cross-match the patient’s blood. Monitor the patient’s vital signs (Table 18-5) and keep reassessing the patient’s condition.
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Table 18-5 Pediatric Vital Signs AGE Newborn 1 year 2 years 4 years 6 years 8 years 10 years
PULSE (BEATS/MIN)
AVERAGE BLOOD PRESSURE (MMHG)
70–170 80–160 80–130 80–120 75–115 70–110 70–110
80/45 95/65 99/65 99/65 100/56 105/56 110/58
RESPIRATION (BREATHS/MIN) 40–90 20–40 20–30 20–25 20–25 15–20 15–20
WEIGHT (KG) 3 10 12 16 20 26 32
Perform a rectal examination and check for blood. Place a Foley catheter; evaluate the meatus or urethra for blood before a placement of the Foley catheter. Place a nasogastric tube. Splint fractures. Keep reevaluating the five key factors of life-threatening conditions: airway, ventilation, spine, shock, and level of consciousness. Obtain radiographs of the cervical spine, abdomen, pelvis, chest, and extremities for suspected fractures. If hypovolemia is suspected, give a 20-ml/kg bolus. Remember that if the patient has stable vital signs that are not deteriorating and the patient is going to the operating room, IV fluids should not be administered. Consult a surgeon as soon as possible.
INDUCTION AND INTUBATION The induction and intubation of pediatric patients who have sustained traumatic injuries should be carried out as follows (Tables 18-6 and 18-7):
Give 100% oxygen by face mask for 3 minutes. Give lidocaine 1 mg/kg IV. Administer a small dose of nondepolarizing relaxant, such as pancuronium 0.01 mg/kg. Give atropine 0.02 mg/kg IV. Give thiopental 1–4 mg/kg or ketamine 1–2 mg/kg IV. Administer succinylcholine 2 mg/kg IV. Perform the Sellick maneuver on the tracheal area.
Table 18-6 Countershocks Atrial arrhythmias ¼ 1 J/kg Defibrillation for ventricular tachycardia or ventricular fibrillation ¼ 2–4 J/kg
1080 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 18-7 Pediatric Resuscitation Medications DRUG Atropine sulfate Sodium bicarbonate Calcium chloride 10% Calcium gluconate 10% Epinephrine Epinephrine infusion Lidocaine Lidocaine infusion Norepinephrine infusion Isoproterenol Dexamethasone Diazepam Dopamine Dobutamine Furosemide (Lasix) Hydrocortisone (Solu-Cortef) Mannitol Methylprednisolone (Solu-Medrol) Insulin, regular Racemic epinephrine 2.25% Glucose D25W Hydralazine Morphine
DOSE 0.02 mg/kg/dose 1–2 mEq/kg/dose or 0.3 base deficit 20 mg/kg/dose 100 mg/kg IV 0.1 mg/kg (0.01 mg/kg) Start at 0.1 ug/kg/min 1 mg/kg/dose 20–50 ug/kg/min Start at 0.1 ug/kg/min Start at 0.1 ug/kg/min 0.25 mg/kg/dose 0.2–0.3 mg/kg/dose every 2–5 minutes 5–20 ug/kg/min IV drip 1–15 ug/kg/min IV drip 1 mg/kg/dose 4–5 mg/kg/dose every 6 hours 0.25–0.5 g/kg/dose every 3–4 hours 1–2 mg/kg/dose every 6 hours
HOW SUPPLIED 0.1 mg/ml 1 mEq/ml 100 mg/kg (10%) 1:10,000 (0.1 mg/ml) (1:1000 1 mg/kg) 10 mg/ml (1%); 20 mg/ml (2%) 40 mg/ml 4% 1 mg/ml 1 mg/5 ml 4 and 24 mg/ml 5 mg/ml 40, 80, 160 mg/ml 250 mg vial 10 mg/ml 11, 200, 500, and 1000 mg vials 200–250 mg/ml 40, 125, 500, and 100 mg vials
DKA: 0.1–0.2 units/kg/hr IV drip 0.05 ml/kg þ 2.5 ml NS 0.5–1 g/kg ¼ 2–4 ml/kg 0.1 mg/kg ¼ 0.1 ml/kg 0.1–0.2 mg/kg
D25W 4 mg/ml 10 mg/ml
IV, Intravenous; DKA, diabetic ketoacidosis.
Intubate the patient orotracheally using the proper size of endotracheal tube. Keep the child paralyzed with pancuronium 0.1 mg/kg.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Pelvic Trauma CHARLES R. BAUER
ICD Codes: Pelvic bone fracture 808.8 (See associated and specific fracture codes.)
Key Points The classification of pelvic fractures can be based on the forces applied leading to the expected fractures. ! Emergency Actions ! During resuscitation of a trauma patient with a pelvic fracture, it is essential to recognize that the potential for significant hypovolemia exists, and efforts must be immediately instituted to control further bleeding. The patient may have intra-abdominal injuries.
DEFINITION AND EPIDEMIOLOGY Pelvic fractures account for 3% of all fractures. Automobile crashes cause 60% of all pelvic fractures with motorcycle crashes and pedestrians struck by automobiles accounting for 9% and 12%, respectively. Falls account for 30%. The mortality rate from pelvic fractures is between 6.4% and 19%. A patient presenting to the ED with a pelvic fracture and hypotension has a 42%–50% mortality rate. Pelvic fracture is the third-leading cause of death from MVCs after traumatic brain injury and blunt aortic disruption.
ANATOMY The pelvis is made up of the sacrum and two innominate bones. The innominate bones are formed by the fusion of ossification centers located within the ilium, ischium, and the pubis. They meet at the triradiate cartilage which fuses by the age of 16 years. The innominate bones are attached to the sacrum by the extremely strong anterior sacroiliac ligaments and, posteriorly, the posterior sacroiliac, sacrospinous, and sacrotuberous ligaments. These ligaments are the strongest in the body and require major forces applied to cause disruption. The posterior pelvis transmits force from the body to the lower extremities while the pubis functions primarily as a strut.
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The iliopectineal, or arcuate, line divides the pelvis into the upper pelvis (which is part of the abdomen and the lower pelvis) and the true pelvis. The iliopectineal line is also part of the femorosacral arch, a subsidiary tie arch. The bodies of the pubic bones and the superior rami support the body in an erect position. The weight-bearing forces transmitted by sitting are supported by the ischiosacral arch and by its ties to the pubic bones, inferior pubic rami, and the ischial rami. When trauma to the pelvis occurs, the first ties to fracture are the pubic symphysis, pubic rami, and the area just lateral to the sacroiliac joint. There are five joints within the pelvis that allow some movement. These are lumbosacral, sacroiliac (2), sacrococcygeal and joints and the pubic symphysis. The acetabulum is a ball-and-socket joint divided into three parts. The ilium portion forms the superior dome and is the weight-bearing portion of the hip joint. The inner wall is made up of the pubis and is thin walled, making it subject to fracture. The posterior acetabulum is made up of the thick ischium. The internal and external iliac vessels are subject to disruption with pelvic fracture with the internal iliac vessels most vulnerable as they wrap around the superior margin of the sciatic notch. There are numerous veins on the anterior surface of the true pelvis that are subject to injury and a major source of retroperitoneal hemorrhage. The flat, cancellous bones of the pelvis are a major source of hematopoiesis. The rich vascularity of the pelvis accounts for the massive amount of blood loss that can occur without visible blood loss recognized. The pudendal nerves and the sacral and lumbar nerve roots are in danger of damage. The reproductive organs, bladder, and lower gastrointestinal tract are all subject to injury and can have significant delayed complications such as infection. Open pelvic fractures with extensive perineal, rectal, or vaginal involvement can have a 40%–50% mortality rate if not properly treated.
MECHANISMS OF INJURY The classification of pelvic fractures can be based upon the forces applied leading to the expected pelvic fractures. Lateral compression forces account for the most common type (50%) of pelvic injury. This may be due to a side impact from a “t-bone” (side-impact) MVC or when a pedestrian is struck from the side. These injuries are associated with a high incidence of traumatic brain injury, which is usually the primary source of morbidity and mortality. Direct AP impact forces tend to fracture the pubic symphysis with dislocation of the sacroiliac joints leading to the “open book” widening of the pubic symphysis (20%–30%). Related injuries may be to the bladder and the membranous portion of the male urethra. Females are less vulnerable to urethral injuries, but both sexes can have urethral and perineal injuries
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from “straddle” injuries with bilateral superior and inferior pubic ramus fractures. Vertical shear forces cause many of the remaining injuries. This can be with a fall from a height, an MVC that occurs while the patient’s leg is extended, or a force applied to the pelvis from above via the spine, such as an object falling on the upper back or shoulders.
ASSOCIATED INJURIES Injuries associated to pelvic trauma are common due to the high amount of energy required to fracture the pelvic ring. A study of more than 1000 patients with pelvic fracture noted neurological injury in 27%, thoracic injuries in 26%, and abdominal injuries in 14%. Urethral injuries (5%– 25%) are common, especially with a pubic symphysis disruption. Bladder injuries are more common with pubic rami fractures (4%–8%), with bone spicules penetrating the bladder wall. There is a risk of aortic disruption due to the forces applied to the body. Damage to the sacral plexus can occur with pelvic injuries of the sacroiliac joints and the sacral notch. Most involve the L5 and S1 nerve roots and the sciatic nerve. The patient should be evaluated for distal motor weakness presenting as inability to dorsiflex and/or plantarflex the great toe. Vaginal and rectal injuries can occur and should be searched out with early use of antibiotics and repair of defects. A diverting colostomy may be required for some rectal injuries. Such injuries constitute an open pelvic fracture and carry an increased morbidity and mortality rate as high as 50%. In one series there was a higher mortality rate, higher injury severity score, greater transfusion requirements, and a higher incidence of hemodynamic instability in Orthopaedic Trauma Association (OTA) classification type A or C fracture patterns or AP compression fracture patterns than in type B or lateral compression patterns. Patients with stable injury patterns likely had injury to both anterior and posterior vessels, whereas those with unstable injury patterns more commonly had posterior vessel injuries. The OTA fracture and dislocation classification is as follows: type A, fracture sparing the posterior arch; type B, incomplete fracture of the posterior arch/partially stable; and type C, complete disruption of the posterior arch/unstable. It is further broken down as unilateral or bilateral and according to the specific location of the fracture line or dislocation.
CLINICAL DIAGNOSIS AND PRESENTATION Type I Pelvic Fractures There are four types of pelvic fracture. A type I pelvic fracture involves individual bones without a break in the pelvic ring. Type I fractures are
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stable fractures and make up one third of all pelvic fractures. Most are stable and can be treated with bed rest and pain control. There are several presentations of type I fractures. Fracture of a single ramus of the pubis or ischium is usually seen in an elderly patient who has had a fall. The patient presents ambulatory but with localized pelvic pain. A femoral neck fracture should be ruled out with a lateral radiograph. These fractures usually heal well without incident. An avulsion fracture of the anterior superior iliac spine results from a violent contraction of the sartorius muscle. The patient presents with pain, swelling, and painful flexion and abduction of the thigh. Radiography will demonstrate minimal displacement of the anterior superior iliac spine. Pain control is usually the only treatment required. Fractures of the coccyx are usually seen in women and are the result of direct trauma to the coccyx such as from a fall or a kick. The patient presents with pain and ecchymosis to the area and painful defecation. During rectal examination, pain can be elicited with palpation and movement of the coccyx. Pain control is the usual treatment. An inflatable ring or cushion may ease the pain when the patient is sitting. Avulsion fractures of the anterior inferior iliac spine occur when the rectus femoris muscle is violently contracted. The patient presents with sharp groin pain, painful and difficult ambulation, and the inability to flex the hip. On an AP radiograph, the fragment will be displaced downward. However, the fragment must be differentiated from the epiphyseal line of the acetabulum. Ischium body fractures are the result of violent external trauma against the ischium. The patient presents with localized pain of the hamstring with movement. On radiography, the fracture of the body of the ischium is demonstrated. It often occurs in a butterfly pattern on the posteroanterior film. Pain medication is usually the only treatment required. An avulsion fracture of the ischial tuberosity results from hamstring contraction and is seen in youths whose apophyses are not united. The patient presents with acute or chronic pain while sitting or upon flexing the thigh with the knee extended. Rectal examination will reveal the tuberosity to be tender. Radiography will show a detachment of the apophysis from the ischium with minimal displacement. The apophysis closes between the ages of 20 and 25 years. An acute sacral fracture usually occurs as the result of massive trauma and is associated with massive pelvic injuries. Direct posteriorto-anterior forces produce a transverse fracture. On rectal examination, there will be pain and movement of the fracture site. These fractures require immediate orthopedic evaluation and a thorough search for internal organ injury. Iliac wing fracture or Duverney’s fracture results from direct trauma to the iliac crest. The patient presents with pain, swelling, and tenderness
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over the iliac wing. There is severe pain and difficulty with ambulation. A positive Trendelenburg’s sign will be present. A thorough evaluation of the internal pelvic organs is necessary, frequently requiring a CT scan. Orthopedic consultation is needed.
Type II Pelvic Fractures A type II pelvic fracture involves a single break in the pelvic ring with little or no displacement and is usually treated with bed rest and pain medications. One fourth of these patients will have soft tissue injuries, visceral injuries, genitourinary injuries, or hemorrhage. They require resuscitation and, when stable, can benefit from a CT scan. Fractures near the subluxation of the symphysis pubis are the result of force applied to the symphysis pubis. This injury, although rare, can occur during or after childbirth. The patient presents with severe pain with some external rotation to the affected side. On examination, compression over the symphysis pubis will produce displacement and pain. Ecchymosis is rarely noted. On radiograph there will be subluxation, fracture, or dislocation. Subluxation will occur in either the coronal or sagittal planes. If dislocated, the midline will overlap by superoposterior or inferoanterior displacement of one articulating surface in relation to the other. Sacroiliac joint disruption or genitourinary injuries are common with these fractures. Fractures of the two rami ipsilaterally result from direct force applied to the femur, which carries the force into the rami as the usual cause. On examination there will be ecchymosis and pain with motion. A hematoma may be palpated. Pain will be present with flexion, abduction, external rotation, or hip extension. On radiograph, minimal or no displacement will be present. A fracture near the sacroiliac joint or subluxation of the sacroiliac joint is secondary to direct force from behind or the patient being struck from behind and laterally. He or she presents with localized pain and pain with ambulation. Pain can be reproduced with compression maneuvers. Often the posterior iliac spine appears more prominent on the traumatized side. On radiograph the sacrum, pelvis, and sacroiliac joint can be noted. A CT scan will help the clinician determine the extent of the fracture.
Type III Pelvic Fractures A type III pelvic fracture of the pelvis involves a double break in the pelvic ring. This fracture is unstable and requires an orthopedic consultation and treatment.
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Multiple pelvic fractures are the result of severe forces applied to the body and have a high incidence of internal organ damage. All multiple pelvic fractures require CT scan when the patient’s condition is stable enough to allow him or her to spend the brief period of time needed in the modern helical CT scanner. Usually, treatment is conservative; however, if the ilium is fractured, adequate reduction is necessitated. Malgaigne’s fracture (i.e., double fracture of the superior or inferior rami) or dislocation of the symphysis in association with a sacral or iliac fracture or sacroiliac joint dislocation occurs because of direct force. The patient presents with crepitans, swelling, contusion, and decreased range of motion on examination. There will be fragment motion with compression over the symphysis pubis. The ipsilateral leg will appear to be shortened. Often, associated internal organ injuries are present. Sacroiliac joint reduction may be difficult and may result in chronic pain. Straddle injuries can result in double vertical fractures or dislocation to the pubis and are a result of direct trauma to the arch or lateral compression of the pelvis occurring with a fall. The patient presents with pain, edema, deformity, and swelling. The fracture is usually treated conservatively, but the patient must be evaluated for soft tissue perineal injuries, especially to the genitourinary tract.
Type IV Pelvic Fractures A type IV acetabular fracture is usually associated with an automobile crash. There are often many other pelvic injuries present with type IV fractures. There are four anatomical types of type IV fracture: posterior, ilioischial, transverse, and iliopubic column fractures. Posterior fractures are the result of direct force applied to the flexed knee and hip. Complications can include sciatic nerve injury and femoral fractures. On radiograph, a posterior acetabular fracture with a posterior hip dislocation is seen. Ilioischial column fractures are seen when there is direct force to the knee with the thigh abducted and flexed. On radiograph, a large medially displaced fragment with central dislocation of the femoral head is noted. There may be associated sciatic nerve injury. Transverse fractures of the acetabulum result from lateral or medial forces over the greater trochanter or forces acting posteriorly to anteriorly on the posterior pelvis with the hip flexed. On radiograph, there will be a central hip dislocation. Iliopubic column fractures are secondary to lateral forces to the greater trochanter with the hip externally rotated. On radiograph, there will be external hip rotation with the ilioischial line disrupted and the anterior lip fractured.
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EXAMINATION The patient with a fractured pelvis has had tremendous forces applied to the body, and there is a high potential for multiple serious injuries. The patient must be resuscitated according to ATLS principles as the evaluation progresses. After the ABCD phase of the primary survey (i.e., ensuring adequacy of airway, breathing, circulation, including volume replacement and bleeding control, and disability), attention can be given to “E” exposure. A visual examination of the patient may reveal seat belt marks, ecchymoses, deformity or swelling over the pelvis, or abnormal position or length of the lower extremities, with or without spontaneous movement. The pelvis should be gently compressed in a lateral-to-medial direction and externally rotated to determine stability. The symphysis pubis must be compressed to evaluate for injury. The movements of pelvic examination should be limited to reduce exacerbation of hemorrhage. The hips are evaluated for pain, with range of motion and deformity representing an acetabular or associated hip fracture. The genitourinary system must be evaluated for injury. In male patients, the clinician should look for blood at the meatus and ecchymosis of the scrotum or perineum, and on rectal examination, a loss of the normal firm feel of the prostate gland replaced with a soft “mushy” hematoma should be noted, if present. Any of these findings may represent trauma to the membranous urethra at the site of its attachment to the symphysis pubis area. If present, a retrograde urethrogram should be completed before urethral catheterization. Once the patient is catheterized, if blood is encountered there must be further evaluation of the bladder and kidneys using a cystogram and CT scan or IVP. Injury to the female urethra is rare; however, the patient with a pelvic fracture should have a minimum of a bimanual pelvic examination, and, if any blood is present, a speculum examination is necessary to search for vaginal laceration, which could represent an open pelvic fracture requiring irrigation, closure in the operating room, and antibiotic therapy. Male and female patients should be evaluated for rectal injuries with appropriate treatment and possible diverting colostomy. A thorough neurological examination must be done to search for injuries related to the lumbosacral plexus and the pudendal and sciatic nerves. Some secondary signs of a pelvic fracture include Destot’s sign, a superficial hematoma above the inguinal ligament or of the scrotum. Roux’s sign occurs when the distance measured from the greater trochanter to the pubic spine is diminished on one side, as compared with the other, as might occur with an overlapping anterior ring fracture. Earle’s sign is present when there is evidence of a large hematoma, an abnormal palpable bony prominence, or a tender fracture line noted on rectal examination.
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RADIOGRAPHS Initial trauma radiographs for a severely injured patient include an AP portable chest and an AP pelvis x-ray. Additional radiographs can be obtained once the patient’s condition has stabilized. An AP and lateral pelvis radiograph should be the minimum taken for a possible pelvic fracture. If the hip is also considered fractured, it should not be put in the frog-leg position. The pelvis must be moved as little as possible until the type of injury is determined to reduce pain and aggravation of bleeding. Stabilization of the patient takes priority over obtaining radiographs. The symphysis pubis is normally less than 5 mm wide. A small offset of 1–2 mm to the left or right is a normal variant. An overlapping symphysis is abnormal. The sacroiliac joint is normally 2–4 mm wide. A fracture of the fifth lumbar transverse process often accompanies a sacroiliac joint disruption or a vertical sacral fracture and is a clue to posterior arch injury. Specialized radiographs of the pelvis can be used to obtain greater detail of the pelvis. The inlet and the tangential projection can be obtained. The inlet view is performed by taking a 30-degree caudal angulation of the beam. The beam is angled 60 degrees to the plate and is perpendicular to the pelvic inlet. This view helps determine whether there is a posterior arch or inward displacement of the anterior arch. The tangential projection is the reverse of the inlet view. The beam is directed cephalad. This view can help to determine whether there is a sacral fracture or a displacement of the sacral joint. A CT scan of a fractured pelvis will further define the fracture and evaluate for internal organ damage and hemorrhage. It should be remembered that the pelvis is a ring. If there is one fracture, the clinician should always look for a second fracture or dislocation.
LABORATORY STUDIES During the initial resuscitation of the patient, as large bore IV lines are placed, blood should be obtained for CBC, INR, PTT, type and crossmatch for at least 6 units of blood, liver profile, and measurements of electrolytes, glucose, beta human chorionic gonadotrophic hormone, and cardiac enzymes, including creatine kinase. An analysis of arterial blood gas with lactate and a urinalysis should be performed.
TREATMENT During resuscitation of a trauma patient with a pelvic fracture, it is essential to recognize that the potential for significant hypovolemia exists and efforts should immediately be instituted to control further bleeding. The patient may have intra-abdominal injuries. FAST can give a quick assessment of possible intra-abdominal bleeding but only assists if apparent fluid is noted and does not reveal retroperitoneal bleeding.
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If the patient’s condition is too unstable to permit a CT evaluation, a DPL may be done searching for bleeding. However, this study is subject to a higher than usual false-positive rate and will not ascertain retroperitoneal hemorrhage. Crystalloid fluids should be infused at a high rate with early use of blood. The pelvis and retroperitoneal area can easily hold 4 liters of blood until the vascular pressure is exceeded and tamponade occurs. Most bleeding may occur from fracture surfaces of the pelvic bones that also have a hematopoietic function with high vascularity. Some are from the iliac arteries and branches and the venous plexus. There are several techniques to assist with the control of pelvic hemorrhage. Before admission to the hospital and transfer to a higher level of care, use of a pneumatic antishock garment may help reduce the pelvic volume by increasing intrapelvic pressure and slowing hemorrhage. The garment limits access to the lower half of the body and, if left on for a prolonged time, may lead to compartment syndrome. An alternate technique is the use of a bedsheet placed around the pelvis and pulled tightly. Once the patient arrives at the facility with the highest level of care available, an orthopedic evaluation should be carried out and the patient may need the application of external fixation in the resuscitation area or internal fixation in the operating suite. Bleeding from major pelvic arteries can be controlled with interventional radiological procedures (e.g., angiography/ embolization) using coils and insufflation of Gelfoam. As more emphasis is placed on early efficient control of bleeding and hypovolemia, there is some advocacy for subjecting patients with severe pelvic fracture to angiography as soon as possible with early mobilization of the angiography team. However, there continues to be need for further study and the developing of protocols based on the capabilities of various treatment centers.
Bibliography Gibbs MA, Bose MJ: Pelvic ring fractures. In Ferrera PC, Colucclello SA, Marx J, et al (eds): Trauma Management: An Emergency Medicine Approach. Mosby: St Louis, 2001. Hak DJ: The role of pelvic angiography in evaluation and treatment of pelvic trauma, Orthopedic Clin North Am 2004;35:439–443. Jerald DA: Pelvic fractures. In Marx JA (ed): Advances in Trauma: Emergency Clinics of North America. Vol. 11.1. WB Saunders: Philadelphia, 1993, pp 147–163. Kaufmann C, Parks SN, Chairs of ATLS Subcommittee: Abdominal trauma. In Student Course Manual: American College of Surgeons Committee on Trauma, ed 7. American College of Surgeons: Chicago, 2004, pp 137–138. Kaufmann C, Parks SN, Chairs of ATLS Subcommittee: Musculoskeletal trauma. In Student Course Manual: American College of Surgeons Committee on Trauma, ed 7. American College of Surgeons: Chicago, 2004. Metz CM, Metz DJ, Goulet JA, Williams D: Pelvic fracture patterns and corresponding angiographic sources of hemorrhage, Orthopedic Clin North Am 2004;35:431–437. Ochsner MG: Pelvic fracture as an indicator of aortic rupture, J Trauma 1989;29:1376.
1090 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Ochsner MG, Hoffman AP, Dipasquale D: Associated aortic rupture-pelvic fracture: An alert to orthopedic and general surgeons, J Trauma 1993;33:429. Orthopaedic Trauma Association Committee for Coding and Classification: Fracture and dislocation compendium, J Orthop Trauma 1996;10(Suppl 1):66–70. Simong RR: Koenigsknecht SJ: Emergency Orthopedics: The Extremities, ed 4. McGrawHill: New York, 2001, p 353. Wilson RF: Pelvic fractures. In Handbook of Trauma: Pitfalls and Pearls, Lippincott, Williams & Wilkins: Philadelphia, 1999, pp 422–429.
Spinal Cord Injuries LON RAMEY
CPT Code: Spinal cord injury not otherwise classified 806.5, Cervical fracture 806.0 (See specific vertebral body fracture type.)
Key Points Spinal cord injuries can be devastating injuries to both patients and their families. Accurate and timely diagnosis is a must when evaluating a trauma patient with these injuries. ! Emergency Actions ! Airway, breathing, and circulation must be addressed and immediate spinal immobilization must be achieved with a cervical collar and rigid back board both on-scene and during transport. The use of the cervical collar and strict precautions—including movement of the patient by log-roll only—must be maintained upon arrival to the ED. Continuous monitoring of vital signs with frequent reassessment is needed to prevent spinal shock and for early recognition of the signs and symptoms of autonomic dysreflexia.
DEFINITION Spinal cord injury is defined as any injury to the spinal nerves resulting in either incomplete or complete loss of motor and/or sensory function at or below the level of injury.
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EPIDEMIOLOGY In the United States, the incidence of spinal cord injury is approximately 50 cases per million population, or about 14,000 patients per year. Approximately 450,000 persons in the United States have sustained traumatic spinal cord injuries. Males account for 82% of all spinal cord injuries and females for 18%. MVCs are the leading cause of spinal cord injury (44%), followed by acts of violence (24%), falls (22%), sports injuries (8%), and other causes (2%). Only about 5% of spinal cord injuries occur in children. However, the fatality rate is higher with pediatric spine injuries.
CLINICAL PRESENTATION Symptoms of spinal cord injury may develop acutely or may occur gradually due to swelling and edema of the spinal cord and from fluid accumulation surrounding the cord at the site of injury. Injuries may either be complete (i.e., with total loss of motor and sensory signals below the level of injury) or incomplete (i.e., with some preserved function below the level of injury). The initial mechanical trauma results from traction and compression forces. Direct compression of neural elements by bone fragments, disk material, and ligaments damages both the central and peripheral nervous systems. Blood vessel damage also leads to ischemia. Rupture of axons and neural cell membranes also occurs. Microhemorrhages occur within minutes in the central gray matter and progress over the next few hours. Massive cord swelling happens within minutes. The cord fills the whole spinal canal at the injury level and leads to further secondary ischemia. Loss of autoregulation and spinal shock cause systemic hypotension and exacerbate ischemia. Spinal fractures account for the majority of spinal cord injuries; however, these injuries can also occur in the absence of fractures when there is total ligament disruption and critical spinal instability. There are multiple types of fractures of the spine that can be classified by either location or type. Atlanto-occipital dislocation can occur as longitudinal distraction, anterior dislocation, or as posterior dislocation. It is two times more likely to occur in children than in adults. Atlantoaxial rotary subluxation occurs when rotary forces disrupt the transverse ligament. With a competent transverse ligament, there can be atlantoaxial rotation without anterior displacement. If the transverse ligament is incompetent, however, there can be anterior displacement, which increases the chance for neurological injury. Jefferson’s fracture or C1 burst fracture occurs with axial loading resulting from vertical compression. It is most commonly seen in diving injuries. The hangman’s fracture is a bilateral fracture through the pars interarticularis of the C2 pedicles. The clay shoveler’s fracture occurs with the avulsion of the C7 spinous process.
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Teardrop fractures occur when a small chip of bone avulses off the anterior inferior edge of the vertebral body. They are often associated with fracture through the sagittal plane of the vertebral body with a large triangular fragment. Anterior compression fractures occur when the middle vertebral column acts as a fulcrum during flexion injuries resulting in wedging of the anterior vertebral body. Burst fractures are the result of axial loading with compression of the whole vertebral body causing failure of the anterior and middle columns. These fractures occur most commonly at the thoracolumbar junction, between T10 and L2. Seat belt fractures are caused by flexion-distraction forces commonly encountered when a lap belt is worn during an MVC. They are fractures through the middle and posterior columns and can occur at one level (Chance fracture) or at multiple levels. Fracture-dislocations occur when all three columns fail as a result of combined compression, tension, rotation, and shear forces. There is almost always unilateral or bilateral facet dislocation associated with these fractures. Complete spinal cord injury is present when there is no motor or sensory function preserved more than three segments below the injured level. Only about 3% of patients diagnosed with complete injuries will show some improvement in function after the first 24 hours. If there is some preservation of function more than three segments below the level of injury, then the spinal cord injury is termed incomplete. There are four major types of incomplete spinal cord injuries: central cord syndrome, anterior cord syndrome, Brown-Séquard syndrome, and posterior cord syndrome. Central cord syndrome is the most common incomplete cord syndrome. It is usually caused from hyperextension injury of the osteoarthritic spine. There is motor weakness and sensory deficit to bilateral upper extremities with more preservation of function in the lower extremities. The cord is injured in the central gray matter that contains the sensory and motor fibers for the upper extremity. Treatment can vary from observation only to surgical decompression at the affected level. Anterior cord syndrome can result from ischemia to the cord because of infarction of the anterior spinal artery or from compression of the anterior cord by either a displaced bone fragment or a traumatic herniated disk. Treatment is to remove the underlying cause of cord injury. Brown-Séquard syndrome is a hemisection injury to the spinal cord. It is most commonly caused by penetrating injury to the spine and results in an ipsilateral loss of motor, proprioception, and vibratory sense and a contralateral loss of pain and temperature sense. Patients with BrownSéquard syndrome have the highest chance for recovery of all the cord syndromes. Posterior cord syndrome is rare and occurs with damage to the posterior cord elements with preservation of anterior cord. Patients experience pain and paresthesias that can be accompanied by paresis.
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In normal adults, the spinal cord usually terminates at the L2/L1 level, which begins the conus medullaris. Injury below this level can result in traumatic herniation of the lumbar disks and injury to the nerve fibers. Cauda equina syndrome occurs due to compression of the nerve fibers by either a herniated disk, tumor, spinal epidural hematoma, or spinal abscess. Symptoms include urinary retention, fecal incontinence, and “saddle anesthesia.” Cauda equina syndrome is a surgical emergency and must be treated immediately to prevent permanent neurological damage. No chapter on spinal cord injury would be complete without mentioning SCIWORA (i.e., spinal cord injury without radiographic abnormality). This phenomenon occurs most frequently in children and is thought to result from increased elasticity of the spinal ligaments and paravertebral soft tissues. The spinal cord may become contused, infracted, or stretched. Plain radiographs and CT scans are of no benefit but must be done to rule out other injuries. Magnetic resonance imaging (MRI) can reveal a lesion in some cases.
EXAMINATION A complete and thorough neurological examination is a must in a patient with spinal cord injury. This includes a head-to-toe testing of all dermatomes for sensory deficits and motor weakness. The examiner should begin by log-rolling the patient and performing a visual assessment of the back and spine. Sensory input should be assessed using fine-touch, pinprick, temperature discrepancy, vibratory sense, and proprioception tests. In the upper extremity, the motor examination includes shoulder shrug, deltoids, triceps, biceps, wrist flexion/extension, hand intrinsics, and grasp. In the lower extremity, the motor examination includes hip flexion/extension, knee flexion/extension, plantar flexion, dorsiflexion, and great toe extension. All sensory data should be recorded as “present” or “absent,” and motor strength is recorded using the 0–5 grading system. Finally, a testing of reflexes is vitally important in a patient with spinal cord injury. These include the biceps, brachioradialis, triceps, patellar, Achilles tendon, cremasteric, bulbocavernosus, Hoffmann’s reflex, abdominal cutaneous, anal wink, and testing for clonus. A rectal examination should be performed on any patient suspected of having a spinal cord injury.
LABORATORY FINDINGS Routine laboratory tests should be performed at the time of admission, including coagulation studies. Repeated hematocrit tests should be performed and the results monitored if internal bleeding is suspected.
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DIAGNOSIS Most spinal cord injuries can be diagnosed with a prudent physical examination and later confirmed by radiological studies. The clinician should be aware for signs of spinal shock, which include hypotension, bradycardia, decreased urinary output, and warm skin. This occurs due to loss of vascular tone and unopposed parasympathetic impulses. Motor weakness and sensory deficits can help the examiner to localize the likely area of injury. Frequent reassessment is mandatory to detect early deterioration noted in the neurological examination. Rapid neurological deterioration will most likely lead to emergency surgical intervention.
RADIOGRAPHS Fractures can be first identified with plain radiographs but are better visualized using CT scanning. Both sagittal and axial cuts are needed, and after the area of injury is determined, a follow-up CT scan with fine cuts 1–3 mm through the area of interest with reconstruction images can aid in making the diagnosis. MRI is considered the “gold standard” for imaging the spinal cord. Whenever a spinal cord injury is suspected, the clinician should perform an immediate MRI scan, with and without contrast, after the patient’s condition has stabilized. For patients too large for the MRI machinery, or for patients that have metallic hardware, a CT myelogram should be performed in place of the MRI scan.
TREATMENT The treatment of any trauma patient begins with basic life support measures. Spinal immobilization must be maintained with a cervical collar and back board while en route to the ED, and strict spinal precautions must be observed once the patient arrives at the ED. If a patient with suspected cervical injuries requires intubation, it should be performed by personnel with experience performing in-line intubation using the Sellick maneuver, or by using fiberoptic guidance if it is readily available. The neurological examination should be performed on a nonintubated, nonsedated patient, if possible. For any patient with evidence of neurological deficit, methylprednisolone is given with an initial bolus dose of 30 mg/ kg over 1 hour, and then continued at 5.4 mg/kg/hr 23 hours. Emergent surgical decompression and stabilization is considered for any patient with MRI findings of acute spinal cord compression by bone fragmentation, herniated or ruptured disk, spinal epidural hematoma, or cauda equina syndrome. Patients with fracture-dislocations will be placed in traction using Gardner-Wells tongs for attempted preoperative closed reduction. Once reduction is accomplished, the patient is usually operated on within a matter of hours. If closed reduction cannot be accomplished,
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then stabilization surgery is performed with hopes of intraoperative reduction at the time of surgery. Patients with stable neurological examination findings will usually be allowed to stabilize for a few days before surgical intervention is planned. Fractures that are nonsurgical are usually treated with bracing for 6–12 weeks, depending on the location and severity. With any spinal cord injury, the success of the treatment depends on the timing from diagnosis to intervention, and the degree of injury sustained. Patients with incomplete injuries will usually have some improvement in their neurological function, whereas patients with initial complete injuries are unlikely to regain any function below the level of injury. Most of the patients from both groups will require long-term rehabilitative treatment. The most common long-term complications in patients with spinal cord injury are pressures ulcers, occurring at a 1-year incidence of 15% and steadily increasing thereafter.
Bibliography Bosch A, Stauffer ES, Nickel VL, et al: Incomplete traumatic quadriplegia: A ten-year review, JAMA 1971;216:473–478. Greenberg MS: Handbook of Neurosurgery, ed 5. Thieme: New York, Stuttgart, 2001. Spinal cord injury. American Association of Neurological Surgeons: November 2005. Available at: http://www.neurosurgerytoday.org. Stauffer ES: Diagnosis and prognosis of acute cervical spine cord injury, Clin Orthop Relat Res 1975;112:9–15.
Thoracic Trauma CHARLES R. BAUER
ICD Code: Trauma 959.9 (See specific injury for specific code.)
Key Points A patient with thoracic trauma may present in a condition ranging from minimal symptoms to frank shock. At initial presentation, the patient should receive evaluation and resuscitation using ATLS ABCDE guidelines. The airway should be accessed and corrective care provided.
1096 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! Any patient who presents to an ED with suspected trauma should have a safety net established: two large-gauge IV lines should be introduced, cardiac monitoring should be initiated, oxygen should be administered, trauma laboratory test samples should be drawn, and acute trauma x-rays should be performed.
DEFINITION Trauma to the thorax can be of blunt or penetrating etiology. It can involve the chest wall, heart, lungs, trachea and bronchi, esophagus, aorta and major vessels, spinal column, and diaphragm. The region of the thoracic cage inferior to the nipple line protects the upper abdominal organs. Chest injuries are directly responsible for more than 25% of trauma deaths annually and contribute significantly to another 25% of trauma fatalities. Fewer than 10% of blunt trauma patients and 15%–30% of penetrating trauma patients require thoracotomy. The remainder can be treated with simple trauma evaluation and treatment.
CLINICAL PRESENTATION AND EXAMINATION A patient with thoracic trauma may present in a condition ranging from minimal symptoms to frank shock. At initial presentation, the patient should have evaluation and resuscitation using ATLS ABCDE guidelines. The airway should be accessed and corrective care provided. The most common cause of airway obstruction continues to be the tongue resting against the retropharyngeal structures. In an unconscious patient, other causes include vomitus, dentures, or blood occluding the larynx or the tracheal-bronchial tree. If the patient is making little or no effort to breathe, the problem may be the result of head or spinal cord trauma or to central nervous system dysfunction resulting from drug ingestion. With little or no air movement, upper airway obstruction should be considered. Breathing is accessed using the look, listen, and feel approach, noting the rise and fall of the chest with respiration and the presence or absence of breath sounds and heart sounds with an obtainable pulse. The trachea should be examined looking for midline deviation, and the presence or absence of neck vein distention should be noted. The entire anterior and posterior of the chest must be examined. Crepitation noted on palpation may represent rib fractures or subcutaneous air. Early in the course of evaluation, a portable AP chest radiograph should be obtained. Specific findings will be addressed with individual pathophysiological entities. During the initial assessment, any life-threatening injuries that are present must be noted and corrected simultaneously. Hypoxia, hypercarbia,
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and acidosis are frequently noted. The patient must receive oxygen via a patent airway, including endotracheal intubation, if needed. Tissue hypoxia and metabolic acidosis are prevented by adequate perfusion. Hypovolemia and any impediments to circulation such as tension pneumothorax or pericardial tamponade must be corrected. Thoracic trauma can be divided into immediately life-threatening conditions and potentially serious conditions.
LIFE-THREATENING INJURIES Airway Obstruction Some rare skeletal injuries may cause airway obstruction due to direct pressure on the trachea or damage to major vessels. A posterior dislocation of the sternoclavicular joint can partially obstruct the airway recognized by stridor. There is evidence of trauma to the upper chest with possible depression of the clavicle. This can be corrected by grasping the clavicle with a clamp such as a towel clip and manually reducing it. Laterally, clavicle fracture fragments can lacerate major vessels and injure the brachial plexus. The sternum can usually be fractured with direct trauma. The scapula is rarely fractured, but when it is, there is a reported 80%–90% associated injury rate. Both sternum and scapula fractures are indicative of significant forces applied to the body.
Open Pneumothorax An open or sucking chest wound can cause ineffective ventilation due to the preferential flow of air through the defect rather than the trachea. This usually requires a defect of at least two thirds the diameter of the trachea. It can be easily corrected temporarily with the application of an occlusive dressing. The dressing is secured with tape on three sides, leaving the fourth side open to relieve excessive intrathoracic pressure if it builds up as an iatrogenic tension pneumothorax. If there is not spontaneous relief, it may be necessary to remove the dressing. If there is still no relief of the tension pneumothorax, a needle decompression may be required. Ultimately, a tube thoracostomy is completed at a site other than the wound. A portable AP radiograph should be obtained noting foreign bodies, fractures, pneumothorax, hemothorax, and mediastinal and diaphragmatic injuries. If the patient is intubated, the position of the tip of the tube relative to the carina should be noted. The tip should usually be 2.0–2.5 cm above the carina. The position of chest tubes should also be noted.
Tension Pneumothorax Tension pneumothorax is a major life-threatening condition that must be recognized by clinical findings and immediately treated. Air from a leak
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in the thoracic wall or the lung becomes trapped in the pleural space, decreasing venous return to the heart and collapsing the opposite lung. The patient presents with signs of hypoxia, hypotension, and tachycardia with decreased breath sounds and hyper-resonance on the side of the trauma. The trachea may be shifted toward the opposite side with or without neck vein distention. The latter may be absent in the presence of hypovolemia. Immediate treatment of a tension pneumothorax consists of the insertion of a large-caliber (14–16 gauge) catheter into the pleural space in the second intercostal space just lateral to the midclavicular line. A rush of air is expected, with temporary relief of the tension pneumothorax. A tube thoracostomy should then be placed on the affected side in the fifth intercostal space just anterior to the midaxillary line and attached to an underwater seal drainage system. If transport is required, a one-way valve system can be attached to the tube. In an emergency, this can be improvised with a glove finger cut off and placed over the tube, leaving the remainder of the glove open. A portable AP chest radiograph is recommended, as noted previously. It is important to note that if a patient were to have bilateral tension pneumothoraces, there may not be a shift of the trachea (mediastinum), but other clinical findings would remain the same. This is a serious condition requiring immediate clinical recognition with treatment including bilateral needle decompression and chest tube placement.
Flail Chest and Pulmonary Contusion A flail chest is the result of trauma to the chest wall with discontinuity of several segments of ribs due to either fractures at more than one site or a fracture and a costochondral separation. This results in inadequate mechanical chest wall movement, compromising ventilation. There may be significant trauma to the underlying lung with hemorrhage, interstitial edema, and fluid within the alveoli. In addition to splinting due to pain and decreased or asymmetrical chest wall movement, the patient may have hypoxia due to respiratory failure. An arterial blood gas analysis may assist with proper diagnosis and treatment. A chest radiograph may reveal rib fractures and patchy areas of hemorrhage and edema representing pulmonary contusion. The treatment of flail chest is based on the condition of the patient. If the patient has significant hypoxia on arterial blood gas analysis with a PaO2 at or below 65 mmHg or SaO2 of 90% or less, the patient should be intubated. Fluid replacement should be adequate to replace blood loss, but the patient should not be overhydrated. Humidified oxygen must be provided. Pain control can be achieved with small IV increments of
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narcotics, intercostal nerve blocks, or, ideally, with epidural spinal anesthesia. Patients with underlying pulmonary disease should be considered for intubation early in treatment, whereas some other patients may not require intubation. Chest wall stabilization with sand bags, towel clips, taping, and other techniques are no longer used.
Massive Hemothorax Massive hemothorax is usually the result of penetrating trauma, but occasionally blunt trauma with the rapid loss of blood into the pleural space is the cause. This condition is defined as the presence of 1500 ml or more of blood or more than one third of the patient’s blood volume in the hemithorax. The source is usually major hilar or systemic vessels. Clinical findings include signs of hypovolemia with tachycardia and hypotension, and hypoxia with decreased breath sounds and dullness found with percussion of the affected hemithorax. Tracheal deviation may not be expected unless there is an accompanying tension pneumothorax. Neck vein distention is seldom seen due to the hypovolemia. Treatment begins with the establishment of an adequate airway and ventilation. Two large-caliber peripheral IV catheters should be used to infuse warmed crystalloid fluid and O-negative or type-specific blood. A thoracostomy tube (men, 36–40 Fr; women, 32–38 Fr) should be placed at the level of the nipple line just anterior to the midaxillary line with the collection system attached to suction. The collected blood should be made available for autotransfusion. A thoracotomy to control bleeding should be considered if the blood loss is over 1500 ml or one third of blood volume or in the case of a significant initial loss noted and a continued loss of 200 ml/hr for 2–4 hours. The thoracotomy should be performed by a qualified, experienced surgeon.
Cardiac Tamponade Cardiac tamponade is usually the result of penetrating trauma, although it can follow blunt trauma. Blood collects within the pericardial sac, decreasing cardiac output. The pericardium is fibrous and inelastic with a limited volume available. As the blood collects in the pericardium, the pressure increases, available volume decreases, and the amount of blood that can enter the heart is decreased. This causes less blood volume per beat and also less stretch of the cardiac muscle for maximum contraction. The diagnosis of cardiac tamponade may be difficult, particularly in the presence of hypovolemia and tension pneumothorax. The classic signs of Beck’s triad—which consists of neck vein distention due to increased
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venous pressure, arterial hypotension, and muffled heart tones—are of limited use in the ED. With hypovolemia there may not be neck vein distention. Hypotension can be due to hypovolemia, tension pneumothorax, and other causes. And muffled heart tones are difficult to hear during the activity of resuscitation. Pulsus paradoxus occurs normally with respiration. There is a decrease in systolic pressure with spontaneous inspiration; however, if this decrease exceeds 10 mmHg, cardiac tamponade may be present. The best way to diagnose cardiac tamponade is to have a high index of suspicion, particularly with penetrating wounds of the mid-anterior chest between the midclavicular lines and posteriorly between the scapulae. Because other causes of decreased cardiac output are excluded, cardiac tamponade should be suspected. A central venous line may show an increased venous pressure. Volume replacement is instituted to increase cardiac output. A chest radiograph usually does not show any expansion of the pericardial sac because of the inelasticity. Sonography, if available, along with examination by experienced clinicians may reveal fluid collected within the pericardial sac. Even small quantities of pericardial fluid can be detected, and this is the study of choice to assess for hemopericardium. The evaluation of the pericardium by placing the sonography probe inferior to the xiphoid angling cephalad is the first step in the FAST examination (see the section “Abdominal Trauma” for details). When sonography is not available and pericardial tamponade is suspected, the patient should be administered a rapid infusion of warm crystalloid. A pericardiocentesis can be both diagnostic and therapeutic. A 15-cm over-the-needle catheter is inserted adjacent to the xiphoid at a 45-degree angle toward the left shoulder and 45 degrees cephalad. If the needle touches the epicardium, a “current of injury” pattern may appear on the cardiac monitor. This may be ST-T wave changes or widened and enlarged QRS complexes. Aspiration of even small amounts of blood may improve cardiac output until definitive treatment can be provided. Unclotted blood that is aspirated is diagnostic, but there may be significant clotted blood within the pericardium. The catheter should be left in position with a three-way stopcock attached for repeated aspiration. If pericardial tamponade is diagnosed or seriously suspected, the patient should be immediately evaluated by a trained, experienced surgical team for definitive treatment. If surgical capabilities are not available, the patient should be transferred with repeat aspirations via the catheter as needed, based on the patient’s status. The surgical treatment may be a pericardial window using the subxiphoid/sternal approach for initial diagnosis. If positive, the patient will require a thoracotomy, pericardiotomy, and repair of the bleeding source. It should be noted that pericardial tamponade may occur rapidly with penetrating injury or slowly and may be exasperated with coagulopathy frequently seen in trauma patients undergoing resuscitation.
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Emergency Department Resuscitation Thoracotomy A qualified surgeon should be available to immediately control hemorrhage and correct life-threatening injuries. Success and appropriate use of resuscitation thoracotomy has been well evaluated over the years. Banney and Moore reviewed results of 2 decades of postinjury ED thoracotomies. When vital signs were present on arrival, there was a survival rate of 3% for blunt trauma and 24% for penetrating trauma, with an overall rate of 13%. When vital signs are absent, the results drop to 1% for blunt injuries, 3% for penetrating, and 2% overall. There is an increased risk of healthcare worker exposure to human immunodeficiency virus and hepatitis that can be minimized with the appropriate application of universal cautions and the selective use of ED thoracotomy. A patient arriving in the ED with a penetrating thoracic injury and ECG activity without a pulse (i.e., pulseless electrical activity) may be a candidate for immediate left anterior thoracotomy by a qualified surgeon. Patients sustaining blunt thoracic trauma who present with electrical activity but have no pulse are not considered candidates for ED thoracotomy. Lifesaving efforts during the ED thoracotomy may include open cardiac massage, which is more efficient than closed massage. The pericardial sac can be quickly evacuated of blood and clots with control of bleeding sites. The hilar vessels can be temporarily cross-clamped to control hemorrhage. The descending aorta can be cross-clamped to decrease intra-abdominal hemorrhage while restoring intravascular volume, allowing perfusion primarily to the heart and brain. A patient with air embolism resulting from bronchovenous fistulae after a penetrating injury or blast lung injury may benefit from hilar cross-clamping and the venting of air from the ventricles and the aortic root.
POTENTIALLY LIFE-THREATENING INJURIES There are a number of other potentially life-threatening injuries that must be identified and for which appropriate treatment must be rendered.
Simple Pneumothorax A simple pneumothorax can be caused by blunt trauma resulting from rib fracture or by penetrating trauma. The clinician should carry a high index of suspicion and should perform a careful examination of the entire thorax looking for wounds, crepitation due to rib fracture, or subcutaneous air and listening for breath sounds. The latter may be difficult to hear but may be best evaluated by listening in the lateral chest infra-axillary area.
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Hemoglobin saturation may be decreased, but blood pressure and pulse will be minimally affected. A chest radiograph will assist with diagnosis. A patient with a minimal collection of pleural space air and no other significant injuries may warrant observation with repeated radiographs. If the patient is to be transported (especially by air), is to undergo surgical procedures with general anesthesia, or is mechanically ventilated, it is appropriate to perform tube thoracostomies to decrease the risk of developing a tension pneumothorax. A tube thoracostomy is placed in the fifth intercostal space and attached to underwater seal drainage. The tube size may vary depending on the presence or absence of blood.
Hemothorax Blood may collect in the pleural space as a result of intercostal or internal mammary artery laceration, laceration of the lung, or other bleeding points. The volume is less than defined for the massive hemothorax. Adequate-sized chest tubes must be placed with evacuation of the blood. This will decrease the risk of later entrapment of the lung with clotted blood requiring surgical removal and will aid with the monitoring of continued bleeding. The diaphragm can be evaluated better for integrity after blood evacuation.
Tracheobronchial Injury Tracheobronchial tree injury can occur from the level of the larynx to the bronchi. It occurs more commonly with blunt than penetrating trauma. A common site for disruption is the main bronchi near the carina. There may be associated pneumothorax, subcutaneous emphysema, air embolism, and pneumomediastinum. When a chest tube is placed there may be a continuous air leak. Additional chest tubes may be placed and high-negative pressure administered with the lung continuing to be collapsed. Further endoscopic evaluation and surgical correction are required.
Traumatic Aortic Disruption and Penetrating Injury Traumatic aortic disruption is usually the result of a rapid deceleration from an MVC with or without ejection or from a fall. Although most are thought to be due to frontal collisions, a significant number is related to side impact. More than 90% of aortic and great vessel injuries are due to penetrating trauma. The most common cause of scene mortality after a MVC or fall from a height is traumatic aortic injury (TAI), accounting for up to 15% of deaths. Between 75% and 90% of patients with TAI die before the arrival of prehospital care responders.
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The key to diagnosing TAI is an awareness of the mechanism of injury and careful evaluation. The patient may present with signs of pericardial tamponade if there is associated bleeding into the pericardial sac. A plain AP chest radiograph may show evidence of a hematoma developing in the area of disruption, which is usually at the ligamentum arteriosum. The expanding hematoma may show a widening of the mediastinum, obliteration of the aortic knob and the aorto-pulmonary window, deviation of the trachea and esophagus to the right, depression of the left mainstem bronchus, presence of a pleural or apical cap, widening of the paratracheal stripe and paraspinal interfaces, and left hemothorax. With the availability of helical contrast-enhanced CT, a physiologically stable patient can be rapidly evaluated for TAI. Chest CT has a sensitivity of 74%–100% and a specificity of 23%–100% for detecting TAI. This is highly dependent on the quality of the equipment and the experience of the interpreters of the studies. If there is continued concern for TAI, the patient should undergo an aortography. Patients with a TAI require immediate evaluation by cardiothoracic surgeons. In the interim, judicious fluid resuscitation permitting moderate hypotension with careful intensive hemodynamic monitoring, the use of beta blockade with propranolol or labetalol titrated according to the heart rate, and nitroprusside infusion for additional blood pressure management are warranted.
Blunt Cardiac Injury Blunt cardiac injuries may result in myocardial contusion and the rupture of cardiac chambers and valves. There may be signs of pericardial tamponade and cardiac failure. The patient may report chest pain. It must be remembered that the initial causative event may have been cardiac, with the trauma being a result, such as in an MVC or a fall. The primary method of diagnosing blunt cardiac injury with myocardial contusion is with the ECG. There may be evidence of infarction, multiple premature contractions, unexplained sinus tachycardia, atrial fibrillation, ST-segment and T-wave changes, and bundle branch block. Transthoracic echocardiography may demonstrate cardiac muscle dysfunction. Based on current literature, cardiac enzymes are considered unreliable in the diagnosis of blunt cardiac injury. Prophylactic antidysrhythmic therapy is not recommended. Dysrhythmias should be treated the same as they are in nontraumatic cases.
Traumatic Diaphragmatic Injury Blunt traumatic rupture of the diaphragm usually occurs on the left hemidiaphragm and is large and radial. It is due to excessive rapid pressure applied to the abdomen. Because of the negative intrathoracic
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pressure with inspiration, there can be increasing amounts of intra-abdominal contents entering the left pleural space, compromising ventilation and cardiac function. There may be decreased breath sounds and dullness to percussion; however, it is rare to hear bowel sounds in the chest. A chest radiograph will reveal obliteration of the diaphragm outline and may show a gas pattern compatible with gastric or large and small bowel gases in the pleural space. If the diagnosis is in doubt, a gastric tube can be passed to be coiled in the stomach within the left chest. Contrast can be injected through the tube to further clarify the diagnosis. The gastric tube will also assist with decompression of the gastrointestinal tract while definitive surgical care is awaited. Thoracostomy tubes, if placed, must be at a slightly higher level, and digital exploration through the incision must be performed to ensure that the stomach and spleen are not injured. The use of a pneumatic antishock garment is contraindicated. Surgical repair of the diaphragm defect is usually accomplished through a transabdominal approach. Defects resulting from penetrating trauma of the diaphragm are usually small and can occur in any area. The defects must be identified and repaired to prevent delayed herniation of intra-abdominal contents, and this can be complicated by strangulation, infarction, perforation, and obstruction. Evaluation may include CT scan with contrast, laparoscopy, thoracoscopy, and open abdominal exploration. Appropriate methods of repair are similar to those associated with blunt defects.
Traumatic Esophageal Injury Esophageal injuries can result from blunt and penetrating trauma. Blunt injuries are frequently associated with a severe force applied to the upper abdomen with gastric contents forced into the distal esophagus. This can produce linear tears into the mediastinum or the left pleural space (the most common side). If undiagnosed, this injury has a mortality rate noted to be 18% in one study. The morbidity and mortality rate rapidly climbs with delay in diagnosis. The initial evaluation can be complicated by signs of sepsis due to mediastinitis. If a chest tube is placed, there may be food particles in the drainage. A chest radiograph may show a pneumomediastinum. The diagnosis of a traumatic esophageal injury is made by esophagoscopy and esophagography using water-soluble contrast. Early surgical repair with wide drainage of the mediastinum and pleural space provides the best outcome with the lowest mortality rate. Penetrating esophageal trauma is rare. It can occur from cervical and thoracic injuries. Diagnosis and treatment are similar to those of blunt injuries.
Bibliography Biffl WL, Moore EE, Johnson JL: Emergency department thoracotomy. In Moore EE, Feliciano DV, Mattox KL (eds): Trauma, ed 5. McGraw Hill: New York, 2004, pp 516–517.
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Kaufmann C, Parks SN, Chairs of ATLS Subcommittee: Thoracic trauma. In Advanced Trauma Life Support for Doctors, ed 7. American College of Surgeons: Chicago, 2004, p 108. Mattox KL, Wall MJ, LeMaire SA: Injury to the thoracic great vessels. In Moore EE, Feliciano DV, Mattox KL (eds): Trauma, ed 5. McGraw Hill: New York, 2004. Mirvis SE: Diagnostic imaging of thoracic trauma. In Mirvis SE, Shanmuganathan K: Imaging in Trauma and Critical Care. WB Saunders: Philadelphia, 2003. Rosen CL, Wolfe RE: Blunt chest trauma, In Ferrera PC, Colucclello SA, Marx J, et al (eds): Trauma Management an Emergency Medicine Approach. Mosby: St Louis, 2001, p 355. Wilson RF, Steiger Z: Thoracic trauma: Chest wall and lung. In Wilson RF, Walt AJ (eds): Management of Trauma: Pitfalls and Practice, ed 2. Williams & Wilkins: Philadelphia, 1996, p 314.
Trauma in the Pregnant Patient CHARLES R. BAUER
Key Points The normal pregnant woman undergoes progressive physiological and anatomical changes that contribute to the complexity of evaluation and care of the mother and fetus. ! Emergency Actions ! Upon arrival, the patient should be evaluated using the principles of ATLS following the primary and secondary assessment survey.
DEFINITION The care of a pregnant patient who has sustained trauma is complicated by the unique changes that come about as the pregnancy progresses and the presence of one or more additional individuals. From early in pregnancy, there are increased risks to the mother and fetus that may be brought about by seemingly relatively minor trauma. Understanding the physiological changes and the potential for adverse outcomes is essential. Appropriate, expedited care of the mother with careful monitoring will give the best chance for survival of the jeopardized fetus.
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EPIDEMIOLOGY Trauma to the pregnant woman may occur intentionally or unintentionally. Domestic violence affects at least 8%–17% of women during pregnancy. MVCs and falls are the most common causes of injury, whereas homicide and suicide account for one third to one half of fatalities. Most injuries are similar to those for nonpregnant patients, with head injury and hypovolemia the most common cause of maternal death. Fetal demise occurs in 80% of pregnancies in which the mother survives hemorrhagic shock.
PHYSIOLOGY OF PREGNANCY A normal pregnant woman undergoes progressive physiological and anatomical changes that contribute to the complexity of evaluation and care of the mother and fetus. The uterus remains a pelvic organ until the 12th week of gestation. It then rises from the pelvis to be at the level of the umbilicus by the 20th week and midway to the xiphoid by 32 weeks. The fundal height reaches the level of the costal margin by 34 to 36 weeks and then begins to descend as the fetal head engages the pelvis. After 24 weeks’ gestation the fetus is potentially viable, and the fetal age can be estimated by the fundal height in centimeters. The uterine wall becomes elastic and pliable as the pregnancy progresses. However, the placenta is inelastic and firm, giving the potential for even minor shearing forces to cause a separation (i.e., abruptio placentae). There is an increase of intravascular volume with a lesser increase of red blood cell mass leading to a relative physiological “anemia of pregnancy,” with a hematocrit of 32%–34% being normal with iron supplementation. Cardiac output increases 20%–30% with most of the increase occurring by the 12th gestational week with a cardiac output of 6–7 L/min. There is increase in the heart rate and a slightly low systolic pressure in early pregnancy that increases to normal during the third trimester. The diastolic pressure may be lower, resulting in a widened pulse pressure. By the third trimester, it is estimated that 20% of CO is received by the uterus and placenta. An otherwise healthy traumatized pregnant patient may lose 1200–1500 ml of blood volume before vital signs and symptoms of hypovolemia become evident. Fetal distress may be apparent with a lesser volume loss and is an early indicator of need for maternal resuscitation. Late in pregnancy, the fundus can cause compression of the inferior vena cava, resulting in decreased venous return and hypotension even in healthy pregnant patients when they are in the supine position. This can be easily alleviated by rotating the entire patient onto her left side. This should be done by elevating the right side of the back board when the patient is immobilized. Care should be taken to prevent lifting the right hip or otherwise causing rotational torsion on the
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spinal column until it has been appropriately cleared of injury. If necessary, the fundus can be manually moved to the patient’s left side, off of the vena cava. The white blood cell count increases to 15,000–18,000 in the third trimester and 25,000 at delivery. Fibrinogen levels increase to 300– 600 mg/dl, compared with 200–400 in a nonpregnant patient; there is no change in prothrombin time (PT) and PTT. A hypercoagulability state exists, with coagulation factor proteins VII, VIII, IX, X, and XII all increased. The presence of normal coagulation factors in a seriously injured pregnant patient should make one concerned for possible disseminated intravascular coagulation (DIC). A pregnant patient develops increased minute volume primarily from increased tidal volume due to stimulation of placental progesterone on the medullary respiratory center. This results in a PCO2 of 30 mmHg being normal during the second trimester. A PCO2 of 35–40 mmHg may indicate impending respiratory failure. During the course of pregnancy, the inspiratory capacity increases while the residual volume decreases. The diaphragm is elevated, and there is flaring of the thoracic cage. Caution must be exercised, requiring the placement of chest tubes one to two intercostal spaces higher than usual. Oxygen consumption is increased, requiring adequate arterial saturation during resuscitation. Because of the low PO2 of fetal hemoglobin (i.e., 32 mmHg) and its left-shifted oxygenhemoglobin dissociation curve, the fetus will benefit from a high maternal oxygen tension. The abdominal cavity changes to meet the intrusion of the pregnant uterus; the viscera elevates, causing varying pain patterns with any intra-abdominal emergency. The bladder is pushed above the pelvic brim, making it more vulnerable to injury, and there is increased hyperemia. Gastric emptying is decreased, necessitating the need for gastric intubation to decrease the risk of vomiting and aspiration. The small intestine is somewhat protected by the enlarging uterus. There is an increase of blood flow to the uterus with marked vascularity in the pelvis and retroperitoneal area. This can allow massive undetected retroperitoneal blood loss further complicated by the patient’s increased intravascular volume. The pituitary gland increases in size during pregnancy. Shock may lead to necrosis of the anterior pituitary with resultant pituitary insufficiency (i.e., Sheehan’s syndrome). The symphysis pubis widens 4–8 mm and the sacroiliac joint spaces increase by the seventh month of pregnancy. These findings need to be taken into consideration by the clinician when reviewing radiographs after trauma. The neurological status of a pregnant trauma patient must be monitored. Eclampsia may occur late in pregnancy and may mimic head injury. Neurological and obstetrical evaluations are needed to differentiate the cause of seizures and altered mental status. Associated findings in
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eclampsia may include proteinuria, hypertension, hyperreflexia, and peripheral edema. The patient may need IV magnesium sulfate at an initial dose of 4 g followed by 2–3 g/hr IVor 5 g IM in each buttock immediately after the loading dose and every 4 hours while deep tendon reflexes remain present. Emergency cesarean section should be considered.
FETAL DISTRESS The normal fetal heart rate is 120–160, and higher or lower rates are cause for concern. The patient should be placed on fetal (cardiotocographic) monitoring as soon as possible, especially after the 20th week of gestation. Signs of fetal distress may include decelerations occurring after uterine contractions (late decelerations), variable decelerations, and beat-tobeat variability noted on the tracing. The fetal distress can be the result of direct fetal injury, fetal hypoxia, maternal hypovolemia, or placental abruption. Direct fetal trauma may result in skull fractures and intracranial hemorrhage, especially after the fetal head is engaged in the pelvis.
PLACENTAL ABRUPTION The second most common cause of fetal death after maternal death is separation of the placenta from the uterine wall; this complicates 1%–5% of minor blunt abdominal trauma cases and, with major abdominal trauma, up to 7%–66%, leading to fetal mortality rates of 30%–68% noted in various studies. Clinical observation with monitoring will aid in recognizing placental injury. The examiner should note any seat belt marks across the pelvis or abdominal wall. Are there uterine tenderness or contractions, vaginal bleeding, amniotic fluid leak, a larger uterus than expected for gestational age, maternal hypovolemia out of proportion to visible bleeding or that associated with fractures, or signs of fetal distress? Vaginal bleeding and abdominal pain may not be present in all cases of abruption. A large volume of blood can be concealed beneath the placenta. Sonography may be of limited value when the placenta is attached to the posterior uterine wall; however, it should be used to assist with maternal and fetal evaluation in looking for fetal activity (cardiac and general), fetal breathing movements, fetal tone, amniotic fluid volume, and position and integrity of the placenta. In the mother, FAST should be used as it is in a nonpregnant patient, with the clinician looking for the accumulation of fluid or blood in the pericardial cavity and the abdominal cavity in the right and left upper quadrants and in the pelvis.
MATERNAL-FETAL HEMORRHAGE Mixing of fetal and maternal blood can occur with trauma, leading to fetal anemia, fetal death, and isoimmunization of the mother. The
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Kleihauer-Betke (K-B) test estimates the volume of fetal blood in the maternal circulation. As little as 0.01–0.03 ml of fetal blood will sensitize an Rh-negative mother, whereas 5 ml are required to yield a positive K-B test result. The K-B test should not be used to determine whether Rh immune globulin (RhoGAM) is to be given to an Rh-negative mother, but it can be used to determine the amount needed. All Rhnegative mothers presenting with a history of abdominal trauma should receive one 300-ug prophylactic dose of RhoGAM. The K-B test should be reserved for Rh-negative patients who have the potential for more than 30 ml of fetal blood entering the maternal circulation, and then an additional dose of RhoGAM should be given for each 30 ml as estimated by the K-B test.
CLINICAL PRESENTATION Pregnant trauma patients will benefit from the resources available at the highest level of trauma care in the community, including trauma surgeons, obstetricians, perinatologists, and neonatologists. Once the patient has been evaluated and her condition stabilized, follow-up care can be designated to the patient’s obstetrician if he or she is at a different location. During prehospital care, the patient should receive oxygen by mask and have large-bore IV lines established. The trauma facility should be alerted to allow time to notify the trauma and obstetrical/pediatric team of the impending arrival of the patient. It may be necessary to transport the patient with the right side of the back board elevated to move the uterus to the left, off the vena cava. Most trauma surgeons would recommend avoiding the use of the pneumatic antishock garment.
EXAMINATION AND TREATMENT Upon arrival, the patient should be evaluated using the principles of ATLS following the primary and secondary assessment survey:
Airway: The airway is evaluated and maintained, providing a definitive airway by endotracheal intubation if needed. High-flow oxygenation is essential. Breathing: Breathing is evaluated. If a tension pneumothorax exists, chest tubes should be placed one to two intercostal spaces higher than the usual fifth intercostal space. Circulation: Two large-bore IV sites should be established with crystalloid and type-specific blood given, as needed, with recognition of the difficulty involved with defining maternal hypovolemia by the usual criteria. Use of vasopressors should be avoided because of its adverse effect on the already compromised placental uterine circulation, leading to further fetal hypoxia.
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Disability: The neurological status of the patient must be noted, with special consideration given to other causes of altered mental status possible in pregnant patients, such as eclampsia. Exposure: The patient should be completely disrobed to enable examination for seat belt marks, ecchymoses, and other signs of trauma. The clinician should be aware of signs of domestic violence. The patient must be log-rolled to allow evaluation of her back. She should be placed in the left lateral decubitus position, with the spinal column protected from any rotational torsion forces until appropriate clearance has been granted.
Upon completion of the primary survey and completion of corrective resuscitation, attention should immediately center on the fetus; fetal heart tones, sonographic evidence of fetal heart activity, and fetal movement should be noted. The height of the fundus should be compared with the stated gestational age. After 24 weeks’ gestation, the fetus is potentially viable outside the uterus. The clinician should note the continuity of the uterus and any firmness, tenderness, or contractions. The examiner should also feel for fetal parts external to the confines of the uterus that would indicate uterine rupture. Pelvic fractures are of greater significance for bleeding due to the marked pelvic vascularity and potential injury to the fetal head if engaged. It is imperative that the pregnant patient’s perineum and vagina be examined to look for external vaginal bleeding, mucosal tears, bony fragments, or vaginal secretions. If no vaginal bleeding is present and the pregnancy is at less than 20 weeks’ gestation, a speculum examination can be performed as needed. After 20 weeks, examination of the cervix may cause bleeding in the presence of placenta previa and should be avoided without specific reasons such as pelvic fracture.
LABORATORY FINDINGS Laboratory studies should include Rh typing. The need for the K-B test can be determined later by the obstetrical consultant. Vaginal vault fluid can be tested with Nitrazine paper, which will turn purple on contact with the alkaline amniotic fluid. It should be noted that the presence of blood can give a false-positive Nitrazine test result. “Ferning” can also be observed on a microscope slide as the amniotic fluid dries. In cases of major trauma, baseline tests for consumptive coagulopathy (i.e., DIC) should be drawn to include platelet count, PT, PTT, and fibrinogen degradation products. The patient’s blood should be type and cross-matched.
RADIOGRAPHS Radiographic studies should be obtained as needed to evaluate the patient, and protective shielding should be used when possible. There
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are numerous reviews available citing the hazardous levels of radiation delivered to both the mother and fetus at various stages of pregnancy. The patient should be monitored in an appropriate setting—usually the obstetrical department. Minor facial laceration repairs and other treatments can be completed in that setting while the patient is monitored in the presence of knowledgeable obstetrical staff close to a delivery room or operating room, in case a cesarean section is warranted. Tetanus prophylaxis should be provided as in a nonpregnant patient. The clinician should be wary of pregnancy-induced hypertension resulting in preeclampsia and eclampsia. Treatment is described earlier. Amniotic fluid embolism is another rare complication of trauma and delivery, associated with maternal mortality rates as high as 80%. The classic presentation is that of sudden dyspnea and hypotension with subsequent cardiac arrest. Treatment is directed at oxygenation, maintaining cardiac output and blood pressure, and correcting any DIC that may develop.
PERIMORTEM CESAREAN SECTION If a mother with a pregnancy at 24 weeks’ gestation or later arrives in the ED within minutes of cardiac arrest, perimortem cesarean section must be considered. Appropriate staff members must be in attendance including trauma surgeons, obstetricians, and neonatologists. If the team is unable to resuscitate the patient with advanced cardiac life support efforts, the maternal-fetal circulation must continue. A thoracotomy with open heart massage without cross-clamping of the aorta should be considered. Perimortem cesarean section is most successful if performed within a minimal time period. There is greatest success if the fetus is older than 26–28 weeks’ gestational age and weighs more than 1000 g. It is estimated that there is a 40%–70% fetal survival rate with best results in those delivered within 5 minutes. There have been reported cases of maternal survival after cesarean section due to the improved hemodynamics in the mother.
Bibliography Agnoli FL, Deutchman ME: Trauma in pregnancy, J Fam Pract 1993;37:588–592. Arvanitis ML, Pasquale JL: External causes of metabolic disorders, Emerg Med Clin North Am 2005;23(3):827–841. Dahmus MA, Sibai BM: Blunt abdominal trauma: Are there any predictive factors for abruptio placentae of maternal-fetal distress? Am J Obstet Gynecol 1993;169:1054–1059. Esposito TJ, Gens DR, Smith LG, et al: Trauma during pregnancy: A review of 79 cases, Arch Surg 1991;126:1073–1078. Ferrera PC, Collucclello SA, Marx J, et al: Advanced Trauma Life Support for Physicians, ed 7. American College of Surgeons 2004, p 276.
1112 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Kass LE, Abbott JT: Trauma in pregnancy, In Ferrera PC, Colucclello SA, Marx J, et al (eds): Trauma Management: An Emergency Medicine Approach, Mosby: St Louis, 2001, pp 489–503. Knutson MM, Rozycki GS, Paquin MM: Reproductive system trauma. In Moore EE, Feliciano DV, Mattox KL (eds): Trauma, ed 5. McGraw-Hill: New York, 2004. Morkovin V: Trauma in pregnancy. In Farrel (ed): Ob/Gyn Emergencies: the First 60 Minutes, Aspen Publishers: Maryland, 1986. Neufeld JDH: Trauma in pregnancy, what if ...? Emerg Clin North Am 1993;11(1):208. Wilson RF: Handbook of Trauma: Pitfalls and Pearls. Lippincott, Williams & Wilkins: Philadelphia, 1999, p 452.
Chapter 19
Urology Emergencies Acute Renal Failure JONATHON ALLEN
ICD Code: Acute renal failure 584.9
Key Points Prerenal acute renal failure (ARF) is the most common cause of a reversible increase in nitrogenous waste products. ! Emergency Actions ! The management of ARF should be directed at restoring the glomerular filtration rate (GFR) and urine output and correcting electrolyte balance. Intravascular volume should be replenished in patients with hypovolemia. Decreased cardiac output should be augmented through increased plasma volume or vasopressors when possible.
DEFINITION Acute renal failure is characterized by a decline in renal function of relatively abrupt onset, usually less than 6–12 weeks. This leads to an accumulation of nitrogenous waste products in the blood. In the acute care setting, ARF is most often identified by an increase in urea or creatinine levels on blood chemistry. Renal failure, both acute and chronic, can be associated with oliguria (i.e., urine output of less than 400 ml/day). ARF can be divided into three categories of causation: (1) prerenal ARF, (2) intrarenal histological damage, and (3) postrenal obstruction.
PATHOLOGY The kidneys are responsible for maintaining both the volume and electrolyte compositions of body fluids; excreting metabolic waste products such as urea, creatinine, and uric acid; and eliminating exogenous drugs and toxins. The GFR is the volume of fluid that passes from the glomerular capillaries into the urinary space in 1 minute. This process of ultrafiltration is driven by hydraulic pressure generated by cardiac systole and is the initial step in the formation of urine. In a normal 70-kg person, approximately 180 L of glomerular filtrate are produced each day. The vast majority of this ultrafiltrate is reabsorbed in the tubules. 1113
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Prerenal ARF is the most common cause of a reversible increase in nitrogenous waste products. It accounts for nearly 60% of cases of ARF. The common feature of prerenal ARF is a reduction in renal blood flow. This results in a decreased GFR and a limited excretory capacity. Prerenal ARF is potentially reversible because no structural histological damage has occurred. Once renal perfusion is restored, kidney function will usually return to normal. Possible mechanisms of prerenal ARF can be separated into three causal categories: intravascular volume depletion, volume redistribution, or decreased cardiac output. Intrarenal histological damage accounts for the minority of ARF seen in the emergency department (ED). This type of ARF results from damage to glomeruli, renal interstitium, intrarenal vasculature, or renal tubules. Acute glomerulonephritis is classically indicated by hematuria, proteinuria, and red blood cell casts. There are many potential causes of acute glomerulonephritis, including systemic diseases such as systemic lupus erythematosus or Goodpasture’s syndrome and primary renal diseases such as poststreptococcal glomerulonephritis. Typically, determining the cause of acute glomerulonephritis is accomplished by renal biopsy and is more appropriately performed in the inpatient setting. ARF resulting from interstitial disease is most commonly linked to an exogenous source, such as medications or infectious organisms. Although the relationship remains poorly understood, the absence of a clear doseresponse relationship and the recurrence with rechallenge suggest an immunologically mediated mechanism. The most common offending pharmacological agents are penicillins, anticoagulants, and nonsteroidal anti-inflammatory drugs (NSAIDs). Numerous infectious sources have been linked to acute interstitial nephritis. Classic signs are rash, fever, eosinophilia, and eosinophiluria. Renal function will usually slowly return to normal after the removal of the offending agent. ARF due to renal vascular insult can occur at any vascular anatomical location. Thrombosis or vasculitis of renal arteries, arterioles, or veins is generally the result of an underlying systemic condition such as atherosclerosis, scleroderma, or sickle cell disease. Patients with prothrombotic disorders such as chronic atrial fibrillation, protein C or S deficiencies, or endocarditis are more likely to encounter acute renal artery thrombosis. Almost 90% of renal artery thromboemboli are cardiac in origin, most commonly left atrial thrombi from chronic atrial fibrillation. The most common clinical form of intrarenal ARF is acute tubular necrosis (ATN). Characterized by oliguria and granular casts containing tubular cells, ATN is most commonly induced by ischemia, direct nephrotoxicity from drugs or intravenous (IV) contrast, or increased levels of intravascular proteins, such as in multiple myeloma or rhabdomyolysis. ATN is generally reversible and typically occurs after causes of other potential causes of ARF are ruled out.
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Postrenal obstruction is an easily reversible cause of ARF and can occur at any level of the genitourinary system. Oliguria and increases in blood urea nitrogen (BUN) and creatinine are not usually seen until urethral or bilateral ureteral obstruction occurs because the nonobstructed kidney can compensate for the loss of contralateral function. Causes of ureteral obstruction include calculi, external compression by intraperitoneal masses, or inadvertent surgical ligature. Urethral obstruction is caused by malfunctioning indwelling catheters, neoplasm, calculi, or prostatitis in males. Although the onset of irreversible renal failure from obstruction is gradual, the underlying cause should be identified and corrected as soon as possible.
CLINICAL PRESENTATION Patients with ARF can present with a spectrum of findings. Patients may report oliguria or anuria, hematuria, or feelings of an inability to completely void. They may present with altered mental status or seizures due to severe electrolyte abnormalities. In nearly all cases, ARF is an incidental finding discovered during the workup of another symptom and may be the result of another disease process such as sepsis, myocardial infarction, or disseminated intravascular coagulation.
PHYSICAL EXAMINATION The examination should be complete, identifying signs of prerenal and postrenal causes. Orthostatic hypotension, decreased skin turgor, and tachycardia point toward volume depletion. A palpable distended bladder or a mass found on rectal or pelvic examination indicates possible postrenal obstruction. The presence of rashes, polyarthritis, fever, or other systemic signs would lead toward an intrarenal etiology of renal failure.
RADIOGRAPHY Radiological studies are most helpful to find the source of obstruction. Ultrasonography is the preferred method to identify significant hydronephrosis. A noncontrasted computed tomography (CT) scan of the abdomen and pelvis can help to identify renal calculi along the urinary tract or obstructive intra-abdominal masses. Intravenous pyelogram (IVP) is typically not performed because the contrast load could worsen the renal failure.
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LABORATORY FINDINGS An evaluation of ARF should begin with a urine chemistry and microscopic analysis. A complete blood count (CBC), serum electrolyte analysis, and an electrocardiogram (ECG) should also be performed. Prerenal ARF is indicated by a high urine specific gravity, a high serum BUN/creatinine ratio, and/or signs or symptoms of volume loss. Postrenal obstruction cannot be ruled out by the ability to void. Postvoid catheterization can document the amount of urine retention and could indicate a possible urethral or bladder neck obstruction. Intrarenal causes are often identified by microscopic urinalysis showing the presence of casts, microscopic red blood cells, white blood cells, or bacteria. The presence of red cell casts points toward glomerular damage, such as vasculitis or glomerulonephritis. Granular casts contain remnants of tubular cells and indicate ATN.
DIAGNOSIS A diagnosis of ARF is obtained by evaluating the history, physical examination findings, serum and urine chemistries and analyses, and radiological study results. In the ED, causes of prerenal and postrenal ARF are often easily identified. Although the specific cause of intrarenal ARF is not always identified, the differential diagnosis can be significantly narrowed.
TREATMENT Management of ARF should be directed at restoring GFR and urine output and correcting electrolyte balance. Intravascular volume should be replenished in patients with hypovolemia. Decreased cardiac output should be augmented through increased plasma volume or vasopressors, when possible. Postrenal obstruction is treated by restoring normal urinary flow. Although bladder outlet or urethral obstruction can be bypassed with a Foley catheter, proximal obstruction may require the placement of a percutaneous nephrostomy tube by a urologist or interventional radiologist. In patients with intrarenal ARF, therapy should be directed toward restoring urine output. Patients with oliguric ARF have a significantly higher mortality rate than those with nonoliguric ARF. In addition, electrolytes in nonoliguric patients are much easier to manage. Mannitol, loop diuretics, and dopamine are the most common agents used to restore urine output. Furosemide (Lasix) has been shown to decrease dialysis requirements and complications from volume overload but has no effect on mortality. The use of “renal-dose” dopamine (1–3 mg/kg/min), with or without loop diuretics, has not been validated to decrease mortality in prospective studies.
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Patients with new-onset ARF should be admitted to the hospital. There are numerous potential complications that require observation and the potential need for emergency treatment. Hyperkalemia is the most common metabolic cause of death in patients with ARF. Doses of many medications require adjustment for decreased GFR. A consultation with a nephrologist should be obtained and will be necessary if the patient requires emergency dialysis.
Bibliography Brady HR, Brenner BM: Acute renal failure, In Kasper DL, Braunwald E, Fauci A, Hauser S (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Sinert R, Peacock PR: Acute renal failure. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Thadhani R, Pascual M, Bonventre JV: Acute renal failure, N Engl J Med 1996;334:1448. Wolfson AB, Maenza RL: Renal failure. In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
End-Stage Renal Disease TERRY EMANUEL
ICD Code: Chronic renal failure 585
Key Points Mortality related to end-stage renal disease (ESRD) is a result of cardiac disease complications 48% of the time. Almost all major organ systems are affected by renal failure. Uremic symptoms (e.g., fatigue, poor appetite, anorexia, nausea, vomiting, leg cramps, restless legs) are almost always present when the GFR decreases to less than 10% of normal. ! Emergency Actions ! Evaluation of fluid volume, cardiac stability, and monitoring of potassium levels will guide the healthcare provider to the urgent treatment of ESRD.
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DEFINITION A patient with end-stage renal disease is by definition very ill and lives in a state in which anemia, coronary artery disease, chronic heart failure (CHF), and metabolic and volume abnormalities are the norm. That said, the appropriate reaction to these common abnormalities is based on the degree of the abnormality. This section describes some of the common abnormalities that must be treated emergently. Problems in patients who are underdialyzed either due to noncompliance or inadequate dialysis may lead to a cachectic, uremic, or simply toxic-looking patient but may not constitute an emergency. Percutaneous hemodialysis and peritoneal dialysis catheters are the source of many infections. This, along with a high likelihood of immunocompromised patients in this population, should always make one consider infection in a toxic-looking patient. Common causes for emergency dialysis in a patient with ESRD include the following:
Hyperkalemia with ECG changes Volume overload with associated CHF, respiratory compromise, or hypertensive emergency Severe acidosis Transplant dysfunction or rejection Other common emergencies in patients with ESRD are as follows:
Anemia Coagulopathy Cardiovascular problems (e.g., myocardial infarction, arrhythmia, CHF, pericarditis) Dialysis disequilibrium syndrome (rare) Diverticulitis Hypertension Hypotension Peritonitis (common to patients receiving peritoneal dialysis) Skeletal abnormalities Syncope Venous or peritoneal access problems
PATHOPHYSIOLOGY Almost all major organ systems are affected by renal failure. Uremic symptoms (e.g., fatigue, poor appetite, anorexia, nausea, vomiting, leg cramps, restless legs) are almost always present when the GFR decreases to less than 10% of normal. The criteria for dialysis are multifaceted, but, generally speaking, dialysis needs to be started when kidney function is 10%–15% of normal. “Normal” is about 120 mg/dl of creatinine found
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in the urine. Some residual function may be maintained for several years in a patient receiving dialysis. In the beginning, this residual function may allow the patient to dialyze fewer times per week or for shorter periods than a patient with more chronic disease. This may also allow for the option of peritoneal dialysis, which in many cases is reliant on some residual function for adequate dialysis. Therefore, clinicians should not be so quick to send a patient with ESRD for a contrast CT scan; this may compromise his or her lifestyle significantly. On the other hand, there is less concern for a patient who has been on dialysis for several years and dialyzes for 4 hours three times a week or more, or for the patient receiving peritoneal dialysis who has been dialyzing for several years or more. Anemia is inevitable in chronic renal failure because of loss of erythropoietin production. The use of synthetic erythropoietin in dialysis patients and IV iron delivered on dialysis is adjusted to maintain hemoglobin of approximately 12 g/dl.
Coagulopathy Abnormalities in white cell and platelet functions lead to increased susceptibility to infection and easy bruising. Platelet dysfunction and prolongation of bleeding time is considered to be multifactorial and should increase the index of suspicion for bleeding as a source of symptoms.
CARDIOVASCULAR COMPLICATIONS OF ESRD ESRD mortality is a result of cardiac disease complications 48% of the time. This is due in part to the often uncontrolled underlying disease processes that often cause renal failure: hypertension, diabetes, and other diseases known to have cardiovascular consequences as well as problems with calcium phosphorus metabolism that form unique plaques on the coronary arteries of patients with ESRD. These calcium phosphorus plaques are often responsible for a geometrical progression of coronary artery disease once dialysis begins. This fact, coupled with extreme volume and metabolic changes associated with intermittent hemodialysis results in very high levels of cardiac morbidity and mortality. It should be noted that hyperkalemia should always be considered as the cause for cardiac arrest in these patients. High-output cardiac failure is a rare complication resulting from welldeveloped arteriovenous fistulas—these are the naturally anastomosed artery and vein that causes hypertrophy of the vein. These large reservoirs of blood can contribute to tachycardia and high-output failure, particularly in the face of anemia and coronary artery disease. Creatine kinase, myocardial-bound creatine kinase, troponin, and brain natriuretic peptide
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levels may all be falsely elevated in a patient with ESRD, but these cannot easily be dismissed in this high-risk population and are most wisely correlated to other clinical markers and diagnostic studies. Pericardial effusion and tamponade are also more common findings in patients with ESRD.
Dialysis Disequilibrium Syndrome Dialysis disequilibrium syndrome occurs when a patient who is relatively new to dialysis is dialyzed for too long a time. This is most likely to occur in the first few months of dialysis and results in central nervous system complications, including confusion, malaise, headache, muscle cramps, seizures, and coma. It is caused by a rapid reduction in serum and extracellular osmolality. Cerebral intracellular osmolality, however, is dependent on intracellular production of osmoles termed idiogenic osmoles, which form to maintain equilibrium in the superosmotic predialysis state. It takes several weeks to months for the intracellular adjustment to take place once the extracellular osmolarity begins to decrease.
Hyperkalemia Dietary indiscretions and missed dialysis treatments are the most likely cause of hyperkalemia in a patient with ESRD. Almost all fruits contain high levels of potassium, particularly bananas and oranges. Tomatoes and potatoes also contain high levels. Potassium levels greater than 6 mEq/liter are a cause for concern, although many patients receiving dialysis have adjusted to above-normal levels of potassium. Weakness is a common symptom of hyperkalemia. Early ECG changes will show peaked T waves, followed by PR-interval prolongation, ST-segment changes, widening QRS complex, atrial standstill, ventricular fibrillation, and asystole. Hyperkalemia in combination with hypocalcemia is common in noncompliant dialysis patients and can contribute to cardiac arrhythmia. The appropriate treatment for hyperkalemia is dialysis, but there is inevitably a delay in dialysis treatment, so immediate treatment consists of the administration of IV calcium to enhance cardiac contractility, IV insulin, concentrated glucose as necessary to maintain serum glucose, and Lasix if the patient is not anuric. Kayexalate may be used but is slow acting, and other measures such as an albuterol nebulizer may be contraindicated in the patient with cardiac compromise.
Hypertension Patients with ESRD are subject to almost all of the same causes of hypertension as patients without ESRD, and the primary cause of fluctuations in
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blood pressure are directly related to volume status. Volume status is affected by compliance with fluid restrictions and sodium restriction. Patients with ESRD cannot excrete a large sodium load and can only compensate by increased intake of free water or dialysis. Ideally, patients will gain 1–2 kg of weight between dialysis periods. However, 5–10 kg is not uncommon. For example, a volume-overloaded patient with a pleural effusion, who receives dialysis on Monday-Wednesday-Friday schedule comes in on a Friday evening. This patient, who routinely gains 5–10 kg of weight between dialysis periods, is clearly noncompliant. He will likely not survive the weekend. Statistically, more patients with ESRD die on a Monday than any other day of the week. Hypertension late in dialysis is not uncommon and is attributed to a catecholamine response to stress, antidiuretic hormone release, and renin secretion in response to hypotension.
Hypotension Patients receiving hemodialysis are weighed before dialysis begins and after it ends. The goal in each dialysis session is to have a euvolemic patient by session’s end. For example, the noncompliant patient described previously may come in for treatment weighing 10 kg more than his estimated dry weight and short of breath, with neck veins bulging and 2þ edema in his lower extremities. The dialysis technician programs the dialysis machine to draw off 10 kg of fluid over 4.0 hours. At 3.5 hours, 8 kg down from his predialysis weight, the patient goes from his predialysis blood pressure of 200/110 to 85/50 mmHg and has a syncopal episode. During this time, his potassium level has also dropped from 6.3 to 2.5 mEq/L. By the time he arrives in the ED, he is still weak and lightheaded but his blood pressure is up to 110/80 mmHg and he feels much better. It takes several hours for the intravascular volume of a patient with ESRD to equilibrate. A small bolus of normal saline (250 ml) may be necessary. The patient’s heart has undergone a very significant stress test, and cardiovascular causes of syncope must be considered. However, in many cases, orthostatic hypotension is the cause.
Skeletal Emergencies The kidney is in part responsible for the absorption of calcium and the expulsion of excess phosphorus. Elevated phosphorus levels are the norm in patients with chronic renal failure or ESRD and are partly controlled by dietary restriction, dialysis, and oral phosphorus binders. Calcium levels are maintained by supplemental oral calcium and calcium in the dialysate. Even with the normalization of calcium levels, patients with ESRD have usually been hypocalcemic for years before the initiation of dialysis.
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In short, patients with ESRD are at risk for occult fractures with minimal trauma. Vascular access complications are similar to those seen in any patient with a vascular surgical procedure (e.g., bleeding, local or disseminated intravascular infections, vessel [graft] occlusion). Vascular complications in ESRD account for more hospitalization days than any other malady. The most common complications are infection, clotting, and hemorrhage. Aneurysms of the grafted vein and pseudoaneurysms—hematomas around the graft site—may also occur. But, these problems do not usually require an ED visit unless they result in systemic infection or significant delays in dialysis with the need for emergency dialysis. A ruptured graft requires a tourniquet for immediate control of bleeding and immediate vascular consult. Bleeding from the venous access graft in the postdialysis period may be caused by the use of heparin during dialysis or a malformation within the graft. These patients may present after dialysis or minor trauma with bleeding from their vascular access. Bleeding usually can be controlled with elevation and firm but nonocclusive pressure. Subclavian vein stenosis is more common with percutaneous devices entering at the internal jugular and subclavian veins and may result in marked edema in the arm. Clotted grafts can also have an impact on venous return with the same effect. Steal syndrome is associated with vascular grafts and is the result of a decrease in flow to the arm and hand distal to the surgical site. This may cause ischemic pain, usually while the patient is receiving dialysis, and can cause atrophy and lead to digit loss. A cool extremity that is painful, blue, and mottled with decreased capillary refill indicates an immediate vascular consult. Methicillin-resistant Staphylococcus aureus infection is endemic in dialysis centers. A peritoneal dialysis catheter subjects patients to the risks of peritonitis and local infection. The catheter acts as a foreign body and provides a portal of entry for pathogens from the external environment.
Transplant Rejection Rejection must always be considered in a renal transplant recipient who presents to the ED with any of the following: abdominal pain, uremic symptoms, or an increase in baseline BUN/creatinine or hyperkalemia. Acute rejection of the transplanted kidney may be associated with infection, noncompliance with medications, or acute or chronic rejection of the transplant (often from the underlying disease that initially caused the renal failure). Trough levels of antirejection medications along with standard laboratory tests and an immediate consultation with a nephrologist are indicated. Patients who find themselves back on chronic dialysis are still subject to rejection with systemic consequences. Immunosuppressive agents must be weaned carefully. Patients being weaned from prednisone
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experience adrenal insufficiency as evidenced by hyponatremia and hyperkalemia.
Peritoneal Dialysis and Peritonitis Peritonitis usually results from a break in sterile technique or spread from around the percutaneous site along the tract of the peritoneal catheter to the peritoneum. The patient will almost always have a diffusely tender abdomen. A sample of the peritoneal dialysate must be drawn under sterile conditions and sent for cell count and differential, Gram stain, and culture, and intraperitoneal antibiotics can be delivered to the peritoneum. IV antibiotics can also be given. Staphylococcal infections are the most common, but a wide variety of gram-negative infection compose about 20% of other common agents. Fungal infections are less common. Vancomycin and gentamicin are commonly used, but consultation with a nephrologist should be undertaken whenever possible before the administration of antibiotics.
LABORATORY FINDINGS Patients experiencing acute or chronic renal failure should undergo a CBC, chemistry-13 panel, albumin measurement, and blood culture if they have a fever. If a patient presents with chest pain, cardiac enzyme analysis and ECG should also be performed.
RADIOGRAPHS Chest radiography should be performed to evaluate for pulmonary edema resulting from fluid overload and to evaluate for cardiomegaly.
TREATMENT Treatment is based on laboratory study findings, chest radiography, and the volume status of the patient. Urgent dialysis is the key to treatment if the fluid overload or electrolyte imbalance makes the patient unstable. Hyperkalemia should be treated medically as soon as possible and before dialysis is initiated.
Bibliography Block GA, Hubert-Shearon TE, Levin NW, Port FK: Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: A national study, Am J Kidney Dis 1998;31:607–617.
1124 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Bloembergen W: Outcome of end stage renal disease, In Greenberg A, Cheung AK, Falk RJ, Coffman TM, Jennette JC (eds): Primer on Kidney Disease, ed 2. Academic Press: San Diego, 1998, pp 422–428. Bushinsky D: Disorders of calcium and phosphorus homeostasis, In Greenberg A, Cheung AK, Falk RJ, Coffman TM, Jennette JC (eds): Primer on Kidney Disease, ed 2. Academic Press: San Diego, 1998, pp 106–113. Fraser CL: Neurological manifestations of renal failure, In Greenberg A, Cheung AK, Falk RJ, Coffman TM, Jennette JC (eds): Primer on Kidney Disease, ed 2. Academic Press: San Diego, 1998, pp 459–464. Hodde LA, Sandroni S: Emergency department evaluation and management of dialysis patient complications, J Emerg Med 1992;10:317–334. Krause RS: Renal failure, chronic and dialysis complications. 2004. Available at: http:// eMedicine.com.
Epididymitis CLAUDIO F. ZEBALLOS
ICD Code: Epididymitis acute 604.99
Key Points In patients younger than 35 years old, chlamydia is the most common infectious organism of the epididymis followed by Neisseria gonorrhoeae. ! Emergency Actions ! Any male who presents with testicular pain must be evaluated for both epididymitis and testicular torsion. Testicular torsion is a true urological emergency.
DEFINITIONS The epididymis is where sperm maturation occurs. The tail of the epididymis is continuous with the vas deferens, which joins to the seminal vesicle and ultimately to the prostate. Epididymitis is an inflammation or infection of the epididymis that, if untreated, can progress to involve the testicle (i.e., epididymo-orchitis). Anatomically, it sits on the posterior pole of the testicle.
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EPIDEMIOLOGY Epididymitis is the most common cause of intrascrotal inflammation and has an incidence of less than 1 per 1000 males per year.
PATHOLOGY Epididymitis is usually caused by retrograde invasion of organisms from the urethra up to the vas deferens. The specific organism varies with the patient’s age at onset. In young boys, this is usually associated with congenital anomalies of the lower urinary tract and will require referral for further workup. In patients younger than 35 years, chlamydia is the most common organism, followed by N. gonorrhoeae. For patients older than 35 years, common pathogens such as Escherichia coli, Klebsiella species, or Pseudomonas aeruginosa are the responsible organisms, and infection is usually due to benign prostatic hypertrophy or urethral stricture.
CLINICAL PRESENTATION Epididymitis presents with gradual-onset testicular or scrotal pain (as opposed to the more acute-onset pain associated with torsion) and tenderness along the epididymis and edematous scrotum. Patients may also report lower abdominal pain, inguinal pain, fever, or nausea. Some report transient relief of symptoms with scrotal elevation or when lying supine, circumstances referred to as a positive Prehn’s sign, although this has been reported to be unreliable.
EXAMINATION A thorough genitourinary examination should be performed to evaluate for penile lesions or discharge, lymphadenopathy, scrotal swelling, and testicular transillumination. Examination of a patient with epididymitis reveals a firm, indurated epididymal cord on the posterior superior aspect of the testicle that is markedly tender to palpation. As inflammation and edema progress, differentiating epididymal tenderness from testicular torsion becomes impossible. More advanced cases with testicular involvement (i.e., epididymo-orchitis) present with significant scrotal swelling, testicular tenderness, and hydrocele.
LABORATORY FINDINGS Urinalysis will show white blood cells in only 50% of cases. Cultures for chlamydia and gonorrhea should be performed when penile discharge is present or if the patient is younger than 35 years of age. Urine cultures may be helpful in a febrile, toxic-appearing patient.
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DIAGNOSIS The diagnosis of epididymitis is made clinically on the basis of history and physical examination findings and with the assistance of Doppler ultrasound.
RADIOGRAPHS Doppler ultrasound is useful in differentiating among testicular torsion, hydrocele, testicular mass, or epididymo-orchitis.
TREATMENT Treatment varies according to severity. For nonfebrile, non–toxic-appearing patients, treatment consists of scrotal elevation with scrotal supporter, application of ice packs, administration of analgesics and oral antibiotics, and instructions to avoid heavy lifting or straining because they may exacerbate symptoms. Patients younger than 9 years of age should be treated with erythromycin (50 mg/kg/day divided four times a day). In patients younger than 35 years old, the clinician should suspect sexually acquired infection and should administer ceftriaxone 250 mg IM plus doxycycline 100 mg PO twice a daily for 10 days. If the patient is allergic to cephalosporins, ofloxacin 300 mg PO twice a day for 10 days or levofloxacin 500 mg PO daily for 10 days can be administered. If the patient is older than 35 years and non-sexually acquired infection is suspected, the healthcare provider can treat epididymitis with ciprofloxacin 750 mg PO twice a day for 10 days. The patient should be referred to a urologist in 5–7 days for follow-up. If a patient is febrile, ill-appearing, or toxic or if testicular abscess is suspected, the patient should be admitted and parenteral IV antibiotics should be administered (cefepime 2 g IV every 8 hours or piperacillin/ tazobactam 4.45 g IV every 8 hours if patient is older than 35 years). Toxic-appearing patients younger than 35 years should be treated with doxycycline 200 mg IV every 12 hours or gatifloxacin 400 mg IV once daily. Emergency consultation with a urologist should be obtained in the case of scrotal abscess.
Bibliography Beers MH, Porter RS, Jones TV, et al. Disorders of the scrotum. In Merck Manual. Merck Research Laboratories, Whitehouse Station, NJ, 2005. Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines 2002. MMWR Morb Mortal Wkly Rep 2002;51(No. RR-6):1.
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Cunha BA: In Antibiotic Essentials 2005. Physicians Press: Royal Oak, MI, 2005. Doble A, Taylor-Robinson D, Thomas BJ, Jalil N: Acute epididymitis: A microbiological and ultrasonographic study, Br J Urol 1989;63:90. Gilbert DN, Moellering RC, Eliopoulus GM, Sande MA: The Sanford Guide to Antimicrobial Therapy 2005, ed 35. Antimicrobial Therapy Inc: Sperryville, VA, 2005. Hawkins DA, Taylor-Robinson D, Thomas BJ, Harris JR: Microbiological survey of acute epididymitis, Genitourin Med 1986;62:342. Holmes KK, Berger RE, Alexander ER: Acute epididymitis: Etiology and therapy, Arch Androl 1979;3:309. McCollough M, Sharieff G: Renal and genitourinary tract disorders, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 2328–2329. Rosenstein D, McAninch JW: Urologic emergencies, Med Clin North Am 2004;88 (2):495–518. Schneider RE:Chapter 95. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 617–618. Siegel A, Snyder H, Duckett JW: Epididymitis in infants and boys: Underlying urogenital anomalies and efficacy of imaging modalities, J Urol 1987;138:1100.
Common Disorders of the Penis CHARLES P. DAVIS
Key Points Disorders of the penis commonly involve the foreskin (i.e. prepuce) penile shaft and glans. In general they commonly result from infection of the structures, malformation of tissues, or trauma to the tissues. ! Emergency Actions ! The reduction of paraphimosis is required to avoid arterial compromise and possible gangrene. Conserving erectile function of the penis is considered an emergency in patients with priapism; detumescence is required in such patients. Patients with a “fractured” penis may require emergent urological surgery.
DEFINITION Balanitis is inflammation of the glans penis; if both the glans penis and foreskin are infected, it is termed balanoposthitis. Phimosis is the inability to retract the foreskin behind the head of the penis, and paraphimosis is the inability to advance the foreskin over the distal penis and glans. Priapism is involuntary pathological erection in which the corpus cavernosa is engorged. Peyronie’s disease is fibrosis of penile tissue that results in
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penis curvature during erection. Penile fracture is a rupture of the tunica albuginea of the erect penis with bleeding into the penile tissue.
EPIDEMIOLOGY Balanitis and balanoposthitis can occur at almost any age. However, the disorders of phimosis (all normal newborn males have physiological phimosis) and paraphimosis usually do not occur until after physiological phimosis disappears (usually after the age of 5 years). Priapism, Peyronie’s disease, and penile fracture usually occur only in sexually active adult males, although the peak incidence for priapism is at 19–21 years and Peyronie’s occurs mainly in middle-aged men (i.e., 30–60 years old).
CLINICAL PRESENTATION Balanitis presents as inflammation of the penile shaft or glans. There is usually erythema with little or no edema, except in rare cases. Balanoposthitis presents similarly except it also involves the foreskin. Phimosis presents with a small opening in the foreskin tip, which cannot be easily expanded to retract past the glans. There may be some crusting, redness, and pain observed when retraction of the foreskin is attempted. Occasionally, swelling of the foreskin may be present. Paraphimosis, in contrast, usually presents with edema of the foreskin, located behind the glans, and usually occurs sometime after the foreskin has been retracted. Inflammation may also be present. The foreskin cannot be placed back in its normal position, and attempts to do so are painful for the patient. Priapism is a persistent erection of the penis that is usually painful, and Peyronie’s disease presents as a painful erection with penile deformity. The deformity usually presents as an abrupt curvature of the penile shaft. Penile fracture presents as a painful partially swollen penile shaft. This disorder usually occurs during vigorous sexual activity, and part of the penile shaft remains swollen after physiological detumescence.
EXAMINATION Obtaining a good history from the patient (especially a sexual history, in adults) and doing a clinical examination of the penis is usually enough to arrive at a diagnosis in all of these conditions. The history is very important in priapism since either predisposing illnesses or chemical/physical penile stimulation by the patient is important to discern. For physical examinations, the clinician should not attempt to forcibly retract the foreskin of an infant or young male (up to about the age of 5 years). Palpation of the flaccid penile shaft may reveal the fibrous plaque responsible for the penile curvature in Peyronie’s disease.
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LABORATORY AND RADIOGRAPHIC FINDINGS Except for priapism with no known predisposing factors, laboratory tests ordered in a clinic or an emergency care center usually are not useful in the diagnosis of these penile conditions. A CBC, urinalysis, reticulocyte count, platelet count, and coagulation profile are recommended to help determine whether leukemia, sickle cell disease, or other predisposing illness is contributing to a patient’s priapism.
TREATMENT AND OUTCOMES Balanitis and balanoposthitis are treated with good penile hygiene; if secondary infection is present, antimicrobial drugs should be prescribed. These methods usually result in the resolution of these disorders. Phimosis can also be improved in some cases by good penile hygiene and occasionally use of antimicrobial drugs, but treatment may be complicated by the necessity to dilate or expand the foreskin opening. Circumcision of the penis may be required. Phimosis is usually resolved by these methods with good outcomes; in addition, circumcision is reported to reduce urinary tract infections (UTIs) in young males and to reduce the risk of developing penile carcinoma. However, social, religious, and sexual practices may need to be addressed before circumcision is done. Also, a urologist needs to be consulted in these cases. Paraphimosis is a medical emergency. Untreated, it can lead to gangrene of the penis. Manual reduction of paraphimosis results in a rapid decrease in penile pain and usually avoids bad outcomes such as impotence or penile loss resulting from gangrene. Manual reduction can be accomplished by placing traction toward the glans with the index and third finger of both hands while simultaneously placing pressure on the glans in the opposite direction with both thumbs. The procedure may take a few minutes of constant pressure to reduce edema and allow the foreskin to resume a normal position over the glans. This procedure is painful for the patient and is likely to require pain medication. If the procedure fails, there are others available such as elastic wrap, dorsal slit, or circumcision. In every case, a urologist should be consulted. Priapism is an emergency because it can result in poor outcomes, including impotence, urinary retention, corpora fibrosis, infections, and other related problems. Initial treatment is 0.25–0.50 mg of terbutaline delivered subcutaneously at the deltoid muscle. Studies also cite oral terbutaline (5 mg PO; twice if first dose is unsuccessful after 15 minutes; resolution should be within a total of 30 minutes). Unfortunately, this may be effective in only one third of patients. If terbutaline fails, or if the painful erection has been sustained for more than 4 hours, detumescence accomplished by aspiration or injection therapy (or both) is
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required. A penile nerve block is first done by injecting 1% plain lidocaine around the base of the penis. After anesthesia, a 19-gauge needle with a 50-ml syringe is injected through the penile shaft at the 2- or 10-o’clock position (not through the corpus spongiosum) and 20–30 ml of blood removed. Pressure on the penis shaft may be required to help remove the blood. If the blood is bright red, the clinician should consider an arterial cause and compress the site and shaft with an elastic bandage. If dark blood is obtained and detumescence is achieved, the disorder may be solved, but urological consultation is still required. However, if the procedures are not successful, aspiration should be repeated followed by injection of phenylephrine solution (10 mg of phenylephrine in 500 ml of 0.9% saline) in a volume equal to the aspirated volume. This process may need to be repeated. Priapism associated with sickle cell disease may require transfusions to increase hemoglobin concentration. Consultation with a urologist is required for patients with priapism. Patients with Peyronie’s disease have spontaneous remissions in up to 50% of patients. An urgent referral to a urologist is imperative for the best treatments and procedural outcomes. Patients with a “fractured” penis require a urological consult because surgical repair will usually be required. Early surgical intervention reportedly gives the best outcomes for patients with penile fracture.
Bibliography Carey MJ: Priapism. eMedicine, 2004. Available at: http://www.emedicine.com/emerg/ topic468.htm. Choe JM, Heiland M: Penile fracture and trauma. eMedicine, 2004. Available at:http:// www.emedicine.com/med/topic3415.htm. Choe JM, Hye K: Phimosis, adult circumcision and buried penis. eMedicine, 2004. Available at:http://www.emedicine.com/med/topic2873.htm. Teichman JMH: In 20 Common Problems in Urology. McGraw-Hill: New York, 2001, p 335. Weiss RM, George N, O’Reilly PH: In Comprehensive Urology. Mosby: New York, 2001, p 724.
Prostatitis
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Prostatitis MARGARET MANN-ZEBALLOS
ICD Code: Prostatitis 601.9
Key Points Prostatitis is an inflammatory disorder of the prostate, commonly caused by bacteria.The condition may be chronic or acute. ! Emergency Actions ! The ED healthcare provider should monitor the vital signs of a patient with prostatitis and provide supportive care in patients exhibiting signs of sepsis. Placement of a Foley catheter should be avoided in men with prostatitis and obstructive symptoms. Suprapubic urine aspiration is indicated in patients who are unable to void to relieve urinary retention or to provide a sample for urine culture.
DEFINITION Prostatitis is an infectious, inflammatory, or irritative condition of the prostate gland. It is classified into four subgroups: 1. Acute bacterial prostatitis 2. Chronic bacterial prostatitis 3. Chronic nonbacterial prostatitis/chronic pelvic pain syndrome, which can be inflammatory or noninflammatory 4. Asymptomatic inflammatory prostatitis In the ED setting, most cases of prostatitis will be treated as an acute or chronic bacterial condition with referral to a urologist for management if nonbacterial chronic prostatitis or pelvic pain syndrome is suspected.
EPIDEMIOLOGY Both acute and chronic bacterial prostatitis are far less prevalent than nonbacterial prostatitis. Acute bacterial prostatitis occurs in 2 of 10,000 patient visits and only 5%–10% of patients with chronic prostatitis having a bacterial cause.
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PATHOLOGY Bacterial prostatitis is caused by gram-negative bacteria (e.g., E. coli, Klebsiella species, and Proteus species) in 80% of cases, though gram-positive enterococci are becoming more prevalent. Chlamydia should be considered in sexually active men, especially those younger than 35 years old. Etiological agents in chronic bacterial prostatitis include those mentioned for acute prostatitis as well as Staphylococcus, Mycoplasma, and Ureaplasma species.
CLINICAL PRESENTATION Patients with acute bacterial prostatitis typically present with dysuria, pelvic or perineal pain, cloudy urine, constitutional symptoms such as fever, chills, and malaise, or obstructive urinary symptoms like hesitancy, dribbling, and urinary retention. Patients may also present with hematospermia, testicular pain, or nonspecific low back pain. Men with chronic prostatitis, in contrast, are generally afebrile and present with nonspecific pelvic discomfort. Obstructive urinary symptoms may be present. These patients typically have a history of or recurrent UTIs or other genitourinary infections and a history of treatment with multiple courses of antibiotics.
EXAMINATION Digital rectal examination with gentle palpation of the prostate will reveal prostate tenderness if prostatitis is present. Aggressive prostatic massage or “milking” of the prostate should be avoided because this may lead to a painful exacerbation of symptoms and bacteremia.
LABORATORY FINDINGS Urinalysis will reveal pyuria or hematuria. Urine cultures should be performed in all cases with a Gram stain, if possible, to direct treatment. CBC may reveal leukocytosis. Gonorrhea and chlamydia testing should be considered in young or sexually active men. Prostate-specific antigen levels will be predictably elevated in cases of prostatitis but should not be routinely measured. Prostate-specific antigen levels will fall with appropriate therapy.
DIAGNOSIS The diagnosis of acute bacterial prostatitis is made on the basis of typical clinical symptoms with the finding of a tender prostate on examination.
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Chronic prostatitis should be suspected in men with recurrent UTIs who have not undergone bladder catheterization. Symptoms may be milder in chronic prostatitis, and the prostate may not be tender on rectal examination. Results of urinalysis and urine cultures will be positive in cases of acute or chronic bacterial prostatitis but may be negative in other chronic prostatitis syndromes.
RADIOGRAPHS Imaging is generally not indicated in the ED setting unless used to clarify the differential diagnosis (i.e., obstruction resulting from renal stones or malignancy) or to work up traumatic hematuria.
TREATMENT Consideration should be given to the patient’s underlying clinical condition when determining treatment. If the patient is able to tolerate oral hydration and therapy and his or her vital signs are stable, an oral antibiotic regimen is appropriate. If the patient appears toxic, is unable to tolerate oral therapy, or has failed a course of oral antibiotics, parenteral antibiotics are indicated. Hospitalization should be considered when parenteral antibiotics will be administered or when the patient is experiencing urinary retention because suprapubic bladder aspiration and a urological consultation will be needed.
ANTIMICROBIAL THERAPY For acute bacterial prostatitis, the duration of therapy is 4–6 weeks. Therapy should ideally be based on initial urine Gram stain results, but if Gram stain is unavailable, empirical therapy should be initiated. Appropriate empirical antibiotic regimens aimed at covering gramnegative organisms include one of the following:
Trimethoprim-sulfamethoxazole (TMP/SMX) DS 1 tablet every 12 hours or A fluoroquinolone: ciprofloxacin 500 mg every 12 hours, levofloxacin 500 mg daily, or other equivalent fluoroquinolone
For gram-positive cocci in chains, enterococcal infection, 500 mg of ampicillin should be given orally every 6 hours or 500 mg of amoxicillin should be given orally every 8 hours. For gram-positive cocci in clusters, Staphylococcus, coverage includes cephalexin 500 mg every 6 hours or dicloxacillin 500 mg every 6 hours.
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For suspected chlamydial infection, both gonorrhea and chlamydia should be treated with either ofloxacin 400 mg (one dose) followed by 300 mg every 12 hours for 10 days or one dose of ceftriaxone 250 mg intramuscularly plus doxycycline 100 mg every 12 hours for 10 days. Inpatient, parenteral antibiotic therapy for gram-negative organisms includes an IV fluoroquinolone plus an aminoglycoside (gentamicin or tobramycin 5 mg/kg daily). Parenteral antibiotic choices for gram-positive organisms include vancomycin 2 g/day divided into four doses IV, cefazolin 1 g IV every 8 hours, or nafcillin 2 g IV every 6 hours. For chronic bacterial prostatitis, patients should be treated for a minimum of 6–12 weeks. In the treatment of chronic bacterial prostatitis, the clinician should initiate treatment with TMP/SMX DS, one tablet twice per day or a fluoroquinolone such as ciprofloxacin 500 mg every 12 hours or levofloxacin 500 mg daily. NSAIDs are the appropriate treatment for analgesia. A 72-hour followup is indicated to confirm clinical improvement and follow cultures. A urological referral should be made in the setting of chronic prostatitis.
Bibliography Dalton DL: Elevated serum prostate-specific antigen due to acute bacterial prostatitis, Urology 1989;33:465. David RD, DeBlieux P: Recommendations for accurate prescribing of antibiotics: Council for Appropriate and Rational Antibiotic Therapy, Am J Med 2005;118(7 Suppl 1):7–13. Gilbert DN, Moellering RC, Eliopoulos et al: The Sanford Guide to Antimicrobial Therapy. ed 35. Antimicrobial Therapy: Bethesda, 2005. National Institute of Diabetes and Digestive and Kidney Disease (NIDDK) Working Group: National Institutes of Health, 1995. Nickel JC, Moon T: Chronic bacterial prostatitis: An evolving clinical enigma, Urology 2005;66(1):2–8. Weidner W, Schiefer HG, Krauss H, et al: Chronic prostatitis: A thorough search for etiologically involved microorganisms, Infection 1991;19(Suppl 3):S119-S125.
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Renal Stones KARI MURPHEY
ICD Code: Kidney stones 592.0
Key Points Risk factors for renal stones include age, sex, family history, and geographical location. Renal calculi affect men more often than women. ! Emergency Actions ! Patients with human immunodeficiency virus (HIV) infection who are taking medication such as indinavir (Crixivan), which is a protease inhibitor, may require an IVP because stones formed from the metabolites of this medication are not visible on CT scans.
DEFINITION Renal stones are urinary calculi originating in the kidney (i.e., nephrolithiasis), usually in the renal pelvis. The stones develop as the result of growth of crystalline components in supersaturated urine and are dependent on pH, ionic strength, and solute concentration. There are five major types of urinary stones: calcium (oxalate and phosphate; 80%), uric acid (5%–10%), magnesium ammonium phosphate (struvite; 5%–10%), cystine (1%), and drug induced (1%). The most common types are composed of calcium; in part because of this, 85% of stones are radiopaque. Uric acid stones may be radiolucent; however, they often have calcium oxalate in their composition and thus can also be radiopaque.
EPIDEMIOLOGY Risk factors for renal stones include age, sex, family history, and geographical location. Renal calculi affect men more often than women. In the United States, the prevalence of renal calculi is 7% in men and 3% in women. Stones may occur in any age group. However, it is less common to find stones in extremes of age. Nearly 70% of all ureteral calculi occur in persons between the ages of 20 and 50 years. Renal colic is more prevalent in areas with elevated temperatures and high humidity. In the United States, the highest incidence of symptomatic ureteral stones is in the southeast.
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Many conditions are associated with an increased risk of renal stone formation. These include chronic UTIs, primary hyperparathyroidism, cystic fibrosis, hyperthyroidism, gout, renal tubular acidosis, sarcoidosis, hyperoxaluria, and conditions that cause chronic diarrhea such as Crohn’s disease, short bowel, inflammatory bowel disease, and laxative abuse. Numerous medications can also encourage calculi formation as a result of their metabolic actions. Vitamin D and calcium supplements, loop diuretics, corticosteroids, and theophylline can induce hypercalciuria. Other drugs may mimic the metabolic changes of renal tubular acidosis; these medications include acetazolamide, amphotericin B, and lithium. With the increasing population of HIV-positive patients, a frequently encountered drug-induced stone is composed of the protease inhibitor indinavir, a medication that is commonly used to treat patients with HIV infection. Pure indinavir stones are difficult to detect. History of a previous renal stone also increases a patient’s risk. The recurrence rate approaches 50% within 5 years after having the first stone.
CLINICAL PRESENTATION The classic presentation of renal colic is the sudden onset of colicky flank pain, usually unilateral, often radiating to the lateral abdomen and groin. The pain may begin as a vague flank pain but evolves into waves of severe pain due to obstruction causing hyperperistalsis. With distal stones, the pain often radiates to the testicles and penis in men and the labia in women; these patients may also have dysuria and urinary frequency. Often, patients have associated nausea and vomiting as a result of stimulation of the celiac plexus. Patients may also report hematuria. A history of fever and chills suggests a complicating secondary infection and should be regarded as a true emergency.
EXAMINATION A complete examination should be performed on patients with this clinical presentation. Symptoms similar to those of renal colic can be caused be noncalculous conditions. Therefore, the physical examination is often more valuable for ruling out non-urological disease. Appendicitis, cholecystitis, diverticulitis, colitis, hernias, and arterial aneurysms may elicit similar pain; a thorough abdominal examination will help localize the pain and rule out palpable masses or fascial defects. Also, the clinician should pay close attention to how the patient looks when he or she enters the examination room; many patients with stones will be constantly moving in attempt to get comfortable, whereas patients with an acute abdominal process are usually very still. Costovertebral angle tenderness is often present in renal colic, but the rest of the examination findings may be unremarkable.
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The patient’s vital signs, including body temperature, should be part of the initial assessment. Patients with renal colic will sometimes be tachycardic and hypertensive as a response to pain. Elevated temperatures in patients suspected to have a kidney stone may be a sign of a complicating infection, and these need a more thorough examination.
LABORATORY FINDINGS A urinalysis with sedimentation rate measurement should be performed. Microscopic hematuria is present in 85% of patients with stones. The presence of pyuria or bacteriuria in these patients should be treated as a true emergency; these findings indicate the possibility of a urinary infection, an infected obstructed renal unit, or pyonephrosis. The pH of urine may be useful in determining the type of stone present; a low urine pH is more indicative of a uric acid stone and a pH greater than 8.0 is more likely to be an infectious stone. When obstruction is suspected, BUN and creatinine measurements are helpful in determining kidney function.
RADIOGRAPHS IVP was the standard for the detection and diagnosis of renal and ureteral stones since 1927, until it was recently displaced by the unenhanced spiral CT scan of the abdomen and pelvis. These CT scans have a sensitivity of 95%–100% and a specificity of 94%–96%. CT scans do not involve contrast materials, eliminating the risk of allergic reactions or renal failure. In current clinical practice, renal colic noncontrast CT scans have become the standard of care in the ED setting. Many urologists still routinely request additional studies such as plain abdominal radiographs (e.g., kidneys, ureters, and bladder) or an IVP to help with management, follow-up, and determination of the need for further intervention. Patients with HIV infection who are taking medication such as indinavir (Crixivan), a protease inhibitor, may require an IVP because stones formed from the metabolites of this medication are not visible on CT scans. Pregnant patients should not be exposed to radiation; therefore, diagnostic options for these patients are limited. Renal ultrasonography may be helpful, but the findings are often inconclusive.
DIAGNOSIS A diagnosis of renal stones is made on the basis of patient history, clinical presentation, urinalysis results, and CT scan.
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TREATMENT The initial treatment of a patient with renal colic in the ED starts with obtaining IV access to allow fluids and medications to be administered. Many of these patients are dehydrated; therefore, the administration of IV fluids is appropriate during the workup. NSAIDs are an excellent alternative to narcotics or they may be used in conjunction with narcotics. Ketorolac is the NSAID often used as a first-line agent; it helps reduce the pain of renal colic by decreasing ureterospasm. Antiemetic agents may also help in the initial management of a patient with nausea. Once the pain and nausea are under control, most patients with renal colic can be discharged from the ED with appropriate referral and instructions; patients should have a follow-up for urologic evaluation within 2 weeks. The patient should be advised to drink a moderate amount of fluids and to take analgesics as needed. He or she should be provided with a strainer, if available, and should be encouraged to strain each void to capture the stone. Stones should be taken to a urologist for analysis to aid in the management and prevention of future stones. Indications for admission to the hospital include severe dehydration, intractable pain or vomiting, evidence of a urinary infection with obstruction, anuria, ARF, or obstruction with a solitary or transplant kidney.
Bibliography Leslie SW: Nephrolithiasis: Acute renal colic. eMedicine, 2005. Available at http://www. eMedicine.com. Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Matlaga BR, Assimos DG: Urologic manifestations of nonurologic disease: Urolithiasis, Urol Clin North Am 2003;30(1):91–99. Morton AR, Iliescu EA, Wilson JW: Nephrology: 1. Investigation and treatment of recurrent kidney stones, Can Med Assoc J 2002;166(2):195. Portis AJ, Sundaram CP: Diagnosis and initial management of kidney stones, Am Fam Phys 2001;63(7):1329–1338. Wasserstein AG: Nephrolithiasis, Am J Kid Dis 2005;45(2).
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Torsion of the Testicle SUMERU GHANSHYAM MEHTA
ICD Code: Torsion of the testicle 608.2
Key Points All patients with suspected testicular torsion should receive emergency urological consultation. ! Emergency Actions ! A testis with evident torsion can be salvaged if a prompt diagnosis can be made (less than 6 hours from the onset of pain).
DEFINITION Torsion of the testis results in obstruction of blood flow, resulting in necrosis and subsequent infarction of the testicle.
EPIDEMIOLOGY It is estimated that torsion of the testicle occurs in two peak periods: the first year of life and at puberty in conjunction with maximal hormonal stimulation. The most common age at presentation is 16.2 years; however, torsion can occur at any time. Torsion is also 10 times more likely in an undescended testis.
CLINICAL PRESENTATION The pain of testicular torsion usually begins suddenly in the scrotum, although the pain may occur in the lower abdomen or may be inguinal. Frequently there is a history of an athletic event, strenuous physical activity, or trauma just before the onset of scrotal pain. Nearly 41% of patients will report a history of similar pain that resolved spontaneously. Although the pain may be constant or intermittent, it is not positional in nature. The pain is often thought to be associated with nausea and vomiting, which is believed to result from the sudden occlusion of the testicular vascular supply. There is a notable absence of urinary symptoms.
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EXAMINATION Extreme pain usually limits the extent of the physical examination, permitting only a superficial examination of the affected hemiscrotum. Generally, the hemiscrotum is swollen, tender, and firm on palpation. A reactive hydrocele may be present. The classic signs of a high-riding testis with a transverse lie are not always detectable. Loss of the cremasteric reflex is associated with torsion. Examination of the contralateral testis may show it to lie in the horizontal axis. Prehn’s sign has been described and used in the past to distinguish torsion from epididymitis. It was believed that relief of scrotal pain by testicular elevation was indicative of epididymitis. This is not a reliable sign, however, and should not be used to distinguish between the two processes.
LABORATORY FINDINGS A urinalysis should be performed, but results will be unremarkable in testicular torsion. A CBC should reveal an absence of leukocytosis. No other laboratory testing is required in the evaluation of suspected testicular torsion.
DIAGNOSIS In patients older than 18 years of age who have a history and physical examination compatible with torsion, no urethral discharge, no cremasteric reflex, and no recent UTIs, the diagnosis of testicular torsion should be strongly considered. If a clinical diagnosis is uncertain, radiographic evaluation can be used to evaluate patients.
RADIOGRAPHS Color-flow duplex Doppler and radionuclide scintigraphy are two imaging modalities that may be used to evaluate patients with indeterminate presentations. Both may be useful, but their use is limited by availability and operator experience. These study results are considered positive for testicular torsion when they demonstrate absent or diminished blood flow to the painful hemiscrotum in comparison with the contralateral testicle. Both modalities have nearly identical reported sensitivity (80%–90%) and specificity (75%–95%) for testicular torsion. Ultrasound has the advantage showing better scrotal anatomy as well as more availability; however, it has the disadvantage of a greater number of indeterminate results compared with scintigraphy.
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TREATMENT In obvious cases of testicular torsion, emergency urological consultation and surgical exploration are recommended. The amount of testicular damage present is related to the duration and extent of vascular obstruction. A salvage rate of 80%–100% is possible if the pain lasts less than 6 hours. Continuous pain for 24 hours is usually associated with testicular infarction. There are no readily available clinical or laboratory parameters to judge either the degree or the duration of testicular ischemia. Therefore, if testicular torsion cannot be excluded by history, physical examination, and imaging, emergency scrotal exploration is the definitive diagnostic test and the procedure of choice. While the patient is waiting for transportation to the operating room, manual detorsion of the affected testis should be attempted. Since most testes undergo torsion in a lateral-to-medial fashion, detorsion should be attempted in a medial-to-lateral fashion, in a manner similar to opening a book. Any relief of pain is a positive end point. A worsening of the pain would indicate that detorsion should be done in the opposite direction.
Bibliography Cummings JM, Boullier JA, Sekhon D, Bose K: Adult testicular torsion, J Urol 2002;167:2109. Edelsberg JS, Surh YS: The acute scrotum, Emerg Med Clin North Am 1988;6:521. Harwood-Nuss AL, Etheredge W, McKenna I: Urologic emergencies, In Rosen P, Barkin R (eds): Emergency Medicine: Concepts and Clinical Practice, ed 4. Mosby: St Louis, 1998, pp 2243–2245. Haynes BE, Bessen HA, Haynes VE: The diagnosis of testicular torsion, JAMA 1983;249:2522. Lindsey D, Stanisic TH: Diagnosis and management of testicular torsion: Pitfalls and perils, Am J Emerg Med 1988;6:42. Schneider RE: Male genital problems. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 635–637.
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Urinary Tract Infections in Adults MARY ANN BROWNING
ICD Code: 599.0
Key Points
Urinary tract infection is defined as bacteriuria plus symptoms. Uncomplicated cystitis may not require laboratory evaluation. Certain factors such as age, sex, comorbidity, resistant pathogens, and pregnancy can help guide the emergency medicine provider to the most effective and cost-effective therapy.
DEFINITION Urinary tract infection is defined as significant bacteriuria plus symptoms. This is a common clinical condition in the ED. Uncomplicated UTI in an otherwise healthy, nonpregnant, nonobstructed young female is generally considered to be easily diagnosed and treated. Most UTIs are caused by pathogens that ascend from the urethra to the bladder. The most common pathogen is E. coli (80%–90% of cases). Staphylococcus saprophyticus accounts for 10%–20% of cases in young women. Traditionally, UTI has been characterized by a bacterial concentration of more than 105 CFU/ml. However, recent research suggests that a colony count as low as 100 CFU/ml may represent significant bacteriuria if associated with symptoms and merits treatment. UTI can involve mucosal tissue of the lower urinary tract (i.e., cystitis) or soft tissue of the upper urinary tract (i.e., pyelonephritis). Complicated UTI is usually accompanied by an underlying condition that increases risk for treatment failure. Rarely, UTI may be acquired via the bloodstream from a distant infectious source, such as pneumonia. Asymptomatic bacteriuria is defined by the presence of more than 105 CFU/ml of one bacterial species on two consecutive urine cultures in a patient without symptoms. Treatment of asymptomatic bacteriuria has not been shown to be beneficial unless the patient is pregnant or a urological procedure is anticipated.
EPIDEMIOLOGY Between 40% and 50% of women will have at least one UTI in their lifetimes. Men have low rates of bacteriuria until advanced age, when the
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incidence rises dramatically. In the United States, UTI accounts for at least 1 million ED visits and 100,000 hospitalizations per year. UTI is primarily a disease of young sexually active women. Other risk factors for women of this age group include spermicidal use, new sex partner, age younger than 15 years at first UTI, and maternal history of UTI. Conversely, wiping patterns, postcoital voiding, hot tub use, pantyhose, douching, and obesity have not been clearly demonstrated as significant risk factors for UTI. In pregnancy, bacteriuria and asymptomatic bacteriuria has been associated with increased risk of pyelonephritis and may lead to preeclampsia, sepsis, or miscarriage. Bacteriuria in men younger than the age of 50 years is rare and may be associated with abnormality of the urinary tract. In men older than 50 years, the incidence of UTI rises dramatically because of the potential for prostate obstruction.
CLINICAL PRESENTATION AND EXAMINATION UTI is typically diagnosed by clinical presentation and a limited amount of physical examination findings. In women, a specific combination of symptoms such as dysuria, frequency, hematuria, and costovertebral angle tenderness raises the probability of UTI to more than 90%. Thus, the diagnosis can be ruled in based on history alone. On the other hand, the probability of UTI is significantly decreased in the absence of dysuria, especially if the patient reports vaginal discharge or other vaginal symptoms. If vaginal symptoms are present, a pelvic examination and cervical culture are indicated to rule out chlamydia, gonorrhea, and other vaginal infections. Renal tenderness or costovertebral angle tenderness may be associated with cystitis because of referred pain. However, additional signs and symptoms such as fever, chills, nausea, and vomiting may indicate pyelonephritis. In younger men, dysuria with urethral discharge usually indicates urethritis or sexually transmitted infection. Older males presenting with fever, dysuria, and back pain should be evaluated for acute bacterial prostatitis or pyelonephritis. If bacteriuria is present and not associated with a sexually transmitted infection or prostatitis, then treatment for UTI is indicated and a urological referral should be considered. A healthy elderly patient who has a UTI is most likely to present with classic symptoms (e.g., frequency, urgency, suprapubic discomfort). New onset of incontinence may also be reported. An elder person with multiple medical problems may present atypically with a decreased
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appetite, change in mental status, or an increase in frequency of incontinent episodes.
LABORATORY FINDINGS A midstream urine sample can be used for dipstick, microscopic urinalysis, and urine culture. Urine dipstick testing is commonly done in ED settings. The presence of leukocyte esterase on a urine dipstick indicates a minimum of eight white blood cells per high-power field and has a sensitivity of 88%–95% and a specificity of 94%–98%. Some uropathogens are capable of reducing dietary nitrates in the urine to nitrite. The presence of both leukocyte esterase and nitrites indicates a likely gram-negative pathogen (e.g., E. coli, Proteus species, Klebsiella pneumoniae). Results of the nitrite test may be falsely negative in patients who have recently voided or in dilute urine. Also, this test does not detect organisms unable to reduce nitrate to nitrite (e.g., enterococci, staphylococci, or adenovirus). Small amounts of protein and red blood cells may also be positive on dipstick test result. A urine culture is important when the diagnosis is not clear or when UTI is recurrent. A urine culture should always be performed in patients who have recently been hospitalized, are seriously ill, have a fever, have a history of frequent UTIs, are pregnant, or have failed treatment or in male patients with suspected UTI. Catheterization specifically for collection of a urine culture sample may be justified if the patient is unable to cooperate to allow the collection of an uncontaminated sample. However, unnecessary catheterization should be avoided because of the possibility of introducing bacteria into the bladder.
DIAGNOSIS The diagnosis of UTI can be proved only by culture of an adequately collected urine sample. A presumptive diagnosis is acceptable in sexually active women in the presence of typical symptoms. However, if a culture is performed, the presence of greater than 102 CFU/ml in the presence of dysuria and other symptoms of UTI confirms the diagnosis. It should be noted that urethritis and prostatitis are far more likely causes of pyuria in young males who are sexually active and report dysuria, regardless of the presence of urethral discharge.
RADIOGRAPHS Renal imaging studies are not indicated in otherwise healthy patients. Elderly, diabetic, or severely ill patients with acute pyelonephritis should
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be considered for imaging, especially if there is a poor response to antibiotic therapy. If an anatomical abnormality or complicating obstructing stone is suspected, imaging of the urinary system is appropriate. Modalities for this include ultrasonography, contrasted CT, or helical CT of the urinary system.
TREATMENT Short-course therapy with an antibiotic is the standard treatment for uncomplicated UTI (Table 19-1). Three days of TMP-SMX, trimethoprim alone, or the quinolones are as effective as longer courses with fewer adverse effects. Beta-lactams are less effective than trimethoprim, TMP-SMX, or the quinolones. Nitrofurantoin is still recommended for a 7-day treatment regimen. Trimethoprim and TMP-SMX have been regarded as the antibiotics of choice but are less appropriate if resistance rates in E. coli and other gramnegative organisms exceed 10%–20%. This information may be obtained from the local laboratory. If the patient has intense dysuria, a bladder analgesic such as phenazopyridine (Pyridium) given for 1–2 days may be helpful. Women with symptomatic UTI during pregnancy should be treated for 7 days, and asymptomatic bacteriuria is usually treated for 3 days. Once the presence of a UTI is documented, monthly urine culture samples should be obtained during the pregnancy. The patient should be advised of this so she can make arrangements for appropriate follow-up. Therapeutic options should be guided by urine culture results. Options include amoxicillin, cephalexin, cefpodoxime, cefixime, Augmentin (amoxicillin and clavulanate), and nitrofurantoin. Nitrofurantoin should be avoided after 36th week of gestation. *
Table 19-1 Oral Treatment Options for Uncomplicated UTI (in Women) AGENT TMP-SMX
DOSAGE
COMMENT
1 DS bid for 3 days
Risk of treatment failure; not recommended in areas where resistance >20% Nitrofurantoin 100 mg bid for 7 days Use only in patients with good renal function; pregnancy risk category B—avoid at 36 weeks’ gestation Ciprofloxacin 250 mg bid for 3 days Avoid use in pregnant patients; not advised in patients aged 18 years and younger; interacts with other medications; other quinolones may be considered but have an increased cost *Adapted from Guidelines from the Infectious Disease Society of America. Warren et al: Guidelines for Antimicrobial Treatment of Uncomplicated Acute Bacterial Cystitis and Acute Pyelonephritis in Women, Clin Infect Dis 1999;745-758. TMP-SMX, Trimethoprim-sulfamethoxazole; bid, twice a day.
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In ED settings serving indigent populations, the incidence of subclinical pyelonephritis may approach 70%. It is necessary to assess each patient’s ability to follow-up. If follow-up compliance is not expected, or if there is a risk of subclinical pyelonephritis, the patient should be prescribed a 10- to 14-day regimen. Women who present with signs and symptoms of pyelonephritis must be treated with vigorous oral or IV fluid and a dose of parenteral antibiotics. A popular regimen, includes 2 L of fluid (IVor orally) and 2 g of ceftriaxone IV. The patient may then be discharged home if she is able to tolerate oral fluid and oral antibiotics. Women with repeated UTIs (two or more over 6 months or three or more over 12 months) may require prophylaxis. She should be advised to follow up with her primary care provider and should receive consideration for referral to a urologist. In the case of a UTI in a male patient, the possibility that infection has ascended to the kidney must be assumed. Outpatient treatment includes TMP-SMX or one of the quinolones such as ciprofloxacin to be taken for a minimum of 10 days. If the patient appears toxic, is unable to tolerate fluid orally, or is unable to care for himself at home, hospital admission should be considered. Appropriate inpatient antimicrobial therapy includes a third-generation cephalosporin, such as ceftriaxone, or an aminoglycoside. Adequate hydration, antipyretics, and pain medicine should also be considered. Consultation with a urologist is necessary; however, this can be done on an outpatient basis.
Bibliography Bent S, Nallamothu B, Simel D, et al: Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002;287:2701–2710. Chambers S: Cystitis and urethral syndromes. In Cohen J, Powderly WG: Infectious Diseases, ed 2. Elsevier: St Louis, 2004, pp 737–743. Fihn S: Acute uncomplicated urinary tract infection in women, N Engl J Med 2003;349:259–266. Fitzgerald M: Urinary tract infection: Providing the best care. Available at: http://www. medscape.com/viewprogram/1920_pnt. Accessed on February 16, 2005. Hooton T, Scholes D, Stapleton A, et al: A prospective study of asymptomatic bacteriuria in sexually active young women, N Engl J Med 2000;343:992–997. Howes D: Urinary tract infection, female. Available at: http://www.emedicine.com/emerg/ topic626.htm. Accessed on February 16, 2005. Howes D: Urinary tract infection, male. Available at: http://www.emedicine.com/emerg/ topic626.htm. Accessed on February 16, 2005. Howes D, Bogner M: Urinary tract infections. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 606–612. Warren J, Abrutyn E, Hebel J, et al: Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women, Clin Infect Dis 1999;29:745–758.
Chapter 20
Transplantation Emergencies Cardiac and Lung Transplantation SCOTT B. JOHNSON, JOHN T. DEEL, SANDEEP J. KHANDHAR, ERIC R. PRESSER, AND JOHN H.CALHOON
ICD Codes: Cardiomyopathy (includes the various kinds) 425, Left heart failure 428.1, Chronic obstructive pulmonary disease 496, Idiopathic pulmonary fibrosis 516.3, Interstitial lung disease 515, Sarcoidosis 135, Pulmonary hypertension 416, Cystic fibrosis 277.02, Emphysema 492.8, Scleroderma 710.1, Complication of transplanted organ, rejection, heart 996.83, Complication of transplanted organ, rejection, lung 996.84, Carditis 429.89, Lung infection 518.89, Pneumonia 486 CPT Codes: Lung transplant, single, without cardiopulmonary bypass 32851, Lung transplant, single, with cardiopulmonary bypass 32852, Lung transplant, double, without cardiopulmonary bypass 32853, Lung transplant, double, with cardiopulmonary bypass 32854, Donor pneumonectomy 32850, Heart transplantation, with or without recipient cardiectomy 33945, Bronchoscopy, rigid or flexible 31622 ! Emergency Actions ! Patients who have had a heart transplant or a lung transplant, or are on the waiting list for the same, usually have one or more of the following problems when presenting to an emergency department: heart failure, pulmonary failure, rejection, or infection. For any of these acute problems, one must remember the simple ABCs: airway, breathing, and circulation. Caregivers who are not familiar with prethoracic or postthoracic transplant recipients may find themselves overwhelmed at times with the complexity of a patient’s illness and the medicines they may be taking to treat their underlying disease or to prevent allograft rejection. If one just keeps in mind that most transplantrelated life-threatening problems are treated with usual supportive care, the caregiver can confidently initiate lifesaving therapy in a more timely fashion. Patients either pretreatment or posttransplant may require emergent intubation and mechanical ventilation. Oxygen saturation monitoring as well as close blood pressure monitoring should be undertaken. Oxygen
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1148 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER should not be withheld if it is needed. Patients on the transplant waiting list may be receiving a continuous infusion of inotropes (e.g., dopamine, milrinone, dobutamine) if experiencing heart failure and waiting for a heart, or they may be receiving pulmonary vasodilators if diagnosed with primary pulmonary hypertension if waiting for a lung—if so, a quick check to make sure that the portable pump is working should be done. Patients experiencing profound heart failure may require inotropes (e.g., milrinone, which decreases afterload, increases inotropy, and may actually decrease the blood pressure; dobutamine, which has similar affect, also decreases afterload and increases inotropy, but probably increases chronotropy more than milrinone) if they are not already taking them, or new ones or higher doses of the same if they already are receiving these medications. If volume is overloaded, a patient may benefit from intravenous furosemide or another diuretic agent. Patients with severe cardiac rejection can present experiencing profound heart failure; likewise, patients with severe pulmonary rejection can present in profound pulmonary failure. Supportive care, rather than definitive care (e.g., high-dose immunosuppressive therapy) should be the mainstay of treatment, at least initially.
DEFINITION Patients who are on the transplant list waiting for an appropriate donor are usually quite ill from their underlying diagnosis. Most of these patients have undergone an intense pretransplant evaluation and hence are quite familiar and knowledgeable about their disease state. Likewise, patients who have already undergone a heart or lung transplant are usually knowledgeable concerning the nuances of their graft and the medicines they are taking to sustain it. Similarly, they are usually quite aware of problems that may be recurring. Therefore, a quick history is often sufficient to determine current problems and to better define the problem. Usually, a patient who is awaiting or has just received a heart or lung transplantation will present with either one or a combination of the following problems: heart failure, pulmonary failure, rejection, or infection. It is important to remember that heart transplantation and lung transplantation trade one problem (heart failure and pulmonary failure, respectively) for another, creating an immunocompromised host who is susceptible to usual as well as to opportunistic infections (e.g., fungal, viral) not commonly seen in otherwise healthy persons.
EPIDEMIOLOGY In 2005, 2125 heart transplants and 1407 lung transplants were performed in the United States. Common diseases that lead to end-stage
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heart disease and the need for cardiac transplantation include cardiomyopathy from any cause (e.g., ischemic, viral, alcoholic, familial, and idiopathic), congenital abnormalities not amenable to surgical correction, and postsurgical pump failure from any cause. Common diseases that lead to end-stage pulmonary disease and the need for lung transplantation include chronic obstructive lung disease, pulmonary fibrosis from any cause, primary pulmonary hypertension, and septic lung disease such as cystic fibrosis. Single lung transplantation is often all that is needed; however, septic lung disease of both lungs necessitates the removal of both lungs and hence is one of the absolute indications for bilateral lung transplantation. Combined heart and lung transplantation is relatively rare but is usually reserved for end-stage disease of both the heart and lungs when surgical correction of either organ is not possible. Most patients awaiting transplant are usually in close proximity to the transplant center where they are receiving care, since they typically have to be able to get to the hospital within a set time period if called for a transplant when a donor becomes available. Patients who have had a transplant likewise are usually in relatively close proximity to the center where the transplant was performed (because of the close follow-up necessary with most of these patients) or at least in close proximity to a transplant center that serves as a surrogate. As a consequence, most of these patients can and should be transferred to the tertiary transplant center familiar with their care once stabilized for transport. Occasionally, however, these patients find themselves relatively far away from a tertiary transplant center. In these cases, the patient may require admission to the hospital to which they present themselves, even though the hospital itself is not specifically trained or equipped to handle services required to either accurately diagnose or definitively treat the presenting problem. In these cases, supportive care in the form of pulmonary and cardiac support should be the mainstay of treatment. Treating a presumed rejection episode with high-dose immunosuppressive agents without a relatively firm diagnosis should be discouraged, since treatment can be fatal if the problem turns out to be infection or sepsis. The ability to distinguish between these two diagnoses strictly on clinical grounds can often be very difficult, and a misdiagnosis and treatment can be potentially fatal (see later text).
CLINICAL PRESENTATION Heart Failure Symptoms of heart failure include shortness of breath, abdominal pain and nausea, weakness or lethargy, and poor mentation or obtundation. Left heart failure typically produces respiratory symptoms (e.g., cough, shortness of breath, frothy sputum), and right heart failure produces peripheral swelling and abdominal symptoms.
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Pulmonary Failure Symptoms of pulmonary failure include shortness of breath, tachypnea, an inability to talk in complete sentences, tachycardia, cough, weakness, and lethargy. This can occur both in patients awaiting lung transplant and in recipients, as well as awaiting or who have received cardiac transplantation.
Rejection Rejection of a transplanted organ can present as either heart failure or pulmonary failure, depending on whether it occurs in a lung or heart transplant recipient. Sometimes symptoms are subtle and can include weakness, malaise, cough, and low-grade subjective fevers.
Infection Infection can occur anywhere in the body, given that most lung and heart transplant recipients are taking immunosuppressive medication. Lung transplant recipients not uncommonly get community-acquired pneumonia that can cause fevers, chills, productive or nonproductive cough, shortness of breath, and pleuritic chest pains. Other common sites of infection include the urinary tract (e.g., dysuria, urgency, and frequency), soft tissue and skin (e.g., redness, pain, and purulence), sinuses (e.g., pain, drainage), biliary tract (e.g., right upper quadrant pain, jaundice), and gastrointestinal tract.
EXAMINATION Heart Failure Examination findings in the presence of heart failure include peripheral swelling, cold/clammy periphery with poorly palpable distal pulses, tachycardia (although bradycardia may be present as well), S3 heart sound audible on cardiac examination, jugular venous distention, pulmonary crackles, diminished breath sounds, pleural effusions, and/or a pulsatile liver. Hypotension is also a common finding, although patients can be experiencing heart failure with high blood pressure as well (though the latter usually implies another cause of heart failure besides primary pump failure).
Pulmonary Failure In the presence of pulmonary failure, examination findings will include a cold/clammy periphery, accessory muscle use, wheezing, cyanosis of the
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lips or fingers, and low oxygen saturations. Patients may present with pneumothoraces (i.e., diminished breath sounds on one side, possible mediastinal shift either toward [nontension] or away [tension] from the side of pneumothorax), pleural effusion (i.e., dullness to percussion, diminished breath sounds on the affected sided), and pulmonary consolidation (i.e., bronchial breath sounds, diminished breath sounds, crackles, and rhonchi in the larger airways).
Rejection Examination findings related to organ rejection can include those of both heart failure and pulmonary failure, depending on whether the patient is a heart or lung transplant recipient. Signs can include those mentioned above and can also mimic infection, especially if it occurs in a lung transplant recipient.
Infection If infection is present, examination findings can be very nonspecific and can include lethargy, weakness, and mental obtundation. More specific findings can include productive cough, fevers, and findings consistent with pulmonary consolidation or pleural effusion, as described previously. Depending on the location of the infection, symptoms can be variable (e.g., redness, purulent drainage if in the skin or soft tissue; abdominal tenderness in the biliary tree or gastrointestinal tract). Signs and symptoms may be very subtle, and what would normally be expected to be present in a nonimmunocompromised patient may be totally absent or only slightly present in an immunocompromised transplant recipient. Any foreign bodies such as pacemakers, automatic implantable defibrillators, central lines, and indwelling implantable venous reservoirs should be carefully examined for any signs of infection (e.g., tenderness, redness, drainage). Indwelling catheter infections are common and must be suspected in any immunocompromised host.
LABORATORY FINDINGS All patients awaiting transplant or transplant recipients with suspected pulmonary and/or heart failure should undergo arterial blood gas examination to determine hypoventilation (carbon dioxide), acid-base balance, and degree of hypoxemia (oxygen saturation), as well as a complete blood count. A basic chemistry panel, including blood urea nitrogen, serum creatinine, and basic electrolytes (including potassium and sodium) as well as blood glucose, should also be performed. A urinalysis should also be performed with microscopic analysis, since many urinary tract infections
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can be asymptomatic in immunocompromised persons. Blood levels of immunosuppressive medications (e.g., cyclosporine, Prograf) should also be performed if available because this can indicate compliance to medication instructions. In addition, certain disease states can radically alter the blood levels of certain immunosuppressive drugs, making the patient more susceptible to other problems such as renal failure, infection, or rejection when an acute change in the patient’s condition occurs. Sputum samples should be collected from patients suspected of having pneumonia, to be sent for immediate Gram stain as well as culture and sensitivity tests. Blood cultures should also be performed in any patient suspected of having bacteremia, and liver/pancreatic enzymes should be measured in anyone suspected of having biliary infections or obstruction.
DIAGNOSIS The diagnosis of heart failure is suspected on both clinical and radiographic grounds. Echocardiography and pulmonary arterial catheterization can help confirm the diagnosis. Pulmonary arterial catheterization will typically reveal a low cardiac output, high pulmonary arterial pressures relative to the systemic pressures, and high pulmonary wedge pressures reflecting high left atrial filling pressures. The diagnosis of pulmonary failure is made mainly on clinical grounds, with radiographic findings aiding in the diagnosis. It is important to remember that although radiographic findings may be subtle or even completely absent, the diagnosis and subsequent treatment of pulmonary failure should not be withheld if clinically apparent. Cardiac rejection in a heart transplant recipient may be difficult to diagnose and usually requires an endomyocardial biopsy to confirm. This is usually done in the heart catheterization laboratory with the patient under local anesthesia. A catheter is inserted into the right jugular vein and guided fluoroscopically into the right ventricle, where a myotome is used to obtain a small piece of endomyocardium for histological analysis. If rejection is suspected, biopsy should be performed as soon as possible by an experienced surgeon or cardiologist. The diagnosis of acute cardiac rejection may be problematic and as such may be made not uncommonly on clinical grounds alone. Rejection in a lung transplant recipient may also be difficult to ascertain and distinguish from infection (e.g., pneumonia), since it may appear quite similar radiographically, and, as a result, usually requires a bronchoscopic transbronchial biopsy to confirm. This is performed in the bronchoscopy suite by an experienced pulmonologist and usually requires a highly skilled pathologist to confirm. Consequently, such a procedure is usually best performed at a lung transplant center with staff skilled in performing such procedures.
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Infection is usually diagnosed clinically with radiographic help and cultures growing confirmatory organisms. Often a responsible organism cannot be isolated, a not uncommon event in cases of viral or fungal infections.
RADIOGRAPHS An upright and lateral chest radiograph should be performed in all patients awaiting heart or lung transplant and in transplant recipients presenting to the emergency department with any of the previously described signs or symptoms. In addition, computed tomography (CT) scanning should be considered in patients with chest findings seen on plain radiography that are considered to be potential sites for infection. In addition, CT scanning of the abdomen and pelvis should be done in immunocompromised patients presenting with abdominal findings. Plain radiographs of the extremities should be performed when soft tissue infections are suspected so that osteomyelitis can be ruled out. It is important to remember that both rejection and infection can often yield similar radiographic findings in lung transplant recipients.
TREATMENT The treatment priority of heart failure, pulmonary failure, rejection, and infection in a patient awaiting cardiac or lung transplant or in a recipient of one of these organs should first be supportive in nature. Addressing the usual ABCs of airway, breathing, and circulation is of paramount importance when dealing with acute decompensation of a thoracic transplant patient. Heart failure is treated with intravenous diuretics and inotropic support with the main goals being to increase cardiac output, decrease afterload, and decrease demand (i.e., rest and mechanical ventilation, if necessary). Common inotropes include milrinone (increases cardiac contraction and decreases afterload), dobutamine (same action as milrinone, although much shorter acting; may also cause more tachycardia than milrinone); dopamine (increases inotropy and increases renal blood flow at low levels), and epinephrine (increases inotropy, increases chronotropy, and at high doses actually increases afterload). Mechanical support may become necessary if the usual pharmacological support fails. Mechanical support may take the form of the insertion of an intra-aortic balloon pump that augments diastolic blood flow (both distally and into the coronary arteries) and diminishes afterload (thereby off-loading and increasing left ventricular ejection). It accomplishes this by means of a sausage-shaped balloon positioned in the proximal descending thoracic aorta that undergoes quick inflation-deflation cycles timed with the ejection cycles of
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the heart. It can be inserted through the femoral artery, usually using fluoroscopic guidance (although in emergency situations can be inserted at the bedside.) In most severe cases, cardiac assist devices may need to be placed emergently by a cardiac surgeon, with the hope being that the underlying acute event is reversible. If the underlying condition is not reversible, mechanical devices can be inserted surgically and occasionally remain in place for months until a new donor heart can be found. Pulmonary failure is first treated with supportive measures in the form of oxygen administration and then mechanical ventilation (if necessary) commensurate with the degree of clinical decompensation. Endotracheal intubation and positive-pressure mechanical ventilation should not be withheld even in the case of relatively recent lung transplant recipients in which the fear of disrupting new bronchial suture lines may be present, so long as peak pressures are kept within reason (i.e., preferably less than 34 cmH2O). Definitive treatment of pulmonary failure must be aimed at the underlying cause, which is usually rejection versus infection versus both in a lung transplant recipient. This can also be true for a heart transplant recipient who has developed pneumonia as a result of being immunocompromised, or who has developed pulmonary edema from left-sided heart failure from primary graft failure from any reason.
REJECTION Once the diagnosis is confirmed, treatment usually occurs in the form of a steroid pulse bolus, followed by a slow taper. More advanced cases of rejection or patients unresponsive to steroid bolus can be treated with cytolytic therapy, usually in the form of OKT3 monoclonal antibody. It is important to remember that treatment of rejection should be first confirmed with biopsy, since infection can actually be made worse, leading to sepsis and then death if misdiagnosed. However, maintenance immunosuppressive therapy should almost never be withheld from a heart or lung transplant recipient, even when he or she is being treated for a life-threatening infection.
INFECTION Treatment of infection can be local (e.g., drainage of an abscess, removal of a necrotic gallbladder or appendix, removal of an infected intravenous line or port) and/or systemic (e.g., administration of intravenous antibiotics). Specific treatment is aimed at the underlying organism. Usually this is bacterial, but the infection can be an opportunistic fungal or viral organism considering the immunocompromised state of the heart or lung transplant recipient. If life-threatening infection is suspected, appropriate therapy should not be withheld once culture samples have been taken,
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even if confirmatory cultures do not yield a specific organism. Often systemic infections are necessarily treated presumptively, once rejection has been ruled out. It is important to remember that infections can occur simultaneously with rejection episodes, and that even certain infections may predispose the transplant recipient to subsequent or concurrent rejection episodes. The overall prognosis in transplant recipients is variable, depending on the patient’s comorbidities, the severity and number of rejection episodes, the severity and underlying cause of infectious events, and the degree of chronic rejection present, which most certainly eventually occurs in all recipients to some degree. It is important to note that all transplant recipients trade one set of problems for another and that transplantation is by no means considered a “cure.”
Bibliography Bag R: Fungal pneumonias in transplant recipients, Curr Opin Pulm Med 2003;9(3):193–198. Collins J: Imaging of the chest after lung transplantation, J Thorac Imag 2002;17 (2):102–112. Emond JC: What’s new in transplantation, J Am Coll Surg 2002;194(5):636–641. Estenne M, Hertz MI: Bronchiolitis obliterans after human lung transplantation, Am J Respir Crit Care Med 2002;166(4):440–444. Faro A, Visner G: The use of multiple transbronchial biopsies as the standard approach to evaluate lung allograft rejection, Pediatr Transplant 2004;8(4):322–328. Grover FL, Barr ML, Edwards LB, et al: Thoracic transplantation, Am J Transplant 2003;3(Suppl 4):91–102. Kaufman DB, Shapiro R, Lucey MR, et al: Immunosuppression: Practice and trends, Am J Transplant 2004;4(Suppl 9):38–53. Knoop C, Haverich A, Fischer S: Immunosuppressive therapy after human lung transplantation, Eur Respir J 2004;23(1):159–171. Kotloff RM, Ahya VN: Medical complications of lung transplantation, Eur Respir J 2004; 23(2):334–342. Nathan SD: Lung transplantation: Disease-specific considerations for referral, Chest 2005;127(3):1006–1016. Pierson RN 3rd, Barr ML, McCullough KP, et al: Thoracic organ transplantation, Am J Transplant 2004;4(Suppl 9):93–105. Ratjen F, Doring G: Cystic fibrosis, Lancet 2003;361(9358):681–689. Stewart KC, Patterson GA: Current trends in lung transplantation, Am J Transplant 2001;1 (3):204–210. Vilchez RA, Dauber J, Kusne S: Infectious etiology of bronchiolitis obliterans: The respiratory viruses connection—myth or reality? Am J Transplant 2003;3(3):245–249. Vilchez RA, Dauber J, McCurry K, et al: Parainfluenza virus infection in adult lung transplant recipients: An emergent clinical syndrome with implications on allograft function, Am J Transplant 2003;3(2):116–120. Zamora MR: Cytomegalovirus and lung transplantation, Am J Transplant 2004;4 (8):1219–1226. Zuckermann A, Klepetko W: Use of cyclosporine in thoracic transplantation, Transplant Proc 2004;36(2 Suppl):331S–336S.
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Liver Transplantation ALFREDO ESPINOZA, K.VINCENT SPEEG, KENNETH WASHBURN, AND GLENN HALFF
ICD Code: Liver failure 572.8
Key Points Hepatitis C virus (HCV) cirrhosis is the most common reason for liver transplantation in the United States. The recurrence rate of HCV is virtually 100% in the transplanted liver and cirrhosis recurs in up to 30% of HCV-infected patients at 5 years. Liver transplant recipients with normal liver function are more likely to acquire unusual infections or tumors relative to the general population but often have common medical illnesses similar to the typical population. It is important to check which medicines interact metabolically with the immunosuppressive medications transplant recipients are taking before prescribing new medications. Renal function is frequently compromised in patients who have received liver transplantation due to a combination of many factors.
DEFINITION Liver transplantation has grown tremendously since Thomas Starzl performed the first orthotopic liver transplantation in 1963. Orthotopic liver transplants occur when a whole donor liver is transplanted into the same location as the recipient’s previous liver. From perfections in surgical technique to the ground-breaking discovery of cyclosporine in 1979, liver transplantation, which was approved as a nonexperimental treatment for end-stage liver disease in 1983, has continued to benefit the lives of thousands of patients and their families. The overall selection of patients for liver transplant is a lengthy and sometimes difficult process. It is dependent on a medical evaluation of other organ systems such as cardiac and pulmonary. A social evaluation is performed to assess whether adequate social support will be present before and after transplant and to determine whether the patient has a history of medical compliance. An evaluation is done to ensure that any substance abuse has stopped for a period of at least 6 months, in combination with counseling, if necessary. This section will primarily focus on the presentation, evaluation, and treatment of some of the complications that occur in patients after they have received a liver transplant.
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SURGICAL PROCEDURE The waiting list for liver transplantation is prioritized based on degree of illness, which is calculated from a formula incorporating laboratory values such as the international normalized ratio (INR), bilirubin, and creatinine. Therefore, most patients who are chosen to receive transplants are the most ill patients, and actual waiting time has little influence on the choice of recipient. The transplant procedure typically takes 3–5 hours with a 7-day hospitalization. Longer posttransplant hospitalizations are common with patients whose conditions are severely deteriorated. The operation involves removing the native cirrhotic liver and reconnecting the donor liver in the same position in which the native liver rested. The vena cava may be connected with an anastomosis below and above the liver (standard) or with only one anastomosis from the cava to the recipient cava (piggy back). The recipient vena cava remains intact with the piggyback technique and the donor cava is a dead end, with one end tied off and the other draining end to the side into the recipient cava. This technical differentiation is important when interpreting a posttransplant ultrasound scan. Living donor liver transplants and pediatric split liver transplants require a piggy back caval anastomosis. The hepatic artery is generally sewn end to end, recipient to donor, but in about 5% an iliac artery graft to the recipient infrarenal aorta is necessary. The portal vein is usually end to end but an iliac vein graft to the superior mesenteric vein may be necessary if the recipient has a thrombosed portal vein. The biliary anastomosis can be done in one of two ways: end to end, in which case a postoperative endoscopic retrograde cholangiopancreatography (ERCP) may be done, or connected to a Roux-en-Y loop of small bowel, in which case an ERCP cannot reach the anastomosis and a percutaneous transhepatic cholangiogram must be done if the biliary system needs to be studied. Magnetic resonance cholangiogram is sometimes helpful to study the biliary system as well. The patients are usually sent home with no drains in place unless a T tube has been inserted in the bile duct. Routine ultrasound scans are done postoperatively to check vessel patency (Tables 20-1 and 20-2).
EPIDEMIOLOGY End-stage liver disease causes 25,000 deaths per year in the United States. According to the United Network for Organ Sharing (UNOS), 17,455 patients were on the liver waiting list as of September 2005 but only 6169 patients were transplanted in 2004. This disparity is a consequence of a donor pool that is unable to keep up with a growing waiting list. Survival after transplant is different for various etiologies of liver disease. Cumulative survival (all etiologies) at 1, 3, and 5 years is 85%, 78%, and 72%, respectively, according to UNOS.
1158 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 20-1 Indications for Liver Transplantation CHOLESTATIC DISORDERS Primary biliary cirrhosis Primary sclerosing cholangitis Biliary atresia
CHRONIC PARENCHYMAL DISEASES Hepatitis C
ACUTE FULMINANT LIVER FAILURE
OTHER
Hepatitis A, B, rarely C, Polycystic liver rarely E disease Toxin ingestion (e.g., Budd-Chiari acetaminophen) syndrome
Hepatitis B
Cryptogenic cirrhosis Wilson’s disease (NASH) Alcohol-related cirrhosis Unknown Autoimmune cirrhosis Hemochromatosis a1 antitrypsin deficiency Wilson’s disease
Primary liver neoplasm Amyloidosis
NASH, Nonalcoholic steatohepatitis.
Table 20-2 Common Immunosuppressive Medications MEDICATION
METABOLISM EXCRETION
Prednisone
Hepatic
Renal
Cyclosporine
Hepatic
Bile
Tacrolimus (Prograf)
Hepatic
Bile
Mycophenolate mofetil (Cellcept)
Hepatic
Renal
Azathioprine (Imuran)
Hepatic
Renal
Sirolimus (Rapamune)
Hepatic
Bile
MAJOR TOXICITIES Hypertension, neurotoxicity, hyperlipidemia, and hyperglycemia Nephrotoxicity, hypertension, hyperkalemia, hypomagnesemia, neurotoxicity (e.g., seizures, tremors), hyperlipidemia, hyperglycemia, and gingival hyperplasia Nephrotoxicity, hyperkalemia, hypomagnesemia, neurotoxicity (e.g., seizures, tremors), hyperlipidemia, and hyperglycemia Leukopenia, anemia, thrombocytopenia, pancreatitis, and gastrointestinal toxicity (e.g., diarrhea) Leukopenia, anemia, thrombocytopenia, and gastrointestinal toxicity (e.g., diarrhea, nausea and vomiting) Leukopenia, anemia, thrombocytopenia, hyperlipidemia, and poor wound healing
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CLINICAL PRESENTATION The posttransplant presentation of a liver transplant recipient can vary widely from that of a completely normal patient to a patient with recurrence of cirrhosis that presents with ascites, encephalopathy, gastrointestinal tract bleeding, or sepsis. It is important to recognize that liver transplant recipients are just as susceptible to common medical problems as they are to more complex ones that are associated with their immunocompromised state.
EXAMINATION Careful evaluation of the patient’s mentation should be one of the initial assessments. Asterixis or flapping tremor of the wrists, which is best seen when the arms are outstretched with the wrists in hyperextension, is a common finding of hepatic encephalopathy. Pretransplant encephalopathy is most commonly related to infection, gastrointestinal tract bleeding, or overdiuresis. Posttransplant encephalopathy may be related to infection or medication adverse effects. A change in mental status usually requires that a head CT or magnetic resonance imaging (MRI) scan be performed to evaluate for intracranial bleeding, tumor, or infection. A yellowish discoloration of the sclera (i.e., icterus) may represent an elevated bilirubin level. The lungs should be examined for the presence of fluid or consolidation. Pleural effusions in the first few months after the transplant are common, as is some degree of ascites. The abdomen should reveal a Mercedes-Benz (inverted Y) incision and should be examined for liver size, tenderness, ascites, or splenomegaly. If edematous, the lower extremities and sometimes upper extremities may give an indication of liver, heart, or kidney failure. The skin may become jaundiced (yellow) in the course of liver failure and spider angiomata (i.e., vascular dermatological aberrations commonly seen in patients with cirrhosis) may be present. If bleeding is suspected, a nasogastric lavage and a rectal examination should be done.
LABORATORY FINDINGS Laboratory data from a liver transplant recipient must be assessed carefully and must be made with reference to the patient’s transplant date and etiology of transplant. For example, most patients’ liver-associated enzyme levels will not have fully normalized at the time of discharge after their transplant. On the other hand, patients with HCV infection may never have fully normalized liver-associated test results. The interpretation of trends is extremely useful to the transplant clinician in compiling a proper diagnostic plan and treatment course. Initial laboratory data in
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the emergency care setting should include complete blood count; coagulation studies (e.g., INR, partial thromboplastin time); measurements of total bilirubin, direct bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, chemistry, and ammonia level; and blood and urine cultures, if infection is suspected. If ascites is present and infection is suspected, a paracentesis should be performed with attention to cell count, Gram stain, and culture. Tacrolimus or cyclosporine trough levels are usually drawn 12 hours after the last dose. The interpretation of a tacrolimus measurement taken too soon after the last dose may produce a falsely high reading, which may in turn lead to an inappropriate lowering of the dose by the transplant clinician. Many liver transplant recipients taking tacrolimus can discontinue all other means of immunosuppression by 1 year posttransplant. Adrenal insufficiency may be present in these patients.
DIAGNOSIS A diagnosis of the complications after transplant can usually be initiated on the basis of laboratory test results. However, more complex problems may require more extensive workup such as Doppler sonography of the hepatic vessels (to evaluate for a thrombosed or stenotic hepatic artery or portal vein or hepatic vein outflow stenosis), liver biopsy (to evaluate for rejection, drug toxicity, or viral infections), CT scan (to evaluate for possible intraabdominal infection), MRI, and sometimes surgical exploration. Thrombosis of the hepatic artery, especially early in the posttransplant period, may cause ischemia of the biliary system and may result in diffuse biliary strictures, bile duct leak, or intrahepatic bilomas. Table 20-3 outlines potential complications.
RADIOGRAPHS Plain radiography such as a chest x-ray or an abdominal series should be tailored to the patient’s presentation. A chest radiograph is necessary Table 20-3 Complications of Liver Transplantation Medical
Diabetes mellitus, hyperlipidemia, hypertension, infections (especially CMV), malignancies, neurological complications (especially seizures), obesity, renal disease, lymphoproliferative disease Postoperative Biliary tract (strictures, leaks, etc.), hepatic artery stenosis, portal vein thrombosis Recurrence of primary Hepatitis C, hepatitis B, PSC, PBC, malignancy disease Rejection Acute, chronic (rare)
CMV, Cytomegalovirus; PSC, primary sclerosing cholangitis; PBC, primary biliary cirrhosis.
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for suspected infection, changes in mentation, or shortness of breath. These can provide a wealth of information and are often sufficient for the diagnosis of pneumonias, bowel obstruction, or ileus. An elevation in the trend of liver-associated enzymes may lead to the suspicion of a biliary or vascular problem. A Doppler ultrasound of the liver should be ordered at this point. If there is still doubt about the findings, an MRI/MR angiograph and MR cholangiopancreatograph or a three-phase CT scan (avoid if renal function is impaired) of the liver may become necessary. If a bile duct problem is suspected, the biliary system should be studied with an ERCP if the patient has a duct-to-duct biliary anastomosis, or with a percutaneous transhepatic cholangiogram if the patient has a Roux-en-Y biliary connection.
TREATMENT As stated previously, most patients after a liver transplant present with common medical problems. These can be treated as they would in the general patient population. However, it is important to understand that commonly prescribed medications can and often do interfere with the immunosuppressant medications (Table 20-4). Biliary and vascular complications will usually involve the multidisciplinary care of a transplant surgeon, a hepatologist, a radiologist, and a biliary endoscopist. Rejection and recurrence of disease can be treated in the transplant clinic or in the acute setting by an experienced transplant clinician. Severe infection may require decreasing the immunosuppression in addition to standard treatment. Adrenal insufficiency may require stress steroids even in the face of infection. Table 20-4 Drug Interactions IF THESE ARE COADMINISTERED, INCREASE DOSES OF CYCLOSPORINE/TACROLIMUS Carbamazepine Phenobarbital Phenytoin Primidone Rifabutin
IF THESE ARE COADMINISTERED, DECREASE DOSES OF CYCLOSPORINE/TACROLIMUS Clarithromycin Daunorubicin Diltiazem Etoposide Erythromycin Fluconazole Grape fruit juice Itraconazole Posiconazole Quinupristin/dalfopristin Ritonavir Saquinavir Vinblastine Verapamil Voriconazole
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If doubt exists about the appropriate treatment of a particular complication, the transplant center or team should always be consulted.
Bibliography Carithers R: AASLD guideline: Liver transplantation, Liver Transplant 2000;6:122. Dedmon M: Liver transplantation: Managing complications in primary care, JAAPA 2005;18(2):41–49. Gane EJ, Portmann BC, Naoumov NV, et al: Long-term outcome of hepatitis C infection after liver transplantation, N Engl J Med 1996;334:815. Killenberg P, Clavien P-A: Medical Care of the Liver Transplant Patient, ed 2. Blackwell Science: Malden, MA, 2001. Kok T, Slooff MJ, Thijn CJ, et al: Routine Doppler ultrasound for the detection of clinically unsuspected vascular complications in the early postoperative phase after orthotopic liver transplantation, Transplant Int 1998;11(4):272–276. Maceneaney PM, Malone DE, Skehan SJ, et al: The role of hepatic arterial Doppler ultrasound after liver transplantation: An “audit cycle” evaluation, Clin Radiol 2000;55 (7):517–524. Saab S, Wang V: Recurrent hepatitis C following liver transplant: Diagnosis, natural history, and therapeutic options, J Clin Gastroenterol 2003;37(2):155–163. Schafer D: Liver transplantation: Looking back looking forward, In Maddrey WC, Schiff ER, Sorrell MF (eds): Transplantation of the Liver, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001. Stein JH, Klippel JH, Reynolds HY, et al (eds): Internal Medicine, ed 5. Mosby: St Louis, 1998, p 2160. United Network for Organ Sharing, Center Data. Available at: http://www.unos.org. Accessed September 17, 2005.
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Renal Transplantation GREG A. ABRAHAMIAN AND ROBERT M. ESTERL
CPT Code: Renal failure 586
Key Points Renal transplant recipients can experience complications that are related directly to the renal graft to immunosuppressive drug therapy to the underlying medical illness that led to their renal disease and to other comorbid medical and surgical problems. An increase in the serum creatinine level is nonspecific and can be due to a number of problems in addition to graft rejection. Transplant recipients are generally monitored closely by their transplant centers and early involvement with that team may yield important insight into the patient being evaluated in the emergency department. ! Emergency Actions ! Emergency action should be dictated by the clinical presentation of the patient, always addressing airway, breathing, and circulation first.
DEFINITION Renal transplantation has become the therapy of choice for patients with end-stage renal disease. More than 16,000 renal transplants are performed annually in the United States for patients with renal disease resulting most commonly from diabetes, hypertension, and glomerulonephritis. Approximately half of the recipients receive organs from living donors and the remainders are from deceased (cadaveric) donors. Many of these patients have associated comorbidities due to their primary disease processes such as coronary artery disease or peripheral vascular disease. Complications arising from chronic immunosuppressive therapy include infections, cancer, metabolic derangements, worsening hypertension and hyperglycemia, and progression or exacerbation of existing illnesses. In addition, a renal transplant recipient is always at risk of rejecting the organ, either acutely or in a chronic fashion.
EPIDEMIOLOGY Early surgical complications involving the renal graft include arterial or venous thrombosis or stenosis, lymphocele formation, ureteral leak with
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“urinoma,” and hemorrhage. Early medical complications involving the grafted organ include rejection, drug toxicities, including tacrolimus or cyclosporine toxicities, infections such as pneumonia or urinary tract infection, and recurrence of the primary disease process. Most opportunistic infections (unusual organisms) do not develop until after the first postoperative month. Late complications affecting the graft and the recipient include rejection, opportunistic infections, arterial stenosis, ureteral stenosis or reflux, cancer, and progression of cardiovascular disease. It is important to note that cardiovascular disease is still the predominant cause of death in patients after renal transplantation.
CLINICAL PRESENTATION The majority of complications in renal transplant recipients are discovered during routine outpatient visits. The following symptoms may be associated with several complications that are unique to the renal transplant recipient. Arterial or venous thromboses are considered catastrophic events after transplantation. Patients may present with sudden graft pain, markedly decreased urine output, and swelling of the ipsilateral leg. Collections that develop around the renal graft include lymphoceles, urinomas, and hematomas. Patients may present with decreased urine output, pelvic pain or fullness, leg swelling, drainage from the incision, and in the case of a hematoma, symptoms related to anemia. Immunosuppressed patients are more susceptible to infections, and in most cases symptoms will be typical for the infected site. Although these persons are at increased risk for opportunistic infections similar to those seen in the patients with human immunodeficiency virus infection, community-acquired bacterial and viral infections still predominate. Cytomegalovirus is the most important viral infection affecting transplant recipients, and symptoms can include fever, diarrhea, dysphagia, fatigue, and evidence of bone marrow suppression on laboratory studies. Patients who develop symptomatic ureteral complications frequently present with recurrent urinary tract infections or graft pyelonephritis. Urinary tract infections are the most frequent cause of bacteremia in renal transplant recipients. Symptoms may include fever, graft tenderness, decreased urine output, and dysuria. The highest incidence of acute rejection occurs within the first 6 months after transplantation. However, it can occur at anytime during the life of the graft. Patients experiencing graft rejection can be asymptomatic or may present with symptoms consistent with acute renal failure. Lowgrade fever, worsening hypertension, weight gain, decreased urine output, graft tenderness, and ipsilateral leg swelling are common symptoms.
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Patients may give a history of having recently stopped or altered their immunosuppressive medications.
EXAMINATION As in most clinical situations, a complete physical examination is necessary. The vital signs noted should always include a temperature, blood pressure, and weight to compare with baseline levels. The general appearance of the patient is important to note because a patient in distress may signify shock or hypoxia due to septicemia or a cardiac or pulmonary event. It is important to palpate the graft to elicit tenderness or the presence of a mass and to auscultate the area to assess for a bruit, which may be associated with an arterial stenosis. Examination of the lower extremities should include notation of the presence or absence of edema. The rectal examination should always include stool guaiac testing. A thorough examination of the skin should be performed, noting any lesions that may be infectious or cancerous.
LABORATORY FINDINGS The serum creatinine measurement is the single most useful test to assess the function of a renal transplant. Most transplant recipients will know their baseline creatinine levels. Elevations in the serum creatinine level may be due to rejection, infection, dehydration, hyperglycemia, vascular or ureteral complications, perinephric fluid collections, recurrent renal disease, and drug toxicities, including tacrolimus or cyclosporine nephrotoxicity. A complete metabolic panel should also be included to assess for other electrolyte abnormalities that may be associated with renal dysfunction. A complete blood count should be performed. Pancytopenia may present in viral infections, most notably cytomegalovirus; however, the diagnosis of a cytomegalovirus infection is most commonly made on the basis of a quantitative polymerase chain reaction analysis. Although immunosuppressed, renal transplant recipients typically will respond to an infection with leukocytosis. A urinalysis with urine culture is necessary to assess for a urinary tract infection as well as for the presence of blood, protein, and glucose. A tacrolimus or cyclosporine serum trough level should be obtained, but to be clinically relevant, samples should only be drawn 10–12 hours after the last dose is administered. Any patient suspected of having bacteremia or sepsis should have blood culture samples drawn from two sites before the initiation of treatment with antibiotics. Drainage from the incision should be sent for Gram stain and culture.
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RADIOGRAPHS A sonogram of the renal recipient is necessary to assess the vasculature and to note the presence or absence of fluid collections or hydronephrosis. A nuclear medicine renal scan may also be performed to further assess graft perfusion and excretion and possibly the presence of a urine leak. Additional radiographs should be ordered based on the patient’s presentation and physical findings.
DIAGNOSIS The diagnosis of a number of complications in renal transplant recipients can be made after a thorough history is taken and physical examination is performed in conjunction with the appropriate laboratory and radiographic data. The diagnosis of rejection, recurrent renal disease, and a small number of unique infections involving the graft can only be made by microscopic examination of the transplant renal biopsy sample. Refer to Tables 20-2 and 20-4 for common immunosuppressive medications and drug interactions, respectively.
TREATMENT Empirical antibiotic therapy should always be initiated early if an infection is suspected. Avoidance of nephrotoxic agents should always be considered, and dosing adjustments made with regard for renal function should be performed. Appropriate culture samples should be obtained before the initiation of therapy. Intravascular volume status should be assessed, and intravenous fluid should be devoid of potassium if renal dysfunction is present. It is important to note that macrolide antibiotics and azole antifungal agents may significantly increase serum levels of tacrolimus and cyclosporine, resulting in drug toxicities. Infections due to opportunistic organisms are often diagnostic dilemmas, frequently requiring multiple tests to achieve the diagnosis. Treatment is geared toward the particular organism identified, often in consultation with infectious disease specialists. If discovered early, most opportunistic infections can be eradicated. Overall, 50% of infections are viral, 30% are bacterial, 5% are fungal, and 15% are polymicrobial. Vascular and ureteral complications, as well as perinephric fluid collections, will frequently require radiological intervention as determined by the transplant team or nephrologists. Surgical intervention is performed after less invasive treatments have failed or are not possible. Treatment for rejection should only be initiated after other causes of renal dysfunction are ruled out and after biopsy confirmation. Often, bolus intravenous steroids are given with adjustments in the maintenance immunosuppression. More potent antibody agents are reserved for bolus steroid
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failures, and treatment is usually undertaken in an inpatient setting. Graft loss due to rejection is rare, with 1-year graft survival rates exceeding 90%.
Bibliography Morris PJ (ed): Kidney Transplantation, ed 5. WB Saunders: Philadelphia, 2001. United Network for Organ Sharing. Available at: http://www.unos.org.
Index AAA. See Abdominal aortic aneurysm ABC. See Airway-breathing-circulation Abdomen. See also Bowel; Gastrointestinal bleeding; Gastrointestinal emergencies anatomy of, 1058 pain in, 389, 509–512, 731–735 clinical presentation, 511 CT scan for, 512 definitions, 510–511 diagnosis, 512 emergency actions, 509–510 endometriosis, 510 examination, 511 geriatric, 389 geriatric emergencies, 389 key points, 509 laboratory findings, 512 pediatric emergencies, 731–735 ultrasound scanning, 512 pediatric emergencies, 731–735, 1078 clinical presentation, 733–734 definition, 732 emergency actions, 731 epidemiology, 732–733 key points, 731 laboratory tests and radiology, 734–735 physical examination, 734 trauma, 1078 treatment, 735 surgical emergencies aortic aneurysm, 1–4 appendicitis, 5–8, 510 cholelithiasis and cholecystitis, 9–14 hernias, 15–18 intestinal obstruction, 18–22 trauma to, 1057–1062, 1078 Abdominal aortic aneurysm (AAA), 1–4 clinical presentation, 2–3 asymptomatic, 2 CT scan/ultrasound for, 4 definition of, 1 diagnosis, 3 emergency actions, 1 epidemiology, 2 examination, 3 key points, 1 laboratory findings, 3
Abdominal aortic aneurysm (AAA), (Continued) pseudoaneurysm, 1 radiographs for, 3–4 treatment and outcome, 4 Abducens nerve examination, 457–458, 458f. See also Cranial nerve examination ABG analysis. See Arterial blood gas analysis Abortion (miscarriage), 510, 525–528. See also Pregnancy Abruptio placentae, 497–499, 510, 1108. See also Pregnancy clinical presentation, 498 definition, 497 emergency actions, 497 epidemiology, 497 etiology, 498 key points, 497 laboratory tests, 498 pathophysiology, 498 traumatic injury causing, 1108 treatment, 499 ultrasound scanning, 499 Abscess, anorectal clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 Abscess, brain Bell's palsy v., 426–427, 426t headaches from, 434 Abscess, breast, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 503–504 mastitis, 504 ultrasound scanning, 503 Abscess, ovarian, 510 A/C ventilation. See Assist-control ventilation Accelerated idioventricular rhythm (AIVR), 51, 51f
1169
1170 INDEX ACE inhibitors. See Angiotensinconverting enzyme inhibitors ACEP. See American College of Emergency Physicians Acetaminophen acute otitis media treatment, 170 genital herpes treatment, 515 pediatric seizures and status epilepticus, 786 thyroid storm treatment, 397 toxicity, 931–936, 934f clinical presentation, 932–933 definition, 931–932 metabolism, 932 diagnosis, 933–935, 934f emergency actions, 931 examination, 933 key points, 931 laboratory findings, 933 overdose nomogram, 933–935, 934f treatment, 931, 935 activated charcoal, 931 Acetylcholine receptor site, myasthenia gravis, 447 Acetylcholinesterase inhibitors, myasthenia gravis requiring, 450 Acetylparaminophenolacetaminophen (APAP), 931. See also Acetaminophen Acid–base emergencies, 311–325 anion gap, 315–317, 324 approach to patients with, 324–325 base deficit/excess, 314 clinical evaluation, 313–314 definition, 312–313 hepatic role in acid-base homeostasis, 314 key points, 311–312 metabolic acidosis, 311, 315–317, 363, 1021, 1023 clinical presentation and examination, 316 definition, 315–316 epidemiology, 316 laboratory findings, 317 treatment and outcome, 317 metabolic alkalosis, 311, 317–320 alkali administration, 318 clinical presentation, 318 contraction alkalosis, 318 definition, 317 epidemiology, 317–318 examination, 319 gastrointestinal Hþ loss, 318 intracellular shifts, 318
Acid–base emergencies, (Continued) laboratory findings, 319 renal Hþ loss, 318 treatment, 319–320 renal excretion and absorption, 313 respiratory acidosis, 312, 320–322, 845 clinical presentation, 320–321 definition, 320 diagnosis, 321–322 epidemiology, 320 examination, 321 laboratory findings, 321 treatment and outcome, 321 respiratory alkalosis, 312, 321–323 clinical presentation and examination, 321–322 definition, 321 diagnosis, 323 etiology, 321 laboratory findings, 323 treatment and outcome, 323 respiratory excretion of volatile acid, 313 theophylline toxicity, 1046 Acidosis alcoholic keto-, 338–343, 339f, 340f, 1021 diabetic keto-, 311, 343–347, 1021. See also Diabetes hyperglycemic hyperosmolar nonketotic coma v., 390–393 pediatric emergencies, 770–774 treatment, 346–347 lactic, 410–413, 411t, 1020 metabolic, 311, 315–317, 363, 1021, 1023 respiratory, 312, 320–322, 845 ACLS. See Advanced cardiac life support Acoustic neuroma, Bell's palsy v., 426–427, 426t Acquired immunodeficiency syndrome (AIDS), 271t. See also Human immunodeficiency virus infection exfoliative dermatitis from, 100, 100b HIV v., 288–289 Activated charcoal. See Charcoal, activated Acute bleeding diathesis, 555–558 clinical presentation, 557 definition, 555 diagnosis, 558 emergency actions, 555 examination, 557 key points, 555 laboratory findings, 557–558
Index Acute bleeding diathesis, (Continued) pathology, 555–556 treatment, 558 Acute compartment syndrome, 596–599 clinical presentation, 597 definition, 596–597 diagnosis, 599 emergency actions, 596 epidemiology, 597 examination, 598 key points, 596 laboratory findings, 598 lower leg, 641 radiographs, 598 treatment, 599 Acute disseminated encephalomyelitis, multiple sclerosis v., 442 Acute mountain sickness (AMS), 184t, 185, 187t, 191 treatment, 188 Acute otitis media (AOM), 169–170, 798–802 barotrauma causing, 207 pediatric emergency, 798–802 Acute renal failure (ARF), 1113–1117. See also End-stage renal disease; Kidneys; Renal disease anti-inflammatory drugs causing, 1114 caustic ingestion causing, 963 clinical presentation, 1115 acute tubular necrosis, 1114 definition, 1113 diagnosis, 1116 emergency actions, 1113 glomerular filtration rate, 1113–1117 key points, 1113 laboratory findings, 1116 lithium poisoning causing, 1018–1019 pathology, 1113–1115 physical examination, 1115 radiography, 1115 treatment, 1116–1117 Acute respiratory distress syndrome (ARDS), 852–854 clinical presentation, 852–853 definition, 852 diagnosis, 853 emergency actions, 852 epidemiology, 852 examination, 853 key points, 852 laboratory findings, 853 PEEP influenced by, 859–861 treatment, 853–854
1171
Acute rheumatic fever (ARF), 774–778 clinical presentation, 775 definition, 775 diagnosis, 775 antecedent GAS infection evidence, 777 Jones criteria for, 775–777 epidemiology, 775 key points, 774 laboratory findings, 777 pathology, 775 treatment, 777 Acute tubular necrosis (ATN), 1114 intrarenal acute renal failure presenting as, 1114 ACV. See Assist-control ventilation Acyclovir, genital herpes treatment, 515 Adnexal torsion, 510 Adrenal insufficiency, 331–338 clinical presentation, 333 consultations with specialists for, 337 definition, 332 differential diagnosis, 334 emergency actions, 331 epidemiology, 332 etiology, 333–334 examination, 333 hospital admission for, 337 key points, 331 laboratory findings, 334 pathophysiology, 332–333 radiographs, 336 treatment, 336–337 Advanced cardiac life support (ACLS), 43, 44 AICD malfunction requiring, 43 lightning injuries requiring, 234 toxic epidermal necrolysis requiring, 103 AED. See Automatic external defibrillator AEDs. See Antiepileptic drugs Aerogastria barotrauma, 207 Aganglionic megacolon (Hirschsprung's disease), 745–748, 748f AICD. See Automatic implantable cardioverter-defibrillator AIDS. See Acquired immunodeficiency syndrome Airway management, 913–916, 914b, 915b. See also Airway-breathingcirculation; Bag-valve-mask device adult clinical presentation, 913 definition, 913
1172 INDEX Airway management, (Continued) equipment for, 673–674 rapid sequence induction COPD patient, 914b head injury patient, 915b treatment, 914–916, 914b, 915b pediatric anesthesia induction, 676 clinical presentation, 671–672 definition, 670 diagnosis, 672 epidemiology, 670 equipment for, 673–674 examination, 672 key points, 670 laboratory findings, 672 neuromuscular blockade, 676–677 pathology, 671 rapid sequence intubation, 672, 674–677 resuscitation formula, 1073–1075, 1074t surgical airway, 677 Airway-breathing-circulation (ABC). See also Airway management; Bag-valvemask device amphetamine overdose, 938 beta-blocker overdose, 954 burns, 196 cardiac arrhythmia emergency securing of, 44 cardiac emergency actions, 58 iron toxicity requiring, 1009–1010 lithium poisoning, 1019 mercury poisoning, 1026 pediatric cardiac arrest, 659, 660 phenytoin toxicity, 1036–1037 theophylline toxicity, 1047 AIVR. See Accelerated idioventricular rhythm Albuterol anaphylactic shock requiring, 921 asthma treatment, 860, 862 Alcoholic ketoacidosis (AKA), 338–343, 339f, 340f, 342, 1021. See also Acidosis; Ethyl alcohol airway and breathing/circulation, 340–341 clinical presentation, 339–340 definition, 339 diagnosis, 342 Soffer and Hamburger's criteria for, 342 disabilities accompanying, 341
Alcoholic ketoacidosis (AKA), (Continued) emergency actions, 338 epidemiology, 339 examination, 340 exposure and secondary survey, 341 key points, 338 laboratory findings, 341–342 pathology, 339, 339f, 340f treatment, 342 Alkalosis. See also Acid-base emergencies metabolic, 311, 317–320 respiratory, 312, 321–323 Allergic conjunctivitis, 164 Alpha–2-adrenergic receptor agonist, 965–968 Alprazolam, panic disorder treatment, 816 ALTE syndrome. See Apparent lifethreatening event syndrome Alternobaric vertigo barotrauma, 207 Altitude-related emergencies, 183–191, 184t, 187t acute mountain sickness, 184t, 185, 187t treatment, 188 cerebral edema, 184t, 185–186, 187t, 189 treatment, 189 definitions, 183 diagnosis, 187–188 epidemiology, 183–185, 184t examination and laboratory findings, 187 key points, 183 peripheral edema, 190 pharyngitis and bronchitis, 190 pulmonary edema, 184t, 186, 187t treatment, 189–190 radiographs, 188 retinopathy, 190 sleep disorders, 191 summary, 191 ultraviolet keratitis, 190–191 Aluminum acetate, toxicodendron dermatitis treatment, 108–109 American Academy of Family Physicians, otitis media treatment, 801 American Academy of Pediatrics, otitis media treatment, 801 American Association for Poison Control Centers, hydrocarbon poisoning, 1004–1005 American Burn Association, 197, 197b
Index American College of Emergency Physicians (ACEP), seizures and status epilepticus, 469, 472 American Psychiatric Association, 815 American Thoracic Society, 883–884 Amide class of anesthesia, 28 Amnesia, high-altitude global, 184t Amniotic fluid embolism, 500–502. See also Pregnancy clinical presentation, 501 definition, 500 emergency actions, 500 epidemiology, 500 etiology/pathogenesis, 500–501 key points, 500 laboratory tests for, 501 radiographs, 501 treatment, 501 Amoxicillin adult bacterial pneumonia, 867, 867t otitis media treatment, 170 pediatric, 801 Amphetamines “ecstasy,” “ice,” 353, 936–937 overdose causing seizures, 938 toxicity, 936–938 clinical presentation, 937 definition, 936 diagnosis, 937 emergency actions, 936 key points, 936 laboratory tests, 937 pathology, 937 treatment, 937–938 Amylase and lipase tests, diverticulitis requiring, 125 Anal fissures clinical presentation, 117 definition, 114 epidemiology, 115 examination, 118 treatment and outcome, 120 Analgesia. See also Morphine; specific type diving injuries treatment, 211 intubated patient, 906–908, 907t contraindicated medications, 908 fentanyl, 907t, 908 hydromorphone, 907t, 908 morphine sulfate, 906, 907t Society for Critical Care Medicine guidelines for, 906 opioid, pulmonary embolism treatment, 903 pediatric, 805–813, 808–809
1173
Analgesia, (Continued) local, 808–809 systemic, 811–812 topical, 808 Anaphylactic reaction, hymenoptera sting causing, 230–233 Anaphylaxis, asthma mimicked by, 857 Anatomy abdominal, 1058 ankle joint, 589–590 central nervous system, 452t foot, 604 forearm and wrist, 609–610 hand, 617–619 hip, 626–627 lower leg, 638–639 neurological examination, 452–453, 452t pelvic, 1081–1082 peripheral nervous system, 452–453 shoulder, 647–648 Anemia conjugated hyperbilirubinemia, 136 hypoalbuminemia state, 315 methemoglobinemia, 964 multiple sclerosis v. pernicious, 442 sickle cell, 570–574 Anesthesia amide and ester classes of, 28 local bupivacaine, 28, 29, 29t EMLA, 28–29 lidocaine, 28, 29, 29t, 914b, 929, 1080 wound management with, 28 pediatric anesthesia induction, 676 pediatric status epilepticus treatment, 787 Aneurysm abdominal aortic, 1–4 geriatric patient susceptibility to, 2 Hunt and Hess Clinical Grading Scale for, 496 pseudo-, 1 Angiotensin-converting enzyme (ACE) inhibitors, 74 Anion gap. See also Metabolic acidosis acid-base problems involving, 315–317, 324 diabetic ketoacidosis causing wide, 1021 isoniazid poisoning causing wide, 1021 lactic acidosis causing wide, 1021
1174 INDEX Anion gap, (Continued) methanol poisoning causing wide, 1021 paraldehyde poisoning causing wide, 1021 Ankle injuries, 589–596 clinical presentation, 590 definitions, 589 diagnosis dislocations, 594 fractures, 593–594 radiographs, 594–595 sprains, 591–592 tendon rupture/dissociation/tear, 592–593 emergency actions, 589 examination, 590–591 joint anatomy, 589–590 key points, 589 laboratory findings, 591 treatment, 595 Anorectal disorders abscess and fistula clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 anal fissures clinical presentation, 117 definition, 114 epidemiology, 115 examination, 118 treatment and outcome, 120 hemorrhoids clinical presentation, 116–117 definition, 114 emergency action, 114 examination, 117–118 laboratory findings, 119 pathology, 115 treatment and outcomes, 119–120 hidradenitis suppurativa, definition, 114 pilonidal disease clinical presentation, 117 cysts, 118 definition, 114 epidemiology, 115 pathology, 116 treatment and outcomes, 120 proctalgia fugax, 114–115 pruritus ani clinical presentation, 117 definition, 115
Anorectal disorders, (Continued) examination, 119 pathology, 116 treatment and outcomes, 120–121 rectal prolapse clinical presentation, 117 definition, 115 examination, 118 pathology, 116 treatment, 120 Antibiotics adrenal insufficiency treatment, 337 adult bacterial pneumonia, 867, 867t AICD infection requiring, 42–43 appendicitis requiring, 8 beta-lactam for toxic shock syndrome, 549 community-acquired pneumonia, 867, 867t diving injury treatment, 211 dosages for neonatal emergencies, 666t endocarditis from prosthetic valve infection, 91–92 epididymitis, 1126 heart transplant complications requiring, 96 hernia requiring, 18 intestinal obstruction requiring, 21 marine fauna envenomation requiring, 240–241 neonatal dosages, 666t otitis externa, 170 otitis media, 801 pediatric urinary tract infection, 757t renal transplant emergency requiring, 1166–1167 rheumatic fever treatment, 777 toxic shock syndrome, 549 urinary tract infection treatment, 1145t, 1146 vasogenic shock requiring, 922 wound management prophylactic, 35 Anticholinergics pediatric asthma treatment, 721–724 toxicity, 938–943 clinical presentation, 940 definition, 939 electrocardiograph, 941 emergency actions, 939 epidemiology, 939 examination, 940–941 history taking, 940 key points, 938 pathology, 939–940
Index Anticholinergics, (Continued) treatment for, 941–943 gastric decontamination, 942 ICU, 942 “safety net,” 941 temperature reduction, 941–942 Anticoagulant agents AICD-associated thrombosis requiring, 43 prosthetic heart valve dysfunction requiring, 91–92 pulmonary embolism requiring, 898, 901, 903–904 Anticonvulsants pediatric seizure treatment, 786 toxicology emergencies requiring, 929 Antidepressant toxicity, 980–984, 982f. See also Cyclic antidepressant toxicity Antiepileptic drugs (AEDs), 471–472, 471t Antihistamines, urticaria treatment requiring, 112 Anti-inflammatory drugs, non-steroidal, 437–438, 1114 Anti-lewisite, 946 Antimicrobial therapy. See also Antibiotics prostatitis requiring, 1133–1134 Antipyretics, thyroid storm treatment, 397. See also Acetaminophen Antisocial personality disorder, 828–829 definition, 828 treatment and outcome, 829 Antivenom, 253, 254 AOM. See Acute otitis media APAP. See Acetylparaminophenolacetaminophen Apparent life-threatening event (ALTE) syndrome, 765–769 Appendicitis, 5–8, 510 abdominal pain from, 510 clinical presentation, 6 definition of, 5 diagnosis, 7 emergency actions for, 5 epidemiology, 5–6 examination, 6–7 key points, 5 laboratory findings, 7 radiography, 7–8 treatment and outcome, 8 ARDS. See Acute respiratory distress syndrome ARF. See Acute renal failure; Acute rheumatic fever
1175
Arrhythmia. See Cardiac arrhythmia Arsenic poisoning, 943–947 clinical presentation, 944 definition, 944 diagnosis, 946 emergency actions, 943 epidemiology, 944 examination, 945 key points, 943 laboratory findings, 945–946 radiographs, 946 treatment, 946–947 Arterial blood gas (ABG) analysis acid-base problems requiring, 312, 324 ARDS diagnostic, 853 hyperglycemic hyperosmolar nonketotic coma, 392 monitoring of, during mechanical ventilation, 877 neonatal emergencies, 668–669 pneumothorax diagnosis, 893 pulmonary embolism diagnostic, 901 shock diagnostic, 919 submersion incident requiring, 245, 246t, 247 toxicology emergencies, 927 Arterial gas embolism (AGE), 205, 208 decompression sickness v., 208 diving injury, 205, 208 Liebermeister's sign, 208 Arteriography, knee pain emergency requiring, 587 Arthralgia, acute rheumatic fever causing, 776 Arthritis. See also Joint and bone infections poly-, acute rheumatic fever causing, 776 septic, 630, 632, 633 Aspergillus, heart transplant infection, 95 Aspirin, 73, 169 acute rheumatic fever treatment, 777 cardiac chest pain treatment, 74 genital herpes treatment, 515 pediatric Kawasaki disease treatment, 794 pediatric seizures and status epilepticus, 786 Assist-control ventilation (ACV), (A/C), 847, 849t, 850–851 Association of Poison Control Centers, iron toxicity, 1007 Asthma, adult, 854–862 clinical presentation, 857
1176 INDEX Asthma, adult, (Continued) definition, 855 diagnosis, 859 disposition, 861–862 emergency actions, 854 epidemiology, 855 examination, 857–858 key points, 854 laboratory findings, 858–859 mechanical ventilator exacerbation of, 876 pathophysiology, 855–857 radiographs, 859 treatment and outcome, 859–861 beta–2 agonists, 860, 861 magnesium sulfate, 223 theophylline, 722 Asthma, pediatric, 714–724, 717t–719t definition, 714 emergency actions, 714 epidemiology, 714–715 evaluation, 716–720 severity classifications, 717t–719t key points, 714 laboratory findings and radiographs, 720–721 pathophysiology, 715–716 presentation, 716 treatment, 721–724 epinephrine, 722 heliox, 223 intubation/mechanical ventilation, 223 magnesium sulfate, 223 methylxanthines, 722 oxygen/beta–2 agonists/ corticosteroids/anticholinergic agents, 721–724 terbutaline, 722 theophylline, 722 Ataxia, dizziness, vertigo, 418–423 cerebellar, 464 clinical presentation, 419–421 CT or MRI scan for, 418, 422 definitions, 418 diagnosis, 422 emergency actions, 418 examination, 421–422 key points, 418 laboratory findings, 422 pathology, 419 subarachnoid hemorrhage causing, 418 syncope, 418 treatment, 422–423
Ataxia, dizziness, vertigo, (Continued) underwater injury causing, 207 ATN. See Acute tubular necrosis Atrial arteries dysrhythmia, heart transplant rejection causing, 95 fibrillation, 49, 49f flutter, 49–50, 50f Atrioventricular bradycardia first-degree, 52, 52f second-degree type I, 52, 52f type II, 52–53, 53f third-degree, 53, 53f Atropine airway management pretreatment, 914b insecticides poisoning antidote, 1033 pediatric trauma medication, 1080 Aural barotrauma, 206. See also Barotrauma Automatic external defibrillator (AED), 658 Automatic implantable cardioverterdefibrillator (AICD), 40–43 Avascular necrosis (AVN), 612–614 AVN. See Avascular necrosis Avoidant personality disorder, 835–836 clinical presentation, 835 definition, 835 diagnosis, 836 epidemiology, 835 key points, 835 treatment and outcome, 836 Azithromycin, adult bacterial pneumonia, 867, 867t Bacillus cereus, infectious disease emergency, 266t Back pain emergency, 577–582, 581t clinical presentation and examination, 578–579 definition, 577–578 diagnosis and specific etiologies, 579–582, 581t emergency actions, 577 key points, 577 laboratory findings, 582 radiographs, 582 treatment, 582 Backward/forward/right pressure (BURP), 915
Index Bacteremia definition, 706–707 pediatric, 706–713, 708t, 710t, 711t Bacteria. See also Infections; Infectious disease emergencies conjunctivitis, 164 infection from, 706–713, 708t, 710t, 711t Bag-valve-mask (BVM) device, 914. See also Airway management pediatric cardiopulmonary resuscitation using, 662, 670 BAL. See British anti-lewisite Balanoposthitis, 1127–1128 Balloon pump, cardiac chest pain treatment, 74 Barbiturate overdose, 948–951 clinical presentation, 949–950 definition, 948 diagnosis, 950 emergency actions, 950 epidemiology, 948–949 key points, 948 laboratory findings, 950 variability of test sensitivity, 950 pathophysiology, 949 treatment, 951 Barium enema, intestinal obstruction diagnosis, 21 Barodontalgia barotrauma, 207 Barotitis media barotrauma, 207 Barotrauma aerogastria, 207 alternobaric vertigo, 207 aural, 206 barodontalgia “tooth squeeze,” 207 barotitis media, 207 inner ear, 207 pulmonary overpressurization syndrome, 206 Bell's palsy clinical presentation, 425 definition, 424 diagnosis, 426–427, 426t differential diagnosis, 426–427, 426t epidemiology, 424 examination, 425–426 herpes virus, 276, 279–280, 286, 423–428, 426t, 484t key points, 423 laboratory findings, 427 pathology, 424 risk factors for, 424–425
1177
Bell's palsy, (Continued) stroke syndromes v., 484t treatment, 427 Benadryl aqueous, 28, 29 urticaria treatment, 111–112 Benign intracranial hypertension (pseudotumor cerebri), headaches from, 434, 435 Benign rolandic epilepsy, treatment, 787 Benzathine penicillin, acute rheumatic fever treatment, 777 Benzodiazepines amphetamine overdose requiring, 938 anesthesia after wound examination, 28 cyclic antidepressant toxicity treatment, 983–984 ethanol withdrawal requiring, 326 panic disorder treatment, 816 Benzoin, wound closure option, 30 Beta–2 agonists, asthma treatment, 860, 861 pediatric, 721–724 Beta-blockers bradycardia as sign of overdose, 953 cardiac chest pain treatment, 74 hyperthyroidism and thyroid storm treatment, 394 norepinephrine as overdose treatment, 952 overdose, 952–955 clinical presentation, 953 definition, 952 diagnostic for, 954 emergency actions, 952 epidemiology, 952–953 examination, 953 key points, 952 laboratory findings, 953 treatment and outcome, 954–955 thyroid storm treatment, 398 Betadine, pre-surgery wound preparation, 29 Beta-lactam antibiotics, toxic shock syndrome, 549 Bicarbonate therapy pediatric diabetes treatment, 773–774 septic shock, 413 Bilevel positive airway pressure (BiPAP) ventilator, 848, 849t Bilirubin conjugated hyperbilirubinemia, 136 measurement, iron toxicity requiring, 1009
1178 INDEX Bilirubin, (Continued) metabolism, 136 BiPAP ventilator. See Bilevel positive airway pressure ventilator Black widow spider bite, 256–258, 259 Bladder injuries, 1064 Bleeding diathesis, 555–558 Blood. See also Blood transfusion; Blood urea nitrogen analysis; Gastrointestinal bleeding; Hemophilia; Hemorrhage; Oncologic and hematologic emergencies; White blood cell count cultures cardiac tamponade requiring, 62 diverticulitis requiring, 125 ethanol withdrawal requiring, 329 heart transplant complications requiring, 94 neonatal emergencies, 668–669 pediatric seizures and status epilepticus, 786 glucose hypoglycemia, 399–405 methanol poisoning treatment, 1022 pediatric diabetes, 773–774 pediatric seizures and status epilepticus, 786 toxicology emergencies, 927–928 nose bleed, 171–172 type and crossmatch abdominal aortic aneurysm requiring, 4 cardiac tamponade requiring, 62 diverticulitis requiring, 125 hip trauma requiring, 630 iron toxicity requiring, 1009 shock diagnostic, 919 Blood transfusion, 559–565, 565 arsine gas intoxication requiring, 943 blood components, 559–562 cryoprecipitated antihemophilic factor, 561–562 iron toxicity requiring, 1009–1010 key points, 559 multiple trauma requiring, 1055, 1055t reactions to delayed hemolytic, 563 febrile, 563–564 hemolytic, 562–563 hemosiderosis causing, 565 hepatitis B and C causing, 565 human immunodeficiency virus causing, 565
Blood transfusion, (Continued) urticarial v. anaphylactic, 565 Blood urea nitrogen (BUN) analysis abdominal aortic aneurysm requiring, 4 caustic ingestion requiring, 964 disseminated intravascular coagulation emergency, 350 diverticulitis requiring, 125 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 pediatric seizures and status epilepticus, 787 salicylates toxicity, 1041 toxicology emergencies, 927–928 Bone and joint infections, 631–637 clinical presentation, 634 emergency actions, 631 epidemiology, 632 imaging, 635–636 key points, 631 laboratory findings, 634–635 osteomyelitis definitions, 631 epidemiology, 632 pathology, 632–633 treatment, 636 septic arthritis definitions, 630, 632 epidemiology, 632 pathology, 633 treatment, 637 Bone marrow studies, exfoliative dermatitis requiring, 101 Borderline personality disorder, 830–831 definition, 830 diagnosis, 831 examination, 830 key points, 830 treatment and outcome, 831 Bordetella pertussis, COPD infection, 884 Botulism, 428–431 clinical presentation, 430 Clostridium botulinum diarrhea from, 744t, 745 infectious disease emergency, 266t definition, 428–429 diagnosis, 430 emergency actions, 428 epidemiology, 429 examination, 430 Guillain-Barré syndrome v., 430 key points, 428
Index Botulism, (Continued) myasthenia gravis v., 430 pathology, 429 risk factors for contracting, 429–430 treatment, 431 Bowel decompression, intestinal obstruction requiring, 21 irrigation of, clonidine overdose treatment, 967–968 irritable bowel syndrome, 126 Bradycardia, 52–53, 52f, 53f AICD causing, 40 atrioventricular first-degree, 52, 52f second-degree type I, 52, 52f type II, 52–53, 53f third-degree, 53, 53f beta-blocker overdose sign, 953 pediatric, 659 sinus, 52, 52f Brain. See also Central nervous system; Head abscess Bell's palsy v., 426–427, 426t headaches from, 434 gray-white matter loss, 487, 490f hyperdense cerebral artery sign, 487, 489f intracerebral hemorrhage, 487f stroke syndromes, 480f subarachnoid hemorrhage, 488f trauma to, 1055, 1067–1072 airway management for, 915b computed tomography scan for, 1055 tumor Bell's palsy v., 426–427, 426t headaches from, 434 stroke syndromes v., 484t Branhamella catarrhalis, COPD infection, 884 Breast abscesses and mastitis, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 503–504 mastitis, 504 ultrasound scanning, 503
1179
Breast, (Continued) gynecomastia (male mammary gland development), exfoliative dermatitis causing, 101 British anti-lewisite (BAL), 946 British Pacing and Electrophysiology Group, pacemaker circuitry types, 84, 85t Bronchiolitis, 687–692, 725–728. See also Bronchitis asthma mimicked by, 857 clinical presentation, 689 definition, 688, 725 diagnosis, 690 emergency actions, 688, 725 epidemiology, 688–689 examination, 689 key points, 725 laboratory findings, 690 radiographs, 690 treatment, 690–692 Bronchitis. See also Bronchiolitis altitude-related emergencies, 190 asthma mimicked by, 857 bronchial injury, 1102 bronchodilators for COPD, 886 Bronchoscopy, prosthetic heart valve requiring, 92 Brown recluse spider bite, 256, 258, 259–260 Brudzinski sign, 464–465 BUN analysis. See Blood urea nitrogen Bundle branch blocks, cardiac arrhythmia from, 53, 54f Bupivacaine, 28, 29 toxicity of, 29, 29t Burns, 192–197, 194f, 196b, 197b. See also Chemical burns American Burn Association, 197, 197b burn department for toxic epidermal necrolysis, 103–106 carbolic acid, 203 child abuse, 763f clinical presentation, first/second/third degree types, 193 definition, 193 emergency actions, 192–193 epidemiology, 193 examination, 193–195, 194f Rule of Nines assessment, 194f hypernatremia etiology involving, 359t key points, 192 laboratory findings, 195 Parkland formula for, 196, 196b
1180 INDEX Burns, (Continued) radiographs, 195–196 sunburn, 100, 100b toxic epidermal necrolysis from, 103–106 treatment, 196–197, 196b “ABC” care, 196 BURP. See Backward/forward/right pressure Burrow's solution, toxicodendron dermatitis treatment, 108–109 Butorphanol tartrate, headache treatment, 437–438 BVM device. See Bag-valve-mask device C1 esterase inhibitor concentrate, urticaria treatment, 112 CAD. See Coronary artery disease Calamine, toxicodendron dermatitis treatment, 108–109 Calcium. See also Hypercalcemia; Hypocalcemia chloride, pediatric trauma medication, 1080 fluid and electrolyte emergencies, 369–377 measurement, toxicology emergencies requiring, 927 pediatric seizure treatment, 787 sign, thoracic aortic dissection diagnosis, 25 toxicology emergencies requiring, 929, 954 Calcium channel blockers (CCBs), overdose, 956–959 clinical examination, 957 congestive heart failure from, 958 definition, 956 diagnosis, 957–958 emergency actions, 956 epidemiology, 957 key points, 956 laboratory findings, 957 treatment, 958–959 Calculi cholelithiasis, 9–14 nephrolithiasis, 511, 1135–1138 sialolithiasis, 175–176 Campylobacter jejuni diarrhea from, 744t infectious disease emergency, 266t Cancer. See also Malignancy; Oncologic and hematologic emergencies; Tumor diverticulitis v., 126
Cancer, (Continued) exfoliative dermatitis from, 100, 100b Candidiasis, treatment, 553–554, 553t CAP. See Community-acquired pneumonia Captopril, hypertensive emergency treatment, 79–80 Carbamate and organophosphorus insecticides poisoning, 1130–1132 Carbamazepine benign rolandic epilepsy, treatment, 787 seizures and status epilepticus, 471t Carbolic acid, chemical burn from, 203 Carbon monoxide poisoning, 959–962 clinical presentation, 960 definition, 960 emergency actions, 960 epidemiology, 960 key points, 959 laboratory findings, 960 metabolic acidosis from, 1021 pathophysiology, 960 treatment, 960–961 Carcinoma, asthma mimicked by, 857 Cardiac arrhythmia, 44–57, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f. See also Cardiac chest pain evaluation; Dysrhythmia bradycardia, 52–53, 52f, 53f AICD causing, 40 atrioventricular first-degree, 52, 52f third-degree, 53, 53f beta-blocker overdose sign, 953 pediatric, 659 sinus, 52, 52f bundle branch blocks, 53, 54f clinical presentation, 45 clonidine overdose monitoring for, 967–968 definition, 44–45 emergency actions, 44 advanced cardiac life support protocols, 43, 44 examination/stable or unstable condition, 45 hypercalcemia, 54, 55f hyperkalemia, 54, 55f hypocalcemia, 54, 55f hypokalemia, 54, 55f key points, 44 laboratory findings, 45 organ rejection causing, 93–96
Index Cardiac arrhythmia, (Continued) pathophysiology of submersion incident, 244 pulmonary embolism causing, 56, 56f radiographs, 45 respiratory acidosis causing, 320 tachycardia, 46–49, 46f, 47f, 48f Wolff-Parkinson-White syndrome, 56–57, 56f Cardiac chest pain evaluation, 68–75, 71f, 72f. See also Cardiac arrhythmia; Cardiac examination; Cardiology clinical presentation, 69–70 definition, 68–69 diagnosis, 73 electrocardiogram findings, 71–72, 71f, 72f emergency actions, 68 epidemiology, 69 examination, 70–71 key points, 68 laboratory findings, 72–73 radiographs, 73 special considerations, 75 treatment and outcome, 73–74 Cardiac enzyme measurements lightning injuries requiring, 236 shock diagnostic, 919 Cardiac examination, 58–60. See also Cardiac chest pain evaluation; Cardiology airway-breathing-circulation emergency actions, 58 clinical presentation, 58 definition, 58 examination, 58–59 key points, 58 radiographs, 59 treatment/outcome, 60 Cardiac life support. See also Advanced cardiac life support Cardiac monitoring calcium channel blockers overdose requiring, 958–959 hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 Cardiac output, exfoliative dermatitis causing increased, 101 Cardiac tamponade, 60–63, 62f, 63f cardiopulmonary arrest from, 664 clinical presentation, 61 definition, 60–61 diagnosis, 62, 62f, 63f epidemiology, 61
1181
Cardiac tamponade, (Continued) etiology, 61 examination, 61–62 key points, 60 laboratory findings, 62 trauma causing, 1099–1100 treatment, 62–63 Cardiac transplantation emergencies, 93–96, 1150, 1151, 1154 Cardiology. See also Cardiac chest pain evaluation; Cardiac examination; Cardiac transplantation emergencies; Toxicology emergencies acute pericarditis, 37–40 advanced cardiac life support, 43, 44 arrhythmias, 44–57, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f atrial dysrhythmia, 95 congestive heart failure, 64–67 defibrillator implantation follow-up, 40–43 examination, 58–60 hypertensive emergencies, 76–80 mitral valve prolapse, 80–82 pacemaker complications, 83–88, 85t pain evaluation, 68–75, 71f, 72f pediatric cardiopulmonary arrest, 655–660 automatic external defibrillator for, 657 laryngeal mask airway for, 657 prosthetic heart valve dysfunction, 89–92, 91b rheumatic carditis, 776 tamponade, 60–63, 62f, 63f thoracic aortic dissection, 22–26 transplantation emergencies, 93–96, 1150, 1151, 1154 Cardiopulmonary arrest, pediatric, 655–660 clinical presentation and physical examination, 656 CPR for, 656, 657–659, 660, 661–664 definition, 655 epidemiology, 655–656 key point, 655 laboratory findings, 656 pathophysiology, 656 summary, 660 treatment, 656–660 asystole/pulseless electrical activity, 659 bradycardia with pulse, 659
1182 INDEX Cardiopulmonary arrest, pediatric, (Continued) unstable tachycardia with pulse, 659–660 ventricular fibrillation/tachycardia without pulse, 658–659 Cardiopulmonary resuscitation (CPR). See also Resuscitation emergencies pediatric emergency, 656, 657–659, 660, 661–664 submersion incidents requiring, 243 Carpal tunnel syndrome, 615. See also Forearm and wrist injuries Cat scratch disease, multiple sclerosis v., 442 Catheter Angiocath, wound preparation requiring irrigation, 30 aspiration for pneumothorax, 895–896 Foley, rhabdomyolysis treatment, 416–417 percutaneous cardiac intervention, 74 Caustic ingestion emergency, 962–965 clinical presentation, 963 definition, 962–963 diagnosis, 964 emergency actions, 962 epidemiology, 963 examination, 963 key points, 962 laboratory findings, 964 radiographs, 964 treatment, 964 CBC. See Complete blood count CDCP. See Centers for Disease Control and Prevention Cefdinir, adult bacterial pneumonia, 867, 867t Cefuroxime, adult bacterial pneumonia, 867, 867t Centers for Disease Control and Prevention (CDC), 271t botulism treatment, 431 Centor criteria for pharyngitis diagnosis, 173 Central nervous system (CNS). See also Brain; Cranial nerve examination; Head; Spinal cord injuries anatomy and function, 452t gliosis, 440 heart transplant infection involving, 95 respiratory acidosis treatment influencing, 322 trauma to, 1067–1072
Central retinal vein occlusion, 165 Cephalexin, marine fauna envenomation requiring, 240–241 Cephalosporins adult bacterial pneumonia, 867, 867t marine fauna envenomation requiring, 240–241 Cerebellar ataxia, 464 Cerebral edema, 184t, 185–186, 187t, 189 Cerebrospinal fluid (CSF) analysis, 271t pediatric infection requiring, 710–712 Cesarean section, postmortem, 1111 Chalazion, 163 Charcoal, activated acetaminophen toxicity treatment, 931 barbiturate overdose treatment, 951 beta-blocker overdose treatment, 954 calcium channel blockers treatment, 958–959 clonidine overdose treatment, 967–968 lithium poisoning treatment, 1019 phenytoin toxicity treatment, 1037 salicylates toxicity treatment, 1042 theophylline toxicity treatment, 1048 Chelation therapy arsenic intoxication requiring, 943 lead poisoning requiring, 1016 Chemical burns, 198–204, 199b. See also Burns airway and breathing, 198 circulation assessment, 199 clinical presentation, 200 definition, 199 types of, 199b diagnosis, 201 emergency actions, 198 epidemiology, 199–200 examination, 200–201 key points, 198 laboratory findings, 201 special situations, 203–204 hydrofluoric acid, 203–204 phenol (carbolic acid), 203 treatment, 202–203 Chemical warfare, cyanide poisoning, 976 Chest evaluation, pediatric trauma requiring, 1078 Chickenpox, 276, 280, 282–283 treatment, 286 Child. See also Pediatric analgesia and sedation; Pediatric bacteremia, sepsis, and meningitis; Pediatric emergencies abuse, 758–765 clinical presentation, 759–761
Index Child, (Continued) definitions, 758–759 emergency actions, 758 epidemiology, 759 examination, 761–763, 762f, 763f marks from burns, 763f marks from instruments, 762f key points, 758 laboratory findings, 764 radiographs, 764 treatment, 764–765 definition of, 657 Chlamydia species, chronic obstructive pulmonary disease from, 884 Chloride, fluid and electrolyte emergencies, 383–385. See also Hyperchloremia Cholelithiasis and cholecystitis, 9–14 clinical presentation, 11 definition of, 9–10 diagnosis, 12 disposition, 14 emergency actions, 9 epidemiology, 10 examination, 12 key points, 9 laboratory findings, 12 Murphy's sign, 12 pathophysiology, 10–11 radiographs, 13 treatments and outcomes, 13–14 Cholesteatoma, Bell's palsy v., 426–427, 426t Chorea, acute rheumatic fever causing, 776 Chronic fatigue syndrome, multiple sclerosis v., 442 Chronic obstructive pulmonary disease (COPD), 46, 49, 883–887, 914b, 915b. See also Respiratory distress syndrome acid-base disorder with, 324 American Thoracic Society definition of, 883–884 asthma mimicked by, 857 clinical presentation, 884–885 definition, 883–884 electrocardiogram, 886 emergency actions, 883 examination, 885 key points, 883 laboratory findings, 885–886 mechanical ventilation required for, 848, 850
1183
Chronic obstructive pulmonary disease (COPD), (Continued) mechanical ventilator exacerbation of, 875–876 pathology, 884 radiographs, 885 stages of, 884 treatment, 886–887 bronchodilators, 886 emergency department, 887 fluid administration, 886 rapid sequence induction, 914b, 915b Cigarette smoking COPD from, 884 pulmonary embolism risk factor, 899 Ciguatera fish poisoning, infectious disease emergency, 270t Cimetidine anaphylactic shock requiring, 921 urticaria treatment, 112 Ciprofloxacin, urinary tract infection treatment, 1145t Clarithromycin, adult bacterial pneumonia, 867, 867t Classic migraine, 433 Clonazepam panic disorder treatment, 816 pediatric status epilepticus treatment, 787 Clonidine hypertensive emergency treatment, 79–80 overdose, 965–968 clinical presentation and examination, 966–967 definition, 965–966 diagnosis, 967 emergency actions, 965 epidemiology, 966 key points, 966 laboratory findings, 967 pathophysiology, 966 pharmacokinetics, 966 treatment, 967–968 Clopidogrel bisulfate, international normalized ratio for, 169 Clostridium botulinum diarrhea from, 744t, 745 infectious disease emergency, 266t Clostridium difficile, diarrhea from, 744t Cluster headache, 434. See also Headache CMV. See Controlled mandatory ventilation; Controlled mechanical ventilation
1184 INDEX CNS. See Central nervous system Coagulation panel analysis heart transplant complications requiring, 94 hip trauma requiring, 630 hymenoptera sting requiring, 232 neonatal emergencies, 668–669 Cocaine toxicity, 969–973 clinical presentation and examination, 970–972 definition, 969 diagnosis, 972 emergency actions, 969 epidemiology, 969–970 key points, 969 laboratory findings, 972 pathology, 970 treatment, 971–973 Colitis, 510 diverticulitis v., 126 Collagen vascular disease, erythema multiforme v., 98 Colonoscopy, diverticulosis requiring, 127 Coma adrenal insufficiency causing, 336 Glasgow Coma Scale, 453, 454t global assessment, 453, 454t head injury examination and disposition, 1071 modified for infants and children, 1076t multiple trauma diagnostic, 1054, 1054t hyperglycemic hyperosmolar nonketotic, 390–393 myxedema, 406–409 submersion incident causing, 246t Community-acquired pneumonia (CAP), 863, 864 antibiotics for, 867, 867t Compartment syndrome, 596–599, 641 Complete blood count (CBC) abdominal aortic aneurysm requiring, 4 cardiac tamponade requiring, 62 caustic ingestion requiring, 964 diabetic patient with otolaryngological emergency, 169 disseminated intravascular coagulation emergency, 350 diverticulitis requiring, 125 exfoliative dermatitis requiring, 101 heart transplant complications requiring, 94 hernias requiring, 17
Complete blood count (CBC), (Continued) hip trauma requiring, 630 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 iron toxicity requiring, 1009 knee pain emergency, 587 lightning injuries requiring, 236 neonatal emergencies, 668–669 ovarian torsion, 534 pediatric seizures and status epilepticus, 786 pneumothorax diagnosis, 893 salicylates toxicity, 1041 shock diagnostic, 919 toxic epidermal necrolysis requiring, 105 toxicology emergencies, 927–928 Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Computed tomography (CT) scan abdominal aortic aneurysm requiring, 4 adrenal insufficiency requiring, 336 angiographic, thoracic aortic dissection requiring, 25 appendicitis requiring, 7–8 ataxia, dizziness, vertigo, 418, 422 cholelithiasis and cholecystitis requiring, 13 with contrast, abdominal trauma, 1060 diverticulitis requiring, 125, 127 diverticulosis requiring, 127 emergent pelvic and abdominal pain, 512 ethanol withdrawal requiring, 329 head -ache, 432 trauma to, 1055 hernia diagnosis, 17 intestinal obstruction diagnosis, 21 methanol poisoning requiring, 1022 multiple trauma, 1052 neonatal emergencies, 668–669 ovarian torsion, 535 pediatric neurological evaluation, 1077 seizures and status epilepticus, 786 pneumothorax diagnosis, 893, 894f pulmonary embolism, 902, 905t Reye's syndrome, 797 seizures and status epilepticus, 469, 789 spinal cord injury, 1055 basilar life-threatening skull fractures, 1068–1069
Index Concussion, 1069. See also Central nervous system; Coma; Head Congenital aganglionic megacolon (Hirschsprung's disease), 745–748, 748f Congestive heart failure (CHF), 64–67 asthma mimicked by, 857 beta-blocker overdose diagnostic, 954 calcium channel blockers causing, 958 clinical presentation and historical findings, 65 definition of, 64 epidemiology, 64 examination, 65 heart transplant rejection causing, 95 key points, 64 laboratory findings, 66 pathophysiology, 64–65 primary prosthetic valve failure causing, 91 radiographs, 66 treatment, 66–67 diuretics, 66–67, 74 Conjugated hyperbilirubinemia, 136 Conjunctivitis, 164 Constipation, pediatric, 736–740 clinical presentation, 738 definition, 736–737 diagnosis, 738–739 emergency actions, 736 epidemiology, 737 examination, 738 key points, 736 laboratory findings, 738 pathology, 737 treatment, 739–740 Contact dermatitis, toxicodendron, 106–109 Continuous positive airway pressure (CPAP), 848 Controlled mandatory ventilation (CMV), 847 Controlled mechanical ventilation (CMV), 849t, 850 Conversion disorder, 819–821 clinical presentation, 820 definition, 820 diagnosis, 821 epidemiology, 820 examination, 820 key points, 819 laboratory findings, 820 treatment, 821 Co-oximetry measurement, toxicology emergencies diagnostic, 927
1185
COPD. See Chronic obstructive pulmonary disease Coral snake bite, 253, 254 Cornea abrasions of, 166–167 foreign bodies on, 167 ulcers of, 164 Coronary artery disease (CAD), 49 graft, after heart transplant, 94 Coronary bypass graft, cardiac chest pain treatment, 74 Cortisol, adrenal insufficiency treatment, 336 Corynebacterium diphtheriae, 261 Coumadin, 169 CPAP. See Continuous positive airway pressure CPR. See Cardiopulmonary resuscitation Cramps, heat, 221, 224 Cranial nerve examination, 456–462, 458f, 459f. See also Abducens nerve examination; Central nervous system CN I (olfactory), 456 CN II (optic), 456 CN III, IV, VI (oculomotor, trochlear, abducens), 457–458, 458f functional layout of extraocular movements and innervations, 458f CN IX, X (glossopharyngeal and vagus), 461 CN V (trigeminal), 459–460, 459f sensory nerve branch divisions, 459f CN VII (facial), 460–461 CN VIII (vestibulocochlear), 461 CN XI (spinous accessory), 461–462 CN XII (hypoglossal), 462 Creatinine study caustic ingestion requiring, 964 diverticulitis requiring, 125 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 pediatric seizures and status epilepticus, 787 toxicology emergencies requiring, 927–928 Crohn's disease, diverticulitis v., 126 Cryoprecipitated antihemophilic factor, as blood transfusion component, 561–562 Cryptosporidium diarrhea from, 745 infectious disease emergency, 268t
1186 INDEX Crystalloid infusion, pulmonary embolism treatment, 903 CSF. See Cerebrospinal fluid analysis CT scan. See Computed tomography scan Cyanide poisoning, 974–980 chemical warfare, 976 clinical presentation, 976–977 definition, 975 diagnosis, 977–978 emergency actions, 975 epidemiology, 975–976 examination, 977 key points, 974 laboratory findings, 977 metabolic acidosis from, 1021 pathology, 976 treatment, 978–980 Cyanosis, ARDS causing, 859–861 Cyclic antidepressant toxicity, 980–984, 982f clinical presentation, 982 definition, 980–982 antagonism of GABA receptors, 982 physiological effects, 981 sodium and potassium-channel blockade, 981 tricyclic antidepressants, 981 diagnosis, 982–983, 982f ECG abnormalities, 981f emergency actions, 980 examination, 982 key points, 980 treatment and outcome, 983–984 Cyclospora diarrhea from, 745 infectious disease emergency, 269t Cysts anorectal disorder, 118 cholecystitis, 9–14 ovarian, 510, 529–532 Pneumocystis carinii pneumonia, 95 Cytomegalovirus (CMV) clinical presentation, 281–282 definition, 277 epidemiology, 278 examination, 283 heart transplant infection, 95 treatment, 287 “Dawn phenomenon,” hypoglycemia from, 402 DCS. See Decompression sickness D-Dimer testing, pulmonary embolism diagnostic, 901
De Quervain's stenosing tenosynovitis, 615–616 DeBakey classification, thoracic aortic dissection, 23 Debridement, wound preparation requiring, 30 Decompression sickness (DCS), 205, 207–208 arterial gas embolism v., 208 Deep tendon reflexes, 462–464, 463t scale for grading of, 463t Defibrillator implantation follow-up automatic implantable cardioverterdefibrillator, 40–43 infection in, 42–43 clinical presentation, 41 diagnosis, 42 emergency defibrillation/cardiac passing, 40 epidemiology, 41 examination, 41–42 key points, 40 laboratory findings, 42 radiographs, 42 treatment, 42–43 pediatric automatic external, 657 Dehydration hyperglycemic hyperosmolar nonketotic coma, 390–393 pediatric emergency, 694–699 clinical presentation/examination, 696 definitions, 694–695 emergency actions, 694 epidemiology, 695 intravenous therapy for severe cases, 698–699 key points, 694 laboratory findings, 696–697 treatment, 697–699 oral rehydration therapy for, 694, 695, 697–699 Delirium haloperidol for intubated patient with, 910–911 respiratory acidosis causing, 320 sedation for intubated patient with, 910–911 Dementia, stroke syndromes v., 484t Demerol, headache treatment, 437–438 Dental emergencies, 154–158 definition, 154–155 diagnosis and treatment, 155–157
Index Dental emergencies, (Continued) emergency actions, 154 epidemiology, 155 examination, 155 key points, 154 “tooth squeeze” barotrauma, 207 Dental trauma, 179–182 definitions, 179–180 emergency actions, 179 epidemiology, 180 examination, 180 key points, 179 radiographs, 181 treatment, 181–182 Dependent personality disorder, 836–838 clinical presentation, 837 definition, 836 diagnosis, 837 epidemiology, 837 examination, 837 key points, 836 treatment and outcome, 837 Depot-testosterone, adrenal insufficiency treatment, 336 Dermatologic emergencies erythema multiforme, 97–99 exfoliative dermatitis, 99–102, 100b lymphadenitis, 101 toxic epidermal necrolysis, 103–106 toxicodendron dermatitis, 106–108, 106–109 urticaria, 109–113 Dermatopathic lymphadenitis, exfoliative dermatitis causing, 101 Detached retina, ophthalmologic emergencies, 166 Dexamethasone adrenal insufficiency treatment, 336–337 pediatric trauma medication, 1080 Diabetes. See also Diabetic ketoacidosis early, with hypoglycemia, 401 hyperglycemic hyperosmolar nonketotic coma, 390–393 insipidus, hypernatremia etiology involving, 359t otolaryngological emergencies with, 169 pediatric, 770–774 clinical presentation, 771 emergency actions, 770 epidemiology, 771 examination, 772 key points, 770 laboratory findings, 772
1187
Diabetes, (Continued) radiographs, 772–773 treatment, 773–774 Type I diabetes mellitus (juvenile diabetes), 770 Type II diabetes mellitus (insulin resistance), 770–771 Diabetic ketoacidosis (DKA), 311, 343–347, 390–393 pediatric, 770–774 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 815–816 Diagnostic peritoneal lavage (DPL), 1060–1061 Dialysis disequilibrium syndrome, 1119 peritoneal, salicylates toxicity treatment, 1043 Diaphragmatic injury, 1103–1104 Diarrhea definition, 272 pediatric, 740–745, 744t clinical presentation, 742 definition, 741 emergency actions, 741 epidemiology, 741–742 examination, 742 key points, 740 laboratory findings and diagnosis, 742–743 treatment, 743–744, 744t common enteropathogens and therapies, 744t Diathesis, acute bleeding, 555–558 Diazepam intubated patient sedation, 911 pediatric status epilepticus treatment, 787 pediatric trauma medication, 1080 DIC. See Disseminated intravascular coagulation Diet fiber-rich, diverticulosis requiring, 127 Third National Health and Nutrition Examination Survey, 1014 vitamin D deficiency (rickets), 371 Diethylenetriamine penta-acetic acid (DTPA), gadolinium complex with chelating agent, 442 Digitalis glycoside toxicity, 984–988 definition, 985–986 diagnosis, 987 emergency actions, 984–985
1188 INDEX Digitalis glycoside toxicity, (Continued) examination, 987 key points, 984 laboratory findings, 987 presentation, 986 treatment and outcome, 987–988 Dihydroergotamine, headache treatment, 437–438 Dilantin, contraindicated for hyperglycemic hyperosmolar nonketotic coma, 393 Diltiazem, thyroid storm treatment, 398 Dimercaprol lead poisoning treatment, 1016 mercury poisoning treatment, 1026 Dimercaptopropanesulfonic acid (DMPS), arsenic intoxication treatment, 946–947 Dimercaptosuccinic acid (DMSA) arsenic poisoning treatment, 946 mercury poisoning treatment, 1026 Dimethyl sulfoxide (DMSO), 204 Diphenhydramine, anaphylactic shock requiring, 922 Diphtheria, 261–264 clinical presentation, 261 definition, 261 diagnosis, 263 emergency actions, 261 epidemiology, 261 examination, 263 key points, 261 pathology, 261 treatment, 263–264 Diplococcus pneumoniae, chronic obstructive pulmonary disease from, 884 Disinfection hair, wound preparation requiring, 29 skin, wound preparation requiring, 29 Dislocation ankle injuries, 594 elbow injuries, 602–603 ED reduced, 603 hand injuries, 620–622 hip injuries, 628 anterior, 628–629 posterior, 629 shoulder injuries, 650–651 Disseminated encephalomyelitis, multiple sclerosis v., 442 Disseminated intravascular coagulation (DIC), 232, 348–350
Disseminated intravascular coagulation (DIC), (Continued) clinical presentation, 349 diagnosis, 349–350 emergency actions, 348 examination, 349 key points, 348 laboratory findings, 350 mechanical ventilation for, 348 pathology, 348–349 treatment, 350 Diuretics congestive heart failure treatment, 66–67, 74 syndrome of inappropriate antidiuretic hormone, 353 Divers Alert Network, hyperbaric chamber referrals, 211 Diverticular hemorrhage, 124, 128 Diverticulitis, 510 acute/uncomplicated, treatment and outcomes, 128–129 clinical presentation, 124 complicated, 125, 129 definition of, 122 differential diagnosis, 125–126 epidemiology of, 122–123 examination, 124 complicated diverticulitis, 125 heart transplant infection, 95 laboratory findings, 125 pathophysiology of, 123 radiographs for, 127 in special situations, 127 treatment and outcome, 128–129 complicated diverticulitis, 129 Diverticulosis clinical presentation, 123–124 differential diagnosis, 125–126 emergency actions, 122 epidemiology, 122–123 examination, 124 key points, 122 laboratory findings, 125 pathology, 123 treatment and outcome, 127 Diving injuries, 205–211, 210b arterial gas embolism, 205, 208 barotrauma aerogastria, 207 alternobaric vertigo, 207 aural, 206 barodontalgia “tooth squeeze,” 207
Index Diving injuries, (Continued) barotitis media, 207 inner ear, 207 pulmonary overpressurization syndrome, 206 clinical presentation, 206 contaminated gases, 209 decompression sickness, 205, 207–208 definitions arterial gas embolism, 205 decompression sickness, 205 diagnosis, 210 focused diving history, 210b Divers Alert Network, hyperbaric chamber referrals, 211 emergency actions, 205 epidemiology, 206 examination, barotrauma, 209 key points, 205 laboratory findings, 210 nitrogen narcosis, 209 treatment, 210–211 analgesics/antibiotics, 211 hyperbaric, 211 rapid recompression, 211 supplemental oxygen, 211 Diving reflex, protective role of, 247–248 Dizziness. See Ataxia, dizziness, vertigo DKA. See Diabetic ketoacidosis DMPS. See Dimercaptopropanesulfonic acid DMSA. See Dimercaptosuccinic acid DMSO. See Dimethyl sulfoxide Dobutamine congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 Domeboro, toxicodendron dermatitis treatment, 108–109 Dopamine congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 Doxepin, urticaria treatment requiring, 112 Doxycycline, adult bacterial pneumonia, 867, 867t DPL. See Diagnostic peritoneal lavage Drowning. See Submersion incidents Drugs. See also Toxicity, drug barbiturate dependence, 949 exfoliative dermatitis from, 100, 100b, 101 hypercalcemia from, 374 hypernatremia etiology involving, 359t
1189
DSM-IV. See Diagnostic and Statistical Manual of Mental Disorders DTPA. See Diethylenetriamine pentaacetic acid Duke criteria for prosthetic heart valve dysfunction, 91b Dysmenorrhea, 510 Dysmetria, 464 cerebellar examination indicating, 464 Dyspnea exfoliative dermatitis causing, 101 pulmonary embolism causing, 898, 903 Dysrhythmia. See also Cardiac arrhythmia beta-blocker overdose sign, 953 cyclic antidepressant toxicity causing, 983–984 heart transplant rejection causing atrial, 95 Reye's syndrome causing, 797 shock causing, 920 theophylline toxicity causing, 1048 E. coli, diarrhea from, 744t, 745 ECF volume. See Extracellular fluid volume ECG. See Electrocardiography Echocardiography neonatal emergencies, 668–669 pulmonary embolism, 902, 905t tetralogy of Fallot, 782 transesophageal, thoracic aortic dissection diagnosis, 25 Eclampsia, 401, 510, 519–525. See also Preeclampsia and eclampsia definition of, 524 “Ecstasy.” See Methylenedioxymethamphetamine Ectopic pregnancy, 505–509 clinical presentation, 506–507 definitions, 505–506 emergency actions, 505 epidemiology, 506 key points, 505 treatment, 507 methotrexate, 507–508 Eczema, exfoliative dermatitis from, 100, 100b ED. See Emergency department Edema cerebral, high-altitude-related, 184t, 185, 187t, 191 treatment, 189 heat, 221, 224
1190 INDEX Edema, (Continued) peripheral, high-altitude-related, 184t, 190 pulmonary, high-altitude-related, 184t, 186, 187t, 191 treatment, 189–190 EEG. See Electroencephalogram Elbow injuries, 600–603 clinical presentation, 601 emergency actions, 601 epidemiology, 601 examination, 601–602 key points, 600 laboratory findings, 602 treatment dislocations, 602–603 ED reduced, 603 fractures, 603 x-ray for diagnosis, 602 Electrical injuries, 212–215. See also Injury clinical observation, 213–214 definitions, 212–213 emergency actions, 212 epidemiology, 213 key points, 212 laboratory findings, 214 treatment, 214–215 Electrocardiography (ECG) anticholinergic toxicity, 941 arrhythmias, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f beta-blocker overdose diagnostic, 953 calcium channel blockers overdose treatment, 958–959 cardiac tamponade, 62, 63f cyclic antidepressant toxicity, 982f hypercalcemia, 375 hypomagnesemia, 378 moderate to severe ethanol withdrawal, 329 pacemaker complications, 86–87 pericarditis, acute, 38–39 permanent pacemakers, 86–87 Electroencephalogram (EEG), status epilepticus diagnostic, 470 Electrolyte and fluid management caustic ingestion requiring, 964 diverticulitis requiring, 125 hernias requiring, 17 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 ovarian torsion, 534
Electrolyte and fluid management, (Continued) pediatric emergencies, 700–705, 701 clinical presentation, 701–703 calculation of deficit fluids, 702–703, 704t calculation of maintenance fluids, 701–702 definition, 701 diagnosis, 703–704 emergency actions, 700 examination, 703 key points, 700 laboratory findings, 703 seizures and status epilepticus, 787 treatment, 704–705 salicylates toxicity, 1041 shock, 920 theophylline toxicity treatment, 1048 thyroid storm treatment, 397 ELISA. See Enzyme-linked immunosorbent assay EM. See Erythema multiforme Embolism. See also Prothrombin time measurement amniotic fluid, 500–502 arterial gas, 205, 208 decompression sickness v., 208 diving injury, 205, 208 Liebermeister's sign, 208 pulmonary, 897–905, 904f, 905t anticoagulant agents for, 898, 901, 903–904 cardiac arrhythmia from, 56, 56f cigarette smoking as risk factor for, 899 crystalloid infusion for, 903 CT scan for, 902, 905t enzyme-linked immunosorbent assay for, 902 Geneva (Wicki) assessment model, 900–901, 900t immuno-turbidimetric D-Dimer assay for, 901, 905t thrombocardiopulmonary arrest from, 664 extracranial sources of, 478f Emergency department (ED) abdominal aortic aneurysm, 4 asthma, 854–862 cholelithiasis and cholecystitis requiring, 12–13 ethanol withdrawal requiring, 330 headache treatment, 437–438
Index Emergency department (ED), (Continued) hymenoptera sting requiring, 232 hyperthyroidism and thyroid storm treatment, 394 pediatric seizures and status epilepticus, 786 snakebite requiring, 253 submersion incident requiring, 246t, 247 urticaria treatment requiring, 112–113 Emergency medical services (EMS) personnel, 236 Emesis arsenic poisoning treatment, 946 hyperemesis gravidarum, 516–518 ovarian torsion causing, 534 theophylline overdose causing, 1048 EMLA local anesthetic, 28–29 EMS personnel. See Emergency medical services personnel Encephalitis, herpes virus causing, 279 treatment, 285–286 Endocarditis erythema multiforme v. bacterial, 98 heart transplant recipient at risk for, 96 prosthetic valve infection, 91–92 Endocrinopathy hypercalcemia from, 374 hypoglycemia from, 402 Endometriosis, 510 Endoscopic retrograde cholangiopancreatography, prosthetic heart valve requiring, 92 Endotracheal tube pediatric emergency use of, 674 pediatric trauma requiring, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t size v. patient age, 1074t End-stage renal disease (ESRD), 1117–1123. See also Renal disease cardiovascular complications with, 1119–1123 dialysis disequilibrium syndrome, 1119 hyperkalemia, 1119, 1123 hypertension, 1119–1121 hypotension, 1121 peritoneal dialysis and peritonitis, 1123 skeletal emergencies, 1121–1122 transplant rejection, 1122–1123, 1158t, 1161t, 1163–1167 chest x-ray, 1123
1191
End-stage renal disease (ESRD), (Continued) definition, 1118 emergency actions, 1117 key points, 1117 laboratory findings, 1123 pathophysiology, 1118–1119 coagulopathy, 1119 treatment, 1123 Enema, barium, intestinal obstruction diagnosis, 21 Enoxaparin sodium, hyperglycemic hyperosmolar nonketotic coma, 393 Entamoeba histolytica diarrhea from, 744t infectious disease emergency, 269t Environmental emergencies altitude-related conditions, 183–191, 184t, 187t burns, 192–197, 194f, 196b, 197b chemical, 198–204, 199b diving injuries, 205–211, 210b electrical injuries, 212–215 frostbite, 215–219 heat injuries, 220–225 hymenoptera sting, 230–233 hypothermia, 225–229 lightning injuries, 234–237 marine fauna envenomations, 238–242 snakebite, 249–254 spider bite and scorpion sting, 255–260 submersion incidents, 242–248, 246t Enzyme-linked immunosorbent assay (ELISA), pulmonary embolism diagnostic, 902 EPAP. See Expiratory positive airway pressure Epididymitis, 1124–1126 clinical presentation, 1125 definitions, 1124 diagnosis, 1126 Doppler ultrasound for differential diagnosis, 1126 emergency actions, 1124 epidemiology, 1125 examination, 1125 key points, 1124 laboratory findings, 1125 pathology, 1125 treatment, 1126 Epilepsy, 465–472, 466t, 468t, 471t. See also Seizures and status epilepticus benign rolandic, treatment for, 787
1192 INDEX Epilepsy, (Continued) juvenile myoclonic, 787 Epinephrine, 28 anaphylactic shock requiring, 921 asthma treatment, 722 pediatric trauma medication, 1080 urticaria treatment with aqueous, 111 vasoconstriction treatment, 28 Epi-Pen autoinjector, urticaria treatment requiring, 112–113 Epistaxis, 171–172 Epstein-Barr virus (EBV) infection, 276–277, 278, 281, 283 multiple sclerosis v., 440 treatment, 287 Erythema marginatum, acute rheumatic fever causing, 776 Erythema multiforme (EM), 97–99 clinical presentation, 97, 98 definition, 97 examination, 98 key point, 97 pathology, 97 treatment, 98 Erythromycin epididymitis, 1126 marine fauna envenomation requiring, 240–241 Escherichia coli diarrhea from, 744t infectious disease emergency, 266t Esophagus transesophageal echocardiography, 25 traumatic injury to, 1104 ESRD. See End-stage renal disease Ester class of anesthesia, 28 Esterase acetylcholinesterase inhibitor, 450 anticholinesterase inhibitor, 942 C1 esterase inhibitor concentrate, 112 Ethanol. See Ethyl alcohol Ethyl alcohol (ETOH), 271t. See also Alcoholic ketoacidosis clinical presentation, 328–329 definition, 326 dispensation, 330–331 emergency actions, 326 epidemiology, 326 examination, 329 intoxication, 989–994 clinical presentation, 991–992 definition, 989 disposition, 993 epidemiology, 989
Ethyl alcohol (ETOH), (Continued) examination, 992 hypoglycemia from, 326 laboratory findings, 992 pathophysiology and pharmacology, 989–991 treatment, 993 key points, 325 laboratory findings, 329 as methanol poisoning treatment, 1022–1023 pathophysiology and pharmacology, 326–328 radiology, 329 treatment, 330 withdrawal, 325–331 Ethylene glycol toxicity, 994–998 clinical presentation, 995–996 definition, 994 disposition, 998 emergency actions, 994 epidemiology, 995 key points, 994 laboratory findings, 996–997 pathophysiology, 995 sequela, 998 treatment, 997–998 ETOH. See Ethyl alcohol Etomidate, airway management treatment, 915b Euvolemia, hyponatremia with, 353, 355–356 Exfoliative dermatitis, 99–102, 100b clinical presentation, 100–101 definition, 99–100 emergency actions, 99 epidemiology, 100 examination, 101 intensive care unit for, 99 key points, 99 laboratory findings and diagnosis, 101–102 pathology, 100, 100b treatment, 102 Exhaustion, pathophysiology of submersion incident, 244 Expiratory positive airway pressure (EPAP), 848 External hordeolum, 163 Extracellular fluid (ECF) volume, 694 Extracellular shifts, hyperkalemia, 366 Eye. See also Ophthalmologic emergencies acute narrow-angle closure glaucoma, 164–165
Index Eye, (Continued) blowout fracture, 168 blunt trauma to, 167–168 chemical injury to, 167 cornea abrasions of, 166–167 foreign bodies on, 167 ulcers of, 164 ultraviolet keratitis, 190–191 vitreous hemorrhage, 165–166 detached retina, 166 emergency examination, 63 glaucoma, acute narrow-angle closure, 164–165 infection Haemophilus influenzae, 164 HIV with ophthalmologic symptoms, 291 ocular herpes simplex virus, 275–276, 279, 285 Staphylococcus aureus, 163 Streptococcus pneumoniae, 164 oculomotor nerve examination, 457–458, 458f red, 164 ruptured globe, 168 Facial nerve examination, 460–461 Fall on outstretched hand (FOOSH), 601 Fasciotomy, acute compartment syndrome treatment, 599 FAST. See Focused abdominal sonography for trauma Female sex organs. See also Obstetrics and gynecology; Pregnancy dysmenorrhea, 510 endometriosis, 510 ovaries, 510, 529–535 sexual assault, 543–545 toxic shock syndrome, 545–549 uterine leiomyoma, 510 uterine perforation, 510 vaginitis, 510 vulvovaginitis, 550–554 Femur herniated, 20 neck, fractured, 627–628 necrosis of, 511 slipped capital femoral epiphysis, 629–630 Fentanyl airway management treatment, 915b intubated patient analgesia, 907t, 908 Fetal distress, 498. See also Pregnancy
1193
Fever acute rheumatic, 774–778 antipyretics, 170, 397, 515, 786, 931–936, 934f blood transfusion causing, 563–564 high, exfoliative dermatitis causing, 101 pediatric, with seizures, 785, 789–792 definition, 789 emergency actions, 789 epidemiology, 789 key points, 789 laboratory findings, 790 pathology, 790 treatment, 790–792 Rocky Mountain spotted, 98 Fibrinolysis, cardiac chest pain treatment, 74 Finkelstein's test, De Quervain's stenosing tenosynovitis diagnostic, 615–616 Fissures, anorectal clinical presentation, 117 definition, 115 examination, 118 treatment and outcomes, 120 Fistula, anorectal clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 Flow-cycle mode mechanical ventilation, 847 Fludrocortisone, adrenal insufficiency treatment, 336 Fluid and electrolyte emergencies, 351–393, 354t, 359t, 369, 382t anaphylactic shock, 921 calcium, 369–377 hypercalcemia clinical presentation, 374–375 definition, 373 diagnosis, 375 drugs causing, 374 ECG findings, 375 endocrinopathies causing, 374 etiology, 373 examination, 375 granulomatous diseases causing, 374 key points, 373 laboratory findings, 375 malignancies causing, 373 medications for, 376–377 redistribution causing, 374 surgery or radiation for, 377
1194 INDEX Fluid and electrolyte emergencies, (Continued) treatment, 376 volume repletion with normal saline, 376 hypocalcemia clinical presentation, 371 definitions, 370 diagnosis, 372 emergency treatment, 372–373 epidemiology, 370 examination, 371 hypomagnesemia, 370 hypoparathyroidism, 371 key points, 370 laboratory findings, 372 pseudohypoparathyroidism, 371 treatment, 372 vitamin D deficiency (rickets), 371 chloride, 383–385 hyperchloremia, 385 hypochloremia, 384 emergency actions, 351 key points, 351 magnesium, 377–380 hypermagnesemia, 379–380 treatment, 380 hypomagnesemia clinical presentation, 378 definition, 377 diagnosis, 379 electrocardiography, 378 epidemiology, 377–378 examination, 378 laboratory findings, 378 treatment, 379 pediatric diabetes treatment, 773–774 phosphorus hyperphosphatemia, 382–383 hypophosphatemia, 380–382 potassium, 361–369 hyperkalemia clinical presentation, 367 definition, 366 diagnosis, 367 epidemiology, 366 examination, 367 extracellular shifts, 366 key points, 365–366 laboratory findings, 367 pseudo-, 366 treatment, 268–369 hypokalemia, 361–365 clinical presentation, 363
Fluid and electrolyte emergencies, (Continued) definition, 362 epidemiology, 362 etiology, 363 examination, 363–364 intracellular shifts, 362 key points, 361–362 laboratory findings, 364–365 sodium, 351–361, 354t, 359t hypernatremia, 357–361, 359t definition, 357 diagnosis, 359–360 epidemiology, 357 etiologies, 359t examination, 358 increased water intake, 357 increased water loss, 357–358 key points, 356–357 laboratory findings, 358–359 presentation, 358 reduced water intake, 357 sodium gain, 358 treatment, 360–361 hyponatremia, 353–356 definition, 352 diagnosis, 354–355 epidemiology, 352–353 etiology, 354t euvolemia with, 353, 355–356 examination, 353 hypervolemia with, 355 hypovolemia with, 355 laboratory studies, 353–354 presentation, 353 treatment, 355 Fluid boluses, intestinal obstruction requiring, 21 Fluid replacement pediatric trauma requiring, 1074t rhabdomyolysis treatment, 416–417 thyroid storm treatment, 397 Flumazenil, pediatric analgesia and sedation reversal, 812–813 Fluoroquinolone, bacterial pneumonia treatment, 867, 867t Fluoxetine, panic disorder treatment, 816 Focused abdominal sonography for trauma (FAST) abdominal trauma, 1060 multiple trauma diagnostic, 1052 thoracic life-threatening injury requiring, 1100 Fomepizole, methanol poisoning treatment, 1022
Index Food and Drug Administration (FDA), haloperidol for intubated patient sedation, 910–911 Foodborne and waterborne illnesses, 264–275, 266t–271t clinical presentation, 265–272, 266t–271t definition, 264–265 diagnosis, 272 emergency actions, 264 epidemiology, 265 examination, 272 FoodNet surveillance for, 274 key points, 264 laboratory findings, 272 radiographs, 273 treatment, 273–274 FoodNet, 274 FOOSH. See Fall on outstretched hand Foot injuries, 604–608 anatomy, 604 definition, 604 emergency actions, 604 examination, 606 forefoot, 606 fractures and punctures, 643–646 hindfoot, 605 key points, 604 laboratory findings, 606–607 midfoot, 605–606 phalangeal, 606 physical examination, 605 radiographs, 607 treatment, puncture wounds, 607 Forced vital capacity (FVC) test, 884 Forearm and wrist injuries, 608–616. See also Tendons anatomy, 609–610 carpal fractures and injuries, 612 clinical presentation, 610–611 definition, 609 emergency actions, 608 examination, 610 forearm, 611–612 key points, 608 wrist nerve entrapment and overuse syndromes, 614–616 carpal tunnel syndrome, 615 De Quervain's stenosing tenosynovitis, 615–616 tendonitis, 615 ulnar tunnel syndrome, 615 Fosphenytoin, toxicity, 1034–1137
1195
Fractures ankle, 593–594 blowout eye, 168 carpal, 612 clavicle, 648 elbow, 603 femoral, 627–628 foot, 607 hand, 619–620 hip dislocations and fracturedislocations, 628 humerus, 649 humoral shaft, 649 intertrochanteric, 628 lower leg, 640–642 multiple long bone, 1056 multiple trauma causing, 1056 open, 643–646 classifications, 644–645 clinical presentation, 643 definition, 643 diagnosis, 644 emergency actions, 643 epidemiology, 643 examination, 644 key points, 643 laboratory findings, 644 radiographs, 645 treatment, 645–646 pelvic type I, 1083–1085 type II, 1085 type III, 1085–1086 type IV, 1086 penile, 1128 scapular, 649 skull, 1068–1069 basilar life-threatening, 1068 tibial tuberosity, 642 trochanteric, 628 Fresh frozen plasma (FFP) acute bleeding diathesis treatment, 558 adrenal insufficiency treatment, 337 as blood transfusion component, 561 urticaria treatment requiring, 112 Frostbite, 215–219 clinical presentation and examination, 217 definition, 216 diagnosis, 217–218 emergency actions, 216 epidemiology, 216 key points, 215
1196 INDEX Frostbite, (Continued) laboratory findings, 218 pathophysiology, 216–217 summary, 219 treatment, 218–219 Furosemide congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 FVC test. See Forced vital capacity test GABA receptors. See Gamma aminobutyric acid receptors GABHS. See Group A beta-hemolytic streptococci GAD. See Generalized anxiety disorder Gadolinium contrast, 442 Gamma aminobutyric acid (GABA) receptors, 330 barbiturate overdose influencing, 949, 950, 951 cyclic antidepressant toxicity influencing, 982 Gamma globulin, pediatric Kawasaki disease treatment, 794–795 GAS infection. See Group A streptococcal infection Gastric lavage arsenic poisoning treatment, 946 iron toxicity requiring, 1009–1010 salicylates toxicity treatment, 1042 Gastric tube, abdominal trauma requiring, 1062 Gastrointestinal bleeding, 130–134 clinical presentation, 131 definition, 130 diagnosis, 133 emergency actions, 130 epidemiology, 131 examination, 131–132 key points, 130 laboratory findings, 132 radiographs, 133 treatment, 133–134 Gastrointestinal emergencies anorectal disorders, 114–121 bleeding, 130–134 diverticulosis and diverticulitis, 122–129 gastroenteritis, 510 jaundice and hepatitis, 135–143, 137f, 138f, 139f metabolic acidosis, 316 pancreatitis, 144–148
Gastrointestinal emergencies, (Continued) peptic ulcer disease, 149–152 Gastrointestinal (GI) system, 271t GCS. See Glasgow Coma Scale Generalized anxiety disorder (GAD), 817–819. See also Panic disorder clinical presentation, 817 definition, 817 diagnosis, 818 epidemiology, 817 examination, 818 key points, 817 laboratory findings, 818 treatment, 818–819 Geneva (Wicki) assessment model, pulmonary embolism risk, 900–901, 900t Genital herpes, 279, 285, 513–515. See also Genitourinary tract; Herpes virus clinical presentation, 513–514 definition, 513 diagnosis, 515 emergency actions, 513 epidemiology, 513 examination, 514 key points, 513 laboratory findings, 514 treatment, 515 Genitourinary tract. See also Genital herpes trauma, 1063–1066 clinical presentation, 1063–1065 genital injuries, 1065 renal contusions/lacerations/ ruptures, 1064 ureter/bladder injuries, 1064 urethral injuries, 1065 definition, 1063 diagnosis, 1066 emergency actions, 1063 examination, 1065–1066 key points, 1063 laboratory findings, 1066 treatment, 1066 Gentamycin, endocarditis from prosthetic valve infection, 91–92 Geriatric patient aneurysm susceptibility, 2 emergencies, 386–393 abdominal pain, 389 clinical presentations, 387 definition, 387 emergency actions, 386 epidemiology, 387 examination and history, 388
Index Geriatric patient, (Continued) myocardial infarction, 388 pneumonia, 388 psychiatric illness, 389 trauma, 389 urinary tract infection, 388–389 glaucoma, acute narrow-angle closure, 164–165 hyperglycemic hyperosmolar nonketotic coma, 390–393 reduced toxicodendron dermatitis sensitivity, 107 retinal artery occlusion in, 165 Gestational hypertension. See also Preeclampsia and eclampsia definition of, 521 GFR. See Glomerular filtration rate GI system. See Gastrointestinal system Giant cell arteritis, ophthalmologic emergencies, 166 Giardia lamblia diarrhea from, 744t infectious disease emergency, 269t Glasgow Coma Scale (GCS), 453, 454t global assessment, 453, 454t head injury examination and disposition, 1071 modified for infants and children, 1076t multiple trauma examination, 1054, 1054t Glaucoma, acute narrow-angle closure, 164–165 Gliosis, 440 Glomerular filtration rate (GFR), 1113–1117 Glossopharyngeal nerve examination, 461 Glucocorticoid replacement therapy, adrenal insufficiency treatment, 337 Glucose level determination hypoglycemia, 399–405 pediatric diabetes, 773–774 pediatric seizures and status epilepticus, 786 toxicology emergencies, 927–928 pediatric trauma medication, 1081 Goodpasture's syndrome, 889–890 Granulomatous diseases hypercalcemia from, 374 Wegener's granulomatosis, 889–890 Group A beta-hemolytic streptococci (GABHS), 173, 174, 802–805
1197
Group A streptococcal (GAS) infection, 774–778 Guillain-Barré syndrome arsenic poisoning v., 946 botulism v., 430 Gynecology. See Female sex organs; Obstetrics and gynecology Gynecomastia (male mammary gland development), exfoliative dermatitis causing, 101 H2 antagonists, urticaria treatment, 112 Haemophilus influenzae type b (HIB) chronic obstructive pulmonary disease from, 884 eye infection, 164 pediatric infection, 708, 708t, 712–713 Hallucinogen toxicity, 999–1003 clinical presentation, 1001–1002 definition, 999 diagnosis, 1002–1003 emergency actions, 999 key points, 999 laboratory findings, 1002 pathophysiology, 999–1001 Haloperidol, delirium requiring, 910–911 Halotestin, adrenal insufficiency treatment, 336 Hand injuries, 617–624 anatomy, 617–619 emergency actions, 617 history (from patient/bystander/ paramedic), 619 key points, 617 physical examination, 619–625 dislocations, 620–622 fractures, 619–620 high-pressure injection injuries, 624 infections, 622–624 radiographs, 624 tendon injuries, 622 HAP. See Hospital-acquired pneumonia HAV. See Hepatitis A virus HBV. See Hepatitis B virus HCV. See Hepatitis C virus Head. See also Brain; Central nervous system trauma to, 1055, 1067–1072 airway management for, 915b computed tomography scan for, 1055 definition, 1067–1068 disposition, 1071–1072 Glasgow Coma Scale, 1071 emergency actions, 1067
1198 INDEX Head, (Continued) hematomas, 1069–1071 epidural, 1069–1070 herniation from, 1070 ICP monitoring for, 1070 subdural, 1070 key points, 1067 minor injuries, 1069 concussion, 1069 outcome, 1072 pathophysiology, 1068 physical examination, 1071 skull fractures, 1068–1069 systemic v. neurologic complications, 1072 Headache, 432–438 clinical presentation, 435–436 CT or MRI scan for, 432 definition, 432 emergency actions, 432 epidemiology, 433 examination, 436 heart transplant infection causing, 95 key points, 432 laboratory findings, 437 migraine, 431–432 classic, 433 common, 433 hemiplegic, 433 ophthalmoplegic, 433 stroke syndromes v., 484t treatment, 437–438 pathology, 433–435 acute narrow-angle glaucoma, 435 brain tumor, 434 classic migraine, 433 cluster headache, 434 common migraine, 433 dural bleeding, 434 hemiplegic migraine, 433 hypertension induced, 434 ophthalmoplegic migraine, 433 post-lumbar puncture, 435 pseudotumor cerebri, 434, 435 subarachnoid hemorrhage, 434–435 temporal arteritis, 435 toxic metabolic, 434 traction induced, 434 trigeminal neuralgia, 435 radiology for, 437 treatment, 437–438 Hearing loss (sudden), 170–171 Heart transplant, 93–96, 1150, 1151, 1154
Heart transplant, (Continued) antibiotic prophylaxis for, 96 definition, 93–94 diagnosis, 94–95 drug toxicity causing, 95 emergency actions for recipient of, 93 endocarditis risk for, 96 epidemiology, 94 examination, 94 infection causing, 94, 95 typical infections, 95 key points, 93 laboratory findings, 94 rejection causing, 93–96, 1150, 1151, 1154 treatment, 95–96 Heat injuries, 220–224 clinical presentation, 221 cramps, 221, 224 definition, 220 diagnosis, 223 edema, 221, 224 emergency actions, 220 epidemiology, 220–221 examination, 222–223 exhaustion, 222, 224 key points, 220 laboratory findings, 223 prickly heat, 222, 224 radiographs, 223 stroke, 222, 225 syncope, 221, 224 treatment, 223–224 Heliox, asthma treatment, 223 HELLP syndrome hemolysis-elevated liver enzyme levels-low platelet count, 401 preeclampsia and eclampsia with, 523 Hematocrit, shock diagnostic, 919 Hematomas Bell's palsy v., 426–427, 426t cranial herniation from, 1069–1071 epidural, 1069–1070 herniation from, 1070 ICP monitoring for, 1070–1071 subdural, 1070 evacuation of, 161 Hemodialysis arsenic intoxication, 943 hyperkalemia requiring, 369 lithium poisoning treatment, 1019 mercury poisoning treatment, 1026
Index Hemodialysis, (Continued) methanol poisoning treatment, 1022–1023 salicylates toxicity treatment, 1043 Hemoglobin analysis, shock diagnostic, 919 Hemoglobinuria, arsine poisoning v., 946 Hemolytic uremic syndrome, infectious disease emergency, 266t Hemophilia, 566–569 clinical presentation, 567–568 cryoprecipitated antihemophilic factor, as blood transfusion component, 561–562 definition, 566–567 diagnosis, 568 emergency actions, 566 epidemiology, 567 examination, 568 key points, 566 laboratory findings, 568 pathophysiology, 567 treatment, 569 Hemoptysis, 888–891 clinical presentation, 889 definition, 888 diagnosis, 890 emergency actions, 888 epidemiology, 888–889 examination, 889 key points, 888 laboratory findings, 889–890 Goodpasture's syndrome, 889–890 systemic lupus erythematosus, 889–890 Wegener's granulomatosis, 889–890 pulmonary embolism causing, 898 treatment, 890–891 surgical intervention, 891 Hemorrhage. See also Blood; Oncologic and hematologic emergencies; Subarachnoid hemorrhage diverticular, 124, 128 maternal-fetal, 1109–1110 MRI of intracerebral, 487f ophthalmologic emergency, 165–166 subconjunctival, 167 ruptured ovarian cyst, 510 salicylates toxicity complication, 1043 shock from, 920 stroke syndromes, 484t, 486–489, 487f, 488f, 489f, 490f, 491f, 492f
1199
Hemorrhoids, 114–120 clinical presentation, 116–117 definition, 114 emergency action, 114 examination, 117–118 laboratory findings, 119 pathology, 115 treatment and outcomes, 119–120 Hemostasis, wound preparation requiring, 29 Heparin cardiac chest pain treatment, 74 contraindications for, 74–75 hyperglycemic hyperosmolar nonketotic coma, 393 low-molecular weight v. unfractionated, 74 pulmonary embolism treatment, 903–904 Hepatic impairment. See also Hepatitis caustic ingestion causing, 964 exfoliative dermatitis causing, 101 hepatitis causing enlargement, 136 hepatomegaly, exfoliative dermatitis causing, 101 hepatotoxicity acetaminophen overdose causing, 931–936, 934f hypoglycemia causing, 401 liver transplantation emergencies, 1156–1162, 1158t, 1160t, 1161t theophylline toxicity, 1046 Hepatitis, 135–143, 137f, 138f, 139f. See also specific type cirrhosis from, 1156 definition of, 136 opioid injection risk of, 1028 Reye's syndrome causing, 797 Hepatitis A virus (HAV), 136, 137, 137f, 139 infectious disease emergency, 268t Hepatitis B virus (HBV), 136, 137–138, 138f, 139 Hepatitis C virus (HCV), 136, 138–139, 139f. See also Liver transplantation emergencies cirrhosis from, requiring liver transplantation, 1156 Hepatobiliary iminodiacetic acid (HIDA), 12–13 cholelithiasis and cholecystitis diagnostic, 12–13 Herniation, 15–20, 797, 1069–1071 abdominal, 15–18
1200 INDEX Herniation, (Continued) cerebral, Reye's syndrome causing, 797 clinical presentation, 16 definition, 15–16 diagnosis, 17 emergency actions for, 15 epidemiology, 16 examination, 16–17 femoral, 20 hematoma causing, 1069–1071 incarcerated, 16, 17, 20 incisional, 16, 20 inguinal, 15, 17, 20 key points, 15 laboratory findings, 17 radiographs for, 17 strangulated, 16, 17 treatment and outcome, 17–18 umbilical, 15 Herpes keratitis, 164 Herpes simplex viruses (HSV), 275–276, 277, 279, 282, 285 Herpes virus, 275–288. See also Genital herpes Bell's palsy clinical presentation, 279–280 definition, 276 differential diagnosis, 426–427, 426t, 484t risk factors for, 424–425 treatment, 286 clinical presentation encephalitis, 279 genital lesions, 279 immunocompromise, 280 oral lesions, 278–279 cytomegalovirus clinical presentation, 281–282 definition, 277 epidemiology, 278 examination, 283 treatment, 287 definition, 275 diagnosis, 284–285 emergency actions, 275 epidemiology, 277 Epstein-Barr virus clinical presentation, 281 definition, 276–277 epidemiology, 278 examination, 283 treatment, 287 heart transplant recipient susceptibility, 95
Herpes virus, (Continued) herpes zoster shingles clinical presentation, 280–281 definition, 276 epidemiology, 277–278 examination, 283 treatment, 287 herpetic whitlow clinical presentation, 280 definition, 276 treatment, 286 key points, 275 laboratory findings, 283–284 ocular HSV clinical presentation, 279 definition, 275–276 treatment, 285 radiographs, 285 simplex viruses 1 and 2 definition, 275 epidemiology, 277 examination, 282 ocular, 275–276, 279, 285 treatment, 285 encephalitis, 285–286 oral and genital lesions, 285 varicella-zoster clinical presentation, 280 definition, 276 epidemiology, 277 examination, 282–283 immune globulin, 96 treatment, 286 Herpes zoster shingles, 276, 277–278, 280–281, 283, 287 Herpetic whitlow, 275, 276, 280 treatment, 286 HIB. See Haemophilus influenzae type b HIDA. See Hepatobiliary iminodiacetic acid Hidradenitis suppurativa, definition, 114 High altitude-related emergencies, 183–191, 184t, 187t global amnesia, 184t headache, 434 High-altitude cerebral edema (HACE), 184t, 185, 187t, 189, 191 High-altitude pulmonary edema (HAPE), 184t, 186, 187t, 189–190, 191 Hip trauma, 625–630 anatomy, 626–627 clinical presentation, 627–630 anterior dislocations, 628–629 femoral neck fractures, 627–628
Index Hip trauma, (Continued) hip dislocations and fracturedislocations, 628 intertrochanteric fractures, 628 Legg-Calvé-Perthes disease, 629 pediatric hip dislocations, 629 posterior dislocations, 629 septic hip or septic arthritis, 630, 632, 633, 637 slipped capital femoral epiphysis, 629–630 trochanteric fractures, 628 definition, 626 emergency actions, 625 epidemiology, 626 examination, 627 key points, 625 laboratory evaluation, 630 radiographs, 630 Hirschsprung's disease (congenital aganglionic megacolon), 745–748, 748f clinical presentation, 746 definition, 746 diagnosis, 747 emergency actions, 746 epidemiology, 746 examination, 746–747 key points, 745 laboratory findings, 747 radiographs, 747, 748f treatment, 747–748 Histrionic personality disorder, 832–833 clinical presentation and examination, 832 diagnosis, 833 epidemiology, 832 key points, 832 treatment and outcome, 833 Hordeolum, 163 Hormone replacement, hypothyroidism and myxedema coma treatment, 408–409 Hospital admission adrenal insufficiency, 337 bacterial pneumonia from, 863 diabetic ketoacidosis, 347 heart transplant complications, 95–96 hyperglycemic hyperosmolar nonketotic coma, 393 hypothyroidism and myxedema coma, 408–409 pediatric emergency dehydration, 699 pediatric Kawasaki disease, 794–795
1201
Hospital admission, (Continued) phenytoin toxicity, 1037 pulmonary embolism risk factor, 899 renal stones, 1138 salicylates toxicity, 1043 theophylline toxicity, 1048 urticaria treatment, 112 Hospital-acquired pneumonia (HAP), 863 HSV. See Herpes simplex viruses Human immunodeficiency virus (HIV) infection, 288–292, 1028 acquired immunodeficiency syndrome, 271t exfoliative dermatitis from, 100, 100b Bell's palsy v., 426–427, 426t clinical presentation, 289–290 definitions, 288 HIV v. AIDS, 288–289 emergency actions, 288 epidemiology, 289 key points, 288 multiple sclerosis v., 442 opioid injection risk of, 1028 pathophysiology, 289 postexposure prophylaxis, 292 renal stones treatment for patients with, 1135, 1137 symptoms central nervous system, 291 cutaneous system, 291–292 gastrointestinal system, 290–291 ophthalmologic system, 291 pulmonary, 290 Human T-lymphotropic virus (HTLV), multiple sclerosis v., 442 Hunt and Hess Clinical Grading Scale, 496 Hydralazine, pediatric trauma medication, 1080 Hydrocarbon poisoning, 1003–1007 clinical presentation, 1005 definition, 1004 diagnosis, 1005–1006 emergency actions, 1004 epidemiology, 1004–1005 examination, 1005 key points, 1003 laboratory findings, 1005 radiographs, 1006 treatment, 1006–1007 Hydrocortisone adrenal insufficiency treatment, 336 hypothyroidism and myxedema coma treatment, 408–409 pediatric trauma medication, 1080
1202 INDEX Hydrocortisone, (Continued) thyroid storm treatment, 397 Hydrofluoric acid, chemical burn from, 203–204 Hydromorphone, intubated patient analgesia, 907t, 908 Hymenoptera sting, 230–233 clinical presentation, 231–232 definition, 230–231 diagnosis, 232 emergency actions, 230 epidemiology, 231 key points, 230 pathophysiology, 231 treatment, 232–233 Hyperbaric chamber referrals, Divers Alert Network for, 211 Hyperbilirubinemia, 136 Hypercalcemia. See also Calcium; Hypocalcemia cardiac arrhythmia from, 54, 55f clinical presentation, 374–375 definition, 373 diagnosis, 375 drugs causing, 374 ECG findings, 375 endocrinopathies causing, 374 etiology, 373 examination, 375 granulomatous diseases causing, 374 key points, 373 laboratory findings, 375 malignancies causing, 373 medications for, 376–377 redistribution causing, 374 surgery or radiation for, 377 treatment, 376 volume repletion with normal saline, 376 Hypercapnia definition of, 845 headaches from, 434 respiratory acidosis causing, 320 Hyperchloremia, 385. See also Chloride, fluid and electrolyte emergencies; Hypochloremia fluid and electrolyte emergencies, 385 Hyperemesis gravidarum, 516–518 clinical presentation, 516 definition, 516 diagnosis, 517 emergency actions, 516 epidemiology, 516 etiology, 516
Hyperemesis gravidarum, (Continued) examination, 517 key points, 515 laboratory findings, 517 treatment, 517–518 Hyperglycemia. See also Hyperglycemic hyperosmolar nonketotic coma theophylline overdose causing, 1046 Hyperglycemic hyperosmolar nonketotic coma (HHNC), 390–393. See also Hyperglycemia clinical presentation, 391–392 definition, 390–391 diabetic ketoacidosis v., 390–393 diagnosis, 392 disposition, 393 emergency actions, 390 epidemiology, 391 key points, 390 laboratory findings, 392 pathophysiology, 391 treatment, 392–393 Hyperkalemia. See also Hypokalemia cardiac arrhythmia from, 54, 55f cardiopulmonary arrest from, 664 clinical presentation, 367 definition, 366 diagnosis, 367 end-stage renal disease causing, 1119, 1123 epidemiology, 366 examination, 367 extracellular shifts, 366 hemodialysis for, 369 key points, 365–366 kidney disease causing, 1119, 1123 laboratory findings, 367 pseudo-, 366 treatment, 268–369 Hypermagnesemia, 379–380. See also Hypomagnesemia; Magnesium treatment, 380 Hypernatremia, 357–361, 359t. Hyponatremia definition, 357 diagnosis, 359–360 epidemiology, 357 etiologies, 359t examination, 358 increased water intake, 357 increased water loss, 357–358 key points, 356–357 laboratory findings, 358–359 presentation, 358
Index Hypernatremia, (Continued) reduced water intake, 357 sodium gain, 358 treatment, 360–361 Hyperosmolarity, hyperglycemic hyperosmolar nonketotic coma, 390–393 Hyperphosphatemia, 382–383. See also Hypophosphatemia Hypertension. See also Hypertensive emergencies; Hypotension acute, 524–525 benign intracranial, 434, 435 chronic, definition of, 520 end-stage renal disease causing, 1119–1121 gestational, 521 headaches associated with, 434 Hypertensive emergencies, 76–80. See also Hypertension; Hypotension asymptomatic, 79–80 definitions, 76 epidemiology, 76–77 examination and history taking, 77 physical, 77 key points, 76 laboratory findings, 77 preeclampsia and eclampsia, 401, 510, 519–525 radiographs, 78 treatment, 78–79 Hyperthermia, 664. See also Hypothermia Hyperthyroidism and thyroid storm, 394–398. See also Hypothyroidism and myxedema coma clinical presentation, 395–396 definitions, 394 diagnosis, 396 emergency actions, 394 epidemiology, 394–395 examination, 396 key points, 394 laboratory findings, 396–397 pathology, 395 treatment, 397–398 Hyperventilation. See also Hypoventilation asthma mimicked by, 857 hypernatremia etiology involving, 359t Hypervolemia, 355. See also Hypovolemia Hyphema, as ophthalmologic emergency, 168 Hypoalbuminemia state, 315 Hypocalcemia. See also Calcium; Hypercalcemia
1203
Hypocalcemia, (Continued) cardiac arrhythmia from, 54, 55f caustic ingestion causing, 964 clinical presentation, 371 definitions, 370 diagnosis, 372 emergency treatment, 372–373 epidemiology, 370 examination, 371 hypomagnesemia, 370 hypoparathyroidism, 371 key points, 370 laboratory findings, 372 pseudohypoparathyroidism, 371 treatment, 372 vitamin D deficiency (rickets), 371 Hypochloremia, 384. See also Hyperchloremia Hypoglossal nerve examination, 462 Hypoglycemia, 326, 399–405, 399f, 434, 484t alcoholic ketoacidosis, 339, 339f causes of “dawn phenomenon,” 402 early diabetes, 401 endocrine disorders, 402 ethanol intoxication, 326, 402 HELLP syndrome, 401 hepatic impairment, 401 hypothyroidism, 408–409 insulinoma, 401 kwashiorkor, 401 medications, 403 meningitis, 401 mesenchymal tumors, 401 renal disease, 402 salicylate intoxication, 403 sepsis, 401 Somogyi syndrome, 402 clinical presentation, 400–403 definition, 399–400 diagnosis, 404 emergency actions, 399 epidemiology, 400 examination, 403 glucose level determination, 399–405 headaches from, 434 hyperosmolar nonketotic, 390–393 insulin-dependent patient, 402 key points, 399 laboratory findings, 403–404 medical emergency, 399–405 mental status alteration from, 404–405
1204 INDEX Hypoglycemia, (Continued) stroke syndromes v., 484t treatment and outcome, 404–405 Hypokalemia, 361–365. See also Hyperkalemia cardiac arrhythmia from, 54, 55f clinical presentation, 363 definition, 362 epidemiology, 362 etiology, 363 examination, 363–364 intracellular shifts, 362 key points, 361–362 laboratory findings, 364–365 metabolic alkalosis causing, 319 theophylline overdose causing, 1046, 1048 Hypomagnesemia, 370, 377–379. See also Hypermagnesemia; Magnesium caustic ingestion causing, 964 clinical presentation, 378 definition, 377 diagnosis, 379 electrocardiography, 378 epidemiology, 377–378 examination, 378 laboratory findings, 378 treatment, 379 Hyponatremia, 353–356. See also Hypernatremia definition, 352 diagnosis, 354–355 epidemiology, 352–353 etiology, 354t euvolemia with, 355–356 examination, 353 hypervolemia with, 355 hypothyroidism and myxedema coma causing, 408–409 hypovolemia with, 355 laboratory studies, 353–354 presentation, 353 treatment, 355 Hypoparathyroidism, 371 pseudo-, 371 Hypophosphatemia, 380–382. See also Hyperphosphatemia Hypopyon, corneal ulcer with, 164 Hypotension. See also Hypertension; Hypertensive emergencies arsenic poisoning causing, 946 beta-blocker overdose sign, 953 clonidine overdose causing, 965, 967–968
Hypotension, (Continued) cyclic antidepressant toxicity causing, 983–984 end-stage renal disease causing, 1121 morphine and nitroglycerin causing, 75 primary valve failure causing, 91 pulmonary embolism causing, 898 respiratory acidosis causing, 321 theophylline toxicity causing, 1048 Hypothermia, 225–229. See also Hyperthermia clinical presentation, 227 definition, 226 diagnosis, 227–228 emergency actions, 226 epidemiology, 226 exfoliative dermatitis causing, 101 hypothyroidism and myxedema coma causing, 409 key points, 225 laboratory findings, 228 pathophysiology, 226–227 pathophysiology of submersion incident, 244 physical examination, 227 submersion incident causing, 246t, 247, 248 summary, 229 treatment, 228–229 Hypothyroidism and myxedema coma, 406–409. See also Hyperthyroidism and thyroid storm clinical presentation and examination, 407–408 definition, 406 diagnosis, 408 emergency actions, 406 epidemiology, 406–407 key points, 406 laboratory findings, 408 pathology, 407 treatment, 408–409 Hypoventilation, metabolic alkalosis causing, 319. See also Hyperventilation Hypovolemia. See also Hypervolemia cardiopulmonary arrest from, 664 hyponatremia with, 355 Hypoxemia cardiopulmonary arrest from, 664 definition of, 845 Hypoxia headaches from, 434 pulmonary embolism causing, 903
Index Hypoxia, (Continued) sudden infant death syndrome, 765–769 “Ice.” See Methylenedioxymethamphetamine ICP. See Intracranial pressure IgM. See Immunoglobulin M Immobilization, pulmonary embolism risk with prolonged, 899 Immunoglobulin G (IgG), toxic shock syndrome requiring, 549 Immunoglobulin M (IgM), 271t Immuno-turbidimetric D-dimer assay, pulmonary embolism, 901, 905t Imuran, myasthenia gravis requiring, 450 IMV. See Intermittent mandatory ventilation Incarcerated hernias, 16, 17, 20 Incisional hernias, 16, 20 Indomethacin, headaches from, 434 INF. See Interferon Infant. See also Child; Pediatric emergencies; Pregnancy definition of, 657 Infections. See also Bacteremia; Bacteria; Infectious disease emergencies; Sepsis; specific pathogen automatic implantable cardioverterdefibrillator, 42–43 bone, 631–637 Epstein-Barr viral, 276–277, 278, 281, 283, 287, 440 hand, 622–624 hand injuries with, 622–624 heart transplant complications, 94, 95 infection risk after marine fauna envenomation, 240–241 joint, 631–637 Listeria, 95 lithium poisoning with, 1018 pharyngitis viral, 172–173 prosthetic valve, 91–92 Staphylococcus aureus, 42, 163, 267t, 502, 1127–1128 Staphylococcus epidermidis, 42 streptococcal group A acute pediatric rheumatic fever from, 774–778 beta-hemolytic, 173, 174, 802–805 pneumoniae, 164, 707–708, 708t toxoplasma, 95 urinary tract, 1142–1146, 1145t pediatric, 388–389
1205
Infections, (Continued) Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Infectious disease emergencies. See also Infections diphtheria, 261–264 foodborne and waterborne illnesses, 264–275, 266t–271t herpes virus, 275–288 human immunodeficiency virus, 288–292 Bell's palsy v., 426–427, 426t multiple sclerosis v., 442 influenza, 292–295 Haemophilus, 164, 708, 708t, 712–713 Isospora belli, 269t knee pain as, 587 malaria, 295–300, 298t–299t, 300t rabies, 301–306 tetanus, 307–310 Inflammatory skin disorders. See also Dermatologic emergencies exfoliative dermatitis from, 100, 100b Influenza, 292–295 carbon monoxide poisoning mimicking, 960 clinical presentation, 293–294 definition, 293 diagnosis, 294 emergency actions, 293 epidemiology, 293 examination, 294 Haemophilus eye infection from, 164 pediatric infection, 708, 708t, 712–713 key points, 293 laboratory findings, 294 radiographs, 294 treatment, 294 Inguinal hernias, 15, 17, 20 Injection drug use Epi-Pen autoinjector, 112–113 high-pressure injection injuries, 624 opioid intoxication, 1027–1030 Injury. See also Caustic ingestion emergency; Trauma; Wound management ankle, 589–596 aortic (traumatic), 1102–1103 diving, 205–211, 210b arterial gas embolism, 205, 208
1206 INDEX Injury, (Continued) inner ear barotrauma, 207 elbow, 600–603 electrical, 212–215 foot, 604–608 forearm and wrist, 608–616 hand, 617–624 head or spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 adult v. child spinal cord, 1077 heat, 220–224 lightning, 234–237 lower leg, 638–642 pediatric, 642 maxillofacial and dental, 158–161 ophthalmologic, 161–168 blunt trauma to eye, 167–168 chemical injury to eye, 167 shoulder, 647–652 INR. See International normalized ratio Insecticides poisoning, 1130–1132 antidotal therapy, 1033 clinical presentation, 1131 SLUDGe mnemonic for, 1131 definition, 1130 emergency actions, 1130 epidemiology, 1131 key points, 1130 laboratory findings, 1033 pathology, 1131 treatment, 1033 Inspiratory positive airway pressure (IPAP), 848 Insulin /glucose, calcium channel blockers overdose treatment, 958–959 infusion diabetic ketoacidosis requiring, 347 hyperglycemic hyperosmolar nonketotic coma, 392–393 pediatric diabetes treatment, 773–774 pediatric trauma medication, 1080 Insulinoma, hypoglycemia from, 401 Intensive care unit (ICU), 271t adrenal insufficiency treatment, 337 beta-blocker overdose treatment, 954 calcium channel blockers overdose treatment, 959 diabetic ketoacidosis requiring, 347 exfoliative dermatitis requiring, 99 hyperglycemic hyperosmolar nonketotic coma, 393 shock, 917–920
Intensive care unit (ICU), (Continued) thoracic aortic dissection requiring, 26 Interferon (INF), 440 Intermittent mandatory ventilation (IMV), 847, 850 Internal hordeolum, 163 International normalized ratio (INR), 169 Intestinal obstruction, 18–22 clinical presentation, 20 CT scan for diagnosis of, 21 definition, 19 diagnosis based on examination and history, 21 emergency actions, 18 epidemiology, 19 examination, 20 key points, 18 laboratory findings, 20 treatment and outcome, 21 Intra-aortic balloon pump, cardiac chest pain treatment, 74 Intracellular shifts, hypokalemia, 362 Intracranial pressure (ICP) headache indicative of, 432 hematomas influencing, 1070–1071 Intubation asthma treatment requiring, 223 hymenoptera sting requiring, 233 patient with delirium requiring, 910–911 primary prosthetic valve failure requiring, 91 Invasive positive-pressure ventilation mechanical ventilation, 849–851 IPAP. See Inspiratory positive airway pressure Iron toxicity, 1007–1010 clinical presentation, 1008 definition, 1008 diagnosis, 1009 emergency actions, 1008 epidemiology, 1008 examination, 1008–1009 key points, 1007 laboratory findings, 1009 metabolic acidosis from, 1021 radiographs, 1009 treatment, 1009–1010 Irradiated blood products, as blood transfusion component, 562 Irrigation whole-bowel clonidine overdose treatment, 967–968 iron toxicity requiring, 1009–1010
Index Irrigation, (Continued) lead poisoning requiring, 1016 lithium poisoning treatment, 1019 theophylline toxicity, 1048 wound preparation requiring, 29–30 Irritable bowel syndrome, diverticulitis v., 126 Ischemia. See also Myocardial infarction diverticulitis v. colitis, 126 MRI of, 491f myocardial, 511 stroke syndromes, 476f, 488, 491f transient ischemic attacks, 469 zones of, 475f Isoniazid poisoning, anion gap from, 1021 Isopropanol toxicity, 1010–1013 clinical presentation, 1011–1012 definition, 1011 diagnosis, 1012 emergency actions, 1011 epidemiology, 1011 examination, 1012 key points, 1010 laboratory findings, 1012 radiographs, 1013 treatment, 1013 Isoproterenol, pediatric trauma medication, 1080 Isospora belli, infectious disease emergency, 269t Jaundice and hepatitis, 135–143, 137f, 138f, 139f clinical presentation and examination, 139–140 definitions of, 136 diagnosis, 142 epidemiology, 136–139, 137f, 138f, 139f key points, 135 laboratory findings, 140–141 radiographs, 141–142 treatment, 142–143 JCAHO. See Joint Commission on Accreditation of Healthcare Organizations Joint and bone infections, 631–637. See also Arthritis clinical presentation, 634 definitions osteomyelitis, 631 septic arthritis, 630, 632 emergency actions, 631 epidemiology, 632
1207
Joint and bone infections, (Continued) osteomyelitis, 632 septic arthritis, 632 imaging, 635–636 key points, 631 laboratory findings, 634–635 pathology osteomyelitis, 632–633 septic arthritis, 633 treatment osteomyelitis, 636 septic arthritis, 637 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), pediatric analgesia and sedation, 806 Jones criteria for acute rheumatic fever, 775–777 Juvenile myoclonic epilepsy, treatment, 787 Kawasaki disease erythema multiforme v., 98 pediatric, 792–795 clinical presentation, 793–794 definition, 792–793 diagnosis, 794 epidemiology, 793 etiology, 793 key points, 792 laboratory findings, 794 treatment, 794–795 Kernig sign, neurological examination, 464–465 Ketamine airway management pretreatment, 914b anesthesia after wound examination, 28 intubated patient sedation, 911 pediatric analgesia and sedation, 812 Ketorolac tromethamine, headache treatment, 437–438 Ketosis, hyperglycemic hyperosmolar nonketotic coma v., 390–393 Kidneys. See also Acute renal failure; Endstage renal disease; Renal disease; Renal transplantation emergency acid-base problems involving, 314, 318 contusions/lacerations/ruptures, 1064 excretion and absorption function, 313 hypernatremia etiology involving, 359t nephrolithiasis, 1135–1138 transplant rejection, 1122–1123, 1158t, 1161t, 1163–1167 urinary tract infection influencing, 1146
1208 INDEX Knee pain emergencies, 583–588 definition, 583 emergency actions, 583 epidemiology, 583–584 key points, 583 laboratory findings, 587 physical examination, 584–586 radiographs, 586–587 RICE therapy for, 587–588 Kwashiorkor, hypoglycemia from, 401 Labetalol, hypertensive emergency treatment, 79–80 Lactate measurements, neonatal emergencies requiring, 668–669 Lactic acidosis, 410–413, 411t, 1020 definition, 410–412, 411t emergency actions, 410 epidemiology, 410 hypoxia causing, 410 key points, 410 summary, 413 treatment bicarbonate therapy in cardiopulmonary resuscitation, 412 bicarbonate therapy in septic shock, 413 wide anion gap from, 1021 Lactulose, hypernatremia etiology involving, 359t Lamotrigine, seizures and status epilepticus, 471t Laryngeal mask airway (LMA), 657 pediatric emergency use of, 674 Laryngoscope blades, airway equipment, 673–674, 915b Lavage diagnostic peritoneal, 1060–1061 gastric arsenic poisoning treatment, 946 iron toxicity requiring, 1009–1010 salicylates toxicity treatment, 1042 Lead poisoning, 1014–1016 clinical presentation, 1015 definition, 1014 diagnosis, 1015 emergency actions, 1014 epidemiology, 1014 key points, 1014 laboratory findings, 1015 pathophysiology, 1014–1015 radiographs, 1015–1016 treatment, 1016
Legg-Calvé-Perthes disease, 629 Leptospirosis, toxic shock syndrome v., 548 Lesions herpes, 278–279 treatment, 285 mass, headaches from, 434 LET local anesthetic, 28, 29 Lethargy, lithium poisoning causing, 1018–1019 Leukocytosis ARDS causing, 859–861 iron toxicity causing, 1009 Leukoreduced blood products, as blood transfusion component, 562 Levetiracetam, seizures and status epilepticus, 471t Levofloxacin, adult bacterial pneumonia, 867, 867t Levothyroxine, hypothyroidism and myxedema coma treatment, 408–409 Lewisite, anti-, 946 Lidocaine, 28, 29 airway management pretreatment, 914b pediatric trauma medication, 1080 toxicity of, 29, 29t toxicology emergencies requiring, 929 Liebermeister's sign, arterial gas embolism diagnostic, 208 Lightning injuries, 234–237 clinical presentation, 235 definition, 234–235 diagnosis, 236 emergency actions, 234 epidemiology, 235 examination, 235–236 key points, 234 laboratory findings, 236 radiographs, 237 treatment and outcome, 237 Listeria monocytogenes heart transplant infection, 95 pediatric infection, 707–708, 708t Lithiasis cholelithiasis, 9–14 nephrolithiasis, 511, 1135–1138 sialolithiasis, 175–176 Lithium battery, 83 Lithium poisoning, 1017–1019 clinical presentation, chronic intoxication, 1018 definition, 1017 diagnosis, 1018 emergency actions, 1017
Index Lithium poisoning, (Continued) hypernatremia etiology involving, 359t key points, 1017 laboratory findings, CNS symptoms v. serum levels, 1018 pathology, 1017–1018 treatment, 1019 Liver function test (LFT), 271t. See also Hepatic impairment; Hepatitis cardiac tamponade requiring, 62 caustic ingestion requiring, 963 diverticulitis requiring, 125 heart transplant complications requiring, 94 lightning injuries requiring, 236 neonatal emergencies requiring, 668–669 Reye's syndrome requiring, 797 toxicology emergencies requiring, 927–928 Liver transplantation emergencies, 1156–1162, 1158t, 1160t, 1161t. See also Hepatic impairment; Hepatitis clinical presentation, 1159 complications of, 1161t definition, 1156 diagnosis, 1160 epidemiology, 1157 examination, 1159 immunosuppressive medications for, 1158t indications for, 1158t key points, 1156 laboratory findings, 1159–1160 organ rejection, 1156–1162, 1158t, 1160t, 1161t radiographs, 1160–1161 surgical procedure of, 1157 treatment, 1161–1162, 1161t drug interactions, 1161t LMA. See Laryngeal mask airway Local analgesics, 808–809 Lorazepam intubated patient sedation, 909t, 910 pediatric status epilepticus treatment, 787 Lower leg injuries, 638–642 anatomy, 638–639 clinical presentation and examination, 639 definition, 638 emergency actions, 638 key points, 638 laboratory findings, 639 pediatric, 642 radiographs, 639
1209
Lower leg injuries, (Continued) treatment Achilles tendon rupture, 641 compartment syndrome, 641 fibular fractures, 640 medial head of gastrocnemius muscle injury, 641 stress fractures, 640–641 tibial fractures, 640, 642 Lumbar puncture ataxia/dizziness/vertigo requiring, 418 headaches from, 434 heart transplant complications requiring, 94 pediatric seizures and status epilepticus, 786 Lung transplantation complications, 1150, 1151, 1154 organ rejection, 1150, 1151, 1154 Lyme disease, multiple sclerosis v., 442 Lymphadenopathy, exfoliative dermatitis causing, 101 Lymphoma, exfoliative dermatitis from, 100, 100b Macrolide, adult bacterial pneumonia, 867, 867t Magill forceps, for upper airway clearing, 662 Magnesium. See also Hypermagnesemia asthma treatment, 860 fluid and electrolyte emergencies, 377–380 measurement for toxicology emergencies, 927 Magnetic resonance imaging (MRI) ataxia, dizziness, vertigo, 418, 422 cholelithiasis and cholecystitis requiring, 13 gadolinium contrast, 442 headache, 432 hemorrhage, 487f hyperdense cerebral artery sign, 489f intracerebral hemorrhage, 487f ischemia, 491f ovarian torsion, 535 pulmonary embolism, 902, 905t subarachnoid hemorrhage, 488f Malaria, 295–300, 298t–299t, 300t, 1028 clinical presentation, 296 definition, 295 diagnosis, 297 emergency actions, 295 epidemiology, 295–296
1210 INDEX Malaria, (Continued) examination, 296 key points, 295 laboratory findings, 296–297 opioid injection risk of, 1028 prevention, 298t–299t treatment, 297, 300t–301t Male mammary gland development (gynecomastia), exfoliative dermatitis causing, 101 Male sex organs epididymitis, 1124–1126 penis disorders, 1127–1130 clinical presentation, 1128 definition, 1127–1128 emergency actions, 1127 epidemiology, 1128 examination, 1128 key points, 1127 laboratory findings and radiographic findings, 1129 penile fracture, 1128 treatment and outcomes, 1129–1130 prostate gland exfoliative dermatitis of, 101 prostatitis, 1131–1134 testicular torsion, 1139–1141 testosterone, 336 Malignancy. See also Cancer; Oncologic and hematologic emergencies; Tumor diverticulitis v., 126 exfoliative dermatitis from, 100, 100b hypercalcemia from, 373 insulinoma, 401 malignant external otitis, 170 mesenchymal tumors, 401 Mannitol arsine gas intoxication requiring, 943 pediatric diabetic emergency requiring, 774 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 Marine fauna envenomations, 238–242 clinical presentation and examination, 239–240 definition, 238 emergency actions, 238 epidemiology, 238–239 key points, 238 pathology, 239 treatment, 240–241 8 hours observation, 242 infection risk, 240–241
Marine fauna envenomations, (Continued) radiographs for sponge envenomation, 241 saltwater v. freshwater, 242 steroids contraindicated, 241 vinegar, 241 Mass lesion, headaches from, 434 Mastitis, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 504 ultrasound scanning, 503 Maxillofacial and dental emergencies dental, 154–158 trauma, 179–182 injuries, 158–161 ophthalmologic, 161–168 otolaryngological, 169–172 pharyngitis, 172–174 sialolithiasis, 175–176 sinusitis, 177–179 MBP. See Myelin basic protein MDI. See Metered dose inhaler MDMA. See Methylenedioxymethamphetamine Measles, toxic shock syndrome v., 548 Mechanical ventilation. See also Pulmonary emergencies asthma treatment, 223 disseminated intravascular coagulation, 348 emergency department basics for, 844–851 indications for, 844–845 types of, 845–851, 849t assist-control ventilation, 850 bilevel positive airway pressure, 848 continuous positive airway pressure as adjunct, 848 controlled mechanical ventilation, 850 expiratory positive airway pressure, 848 flow-cycle mode, 847 inspiratory positive airway pressure, 848 invasive positive-pressure ventilation, 849–851
Index Mechanical ventilation, (Continued) negative-pressure ventilation, 845–846 noninvasive positive-pressure ventilation, 847–848 positive-pressure ventilation, 91, 846–851 pressure support ventilation, 849–850, 849t pressure-cycled v. volume-cycled modes, 846–847, 849t Mechanical ventilator alarms, 882 complications, 882 monitoring, 877–881, 881t acronyms, 881t arterial blood gas, 877 equipment, 877 oxygenation, 877–878 patient positioning, 877 peak and plateau pressures, 878–881, 879t–880t PEEP and auto-PEEP, 846, 849t, 859–861, 881 ventilation, 878 settings, 872–876, 875t initiating, 872–875, 875t fraction of inspired oxygen, 873–874 inhalation/exhalation ratio, 874–875 positive end-expiratory pressure, 874 respiratory rate, 872–873 tidal volume, 849t, 873 special considerations, 875–876, 876t acute respiratory distress syndrome, 876 asthma exacerbation, 876 COPD exacerbation, 875–876 pregnancy, 876 Medical emergencies acid-base imbalances, 311–325 adrenal insufficiency, 331–338 alcoholic ketoacidosis, 338–343, 339f, 340f diabetic ketoacidosis, 343–347 disseminated intravascular coagulation, 348–350 ethyl alcohol withdrawal, 325–331 fluid and electrolyte, 351–393, 354t, 359t, 382t geriatric, 386–393 hyperthyroidism and thyroid storm, 394–398
1211
Medical emergencies, (Continued) hypoglycemia, 399–405 hypothyroidism and myxedema coma, 406–409 lactic acidosis, 410–414, 411t rhabdomyolysis, 414–417 seizures and status epilepticus, 465–472, 466t, 468t, 471t stroke syndromes, 473–496, 475f, 476f, 477f, 478f, 480f, 484t, 485t, 487f, 488f, 489f, 490f, 491f, 492f, 494t Medications hypoglycemia from, 403 multiple sclerosis v. toxicity from, 442 Meningitis, 706–713, 708t, 710t, 711t Bell's palsy v., 426–427, 426t definition of, 706, 707 erythema multiforme v., 98 heart transplant infection, 95 hypoglycemia from, 401 Neisseria meningitidis, pediatric infection, 707–708, 708t, 710t, 711t, 712–713 pediatric, 706–713, 708t, 710t, 711t Meningoencephalitis, stroke syndromes v., 484t Mental status hyperglycemic hyperosmolar nonketotic coma, 392–393 hypoglycemia, 404–405 lithium poisoning impairing, 1018–1019 monitoring of, for hypothyroidism and myxedema coma, 408–409 salicylates toxicity influencing, 1043 Meperidine hydrochloride, headache treatment, 437–438 Mercury poisoning, 1024–1026 clinical presentation, 1025 definition, 1023 diagnosis, 1025 emergency actions, 1023 epidemiology, 1023 key points, 1023 laboratory findings, 1025–1026 pathophysiology, 1024–1025 radiographic findings, 1026 treatment, 1026 Mesenchymal tumors, hypoglycemia from, 401 Mestinon, myasthenia gravis requiring, 450
1212 INDEX Metabolic acidosis, 315–317, 363, 1021, 1023. See also Anion gap alcoholic ketoacidosis causing, 1021 carbon monoxide poisoning causing, 1021 caustic ingestion causing, 964 clinical presentation and examination, 316 cyanide poisoning causing, 1021 definition, 315–316 epidemiology, 316 iron poisoning causing, 1021 isoniazid poisoning causing, 1021 laboratory findings, 317 methanol poisoning causing, 1021, 1023 MUDPILES mnemonic for causes of, 315 toluene poisoning causing, 1021 treatment and outcome, 317 uremia causing, 1021 Metabolic alkalosis, 311, 317–320 alkali administration, 318 clinical presentation, 318 contraction alkalosis, 318 definition, 317 epidemiology, 317–318 examination, 319 gastrointestinal Hþ loss, 318 intracellular shifts, 318 laboratory findings, 319 renal Hþ loss, 318 treatment, 319–320 saline-resistant alkalosis, 320 saline-responsive alkalosis, 319–320 Metabolic panel, iron toxicity requiring, 1008 Metered dose inhaler (MDI), 854 asthma treatment, 860, 862 Methanol poisoning, 1020–1023 clinical presentation, 1021 CT scan of head, 1022 definition, 1020 diagnosis, 1021 emergency actions, 1020 epidemiology, 1021 examination, 1021 key points, 1020 laboratory findings, 1021 treatment and outcome, 1022 Methemoglobinemia, caustic ingestion causing, 964 Methicillin-resistant Staphylococcus aureus (MRSA), 502
Methimazole, thyroid storm treatment, 397 Methohexital, airway management treatment, 915b Methotrexate, ectopic pregnancy treatment, 507–508 Methylenedioxymethamphetamine (MDMA), 353, 935–936 Methylprednisolone anaphylactic shock requiring, 921 multiple sclerosis treatment, 439 pediatric trauma medication, 1080 urticaria treatment, 112 Metoprolol, cardiac chest pain treatment, 74 MFAT. See Multifocal atrial tachycardia MG. See Myasthenia gravis MI. See Myocardial infarction Michaelis-Menton elimination (toxicology diagnostic), 924 Midazolam, intubated patient sedation, 909t, 910 Migraine headache, 431–432 stroke syndromes v., 484t treatment, 437–438 Miscarriage (abortion), 525–528 definition, 526 emergency actions, 525 epidemiology, 526 etiology, 526–527 examination, 527 key points, 525 laboratory findings, 527 treatment, 527–528 ultrasound scan, 527 Mitral valve prolapse (MVP) clinical presentation, 81 definition of, 80 diagnosis, 81 epidemiology, 80–81 key points, 80 laboratory and ancillary findings, 82 pathology, 81 physical examination, 81 treatment, 82 Mittelschmerz, 510 Molar pregnancy, 510 MONA. See Morphine-oxygennitroglycerin-aspirin Morphine caution for, 75 congestive heart failure treatment, 66–67 hydromorphone, 907t, 908 intubated patient analgesia, 906, 907t morphine-oxygen-nitroglycerin-aspirin, 73
Index Morphine, (Continued) pediatric trauma medication, 1080 tetralogy of Fallot requiring, 779 Morphine-oxygen-nitroglycerin-aspirin (MONA), cardiac chest pain treatment, 73 Motor examination, 455–456, 456t Mountain sickness, 184t, 185, 187t, 191 MRI. See Magnetic resonance imaging MRSA. See Methicillin-resistant Staphylococcus aureus MS. See Multiple sclerosis MUDPILES mnemonic, for causes of metabolic acidosis, 315 Multifocal atrial tachycardia (MFAT), 48–49, 48f Multiple myeloma, multiple sclerosis v., 442 Multiple sclerosis (MS), 438–447 Bell's palsy v., 426–427, 426t clinical presentation, 441 definition, 439 diagnosis and laboratory findings, 442–443 disseminated encephalomyelitis v., 442 emergency actions, 439 epidemiology, 439 examination, 441 key points, 438 myelin basic protein, 440 pathology, 439–440 relapsing-remitting, 443–444 risk factors, 440–441 treatment, 443–446 methylprednisolone, 439 Multiple trauma. See also Injury; Trauma challenges to treatment of, 1056 coma, Glasgow Coma Scale for, 1054, 1054t computed tomography for, 1052 focused abdominal sonography for, 1052 fractures, 1056 pregnant patient with, 1056 Multiple trauma requiring, blood transfusion for, 1055, 1055t Murphy's sign, 12 Musculoskeletal disorder, 511 MVP. See Mitral valve prolapse Myasthenia gravis (MG), 447–450 acetylcholine receptor site blockage, 447 Bell's palsy v., 426, 426t botulism v., 430 clinical presentation, 448–449 definition, 447
1213
Myasthenia gravis (MG), (Continued) diagnosis, 449–450 Tensilon test for, 449 emergency action, 447 epidemiology, 447 examination, 449 key points, 447 pathology, 448 treatment, 450 Mycoplasma species, chronic obstructive pulmonary disease from, 884 Myelin basic protein (MBP), 440 Myocardial infarction (MI). See also Ischemia clonidine overdose causing, 967–968 geriatric emergency, 388 shock, 920 zones of cerebral infarction and ischemia, 475f Myxedema coma, 406–409 Naloxone clonidine poisoning treatment, 965 opioid intoxication, 1030 pediatric analgesia and sedation reversal, 812–813 pharmacological shock requiring, 921 phenytoin toxicity treatment, 1037 Narcissistic personality disorder, 833–835 clinical presentation, 834 definition, 834 diagnosis, 834 epidemiology, 834 key points, 833 treatment and outcome, 834–835 Narcotics anesthesia after wound examination, 28 pharmacological shock from, 921 Nasogastric tube, intestinal obstruction requiring, 21 Nasopharyngeal airway device, airway equipment, 673–674 National Heart, Lung, and Blood Institute, pulmonary embolism epidemiology, 898 National Institute of Child Health and Human Development (NICHD), SIDS prevention, 766–769 National Institutes of Health (NIH) stroke severity scale, 485t Necrosis. See also Caustic ingestion emergency acute tubular, 1114 avascular, 612–614
1214 INDEX Necrosis, (Continued) femoral, 511 toxic epidermal necrolysis from burns, 103–106 ACLS for, 103 Negative-pressure ventilation, 845–846 Neisseria gonorrhoeae, epididymitis from, 1124–1126 Neisseria meningitidis, pediatric infection, 707–708, 708t Neomycin, otitis externa treatment, 170 Neonatal emergencies. See also Pediatric emergencies antibiotic dosages for, 666t clinical presentation, 665–667 definition, 665 emergency actions, 664–665 examination, 667 key points, 664 laboratory findings, 668–669 patent ductus arteriosus, 666–667 treatment, 669 vital signs, 667–668 Neonate. See also Neonatal emergencies definition of, 657 Neoplasm, 510 Nephrolithiasis, 511, 1135–1138. See also Kidneys; Renal disease Nesiritide, congestive heart failure treatment, 66–67 Neurological emergencies ataxia, dizziness, vertigo, 418–423 Bell's palsy, 423–428 botulism, 428–431 examination, 451–465, 451t, 452t, 454t, 456t, 458f, 459f, 463t headaches, 432–438 multiple sclerosis, 438–447 myasthenia gravis, 447–450 Neurological examination anatomical considerations, 452–453, 452t central nervous system anatomy and function, 452t Brudzinski sign, 464–465 cerebellar examination, 464 cerebellar ataxia, 464 dysmetria, 464 point-to-point test, 464 Romberg test, 464 cranial nerve examination, 456–462, 458f, 459f CN I (olfactory), 456 CN II (optic), 456
Neurological examination, (Continued) CN III, IV, VI (oculomotor, trochlear, abducens), 457–458, 458f functional layout of extraocular movements and innervations, 458f CN IX, X (glossopharyngeal and vagus), 461 CN V (trigeminal), 459–460, 459f sensory nerve branch divisions, 459f CN VII (facial), 460–461 CN VIII (vestibulocochlear), 461 CN XI (spinous accessory), 461–462 CN XII (hypoglossal), 462 deep tendon reflexes, 462–464, 463t scale for grading of, 463t global assessment, 453 Glasgow Coma Scale, 453, 454t indications for, 451, 451t Kernig sign, 464–465 motor examination, 455–456, 456t pediatric trauma, 1075–1077, 1076t adult v. child spinal cord, 1077 CT scan, 1077 head injury, 1076–1077 modified Glasgow Coma Scale, 1076t sensory function examination, 454–455 pain sensation, 455 vibration sense, 454–455 Neurologist consultation, head or spinal cord injury requiring, 1055 NHANES III. See Third National Health and Nutrition Examination Survey NICHD. See National Institute of Child Health and Human Development Nifedipine, hypertensive emergency treatment, 79–80 Nitrates, congestive heart failure treatment, 66–67 Nitrofurantoin, urinary tract infection treatment, 1145t Nitrogen narcosis, diving injury, 205 Nitroglycerin caution for, 75 congestive heart failure treatment, 66–67 headaches from, 434 Nitroprusside, congestive heart failure treatment, 66–67 Nocardia, heart transplant infection, 95 Noninvasive positive-pressure ventilation mechanical ventilation, 847–848
Index Nonpharmacological anxiolysis, pediatric analgesia and sedation, 807 Nonsteroidal anti-inflammatory drugs (NSAIDS), headache treatment, 114, 437–438 Norepinephrine. See also Epinephrine beta-blocker overdose treatment, 954 North American Society of Pacing and Electrophysiology, pacemaker circuitry types, 84, 85t Norwalk/Norwalk-like viruses, infectious disease emergency, 268t Nose bleed, 171–172 NSAIDS. See Nonsteroidal antiinflammatory drugs Oatmeal baths, toxicodendron dermatitis treatment, 108–109 Obesity, pulmonary embolism risk factor, 899 OB/GYN. See Obstetrics and gynecology Obsessive-compulsive personality disorder, 838–839 clinical presentation, 838 definition, 838 diagnosis, 839 epidemiology, 838 examination, 838 key points, 838 treatment and outcome, 839 Obstetrics and gynecology (OB/GYN). See also Female sex organs; Pregnancy abruptio placentae, 497–499, 510, 1108 amniotic fluid embolism, 500–502 breast abscesses and mastitis, 502–504 ectopic pregnancy, 505–509 emergent pelvic and abdominal pain, 509–512 fetal distress, 498 genital herpes, 279, 285, 513–515 hyperemesis gravidarum, 515–518 miscarriage (abortion), 525–528 ovarian cysts, 529–532 pelvic inflammatory disease, 536–540 placenta previa, 540–542 Obstructive sleep apnea, high-altitudeexacerbated illness, 184t Occult bacteremia, 707. See also Bacteremia Ocular herpes simplex virus, 275–276, 279, 285 Oculomotor nerve examination, 457–458, 458f Ogilvie's syndrome, 19
1215
Olfactory sense, cranial nerve examination, 456 Oncologic and hematologic emergencies. See also Cancer; Malignancy; Tumor acute bleeding diathesis, 555–558 blood transfusions, 559–565 hemophilia, 566–569 sickle cell anemia, 570–574 Operating room (OR), open fractures, 646 Ophthalmologic emergencies, 161–168. See also Eye clinical presentation, 162 definition, 162 diagnosis based on eye examination, 63 epidemiology, 162 examination, 162–163 key points, 162 ocular herpes simplex virus, 275–276, 279, 285 radiographs, 63 treatment, 163–168 blowout fractures, 168 blunt trauma, 167–168 cellulitis, 164 chemical injury, 167 conjunctivitis, 164 corneal abrasions, 166–167 corneal foreign bodies, 167 corneal ulcers, 164 glaucoma, 164–165 herpes keratitis, 164 hyphema, 168 ruptured globe, 168 subconjunctival hemorrhage, 167 ultraviolet keratitis, 167 vision loss (painless), 165 central retinal artery or vein occlusion, 165 detached retina, 166 giant cell arteritis, 166 optic neuritis, 166 temporal arteritis, 166 vitreous hemorrhage, 165–166 Opioids as analgesic for pulmonary embolism, 903 intoxication, 1027–1030 clinical presentation, 1028–1029 clonidine overdose mimicking, 967–968 definition, 1027 diagnosis, 1030 emergency actions, 1027
1216 INDEX Opioids, (Continued) epidemiology, 1028 examination, 1029 history taking, 1029 HIV/malaria/tetanus infection risk with, 1028 injection drug use complications with, 1028 key points, 1027 laboratory findings, 1029 pathology, 1028 treatment and disposition, 1030 Optic nerve. See also Eye; Ophthalmologic emergencies examination of, 456 neuritis emergency, 166 OR. See Operating room Oral contraceptives. See also Pregnancy headaches from, 434 pulmonary embolism risk factor, 899 Oral rehydration therapy (ORT), pediatric dehydration requiring, 694, 695, 697–699 Orbital cellulitis, 164 Organ rejection. See also Transplantation emergencies cardiac, 93–96, 1150, 1151, 1154 liver, 1156–1162, 1158t, 1160t, 1161t lung, 1150, 1151, 1154 renal, 1122–1123, 1158t, 1161t, 1163–1167 Organophosphorus and carbamate insecticides poisoning, 1130–1132 Oropharyngeal airway device, 673–674 Orthopedic emergencies acute compartment syndrome, 596–599 ankle injuries, 589–596 back pain, 577–582, 581t elbow injuries, 600–603 foot injuries, 604–608 forearm and wrist injuries, 608–616 hand injuries, 617–624 hip trauma, 625–630 infections of bones and joints, 631–637 knee pain, 583–588 lower leg injuries, 638–642 principles of, 575–577 examination, 576–577 shoulder injuries, 647–652 Osgood-Schlatter disease, pediatric lower leg injury, 642 Osteomyelitis, 631, 632–633, 636 definitions, 631
Osteomyelitis, (Continued) epidemiology, 632 pathology, 632–633 treatment, 636 Otitis externa, 170 Otitis media, 169–170, 798–802 barotrauma causing, 207 pediatric emergency, 798–802 clinical presentation, 800 complications of, 802 definition, 169–170, 799 diagnosis, 800 emergency actions, 798 epidemiology, 799 etiology, 799–800 examination, 800 key points, 798 laboratory findings, 800 treatment, 800–802 American Academy of Pediatrics guidelines on, 801 Otolaryngological emergencies, 169–172 definitions epistaxis, 171–172 hearing loss (sudden), 170–171 malignant external otitis, 170 otitis externa, 170 otitis media, 169–170, 798–802 emergency actions, 169 key points, 169 for diabetic patients, 169 laboratory findings, 172 radiographs, 172 Ovaries. See also Female sex organs abscess, 510 cysts, 510, 529–532 clinical presentation and examination, 530–531 definition, 529 diagnosis, 531 emergency actions, 529 key points, 529 laboratory findings, 531 pathophysiology, 529–530 treatment, 531–532 torsion, 532–535 clinical presentation, 533 definition, 532 diagnosis, 534 epidemiology, 533 examination, 533–534 key points, 532 laboratory findings, 534
Index Ovaries, (Continued) magnetic resonance imagining and CT scanning, 535 radiographs, 534–535 treatment, 535 Overdose. See Caustic ingestion emergency; Toxicology emergencies Oxygen carbon monoxide poisoning treatment, 960 saturation monitoring for pediatric airway compromise, 672 supplemental adrenal insufficiency treatment, 336 hyperglycemic hyperosmolar nonketotic coma, 392 iron toxicity requiring, 1009 mercury poisoning treatment, 1026 methanol poisoning treatment, 1022 monitoring of, during mechanical ventilation, 877–878 pneumothorax treatment, 894 pulmonary embolism treatment, 903 seizures and status epilepticus, 786 tetralogy of Fallot requiring, 779 toxicity, diving injury causing, 205 Pacemakers complications, 83–84, 85t chest radiograph identification, 84, 85t, 87 circuitry, 84, 85t clinical observation, 84, 86 definition, 83–84, 85t electrocardiography for, 86–87 emergency actions, 83 epidemiology, 84 examination, 86 five-letter pacemaker code, 84, 85t key points, 83 magnet rate, 84 treatment, 87–88 acute intervention, 88 types of, 84, 86–87 North American Society of Pacing and Electrophysiology circuitry types, 84, 85t permanent, 86–87 Packed red blood cells, as blood transfusion component, 560 PACs tachycardia. See Premature atrial contractions tachycardia Pain abdominal, 389, 509–512, 731–735
1217
Pain, (Continued) CT scan for, 512 geriatric, 389 abortion (miscarriage), 510 abruptio placentae, 510 abscess, ovarian, 510 adnexal torsion, 510 appendicitis, 510 arteriography, knee pain emergency requiring, 587 aspirin for, 74 back, 577–582, 581t cardiac chest, 74 chest evaluation of, 68–75, 71f, 72f fibrinolysis for, 74 morphine-oxygen-nitroglycerinaspirin for, 73 colitis, 510 diverticulitis, 510 dysmenorrhea, 510 endometriosis, 510 knee emergencies, 583–588 RICE therapy for, 587–588 molar pregnancy, 510 musculoskeletal disorder, 511 neoplasm, 510 nephrolithiasis, 511 obstetric and gynecological, 509–512 orthopedic emergencies, 577–582, 581t ovarian cysts, 510 pancreatitis, 511 pediatric abdominal, 731–735 patient's underestimation of pain, 806 pelvic, 731–735, 806 pelvic, 509–512, 731–735, 806 pelvic inflammatory disease, 510 pulmonary embolism, 511 pyelonephritis, 511 sensory function examination, 455 sickle cell anemia, 510 Pancreatitis, 144–148, 511 clinical presentation, 145–146 definition, 144 diagnosis, 147 epidemiology, 144–145 examination, 146 infectious agents, 145 key points, 144 laboratory findings, 146 medical treatment, 145 radiographs, 147 Reye's syndrome causing, 797
1218 INDEX Pancreatitis, (Continued) treatment and outcome, 147–148 Pancuronium, intubated patient sedation, 912 Panic disorder, 814–816. See also Generalized anxiety disorder asthma mimicked by, 857 clinical presentation, 816 definition, 814, 815–816 diagnosis, 816 emergency actions, 814 epidemiology, 814 examination, 816 key points, 814 laboratory findings, 816 radiographs, 816 treatment, 816 Paraldehyde poisoning, anion gap from, 1020 Paralytic shellfish poisoning, infectious disease emergency, 271t Paranoid personality disorder, 823–824 diagnosis/treatment/outcome, 824 epidemiology, 824 key points, 823 Paraphimosis, 1127–1128 Parathyroidism, 371 Parkland formula for burn treatment, 196, 196b Parotid tumor, Bell's palsy v., 426–427, 426t Paroxetine, panic disorder treatment, 816 Partial thromboplastin time (PTT) diabetic patient with otolaryngological emergency, 169 disseminated intravascular coagulation emergency, 350 iron toxicity requiring, 1009 pneumothorax diagnosis, 893 Patent ductus arteriosus (PDA), 666–667 PCI. See Percutaneous coronary intervention PCR. See Polymerase chain reaction PDA. See Patent ductus arteriosus PE. See Pulmonary embolism Peak expiratory flow rate (PEFR), 858, 859, 861–862 Pediatric analgesia and sedation, 805–813 definition complications, 807 equipment, 806–807 fasting/aspiration risk, 806 Joint Commission on Accreditation of Healthcare Organizations, 806
Pediatric analgesia and sedation, (Continued) monitoring, 807 qualified personnel, 807 subjectivity and underestimation of pain, 806 local, 808–809 local analgesics, 808–809 nonpharmacological anxiolysis, 807 reversal agents, 812–813 systemic, 809–812 analgesics, 811–812 combined analgesia and sedation, 812 sedatives, 809–811 topical analgesics, 808 Pediatric bacteremia, sepsis, and meningitis, 706–713, 708t, 710t, 711t clinical presentation, 708–709 definitions, 706–707 emergency actions, 706 epidemiology, 707–708 examination, 709 Haemophilus influenzae type b, 708, 708t, 712–713 key points, 706 laboratory findings, 710, 710t treatment meningitis, 711t, 712–713 occult bacteremia, 710–712, 711t sepsis, 711t, 712 Pediatric emergencies. See also Neonatal emergencies abdominal pain, 731–735 airway management, 670–678, 1073–1075, 1074t analgesia and sedation for, 805–813 approach to, 652–654 asthma, 714–724, 717t–719t bacteremia, sepsis, and meningitis, 706–713, 708t, 710t, 711t bronchiolitis, 725–728 cardiopulmonary arrest, 655–660 cardiopulmonary resuscitation, 656–664 child abuse, 758–765, 762f, 763f constipation, 736–740 CPR, 656, 657–659, 660, 661–664 dehydration, 694–699 diabetes and diabetic ketoacidosis, 770–774 diarrhea, 740–745 electrolyte and fluid management, 700–705
Index Pediatric emergencies, (Continued) Hirschsprung's disease (congenital aganglionic megacolon), 745–748, 748f Kawasaki disease, 792–795 neonatal, 664–669 otitis media, 798–802 overview of child development, 652 pharyngotonsillitis, 802–805 pneumonia, 728–731 pyloric stenosis, 749–753, 751f, 752f questions to ask, 653 Reye's syndrome, 795–798 rheumatic fever, 774–778 seizures and status epilepticus, 783–788 sudden death syndrome and lifethreatening event syndrome, 765–769 tetralogy of Fallot, 778–782, 781f, 782f trauma, 629, 1073–1080, 1074t, 1076t, 1079t, 1080t abdomen evaluation, 1078 airway management for, 1073–1075, 1074t blood pressure, 1074t cardiovascular management, 1075 chest evaluation, 1078 endotracheal tube size v. age, 1074t evaluation and stabilization, 1078–1079, 1079t vital signs, 1079t fluid resuscitation, 1074t hip dislocation, 629 induction and intubation, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t neurological evaluation, 1075–1077, 1076t adult v. child spinal cord, 1077 CT scan, 1077 head injury, 1076–1077 modified Glasgow Coma Scale, 1076t renal perfusion assessment, 1075 upper respiratory, 678–692 urinary tract infections, 753–757, 757t PEEP. See Positive end-expiratory pressure PEFR. See Peak expiratory flow rate Pelvic inflammatory disease (PID), 510, 536–540. See also Pelvis clinical presentation, 537–538 definition, 536
1219
Pelvic inflammatory disease (PID), (Continued) diagnosis, 538 emergency actions, 536 epidemiology, 536 key points, 536 laboratory findings, 538 pathology, 537 treatment, 538–539 inpatient therapy, 539 outpatient therapy, 539–540 Pelvis. See also Pelvic inflammatory disease anatomy of, 1081–1082 pain in, 509–512, 731–735, 806 clinical presentation, 511 definitions, 510–511 diagnosis, 512 emergency actions, 509–510 examination, 511 key points, 509 laboratory findings, 512 pediatric, 731–735, 806 ultrasound scanning, 512 pelvic inflammatory disease, 536–540 trauma to, 1081–1089 associated injuries, 1083 clinical diagnosis and presentation type I fractures, 1083–1085 type II fractures, 1085 type III fractures, 1085–1086 type IV fractures, 1086 definition and epidemiology, 1081 emergency actions, 1081 examination, 1087 key points, 1081 laboratory studies, 1088 mechanisms of injury, 1082–1083 radiographs, 1088 treatment, 1088–1189 Penicillin benzathine, as rheumatic fever treatment, 777 marine fauna envenomation requiring, 240–241 vasogenic shock requiring, 921 Penis disorders, 1127–1130. See also Male sex organs clinical presentation, 1128 definition, 1127–1128 emergency actions, 1127 epidemiology, 1128 examination, 1128 key points, 1127
1220 INDEX Penis disorders, (Continued) laboratory findings and radiographic findings, 1129 treatment and outcomes, 1129–1130 Peptic ulcer disease, 149–152 clinical presentation, 150 definition, 149 epidemiology, 150 examination, 150–151 key points, 149 laboratory findings, 151 radiographs, 152 treatment, 152 Percutaneous coronary intervention (PCI), cardiac chest pain treatment, 74 Pericarditis, acute, 37 clinical presentation, 38 diagnosis, 39 electrocardiographic findings, 38–39 emergency actions, 37 epidemiology, 37–38 examination, 38 key points, 37 laboratory findings, 39 radiographs, 39 treatment, 39 Peripheral nervous system anatomy and function, 452–453 edema of, as high-altitude-related illness, 184t Personality disorders, 822–839, 822t. See also Psychiatric emergencies classifications of, 822t definition, 822–823 treatment and outcome, 823 types of, 823–839 Peyronie's disease, 1127–1130 Pharyngitis, 172–174 acute pediatric rheumatic fever, 774–778 altitude-related emergencies, 190 definition, 172 diagnosis, 173 Centor criteria, 173 epidemiology, 172–173 group A beta-hemolytic streptococci causing, 173, 174 laboratory findings, 173 treatment, 174 Pharyngotonsillitis, 802–805 clinical presentation, 803–804 definition, 802 diagnosis, 804 emergency actions, 802
Pharyngotonsillitis, (Continued) epidemiology, 802 key points, 802 laboratory findings, 804 physical examination, 804 treatment, 804–805 Phenformin, wide anion gap from, 1021 Phenobarbital activated charcoal for overdose of, 951 pediatric status epilepticus treatment, 787 seizures and status epilepticus, 471t Phenylephrine, beta-blocker overdose treatment, 954 Phenytoin pediatric seizures and status epilepticus, 786 seizures and status epilepticus, 471t toxicity, 1034–1037 clinical presentation, 1035–1036 definition, 1034 diagnosis, 1036 emergency actions, 1034 epidemiology, 1034 key points, 1034 laboratory studies, 1036 pathophysiology, 1034–1035 pharmacokinetics, 1035 treatment, 1036–1037 Phimosis, 1127–1128 Phosphorus, fluid and electrolyte emergencies, 380–383. See also Hyperphosphatemia; Hypophosphatemia Physostigmine, anticholinesterase inhibitor, 942 PID. See Pelvic inflammatory disease Pilonidal disease clinical presentation, 117 cysts, 118 definition, 114 epidemiology, 115 pathology, 116 treatment and outcomes, 120 Placenta previa, 510, 540–542. See also Pregnancy definition, 541 diagnosis, 541–542 emergency actions, 540 epidemiology, 541 key points, 540 laboratory findings, 542 presentation, 541 radiographs, 542 treatment, 542
Index Platelets, as blood transfusion component, 560–561 Plavix, 169 international normalized ratio for, 169 Pneumocystis carinii pneumonia, heart transplant infection, 95 Pneumonia, 510; See also specific pathogens aspiration, 868–870 clinical presentation, 869 definition, 868 diagnosis, 870 epidemiology, 868 laboratory findings, 869 physical examination, 869 radiographs, 869 treatment, 870 bacterial, 863–867, 867t antibiotic therapy, 867, 867t asthma mimicked by, 857 clinical presentation, 865 community-acquired, 863, 864 definitions, 864 diagnosis, 865 disposition, 866–867 emergency actions, 863 epidemiology, 864 geriatric, 388 hospital-acquired, 863 key points, 863 laboratory findings, 866 pathophysiology, 864–865 Diplococcus pneumoniae, 884 pediatric, 728–731 clinical presentation, 729 definition, 729 diagnosis/treatment, 730–731 documentation by chest radiograph, 731 emergency actions, 728 epidemiology, 729 examination, 729–730 key points, 728 laboratory findings, 730 pneumocystis carinii, heart transplant infection, 95 respiratory acidosis from, 321 Streptococcus pneumoniae eye infection from, 164 pediatric infection, 707–708, 708t Pneumothorax, 891–896, 894f clinical presentation, 893 definition, 892 diagnosis, 893, 894f disposition, 896
1221
Pneumothorax, (Continued) emergency action, 892 iatrogenic, 892 key points, 891 laboratory findings, 893 radiograph, 893 spontaneous, 892 tension, 892 treatment goals, 894–896 catheter/needle aspiration, 895–896 tube thoracostomy, 895–896 Point-to-point test (cerebellar examination), 464 Poison ivy/poison oak, toxicodendron dermatitis, 106 Polymerase chain reaction (PCR), 271t Polymyxin B-hydrocortisone, otitis externa treatment, 170 POPS. See Pulmonary overpressurization syndrome Porphyria, arsenic poisoning v., 946 Positive end-expiratory pressure (PEEP), 846, 849t, 881 ARDS treatment, 859–861 ventilator setting, 874 Positive-pressure ventilation, 846–851 primary prosthetic valve failure requiring, 91 Postictal Todd's paralysis, stroke syndromes v., 484t Postmortem cesarean section, 1111 Potassium fluid and electrolyte emergencies, 361–369 hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 intracellular shifts in, 362 pediatric diabetes treatment, 773–774 replacement of, diabetic ketoacidosis requiring, 347 Pralidoxime, insecticides poisoning antidote, 1033 Prednisone myasthenia gravis requiring, 450 toxicodendron dermatitis treatment, 108–109 Preeclampsia and eclampsia, 510, 519–525. See also Pregnancy HELLP syndrome, 523 hypoglycemic emergency with, 401 treatment, 522–523
1222 INDEX Pregnancy. See also Abortion (miscarriage); Obstetrics and gynecology; Oral contraceptives abruptio placentae, 497–499, 510, 1108 amniotic fluid embolism, 500–502 fetal distress, 498 hyperemesis gravidarum, 515–518 hypertension, 521 hypoglycemic emergency with, 401 mechanical ventilation during, 876 miscarriage, 525–528 multiple trauma during, 1056 physiology of, 1106–1108 placenta previa, 510, 540–542 preeclampsia and eclampsia, 401, 510, 519–525 preterm labor, 510 prevention of, post sexual assault, 545 traumatic injury during, 1105–1111 clinical presentation, 1109 definition, 1105 emergency actions, 1105 epidemiology, 1106 examination and treatment, 1109–1110 fetal distress, 1108 key points, 1105 laboratory findings, 1110 maternal-fetal hemorrhage, 1108–1109 placental abruption, 1108 postmortem cesarean section, 1111 radiographs, 1110–1111 urinary tract infection during, 1145–1146, 1145t Pregnancy test, diverticulitis requiring, 125 Premature atrial contractions (PACs) tachycardia, 46, 46f Premature ventricular contractions (PVCs) tachycardia, 46, 47f Pressure support ventilation (PSV), 849–851, 849t Preterm labor, 510 Priapism, 1127–1128 Primidone, seizures and status epilepticus, 471t Prochlorperazine, headache treatment, 437–438 Proctalgia fugax, 114–115 Propofol, intubated patient sedation, 909t, 910 Propranolol, thyroid storm treatment, 398
Prostate gland. See also Male sex organs exfoliative dermatitis causing enlargement of, 101 prostatitis, 1131–1134 clinical presentation, 1132 definition, 1131 diagnosis, 1132–1133 emergency actions, 1131 epidemiology, 1131 examination, 1132 key points, 1131 laboratory findings, 1132 pathology, 1132 radiographs, 1133 treatment, 1133–1134 Prosthetic heart valve dysfunction, 89–92, 91b clinical presentation, 90 definition, 89–90 diagnosis, 90–91, 91b epidemiology, 90 examination, 90 laboratory findings, 90 radiographs for, 91 treatment, 91–92 Prothrombin time (PT) measurement, 350. See also Embolism iron toxicity requiring, 1009 pulmonary embolism diagnostic, 901 salicylates toxicity, 1041 shock diagnostic, 919 Pruritus ani clinical presentation, 117 definition, 115 examination, 119 pathology, 116 treatment and outcomes, 120–121 Pseudoaneurysm, 1 Pseudohyperkalemia, 366 Pseudohypoparathyroidism, 371 Pseudotumor cerebri, headaches from, 434, 435 PSV. See Pressure support ventilation Psychiatric emergencies, 814–844. See also Suicide American Psychiatric Association, 815 conversion disorder, 819–821 generalized anxiety disorder, 817–819 geriatric, 389 panic disorder, 814–816 personality disorders, 822–839, 822t antisocial personality disorder, 828–829
Index Psychiatric emergencies, (Continued) avoidant personality disorder, 835–836 borderline personality disorder, 830–831 dependent personality disorder, 836–838 histrionic personality disorder, 832–833 narcissistic personality disorder, 833–835 obsessive-compulsive personality disorder, 838–839 paranoid personality disorder, 823–824 schizoid personality disorder, 825–826 schizotypal personality disorder, 826–828 suicide, 840–843 PT. See Prothrombin time PTT. See Partial thromboplastin time Pulmonary edema, 184t, 186, 187t beta-blocker overdose diagnostic, 954 treatment, 189–190 Pulmonary embolism (PE), 897–905, 904f, 905t cardiac arrhythmia from, 56, 56f clinical presentation, 898–899 definition, 898 diagnosis, 902–903 likelihood ratio, 905t stepwise approach to, 903, 904f emergency actions, 897–898 epidemiology, 898 key points, 897 laboratory findings, D-Dimer testing, 901, 905t National Heart, Lung, and Blood Institute on, 898 pelvic and abdominal pain from, 511 risk factors, 899–901 clinical gestalt, 899 Geneva criteria, 900–901, 900t laboratory findings, 901 arterial blood gas analysis, 901 ELISA and immuno-turbidimetric assays, 902 prothrombin time/activated PTT, 901 radiographs, 902 Wells criteria, 899–900, 900t tachycardia from, 899 treatment, 903, 905
1223
Pulmonary emergencies, 844–913. See also Mechanical ventilation acute respiratory distress syndrome, 852–854 asthma, 854–862 chronic obstructive pulmonary disease, 883–887 hemoptysis, 888–891 pneumothorax, 891–896, 894f pulmonary embolism, 897–905 905t, 904f pulmonary overpressurization syndrome, 206 sedation and analgesia for intubated patient, 906–913 ventilator management in ED, 844–851 Pulmonary overpressurization syndrome (POPS), 206 Pulmonary wedge pressure, ARDS influencing, 853 Pulse generator, 83 PVCs tachycardia. See Premature ventricular contractions Pyelonephritis, 511 urinary tract infection with, 1146 Pyloric stenosis, pediatric, 749–753, 751f, 752f clinical presentation, 750 definition, 749 diagnosis, 751 emergency actions, 749 epidemiology, 749–750 examination, 750 key points, 749 laboratory findings, 751 radiographs, 751–752, 751f, 752f “should sign” created by barium collection, 752f sonogram, 751f QRS voltage on electrocardiogram, heart transplant rejection causing, 95 Rabies viral infection, 301–306 clinical presentation, 302–303 definitions, 301 diagnosis, 304 emergency actions, 301 epidemiology, 301–302 examination, 303 key points, 301 laboratory findings, 303 pathology, 302
1224 INDEX Rabies viral infection, (Continued) quarantine, 304–305 radiographs, 304 treatment and outcomes, 304 Racemic epinephrine, pediatric trauma medication, 1080 Radiation, hypercalcemia requiring, 377 Radiopaque markers, permanent pacemaker, 84 Rapid sequence intubation (RSI), 672, 674–677. See also Airway management Rapid ventricular response (RVR), 49 Rectal prolapse clinical presentation, 117 definition, 115 examination, 118 pathology, 116 treatment, 120 Red blood cells bilirubin formation from, 136 as blood transfusion component, 560 Red eye, 164 RED MAN mnemonic, exfoliative dermatitis pathology identification, 100, 100b Rehydration adrenal insufficiency treatment, 337 appendicitis requiring, 8 hernia requiring, 18 salicylates toxicity treatment, 1042 Relapsing-remitting multiple sclerosis (RRMS), 443–444 Renal disease. See also Acute renal failure; Kidneys; Renal stones; Renal transplantation emergency end-stage renal disease, 1117–1123 hypoglycemia from, 402 rhabdomyolysis from, 414–417 Renal failure, 1113–1117. See also Endstage renal disease; Kidneys anti-inflammatory drugs causing, 1114 caustic ingestion causing, 964 clinical presentation, 1115 acute tubular necrosis, 1114 definition, 1113 diagnosis, 1116 emergency actions, 1113 glomerular filtration rate, 1113–1117 key points, 1113 laboratory findings, 1116 lithium poisoning causing, 1018–1019 pathology, 1113–1115 physical examination, 1115
Renal failure, (Continued) radiography, 1115 treatment, 1116–1117 Renal stones, 1135–1138. See also Renal disease clinical presentation, 1136 definition, 1135 diagnosis, 1137 emergency actions, 1135 epidemiology, 1135–1136 examination, 1136–1137 HIV-infected patients with, 1135, 1137 key points, 1135 laboratory findings, 1137 radiographs, 1137 Renal transplantation emergency, 1122–1123, 1158t, 1160t, 1161t, 1163–1167. See also End-stage renal disease; Kidneys clinical presentation, 1164–1165 definition, 1163 diagnosis, 1166 emergency actions, 1163 epidemiology, 1164 examination, 1165 immunosuppressive medications for, 1158t key points, 1163 laboratory findings, 1165–1166 radiographs, 1166 treatment, 1166–1167 drug interactions, 1161t Respiratory acidosis, 312, 320–322, 845 clinical presentation, 320–321 definition of, 320, 845 delirium from, 320 diagnosis, 321–322 epidemiology, 320 examination, 321 laboratory findings, 321 treatment and outcome, 321 Respiratory alkalosis, 321–323 clinical presentation and examination, 321–322 definition, 321 diagnosis, 323 etiology, 321 laboratory findings, 323 treatment and outcome, 323 Respiratory distress syndrome, 852–854. See also Chronic obstructive pulmonary disease clinical presentation, 852–853 definition, 852
Index Respiratory distress syndrome, (Continued) diagnosis, 853 emergency actions, 852 epidemiology, 852 examination, 853 key points, 852 laboratory findings, 853 treatment, 853–854 Respiratory failure, Reye's syndrome causing, 797 Respiratory system, theophylline overdose influencing, 1046 Rest, intestinal obstruction requiring, 21 Resuscitation emergencies. See also Cardiopulmonary resuscitation airway management, 913–916, 914b, 915b pediatric, 1073–1075, 1074t shock, 917–921 Retinal artery occlusion, 165 Reye's syndrome, 795–798 clinical presentation and examination, 796–797 diagnosis, 797 emergency actions, 796 epidemiology, 796 imaging findings, 797 key points, 798 laboratory findings, 797 pathology, 796 treatment, 797–798 intracranial pressure, 797–798 Rhabdomyolysis, 414–417 clinical presentation, 415 definition, 414 diagnosis, 416 emergency actions, 414 epidemiology, 414–415 examination, 415 key points, 414 laboratory findings, 415–416 treatment, 416–417 Rheumatic fever, 774–778 clinical presentation, 775 definition, 775 diagnosis, 775 antecedent GAS infection evidence, 777 Jones criteria for, 775–777 epidemiology, 775 key points, 774 laboratory findings, 777
1225
Rheumatic fever, (Continued) pathology, 775 treatment, 777 Rheumatoid factor analysis, knee pain emergency, 587 RICE therapy, knee pain treatment, 587–588 Rickets (vitamin D deficiency), hypocalcemia, 371 Rocky Mountain spotted fever erythema multiforme v., 98 toxic shock syndrome v., 548 Roentgenogram, tetralogy of Fallot, 782 Romberg test, 464 cerebellar examination including, 464 Rotavirus, infectious disease emergency, 268t RSI. See Rapid sequence intubation Rule of Nines assessment for burns, 194f Rumack-Matthew acetaminophen overdose nomogram, 933–935, 934f RVR. See Rapid ventricular response SADPERSONS scale, 842t Salicylate toxicity, 1038–1043 clinical presentation, 1040 definition, 1038 diagnosis, 1041 emergency actions, 1038 epidemiology, 1038–1039 hypoglycemia from, 403 key points, 1038 laboratory findings, 1040–1041 pathology, 1039–1040 radiography, 1041 treatment, 1042–1043 altered mental status, 1043 gastric lavage, 1042 hemodialysis, 1042 hemorrhagic complications with, 1043 hospital admission, 1043 peritoneal dialysis, 1043 rehydration, 1042 sodium bicarbonate, 1042 wide anion gap from, 1021 Saline solution hypercalcemia requiring, 376 hyperglycemic hyperosmolar nonketotic coma requiring, 390 rhabdomyolysis treatment, 416–417 -washed blood products, 562 wound irrigation with, 30
1226 INDEX Salmonella diarrhea from, 744t, 745 non-typhoid v. typhoid, 266t Sandimmune, myasthenia gravis requiring, 450 Sarcoidosis asthma mimicked by, 857 Bell's palsy v., 426–427, 426t multiple sclerosis v., 442 SBI. See Serious bacterial infection SCCM. See Society for Critical Care Medicine Schizoid personality disorder, 825–826 Schizotypal personality disorder, 826–828 clinical presentation, 827 definition, 826 diagnosis, 827 epidemiology, 827 key points, 826 treatment and outcome, 827–828 Scombroid poisoning, infectious disease emergency, 271t Scorpion sting, 256, 257, 259 Second-degree atrioventricular bradycardia type I, 52, 52f type II, 52–53, 53f Sedation intubated patient, 906, 908–913, 909t analgesics with, 906–908, 907t, 912–913 conclusion, 912 delirium, 910–911 dosages/durations/advantages, 909t last resort paralytics, 911–912 lorazepam, 909t, 910 midazolam, 909t, 910 propofol, 909t, 910 pediatric, 805–813 toxicology emergencies requiring, 929 Seizures and status epilepticus, 465–472, 466t, 468t, 471t amphetamine overdose causing, 938 antiepileptic drugs for, 466t, 471–472, 471t arsenic poisoning causing, 946 beta-blocker overdose sign, 953 clinical presentation, 467–469 clonidine overdose causing, 967–968 CT scan for, 469 cyclic antidepressant toxicity, 982 definitions, 466–467 EEG for, 470 emergency actions, 466 epidemiology, 467
Seizures and status epilepticus, (Continued) key points, 465 laboratory findings, 470 pathology, 467 pediatric, 783–788 clinical presentation, 785–786 definitions, 783–784 diagnosis, 786 emergency actions, 783 epidemiology, 784 examination, 786 febrile, 785, 789–792 definition, 789 emergency actions, 789 epidemiology, 789 key points, 789 laboratory findings, 790 pathology, 790 treatment, 790–792 key points, 783 laboratory findings, 786 pathology, 784–785 age-related, 784–785 metabolic-related, 785 treatment, 786–788 adverse effects of medications, 788 anticonvulsants, 786 oxygen, 786 post-trauma, 786–787 predisposing factors for, 468t theophylline overdose causing, 1046, 1047 treatment, 470–472, 471t antiepileptic drugs, 471t Selective serotonin reuptake inhibitors (SSRIs), panic disorder treatment, 816 Sensory function examination, 454–455 pain sensation, 455 vibration sense, 454–455 Sepsis, 706–712, 708t, 710t, 711t. See also Infections; Infectious disease emergencies definition, 706, 707 hypoglycemia from, 401 pediatric, 706–713, 708t, 710t, 711t Septic arthritis, 630, 632, 633, 637 definitions, 630, 632 epidemiology, 632 pathology, 633 treatment, 637
Index Septic shock, 413, 707 Serious bacterial infection (SBI), 706–713, 708t, 710t, 711t Sertraline, panic disorder treatment, 816 Serum acetaminophen, toxicity evaluation, 931 Serum electrolyte measurement, toxicology emergencies, 927–928 Serum glucose, hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 Serum glutamate oxaloacetate transaminase (SGOT), 548 Serum glutamate pyruvate transaminase (SGPT), 548 Serum iron test, iron toxicity requiring, 1009 Serum ketones absence of, 390–393 hyperglycemic hyperosmolar nonketotic coma, 392 Sexual assault, 543–545 definition, 543 emergency actions, 543 epidemiology, 543 examination, 543–544 key points, 543 laboratory findings, 544 treatment, 544–545 pregnancy prevention, 545 Sexually transmitted disease (STD), 544. See also Human immunodeficiency virus infection genital herpes, 279, 285, 513–515 syphilis erythema multiforme v., 98 multiple sclerosis v., 442 treatment, 554 Sézary cells, exfoliative dermatitis associated with, 101 SGOT. See Serum glutamate oxaloacetate transaminase SGPT. See Serum glutamate pyruvate transaminase Shigella diarrhea from, 744t, 745 infectious disease emergency, 267t Shingles, 276, 277–278, 280–281, 283, 287 treatment, 287 Shock, 917–921 beta-blocker overdose causing, 953 clinical presentation anaphylactic, 919 treatment, 920
1227
Shock, (Continued) dysrhythmia, treatment, 920 hemorrhage, 920 hypovolemic (nontraumatic), 917–918 treatment, 920 myocardial infarction, treatment, 920 neurogenic, 919 treatment, 921 pharmacological, 919 treatment, 920 traumatic cardiogenic, 918 treatment dobutamine, 920 dopamine, 920 goals, 920 pericardiocentesis, 920 thoracotomy, 920 vasogenic, 919 treatment, 921 definition, 917 laboratory findings, 919 pathology, 917 treatment, 919–921 Shoulder injuries, 647–651 anatomy, 647–648 clinical presentation acromioclavicular joint injuries, 650 clavicle fractures, 648 humoral shaft fractures, 649 proximal humerus fractures, 649 rotator cuff tears, 651 scapular fractures, 649 shoulder dislocations, 650–651 sternoclavicular joint injuries, 649–650 definition, 647 emergency actions, 647 key points, 647 laboratory findings, 648 radiographs, 648 SIADH. See Syndrome of inappropriate antidiuretic hormone Sialolithiasis, 175–176 definition, 175 emergency actions, 175 examination, 176 key points, 175 treatment, 176 Sickle cell anemia, 570–574 clinical presentation, 571–572 definition, 570 diagnosis, 573 emergency actions, 570
1228 INDEX Sickle cell anemia, (Continued) examination, 572 high-altitude-exacerbated illness, 184t key points, 570 laboratory findings, 572–573 pain from, 510 pathology, 570–571 treatment, 573 SIDS. See Sudden death syndrome Sigmoidoscopy, diverticulosis requiring, 127 SIMV. See Synchronized intermittent mandatory ventilation Sinus bradycardia, 52, 52f Sinus tachycardia, 46 Sinusitis, 177–179 clinical presentation, 178 definition, 177 emergency actions, 177 epidemiology, 177 key points, 177 treatment, 178–179 Sitz bath, genital herpes treatment, 515 Skeletal emergency, end-stage renal disease causing, 1121–1122 Skin biopsy, exfoliative dermatitis requiring, 101 hypernatremia etiology involving, 359t tape, wound closure option, 30 Sleep disorders high altitude-related, 191 obstructive sleep apnea, 184t SLUDGe mnemonic, insecticide poisoning signs, 1131 Snakebite, 249–254 clinical presentation, 251 definition, 249–250 diagnosis, 252 emergency actions, 249 epidemiology, 250 examination, 251–252 key point, 249 laboratory findings, 252 pathology, 250–251 treatment, 252–254 antivenom, 253, 254 coral snake, 253, 254 limb elevation, 253 pertinent history taking for, 253 tetanus immunization, 253 Society for Critical Care Medicine (SCCM), analgesia and sedation for intubated patient (over 12 years old), 906
Sodium, 351–361, 354t, 359t fluid and electrolyte emergencies, 351–361, 354t, 359t intake, hypernatremia from, 359t Sodium bicarbonate cyclic antidepressant toxicity treatment, 983–984 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 salicylates toxicity treatment, 1042 tetralogy of Fallot requiring, 779 Soffer and Hamburger's criteria for alcoholic ketoacidosis, 342 Solu-Medrol, urticaria treatment, 112 Somogyi, hypoglycemia from, 401 Sorbitol, theophylline toxicity treatment, 1048 Spider bites and scorpion stings, 255–260 clinical presentation black widow spider, 257–258 brown recluse spider, 258 scorpion, 257 definitions, 255–256 diagnosis, 258 emergency actions, 255 epidemiology black widow spider, 256–257 brown recluse spider, 256 scorpion, 256 examination, 258 key points, 255 laboratory findings, 258 tarantula spiders, 260 treatment and outcome black widow spider, 259 brown recluse spider, 259–260 scorpion, 259 Spinal cord injuries, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095. See also Trauma clinical presentation, 1091–1093 definition, 1090 diagnosis, 1094 emergency actions, 1090 epidemiology, 1091 examination, 1093 key points, 1090 laboratory findings, 1093 multiple, 1055 radiographs, 1094 treatment, 1094–1095 Spinous accessory nerve examination, 461–462
Index Splenomegaly, exfoliative dermatitis causing, 101 SSRIs. See Selective serotonin reuptake inhibitors St. Vitus' dance, acute rheumatic fever causing, 776 Stanford classification of thoracic aortic dissection, 23 Staphylococcal TSS (STSS), toxic shock syndrome from, 545–549 Staphylococcus aureus, 267t AICD infection, 42 balanoposthitis from, 1127–1128 breast abscesses from, 502 eye infection, 163 infectious disease emergency, 267t methicillin-resistant, 502 Staphylococcus epidermidis, AICD infection, 42 Staples, wound closure option, 30 STD. See Sexually transmitted disease Steroids contraindicated for marine fauna envenomations, 241 cortico-, asthma treatment, 721–724 non-steroidal anti-inflammatory drugs, 437–438, 1114 toxicodendron dermatitis treatment, 108–109 STIC pressure monitor, acute compartment syndrome diagnosis, 599 Stool cultures foodborne and waterborne illness diagnosis, 272 heart transplant complications requiring, 94 softeners, anorectal disorders treatment, 120 Strangulated hernias, 16, 17 Streptococcal infection group A acute pediatric rheumatic fever from, 774–778 beta-hemolytic, 173, 174, 802–805 pneumoniae eye infection from, 164 pediatric infection, 707–708, 708t Working Group on Severe Streptococcal Infection, 548 Stroke syndromes. See also Embolism Bell's palsy v., 484t definition, 473
1229
Stroke syndromes, (Continued) diagnosis, 486–489, 487f, 488f, 489f, 490f, 491f, 492f gray-white matter loss, 488, 490f hemorrhagic v. nonhemorrhagic, 484t, 486–489, 487f, 488f, 489f, 490f, 491f, 492f hypoattenuation in middle cerebral artery, 488 hypodensity or ischemia, 488, 491f intracerebral hemorrhage, 487f subarachnoid hemorrhage, 486, 488f sulcal effacement in middle cerebral artery, 488, 492f differential diagnosis, 484t epidemiology, 473–494 laboratory findings, 485–486, 485t NIH stroke severity scale, 485t pathophysiology, 474–479, 475f, 476f, 477f, 478f arterial circle of Willis, 477, 477f brain control centers, 480f collateral blood flow to ischemic penumbra, 476f extracranial sources of thromboemboli, 478f homunculus distribution of innervation on parietal cortex, 480f zones of cerebral infarction and ischemia, 475f physical examination, 483–485, 484t risk factors for, 474 treatment, 490–496 tissue plasminogen activator, 494t STSS. See Staphylococcal TSS Subarachnoid hemorrhage (SAH). See also Hemorrhage headache indicative of, 432 headaches from, 434 Hunt and Hess Clinical Grading Scale for, 496 MRI of, 488f radiology for, 437 Submersion incidents, 207, 242–248, 246t ataxia, dizziness from, 207 clinical presentation, 245 definitions, 243 diagnosis, 246 emergency actions, 243 epidemiology, 243–244 key points, 242 laboratory findings, 245
1230 INDEX Submersion incidents, (Continued) pathophysiology, 244 physical examination, 245 radiographs, 246 treatment and outcome, 246–248, 246t Succinylcholine airway management pretreatment, 914b airway management treatment, 915b Sudden death syndrome (SIDS), 765–769 clinical presentation, 767 definitions, 766 diagnosis, 768 emergency actions, 765–766 epidemiology, 766–767 examination, 768 key points, 765 laboratory findings, 768 NICHD's recommendations, 769 pathology, 767 radiographs, 768 treatment, 768–769 Sudden hearing loss, 170–171 Suicide, 840–843. See also Psychiatric emergencies clinical presentation, 841 definition, 840 diagnosis, 841–842 SADPERSONS scale, 842t emergency actions, 840 epidemiology, 841 key points, 840 laboratory findings, 841 radiographs, 842 treatment, 842–843 Sulfonylureas, hypoglycemia from, 401 Sumac, toxicodendron dermatitis from, 106 Sunburn, exfoliative dermatitis from, 100, 100b Supraventricular tachycardia (SVT), 47–48, 47f, 48f AICD causing, 43 Surgery, hypercalcemia requiring, 377 Surgilope lubricating jelly, 204 Sutures removal of, 35, 36t wound closure, 30–34, 31t, 32t, 33f–34f SVR. See Systemic vascular resistance SVT. See Supraventricular tachycardia Sweating, hypernatremia etiology involving, 359t Sydenham's chorea, acute rheumatic fever causing, 776
Synchronized intermittent mandatory ventilation (SIMV), 847, 849t, 850–851 Syncope ataxia, dizziness, vertigo and, 418 heat, 221, 224 pulmonary embolism causing, 899 Syndrome of inappropriate antidiuretic hormone (SIADH), 353 Synovial fluid analysis knee pain emergency, 587 septic arthritis diagnostic, 637 Syphilis. See also Sexually transmitted disease erythema multiforme v., 98 tertiary, multiple sclerosis v., 442 Systemic analgesia and sedation, 809–812 Systemic lupus erythematosus (SLE), 889–890 multiple sclerosis v., 442 Systemic vascular resistance (SVR), clinical presentation, 779–780 Tachycardia, 46–49, 46f, 47f, 48f ARDS causing, 859–861 exfoliative dermatitis causing, 101 pediatric, 658–659, 659–660 pulmonary embolism causing, 899 supraventricular, 50, 50f AICD causing, 40, 43 Tachypnea ARDS causing, 859–861 pulmonary embolism causing, 899 TAI. See Traumatic aortic injury Tamponade. See Cardiac tamponade TEE. See Transesophageal echocardiography Teeth. See Dental emergencies; Dental trauma Telemetry unit observation, AICD malfunction requiring, 43 Temporal arteritis, ophthalmologic emergencies, 166 TEN. See Toxic epidermal necrolysis Tendons. See also Forearm and wrist injuries Achilles tendon rupture, 641 ankle tendon rupture/dissociation/tear, 592–593 deep tendon reflexes, 462–464, 463t scale for grading of, 463t hand injuries, 622 tendonitis, 615
Index Tensilon test, myasthenia gravis diagnostic, 449 Tension pneumothorax, cardiopulmonary arrest from, 664 Terbutaline, asthma treatment, 722 Testicles epididymitis, 1124–1126 torsion of, 1139–1141 clinical presentation, 1139 definition, 1139 diagnosis, 1140 emergency actions, 1139 epidemiology, 1139 examination, 1140 key points, 1139 laboratory findings, 1140 radiographs, 1140 treatment, 1141 Testosterone, depot-, 336 Tetanus, 307–310, 1028 clinical presentation, 308–309 definition, 307 diagnosis, 309–310 emergency actions, 307 epidemiology, 307 etiology, 308 immunization for snakebite, 253 wound management, 35 for wound management, 35 key points, 307 laboratory findings, 309 opioid injection risk of, 1028 pathophysiology, 308 treatment, 310 Tetracycline, adult bacterial pneumonia, 867, 867t Tetralogy of Fallot, 778–782, 781f, 782f clinical presentation, 779–780 definition, 779 diagnosis, 780 emergency actions, 779 epidemiology, 779 examination, 780 key points, 778 laboratory findings, 780 radiographs, 780, 781f, 782f treatment, 781–782 Tetrodotoxin fish poisoning, infectious disease emergency, 271t Thallium poisoning, arsenic poisoning v., 946 Theophylline overdose, 1044–1049 clinical presentation, 1045
1231
Theophylline overdose, (Continued) definition, 1044–1045 diagnosis, 1047 emergency actions, 1044 emesis from, 1048 epidemiology, 1045 examination cardiovascular, 1045–1046 gastrointestinal, 1046 respiratory system, 1046 seizures, 1046 hyperglycemia from, 1047 hypokalemia from, 1046, 1048 intentional, 1047 key points, 1044 laboratory findings, 1046 liver function impairment, 1047 pediatric seizures and status epilepticus, 786 radiographs, 1047 serum levels, 1047 treatment “ABC” care, 1047 cardiac and respiratory stabilization, 1047 electrolyte disturbances, 1048 seizures, 1047 Thiamin, ethanol withdrawal requiring, 330–331 Thiopental, airway management treatment, 915b Third National Health and Nutrition Examination Survey (NHANES III). See also Diet lead poisoning, 1014 Third-degree atrioventricular bradycardia type II, 53, 53f Thorax American Thoracic Society, 883–884 thoracic aortic dissection, 22–26 classification of, 23 clinical presentation, 24 definition of, 22–23 diagnosis, 22–26, 25 emergency actions, 22 epidemiology, 23 examination, 24 key points, 22 laboratory findings, 24 radiograph, 25 Stanford classification, 23 transesophageal echocardiography for, 25 treatment and outcome, 25–26
1232 INDEX Thorax, (Continued) thoracotomy, 920 trauma to, 1095–1104 al presentation, 1096 clinical presentation and examination, 1096–1097 definition, 1096 emergency actions, 1096 emergency department resuscitation thoracotomy, 1101 key points, 1095 life-threatening injuries, 1100 airway obstruction, 1097 cardiac tamponade, 1099–1100 FAST examination, 1100 flail chest and pulmonary contusion, 1098–1099 massive hemothorax, 1099 open pneumothorax, 1097 tension pneumothorax, 1097–1098 potentially life-threatening injuries aortic disruption and penetrating injury, 1102–1103 blunt cardiac injury, 1103 esophageal, 1104 hemothorax, 1102 simple pneumothorax, 1101–1102 tracheobronchial injury, 1102 traumatic diaphragmatic injury, 1103–1104 tube thoracostomy, 895–896 Thromboembolism. See also Embolism; Stroke syndromes cardiopulmonary arrest from, 664 extracranial sources of, 478f thrombolytic agents for, 904 Thrombolytic agents. See also Embolism prosthetic heart valve dysfunction requiring, 91–92 pulmonary embolism treatment, 904 Thyroid glands, exfoliative dermatitis causing enlargement of, 101 TIAs. See Transient ischemic attacks Tibial tuberosity fractures, 642 Tidal volume (Vt), 849t, 873 Tissue adhesives, wound closure option, 30 Tissue plasminogen activator (tPA), 494t TMP/SMX. See Trimethoprimsulfamethoxazole Toluene poisoning, metabolic acidosis from, 1021
“Tooth squeeze” barotrauma, 207 Topical analgesics, 808 Topiramate, seizures and status epilepticus, 471t Torsades de pointes, 51, 51f Toxic epidermal necrolysis (TEN), 103–106 clinical presentation, 104 definition, 103–104 emergency actions, 103 epidemiology, 104 examination, 104–105 key points, 103 laboratory findings, 105 treatment and outcome, 105–106 Toxic metabolic headaches, 434 Toxic shock syndrome (TSS), 545–549 clinical presentation and examination, 547 definition, 546 diagnosis, 547–549 emergency actions, 545 epidemiology, 546 erythema multiforme v., 98 examination, 549 key points, 545 laboratory findings, 549 pathology, 546–547 treatment, 549 Toxicity, drug. See also Toxicology emergencies cardiopulmonary arrest from, 664 heart transplant complications from, 95 toxic epidermal necrolysis from, 103–106 Toxicodendron dermatitis, 106–108 clinical presentation, 107–108 definition, 106 demographics and epidemiology, 107 key points, 106 nomenclature and plant identification, 107 pathophysiology, 107 treatment, 108–109 water irrigation for, 108–109 Toxicology emergencies, 923–930. See also Toxicity, drug acetaminophen, 931–936, 934f amphetamines, 936–938 anticholinergics, 938–943 antidotes, 929–930 arsenic, 943–947 barbiturates, 948–951
Index Toxicology emergencies, (Continued) beta-blockers, 952–955 calcium channel blockers for, 956–959 carbon monoxide, 959–962 caustic ingestion, 962–965 clonidine overdose, 965–968 cocaine toxicity, 969–973 cyanide poisoning, 974–980 cyclic antidepressant toxicity, 980–984, 982f decontamination, 928 definition, 923 digitalis glycoside, 984–988 disposition, 930 electrocardiogram, 927 enhanced elimination techniques, 930 epidemiology, 923 ethanol intoxication, 989–994 ethylene glycol, 994–998 examination, 926–927 hallucinogens, 999–1003 history-taking of event, 926 hydrocarbon poisoning, 1003–1007 iron toxicity, 1007–1010 isopropanol toxicity, 1010–1013 laboratory findings, 927–928 lead poisoning, 1014–1016 lithium poisoning, 1017–1019 mercury, 1024–1026 methanol poisoning, 1020–1023 opioid intoxication, 1027–1030 organophosphorus and carbamate insecticides poisoning, 1130–1132 phenytoin, 1034–1037 “safety net” and initial evaluation, 925 salicylates, 1038–1043 supportive care, 928–929 drug-associated agitation medications, 929 IV fluids, 929 lidocaine, 929 sedatives, 929 seizure medications, 929 serum calcium, 929 theophylline, 1044–1049 toxicokinetics and pharmacokinetics, 923–924 first-order (renal elimination), 924 Michaelis-Menton elimination, 924 questions to ask, 924 zero-order (enzyme kinetics), 924 treatment approach, 924–925
1233
Toxicology screening, neonatal emergencies requiring, 668–669 Toxoplasma, heart transplant infection, 95 TPA. See Tissue plasminogen activator Transdermal therapeutic system (TTS), 965–966 Transesophageal echocardiography (TEE), thoracic aortic dissection diagnosis, 25 Transient ischemic attacks (TIAs), 469 Transplantation emergencies, 1147–1167. See also Organ rejection cardiac and pulmonary, 93–96, 1150, 1151, 1154 clinical presentation heart failure, 1149–1150 infection, 1150 organ rejection, 1150 pulmonary failure, 1150 definition, 1148 diagnosis, 1152–1153 emergency actions, 1147–1148 epidemiology, 1149 examination heart failure, 1150 infection, 1151 organ rejection, 1151 pulmonary failure, 1151 laboratory findings, 1151–1152 radiographs, 1153 treatment, 1153–1154 infection, 1154–1155 organ rejection, 1154 liver transplantation, 1156–1162, 1158t, 1160t, 1161t renal, 1122–1123, 1158t, 1160t, 1161t, 1163–1167 Trauma. See also Injury; Wound management abdominal, 1057–1062 anatomy, 1058 clinical presentation and examination, 1059 CT scan with contrast, 1060 definition, 1058 diagnosis, 1059–1060 diagnostic peritoneal lavage, 1060–1061 emergency actions, 1057 FAST examination, 1060 key points, 1057 treatment, 1061–1062 gastric tube placement, 1062
1234 INDEX Trauma, (Continued) barotrauma, 206–207 brain, 915b, 1055, 1067–1072 genitourinary tract, 1063–1066 geriatric emergency, 389 head, 915b, 1055, 1067–1072 headaches from, 434 multiple injury, 1050–1056, 1054t, 1055t hip, 625–630 life-threatening injuries airway obstruction, 1097 cardiac tamponade, 1099–1100 FAST examination, 1100 flail chest and pulmonary contusion, 1098–1099 massive hemothorax, 1099 open pneumothorax, 1097 tension pneumothorax, 1097–1098 maxillofacial and dental emergencies, 179–182 multiple injury blood transfusion for, 1055, 1055t bone fracture from, 1056 clinical presentation, 1053 diagnosis, 1056 epidemiology, 1050–1051 examination, 1053–1056 Glasgow Coma Scale, 1054, 1054t head or spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 CT scans, 1052, 1055 FAST, 1052 neurologist consultation, 1055 ophthalmologic, 167–168 pediatric, 629, 1073–1080, 1074t, 1079t, 1080t abdomen evaluation, 1078 adult v. child spinal cord, 1077 airway management for, 1073–1075, 1074t blood pressure, 1074t cardiovascular management, 1075 chest evaluation, 1078 endotracheal tube size v. age, 1074t evaluation and stabilization, 1078–1079, 1079t fluid resuscitation, 1074t induction and intubation, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t
Trauma, (Continued) neurological evaluation, 1075–1077, 1076–1077, 1076t CT scan, 1077 Glasgow Coma Scale (modified), 1076t renal perfusion assessment, 1075 seizures and status epilepticus, posttrauma, 786–787 vital signs, 1079t pelvic, 1081–1089 anatomy, 1081–1082 associated injuries, 1083 emergency actions, 1081 examination, 1087 key points, 1081 laboratory studies, 1088 mechanisms of injury, 1082–1083 treatment, 1088–1189 type I fractures, 1083–1085 type II fractures, 1085 type III fractures, 1085–1086 type IV fractures, 1086 potentially life-threatening injuries aortic disruption and penetrating injury, 1102–1103 blunt cardiac injury, 1103 diaphragmatic injury, 1103–1104 esophageal, 1104 hemothorax, 1102 simple pneumothorax, 1101–1102 tracheobronchial injury, 1102 pregnant patient with, 1105–1111 pulmonary embolism risk factor from, 899 spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 thoracic, 1095–1104 clinical presentation and examination, 1096–1097 definition, 1096 emergency actions, 1096 emergency department resuscitation thoracotomy, 1101 key points, 1095 life-threatening injuries, 1100 Traumatic aortic injury (TAI), 1102–1103 Tremors, respiratory acidosis causing, 320 Trendelenburg's position, hernia treatment requiring, 17 Trichomonas vaginalis, treatment, 553–554, 553t
Index Trigeminal nerve examination, 459–460, 459f Trimethoprim-sulfamethoxazole (TMP/ SMX), 271t urinary tract infection treatment, 1145t, 1146 Trochlear nerve examination, 457–458, 458f TSS. See Toxic shock syndrome TTS. See Transdermal therapeutic system Tubular necrosis, 1114 intrarenal acute renal failure presenting as, 1114 Tumor. See also Malignancy; Oncologic and hematologic emergencies acoustic neuroma, 426–427, 426t parotid, Bell's palsy v., 426–427, 426t Tzanck smear and culture, genital herpes diagnosis, 515 Ulcer colitis v diverticulitis, 126 gastric or duodenal, 511 Ulnar tunnel syndrome, 615. See also Forearm and wrist injuries Ultrasonography abdominal aortic aneurysm requiring, 4 abdominal pain, 512 abruptio placentae, 499 abscesses of breast requiring, 503 appendicitis, 7–8 cholelithiasis and cholecystitis, 13 Doppler epididymitis differential diagnosis, 1126 testicular torsion, 1140 focused abdominal sonography for trauma, 1052, 1060, 1100 hernia diagnosis, 17 hyperemesis gravidarum, 517 mastitis, 503 miscarriage (abortion), 527 pelvic pain, 512 pulmonary embolism, 905t Ultraviolet keratitis, as altitude-related emergency, 190–191 Ultraviolet keratitis, ophthalmologic emergency, 167 Umbilical hernias, 15 Unconjugated hyperbilirubinemia, 136 Upper respiratory pediatric emergencies, 678–692 bronchiolitis, 687–692 clinical presentation, 689
1235
Upper respiratory pediatric emergencies, (Continued) definition, 688 diagnosis, 690 emergency actions, 688 epidemiology, 688–689 examination, 689 laboratory findings, 690 radiographs, 690 treatment, 690–692 clinical presentation, 680–681 definitions, 678–679 diagnosis, 683–684 emergency actions, 678 epidemiology, 679–680 examination, 681–682 key points, 678 laboratory findings, 682–683 radiographs, 684–685 treatment, 685–687 Uremia, metabolic acidosis with, 1021 Ureter injuries, 1064 Urethra dilation of, prosthetic heart valve requiring, 92 injuries to, 1065 Urinalysis hip trauma requiring, 630 hymenoptera sting requiring, 232 lightning injuries requiring, 236 neonatal emergencies, 668–669 ovarian torsion, 534 toxicology emergencies, 927–928 Urinary tract infection (UTI), 1142–1146, 1145t. See also Urology emergencies clinical presentation and examination, 1143–1144 definition, 1142 diagnosis, 1144 epidemiology, 1143 geriatric emergency, 388–389 key points, 1142 laboratory findings, 1144 pediatric, 753–757, 757t clinical presentation, 754–755 definition, 753 diagnosis, 755 emergency actions, 753 epidemiology, 754 examination, 755 key points, 753 laboratory findings, 756 pathology, 754
1236 INDEX Urinary tract infection (UTI), (Continued) treatment, 756, 757t antibiotics, 757t radiographs, 1145 treatment, 1145–1146, 1145t oral medications, 1145t Urine culture pediatric urinary tract infection diagnostic, 755 shock diagnostic, 919 Urology emergencies. See also Urinary tract infection adults, urinary tract infections, 1142–1146, 1145t epididymitis, 1124–1126 penis disorders, 1127–1130 prostatitis, 1131–1134 renal failure, 1113–1117 testicular torsion, 1139–1141 Urticaria, 109–113 clinical presentation, 111 definition, 110 emergency actions, 109 epidemiology, 110 etiology, 110 examination, 111 hymenoptera sting causing, 232 key points, 109 laboratory findings, 111 pathophysiology, 110–111 treatment, 111–113 Uterine perforation/leiomyoma, 510 UTI. See Urinary tract infection Vaginitis, pelvic and abdominal pain from, 510 Vagus nerve examination, 461 Valproate, pediatric seizures and status epilepticus, 786 Valproic acid, seizures and status epilepticus, 471t Valsalva maneuver, hernia diagnosis, 17 Vancomycin AICD infection requiring, 42–43 endocarditis from prosthetic valve infection, 91–92 vasogenic shock requiring, 921 Varicella-zoster virus, 276, 280, 282–283 immune globulin, 96 treatment for, 286 Vasoconstriction, epinephrine for, 28 Vecuronium, airway management pretreatment and treatment, 915b, 916
Venous blood gas analysis, hyperglycemic hyperosmolar nonketotic coma, 392 Ventilation/perfusion (V/Q) scanning, pulmonary embolism, 902, 905t Ventricular fibrillation (VF), 50–51, 51f AICD causing, 40 Ventricular septal defect (VSD), 779–782, 782f Ventricular tachycardia (VT), 50, 50f AICD causing, 40, 43 Versed, airway management treatment, 916 Vertigo, 418–423. See also Ataxia, dizziness, vertigo alternobaric vertigo barotrauma, 207 Vestibulocochlear nerve examination, 461 VF. See Ventricular fibrillation Vibration sense, sensory function examination, 454–455 Vibrio cholerae diarrhea from, 744t, 745 infectious disease emergency, 267t Vinyl gloves, toxicodendron dermatitis treatment requiring, 108–109 Viral conjunctivitis, 164 Viral hepatitis, 135–143, 137f, 138f, 139f definition of, 136 Vital signs, pediatric trauma evaluation, 1079t Vitamin D deficiency (rickets), hypocalcemia, 371 Vocal cord dysfunction, asthma mimicked by, 857 Vomiting arsenic poisoning treatment, 946 hyperemesis gravidarum, 515–518 ovarian torsion causing, 534 theophylline overdose causing, 1048 VT. See Ventricular tachycardia Vt. See Tidal volume Vulvovaginitis, 550–554 clinical presentation and examination, 552 definition, 550–551 diagnosis and laboratory findings, 552–554 emergency actions, 550 epidemiology, 551 key points, 550 pathology, 551–552 treatment, 553–554, 553t Water -borne illnesses, 264–275, 266t–271t fluid and electrolyte emergencies, 351–393, 354t, 359t, 382t
Index Water (Continued) intake, 357–358 hypernatremia from reduced, 359t increased, 357 reduced, 357 irrigation with, toxicodendron dermatitis requiring, 108–109 marine fauna envenomations, 238–242 submersion incidents, 207, 242–248, 246t WBC count. See White blood cell count Wegener's granulomatosis, 889–890 Wells assessment model, pulmonary embolism risk, 899–900, 900t White blood cell (WBC) count appendicitis requiring, 7 as blood component, 559 Whitesides apparatus, acute compartment syndrome diagnosis, 599 Whole blood, as blood transfusion component, 560 Wicki (Geneva) assessment model, pulmonary embolism risk, 900–901, 900t Wolff-Parkinson-White syndrome, 56–57, 56f Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Wound management, 26–36, 29t, 31t, 32t, 33f, 34f, 36t. See also Injury anesthesia after examination, 28 antibiotic prophylaxis, 35 closure, 30–34, 31t, 32t, 33f, 34f disposition, 35–36, 36t dressings, 34–36
1237
Wound management, (Continued) epidemiology of traumatic wounds, 27 foot injuries, 607 key points, 26 medical history required for, 27–28 physical examination, 28 preparation, 29–30 radiographs, 36 stages of healing, 27 tetanus immunization, 35 Wrist and forearm injuries, 608–616 X-ray chest adrenal insufficiency requiring, 336 cardiac chest pain evaluation, 73 cardiac tamponade, 62 ethanol withdrawal requiring, 329 hypertensive emergencies, 78 isopropanol toxicity, 1012 respiratory acidosis requiring, 321 Reye's syndrome, 797 submersion incident requiring, 246 elbow injury diagnosis, 602 neonatal emergencies, 668–669 permanent pacemakers, 87 Yersinia, infectious disease emergency, 267t Zantac, urticaria treatment, 112 Zonegran, seizures and status epilepticus, 471t Zonisamide, seizures and status epilepticus, 471t Zyrtec, urticaria treatment requiring, 112
